Psychopathology and Psychotherapy
In introducing the scientific study of mind and behavior, we have focused primarily on adaptive behavior, and the normal mental processes that underlie it. There have been occasional references to cases of brain insult, injury, and disease, for the light they shed on normal mental life. Now we wish to examine mental illness in its own right:
- abnormal and maladaptive behavior;
- the disordered mental processes that underlie it;
- and interventions that treat and prevent mental illness.
The term psychopathology is, obviously, derived from two Greek roots:
- psycho, from the Greek psyche, soul, referring to the mind;
- pathology, from the Greek pathos, suffering, referring to disease or illness.
The term makes it clear that mental illness is analogous to physical illness. Just as physical illness involves abnormalities of bodily structure (anatomy) and function (physiology), so mental illness involves abnormalities of mental structure and function -- abnormalities of cognition, emotion, and motivation -- that result in abnormal, deviant behavior.
It has not proved easy to define psychopathology in the abstract.
By analogy with the concept of pathology in medicine, psychopathology may be defined as abnormalities in mental structures, processes, and states that give rise to abnormal, deviant behavior. But the concept of abnormality implies an opposite construct of normality, from which abnormality deviates. So what do we mean by normality?
Normal mental and behavioral
functioning is characterized by:
- Accurate and Efficient Cognition: Normal people generally see the world the way it is, remember things the way they happened, think clearly, and communicate comprehensibly. And beyond cognition, they tend to have feelings and desires that are appropriate to the situation.
- Self-Awareness: Normal people generally are aware of their thoughts, feelings, and desires, and of their behavior and its impact on other people.
- Self-Control Normal people generally are able to control their impulses and emotions, and to delay gratification.
- Self-Esteem: Normal people generally think reasonably well of themselves.
- Social Relations Based on Affection: Normal people generally treat others with respect, and not like objects.
- Productivity and Creativity: Normal people are generally productive at work, at play, and in their family lives; and although most of us can't become great artists, we are nevertheless able to create things on our own.
(Note: I am pretty certain that I derived this list of features of normality from an early edition of a textbook in abnormal psychology written either by Richard Bootzin, or one by Gerald Davison and John Neale, but I can no longer identify the source precisely.)
But having defined a sort of prototype for "normality", what do we mean by deviance?
Deviations from normality can be
defined in various ways:
- Deviance from Statistical Norms: By statistical
convention, a score is "abnormal" if it lies more than 2
standard deviations above or below the population mean.
- This frequency criterion is certainly
objective, but it has some problems attached to it --
not the least of which is the problem of estimating
population means for all the various mental
characteristics on which people might deviate.
- There is also the problem of what to do about positive deviations. An IQ less than 70 is more than 2 standard deviations away from the mean IQ of 100, and (if other factors are also present) can lead an individual to be classified as intellectually disabled (what used to be known as "mental retardation"). But an IQ of more than 130 is also more than 2 standard deviations away from the mean, and can lead an individual to be classified as a "genius". But while intellectual disability is a form of mental illness, we usually don't think of genius that way. A further problem is that even negative deviations are not necessarily signs of mental abnormality. For example, a person who is more than 2 standard deviations below the mean on Extraversion might be merely shy.
- Deviance from Social Norms: Every group, organization, and society imposes certain expectations and demands on its members, and some people simply don't do what they are supposed to do. Given that human experience, thought, and action takes place in an expressly social context, this compliance criterion may well be useful for evaluating which deviations we should pay attention to, but it also has its problems.
- Norms vary across societies. In the former Soviet Union, political dissidents could be classified as mentally ill, and confined to mental hospitals, simply for disagreeing with their government.
- Norms also vary across epochs within societies. When I began my graduate studies, in 1970, homosexuality listed in the official Diagnostic and Statistical Manual of Mental Disorders. Then, about 1973, the American Psychiatric Association took a vote and decided that it wouldn't call homosexuality a mental illness any longer.
- One may agree with the vote (as I do), but the essentially political process by which the status of homosexuality was changed should give us pause. If we are looking for an objective standard by which to evaluate deviance, we want one that is constant across groups. The length of a foot or a yard doesn't vary from Denmark to Ghana -- why should the criteria for mental disorders be any different?
- Personal Distress: mental illness is usually manifested in symptoms that create problems for the patient, and cause considerable concern. This subjective criterion may be important in leading the patient to seek the help of a professional, but it too has a couple of problems.
- People's self-perceptions are not always accurate.
Some people believe they are ill when they are not; but
more important in the present context, some mentally ill
people do not believe that they are mentally ill, and
resist diagnosis and treatment. This is a particular
problem in schizophrenia and the personality disorders.
- Even when people's self-perceptions are accurate, we would not want to substitute self-diagnosis for an objective assessment by a trained professional. We don't let patients self-diagnose cancer and heart disease -- why should we allow them to self-diagnose depression and anxiety disorder?
- Maladaptiveness: Mental illness often leads
people to engage in behaviors that are harmful to
themselves and others. For example, people with depression
may be at elevated risk for suicide. People with
antisocial personality disorder, by definition, engage in
antisocial behaviors. Normal mental function is by
definition adaptive, because the purpose of the mind is to
aid the organism's adaptation to its environment, so a harmfulness
criterion is helpful in diagnosing mental illness. On the
- Not all maladaptive behavior is a sign of mental illness. Criminal behavior is maladaptive, harmful to the people against whom the crime is perpetrated, and harmful to the criminal when he or she is caught and punished. But we do not label all criminal behavior as the product of mental illness. In fact, the insanity defense is attempted in only a very small minority of criminal cases, and it is successful in only a very small minority of these.
The Insanity Defense
In 1981, John Hinckley attempted to assassinate
President Ronald Reagan: one of his gunshots
actually hit Reagan, and others seriously injured
James Brady, Reagan's press secretary, a Secret
Service agent, and a District of Columbia
policeman. Hinckley's motive was a desire to
impress Jodie Foster, an actress, with whom he was
infatuated. At his trial, in 1982, a jury
found him not guilty by reason of insanity.
More than 30 years later, he remains confined to St.
Elizabeth's Hospital, a federal facility in
Up until the late 18th century, the mentally ill
were treated little differently than
criminals. It wasn't until after the French
Revolution that Jean-Etienne Dominique Esquirol
formally distinguished between insanity, mental
deficiency, and criminality, and his protege
Phillippe Pinel "freed the insane from their
chains". As medicine developed further,
however, psychiatrists began to understand that, in
certain instances, criminal behavior could be a
product of insanity. If that were the case,
then the "criminal" could not be held morally and
legally responsible for his or her criminal acts.
At lest since the 17th century, English common law
has required that a criminal act (actus rea,
or "guilty act") be accompanied by criminal intent (mens
rea, or "guilty mind". There is no
criminal liability for injuries committed
involuntarily (e.g., because of a reflex, or while
The formal insanity defense has its beginnings in
1843, when Daniel McNaughton tried to kill Robert
Peel, the British prime minister (he shot and killed
his secretary instead). At his trial,
McNaughten testified that he believed that the
British government was plotting against him, and he
was acquitted of murder. The McNaughton
Rule requires that a criminal defendant (1)
not know what he was doing at the time or (2) not
know that his actions were wrong (because of his
delusional belief, McNaughton thought he was
In the United States, the next advance in the
insanity defense was The Durham Rule or
"product test" adopted in 1954, which states that
"... an accused is not criminally responsible if his
unlawful act was the product of mental disease or
defect". This "product test" was overturned in
1972, largely because its ambiguous reference to
"mental disease or defect" places undue emphasis on
subjective judgments by psychiatrists, and can
easily lead to a "battle of the experts".
Many states now adopt a version of guidelines set
out by the American Law Institute in 1962, which
allows the insanity defense if, by virtue of mental
illness, the defendant (1) lacks the ability to
understand the meaning of their act or (2) cannot
control their impulses. This is sometimes
known as the "irresistible impulse test".
Other states allow for a compromise verdict of
"guilty but mentally ill", resulting in commitment
to a mental institution for treatment, rather than
incarceration in a prison for punishment.
In whatever form, the insanity defense requires
both that the defendant meet the criteria for some
psychiatric diagnosis and that his
ostensibly criminal act be attributed to his mental
Hinckley clearly met this criterion, but the
insanity defense is rarely successful. It has
been estimated that it is invoked in only about 1%
of criminal trials, and it succeeds in fewer than
25% of those cases. And while commitment to a
mental hospital is arguably better than
incarceration in a prison, there is a definite
downside. Prison terms lapse, and prisoners
can be released or paroled. But commitment to
a mental hospital can be forever -- until the
relevant medical authorities can persuade a judge
that their patient's illness has been
Each of these definitions has certain assets and liabilities. Taken together, these two lists of definitions -- of normality and of deviance -- comprise a kind of "prototype" of the "typical" case of mental illness. Not every mentally ill person will lack all the criteria of normality, or display all the criteria of deviance. But most mentally ill people will display some or most of them, so that the mentally ill are related to each other by a principle of family resemblance.
Syndromes of Mental Illness
In actual practice, mental illnesses are not identified by abstract conceptual definitions of mental abnormality and deviance, but rather in terms of various syndromes characterized by particular signs and symptoms.
The Diagnostic Nosology
identify nine (9) major categories of mental illness.
Warning: these groupings differ somewhat from such "official"
classifications as the Diagnostic and Statistical Manual
of the American Psychiatric Association, but the overlaps are
1. Organic Brain Syndromes,in which there are gross impairments in mental function resulting from known insult, injury, or disease in the central nervous system.
- Alzheimer's disease is a clear example: here the patient suffers memory loss and other aspects of dementia resulting from plaques and tangles in cortical tissue.
- Other examples are the amnesic syndrome (such as
Patient H.M.) associated with damage to the hippocampus
and related areas,
- and the various forms of aphasia associated with damage to Broca's and Wernicke's areas.
Disorders,in which there is an abnormal pace of
development in one or more mental functions since birth.
- The classic example is intellectual disability, in which the individual shows subnormal levels of mental function (as indexed by an IQ less than 70), in degrees ranging from mild to profound, accompanied by an inability to meet the demands of his or her environment.
- Henry H. Goddard, an early authority on intelligence, classified what was then known as "mental retardation" into three subcategories -- moron, idiot, and imbecile -- based strictly on IQ test scores.
- More recent practice has abandoned these offensive terms, but more importantly assess intellectual disability not just in terms of test scores, but also in terms of the individual's ability to cope with environmental demands. If people with low IQs can get along effectively in their environment, there is no reason to classify them as intellectually disabled.
- DSM-5 assesses the severity of intellectual disability from mild t profound, taking account of the individual's ability to adapt in the social and practical as well as the purely intellectual domains.
- Similarly, the American Association for Intellectual
and Developmental Disabilities (formerly the American
Association for Mental Retardation) takes account of
how much environmental support the individual needs,
from intermittent to pervasive.
- Another example is autism, a disorder characterized by a severe inability to relate to, and communicate with, other people. Autism is now often referred to as autism spectrum disorder, an umbrella term that covers conditions like Asperger's syndrome as well.
- Traditionally, classical autism was characterized by three criteria: impairment in social interaction; impairment in social communication (language); and restricted, repetitive and stereotyped patterns of behavior, interests, and activities. Asperger's syndrome was used for patients who displayed impairments in social interaction but not impairments in language. The 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) collapses social interaction and social communication into a single criterion, and has been very controversial.
- Attention deficit hyperactivity disorder (ADHD), a relatively new syndrome, is typically diagnosed in children. Originally, it was thought that children would "outgrow" ADHD with time, but in fact many children with ADHD grow up to be adults with ADHD, and the syndrome is now diagnosed and treated in adults as well.
- Originally, the syndrome was called "hyperactivity" or "hyperkinetic disorder".
- The syndrome entered the diagnostic nomenclature as Minimal Brain Dysfunction (MBD) in DSM-II (1968) -- "minimal" because there was no physical evidence of any brain damage.
- Following an argument by Virginia Douglas (1972), a Canadian psychologist, that the basic problem in "hyperkinesis" was insufficient attention, the syndrome was renamed at Attention Deficit Disorder (ADD) in DSM-III (1980)
- In DSM-IIIR (1987), the diagnosis was expanded to Attention deficit Hyperactivity Disorder (ADHD).
Intellectual Disability and the Death Penalty
In 2002, in the case of Daryl R. Atkins (Atkins
v. Virginia), a convicted murderer with an IQ of 59,
the United States Supreme Court prohibited the execution of
intellectually disabled prisoners. However, the Court did
not provide guidelines for determining who is intellectually
disabled. Instead, the Court left it up to individual
states to determine the standards by which intellectual
disability is diagnosed -- provided that they are "informed
by the medical community's diagnostic framework" (Hall v.
Florida, 2014). Accordingly, some two years
later, Atkins still faced the death penalty ("New Challenge
for Courts: How to Define Retardation" by Adam Liptak,New
York Times, 03/14/04).
One problem is the way intellectual disability
is defined in the psychiatric nosology: subnormal IQ plus
a demonstrated inability to meet environmental demands. The
reasonable approach would be to adopt the standards set by
the DSM or the similar standards promoted by the
AAIDD. But even so, low test scores can be faked, and
judgments of adaptiveness are inherently subjective. These
problems are confounded by the theory, promoted by some
prosecutors and other proponents of the death penalty, that
certain murders (such as the one Atkins was convicted of
committing) require highly sophisticated planning, and
therefore are beyond the capacity of the intellectually
disabled. Even "low IQ" is problematic: an IQ below 70
is two standard deviations below the mean, but all such
measurements are somewhat unreliable. Should someone
with an IQ of 71 be put to death just because he or she
A 2004 ruling by the Texas Court of Criminal
Appeals (ex parte Brisno) essentially adopted
Virginia's reasoning, effectively ruling intellectual
disability out in cases where a crime entailed "forethought,
planning, and complex execution of purpose". The ruling
poses an interesting "Catch-22": a defendant's crime can be
used to impeach the claim that he or she is intellectually
disabled! As it happens, the standards in Texas,
whose public officials have an inordinate fondness for the
death penalty, are not only outmoded, they include various
stereotypes about the intellectually disabled, which have no
scientific basis. In fact, Judge Cochran, writing for
the Texas CCA, referred to Lennie Small, the "retarded"
character in John Steinbeck's novel, Of Mice and Men
(1937) -- she actually talked of "the Lennie standard"
("Supreme Court to Consider Legal Standard Drawn from 'Of
Mice and Men'" by Adam Liptak, New York Times,
08/22/2016). The effect of these standards, if that is
what they are, is to severely limit those who would qualify
as intellectually disabled.
Moore v Texas, a case brought before the Supreme Court in 2016, challenges the Texas standards in a case of a man convicted in 1980 of murder in the course of a robbery. Moore's death sentence was overturned by a lower court, which used modern medical standards to determine that he was intellectually disabled, and thus could not be executed. The Texas CCA reversed that decision, expressly criticizing the lower court judge for applying contemporary scientific standards, instead of the ones set out in earlier decisions by the CCA. These standards, in the CCA's view, more closely reflect the beliefs about intellectual disability held by ordinary Texans -- scientific evidence and medical standards be damned. In 2017, the Court overturned the Texas decision by 5-3, ruling that the Texas court relied too heavily on IQ scores -- not to mention outmoded stereotypes about the intellectually disabled. The Court advanced a new three-point standard for identifying the intellectually disabled:
- "Subaverage intellectual functioning", meaning IQ scores lower than "approximately 70".
- Lack of fundamental social and practical skills.
- Presence of both of these conditions before the age of
Three justices dissented, on the grounds that Moore's two
"reliable" IQ scores were both over 70 -- high enough to
permit his execution.
in which there are gross impairments in reality testing.
Psychoses are often labeled as "functional", meaning that they
have no organic cause. However, these disorders are almost
certainly "organic" in nature, and as their underlying brain
pathology becomes known they may well be shifted to the
category of organic brain syndromes.
- Schizophrenia, characterized by disordered language and thought processes.
- Very early medical texts, going back to the Egyptian Book
of Hearts and the Chinese Yellow emperor's
Classic of Internal Medicine describe illnesses
resembling modern-day schizophrenia.
- In 1809, Phillippe Pinel described a "premature dementia" in young patient
- In 1896, Emile Kraepelin renamed the disorder dementia
praecox, or "early dementia", distinguishing the
disorder from the "senile dementia" associated with
- The term schizophrenia was introduced by Eugen Bleuler (1911), who distinguished among five subtypes:
- Hebephrenic (childlike)
- Catatonic (immobile)
- Paranoid (delusional)
- Chronic Undifferentiated
- Schneider (1959) characterized schizophrenia in terms of a set of "first-rank" symptoms:
- Auditory hallucinations, particularly voices speaking to the patient (arguing or giving instructions.) or about the patient (commenting on the patient's actions).
- Schneider considered other hallucinations to be "second-rank" symptoms.
- Experience of one's mind or body being controlled.
- Thought disorder:
- That one's thoughts are being heard aloud.
- Thought withdrawal/
- Thought insertion.
- Thought broadcasting.
- Delusional perceptions, in which an actual stimulus event (not a hallucination) is given a bizarre interpretation.
- A variety of affective disorders, primarily
affecting emotional functioning (as their name implies),
- major depressive disorder (also known as unipolar
- bipolar disorder (also known as manic-depressive
- and pure mania.
4. Neuroses, a set of
syndromes that share primary symptoms of anxiety in common.
These are also "functional" in nature, but in contrast to the
psychoses there is less question of organic involvement;
rather, they are commonly attributed to the patient's
experiential history of social learning.
- A variety of phobic disorders, entailing
excessive, unwarranted, and irrational fears of specific
objects or situations, such as snakes and spiders,
heights, open spaces, or public places.
- In contrast, anxiety disorder is characterized by
a free-floating state of apprehension and worry,
unattached to any object.
- Sudden, unexpected waves of anxiety are characteristic
of panic disorder.
- For an excellent personal account of anxiety disorder,
see My Age of Anxiety: Fera, Hope, Dread, and the
Search for Peace of Mind by Scott Stossel.
- Obsessive-compulsive disorder (OCD) is
characterized by recurring, unwanted ruminations about
certain events (past or future), often accompanied by
overt behaviors intended to reduce the impact of these
events, or the likelihood that they will occur.
- As its name implies, post-traumatic stress disorder occurs in some individuals who have been exposed to high levels of stress, such as soldiers on a battlefield, victims of sexual assault and other violent crimes, and victims of natural disasters such as earthquakes and hurricanes (for a review, see Rosen & Lilienfeld, 2008).
- The syndrome was first recognized in World War I: the term "shell shock" first appeared in the Lancet, a British medical journal, in 1915. As its name implies, it was originally attributed to a kind of concussion, caused by artillery shells exploding near the soldier, and the resulting "commotion" in the brain. Affected soldiers received a war ribbon and a disability pension. However, cases began to be diagnosed in soldiers who had been nowhere near exploding ordnance, leading psychiatrists to shift their thinking. Now, "shell shock" was called "war neurosis", and viewed as reflecting a "nervous breakdown" or neurasthenia -- emotional shock, if you will, rather than concussion or "commotional" shock. Instead of recovering from their putative brain injuries in hospitals, they were now sent to convalesce in mental hospitals. (See "the Shock of War" by Caroline Alexander, Smithsonian, September 2010).
- War neurosis was diagnosed in World War II, as well, where it was the subject of an important documentary film, Let There Be Light, directed by by John Huston -- a film that the War Department censored, worried that the public would balk at learning about the psychological damage wreaked by warfare.
- And, in retrospect, war neurosis occurred before
World War I, as well.
- In the Civil War, is was known as "irritable
heart", or Da Costa's Syndrome" (see "PTSD: The
Civil War's Hidden Legacy" by Tony Horwitz, Smithsonian
- War neurosis, redefined as PTSD, surfaced with a vengeance during the Vietnam War (it was originally called "post-Vietnam syndrome"), and again in the post-9/11 wars in Afghanistan and Iraq (as well as en epidemic of concussive head injuries caused by improvised explosive devices, or IEDs).
- At roughly the same time, mental health professions began to appreciate the effects of trauma off the battlefield, especially in victims of sexual assault and of childhood sexual and physical abuse. PTSD formally entered the diagnostic nosology with the third edition of the Diagnostic and Statistical Manual for Mental Disorders (DSM-III), in 1980 (Scott, 1990).
- One positive result of the wars in Iraq and
Afghanistan is that soldiers suffering from PTSD can
now receive disability benefits -- even if they did
not directly experience the trauma in question.
Just being in the vicinity, apparently, was
traumatic enough. This policy change, however,
only served to increase the controversy over the
diagnosis. Contributing to the debate was the
proposal that veterans with PTSD receive a medal,
analogous to the Purple Heart, to recognize their war
injuries -- mental injuries, rather than physical
injuries, but injuries just the same.
- Usually we think of PTSD we think about victims of violent crime, or war, or natural disaster. And that's how psychiatrists usually think about it, too. The Diagnostic and Statistical Manual of Mental Disorders (DSM) defines stress as experiencing, or witnessing, "actual or threatened death or serious injury, or a threat to the physical integrity of self or others". But as we discussed earlier, "stress" is defined psychologically as any event which challenges the organism's current level of adaptation. Divorce, being laid off, or losing a close friend are examples. Exposure to unpredictable and uncontrollable aversive events is inherently stressful. Even positive events can be stressful, though they rarely play a role as instigators of PTSD.
- Documented exposure to trauma, as defined in DSM, is necessary for the diagnosis of PTSD. But it is not sufficient. Most people -- perhaps as many as 95% -- who are exposed to trauma do not develop PTSD (Bonanno, 2011). This is true even when the exposure is prolonged or severe.
- However, some clinicians diagnose PTSD even in the
absence of such documentation, in patients who "have the
symptoms" of PTSD. Sometimes, the clinician
assumes that the patient has "repressed" or
"dissociated" his memory for the traumatic event.
It's as if they figure, "They have the symptoms, so they
must have been traumatized". But this is backwards
reasoning -- technically, the error of asserting the
consequent discussed in the lectures on Thought
and Language. In fact, patients can show
some of the symptoms of PTSD even in the absence of
exposure to trauma: for example, hyperarousal is
symptomatic of anxiety disorder, and poor sleep is
symptomatic of depression. Just because someone is
anxious and/or depressed doesn't mean that they've been
traumatized. They might be anxious or depressed for some
other reason. This error in reasoning was, in my view,
largely responsible for the "epidemic" of claims of
childhood sexual abuse that arose in the 1980s.
5. Psychosomatic Disorders (also known as psychophysiological disorders) involve actual damage to some organ enervated by the autonomic nervous system, usually associated with psychological stress.
- So-called psychosomatic ulcers are the classic example: here, peptic ulcers of the stomach (gastric ulcer) or small intestine (duodenal ulcer) occur in the context of high levels of psychological stress.
- "Type A" behavior -- very high levels of stress, usually self-imposed through a regime of high activity levels, aggressiveness, and competitiveness -- has been associated with increased risk of coronary heart disease.
- Other instances of anatomical damage or physiological malfunction may also be stress-related, as when stress leads to a breakout of acne or a temporary disruption of the menstrual cycle. Of course, both acne and dysmenorrhea can have purely physical causes, but sometimes they do occur under conditions of stress (like prom night).
Disorders are characterized by physical complaints that
have no organic basis. In this respect they are similar to the
dissociative disorders, except that the symptoms mimic
conditions arising outside the nervous system.
- In hypochondriasis, the patient is excessively concerned with the risk or threat of disease.
- Somatization disorder (also sometimes known as Briquet's syndrome or just plain "hysteria", involves multiple, constantly changing physical complaints.
- Somatoform pain disorder is characterized by constant, frequent complaints of pain in various body parts, in the absence of any evidence of a physical condition that could cause this pain.
- Body dysmorphic disorder is characterized by an excessive concern that particular features of the body, such as one's nose or ears, are "not right". Individuals with body dysmorphic disorder are commonly found in the waiting rooms of plastic surgeons, many of whom are only to happy to have them as returning customers. Somehow, though, the problem never seems to get fixed.
- A controversial case is irritable bowel syndrome, in which the patient experiences abdominal pain, cramping, bloating, diarrhea, and constipation. Aside from these symptoms, physical examination doesn't typically reveal inflammation or other damage to the colon or other parts of the gastrointestinal system -- leading some authorities to suggest that it is a form of somatization disorder. On the other hand, it could be a physical illness, perhaps stress-induced, whose underlying pathology is still unknown. Or, it could be a straightforward physical illness, whose etiology has nothing to do with stress.
- Something similar could be said about chronic fatigue syndrome (CFS), where the patient suffers from profound exhaustion, disordered sleep, and pain in the muscles and joints -- sometimes so severe that the patient cannot get out of bed, or engage in his or her normal physical activities. Again, the frequent absence of physical findings has led some authorities to suggest that CFS is a somatoform disorder -- "all in the patient's head", or perhaps depression masquerading as a physical illness. But, as with IBD, this assertion is highly controversial, and there are reputable medical researchers who suspect that CFS stems from an underlying, if still unknown, viral infection, or perhaps a form of autoimmune disease.
7. Dissociative Disorders,
including conversion disorders, in which there is a
disruption of conscious awareness and control.
- In the dissociative disorders, such as
- dissociative amnesia (also known as functional or psychogenic amnesia),
- dissociative fugue (also known as psychogenic fugue), and
- dissociative identity disorder (also known as multiple personality disorder), the dissociation affects conscious awareness of identity and autobiographical (episodic) memory.
- In the conversion disorders, traditionally
collected under the rubric of hysteria, the
dissociation affects sensory-perceptual awareness
- as in psychogenic or functional blindness,
- deafness, or
- and/or the voluntary control of action (as in psychogenic or functional paralysis).
The dissociative and conversion disorders sometimes mimic the effects of damage to the peripheral or central nervous systems, but in these syndromes there is no evidence of brain insult, injury, or disease.
Disorders (e.g., borderline personality, antisocial
personality or psychopathy) are deeply engrained --
longstanding, inflexible, and pervasive -- patterns of
maladaptive behavior which typically develop in adolescence.
In contrast to the psychoses and neuroses, whose symptoms are
"ego-dystonic" (experienced as alien and unwanted), the
symptoms of personality disorders are "ego-syntonic" --
experienced as a part of their normal personality.
- In antisocial personality disorder (also known as psychopathic personality disorder,psychopathy, or sociopathy, the person engages in a pattern of incorrigible antisocial behavior.
- In borderline personality disorder the person experiences a blurring of the boundaries between self and other, difficulty managing affect, etc.
The classical term for antisocial personality
disorder is psychopathy, first described by Philippe
Pinel, the French physician who famously freed the insane
from their chains, in 180, as mania without delirium,
because the patient did not display delusions or other
typical signs of psychosis. Later, Benjamin Rush, an
American physician who pioneered in the medical treatment of
the mentally ill, characterized the same syndrome as moral
derangement because violent and other antisocial
behavior featured so prominently in the cases he observed.
This term was replaced by moral insanity, and then
The classical clinical description of "primary
psychopathy" was provided by Hervey Cleckley's book The
Mask of Sanity (1941):
- emotionally shallow
- lacking empathy
- lacking insight.
(Cleckley was also co-author, with Corbett Thigpen, of The Three Faces of Eve, a classic case study of multiple personality disorder that was made into an Oscar-winning film starring Joanne Woodward.)
There are also "secondary" or "neurotic" psychopaths, whose antisocial behavior occurs in the context of conflict and anxiety. One classic case of neurotic psychopathy is Robert Lindner's Rebel Without a Cause: Hypnoanalysis of a Criminal Psychopath, which -- I swear this is true -- was made into the famous movie starring James Dean, Natalie Wood, and Sal Mineo.
Cleckley's characterization of psychopathy is summarized by John Seabrook in "Suffering Souls: The Search for the Roots of Psychopathy" (New Yorker, 11/10/2008, p. 67):
"Beauty and ugliness, except in a very superficial sense, goodness, evil, love, horror, and humor have no actual meaning, no power to move him," Cleckley wrote.... The psychopath talks "entertainingly,"... and is "brilliant and charming," but nonetheless "carries disaster lightly in each hand." Cleckley emphasized his subjects' deceptive, predatory nature, writing that the psychopath is capable of "concealing behind a perfect mimicry of normal emotion, fine intelligence, and social responsibility a grossly disabled and irresponsible personality." This mimicry allows psychopaths to function, and even thrive, in normal society.
In the 1930s, the alternative label psychopath
was coined by G.E. Partridge, and psychopathy entered the
first edition of the DSM as sociopathic
personality. In the 2nd edition of DSM, the
syndrome was renamed antisocial personality disorder.
- Actually, psychopathy is quite not the same thing as
antisocial personality disorder. Only a minority of
individuals with the diagnosis of antisocial personality
disorder are psychopaths, as defined by Cleckley and Hare.
Psychopaths would seem to be excellent
candidates for the insanity defense -- after all, they
suffer from a particular mental disorder which, by its very
definition, disposes them to antisocial and criminal
behavior. Unfortunately, psychopathy is generally
excluded from the insanity defense from other
considerations. Not the least of which is that most
psychopaths, when asked will freely admit that their conduct
is immoral or illegal or unethical. So they do
appreciate the difference between right and wrong. And
in other respects, they can appear quite intelligent and
charming. They don't hallucinate, they're not
delusional. So, to all outward appearances, they would
seem both to understand the difference between right and
wrong and to be able to conform their conduct to societal
rules. But they don't and that makes them look like
they're criminals, not mentally ill. And they're
treated as such: it's been estimated that as many as 1/4-1/3
of prisoners in American jails are psychopaths.
Disorders consist of specific maladaptive behaviors that
occur in the absence of signs of any associated mental
disorders (e.g., psychosis, neurosis, or personality
- Alcoholism and alcohol abuse is a widely recognized form.
- Drug addiction and other forms of substance abuse are also classified under this label.
- Addictions to sex, gambling, and other activities are also recognized as behavioral disorders. Whether these are "real" addictions, like the physical addiction caused by some drugs, is a matter of some controversy.
addition to these forms of mental illness, there are more
mundane problems in living (a phrase coined by T.S.
Szasz, a famous critic of psychiatry, in his book The Myth
of Mental Illness). These include:
- marital stress
- sexual dysfunction
- adjustment problems
- stress reactions
- vocational quandaries.
These problems don't remotely resemble
mental illness, but they can be extremely distressing to the
people involved. Accordingly, they are often treated by mental
health professionals, including counseling psychologists as
well as clinical psychologists, psychiatrists, and clinical
and anxiety disorder, like cancer, heart disease, and measles,
are found everywhere -- though their incidence and precise
manifestation can vary from culture to culture. While
this mean seem puzzling at first, the existence of
culture-specific syndromes only underscores the point that the
individual's mind and behavior exist in and are shaped by
sociocultural context, which is why psychology is both a
biological and a social science.
In addition, there are
certain forms of mental illness that are encountered only in
particular cultures. For example:
- Latah, observed in Southeast Asia and Malaysia, is characterized by sudden, extreme startle reactions, loss of behavioral control, and profanity.
- Ataque de nervios, observed in Latin America, is characterized by shouting, tremors, cursing, feelings of loss of control, and extremely high levels of fear, and can be accompanied by interpersonal violence or suicidal behavior.
- In koro, observed in Southeast Asia and Africa, the person is obsessed by the idea that his genitalia are shrinking and disappearing.
- In amok, observe din Malaysia, men (mostly) withdraw and brood, followed by a bout of uncontrolled violence -- hence the English phrase, "running amok".
- In 2-D love, some Japanese men (again, mostly)
develop romantic infatuations with animated characters (anime).
These syndromes are rarely seen in
western developed countries -- except, perhaps, among recent
immigrants from these regions.
An interesting recent case is uppgivenhetsyndrom ("resignation syndrome"), which has been diagnosed among refugee children in Sweden who face deportation -- only in Sweden (at least so far), and only in refugee children (not adults). These children (and, for that matter, their parents) are under constant, prolonged stress -- first from the conflict that made them refugees in the first place, then from the difficult migration from their home country through Europe to Sweden, and then from the uncertainties of refugee life: How long will they be able to stay? How will they live while they are here? When will they be able to return home? What will things be like when they get there? In fact, some refugees are denied asylum, even in a country like Sweden, and it's in these children that uppgivenhetsyndrom is diagnosed. A typical patient appears to be unconscious, even comatose: “totally passive, immobile, lacks tonus, withdrawn, mute, unable to eat and drink, incontinent and not reacting to physical stimuli or pain.” However, they are not in a coma. Their reflexes are normal, as are cardiovascular signs such as pulse rate and blood pressure. In fact, they show no signs of neurological or any other physical illness. For this reason, even though these children are obviously under a great deal of stress, uppgivenhetsyndrom is not a stress-related psychophysiological disorder, precisely because there is no evidence of any organic damage -- as you would find in extreme cases of Selye's General Adaptation Syndrome (discussed in the lectures on "The Biological Bases of Mind and Behavior"). In our terms, uppgivenhetsyndrom appears to be a culture-specific form of somatization disorder. Cases started appearing in the early 2000s, and by 2005 more than 400 cases had been diagnosed. The children typically recover if their families are permitted to stay in Sweden, especially if they (and their families) also receive psychotherapy aimed at their underlying state of fear and hopelessness (Bodegard, Acta Paediatrica, 2005; see also "The Apathetic" by Rachel Aviv, New Yorker, 04/03/2017, which also discusses culture-specific syndromes in general).
Cultural differences can also work in reverse, preventing "universal" illnesses from being recognized. The Hmong people of Laos recognize a condition known as quag dab peg -- literally, “the spirit catches you and you fall down”; it is treated through religious rituals. In the West, this same condition is known as epilepsy, and is usually treated quite effectively with drugs. For an excellent treatment of this problem among Hmong refugees in the Unites States, see The Spirit Catches You and Then You Fall Down: A Hmong Child, Her American Doctors, and the Collision of Two Cultures by Anne Fadiman (1997).
Although there are some culture-specific
forms of mental illness, for the most part the major
psychiatric syndromes are considered universal. In Crazy
Like Us: The Globalization of the American Psyche
(2010), Ethan Watters argues that DSM has become a
kind of cultural export, shaping non-Western views of mental
illness and its treatment. Watters suggests that this is
a bad thing -- a kind of intellectual colonialism. On
the other hand, nobody complains when other aspects of Western
science and medicine are exported to non-Western countries, as
in the case of treatments for HIV/AIDS, Ebola, or Zika.
