| Article Access Statistics|
| Viewed||9169 |
| Printed||202 |
| Emailed||10 |
| PDF Downloaded||1092 |
| Comments ||[Add] |
| Cited by others ||5 |
Click on image for details.
D.L.N. MURTHY RAO ORATION
|Year : 2006
: 48 | Issue : 1 | Page
|Cognitive deficits in psychiatric disorders: Current status
Department of Psychiatry, King George Medical University, Lucknow 226006, Uttar Pradesh, India
Click here for correspondence address and
| 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
|How to cite this article:|
Trivedi J K. Cognitive deficits in psychiatric disorders: Current status. Indian J Psychiatry 2006;48:10-20
| Introduction|| |
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.
This oration summarizes the studies investigating cognitive 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, motivation, 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 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. Cognitive deficits may result in the inability to:
- pay attention
- process information quickly
- remember and recall information
- respond to information quickly
- think critically, plan, organize and solve problems
- initiate speech
The following questions need to be addressed in relation to psychiatric disorders and cognitive impairment:
- Is there anything specific about the profile of cognitive impairment in these disorders?
- How do these impairments relate to the underlying psychopathology/neuroanatomy of these disorders?
- Do these cognitive impairments vary over a course of time?
- 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 [Figure - 1]. 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.
| 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.
| 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 schizophrenia 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;
-are relatively stable over time, with progressive deterioration after the age of 65 years in some patients;
-persist on the remission of psychotic symptoms;
-are related to but separate from negative symptoms;,and
-determine the functional impairment characteristics of patients with this disorder.
An important domain of schizophrenia that appears closely related to functional outcome involves cognitive deficits., The range of cognitive deficits is broad and includes problems in perception, attention, memory and problem-solving.
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.,,, WM deficits have been found to correlate significantly with formal thought disorder, and may result in loose association and derailment. Deficits in strategic long-term memory (e.g. free recall, memory for temporal order) could be accounted for by deficits in WM.
Patients with schizophrenia also show deficits in measures of EF., 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. Performance on the measures of executive functioning has been found to be linked to insight of illness, and hence to poor medication compliance, self-injurious behaviour and assaultiveness.,,
Deficits in attention and information processing might be central to schizophrenia because these can contribute to deficits in EF and WM. Attention deficits are also trait and vulnerability markers seen during remission in children of schizophrenic parents and individuals with schizotypal personality. Attention deficits have been found to be robustly associated with deficit syndrome. Distractability has been associated with higher levels of formal thought disorder.
Although there appears to be a group of patients who are impaired only minimally,,, 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.,,
Some deficits including verbal memory and learning, visual memory, abstraction, attention and language abilities have been found even in untreated, first-episode patients.,,,
Cognitive impairments differ according to the clinical symptomatology-the deficits may be related more with disorganized and negative symptoms and less with psychotic symptoms.,,,, 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.[Figure - 2]
| Improving Cognition In Schizophrenia|| |
Newer antipsychotic medications have been shown to have neurocognitive advantages over conventional antipsychotic medications.,,, 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., 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, particularly for WM. Adjunctive pharmacological interventions, with some reported effectiveness include nicotinic treatment for attentional difficulties, tandospirone for memory problems, donepezil,, and NMDA receptor stimulating agents.
Such newer psychopharmacological and neuropsychological 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. 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, sustained attention,, focusingexecution, abstract reasoning and visuomotor skills, verbal memory,, verbal fluency, visuospatial ability, 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.,,,, 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.
| 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., 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.,, There is now substantial evidence that cognition is a good predictor of functional outcome in schizophrenia as well as bipolar-I disorder. 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.,,,
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.,
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 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.
| 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 understanding 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. Recently, cognitive assessments have been performed in bipolar patients when they are euthymic. Studies of this nature aim to identify traitdependent 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. Euthymia is often poorly defined.,
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 epiphenomena.
A high incidence of psychosocial difficulties has been reported during remission, which raises questions about socalled complete recovery. Patients in either acute manic or euthymic states have demonstrated significant impairment on the Stroop test, a test for EF.
Zubeita et al.  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 nonverbal 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 recitation and word list recall 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 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.
| 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.  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.  suggested deficits in the executive control of WM to be a trait deficit. Zalla et al.  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.  found significant impairment on executive and nonverbal 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.,, 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. 
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 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.
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 highrisk 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 neuropsychological deficits in actually depressed patients with verbal and visual memory as well as EF.,, 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. Prominent cognitive disturbances may be one of the presenting symptoms of depression. Drevets et al.  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.
