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10 Trivedi: Cognitive deficits in psychiatric disorders: Current status

D.L.N. MURTHY RAO ORATION

Cognitive deficits in psychiatric disorders: Current status

J.K. TRIVEDI

ABSTRACT
Cognition denotes a relatively high level of processing of specific information including thinking, memory,
perception, motivation, skilled movements and language. Cognitive psychology has become an important
discipline in the research of a number of psychiatric disorders, ranging from severe psychotic illness such as
schizophrenia to relatively benign, yet significantly disabling, non-psychotic illnesses such as somatoform
disorder. Research in the area of neurocognition has started unlocking various secrets of psychiatric disorders,
such as revealing the biological underpinnings, explaining the underlying psychopathology and issues
related to course, outcome and treatment strategies. Such research has also attempted to uproot a number of
previously held concepts, such as Kraepelin’s dichotomy. Although the range of cognitive problems can be
diverse, there are several cognitive domains, including executive function, attention and information processing,
and working memory, which appear more frequently at risk. A broad range of impairment across and within the
psychiatric disorders are highlighted in this oration. The oration summarizes the studies investigating cognitive
processing in different psychiatric disorders. I will also discuss the findings of my own research on
neurocognitive deficits in mood disorders, schizophrenia, obsessive–compulsive disorder, somatoform disorder,
including studies on ‘high-risk’ individuals. Tracing the evaluation of neurocognitive science may provide
new insights into the pathophysiology and treatment of psychiatric disorders.
Keywords: Cognitive deficits, neurocognition, treatment of psychiatric disorders
Indian J Psychiatry 2006;48:10–20

INTRODUCTION This oration summarizes the studies investigating cognitive

To begin with, I am immensely thankful to the Indian
Psychiatric Society for bestowing the honour on me—to
deliver this prestigious oration. This oration has enabled me
to pay my tributes to Late Dr DLN Murthy Rao—the renowned
psychiatrist who has helped many in the Indian psychiatry to
reach the present height. I wish to pay my gratitude and sincere
thanks to my teachers Late Professor B.B. Sethi, Professor
A.K. Agarwal, Professor Narottam Lal, Professor S.C. Gupta
and Shri P.K, Sinha for their blessings and support. I feel
extremely privileged as I stand before you and focus on one
of the most interesting topic in psychiatry—‘Cognition’.
Cognitive psychology has become an important area of
research in a number of psychiatric disorders, ranging from
severe psychotic illness such as schizophrenia to relatively
benign, yet significantly disabling, non-psychotic illnesses
such as somatoform disorder. Research in the area of
neurocognition has started unlocking various secrets of
psychotic disorders, such as revealing the biological
underpinnings, explaining the underlying psychopathology
and issues related to course, outcome and treatment strategies.
processing in different psychiatric disorders, with an emphasis
on recent concepts. I will also discuss the findings of my
team’s research on neurocognitive deficits in mood disorder
(including a high-risk group study), schizophrenia, obsessive–
compulsive disorder and somatoform disorder carried out in
the Department of Psychiatry, K.G. Medical University,
Lucknow. Tracing the evolution of neurocognitive science
may provide new insights into the pathophysiology and
treatment of psychiatric disorders.
COGNITION
Cognition in a broad sense means information processing. It
denotes a relatively high level of processing of specific
information including thinking, memory, perception, motiva­
tion, skilled movements and language. The hippocampus
contains the neural circuitry crucial for cognitive functions
such as learning and memory. It refers to the perceptual and
intellectual aspects of mental functioning. Among the specific
functions that may be assessed in determining the intactness
or adequacy of cognition are orientation, the ability to learn

Indian Journal of Psychiatry 2006;48:10–20

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Trivedi: Cognitive deficits in psychiatric disorders: Current status
necessary skills, solve problems, think abstractly, reason and
make judgements, the ability to retain and recall events,
mathematical ability and other forms of symbol manipulation,
control over primitive reactions and behaviour, language use
and comprehension, attention, perception and praxis. 1
Cognitive deficits may result in the inability to:
1. pay attention
2. process information quickly
3. remember and recall information
4. respond to information quickly
5. think critically, plan, organize and solve problems
6. initiate speech
The following questions need to be addressed in relation
to psychiatric disorders and cognitive impairment:
1. Is there anything specific about the profile of cognitive
impairment in these disorders?