It's likely that schizophrenia, depression, anxiety, and other
major mental illnesses are, indeed universal. But still,
non-Western countries likely have something to teach us about
prevention and treatment. For example, epidemiological
studies have found that the prospects for recovery from
schizophrenia are much better in some cultures than others -
-suggesting that, when it comes to mental illness, it's not
all in the genes and neurotransmitters.
Structure and Function
In many ways, mental
illnesses are analogous to the physical illnesses diagnosed
and treated by physicians and other medical professionals.
Just as physical illness stems from abnormalities in bodily
structure or function -- a weak heart valve, or bacterial
infection, or whatever -- so mental illness stems from
abnormalities in mental structure or function -- a
defect in the system for affect regulation, perhaps, or just
acquiring, through learning, some maladaptive belief or
- Abnormalities in cognition are prominent in Alzheimer's disease and other forms of dementia, and in schizophrenia.
- Abnormalities in emotion are prominent in the anxiety disorders, and in the affective disorders.
- Abnormalities in motivation are prominent in psychopathy.
The Medical Model of Psychopathology
- mental patients,
- with acute mental illnesses,
- associated with a particular etiology,course, and prognosis,
- treated in mental hospitals,
- which also have rehabilitation programs for the chronically mentally ill, and
- programs of mental hygiene to prevent mental illness from occurring in the first place.
Mental illness is diagnosed
- symptoms, or publicly observable manifestations of psychopathology (as when a patient complains about being depressed), and
- signs, manifestations of psychopathology that are identifiable by a trained professional (perhaps by the results of formal psychological testing).
These symptoms and signs
of mental illness may be grouped into
- syndromes, or clusters of symptoms that tend to
- diseases, which are syndromes whose underlying
cause is known; and
- illness, which is the subjective experience of disease
Mental illnesses run a particular time course:
- There is an acute phase, between the onset of illness and its remission (whether the illnesses is treated or not).
- If the illness does not remit, the patient proceeds to the chronic phase.
- Prognosis refers to the likelihood that remission will improve (with treatment or not).
- Relapse refers to a return of symptoms after a patient has shown some improvement.
- Recurrrence refers to a new acute episode of
illness after a patient has achieved remission.
These analogies are one aspect of the medical model of psychopathology.
Beyond these analogies, the medical model also has implications for the nature of mental illness. However, these implications are commonly misunderstood. It is commonly believed that the medical model ascribes mental illnesses to organic causes. That every psychiatric syndrome is ultimately an organic brain syndrome. As Ralph Gerard, one proponent of this viewpoint, once put it:
"Behind every twisted thought there lies a twisted molecule".
Similarly, Eric Kandel, the psychiatrist
who won the Nobel Prize for his studies of long-term
potentiation in Aplysia, discussed in the lectures on "Learning", has stated
that "All mental processes are brain processes, and therefore
all disorders of mental functioning are biological
diseases.... The brain is the organ of the mind.
Where else could [mental illness] be if not in the brain?"
(quoted by Kisten Weir in "the Roots of Mental Illness", Monitor
on Psychology, 06/2012).
This "somatogenic" view of mental illness is quite popular, but it is not what the medical model is about. All the medical model asserts is that mental illness has natural causes.According to the medical model, the causes of mental illness may be biological in nature, or they might be psychosocial in nature. All that matters is that they are natural causes that can be ascertained through the methods of empirical science -- namely psychology and related fields. By extension, the medical model holds that mental illness can be treated and prevented by methods derived from scientific research.
Misunderstanding the Medical Model
However, there are considerable misunderstandings abroad about the nature of the medical model -- including misunderstandings perpetrated by many writers of introductory textbooks in psychology. For example, the 4th edition Gleitman's Psychology (1995, p. 722), the book that I have used most often in teaching introductory psychology, described the medical model as follows:
Some authors endorse the medical model, a particular version of the pathology model [which assumes that symptoms are produced by an underlying pathology, and that the main goal of treatment is to discover and remove this pathology], that assumes... that the underlying pathology is organic. Its practitioners therefore employ various forms of somatic therapy such as drugs. In addition, it takes for granted that would-be healers should be members of the medical profession.
Many other introductory textbooks (as well as texts in abnormal and clinical psychology) have similar passages. For the most part, they are intended to distinguish an ostensibly somatogenic medical model from the psychogenic models associated with cognitive and behavioral therapy, or to distinguish the profession of psychiatry, with its emphasis on drugs and other physical treatments, from clinical psychology, with its emphasis on behavioral interventions. This common association of the medical model with somatogenic theories and biological treatments reflects a deep misunderstanding, and what I have presented here follows is an attempt to give an alternative perspective on this issue, based on Siegler and Osmond's (1974b) sociological analysis of the medical model,Models of Madness, Models of Medicine (see also Shagass, 1975).
Interestingly, the Osmond of Siegler & Osmond is Humphrey Osmond (1917-2004), a pioneering LSD researcher who (in 1957) coined the word psychedelic to describe the effects of that and other hallucinogenic drugs. Osmond gave LSD to Aldous Huxley, who wrote The Doors of Perception about the experience -- a book from which the rock group The Doors, led by Jim Morrison, took their name. Initially, Osmond thought that LSD would serve as a laboratory model (see below) of schizophrenia (or, at lest, of schizophrenic hallucinations), but he later focused his attention on the potential of it and other psychedelic drugs to treat alcoholism and promote "transcendent" alterations in consciousness (Osmond's obituary appeared in the New York Times, 02/22/04).
According to Siegler and Osmond, the history of psychology can be traced in terms of three major models of psychopathology. The supernatural model prevailed before the 18th century Enlightenment. It assumes that psychology reflects the possession of the individual by demons; by implication, the proper response to psychopathology is exorcism. The moral model, which prevailed in the late 18th and early 19th centuries, assumes that psychopathology -- or, more precisely, abnormal behavior -- is deliberately adopted by the individual, much in the manner of criminal behavior; by implication, the proper response to psychopathology is confinement and other forms of punishment. The medical model, which began to emerge in the 19th century, assumes only that psychopathology is the product of natural causes that can be identified by the techniques of empirical science. By implication, the proper response to psychopathology is diagnosis according to a scientifically validated system, and attempts at cure or rehabilitation by means of scientifically proven methods. Contrary to the popular view, the medical model does not assert that psychopathology is the product of an abnormal biological condition, or that it should be treated only with drugs or surgery. Rather, the medical model is centered on particular rules regulating two primary social roles: the doctor and the patient.
To illustrate the differences between these models, consider the 1973 decision by the American Psychiatric Association, to "de-list" homosexuality as a mental illness. As Charles Silverstein (2011) has noted -- he was one of the psychologists who persuaded the psychiatrists to change their position -- at the time, "homosexuality was considered a crime, a sin, and a mental pathology". So, in that case, homosexuality fell under both the supernatural model (it was considered to be a sin, the work of the Devil), the moral model (it was considered to be a crime, a willful antisocial act), and it was considered to be an illness (a sexual pathology).
The doctor (who does not have to be a physician, or even hold a doctoral degree) possesses a special kind of authority called Aesculapian (after Aesculapius, the Greek god of medicine). Aesculapian authority is a combination of three other kinds of authority recognized by sociologists:sapiential authority, by virtue of the doctor's special knowledge and expertise;moral authority, by virtue of the doctor's concern for the afflicted individual; and charismatic authority, by virtue of the afflicted person's faith that the doctor will be of help. Note that doctors lack structural authority: they cannot enforce their prescriptions, resulting in a markedly low rate of compliance. The doctor's role is to investigate the disorder at hand, by means of procedures that might be unpleasant, intrusive, or even frightening. On the basis of this investigation the doctor makes a diagnosis, informs the afflicted person about the nature of his or her problem, absolves the patient of blame (it is critical to medical ethics that people are not blamed, and thus punished, for their illnesses), and finally creates the conditions for the afflicted person to return to health and his or her proper role in society.
The patient enacts his or her part by taking on the sick role: he or she must seek help from the doctor, and cooperate with treatment; in return, the patient is exempt from some or all of his or her responsibilities during treatment. Note that a doctor's order has supreme authority in society -- it can exempt the person from jury duty, military service, and final examinations. It has this power by virtue of our society's implicit adoption of the medical model and the sick role. However, patients cannot remain in the sick role forever: they must leave it eventually, either by recovering or dying.
A special case is when the illness is chronic, and nothing more can be done to achieve a cure. Under these circumstances the role relationships change. It is the responsibility of the doctor to remove the sick role, and confer the impaired role on the afflicted patient. At this point the patient must leave the hospital and active treatment. What once was an illness is transformed into a handicap; and the doctor is replaced by a rehabilitation specialist. Patients are no longer absolved from their responsibilities: they must return to some socially productive activity, do things for themselves, and cope with their handicaps as well as possible.
What has just been
described is what Siegler and Osmond (1974) call the clinical
medical model, which is one of many different versions.
All versions of the medical model assume that disease is the
product of natural causes, and that the proper response is
scientifically based treatment. However, they differ in terms
of their role relationships. In the clinical medical model,
the goal is to cure disease in an individual, and the role
relationships are doctor and patient.
- In the public health medical model, the goal is to cure illnesses that cannot be controlled on an individual basis. Its focus is on prevention of disease in a population, rather than an individual, and in fact its prescriptions for public health may damage some individuals; moreover, the public health official may decide to permit some diseases to occur, perhaps for economic reasons. Note that the role relationships differ in the public health medical model. The doctor is replaced by the public health official, who has structural as well as sapiential authority -- he or she has the power of the law and the courts to enforce "doctor's orders", and to force us to fluoridate our water, or be immunized against smallpox and polio. And the patient is replaced by the citizen, who by his or her vote can place limits on the public health official's authority to act.
- In the scientific medical model, there is no direct interest in intervention (prevention or cure), but interest only in the acquisition of scientific knowledge about the nature of disease. Again, the role relationships change. The doctor is replaced by the investigator who has only sapiential authority. The investigator has no obligation to cure and prevent disease, and in certain circumstances may even inflict disease (or allow it to occur) as part of a controlled experiment. The patient is replaced by the subject who volunteers his or her services. Subjects are under no obligation to participate in research, and do so only when they are compensated in some way for their services. Subjects have rights that patients and citizens do not: they must be protected from harm, and must be assured that the procedures to which they are subjected are worthwhile; their only responsibility is to honor their commitment to the study.
So much detail has been devoted to the medical model because it has been subject to so much misunderstanding -- and also because it gives us the opportunity to unite two social sciences, psychology and sociology, at least for a moment. However, the interested reader should reflect on the implications of the medical model(s) for understanding psychopathology -- its nature, causes, treatment, and prevention. And also reflect on the proposition that many of the abuses frequently attributed to mental health professionals -- such as the confinement of mental patients in the back wards of mental hospitals, without any active treatment -- actually represent violations, not expressions, of the medical model.
Excerpted from Kihlstrom, J.F. (2002), "To honor Kraepelin...: From symptoms to pathology in the diagnosis of mental illness". In L.E. Beutler & M.L. Malik (Eds.),Alternatives to the DSM (pp. 279-303). Washington, D.C.: American Psychological Association.
Diagnosis as Categorization
The diagnosis of mental
illness is an act of categorization in which patients (or
their illnesses) are assigned to categories based on the same
feature-matching process we use to categorize other objects.
- The patient's symptoms and signs serve as features.
- The clinician compares the patient's symptoms and signs to those that are associated with various diagnostic categories, as listed in the Diagnostic and Statistical for Mental Disorders (DSM), published by the American Psychiatric Association. The DSM is the "official" list of mental illnesses recognized by the psychiatric profession in America, and has been adopted by other helping professions, such as clinical psychology and clinical social work, as well.
- The patient's illness is diagnosed in terms of the illness that most closely fits his or her symptoms.
- Sometimes a patient receives more than one diagnosis, a situation known as comorbidity. For example, anxiety disorder is often "comorbid" with depressive disorder.
- There is a natural linguistic tendency to confuse the patient with the illness -- that is, to refer to "schizophrenics" and "depressives" instead of "patients with schizophrenia" or depression. This transformation of a category of illness into a category of people is politically incorrect, and a source of great annoyance to many mental patients and their families. But we can't really help engaging in such linguistic shorthand, anymore than we can help referring to people as "Asians" or "Hispanics" -- or, for that matter, "extraverts" or "homosexuals".
Formal psychiatric diagnosis essentially began with a French physician, Jean-Etienne Dominique Esquirol (1772-1840), who drew a fundamental distinction between the insane, the mentally deficient (today we use the term intellectually disabled), and the criminal. In the 19th century, Emil Kraepelin (1856-1926) divided the psychoses into two major categories --dementia praecox (early dementia, or what we now call schizophrenia) and manic-depressive illness (what we now call affective disorder). And a little later, Pierre Janet (1859-1947) did for the neuroses what Kraepelin had done for the psychoses, dividing them into two major categories --hysteria (including what we now call the dissociative and conversion disorders) and psychasthenia (including anxiety disorders and some forms of depression).
Since the 19th century, the number of recognized mental illnesses has grown markedly. The first edition of the Diagnostic and Statistical Manual for Mental Disorders (DSM-I), published in 1952, listed only about 100 different syndromes. The latest edition,DSM-V, published in 1994, listed almost 300.DSM-VI is due to be published sometime around 2012, and we'll see how many mental illnesses there are then!
Whatever its edition,DSM is essentially a catalog of mental illnesses, with a list of the symptoms characteristic of each. Diagnosis is essentially a feature-matching process that asks whether a patient has the symptoms associated with a particular syndrome or disease. In other words, diagnosis is an act of categorization, so it is interesting to look at what kind of categories the diagnostic categories are.
Diagnostic Categories as Proper Sets
In the past, the
diagnostic categories of mental illness were at least tacitly
construed as proper sets, where sets of symptoms served as
defining features of a syndrome, singly necessary and jointly
sufficient to define an illness (such as schizophrenia) or a
person (such as a schizophrenic) as having some illness.
- For example, traditionally mental illnesses were classified as organic (associated with demonstrable brain insult, injury, or disease) or functional (occurring in the absence of obvious brain damage).
- The functional mental illnesses were also characterized as psychotic (featuring a loss of reality testing) or neurotic (featuring symptoms of anxiety).
- The functional psychoses were classified (by Ernst Kraepelin, a 19th-century psychiatrist) into two broad groups,dementia praecox (what we now call schizophrenia, featuring symptoms of cognitive disorder) or manic-depressive illness (featuring symptoms of affective disorder).
- The neuroses were also classified (by Pierre Janet, another psychiatrist of the late 19th and early 20th century) into two broad groups,psychasthenia (syndromes such as anxiety disorder, obsessive-compulsive disorder, hypochondriasis, and "neurotic" depression, where the patient is aware of what is wrong), and hysteria (such as psychogenic amnesia, blindness, or paralysis) where the patient suffers a constriction in awareness.
In this way, the traditional psychiatric nosology formed a conceptual hierarchy with superordinate categories (organic vs. functional, psychotic vs. neurotic) at the top. Subordinate categories were then created by adding symptoms (such as loss of reality testing or problems with anxiety) as defining features.
The Case of Schizophrenia
The nature of traditional
psychiatric diagnosis, as a perfectly nested hierarchy of
proper sets, is exemplified by the work of Eugen Bleuler, a
Swiss psychiatrist who in 1911 redefined dementia praecox as
"the group of schizophrenias".
- Bleuler accepted Kraepelin's classification of "dementia praecox" as a functional psychosis; but he did not believe, as Kraepelin's name implied, that the syndrome was merely a form of dementia that occurred relatively early in life, as opposed to the "senile dementia" associated with old age.
- Instead, Bleuler believed he had discovered a new form of illness characterized by a discordance among basic mental faculties of cognition, emotion, and motivation -- hence his label,schizophrenia.
- In Bleuler's view, all schizophrenics shared four symptoms in common -- his "Four As":
- associative disturbance, manifested in a certain disorganization in the logical organization of thought ("thinking crookedly"), neologisms (made-up words), "word salad" consisting of loose, "clang", and chained associations, and a tendency toward overinclusiveness in categorization;
- anhedonia, an inability to experience positive emotions -- and, more generally,blunted or inappropriate affect (emotional responses that are not correctly tuned to the situation);
- ambivalence, a lack of initiative and a diminished motivation to comply with others' wishes; and
- autism, withdrawal from others and a general detachment from reality.
- There were also four subtypes, characterized by additional defining symptoms:
- simple, as described above;
- hebephrenic, characterized by childlike demeanor;
- catatonic, characterized by immobility; and
- paranoid, characterized by delusions.
Bleuler clearly construed
the 4 As as defining features of schizophrenia:
- Every schizophrenic patient displayed all four symptoms in one form or another.
- Every patient who displayed all four symptoms was a schizophrenic.
The boundaries between schizophrenia and manic-depressive illnesses were clear: you could have one illness or the other, but not both. And the boundaries between schizophrenic subtypes were also clear: you could be hebephrenic or catatonic, but not both.
A similar hierarchy of syndromes developed around manic-depressive illness.
Problems with the Diagnostic Categories
This view of the diagnostic categories as proper sets, recognized by symptoms that were singly necessary and jointly sufficient to define the diagnosis. And early editions of the DSM were at least implicitly structured around this conceptualization, in terms of the "textbook cases" it used to characterize each syndrome.
However, the traditional
view quickly encountered problems of a sort that are familiar
from the critique of the classical view of categories as
proper sets (discussed in the lectures on Thought and
Language).The simple fact was that very few patients actually
resembled the textbook descriptions of the various syndromes.
- Partial Expression: Many patients displayed some but not all of the symptoms that defined a particular syndrome. In the case of schizophrenia, this led to the introduction of new syndromes such as schizoid personality disorder,schizotypical personality disorder, and paranoid personality disorder. There were also many different forms of depression.
- Combined Expression: Many patients displayed defining symptoms of several different categories. In the case of schizophrenia, again, this led to the introduction of new syndromes such as pseudoneurotic schizophrenia,pseudopsychopathic schizophrenia,schizoaffective disorder. The term borderline personality disorder was introduced to cover patients who displayed the symptoms of both psychosis and neurosis -- they were literally "on the border" between these major diagnostic categories.
Psychiatric Syndromes as Fuzzy Sets
Accordingly, for the third
edition of DSM (DSM-III), published in 1980,
the diagnostic system was reformed to take into account a new
understanding of the structure of natural categories offered
by cognitive psychology. Under this "revisionist" view:
- The diagnostic categories were construed as fuzzy sets, rather than proper sets: there is no clear boundary that distinguishes schizophrenia or anxiety disorder from other forms of mental illness.
- Symptoms are considered to be characteristic rather than defining features, only probabilistically associated with various syndromes: delusions may be highly likely to occur in schizophrenia, but they do not define schizophrenia because they are also observed in other syndromes.
- Specific instances of the categories sharing a family resemblance, resulting in a great deal of heterogeneity among patients carrying the same diagnosis.
- Each syndrome is represented by a "prototypical" patient who has many, but not necessarily all, of its characteristic symptoms.
Consider, for example, several prominent psychiatric diagnoses, as listed in DSM-5 (2013):
A statistical technique called network analysis can be used to show the relations among the various categories of psychopathology. Denny Borsboom, a Dutch psychologist, and his colleagues created a simple spreadsheet showing the co-occurrence of all the symptoms listed in DSM-IV -- that is, how many times insomnia and fatigue are listed as characteristic symptoms of the same syndrome (such as sleep disorder or depression). The obtained a graph in which each symptom is represented by a node, and nodes are connected whenever two symptoms are characteristic of the same disorder. They then colored each of the nodes, according to the major category of mental illness in which each symptom occurred. The resulting graph shows the extent of symptom overlap in DSM-IV. in which
Regardless of diagnostic category, there
was no expectation that all of the symptoms listed under a
syndrome will be present in any particular case. In principle,
we can observe all possible combinations of characteristic
symptoms. Diagnosis, then, is a matter of judgment under
uncertainty. Studies of the diagnostic process by Nancy
Cantor and her associates show that the certainty with which a
diagnosis of schizophrenia is made, for example, will be a
function of the number of the patient's symptoms that are
highly characteristic of schizophrenia, and the number of
symptoms that are more characteristic of other diagnostic
categories. In this system, "textbook cases" serve as category
prototypes, and there is explicit recognition of heterogeneity
among actual patients.
The Diagnostic and Statistical
Manual for Mental Disorders (DSM) was
first published in 1952, with a second edition appearing in
1968. Both manuals were as much literary productions as
scientific ones. They were heavily influenced by
Freudian psychoanalysis, centered on the distinction between
psychoses and neuroses, and didn't really include clear
criteria for making various diagnoses. All that changed
with DSM-III in 1980 (a revised edition, known
as DSM-II-TR, for "Text Revision", came out in 1987),
and DSM-IV in 1994. In these editions, serious effort
went into producing checklists of symptoms by which the
various disorders could be reliably diagnosed.
The fifth edition of DSM,
known as DSM-5, retains the "fuzzy set" structure of
the diagnostic categories, while sometimes revising the
criteria for specific disorders.
- For example, in DSM-IV, the diagnosis of
schizophrenia required the presence of any two
"characteristic symptoms", whether positive or
negative. In DSM-5, the diagnosis requires
that at least one of these "characteristic symptoms" be a
"positive" symptom such as delusions, hallucinations,
disorganized speech, or grossly disorganized behavior.
- Moreover, it abandons the Bleulerian" subtypes of simple, hebephrenic, catatonic, and paranoid schizophrenia.
- DSM-IV diagnosed autism based on three criterial
symptoms: impairments in social interaction, impairments
in social communication (language), and restricted,
repetitive, and stereotyped patterns of behavior,
interests, and activities. DSM-5 lumps the
two kinds of social impairments together, so that
Asperger's syndrome joins classic autism in a single
category of autistic spectrum disorder.
- The implication is that autism and Asperger's syndrome
differ only in degree, quantitatively, not in kind,
qualitatively. Many in the autism/Asperger's
community disagree, including Temple Grandin, whose
vigorous critique-from-the-inside of DSM-5 is
included in her 2013 book, the Autistic Brain:
Thinking Across the Spectrum (2013, written with
However, DSM-5 abandons
certain other features of previous editions.
- Previous editions were arranged hierarchically, with major sections devoted to the psychoses, mood disorders, anxiety disorders, and the like. DSM-5 is organized developmentally, with the earliest chapters covering disorders that first appear in childhood.
- Reflecting increasing cultural diversity, DSM-5
pays more attention to "culture-specific" syndromes, as
well as cultural factors that may affect diagnosis.
- Earlier editions made liberal use of a subcategory Not
Otherwise Specified (NOS), as in "Psychotic
Disorder -- Not Otherwise Specified", for use with
patients who displayed some features of psychosis, but not
enough to enable a more specific diagnosis. Previously, a
remarkably high proportion of psychiatric patients
received diagnoses containing the NOS suffix. This
was especially true of the personality disorders and
pervasive developmental disorder (autism). NOS allowed
psychiatrists too much leeway to diagnose anyone
with a mental illness, without being specific as to
precisely what illness he or she had: the suffix is now
- At the same time, DSM-5 also allows practitioners to assess a disorder's degree of severity in the particular patient -- much as medical disorders are rated as mild, moderate, or severe. So, a patient could meet all the criteria for schizophrenia, even though each of the relevant symptoms was present only to a mild or moderate degree.
- Previous editions classified patients according to
- Axis I referred to the mental disorder itself, such as
schizophrenia or bipolar disorder.
- Axis II referred to background personality
characteristics, and included the personality disorders
themselves, as well as intellectual disability.
- Axis III concerned general medical conditions that
might relate to diagnosis or treatment.
- Axis IV referred to socioeconomic factors, such as
poverty, that might be relevant to diagnosis or
- Axis VI consisted of a global assessment of
Aside from Axes I and II, none of these dimensions got much use in real-world, everyday diagnosis, and so they were dropped.
Some of the changes in DSM-5 are highly controversial.
- Although it eliminates the NOS subcategory for specific
mental disorders such as schizophrenia, it includes a new
category of Unspecified Mental Disorder,
specifically for patients who "do not meet the full
criteria for any mental disorder" (p. 708).
- And it also revives NOS in another guise, as in the new category of Unspecified Schizophrenia Spectrum Disorder and Unspecified Attention -Deficit/Hyperactivity Disorder.
- DSM-5 collapses Autistic Disorder and Asperger's Syndrome into a single category of Autistic Spectrum Disorder. The implication is that Asperger's Syndrome differs from Autistic Disorder only in terms of severity. But autism and Asperger's Syndrome don't just differ quantitatively, in terms of severity. They also differ qualitatively, in that patients with Asperger's Syndrome have language abilities that patients with Autistic Disorder simply don't have. Moreover, people with Asperger's Syndrome have an interest in interpersonal relations, even if they lack the skills to build or maintain them. Classifying a child with Asperger's Syndrome as "autistic" may mean that the child will not receive optimal treatment.
- As another example, DSM-5 eliminates the "bereavement exclusion" for the diagnosis of Major Depressive Episode. Previously, people who showed signs of depression immediately following the loss of a loved one (spouse, child, parent, pet, friend, etc.) were not diagnosed as "depressed" unless their depression continued for more than two months after the onset of symptoms. But now, patients can be diagnosed as "depressed" even though they are still mourning a loss.
- The diagnosis of bipolar disorder has come to be used more frequently with children, a trend that is highly controversial in itself. Compounding the controversy, DSM-5 introduces a new diagnostic category of disruptive mood dysregulation disorder -- which, critics suggest, might apply to any child who has frequent temper tantrums.
- In addition to anorexia and bulimia, DSM-5 introduces the opposite side of the eating-disorder coin, binge-eating disorder, applied to anyone who eats to excess at least once per week.
- Hoarding is now a full-fledged mental disorder in
its own right, not just one possible symptom of
Some commentators have expressed the
fear of diagnostic inflation -- that these kind of
changes may make it possible to diagnose anyone with a
mental illness -- or, at least, that DSM threatens to
"pathologize normality" by classifying normal mental states,
like bereavement or even shyness (which can resemble
depression), as mental illnesses. (Benjamin Wolman, a
leading psychoanalytic psychotherapist, once wrote a book
entitled Call No Man Normal.) Overdiagnosis, of
course, inevitably leads to overtreatment.
In addition, some of those responsible
for formulating the DSM-5 criteria had unacknowledged
links with the pharmaceutical industry, raising the
possibility that increasing the number of people who can be
diagnosed with some form of mental illness, however mild, will
effectively expand the market for psychiatric
medications. At the very least, these affiliations might
have biased the Manual developers toward biological diagnoses
and treatments. At the worst, it raises the possibility
that Big Pharma might encourage clinicians to formulate new
diagnoses that expand the market for available psychotropic
drugs -- what Marcia Angell, the former editor of the New
England Journal of Medicine, has called a
"patent-extending game" (see her book, the Truth About
Drug Companies: How They Deceive Us and What We Can Do About
- In 1993, the editors of DSM-IV considered, but rejected, a proposal for a new diagnosis of Pre-Menstrual Dysphoric Disorder (PMDD), a severe form of Premenstrual Syndrome (PMS) experienced by some women of childbearing age: previously, it was known as Late Luteal Phase Dysphoric Disorder (LLPDD). At roughly the same time, SmithKline, a major pharmaceutical company, was losing its patent on Prozac, a drug used in the treatment of depression; SmithKline repackaged Prozac as Serafem (changing little more than the color of the pill), and began recommending the "new" drug for the treatment of this "new" disorder. PMDD was given official recognition in DSM-5. Many commentators entertain the suspicion that PMDD was proposed as part of a strategy to legitimize extending the patent on Prozac.
- Aricept is a drug commonly prescribed for symptom relief
in cases of mild to moderate Alzheimer's Disease
(AD): it doesn't reverse, or even slow, the progression of
the disease, but it does provide temporary relief from
some symptoms. In 1999, some researchers began to
talk about Mild Cognitive Impairment (MCI) as a
"prodromal" or incipient phase of Alzheimer's
disease. Diagnosis of MCI requires objective
evidence of memory impairment -- worse than normal
cognitive aging, but not as severe as AD. But in
2013, some researchers began touting a new syndrome of Subjective
Memory Impairment (SMI) to cover cases where
the patient (or his family) complains about memory
impairment, but does not perform poorly on objective
memory tests. Obviously (just think about the normal
bell-shaped curve for a moment) there are more people with
MCI than with AD, and probably more people with SMI than
MCI -- thus potentially expanding the clientele for drugs
- If college students take Ritalin as a "smart drug",
why shouldn't their grandparents take Aricept for the
Other commentators worry that many DSM-5
diagnoses simply lack validity to begin with. In an
important early paper, Robins and Guze (1970) outlined the
criteria for establishing the validity of any diagnostic
- Distinguish the target diagnosis (e.g., schizophrenia) from other possible diagnoses (e.g., bipolar disorder).
- Predict performance on laboratory tests involving psychological and biological variables.
- Correlate with family history of mental disorders.
- Predicts the course of the illness.
- Predicts the outcome of treatment.
By these standards, more than 40 years later, many DSM diagnoses do not fare too well. For example, the American Psychiatric Association proposed to "field-test" DSM-5 before its actual publication, to make sure that clinicians could use it reliably to make diagnoses. Unfortunately, DSM-5 failed its field trials, in that the rate of disagreement between two clinicians, applying the same criteria to the same patient, was unacceptably high.
This state of affairs has led some
investigators to propose alternatives to the DSM.
- Some theorists have proposed that diagnosis move from a
categorical structure to a dimensional structure. In
such a system, patients would be assessed along continuous
dimensions representing various aspects of cognition,
emotion, motivation, and behavior -- much as personality
assessment is guided by the Big Five dimensions of
personality.Of course, the precise nature of these
dimensions is something for future research to establish.
- Other theorists have proposed moving toward a biological classification -- perhaps in terms of neurotransmitter activity. This assumes that all mental illnesses involve underlying biological abnormalities -- an assumption which isn't self-evidently true. Some mental illnesses, such as phobias and certain types of depression, may reflect maladaptive social learning by patients whose neural functioning is essentially normal.
- Other theorists, including yours truly, have proposed that the diagnostic categories be based on the results of laboratory tests -- but laboratory tests of psychopathology, not of pathological anatomy and physiology. What these tests might look like is foreshadowed in the next section, on Experimental Psychopathology.
For now, though, DSM-5 is what
we've got. The Social Security administration won't pay
disability benefits, insurance companies won't pay for
treatment, and courts won't consider the insanity defense, in
the absence of an official psychiatric diagnosis, and DSM
is how psychiatrists officially diagnose patients. It's
as simple as that.
Research Domain Criteria
One possible alternative diagnostic system, embraced by the National Institute of Mental Health, is the Research Domain Criteria (RDoC). Instead of employing traditional diagnostic categories, such as schizophrenia and bipolar disorder, RDoC classifies mental processes into several domains, constructs, and sub-constructs, with each construct and sub-construct hypothetically linked to a different neural circuit in the brain.
- For example, negative emotionality includes fear, which is linked to the amygdala.
Here is a list of the domains and subdomains, as listed in a document published by NIMH in 2011.
- Negative Valence Systems
- Acute Threat ("Fear")
- Potential Threat ("Anxiety")
- Sustained Threat
- Frustrative Nonreward (i.e., frustration due to the
withholding of reinforcement for previously reinforced
- Positive Valence Systems
- Approach Motivation
- Reward Valuation
- Effort Valuation/Willingness to Work
- Expectancy/Reward Prediction Error
- Action Selection/Preference-Based Decision Making
- Initial Responsiveness to Reward
- Sustained Responsiveness to Reward
- Reward Learning
- Cognitive Systems
- Visual Perception
- Auditory Perception
- Olfactory/Somatosensory/Multimodal Perception
- Declarative Memory
- Language Behavior
- Cognitive (Effortful) Control
- Goal Selection
- Representation and Maintenance
- Response Selection, Inhibition or Suppression
- Working Memory
- Active Maintenance
- Flexible Updating
- Limited Capacity
- Interference Control
- Systems for Social Processes
- Affiliation and Attachment
- Attachment Formation and Maintenance
- Social Communication
- Reception of Facial Communication
- Production of Facial Communication
- Reception of Non-Facial Communication
- Production of Non-Facial Communication
- Perception and Understanding of Self
- Perception and Understanding of Others
- Animacy Perception
- Action Perception
- Understanding Mental States
- Arousal and Regulatory Systems
- Circadian Rhythms
- Sleep and Wakefulness
Following the medical model, it's important to get beyond surface symptoms and signs to underlying pathology. DSM-5 doesn't do that, it's diagnoses are solely based on signs and symptoms. Diagnosis in the rest of medicine is of diseases, , and the RDoC is a step in this direction. At the same time, we can worry about the underlying assumption, which is that each element of underlying pathology is linked to a dysfunction in some brain circuit (Insel, "Faulty circuits", Scientific American, April 2010). It's not at al clear that a faulty brain circuit must be involved in every instance of mental illness. Moreover, the identification of such circuits is years, decades, maybe centuries away. The whole project of identifying the circuits of the brain, which is the raison d'etre of the Human Connectome Project announced by President Obama in 2013, begins with extremely simple nervous systems, such as aplysia (the sea slug studied by Eric Kandel and others), and then move up to the mouse, and only later to the human -- at which point the process of linking neural circuits to the various domains can begin. Not in my lifetime, nor yours.
In the meantime, diagnosis needs to
move beyond signs and symptoms to the identification of
underlying pathology through laboratory tests -- underlying psychopathology.
For now, though, and for the foreseeable
future, psychiatric diagnosis is going to be based on symptoms
and signs, and organized by something very much like DSM-5.
This line of research in experimental psychopathology
has a long and distinguished history, going back to Emil
Kraepelin's studies of schizophrenia using Donders's
reaction-time methodology. While the RDoC claims to be
"agnostic" about the traditional diagnostic categories
(actually, far from being agnostic, it rejects them),
experimental psychopathology takes them as a starting point,
and tries to identify the pathological mental processes that
underlie them. One result of this work should be the
more fine-grained classification, moving beyond superficial
symptoms and signs, that the RDoC seeks -- but without the
For critiques of psychiatric diagnosis and DSM, see:
- The Selling of DSM (1992) and Making Us Crazy (1997) by Herb Kutchins.
- They Say You're Crazy (1996) by Paula Caplan.
- "The Epidemic of Mental Illness: Why?" and "The Illusions of Psychiatry" an essay-review of several books critical of psychiatry by Marcia Angell (New York Review of Books, June 23 and July 14, 2011).
