Developmental Theory for a Cognitive
Enhancement Therapy of Schizophrenia
by Qerard E. Hogarty and Samuel Flesher
While improved outcomes have clearly been achieved
with contemporary psychosocial treatments, most would
acknowledge that a more complete social and vocational
recovery remains an elusive goal for many patients with
schizophrenia. Outcomes other than symptom improvement and relapse prevention have not been well documented (Lehman et al. 1995). Perhaps as many as 10 percent of all incapacitated persons in the United States, for
example, are disabled by schizophrenia (Rupp and Keith
1993). Only 10 percent to 30 percent of schizophrenia
patients on average are employed at any time (Attkisson
et al. 1992), and few of these are able to maintain their
vocational gains (Policy Studies Associates 1989).
Quality of life and the relationships needed to sustain it
are often marginal for patients with schizophrenia
(Lehman et al. 1982). This is not to say that psychosocial
interventions are without important and well-established
effects. Symptom alleviation, delay of relapse and rehospitalization, and the acquisition of behavioral skills and
interpersonal effectiveness have been variably associated
with assertive community treatment and case management
(Scott and Dixon 1995a); family intervention (Dixon and
Lehman 1995); and psychotherapeutic approaches, primarily social skills training (Scott and Dixon 1995fc). Yet
even the recent and most successful of our behavioral
attempts to enhance the personal and social adjustment of
schizophrenia patients with a disorder-relevant psychotherapy led us to conclude that while patients were
significantly improved in work and relationship roles
compared with controls, few were able to equal their own
"at best" premorbid functioning in these areas (Hogarty et
al. 1997). More recently, cognitive rehabilitation of schizophrenia patients has shifted to the sequential remediation
Abstract
Recent findings on psychosocial and neurodevelopmental anomalies in schizophrenia patients
indicate that deficits related to social cognition—the
ability to act wisely in social interactions—may be
important constraints on complete social and vocational recovery. Social cognition is acquired over many
decades and appears to be partially independent of
formal IQ and neuropsychological problems. It invites
a more developmental approach to the rehabilitation
of schizophrenia, one that we call Cognitive Enhancement Therapy (CET). CET draws on an emerging literature that implicates both pre- and postonset neurodevelopmental difficulties, as well as a complementary
literature on diffuse neuropsychological impairments
that supports the notion of a neurodevelopmental
insult. We analyzed evidence for an associated developmental basis to social cognitive impairment in the
context of a model that addressed both the acquisition
of interpersonal wisdom and the adaptive process that
might follow developmental failures.
A contemporary model of human cognition is then
used to identify the metacognitive functions that characterize the developmental acquisition of normal cognition and, by inference, the associated difficulties of
many patients with schizophrenia. A rehabilitation
strategy for schizophrenia, designed to facilitate the
metacognitive transition from prepubertal to young
adult social cognition, would thus emphasize developmental learning experiences during the remediation of
social cognitive deficits. A "gistful" appraisal of interpersonal behavior and novel social contexts best
reflects the theoretical intent of this new intervention.
Key words: Social cognition, cognitive rehabilitation.
Schizophrenia Bulletin, 25(4): 677-692,1999.
Reprint requests should be sent to Mr. G. Hogarty, Western
Psychiatric Institute and Clinic, University of Pittsburgh School of
Medicine, 3811 O'Hara Street, Pittsburgh, PA 15213.
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G.E. Hogarty and S. Flesher
of nonsocial cognitive impairments and social problemsolving deficits that might underlie interpersonal and
vocational dysfunction. Published results to date have
suggested the potential for further patient recovery.
However, outcomes indicate that these improvements in
symptom state and selected aspects of neuropsychological
and behavioral functioning are without broad generalization to areas of community adjustment (Hodel and
Brenner 1994).
In light of the poorly understood rate-limiting factors
to a fuller social and vocational recovery, we share a reevaluation that has influenced the conceptualization and
implementation of a developmental approach to cognitive
rehabilitation called Cognitive Enhancement Therapy
(CET). We hope this initiative will respond to the recent
recommendation that the study and treatment of cognition
in schizophrenia should move beyond the focus on neuropsychological tasks and social problem solving to
include (1) the processes that support socialization; (2) the
reciprocal influence of memory and affect associated with
past social exchanges and current functioning; and (3) the
representation of multidisciplinary contributions to the
study of social cognition, including contemporary models
of normal cognition (Silverstein 1997). Operational theory, in our experience, has systematically, effectively, and
confidently guided clinical practice with patients whose
disorders had remained enigmatic and suboptimally
responsive to previous psychosocial interventions
(Anderson et al. 1980; Hogarty et al. 1995).
In this discussion, we propose that the recently suggested neurodevelopmental anomalies of schizophrenia
might also implicate a developmental disability in social
cognition that requires an appropriate developmental therapeutic response. Our distinction between "developmental" and "behavioral" rehabilitation are relative rather than
absolute, because in practice cognitive rehabilitation
would likely include features of both approaches. When
we use the term developmental, we wish to imply a
greater emphasis on real-life (unrehearsed but clinically
guided) interpersonal experiences that are targeted to the
secondary socialization process of attaining age-appropriate social cognitive milestones that reasonably stable and
less severely impaired outpatients might not yet have
achieved. A behavioral approach, on the other hand,
would more likely be characterized by stepwise, didactic
training to the criteria of topographic behavioral or cognitive tasks that are usually prescribed for severely impaired
and often acutely ill inpatients through primary socialization experiences. Normal neurodevelopmental processes
that reinforce crucial neural connections could have failed
in schizophrenia (Feinberg 1997; Lewis 1997a), and
remediation of neuropsychological sequelae might likely
be difficult to achieve (Benedict et al. 1994). But we shall
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suggest that the acquisition of context appraisal and perspective taking that are acquired through secondary
socialization are central to adult social cognition and its
"practical intelligence" and seem at least partially independent of neuropsychological integrity (Penn et al. 1997)
and generalized intelligence (Sternberg et al. 1995).
