The Charcot Effect: The Invention of Mental Illnesses

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The Charcot Effect: The Invention of Mental Illnesses
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THE CHARCOT EFFECT: THE INVENTION

OF MENTAL ILLNESSES
MARINO PÉREZ-ÁLVAREZ
Department of Psychology, University of Oviedo, Oviedo, Spain
JOSÉ M. GARCÍA-MONTES
Department of Psychology, University of Almerı́a, Almerı́a, Spain
This article proposes the Charcot effect, in which clinicians describe what
they themselves prescribe. It is argued that the Charcot effect can be a critical
instrument for exposing how mental illnesses are invented in the process of
developing diagnostic systems and conducting psychopharmacological research.
We argue that the Charcot effect helps explain the expansion of depression
to epidemic proportions, the promotion of social phobia as a pharmaceutical
marketing strategy, the profile of panic disorder according to the available
medication, and the worse prognosis of schizophrenia in developed countries than
in developing countries. Having undertaken this review, we situate the Charcot
effect in relation to constructivist psychology.
We propose something called the Charcot effect, which takes its

name from the eminent French neuropathologist of the late
nineteenth century, Jean-Marie Charcot (1825–1893). Charcot is
relevant here because he was well known for inducing an attack
of hysteria under the assumption that he was describing it. This
presumed description actually functioned as a prescription of
what was to be observed, so that Charcot himself was immersed
in a self-confirmatory system. The admiration of the audience at
his lectures served only to confirm this effect. The Charcot effect
is as much a historical fact as a general clinical phenomenon.
As an historical fact it refers to Charcot’s study of hysteria
from 1864 to 1893 at La Salpêtrière, where he described the
grand attaque de l’hystérie (Shorter, 1992). As a general clinical
phenomenon, the Charcot effect may well be a phenomenon that
occurs, to a greater or lesser extent, in all psychodiagnostic and
Received 1 March 2006; accepted 1 September 2006.
This work was supported in part by Research Grant MEC-05-SEJ2005–00455.
Address correspondence to Marino Pérez-Álvarez, Departamento de Psicologı́a,
Universidad de Oviedo, Plaza Feijoo, s/n. 33003-Oviedo, Spain. E-mail: marino@uniovi.es
309
310 M. Pérez-Álvarez and J. M. Garcı́a-Montes
psychotherapeutic processes (Berkenkotter & Ravotas, 2002). In

principle, it is not difficult to accept that a certain structuring
of patients’ problems in accordance with clinical theory and

procedures is found to some extent in all approaches. What draws
our attention to the case of Charcot is its theatricality. In any
case, the distance that allows us to consider it as an “historical
fact” also permits us to use it as a model for perceiving the
same phenomenon today, with ourselves as either the potential
“Charcots” or his admiring followers.
In fact, the phenomenon designated here as the Charcot
effect was already identified by Karl Popper, in relation to psycho-
analysis, under the name Oedipus effect, “to describe the influence
of a theory or expectation or prediction upon the event which it
predicts or describes: it will be remembered that the causal chain
leading to Oedipus’ parricide was started by oracle’s prediction
of this event” (Popper, 1963, p. 39). In any case, let us introduce
the expression Charcot effect, which is probably more appropriate
for the phenomenon in question here. In examining the Charcot
effect, first we show its current relevance, with particular refer-
ence to psychiatry. Second, we review four mental disorders (de-
pression, social phobia, panic attack, and schizophrenia) within
the perspective of their construction—or rather, “invention,” to
use a more critical term. Third, we situate the Charcot effect
squarely within constructivist psychology. Finally, we point out
some perverse consequences of the Charcot effect for psychiatry
and clinical psychology, and some possible alternatives.
The Charcot Effect Today
The Charcot effect remains with us, mutatis mutandis, in psychiatry

today. And although psychiatry is the main concern of the present
work, clinical psychology is by no means exempt from the effects
of this phenomenon. Within current psychiatry, the Charcot effect
can be discerned in diagnostic systems and psychopharmacologi-
cal research, not to mention an entire serotonin culture.
With regard to diagnostic systems, taking the Diagnostic and
Statistical Manual of Mental Disorders (DSM) as a reference, the first
thing we notice is the proliferation of typified disorders, especially
since 1980 and the publication of DSM-III. Specifically, the 163
disorders in the DSM-II (American Psychiatric Association, 1968)
The Charcot Effect 311
become 224 in the DSM-III (APA, 1980), and reach 374 by the
DSM-IV (APA, 1994; with no additions in the revised text of 2000,
which was merely a text revision).

Such a proliferation cannot reasonably be attributed to the
discovery of new natural entities that were “out there” waiting for
more accurate diagnostic procedures. Nor does this mean that the
previous categories were natural entities. Indeed, our perspective
holds that mental disorders are not natural kinds, but rather
practical kinds arising more out of pragmatic conventions than
supposed objective essences (Zachar, 2001, 2003). In any case,
what is important to stress is that the classification systems for
mental disorders serve various interests other than those of scien-
tific progress. These would include the legitimization of psychiatry
as a medical specialization dealing with supposed illnesses, the
requirements of pharmaceutical companies for commercializing
drugs, and the system of third-party payers. According to Horwitz
(2002), “The application of this system to the broad range of
problems of psychiatric clients was not a triumph of science over
ideology, but rather a use of the ideology of science to justify
current social practices” (p. 74).
The greatest problem with diagnostic systems is that they end
up creating their own objectivity. There is a process of naming
and framing (Brown, 1995) through which diagnoses appear to
reveal illnesses that are just beyond our ability to measure them,
when, to the contrary, they are largely socially constructed. This
process is somewhat complex, as it includes a whole series of
academic, scientific, professional, and everyday practices, from
the training of clinicians (text books and so on) and the scientific
style of thought (theories, vocabulary, procedures) to professional
roles (diagnosing illnesses) and common sense itself (now duly
“educated” by pharmaceutical marketing).
As far as psychopharmacological research is concerned, an
important aspect to highlight is the strategy of defining disorders
by the effects of the drugs prescribed for them. The notion of
“listening to the drug” was popularized by Kramer’s (1993) book,
Listening to Prozac. The point is that the psychological changes in-
duced by a drug are taken as a diagnostic criterion of the patient’s
problem, and, in turn, the supposed deficit remedied by the drug
is taken as the cause of that problem. Thus, the improvement
in mood produced by Prozac defines the depression, and the
supposed serotonin deficit for which it compensates would be its