- "Head Case: Can Psychiatry Be a Science?" by Louis Menand (New Yorker, March 1, 2010).
- The Book of Woe: The DSM and the Unmaking of Psychiatry (2013) by Gary Greenberg, who doesn't seem to like diagnosis at all (he also wrote another book, entitled Manufacturing Depression).
- Saving Normal: An Insider's Revolt Against Out-of-Control Psychiatric Diagnosis, DSM-5, Big Pharma, and the Medicalization of Ordinary Life (2013) by Allen Frances (who led the task force that prepared DSM-IV, but thinks that DSM-5 takes an approach to diagnosis that has become outmoded).
Current diagnostic practices classify illness based on surface symptoms, but the symptoms are not the disease. Rather, symptoms are assumed to be caused by some underlying disease process --pathology.
Beyond Surface Symptoms to Underlying Pathology
In medicine, symptoms are not the disease, and progress in medical understanding is marked by a shift in focus from symptoms to underlying disease processes -- to underlying pathology revealed by laboratory analyses of structure and function whose results are interpreted in the light of a theoretical understanding of normal function.
Consider the example of fever, manifested by chills (a symptom about which patients complain) and increased body temperature (a sign, indicated by a thermometer). Well into the 19th century the medical nosology included a large number of different "types" of fever, based on the symptoms accompanying the fever and the circumstances under which the fever occurred. In fact, Benjamin Rush, the pioneering American physician of the Revolutionary War era, thought there was only one disease -- fever. But nobody diagnoses and treats fever anymore, because fever is viewed as a symptom of an underlying bacterial infection. Physicians may try to reduce a patient's fever, as an emergency measure, but most of their efforts are devoted to identifying the underlying infection (through blood tests) and then treating it (through antibiotics).
In "Rocky Mountain spotted fever" the patient presents with chills and elevated body temperature, as well as a petechial rash beginning on the wrists and ankles; the illness was first diagnosed in the Rocky Mountain area of the United States. Initially, treatment focused on bring the fever down with cold compresses, or else simply letting the fever "run its course". Now, however, a physician who suspects that a patient suffers from this disease will order a laboratory test to look for serum antibodies to the Rickettsia rickettsii virus, which is transmitted by a wood tick found in the western United States. Treatment entails finding the tick and removing it from the patient's skin, followed by a course of antibiotics to eliminate the infection. This treatment, applied in a timely fashion, results in a complete cure, not just symptom relief. Similarly, efforts at preventing the disease are aimed at eliminating the tick from the environment through insecticide sprays.
The Way We Diagnose Now (in the Rest of Medicine)
Lisa Sanders, a physician on the faculty of
the Yale School of Medicine, occasionally contributes a
column to the New York Times Magazine in which she
shows how a puzzling medical diagnosis was resolved through
the interpretation of laboratory tests that went beyond the
usual symptoms, signs, and history. Here are a couple of
examples from her 2003 columns:
- A middle-aged man with a history of diabetes, hypothyroidism, and bone marrow dysfunction leading to anemia complained of pain in the hips and buttocks and difficulty walking; he was comfortable so long as his legs were not bearing weight. An initial diagnosis of sciatica, based on the patient's symptoms, didn't quite fit. X-rays were negative, as were blood tests for infection or destruction of muscle tissue. However, an MRI revealed an obstruction in an artery leading to his thigh, a complication of diabetes, that was a condition similar to a heart attack, including "ischemic" muscle pain (09/07/03).
- A young man with morbid obesity (5'7", 350 pounds) was admitted to the Intensive Care Unit complaining of difficulty breathing and extreme fatigue. A test showed that the oxygen in his blood was only 88% of normal. Blood tests suggested an infection in the lungs, while X-rays revealed pneumonia. The patient's obesity was preventing him from clearing carbon dioxide from his blood, and the buildup was causing his sleepiness. The disease, hypoventilation syndrome, is also known as Pickwickian syndrome, after an obese, chronically sleepy character in Charles Dickens's Pickwick Papers (09/21/03).
- A plump woman in her 50s was taken to the emergency room after a fall. She complained of chronic back pain. An X-ray revealed a collapsed vertebra in her lower spine, and the mottled appearance of surrounding vertebrae suggested cancer. In fact, further physical examination, confirmed by further tests, revealed a cancer which had metastasized from her breast to her ribs, hips, and spine (10/19/03).
- A young woman with complained of looking like a man, and being mistaken for male. She presented with a somewhat "masculine" appearance, including facial hair, bearing, and voice. Her menstrual periods were irregular. She had no signs of a hormonal abnormality such as congenital adrenal hyperplasia (discussed in the lecture supplements on Psychological Development). Physical examination revealed male pattern baldness, and patches of darkened skin often associated with high levels of circulating insulin. In the absence of a test that could definitively confirm the diagnosis, the patient was treated with medication that would improve her response to insulin, and thus lower her levels of circulating insulin. In response, the patient lost some weight and regained menstrual regularity, consonant with the diagnosis. But the patient was also referred to an endocrinologist for further laboratory tests of hormonal dysfunction.
- A man in his 50s, being treated for high cholesterol but with no other health problems, complained of shortness of breath, but no other symptoms. The absence of fever or cough ruled out pneumonia. Evaluations of cardiovascular function ruled out heart disease. A course of antibiotics had no effect, ruling out infection. A bronchoscopy was negative for both infection or cancer. The pattern of negative findings led to a diagnosis of interstitial lung disease by default -- it was the only remaining possible cause of the patient's symptoms. In fact, a review of the bronchoscopy results did reveal a white blood cell anomaly consistent with ILD, which may have been triggered by the Lipitor the patient was taking to control his cholesterol levels. The patient's condition improved when he was taken off the Lipitor and put on anti-inflammatory steroids -- an outcome consistent with the diagnosis of ILD.
These examples illustrate how diagnosis is
done in advanced, scientific medicine:
- The patient's symptomatic complaints, and signs revealed by physical examination, lead the physician to generate a hypothetical -- that the patient has a particular disease, which accounts for for the observed signs and symptoms.
- This diagnosis is then confirmed or disconfirmed through laboratory tests.
- If the tests are positive, treatment proceeds in accordance with the confirmed diagnosis.
- If the tests are negative, a new hypothesis is generated, and new tests are performed.
- If no definitive tests are available, a diagnosis may be supported retrospectively through the patient's response to treatment.
- If the patient responds positively, then the diagnosis is provisionally confirmed.
- But if the patient does not respond positively, a new diagnosis may be hypothesized, and a new treatment ordered in an attempt to confirm the hypothesis.
In any event, the patient's response to treatment is assessed by laboratory tests: if the diagnosis is correct, and the treatment is working, the patient's scores will improve on the very tests that generated the diagnosis in the first place.
On occasion, the correlation between symptoms and disease may be so high that no tests are ordered. But in most cases, medical diagnosis is based on laboratory tests, not presenting symptoms, and the success of treatment is confirmed by laboratory tests as well.
In medicine, pathology affects bodily functions through lesions in anatomical structures (e.g., a skull fracture or lung cancer), abnormalities in physiological functions (e.g., hypertension or sinus arrhythmia), or infection by micro-organisms (e.g., the influenza virus; in addition to viral infections, there are also infections by bacteria, fungi, chlamydiae, rickettsiae, and microplasmas). Modern medical diagnosis is based on evidence of these pathological conditions, as revealed by objective laboratory tests.
There are parallels in the
medical model of psychopathology:
- Abnormalities in Mental Structures and Processes, roughly analogous to the anatomical and physiological abnormalities in physical medicine. In these cases of psychological deficit,something has gone wrong with the patient's basic mental apparatus -- the cognitive, emotional, and motivational systems governing the person's experience, thought, and action. Presumably, there is also some underlying biological abnormality contributing to the abnormal mental function.
- Abnormalities in Mental States (thoughts, feelings, and desires) constructed by mental structures and functions (and their biological substrates) that are essentially intact. These abnormal mental states -- beliefs, expectations, thoughts, feelings, and desires -- are the mental analogies of infections.
In medicine, underlying
pathology is revealed by laboratory analyses interpreted in
the light of our understanding of normal structure and
function. In psychopathology, such laboratory research is
known as experimental psychopathology. Experimental
psychopathology tries to identify the causes of the patient's
manifest symptoms. It is basic research on psychopathology, as
opposed to applied research on diagnosis and treatment, and it
comes in two major forms:
- laboratory studies of psychological deficit and
- laboratory models of psychopathology.
Attentional Deficits in Schizophrenia
Studies of psychological deficit in schizophrenia have a long history, dating back to experimental work by Kraepelin, in Wundt's laboratory, who used Donders' reaction time technique to measure the speed of mental processes in patients with dementia praecox (presenile dementia), the syndrome later renamed schizophrenia. One highly prominent theory of schizophrenia holds that the psychological deficit underlying the patient's presenting symptoms affects the attentional system. According to this theory, schizophrenics suffer from a breakdown in selective attention that renders them highly distractable and unable to filter out irrelevant ideas. The patient shows thought and language disorder because he cannot keep track of what he is thinking and saying; he withdraws socially to shut out this chaos of stimulation. And, in fact, laboratory tests confirm that patients with schizophrenia have a number of difficulties with attention.
information-processing deficits in schizophrenia appear to
begin at the very beginning of the information-processing
of the multi-store model discussed in the lectures on
memory. In that
model, stimulus information is briefly held in
modality-specific sensory registers, from which it is
extracted into short-term or working memory for further
processing, and then encoded into long-term memory. Studies of
information-processing in schizophrenia have focused on the
sensory registers, working memory, and attention. If things go wrong
at these earliest stages of information processing, lots of
other things will go wrong as well.
Consider, for example, a study by Wishner and Wahl (1974) of dichotic listening in schizophrenia (there are other studies of this topic, but I chose this one because Wishner was a teacher of mine in graduate school and Wahl was a graduate-student colleague).In this paradigm, different messages are played through earphones to the two ears, and the subject is instructed to shadow one message, repeating its words aloud as they are spoken, and ignore the other. There is little or no impairment when normal subjects shadow a single message, with no distracting message coming over the other ear. When the distracting channel is added, however, subjects begin to make shadowing errors: omissions of parts of the target message and intrusions of the irrelevant message, and recall of the target message.Wishner and Wahl found that schizophrenics were particularly prone to make shadowing errors: more omissions and more intrusions, especially when the target message was played at a relatively fast speed;, and poorer recall of words from the target message, even when no distractor was present. These results are consistent with the hypothesis that schizophrenics suffer from an attentional deficit.
findings were obtained in a study of visual attention by
Saccuzzo and Shubert (1981) employing the backward masking
paradigm. In this procedure, an array of digits or letters is
presented very briefly, so that there is not much opportunity
for it to register in a very short-term memory store known as
iconic memory (see the lecture supplements on Memory).
Presentation of this array is followed by a "masking" stimulus
that effectively displaces the array from iconic memory,
preventing it from being further processed in "primary",
"short-term, or "working" memory. Therefore, identification of
the elements in the array requires highly focused attention,
so that the subject can process the information from the array
into primary memory before its representation disappears from
iconic memory. In the experiment, subjects had to search for
the letter T in an array of As, or for the
letter A in an array of Ts: if it is present,
they simply say "yes" and another trial begins.The investigators varied the
"stimulus-onset asynchrony" (SOA), or the interval between the
onset of the array and the onset of the mask -- essentially,
the amount of time that a representation of the array resides
in iconic memory. They found that schizophrenics were
generally poorer at target detection than controls, especially
at longer SOAs. They concluded that it takes longer for
schizophrenics to transfer information from iconic to primary
memory. By virtue of this slower rate of information
processing, schizophrenics miss a lot of what goes on around
them, and are more distractable.
In recent years, much attention has focused on working memory in schizophrenia. You’ll remember from an earlier lecture that working memory enables an individual to maintain information in an active state, over short periods of time, while it is being manipulated by other cognitive processes. This information may be extracted from perception or retrieved from memory. As such, working memory is critical for a wide variety of cognitive processes, such as selective attention, including both focusing on needed information and inhibition of irrelevant information. A problem in working memory can permeate far into cognitive function, affecting memory, reasoning, problem-solving, and language. 10
Working memory is often studied with variants of the Sternberg task, discussed at length in the lecture on methods and statistics. In the Sternberg task, a subject is asked to memorize a small set of items, and then to search that set for a particular target. It’s different from the Sperling task. In the Sperling task, subjects have to inspect a study set presented as a visual array. In the Sternberg task, they have to hold a representation of the study set in working memory while they search it. Sternberg’s basic finding, you’ll remember, was that response latency varied with the size of the search set, indicating a serial, self-terminating search process. An experiment by Paul Metzak and his colleagues compared schizophrenic patients with a group of normal control subjects who had been matched with the patients on such demographic variables as age and education.
Like Sternberg, Metzak found that accuracy decreased, and response latency increased, with the size of the study set. But this variable had a greater effect on the performance of the schizophrenic patients than on the normal subjects. Performance especially deteriorated at the largest set size. It’s as if the patients were overwhelmed by the information they had to process – maybe because they’re processing information so slowly, as in the Saccuzzo experiments in iconic memory.
Working memory consists of several different components. First, there are modality-specific buffers which maintain information in an active state. These elements are similar to the traditional concept of short-term memory, and there appears to be no problem with them in schizophrenia. Then there is a central executive, which actually guides various information-processing tasks, manipulating and transforming information held by the buffers. Here is where the psychological deficit in schizophrenia appears to be located. Other research shows that there is a particular problem with a component of the central executive that represents and maintains contextual information that is relevant to current tasks – information about the task being performed, other information that has been recently processed, and what’s coming next. This central executive appears to be mediated by the dorsolateral prefrontal cortex. Interestingly, this region of the brain is part of a system modulated by dopamine, and the antipsychotic drugs used in the treatment of schizophrenia are antagonists of this neurotransmitter.
of dichotic listening, backward masking, and working memory
illuminate schizophrenic deficiencies in central mechanisms of
attention, but attention is also regulated by peripheral
mechanisms -- as when we turn our heads or eyes to shift our
attention from one object to another. Holzman and his
colleagues have studied the peripheral mechanisms of attention
with an eye-tracking paradigm in which subjects are
asked to hold their head in a fixed position and move their
eyes to track a target moving smoothly across a screen; they
then examine the subjects' pursuit eye movements (PEMs) as
they follow the target. Some aspects of these eye movements
are not consciously perceptible to the subject, but can be
recorded by an electrooculogram (EOG) similar to that used in
sleep research, or by special infrared devices.
Holzman et al. have found that in
contrast to the smooth pursuit eye movements (SPEMs)
characteristic of normals, schizophrenics show eye movements
that are more jagged.About
70% of schizophrenic patients show anomalous PEMs, but PEM
anomalies also show up in relatives of patients who are not
themselves diagnosed with schizophrenia.Accordingly, Holzman has
suggested that abnormal PEMs might be a biological marker
for schizophrenia, perhaps indicating an underlying
malfunction in the frontal-lobe of the brain, particularly in
those centers involved in the peripheral control of attention.
Interestingly, Holzman and his colleagues have found that
abnormal PEMs are related to various aspects of thought
disorder, as measured in patients' verbal protocols. However,
abnormal PEMs are associated with thought disorder across a
wide variety of diagnoses, so this aspect of attentional
deficit may not be specific to schizophrenia.
experimental studies of schizophrenia focus on various aspects
of cognitive function, such as attentional deficits, but
schizophrenia can involve problems with emotional function as
well. Consider anhedonia, one of the classic "Four As"
of schizophrenia. Many schizophrenics show flat or bunted
affect, or else affect that is inappropriate to the situation.
But that's their display of affect. Recall Lang's
multiple systems view of attention, according to which
emotional responses have three different components: a
subjective feeling state, overt behavior, and covert
In one experiment, Kring and Neale (1998) showed emotional (positive and negative) and neutral films to schizophrenic patients and controls, and measured all three components of emotional response. In terms of facial expressions, schizophrenics were, indeed, less reactive than controls -- in terms of the frequency, intensity, and duration. But they were actually more reactive when their covert physiological responses were measured by a psychophysiological index known as skin conductance. The self-reported emotional responses of schizophrenic patients were somewhat muted, compared to controls, but both patients and controls showed the same pattern of response to positive and negative films. So, schizophrenics do not appear to be emotionally responsive, in terms of their facial expressions. But in terms of their subjective feeling states, and their physiological response to emotional stimuli, they appear to be experiencing emotion -- even if they aren't showing it in their behavior.
The problem with diagnosing mental illness based on symptoms is illustrated by attention deficit hyperactivity disorder (ADHD), which is typically diagnosed in children based on such symptoms as failure to pay attention in school or play, running around the room, climbing on things, fidgeting and squirming, and the like. But adults with ADHD don't necessarily do these things. Instead, they display other, more age-appropriate symptoms such as difficulties in "wrapping up" the final details of a project, getting and keeping things in order, remembering appointments, and the like. Both sets of symptoms may have a common origin in some attentional dysfunction, and perhaps a common standard for diagnosis, applicable to children and adults alike, could be achieved by the development of laboratory tests that assess attentional functions directly.
Laboratory Models of Psychopathology
In addition to studies of
psychological deficit, it is sometimes possible to create
laboratory models of psychopathology, inducing in normal
individuals a syndrome that, in at least some respects,
resembles some form of actual mental illness. Laboratory
models are rarely if ever exact replicas of mental illnesses,
down to the last detail; rather, they usual mimic one or more
characteristic symptoms of some syndrome. In a sense,
laboratory models constitute theories of how symptoms arise in
actual patients, because they are based on the assumption that
the causative agents that effectively produce symptoms in the
lab parallel those that are present in the real world outside
the laboratory. Thus laboratory models can be used to test
proposals concerning the origins, treatment, and prevention of
mental illness. As such, they can be evaluated on a number of
- behavioral (i.e., descriptive features of symptoms and syndromes);
- prevention; and
- underlying biological structures and processes.
Like studies of psychological deficit, laboratory models of psychopathology have a history that goes fairly far back in time -- but this time, to Pavlov's laboratory rather than Wundt's. In some early studies of discrimination learning, dogs were conditioned to salivate to a circle or an ellipse, and then the axes of the stimulus were progressively changed, so that the circle became more elliptical, or the ellipse more circular. The result was that, at some point, the dogs became distressed -- seemingly anxious -- a phenomenon that became known as experimental neurosis. One explanation (proposed by Sue Mineka and myself) was that this increase in anxiety occurred because the animals could no longer predict the onset of the food US. Unpredictability causes anxiety (hold this thought, because in a little while we'll discuss another laboratory model that indicates that uncontrollability causes depression).
In addition, conditioned
fear has served as a laboratory model of phobia, while
conditioned avoidance has served as a laboratory model for
- In conditioned fear, the animal becomes afraid of a previously neutral stimulus that is associated with fear, such as a tone that predicts shock.
- In 1920, John B. Watson (who gave us the doctrines of behaviorism) and his student Rosalie Rayner showed that they could condition phobia-like levels of fear of furry things in an infant, known to us as "Albert B.", or more colloquially "Little Albert", by making a loud noise whenever he came into close proximity to an otherwise-harmless white rat.Link to a a video of the Little Albert study.
- The case was controversial, not just on the obvious ethical grounds that they were inducing fear in a child who was not fearful before, but because they didn't engage in an extinction procedure that would have eliminated Albert's fear response.
- Inevitably, questions are often asked about what
happened to Little Albert. We don't know for
sure, because Watson left academia shortly thereafter
(following an affair with Rayner, which led to his
divorce) -- he turned to a career in advertising with
the firm of J. Walter Thompson, for whom he invented
the concept of the coffee break" as part of a campaign
for Maxwell House. When he died, his wife,
following his instructions, burned all of his papers.
- In 2009, "Little Albert" was plausibly identified as Douglas Merritte, son of a wet nurse at Johns Hopkins Hospital. A 2012 article also suggests, based on films of Albert, that he was not exactly "normal" to begin with: he may have suffered from a form of hydrocephalus, an accumulation of cerebrospinal fluid in the brain. Douglas died when he was six years old, presumably of the consequences of his neurological condition (Beck et al., 2009; Fridlund et al., 2012)).
- But in 2014, another group of investigators pointed to another child, William Albert Barger, who had been born at about the same time as Merritte, who died in 2007 (Powell et al., 2014)..
- But in the absence of any followup documentation, we'll never know for sure.
- In 1958, Joseph Wolpe reported a series of studies of conditioned fear and its extinction in cats, which laid the scientific foundation for systematic desensitization, an early form of behavior therapy.
- Research by Sue Mineka (already described in the lectures on Learning) on the acquisition of snake fear in lab-reared rhesus monkeys showed that conditioned fear could be acquired vicariously, without direct exposure to the shock, which offered an explanation for why many phobics report not having had unpleasant encounters with the objects of their phobia.
- Although in principle we can acquire phobic-like fears of just about anything, including teddy bears, in practice the phobias encountered clinically are restricted to a relatively narrow range of objects: heights, darkness, being stared at by other people, things that crawl or slither -- you get the idea. It's been suggested that, like snake fear in lab-reared rhesus monkeys, clinical phobias represent highly prepared fear responses, part of our evolutionary heritage.
- In much the same way, avoidance learning can serve as a laboratory model of obsessive-compulsive disorder.
- Many compulsions -- like constantly checking the door to see if it is locked -- seem to reflect the patient's attempt to avoid or prevent some undesirable outcome. And, of course, the behavior is reinforced by the fact that the undesirable outcome never occurs. So the patient continues doing it. Similarly, avoidance responses are very difficult to extinguish -- precisely because they succeed so well that the animal never learns that the shock has been turned off!
For a personal account of OCD, as well as good coverage of the scientific literature, see the Man Who Couldn't Stop: OCD and the True Story of a Life Lost in Thought by David Adam (2015). Adam himself fell into the clutches of OCD after having unprotected not-quite sexual intercourse as a college student. He became obsessed with the idea that he might contract HIV-AIDS, and went to great lengths to ward off that outcome.
Learned Helplessness and Depression
Of particular interest is the development of learned helplessness as a laboratory model of depression. As discussed earlier (in the lectures on Learning), learned helplessness was initially observed in studies designed to test Mowrer's "two-factor" theory of avoidance learning. In avoidance learning, a conditioned stimulus (such as a tone) is followed by prolonged shock as an unconditioned stimulus. If the animal makes a certain conditioned response (such as moving from one side of the shuttlebox to the other) after the onset of the US, it can turn the US off; termination of the US constitutes reinforcement of an escape response. If it makes the CR after the onset of the CS, but before the onset of the US, the US is prevented from occurring at all; this reinforces an avoidance response. Martin Seligman and his colleagues discovered that prior exposure to inescapable shock interfered with escape and avoidance learning. In their analysis, prior experience with inescapable shock taught the animal that shock was uncontrollable, and this learning generalized to the new situation of the shuttlebox. The learned helplessness experiments underscore the principle that in instrumental conditioning the organism is learning to control its environment.
The animals in these experiments learned to be helpless, but Seligman and his colleagues also observed that they looked and behaved as if they were "depressed" (if you've ever seen a sad dog, you know what they meant). This led Seligman to propose that learned helplessness is a laboratory model for some forms of depression -- i.e., that some people become depressed by virtue of a history of uncontrollable aversive events in their lives.
Subsequent research by
Seligman and others, including Steven Maier, Lyn Abramson, and
Lauren Alloy, identified a number of parallels between learned
helplessness and depression:
- Symptoms: depression, like LH, is characterized by symptoms of passivity, negative expectations, lack of aggression, and loss of appetite and sexual interest; in both learned helplessness and depression, these symptoms dissipate with time.
- Cause: some depressives, like animals in the LH experiments, have histories of life experiences from which they learned that outcomes were independent of their behavior.
- Cure: depression, like LH, can often be overcome by treatments that change the patient's beliefs and expectations (this is what cognitive therapy explicitly tries to do). Just as electroconvulsive therapy (ECT) can successfully treat depression, so electroconvulsive shock (ECS) can alleviate LH. Just as depressed patients respond to antidepressant drugs, so helpless animals respond positively to drugs that stimulate the norepinephrine system.
- Prevention: individuals who are relatively invulnerable to depression often have a life history characterized by many mastery experiences; similarly, animals can be "inoculated" against LH by giving them prior experience with control.
- Biological Substrates: animals who have undergone LH treatments give evidence of norepinephrine depletion.
learned helplessness model of depression, as originally
formulated, is not complete, and nobody claims that LH
underlies all forms of depression. But Abramson and Alloy have
suggested that a certain type of depression, which they label
helplessness depression, is caused by the kinds of
experiences modeled in the LH experiments.
Alloy, and their colleagues subsequently modified Seligman's
theory with the hopelessness theory of depression.
They argued that the experience of uncontrollable aversive
events was not enough to make people (or dogs, for that
matter) depressed. Sometimes, people (and dogs) respond to
uncontrollable aversive events with anger, instead.
Abramson and Alloy
proposed that uncontrollability led to depression only when
the individual made a certain causal attribution
concerning the uncontrollability. They argued that the
explanations that people make for various events vary on
- Internal vs. external -- does responsibility for the event lie with the person himself, or with some external agent?
- Stable vs. variable -- does the event always work out that way, or is the outcome sometimes different?
- Global vs. local -- is it everything that goes this way, or just some specific thing.
They proposed that uncontrollability causes depression only when the individual makes an internal, stable, global attribution for the helplessness -- as if to say, I can't control this thing, it's my fault that I can't control it, I can never control this or anything else. If you thought like this, you'd get depressed, too, and that's the point.
Abramson and Alloy pointed out that, in contrast to non-depressed people, depressed people are often starkly realistic about their inability to control events -- a characteristic of depressive realism that they contrasted to the illusion of control that is characteristic of non-depressed thought. That is, non-depressed individuals often have an unrealistically elevated sense of control (which is why many of us think we can control chance events by picking "lucky" lottery numbers), while depressed individuals are often quite realistic about the prospects.
Abramson and Alloy identified this pessimistic attributional style as a risk factor for what they called hopelessness depression. They and their colleagues also constructed a personality questionnaire, the Attributional Style Questionnaire (ASQ) to identify people who might be "at risk" for depression, based on this aspect of cognitive style.
Seligman, for his part, took off from his studies of helplessness and depression to focus on the other side of things, and proposed that positive psychology should focus on the sunny side of life, and the positive characteristics that enabled people to be resilient in the face of unpleasant circumstances. In particular, Seligman has proposed that giving experiences of control to children who are at risk for depression (by virtue of their pessimistic attributional style) may help these children avoid actual episodes of depression.
In the domain of the psychoses,amphetamine psychosis can serve as a laboratory model of schizophrenia. High doses of amphetamines, which increase dopamine activity in the brain, lead to psychological symptoms similar to those found in acute schizophrenia -- hallucinations, thought disorder, and paranoid delusions. The behavioral parallels between amphetamine psychosis and schizophrenia is one source of the dopamine hypothesis of schizophrenia, discussed below.
Hypnosis and "Hysteria"
While most laboratory
modeling has focused on various anxiety disorders, some
investigators -- again, beginning in the late 19th and early
20th century -- noticed a phenotypic similarity between some
of the phenomena of hypnosis (e.g., suggested blindness,
deafness, and analgesia; suggested paralysis; posthypnotic
amnesia) and some of the characteristic symptoms of
"hysteria", a cluster of syndromes now known as the
dissociative and conversion disorders.
- In both hypnosis and "hysteria", pseudoneurological "symptoms" occur in the absence of brain insult, injury, or disease.
- Both hypnosis and "hysteria" affect explicit, conscious perception, memory, and action (like conscious perception or recall), while largely sparing their implicit counterparts (like priming).
This has suggested that understanding
the mechanisms of hypnosis might help us to understand these
forms of mental illness as well. In fact, it's been proposed
that both the dissociative and conversion disorders result
from a division of consciousness that prevents certain
percepts and memories from being represented in conscious
Linking Laboratory Models to Psychological Deficits
laboratory models and studies of psychological deficit go
hand-in-hand. Consider experimental research on psychopathy,
or antisocial personality disorder. One feature of psychopathy
is that these individuals tend not to be responsive to
aversive stimulation. On experimental tests, psychopaths often
show a failure of avoidance learning, and they also show a
failure to respond to punishment. Gorenstein and Newman (1980)
observed a similar pattern of behavior in laboratory rats who
had surgical lesions in a subcortical area of the brain known
as the septum. Rats with septal lesions do not freeze
when they are punished, they have difficulty with passive
avoidance learning (i.e., learning not to do something
in order to avoid punishment), and they also have difficulty
with delay of gratification. All of these phenomena, of
course, closely resemble the characteristic symptoms of
psychopathy. This has led to a theory that, by virtue of some
kind of brain disorder, psychopaths, like septal rats, are
unable to suppress habitual behaviors in order in order to
avoid the aversive consequences of these behaviors.
Experimental research by Newman and
others have further clarified the psychological deficit in
psychopathy to problems linking attention to the reward
system. In one experiment, subjects played a
computerized card game: if they turned over a card they would
gain a point if it was a face card, and lose a point if
not. The deck was arranged so that 9 of the first 10
cards were face cards, then 8 of the next ten, 7 of the next
10, and so on, and they could stop whenever they wanted.
Of course, with the deck arranged in this manner, the subjects
began accruing lots of points, and then started losing.
Normal subjects generally stopped playing after about 50
cards, while they were still ahead; but the psychopaths
continued playing, losing everything they had won -- and more.
Newman's latest theory of psychopathy
implicates attention rather than reward per se. The
general idea is that psychopaths have difficulty updating
working memory with new information, once their attention has
been engaged. They can focus attention, but they can't
disengage and shift it very easily.
Still, there does seem to be something
missing in psychopaths' emotional lives. They don't
accurately pick up on other people's facial and vocal
expressions of emotion, especially fear; don't respond
normally to words with positive or negative emotional
Returning to Newman's septal rats, Kent
Kiehl (2006) has used fMRI to record brain activity in
psychopaths during various types of tasks. He has found
deficits in a a system of subcortical brain areas known as the
- the anterior cingulate, which is important for decision making and other aspects of executive control;
- the amygdala, which generates emotional responses, especially fear;
- the orbitofrontal cortex, important for learning under conditions of reward and punishment;
- the posterior cingulate, involved in emotional processing;
- the insula, which mediates perception of pain and other bodily states;
- the temporal pole, involved in the integration of emotion and perception.
For more on psychopathy, see "Inside the Mind of a Psychopath" by Kent A. Kiehl and Joshua W. Buckholtz, Scientific American Mind, September-October 2010.
Linking the Laboratory and the Clinic
We're going to get back to the clinic in a moment, but the point of this whole exercise is that the clinical enterprise of understanding and treating mental illness is not divorced from the sort of basic research that goes on in university laboratories. We can use various research paradigms of the sort discussed earlier in this course -- classical and instrumental conditioning, dichotic listening, and the like -- to understand the basic mechanisms by which mental illness occurs -- as well as ways in which we might more effectively treat mental illness and prevent it from occurring in the first place.
By virtue of basic laboratory research we can move beyond the surface signs and symptoms of mental illness to understand its underlying pathology. And by better understanding its underlying pathology, we will be able to formulate better theories of the causes and cure of mental illness, and better tools for diagnosis, treatment, and prevention.
In fact, laboratory
research helps us to identify two different ways that mental
illness can occur.
- Some forms of psychopathology reflect psychological deficits -- disruptions affecting basic psychological functions.
- Schizophrenia seems to involve malfunctioning of the attention system.
- Autistic children (and adults) appear to lack a theory of mind.
- Major forms of depression may be caused by a defect in the system affecting positive or negative affect.
- Attention-deficit disorder also, obviously, seems to involve a malfunctioning of the attention system -- though presumably a different malfunction from the one implicated in schizophrenia.
- Other forms of psychopathology reflect maladaptive social learning, in the absence of any particular psychological deficits. The mind is working OK, but the person has somehow acquired maladaptive knowledge, expectations, and beliefs.
- In phobia, the person has learned to fear and object that is not, objectively fearsome.
- In obsessive-compulsive disorder, the person performs an avoidance response that isn't, objectively, necessary.
- In hopelessness depression, the person makes inappropriate causal attributions for unpleasant events.
- Some of the psychophysiological disorders appear to reflect the effects of environmental stress on internal organs supplied by the autonomic nervous system -- effects that might not occur of the person learned how to handle stress better.
The Biology of Mental Illness
Where mental illness appears to reflect maladaptive social learning, we generally assume that the architecture of the individual's basic mental structures and processes is largely intact, as are the neural substrates of that mental architecture. However, where mental illness appears to reflect an underlying psychological deficit, there are good reasons to think that the neural substrates of that mental architecture are malfunctioning as well -- that is, that the mental disorders are ultimately neurological disorders. This idea is expressed in Ralph Gerard's old adage that
"behind every twisted thought there lies a twisted molecule".
The idea that mental illness have
underlying biological causes goes back at least as far as the
19th century -- which is to say, it is almost as old as
scientific medicine and scientific psychology themselves. In
fact, the history of psychiatry and clinical psychology may be
characterized as a cycle in which prevailing views alternate
between "somatogenic" theories that mental illness is due to
biological causes (i.e., brain insult, injury, or disease) and
"psychogenic" theories that mental illness is due to
environmental causes, and that the biology of the nervous
system is no more relevant to mental illness than it is to
normal mental and behavioral functioning.
From Somatogenesis to Psychogenesis and Back
The earliest scientific theories of
mental illness were neurological theories, based on the
assumption, mostly unproven, that patients' symptoms were due
to lesions or infections affecting brain tissue.
With the emergence of Freudian
psychoanalysis, in the late 19th and early 20th centuries, the
predominant theory of mental illness shifted from somatogenic
to psychogenic. Put briefly, Freud and his followers
taught that mental illnesses, particularly the neuroses, had
their origins in conflict and defense. Psychoanalysis,
both Freudian and neo-Freudian, dominated psychiatry well into
Another important influence on American
psychiatry was Adolph Meyer, who argued that mental patients'
problems had their origins in their life histories, not their
The pendulum began to shift back toward somatogenesis in the 1950s, with the introduction of the first psychotropic ("mind-moving") drugs: Thorazine (1954), a "major tranquilizer" used in the treatment of schizophrenia; Milltown (1955), a "minor tranquilizer" used to treat anxiety; and Marsilid (1957), a "psychic energizer" used in the treatment of depression. These drugs were discovered more or less accidentally, but it was soon learned that they (and other drugs like them) altered the levels of certain neurotransmiters in the brain. This led to the hypothesis that schizophrenia, depression, and other forms of major mental illness were caused by abnormal levels of these substances.