2. How do these impairments relate to the underlying
psychopathology/neuroanatomy of these disorders?
3. Do these cognitive impairments vary over a course of time?
4. What impact do these impairments have in terms of
treatment implications?
Cognitive deficits have a relationship with different levels
of the disease process, as depicted in Fig. 1.2 Before discussing
specific cognitive deficits in different psychiatric disorders,
the following cognitive domains need to be elucidated.
WORKING MEMORY
Working memory (WM) function is thought to be sustained
by a network of temporary memory systems. It plays a crucial
role in many cognitive tasks, such as reasoning, learning and
understanding. It refers to the ability to hold the stimuli ‘online’
for a short time, then either use it directly after a short delay or
process or manipulate it mentally to solve cognitive and
behavioural tasks. WM involves active rehearsing, processing
and manipulation of information. WM seems to depend on
the function of the prefrontal cortex.3
Pathology level Impairment level
Abnormality in EEG, event- Impairments in sustained
related potential, eye-tracking, attention, disinhibition, and
imaging and neuroimaging switching between attention,
data, e.g. functional magnetic e.g. Stroop test and Wisconsin
resonance imaging paradigm Card Sorting test
and eye-tracking machine
Fig. 1 Levels of disease process and types of assessments—relationship
Indian Journal of Psychiatry 2006;48:10–20
11
EXECUTIVE FUNCTION
Executive function (EF) refers to the ability to use abstract
concepts, to form an appropriate problem-solving test for the
attainment of future goals, to plan one’s actions, to work out
strategies for problem-solving, and to execute these with the
self-monitoring of one’s mental and physical processes.
Executive skills are most important in dealing with novel or
complex situations. Physiologically, EF is linked to the
cortical–subcortical circuits and frontal lobes.4
ATTENTION AND INFORMATION PROCESSING
Attention refers to the ability to identify relevant stimuli, focus
on these stimuli rather than others (selective attention), ability
to perform a task in the presence of distracting stimuli (focused
attention), sustain focus on the stimulus until it is processed
(sustained attention or vigilance), and allow for the transfer of
the stimulus to higher-level processes. The Continuous
Performance Test (CPT) is commonly used for measuring
attention.
Cognitive deficits have been an area of research in many
psychiatric disorders, the ‘prototype’ work being in
schizophrenia. I will begin with the review of the research on
cognitive deficits in schizophrenia.
COGNITIVE DEFICITS IN SCHIZOPHRENIA
The understanding of the fundamental deficits in schizo­
phrenia comes full circle as it begins to be accepted that
cognitive dysfunctions play a central role in the illness, as
Kraepelin and Bleuler had suggested. Cognitive deficits are a
core feature of schizophrenia which
—may precipitate psychotic and negative symptoms;5
—are relatively stable over time, with progressive deterioration
after the age of 65 years in some patients;6
—persist on the remission of psychotic symptoms;7
—are related to but separate from negative symptoms;8,9 and
—determine the functional impairment characteristics of
patients with this disorder.10
Disability level Handicap/participation level
Disability in reading a Being handicapped in
newspaper or listening to a performing the proper role of
lesson a housewife or manual worker
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12 Trivedi: Cognitive deficits in psychiatric disorders: Current status
An important domain of schizophrenia that appears closely
related to functional outcome involves cognitive deficits.11,12
The range of cognitive deficits is broad and includes problems
in perception, attention, memory and problem-solving.13
WM deficits in schizophrenia reflect hypofunction of the
prefrontal cortex (PFC). Neuropsychological and imaging
studies suggest that the WM system is of a limited capacity
in patients with schizophrenia.14–17 WM deficits have been
found to correlate significantly with formal thought disorder,18
and may result in loose association and derailment.19 Deficits
in strategic long-term memory (e.g. free recall, memory for
temporal order) could be accounted for by deficits in WM.20
Patients with schizophrenia also show deficits in measures
of EF.21,22 Severity of negative symptoms such as affective
flattening, alogia, social withdrawal or avolition has been found
to be associated with poor performance on measures of EF.23
Performance on the measures of executive functioning has
been found to be linked to insight of illness23,24 and hence to
