In Review
The Negative Symptoms of Schizophrenia: A Cognitive
Perspective
Neil A Rector, PhD1, Aaron T Beck, MD2, Neal Stolar, MD-PhD3
Recent reports of improvement in the negative symptoms of schizophrenia following targeted
cognitive interventions have prompted interest in the cognitive underpinnings of these symptoms.
This review integrates current experimental research with the phenomenological accounts of patients
participating in cognitive therapy for these specific symptoms. We propose that, in addition to the
well-established role of neurobiological factors in their development and maintenance, specific
cognitive appraisals and beliefs play a role in the expression and persistence of negative symptoms.
This cognitive model of negative symptoms is based on a diathesis–stress formulation: a continuum
of predispositional traits from the premorbid personality to the full-blown negative symptomatology,
the incorporation of negative social and performance attitudes within these traits, and low
expectancies for pleasure or success in goal-oriented activities. We suggest that negative symptoms
represent, in part, a compensatory pattern of disengagement in response to threatening delusional
beliefs, perceived social threat, and anticipated failure in tasks and social activities. A psychological
aspect of this motivational and behavioural inertia appears to be the patient’s perception of limited
psychological resources—a perception that motivates patients to conserve energy by minimizing
investment in activities requiring effort.
(Can J Psychiatry 2005;50:247–257)
Information on author affiliations appears at the end of the article.
Clinical Implications
· Active psychological processes contribute to what appear to be mere behavioural and emotional
deficiencies and can be targeted in psychological treatments.
· Pharmacotherapy has been shown to improve the psychophysiological underpinnings of negative
symptoms, and there is evidence that cognitive therapy can help in mobilizing patients ’ latent resources
to promote emotional reengagement.
Limitations
· Additional experimental and clinical research is required to test some of the theoretical assertions
established in our cognitive model of negative symptoms
Key Words: cognitive therapy, schizophrenia, negative symptoms, cognitive appraisals, dysfunctional
beliefs
he past decade has seen considerable progress in the
development and delivery of effective cognitivebehavioural therapy (CBT) interventions for persistent symptoms of schizophrenia, such as delusions and hallucinations.
Recent randomized controlled trials (RCTs) have demonstrated the ability of CBT to significantly and sustainably
reduce distress caused by the experience of positive symptoms (1–3). Much less attention has been given to understanding and treating the negative symptoms of schizophrenia.
Nevertheless, a growing number of studies have found that
CBT also leads to clinically significant reductions in second-
T
Can J Psychiatry, Vol 50, No 5, April 2005 W
ary negative symptoms (2,3). In a recent RCT comparing CBT
plus enriched standard care with enriched standard care alone
(4), CBT was shown to significantly reduce both positive and
negative symptoms. Further, the changes in these symptoms
were relatively independent: changes in negative symptoms
were not simply a secondary consequence of change in positive symptoms (or depression or medication). In view of this
preliminary evidence, it is desirable to provide a cognitive formulation for these symptoms as a guide to therapy and future
research.
247
The Canadian Journal of Psychiatry—In Review
The Negative Symptoms of Schizophrenia
The importance of deterioration in emotional expression,
motivation, and behaviours has been central to schizophrenia
since it was first described: as Kraepelin stated, the 2 fundamental processes underlying dementia praecox were “weakening of the mainsprings of volition” and “the destruction of
the personality” (5). Similarly, Bleuler observed that “the
emotional deterioration stands in the forefront of the clinical
picture . . . many sit about the institutions to which they are
confined with expressionless faces, hunch-up, the image of
indifference” (6). These early descriptions of emotional and
motivational dysfunction are closely aligned with the current
nosological description of negative symptoms as restrictions
in the range and intensity of emotional expression (affective
flattening), in the fluency and productivity of thought and
speech (alogia), and in the initiation of goal-directed behaviour (avolition) (7). The loss of ability to feel pleasure
(anhedonia) has also been identified as an associated feature
(7), although controversy exists regarding the significance of
this observation (see below).
Conceptually, the identification of negative symptoms as
characterized by loss of normal functioning and distinct from
positive symptoms characterized by active excesses of normal
functioning has been articulated for over 150 years (8) and has
remained central to the conceptualization of the psychopathological processes of schizophrenia (9–12). At the phenomenological level, an extremely large extant literature of
factor-analytic studies of schizophrenia has extracted 2 distinct and often independent symptom factors, one reflecting
positive symptoms and a second measuring negative symptoms, providing empirical support for their distinction (13).
Patients experiencing flat affect may speak in a monotone,
stare vacantly, and generally appear unresponsive to things
going on around them. Brief and empty replies reflect alogia,
translated literally to mean “without speech” or “poverty of
speech.” Alogia often takes the form of delayed comments or
slow responses to questions. Avolition is characterized by an
inability to initiate and persist in goal-directed activities,
including basic functions of personal hygiene. While affective flattening, alogia, and avolition comprise the diagnostic
description of negative symptoms in the DSM-IV, other
symptoms have also been included, depending on the
conceptual scheme (9,14).
Diathesis–Stress Model of Negative Symptoms
The starting point is an explicit diathesis–stress model of
schizophrenia, according to which, as a result of a complex
combination of genetic and environmental factors, certain
individuals become susceptible to the development of negative symptoms during youth and adolescence (15). Quantitative reviews of the extant literature have demonstrated a
248
greater genetic contribution to the emergence of negative
symptoms opposed to positive symptoms (16,17). Further,
obstetric complications in schizophrenia are more directly
associated with the subsequent development of negative
symptoms, compared with positive symptoms (18). The
genetic and obstetric factors are hypothesized to result in
structural abnormalities, such as enlarged ventricles (19),
which have been found in turn to be specifically associated
with negative symptoms (20). Ventricular enlargement likely
predates the onset of psychosis (21), since retrospective recall
has linked it to childhood motor abnormalities (22). Enlargement of the ventricles may be secondary to diminished volumes of cortical structures resulting from abnormal cell
migration, programmed cell death during gestation (23), and
(or) abnormal pruning during adolescence (24). These
neuronal insults may produce aberrant connectivity between
various brain regions, leading to poor integrative functioning
of the brain (25) and, hence, limited processing resources and
poor neurocognitive performance (23). Such cognitive deficits and the limited availability of processing resources (26)
likely render patients with negative symptoms particularly
vulnerable and provoke such adverse developmental stressors
as social and academic failure (27).
The seminal role of neurobiological and neurocognitive deficits in the pathogenesis of negative symptoms is established.
