Neuropsychological profile in patients with schizotypal personality disorder or schizophrenia

Neuropsychological impairments have been consistently reported in patients with schizophrenia. As little is known whether subjects with schizotypal personality disorder exhibit neurocognitive dysfunction similar to that in schizophrenia, we assessed the neuropsychological profile of 15 subjects with schizotypal personality disorder and compared it with that for 15 patients with schizophrenia and for 15 psychiatrically normal volunteers. All participants were administered a standard neuropsychological battery assessing language ability, spatial ability, visuomotor function, verbal memory, visual memory, auditory attention, visual attention, and executive function. Performance on most of the cognitive domains was impaired in patients with schizotypal personality disorder but less than patients with schizophrenia. Specifically, impairment in verbal memory and visuomotor ability in patients with schizotypal personality disorder and patients with schizophrenia were comparable, while patients with schizophrenia performed worse on the test of executive function than did patients with schizotypal personality disorder. As a whole, cognitive deficits in patients with schizotypal personality disorder were qualitatively similar to, but quantitatively milder than, those for patients with schizophrenia. The results suggest that cognitive abilities related to frontotemporal lobe function are disturbed across these schizophrenia-spectrum disorders.     

Turning it Upside Down: Areas of Preserved Cognitive Function in Schizophrenia

Patients with schizophrenia demonstrate marked impairments on most clinical neuropsychological tests. These findings suggest that patients suffer from a generalized form of cognitive impairment, with little evidence of spared performance documented in several large meta-analytic reviews of the clinical literature. In contrast, we review evidence for relative sparing of aspects of attention, procedural memory, and emotional processing observed in studies that have employed experimental approaches adapted from the cognitive and affective neuroscience literature. These islands of preserved performance suggest that the cognitive deficits in schizophrenia are not as general as they appear to be when assayed with clinical neuropsychological methods. The apparent contradiction in findings across methods may offer important clues about the nature of cognitive impairment in schizophrenia. The documentation of preserved cognitive function in schizophrenia may serve to sharpen hypotheses about the biological mechanisms that are implicated in the illness.     

Optimizing treatment of schizophrenia. Enhancing affective/cognitive and depressive functioning

Recognition and treatment of schizophrenia has largely focused on positive symptoms of the disorder, such as delusions, hallucinations, and disorganization. However, other important symptoms, such as depression, cognition, and social functioning, have not received comparable attention. Fifty percent of schizophrenic patients suffer from comorbid depression, which is a major risk factor for suicide in this population, while 10% to 25% suffer from comorbid obsessive-compulsive disorder. Cognitive deficits commonly observed in patients with schizophrenia include problems with concentration, attention, and memory, as well as problem-solving and verbal skills. These deficits are observed at early stages of the illness and can predict deficits in functional capabilities, such as occupational and social skills, educational attainment, and the ability to live independently. The severity of such impairments affects all patient in this population, including up to 10% of patients working full time and up to one third of those working part time. In light of the debilitating effects of depression, cognitive impairment, and other aspects of affective functioning on the quality of life of patients with schizophrenia, physicians need to partner with their patients to address these concerns and determine an appropriate treatment regimen. This can be done with simple functional-based cognitive questioning, the use of evidence-based psychosocial practices, and psychoeducation on the many pharmacotherapeutic options. It is recommended that depressive or suicidal symptoms of schizophrenia be treated with an antidepressant or mood stabilizer only if the symptoms have not subsided after treatment of the psychosis with an atypical antipsychotic. Additionally, relative to older medications, atypicals have demonstrated benefit in improving some of the cognitive impairments.     

Cognitive deficits in major depression

Major depression is a mood disorder that is often accompanied by the impairment of cognitive functions. Although suggestive, the large range of existing neuropsychological, neuropsychiatric, and, lately, neuroimaging investigations have not yet given a consistent picture of the psychological and biological disturbances involved in this psychiatric disorder. The present study of the cognitive functions in depression was part of an extensive investigation, including neuropsychological testing, psychiatric examination, and neuroimaging. A representative sample of 40 severely depressed hospitalized patients and a group of 49 closely matched control subjects were tested with an extensive neuropsychological test battery. Results, corrected for various confounding factors, confirmed the current notion that depressed patients suffer from wide-spread cognitive impairments. The group analysis did not allow any hypothesis on a possible pattern to the dysfunctions, but heterogeneity in the test performances calls for further analysis of the data in patient subgroups in relation to neuroimaging results.     