In the acute phase of depression, patients produce more errors of attention compared with matched controls.Austin et al.  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.,
Non-verbal memory has also been reportedly impaired in depressed patients. Implicit non-declarative memory has not been found to be impaired in depressed patients.
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 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.
| 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.,,, These EF deficits may explain partly the performance difficulties seen in patients with OCD in other cognitive domains. Okasha et al.  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.,
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., Savage et al.  indicate that retrieval is also faulty, while storage is intact. Deckersbach et al.  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.,, Patients with OCD demonstrate normal general intelligence and language abilities. Different subtypes of OCD may have varying neuropsychological deficit profiles.
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.
| 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. About 50%-85% of patients with somatoform/ chronic fatigue syndrome (CFS) report cognitive problems, which contribute considerably to their social and occupational dysfunction.,
Studies have revealed that impaired attention- concentration abilities and spatial working memory in patients of somatoform disorder,,, 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.  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 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.
| 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., Burgees revealed a link between attention and memory impairment and self-injury. O'Leary et al.  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.  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.
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., In particular, converging evidence points to a prominent disturbance of EF.,, Various execution functions that have been studied in relation to ADHD are: cognitive flexibility, initiation, interference control, planning and organization, response inhibition, self-monitoring and WM. Further research using cognitive tasks assessing EF in 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.  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.  showed that an explicit memory process may have utility for predicting readiness to change drinking behaviour. Lyvers et al.  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., Deficits exist in novel problem-solving, abstract reasoning, and learning and recalling information., Deficits in perceptual-motor abilities, abstract reasoning, and non-verbal learning and memory can persist for months or years.,, Neuropsychological test findings with substance-dependent populations also might influence the design of treatment programmes.,
| 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 psychopathology 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 achievements 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 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.
| References|| |
|1.||Campbell RJ. Campbell's psychiatric dictionary, 8th ed. Oxford: Oxford University Press 2004; 131. |
|2.||Chan RCK, Chen EYH. Assessment of executive functions for schizophrenia in Hong Kong. Hong Kong J Psychiatry 2005;15:23-8. |
|3.||Goldman-Rakic PS. Working memory dysfunction in schizophrenia. J Neuropsychiatry Clin Neurosci 1994;6: 348-57. [PUBMED] |
|4.||Cummings JL. Frontal-subcortical circuits and human behavior. Arch Neurol 1993;50:873-80. [PUBMED] |
|5.||Crow TJ, Done DJ, Sacker A. Childhood precursors of psychoses as clues to its evolutionary origins. Eur Arch Psychiatry Clin Neurosci 1995;245:61-9. [PUBMED] |
|6.||Friedman JI, Harvey PD, Coleman T, et al. Six-year follow-up study of cognitive and functional status across the lifespan in schizophrenia: A comparison with Alzheimer's disease and normal aging. Am J Psychiatry 2001;158:1441-8. [PUBMED] [FULLTEXT]|
|7.||Heaton RK. Wisconsin Card Sorting Test. Psychological Assessment Resources; 1993. |