cause.
The use of medication for specifying the diagnosis also has

been incorporated into clinical practice. Thus, for example, as
Luhrmann (2000, p. 49) noted,
if a supposed manic-depressive does not respond to lithium or to another

of the mood stabilizers, a psychiatrist will wonder whether after all he’s
schizophrenic. If a supposed schizophrenic is managed effectively on
antianxiety agents or even without medication, a psychiatrist will question
whether she is, in fact, schizophrenic.
This strategy of listening to the drug involves the reduction

of a disorder to a list of symptoms. And we need scarcely add that
these symptoms are those selected according to their sensitivity
to the effects of the medication in question. In this way, there
is a kind of teleological adjustment of the diagnosis to the treat-
ment. The psychiatric patient him- or herself ends up adapting
the explanation of his or her problems (social and emotional)
to a medical protocol devoid of any contextual consideration
(Berkenkotter & Ravotas, 2002; Borges & Waitzkin, 1995).
Although this way of proceeding invalidates the diagnosis,
it does not challenge either the convention or the conviction of
the existence of an organic illness. Thus, the current psychiatric
lore largely endorses a psychopharmacological model of illness.
Specifically, experts usually postulate some type of biochemical
imbalance, most commonly in relation to serotonin. Regardless
of the confirmation of some biochemical imbalance correlative
to a mental disorder, the point is that such an imbalance does
not in itself explain the experience of the disorder (depressive
or psychotic, for example). Neurochemical hypotheses do not
substitute for or excuse social and personal construction. Indeed,
it could be said that the imbalance theory in psychiatry functions
more as a rhetorical device than as scientific evidence (Valenstein,
1998).
The truth is that we are living in a serotonin culture (Healy,
2004a), where it is taken for granted that serotonin deficit is the
cause not only of depression but of a whole series of conditions
that, curiously enough, improve on taking selective serotonin
reuptake inhibitors (SSRIs), such as Prozac, Zoloft, or Paxil. A
biobabble has emerged that, despite using the language of chem-

istry, is no more scientific than the psychobabble of earlier times.
As Healy (2004a) put it, “now this psychobabble has been all
but replaced by an equally vacuous biobabble, which in turn has
consequences for how we view ourselves, how we view the turmoil
of adolescence or school underachievement or, finally, moral and
criminal culpability” (p. 264). It is in such a cultural context that
we can identify the concept of neurochemical selves (Rose, 2003).
The paradox in all of this is that, as Horwitz (2002) argued, “the
ascendant belief that ‘mental illnesses are brain diseases’ is due
far more to the cultural belief that only biologically-based illnesses
are ‘real’ illnesses than to any empirical findings that the causes
of mental disorder are brain-based” (p. 156).
If against such a background we consider the fact that psy-
chopharmacological research and the corresponding diagnostic
expansion make use of marketing, it is easy to understand the
culture that has been created. As far as psychopharmacological
marketing is concerned, it suffices to recall that it includes a
wide variety of strategies, such as direct propaganda that reaches
patients via the media; the promotion of illnesses for the com-
mercialization of drugs; the provision of symptom lists to gen-
eral practitioners for quick diagnoses; the continual “education”
of psychiatrists; the sponsoring of conferences, symposia, and
commissions; financial support for research; influencing scientific
publications; and the financing of patients’ associations that
defend the illness model. Those still unaware of the current
situation can be enlightened by authors such as Healy (2004a),
Moncrieff (2003), Moynihan and Cassels (2005), or Valenstein
(1998). The culture created is the serotonin culture we have
described, incorporating the concept of neurochemical selves.
Having explained how the Charcot effect can still function
today, we will describe how disorders are invented through it.
The term “invention” is used here in a critical sense, to highlight
the artifactual aspect, in contrast to the supposed objective reality
in which mental disorder categories are portrayed via diagnostic
systems and psychopharmacological research. This critical sense
has both an epistemological dimension, related to the way in
which pharmaceutical matters are understood (Barry, 2005), and
an anthropological dimension, given the harmony of illusions
that can be achieved in a new diagnosis (Young, 1995). On the
other hand, the term “construction” is reserved for referring to

the actual construction of frames of meaning in the context of
psychotherapy (Gergen, 2004; McNamee, 2002).

As a general phenomenon, the Charcot effect can be recog-
nized in all mental disorders (and even in some general medical
disorders). A particular history of each disorder would be neces-
sary in order to perceive the part of their conception attributable
to clinical theories and procedures, not to mention conventions
and interests. It would be a contextual history, as distinct from
internal histories such as, for example, that of Berrios (1996),
whose supposed objective description of symptoms trimmed out
their phenomenological, social, and historical background. After
all, mental symptoms do not come through like teeth.
A contextual history can be found in Szasz’s (1961) history
of hysteria in his illustration of the “myth of mental illness”;
in Hacking’s (1995) and Spanos’s (1996) histories of multiple
personality, reconstructing the social processes surrounding this
disorder; and in Young’s (1995) history of posttraumatic stress
disorder, showing the “harmony of illusions” on which it has
been invented. Leaving aside hysteria as an historical model, both
multiple personality and posttraumatic stress constitute good
examples of the current tendency for the creation of mental
illnesses following the Charcot method, despite the fact that
psychopharmacological research is not especially implicated in
their construction. Because we are primarily concerned here with
psychopharmacological research (as well as the DSM diagnostic
system), we will concentrate on other disorders. Among the
most eligible candidates are depression, social phobia, and panic
disorder, without forgetting schizophrenia.
The Growth of Depression to Epidemic Proportions
Although the term “depression” dates from the second half of the
nineteenth century (Berrios, 1996, p. 299), it did not become the
widespread diagnosis it is today until the late twentieth century.
It is, indeed, precisely with the advent of new antidepressants
that depression increased with respect to other diagnoses (Healy,
2004b; Shorter, 2001). If we have to fix a date, this could be said
to have occurred after 1987, the year of the revised DSM-III and
the approval of Prozac.
Until publication of the DSM-III-R (APA, 1987), depression