Normal subjects, at least, appear able to acquire practical
intelligence over much of the life cycle (Sternberg et al.
1995).
Secondary socialization is a lifelong process that
includes context appraisal, or the acquired ability to
apprehend and appropriately respond to the informal rules
of conduct that characterize diverse social contexts and
roles, particularly those that change spontaneously and
often in unexpected ways (Berger and Luckman 1966;
Brim 1966; Hay 1994). Secondary socialization also
includes perspective taking, a cognitive skill that requires
rapid and correct assessment, attribution, and inferencemaking regarding one's own and another's thinking and
feeling and the subsequent prediction of behavior (Berger
and Luckman 1966; Baldwin 1992). CET is guided by
cognitive theory that facilitates a less demanding and
more intuitive, abstracting, "gistful" approach to acquiring these secondary socialization skills (Brainerd and
Reyna 1990), rather than one that relies on the controlled,
effortful, cognitive processing that often characterizes
schizophrenia (Nuechterlein and Dawson 1984) as well as
much of its psychosocial treatment (Bellack et al. 1989;
Bellack and Mueser 1993). In deference to space and to
our personal limitations in basic neuroscience as well as
developmental, social, and cognitive psychology (we are
neither neuropsychologists nor theorists), we rely on
authoritative reviews of this extensive literature. Our primary objective is simply to bring theoretical concepts into
the service of treatment development.
Our formulation is admittedly selective, but it is compatible with evidence from a broad interdisciplinary literature. No psychosocial treatment, to our knowledge, has
attempted to accommodate all possible theoretical models. Our theoretical premises are not intended to be deterministic, linear, or reductionistic in nature. They do not,
for example, imply an "inside-out," etiopathophysiologic
cascade of effects that begins with impairments in neuroanatomy and extends to those that are neuropsychological
in nature, which in turn determine impairments in cognition, symptomatic response, and ultimately dysfunctional
behavior. This often-assumed connection between neuroscience and phenomenology seems decidedly incomplete
(Mortimer and McKenna 1994). Rather, our postulates
recognize the inevitable synergy and hence interaction
between acquired cognitive impairments, both social and
nonsocial, as well as the individual dysfunctional adaptations to such and the potential for improvement that is
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Schizophrenia Bulletin, Vol. 25, No. 4, 1999
(Keshavan and Murray 1997). Moreover, these observations are compatible with broad evidence that supports
dynamic disruptions in schizophrenia patients in the interconnected, parallel distributed neural systems that are
subsumed within the heteromodal association cortex
(HASC; Pearlson et al. 1996). The cerebral areas involved
(the dorsolateral prefrontal cortex, Broca's area, the superior temporal cortex, and the inferior parietal cortex) are
the most recently evolved, phylogenetically, and are fundamental to normal human cognition, including such
higher order social cognitive abilities as foresightfulness
and reflectiveness. Associated evidence from neuroimaging studies (McCarley et al. 1996), when integrated with
the neuropathologal findings of the HASC (Pearlson et al.
1996) and limbic system anomalies (Kirkpatrick and
Buchanan 1990) in schizophrenia, lends support to the
possibility of a neurodevelopmentally based impairment
in the structures that influence social cognition.
offered by neuroplasticity (i.e., the possibility of neural
circuit response to developmental exercises and experiences that are targeted to social cognitive enhancement).
Neurodevelopment and Schizophrenia
Converging lines of evidence increasingly indicate that
schizophrenia has many developmental aspects (PogueGeile 1997). The evidence supporting a neurodevelopmental basis to schizophrenia, as critically reviewed by
Weinberger (1996), extends from the less consistent findings associated with neurological soft signs, obstetrical
complications, and fetal infection to the better documented problems in premorbid, nonsocial cognition and
to the more compelling and recent findings from cytoarchitectonic studies. The latter suggest a neurodevelopmental vulnerability to later-life psychosis among some
patients that follows an in utero, displaced migration of
neurons to essential cortical plates. The result is an inappropriate decrease in neural connectivity in superficial
cortical layers that is accompanied by an equally suspect
increase in neural density in deeper white matter layers.
Early inconsistencies in these observations have increasingly been clarified (Glantz and Lewis 1995; Akbarian et
al. 1996).
The potential causes of neurodevelopmental insult
have been variably attributed to neonatal malnourishment
(Susser and Lin 1992), obstetrical complications (McNeil
1988), and viral infection (Mednick et al. 1988), either as
isolated events or more likely as the result of a "double
whammy" (Bracha et al. 1992) when combined with
genetic vulnerability (Fish et al. 1992). Weinberger (1987)
suggested that these early problems of neural connectivity, particularly in the temporal-limbic and prefrontal cortices, might not become manifest until early adult life
(perhaps as schizophrenia), a speculation supported by
neonatally lesioned animals that show a delay both in the
manifestation of abnormal behavior and in an associated
dopaminergic hyperresponsiveness (Lipska et al. 1993).
Such abnormalities have yet to be found in all cases of
schizophrenia studied, and, according to Weinberger
(1996), it remains unclear how such findings, often subtle
in nature, might explain the clinical syndrome itself.
Others (McCarley et al. 1996) minimize the "first hit"
hypothesis and cite later developmental changes that follow the onset of schizophrenia (the "second hit"), such as
(1) reductions in temporal and frontal lobe volume in the
first years post onset, (2) an increasing delay of P300
latencies, (3) production of free radical or secondary neurotoxins, and (4) N-methyl-D-aspartate receptor dysfunction. Still, growing evidence that suggests a perinatal and
young adult neurodevelopmental basis to schizophrenia,
though incomplete and indirect, is not easily dismissed
Neuropsychology and Schizophrenia
Volumes have been written on the nature of neuropsychological deficits in schizophrenia, and it is not our intent to
discredit either their importance in understanding the
pathophysiology of this disorder or their contribution to
social dysfunction. Rather, we wish simply to encourage a
greater clinical awareness of the social cognitive components that appear to us to have been de-emphasized in
contemporary neuroscience and cognitive rehabilitation.