|8.||Harvey PD, Lombardi J, Leibman M, et al. Cognitive impairment and negative symptom in geriatric chronic schizophrenic patients: A follow-up study. Schizophr Res 1996;22:223-31. |
|9.||Hughes C, Kumari V, Soni Q, et al. Longitudinal study of symptoms and cognitive function in chronic schizophrenia. Schizophr Res 2002;123:243-55. |
|10.||Green MF. What are the functional consequences of neurocognitive deficits in schizophrenia? Am J Psychiatry 1996;153:321-30. |
|11.||Goldberg TE, Gold GM. Neurocognitive functioning in patients with schizophrenia. In: Bloom FE, Kupfer DJ (eds). Psychopharmacology: The fourth generation of progress. New York: Raven Press; 1995; 1245-57. |
|12.||Green MF, Kern RS, Braff DL, et al. Neurocognitive deficits and functional outcomes in schizophrenia: Are we measuring the right stuff? Schizophr Bull 2000;26:119-36. |
|13.||Green MF. Schizophrenia revealed: From neurons to social interactions. New York: WW Norton; 2001. |
|14.||Stuss DT, Kaplan EF, Bensoon DF, et al. Evidence for the involvement of orbitofrontal cortex in memory functions: An interference effect. J Comp Physiol Psychol 1982;96: 913-25. |
|15.||Bressi S, Miele L, Bressi C, et al. Deficits of central executive component of working memory in schizophrenia. New Trends Exp Clin Psychiatry 1996;12:243-52. |
|16.||Gold JM, Carpenter C, Randolph C, et al. Auditory working memory and Wisconsin Card Sorting Test performance in schizophrenia. Arch Gen Psychiatry 1997;54:159-65. |
|17.||Buchsbaum MS, Hazlett EA. Positron emission tomography studies of abnormal glucose metabolism in schizophrenia. Schizophr Bull 1998;24:343-64. |
|18.||Spitzer M. The psychopathology, neuropsychology, and neurobiology of associative and working memory in schizophrenia. Eur Arch Psychiatry Clin Neurosci 1993;243:57-70. |
|19.||Rochester SR. Are language disorders in acute schizophrenia actually information processing problems? J Psychiatry Res 1978;14:275-83. |
|20.||Stone M, Gabrieti JDE, Stebbins T, et al. Working and strategic memory deficits in schizophrenia. Neuropsychology 1998; 12:278-88. |
|21.||Goldberg TE, Saint-Cry JA, Weinberger DR. Assessment of procedural learning and problem solving in schizophrenia patients by Tower of Hanoi type tasks. J Neuropsychiatry Clin Neurosci 1990;2:165-73. |
|22.||Braff DL, Heaton R, Kuck J, et al. The generalized pattern of neuropsychological deficits in outpatients with chronic schizophrenia with heterogeneous Wisconsin Card Sorting Test results. Arch Gen Psychiatry 1991;48:891-8. |
|23.||Voruganti LN, Heslegrave RJ, Awad AG. Neurocognitive correlates of positive and negative syndromes in schizophrenia. Can J Psychiatry 1997;42:1066-71. |
|24.||Young DA, Davila R, Scher H. Unawareness of illness and neuropsychological performance in chronic schizophrenia. Schizophr Res 1993;10:117-24. |
|25.||Garavan J, Browne S, Gervin M, et al. Compliance with neuroleptic medication in outpatients with schizophrenia: Relationship to subjective response to neuroleptics: Attitudes to medication and insight. Compr Psychiatry 1998;39:215-19. |
|26.||Meltzer HY. Treatment of suicidality in schizophrenia. Ann N Y Acad Sci 2001;932:44-58. |
|27.||Arango C, Calcedo BA, Gonzalez S, et al. Violence in inpatients with schizophrenia: A prospective study. Schizophr Bull 1999;25:493-503. |
|28.||Braff DL. Information processing and attention dysfunctions in schizophrenia. Schizophr Bull 1993;19:233-59. |
|29.||Nuechterlein KH. Childhood precursors of adult schizophrenia. J Child Psychol Psychiatry 1986;27:133-44. |
|30.||Cornblatt BA, Erlenmeyer-Kimling L. Global attentional deviance as a marker of risk for schizophrenia: Specificity and predictive validity. J Abnorm Psychol 1985;94:470-8. |
|31.||Trestman RL, Keefe RS, Mitropoulou V, et al. Cognitive function and biological correlates of cognitive performance in schizotypal personality disorder. Psychiatr Res 1995;59:127-36. |
|32.||Ross DE, Thaker GK, Buchanan RW, et al. Eye tracking disorder in schizophrenia is characterized by specific ocular motor defects and is associated with the deficit syndrome. Biol Psychiatry 1997;42:781-96. |