Let us just note, in passing, that the
logic of this inference is far from airtight. In fact,
it's a variant on the logical error of denying the
antecedent, discussed in the Lecture Supplement on Thinking. The logic
seems to go something like this.
- Thorazine relieves the symptoms of schizophrenia.
- Thorazine decreases dopamine levels in the brain.
- Therefore, schizophrenia must result from excessive dopamine levels in the brain.
The problem is that the efficacy of a
treatment says nothing about the cause of the illness.
Nobody thinks that a lack of aspirin causes fever to occur.
And, as it happens, the evidence for the
dopamine theory of schizophrenia, and similar theories, is not
completely convincing. There has never been any
convincing demonstration that, prior to treatment,
schizophrenics or depressives actually suffer from any kind of
chemical imbalance in their brains. Still, theories
about chemical imbalances remain very popular.
In fact, over the past 100 years or so,
biological causes have been uncovered for a number of mental
illnesses, whose biological causes were unknown at the time
they were described, and which had previously been attributed
to environmental causes. In this way, some "functional" mental
illnesses have been reclassified as "organic" in nature.
- The first of these was a form of dementia associated with syphilis, a venereal disease, and which is now known to be caused by infection by the syphilis spirochete, and which can be cured by timely administration of antibiotics.
- Alzheimer's disease, once labeled as presenile dementia, is now known to be caused by the build up of plaques and tangles in brain tissue.
- Autism, a developmental disorder once known as Kanner's syndrome, was once attributed to poor parenting -- and especially by so-called "refrigerator mothers" (it's always the mother, isn't it?) who failed to display emotional warmth toward their children. This was the theory proposed by Bruno Bettelheim, a prominent psychoanalyst, and is now known to be completely wrong (the score is now "Psychoanalysis Zero", while scientific Psychology is batting much closer to 1000). Kanner himself, who first described the syndrome in 1943, believed that it was caused by bad parenting. These beliefs did not change until autism was diagnosed in the first child of Bernard Rimland, a biologically oriented psychologist, and his wife. They knew that they hadn't been bad parents, not least because their child had been autistic since birth -- that is, before they had even had a chance to be bad parents. In 1964, Rimland published Infantile Autism, a classic monograph on the subject, in which he proposed that autism had an organic cause. Although we still do not know what the precise causes of autism are, we are now quite certain that they lie not in the environment, or in the patients' childhood experiences, but presumably reflects malfunctioning in certain brain systems.
Current Biological Approaches to Mental Illness
According to the dopamine
hypothesis of schizophrenia , the symptoms of
schizophrenia, and their underlying psychopathology, are
caused by excess activity of dopamine, a neurotransmitter
substance. Evidence for the dopamine hypothesis includes:
- increased levels of dopamine metabolites in schizophrenic patients;
- the positive effects of antipsychotic medications, many of which operate to reduce dopamine levels.
In fact, autopsy studies, and also some brain imaging studies, indicate that there are increased levels of dopamine metabolites in schizophrenic patients. And that's consistent with the dopamine hypothesis. Moreover, phenothiazine drugs, which are used in the treatment of schizophrenia, block the neural receptors for dopamine, impairing the uptake of dopamine by post-synaptic neurons. So the fact that there are increased levels of dopamine metabolites found in schizophrenic patients, and that antipsychotic medications operate to reduce dopamine levels -- these are both factors that are consistent with the dopamine hypothesis of schizophrenia.
another piece of evidence comes from a laboratory model of
schizophrenia known as amphetamine psychosis. Solomon Snyder and
his colleagues, working at the National Institute of Mental
Health, found that the administration of certain drugs known
as amphetamines can actually produce some of the symptoms of
psychosis, particularly schizophrenia, in rats and other
laboratory animals. They
also noticed that the habitual heavy use of amphetamines by
humans can produce some of the symptoms of schizophrenia as
well -- particularly hallucinations, thought disorder, and
amphetamine drugs, such as Benzedrine (amphetamine),
Dexedrine (dextroamphetamine), and methedrine
(methamphetamine) may cause the user to experience
hallucinations, while habitual, heavy use can cause thought
disorder and paranoid symptoms as well.have
the effect of increasing dopamine activity in the brain. So this laboratory
model -- first studied in rats, then in monkeys, and then in
humans who abuse amphetamine recreationally -- provides
further support for the dopamine hypothesis of
schizophrenia.In these ways, amphetamine psychosis
seems to mimic at least some of the symptoms usually
associated with schizophrenia.
According to the monoamine
hypothesis of depression, the symptoms of depression,
and their underlying psychopathology, are caused by lowered
levels of another class of neurotransmitters, the monoamines,
which include norepinephrine and serotonin. Evidence for the
monoamine hypothesis includes:
- decreased levels of monoamine metabolites in depressed patients;
- the positive effects of antipsychotic medications, many of which operate to increase the levels of monoamines in the brain; in particular, the selective serotonin reuptake inhibitors, effectively increase the availability of serotonin by preventing premature reuptake of the neurotransmitter by presynaptic neurons.
Is Depression Adaptive?
Depression is so frequent (it has been called "the common cold of psychiatry"), and has been around for so long (Robert Burton published The Anatomy of Melancholy in 1621), that some evolutionary psychologists have suggested that, counter-intuitively, a tendency toward depression might actually be an adaptive trait. According to one argument, the ruminative thinking that is one of the characteristic symptoms of depression facilitates problem-solving. The only problem is that depressives don't solve their problems -- they just stay depressed.
Actually, that's just one of the problems
with the evolutionary argument. Here are some others:
- It's not clear that clinically depressed patients are all that good at thinking and problem-solving. Most of the research either involves experimentally manipulated emotional states, or states of mild depressed mood that aren't anywhere near clinical severity.
- Moreover, the evolutionary argument assumes that depression is somehow a response to some kind of instigating psychosocial event -- i.e., whatever problem the patient is confronting in his or her environment. But sometimes depression just happens, and it's difficult or impossible to find an instigating event of sufficient magnitude to cause such a severe change in mood.
- Even assuming that there is such an event, clinically significant depression is typically a chronic condition -- you'd think that, if depression helped people solve the problems that set their depression off in the first place, it wouldn't come back so readily.
- And finally, a significant proportion of depressed patients -- not all, or even a majority, but enough -- commit suicide (or attempt it). And suicide is definitely maladaptive (though I suppose that evolutionary psychologists could make up a just-so story about the adaptiveness of suicide, as well!).
This points out the problem with the adaptationist fallacy that lies at the heart of so many speculations by evolutionary psychologists. Depression exists as a human psychological trait, human psychological traits, like human physical traits, a product of natural selection; therefore, depression must be adaptive in the Darwinian sense. A similar argument has been made about homosexuality (which, of course, isn't a mental illness), and even about grandmothers (who aren't necessarily mentally ill either!). But the whole thing begins with a fallacious assumption, which is that every human trait, whether biological or psychological, but be adaptive.
It should be understood that these are only hypotheses about the underlying biology of these syndromes, and that these hypotheses are surely incomplete.
And sometimes biological hypotheses are just wrong. In 1998, a paper published in Lancet by Andrew Wakefield, a British physician, suggested a link between autism and the childhood vaccine for measles, mumps, and rubella (MMR). The resulting concern led to a worldwide reduction in MMR vaccination, as parents hoped to prevent their children from getting autism. The methodology of the study was subsequently criticized, and 10 of Wakefield's 12 co-authors subsequently retracted the paper -- as did the journal in which it was originally published, and Wakefield lost his license to practice medicine in Britain (he relocated to the US). In 2011, an investigation published in the British Medical Journal asserted that Wakefield's paper was not just methodologically weak but actually fraudulent.In fact, subsequent, better designed studies show that there is no evidence for a role of MMR or any other childhood vaccination in autism. Nevertheless, as of 2011, Wakefield (who has relocated to the US) continues to assert such a link, and worldwide MMR vaccination rates have never returned to their pre-1998 levels -- increasing the risk of childhood diseases that are entirely preventable.
For an excellent introduction to the roe of neurotransmitters in mental illness, and the basics of psychopharmacology, see Drugs and the Brain (Rev. Ed., 1996) by Solomon Snyder, one of the deans of psychopharmacology. Because the pharmaceutical industry is constantly developing new products, the information on specific drugs is necessarily a little dated. But the basic ideas haven't changed much, and neither has the underlying neuroscience. It's a good place to sstart..
Etiology of Mental Illness
Somatogenic and psychogenic theories of mental illness are, first and foremost, theories about the role of nature and nurture, and we have now learned that the proper formulation is nature-nurture questions is not "Which is right?" but rather "How do nature and nurture interact?". The etiology of mental illness is no exception.
Genetics of Mental Illness
One place to look for the origins of psychopathology is in the genes: perhaps certain forms of mental illness, or at least risk factors for them, are passed through families through genetic inheritance. We know that, for many diagnoses, having a family member with mental illness increases the risk for mental illness in other family members. Of course, this effect could be environmental as well as genetic.
The genetic contribution to mental illness can be assessed by means of the twin-study method described in the lectures on Psychological Development: by comparing the similarity of MZ and DZ twins, we can estimate the contributions of genetics, the shared environment, and the nonshared environment. When it comes to personality characteristics, such as the Big Five personality traits, similarity is measured by means of the correlation coefficient. In psychiatric genetics, similarity is more commonly measured by means of the concordance rate -- that is, the probability that two twins will have the same psychiatric disorder. The calculations for heritability differ a little, but the underlying logic is the same:
- If a mental illness is completely inherited, the
concordance rate for MZ twins should be 100%, and for DZ
twins should be 50%.
- To the extent that the MZ concordance rate is less than a perfect 100%, there is a contribution from the nonshared environment.
This table reflects our best understanding of the heritability of major forms of mental disorder, as of 2012. The heritability coefficients vary widely, from a low of .37 for Major Depressive Disorder to a high of .80 for Autism Spectrum Disorder and .81 for Schizophrenia. Note, however, two points about this table:
- There are many forms of mental illness that are not represented here -- either because they have not been studied, or because existing research has yielded low heritability coefficients.
- None of the heritability coefficients is a perfect 1.0. Even for autism and schizophrenia, genetics is not destiny, and there are plenty of families with an autistic or schizophrenic family member where the rest of the family has no significant mental illness.
So, as is generally the case, the
origins of mental illness are not to be found in the genotype
alone. Rather, they will have to be found in gene-by-environment
Still, once researchers have established
a significant level of heritability for a mental illness, it
makes sense to start searching for the genes responsible (for
a review, see Duncan et al., 2014). Before the 21st
century, this was not really possible. We didn't know
enough about the human genome, and we didn't have the
technology. And even with the mapping of the human
genome, and the availability of (relatively) inexpensive
technology, the task is daunting:
- There are some 20-25,000 candidate genes -- not to mention all that "intergenic" and "intronic" regions in the genome that are not, technically, genes.
- To obtain reliable results, researchers typically need huge sample sizes.
Until recently, researchers had to propose, on the basis of some theory, what genes to look for. So, for example, if they were interested in schizophrenia, they might look at genes that are involved in the production and metabolism of the neurotransmitter dopamine; for depression, they might look for genes involved with the production and metabolism of the neurotransmiters norepinephrine or serotonin. This is known as the candidate gene strategy. However, advances in technology have permitted researchers to go on "fishing expeditions" in which they cast their nets more widely, over thousands or millions of candidate genes and their variants, in what are known as genome-wide association studies (GWAS). These studies have begun to yield results -- and, interestingly, they have been turning up evidence of genes involved in mental illness other than those "candidates" hypothesized by various biochemical theories of mental illness!
It's pretty clear that the search for
"the gene" that is "for" schizophrenia, or any other form of
mental illness, is going to be complicated (Duncan et al.,
- In the first place, there's almost certainly no such
single gene, not for any form of mental illness.
Instead the genetic contribution is more likely to be polygenic
in nature, consist of the accumulation of many different
- For example, there are at least 40 different genetic loci associated with height.
- A recent GWAS identified more than 100 different
genetic loci, and more than 8,000 genetic variants on
these loci, associated with increased risk for
- And these genes, themselves, are not "for" mental
illness in any sense. Any single gene will have
different effects, depending on its local (physical)
- For example, one of the gene loci associated with
schizophrenia also plays a role in the auto-immune
- Genetic influences may be pleitropic, meaning
that a single genetic variant may have more than one
- For example, some genetic loci are associated with both schizophrenia and bipolar disorder, suggesting that they may well be risk factors for major mental illness (or psychotic disorders) generally.
- Some genetic factors may be rare variants,
present in only a very small number of individuals.
- And then there is the problem of missing
heritability -- that is, the difference between the
proportion of variance in some phenotype (such as
schizophrenia) that is explained by heritability, and the
proportion explained by specific genetic variants.
- For example, we know that approximately 80% of
population variability in height is accounted for by
genetic factors; but the specific genetic loci "for"
height discovered so far account for only 5% of
population variance -- leaving 75% of genetic
- And finally, there are the problems of epigenetics discussed in the lectures on Psychological Development.
Once we've determined that there is, in
fact, a genetic contribution to some mental illness, the next
step is to determine what genes are involved. I say
"genes", plural, because it's clear that there's no single
gene "for" schizophrenia, like the gene for blue or brown eyes
presented in standard elementary accounts of Mendelian
genetics. Rather, much as wth intelligence, the genetic
basis for schizophrenia is most likely to involve the
cumulative effects of many genes -- dozens, perhaps hundreds.
Recent advances in understanding the
genetics of schizophrenia offer interesting insights into the
genetic contribution to mental illness more generally.
These advances have been made possible by the Human Genome
Project, which in 2003 delivered a map of the human genome,
indicating the location of each of our roughly 22,500 genes on
our 23 chromosome pairs. Then began the process of
determining the function of each of these genes. Over
the years, gene-mapping has become less expensive and
time-consuming, so it is now possible to search the genomes of
large numbers of individuals for genes that are associated
with various illnesses, employing such techniques candidate
gene association, common variant association,
and copy number variation.
This isn't a course in genetics, and if you want details of each of these methods, there's an excellent, highly accessible account of this work in "Runs in the Family" by Siddhartha Mukherjee (New Yorker, 03/28/2016), and a more technical survey in "Genome-Scale Neurogenetics Methodology and Meaning" by McCarroll, Feng, and Hyman (Nature Neuroscience, 2014). This discussion is largely drawn from these sources.
With data available on a very large number of individuals, investigators are able to identify asociations between schizophrenia (and other forms of major mental illness, such as bipolar disorder and autism) with various portions of the human genome. This task has been undertaking by a group known as the Psychiatric Genomics Consortium (PGC). The "Manhattan plot" at left (so named because it looks like the New York City Skyline), taken from one such study involving more almost 37,000 patients and more than 110,000 controls, sampled from 20 countries, shows which specific loci on each chromosome is significantly associated with schizophrenia (Sekar et al., Nature 2016). Of course, with 22,500 genes, a number of these associations could appear just by chance, so the investigators employed appropriate statistical corrections. .
- As expected, based on the hypothesis of polygenic
inheritance, there were lots of such segments -- more than
100, in fact..
- Some of these gene loci are known to be associated with
certain neurotransmitters, and others were associated with
axonal transmission and other activity within individual
neurons. Presumably, particular alleles of these genes
predispose the individual to schizophrenia (or bipolar
disorder, or autism, etc.) -- and as more of these alleles
accumulate in the individual's genome, his or her risk for
major mental illness increases.
These sorts of findings would be
expected if, as most theorists believe, major mental illness
is fundamentally a disorder of the central nervous system. But
other findings were more surprising. For example, the
strongest association (the talest "skyscraper" in the
Manhattan plot above) was on Chromosome 6, in a region known
as the major histocompatibility complex (MHC), whose genes are
linked to the immune system. But how do we get from
the immune system to schizophrenia? Here's one
prominent theory (Sekar et al., Nature, 2016).
- The immune system protects the body against disease by detecting and attacking varous pathogens in the body. The genes in question control what are known as complement components (CCs), which identify varous viruses, bacteria, and the like for destruction by immune cells. However, CCs also identify synapses for destruction. But why would anyone want to destroy synapses?
- Actually, this is a major feature of neural development. During the course of fetal development, brain activity creates large numbers of synaptic connections, ready for use when the newborn infant encounters the world. During learning, neurons that fire close together in space and time (remember long term potentiation?) strengthen their synaptic connections; other, unused synaptic connections are lost, in a process known as pruning (as in pruning trees and bushes). This pruning process, which goes on for about the first 30 years of life, is a normal process of neural development and plasticity. The same CCs that identify pathogens for destruction also identify synapses for pruning.
- A gene in the MHC region of Chromosome 6, known as C4,
comes in two forms, known as C4A and C4B, and individuals
vary in terms of how many C4A and C4B genes they have, and
in what combinations. C4A and C4B generate
- A particular variant on C4 elevates the risk for schizophrenia from 1% to 1.27%. Yes, you read that right. An elevation of 27%, which sounds like a lot, but in absolute terms still a very small risk. So C4 alone is not by any means the solution to the genetics of schizophrenia.
- About 27% of the schizophrenic patients in the PGC study
had this variant on C4. But so did 22% of the normal
- Mice that lack the C4 gene underprune their
- And it is known that the brains of schizophrenic patients
contain fewer synapses than those of normal controls.
- A certain combination of C4 alleles promoting excessive
- This overactivity in the CC system identifies too many synapses for pruning.
- Overpruning of synapses results in the dificulties in attention and thinking that are characteristic of schizophrenia.
- The normal process of synapse-pruning begins at birth and
continues for 20-30 years. Thus, overpruning of
synapses results in the typical onset of schizophrenia in
late adolescence or the patient's 20s and 30s (schizophrenia
used to be called dementia praecox, or "early
Understand: I'm not saying that this
theory is the neuroimmunological cue to the secret of the
origins of schizophrenia. It might very well be wrong --
just like most past hypotheses concerning the genetic origins
At the same time, other researchers have
turned their attention to the environment, and in particular
to those features of the environment that interact with one's
For more on the search for the genetic basis of schizophrenia, including a plea that researchers spend more time searching for environmental factors that might interact with genetic predispositions, see "Schizophrenia's Unyielding Mysteries" by Michael Balter, Scientific American, 05/2017.
The Diathesis-Stress Model
The origins psychopathology (etiology) may be viewed within the framework of the diathesis-stress model of psychopathology proposed initially by Meehl (1962) and Rosenthal (1963), and elaborated more recently by Monroe and Simons (1991) and Belsky and Pleuss (2009). According to the model:
- Diathesis represents a predisposition toward a specific breakdown in normal mental functioning. Its source may lie in the person's biological (genetic -biochemical) endowment, experiential history of social learning, or both. The diathesis renders the person vulnerable to, or at risk for, some specific form of psychopathology (not psychopathology in general). Every person achieves a more or less successful adaptation to this genetic or psychosocial "inheritance".
- Stress refers to any event (or series of events) which challenges the person's current level of adaptation to the diathesis. Again, stress factors may be either biological or psychosocial in nature.
- The interaction of diathesis and stress precipitates an acute episode of mental illness -- what used to be called a "nervous breakdown".
- Looking backward from the acute episode, we can examine the patient's level of premorbid adjustment, or what is sometimes called premorbid personality. In medicine, the term "premorbid" refers to the patient's status before he or she became ill.
- Individuals with good premorbid personality have "inherited" relatively little diathesis, whether through genes or social learning, or made a relatively successful adjustment to a relatively high level of diathesis.
- Individuals with poor premorbid personality have "inherited" a relatively high amount of diathesis, or made a relatively unsuccessful adjustment to a relatively low level of diathesis.
The diathesis-stress model of psychopathology is a special case of the person-by-situation interaction, where diathesis is an attribute of the person and stress is an attribute of the environment.
In principle, diathesis and stress factors could combine in a number of ways.
In an additive model, diathesis and stress are independent of each other, and the likelihood of an acute episode is simply a function of the sum of diathesis and stress factors. Following Lewin, we might symbolize this situation as E =f(D + S).
- For individuals carrying substantial levels of diathesis, relatively little stress would be required to precipitate an acute episode of mental illness, and the individual would likely show relatively poor premorbid adjustment.
- On the other hand, catastrophic levels of stress would likely produce an acute episode even in individuals who carry little or no pre-existing diathesis, and who would show relatively good premorbid adjustment.
- If diathesis levels are within normal limits, an acute episode would occur as a function of stressors in the individual's life.
- If stressors are within normal limits, an acute episode would occur as a function of the individual's level of diathesis.
Note that diathesis factors are
specific to particular forms of mental illness. In theory,
some particular diathesis predisposes an individual to
schizophrenia, but other specific diathesis would be relevant
to depressive disorder, anxiety disorder, etc. In this way, if
stress precipitates an acute episode of mental illness, that
illness will take a specific form.
Diathesis and Stress in Theory and Practice
Schizophrenia. The diathesis-stress approach was first articulated in the context of schizophrenia. With respect to diathesis, there is a clear genetic component to schizophrenia. Compared to a base rate of about 1% in the population at large, the concordance rate for schizophrenia is clearly elevated among relatives. In monozygotic twins, the concordance rate is about 38%; for dizygotic twins, 8%. Risk for schizophrenia is also increased if a first-degree relative (father, mother, brother, sister) is schizophrenic. Among adoptees, risk is increased if one's biological parent has schizophrenia, but not if one's adoptive parent has schizophrenia. These figures are consistent with the proposition that people can inherit a predisposition to schizophrenia. But note that the concordance rate is far from a perfect 100% (in fact, it appears to be far from even 50%), suggesting that genes are not solely determinative . Any difference between monozygotic twins must be due to the unshared environment, and that is where differences in stress probably come into play. In any event, schizophrenia appears to occur as the product of the combination is of a shared genetic diathesis and an unshared environmental stress.
Rosenthal (1963) originally got his idea about diathesis and stress from the Genain Quadruplets -- identical quadruplet girls, born in 1930 into a family with a history of mental illness, three of whom were hospitalized for schizophrenia on at lest one occasion. "Genain" is a pseudonym, derived from the Greek words for "dire birth", intended to protect the identity of the girls and their family. Because they were studied intensively at the National Institute of Mental Health, they are known as Nora, Iris, Myra, and Hester. What was particularly interesting about the twins was that not all of them fell ill -- at least, Myra was never actually hospitalized. Thus, schizophrenia is not purely a result of genetics -- or else, these identical twins would all have had identical outcomes. Instead, Rosenthal hypothesized that a genetic diathesis interacted with some environmental stress to precipitate schizophrenia in some of the children, but not in all.
One environmental stressor that has been implicated in schizophrenia is socioeconomic status: schizophrenia is rare, affecting less than 1% of the population, but it is more likely to be observed in individuals with relatively low socioeconomic status. One theory is that the stresses of lower-class living interact with a genetic diathesis for schizophrenia, resulting in the higher incidence -- an idea known as sociogenesis. However, careful epidemiological studies have shown that low SES follows, rather than precedes, the onset of schizophrenia. That is, schizophrenia occurs in all socioeconomic strata, but when it happens to upper-class individuals, they tend to drift down to lower socioeconomic strata -- a phenomenon known as social drift.
However, the failure of the sociogenic
hypothesis does not rule out environmental contributions to
schizophrenia. Other environmental influences that have been
causally linked to schizophrenia include:
- Coping failures, including losses and frustrations of various sorts. Loss, frustration, and coping failure do not by themselves cause schizophrenia, but they appear to be the sorts of things that can precipitate an episode of schizophrenia in someone who is at risk for it.
- Expressed emotion: Schizophrenics who have recovered from an episode of the illness, and then are discharged into a home environment in which criticism and other negative affect is directed at them, or family members and others become overly emotionally involved with the patient, are more likely to relapse, and have another episode.
- Lack of Social Support: Schizophrenia is often
associated with a poor prognosis, and the expectation that
schizophrenia is a chronic disease from which patients
never recover. But it turns out that it's possible
for schizophrenics to make a pretty good re-entry into
ordinary, everyday life -- especially if they had made a
good premorbid adjustment before their initial
episode. One key to this recovery is medication, for
symptom control. But another key, equally important,
is social support. If schizophrenic patients learn
to cope with their residual symptoms, and they receive the
support and encouragement of family, friends, neighbors,
and coworkers, the prognosis for successful recovery is
actually pretty good (think about John Nash, subject of A
Beautiful Mind by Silvia Nasr, who won the Nobel
Prize in Economics). If social support can lead to
successful recovery, the implication is that social
support might have prevented the initial episode in the
One environmental stressor that has received a great deal of research attention is deviant communication: Vague and fragmented verbal exchanges, especially on the part of family members. A longitudinal research project known as the Finnish Adoptive Family Study of Schizophrenia examined the long-term outcome of "high risk" children who were born to 167 women hospitalized for schizophrenia and control children born 202 women hospitalized for other illnesses. On medical advice, the children of these women were given up for adoption. In one study, Wahlberg, Wynn, and their colleagues tested the adoptive families for signs of communication deviance, and then tested the adopted children themselves (known in medical terminology as "probands", because their family history gives them an elevated probability of becoming ill) on an index of thought disorder characteristic of schizophrenia.
- When there was little communication deviance in the adoptive family, the high-risk probands of the schizophrenic women showed little evidence of thought disorder.
- But with increased levels of communication deviance in the adoptive family, the incidence of thought disorder in the schizophrenic probands progressively increased -- but no such increase was seen in the non-schizophrenic probands.
This is exactly the kind of person-environment interaction anticipated by the diathesis-stress model: the combination of high genetic risk (being the child of a schizophrenic mother)and high environmental stress (being exposed to communication deviance in one's adoptive family) leads to increased occurrence of schizophrenic symptoms. No such trend occurred, however, in children who were not already at risk for schizophrenia.
Now look carefully at the graph. Note that the level of communication deviance in the adoptive families of control children "maxes out" at 8 units, while the level observed in the adoptive families of the high-risk probands goes as high as 10 units. Perhaps, by some stroke of bad luck, these high-risk probands were adopted into families who were carrying more than their fair share of schizophrenic diathesis. More likely, the high-risk probands contributed to the high levels of communication deviance observed in their adoptive families -- communication deviance that might not have been present, but for the probands themselves. Perhaps this is another instance of the person creating the environment to which s/he responds.
Mood Disorder. Studies of
bipolar and (especially) unipolar affective disorder show the
same patterns: clear evidence for a genetic diathesis, but
equally clear evidence for an unshared environmental stress
(we cannot calculate the contributions of genetics, shared
environment, and nonshared environment from concordance rates
in exactly the same way you can for twin correlations, but the
logic is the same).
Ulcers. The diathesis-stress
approach is also relevant to psychosomatic ulcers,
where lesions in the lining of the gastrointestinal system
(that's what peptic ulcers are) occur to people who are under
a high amount of stress.
- Gastric ulcers affect the lining of the stomach.
- Duodenal ulcers affect the lining of the small intestine (or duodenum).
- There are also esophageal ulcers, which don't concern us here.
The psychosomatic nature of peptic ulcers has recently been discounted by some physicians, who note the presence of a particular bacterial infection,helicobacter pylori, in the stomachs and small intestines of as many as 80% of ulcer patients. But while almost everyone who suffers from ulcers is infected with h. pylori, not everyone infected with h. pylori has ulcers. In fact,h. pylori is also found in the gastrointestinal systems of 70% of patients who do not have ulcers! What makes the difference? Plausibly, stress. Part of the stress response is to secrete acid into the stomach (to aid in the digestion process; when it doesn't encounter food, it eats away at the stomach lining, creating ulcers (gastric ulcers are lesions in the stomach; duodenal ulcers are lesions in the small intestine). Infection by h. pylori increases the gastrointestinal system's vulnerability to ulceration: it is a genuine diathesis factor. But, prolonged stress-related autonomic activation (see the discussion of Selye's general activation syndrome in the lecture supplements on the Biological Basis of Mind and Behavior) can interact with the bacteria to make ulcers even more likely to occur.
The diathesis-stress hypothesis is supported by a laboratory model of ulcers developed by Steven Maier (one of the investigators involved in the discovery of learned helplessness). In this model, rats are infected with h. pylori bacteria, and then are exposed to stress in the form of unpredictable and uncontrollable shock. This combination is particularly likely to produce ulcers, compared to conditions in which neither diathesis nor stress, or only one factor but not the other, are present.
Phobias. In experimental psychopathology, phobias are a classical example of psychopathology acquired through learning -- particularly, fear conditioning. As such, phobias would seem to be a case of all stress and no diathesis: the stress is the anxiety that accompanies exposure to the feared object. So, if a person has a negative encounter with a snake, he or she will come to fear snakes. In this conditioning theory of phobia, the snake is a CS that predicts unpleasant consequences.
This is a fine theory, so far as it goes, but it has two problems.
One problem is that people with phobias don't always, or even usually, have histories of negative experiences with the objects of their fears. Readers who have phobias concerning snakes, for example, might ask themselves what snakes have ever done to them. Once in a while a snake phobic has been bitten by a snake, but not too often. Instead of resulting from direct experience with the phobic object, it is more likely that the snake phobia has been acquired through social learning or vicarious conditioning. That is, people become afraid of snakes because they know other people who are afraid of snakes. We learn to fear what other people fear, without having frightening experiences ourselves.
The second problem is that people don't always acquire phobias following association of an object with negative consequences. To use an example from Seligman (the same theorist who proposed the learned helplessness model of depression), when we have a bout of food poisoning we don't become afraid of the crockery and cutlery; we become afraid of the food. And not just any food we may have eaten; we tend to become afraid of thinks like Lima beans and cream sauces. In fact, clinical phobias are largely limited to a relatively small number of situations: open spaces, high places, the gaze of other people, and wriggly, slimy things. According to Seligman, we are prepared by evolution to easily and quickly acquire conditioned fear responses to these sorts of objects and situations. In this view, the diathesis in phobia is a set of "prepared" associations, a part of the organism's evolutionary heritage, which predispose the individual to acquire intense fears even with minimal exposure.And the stress is a negative event. The stressful event can result in phobic levels of fear, but only by virtue of these prepared associations.
A laboratory model of phobias incorporating both social learning and preparedness has been studied by Mineka and her colleagues in research described in the lecture supplement on Learning. MIneka and her colleagues showed that observational learning was sufficient to produce intense conditioned fear in monkeys who themselves had no experience of negative consequences in association with the CS: they learned to fear what other monkeys feared. But Mineka et al. also found that observational learning didn't produce fear of just anything. Through vicarious learning, monkeys acquired conditioned fear responses to snakes, but not flowers. According to the preparedness argument, a disposition to fear snakes is built into monkeys by evolution, and can produce full-blown snake-fear even in with little or no direct experience.
The Dunedin Studies. The interaction of a biological diathesis with environmental stressors can be illustrated by two studies by Avshalom Caspi, Terrie Moffitt, and their associates, based on data collected in the "Dunedin Multidisciplinary Health and Development Study". In this project, longitudinal data was collected from a "birth cohort" of 1,037 children (roughly half of them males) born near Dunedin, New Zealand, and tested approximately every two or three years from ages 3 to 26 (actually, they're still being followed).
In one study, Caspi et al. (2002) examined the role that the MAOA gene played in adolescent conduct disorder. This gene, located on the X chromosome, promotes monoamine oxidase A, a substance that metabolizes many different neurotransmitters, and which has been linked to increased aggression in both laboratory mice and humans. Caspi et al. also explored the role of stress in conduct disorder -- particularly a history of childhood and adolescent maltreatment, which some theorists have proposed initiates an intergenerational "vicious cycle of violence" in which maltreated boys become maltreating fathers, producing maltreated boys who also become maltreating fathers. In fact, subjects with high levels of MAOA activity showed a relatively low incidence of conduct disorder, regardless of their history of maltreatment. However, subjects with low levels of MAOA activity, who also had a history of severe maltreatment, showed a very high incidence of conduct disorder. The MAOA gene is a diathesis which interacts with severe maltreatment to produce conduct disorder.
In another study, Caspi et al. (2003) examined the role of the 5-HTT gene in major depressive disorder. This gene, located on chromosome 17q11.2, comes in two forms, "short" and "long", yielding four genotypes: SS, SL, LS, or LL. Caspi et al. also explored the role of life stress in depression, by counting the number of stressful events occurring in the life of each subject between ages 21 and 26 (in psychology, a "stressful" event can include getting married as well as getting divorced). Subjects with the LL form of the genotype showed a relatively low incidence of depression, regardless of their history of life stress. However, subjects with the "short" form of the genotype (with at least one short allele, as in SS, SL, or LS), combined with a history of many stressful events during the previous five years, showed a much higher incidence of depression.
Similarly, Fox et al. studied the role of
the 5-HTT gene in pathological shyness -- children and
adults who are severely withdrawn. Their study actually
involved multiple assessments of children's temperament -- how
inhibited the children were in the presence of strangers, and
their mothers' ratings of their shyness. The mothers also
provided ratings of the amount of social support (e.g.,
friends) their children had. The results of the study showed a
clear gene x environment interaction:
- Children with the "short" allele of the 5-HTT gene,
coupled with poor or very poor social support, showed much
higher levels of behavioral inhibition, compared to
children with the "long" allele, or good levels of social
- Similarly, children who combined the short allele with poor social support received much higher ratings of shyness -- by which, of course, we mean pathological shyness, not the ordinary sort of shyness that children (and adults) can display.
Notice the shape of the graphs in the Fox et al. study of pathological shyness, which combines the "crossover" and "fan" effects that are so characteristic of the person-by-situation interaction.
Still another study from the Caspi-Moffitt group focused on marijuana and psychosis. It’s long been known that some people who smoked marijuana as adolescents develop a form of psychosis as adults, but the precise pathway has been unclear. Certainly, most adolescents who smoke marijuana don’t develop psychosis, but it does appear to be a risk factor. Caspi and Moffitt focused their attention on yet another gene, known as COMT, located on Chromosome 22. COMT is involved in the metabolism of dopamine, which has been linked to schizophrenia. The gene comes in two forms, methionine (“Met”), and valine (“Val”). Individuals who have two copies of the “Met” allele show the fastest breakdown of dopamine; those with two copies of “Val”, the slowest; and those with one of each, somewhere in between. So, if you’re a “MetMet” person, dopamine metabolizes faster, and resides in your system for less time. Again using subjects from the Dunedin study, Caspi and Moffitt classified their subjects according to the form of the COMT gene, and also by their history of adolescent marijuana use. And when they looked at the incidence of psychotic symptoms in these subjects when they were young adults, they found a clear gene-by-environment interaction. The affected subjects didn’t always show full-blown schizophrenia or any other psychotic syndrome. Still, their risk for delusions, hallucinations, and other “schizophreniform” symptoms was greatly increased if they had two copies of the “Val” allele, coupled with frequent marijuana use as adolescents. If they had only one copy of “Val", or two copies of “Met”, their risk was greatly reduced.