An impartial overview of the neuropsychological literature would likely lead to the conclusion that nonsocial
cognitive impairments are more diffuse and global than
not (e.g., Goldstein 1978; Heaton et al. 1978; Seedman
1983; Straube and Oades 1992; Blanchard and Neale
1994), an observation that is consistent with neurodevelopmental anomalies and with a growing literature that
implicates impairments among many cerebral structures
and their interconnected neural circuitry in schizophrenia
(Buchanan et al. 1997). (We do acknowledge findings of
focal impairment and specific functional deficits in
selected samples; see Gur 1978; Kolb and Whishaw 1983;
Hoff et al. 1992; Pilowsky et al. 1993; Buchanan et al.
1994; Perry et al. 1995; Servan-Schreiber et al. 1996. But
a broad literature appears clearly to favor a global impairment.) A frequently cited characteristic of these diverse
neuropsychological deficits is a pervasive slowness in
behavioral responses to information processing and attentional tasks (Nuechterlein and Dawson 1984). This slowness may be a general indicator of the effortful (controlled) processing that follows extensive demands on
cognitive capacity (Asarnow et al. 1994), at least with
regard to laboratory tasks. (We shall return to this cognitive feature when we expand on the developmental acqui-
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G.E. Hogarty and S. Flesher
sition of "normal" cognition.) Many patients with schizophrenia have a nonspecific task difficulty in establishing a
cognitive set, sustaining vigilance especially in the face of
competing stimuli, and shifting a focused alertness
(Nuechterlein and Dawson 1984). Failures in short-term
spatial and verbal memory functioning are also frequently
observed (Park and Holzman 1992; Tamlyn et al. 1992),
as are executive function difficulties (Morice and
Delahunty 1996). Psychophysiological studies show problems in arousal, electrodermal activity, and evoked potentials, functions that also interact with and influence
impaired information processing capacities (Dawson and
Nuechterlein 1984; Brekke et al. 1997). However, it is
important to remember that no brain structure can singularly explain the nature of any cognitive impairment, be it
in attention, memory, or problem solving (Posner and
Rafal 1987; Mesulum 1990; Hoffman and McGlashan
1993). Further, the brain has a long-term, albeit decreasing, plasticity that appears to be dynamically engineered
by experience, such as those that characterize more "procedural" (ongoing experiential learning) than "declarative" (rote memory) rehabilitation programs (Kami 1997).
It is appealing to suggest that the problems of cortical
connectivity implied by the cytoarchitectonic studies are
responsible for neuropsychological test failures, which in
turn might account for symptoms or social and vocational
dysfunctioning. But such a conclusion has been viewed
both as speculative (Weinberger 1996) and hazardous
(Mortimer and McKenna 1994). Evolutionary evidence
describing human and nonhuman primates, for example,
has led others to conclude that social cognition preceded
and shaped neocortical functions (Brothers 1990), and
that social cognition itself might represent more basic,
evolutionary cognitive processes of domain-specific "reasoning instincts" (Cosmides and Tooby 1989, 1994).
These authors argue that the cognitive process of "social
exchange" (e.g., memory for prior interactions or the
communication of values) was likely influenced by the
Pleistocene conditions of natural selection and thus
required rational instincts for specific adaptive functions
and species survival. The authors also extend an invitation
to cognitive science to study what the brain has been programmed to do and why, as much as how it operates.
(From this perspective, the rehabilitation of maladaptive
social cognition should become an essential, rather than
simply a desirable, goal of treatment.) The integrity of
memory, attention, and problem solving are closely associated with individual attributions of importance to specific interpersonal stimuli as well as to motivation and
environmental context (Baldwin 1992). Attention to and
memory for cognitive content depend on the uniquely personal meaning and emotions associated with important
experiences (Prigatano 1987; Clark 1994), which is an
680
integration of affect and cognition that seems central to
clinical change (Greenberg and Safron 1984). Failures in
laboratory measures of nonsocial cognition might reflect
neglected stimuli that are not endowed with affective significance or that do not elicit a motive to respond (Ciompi
1988). In fact, following an extensive review, Brothers
(1990) concluded that "the core process which distinguishes social cognition is an intimate tie to affect." In
this regard, we are reminded of the age-old tenet: "We do
what we think, but what we think is what we feel" (cited
in Straube and Oades 1992).
Recent literature in schizophrenia does show important but modest correlations between the nonsocial cognitive functions of verbal memory and vigilance and the
broad indices of social functioning (Green 1996). However, few longitudinal studies assess the important relationships between neuropsychological or psychophysiological indices and social competencies over time (Green
1996; Brekke et al. 1997). Also, much remains unknown
about the real-world significance of nonsocial cognitive
functions that are measured in the laboratory (Hogarty
and Flesher 1992). Failure in the laboratory, it has been
argued, is not failure in life (Berrol 1990). Subjects might
avoid tasks in the community that would lead to "fluid
intelligence" failures in the laboratory (more akin to formal IQ) and compensate by using "crystallized intelligence" (a practical intelligence) through the pursuit of
personally meaningful, familiar, and less demanding tasks
(Salthouse 1987). Once again, this distinction implies the
existence of cognitive processes and perhaps neural circuits that evolved in response to specific adaptive requirements (Cosmides and Tooby 1989, 1994). As comprehensively reviewed by Penn et al. (1997), neuropsychological
assessment of basic (nonsocial) cognition is often made
through a subject's response to variables that might hold
little or no personal significance, such as objects, colors,
lights, numbers, or tones (e.g., "cold" cognition). The
social-cognitive competence that is fundamental to a successful life, however, is developed and assessed through
the independent and reciprocal interaction between the
subject and another person (e.g., "hot" cognition).
Neuropsychological markers may well have high diagnostic sensitivity in schizophrenia, but very little specificity
has been shown (Szymanski et al. 1991; Keefe 1995).