was a minor diagnosis. At the end of the nineteenth and in
the early twentieth century, “melancholia” was a more promi-

nent notion than “depression.” Later in the century, with the
doctrinal dominance of psychoanalysis, anxiety disorders were
diagnosed far more frequently than was depression. Depression
was considered nothing more than a depressive neurosis, as
reflected even in the DSM-II (APA, 1968). By the time the DSM-III
arrived (APA, 1980), we were still in the era of anxiety (Healy,
2004b; Shorter, 1997). It was not until 1987 and the DSM-III-R
that depression caught up with anxiety in terms of its social
importance, and perhaps overtook it. In psychopharmacological
terms, the antidepressant era was beginning (Healy, 1997). The
hegemony of Valium was giving way to that of Prozac. Today,
the prevalence of depression is estimated at 10% to 15% of
the population, having reached epidemic proportions (Pignarre,
2001).
The first antidepressants (imipramine and iproniazid) were
actually developed in the late 1950s, but because depression was
not at the time a relevant disorder, the laboratories involved
(Geigy, Ciba, and Sandoz, later merging to become Novartis)
took no interest in their promotion. Nevertheless, in 1961 Merck,
in its efforts to launch amitriptyline (practically identical to
imipramine), distributed 50,000 copies of a book published that
same year, Recognizing the Depressed Patient, by Frank Ayd, with
a view to sensitizing doctors about the presence of depression
in general medicine. Although amitriptyline (Elavil/Triptizol)
brought considerable advantages, we were, of course, in the era of
Valium and Librium; antidepressants and depression had to wait
for their time to come (Healy, 1997, Chapter 2). This time would
arrive with the approval of Prozac in 1987.
The rest of the story concerns the launching of Prozac. Its
approval by the Food and Drug Administration in 1987 was essen-
tially a passport to fame. This approval meant no more, in reality,
than that the product could be called an antidepressant because
it showed itself to have some effect on depression (fulfilling, in
fact, the minimum criteria). The drug’s license did not mean it
was effective in the sense that people should see it as the solution
to the diagnosed disorder (Healy, 2004a, p. 35). Marketing has
done the rest.
For a start, the very trade name, Prozac—and even the

description of its pharmacological action, “selective serotonin
reuptake inhibitor” (SSRI)—shows commercial intelligence. The

name Prozac, rather than alluding to pharmacological properties,
as trade names usually do, suggests, on the one hand, profes-
sionalism, pro-, and on the other, hitting the right spot, -zac. In
turn, the description of the chemical action also hints that we
are dealing with an “intelligent” drug, using the words selective
inhibitor when, in fact, it does not act on a particular area of
the brain (serotonin is present virtually all over the brain, and
not exclusively in the brain). In any case, there is a remarkable
lack of connection between the advertisements and the scientific
literature (Lacasse & Leo, 2005). We are undoubtedly witnessing
a triumph of marketing over science (Antonuccio, Burns, &
Danton, 2002), within an unhealthy relationship between the
pharmaceutical industry and depression (Healy, 2004a).
In addition to using these clever names, the manufacturing
company, Eli Lilly, would take it upon itself to sell, in addition
to the drug’s efficacy, its safety (compared to the early antide-
pressants, with their side-effects) and its freedom from addictive
effects (which had been the downfall of the benzodiazepines).
Furthermore, the effectiveness of Prozac would not be reduced
to the remedy for a disorder (first depression and then others),
limited to helping us “get well,” but would help us to get “better
than well,” paving the way for cosmetic psychopharmacology. As
the reader may recall, the expressions “better than well” and
“cosmetic psychopharmacology” come from the work by Kramer
(1993). What highlights the success of these expressions is that
solutions such as Prozac fit in perfectly with current values (Elliott,
2003; Elliott & Chambers, 2004). Thus, Prozac is represented
in popular culture through metaphors such as magic bullet, life-
saver , upper/elevator , or genetic corrector , and is associated with
experiences such as life change, happiness, self-esteem, and new
personality (Montagne, 2001).
The reality is that the new antidepressants represented by
Prozac are not as effective as the classical ones, particularly in se-
vere depression (Anderson, 2000; Fremantle, Anderson, & Young,
2000); nor are they immune from side effects, among them
suicide, violence, and mania (Breggin, 2003/2004; Glenmullen,
2000; Healy, 2005, Chapter 4). But by the time this became
evident, depression had already grown to epidemic proportions

and was understood in chemical terms. Indeed, people have
learned to frame a large proportion of life problems in terms of

depression, including those that are closer to the cosmetic realm
than that of treatment per se. At the same time, they have learned
to see depression in chemical terms. However many possible
psychological and psychosocial explanations of depression there
are, and however obvious it is to see it as a life experience, people
have been converted to a belief in chemistry. “Like religious con-
version, capitulation to a biological version of depression’s causes
and proper treatment is accomplished through a socialization
process that entails a radical transformation of identity, a ‘process
of changing a sense of root reality’“ (Karp, 1996, p. 82).
This capitulation to the biological version of depression is a
case of what Gergen (1994) called the cycle of progressive infirmity,
discussed further below. In any case, it is worth mentioning
here something of great interest to constructivist psychology:
personal responsibility within social influence. According to our
conception of constructivism, individual persons are essentially
the authors of the systems of meanings about their worlds and
experiences (Pérez-Álvarez & Garcı́a-Montes, 2004, 2006). The
problem represented by depression is especially relevant for ap-
proaching this question, given the fact that it concerns—perhaps
more clearly than other disorders—personal meaning and experi-
ence of the world and of one’s own life. People’s adherence to bi-
ological explanations and solutions (in this case, for depression),
however strongly influenced by the propaganda, is nevertheless a
personal decision and creation. Such adherence, far from being
inevitable, occurs in the context of other possible constructions.
Thus, for example, both common sense and psychological thera-
pies offer alternative constructions. It is suggested that biological
capitulation may be related to the personal construction consist-
ing in self-exempting oneself from responsibility, preferring to
blame the brain (Valenstein, 1998) and take Prozac as a way of
life (Elliott & Chambers, 2004).
The Promotion of Social Phobia as a Commercial Strategy
The promotion of social phobia as a distinct clinical entity has

become a classic example of pharmaceutical marketing of a
commercial strategy for the promotion of drugs (Moynihan,