poor medication compliance, self-injurious behaviour and
assaultiveness.25–27
Deficits in attention and information processing might be
central to schizophrenia because these can contribute to
deficits in EF and WM.28 Attention deficits are also trait and
vulnerability markers seen during remission29 in children of
schizophrenic parents30 and individuals with schizotypal
personality.31 Attention deficits have been found to be robustly
associated with deficit syndrome.32 Distractability has been
associated with higher levels of formal thought disorder.33
Although there appears to be a group of patients who are
impaired only minimally,34–36 most patients are characterized
as having at least some impairment across a number of
domains. More specific deficits in schizophrenia occur within
the context of diffuse cognitive impairment—especially in
areas of verbal episodic memory and vigilance.37–39
Some deficits including verbal memory and learning, visual
memory, abstraction, attention and language abilities have
been found even in untreated, first-episode patients.40–43
Cognitive impairments differ according to the clinical
symptomatology—the deficits may be related more with
disorganized and negative symptoms and less with psychotic
symptoms. 44–48 There appears no pathognomonic
neuropsychological profile in schizophrenia, likely due in part
to aetiological heterogeneity within the disorder.
Cognitive deficits and functional impairment manifest a
specific pattern of relationship in schizophrenia.
Functional domain Cognitive correlates
Social function Declarative memory,
vigilance, EF
Occupational functioning EF, declarative memory, WM,
vigilance
Independent functioning EF, declarative memory, WM
EF: executive function; WM: working memory
Indian Journal of Psychiatry 2006;48:10–20
IMPROVING COGNITION IN SCHIZOPHRENIA
Newer antipsychotic medications have been shown to have
neurocognitive advantages over conventional antipsychotic
medications.49–52 Atypical antipsychotic medications differ in
their profiles of cognitive efficacy; for example, risperidone
shows relatively greater improvement in memory; olanzapine
causes greater improvement in processing speed. 53,54
Determining and characterizing the cognitive profile of each
atypical antipsychotic medication is an important task, as this
information could be used to target the cognitive problems of
individual patients.
Although atypical antipsychotic medications appear to
have some benefit on cognitive function, further efforts are
required to improve cognitive function. Such methods may be
pharmacological and psychological such as cognitive
remediation. Cognitive remediation targets three domains—
EF, attention and memory, and there is evidence for gains in
performance across all three domains,55 particularly for WM.56
Adjunctive pharmacological interventions, with some reported
effectiveness include nicotinic treatment for attentional
difficulties,57 tandospirone for memory problems,58 donepezil59–
61
and NMDA receptor stimulating agents.62
Such newer psychopharmacological and neuropsychol­
ogical remediation programmes may provide clinicians with a
variety of means to improve cognitive and social functioning
in schizophrenia.
COGNITIVE IMPAIRMENTS IN MOOD DISORDERS
Neurocognitive deficits are present in mood disorders. In major
depression, cognitive impairment can be severe and global,
mimicking dementia.63 In the acute phase of bipolar disorder,
impairment of cognition may progress to a stuporous state.
Cognitive deficits in mood disorders include impaired
performance in tests of attention, EF and memory. Increased
cognitive dysfunction is associated with greater severity of
symptoms. Owing to the presence of cognitive deficits even
during the euthymic/remitted states, it is suggested that certain
cognitive deficits are fundamental trait characteristics.
Impairment of WM, 64 sustained attention, 65,66 focusing-
execution,67 abstract reasoning and visuomotor skills,68 verbal
memory,69,70 verbal fluency,71 visuospatial ability,72 have all
been reported, even in the euthymic phase of the illness.
The deficits have been shown to correlate with both the
number of affective episodes and the overall duration of
illness.65,71,73,74,76, Performance on memory and executive tasks
were most likely to correlate with illness episodes.
The relationships between mood and cognition are dynamic
ones, with components that are trait-dependent and others
that are state-dependent. Because of their relatively static
nature, trait characteristics of cognitive and neurological
manifestation may provide insights into core brain anomalies
that give rise to severe mood disorders.