This paper aims to outline what we believe to be important
psychological variables, the conceptualization and treatment
of which require further investigation and attention. We followed 2 lines of inquiry in examining evidence that might support our formulations. First, we reviewed historical
antecedents of the negative symptoms model and the subsequent experimental literature relevant to our hypothesis;
second, we drew on clinical material that illustrates the interaction of beliefs and interpretations with negative symptoms
as well as with retrospective accounts of cognitive precursors
to psychosis. We propose that certain active psychological
processes contribute to what on the surface seem to be mere
behavioural and emotional deficiencies.
Continuity and Predisposition
It is important initially to determine whether negative symptoms represent a coherent construct that can be analyzed in
terms of its relation to relevant beliefs and expectancies. Are
the negative symptoms relatively stable over time? Do they
have trait-like characteristics that would suggest continuity
with premorbid characteristics? The identification of
subclinical precursors that overlap the clinical picture would
suggest that the negative symptomology represents an
exacerbation of these precursor attributes.
While most patients experience waxing and waning of their
negative symptoms, only a small subgroup of patients
W Can J Psychiatry, Vol 50, No 5, April 2005
The Negative Symptoms of Schizophrenia: A Cognitive Perspective
(approximately 15% to 20%, 28) appear to demonstrate
greater stability in a constellation of core negative symptoms,
termed the “deficit syndrome” (28). The deficit syndrome is
defined as the presence of 2 negative symptoms (specifically,
restricted affect, diminished emotional range, poverty of
speech, curbing of interests, diminished sense of purpose, or
diminished social drive) for a period of 12 months that are
determined not to be secondary to anxiety, medications, positive symptoms, cognitive deficits, and (or) depression (29).
Studies have established the relative stability of the core negative symptoms (28,30). Patients with core negative symptoms
may also have changes in symptom intensity and superimposed secondary negative symptoms, but a primary and
enduring core of negative symptoms is hypothesized to persist
(28). For instance, a prospective study aimed to examine the
stability and exacerbation of negative symptoms over 6 time
points in patients assessed within 2 years of onset (31). In this
study, patients receiving the deficit classification were found
to have more consistent elevations of negative symptoms,
compared with nondeficit patients (suggesting greater stability), but the deficit patients were also found to experience clinically significant fluctuations in their negative symptoms. The
relative stability and continuity of these symptoms superimposed on periodic exacerbations could suggest that the more
enduring negative symptoms emerge from fixed neurobiological deficits. However, it is also possible that greater
stability of symptoms in some patients could be related to
stable behavioural patterns and personality traits that existed
prior to psychosis onset.
Many authors have identified relevant preexisting personality
and behavioural patterns and generally related them to the
negative symptoms in schizophrenia (6,32,33). Kretschmer
suggested that anesthetic (that is, trait) indifference is often a
precursor to the development of schizophrenia, whereas
hyperesthetic (that is, reactive) avoidance is not (33). He also
asserted that anesthetic indifference could be considered as
both a clinical manifestation of schizophrenia and as a trait of
normal temperament that predisposes to schizophrenia. This
dimensional view of schizophrenia resting on a continuum of
expression of schizoid withdrawal has been retained in the
current DSM classification of schizoid personality disorder.
Persons with a schizoid personality disorder neither desire nor
enjoy close relationships; choose solitary activities; have little
interest in experiences; take pleasure in few, if any, activities;
lack close friends; appear indifferent to the praise or criticism
of others; and show emotional coldness, detachment, and flattened affect (7). The dimensional view of schizophrenia is
also captured in the current diagnostic criteria for schizotypal
personality disorder, which not only emphasize attenuated
forms of positive symptoms (for example, ideas of reference,
odd and magical ideation, and suspiciousness) but also
Can J Psychiatry, Vol 50, No 5, April 2005 W
highlight the restriction of social affiliation, described as a
pervasive pattern of social and interpersonal deficits marked
by acute discomfort with, and reduced capacity for, close
relationships (7).
Importantly, patients with schizophrenia demonstrate significant elevations of these traits prior to the onset of their illness.
These traits are also specifically associated with the expression of negative symptoms following illness onset, but they
appear to be unrelated to positive symptoms. Solano and De
Chavez found that 85% of outpatients with schizophrenia had
a history of premorbid personality disorders with schizoid,
schizotypal, and avoidant personality disorders being most
common (34). Peralta and colleagues found schizoid and
schizotypal personality disorders in 39% of a large sample of
inpatients with schizophrenia (35). Most critical to our argument, the presence of schizoid-schizotypal personality disorders was specifically associated with more frequent and
severe affective flattening and alogia but entirely unrelated to
the positive symptoms of schizophrenia. Similarly,
Lindstroem and colleagues found that outpatients suffering
from schizophrenia with schizoid, schizotypal, and cluster A
personality disorders were likely to display more prominent
negative than positive symptoms (36). These studies provide
some support for the specific association between premorbid
schizoid withdrawal and negative symptom expression. Further support for the predisposing role of schizoid traits comes
from research on the presence of these traits in nonaffected
first-degree relatives. Battaglia and colleagues found that the
first-degree relatives of patients with schizotypal personality
disorder (and other personality disorders) have a greater risk
for schizoid and schizotypal personality disorders (as well as
schizophrenia), compared with a nonpsychiatric control
group (37).
The importance of the dimensionality of “schizoidness” as
both a trait disposition to and clinical manifestation of negative symptoms in schizophrenia has been further examined
within the research tradition on schizotypy (38–40). Mata and
colleagues found that premorbid schizoid and schizotypal
traits in patients with schizophrenia predicted dimensional
schizotypy scores in nonaffected first-degree relatives (41).
An important component of the schizoid traits and behavioural disposition centres on negative beliefs, attitudes, and
appraisals related to social engagement.
In summary, negative symptoms are expressed along a continuum. In some cases, negative symptoms may persist throughout the illness (independent of other symptoms, that is, the
deficit syndrome). Alternatively, they may appear only in
response to positive symptoms, to stressful events, or to
neurocognitive medication side effects (7). We propose that
this continuum of expression is related, in part, to the intensification of the negative beliefs about the self and others that are
249
The Canadian Journal of Psychiatry—In Review
embedded in the schizoid traits. As these beliefs become
hypervalent, patients resort to a familiar strategy of buffering
themselves from external threat and painful symptoms. This is
manifested not only in social isolation but also in blank faces,
poverty of speech, and diminished motivation for ordinary
activities. Their attenuated verbal behaviour becomes alogia;
their diminished drive is perceived as amotivation, their limited facial expressiveness as affective blunting, and their
hopelessness as apathy.