CANTAB explicit memory is less impaired in addicted schizophrenia patients

It has been suggested that in order to sustain the lifestyle of substance abuse, addicted schizophrenia patients would have less negative symptoms, better social skills, and less cognitive impairments. Mounting evidence supports the first two assumptions, but data lack regarding cognition in dual diagnosis schizophrenia. Seventy-six schizophrenia outpatients (DSM-IV) were divided into two groups: with (n = 44) and without (n = 32) a substance use disorder. Motor speed and visuo-spatial explicit memory were investigated using CANTAB. As expected, dual diagnosis patients showed a better cognitive performance. Our results suggest either that substance abuse relieves the cognitive deficits of schizophrenia or that the patients with less cognitive deficits are more prone to substance abuse.     

Neuropsychological profile and neuroimaging in patients with 22Q11.2 Deletion Syndrome: a review.

22q11.2 Deletion Syndrome is associated with cognitive, behavioural, and psychiatric problems and is known to affect brain structure. Recently, 22q11.2 Deletion Syndrome has been proposed as a disease model for a genetic subtype of schizophrenia. In this paper we discuss the currently available literature on neurocognitive functioning and brain anatomy in patients with 22q11.2 Deletion Syndrome, and how this contributes to our understanding of the neurobiology of schizophrenia. Research on cognitive functioning in 22q11.2 Deletion Syndrome patients suggests a specific cognitive profile with impairments on arithmetical, visuo-spatial, and executive tasks and relatively preserved language skills. Prominent findings of neuroimaging studies in 22q11.2 Deletion Syndrome patients are: reduction of overall brain volume, midline defects, structural alterations of cerebellum and frontal lobe, white matter abnormalities, and decreased grey matter volumes in parietal and temporal areas. We describe how brain abnormalities in patients with 22q11.2 Deletion Syndrome may contribute to the understanding of the clinical syndrome including cognitive impairments, psychotic symptoms, and social and communication problems.     

Episodic Memory in Schizophrenia

Episodic memory impairments in individuals with schizophrenia have been well documented in the literature. However, despite the abundance of findings, constituent cognitive, neural, behavioral, and genetic components of the deficits continue to elude full characterization. This review provides a characterization of these deficits by organizing findings within three frameworks of interest: 1) neuroanatomical; 2) genetic; and 3) behavioral. Within each approach, evidence from imaging studies as well as behavioral studies is examined. The hope is that by synthesizing the cognitive science paradigms, molecular genetic neurophysiological findings, and computational algorithms applied to medial temporal lobe subregions, we will be able to expand our understanding of the types of compromises in episodic memory systems of individuals with schizophrenia.     

The posterior parietal paradox: Why do functional magnetic resonance imaging and lesion studies on episodic memory produce conflicting results?

Recent functional magnetic resonance imaging (fMRI) studies addressing healthy subjects point towards posterior parietal cortex (PPC) involvement in episodic memory tasks. This is noteworthy, since neuropsychological studies usually do not connect parietal lesions to episodic memory impairments. Therefore an inventory of the possible factors behind this apparent paradox is warranted. This review compared fMRI studies which demonstrated PPC activity in episodic memory tasks, with findings with studies of patients with PPC lesions. A systematic evaluation of possible explanations for the posterior parietal paradox indicates that PPC activation in fMRI studies does not appear to be attributable to confounding cognitive/psychomotor processes, such as button pressing or stimulus processing. What may be of more importance is the extent to which an episodic memory task loads on three closely related cognitive processes: effort and attention, self‐related activity, and scene and image construction. We discuss to what extent these cognitive processes can account for the paradox between lesion and fMRI results. They are strongly intertwined with the episodic memory and may critically determine in how far the PPC plays a role in a given memory task. Future patient studies might profit from specifically taking these cognitive factors into consideration in the task design.     