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Trivedi: Cognitive deficits in psychiatric disorders: Current status
COGNITIVE DEFICITS: A CHALLENGE TO
KRAEPELIN’S DICHOTOMY
In 1896, Kraepelin proposed the classification of the
psychoses into dementia praecox and manic–depressive
insanity. The latter was characterized by an episodic course
and benign prognosis, and formed the basis of the concept of
bipolar disorder. Recent investigations, which demonstrate
neuropsychological impairment in euthymic bipolar patients,
have posed a challenge to Kraepelin’s dichotomy.
Schizophrenia and mood disorders have significant overlap
in genetic and neuroimaging studies as well.77,78 In contrast to
the concepts of Kraepelin, bipolar disorders may be chronic;
hence, long-term therapy may be needed for bipolar disorder,
as is true for schizophrenia.
COGNITIVE DEFICITS IN BIPOLAR DISORDER AND
SCHIZOPHRENIA: A COMPARISON
Similar cognitive profiles have been reported in patients with
bipolar disorder and schizophrenia, but the severity of
impairment appears greater in schizophrenia.79–81 There is now
substantial evidence that cognition is a good predictor of
functional outcome in schizophrenia as well as bipolar-I
disorder. 12 Controversies, however, exist regarding the
specificity of domains or the generalizability.
Comparisons of cognition between these patient groups
are problematic due to the fact that differences in illness
characteristics and current symptoms are not always assessed
and may confound neuropsychological test performance.80–83
A major limitation is differing medication regimens. Patients
with bipolar disorder usually receive mood stabilizers (e.g.
lithium, anticonvulsants) whereas patients with schizophrenia
often take antipsychotic medications. Also, it is impossible to
assess the degree of the patient’s cognitive impairment if
studies fail to include a normal control group.83,84
In a study conducted at our centre (tertiary-care psychiatric
hospital), 15 stable maintained schizophrenic patients and 15
euthymic bipolar-I patients attending the outpatient clinic were
compared with each other as well as with 15 age- and
education-matched controls. Stable schizophrenic patients
were clinically assessed using the Positive and Negative
Syndrome Scale for Schizophrenia (PANSS) and Hamilton
Depression Rating Scale (HDRS) while euthymic patients were
clinically assessed using the Young Mania Rating Scale
(YMRS) and HDRS. Neurocognitive assessments were done
using the WCST, Spatial Working Memory Test (SWMT) and
CPT—all are computer-based. Stable schizophrenic patients
performed poorly on all the neurocognitive parameters as
compared with both controls and bipolar euthymic patients.
Euthymic bipolar patients showed a significant difference in
the domain of EF compared with normal controls, while the
schizophrenic and bipolar euthymic patients were comparable.
Thus, our study suggested that bipolar patients in the
euthymic/remitted phase also have some types of cognitive
processing deficits. Patterns of cognitive disturbances in tasks
Indian Journal of Psychiatry 2006;48:10–20
13
of EF are similar in both the groups but are quantitatively
more marked in schizophrenia. Euthymic bipolar subjects
showed significant impairment only on EF when compared
with the control group.85
COGNITION DURING REMISSION IN
BIPOLAR DISORDER
Cognitive deficits in attention, EF and memory have been
recorded in bipolar patients. Cognitive deficits persist during
remission and indicate some type of cognitive processing
deficits that may be fundamental trait characteristics. Examining
the deficits during remission may help in a better under­
standing of the course of non-affective symptoms associated
with mood disorders.
Although cortical dysfunction undoubtedly plays a role in
the development of abnormal mood states, the use of
neuropsychological assessments as a tool to probe such
dysfunction is limited by a number of non-specific factors.
Poor performance on neuropsychological tests may be due to
reduced motivation, non-cooperation or failure to remain
engaged in a formal test setting. 75 Recently, cognitive
assessments have been performed in bipolar patients when
they are euthymic. Studies of this nature aim to identify trait-
dependent rather than state-dependent neuropsychological
deficits, which may be indicative of underlying neurobiological
disturbances associated with the pathophysiology of bipolar
disorder. Results from various studies are not consistent and
therefore raise questions about the generalization of the
findings. Some studies fail to control for differences in age,
gender and premorbid intelligence between patients and
control subjects.86 Euthymia is often poorly defined.73,83
Different neuropsychological measures used by investigators
to study neurocognitive functions of bipolar disorder further
limit the interpretability and generalizability of the findings.