Heath, & Henry, 2002). Thus, it is no coincidence that social
phobia has gone from being a rare disorder in 1980 to being the
third most common psychiatric diagnosis, after depression and
alcoholism, by the end of the 1990s (Moncrieff, 2003). In the
space of some 10 years, it nearly quintupled its prevalence, going
from 2.75% at the beginning of the 1980s to 13.3% by the early
1990s (Horwitz, 2002, p. 95).
Even though social phobia is clearly a questionable diagnostic
category, given the heterogeneity of its symptoms (Hofmann,
Heinrichs, & Moscovitch, 2004), and in any case its markedly
interpersonal condition (Alden & Taylor, 2004), it has the status of
a clinical entity, and indeed functions as a mental disorder (APA,
2000). From the constructivist point of view, it is interesting to
consider how this has come about.
Above all, it should be pointed out that social phobia repre-
sents a clear case of the conversion of a social and personal prob-
lem into a medical one (Moynihan et al., 2002). The initial prob-
lem would be none other than shyness (in turn a construction,
in this case more mundane than clinical). Although traditionally
shyness was not a problem, but rather a personal characteristic
and even a social style, it began to be problematized in the
1970s in response to certain social changes. These changes had
to do, above all, although not exclusively, with heterosexual roles,
whereby both feminine shyness and masculine shyness (“reserve”)
ceased to be the acceptable patterns they had been (McDaniel,
2001). The fact that social phobia affects males and females
equally (or even, unlike other phobias, affects males more; APA,
2000) is in line with these social changes that became discernible
in the mid-1970s, when women’s liberation movements began to
challenge male privilege in many fields (McDaniel, 2001).
What is important to emphasize is that these personal social
problems were shrewdly capitalized upon by the pharmaceuticals
industry, becoming among the most widespread medical prob-
lems in clinical psychiatry at the end of the 1990s. Thus, this con-
version into a clinical problem is concerned more than anything
with the history of psychopharmacology (Healy, 1997, 2004a).
In this regard, one of the leading players was the pharmaceu-
tical company GlaxoSmithKline (GSK). GSK set out to market the
SSRI-type drug paroxetine (Paxil in the United States and Seroxat
in Europe). Although Paxil is known as an antidepressant, the
depression “market” was already covered by Prozac. Thus, it be-

came necessary to find another niche—namely, social phobia or,
more generally, social anxiety. Indeed, social phobia became more

commonly known as social anxiety, a less stigmatizing term, and
a wider one, so that it included a larger number of people who
recognized themselves as socially self-conscious (Healy, 2004a, pp.
27–28). For the launching of Paxil, GSK hired the advertising
agency of Cohn & Wolfe, so as “to position social anxiety disorder
as a severe condition. This occurred before Paxil was even ap-
proved for the treatment of this condition, in order to give Cohn
& Wolfe time to start ‘cultivating the marketplace’“ (Moynihan &
Cassels, 2005, p. 121). The objective was to promote social phobia
so as to create widespread recognition of Paxil as the first and only
treatment for the condition, as can be seen on the Cohn & Wolfe
(n.d.) website. The strategy consisted in sensitizing the public to a
neglected disorder. The awareness-raising campaign was based on
this slogan: “Imagine being allergic to people. You blush, sweat,
shake—even find it hard to breathe. That’s what social anxiety
disorder feels like” (Moynihan & Cassells, 2005, pp. 121–122).
Obviously, this problem has a remedy, which is none other than
the advertised drug.
The propaganda of the drug advertisers implied that the
problem preceded the solution—namely, that awareness of the
disorder came first, and that invention of the medication was
a subsequent event motivated by this discovery. The reality of
the constructive process was, in fact, very different. In reality, it
began with a solution, a medication that needed to be marketed
and therefore required a problem to which it could be applied.
Although the solution preceded the problem, in the end things
were arranged so as to make it seem that the problem preceded
the solution—as though social phobia had been out there without
being diagnosed, just waiting to be discovered. This process in
no way means that people do not, in fact, have the experience
of social phobia or anxiety. After all, the social construction of a
disorder implies the experience of illness (Brown, 1995).
The Construction of Panic Disorder in Accordance

with the Medication
Panic disorder provides another example of the promotion of a

condition in accordance with the marketing of a drug. Indeed,
it is now considered a typical case of this phenomenon in the

history of psychiatry (Shorter, 1997). Even so, panic disorder
merits a comment here, more than merely a mention, insofar

as it illustrates certain aspects of the invention of mental illness
categories that, although present in those already mentioned
(hyperactivity, depression, social phobia), can more easily be seen
in relation to this diagnostic category. We are referring specifically
to the construction of the clinical condition according to the
medication, listening to the drug instead of to the patient.
For a start, we should bear in mind that panic disorder ac-
tually constitutes anxiety trimmed down to its somatic symptoms,
in particular, the paroxystic state it involves. Thus, panic seems
to lend itself to medication. In fact, panic disorder became a
disorder in its own right in the DSM-III (APA, 1980) due to
the influence of promoters interested in seeing its response to
medication—specifically, to antidepressants (Healy, 1997, p. 193).
However, at that time panic disorder was an uncommon diagnosis
(as were depression and social phobia). It would have to wait
for its promotion throughout the 1980s to become a frequently
diagnosed disorder and to reach the epidemic proportions of the
1990s, as Shorter (1997) pointed out.
This promotion, as is well known (see, e.g., Healy, 1997;
Shorter, 1997; Valenstein, 1998), was mainly the responsibility of
Upjohn laboratories, bent on opening up a market for a new
benzodiazepine called alprazolam, which would be sold under
the brand name Xanax. It was therefore not surprising that panic
disorder was known colloquially as the “Upjohn illness.” Thus, it
could be said that the determination to find a new space for an
antidepressant such as alprazolam was due in large part to the
fact that the field of depression was already being cornered by the
SSRIs (i.e., Prozac).
When all is said and done, the question, of course, is whether
alprazolam works for the problem of anxiety called panic disorder.
The answer is yes, but not sufficiently for it to be considered
a therapeutic advance. Indeed, the presentation of its results at
conferences and in scientific journals was not without controversy.
Worthy of note in this regard are the criticisms leveled by British
psychiatrist I. Marks, who claimed that studies on alprazolam had
been controlled in a biased manner by Upjohn and who drew
attention to the fact that behavioral therapy had shown more
lasting effects than alprazolam in an independent study (Healy,