Neuropsychological deficits also occur among individuals
without clinical syndromes of mental illness or current
social dysfunction (Brunke et al. 1991), although such
deficits might constrain social competence potential.
Thus, it is at least plausible that the neuropsychological deficits of schizophrenia patients that are usually targeted by rehabilitation programs might arise from one or
more compromised cerebral structures that directly or
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indirectly influence other neural structures or circuits that
support social cognition. (See Benes [1997] and Lewis
[1991b] for descriptions of how secondary neural influences might evolve.) Among nonhuman primates, for
example, sophistication in expressing "empathy," conflict
resolution, reciprocity, and maintenance of a collaborative
social order suggest relatively distinct neural circuits for
social cognition (including orbital frontal cortex, basal
ganglia, and amygdala) that likely predate human intelligence and the neocortex (Brothers 1990). The potential
influence of basal ganglia and amygdala impairment on
cognition in schizophrenia has recently been described,
but these structures and their associated circuitry have
been relatively neglected in the study of schizophrenia
(Graybiel 1997; Haber and Fudge 1997). Again, as argued
by Cosmides and Tooby (1989, 1994), these important
aspects of social cognition might well have required specialized and evolutionary reasoning circuits for species
survival. (Selecting a mate and selecting from a restaurant
menu clearly necessitate different cognitive processes, to
cite an example of these authors.) That social cognitive
operations are directly represented in the results of nonsocial, neuropsychological assessment and treatment of
schizophrenia patients has been questioned (Penn 1991).
As Penn and his colleagues concluded, social and nonsocial cognition require very different levels of analyses,
and the latter measures "do not adequately explain the
social impairment and symptomatology of the disorder"
(Penn et al. 1997).
If neuropsychological deficits themselves are the
principal rate-limiting factors against normative functioning, systematic remediation should facilitate social and
vocational recovery. But the case for systematic remediation and recovery is equivocal, if not weak (Benedict et al.
1994). Many studies have indeed shown improvements in
reaction time, vigilance, memory, and cognitive flexibility
following training (Bellack and Mueser 1993), but when
such training was used as a precursor to social skills
acquisition, evidence of durability and generalization to
other real-life contexts is lacking (Hodel and Brenner
1994). Our understanding of the neuropsychological literature, as it relates to schizophrenia rehabilitation, is as follows: (1) There is clear evidence that the acquisition of
social skills is indeed constrained by neuropsychological
deficits (Mueser et al. 1991; Kern et al. 1992; Bowen et
al. 1994), thus establishing the need to clinically accommodate nonsocial cognitive impairments. (2) Many studies indicate that nonsocial, cognitive deficit training is at
least possible (see Spring and Ravden 1992; Hodel and
Brenner 1994). But, with a recent exception (Spaulding et
al. 1999, this issue), little or no evidence of generalization
to untrained social behaviors has been observed (although
many efforts did not have generalization as a goal). (3)
Suggestive, but poorly replicated, evidence shows that
broad cognitive "modification" improves untrained
nonsocial cognition deficits (Meichenbaum and Cameron
1973; Lowe and Higson 1981; Spring and Ravden 1992).
(4) The effects of existing and "integrated" nonsocial and
social cognitive (behavioral) approaches are decidedly
modest on social and vocational recovery in the community (Bellack 1992; Liberman and Green 1992; Bellack
and Mueser 1993; Hodel and Brenner 1994). Thus,
regarding the components of social and nonsocial cognition, questions remain that require a more direct therapeutic response as well as the method (e.g., developmental or
behavioral) that might better address specific, functionally
disabling deficits. While recent studies of behavioral
interventions have indeed moved from the micro training
of specific behavioral deficits to more macro "social problem-solving" exercises (Bellack et al. 1989), there is a
growing consensus that such skills are ultimately dependent on the hierarchical capacity of social abstraction. As
Corrigan and Green (1993a) recently concluded, "The
schizophrenic patient's relative insensitivity to abstract
(social) cues may explain their limited repertoire of social
skills." Sensitivity to abstract social cues appears to be a
key precursor of social problem-solving ability (Corrigan
and Toomey 1995). Rather than skills training targeted to
"topographic behaviors," Corrigan et al. (1996a) have
argued from their extensive and relevant studies that:
Patients with schizophrenia have most difficulty with
abstract components (associated with) the identification of goals and affect. Therefore, schizophrenic
patients . . . need to learn the rules and goals that
guide interpersonal situations. In this way, they can
'generate' behaviors that meet the demands of a particular situation. This is a skill area that has largely
been overlooked in current social skills training programs, (p. 82)
As such, behavioral approaches to the remediation of
neuropsychological deficits have clearly improved the
lives of many patients. It appears, however, that more
optimal recovery of function, at least among less severely
impaired and medication-responsive schizophrenia outpatients who have greater rehabilitation potential (i.e., the
better half of patients), might require a developmental
approach that addresses capacities that are broadly associated with an abstracting social cognition, one that itself is
developmentally acquired.
Social Cognition and Schizophrenia
Much like the neurodevelopmental literature, evidence
concerning social cognitive impairment in schizophrenia
is recent and its assessment has largely relied on discrete
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G.E. Hogarty and S. Flesher
and predominantly indirect components of social cognition such as affect perception, social knowledge, social
problem solving, and processing bias (Penn et al. 1997).
Only recently have these components been viewed in the
broader context of social cognitive processes that remain
largely unassessed (Silverstein 1997). As is the case with
neuropsychological deficits, the evidence supporting
social cognitive impairment is also nonspecific to schizophrenia, insofar as persistent social disability has increasingly been shown to characterize other psychiatric disorders as well (Coryell et al. 1993; Olfson et al. 1997).