Yet, patterns that emerge from the literature demonstrate the
fact that neurocognitive impairments form an important clinical
component of bipolar illness and are not merely epi­
phenomena.
A high incidence of psychosocial difficulties has been
reported during remission, which raises questions about so-
called complete recovery. Patients in either acute manic or
euthymic states have demonstrated significant impairment on
the Stroop test, a test for EF.87
Zubeita et al.88 found that euthymic patients did not show
significant impairment on CPT, however, on WCST patients
committed more errors than healthy controls. The same study
also showed impairment in verbal memory, but not in non­
verbal memory. Subjective memory complaints are often
reported during the euthymic state in bipolar patients.
Impairment of memory has been reported during the depressed,
manic and euthymic phases of the illness. Impairments in story
recitation88 and word list recall69 have been recorded in the
euthymic phase.
In a study conducted at our centre on 30 patients meeting
the DSM-IV criteria for bipolar affective disorder, currently
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14 Trivedi: Cognitive deficits in psychiatric disorders: Current status
euthymic, were assessed using WCST for EF, CPT for
performance on continuous tasks administering and SWMT
for spatial working memory. Fifteen controls matched for age
and sex were also assessed. All the patients and controls
were educated at least up to standard VIII. The patients’
performance was impaired on WCST, implying poor EF as
compared with controls, and indicating residual cognitive
deficits. The performance on tests of attention, concentration
and memory was not significantly different from that of the
matched controls.89
HIGH-RISK STUDIES: EVIDENCE FOR TRAIT
MARKERS
Neurocognitive deficits in individuals with bipolar disorder
are not merely the product of affective symptomatology or
medication use, but are reflective of premorbid developmental
abnormalities. Support for this theoretical position is derived
from a variety of methodological approaches: twin studies,
comparison of cases with positive and negative family histories,
retrospective analyses of premorbid function and assessment
of unaffected biological relatives. ‘High-risk’ individuals are
those who have an increased genetic risk for bipolar disorder
(e.g. monozygotic twins, first-degree relatives) but without
outright expression of the illness. Studies on these individuals
are unlikely to be confounded by medication or effects of
chronicity of illness. Few studies of bipolar disorder have
employed a high-risk paradigm model (unlike large number of
studies on schizophrenia).
Keri et al.90 showed that the unaffected relatives of bipolar
patients showed a greater degree of verbal recall difficulties
than a group of unrelated controls. Chowdhury et al. 91
suggested deficits in the executive control of WM to be a trait
deficit. Zalla et al.92 found that the unaffected relatives of
bipolar patients performed poorly on the Stroop test, i.e. a
dysfunction of anterior cingulate cortex. McDonough–Ryan
et al.93 found significant impairment on executive and non­
verbal intelligence test—associated tasks in children with at
least one parent with bipolar disorder.
However, not all studies of ‘at risk’ relatives of bipolar
patients have reported the presence of cognitive deficits.94–96
The plastic changes associated with a mood-driven
disturbance of attention may adversely affect cognition
particularly in the acute stage of the bipolar illness. Analysis
of executive-type cognitive traits may constitute a key
endophenotype (vulnerability marker) for genetic studies of
bipolar disorder. 97
We conducted a study to assess neurocognitive functions
in 10 first-degree healthy relatives of patients with bipolar
disorder and compared them with 10 age-, gender- and
education-matched healthy controls with no family history of
any neuropsychiatric disorder. In this study, EF assessed using
WCST showed that healthy first-degree relatives of patients
with bipolar disorder completed less categories and committed
more perseverative errors than did normal controls, i.e. they
Indian Journal of Psychiatry 2006;48:10–20
had impaired EF.
On CPT, attention and concentration abilities were found
to be significantly impaired; and first-degree healthy relatives
of bipolar patients committed more mistakes (errors of
commission), had more missed responses (errors of omission)
and took more time to respond then normal controls.