Measuring emotion recognition: Added value in diagnosing dementia of the Alzheimer’s disease type

Neuropsychological tests, particularly for episodic memory, are used to classify patients in memory clinics. Still, the differential diagnosis between dementia of the Alzheimer’s disease type (Dementia-AD), mild cognitive impairment (MCI), or major depressive disorder (MDD) is challenging. However, impairments in other domains, such as emotion recognition, an aspect of social cognition, might have additional value in distinguishing Dementia-AD from MCI and MDD and hence signal progression of neurodegeneration. We evaluated this in patients visiting a memory clinic. Sixty healthy controls (HC) and 143 first time attendants of an academic hospital memory clinic who were eventually classified as Dementia-AD (n = 45), MCI (n = 47), MDD (n = 27), or No Impairment (NI, n = 24) were included. We assessed group differences in Emotion Recognition (Ekman 60 Faces Test (EFT)) and episodic memory (Dutch Rey Auditory Verbal Learning Test (RAVLT)). With multinomial and binomial regression analysis, we assessed whether EFT was added to RAVLT in distinguishing patient groups. Dementia-AD patients had significantly worse emotion recognition than HC, MCI, MDD, and NI groups, but no other between-group differences were found. Episodic memory was impaired in Dementia-AD and MCI patients. We found no memory impairments in the MDD and NI groups. Emotion recognition in addition to episodic memory was significantly better in predicting group membership than episodic memory alone. In conclusion, emotion recognition measurement had added value for differentiation between patients first visiting memory clinics, in particular in distinguishing Dementia-AD from MCI. We recommend the standard inclusion of emotion recognition testing in neuropsychological assessment in memory clinics.     

Neuropsychology,genetic liability,and psychotic symptoms in those at high risk of schizophrenia

Neuropsychological assessments were compared among individuals at enhanced genetic risk of schizophrenia (n = 157) and controls (n = 34). The relationship between cognitive impairments and the presence of psychotic symptoms and measures of genetic risk was explored in the high-risk subjects. Neuropsychological differences were identified in many areas of function and were not accounted for by the presence of psychotic symptoms. Genetic liability was not associated with neuropsychological performance or with psychotic symptoms, but exploratory analysis showed some tests were associated with both liability measures. These results suggest that what is inherited is not the disorder itself but a state of vulnerability manifested by neuropsychological impairment, occurring in many more individuals than are predicted to develop the disorder.     

Schizophrenia, ketamine and cannabis: evidence of overlapping memory deficits

Drug models of mental illness are considered useful if they provoke its characteristic symptoms. In this respect, ketamine and tetrahydrocannabinol (cannabis) are coming under increasing scrutiny as models for schizophrenia. However, although both undoubtedly produce psychotic symptoms characteristic of the disorder, we argue here that, because schizophrenia is also accompanied by cognitive deficits, a full understanding of the impact of these drugs on cognition will be crucial in taking these models further. Memory deficits are pronounced in schizophrenia and we focus upon patterns of working and episodic memory impairment produced by ketamine and cannabis, identifying overlaps between drug and illness. We suggest that close attention to these deficits can offer insights into core pathophysiology of schizophrenia.     

Frontal lobe dysfunctions in borderline personality disorder? Neuropsychological findings

This study aims to determine whether specific neuropsychological performance impairments in borderline patients can be objectified and whether these findings indicate frontal dysfunctions. Twenty-three patients with borderline personality disorder and 23 normal controls were examined using a neuropsychological test battery to assess intelligence, attentiveness, proneness to interference, learning and memory, as well as planning and problem solving. All subjects filled out standardized questionnaires to assess aggressiveness and impulsiveness in the context of these cognitive performance areas. The neuropsychological test results of the borderline patients were comparable to those of the controls. Although there were no indications of frontal dysfunction of cognitive information processing, inverse correlations were found between the severity of borderline-related personality traits regarding impulsiveness and various areas of cognitive performance. Borderline personality patients show no indications of frontal cognitive dysfunction. Further research is needed to clarify the relationship between impulsiveness and cognitive information processing in borderline personality disorder, including a dimensional approach to personality and personality disorder.     