Negative Beliefs and Negative Expectancies
Social Distancing Beliefs
Several studies have shown that an important component of
the schizoid personality pattern centres on negative attitudes
toward social engagement. The most widely used scale, the
inexactly labelled “Social Anhedonia Scale” (42,43), is
loaded primarily with items minimizing the value of interpersonal affiliations: “Having close friends is not as important as
many say,” “I attach very little importance to having close
friends,” and “I prefer hobbies and leisure activities that do
not involve other people.”
The values and preferences detailed in this questionnaire
seem to be connected to the social withdrawal manifested by
individuals with schizoid traits and conceivably function as a
partial determinant of them. Several studies, for example,
have shown that negative attitudes toward social affiliation, as
measured by the Chapman scale, are a characteristic feature of
those showing psychosis proneness (44,45). These attitudes
are also prominent in the biological relatives of individuals
diagnosed with schizophrenia (46). For instance, Kendler and
colleagues compared relatives of matched control subjects
with relatives of 5 proband groups: schizophrenia, psychotic
affective illness, nonpsychotic affective illness, other
nonaffective psychoses, and nonpsychiatric control subjects
(46). They found that negative attitudes toward social affiliation were the only self-report dimension to differentiate the
relatives of schizophrenia probands from the relatives of other
psychopathological groups.
Although social distancing is characteristic of other
psychopathological states (for example, depression), the persistence of these difficulties in patients with schizophrenia
may distinguish them from patients with other conditions. For
instance, Blanchard and colleagues found that patients with
schizophrenia evidenced greater stability in their (negative)
attitudes toward social affiliation than did a nonpsychiatric
control group (47). A more recent study, following inpatient
admissions for acute treatment over a 1-year period, found
that preference for social withdrawal remained stable in a
schizophrenia patient sample but was only transiently related
to symptom severity in depression patients (48). Interestingly,
250
the 2 samples did not differ in clinician-rated measures of
social affiliation at baseline.
The problem of distinguishing between social and emotional
withdrawal as part of the negative symptom constellation vs
syndromal depression has been recognized since its earliest
description (5,6). Depressive symptoms may be present at
each phase—premorbidly, at acute onset, in the postacute
period, and at the time of relapse—with epidemiologic and
clinical studies converging on a 25% modal occurrence during the longitudinal course of the disorder (49,50). However,
numerous factor-analytic and longitudinal studies have
shown that secondary depressive symptoms can be reliably
distinguished from the negative symptoms of schizophrenia
(14). Fewer studies like that by Blanchard and colleagues (48)
have been conducted to test whether there are qualitatively
distinct and enduring attitudinal differences toward affiliation
that distinguish these conditions. Blanchard and colleagues
found that negative attitudes toward social affiliation were
more stable in patients with schizophrenia than in patients
with depression.
Negative Beliefs About Performance
A cross-sectional examination of patients’ beliefs and attitudes as assessed by the Dysfunctional Attitude Scale (DAS)
was compared with symptom expression assessed by
responses to the Positive and Negative Syndrome Scale
(PANSS) (51,52). Endorsement of items on the DAS such as
“Taking even a small risk is foolish because the loss is likely to
be a disaster” and “If a person avoids problems, the problem
tends to go away” were significantly correlated with symptoms comprising the negative syndrome and were independent of positive symptoms. The association between these
autonomous beliefs and negative symptoms held after depression was controlled for. Table 1 shows selective DAS items
that correlated significantly with the social and emotional
withdrawal symptom ratings of the PANSS.
Taken from the observed associations in Table 1, the pattern
of responding on the DAS suggests that some patients are
prone to attach negative meanings to themselves for perceived
substandard performance. Attitudes such as “If I fail partly, it
is as bad as being a complete failure,” “If you cannot do something well, there is little point in doing it at all,” and “If I fail at
work, I”m a failure as a person” feed into avoidance, apathy,
and passivity. Significantly, these patients disagree with the
statement, “Being isolated from other people leads to unhappiness”—consistent with their sense that isolation protects
them from the pain of rejection and, ergo, leads to happiness.
This response obviously contrasts with the usual response of
depression patients, who would agree with the statement (53).
Further, Barrowclough and colleagues found a significant
negative correlation between negative symptoms in
W Can J Psychiatry, Vol 50, No 5, April 2005
The Negative Symptoms of Schizophrenia: A Cognitive Perspective
Table 1 Dysfunctional attitudes associated with social and emotional withdrawal in schizophrenia
r
P
If I fail at my work, then I am failure as a person.
0.437
0.001
If you cannot do something well, there is little point in doing it at all.
0.346
0.009
If I fail partly, it is as bad as being a complete failure.
0.265
0.048
If a person asks for help, it is a sign of weakness.
0.289
0.031
If I do not do as well as other people, it means I am an inferior human being.
0.358
0.007
Taking even a small risk is foolish because the loss is likely to be a disaster.
0.359
0.007
People will probably think less of me if I make a mistake.
0.265
0.048
If I ask a question, It makes me look inferior.
0.374
0.004
I should be upset if I make a mistake.
0.374
0.005
One can get pleasure from an activity regardless of the end result.
–0.425
0.001
Dysfunctional Attitude Scale items
schizophrenia and patients’ evaluation of their positive attributes, as well as a similar correlation with their positive attitudes about their role (54). Patients’ evaluation of personal
worth seems to be grounded in their presumed deficits (for
example, perceived lack of such personal attributes as attractiveness, intelligence, and social skills) together with perceived deficiencies in various domains (for example, social,
interpersonal, or occupational). It is conceivable that dysfunctional attitudes and perceived personal and interpersonal inadequacies converge to steer these patients to a “point of safety.”
In summary, preliminary evidence links negative symptoms
with related preexisting personality traits. The consolidation
of negative attitudes toward affiliation and preference for
social distancing prior to the onset of the illness may potentiate the activation of negative symptoms following activation
of the disorder. Specific attitudes and beliefs pertaining to
negative performance evaluation in patients experiencing
prominent negative symptoms are also hypothesized to be
associated with the persistence of negative symptoms.
Negative Beliefs Activated by Positive Symptoms
There is considerable interaction and overlap between negative symptoms and positive symptoms (7). For instance, to
mitigate social threats, patients suffering from paranoia
engage in interpersonal avoidance and other active safety
behaviours. These patterns of emotional and social disengagement are said to constitute “secondary” negative symptoms as opposed to the so-called “primary” negative
symptoms that are defined as independent of other emotional,
environmental, or pharmacologic factors. In support of the
secondary activation of negative symptoms in response to
positive symptoms, recent research following patients prospectively over an average period of 3 years found that negative symptom exacerbations (that is, blunted affect, emotional
Can J Psychiatry, Vol 50, No 5, April 2005 W
withdrawal, and [or] psychomotor retardation) were concurrent with positive symptom exacerbations to a greater extent
than by chance (31).