Thorndike first described social cognition as a product of
social intelligence, or the ability to "act wisely," eight
decades ago (Walker and Foley 1973; Taylor 1990). Since
then, more than 100 definitions and attempts at measurement have followed (Wyer and Srull 1994). Over the
years, certain commonalities have survived its analysis
(Eisenberg and Harris 1984): (1) an acquired ability in
perspective taking, (2) interpersonal problem solving, (3)
relationship maintenance, (4) moral judgment, and (5)
communication skills. Social problem solving has
received the most attention in the skills training literature
(Bellack et al. 1989). Our functional definition of social
cognition has resolved to the essential elements identified
by others: the ability to understand, predict, and appropriately respond to the thinking (including attributions and
intentions), feeling, and likely behavior of self and others
in diverse and often unrehearsed social contexts (e.g.,
Gazzaniga 1985; Taylor and Cadet 1989; Brothers 1990;
Newman and Uleman 1993). We believe that these essential characteristics of social cognition are best represented
by the secondary socialization abilities of perspective taking and context appraisal (Brim 1966; Baldwin 1992;
Berger and Luckman 1966). We frequently use the term
"social cognition" interchangeably with such terms as
"practical," "tacit," or "social" intelligence when attempting to convey a form of interpersonal wisdom that seems
both quasi-independent of formal IQ and neuropsychological integrity and capable of being developmentally
acquired throughout life.
While the social cognitive abilities that determine
social intelligence (and its associated and increasingly
popular "emotional intelligence" [Goleman 1995]) appear
to be part of generalized intelligence, they differ qualitatively from the abilities that determine formal IQ (Taylor
1990). Depending on methodology and criteria, the shared
variance between the practical intelligence that determines social performance and the generalized intelligence
measured by IQ is alleged to be only 4 percent to 25 percent (Sternberg et al. 1995). Traditional measures of IQ,
for example, largely tap the verbal and logical skills associated with academic test taking; however, the awareness
of the self and others that is necessary for a successful life
682
remain unassessed (McClelland 1973). Abstract social cue
perception, a likely component of social cognition, has
been shown to be at least partially independent of formal
IQ in normal subjects as well as in schizophrenia patients
(Corrigan 1994). Social intelligence is thought to be the
"compensatory" intelligence in those with modest intellectual ability who nonetheless lead interpersonally wise
and productive lives (Salthouse 1987). Conversely, social
intelligence can be impaired among otherwise intellectually gifted individuals (Selman and Schultz 1990), such as
the scientist who has a highly developed formal IQ but is
interpersonally inept. We do not imply that social intelligence is independent of IQ across the entire spectrum of
general intelligence. Even mild mental insufficiency, for
example, can be the reason for a lack of great social wisdom in a person (an appreciation that has led to the exclusion of patients from CET whose IQ is < 80). The awareness of relationship features that is central to social
intelligence has been described as a dynamic ability that
is continuously influenced by changing contextual knowledge and experience (Salovey and Mayer 1990; Taylor
1990). Formal IQ likely plateaus in early adult life, while
social intelligence appears to increase over many decades
(Sternberg et al. 1995), a phenomenon that invites therapeutic intervention.
Our focus on social cognition as a potential rate-limiting factor to social and vocational recovery in schizophrenia arose from observations in our clinical experience
with schizophrenia patients that appear to have growing
empirical support (Corrigan et al. 1996b). Many patients
appeared to have become affectively and cognitively dysregulated by unpredictable changes in novel (untrained)
social contexts and by a resulting inability to get "the big
picture" regarding the nuances of interpersonal relationships and expected behavior (i.e., secondary socialization
problems in context appraisal and perspective taking). As
we describe below, evidence for our clinical observations
is largely indirect at this time.
The social cognitive impairments of many schizophrenia patients may arise from neurodevelopmental
insult, but similar social cognitive deficits also appear to
characterize those that are unequivocally compromised by
reason of traumatic brain injury. Intensive case studies of
focal injury clearly illustrate the relationship between
brain trauma and pervasive disabilities in social and emotional intelligence (Damasio 1994). In dramatic cases, IQ
and memory may be preserved but social judgment is
inoperative (Brothers 1990). Relatives of those with traumatic brain injury describe the most burdensome, longterm sequelae of injury not as abiding problems in neuropsychological competence, but as changes in
"personality" (Brooks and McKinlay 1983). Some investigators have characterized this phenomenon as "social
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Schizophrenia Bulletin, Vol. 25, No. 4, 1999
cognitive regression" to earlier developmental levels
(Santoro and Spiers 1994). We cite references to the traumatic brain injured simply to indicate that the mild focal
insult of the traumatically injured and the diffuse insults
of the developmentally compromised often share important functional impairments in the exercise of social cognition, i.e., a final common pathway of cerebral insult. We
do not imply, however, that this is the psychoanalytic
mechanism of "regression to primitive processing" in
schizophrenia. Rather, we are inclined to view the social
cognition of schizophrenia patients as reflecting an inappropriate reliance on earlier acquired controlled or serial
processing styles that served a necessary purpose prepubertally but render the automatic and abstract (parallel)
processing of adult life more difficult.
Indirect evidence that social cognition might be
developmentally compromised in schizophrenia has a rich
history. Researchers have reported on the poor premorbid
social dysfunctioning of many adult patients (Klorman et
al. 1977), neuropsychological problems among high-risk
children (Asarnow 1988), the social adjustment problems
of adolescents with mothers who have schizophrenia
(Dworkin et al. 1994), the developmental difficulties of
some children who later develop schizophrenia (Watt
1978), and the preschizophrenia child's inclination toward
atypical emotional expression (Walker and Lewine 1990).