1997, pp. 196–197).
It is important, therefore, to see how, after all of this, panic

disorder is dealt with in the DSM-IV-TR (APA, 2000). It is defined
by the “temporary and isolated appearance of intense fear or un-
ease, accompanied by four (or more) of the following symptoms”
from a list of 13: palpitations, sweating, trembling, sensations
of shortness of breath, feeling of choking, chest pain, nausea,
feeling dizzy, disrealization, fear of losing control, fear of dying,
paresthesias, and chills. Note that the condition has now not only
been trimmed down to the somatic symptoms (with respect to the
traditional anxiety condition), but all possible antecedents and
consequents have been omitted, as though the crisis were an “out-
break” without sense and, as described, “isolated.” Given that the
diagnosis concentrates on the subjective phenomenology of the
symptoms (Did it happen suddenly? Was your heart beating fast?
Did you feel as if you were going to die?), it is easy to imagine how
the clinician’s questions find confirmation in the patient, who in
turn senses confirmation on hearing such appropriate questions,
thus completing a self-explanatory circle (à la Charcot).
Consequently, the symptoms of the disorder are more likely
to serve the statistical protocol than clinical understanding and
explanation. Thus, there is a tendency to listen to the medication
rather than to the patient. “Listening to Xanax” would, in this
case, be an appropriate title. If we listened to the patient, we
would see that the panic has its antecedents (its “why?”) and its
consequents (its “what for?”)—or, as Capp and Ochs (1995) would
say, its grammar—which certainly falls outside of the defined
disorder. What is certainly the case is that, once more, the clinical
discourse fails to correspond to the sense of the disorder within
the person’s life (Borges & Waitzkin, 1995). Thus, far from being
an isolated outbreak, as though it emerged from the void (as
accepted by clinician and patient), it has its causes: its material
cause or content in problematic situations and its final cause in
the attempt to resolve those situations. What we are talking about
here is a “grammar of panic,” in which clinicians of a nosographic
bent would be illiterate, a grammar that can be interpreted in a
variety of ways, such as through discourse analysis (Capp & Ochs,
1995), clinical behavior analysis (Dougher, 2000), or social games
(Szasz, 1961).
Whether or not panic has much to do with hysteria, psychi-

atric research can be seen as a kind of hysteria in the sense of
being satisfied with playing out a “methodological drama” (Orr,

2000). Orr, a social researcher, actually passed herself off as a
patient in a clinical trial with Xanax in the 1980s. As a result,
Orr (2000) dismisses psychiatric research that defines diagnostic
conditions based on their symptoms’ sensitivity to medication,
calling such research “performance methodology.” On constitut-
ing a teleological spectacle in which the diagnosis is established
by the treatment, as Orr argues, the psychiatry itself demonstrates
hysteria because it confuses the real event in the patient’s life with
the event resulting from the method that supposedly establishes
its empirical character (2000, p. 63).
The Poor Prognosis of Schizophrenia as a Possible Effect

of Clinical Practice
Schizophrenia is often presented as the last bastion of mental

illness with a neurobiological basis, so that it would not be subject
to a process of construction as are other disorders, such as
those already discussed. Thus, Horwitz (2002) himself marked out
schizophrenia as an exception, together with manic–depressive
psychosis and psychotic depression, from the creation of men-
tal illnesses. Horwitz endorsed the concept of mental disorder
proposed by Wakefield (1992), according to which there would
be some internal dysfunction at the base of such disorders. In
this regard, the universality of schizophrenia usually is seen as
corroboration of its condition as independent of culture.
Wakefield’s (1992) conception assumes a natural design of
mental functioning, with respect to which we can define “internal
dysfunction.” In this sense it is an essentialist conception, as
the author himself acknowledged (Wakefield, 1999). However,
it is problematic to assume that there are essences or inherent
qualities in an individual that would represent the truth of his or
her abnormality. Indeed, abnormality, far from being a human
essence, is more a social construction (Stanley & Raskin, 2002).
As Zachar argued in relation to Wakefield’s conception, mental
disorders are not “natural kinds” but, rather, “practical kinds”
constructed on a pragmatic basis (Zachar, 2001, 2003). At the
same time, neither can schizophrenia’s supposed universality be
taken as proof of biological pathogeny, because there are also

cultural universals, such as norms, prohibitions, role transitions,
deviations, and so on. Thus, even without denying some possible

biological condition, it seems clear that schizophrenia is not
exempt from the processes found in other disorders. In this
regard, the data show that patients today, in the psychotropic
era, spend on average more time in the course of a psychiatric
career in a hospital than they did before modern drugs came “on
stream” (Healy, 2004b, p. 236). Likewise, it is important to note
the current tendency advocating early preventive intervention
with psychosis, which may extend diagnoses and expose to the
adverse effects of medicines people who might never actually
develop psychoses or schizophrenia (Moncrieff, 2003).
However, the area of greatest interest here almost certainly
concerns the different course and results in schizophrenia be-
tween developed and developing countries, according to the
international studies commissioned by the World Health Organi-
zation, begun in 1967 and 1978. The major conclusion of these
studies—perhaps unexpected, but repeatedly confirmed—is that
schizophrenia has a better course and result in developing coun-
tries than in developed countries (Hopper & Wanderling, 2000;
Warner, 2004). This finding seems paradoxical, if we consider that
developed countries have better treatment conditions, includ-
ing antipsychotic medication. Indeed, only 16% of developing-
world subjects, versus 61% of cases in the developed world,
were taking antipsychotic medication throughout the follow-up
period (Warner, 2004, p. 167). It would seem that the better
the treatment, the poorer the prognosis. Indeed, it looks as
though people in less developed countries also fail to develop
such an “advanced” schizophrenia as those in more developed
ones. It should be stressed, moreover, that these findings are
resistant to possible sources of bias that could discredit them,
such as differences in follow-up, arbitrary grouping of centers,
diagnostic ambiguities, selective outcome measures, gender, and
age (Hopper & Wanderling, 2000).
How can this be? Naturally, nobody is saying it is antipsy-
chotic medication that makes things worse. Even so, antipsychotic
medication, as the chosen treatment it is in developed countries,
goes hand-in-hand with a whole series of social practices befitting
a conception of illness (with supposed biological basis and a
tendency toward chronicity). This involves, in turn, a neglect of