Behavioural responses conceptualized as secondary to active
hallucinations and delusions can often be understood in terms
of the person’s fears, attitudes, beliefs, wishes, and the like.
Negative symptoms associated with threatening delusions
and hallucinations often reflect compensatory strategies that
serve as a form of protection against the putative threat. For
example, one patient with an encapsulated paranoid delusion
spent the entire day in bed to alleviate his fears of being monitored by government officials outside his home. Another
patient, hearing voices attesting to her “worthlessness,” quit
her part-time job and continuing education course and withdrew from family and friends because she feared making mistakes, which would trigger a voice stating “You’re
worthless.” Chadwick and Birchwood (55,56) found that
patients’ idiosyncratic delusional beliefs about voices’ power
and authority determine whether they become engaged with
the voices or, alternatively, whether they become disengaged
and withdrawn (57). In this way, beliefs and appraisals about
the voice activity are more predictive of the emergence of secondary negative symptoms than is the mere occurrence of the
voice activity itself.
In other instances, specific negative symptoms appear to follow from idiosyncratic delusional beliefs. One patient, for
instance, was severely bullied throughout early grade school.
Although he had previously shown excellent academic promise, he began to isolate himself and skip classes. When he did
attend class, he spent most of his time daydreaming and fantasizing about girls; on occasion, this produced erections in
class, of which he was deeply ashamed. He stopped attending
classes altogether and spent his time isolated in his room.
251
The Canadian Journal of Psychiatry—In Review
Table 2 Negative expectancy appraisals associated with DSM-IV negative symptoms
Appraisals
Symptoms
Low self-efficacy (success)
Low satisfaction (pleasure)
Affective flattening
If I show my feelings, others I don’t feel the way I used
will see my inadequacy.
to.
Alogia
I’m not going to find the
right words to express
myself.
I take so long to get my
I’m going to sound weird,
point across that it’s boring. stupid, or strange.
Avolition
Why bother, I’m just going
to fail.
It’s more trouble than it’s
worth.
Upon assessment, all negative symptoms were rated as present but were seen to be secondary to his delusional beliefs.
The patient was afraid to speak to people for fear that he might
have an erection in their presence and so kept all conversation
to a bare minimum (reflecting alogia). To prevent arousal, he
intentionally minimized all activities and directed significant
mental and physical energy to attempting to control his
thoughts (reflecting anergia and withdrawal).
Cognitive Factors in the Expression of
Negative Symptoms Independent of Positive
Symptoms
There also appear to be characteristic cognitive factors that
contribute to negative symptoms, independent of positive
symptoms. Specifically, a cognitive set characterized by low
expectancies for pleasure, success, and acceptance, as well as
the perception of limited resources, contributes to the persistence of negative symptoms. As Table 2 illustrates, we propose that negative expectancy appraisals in part form the
specific expression of negative symptoms. We address the
form and content of each negative expectancy in sequence.
Low Expectancies for Pleasure
When provided with the opportunity to participate in pleasurable activities, patients often respond by stating (or simply
thinking) “What’s the point?” “Why should I bother?” “It’s
too much work,” and the like. For instance, a patient who
spent several hours lying in bed decided to get his guitar from
the closet. He began to play a few chords and quickly realized
that the strings needed tuning. He thought, “Why bother? It’s
more work than it’s worth,” and he turned on the television
instead. Patients not only appear to expect little enjoyment for
their efforts but also focus on their high expectation of displeasure. DeVries and Delespaul found that, compared with
nonpatient control subjects, patients with schizophrenia
report experiencing more negative emotions and fewer positive emotions in their daily lives, perhaps as a function of
252
Low acceptance
Low available resources
My face appears stiff and
contorted to others.
I don’t have the ability to
express my feelings.
It takes too much effort to
talk.
It’s best not to get involved. It takes too much effort to
try.
participating in fewer activities that are likely to elicit pleasant
emotions (58).
Experimental studies have shown that patients with schizophrenia tend to exhibit significantly fewer positive and negative facial expressions in response to emotional stimuli than
do control subjects (59,60), especially if they have enduring
negative symptoms (61). By contrast, their subjective reports
of emotional experience during exposure to emotional stimuli
indicate that they experience the full range of positive and
negative emotions and do so to the same degree as, or even
more so, than nonpatient control subjects (59,60). Even
patients with chronic and severe negative symptoms report
experiencing the same range of positive and negative emotions as those without enduring negative symptoms (although
there is less expressivity in the former). As such, when
patients, including those with prominent and severe negative
symptoms, are presented with pleasurable stimuli, they can
and do derive pleasure from these experiences.
Germans and Kring resolved this inconsistency by suggesting
that patients do not anticipate that pleasurable activities will
indeed be pleasurable, even though they do experience pleasant emotion when presented with pleasurable stimuli (62).
This explanation follows the distinction between appetitive
pleasure (that is, anticipating that something will bring pleasure) and consummatory pleasure (that is, the actual level of
pleasure experienced from participating in an activity). Gard
and colleagues compared patients with schizophrenia (n = 45)
with nonpatient control subjects (n = 40), using a wellvalidated measure of anticipatory and consummatory pleasure (63). While patients with schizophrenia reported lower
scores on anticipatory pleasure, they had the same degree of
consummatory (actual) pleasure as did nonpsychiatric control
subjects. Hence research supports the hypotheses that patients
with schizophrenia maintain low expectancies for pleasure
but, once engaged, show little impairment in their ability to
derive pleasure. This hypothesis is in line with the distinction
made between a dopaminergic system involved in responses
W Can J Psychiatry, Vol 50, No 5, April 2005
The Negative Symptoms of Schizophrenia: A Cognitive Perspective
to expectations of reward (through associative learning) and
an enkephalin system involved in direct experiences of
reward (64), according to which only the former has been
found to be diminished in those with prominent negative
symptoms.
Despite their low expectancy for pleasure, patients do experience some enjoyment once they are engaged in a task. For
instance, one patient whose daily routine had been reduced to
sleeping, eating, and attending doctors’ appointments identified a list of activities in which she used to take pleasure but no
longer anticipated enjoying. These included calling family,
vacuuming the house, taking baths, watching television, and
praying. Although the initial ratings of expected pleasure
were close to zero, she subsequently reported experiencing
mild satisfaction when vacuuming, moderate enjoyment during the bath and watching television, and high pleasure when
speaking with her mother on the telephone. It is important to
obtain ratings at the time of the event because, upon recall, it is
frequently noted clinically that patients tend to underestimate
their level of enjoyment. Of course, negatively biased recollections serve to reinforce a negative view of the situation and
to minimize the pleasure taken.