|33.||Perry W, Braff DL. Information-processing deficits and thought disorder in schizophrenia. Am J Psychiatry 1994;151:363-7. |
|34.||Allen DN, Goldstein G, Warnick E. A consideration of neuropsychologically normal schizophrenia. J Int Neuropsychol Soc 2003;9:56-63. |
|35.||Palmer BW, Heaton RK, Paulsen JS, et al. Is it possible to be schizophrenic yet neuropsychologically normal? Neuropsychology 1997;11:437-46. |
|36.||Silverstein ML, Zerwic MJ. Clinical psychopathologic symptoms in neuropsychologically impaired and intact schizophrenics. J Consult Clin Psychol 1985;53:267-8. |
|37.||Saykin AJ, Gur RC, Gur R, et al. Neuropsychological function in schizophrenia: Selective impairment in memory and learning. Arch Gen Psychiatry 1991;48:618-24. |
|38.||Goldberg TE, Weinberger DR, Berman KF, et al. Further evidence for dementia of the prefrontal type in schizophrenia? Arch Gen Psychiatry 1987;44:1008-14. |
|39.||Cirillo MA, Seidman LJ. Verbal declarative memory dysfunction in schizophrenia: From clinical assessment to genetics and brain mechanisms. Neuropsychol Rev 2003;13:43-77. |
|40.||Censits DM, Ragland JD, Gur RC, et al. Neuropsychological evidence supporting a neurodevelopmental model of schizophrenia: A longitudinal study. Schizophr Res 1997;24:289-98. |
|41.||Saykin AJ, Shtasel DL, Gur RE, et al. Neuropsychological deficits in neuroleptic naive patients with first-episode schizophrenia. Arch Gen Psychiatry 1994;51:124-31. |
|42.||Lussier I, Stip E. Memory and attention deficits in drug naive patients with schizophrenia. Schizophr Res 2001;48:45-55. |
|43.||Schuepbach D, Keshavan MS, Sweeney JA. Selective attention in neuroleptic-naive first-episode schizophrenia: A two-year follow up. Biol Psychiatry 2002;51:118S-19S. |
|44.||Bilder RM, Goldman RS, Robinson D, et al. Neuropsychology of first-episode schizophrenia: Initial characterization and clinical correlates. Am J Psychiatry 2000;157:549-59. |
|45.||Liddle PF. Schizophrenic syndrome, cognitive performance, and neurological dysfunction. Psychol Med 1987;17:49-57. |
|46.||Brazo P, Marie RM, Halbecq I, et al. Cognitive patterns in subtypes of schizophrenia. Eur Psychiatry 2002; 17:155-62. |
|47.||Frith CD, Leary J, Cahill C, et al. Performance on psychological tests: Demographic and clinical correlates of these results. Br J Psychiatry 1991;159:26-9. |
|48.||O'Leary DS, Flaum M, Kesler ML, et al. Cognitive correlates of the negative, disorganized, and psychotic symptom dimensions in schizophrenia. J Neuropsychiatry Clin Neurosci 2000;12:4-15. |
|49.||Purdon SE. Cognitive improvement in schizophrenia with novel antipsychotic medications. Schizophr Res 1999;35:S51-S60. |
|50.||Harvey PD, Keefe RSE. Studies of cognitive change in patients with schizophrenia following novel antipsychotic treatment. Am J Psychiatry 2001;158:176-84. |
|51.||Keefe RSE, Silva SG, Perkins DO, et al. The effects of atypical antipsychotic drugs on neurocognitive impairment in schizophrenia: A review and meta-analysis. Schizophr Bull 1999;25:201-22. |
|52.||Meltzer HY, McGurk SR. The effect of clozapine, risperidone, and olanzapine on cognitive function in schizophrenia. Schizophr Bull 1999;25:233-55. |
|53.||Bilder RM, Goldman RS, Volavka J, et al. Neurocognitive effects of clozapine, olanzapine, risperidone, and haloperidol in patients with chronic schizophrenia or schizoaffective disorder. Am J Psychiatry 2002;159:1018-28. |
|54.||Sharma T, Antonova L. Cognitive function in schizophrenia. Deficits, functional consequences, and future treatment. Psychiatr Clin North Am 2003;26:26-40. |
|55.||Kurtz MM, Moberg PJ, Gur RC, et al. Approaches to cognitive remediation of neuropsychological deficits in schizophrenia: A review and meta-analysis. Neuropsychol Rev 2001;11:197-210. |
|56.||Galletly CA, Clark CR, MacFarlane AC. Treating cognitive dysfunction in patients with schizophrenia [comment]. J Psychiatry Neurosci 2000;25:117-24. |
|57.||Levin ED, Rezvani AH. Nicotinic treatment for cognitive dysfunction. Curr Drug Target CNS Neurol Disord 2002;1: 423-31. |
|58.||Sumiyoshi T, Matsui M, Yamashita I, et al. The effect of tandospirone, a serotonin (1A) agonist, on memory function in schizophrenia. Biol Psychiatry 2001;49:861-8. |