other conditions of a vital (more than biological) nature. It is
precisely these other conditions of a vital nature on which may

depend a better prognosis, and therefore the better recovery from
schizophrenia in developing countries.
These conditions imply a wholly different conception of the
disorder. Thus, psychosis may be seen in traditional cultures as a
transitory delirium, from which the person will not take long to
recover. The belief system itself probably offers an explanation
of external causes, liberating the patient and his or her family
from possible stigma. Likewise, there is no separation of patients
from their social roles; rather, they maintain their integration in
the group to which they belong. Consequently, neither personal
identity nor social status is at stake. In sum, greater normalization
of the psychotic episode seems to bring with it better chances of
recovery.
On the other hand, in Western societies, with their clinical
culture, a first psychotic episode would probably be seen as a
symptom of a mental illness requiring immediate antipsychotic
medication. The symptom, particularly if it is hallucinations or
delusions, alarms both the family and the clinician, while its
attenuation through medication brings calm as well as confir-
mation of its appropriateness (Lally, 1989). Observation and
rest, probably including hospitalization, would be the subsequent
steps. Consequently, listening to the drug becomes the clinician’s
main task. Normally, if the symptoms subside, the medication is
maintained for a period; if they do not subside, it is increased or
changed. In the meantime, hospitalization and medication—part
and parcel of being ill (in this case, mentally ill)—separate the
patient from current or expected social roles. As discussed below,
this may constitute the beginning of a dislodging from normal
social roles and enrollment instead in a schizophrenic pathway.
An abundant literature on labeling theory analyzes this process
(e.g., Scheff, 1999).
Thus, the course and result of schizophrenia are found to be
linked to the society of reference, and we encounter the paradox
that more developed clinical practices also appear to bring a
greater “development” of schizophrenia. This may indicate that,
given an “onset and prodromal phase,” there is a certain margin
with regard to whether schizophrenia develops into a chronic
problem. It is therefore relevant to consider studies about the

onset of schizophrenia.
These studies show that the main antecedent of schizophre-

nia is the loss of expectable social roles, together with anxiety
and depression (Häfner et al., 1999; see also Dohrenwend, 1999).
Furthermore, it should be borne in mind that this onset tends
to occur in early adolescence, when the adoption of social roles
is decisive for personal identity (Harrop & Trower, 2001)—such
identity being implicated in schizophrenia (Estroff, 1989; Fab-
rega, 1989). Thus, if we consider how the alarm produced by
“psychotic episodes” leads to the immediate prescription of med-
ication, we can see how social-role dislodgement can result in
adopting instead the role of a mental patient.
Against this background, it is relevant to introduce the notion
of career mental patients (Aneshensel, 1999; Karp, 1996). In
the case of schizophrenia, this process of engulfment, as Lally
(1989) put it, is marked by important transitional events (such
as hallucinations, repeated hospitalizations, medication or sup-
plementary security income), which weave the patient into the
course of the illness. This process is now so normalized in Western
society that we cannot say societal forces convert patients into a
stereotypically defined role and identity, or that patients want to
take advantage of the “good deal” hospitals provide. Rather, it is
the case that patients strive to maintain a positive view of the self as
competent (Lally, 1989, p. 263). The point here, however, is that
mental illness in accordance with the established clinical practices
may function as an alternative career to more productive life
careers.
However, the career of schizophrenia is not inevitable, to
judge from the differences in prognoses between countries.
Despite the fact that the clinical standards of Western society
encourage the concept of career mental illness, they could equally
be reoriented toward normalization, amounting to a move from
biological psychiatry to social psychiatry. Worthy of mention in
this regard are the research and clinical procedures developed by
Romme and Escher (2000). The primary aim of their approach
“is to make explicit the relationship between individual history
and the voices. In other words, to take it out of the realm of
psychopathology and put it into the context of people’s life-
problems and their personal philosophy” (2000, p. 10).
Romme and Escher’s approach involves, then, a new analysis

of the experience of hearing voices outside the illness model.
Note, first, that they speak of “hearing voices,” rather than

“auditory hallucinations.” Thus, it is still possible in developed
countries to normalize unusual experiences and perhaps, in turn,
improve the prognosis for schizophrenia. Relevant studies in this
regard would be those referring to the Open Dialogue Model
(Seikkula, Alakare, & Aaltonen, 2001a; 2001b; Seikkula & Olson,
2003) and the Dialogical Model (Lysaker & Lysaker, 2004, 2006).
Situating the Charcot Effect on the Map of Constructivism
We have used the Charcot effect, an historical case, as a critical

instrument for exposing clinical practices, in particular those
of psychopharmacology. Our analysis has shown how mental
disorders, far from being the supposed natural entities with
biological bases they are claimed to be, are constructed entities
of a historical–social nature. Having said this, there is a need
for greater specification of constructivism as understood here,
given the variety of constructivist theories. To this end, the most
appropriate approach seems to be to situate the Charcot effect
on the map of constructivist psychology drawn up by Raskin
(2002), which distinguishes three broad types of constructivism:
personal construct psychology, radical constructivism, and social
constructivism, each with its variants.
In general, it could be said that the Charcot effect fits in
with Gergen’s (1994, 2004) cycle of progressive infirmity. As the
reader will recall, four interconnected phases can be identified
in this cycle: (1) deficit translation, whereby life’s problems are
converted into the sacred or professional language of mental
disorder; (2) cultural dissemination, which turns mental disor-
ders into common, everyday concepts; (3) the cultural construc-
tion of illness, consisting in the social practices that teach us
to be mentally ill; and (4) vocabulary expansion, which estab-
lishes a thorough medicalization and psychologization of every-
day life. The disorders previously analyzed provide an excellent
demonstration of this cycle of progressive infirmity. Thus, the
Charcot effect would fall within the frame of Gergen’s social
constructionism.
Nevertheless, our conception presents certain differences