For spatial working memory on SWMT, healthy first-degree
relatives of patients with bipolar disorder were found to be
significantly impaired (scored less correct responses) at 0 sec
delay (i.e. error in recognition) but no significant differences
were reported between subjects (relatives) and controls at 20
sec delay (i.e. no error in recall). No significant differences were
seen regarding non-adjacent errors at 0 sec and 20 sec delays.98
The evidence suggests that the presence of cognitive
dysfunction in bipolar affective disorder is a core and enduring
deficit of the illness. The association between cognitive
impairment and the number of affective episodes suggests
that each affective episode is not biologically benign and
early diagnosis followed by active treatment could potentially
reduce cognitive morbidity. Future studies are required
employing a variety of study designs such as the use of high-
risk groups and first-episode patients, in conjunction with
longitudinal assessments. Understanding the mechanism that
underlies mood and cognition may help to devise better
treatment options to address dysfunctions during euthymia.
COGNITION IN DEPRESSION
Numerous studies have demonstrated the presence of neuro­
psychological deficits in actually depressed patients with
verbal and visual memory as well as EF.99–101 The decrement in
cognition has been attributed to reduced motivation,
attenuated attentional capacity, impaired concentration,
intrusive thought and slowness. Cognitive deficits are more
pronounced in melancholic than non-melancholic
depression.102 Prominent cognitive disturbances may be one
of the presenting symptoms of depression. Drevets et al.103
showed reduced blood flow to the subgenual area of the
prefrontal cortex in bipolar and unipolar depression. Core
cognitive deficits may be present in unipolar depression which
is independent of the depressed state.87
In the acute phase of depression, patients produce more
errors of attention compared with matched controls.104 Austin
et al.105 showed impairment in EF in the Trail Making Test,
part B, which worsened with the level of depression. Verbal
memory impairment, such as story recitation and word list
recall, has been reported.88,105
Non-verbal memory has also been reportedly impaired in
depressed patients.106 Implicit non-declarative memory has
not been found to be impaired in depressed patients.107
We carried out a study at our centre on 30 patients with
depression and 15 matched controls, and compared their
performance on the tests of EF, attention–concentration and
WM. The findings of the study suggest that depression
induces significant impairment in the abilities of sustained
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Trivedi: Cognitive deficits in psychiatric disorders: Current status
attention as shown by the fewer correct responses and more
missed responses (errors of omission), and this impairment
increases with severity. The number of wrong responses,
however, was similar in controls and patients (errors of
commission). Reaction time also increases due to depression,
which further increases with severity.
Significant impairment in spatial working memory after a
delay (error in recall) is seen as compared with controls, its
extent, however, is similar across the variable severity.
Patients performed similar to controls at 0 sec (recognition).
On WCST, executive dysfunction was significant in the patient
group; more severe illness was associated with greater
impairment in EF.108
COGNITIVE DEFICITS IN OBSESSIVE–COMPULSIVE
DISORDER (OCD)
A recent area of research has been the characterization of
neuropsychological deficits in patients with OCD. This has
contributed to the understanding of biological underpinnings
of the illness. Cognitive deficits could be functioning as an
intermediate variable between neurobiological abnormalities
and OCD symptoms. Reductions in social competence and
the capacity for independent living and vocational success
may be the result of neurocognitive compromise.
EF deficits have been seen in several studies among OCD
patients.109–112 These EF deficits may explain partly the
performance difficulties seen in patients with OCD in other
cognitive domains.113 Okasha et al.114 suggested that patients
with OCD are unable to disregard irrelevant stimuli and may
become overwhelmed by this information.
Visuospatial and visuoconstructional deficits are among
the most consistent findings in neuropsychological
assessment studies of patients with OCD.114,115
OCD patient groups have shown impairment on numerous
tests of non-verbal memory including visual reproduction and
delayed recognition of figures, maze learning and intermediate
and delayed figure copying. Most studies suggest that
encoding and retrieval are impaired in OCD, while storage of
information remains intact. Some studies suggest that deficits
in encoding of new information are primarily responsible for
these performance problems.111,116 Savage et al.117 indicate
that retrieval is also faulty, while storage is intact. Deckersbach
et al.118 reported that OCD patient groups have deficits in the
implicit memory domain of procedural learning in dual task
condition. This finding was interpreted as consistent with
frontostriatal dysfunction.