|59.||Buchanan RW, Summerfelt A, Tek C, et al. An open-labeled trial of adjunctive donepezil for cognitive impairments in patients with schizophrenia. Schizophr Res 2003;59:29-33. |
|60.||Friedman JI, Alder DN, Howanitz E, et al. A double blind placebo controlled trial of donepezil adjunctive treatment to risperidone for the cognitive impairment of schizophrenia. Biol Psychiatry 2002;51:349-57. |
|61.||MacEwan GW, Ehmann TS, Khanbhai I, et al. Donepezil in schizophrenia-is it helpful? An experimental design case study. Acta Psychiatr Scand 2001;104:469-72. |
|62.||File SE, Fluck E, Fernandes C. Beneficial effects of glycine (bioglycine) on memory and attention in young and middleaged adults. J Clin Psychopharmacol 1999;19:506-12. |
|63.||Rabins PV, Merchant A. Criteria for diagnosing reversible dementia caused by depression: Validation by 2-year follow up. Br J Psychiatry 1984;144:488-92. |
|64.||Ferrier IN, Stanton BR, Kelly TP, et al. Neuropsychological function in euthymic patients with bipolar disorder. Br J Psychiatry 1999;175:246-51. |
|65.||Clark LD, Iversen SD, Goodwin G. Sustained attention deficit in bipolar disorder. Br J Psychiatry 2002;180:313-19. |
|66.||Harmer CJ, Clark L, Grayson L, et al. Sustained attention deficit in bipolar is not a working memory impairment in disguise. Neuropsychologia 2002;40:1586-90. |
|67.||Jones BP, Duncan CC, Mirsky AF, et al. Neuropsychological profiles in bipolar affective disorder and complex partial seizure. Neuropsychology 1994;8:55-64. |
|68.||Ali SO, Denicoff KD, Altshuler LL, et al. A preliminary study of the relation of neuropsychological performance to neuroanatomic structures in bipolar disorder. Neuropsychiatry Neuropsychol Behav Neurol 2000;13:20-8. |
|69.||Van Gorp WG, Altshuler L, Theberge DC, et al. Declarative and procedural memory in bipolar disorder. Biol Psychiatry 1999;46:525-31. |
|70.||Van Gorp WG, Altshuler L, Theberge DC, et al. Cognitive impairment in euthymic bipolar patients with and without prior alcohol dependence. Arch Gen Psychiatry 1998;55:41-6. |
|71.||Lebowitz BK, Shear PK, Steed MA, et al. Verbal fluency in mania: Relationship to number of manic episodes. Neuropsychiatry Neuropsychol Behav Neurol 2001;14:177-82. |
|72.||Sapin LR, Berrettini WH, Nurnberger JI Jr, et al. Mediational factors underlying cognitive changes and laterality in affective illness. Biol Psychiatry 1987;22: 979-86. |
|73.||El-Badri SM, Ashton CH, Moore PB, et al. Electrophysiological and cognitive function in young euthymic patients with bipolar affective disorder. Bipolar Disord 2001;3:79-87. |
|74.||Denicoff KD, Ali SO, Mirsky AF, et al. Relationship between prior course of illness and neuropsychological functioning in patients with bipolar disorder. J Affect Disord 1999;56:67-73. |
|75.||Clark LD, Iversen SD, Goodwin G. A neuropsychological investigation of prefrontal cortex involvement in acute mania. Am J Psychiatry 2001;158:1605-11. |
|76.||Cavanagh JTO, Van Beck M, Muir W, et al. Case-control study of neurocognitive function in euthymic patients with bipolar disorder: An association with mania. Br J Psychiatry 2002;180:320-6. |
|77.||Bramon E, Shan PC. One common genetic liability between schizophrenia and bipolar disorder: A review. Curr Psychiatry Rep 2001;3:332-7. |
|78.|| Berrettini WH. Are schizophrenic and bipolar disorders related? A review of family and molecular studies. Biol Psychiatry 2000;48:531-8. |
|79.|| Bearden CE, Hoffman KM, Cannon TD. The neuropsychology and neuroanatomy of bipolar affective disorder: A critical review. Bipolar Disord 2001;3:106-50. |
|80.|| Martinez-Aran A, Penades R, Vieta E, et al. Executive function in patients with remitted bipolar disorder and schizophrenia and its relationship with functional outcome. Psychother Psychosom 2002;71:39-46. |
|81.|| Seidman LJ, Kremen WS, Koren D, et al. A comparative profile analysis of neuropsychological functioning in patients with schizophrenia and bipolar psychoses. Schizophr Res 2002; 53:31-44. |
|82.|| Neu P, Kiesslinger U, Schlattmann P, et al. Time-related cognitive deficiency in four different types of depression. Psychiatry Res 2001;103:237-47. |