that preclude it from complete identification with social construc-
tionism, and especially its postmodern variant. These differences

specifically concern the relativist and relational emphasis of so-
cial constructionism (Raskin, 2002). In contrast to this relativist
emphasis, the constructivism defended here is committed to the
idea that some constructions can be better than others. Thus, we
have used the term “invention” to characterize the construction of
mental disorders promoted by psychopharmacological research,
largely for commercial reasons. The constructions of disorders
derived from listening to the person (rather than to the drug)
are considered here as more appropriate to the nature of the
problem. In contrast to social constructionism’s emphasis on the
relational and conversational as the source of individual mental
life, here we defend the role of people themselves in the con-
struction of their personalities, including forms alternative to the
dominant tendencies—for example, as authors responsible for
their own lives rather than as patients dependent on the Charcot
effect of the moment. These differences with respect to social con-
structionism lead to personal constructivism, in relation to which
we need scarcely mention the personal construct psychology of
George Kelly. Kelly’s perspective stresses humanistic aspects more
than cognitive ones, through an emphasis on self-determination
and the creation of personal meaning (Raskin, 2002). Even so,
it would be necessary to consider personal construct theory in
terms of a conative psychology, of behavioral and contextual flavor
along the lines, for example, of Sarbin (1997). In this context,
we might highlight the self-constructive nature of the personality
as a work of art, including the poetry of subjective experience
(Pérez-Álvarez & Garcı́a-Montes, 2004, 2006).
Our approach also has implications related to radical con-
structivism. Here once again it differs in relation to the theories
of reference (e.g., Maturana, 1988; von Glaserfeld, 1995). In
contrast to the epistemological constructivism that characterizes
radical constructivism, according to which human beings are
closed systems that cannot accede directly to external reality
(Raskin, 2002), our constructivism would constitute a kind of
hermeneutic constructivism. But even within the hermeneutic
perspective, ours would be more of a behavioral hermeneutics, in
Geertz’s (1986, p. 379) sense. Behavioral hermeneutics has its root
metaphor in drama, as employed in anthropology (e.g., Turner,

1982). In relation to the issue in question here, dramaturgical
theory does not involve consideration of the person as a closed

system, but rather as being in contact with others (as radical
constructivism in some way involves). The person would always be
situated in a context of action, in accordance with a contextualist
ontology (Mancuso, 1993). Even places themselves contribute to
the human drama (Sarbin, 2005). This means that the world
around us is considered an objective reality, previous to the entry
on the stage of any person in particular. After all, as Bruner (1990)
pointed out, when we enter life the play is already well under way.
But just because objective reality is real and objective does
not mean that it is not constructed; or put another way, the fact
that it is constructed does not mean it is not real and objective.
Thus, we would have to talk about the cultural construction
of clinical reality, in the sense established by Kleinman (1980,
pp. 35ff ). The phenomenon designated as the Charcot effect
would be a clinical reality of this type. However, precisely because
it is a constructed reality, this reality is susceptible to alternative
constructions, in Kelly’s sense, once more. Thus, for example, if
different roles from the normal ones are brought into play, both
for patients and professionals, alternatives to accepted clinical
realities can be constructed. This state of affairs may appear
quixotic. But perhaps precisely what is required is a quixotic
attitude, consisting in beginning to act in another way, as the
starting point for thorough personal and social change. We refer
here to the “quixotic principle” introduced in psychology by
Sarbin (see Pérez-Álvarez, 2005; Pérez-Alvarez & Garcı́a-Montes,
2004), in which we recognize the fixed role therapy proposed
by Kelly. If many of the patients who have succumbed to the
role of mentally ill are encouraged to play a different role in
their everyday lives, they would probably have opportunities to
incorporate new perspectives on life and on their experience of
themselves.
This is precisely what occurs in behavioral activation therapy
(Jacobson, Martell, & Dimidjian, 2001). This therapy consists
basically in replacing the pattern of avoidance characteristic of the
depressive situation by one of behavioral activation. The objective
is that clients engage in their lives in ways that modify their
environment to increase their contact with sources of positive
reinforcement. The result is that the behavioral activation itself

changes cognitions and emotions, being thus more parsimonious
than cognitive therapy (whose efficacy is perhaps due, in reality,

to its element of behavioral activation). Although behavioral
activation does not refer to fixed role therapy, it is easy to perceive
a certain affinity between the two. As far as our issue here is
concerned, both would be seen as demedicalized alternatives
to “mental disorders.” In sum, if we had to briefly define the
constructivism endorsed here, we might say that it is a personal
constructivism of a dramaturgic nature.
The Charcot Effect and Its Consequences for Psychiatry

and Clinical Psychology
In addition to the cultural consequences associated with the cycle

of progressive infirmity, the invention of mental disorders also
has perverse consequences for psychiatry and clinical psychology
themselves. For while the culture of therapy gives prominence
to psychiatrists, it also carries a threat. As people in general
discover for themselves the nature of their disorders and the
recommended treatments, the clinician’s specialized knowledge
becomes redundant. Thus, for example, the biologically oriented
psychiatrist is practically reduced to being a dispenser of pre-
scriptions, and indeed, much of this work can be and is done by
general practitioners—and it is no coincidence that this role for
primary care agents is a priority objective of psychopharmaceuti-
cal marketing. If patients do not arrive with their own diagnosis,
the general practitioner can apply a brief questionnaire sufficient
for making the corresponding prescription (Spitzer, Kroenke, &
Williams, 1999). On the other hand, if psychiatry were actually
capable of identifying the supposed biological causes of disorders,
it would die of its own success, because such disorders would cease
to be psychiatric and become neurological or of another medical
specialization, in a process that has occurred over the history of
psychiatry (Shorter, 1997). In the meantime, and paradoxically,
psychiatry survives by virtue of the failure to discover the alleged
biological causes that legitimate it as a branch of medicine.
As far as the perverse consequences for clinical psychology
are concerned, these are perceived in its adherence to the medical
model, consisting of a psychological discourse of deficits parallel
to that of neurobiology. Thus, in place of the neurobiological