Patients with OCD often function remarkably well in their
daily lives, despite severe symptomatology and cognitive
difficulties, which are apparent only on specific testing. In
contrast to non-verbal memory deficits, verbal memory is
generally preserved in studies of patients with OCD.115,119,120
Patients with OCD demonstrate normal general intelligence
and language abilities. Different subtypes of OCD may have
varying neuropsychological deficit profiles.121
Indian Journal of Psychiatry 2006;48:10–20
15
In a study we aimed to evaluate the EF, spatial working
memory and performance on continuous tasks of 30 patients
with OCD compared with 30 normal matched healthy controls,
and to observe the effect of severity and duration of
psychopathology on them.
Findings of the study suggested that OCD induces
significant impairment in the EF as lesser categories were
completed and more perseverative errors were committed by
patients, and that the degree of impairment increases with the
severity of the illness.
OCD induces significant impairment in sustained attention
abilities, as shown by fewer correct responses and more missed
and wrong responses; the degree of impairment does not
increase with severity.
Reaction time was, however, not significantly different
between the patients and controls.
Significant impairment in spatial working memory was seen
as compared controls after a delay (error in recall); its extent
also increased with increasing severity. The patients performed
similar to controls at 0 sec (recognition).
No effect was found of the duration of illness on
performance in any of the domains.
Ascertaining whether cognitive impairment is a function
of the present disease state or a long-term stable trait has
both heuristic and clinical implications.122
COGNITION IN SOMATOFORM DISORDER
Somatoform disorder includes somatic, psychopathological
and neuropsychological symptoms. Cognitive complaints
reported frequently by patients include poor concentration,
decreased memory for recent events and poor word-finding
abilities.123 About 50%–85% of patients with somatoform/
chronic fatigue syndrome (CFS) report cognitive problems,
which contribute considerably to their social and occupational
dysfunction.124,125
Studies have revealed that impaired attention–
concentration abilities and spatial working memory in patients
of somatoform disorder126–129 also reported significantly slow
responses. Cognitive problems in severe somatization provide
a challenge to future research as well as diagnostic and
treatment options. Early identification of the cognitive
dysfunction in somatoform disorder, namely slowed
processing speed, impaired working memory, poor learning
information, poor set shifting and planning ability, would
enable us to offer appropriate advice on coping with these
and provide considerable benefit to patients.
Niemi et al.130 showed that patients of somatoform disorder
performed at a lower level than controls in tests involving
semantic memory, verbal episodic memory and visuospatial
tasks, and the fact that they were slower in attentional tasks
may further suggest that somatization is associated with brain
dysfunction, especially impaired anterior control of attention
and memory.
In a study between 1 May and 31 July 2004, we assessed
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16 Trivedi: Cognitive deficits in psychiatric disorders: Current status
20 patients who met the ICD-10 criteria for somatoform disorder
by using the test for EF on WCST, performance on continuous
task on CPT and spatial working memory on SWMT. Fifteen
controls (age-, education- and gender-matched) were also
assessed. All the patients and controls were educated at least
up to standard VIII. The patients’ performance was impaired
on WCST implying poor EF as compared with controls. The
performance on tests of attention–concentration was also
significantly poorer than that of the controls. On the SWMT,
however, significant difference was found only in delayed
retrieval and not in immediate recall. The study suggested
that enduring cognitive deficits in EF, attention–concentration
and memory may be contributing to the poor psychosocial
functioning in patients with somatoform disorders.131
COGNITIVE DEFICITS IN OTHER PSYCHIATRIC
DISORDERS
Studies related to neuropsychological dysfunction are
invading many other psychiatric disorders as well. Some
important psychiatric disorders are discussed below.
Cognitive deficits in borderline personality
disorder (BPD)
Neuropsychological and psychopathological factors in
personality disorders seem to be related thus, they challenge
the assumption that personality traits are responsible for the
behavioural and emotional experiences associated with BPD.