Psychogenic amnesia – A malady of the constricted self

Autobiographical–episodic memory is the conjunction of subjective time, autonoetic consciousness and the experiencing self. Understanding the neural correlates of autobiographical–episodic memory might therefore be essential for shedding light on the neurobiology underlying the experience of being an autonoetic self. In this contribution we illustrate the intimate relationship between autobiographical–episodic memory and self by reviewing the clinical and neuropsychological features and brain functional imaging correlates of psychogenic amnesia – a condition that is usually characterized by severely impaired retrograde memory functioning, in absence of structural brain damage as detected by standard imaging. We demonstrate that in this disorder the autobiographical–episodic memory deficits do not exist in isolation, but occur with impairments of the autonoetic self-consciousness, emotional processing, and theory of mind or executive functions. Furthermore functional and metabolic brain alterations involving regions that are agreed upon to exert crucial roles in memory processes were frequently found to accompany the psychogenic memory “loss”.     

The Impact of Neuropsychological Deficits on Functional Stroke Outcomes

This review examines the available literature on neuropsychological outcomes of stroke and the literature on the ability of specific areas of neuropsychological deficit to predict functional stroke outcome. The literature reviewed indicates that post-stroke deficits in executive function, memory, language, and speed of processing are common, with those identified as having progressive ‘post-stroke dementia’ presenting with a similar, though more impaired profile, with increased impairments particularly noted in the area of memory. It is clear that some aspects of neuropsychological functioning (e.g., presence of neglect, aphasia, anosognosia; and verbal memory and attention deficits) show promise as a means of predicting post-stroke functional outcomes. Examining the available literature, it becomes evident that there is a need for long-term, large scale (i.e., population based) follow-up studies, evaluating likely long-term neuropsychological outcomes of stroke and their prognostic utility.     

Cognitive impairments and disordered speech in schizophrenia: thought disorder, disorganization, and communication failure perspectives

This article posits that basic cognitive impairments in schizophrenia are more highly related to speech disorder measured as communication failures than speech disorder measured as thought disorder or disorganization. The author tested 47 schizophrenia patients and 36 control participants for sustained attention, sequencing, and conceptual sequencing ability. Their speech was also rated for communication failures, thought disorder, and conceptual disorganization. Attention and sequencing impairments, examined hierarchically, explained a substantial 38% of the variance in the communication measure of speech disorder but little of the variance in formal thought disorder or conceptual disorganization. The author concludes that (a) impairments in attention and sequencing abilities contribute substantially to schizophrenic communication failures, and (b) it is important to consider lower level cognitive "3rd variables" when examining higher level cognitive associates of speech disorder.     

What Do We Know About Neuropsychological Aspects Of Schizophrenia?

Application of a neuropsychological perspective to the study of schizophrenia has established a number of important facts about this disorder. Some of the key findings from the existing literature are that, while neurocognitive impairment is present in most, if not all, persons with schizophrenia, there is both substantial interpatient heterogeneity and remarkable within-patient stability of cognitive function over the long-term course of the illness. Such findings have contributed to the firm establishment of neurobiologic models of schizophrenia, and thereby help to reduce the social stigma that was sometimes associated with purely psychogenic models popular during parts of the 20th century. Neuropsychological studies in recent decades have established the primacy of cognitive functions over psychopathologic symptoms as determinants of functional capacity and independence in everyday functioning. Although the cognitive benefits of both conventional and even second generation antipsychotic medications appear marginal at best, recognition of the primacy of cognitive deficits as determinants of functional disability in schizophrenia has catalyzed recent efforts to develop targeted treatments for the cognitive deficits of this disorder. Despite these accomplishments, however, some issues remain to be resolved. Efforts to firmly establish the specific neurocognitive/neuropathologic systems responsible for schizophrenia remain elusive, as do efforts to definitively demonstrate the specific cognitive deficits underlying specific forms of functional impairment. Further progress may be fostered by recent initiatives to integrate neuropsychological studies with experimental neuroscience, perhaps leading to measures of deficits in cognitive processes more clearly associated with specific, identifiable brain systems.     