Low Expectancies for Success
Patients also show bias in their reported low expectation of
success in a proposed task. They often expect to fail to meet
given goals. If they meet their goals, they tend to perceive
their performance as substandard, compared with their
expected performance. This negative outlook affects their
motivation to initiate and sustain goal-directed behaviour,
especially when under stress. Among patients, the impaired
role of executive functioning in maintaining goal-directed
thoughts, especially on complex tasks (65,66), does not adequately account for the fact that patients do not at times complete simple tasks or the fact that they are engaged and making
an effort toward a specific goal one day but not the next.
Moreover, when sufficiently motivated, patients can carry out
complex tasks that seem to be beyond their capacity.
Many patients show negative expectations that interfere with
motivation and action. One socially isolated patient, for example, would pick up the phone to make a call but would then
quickly hang up. The patient’s thought was “I’m not going to
sound right; I’ll have nothing to say.” Attending day-hospital
groups, he was able to recognize similar performance-related
concerns when he thought about speaking to others (“I’m
going to take too long to say everything that I’ll want to say”),
going to the gym (“I won’t be able to get through all the
weights”), and playing soccer (“I’m not going to be good
enough”)—areas that he listed at the beginning of treatment as
areas wherein he was “lacking motivation.” As he recognized
Can J Psychiatry, Vol 50, No 5, April 2005 W
the deterrents to action, he became motivated to follow
through on a given goal.
Since some patients do indeed report having greater difficulties with concentration, fine motor skills, and sustained effort
to see things through to the end, the following question
emerges: Is this negative view of likely success accurate? A
core difficulty contributing to negative performance expectation is that patients are easily defeated and consequently disappointed in their performance. In addition to the frustration
that follows from failing to meet self-directed goals, patients
with prominent negative symptoms also experience considerable guilt in the perception that they have failed to meet others’ past and present expectations. The double burden of
persistently believing that they have failed to meet their own
and others’ expectations consolidates core beliefs of being a
“failure,” “useless,” “worthless,” and “a bum.” Patients
become hypervigilant and exquisitively sensitive to the perception of criticism. For example, one patient, encouraged by
his mother to awake and get dressed for a doctor’s appointment, reported feeling annoyed as he thought to himself, “I’m
always being hassled,” “I’m too tired,” and “They expect too
much from me.” He responded by going back to bed.
Barrowclough and colleagues found that the degree of perceived critical comments from family members predicted the
presence and severity of negative symptoms but not positive
symptoms (54). Conversely, when relatives were perceived as
warm and supportive, patients evaluated their performance
more positively.
Low Expectancies Owing to Stigma
Previous reviews have extensively described the adverse
effect of a schizophrenia diagnosis (67,68). This adverse
effect also figures prominently in published first-person
accounts (see Schizophrenia Bulletin). Patients with prominent negative symptoms characteristically experience defeat
when their persistent symptoms interrupt their life goals, create great personal distress, and are frequently misconstrued as
signs of laziness, ineptitude, or a “bad attitude.” The demoralization resulting from the diagnosis of schizophrenia is significant: many patients refer to it in different ways as a type of
death sentence. Some patients painfully recognize that they
have missed our broader cultural goals—to work, have a life
partner, and enjoy leisure pursuits—even though they have
not relinquished the desire for these goals. Many patients have
previously developed negative beliefs that they are worthless,
incompetent, or unsuccessful, which they view as validated
by the limitations imposed by their disorder.
In addition to the real limitations produced by schizophrenia
symptoms, patients with prominent negative symptoms incorporate these stigmatizing views into their self-construals.
These symptoms have a negative influence on patients’
253
The Canadian Journal of Psychiatry—In Review
Figure 1 Cognitive expectancies in the production of negative symptoms
Low
Expectancies for
Pleasure
Low
Expectancies for
Success
Negative Symptoms
Affective
Flattening
Anergia
Low
Expectancies for
Acceptance
perceived self-efficacy when they are faced with life challenges. The following statements are common: “What do you
expect, I’m mentally ill”; “It doesn’t matter what I do, it’s not
going to change the fact that I’m just a schizophrenic”; or
“There’s no hope for me , since I’ve got schizophrenia.”
One patient, who used to enjoy playing badminton, developed
a sense that he was being “judged for being crazy” when he
played. This patient stated that he knew he was being criticized because he perceived a “weird sensation” in his stomach
whenever he played—an experience similar to the misinterpretation of bodily sensations as confirmation of delusional
beliefs (69). The fear of being judged “crazy” led him to avoid
playing badminton, although it had given him great pleasure.
Another patient stated, “I’m just a label living in a bubble.”
When presented with the opportunity to work as a volunteer,
he said, “Why bother, I’ve already been left behind. It’s as if I
have a yellow stripe down my back.”
Perception of Limited Resources
Beliefs about the perceived personal costs of expending
energy in making an effort also contribute to a pattern of passivity and avoidance. When presented with the opportunity to
participate in a putative pleasant activity, patients will state,
“It’s too much,” or “I can’t handle it,” or “Why bother, it’s too
much.” For instance, one patient referred for cognitive therapy was concerned primarily about “low motivation and low
energy.” Even lifting his head from the pillow “took too much
effort.”
Patients’ subjective accounts of limited resources likely
reflect, in part, an accurate perception of diminished
254
Alogia
Avolition
Anhedonia
Perception
of
Limited Resources
resources. For instance, a voluminous literature attests to
reduced processing capacity for task-relevant cognitive operations—including but not limited to reduced ability to sustain
concentration, maintain a task set, and establish an optimal
level of readiness for processing (26). Further, it has been suggested that a reduced “pool of nonspecific resources” can lead
to apathy, alogia, affective flattening, and emotional withdrawal (70). However, we also propose that patients with
prominent negative symptoms exaggerate the limited availability of resources as a result of their rigid defeatist cognitive
set.
Cognitive and behavioural avoidance of effortful engagement
may be similar to the cognitive processes at work in chronic
pain and may reflect, in part, conscious and strategic attempts
to limit “reinjury.” Patients with prominent negative symptoms often highlight “discomfort” and “low energy” when
confronted with personal challenges and fear that undertaking
an effortful activity will generate uncomfortable and unsustainable expectations from others. In this way, patients relinquish goals to establish a more acceptable comfort level.