Among those already affected with schizophrenia, more
direct evidence demonstrates impairment in various social
cognitive abilities. Bellack et al. (1994) found that schizophrenia patients and other psychiatrically impaired
patients are greatly compromised in their ability to generate, evaluate, and implement solutions to interpersonal
problems, a difficulty that Corrigan and Toomey (1995)
and Penn et al. (1996) relate more to social cognitive
deficits than to nonsocial, neuropsychological impairments. Extensive failures in the relevance and depth of
social problem solving among schizophrenia patients and
other severely mentally ill patients have also been demonstrated by others (Donahoe et al. 1990), another indication
of the importance, albeit nonspecific, of social cognitive
deficits. Corrigan and colleagues (Corrigan and Green
1993a; Corrigan and Toomey 1995) have shown that the
schizophrenia patient's insensitivity to social cues, particularly abstract cues, is in part also related to aspects of
negative symptoms. The most socially isolated and vocationally disadvantaged patients, for example, seem to be
those characterized by negative symptoms (Andreasen
1985; Jackson et al. 1989). Corrigan and Green (19936)
further cite patient recognition of concrete rather than
abstract situational features of social contexts that govern
appropriate behavior. Moreover, continuing studies suggest that these abstracting deficits might be influenced by
the "unfamiliar" social situations that patients find
"uncomfortable," another important directive for social
cognitive rehabilitation (Corrigan et al. 19966). Further,
affect perception among chronic schizophrenia patients is
also thought to be impaired (Mueser et al. 1997), as is
social knowledge, which has been described as social
naivete (Cutting and Murphy 1990), the converse of interpersonal wisdom. More recently, these social knowledge
deficits have also been associated with impairments in
nonsocial cognition as well (McEvoy et al. 1996). In a
rare repeated assessment study, Penn et al. (1993) have
shown that social cognitive problems persist in schizophrenia from the acute through remission stages.
However, most published studies of social problem solving appear to be cross-sectional assessments of a behavioral approach involving hospitalized schizophrenia
patients (Bellack et al. 1989; Green 1996). To our knowledge, relevant social cognitive deficits and their potential
response to a developmental intervention have not been
examined longitudinally among rehabilitation-ready and
symptomatically stable schizophrenia outpatients.
Again, while social cognitive impairment is not specific to a diagnosis of schizophrenia, it does have therapeutic relevance for schizophrenia. Clearly, individuals
afflicted with, for example, childhood autism or mental
retardation, also display pronounced social cognitive
deficits. However, the nature and subsequent remediation
of social cognitive deficits would be very different when
the developmental sequelae were usually manifest in late
adolescence or early adulthood, as with schizophrenia,
and thus affected the acquisition of secondary socialization skills, than when the functional disabilities were first
apparent in childhood and adversely affected primary
socialization skills.
Some might also challenge the concept of a developmentally compromised social cognition in schizophrenia
by citing evidence of good premorbid functioning in
many adult patients. Clearly, neurodevelopmental anomalies have not been found in all cases of schizophrenia
studied (Weinberger 1996). However, the developmental
hypothesis implies a delay in manifest problems; namely,
that latent social cognitive deficits in allegedly good premorbid patients might not become apparent until challenged by the interpersonal demands of early adult life
(Carter and Flesher 1995). For example, educationally
appropriate employment, courtship, marriage, and childrearing tasks seldom appear to be realized among most
male patients with schizophrenia, independent of premorbid status (Hogarty 1988). Elsewhere, indirect but supporting evidence suggests that schizophrenia patients
function better in sheltered vocational settings (Bond and
Boyer 1988) and achieve superior outcomes in cultures
that are less socially demanding and complex (Warner
1983); in other words, good premorbid status could be an
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Schizophrenia Bulletin, Vol. 25, No. 4, 1999
G.E. Hogarty and S. Flesher
artifact of unchallenging environments. Many nonpatients
also fail to achieve higher levels of "operational intelligence" (a form of practical intelligence) in the Piagetian
sense, but they still manage successful social and vocational lives. Again, this seeming paradox might also
reflect a self-selection process or fortuitous environments
that don't require complex instrumental and expressive
roles and the associated social cognitive skills.
. Finally, one could question the validity of existing
premorbid measures as indicators of social cognitive competence. All measures (Klorman et al. 1977) variably
assess, retrospectively, the most global of behavioral
domains, such as peer friendships; levels of isolation; and
interest in school activities, hobbies, or members of the
opposite sex. No epidemiological study of high-risk, prepubertal children, to our knowledge, has assessed the
essential components of social cognition, such as perspective taking, context appraisal, negotiation, and foresightful planning. Most studies assess only broad aspects of
mood and behavior as measures of social competence
(Olin and Mednick 1996). The existing evidence largely
indicates that prepubertal deficits in neuropsychological
(nonsocial) cognition might predict failure in social cognition during adolescence or adulthood or that adolescent
social cognition predicts adult mental status (Asarnow
1988). Longitudinal studies could be interpreted as indicating that high-risk children who eventually develop
schizophrenia simply failed to advance social cognition in
step with their unaffected peers, rather than having suffered a progressive deterioration of social cognitive ability from a good premorbid, pre- or early adolescent baseline. It is more likely that the good premorbid competence
assessed by traditional measures simply reflects a mastery
of primary socialization skills, but not secondary socialization skills (Carter and Flesher 1995).
In summary, the functional deficits of schizophrenia
are at least associated with problems in social cognition,
and, as might be true with neuropsychological deficits,
could also have been developmentally compromised in
many patients. Rehabilitation might thus require a developmentally guided approach to their remediation.
Developmentally, there is a prepubertal stage of life
(ages 7 to 10) where significant limitations in selective
attention, effective inhibition, working memory, and problem solving are, in fact, the norm (Spreen and Strauss
1991; Howe and Pasnak 1993). Moreover, the main characteristic of cognitive processing during this period is its
slowness (Kail 1993). Evidence for this has been well
established from (1) studies that document perseveration
errors and fewer categories achieved on the Wisconsin
Card Sort Test (Chelune and Baer 1986); (2) errors on the
Stroop Test (Comalli et al. 1962); (3) average evoked
potential anomalies (Taylor 1988); (4) failures of anterior
lobe activation (Matsuura 1985); and (5) performance
deficits in language, attention, and field independence
tests (Dempster 1993). Concurrently, there are also inefficient, but age-appropriate, prepubertal social cognitive
strategies that have been described by such pioneers as
Piaget, Mead, Cameron, Kohlberg, Baldwin, and Sullivan.