Studies have revealed poor decision-making skills.132,133
Burgees134 revealed a link between attention and memory
impairment and self-injury. O’Leary et al.132 showed that
although verbal memory skills of BPD patients were impaired,
their memory improved with the use of cues. Thus, clinicians
might make use of cueing strategies when working with these
patients. Paris et al.135 found significant impairment on tests
of frontal lobe and executive functions in children with BPD,
and also showed inconsistent levels of attention, poor
orientation to task and slower reaction on CPT. In fact, suicide
risk in BPD patients has been linked to cognitive functioning
and not to level of depression.134
Cognitive deficits in attention deficit/
hyperactivity disorder (ADHD)
In general, poor performance on tests of EF, sustained attention
and memory tend to be the most common neuropsychological
deficits reported in children and adults with ADHD. There is
little evidence for deficits in basic motor, visuospatial or sensory
functioning in ADHD, with the possible exception of olfactory
processing.136,137 In particular, converging evidence points to
a prominent disturbance of EF.136,138,139 Various execution
functions that have been studied in relation to ADHD are:
cognitive flexibility, initiation, interference control, planning
and organization, responssssse inhibition, self-monitoring and
WM. Further research using cognitive tasks assessing EF in
Indian Journal of Psychiatry 2006;48:10–20
combination with functional imaging techniques will provide
insights into the aetiology of the disorder.
Cognitive impairments in substance abuse
Cognitive dysfunctions have been demonstrated following
substance abuse. These functions include mental activities
that involve acquiring, storing, retrieving and using
information. These cognitive functions could play an important
role in the development of the addictive process and
rehabilitation of substance abusers. Prochaska et al. 140
postulated that cognitive skills are critical for drinking
behaviour change. Memory and EF are likely to influence the
execution of skills that are implicated for both motivating and
sustaining drinking behaviour change. Blume et al.141 showed
that an explicit memory process may have utility for predicting
readiness to change drinking behaviour. Lyvers et al.142
showed that opioid dependence such as alcohol addiction is
associated with cognitive dysfunctions. Newly detoxified
alcoholics exhibit relatively intact verbal and general
intellectual abilities, but impaired non-verbal abilities.143,144
Deficits exist in novel problem-solving, abstract reasoning,
and learning and recalling information. 144,145 Deficits in
perceptual–motor abilities, abstract reasoning, and non-verbal
learning and memory can persist for months or years.145–147
Neuropsychological test findings with substance-dependent
populations also might influence the design of treatment
programmes.143,148
CONCLUSION
Although the range of cognitive problems can be diverse,
there are several cognitive domains, including executive,
attentional and memory, that appear most frequently at risk.
Without a doubt, there is more to be learned about the
specificity of cognitive impairment across disorders, the
relationship of these deficits with the underlying psycho­
pathology and neuroanatomy of these disorders, and the
impact of the impairments on treatment implications. Early
identification of these dysfunctions would provide
considerable benefit to patients and suggest ways of coping
with these dysfunctions.
ACKNOWLEDGEMENTS
Prayers, rather than thanks, need to be offered to the Almighty
God, my parents and my teachers—the blessings bestowed
by them have paved the way for my existence and achieve­
ments so far.
I am immensely thankful for the caring attitude of my family,
who always stood by my side—at times, sacrificing their
personal needs for me and my work.
Words to thank my colleagues, friends, students and all
other associates are few, who perpetually helped me in my
progress of learning.
I am especially thankful to Professor Roy Abraham
[Downloaded free from http://www.indianjpsychiatry.org on Monday, November 19, 2018, IP: 120.188.81.212]
Trivedi: Cognitive deficits in psychiatric disorders: Current status
Kallivayalil, Dr Rajul Tandon, Dr Manisha Mishra, Dr Mohan
Dhyani, Dr Sachin Sharma, Dr Amol Pargaonkar, Dr Anand
Pratap Singh and a very dear friend Shri P.K. Sinha for their
useful suggestions and inputs.
Last, but not the least, I am thankful to all the patients who
participated in the studies conducted by our team.
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J.K. Trivedi Professor
J.K. Trivedi, Department of Psychiatry, King George Medical
University, Lucknow 226006, Uttar Pradesh
e-mail: drjktrivedi@sify.com, drjktrivedi@sancharnet.in,
jktrivedi@hotmail.com, jitendra.trivedi@gmail.com