As the bidirectional arrows in Figure 1 indicate, the presence
of a negative expectancy can serve as a catalyst for the activation of other expectancies: the patient who habitually expects
to fail at task pursuits is also likely to expect to derive little satisfaction from those pursuits; the patient who expects not to
have the energy to talk at a social gathering is more likely to
expect to come across as detached and “strange.” Also, the
relation between negative expectancies and negative symptoms is bidirectional, so the worsening of negative symptoms
W Can J Psychiatry, Vol 50, No 5, April 2005
The Negative Symptoms of Schizophrenia: A Cognitive Perspective
further primes negative expectancy appraisals, creating a
vicious downward spiral.
Summary and Conclusions
We have proposed a cognitive perspective on the negative
symptoms that highlights the interaction of neurologic deficits, stressors, personality vulnerability, dysfunctional
beliefs, and negative expectancies in the development,
expression, and persistence of these symptoms. We have presented supporting evidence based on empirical and clinical
studies. The continuity of negative symptoms is supported by
the finding of attenuated negative symptoms in youths who
eventually develop schizophrenia. The concept of an organized pattern is supported by the finding of schizoid,
schizotypal, and avoidant personality disorders in patients
who develop schizophrenia. The hypothesis that a cluster of
beliefs is associated with negative symptoms is supported by
the finding of asocial or autonomous beliefs during the
schizophrenic episode. The concept of expectancies of
nongratification is supported by experimental work with
expectancies. The tendency to withdraw when confronted
with demanding situations is supported by clinical case
reports. Finally, the effect of psychotherapeutic interventions
also provides a quasi-experimental line of evidence.
To date, there has been very little psychological theorizing or
experimentation on the negative symptoms of schizophrenia,
and there are gaps in the empirical evidence for our proposed
perspective. Prospective research is needed to assess whether
the severity of dysfunctional attitudes assessed in the
premorbid phase predicts the onset and later exacerbation of
negative symptoms throughout the disorder’s course. Prospective research should also address important issues pertaining to the “directionality” of symptom and cognitive
changes. Psychometric development is needed for the reliable
and valid assessment of expectancy appraisals, so that
cross-sectional and prospective research can be conducted on
their role in producing and maintaining negative symptoms.
Such research should also seek to determine the extent to
which negative expectancies are unique to patients with negative symptoms or other psychiatric conditions. Support for the
model would also be garnered if treatment studies were able to
demonstrate that reduced negative symptoms are associated
with a corresponding (and correlating) reduction in dysfunctional attitudes and (or) negative expectancy appraisals.
Finally, advances in the psychological understanding of negative symptoms will be contingent on the study of corresponding neurobiological factors that likely potentiate and interact
with these processes. For instance, negative symptoms have
been found to be associated with decreased frontal activity
(71) and diminished dopamine activity (as well as other associated neurotransmitter disruptions) in the prefrontal cortex
Can J Psychiatry, Vol 50, No 5, April 2005 W
(72). These physiological disruptions may be primary antecedents to the lack of goal-directed activities or, alternatively,
may reflect in part the neurophysiological consequences of
repetitive priming of negative expectancies.
The understanding and management of negative symptoms is
especially important given their association with poor
long-term functioning (73). Pharmacotherapy has been
shown to improve the psychophysiological underpinnings of
negative symptoms, and as described, psychosocial interventions have successfully mobilized patients’ latent resources to
promote emotional reengagement. By focusing on patients’
latent resources (or “neuroplasticity”), clinicians can help to
move them toward a more fulfilling, less distressing life.
Acknowledgements
We thank Dr C Cather, Dr A David, Dr D Fowler, Dr D Fowles,
Dr E Granholm, Dr P Grant, Dr D Kingdon, Dr R Lewine, Dr J
McQuaid, Dr E Peters, Dr M Sosland, Dr D Turkington, Dr D
Warman, Dr J Wright, and Dr T Wykes for their comments on an
earlier draft of this manuscript.
References
1. Rector NA, Beck AT. Cognitive behavioral therapy for schizophrenia: an
empirical review. J Nerv Ment Dis 2001;189:278–87.
2. Tarrier N, Wykes T. Is there evidence that cognitive behaviour therapy is an
effective treatment of schizophrenia? A cautious or cautionary tale? Behav Res
Ther 2004;42:1377–401.
3. Gould RA, Mueser KT, Bolton E, Mays V, Goff D. Cognitive therapy for
psychosis in schizophrenia: an effect size analysis. Schizophr Res
2001;48:335–42.
4. Rector NA, Seeman MV, Segal ZV. Cognitive therapy of schizophrenia: a
preliminary randomized controlled trial. Schizophr Res 2003;63:1–11.
5. Kraepelin E. “Dementia praecox.” Barclay RM, translator (1919). Psychiatrica.
8th ed. Melbourne (FL): Robert E Krieger; 1913.
6. Bleuler E. Dementia praecox or the group of schizophrenics. Kinkin J,
translator. New York: International Universities Press Inc; 1950.
7. American Psychiatric Association. Diagnostic and statistical manual of mental
disorders. 4th ed. Text revision. Washington (DC): American Psychiatric
Association; 2000.
8. Berrios GE. Positive and negative symptoms and Jackson: a conceptual history.
Arch Gen Psychiatry 1985;42:95–7.
9. Andreasen NC. Negative symptoms in schizophrenia: definition and reliability.
Arch Gen Psychiatry 1982;39:784–8.
10. Crow TJ. Positive and negative schizophrenic symptoms and the role of
dopamine: II. Br J Psychiatry 1980;137:383–6.
11. Crow TJ. The two-syndrome concept: origins and current status. Schizophr Bull
1985;11:471–86.
12. Strauss JS, Carpenter WT, Bartko JJ. Speculations on the processes that underlie
schizophrenic symptoms and signs: III. Schizophr Bull 1975;11:61–9.
13. Earnst KS, Kring AM. Construct validity of negative symptoms: an empirical
and conceptual review. Clin Psychol Rev 1997;17:167–90.
14. Kay SR, Opler LA, Lindenmayer JP. The Positive and Negative Syndrome Scale
(PANSS): rationale and standardisation. Br J Psychiatry 1989;155:59–65.
15. Zubin J, Spring B. Vulnerability—a new view of schizophrenia. J Abnorm
Psychol 1997;86:103–26.
16. Dworkin RH, Lenzenwenger MF. Symptoms and the genetics of schizophrenia:
implications for diagnosis. Am J Psychiatry 1984;141:1541–6.