|83.|| Dickerson FB, Sommerville J, Origoni AE, et al. Outpatients with schizophrenia and bipolar I disorder: Do they differ in their cognitive and social functioning. Psychiatry Res 2001; 102:21-7. |
|84.|| Borkowska A, Rybakwwski JK. Neuropsychological frontal lobe tests indicate that bipolar depressed patients are more impaired than unipolar. Bipolar Disord 2001;3:88-94. |
|85.|| Trivedi JK, Tandon R, Singh AP, et al. Neurocognitive functions in patients with stable schizophrenia and euthymic state of bipolar disorder: A comparative study. Poster presentation at 'Regional and Intersectional Congress of the World Psychiatric Association', 12-15 March 2005, Athens, Greece. |
|86.||Wolder-Willis KE, Sax KW, Rosenberg HL, et al. Persistent attentional dysfunction in remitted bipolar disorder. Bipolar Disord 2001;3:58-62. |
|87.|| Paradiso S, Lamberty GJ, Gravey MJ, et al. Cognitive impairment in euthymic phase of chronic unipolar depression. J Nerv Ment Dis 1997;185:718-54. |
|88.|| Zubieta JK, Huguelet P, O'Neil RL, et al. Cognitive function in euthymic bipolar I disorder. Psychiatry Res 2001;102:9-20. |
|89.|| Trivedi JK, Tandon R, Singh AP, et al. Neurocognitive functions in remitted patients of bipolar I disorder. Bipolar Disord 2004;6:29. |
|90.|| Keri S, Kelemen O, Benedak G, et al. Different trait markers for schizophrenia and bipolar disorder: A neurocognitive approach. Psychol Med 2001;31:915-22. |
|91.|| Chowdhury R, Ferrier IN, Thompson HM. Cognitive dysfunction in bipolar disorder. Curr Opin Psychiatry 2003;16:7-12. |
|92.|| Zalla T, Joyce C, Szoke A, et al. Executive dysfunctions as potential markers of familial vulnerability to bipolar disorder and schizophrenia. Psychiatry Res 2004;121:207-17. |
|93.|| McDonough-Ryan P, DelBello M, Shear PK, et al. Academic and cognitive abilities in children of parents with bipolar disorder: A test of the nonverbal learning disability model. J Clin Exp Neuropsychol 2002;24:280-5. |
|94.|| Kremen WS, Faraone SV, Seidman LJ, et al. Neuropsychological risk factors for schizophrenia: A preliminary study of female relatives of schizophrenic and bipolar probands. Psychiatry Res 1998;79:227-40. |
|95.|| Gilvarry C, Takei N, Russell A, et al. Premorbid IQ in patients with functional psychosis and their first degree relatives. Schiz Res 2000;41:417-29. |
|96.|| McNeil TF, Schubert EW. Do schizophrenia and bipolar disorder belong to the same neurobiological continuum? Neurodeviation in high-risk offspring form birth to adulthood. Schiz Res 2003;60:22. |
|97.|| Savitz J, Solms M, Ramesar R. Neuropsychological dysfunction in bipolar affective disorder: A critical opinion. Bipolar Disord 2005;7:216-35. |
|98.|| Trivedi JK, Sharma S, Tandon R, et al. Neurocognitive functions in healthy first degree relatives of bipolar affective disorder: A study from Northern India. Presented in 'Evolving trends in Psychiatry' at Malaysia, 23-25 June 2005. |
|99.|| Muller WR. Psychological deficit in depression. Psychol Bull 1975;82:238-60. |
|100.|| Elliot R, Baker SC, Rogers RD, et al. Prefrontal dysfunction in depressed patients performing a complex planning task: A study using positron emission tomography. Psychol Med 1997; 27:931-42. |
|101.|| Elliot R, Sahakian BJ, McKay AP, et al. Neuropsychological impairments in unipolar depression: The influence of perceived failure on subsequent performance. Psychol Med 1996;26: 975-89. |
|102.|| Austin MP, Mitchell P, Wilhelm K, et al. Cognitive function in depression: A distinct pattern on frontal impairment in melancholia. Psychol Med 1999;29:73-85. |
|103.|| Drevets WC, Price JL, Simpson JR. Subgenual prefrontal cortex abnormalities detected in bipolar affective disorder using MRI. Arch Gen Psychiatry 1997;47:55-9. |
|104.|| Brand N, Jolles J. Information processing in depression and anxiety. Psychol Med 1987;17:145-53. |
|105.|| Austin MP, Ross M, Murray C, et al. Cognitive function in major depression. J Affect Disord 1992;26:127-37. |
|106.|| Calev A, KorinY, Shapira B, et al. Verbal and non-verbal recall by depressed and euthymic affective patients. Psychol Med 1986;16:789-94. |
|107.|| Ilsley JE, Moffoot AP. An analysis of memory dysfunction in major depression. J Affect Disord 1995;35:1-9. |