This literature, as reviewed by Selman and Schultz
(1990), provides a theoretical grounding for our social
cognitive approach. The evidence describes a concrete or
egocentric understanding of other people prepubertally; a
relative underdevelopment of language meaning, reciprocity, perspective taking, negotiation, empathy, reflection, context appraisal, planning, and foresight; and the
use of "procedural" (if . . . then) relational cognitive
scripts (Baldwin 1992) that appear central to adult social
cognition. These social cognitive capacities can eventually be acquired developmentally through meaningful secondary socialization experiences across the life span, as
described by Brim (1966) and tested by Selman and
Schultz (1990). The processes that underlie secondary
socialization are useful in understanding both the normal
acquisition of social cognition and the consequences that
follow the socialization failures in schizophrenia.
Primary socialization involves an apprehension of the
social structure and concrete rules that govern the "objective world." As described by Berger and Luckman (1966)
these basic skills are developmentally acquired by children through the instruction and sanction of adults, particularly parents (e.g., "Don't spill your milk," "Watch your
tone of voice," "Don't hit your sister"). Secondary socialization arises from but extends far beyond primary socialization. It includes the independently acquired "subjective
subworlds" that necessitate practical knowledge of the
affects, vocabulary, and informal rules of conduct associated with the expanded and more adult roles that one
encounters in new social contexts (such as becoming a
clinician or a neuroscientist). In contemporary, nonlinear
models of social cognition, feedback loops are thought to
exist not only among the various stages of social cognitive processing (such as encoding, interpreting, response
Normal Cognitive Development
and Schizophrenia
If one accepts a developmental basis to social cognitive
dysfunctioning in schizophrenia, the next step is to examine the developmental stages at which normal subjects
acquire nonsocial and social cognitive competencies.
These insights from developmental and social psychology
might serve to place in perspective both the nature and the
age relevance of developmental failures in schizophrenia
that require rehabilitation.
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Schizophrenia Bulletin, Vol. 25, No. 4, 1999
selection, and enactment) but also between the feedback
recalled from prior peer evaluations and the initiation of a
new response (Crick and Dodge 1994). Thus normal
social cognition arises from continuing and hence developmentally acquired secondary socialization experiences
that include one's working memory for past social goals;
past outcomes; the appraisal of prior social contexts,
including the intentions and behavior of others; and an
evaluation of one's own responses and associated affects.
Spontaneous awareness of social exchanges from past and
present experience is thus thought to slowly shape the
development of social cognition.
Through these reciprocal interactions, healthy adults
routinely socialize with each other over their lifetime as
environments and contexts change. However, when one
adult routinely appears not to get "the big picture," as is
likely among many patients with schizophrenia (i.e., when
a patient fails to correctly encode, remember, interpret, or
respond to the subtle cues regarding context-specific
rules, affects, and language), then other adults will often
cease or greatly limit further interaction. This process of
"desocializing" a person with poorly developed social
cognitive skills has been well described and includes the
consequences that lead to increased deviance and idiosyncratic behavior. Various authors (e.g., Cameron and
Margaret 1951) cite the functional disabilities of schizophrenia that follow upon the desocialization process,
including social withdrawal, progressive isolation, and
broad social dysfunctioning. These behaviors have
recently been shown to characterize the adjustment of
patients for more than 2 years prior to schizophrenia onset
(Hafner et al. 1998), and they effectively preclude the
acquisition and maintenance of social cognitive skills that
depend on continuing secondary socialization.
While the characteristics of prepubertal social cognition that have not been advanced through secondary
socialization might resonate among clinicians as being
all-too-common features of adult schizophrenia, it is again
necessary to indicate that only indirect evidence of such
impairments in schizophrenia exist. To our knowledge,
few if any of the above indicators of social cognition have
been measured prospectively, or retrospectively, among
patients with schizophrenia, either in the epidemiology,
high-risk, phenomenology, or rehabilitation literatures.
Clearly, many of the better established nonsocial cognitive problems of schizophrenia patients (e.g., ineffective
attentional inhibition [Nuechterlein and Dawson 1984]
and working memory difficulties [Goldman-Rakic 1990])
are more similar to prepubertal function. But again, the
neural connectivity and hence underlying mechanisms
among patients are likely to be different. Some might
argue that even suggesting associations between adult
schizophrenic cognition and that of normal prepubertal
subjects is akin to using childhood stature as a clue to
adult dwarfism. But this would misconstrue our central
message from developmental psychology (although studies of childhood growth hormone function ultimately did
provide insights into the nature of arrested stature). Rather,
what is important are the developmental processes that
emerge in most normal preadolescents whereby they eventually resolve their sensitivity to performance interference
and slowness of processing, and concurrently achieve a
level of intimacy and empathic understanding, a skill at
negotiating role complexities, a foresightful planning
capacity, and a more meaningful use of language, all of
which seem associated with successful social and vocational functioning (Selman and Schultz 1990). Obviously,
if many schizophrenia patients have cerebral insults, these
might preclude certain normal neurodevelopmental
processes perinatally or during young adult life (Feinberg
1997) and, in fact, might provoke atypical cerebral activation (Weinberger 1996). But a rehabilitation approach that
could stimulate the normative developmental processes of
social cognition might prove useful given the potential of
neuroplasticity and the acquisition of social intelligence
through many decades (Sternberg et al. 1995). But the key
elements of metacognition would have to be identified and
incorporated in an operational clinical strategy. Without
ongoing opportunities for clinically guided secondary
socialization experiences, schizophrenia patients would
likely be at a marked disadvantage in acquiring and elaborating the metacognitive components of social cognition.