Common and specific cognitive deficits in schizophrenia: relationships to function

The goals of the present study were to assess the interrelationships among tasks from the MATRICS and CNTRACS batteries, to determine the degree to which tasks from each battery capture unique variance in cognitive dysfunction in schizophrenia, and to determine the ability of tasks from each battery to predict functional outcome. Subjects were 104 schizophrenia patients and 132 healthy control subjects recruited as part of the CNTRACS initiative. All subjects completed four CNTRACS tasks and two tasks from the MATRICS battery: Brief Assessment of Cognition in Schizophrenia Symbol Coding and the Hopkins Verbal Learning Test. Functional outcome was also assessed in the schizophrenia subjects. In both the patient and control groups, we found significant intercorrelations between all higher order cognitive tasks (episodic memory, goal maintenance, processing speed, verbal learning) but minimal relationships with the visual task. For almost all tasks, scores were significantly related to measures of functional outcome, with higher associations between CNTRACS tasks and performance-based measures of function and between one of the MATRICS tasks and self-reported functioning, relative to the other functioning measures. After regressing out variance shared by other tasks, we continued to observe group differences in performance among task residuals, particularly for measures of episodic memory from both batteries, although these residuals did not correlate as robustly with functional outcome as raw test scores. These findings suggest that there exists both shared and specific variance across cognitive tasks related to cognitive and functional impairments in schizophrenia and that measures derived from cognitive neuroscience can predict functional capacity and status in schizophrenia.     

The impact of borderline personality disorder and anxiety on neuropsychological performance in major depression

Previous studies of neuropsychological performance in borderline personality disorder (BPD) have exhibited mixed results. The high rate of co-occurring major depressive disorder (MDD) in BPD makes it difficult to specify whether neuropsychological deficits in BPD predominantly reflect co-occurring MDD or unique aspects of their psychopathology. To address this issue, 22 participants with borderline personality disorder and concurrent major depressive disorder (BPD-MDD) and 33 participants with MDD and no concurrent personality disorder were compared on a neuropsychological battery that assessed seven domains of performance: general intellectual functioning, motor skill, psychomotor speed, attention, memory, working memory, and executive function. Neuropsychological performance did not differ between BPD-MDD and MDD. However, BPD-MDD participants reported higher levels of anger, anxiety, and of overall emotional distress compared to MDD. When levels of anxiety were controlled, BPD-MDD participants exhibited superior general intellectual performance, psychomotor speed, and attention. Deficits found in previous BPD samples may reflect their susceptibility to co-occurring MDD. The impact of anxiety on neuropsychological performance in BPD, though, indicates a need for future experimental studies of the effects of mood on cognitive function to determine whether mood dysregulation, rather than core depressive symptoms, underlie cognition impairments in BPD.     

Neuropsychological findings and depressive symptoms in patients with Huntington''s disease

Twenty patients with Huntington's disease (HD) and a comparison group were studied by a depression scale (MADRS) and a neuropsychological test-battery assessing central areas of cognitive function. The main purpose was to analyze the consistency of findings across patients and focus on the role of specific factors in the impairments. The HD-patients are impaired relative to norms and the comparison-group in all areas but verbal conceptual function. We further divided the HD-patients into subgroups according to severity of neuropsychological impairment. The groups generally show a pattern of increasing deficits. Early changes are found in tests of cognitive efficiency, memory and sensomotor function, but the pattern of impairment is variable. The more severely affected subgroups show an increased decline in performance and progressive involvement of a broader range of functions. The pattern of depressive symptoms in HD-patients indicates that cognitive symptoms of concentration difficulties and lassitude are prominent in all subgroups.