17. Dworkin RH, Lenzenwenger MF, Moldin SO. Genetics and the phenomenology
of schizophrenia. In: Harvey PD, Walker EF, editors. Positive and negative
symptoms of psychosis. Hillsdale (NJ): Erlbaum; 1987.
18. Cannon TD, Mednick SA, Parnas J. Antecedents of predominantly negative and
predominantly positive symptom schizophrenia in a high-risk population. Arch
Gen Psychiatry 1990;47:622–32.
19. Pahl JJ, Swayze VW, Andreasen NC. Diagnostic advances in anatomical and
functional brain imaging in schizophrenia. In: Kales A, Stefanis CN, Talbott JA,
editors. Recent advances in schizophrenia. New York: Springer-Verlag; 1990.
p 163–89.
255
The Canadian Journal of Psychiatry—In Review
20. Andreasen NC, Olsen SA, Dennert JW, Smith MR. Ventricular enlargement in
schizophrenia: relationship to positive and negative symptoms. Am J Psychiatry
1982;139:297–302.
21. Foerster A, Lewis SW, Murray RM. Genetic and environmental correlates of the
positive and negative syndromes. In: Greden JF, Tandon R, editors. Negative
schizophrenic symptoms: pathophysiology and clinical implications Washington
(DC): American Psychiatric Press; 1991. p 187–202.
22. Walker E, Lewine RJ, Neumann C. Childhood behavioral characteristics and
adult brain morphology in schizophrenia. Schizophr Res 1996;22:93–101.
23. Bunney WE, Bunney BG. Neurodevelopmental hypothesis of schizophrenia. In:
Charney DS, Nestler E, Bunney BS, editors. Neurobiology of mental illness.
New York: Oxford University Press; 1999. p 225–35.
24. Feinberg I. Schizophrenia: caused by a fault in programmed synaptic elimination
during adolescence. J Psychiatr Res 1983;17:319–34.
25. McGlashan TH, Hoffman RE. Schizophrenia as a disorder of developmentally
reduced synaptic connectivity. Arch Gen Psychiatry 2000;57:637–48.
26. Nuechterlein KH, Dawson ME. Information processing and attentional
functioning in the developmental course of schizophrenic disorders. Schizophr
Bull 1984;10:160–203.
27. Lencz T, Smith CW, Auther A, Correll CU, Cornblatt B. Nonspecific and
attenuated negative symptoms in patients at clinical high-risk for schizophrenia.
Schizophr Res 2004;68:37–48.
28. Carpenter WT, Heinrichs DW, Wagman AMI. Deficit and nondeficit forms of
schizophrenia: the concept. Am J Psychiatry 1988;145:578–83.
29. Kirkpatrick B, Buchanan RW, McKenny PD, Alphs LD, Carpenter WT Jr. The
schedule for the deficit syndrome: an instrument for research in schizophrenia.
Psychiatr Res 1989;30:119–23.
30. Subtonik KL, Nuechterlein KH, Ventura J, Green MF, Hwang SS. Prediction of
the deficit syndrome from initial deficit symptoms in the early course of
schizophrenia. Psychiatr Res 1998;80:53–9.
31. Ventura J, Nuechterlein KH, Green MF, Horan WP, Subotnik KL, Mintz J. The
timing of negative symptom exacerbations in relationship to positive symptom
exacerbations in the early course of schizophrenia. Schizophr Res
2004;69:333–42.
32. Hoch A. On some of the mental mechanisms in dementia praecox. J Abnorm
Psychol 1910;5:255–73.
33. Kretschmer E. Physique and character. London: Kegan Paul, Trench, Trubner
and Co; 1925.
34. Solano JJR, De Chavez GM. Premorbid personality disorders in schizophrenia.
Schizophr Res 2000;44:137–44.
35. Peralta A, Cuesta MJ, de Leon J. Premorbid personality and positive and
negative symptoms in schizophrenia. Acta Psychiatr Scand 1991;84:336–9.
36. Lindstroem E, von Knorring L, Ekselius L. Self-reported personality disorders in
patients with schizophrenia and the relationship to symptoms, side effects, and
social functioning. Nord J Psychiatr 2000;54:341–6.
37. Battaglia M, Bernardeschi L, Franchini L, Bellodi L, Smeraldi E. A family study
of schizotypal disorder. Schizophr Bull 1995;21:33–45.
38. Rado S. Dynamics and classification of disordered behaviour. Am J Psychiatry
1953;110:406–16.
39. Meehl PE. Schizotaxia, schizotypy and schizophrenia. Am Psychol
1962;17:827–38.
40. Claridge G. Theoretical background and issues. In: Claridge G. Schizotypy:
implications for illness and health. Oxford: Oxford University Press; 1997.
p 3–18.
41. Mata I, Sham PC, Gilvarry CM, Jones PB, Lewis SW, Murray RM. Childhood
schizotypy and positive symptoms in schizophrenic patients predict schizotypy
in relatives. Schizophr Res 2000;44:129–36.
42. Chapman LJ, Chapman JP, Raulin ML Scales for physical and social anhedonia.
J Abnorm Psychol 1976;85:374–82.
43. Chapman LJ, Chapman JP, Miller EN. Reliabilities and intercorrelations of 8
measure of proneness to psychosis. J Consult Clin Psychol 1982;50:187–95.
44. Chapman LJ, Chapman JP, Kwapil TR, Eckblad M, Zinser MC. Putatively
psychosis-prone subjects 10 years later. J Abnorm Psychol 1994;103:171–83.
45. Miller P, Byrne M, Hodges AN, Lawrie SM, Owens DGC, Johnston EC.
Schizotypal components in people at high risk of developing schizophrenia:
early findings from the Edinburgh high-risk study. Br J Psychiatry
2002;180:179–84.
46. Kendler KS, Thacker L, Walsh D. Self-report measures of schizotypy as indices
of familial vulnerability to schizophrenia. Schizophr Bull 1996;22:511–20.
47. Blanchard JJ, Mueser KT, Bellack AS. Anhedonia, positive and negative affect,
and social functioning in schizophrenia. Schizophr Bull 1998;24:413–24.
48. Blanchard JJ, Horan WP, Brown SA. Diagnostic differences in social anhedonia:
a longitudinal study of schizophrenia and major depressive disorder. J Abnorm
Psychol 2001;11:363–71.
49. Siris SG. Diagnosis of secondary depression in schizophrenia: implications for
DSM-IV. Schizophr Bull 1991;17:75–98.
256
50. Siris SG. Depression in schizophrenia. In: Shriqui CL, Nasrallah HA, editors.
Contemporary issues in the treatment of schizophrenia. Washington (DC):
American Psychiatric Press; 1995.