|108.|| Trivedi JK, Tandon R, Singh AP, et al. Executive functions in depression: A clinical report. Indian J Psychiatry 2002;44: 343-7. |
|109.|| Savage CR, Baer L, Keuthen NJ, et al. Organizational strategies mediate non-verbal memory impairment in obsessive- compulsive disorder. Biol Psychiatry 1999;45:905-16. |
|110.|| Behar D, Rapoport JL, Berg CJ, et al. Computerized tomography and neuropsychological test measure in adolescents with obsessive-compulsive disorder. Am J Psychiatry 1984;141: 363-8. |
|111.|| Aronowitz BR, Hollander E, DeCaria C, et al. Neuropsychology obsessive-compulsive disorder: Preliminary findings. Neuropsychiatr Neuropsychol Behav Neurol 1994;7:81-6. |
|112.|| Dirson S, Bouvard M, Cottraux J, et al. Visual memory impairment in patients with obsessive-compulsive disorder: A controlled study. Psychother Psychosom 1995;63:22-31. |
|113.|| Savage CR. Neuropsychology of subcortical dementias. Psychiatr Clin North Am 1997;20:911-31. |
|114.|| Okasha A, Rafaat M, Mahallawy N, et al. Cognitive dysfunction in obsessive-compulsive disorder. Acta Psychiatr Scand 2000;101:281-5. |
|115.|| Christensen KJ, Kim SW, Dysken MW, et al. Neuropsychological performance in obsessive-compulsive disorder. Biol Psychiatry 1992;31:4-18. |
|116.||Cohen LJ, Hollander E, DeCaria CM, et al. Specificity of neuropsychological impairment in obsessive-compulsive disorder. J Neuropsychiatry Clin Neurosci 1996;8:99-103. |
|117.||Savage CR, Keuthen NJ, Jenike MA, et al. Recall and recognition memory in obsessive-compulsive disorder. J Neuropsychiatry Clin Neurosci 1996;8:99-103. |
|118.||Deckersbach T, Savage CR, Curran T, et al. A study of parallel implicit and explicit information processing in obsessive- compulsive disorder. Am J Psychiatry 2002;159:1780-2. |
|119.||Boone KB, Ananth J, Philpott L, et al. Neuropsychological characteristics of non-depressed adults with obsessive-compulsive disorder. Neuropsychiatry Neuropsychol Behav Neurol 1991;4:96-109. |
|120.||Zielinski CM, Taylor MA, Juzwin KR. Neuropsychological deficits in obsessive-compulsive disorder. Neuropsychiatry Neuropsychol Behav Neurol 1991;4:110-26. |
|121.||Malloy P. Frontal lobe dysfunction in obsessive-compulsive disorder. In: Perecman E (ed). The frontal lobes revisited. New York: The IRBN Press; 1987:207-23. |
|122.||Trivedi JK, Sharma S, Tandon R, et al. Neurocognitive functions in the patients of obsessive compulsive disorder. Poster presentation at XIII World Congress of Psychiatry, Cairo, Egypt, 10-15 September 2005. |
|123.||Barrows DM. Functional capacity evaluation of persons with chronic fatigue immune dysfunction syndrome. Am J Occup Ther 1995;49:327-37. |
|124.||Kamaroff AL, Buchwald D. Symptoms and signs of CFS. Rev Infect Dis 1991;13 (Suppl. 1):8-11. |
|125.||Abbey SE, Garfenkel PE. Chronic fatigue syndrome and depression: Cause, effect, or covariate. Rev Infect Dis 1991;13 (Suppl. 1):73-83. |
|126.||Stuss DT, Shallice T, Alexander MP, et al. A multidisciplinary approach to anterior attentional function. Ann NY Acad Sci 1995;769:191-211. |
|127.||Michiels V, Cluydts R, Fichler B, et al. Cognitive functioning in patients with chronic fatigue syndrome. J Clin Exp Neuropsychol 1996;18:666-77. |
|128.||Kane RL, Gantz NM, Dipino RK. Neuropsychological and psychological functioning in CFS. Neuropsyhciatr Neuropsychol Behav Neurol 1997;10:25-31. |
|129.||Vollmer Conna UTE, Wakefield D, Lloyd A, et al. Cognitive deficits in patients suffering from chronic fatigue syndrome, acute infective illness or depression. Br J Psychiatry 1997; 171:377-81. |
|130.||Niemi PM, Portin R, Aalto S, et al. Cognitive functioning in severe somatization: A pilot study. Acta Psychiatr Scand 2002;106:461-3. |
|131.||Trivedi JK, Tandon R, Singh AP. Neurocognitive functions in patients of somatoform disorder. Poster presentation at VIII World Congress of Biological Psychiatry, 28 June-3 July 2005, Vienna, Austria. Submitted for publication in Hong Kong J Psychiatry, 2005. |
|132.||O'Leary KM, Brouwers P, Gardner DL. Neuropsychological testing of patients with borderline personality disorder. Am J Psychiatry 1991;148:106-11. |