explanation would be a psychological one, also relating to inter-
nal mechanisms; in place of medication would be therapeutic

techniques, assuming a specificity that does not exist either in
psychopharmacology or in psychotherapy. Indeed, specificity in
psychotherapy is by no means established, despite all its claims
(Baskin, Tierney, Minami, & Wampold, 2003; Wampold, 2005).
The point is that the medical model of psychotherapy is detri-
mental to a contextual model (psychosocial, interpersonal, and
cultural), which would be more in keeping with psychology. In
fact, the great debate in psychotherapy is between the medical
model and the contextual model (Wampold, 2001). Thus, the
mission of the contextual model would be twofold: on the one
hand, to promote the demedicalization of clinical psychology and,
on the other, to develop its own line as an alternative.
It is interesting to note that the controversy is not between
psychiatry and psychology. Although psychiatry is currently domi-
nated by psychopharmacology, it has a critical (“antipsychiatric”)
tradition that would not be out of place in the contextual per-
spective. Relevant approaches in this respect would be, among
others, critical psychiatry (Moncrieff, 2003), social psychiatry
(Romme & Escher, 2000), the cultural phenomenology of expe-
rience (Jenkins & Barrett, 2004), and postpsychiatry (Bracken
& Thomas, 2005). For its part, clinical psychology, however
cognitive–behavioral, subscribes nevertheless to a medical model,
as already argued. Thus, the “medical model versus contextual
model” debate is not between psychiatry and psychology, but
between, on the one hand, a discourse of deficit and the cor-
responding cycle of progressive infirmity and, on the other, the
development of alternative constructions and the consequent em-
powerment of persons. Nor is it a question, obviously, of whether
disorders are constructions but, rather, of what type of construc-
tions they are. Here we have criticized constructions as mental
illnesses and have, in fact, spoken of “inventions.” But we endorse
constructions as transformations of sense open to new meanings
(Gergen, 2004; McNamee, 2002; Raskin & Lewandowski, 2000).
In any case, escape from this discourse of deficit and cultural
weakening that has resulted from the invention of mental dis-
orders is no easy task. Nevertheless, given that we are dealing
with cultural constructions, there is a possibility that things can
be reconstructed in another way. Even so, it would be a gradual

process that has to begin by making an alternative presence felt
in a context where things are already functioning in a particular

way. A key point in this process, as Gergen (2004) argued, is
to break the existing circle that links the vocabulary of deficit
and payment of the costs of medical attention. That is, it would
be a question of eliminating the requirement of diagnosis and
reducing dependence on medication. If only to demonstrate that
this process is no utopia, we might cite some alternatives to the
treatment of “psychotic symptoms” because, in the end, these
“symptoms” constitute the bulwark of the medical model that
dominates in psychiatry and clinical psychology. Of relevance in
this respect would be Making Sense of Voices (Romme & Escher,
2000), Open Dialogue (Seikkula & Olson, 2003), and the Dialogical
Model (Lysaker & Lysaker, 2004; 2006); in a similar line, we might
also mention the reconstruction of a personal narrative (Dimag-
gio, 2006). All of these approaches—which basically consist of
listening to the voices of people with psychotic crises, instead
of “listening to the antipsychotics”—show a notable reduction in
the need for medication and hospitalization and, in the end, for
diagnoses of mental illnesses.
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The Charcot Effect: The Invention of Mental Illnesses

Article in Journal of Constructivist Psychology · August 2007

Pérez-Álvarez, Marino José Manuel García-Montes

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THE CHARCOT EFFECT: THE INVENTION

We propose something called the Charcot effect, which takes its

psychotherapeutic processes (Berkenkotter & Ravotas, 2002). In

of patients’ problems in accordance with clinical theory and

The Charcot Effect Today

The Charcot effect remains with us, mutatis mutandis, in psychiatry

which was merely a text revision).

supposed serotonin deficit for which it compensates would be its

The use of medication for specifying the diagnosis also has

if a supposed manic-depressive does not respond to lithium or to another

This strategy of listening to the drug involves the reduction

biobabble has emerged that, despite using the language of chem-

other hand, the term “construction” is reserved for referring to

psychotherapy (Gergen, 2004; McNamee, 2002).

The Growth of Depression to Epidemic Proportions

Until publication of the DSM-III-R (APA, 1987), depression

the early twentieth century, “melancholia” was a more promi-

For a start, the very trade name, Prozac—and even the

reuptake inhibitor” (SSRI)—shows commercial intelligence. The

evident, depression had already grown to epidemic proportions

learned to frame a large proportion of life problems in terms of

The Promotion of Social Phobia as a Commercial Strategy

The promotion of social phobia as a distinct clinical entity has

commercial strategy for the promotion of drugs (Moynihan,

depression “market” was already covered by Prozac. Thus, it be-

more generally, social anxiety. Indeed, social phobia became more

The Construction of Panic Disorder in Accordance

Panic disorder provides another example of the promotion of a

it is now considered a typical case of this phenomenon in the

merits a comment here, more than merely a mention, insofar

lasting effects than alprazolam in an independent study (Healy,

It is important, therefore, to see how, after all of this, panic

Whether or not panic has much to do with hysteria, psychi-

being satisfied with playing out a “methodological drama” (Orr,

The Poor Prognosis of Schizophrenia as a Possible Effect

Schizophrenia is often presented as the last bastion of mental

taken as proof of biological pathogeny, because there are also

deviations, and so on. Thus, even without denying some possible

tendency toward chronicity). This involves, in turn, a neglect of

precisely these other conditions of a vital nature on which may

problem. It is therefore relevant to consider studies about the

These studies show that the main antecedent of schizophre-

Romme and Escher’s approach involves, then, a new analysis

Note, first, that they speak of “hearing voices,” rather than

Situating the Charcot Effect on the Map of Constructivism

We have used the Charcot effect, an historical case, as a critical

Nevertheless, our conception presents certain differences

tionism, and especially its postmodern variant. These differences

metaphor in drama, as employed in anthropology (e.g., Turner,

theory does not involve consideration of the person as a closed

reinforcement. The result is that the behavioral activation itself

than cognitive therapy (whose efficacy is perhaps due, in reality,

The Charcot Effect and Its Consequences for Psychiatry