The Normative Metacognitive
Processes of CET
Having suggested the nature and the age relevance of
social cognitive failures in schizophrenia, we turn to the
abstracting processes that facilitate the achievement of
these developmental milestones in normal subjects. As
recently summarized by Silverstein (1997), the problem
faced by the field of cognitive rehabilitation "is not the
relevance of cognitive tasks to social skill remediation in
schizophrenia; rather, it is the definition of those underlying processes related to social functioning in schizophrenia . . . and the interventions to improve them." (Italics
added.) We hope that the identification of one or more
processes that might be clinically enhanced could lead to
the formation of a developmentally appropriate and hence
more effective intervention.
While various cognitive models historically have
been used to explain the cross-sectional assessments of
schizophrenic cognition that were measured in the laboratory (Straube and Oades 1992), these deficits have rarely
been examined from a developmental perspective. The
685
G.E. Hogarty and S. Flesher
Schizophrenia Bulletin, Vol. 25, No. 4, 1999
colleagues (1994) suggest in their extensive studies of
schizophrenic cognition that schizophrenic "deficits in controlled processing may lead to deficient development of
automatic operations. Conversely, deficient automaticity
results in overutilization of controlled processes." This
"serial search defect," which is characteristic of childhood
and adult schizophrenia, appears to be associated with
increased demands (and processing activity) on a limited
capacity system (Strandburg et al. 1994), a phenomenon
that suggests to us a strong reliance on verbatim memory.
Some argue that these controlled, serial search deficits are
particularly characteristic of paranoid individuals (Magaro
1981). Perhaps Bellack et al.'s (1989) criticism regarding
social problem-solving approaches to schizophrenia (i.e.,
that normal subjects do not consciously engage in sequential, stepwise processing) represents an appeal similar to
Corrigan et al.'s (1996a) to enhance the requisite abstracting ability of normal social cognition for schizophrenia
patients, much like the wise individual who is actually cognitively "sloppy," ignoring details by going straight to the
heart or "gist" of the problem (Brainerd and Reyna 1993).
Thus to reduce information complexity, nature is
inclined to "making it simple" by getting to the "essence"
of things. This process seems to involve a decreasing
reliance on both verbatim memory and serial, controlled
processing (characteristic of schizophrenic and normal
prepubertal cognition) and an increasing use of less
demanding cognitive strategies such as intentional forgetting and extraction and enhancement of gists in a parallel,
automatic processing mode (i.e., the features of normal,
young adult cognition). These developmental cognitive
processes might profitably be addressed in a rehabilitation
program designed to facilitate a more abstracting social
cognition for schizophrenia patients. When operationalized through the use of developmental exercises targeted
to the acquisition of secondary socialization abilities, such
as context appraisal and perspective taking, the resulting
approach might ultimately represent a Cognitive Enhancement Therapy for schizophrenia.
development perspective elaborates the progressive shift
from a prepubertal reliance on relatively concrete, effortful processing to the more abstracting and less demanding
cognitive processing of late adolescence and early adulthood (Howe and Pasnak 1993). In contemporary cognitive models, children have been shown to be developmentally endowed with the capacity to acquire highly concrete
schemata, called verbatim memory (Brainerd and Reyna
1993). Following the well-established Principle of Least
Effort in human cognition (Zipf 1949), nature slowly provides an easy way out of the growing problem of acquiring and remembering multiple pieces of information
through a process of cognitive "downsizing" or "reduction to essence," whereby only fuzzy trace elements of
verbatim memory stores persist (Brainerd and Reyna
1990). These elements are called "gists." Social gists, for
example, would include the personally meaningful and
abstract relational schemata, attributions and inferences,
and rules and principles that underlie perspective taking
and context appraisal. As elaborated by Brainerd and
Reyna (1990, 1993), with age and cerebral maturation
(including neural pruning and the reinforcement of crucial
neural circuits [Keshavan and Murray 1997]), primary
gists are increasingly extracted from stimuli as new
sources of meaning are used to elaborate and reconstruct
existing gists. Verbatim stores are unstable, quick to fade
from memory, extremely hard to recall, and greatly subject to interference—all cognitive features that are common in schizophrenia. Gists, on the other hand, require far
less effort to recall. Perhaps, as is true for schizophrenia
patients and those among them who are treated with
sequential behavioral strategies, individuals who process
information in the serial fashion of a specific response
paradigm tend to become subject to cognitive interference. A problem subsequently arises, for example, in having to continuously edit or inhibit existing verbatim or
semantic memory stores or an earlier acquired primitive
gist (Brainerd and Reyna 1993). A developed gist-acquisition capacity, on the other hand, leads to multiple and
spontaneous behavioral responses rather than discrete,
controlled, situation-defined responses. Corollary evidence for gistful cognition can be found in recent developmental studies of effective inhibition (Dempster 1993;
Harnishfeger and Bjorkland 1993). In a compensatory
manner, nature again provides the growing child with the
capacity for "intentional forgetting and selective remembering" (Lehman and Bovasso 1993). The relatively fewer
stimuli that are remembered likely represent the trace
stores that contain the gist of things, a process greatly
facilitated by a developmental shift from serial (controlled) to parallel (automatic) processing.
While controlled and automatic processing appear to
be highly interrelated (Schneider et al. 1984), Asarnow and
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Acknowledgments
The development and testing of Cognitive Enhancement
Therapy has been supported by Grant MH-30750 from the
National Institute of Mental Health (NIMH) and by the
contributions of Mary Carter, Ph.D., Deborah Greenwald,
Ph.D., Susan Cooley, M.N.Ed., Ann Louise DiBarry,
M.S.N., Ann Garrett, Ph.D., Sander Kornblith, Ph.D.,
Richard Ulrich, M.S., and Hari Parepally, M.D., who are
members of the Environmental/Personal Indicators in the
Cause of Schizophrenia research program. We gratefully
acknowledge and attempt to incorporate responses to the
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The Authors
Gerard E. Hogarty, M.S.W., is Professor of Psychiatry at
the University of Pittsburgh, School of Medicine, and
Samuel Flesher, Ph.D., is Senior Research Psychologist,
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