|133.||Bazanis E, Rogers RD, Dowson P. Neurocognitive deficits in decision-making and planning of patients with DSM-III-R borderline personality disorder. Psychol Med 2002;32: 1395-405. |
|134.||Burgees JW. Relationship of depression and cognitive impairment to self-injury in borderline personality disorder, major depression, and schizophrenia. Psychiatry Res 1991;38:77-87. |
|135.||Paris J, Zelkowitz P, Guzder J, et al. Neuropsychological factors associated with borderline pathology in children. J Am Acad Child Adolesc Psychiatry 1999;38:770-4. |
|136.||Woods SP, Lovejoy DW, Ball JD. Neuropsychological characteristics of adults with ADHD: A comprehensive review of initial studies. Clin Neuropsychol 2002;16:12-34. |
|137.||Murphy KR, Barkley RA, Bush T. Executive functioning and olfactory identification in young adults with attention-deficit/ hyperactive disorder. Neuropsychology 2001;15:211-20. |
|138.||Seidman LJ, Biederman J, Faraone SV, et al. Toward defining a neuropsychology of attention-deficit/hyperactivity disorder: Performance of children and adolescents from a large clinically referred sample. J Consult Clin Psychol 1997;65:150-60. |
|139.||Shallice T, Marzocchi GM, Coser S, et al. Executive function profile of children with attention-deficit/hyperactivity disorder. Dev Neuropsychol 2002;21:43-71. |
|140.||Prochaska JO, Dectemente CC. Transtheoretical therapy: Towards a more integrative model of change. Psychotherapy, Theory, Research and Practice 1982;19:276-88. |
|141.||Blume AW, Schmaling KB, Marlatt GA. Memory, executive cognitive function and readiness to change drinking behaviour. Addict Behav 2005;30:301-14. |
|142.||Lyvers M, Yakeimoff M. Neuropsychological correlate of opioid dependence and withdrawal. Addict Behav 2003;28: 605-11. |
|143.||Fals-Stewart W, Schafer J, Lucente S, et al. Neurobehavioural consequences of prolonged alcohol and substance abuse: A review of findings and treatment implications. Clin Psychol Rev 1994;14:775-88. |
|144.||Rourke SB, Lorberg T. The neurobehavioural correlates of alcoholism. In: Grand I, Adams KM (eds) Neuropsychological assessment of neuropsychiatric disorders. 2nd ed. New York: Guilford; 1998:423-85. |
|145.||Allen DN, Landis RKB. Neuropsychological correlates of substance use disorders. In: Snyder PJ, Nassbaum PD (eds). Clinical neuropsychology: A pocket handbook for assessment. Washington (DC): American Psychological Association; 1998: 591-612. |
|146.||Bates ME, Bowden SC, Barry D. Neurocognitive impairment associated with alcohol use disorders: Implications for treatment. Exp Clin Psychopharmacol 2002;10:193-212. |
|147.||Goldman MS. Experience-dependent neuropsychological recovery and the treatment of chronic alcoholism. Neuropsychol Rev 1990;1:75-101. |
|148.||Mc Crady BS, Smith DE. Implications of cognitive impairment for treatment of alcoholism. Alcohol Clin Exp Res 1986;10: 145-9. |
J K Trivedi
Department of Psychiatry, King George Medical University, Lucknow 226006, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
[Figure - 1], [Figure - 2]
|This article has been cited by|
||Family-based association study of the arsenite methyltransferase gene (AS3MT, rs11191454) in Korean children with attention-deficit hyperactivity disorder
| ||Subin Park,Jong-Eun Park,Hee Jeong Yoo,Jae-Won Kim,Soo-Churl Cho,Min-Sup Shin,Jae Hoon Cheong,Doug Hyun Han,Bung-Nyun Kim |
| ||Psychiatric Genetics. 2015; 25(1): 26 |
|[Pubmed] | [DOI]|
||Is cognitive impairment associated with suicidality? A population-based study
| ||Elvira Lara,Beatriz Olaya,Noé Garin,Jose Luis Ayuso-Mateos,Marta Miret,Victoria Moneta,Josep Maria Haro |
| ||European Neuropsychopharmacology. 2014; |
|[Pubmed] | [DOI]|
||Neuropsychological impairments in panic disorder: a systematic review
| ||Kate OæSullivan,Emily F. Newman |
| ||Journal of Affective Disorders. 2014; |
|[Pubmed] | [DOI]|
||Neuronal substrates and functional consequences of prenatal cannabis exposure
| ||Daniela Calvigioni,Yasmin L. Hurd,Tibor Harkany,Erik Keimpema |
| ||European Child & Adolescent Psychiatry. 2014; |
|[Pubmed] | [DOI]|
||Cognitive deficits in schizophrenia
| ||S Chattopadhyay,RB Nayak,NM Patil,SS Chate |
| ||Journal of the Scientific Society. 2012; 39(2): 57 |
|[Pubmed] | [DOI]|