Another study showed how the COMT
genotype interacted with stress to affect performance on a
academic tests (Yeh et al. 2009) -- not, admittedly, a major
mental illness, but perhaps indicative of GxE interactions in
anxiety disorders. Every year, Taiwanese students who
wish to move on from junior to senior high school must take a
rigorous test known as the Basic Competence Test, which
measures educational achievement in a number of subjects,
including Chinese and English language, mathematics, science,
social science, and writing. The BCT is an extremely
stressful "high-stakes" test, because its outcome determines
whether the student will have any chance of going to college
(at least in Taiwan). Yeh drew a sample of 779 Taiwanese
high-school students (i.e., who had already passed the BCT),
and examined their scores on the BCT subtests as a function of
their COMT genotype.
- Students with the Met/Met genotype consistently performed more poorly than those with the Val/Val or Met/Val genotype.
- There were no differences between students with the Val/Val or Met/Val genotypes.
The conclusion is that having two
copies of the Met genotype renders the person vulnerable to
high levels of stress, to the detriment of performance.
Some of these gene-environment interactions are controversial.
- The specific findings of Caspi and Moffitt, as well as
those of have proved difficult to replicate, possibly
because of the highly unusual population from which they
drew their samples (Duncan et al. 2014).
- The interpretation of the gene-by-environment effects
is also subject to controversy.
- I have presented them as illustrative of the diathesis-stress approach, with -- for example -- the short allele of the 5-HTT gene functioning as a kind of risk factor, rendering a person more vulnerable to the effects of a stressful environment.
- An alternative view is that the 5-HTT gene, and
presumably others like it, acts as a kind of
"sensitivity gene", amplifying the effects of the
- Possessing the short allele will magnify the negative effects of exposure to a negative, stress-filled environment.
- But possessing the same short allele will magnify the positive effects of exposure to a positive, pleasure-filled environment.
In particular, the gene-by-environment interaction in depression, involving the 5-HTT gene, has stimulated a great deal of interest, but it’s also been controversial. Some researchers have failed to replicate Caspi and Moffitt’s findings, while some critics have complained about the assessment of stress. Katja Karg and her colleagues recently surveyed 56 studies, involving more than 40,000 subjects, and found that, overall, these studies confirmed the G-by-E effect. A history of stress, especially defined by childhood maltreatment or life-threatening or chronic medical conditions, coupled with the “short” form of the 5-HTT gene, greatly increases one’s risk for a major depressive episode. So please note that the findings on 5-HTT or COMT, for example, are not to be taken as firm. Rather, I cite them here simply as illustrations of a particular approach, using the diathesis-stress model, that is commonly used to identify the genetic and environmental contributions to mental illness. So stay tuned!
The Nature of Diathesis and Stress
In standard presentations of the
diathesis-stress model, the diathesis is often biological
(like the 5-HTT gene) and the stress is often psychosocial
(like stressful life events), but this need not necessarily be
Usually, we think of biological stressors as specific genes, like MAO-A or 5-HTT. But it's possible that there is a genetic diathesis for a broader group of mental illnesses. Smoller and his colleagues (2013) conducted the largest study to date of the genetics of mental illness, including more than 60,000 subjects from 19 countries (roughly half were patients carrying a psychiatric diagnosis). They found that five different disorders -- schizophrenia, bipolar disorder, depression, attention deficit hyperactivity disorder, and autism -- shared a relatively small set of genetic aberrations in common. For example, one identical twin might develop schizophrenia, while another might develop bipolar disorder. These investigators suggested that there might be a genetic diathesis for these major forms of mental illness in general, and that whatever specific mental illness an affected individual develops would depend on other factors (perhaps environmental, perhaps genetic as well).
In some instances, stress is better conceptualized as biological rather than psychosocial in nature.
For example, prenatal and perinatal
complications are often found in the life histories of people
who eventually develop schizophrenia. These are environmental
stressors, but the fact that they occur in the prenatal or
perinatal environment mark them as more biological than
psychosocial in nature. A difficult birth doesn't have the
same meaning for a person as a difficult childhood or
In other instances, diathesis is better conceptualized as psychosocial rather than biological in nature
For example, people may be
predisposed to depression by histories of social
learning that lead them to acquire certain beliefs.
- Beck has noted the presence of depressogenic schemata -- what he calls the depressogenic triad negative views of the self, the world, and the future -- in the belief systems of many depressed patients. In Beck's view, these cognitive structures of knowledge and belief render the person vulnerable to depression and all its symptoms -- sadness, anhedonia, guilt, withdrawal, inactivity, and loss of appetite -- in the face of adverse life events.
- Beck has recently expanded his cognitive theory of
depression (Beck & Bredemeier, 2016) to include yet
another diathesis factor: a heightened reactivity to
stress, which causes the individual to view
any loss of "essential human resources" as particularly
"devastating and insurmountable". As a result, it
takes relatively little stress to activate the
depressogenic schemata, leading to the development of
the symptoms of full-blown depression.
- Similarly, Abramson and Alloy noted that many depressed patients displayed a particular attributional style in which they tended to explain events in terms of stable, global, internal factors (as opposed to unstable, local, external ones). In their view, way of thinking rendered people vulnerable to depression -- because they tend to think that negative events are uncontrollable even when they aren't.
- Another psychosocial diathesis for depression was noted
by Nolem-Hoeksema (1991; Nolem-Hoeksema et al., 2008):
rumination, as opposed to self-distraction, perpetuates
the symptoms of depression. Especially in women, a
tendency toward rumination may serve some of the same
maladaptive functions as Beck's depressogenic schemata or
Abramson and Alloy's depressogenic attributional style.
Consider how this "reversal" of the standard account of diathesis and stress might help explain the incidence of postpartum depression, which occurs in some (but not all) women who have recently given birth. Sudden biochemical changes associated with pregnancy and childbirth may alter the person's characteristic mood states and activity levels. These particular alterations may be similar to those that occur in depression, but they do not necessarily result in a depressive episode. However, if these changes are interpreted in terms of Beck's "depressogenic schemata" or Abramson and Alloy's "depressive attributional style", they may well be interpreted in such a manner precipitate an episode of depression. In this case, the diathesis factor is psychosocial in nature -- a "depressogenic" way of thinking. But mental illness doesn't occur unless this diathesis interacts with a stressor-- and in this case, the stressful events are biochemical in nature, consisting of certain biochemical changes that occur naturally with pregnancy and parturition.
A similar account could be given of the depression which occurs in some (but not all) women who are going through menopause.
Post-traumatic stress disorder
(PTSD) would, at first glance, appear to be an almost "pure"
case of stress-related mental illness. But, in fact, only a
minority of people actually exposed to traumatic levels of
stress actually go on to develop PTSD (there is, of course, an
acute stress disorder affecting large proportions of
trauma victims, but even this isn't universal). This
variability was noted even as far back as World War I, where
it was attributed to individual differences in soldiers'
predisposition to stress. This diathesis might be
biological -- perhaps something related to the functioning of
the hypothalamic-pituitary-adrenal (HPA) axis, or perhaps a
genetic predisposition. Or it might be something
psychological, analogous to the depressogenic schemata and
attributional styles implicated in some forms of
depression. But the basic point is that even in PTSD,
the stressor alone is rarely sufficient to cause the disorder
all by itself; the stressor has to combine with a
predisposition or vulnerability.
Interestingly, the role of diathesis or predisposition in PTSD has contributed to the reluctance to award honors or disability benefits to some soldiers suffering from PTSD. The argument is that the soldiers' disabilities weren't caused by the stress of war, but rather are related to personality problems that predated the war -- much as insurance companies will sometimes deny medical coverage on grounds of a "pre-existing condition". Setting this policy issue aside, PTSD may be an example where both the diathesis and the stress are psychosocial in nature.
Diathesis is often biological, and stress is often psychosocial, in nature. But the really important feature of diathesis is that it is something that the person carries with him into a situation, either as a biological or a psychosocial "trait". By the same token, the really important feature of stress is that it is something that happens to the person in a particular situation, ether as a biological or psychosocial event (or series of events).
Treatment of Mental Illness
The diathesis-stress model for the
origins of mental illness offers a framework for understanding
their treatment and prevention as well. So, if mental illness
is caused by the interaction of diathesis and stress, then
effective interventions should alter diathesis factors, stress
factors, or both.
To orient ourselves, let's first examine
what happens during an episode of mental illness. As in
earlier lectures in this module, we'll be using language
derived from medicine patient, symptom, syndrome,
and so on, to identify what we can call, following Steven
Hollon, a prominent depression researcher at Vanderbilt
University, and others, the 5 Rs of Mental Illness.
I'll use depression as my example, but the same
general points would apply to any syndrome of mental illness.
let's assume that the patient begins at a more-or-less
"normal" state, with no identifiable symptoms of mental
illness. At some point, however, given a certain
combination of diathesis and stress, he or she begins to show
symptoms of some form of mental illness -- depression, or
anxiety disorder, or schizophrenia. At some point,
enough symptoms develop, with enough severity, to compromise
normal functioning, at which point we can say that the person
has "progressed" -- that's the medical term -- to a full-blown
acute episode of mental illness.
- Remission. With time, even without active
intervention, the symptoms may disappear on their own, in
which case we would talk about spontaneous remission
of the illness. "Remission". Spontaneous
remission is surprisingly common in depression, which tends
to come and go in its natural course. But it also
takes time, maybe 6-9 months, so rather than wait the
illness out, it's probably better to get some sort of acute
- Response. Now let's suppose that the patient
does receive some active treatment, whether it's
psychotherapy, or some kind of biological treatment, like
medication. Many patients will respond positively to
whatever treatment they receive. If they don't, the
therapist may switch to a different form of treatment -- a
different approach to therapy or perhaps a different drug --
until something seems to work.
- Recovery. In depression, subjects may respond
positively after a couple of weeks of appropriate treatment,
but it may take a while before they really get back to
normal -- a complete recovery, in which they are symptom
free. Alternatively, may show a partial recovery, in
which some symptoms remit completely, but not others; or
there may be a clinically significant reduction in the
severity of symptoms. Sometimes, unfortunately,
recovery doesn't occur at all, in which case the patient
proceeds from an acute to a chronic illness, calling for
- Relapse. Even with a complete recovery, there
is some chance that the symptoms may come back, perhaps not
as severely as before, but enough to interfere with normal
functioning. In depression, for example, the
likelihood of a relapse even after what appeared to be a
complete recovery is about nine times the risk of depression
occurring in the general population. Apparently the
acute episode is still going on, appearances to the contrary
notwithstanding. For this reason, most therapists
don't stop treatment immediately once the patient has
recovered, but continue it for awhile.
- Recurrence. Even after a patient has
completely recovered, there is still some chance that
another acute episode can occur later. If a person has
recovered from an acute episode of depression, there is
still a chance that another acute episode will occur --
about three times more risk than in the general
population. For this reason, even patients who have
completely recovered may want to maintain some degree of maintenance
The first goal of treatment is to
achieve a cure. Genuine cures will do more than suppress
superficial symptoms: they will eliminate underlying
pathology, or reduce it to a clinically significant extent,
returning the person's level of functioning to "within normal
limits" even after active treatment has stopped. In the
absence of a cure, treatment focuses on the amelioration of
symptoms, or rehabilitation regimes that permit the patient to
cope with a chronic condition.
Historically, the scientific treatment of mental illness has come in three basic forms. Up until the 20th century, there were really no active treatments available for mental illness, so intervention focused largely on custodial care -- chiefly the warehousing of the mentally ill in public hospitals or private asylums. Pennsylvania Hospital, America’s first hospital, was founded by Benjamin Franklin and Thomas Bond in 1751, when Pennsylvania was still a British colony, for the care of the indigent and the mentally ill. New York Hospital and the Virginia Asylum were also chartered for the care of “Lunaticks” before the Revolutionary War, but did not open their doors until after the War was over. Still, the patients there were mostly “warehoused”, out of sight of the rest of the community. After the Civil War, Silas Weir Mitchell gave a more positive spin to “warehousing” by prescribing a “rest cure” for “mental exhaustion – famously depicted in The Yellow Wallpaper, an early feminist classic by Charlotte Perkins Gilman.
- For insight into the state mental hospital system, see The Lives They Left Behind: Suitcases from a State Hospital Attic by Darby Penney and Peter Stastny (2007), based on artifacts collected from Willard State Hospital in Romulus, New York. Link to the accompanying website: www.suitcaseexhibit.org.
- Beginning in December 2013, this exhibition can be viewed at the Exploratorium in San Francisco.
- Sometimes, the mentally ill were confined at home, in back bedrooms and attics, as in the character of Mrs. Rochester in Charlotte Bronte's Jane Eyre (1847) -- the original "madwoman in the attic".
Beginning in the late 19th century, various forms of psychotherapy were introduced. These interventions, one way or another, were intended to alter the patients' pathological mental states -- their abnormal beliefs and feelings and desires, which were thought to underlie the various symptoms of mental illness. By changing these abnormal, maladaptive mental states, mental health professionals sought to change the maladaptive patterns of behavior that brought patients to the attention to the professionals in the first place. Beginning in the 20th century, a wide variety of biological treatments were introduced for mental illness. These began with procedures like electroconvulsive therapy, and even psycho-surgery where physicians operated on various brain centers that were presumed to be implicated in the patient's problems. But more recently, a wide variety of medications have been introduced for the treatment of various metal illnesses, beginning with schizophrenia. These medications have largely supplanted psychosurgery and ECT, though both still have a place in selected cases.
- For histories of the beginnings of mental-health treatment in America, see:
- American Nervousness: Its Causes and Consequences by George M. Beard (1881 -- note the date!);
- American Nervousness, 1903 by Tom Lutz (1991).
- Before Prozac (2008) and How Everyone Became Depressed: the Rise and Fall of the Nervous Breakdown (2013) by Edward Shorter, the pre-eminent historian of the psychiatry in America.
- Beginning in the mid-20th century,a wide variety of psychotropic medications were introduced for the treatment of various mental illnesses, beginning with schizophrenia. Mental health has been a full participant in the "pharmaceutical revolution" that has swept modern medicine.
Where biological causes are the primary factor in mental illness, strictly biological treatments may effect a complete cure. Of course, such biological cures require an understanding of the biological basis of some form of mental illness.
Biological cures are
exemplified by treatments available for two specific forms of
- Phenylketonuria is a metabolic disorder that interferes with the myelinization of neural tissue. If a child with phenylketonuria is put on a strict low-protein diet until about age 6, this form of intellectual disability can be prevented entirely. Unfortunately individuals with PKU must stay on a somewhat restricted diet for the rest of their lives. In 2007, the Food and Drug Administration approved Kuvan, the first drug treatment for the disorder, while will allow for a somewhat more relaxed dietary regimen, allowing affected individuals to eat things like cheese and pizza (if only in moderation).
- Cretinism, another form of intellectual disability, is caused by thyroxine deficiency, a hormone imbalance due to a lack of iodine in a pregnant woman's diet. This illness can be prevented entirely by treating the infant with thyroid extract during the first year of life (it can also be prevented entirely by giving the mother the iodine she needs during pregnancy).
There are many other biological treatments for mental illness, including many different medications but also psychosurgery and electroconvulsive therapy. These are often very effective, but they do not reach the level of a cure, because the illness returns when the treatment is discontinued.
Psychosurgery, especially prefrontal
lobotomy (the destruction of the prefrontal cortex of
the brain) was once rather popular: Egas Moniz, the Portuguese
neurologist who pioneered the technique of "prefrontal
leukotomy", even won the Nobel Prize for Physiology or
Medicine in 1949. The technique has now been completely
repudiated, and Moniz' prize considered something of an
embarrassment. However, as our understanding of brain
function advances more nuanced surgical approaches to mental
illness are sometimes proposed. For a history of
psychosurgery, see Great and Desperate Cures: The Rise and
Decline of Psychosurgery and Other Radical Treatments for
Mental Illness (1986) by Elliot Valenstein, a
distinguished neuroscientist. Valenstein's other books are
also of interest:Brain Control: A Critical Examination of
Brain Stimulation and Psychosurgery (1977) and Blaming
the Brain : The Truth About Drugs and Mental Health
Although nobody does lobotomies anymore,
psychosurgeries are still performed (of course, brain surgery
is frequently performed for strictly neurological disorders
like epilepsy). Most of these operations occur in cases
of obsessive-compulsive disorder or depression, and they are
pretty rare -- although, with increasing evidence of efficacy
and safety, their use is increasing (though they are not
risk-free). Most of these "surgeries" are performed by
means of electrical stimulation through microelectrodes, as
opposed to with a scalpel (as was the case, for example, with
the earlier lobotomies).
- Cingulotomy, destruction of a portion of the anterior cingulate gyrus, which disrupts a circuit that connects emotional enters in the limbic system to the frontal cortex.
- A related procedure, known as capsulotomy,
targets the internal capsule, a bundle of white
matter that connects midbrain and forebrain structures.
- One new form of surgery involves deep brain stimulation -- surgically implanting electrodes in the brain, using much lower levels of current to stimulate specific brain areas -- sort of like the pacemakers that are implanted to treat certain forms of heart disease. Originally developed as a treatment for Parkinson's disease, and later extended to Tourette's syndrome (both more properly regarded as neurological syndromes with behavioral consequences than as mental illnesses per se), deep brain stimulation is now being performed in some cases of depression and obsessive-compulsive disorder as well.
- For depression, the electrodes are typically implanted in the subcallosal cingulate gyrus (Brodmann's area 25).
- For a a recent discussion of this technique, which as of 2015 had not yet been approved for routine therapeutic use, see "Treating Depression at the Source" by Andres M. Lozano & Helen S. Mayberg, Scientific American, 02/2015.
- A variant on deep-brain stimulation for depression,
which has been approved for routine use, is transcranial
magnetic stimulation, stimulates the brain with
short bursts of magnetic pulses focused on the left
prefrontal cortex -- a little like electroconvulsive
therapy, though without the convulsive seizures or
transient confusion and memory loss.
- Both DBS and TMS have been proposed for use with
depressed patients who are not responsive to
conventional psychotherapeutic or pharmacological
- For obsessive-compulsive disorder, the electrodes are implanted in the nucleus accumbens.
- A newer technique, which doesn't employ electrical
stimulation at all, is gamma knife surgery,
derived from a radiological treatment for cancer, which
focuses a large number of beams of radiation on a very
small area of brain tissue. Each beam is, itself,
completely benign, but the cumulative effect of all the
beams is sufficient to destroy tissue precisely at the
point of focus.
The treatments are strictly
experimental, and they can have powerful and unpleasant
side-effects, so they are typically performed only under a
"humanitarian device exemption", where no other treatment has
worked. For this reason, deep brain stimulation has not
been subject to the kinds of controlled clinical trials that
are required for approval of new medications and other medical
Electroconvulsive Therapy (ECT) is sometimes used as a treatment for severe depression. ECT employs a brief electrical current applied to the scalp to induce a brief seizure somewhat similar to that seen in epilepsy. ECT has a somewhat unsavory history, having been misused in the past, but the fact is that a short course of ECT, judiciously applied, can often produce rapid remission of depressive symptoms. ECT is often avoided because of its presumed side-effects, which (when misapplied) can include brain damage. However, ECT does not hurt (because the patient is unconscious during the treatment). ECT applied bilaterally (with electrodes placed on both sides of the head) can produce an amnesia similar to that which occurs following a concussive blow to the head; but memory impairment can be reduced substantially if the treatment is applied unilaterally, so the seizure is confined to one (usually the nondominant) hemisphere. Biologically, ECT increases levels of norepinephrine and serotonin in the brain, which is interesting in light of the "monoamine" hypothesis of depression.
- ECT and TMS are sometimes referred to as "jump-starting the brain", but we don't really have a good idea why they work -- when they do.
By far the most popular and effective biological treatments for mental illness involve medications: beginning in the 1950s, psychiatry has been a full participant in the "pharmaceutical revolution" in medicine.
variety of antipsychotic medications are used in the
treatment of schizophrenia. Most common, perhaps, are
the phenothiazines, which appear to decrease dopamine
levels in the brain. Typical brand names are Thorazine,
Stelazine, Prolixin, and Mellaril. Haldol (a butyrophenone),
and Navane (a thioxanthene) are also widely used. There is
also a group of "atypical" antipsychotics like Clozaril,
Resperidal, Zyprexa, and Abilify, which are as effective as
the earlier antipsychotic agents, but cause fewer
To be honest, though, most of the drugs used in the treatment of schizophrenia are really nothing more than major tranquilizers, which calm the patient, reducing the tendency to report and act on hallucinations if not to have them.Setting aside the dopamine hypothesis of schizophrenia, nobody thinks that these drugs act directly on the patient's underlying pathology. However, these drugs do make patients more manageable, and their introduction made everybody's life better, staff and patients, inside mental hospitals -- and made it possible for many people with schizophrenia to be released from mental hospitals to live with their families or elsewhere in the community. But, as with many psychiatric drugs, you've got to keep taking them. And once released from direct supervision, this is something that many schizophrenics just aren't inclined to do.
- The tricyclic antidepressants, drugs like
Elavil, Tofranil, and Sinequan, increase levels of
norepinephrine and serotonin.
- Another group of antidepressants, known as the MAO inhibitors -- Nardil and Parnate are examples -- inhibit monoamine oxidase, a substance which, in turn, deactivates norepinephrine and serotonin. Both the tricyclics and the MAO inhibitors act by increasing the release of norepinephrine and serotonin into the synapse
- Recently, these earlier generations of drugs have begun
to be replaced by a newer generation of selective
serotonin reuptake inhibitors(SSRIs) such as
Prozac, Zoloft, Paxil, Celexa, and Lexapro. As their name
implies, these drugs act selectively on serotonin, and
have little or no effect on norepinephrine; and rather
than increasing the release of serotonin, they act to
prevent its reuptake by the presynaptic neuron -- thus,
effectively, increasing the levels of serotonin available
at the synapse.
- There is also a class of drugs called selective serotonin and norepinephrine reuptake inhibitors, or SNRIs, such as Cymbalta, which act on both serotonin and norepinephrine -- thus accomplishing the same effect as the MAO inhibitors, but through a different mechanism.
- And, of course, there are now selective norepinephrine reuptake inhibitors, also known as an NRIs, including Strattera
The SSRIs and SNRIs are as effective as
the earlier tricyclics and MAO inhibitors -- a fact that has
led to the revision of the general monoamine hypothesis of
depression by the more specific serotonin hypothesis of
For a discussion of recent advances in the drug treatment of depression, see
- Lifting the Black Cloud" by R.M. Henig,Scientific American, 03/2012.
Also within the category of mood disorders,lithium carbonate has proved to be a very effective treatment for bipolar disorder, also known as "manic-depressive illness". Treatment with lithium reduces or eliminates episodes of mania in as many as 70% of cases, and also reduces episodes of depression. However, because lithium is toxic, its use must be carefully monitored.
early drug treatment of anxiety disorder focused on
sedatives such as the barbiturates (e.g. Nembutol and
Seconol), propanediols (e.g., Miltown, Equanil), and
benzodiazepines (e.g., Librium, Valium, and Xanax). The
20th century was known as the "Age of Anxiety", and popular
literature and movies concerned with American middle-class in
the 1950s and 1960s are full of references to these drugs.
These drugs are also, essentially, tranquilizers -- though far
less potent than those used in the management of
schizophrenia. Specifically, they increase the activity of the
neurotransmitter GABA, which in turn suppresses activity in
the hypothalamic-pituitary-adrenal axis (HPA).
As with the antipsychotic medications,
there is also a group of atypical anxiolytics, such as
Buspirone, which are as generally effective as the earlier
sedatives but with fewer side-effects.
Whether "typical" or "atypical", all
psychotropic drugs in a particular class have the same basic
pharmacological mechanism of action:
- The antipsychotics, like Thorazine, decrease levels of dopamine.
- The antidepressants, like increase serotonin, dopamine, or norepinephrine.
- The anxiolytics increase GABA.
Newer drugs within a class are sometimes called "me-too" drugs, because they all have the same basic effects -- put another way, the newer drugs are little more than copycats of the older ones. The newer drugs may have fewer side-effects, and be somewhat safer and easier to tolerate. But the basic underlying pharmacological action is no different. So why are new drugs introduced? Mostly because the patents are running out on the old ones. And, in fact, the pharmaceutical industry isn't devoting that much research to the development of truly new psychotropic drugs, because -- despite their popularity -- there isn't that much to be gained financially from them. There is much ore money to be made from drugs that treat cancer, heart disease, or diabetes.
Because of the co-morbidity between
anxiety and depression, anxiety disorder is sometimes treated
with SSRIs such as Paxil. The rationale for this strategy
isn't completely clear -- maybe it's to help patients feel
less depressed about being anxious!
In many instances, specific drug treatments are developed based on a specific somatogenic theory of the illness in question. In theory, at least, psychotropic medications work because they address the biological bases of mental illness. Thus, according to the dopamine hypothesis of schizophrenia, drugs that alter the processing of dopamine should be effective treatments for schizophrenia but not depression; and according to the amine hypothesis of depression, drugs that alter the processing of monoamine neurotransmitters should be effective treatments for depression but not for schizophrenia. The SSRIs, which act specifically to enhance the availability of serotonin in depressed patients, are perhaps the clearest expression of this connection between theory and treatment.
But sometimes drug treatments are simply
empirical, meaning that they are prescribed simply
because they are known to help, and not because their efficacy
is predicted by any theory of the illness in question.
A good example of such an empirical
treatment is the prescription of amphetamine, such as Ritalin,
for the treatment of ADHD.
- A report by Bradley (1937) had noted that Benzedrine, a
trade name for amphetamine, had positive, and paradoxical,
effects on a group of schoolchildren with various
"behavioral issues" -- what we would now recognize as
ADHD. Bradley originally prescribed the drug to treat
headaches, and noticed that it affected their behavior as
- That same year, interestingly, news media carried
reports of college students taking amphetamine as a study
aid. Plus ca change....
- Ritalin, another proprietary form of amphetamine, was put
on the market in 1956, and a study soon showed that it, too,
produced positive effects on children with various
behavioral disturbances (Ritalin was named after the wife of
the chemist who formulated the drug).
- In 1970, amphetamines were placed under tight restrictions (Schedule II) by the Controlled Substances Act. Initially, sales of Ritalin and other amphetamines declined substantially, but recovered as more children were diagnosed with hyperactivity disorder or ADD/ADHD.
- Another proprietary amphetamine, Adderall, was introduced in 1996. Essentially the same drug was formerly marketed as Obetrol, for the control of obesity; its new name is a contraction of "ADD for all", which should tell you something.
- Concerta was introduced in 2000.
- The landmark "MTA" study (the acronym stands for
"Multimodal Treatment of Children with ADHD") found that 68%
of children who received Ritalin or Concerta with behavior
therapy showed improvement; comparable figures for
medication alone were 56%, behavior therapy alone 34%, and
25% for an untreated control group. This study
effectively set medication as the "standard of care" for
There's no good reason why Ritalin should work in these cases -- and given that amphetamine is a central nervous system stimulant, there would be every good reason to think that it would make things worse. Such "off-label" use of medications is a fairly common practice in medicine: physicians may "experimentally" prescribe drugs for conditions other than those indications approved by the Food and Drug Administration following controlled studies of safety and efficacy). But exactly how it occurred to anyone to try Ritalin in the first place isn't clear. Perhaps it was simply an act of desperation after everything else failed. But it does work, at least for many patients with ADHD, and is now the standard of care for both children and adults carrying the diagnosis -- ADHD is now a "labeled" indicator for Ritalin and similar drugs, rather than an "off-label" use. But there's still no theory that explains the paradoxical effects of Ritalin on ADHS. One theory is that amphetamines activate brain centers for the control of attention which are relatively inactive in patients with ADHD -- but this is just a theory, and a rather post-hoc one at that, and as yet there's no evidence supporting it.
Actually, there is a double paradox here, because the evidence for the efficacy of amphetamines in the treatment of ADHD is somewhat ambiguous. Laboratory tests show that Ritalin (and similar drugs) improves performance on laboratory tests of attention and working, and also has positive effects on brain centers involved in these cognitive functions. But other studies show that there is no corresponding improvement in student academic performance, as measured by grade-point averages, achievement-test scores, or even the likelihood of repeating a grade. of elementary and secondary-school. So, whatever is going on in the laboratory, and the brain, doesn't seem to translate into the real life of the classroom. One possibility is that these children, and their families, come to rely too heavily on the drugs. In the absence of proper study skills, and a home environment conducive to and encouraging of study, academic performance won't improve just by taking a pill.
Notes on Cosmetic Neurology
Advances in neuroscience, pharmacology, and gaming have conspired to usher in a new age of what can only be called cosmetic neurology (Chatterjee, 2004, 2007) -- that is, the use of neuroscientific and pharmaceutical techniques to enhance performance in healthy people -- much like cosmetic surgery is intended to enhance physical appearance in healthy clients who have "normal" physical traits. Cosmetic neurology raises a host of ethical issues, but the first issues they raise are scientific and medical -- namely:
- Do these techniques work?
- Do they do any harm?
- What are the cost-benefits ratios attached to them?
Let's look at some cases.
1. "Study Drugs"
Actually, a number of "stimulant" drugs are now prescribed for ADHD, including methylphenidates such as Ritalin, Focalin, and Concerta, and amphetamines such as Adderall and Vivanse. All have the "paradoxical" effect of focusing the concentration of patients with ADHD. But maybe these "paradoxical" effects are not paradoxical at all, and that these and other drugs may improve focus and concentration in anyone.
Other psychostimulants include:
- Modafinil (trade name Provigil), used in the treatment of narcolepsy and excessive sleepiness.
- Donepezil (trade name Aricept), used in the treatment of Alzheimer's disease.
In fact, these alleged "brain boosters"have
been increasingly used by high-school and college students
who do not have ADHD as "study drugs" -- that is, as
pharmaceutical aids for studying and test-taking. Students
have been known to fake the symptoms of ADHD in order to get
a prescription, and there is apparently a vigorous black
market in the drugs. A 2007 survey by the Centers for
Disease Control and Prevention found that 2.7 million
children and adolescents were taking prescribed medication
for ADHD. Some of that medication, perhaps as much as
20%, is "diverted" to others for non-prescribed use.
In addition, some students persuade their family physicians
to prescribe stimulants to help them get through academic
exercises such as the SAT.
It should be noted, first of all, that these
drugs are controlled substances (in Schedule II, right up
there with cocaine and morphine): possession and use without
a prescription is illegal, and even giving them away can
lead to felony charges.
It should also be understood that, like all
psychoactive drugs, there is a danger of addiction.
Habitual overuse of stimulants can lead to episodes of
psychosis, and even suicide. So stimulants should
never be taken unless actually prescribed by a physician;
and the medication regime should be continually
monitored. N For a cautionary tale, see "Drowned in a
Stream of Prescriptions" by Alan Schwartz (New York Times,
02/03/2013) -- the cautionary tale of Richard Fee, the
pre-med president of his college class, who faked ADHD to
get a prescription for Adderall, and hanged himself when his
prescription ran out.
These are powerful
drugs. And this is your brain, and you only get one
From a scientific point of view, it has to
be said that, until recently, claims about the effectiveness
of Ritalin and similar drugs as study drugs for "normals"
are largely anecdotal. A formal review of this literature by
Elizabeth Smith and Martha Farah (Psychological Bulletin,
2011). They found that there was little
evidence that stimulants improved the cognitive performance
of normal, healthy individuals. There may be some
positive effects, but they seem to be small and variable,
and do not necessarily translate into improved academic
From a medical standpoint, however, it should be understood that, like all psychoactive drugs, these substances have negative side effects. Chief among these are that they are highly addictive. It is very easy for students to become dependent on these drugs, and for their prolonged use to lead to the addictive cycle of tolerance and withdrawal.
So, the word from here is: as tempting as it may sometimes be,don't do it; don't even start. Just study hard and do your best!
For a discussion of the scientific and ethical issues involved, see:
- "Turbocharging the Brain" by Gary Stix,Scientific American, October 2009.
- ADHD Nation: Children, Doctors, Big Pharma, and the Making of an American Epidemic (2017) by Alan Schwarz, based on a series he wrote for the New York Times in 2012. Schwarz is clear that ADHD is a legitimate diagnosis, and he acknowledges that methamphetamines can be an effective treatment for the disorder. But he also thinks that the syndrome is vastly overdiagnosed, and that Ritalin and similar drugs are vastly overprescribed, leading to a serious epidemic of drug abuse.
2. "Brain Training"
"Smart drugs" may not be the only way to
enhance cognitive performance (if, in fact, that's what they
do). Lately, some entrepreneurial psychologists have
begun to promote "brain training" programs, ostensibly based
on cognitive neuroscience. These are, essentially,
adult video games, aimed especially at baby-boomers (like
yours truly), and intended to stave off the cognitive
decline that comes naturally with age -- not to mention
Alzheimer's disease. Also to promote things like
"neuroplasticity", "fluid intelligence", and "working
These products go by a number of brands.,
most of which is some variant on "Brain Fitness".
According to a report by Sharp Brains, an industry group,
more than $1 billion was spent on brain-fitness programs of
various sorts, mostly software, in 2012 alone -- and the
industry is expected to reach $6 billion by 2020. I
don't intend to promote or criticize any particular product,
but I do want to offer some cautions about the whole
enterprise of "brain training".
- One leading product is BrainHQ, sold by Posit Science,
co-founded by Michael Merzenich, a neuroscientist at UC
- Another is Lumosity, offered as a subscription service, with new "brain games" every month.
- There are lots of others, some with UC or Stanford
The rationale for these programs is simple
enough. We know from the literature on brain
plasticity that mental exercise can stimulate the growth of
neural connections, if not neurogenesis itself. And
these exercises do activate brain regions, especially in the
prefrontal cortex, that are known to be involved in working
memory, attention, and other executive functions.
Therefore, it only makes sense that these games would result
in improvements in brain function.