51. Rector NA. Dysfunctional attitudes and symptom expression in schizophrenia:
differential associations with paranoid delusions and negative symptoms. J Cog
Psychother: Int Q 2004;18:163–73.
52. Rector NA, Beck AT. Dysfunctional attitudes and symptom expression in
schizophrenia: associations with behavioural and social withdrawal. Paper
presented at the meeting of the Society for Psychopathology Research; October
2003; Toronto (ON).
53. Weissman AN, Beck AT. Development and validation of the Dysfunctional
Attitude Scale: a preliminary investigation. Paper presented at the meeting of the
American Psychological Association; 1978; Toronto (ON).
54. Barrlowclough C, Tarrier N, Humphreys L, Ward J, Gregg L, Andrews B.
Self-esteem in schizophrenia: relationships between self-evaluation, family
attitudes, and symptomatology. J Abnorm Psychol 2003;112:92–9.
55. Birchwood M, Chadwick P. The omnipotence of voices: testing the validity of a
cognitive model. Psychol Med 1997;27:1345–53.
56. Chadwick P, Birchwood M. The omnipotence of voices: I. A cognitive approach
to auditory hallucinations. Br J Psychiatry 1994;164:190–201.
57. Beck AT, Rector NA. A cognitive model of hallucinations. Cognitive Ther Res
2003;27:19–52.
58. DeVries MW, Delespaul PA. Time, context, and subjective experiences in
schizophrenia. Schizophr Bull 1989;15:233–44.
59. Berenbaum H, Oltmans TF. Emotional experience and expression in
schizophrenia and depression. J Abnorm Psychol 1992;101:37–44.
60. Kring AM, Neale JM. So schizophrenic patients show a disjunction amount
expressive, experiential, and psychophysiological components of emotion? J
Abnorm Psychol 1996;105:249–57.
61. Earnst KS, Kring AM. Emotional responding in deficit and non-deficit
schizophrenia. Psychiatr Res 1999;88:191–207.
62. Germans MJ, Kring AM. Hedonic deficit in anhedonia: support for the role of
approach motivation. Pers Indiv Differ 2000;28:659–72.
63. Gard DE, Germans Gard MK, Horan WP, Kring AM, John OP, Green MF.
Anticipatory and consummatory pleasure in schizophrenia: a scale development
study. Paper presented at the Annual Meeting of the Society for Research in
Psychopathology; October 2003; Toronto (ON).
64. van Reel JM, Gerrits MAFM, Vanderschuren LJMJ. Opioids, reward and
addiction: an encounter of biology, psychology, and medicine. Pharmacol Rev
1999;51:341–96.
65. Berman I, Viegner B, Merson A, Allan E, Pappas D, Green AI. Differential
relationships between positive and negative symptoms and neuropsychological
deficits in schizophrenia. Schizophr Res 1997;25:1–10.
66. Stolar N, Berenbaum H, Banich MT, Barch D. Neuropsychological correlates of
alogia and affective flattening in schizophrenia. Biol Psychiatry 1994;35:164–72.
67. Estroff SE. Self, identity, and subjective experiences of schizophrenia: in search
of the subject. Schizophr Bull 1989;15:189–96.
68. Kingdom D, Turkington D. Cognitive behavioural therapy of schizophrenia.
New York: Guilford; 1994.
69. Beck AT, Rector NA. Delusions: a cognitive perspective. J Cogn Psychother
2002;16:455–68.
70. Nuechterlein KH, Edell WS, Norries M, Dawson ME. Attentional vulnerability
indicators, thought disorder, and negative symptoms. Schizophr Bull
1986;12:408–26.
71. Liddle PF. Disordered mind and brain: the neural basis of mental symptoms.
London (UK): Gaskell; 2001.
72. Weinberger DR, Egan MF, Bertolino A, Callicot JH, Mattay VS, Lipska BK, and
others. Prefrontal neurons and the genetics of schizophrenia. Biol Psychiatry
2001;50:825–44.
73. McGlashan TH, Fenton WS. Subtype progression and pathophysiologic
deterioration in early schizophrenia. Schizophr Bull 1993;19:71–84.
Manuscript received and accepted January 2005.
1
Psychologist, Mood and Anxiety Program, Centre for Addiction and
Mental Health, Toronto, Ontario; Associate Professor, University of
Toronto, Toronto, Ontario.
2
Emeritus Professor, Department of Psychiatry, University of
Pennsylvania, Pittsburgh, Pennsylvania.
3
Assistant Professor, Department of Psychiatry, University of
Pennsylvania, Pittsburgh, Pennsylvania.
Address for correspondence: Dr NA Rector, Mood and Anxiety Program,
Centre for Addiction and Mental Health, 250 College Street, Toronto, ON
M5T 1R8
e-mail: [email protected]
W Can J Psychiatry, Vol 50, No 5, April 2005
The Negative Symptoms of Schizophrenia: A Cognitive Perspective
Résumé : Les symptômes négatifs de la schizophrénie : une perspective cognitive
Des études récentes sur l’amélioration des symptômes négatifs de la schizophrénie, par suite
d’interventions cognitives ciblées, ont suscité l’intérêt pour les fondements cognitifs de ces
symptômes. Cet article intègre la recherche expérimentale actuelle avec les témoignages
phénoménologiques de patients participant à une thérapie cognitive pour ces symptômes spécifiques.
Nous proposons qu’outre le rôle bien établi des facteurs neurobiologiques dans leur développement et
leur maintien, les évaluations et croyances cognitives spécifiques jouent un rôle dans l’expression et
la persistance des symptômes négatifs. Ce modèle cognitif des symptômes négatifs se fonde sur une
formulation diathèse-stress : un continuum de traits de prédisposition, de la personnalité prémorbide à
la symptomatologie négative complète, l’incorporation d’attitudes sociales et performantes négatives
dans ces traits, avec de faibles attentes de plaisir et de faibles attentes de succès dans des activités
visant l’atteinte d’objectifs. Nous suggérons que les symptômes négatifs représentent, en partie, un
modèle compensatoire de désengagement en réponse à des croyances délirantes menaçantes, à une
menace sociale perçue, et à un échec anticipé des tâches et activités sociales. Un aspect psychologique
de cette inertie comportementale et motivationnelle semble être la perception du patient de ses
ressources psychologiques limitées—une perception qui motive les patients à conserver leur énergie
en minimisant l’investissement dans des activités nécessitant un effort.
Can J Psychiatry, Vol 50, No 5, April 2005 W
257