But, at least as of 2013, none of the
commercially available programs has received anything like
the kind of approval that new drugs must receive from the
Food and Drug Administration. Most of the research
demonstrating their effectiveness is proprietary, and has
not been subjected to peer review. And while the
published studies may report statistically significant
increases in brain activity, or gains in performance on
cognitive tasks, they don't necessarily show that these statistically
significant improvements lead to clinically
significant improvements outside the laboratory, in the
ordinary course of everyday living. Nor, for the most
part, have the published studies shown that using the
(fairly expensive) games produces improvements in
performance over and above any other kind of mental
exercise, such as doing a crossword puzzle, watching Jeopardy!
and Wheel of Fortune -- or, for that matter,
engaging in physical exercise for 30 minutes a day, five
days a week.
The rationale for "brain games" appears to be
be based on the idea that the brain is a muscle, which is
strengthened by use and weakened by disuse (a principle
you'll remember from Thorndike's Law of Exercise, translated
into neuroscientific terms). And it's rue that
practice on a task will make you better at that task -- and
with enough practice (like the "10 Thousand Hour Rule"),
even automatize the underlying processes such that task
performance occurs automatically, and consumes few or no
cognitive resources -- thus freeing up those resources to be
devoted to some other task. But the analogy is
inexact. We know from the Doctrine of Modularity that the
brain isn't like a muscle: if anything, it's like a whole
collection of muscles, each corresponding to a module.
The human body contains about 650 different skeletal
muscles, after all (maybe more, depending on how you count,
and we're not counting involuntary muscles, such as the ones
in the heart). There's no reason to think that
exercising the triceps brachii of the upper arm has any
effect on the triceps surae of the leg. You've got to
exercise them both, if you want to increase your total body
Another, related point: practice with any
game will make you get better at that game. That's
just learning. But there is little evidence that
getting better at any game actually improves cognitive
abilities or overall brain function.
So, as with any other treatment, drug, or psychotherapy, or brain-fitness software, caveat emptor -- which, freely translated from the Latin, means check out the efficacy studies.
And, in fact, as of early 2017, there was
precious little evidence that these "brain-training"
programs actually accomplish their goals. Playing a
particular game may enhance a person's ability to perform
the tasks required by that particular game (no surprise
there!), but there is little evidence that the skills
acquired in one game generalize to other cognitive skills --
let alone prevent Alzheimer's Disease.
- In October 2014, a large group of cognitive
psychologists and cognitive neuroscientists, organized by
the Stanford Center for Longevity and the Max Planck
Institute for Human Development issued "A
Consensus on the Brain-Training Industry from the
Scientific Community" arguing that claims that
"brain games" can "reduce or reverse cognitive decline"
are unsupported by scientific evidence from controlled
experiments. In response, another 100 cognitive
psychologists and cognitive neuroscientists published an open letter
attempting to make the case that cognitive training
actually improves cognitive function.
- In December of that same year, however, a large international group countered that "a substantial and growing body of evidence shows that certain cognitive-training regimens can significantly improve cognitive function, including in ways that generalize to everyday life".
- On January 5, 2016, the Federal trade Commission fined the creators and marketers of Lumosity, a popular "brain-training" program, $2 million for deceptive advertising (actually, the initial fine was for $50 million, but after the FTC discovered that Lumosity had no hope of ever paying it, the fine was reduced to something more manageable). The FTC determined that Lumos Labs, the makers of Lumosity, had systematically deceived its 1,000,000+ subscribers, who paid $14.95/month -- you do the math -- by making "unfounded claims that Lumosity games can help users perform better at work and in school, and reduce or delay cognitive impairment associated with age and other serious health conditions".
- A comprehensive review by Daniel Simons and his colleagues concluded that there was "extensive evidence that brain-training interventions improve performance on the trained tasks, less evidence that such interventions improve performance on closely related tasks, and little evidence that training enhances performance on distantly related tasks or that training improves everyday cognitive performance." They also found "that many of the published intervention studies had major shortcomings in design or analysis that preclude definitive conclusions about the efficacy of training, and that none of the cited studies conformed to... the best practices... essential to drawing clear conclusions about the benefits of brain training for everyday activities" ("Do 'Brain-Training' Programs Work?", Psychological Science in the Public Interest, 2016).
So what are the problems with
brain-training? Chiefly, purveyors of brain-training
games, like Lumosity, have not conducted proper research,
modeled after clinical trials, to demonstrate that their
products actually are effective.
- True, customers who practiced their games, like one in
which they were asked to remember the location of colored
squares on a grid, got better at those games, and other
games very much like them (what is known as "near
transfer"); and they might have felt,
subjectively, that their cognitive skills had
- But there is no evidence that these gains generalize beyond the games themselves ("far transfer") -- much less that they stave off dementia or even normal age-related cognitive decline.
- Moreover, most of the available studies have employed
inadequate control groups, such as "no treatment"
controls, who do nothing while the experimental group is
playing the games. The best study would have a
placebo control, like a drug trial.
Cognitive training has potential, so it would
be too bad if actions like the FTC's stopped research and
development dead in its tracks. But at the same time,
the claims of the brain-training industry far exceed the
available evidence. Worse, it seems like the purveyors
of brain-training games haven't even tried very hard to
document the effects of their products. They have,
however, been very eager to take consumers' money.
For an interesting first-hand account of some of these programs, see "Mentally Fit: Workouts at the Brain Gym" by Patricia Marx, New Yorker, 07/29/2013.
See also "Can You Train Your Brain" by Simon Makin, Scientific American, July/August 2015.
Another fad has been Transcranial
Direct Current Stimulation (TDCS), in which a low
electrical current is applied to certain brain areas --
e.g., the left prefrontal cortex -- by means of electrodes
attached to a power source (often, nothing more than a
9-volt battery!) and an interface which controls the amount
of current and the duration of stimulation. Sort of
like EEG in reverse, but not nearly as strong as
Transcranial Magnetic Stimulation. You can buy these
things on the market (e.g., the Foc.us), or make them at
home, and a recent review shows that it might actually
improve performance on some cognitive tasks (Chrysikou et
al., 2013). But as of 2013 the device was not approved
by the Food and Drug Administration, and because the device
is so new there is no data on any harmful effects of
long-term use -- and there is every reason to think that the
long-term effects can be very harmful indeed.
4. "Baby Apps"
While we're on the subject, there has been a
proliferation of baby apps for smartphones and
tablets, advertised as enhancing infants and children's
cognitive skills. The progenitors of these were the 'Baby
Einstein" videos marketed in the days before smartphones and
tablets. These days, "baby apps" are promoted as ways
to teach infants motor and spatial skills, numbers, and
Again, on first blush, the idea seems
plausible. But in fact, there is very little evidence
that these "baby apps" do what is claimed for them.
The published research is paltry and ambiguous, and even
some of the software developers admit that they don't have
the research to back up their claims. These apps may
entertain and distract children, but there is no good
evidence that they actually teach them anything.
Mostly, it seems, they make parents feel better about using
screens to distract their kids during dinner or cocktail
And there are some reasons to think that they
may actually be harmful, by consuming time and effort that
might actually be devoted productively to creative play,
person-to-person interactions with parents and older
siblings, and the like. The American Academy of
Pediatrics recommends that children not be exposed to
"screen media" of any kind, including television, for at
least the first 30 months (2-1/2 years).
In 2013, the Campaign for a Commercial-Free
Childhood, an advocacy organization, filed a complaint with
the Federal Trade Commission intended to put the brakes on
the "baby genius industry". Either they provide
evidence to back up their claims, or they stop making the
claims. The group was successful in an earlier effort
against the "Baby Einstein" videos, forcing the Walt Disney
Company to offer refunds to consumers who bought them for
their educational value.
So, to repeat: As with any other treatment, drug, or psychotherapy, brain-fitness or educational software, or indeed any innovation of this sort, caveat emptor -- which, freely translated from the Latin, means What's the evidence?
pharmaceutical revolution in mental health has been a genuine
revolution, providing a degree of symptom relief that simply
was not available previously, and enabling the
de-institutionalization of large numbers of patients from
mental hospitals, which offered mostly custodial care, back to
their homes and into the community; it also improved the lives
of a large number of individuals who were being treated on an
outpatient basis by psychiatrists and other mental health
The effectiveness of these
drugs also has theoretical implications for our understanding
of the biological mechanisms involved in certain forms of
- The effectiveness of the phenothiazines supports the dopamine hypothesis of schizophrenia.
- The effectiveness of the tricyclics supports the monoamine hypothesis of depression, just as the effectiveness of the SSRI supports the revised serotonin hypothesis.
- The effectiveness of the benzodiazepines supports the GABA hypothesis of anxiety.
In theory, these drugs attach the biological bases of the symptoms of these disorders -- the biological bases of their underlying psychological deficits. But note that the reasoning here is somewhat circular: How do we know that dopamine is implicated in schizophrenia? Because the phenothiazines, which act on dopamine circuits in the brain, are effective in the treatment of schizophrenia. Why do the phenothiazines work so well? Because excess dopamine is the cause of schizophrenia. What we really need is independent evidence that these neurotransmitters are specifically involved in these forms of mental illness.
Setting aside the positive effects of
these drugs, it's also the case that pharmacotherapy
has some problems:
- In many instances, the drugs just don't work. A large portion of patients for whom antidepressant drugs are prescribed do not respond to them fully, so their depression never really lifts. In other cases, the patients will relapse into depression even though they remain on a drug that seemed to work at first.
- It is not easy to predict which of the available drugs
will work for a particular patient. The result is that
many patients must go through an extended period of
"adjusting their medication" until their therapist
stumbles on the one that works for them. If depression
were simply a matter of making more serotonin (or
norepinephrine) available at the synapse, we would expect
all of the antidepressant drugs to have pretty much the
- Many medications have undesirable side effects, such as
the "Parkinsonism" (mimicking the symptoms of Parkinson's
disease) and tardive dyskinesia that frequently
accompanies the use of antipsychotic medications.
- There is a certain lack of specificity in the actions of
drugs -- as when Paxil, an SSRI, is used to treat anxiety
as well as depression.
- Along these lines, there is good evidence that the effects of many psychiatric drugs, including the SSRIs, are heavily loaded with placebo effects. According to one estimate, fully 75% of the effect of antidepressant medication is attributable to placebo, rather than any specific pharmacological action.
- Link to a segment of 60 Minutes, interviewing Prof. Irving Kirsch and others on placebo effects in the drug treatment of depression, broadcast on CBS 02/19/2012.
- But that doesn't mean that antidepressants are just placebos. There is good evidence that they are especially effective for patients with severe or very severe episodes of depression -- less so in patients with mild to moderate depression (Fournier et al., 2010).
- Patients with mild to moderate depression may be
helped just as much, if not more, by psychotherapy as
opposed to medication.
- Psychiatric drugs provide symptom relief, but they do
not provide a cure, in the sense of reversing underlying
biological and psychological deficits. Patients on
medication will often relapse if their medication is
- The prospects of relapse are likely to be diminished if medication is combined with psychotherapy (see below).
- On the other hand, there is some evidence that
medication can actually interfere with
psychotherapy (Forand et al., 2013).
Perhaps the most important consequence of the pharmaceutical revolution in mental health has been to give practitioners, and therapists, a means for managing chronic mental illnesses. In this way, the pharmacological treatment of major mental illness is analogous to the use of insulin to treat diabetes. Patients with schizophrenia will still have schizophrenia, and patients with depression will still have depression, but with medication they can better deal with their illnesses, and lead more productive lives. That's a nontrivial benefit, but genuine cures for mental illness are going to have to wait for further pharmaceutical advances -- or, perhaps, another approach entirely.
Pharmaceutical companies can't just market any old
drug for any old purpose. In the United States, the
Food and Drug Administration (FDA) must approve
specific formulations for specific purposes, with
specific warnings about contraindications and
side-effects, based on research known as a clinical
trial. Clinical trials take place across
a sequence of several phases:
Typically, the FDA requires two separate trials
showing a statistically significant difference
between treatment with the investigational new
drug (IND) and placebo. Sometimes
the IND is compared to the standard of care
-- which is often an older drug. Only about 20% of
IND applications result in actual approval by the
In meeting the FDA standards, it does not matter
how many failed trials have been conducted -- that
is, trials which fail to yield a significant
difference between the IND and placebo. Given
the standard of p < .05, meaning that a
statistically significant difference between two
conditions would be expected to occur less than 5
times out of 100 just by chance, in principle this
means that a pharmaceutical company could conduct as
many as 50 or 100 studies, and just report the
studies that happened to yield significant results just
by chance! In fact, something like this
seems to have happened in the case of some
antidepressants: some pharmaceutical companies
reported only the results of positive trials -- a
phenomenon known as the file drawer problem
(for more details, see The Emperor's New Drugs
by Irving Kirsch). In other cases, the company
will conduct a meta-analysis, combining many
small trials, only some of which have yielded a
statistically significant result, into a much larger
study that shows an overall positive effect.
For this reason, the FDA now requires drug companies
to register all their clinical trials in advance, so
it can be determined how many negative studies were
left "in the file drawer".
After the Phase III clinical trial has been
successfully concluded, and the drug has been
approved for use, research still isn't done.
FDA review and approval is then followed by post-marketing
surveillance intended to identify additional
adverse reactions, other side-effects, and
contraindications that did not show up during the
formal clinical trials. This information may result
in withdrawal of FDA approval, or a requirement to
provide additional warnings or other information on
the drug's label.
A similar sequence of clinical trials is required
for the approval of non-pharmaceutical treatments,
such as heart pacemakers, or new surgical
No research at all is required for the marketing
of herbal remedies, such as St. John's Wort.
This is because these substances occur naturally, in
nature, and are classified as "foods" rather than
"drugs". For this reason, herbal remedies are
often marketed with no, or very poor, research to
back up the marketer's claims.
Once a pharmaceutical firm has developed a drug,
the clinical trials have to be run by physicians
with patients who might benefit from them.
Unfortunately, there are often strong financial ties
between these physicians and the drug companies --
ties that are so strong that they might bias the
physicians' evaluations of the drugs. To help
allay this problem, in 2013 Congress passed the
"Physician Payments Sunshine Act", which requires
pharmaceutical firms and medical-device
manufacturers to disclose most of their financial
relationships with the physicians who perform
research for them -- most, that is, but not
The Life History of a Psychotropic Drug
The process of drug approval can take years and be
very expensive. Consider the example of
Cymbalta, a popular SSRI (as described by Sarah
Amandolare in "Life of a Drug", Scientific
American Mind, September-October 2013).
Psychotropic Medication: A Guide for the
is a relatively new approach to the treatment of mental
illness. Historically, the active treatment of mental illness
was limited to various forms of psychotherapy, a
"talking cure" in which a therapist engaged in activities that
were intended to change the contents of the patient's mind: to
alter patients' beliefs, feelings, desires -- and thus their
behavior. Although there were important precursors, the birth
of psychotherapy is commonly given as 1893, when Sigmund Freud
and Joseph Breuer began publishing the articles that were
eventually collected as their Studies in Hysteria.
- Pharmacotherapy attempts to alter mental functions indirectly, by altering the chemistry of the brain.
- Psychotherapy attempts to alter the mind directly, through various sorts of learning experiences.
There are literally
hundreds of different psychotherapies, but they can all be
classified under three major headings:
- Psychodynamic, Insight-Oriented Psychotherapy, such as Freudian psychoanalysis. In this technique, the therapist helps the patient gain insight into unconscious conflicts that presumably lie at the root of his or her symptoms. For Freud, these conflicts involved primitive, unconscious sexual and aggressive urges, which gave rise to anxiety, which the patient reduced by engaging in repression and other psychological defenses, which in turn caused symptoms to occur. Psychoanalysis was intended to help the patient become aware of these conflicts, and acknowledge his primitive urges, so that the defenses would no longer be needed and the symptoms would disappear.
- "Neo-Freudian" psychoanalysis retained the emphasis on unconscious conflict, but de-emphasized biological drives having to do with sex and aggression, and focused instead on conflicts the patient encountered in the "real world". Classic psychoanalysis was a 5-times-per-week affair; what is known as psychoanalytic psychotherapy is less intense, but follows much the same rationale as the classic form.
- Behavior Therapy began in the 1950s as a behavioristic reaction to the "mentalism" of psychoanalysis. Rather than resolving the unconscious conflicts that supposedly underlay the patient's symptoms, behavior therapists like Joseph Wolpe sought to modify the symptoms themselves, directly, by means of techniques derived from learning theory. From their point of view, symptoms were not caused by disease; rather, the symptoms were the disease. In some cases, such as phobias and obsessive-compulsive behaviors, the assumption was that the symptoms were learned behaviors that could be unlearned; even if the symptoms were not acquired through learning, however, it was assumed that they could be modified by learning (some forms of behavior therapy were called behavior modification).
- Cognitive Therapy: Later, in the aftermath of the "cognitive revolution" in psychology, which supplanted behaviorism,behavior therapy was supplanted by a cognitive therapy which attempted to alter the patient's behaviors, whether overt or covert), by changing the patient's cognitions; early proponents of cognitive therapy were Aaron (Tim) Beck, known for his cognitive theory of depression, and Albert Ellis who practiced what he called rational-emotive psychotherapy. In 2006, Beck received the prestigious Lasker Award for clinical research -- the first ever given to a psychiatrist for research on treatment. The chairman of the award jury noted that cognitive therapy "is one of the most important advances -- if not the most important advance -- in the treatment of mental diseases in the last 50 years" (New York Times, 09/17/06).
- Cognitive-Behavioral Therapy: Even with the new "mentalism" of cognitive psychology, the goal of cognitive therapy was to change the patient's behavior, so the hybrid term cognitive-behavioral therapy (CBT) became popular. Whereas psychodynamic therapy focuses on the patient's past, especially his childhood, CBT focuses on the "here and now" of the patient's life.
- Humanistic Psychotherapy emerged as a reaction to both psychoanalysis and behavior therapy. In both kinds of therapy, the therapist was extremely directive; but -- either keeping the patient focused on unconscious conflicts, or Both , which were perceived as much too directive. Carl Rogers introduced a client-centered therapy in which the patient set the therapeutic agenda, and the therapist helped create an environment of unconditional positive regard in which the patient could achieve self-actualization (a term introduced by another humanistic psychologist, Abraham Maslow). Rogers' language is very revealing here: "patients" are passive recipients of the action of "agents"; but "clients" hire people, like lawyers, to work for them.
Contemporary psychodynamic psychotherapy has its origins in classical Freudian psychoanalysis. But just as "neo-Freudian" theories of personality were de-biologized and de-sexualized, so has contemporary psychodynamic psychotherapy.
Jonathan Shedler (2010) has summarized
the main principles of contemporary psychodynamic
psychotherapy as follows:
- Focus on the experience, expression, and discussion of emotion (in contrast to the focus of cognitive-behavioral therapy on thoughts and behaviors).
- Exploration of the patient's attempts to avoid, resist, and defend against distressing thoughts and feelings.
- Identification of recurring themes and patterns in the patient's relationships.
- Discussion of past experiences, especially the ostensibly formative experiences of childhood.
- Focus on interpersonal relations and attachments.
- Focus on the therapeutic relationship between patient and therapist, which may reflect repetitive themes in the patient's relationships with others outside of therapy.
- Exploration of fantasy life, including dreams and fantasies, but generally allowing the patient to give free expression to whatever is on their minds, instead of following an agenda set by the therapist.
Shedler points out that modern
psychodynamic therapy, while rooted in Freud, has shed most of
the trappings of classical psychoanalysis. There is
little attention paid to the Oedipus conflict and castration
anxiety, for example1 Patients don't necessarily lie on
a couch and free associate for 50 minutes a session, five
sessions per week. Rather, modern psychodynamic
psychotherapy is practiced as an open-ended vehicle for
self-examination -- which means that it might be useful even
for people who don't suffer from depression, anxiety, or some
other form of mental illness.
For a first-person account by a writer who spent most of her adult lifetime (and, for that matter, a considerable amount of her childhood) in psychoanalysis, see "My Life in Therapy" by Daphne Merkin (New York Times Magazine, 08/08/2010) -- or, for a longer treatment,Mockingbird Years: A Life In and Out of Therapy (2000), a book-length memoir from Emily Fox Gordon. For some patients in long-term psychodynamic psychotherapy (and here we think of Woody Allen), the treatment -- especially if it includes hospitalization at an institution like Austen Riggs, or the MacLean Hospital, or the Menninger Clinic -- takes on a kind of Romantic feeling, not unlike the tuberculosis sanitarium depicted in Thomas Mann's novel,The Magic Mountain.
Especially where maladaptive social learning lies at the heart of the patient's illness, psychotherapy can achieve a full-fledged cure through what are essentially re-education techniques -- that is, by arranging new learning experiences that undo, or modify, the effects of old ones. Even when the patient's symptoms are not acquired through learning, at least in the usual sense, cognitive-behavioral therapy can help patients to acquire new modes of thought, and new behaviors, that will counteract the effects of their illness.
- Systematic Desensitization, involving a progressive, graded exposure to a phobic stimulus; and
- Flooding, also known as Implosion Therapy (there are technical differences between these), in which the patient is immediately immersed in the most frightening situation -- either direct contact with the phobic object, or rehearsal of an obsessive thought and prevention of compulsive behavior.
In both cases, the patient can
experience complete alleviation of anxiety, which will never
return -- the very definition of a cure -- through the
extinction of fear, aversion, or other response, and the
acquisition of more appropriate, adaptive behaviors. In the
treatment of phobias, systematic desensitization and flooding
are equally effective. Flooding is more efficient, but it is
also somewhat more dangerous: if done improperly, the patient
will be left worse off than when he started, so don't try
this at home.
For the psychophysiological (psychosomatic) disorders, the best treatment is to eliminate the stressor from the patient's environment. However, this is not always possible, in which case the therapy involves modifying the patient's response, including physiological responses mediated by the autonomic nervous system, to the stressor.
- Relaxation Training seeks to achieve a general reduction in the patient's emotional reaction to the stressor, essentially modulating the general adaptation syndrome (see the lecture supplements on the Biological Bases of Mind and Behavior).
- Biofeedback permits the patient to gain some voluntary control over the functioning of some element of the autonomic nervous system, such as heart rate or blood pressure. Because ANS activity is not accessible to conscious awareness, the therapist must use special physiological monitoring devices, such as the EKG or EMG, to provide information to the patient about his or her internal physiological state. In biofeedback, the apparatus signals the patient's level of physiological activity, and the patient learns, through a feedback process similar to instrumental conditioning, to control his own physiological state.
- According to Beck's original cognitive theory, depression is caused by a particular set of beliefs, as well as a cognitive style that maintains those beliefs. Similarly, following the learned helplessness model of Seligman, Abramson, and Alloy, depression may be caused by the patient's belief that important, particularly aversive events, are uncontrollable.
- Similarly, anxiety may be caused by the patient's belief that such events are unpredictable.
- Delusions may reflect the patient's inappropriate attempts to explain the anomalous experiences associated with schizophrenia and the manic-depressive mood swings of bipolar disorder.
In these cases, the goal
of cognitive therapy is to change the patient's underlying
cognitive structures, or schemata:
- Confront the patient with schema-incongruent information that will stimulate schema change.
- Provide a more adaptive way of construing the patient him- or herself, others, various social situations, the past, present, and future;
- Change the patient's interpretation of the situation, and construal of experience;
- Alter the patient's expectations of the future.
Beck's cognitive therapy for depression entails altering the patient's depressogenic schemata -- the "depressogenic triad" of negative beliefs concerning oneself, the world, and the future. Cognitive therapy also seeks to alter the patient's tendency toward arbitrary inference, selective abstraction, overgeneralization, magnification, and minimization that maintain these schemata once established.
Based on the learned helplessness theory of depression, Seligman, Abramson, Alloy, and their colleagues have suggested that depression may be alleviated by changing the individual's "depressogenic" attributional style that leads to feelings of helplessness and hopelessness, so that the patient will make more realistic, adaptive causal attributions about events.
CBT for Insomnia
A good example of how behavioral and cognitive therapy can be combined is Cognitive-Behavioral Therapy for Insomnia
(CBT-I). I go into detail on this
treatment because sleep is such an issue for college students
-- and for so many other people, too.
CBT-I has five major components:
- Stimulus Control: Strengthening the association between the bed and sleeping.
- Go to bed only when you are actually tired.
- Do nothing in bed except sleep and have sex.
- Get out of bed at the same time every morning.
- If you do not fall asleep within 10 minutes of going
to bed, get up, move to another room, and do something
relaxing until you feel sleepy.
- Sleep Hygiene: Altering the environment to make it more conducive to sleep.
- Within 4 to 6 hours of going to bed, limit the intake of substances such as caffeine, nicotine, and alcohol that interfere with sleep.
- Take a light snack, such as milk or peanut butter, instead.
- Avoid stimulating activity prior to sleep
- Get rid of all distractions: No TV, no computer games; Turn off the cell phone!
- Read a book, write an e-mail, take a warm bath.
- Sleep Restriction: Control the time you spend in bed, to maximize "sleep efficiency" and restore "sleep homeostasis" -- that is, the biological need to sleep.
- Sleep Efficiency (SE) = Total Sleep Time (TST) / Time in Bed (TIB), with the ratio expressed as a percentage.
- Increase TIB if SE > 90%
- Decrease TIB if SE < 80%
- Sleep Restriction involves paradoxical intention,
a concept first articulated by Viktor Frankl, founder of
existential psychiatry, in 1959. It also played a
prominent role in the techniques of an American maverick
psychotherapist, Milton Erickson, as detailed by an
early disciple, Jay Haley (Strategies of
Psychotherapy, 1963; Uncommon therapy,
- Relaxation Training is a set of techniques,
imported from systematic desensitization and
stress-reduction therapies, intended to promote physical
- Cognitive Therapy includes educating the patient
about sleep, changing any dysfunctional attitudes or
beliefs that the patient may have about sleep, and
controlling the patient's worries about losing
Social Skills Training
Many behavioral disorders and
annoying problems in living often result from the
individual's inadequate social skills.
Public-speaking anxiety, while not necessarily rising to the level of a full-fledged social phobia, can be extremely debilitating, but can be relieved simply by giving the person practice in public speaking in a controlled, friendly environment. Many people have a great deal of trouble saying "no" to people, including their parents (or children) or spouses. In this case,assertiveness training can help people make, and respond to, demands more adaptively. People's sexual problems are not limited to impotence or frigidity. Often, the difficulties that people have in maintaining sexual arousal, or achieving orgasm (in oneself or one's partner) reflects a simple lack of knowledge about how to make love (sex is a biological function, and in that sense natural, but the pleasure-giving and -receiving aspects of lovemaking don't come naturally -- as almost anyone who remembers his or her first sexual experiences can attest. Many people learn to make love through practice, but many people need instruction in the form of sex therapy -- not necessarily from a sexual surrogate, but sometimes just some friendly advice.
Cognitive-Behavioral Therapy and Social Intelligence
Whereas pharmacotherapy attempts to alter the disordered mind by altering the chemistry of the brain, psychotherapy attempts to alter the disordered mind directly through learning experiences.
Much of cognitive-behavioral therapy seeks to alter the patient's declarative knowledge about what to believe and expect in various situations, social skills training, like relaxation training and biofeedback, seeks to alter the patient's procedural knowledge about what to do in those situations. Taken together, the cognitive-behavioral therapies work by altering the individual's social intelligence -- his or her fund of knowledge about self and others, and repertoire of interpersonal skills -- that he or she uses to navigate in the social world (see the lecture supplement on Personality and Social Interaction).
Outcomes of Psychotherapy
notion of psychotherapy is fine in principle, and it's made a
healthy living for several generations of psychiatrists,
clinical psychologists, clinical social workers, and other
mental health professionals. But does it really work?
Psychotherapy is plagued by what might be called the Woody
Allen Bugaboo -- after the characters played by the
actor-director, who go through years, decades, of
psychoanalysis but never seem to change.
In fact, psychotherapy came to a crisis in the 1950s when Hans Eysenck, a British psychologist, reviewed the literature and claimed that psychotherapy was ineffective -- that people who received psychotherapy had no better outcomes than those who received no treatment at all. Along with the evident success of pharmacotherapy, and lingering doubts such as expressed by the Woody Allen Bugaboo, therapists were challenged to demonstrate, scientifically, that psychotherapy really helps people with mental illness.
Since Eysenck's original study, a large body of empirical research shows that, contrary to his conclusions, psychotherapy can be an effective treatment for mental illness. For example, a classic study by Smith, Glass, and Miller (1980) employed a technique called meta-analysis (see the lecture supplement on Statistics and Methods) to combine the results of a large number of studies that compared adult patients who received various forms of psychotherapy to control patients who were untreated. Quantifying psychotherapy outcome isn't easy, but it can be done, and it's necessary if we're going to analyze the effects of psychotherapy statistically. Typically, the control patients were not denied treatment, but were merely put on a "waiting list" until a therapist became available. So, the question can be reformulated along these lines: given X months or years since their diagnosis, have patients who received psychotherapy improved more than those who did not? The answer is yes: in the Smith et al. analysis, that the median patient receiving psychotherapy did better than about 75% of the control patients.
Another finding of the Smith et al. study
was that patients who received psychotherapy did better than
those who did not, regardless of what form of therapy they
received. This finding led some commentators to conclude that
all forms of therapy are equivalent. It doesn't matter what
the therapist does, so long as the patient sees one. Lester
Luborsky (1975), a psychoanalyst and prominent psychotherapy
researcher at the University of Pennsylvania (and thus a
colleague of Gleitman's), has expressed this point of view as
the Dodo Bird Verdict, after an episode in Lewis
Carroll's Alice's Adventures in Wonderland (1865).
When Alice discovered that she would not get out of the rabbit hole, she was engulfed in a pond of her own tears, which also drenched a number of animals, such as The Mouse. The Dodo Bird suggested that the animals run a Caucus Race to get dry. The animals ran around until they ran out of breath and stopped. When Alice asked who had won the Caucus Race, the Dodo Bird replied that "everyone has won and all must have prizes".
The Dodo Bird verdict has been a source of comfort to some psychotherapists who prefer to use those psychodynamic forms of therapy that have come under attack by modern scientific psychology, as well as those who believe that the therapeutic relationship between therapist and patient is more important than anything the therapist does (e.g., Frank, 1961; Wampold, 1997, 2001)). Put another way, the "tie-score effect" is taken as indicating that the various forms of therapy have more in common than appears on the surface (see, for example, the Great Psychotherapy Debate: Models, Methods, and Findings by Bruce E. Wampold, 2001). But the Dodo Bird Verdict is troubling, too, because is suggests that the effects of psychotherapy are nonspecific -- that is, that there is no particular "active ingredient" that makes therapy effective. Put another way, it suggests that psychotherapy is simply a kind of placebo. And since psychiatric medications are approved for use precisely because they have been shown to be better than placebo, that suggests that psychotherapy is inferior to pharmacotherapy.
Fortunately, the Smith et al. study contained an analysis that showed that the Dodo Bird Verdict is not quite right: some psychotherapies work better than others. This is already evident in the data presented earlier, which showed that patients who received cognitive-behavioral forms of therapy did even better, compared to controls, than patients who received psychodynamic or humanistic forms of therapy. To examine this issue further, Smith et al. computed measures of effect size (see the lecture supplement on Methods and Statistics) for each of the studies included in their analysis.
The effect size d is a measure of the difference in mean outcomes between two treatments, expressed in standard deviation units. Thus, an effect size of 1.0 means that the average subject in the experimental group scored 1 standard deviation higher than the average subject in the control group. According to Cohen (1977), effect sizes in behavioral and social research can be classified as follows:
- d = .20: a small effect;
- d = .50: a moderate effect;
- d = .80: a large effect.
Smith et al. calculated the average effect size for different
types of therapies, all forms of therapy were shown to have at
least moderate-sized effects, consistent with the Dodo Bird
Verdict. However, the effect sizes associated with the
cognitive and behavioral therapies were much larger than those
associated with the psychodynamic and humanistic forms.
In the Smith et al. meta-analysis, the effect of psychotherapy overall, without regard to the form of therapy or the condition being treated, was quantified as an "effect size" of 0.85 -- which is generally considered a "large" effect in medical, psychological, and social-science research.
A later review by Lipsey and Wilson (1993) -- actually, a mega-analysis, or meta-analysis of published meta-analyses (18 in all), obtained a median effect size of .75 -- which is a substantial effect by any standard.
Other studies have also demonstrated the
general superiority of cognitive-behavioral therapies:
- Chambless and Ollendick (2001) reviewed studies of treatment of the anxiety disorders, and also of depression and behavior problems in children and adolescents.
- Tolin (2010) reviewed studies of the treatment of anxiety and mood disorders.
Based on these studies, and others like them, it appears that all psychotherapies are not created equal: as a rule, cognitive and behavioral therapies are more effective than psychodynamic and humanistic therapies.
Other considerations also
suggest that the Dodo Bird Verdict is wrong:
- For specific illnesses, some forms of therapy are more effective than others: in general the cognitive and behavioral disorders are more effective than insight-oriented therapies in the treatment of a wide variety of mental illnesses, especially the anxiety disorders.
- Moreover, the cognitive-behavioral therapies are more efficient than the insight therapies, achieving their results in less time, and therefore with less expense to the patient or insurance companies.
- And some forms of therapy may even be harmful. For
example, crisis debriefing does not appear to help
patients suffering from post-traumatic stress disorder,
and may even make their problems worse.
- Therapies can be harmful when they are based on the
wrong theory of illness -- as, for example, when a
patient's symptoms are attributed to "repressed
memories" of childhood sexual abuse.
For that reason, cognitive-behavioral treatments are quickly emerging as the "standard of care" in the psychological treatment of mental illness and problems in living.
This does not mean, however, that psychodynamic psychotherapy is not effective. Although classical psychoanalysis, which is what Eysenck studied in the 1950s, does not seem to be more effective than no treatment, better results have been obtained with contemporary forms of psychodynamic therapy.
For example, Shedler (2010) cited a 2006 meta-analysis of psychodynamic therapy that yielded an overall effect size of 0.97.
The real question, though,
is not the comparison of overall effect sizes. Questions about
the efficacy of psychotherapy are better framed more
- What kind of treatment works best for each particular disorder?
- And when two different treatments are effective, which one is more efficient, and less expensive?
- What are the particular mechanisms by which a treatment achieves its successful outcomes?What are the particular mechanisms by which a treatment achieves its successful outcomes?
As a rule, psychodynamic therapy appears to be based on the theory that mental illness is rooted in unconscious conflicts -- not necessarily conflicts over sex and aggression like the Oedipus conflict, but unconscious conflicts nonetheless; and that uncovering these conflicts is the key to successful therapy. However, there is very little scientific evidence that unconscious conflict lies at the root of major forms of mental illness, such as schizophrenia, anxiety disorder, or depressive disorder. And there is no scientific evidence that the primary goal of psychodynamic psychotherapy, which is to bring such conflicts into the daylight of consciousness, is the key to successful treatment. Rather, the evidence seems to indicate that the success of psychodynamic psychotherapy, where it achieves such successes, is produced by the same sorts of techniques employed by cognitive-behavioral psychotherapists -- namely, a focus on the here and now, as opposed to the there and then.
There is also the matter of utility. If psychodynamic psychotherapy achieves its positive outcomes by the same mechanisms as cognitive-behavioral therapy, but takes longer and costs more, then cognitive-behavioral therapy is to be preferred on grounds of cost-effectiveness. CBT is not just based on more scientifically valid conceptualizations of mental illness -- it also delivers more bang for the buck.
On those grounds, it seems that CBT
still has an edge over psychodynamic psychotherapy. But again,
a precise answer to the question will depend on the particular
disorder being treated.
Psychotherapy vs. Medication
How does psychotherapy
stand up, in comparison to medication? This question
has often been investigated in the context of
depression. In a provocative article entitled
"Listening to Prozac But Hearing Placebo", Kirsch
& Sapirstein (Prevention & Treatment,1998) conducted a
meta-analysis of 19 published studies in which an
antidepressant medication (such as Prozac) was
compared to placebo, and another
19 studies comparing psychotherapy with a
wait-list or no-treatment control. Putting
the four conditions together, they
provided a comprehensive
overview of the outcomes of
varous treatments for
- The median effect size (D) for the drug groups was 1.55 standard deviations (SDs), while D for the placebo was 1.16 SDs.
three types of antidepressant medication used
in these studies did not differ
significantly in effect size: tricyclic and
tetracyclic, D = 1.52; SSRIs, D
= 1.68; Other, D = 1.43.
- The mean D for psychotherapy was
1.60, about the same as for drug
treatment (this is a common
finding), compared to D =
0.37 for the controls.
- Unfortunately, K&S did not
compare different forms of
So, some depressed patients get better on
their own, without any treatment -- a phenomenon called spontaneous
remission. Apparently, over
the natural history of an acute
episode, depression sometimes goes
away all by iteself.
Active treatment improves the prospects of a good outcome
considerably, but the outcome with
psychotherapy alone is about the same as the outcome with
drugs alone. And so is the outcome with placebo
medication -- though, frankly, if you think about it,
the placebo group is really another
form of psychotherapy. The patients who received
placebo received all the attention, social support,
and the like that the drug patients received -- only
without the active drug (it's findings
like this that give rise to the Dodo Bird Verdict)..
On the basis of their results, K&S concluded that the active ingredients in antidepressant medications accounted for about 25% of the outcome in the drug treatment of depression; spontaneous remission (natural history) accounted for another 24%, and placebo accounted for approximately 51%.
As you might imagine, this claim drove psychiatrists, who generally favor drugs over psychotherapy, and even some psychologists (who sometimes envy psychiatrists' ability to prescribe drugs; ), quite crazy. Kirsch's title was, in fact, a deliberate play on Listening to Prozac (1993), a pean to the drug by psychiatrist Peter D. Kramer. Kirsch presented additional analyses in a book, The Emperor's New Drugs: Exploding the Antidepressant Myth (2011), that was highly critical of the use of antidepressants. In response, Kramer recently published a new book, Ordinarily Well: The Case for Antidepressants (2016), which conceded that antidepressant medication works best for the most severely depressed patients, but argues that a combination of medication and psychotherapy is good for everyone.
The point of all this is not to diminish the value of antidepressants: there's that 24%, which is not nothing. Kirsch's data are convincing, but Kramer's response is probably correct: when people are depressed, the combination of drugs and psychotherapy can be very helpful. The point is that even powerful psychoactive drugs have substantial placebo components, and this is likely to be true for the major and minor psychedelics as well. As Kirsch et al. (2002) point out, "Placebo alcohol produces effects that are not observed when alcohol is administered surreptitiously...".
If pharmacotherapy is effective, and
psychotherapy is effective, what about the combination of the
two?Here the data is
somewhat in flux, but it appears that the combination of drugs
and psychotherapy is rather promising. In a study by Keller et
al. (2000), depressed patients who received
cognitive-behavioral therapy did about as well as those who
received Serzone (Nefazodone), an SSRI, but those who received
them both did especially well.
Here's another example. Obsessive-compulsive disorder, like many other anxiety disorders, is commonly treated with SSRIs -- even though there are perfectly good cognitive-behavioral therapies for this problem. But SSRIs aren't always effective, or at least they aren't always as effective as we'd like them to be. In a randomized clinical trial, Simpson et al. (JAMA 2013) studied a group of patients with OCD who did not respond positively to a course of treatment with SSRIs. One subgroup got an additional medication, the antipsychotic Risperidone (remember, "antipsychotic" drugs are really little more than major tranquilizers); another got a placebo pill; and a third group got a course of cognitive-behavioral therapy emphasizing exposure and response prevention (i.e., a variant on flooding). The outcome was measured with the Yale-Brown Obsessive-Compulsive Scale, a standardized instrument used in the diagnosis of OCD. The risperidone didn't help much: only about 23% of the patients got better 13% were essentially "cured"), compared to 15% (5% "cured") for placebo. But the cognitive-behavioral therapy helped a lot: 80% of the patients in this treatment group got significantly better, and 43% were essentially "cured". One wonders what would have happened if these patients had simply gotten the CBT, without any drugs at all. Or, whether patients who responded well to the SSRI would have done just as well, or even better, if they received CBT as well. Or, if those patients had just gotten CBT, without any drugs at all.
The fact of the matter is that, for
people with mild or moderate cases of depression, anxiety, and
many other mental illnesses, psychotherapy -- especially some
form of cognitive-behavior therapy -- works about as well as
medication. Medication really boosts treatment outcome
only in severely ill patients. For people with mild to
moderate illnesses, psychotherapy alone reduces side effects
(obviously, becuse patients don't get medication in the first
place) as well as the risk of relapse as the treatment
proceeds and the patient is improving and recurrence of a new
acute episode after full remission.
There is also evidence that psychotherapy is associated with lower relapse rates than medication. In a study of depression, patients were administered either an antidepressant SSRI or cognitive-behavioral therapy. Patients in both groups responded equally well to treatment. But when the patients were followed up some time after their medication was discontinued, or therapy terminated, the patients in the medication group were much more likely to have relapsed -- that is, to have experienced another episode of depression. In other words, psychotherapy came closer than drugs to providing a cure for depression.
And a meta-analysis by Swift et al. (Psychotherapy, 2017) found that patents who receive psychotherapy are less likely to drop out of treatment, or to refuse treatment in the first place. These investigators analyzed studies that compared psychotherapy and pharmacotherapy, alone and in combination. It is standard practice in these sorts of studies to report the number of patients who refused their assigned treatment, as well as the number who dropped out before completing it. Patients assigned to pharmacotherapy alone were more likely to refuse treatment than those assigned to psychotherapy alone, or to a combination. Similarly, patients were more likely to prematurely terminate treatment if assigned to pharmacotherapy alone. People seeking help for mental and behavioral problems appear to prefer the personal contact that comes with psychotherapy; if they're going to get medication, they want the dialog and social support that comes with a live therapist, too. So, even if mediation is the primary vehicle for treatment, supplying adjunctive psychotherapy may help patients stay on course.
Combining psychotherapy with medication often seems like the optimal approach to treatment. Presently available psychiatric drugs offer a fair measure of symptom relief, but not a cure. Psychotherapy gives the patient the knowledge and skills to overcome his illness, or at least to cope with it more effectively. In the Keller study, patients who got Serzone experienced a temporary boost in their mood, and that's not a trivial outcome. But patients who got active psychotherapy learned to deal with their depression on an ongoing basis, and to adjust to the life after the depression went away. More generally, patients can suffer relapses when their drugs are withdrawn, but in a sense new knowledge and skills, acquired through the experience of cognitive-behavioral therapy, never go away. They remain permanently available to the patient, as part of his repertoire of social intelligence.
It's probably for this reason that
patients who receive psychotherapy, regardless of whether or
not they also receive drugs, are less likely to relapse before
full remission, or to experience a recurrence of another acute
episode. On the other hand, there is some evidence that
medication can actually interfere with psychotherapy
(Forand et al., 2013). For mild to moderate cases,
psychotherapy does about a well as drugs -- with fewer
side-effects and less risk or relapse or remission.
Drugs are most effective for the most severe cases -- and even
then, psychotherapy can help, by giving the patient new
knowledge and skills.
And of course, effective psychotherapy
avoids the unpleasant and harmful side-effects of
medications. A good example is insomnia, a
fairly common sleep disorder, and one of the prominent
symptoms of depression. Patients with insomnia are often
treated with prescription medications such as Ambien and
Lunesta, as well as sedative drugs like the benzodiazepines,
and over-the-counter "sleep aids" such as ZzzQuil. But
all of these drugs carry a risk of dependence, if not
addiction; they can make the patient feel groggy even during
the daytime; they can disrupt the REM (dreaming) stage of
sleep. But an effective psychological treatment,
Cognitive-Behavioral Therapy for Insomnia (CBT-I), achieves
the same success rate as medications, without the side effects
(Morin et al., 1994, 2006).
- Interestingly, a course of CBT-I is also effective in lifting depression, roughly doubling the effectiveness of conventional treatments. What's interesting about this is that we usually think of insomnia as a symptom of depression -- that is, as something that is caused by an underlying mental illness. But it's also possible that the relation between depression and sleep is bidirectional -- that is, that insomnia may exacerbate the individual's depression, and treating the insomnia will also cause the depression to life, at least a little. At least the patient won't be depressed about not getting enough sleep!
- Or, it may be that conventional treatments don't do anything for the disordered-sleep component.
- Or, it may be that gaining control over sleep may
improve the patient's sense that he can get control over
the other symptoms, as well.
The combination of drugs and psychotherapy is probably no less important in schizophrenia than it is for depression. We know that a wide range of social stressors can be implicated in the onset of schizophrenia, and it makes sense that eliminating or at least modulating these aspects of the environment would promote successful treatment. Equally important, people with schizophrenia may have to learn how to live with their disability, and these cognitive and social skills must be learned through active rehabilitation programs. (See "A Social Salve for Schizophrenia" by Matthew M. Kurtz, Scientific American Mind, March-April 2013).
- Recent reviews show that these programs can, in fact, be
successful (Horan et al., 2011; Kurtz & Richardson,
- Identifying people at risk for schizophrenia, and helping them acquire these skills, may even prevent the occurrence of the illness in the first place.
Give a man a fish and he eats for a day. Teach a man to fish and he eats for a lifetime.
Giving a patient drugs is like giving a
man a fish: when they're gone they're gone. But the learning
that comes through active cognitive-behavioral psychotherapy
stay forever, as a permanent resource for the patient.
The Social Context of Psychopathology
Traditional forms of psychotherapy, including psychodynamic and cognitive-behavioral forms of therapy, tend to treat the individual patient in isolation -- there's the therapist, and there's the patient, and that's about it. This tradition follows from the medical model, in which the patient has some illness that the doctor treats with an antibiotic, or surgery, or whatever. But psychologically speaking, we've already argued that, as the poet John Donne put it "no man is an island". Psychology explains the individual's behavior in terms of his or her individual mental states, and that goes as well for abnormal behavior, as well as for the psychological deficits and maladaptive social learning that account for it. Individuals live their lives in the context of other people, and it would be foolish to assume that the social context has no influence on individual mental patients and the course of mental illness.
In fact, we've already seen how certain anxiety disorders, such as phobias and obsessive-compulsive disorder, can be acquired through social learning, as well as through direct experience. And also how expressed emotion -- how other family members view and behavior toward the patient -- can influence the prospects for recovery and relapse in patients with schizophrenia.
The role of social factors in
psychopathology can be seen in the various "epidemics" of
- Multiple Personality Disorder in the 1980s
- Attention deficit Hyperactivity Disorder in the early
Group and Family Therapy
Some therapists have gone so far as to assert that it is not enough to treat the individual patient, precisely because, in some psychologically real sense, it's not just the patient who is mentally ill. And if it's not just the patient who is mentally ill, then it's a mistake to treat the individual patient as if he or she were the only person that mattered. If the real problem is with the patient's relationship with other people, then it's the relationship that has to be treated. At the very least, other people have to be enrolled somehow in the treatment process.
This is obviously the case with many problems in living, such as marital difficulties, that are often treated by psychotherapists. If a marriage is in trouble, you can't hope to fix it by working on only one partner. Both partners have to be in the therapy, together.
Many patients are treated in groups in
addition to, or instead of, individual therapy sessions.
Group therapy has obvious economic advantages, and
psychological advantages as well. Patients can learn
that other people have problems like theirs, and learn how
others deal with them. Individual patients can find
social support and encouragement for their own efforts to get
better, and models for improvement. Some patients'
problems are best observed in a group context. And the
group provides a "safe place" where patients can try out new
ideas, feelings, and behaviors.
Alcoholics Anonymous is an informal setting , created and maintained by recovering alcoholics themselves, which provides many of the benefits of group therapy.
the earliest and most vigorous proponents of this idea was
Salvador Minuchin (Minuchin et al., 1974), a psychiatrist who
has specialized in the treatment of eating disorders in
adolescents. Minuchin argued that mental illness should not be
construed as "contained within the individual"; nor should the
mental patient be viewed as a "passive recipient of noxious
environmental [or biological] influences. Rather, Minuchin
argued that family (and other social) interactions may be
responsible for certain forms of mental illness; and that
these family interactions are truly interactional in
nature, in that the patient plays a role in shaping the
environment to which he or she, in turn, responds.
systems model of psychopathology and psychotherapy
"[broadens] the focus from the sick child to the sick child
within the family" and "redefines the nature of pathological
disorder and the scope of therapeutic change" (Minuchin et
al., 1974). The open systems model postulates that:
- The way the family is organized is triggers the development and maintenance of the child's symptoms.
- The child's symptoms themselves help maintain that very same family organization.
Minuchin et al. conclude: "Therefore, therapy must be directed toward changing the family processes that trigger and maintain the child's... symptoms and toward changing the use of these symptoms within the family." Obviously, that can't be done with the child alone; and it can't be done by working on one family member at a time. The whole family has to be enrolled in the treatment of the child, and the whole family has to change.
Minuchin et al. go on to
describe a pathological family organization in terms of
several family transactional characteristics:
- Enmeshment, or a high degree of responsiveness and involvement with the child, so that any change in one family member will "reverberate throughout the family system".
- Overprotectiveness, in which family members' concerns for each others' welfare go far beyond the bounds of any individual's illness.
- Rigidity, such that family members are committed to maintaining the status quo in the family, to such an extent that, quite literally, they prevent the child from getting better -- precisely because any change in the child would disrupt the family's organization.
- Lack of conflict resolution, which prevents families from acknowledging and negotiating various problems.
Minuchin et al. devised a form of family therapy that was expressly designed to identify, challenge, and break down these four characteristics, and thus create a family environment in which the child is permitted, and encouraged, to get well. For example, it wasn't just the individual child who was hospitalized for treatment; the whole family had to stop what it was doing and mobilize for treatment. Minuchin's system was further developed by a group of therapists at the Maudsley Hospital in London (yes, that's the old "Bedlam", now much reformed and one of the world's leading centers for research on psychopathology and psychotherapy), and is now known as the "Maudsley model" for family treatment of adolescent eating disorders.
In their initial 1974
study, Minuchin et al. reported about 86% success in treating
48 children with "superlabile" diabetes, "intractable" asthma,
or anorexia nervosa, but they did not have a comparable group
that received traditional individual therapy. The comparison
of family vs. individual therapy has been carried out mostly
by the Maudsley group, who largely confirmed Minuchin's
- For example, Russell et al. (1987) reported that, after 1 year of treatment, family-based treatment (FBT) for eating disorder (both anorexia and bulimia) produced significantly better outcomes than individual treatment (IT), especially for patients whose illness had began in childhood or adolescence.
- Interestingly, a 5-year followup of these patients by Eisler et al. (1997) found no difference between the two groups, indicating that the patients who had received individual treatment eventually got better as well. But that doesn't mean that the FBT and were equally effective. Most patients with eating disorder will, eventually, "grow out" of their disorder in the natural course of time. But in the meantime their lives, and their families' lives, are hell, and there are significant risks to the patients' health while the illness runs its course. So anything that gives the natural course of the illness a boost is a good thing -- and FBT is a much better booster than IT.
Chronic Disease Management and Rehabilitation
What about instances of
mental illness where a cure is impossible? There are lots of
such disorders, including:
- the organic brain syndromes (brain damage is, for all intents and purposes, irreversible);
- intellectual disability (most syndromes can't be reversed or prevented);
- schizophrenia (the tranquilizers are tranquilizers, not cures);
- autism (no cure yet, though some behavioral treatments can effectively convey important social skills);
- relapsing mood or anxiety disorders (relapse is likely when the drugs are discontinued).
After the acute phase of mental
illness, after efforts at treatment have gone as far as they
can, the patient may move into a chronic phase. Such
circumstances call for rehabilitation programs to help
patients and others cope with their chronic disability, get
out of the institution, back to their families and
communities, and make an optimal social adjustment despite
Before the 19th century, there was little by way of active treatment or rehabilitation. Psychology wasn't yet a science, nor was psychiatry a branch of medicine -- and never mind that medicine wasn't all that scientific, either!
For the most part, mental patients, when they became too much trouble, were simply warehoused -- often, kept in prisons along with criminals. Sometimes, they were housed in special "insane asylums", separate from convicts. A good example of an 18th-century insane asylum is the Royal Bethlehem Hospital in London, founded in 1337 as a religious charity, then taken under royal auspices in the 16th century. But even these hospitals could offer little more than custodial care, and conditions in most of them progressively deteriorated. Which is how the Royal Bethlehem Hospital got the nickname "Bedlam". In fact, the middle and upper classes used to pay a fee to visit the hospital and watch the antics of the patients as a form of Sunday-afternoon entertainment.
"Bedlam" and The Rake's Progress
The word bedlam has come to mean "a state of uproar or confusion", but the word has its origins as the popular name of the Royal Hospital of St. Mary of Bethlehem, in London. Bedlam, originally founded as a charity hospital in the 14th century, had by the 18th century become a notorious madhouse, and was depicted in William Hogarth's A Rake's Progress, a series of eight paintings (also published as engravings, with the images reversed) produced in 1733-1735. In the sequence, Tom inherits a fortune from his father, abandons his finance, Sarah Young, who is pregnant with his child, and moves to London to live the high life. He leads a life of increasing dissolution, falls into debt, and marries a rich but ugly spinster, but he gambles away her fortune as well. He is incarcerated in debtors' prison, but goes mad (perhaps suffering from dementia caused by syphilis) and is consigned to Bedlam.
The Bedlam scene has been described as an authentic representation of the interior of the hospital as it existed in the 18th century -- with individual cells, men's and women's quarters separated by an iron grate, hospital staff, potentially suicidal patients (like Tom) chained to the walls, sightseers who paid a tuppence to view the patients' antics, and Sarah kneeling beside Tom.
See "A Rake's Progress: 'Bedlam'" by James C. Harris,Archives of General Psychiatry, 2003). Hogarth's series of engravings was the inspiration for The Rake's Progress, an opera by Igor Stravinsky, with libretto by W.H. Auden and Chester Kallman (1951).
Even though Esquirol distinguished between the mentally ill (in his terms, the insane), the intellectually disabled (in his terms, the mentally deficient), and mere criminals, they were still all housed together (except for insane members of upper-class families, who were more likely to be consigned to the attic, as in Charlotte Bronte's Jane Eyre). Things began to change when Philippe Pinel (1745-1826), became the superintendent of the Bicetre, an asylum in Paris, and later the Salpetriere, a large mental hospital (which you can still see when you visit the city). Along with his mentor, Jean-Baptiste Pussin (1745-1811), Pinel pioneered the "moral" treatment of those who, although mentally ill, still deserved respect as "citizens". Pinel is also credited with freeing the mentally ill from their chains -- although it was actually Pussin who did this (and he replaced the chains with straitjackets!).
moral, humane treatment of the mentally ill quickly spread to
England and America. Bethlem Hospital was reformed. In 1792,
Benjamin Rush (1745-1813), a physician who had been one of the
signers of the Declaration of Independence, founded a division
of the Pennsylvania Hospital (itself the first hospital in
America, after New York's Belledvue), devoted to the moral
treatment of the insane. Rush's treatise, Medical
Inquires and Observations Upon diseases of the Mind
(1812) was the first textbook of psychiatry published in
America. Anotehr book, On the Construction,
Organization, and General Arrangements of Hospitals for the
Insane (1854), by Thomas Kirkbride, the first
superintendent and physician-in-chief of the Institute,
remained influential even into the 20th century. (I worked at
The Institute as a graduate student at the University of
Pennsylvania). See "Rush's Remedies" by Susan Frith, Pennsylvania
There was also an extensive system of private mental hospitals, catering mostly to the wealthy. An early example was the Sidis Institute at Maplewood Farms, a large estate in Portsmouth, New Hampshire. Established by Boris Sidis, a friend of William James, and leader of the "Boston School" of psychotherapy (and father to William James Sidis, at the time the youngest person ever to enter Harvard College, at age 11), the Institute offered all the latest treatments, including psychotherapy in an environment of "beautiful grounds, private parks, rare trees, greenhouses, sun parlors, palatial rooms, luxuriously furnished private baths, private farm products". By 1916, there were more than 20 such institutions in Massachusetts alone.Link to the Sidis Institute website.
Still, some of these asylums were awful
places, little better than bedlam. In 1845, the British
government set up the independent Lunacy commission to set and
enforce standards for private mental hospitals. For a
history of mental-hospital reform in Victorian England, see Inconvenient
People by Sarah Wise (2013).
the late 19th century publicly supported mental hospitals were
a feature of virtually every state health system. These were
often glorious structures, architecturally distinctive
-- following the precepts laid down by Thomas Kirkbride (see Asylum:
Inside the Closed World of State Mental Hospitals by
Christopher Payne (2010).
- Binghamton State Hospital, near where I grew up in New York State, was a neo-Gothic structure, built in 1858, and situated on a hill overlooking the city like some medieval castle. It's on the National Register of Historic Places.
- Napa State Hospital, erected in Northern California in 1872, also a neo-Gothic structure, included farming operations designed to make the hospital self-sufficient, and also to provide a kind of occupational therapy for the residents.
- Oregon State Hospital, in Salem, was the setting for Ken Keesey's novel, One Flew Over the Cuckoo's Nest -- location for the film made from the book. Its classic building has now been repurposed as a Museum of Mental health, which tells the story of public, state-funded mental hospitals.
Here are some more classic state mental hospitals.
|The Trans-Allegheny Lunatic Asylum, built between 1858 and 1881, in Weston, West Virginia. Now closed, it still hosts guided tours. See "Getting Into the Spirit" by John Searles, New York Times 10/13/2013.|
|Greystone Park Mental Hospital, in New
Jersey. Like the Trans-Allegheny Asylum, Greystone was
designed as a "Kirkbride
building", following the principles of "moral
treatment" of the insane promoted by Thomas Story
Kirkbride, who trained, and later ran, the Institute
of the Pennsylvania Hospital in Philadelphia.
Woody Guthrie, the American folksinger, was a patient
here from 1956 to 1961 (when Guthrie told the staff
that he had written 8,000 songs, he was diagnosed as
having "grandiose ideas" and as lacking in "judgment"
and "insight". As of 2015, Greystone Park was
slated to be demolished, although a group of
preservationists were trying to save it as an
important historical landmark. See
"Preservationists Fight to Save a Former Mental Asylum
in New Jersey" by Dan Hurley, New York Times,
But as good and humane as these
hospitals were intended to be, they still offered little more
than custodial care until the beginning of the 20th century,
when advances in psychology and psychiatry began to afford the
possibility of active treatment of the mentally ill. In the
20th century, reflecting our progressively increased
understanding of mental illness, public and private mental
hospitals offered active treatments as well as custodial care:
biological treatments like psychosurgery, ECT, and later drug
treatments of various kinds, as well as psychotherapy by
psychologists and social services by social workers.
A 1946 expose by Life magazine described many American asylums as "little more than concentration camps".
All that came to a screeching halt with
the de-institutionalization movement that began in the
1960s, when the mental hospitals began to be emptied and their
residents discharged back to their families and communities.
Partly this was a result of the early successes of the
pharmaceutical revolution, which made many schizophrenics more
manageable, and afforded symptom relief to many with patients
suffering from depression and anxiety disorder. In addition,
most public mental hospitals suffered from overcrowding, and
budget difficulties led to a lack of properly trained and
supervised staff, and corresponding scandals of the sort
exposed by Life magazine. But there were also
other contributing factors:
- There arose an anti-psychiatry movement which questioned not only the existence of mental hospitals, but the whole idea of the mental-health professions.
- Thomas Szasz (1920-), influenced by a radically libertarian political philosophy, argued in his book,The Myth of Mental Illness (1960) that, aside from actual neurological disorders, most of what we call "mental illnesses" were simply "problems in living" and psychiatry ought to mind its own business.
- Theodore Sarbin (1911-2005), a social psychologist (who taught at Berkeley before moving to the then-new UC campus at Santa Cruz), also argued that mental illness was a myth, born of a mistaken metaphor with physical illness. For Sarbin, mental illnesses was a role imposed on individuals whose behavior deviated from prevailing social norms.
- R.D. Liang (1927-1989), influenced by the 60's passion for psychedelic drugs, argued that, far from being symptoms of some kind of medical disorder, what we call "mental illness" was really an episode of transformation not unlike what Native Americans experience in their "vision quests".
- The burgeoning civil rights movement of the 1950s and 1960s expanded into a movement for the rights of disabled people -- including the mentally disabled. Under a doctrine of "least restrictive conditions", the law came to the view that disabled people had a right to live with the least restrictions possible. For people in wheelchairs, that meant that public accommodations had to build ramps, and widen their doorways. For people with mental illnesses, that meant no more confinement in mental institutions.
- In 1967, the New York Civil Liberties Union stablished its project on Civil Liberties and Mental Illness.
- In 1971, Frank Johnson, a federal district court judge in Alabama, decided (in Wyatt v. Stickney) that patients in a state mental hospital had a constitutional right to treatment, not mere confinement.
- In 1972, a similar case in New York, concerning the
residents of the Willowbrook State School for what was
then called the "mentally retarded" (New York ARC v.
Rockefeller), required the state to facilitate
community placement of intellectually disabled
- In 1973, the American Civil Libertis Union followed suit, with its Mental health Law Project.
- In 1975, the United States Supreme Court unanimously
decided (in O'Connor v. Donaldson, also argued
by Ennis) that patients involuntarily confined to mental
hospitals were constitutionally entitled to effective
treatment. Agreeing with a lower court decision,
the Court declared : "a State cannot constitutionally
confine... a non-dangerous individual who is capable of
surviving safely in freedom by himself or with the help
of willing and responsible family members or
- In 1990, the Americans with Disabilities Act (ADA) required that individuals with physical and mental disabilities be allowed to live in the least restrictive setting possible; and, wherever possible, to be integrated with non-disabled individuals.
- In 1999, the requirement that mentally ill people be able to live in the least restrictive settings possible was affirmed by the United States Supreme Court in Olmstead vs. L.C.
- In 2010, the Affordable Care Act (ACA, aka Obamacare)
listed mental health and substance abuse services among
10 "essential health benefits", and mandated parity
between physical and mental illnesses. The ACA
also included federal subsidies permitting individuals
under 65 years of age to receive community mental health
services (individuals over 65 were already covered in
this respect under Medicare), and expanded mental-health
coverage for the poor under Medicaid.
- And then, of course, there was the economy. Hospitalization is expensive, and as states looked for ways to tighten their budgets, public mental hospitals were an easy target.
The federal government encouraged
de-institutionalization as well, for both economic and legal
reasons. But the funds promised to support community and
family treatment of de-institutionalized mental patients never
were forthcoming -- with the result that homeless people with
mental illness and substance abuse are found on the streets of
every major city (if you don't believe me, check out Peoples'
Park in Berkeley, or Civic Plaza in San Francisco).
De-institutionalization was not a bad
idea. There were, admittedly, lots of people confined to
mental hospitals who didn't need to be there. At the same
time, it's not at all clear that the homeless mentally ill are
better off on the streets of Berkeley and San Francisco than
they would be within the walls of Binghamton or Napa State
Hospital. Moreover, mental hospitals could have created an
environment for the active rehabilitation of the mentally ill,
preparing them for lives in the community and with their
families. Such environments are going to look
increasingly attractive as an aging population of Baby Boomers
increases the number of individuals with Alzheimer's Disease
and other forms of dementia, and individuals on the autism
spectrum outlive their parents and other family members who
have cared for them.
And community mental health treatment
isn't always all it's cracked up to be, either. All too
often, substandard care in large state institutions has been
replaced by substandard care, barely better than custodial
care, in small group homes, run on tight budgets, by
individuals who, however well-intentioned they may be, often
lack proper training and supervision. And then again,
many of these group homes are run on a for-profit basis,
further limiting the care and support that the
non-institutionalized mentally ill receive. Many
homeless mentally ill and up in local jails, for want of any
other way of housing them -- a step backward, I suppose,
toward the moral model of mental illness.
For this reason, some prominent
psychiatrists have begun to advocate for a revival of the
state mental hospital system for the care of the chronically
mentally ill (see "Improving Long-Term Psychiatric Care: Bring
Back the Asylum" by D.A. Sisti, A.G. Segal, and E.J. Emanuel,
Journal of the American Medical Association,
2015). The same legitimate concerns that led to
de-institutionalization in the first place will probably
oppose any such move (see, for example, "Under Lock & Key:
How Long?" by Aryeh Neier & David J. Rothman, New York
Review of Books, 12/17/2015). But if re-institutionalization
occurs, we can hope that it avoids the problems that cropped
up in the 20th century. That will take money, for proper
facilities and proper staffing; and strict enforcement of the
legal principle of "least restrictive treatment". The
mental hospital may have its place in public policy, but
nobody should be sent there who can't receive safe, effective
treatment in the community.
For better and for worse,
de-institutionalization is a fact of life in the United
States, and many other developed countries as well. But
in underdeveloped countries, institutionalization remains the
norm, and the institutions themselves are often little more
than warehouses for the mentally ill. In 2013, the World
health Organization introduced a "global mental health plan"
to move from centralized mental hospitals to community-based
care. But this takes money -- money that is hard to come
by even in a rich country like the United States, and even
harder to come by for the underdeveloped countries of the
Third World. (For more information, with a special focus
on developments in Guatemala, see "Where Mental Asylums Live
On" by John Rudolf, New York Times, 11/05/2013.)
Even in the case of the organic brain
syndromes, developmental disorders, and functional psychoses,
behavioral treatments such as token economies,
employing the principles of instrumental or operant
conditioning, can facilitate the acquisition of new, more
adaptive behaviors in individuals with actual or presumed
brain pathology. In token economies, patients receive tokens,
such as poker chips, contingent on their performance of
certain actions, such as cleaning their living area or
dressing themselves; these tokens may then be exchanged for
goods at the hospital canteen or other privileges. In the
language of instrumental conditioning, then, the tokens are
secondary reinforcers. Perhaps as much as medication, these
training procedures help chronic mental patients return to
their families, and live in the community, by providing them
with the repertoire of behaviors they need to live outside the
confines of the mental hospital. (Token economies can also
serve as laboratory models of national economies, but for some
reason behavioral economists haven't taken much interest in
Social Interventions for Autism
Autism is one of the most challenging
chronic mental illnesses. Psychotropic medication can
help manage some of the secondary symptoms of autism, such as
the mood swings, temper tantrums, and irritability that
autistic children display, but have essentially no impact on
the child's primary deficits in communication and other
aspects of social interaction. For that, the best hope
lies in psychosocial interventions (though injections of
oxytocin have been recommended!).
One intervention technique, derived from
instrumental conditioning, is applied behavior analysis
(ABA), first devised by O. Ivar Lovaas for the treatment of
children with autism. This treatment program involves an
intensive regime, perhaps 40 hours a week (i.e., a full-time
job for both the child and his therapists), beginning very
early (as young as 3 years of age). ABA involves an extensive
system of rewards and punishments intended to shape and
reinforce desirable behaviors, such as making eye contact and
sitting quietly, and to eliminate or discourage undesirable
ones, like yelling or head-banging. Early applications of ABA
sometimes used punishments such as slapping or even electrical
shocks (delivered by an instrument that looked disconcertingly
like a cattle prod), resulting in considerable criticism. Yet
Lovaas contended that his methods delivered results when other
strategies did not, and he eventually gave up punishment in
favor of a regime based entirely on positive reinforcement (in
this respect, following Skinner's dictum that positive
reinforcement is much better than punishment for controlling
behavior). In 1987, Lovaas reported that his treatment had a
50% success rate (a 1993 follow-up showed that most of the
patients had maintained their treatment gains). Subsequent
studies have not reported about a 30% success rate, which is
still better than most other treatments for autism. ABA is
phenomenally expensive, unless you consider the alternatives,
and it is now a standard treatment for autism.
A number of other interventions have combined techniques from ABA with more cognitive approaches derived from the study of social development and the "theory of mind". For example, the Early Start Denver Model (ESDM) focuses on getting the child to pay attention (and respond appropriately) to social cues such as facial expressions, gestures, and -- last but not least -- speech. Studies have shown that ASDM is effective, but it isn't easy, one study employing more 2000 hours of therapy delivered over the course of two years.
Some variant of ABA is the most popular,
and effective, approach to treatment currently available for
autism spectrum disorders (ASD). There is no medication
available, other than sedatives. And although we
generally think of autism as a "chronic" mental illness, from
which a patient will never fully recover, in fact the
prospects for improvement are not trivial. As with
schizophrenia, it is possible for an autistic individual to
make a substantial-enough recovery that he or she will no
longer qualify for ASD.
- Fein and her colleagues (2013) identified a group of 34 individuals who had been diagnosed with autism in childhood but who, as adolescents or young adults, no longer qualified for the diagnosis. Not all of these individuals had received ABA, or any formal behavioral treatment, but most of them, when they did carry the diagnosis, had milder social symptoms than a comparison group with "high-functioning" autism.
- Lord and her colleagues (2014) followed a group of patients who had been diagnosed with autism at age 2 (about as early as the diagnosis can be made). By age 22, about 10% of this group no longer qualified for the diagnosis. Interestingly, this subset had higher IQs than those who did not make an "optimal" recovery.
One conclusion from these studies is that, as with schizophrenia, prognosis is related to premorbid personality as well as to active treatment. Those patients who do better, achieving an optimal outcome of their illness, may be those who have better resources at the start: better social skills, higher intelligence, and the like.
Cognitive Restructuring -- Again
As discussed earlier, a number of theorists have proposed that paranoid delusions reflect schizophrenic patients' inappropriate attempts to explain the anomalous experiences they have as a result of their illness. Accordingly, another aspect of rehabilitation may be to give delusional patients more appropriate and adaptive explanations for what is happening to them.
When I visited China in 1985, as part of a delegation of mental health specialists, the mental-health authorities we meat stressed that the incidence of schizophrenia in the People's Republic of China was no different than that in other countries -- which is what we would expect if schizophrenia was due largely to genetic and biochemical factors. However, we were also informed that the incidence of paranoid schizophrenia was lower in China than in other countries. I have no independent knowledge of whether this is so, but the attributional account of delusions offers an explanation for this fact (assuming it is true): in China, social organization is such that the mentally ill are detected very early in the acute phase of their illness, and are brought to local mental hospitals for treatment. At least at the time of my visit, it was routine for these acute patients to be given antipsychotic medication followed by a series of lectures on the nature of their illness. Perhaps, when schizophrenics in the acute stage of their illness are given correct information about what is happening to them, they have no need or opportunity to develop delusional explanations for themselves.
Rehabilitation is an important aspect of mental-health
treatment because, at least for the present, most serious
mental illnesses, such as schizophrenia, autism, and the more
serious forms of mood disorder, are chronic diseases:
psychiatric medications provide only symptomatic relief, and
psychotherapy can only go so far. For mental health, as for
the rest of medicine, in the face of incurable illness we do
not simply throw up our hands and walk away from the patient.
Nor, for that matter, do we continue fruitless attempts to
cure the patient's illness. Rather, in chronic illness the
goal of treatment shifts from cure to rehabilitation -- to
help the mentally ill become at least partly self-sufficient,
to live on their own or with their families, or in halfway
houses and other protected living environments. In mental
health, as in the rest of medicine, permanent hospitalization
is the last resort.
Stigma, Stereotypes, and the Self-Fulfilling Prophecy
Unfortunately, the prospects of
successful treatment of mental illness -- whether success
comes in the form of a cure or rehabilitation -- is hampered
by the social context in which mental illness occurs.
- People frequently overemphasize the statistical or social criteria for mental illness, labeling as "sick" behavior that is simply unusual, infrequent, or nonconforming. An extreme example of this tendency is the use of psychiatric diagnosis as a means of social control -- as in the former Soviet Union, where political dissidents where frequently diagnosed as mentally ill, and incarcerated in mental hospitals, simply on the basis of their disagreement with government policies.
- There is also a tendency to embrace the moral rather than the medical model of mental illness, so that the mentally ill are perceived as socially undesirable -- as bad, immoral, or even evil; and as somehow responsible for their own problems (or, at least, their failure to overcome them). As a result, people impose a "criminal" role on mental patients, instead of the "sick" or "impaired" role, emphasizing restraint and punishment as opposed to cure or rehabilitation. A familiar example of this tendency is the stereotypical association of mental illness with violence and criminal behavior, as well as the tendency to NIMBYism (as in Not In My Back Yard) when it comes to the establishment of halfway houses and other facilities for the community care of the mentally ill.
- And, finally, there is a tendency to identify people
with their illnesses -- particularly their mental
illnesses, by referring to people as schizophrenics
or depressives, rather than people with
schizophrenia or people with depression.
More subtle, perhaps, is the frequent occurrence of stereotyping when it comes to the mentally ill, as well as the dominance of first impressions -- psychiatric diagnoses, once made, tend to stick so that the person never sheds the label of "schizophrenic", "manic-depressive", etc., or for that matter the sick or impaired role. Generally, there is a popular refusal to admit the possibility of a good outcome in mental illness -- a successful treatment, whether cure or rehabilitation, that would allow the person to leave the sick role and assume his or her proper role(s) in society.
Erving Goffman, a sociologist, analyzed what he called the stigma of mental illness. For Goffman, a stigma is "an attribute that is deeply discrediting" -- which turns a "whole person" into a "tainted, discounted one". Many physical stigmata (that's the plural of stigma) are immediately apparent. But others, like the stigma of mental illness, are not readily apparent. The mentally ill only become stigmatized when their mental illness becomes known to others. Before their conditions become known, the mentally ill, with their secret stigma, are discreditable; after their condition becomes known, the mentally ill are actually discredited.
- Concealability: Some stigmata (that's the plural of stigma) can be concealed, while others cannot. In an earlier time, being black was stigmatized, but light-skinned African-Americans were often able to "pass" for white, and be accepted by white society. The stigmata of mental illness are not immediately apparent, allowing mentally ill people can "pass" for "normal".
- The course of the mark refers to the extent to which the stigma can be concealed over time. It might be possible for a mentally ill individual to conceal his condition for a period of time, but the more time he spends with other people, the more likely it is that he will inadvertently reveal his stigma.
- Disruptiveness has to do with the extent to which the stigma can impair the individual's social interactions.
- Aesthetics has to do with other people's reactions to the stigma.
- The origins of the stigma may be congenital (present at birth) or acquired; if the latter, it may have been acquired accidentally or deliberately, perhaps due to some misbehavior on the part of the individual.
- Peril has to do with the danger, or the apparent danger, that the stigma poses to other people.
- Social selection is the process by which people identify and label the differences that are important to them. Most people don't care whether someone has a physical illness (unless, perhaps, it's contagious). But Link and Pheelan argue that people are very much concerned about mental illness. If someone knows that you've been diagnosed with schizophrenia, that makes a difference to them in a way that knowing that you've been diagnosed with asthma does not.
- Stereotyping is the process by which the person's label, as mentally ill, is linked to a whole list of undesirable characteristics. If you've got heart disease, it doesn't matter. But if you've got a mental illness, or so people think, maybe you shouldn't be around children, or you're the wrong person for a particular job.
- Social selection inevitably leads to a separation between "Us" and "Them", the stereotyping group, and the group that gets stereotyped.
- The distinction between "Us" and "them" inevitably leads to discrimination against "Them", and Their loss of status. This is the discrediting that Goffman talked about. The discrimination can be direct ("the mentally ill need not apply") or structural (built into the structure of society, as when mental hospitals are set apart from other hospitals). If halfway houses for the mentally ill are located in less-desirable areas of towns and cities (as they often are), that carries the implication that the mentally ill are also undesirable. And when stigmatized individuals incorporate their stigma into their self-concept, they may begin to view themselves as undesirable as well.
- And then there is the exercise of power: medical patients are supposed to follow their doctors' orders, but they can question them, and challenge them, and seek second opinions, and do what they want. Mental patients, because they are presumed to be incompetent mentally, don't have this same kind of countervailing power.
- Applying the statistical and social standards for abnormality, we can label unusual or nonconforming behavior as "sick", leading to an inappropriate diagnosis of mental illness. In the former Soviet Union, people who were opposed to communism were often diagnosed as mentally ill and confined to mental hospitals. This still happens in the People's Republic of China, even today.
- Applying the moral vs. the medical model, it is easy to view the mentally ill not just as socially undesirable, but also as responsible for their own afflictions. It is this emphasis on the "criminal role" that led, in the 18th century, to the confinement of the mentally ill with paupers and criminals in asylums like Bedlam.
Also subtly keeping the
mentally ill "sick" is the self-fulfilling prophecy
(discussed in the lecture supplements on Personality and
- the diagnosis of mental illness creates expectations concerning the patient;
- these expectations lead to behavior on the part of others that elicits abnormal rather than normal behavior from the patient;
- they also lead the patient's normal or ambiguous behavior to be interpreted by others as "abnormal";
- in either case, the patient's behavior is taken as confirming the diagnosis of mental illness.
Such a process can lead patients to
define themselves as incurably ill, diminishing their
motivation for therapeutic change. It can also lead those who
care for mental patients to substitute custodial care and
medication for active treatment that might return patients to
their normal role(s) in society. If there are few or no
attempts at cure or rehabilitation, we can virtually guarantee
that mental patients will never get well.
A good example comes from schizophrenia, which is generally thought to have a poor prognosis. In fact, people with schizophrenia can show a remarkably good recovery, with treatment, so long as they get the right treatment, in the right environment -- and, perhaps, have a "better" premorbid personality to begin with.
Yet another approach to the stigma of
mental illness is simply to deny it. Some individuals
with autism, for example, deny that autism is a mental illness
which should be treated an eliminated. Instead, they
argue that autism exemplifies neurodiversity. In
this view, autistic individuals are not mentally ill -- they
just have brains that operate differently than most other
people. And while they may need help and accommodation
in some respects, they assert that autism isn't something to
be eliminated. Rather, they incorporate autism into
their personal identities.
- Temple Grandin is a case in point. Diagnosed with autism as a child, she grew up to get a PhD and have a substantial career as a specialist in animal behavior, on the faculty at Colorado State University. She argues that her autism gives her a special ability to understand the interior lives of livestock and other domestic animals.
The "Pseudopatient" Study
The deleterious effects of the social
context on the treatment of the mentally ill are illustrated
by a controversial study performed by David Rosenhan, a
professor of psychology and law at Stanford University, in the
1970s. In this study, Rosenhan, as well as some colleagues and
students, sought and gained admission to a number of different
mental hospitals, public and private, by falsely reporting
some symptoms commonly associated with mental illness. All the
"pseudopatients" were in their mid-30s (except perhaps for
Rosenhan himself), gainfully employed, with no prior history
of psychopathology, and during the admission interview all the
patients told the truth about themselves except for two
- they did not reveal that they were academic researchers, or that they worked in an academic organization;
- they claimed to be experiencing auditory hallucinations in which voices spoke such words as "empty", "hollow", and "thud" (a voice said thud? -- never mind).
Given that hallucinations are serious symptoms, it is not surprising that all of the pseudopatients were admitted to the hospital for observation. What is surprising is what happened next.
Immediately upon their
admission, the pseudopatients ceased their simulation, and
behaved normally in every way (except for identifying
themselves explicitly as simulators). Other patients on the
ward frequently noticed the change, but by and large the
professional staff did not. In fact, Rosenhan reports that the
pseudopatients were largely ignored by the staff.
- Most were given a diagnosis of schizophrenia, and their behavior was interpreted in terms of the diagnosis. For example, all the pseudopatients kept journals of their experiences. In the chart of one pseudopatient, this was described as "patient engages in writing behavior" -- although if the staff had bothered to read what the patient was writing, his deception would have been uncovered immediately.
- The pseudopatients were given mostly custodial care, including medications of various sorts averaging 14 capsules per day (they tongued" these pills, and then disposed of them when they could do so unobserved).
- The pseudopatients stayed in the hospital an average of 19 days, at which time most were discharged with the diagnosis of "schizophrenia in remission" -- notice how the diagnostic label stuck?
A possibly apocryphal story: In one particular episode, Rosenhan spent a sabbatical quarter as a pseudopatient. At the end of the term, when Rosenhan was obliged to return to his teaching duties, he informed the attending psychiatrist that he was Prof. David Rosenhan of Stanford University. The response was "Oh,sure you are!". Rosenhan's wife had to secure a legal write of habeas corpus to get him discharged.
And another one. In another episode, one of Rosenhan's colleagues, an international authority on depression, while masquerading as a pseudopatient, noticed that a particular patient was being treated for depression with an inappropriate drug. The colleague, while staying in his pseudopatient role, approached one of the ward psychiatrists to discuss the matter -- identifying himself merely as someone who had read a lot about depression. After the discussion, the psychiatrist made a notation on the pseudopatient's chart that he displayed "grandiosity", and increased his medication!
That Rosenhan and his collaborators were admitted to mental hospitals is unremarkable. Anyone who reports auditory hallucinations deserves some further investigation. But after their admission, the treatment of the pseudopatients can only be described as gross negligence. There was little or no investigation of the "presenting complaints" that brought them to the hospital in the first place, and the clinical staff failed to notice that their symptoms had "remitted". There was little or no active attempt at cure or rehabilitation, or apparently any consideration that active treatment was possible.
Although the pseudopatient study is
often cited as an example of the negative effects of the
medical model in psychiatry, it would be more accurate to say
that the problems encountered by the pseudopatients occurred precisely
because the clinicians failed to adhere to the medical model.
If the psychiatrists and others had acted in accordance with
the medical model, they would have discovered much sooner that
the patients' symptoms had disappeared; they would have been
more observant of their behavior; and they would not have been
so quick to dispense medication to patients who did not need
Nellie Bly, Nellie Bly...
his colleagues were perhaps inspired by Nellie Bly (the
pen-name -- taken from the song by Stephen Foster -- of
Elizabeth Jane Cochrane Spearman, 1864?-1922), a pioneering
("daredevil" woman investigative journalist. Bly began her
career with the Pittsburgh Dispatch, but became
famous on the staff of the New York World, published
by Joseph Pulitzer (he of the prizes). In 1888, she feigned
insanity to gain admission to New York's infamous
Blackwell's Island insane asylum to gather material for an
expose of patient mistreatment that led to a number of
important reforms in the mental-health system. The series
was subsequently published as a book,Ten Days in a Mad
But this was not by any means Bly's only
accomplishment. In 1890, she beat Jules Verne's fictional
record by traveling around the world in less than 80
days (72 days, 6 hours, 11 minutes, and 14 seconds, to be
exact). After retiring from journalism to run her deceased
husband's companies, she introduced a number reforms for the
treatment of industrial workers, including the provision of
"managed" health care. On vacation in Europe when World War
I broke out, Bly returned to journalism as a war
correspondent for the New York Evening Journal. (By
the way, Bly took her pen name from the popular song by
Stephen Foster, not the reverse.)
Following the Rosenhan study, a Dutch
psychiatric hospital actually commissioned a consulting firm
to plant pseudopatients in its own wards, as a check on
staff behavior and other conditions ("The Doctors Were Real,
the Patients Undercover" by Douglas Heingartner, New
York Times, 12/01/2009).
The issue of how we label people with mental illness has come to the fore with the "disability rights" movement, and the objection of people who have various disabilities to be identified with their disabilities (a similar issue has been raised in racial, ethnic, and sexual minority communities as well).
One important question is how to refer to people with various disabilities. Put bluntly, should we say that "Jack is a schizophrenic or "Jack is a person who ha schizophrenia"? Or substitute any other diagnostic label, including neurotic, depressive, or autistic.
Dunn and Andrews (American Psychologist, 2015) have traced the evolution of models for conceptualizing disability -- some of which also apply to other ways of categorizing ourselves and others. The current debate offers two main choices:
- A "person-first" approach -- as in, "Jack is a person with a disability". In this social model (Wright, 1991), disability is presented "as a neutral characteristic or attribute, not a medical problem requiring a cure, and not a representation of moral failing" (p. 258) -- or, it might also be said, as a chronic condition requiring rehabilitation. Instead, disability itself is seen as a sort of social construction -- or, at least, a matter of social categorization.
- An "identity-first" approach -- as in, "Jack is a disabled person". While this might seem a step backward, this minority model (Olkin & Peldger, 2003) "portrays disability as a neutral, or even positive, as well as natural characteristic of human attribute" (p. 259). Put another way, disability confers minority -group status: it connotes disabled people, with their own culture, living "in a world designed for nondisabled people".
Until recently, the treatment of the mentally ill was left pretty much in the hands of physicians, with minimal regulation. Historically, legislatures and courts have not intruded on issues of medical treatment -- relying, implicitly on physicians' Hippocratic Oath to "do no harm" -- and also out of respect for the sapiential authority of physicians, who are assumed to have more expertise in matters of diagnosis and treatment than laypeople do.
This situation changed sharply in 1971, in Wyatt v. Stickney, a landmark class-action case brought against the Alabama state mental hospitals in 1971. Ricky Wyatt (1954-2011) had a record of youthful misbehavior, as a result of which his juvenile probation officer arranged to have him committed to Bryce State Hospital at the age of 14 -- the youngest patient there (the procedures for such institutional commitment were pretty lax at the time). Despite the fact that he never actually received a psychiatric diagnosis, Wyatt was "treated" with large doses of Thorazine and other antipsychotic medications, and suffered many other indignities. The Federal judge in the case, Frank Johnson, ruled in favor of the plaintiffs and placed the entire state hospital system under federal receivership (where it stayed until 2003). He also issued a set of guidelines for the proper treatment of mental patients, now known as the "Wyatt Standards", that are now applied nationwide. Chief among these is the concept of least restrictive treatment -- that if mentally ill or intellectually disabled persons must be institutionalized, they have a right to as much freedom as practicable. They also have a right to human treatment, sufficient staffing, and individualized treatment plans, plus certain minimal standards for diet and nutrition. It is no accident that the same judge who ruled in Wyatt had also earlier placed Alabama's schools and prisons under federal receivership. The case is a landmark of civil rights law, and the Wyatt Standards are sometimes known as the Mental Patients' Bill of Rights.
Another major change in mental-health policy occurred in 1999, with the White House Conference on Mental Health and the issuance of the Surgeon General's Report on Mental Health. The Surgeon General argued that "mental health is fundamental to health" -- that a sound mind is part and parcel of a sound body. It also stressed that "mental health disorders are real health conditions", not figments of someone's imagination or excuses for not working. It asserted that "the efficacy of mental health treatments is well documented" -- a real change from the Eysenck study of the 1950s, and the Woody Allen Bugaboo. And it noted that "a range of treatments exists for most mental disorders", including both biological treatments (like drugs) and psychotherapy. This was the first time that federal policy formally recognized the problem of mental illness.
Mental Health Parity
Before this time, mental illness was treated quite differently from physical illness. While many consumers has insurance policies like Blue Cross and Blue Shield to help pay medical bills, they had to pay for psychotherapy out of their own pockets. And even "Cadillac" health-insurance plans imposed annual or lifetime dollar limits on expenditures for treatment for mental illness and substance abuse. For example, my own health policy at the University of California, pays for only 28 days of inpatient mental-health treatment, and outpatient psychotherapy had to be authorized in a way that outpatient medical treatment did not.
Now, however, by federal
law, such as the Mental Health Parity Act of 1996,
there is parity between "medical" and "mental" illness.
- Health insurance must cover mental health.
- Mental health benefits must be subject to the same annual and lifetime dollar limits as medical and surgical benefits.
- There must be the same schedule of deductibles and co-payments.
- And coverage cannot exempt treatments for behavioral disorders such as alcoholism, substance abuse, and chemical dependency.
Still, there remained important gaps between mental health and other medical services. In particular, the MHPA control issues like cost-sharing, limits on number of therapy visits or days of inpatient hospitalization, and the like. As a result, employers and insurance companies were able to circumvent the intention of the Act by increasing patient co-pays for mental-health services, and imposing limits on the number of visits or the days of coverage.
The Mental Health Parity and Addiction
Equity Act of 2008 was intended to strengthen parity even
further, by closing the loopholes in the MHPA. It
required that all financial requirements, including
co-payments and caps on visits or days of treatment be the
same for mental-health services as for medical and surgical
So did the Affordable Care Act of 2010 (aka ObamaCare) reinforced parity -- in fact, one Administration official was quoted as saying that it was "kind of the final word on parity" ("Rules to Require Equal Coverage for Mental Ills" by Jackie Calmes and Robert Pear, New York Times, 11/08/2013).
- Its final rules, issued in 2013, concerning "essential health benefits" mandated that all insurance policies cover mental-health and substance-abuse treatments.
- Co-payments, deductibles, and other limits may not be "more restrictive" or "less generous" than those that apply to medical and surgical treatments.
- Geographical and facility limitations were also equalized. If a California resident is covered for cancer treatment at the Mayo Clinic, in Minnesota, then a Minnesotan is covered for substance-abuse treatment at the Betty Ford center in Palm Springs, California.
- Whereas the MHPA applied only to group health plans, the
provisions of the ACA apply to all forms of health
- The precise menu of coverage and services will differ from state to state, and also depending on the level of the individual's plan (bronze, silver, gold, or platinum). The fact that so much variance is permitted under the ACA does undercut mental-health parity to some extent, as states and plans may skimp on mental-health and substance-abuse services. But at least some coverage is mandatory.
Again, any requirements and restrictions
(such as pre-authorization for treatment) must be the same for
mental health as for other medical care. Still, talk
(legislation) is cheap: the real issue now is enforcement, in
which other budgetary priorities may conspire with the stigma
associated with mental illness, and skepticism about the value
of mental-health treatments, to prevent mental-health services
from actually achieving parity.
Similar issues arise at the state level.
In 1999, California passed the
California Mental Health Parity Act to implement and extend
the federal MHPA.
- In a landmark 2011 case (Harlick v. Blue Cross and Blue Shield of California), the 9th Circuit Court of Appeals ruled that health insurers must cover "medically necessary" inpatient treatment -- not just outpatient treatment -- for nine categories of "severe mental illness": autism, bipolar disorder, (major) depression, eating disorders, obsessive-compulsive disorder, panic disorder, schizophrenia, schizoaffective disorder, and "serious emotional disturbances" in children and adolescents. Up until then, many insurers had refused to cover inpatient treatment for these illnesses, favoring less-expensive outpatient treatment instead. In fact, Ms. Harlick's health-insurance policy did cover outpatient treatment for mental illnesses, as well as short-term inpatient treatment. But the 9th Circuit found that, in many cases, long-term inpatient treatment was "medically necessary", and so must be included in coverage to insure that mental illnesses are covered to the same degree as physical illnesses.
Despite the movement toward parity, many psychiatrists claim that they are not paid enough for their services. As a result, they do not accept insurance, and require that their patients pay out of pocket. A 2013 study by Bishop et al. (JAMA Psychiatry) found that only 55% of psychiatrists accepted private insurance, compared with 89% of other physicians, and only 55% of psychiatrists accept Medicare patients, compared to 86% of other specialists, and only 43% accept Medicaid patients, compared to 73% of their colleagues. Whether these disparities reflect a problem with reimbursement for mental-health services, or the mendacity of some mental-health professionals, isn't clear. mental-health. But it makes clear that mental-health parity is only part of the problem of delivering mental-health services. In addition to balking at (allegedly) low payments, these psychiatrists may also resist the kind of intrusive review that comes with third-party payments. To be fair, many psychiatrists are solo practitioners, and simply don't have the office staff needed to cope with the paperwork that comes with insurance -- and solo practitioners in all specialties are less likely to take insurance than are physicians in any sort of group practice. Then again, psychotherapy takes time, and so long as insurers (including Medicare and medicaid) reimburse on a fee-for-service basis, psychotherapists will never be able to move as many patients through their practice, or deliver as many services per unit time, as other physicians (or, for that matter, psychiatrists who do little more than dispense medication).
Perhaps for this reason, there aren't
enough psychiatrists and other mental-health professionals to
meet the demand. A 2012 study by the US Department of
health and Human Services found that fully 55% -- that's more
than half -- of the nation's 3100 counties have no practicing
psychiatrists, psychologists, or social workers.
And mental-health workers don't earn as
much as other medical professionals. A 2012 survey by
Medscape showed that the average income for psychiatrists is
only $186,000/year, ranking psychiatry 19th out of 25 medical
specialties. Now, $186,000 is not chump change -- but
it's not nearly as much as other physicians make.
So it's a system, and it can't be fixed
simply by mandating parity. Mental-health professionals
don't get paid enough, so there aren't enough of them.
Still, if psychotherapists could show
that what they do really works, then insurers would have
little choice but to pay for the services they deliver.
Which brings us to the most important feature of the current
mental-health environment, which is the move toward
these changes in mental-health policy and practice come with a
price, which is that, for the first time, mental-health
practitioners have to demonstrate that they know what they're
doing -- that their diagnoses are valid, and that their
Frankly, up until these changes in policy, people didn't care much what went on in psychotherapy -- largely because they weren't paying for it. People can do what with their own money, the thinking went -- they can buy cigarettes, or speedboats, or psychotherapy. But if they're going to spend my money, whether in the form of insurance premiums or taxes, they better be spending it on something they really need, like a valid diagnosis, and something that really works, like an effective treatment. And also, frankly, "third-party" payers were still suspicious that mental illness was a bogus concept, and psychotherapy a bogus treatment. If people wanted to waste their own money on such self-indulgence, that was fine. But they weren't going to waste mine.
The upshot of all of this is that mental-health parity was a huge boon for mental-health practitioners, because they became eligible for third-party payments from government and insurance companies -- not to mention that parity also helped reduce the stigma of mental illness. But parity came with a price -- which is that mental-health practitioners actually had to prove, for the first time, that their treatments actually worked.
But of course, the very question of EBPs suggests that there are some treatments that don't work, and some practices that aren't empirically valid. Could this possibly be true?The simple, straightforward answer is "Yes" -- but this is also true for medicine in general, not just psychotherapy. The medical profession has long cloaked itself with the mantle of science, but until relatively recently physicians had relatively few effective treatments for disease. Mostly, their treatments were palliative in nature, intended to ameliorate the patient's symptoms, and make the patient comfortable, while nature took its course; or else they simply removed diseased organs and tissues through surgery. Scientific medicine really only began with the microbe-hunting of Louis Pasteur and Robert Koch in the 19th century, and successive phases of the pharmaceutical revolution of the 20th century. It is only relatively recently that medical researchers have begun to test medical practices to determine whether they actually work, which ones work better than others, and which are cost effective. Evidence-based medicine is epitomized by the clinical trials that new drugs must go through, to demonstrate their safety and efficacy, before they are marketed for the treatment of specific diseases.
Something similar is now happening to
psychotherapy. For a long time, psychotherapists, including
psychiatrists and clinical social workers as well as clinical
psychologists, have had to operate "in the dark" about whether
their treatments were actually effective. Many
psychotherapists were loathe to measure the effects of their
treatments quantitatively. And so long as patients were paying
out of their own pockets, and so long as they believed
that they were being helped by their therapists, there was
little incentive for psychotherapists to validate their
practices scientifically. In the 20th century, as standards
for medical practice changed, psychotherapists felt under
increasing pressure to demonstrate that their practices, too,
"really worked". The pressure increased as responsibility for
paying for psychotherapy gradually shifted to "third parties"
(patients and their therapists were the first an second
parties) such as employers and health-insurance firms. These
third-party payees naturally want to make sure that they were
getting value for their money: and so they demanded that
psychotherapists, like other health professionals, show that
their practices were both effective and cost-effective.
Although there is an increasing literature on the validity of
various assessment practices, such as comparing "objective"
and "projective" techniques (see, e.g., "Clinical Assessment"
by J.M Wood, H.N. Garb, S.O. Lilienfeld, M.T. Nezworski,Annual
Review of Psychology, 2002), most practice research
focuses on treatment practices.
And, for that matter, something similar
is happening in other fields of public policy.
Under the Obama Administration, the federal Office of
Management and Budget has tried to promote experiments
structured like clinical trials, with random assignment of
subjects (or, for that matter, organizations) to conditions,
as a rational basis for policy changes. This trend is
most advanced in the field of education. Beginning with
the passage of the No Child Left behind Act during the George
W. Bush (43) Administration, the US Department of Education
has posted the findings of "clinical trials" of educational
innovations on its What
Works Clearinghouse website. Included among these
innovations are many of the teaching and learning strategies
discussed in the Exam Information
Another name for evidence-based treatments is "empirically supported treatment", or EST. The term "evidence-based practice" (EBP) extends the scope of the EST movement to procedures employed for diagnosis and assessment.
present, the standards for evidence-based practice in
psychotherapy are roughly modeled on the clinical trials
required before drugs are marketed (see, e.g., "Empirically
Supported Psychological Interventions: Controversies and
Evidence" by D.L. Chambless & T.H. Ollendick,Annual
Review of Psychology, 2001). In order to qualify as
"empirically supported", a treatment must yield outcomes that
are significantly better than those associated with an
adequate control (typically, patients who receive no treatment
at all) in at least two studies, preferably conducted by
independent research groups. An ongoing list of treatments
that meet current standards is maintained by Division 12
(Clinical Psychology) of the American Psychological
- For example, some practitioners argue against any
standards at all, on the grounds that therapists should be
free to pick whatever treatment they think will be best
for the individual patient. Often they argue that
psychotherapy is an "art", not a science. But
physicians don't have this freedom: they have to conform
their practices to the available evidence -- and where
evidence is lacking, to the prevailing standard of
care. When physicians refer to the "medical arts",
they refer to the individual practitioner's skill -- but
even so, those "arts" are practiced within the bounds of
- Others, including some clinical scientists, believe that the "efficacy" research that provides the basis for ESTs is inappropriate, because the studies are conducted under somewhat artificial conditions that do not represent the problems that are encountered in actual practice. Instead, they propose that ESTs be based on "effectiveness" research, which they argue is more "ecologically valid". But the distinction between efficacy research and effectiveness research seems strained. Research is research. Clinical drug trials are somewhat artificial too, but their artificiality does not prevent physicians from prescribing effective drugs in actual practice. Moreover, "effectiveness" research often doesn't seem to be very good research. In the highly touted Consumer Reports study, for example, the outcome of psychotherapy was measured by patients' self-reported satisfaction with their treatment, instead of objective evidence of actual improvement (see "The Effectiveness of Psychotherapy: The Consumer Reports Study" by M.E.P. Seligman,American Psychologist, December 1995; commentary on Seligman's article was published in the October 1996 issue of the same journal. There were no controls for sampling bias, nor any untreated control group, for example. If the CR study is an example of effectiveness research, then effectiveness research is a step backward, not a step forward.
- Still other practitioners hold that empirical evidence of efficacy and effectiveness is only part of the equation -- that the choice of treatment should also be based on the clinician's expert judgment, and also on the patient's values. While it's true that clinical expertise is important, personal expertise should not trump scientific evidence. An awful lot of common wisdom in mental health proves, on examination, to be little more than folklore. That is why physicians and surgeons rely on practice guidelines, so that they can choose which of several empirically valid treatments to recommend to their patients. And while patients' values will help determine which treatment they should receive, patient values don't trump empirical evidence any more than clinical expertise does. A cancer patient might want to be treated with avocado extract instead of radiation and chemotherapy, and that's his choice; but no third-party should be expected to pay for a treatment that doesn't work.
Right now, the standards for EST are pretty minimal. They are a good start, but the standards need to be ratcheted up (the opposite of dumbing down, I guess) over time to improve the quality of psychotherapeutic practice.
- For example, some might wish to drop no-treatment control as an appropriate comparison group, in favor of an appropriate placebo. And should a new treatment simply be comparable to the available standard of care, or should it somehow be better that what is available? These are the same kinds of questions that are raised in drug research.
- As another example, there is the matter of clinical vs. statistical significance. A statistically significant change in patient status may not be clinically significant in terms of the ordinary course of everyday living. The question is, what are the standards for clinical significance?
- As another example, two studies out of how many? The current EST standard is modeled on current FDA standards, which require only two positive trials, regardless of how many negative or inconclusive trials there are, raising the file-drawer problem and the issue of selective publication of positive results.
- As another example, and I think this is the really interesting one, there is the question of mechanism. Since the 19th century, medicine has generally rejected mere "empirical" treatments, which are simply known to work, in favor of treatments whose mechanisms of action can be interpreted within the framework of existing knowledge of anatomy and physiology. Not to say that new treatments can't teach us something new about structure and function (this is one of the reasons that people find hypnosis so interesting), but you do expect a broad consistency. And if a proposed treatment is inconsistent with what we already know, that may be a reason to reject it regardless of whether it works.
- To take an example from the history of hypnosis (see my paper in the International Journal of Clinical & Experimental Hypnosis, October 2002), Mesmer's animal magnetism wasn't rejected by the Franklin Commission because it didn't work. Everyone agreed that it did work. Animal magnetism was rejected because Mesmer's theory was wrong, and nobody had a good theory to replace it (psychology not having been invented yet). Exorcism might work, empirically, but even if it did medicine would reject it as a legitimate treatment because its underlying theory -- that disease is caused by demon possession -- is inconsistent with everything we know about how the body works. In fact, Mesmer (and everyone else) agreed that Fr. Gassner's exorcisms worked. But Mesmer won the debate with Gassner because (at the time) he offered a materialistic, and thus scientifically acceptable, theory to account for his effects (the Franklin Commission came along later).
It would represent a major "ratcheting
up" of the EST requirements if we required not just that the
treatment be efficacious, but that the theory on which the
treatment is based be scientifically valid as well. But it may
be exactly what we need (see below for more on this subject).
These are all points for debate within the field. The actual standards for EST are the result of a political process, and inevitably involve some compromise. But once they are established, the important thing is that (1) they are adhered to and (2) that if they are changed the change is in the direction of tightening not loosening. If practice is to be based on science, and science goes forward, there can be no going back for practice.
It took a Supreme Court case, Virginia Academy of Clinical Psychologists, and Robert J. Resnick, Ph.D. v. Blue Shield of Virginia, (1977), to establish psychologists' legal right to practice, and receive reimbursement, without being supervised by psychiatrists or other physicians. Clinical psychology owes is autonomy from psychiatry, and its eligibility for third-party payments, to the assumption that its practices rest on a firm scientific foundation. Therefore, clinical psychology, and the rest of the mental-health profession, departs from scientific evidence at its own risk.
Putting Mental Illness in Social Context
study illustrates an important general point about mental
illness, and for that matter about normal mental and
behavioral functioning as well.
- We assume (based on Chicago functionalism, described in the lecture supplements on the Biological Bases of Mind and Behavior) that the individual's mental life takes place in a social context.
- We know from the person-by-situation interaction (described in the lecture supplement on Personality and Social Interaction) that we cannot extricate the individual from his or her surrounding social and cultural context.
What is true for normal mental functioning is true for mental illness as well. We simply cannot treat mental illness successfully by operating on the individual alone. We must also act to change the social environment in which the person lives.
For therapy to succeed,
mental-health professionals must do more than address the
individual's underlying psychopathology -- psychological
deficits, maladaptive social learning, diathesis and stress,
biological substrates, and so on.
- They must also work with the patient's family members, friends, neighbors, employers, and co-workers.
- They -- and we -- must also work to change social attitudes so that the mentally ill can live in an environment that permits maximum recovery and adaptation.
This page last revised 09/05/2017.