A constant current source for extracellular microiontophoresis

There is evidence that some schizophrenic patients have deficits on tests of cognitive function, particularly tests of executive function, including the Wisconsin Card Sorting Test (WCST) and the Trail-making Test, Part B. This study was conducted to determine the generalizability of these findings across the schizophrenia spectrum to schizotypal personality disorder (SPD). Forty DSM-III SPD patients, 56 nonschizophrenia-related other personality disorder (OPD) patients, and 32 normal volunteers from two medical centers performed tests of executive function such as the WCST, Trail-making Part B, Stroop Word-Color Test, and Verbal Fluency, as well as tests of more general intellectual functioning such as the Wechsler Intelligence Scale-Revised Vocabulary and Block Design subtests, and Trail-making Part A. SPD patients performed more poorly on the WCST and on Trail-making Part B than did OPD patients or normal subjects; the groups did not differ on tests of general intellectual functioning. SPD patients may share some of the cognitive deficits observed in schizophrenia.     

Inferior parietal perfusion, lateralization, and neuropsychological dysfunction in Alzheimer's disease

The severity of inferior parietal perfusion deficits in Alzheimer's disease (AD) is strongly associated with global intellectual decline. The relationship to specific losses of neuropsychological functioning, however, is less clear, as is the relative importance of the side (left vs. right) of hemispheric deficit. In this study, 53 patients with probable AD and 35 elderly controls received both a resting 133Xe rCBF measurement and neuropsychological examination. AD patients demonstrated the expected bilateral deficits in inferior parietal perfusion, as well as impairment on measures of mental status, intelligence verbal and visual memory, attention, language, and construction abilities. The severity of this bilateral parietal deficit, in turn, was associated with virtually all of these AD-related neuropsychological impairments, most strongly with declining Performance IQ. Left-sided deficits correlated better with overall declines in IQ, as well as with declining attention and language fluency. Right-sided deficits, on the other hand, correlated best with declines in mental status and--paradoxically--verbal memory and contributed independently to declines in Full Scale and Performance IQ. In terms of the number and strength of their association to neuropsychological measures, left-sided deficits appear much more predicative of cognitive decline in AD. Right-sided deficits, however, may be most important in predicting aspects of performance skill that are only indirectly assessed in standard paper-and-pencil format. Overall, it appears that both sides make significant, but independent contributions to general functional decline in AD, but that left-sided deficits are more closely associated with cognitive decline in measured by most standard neuropsychological measures.     

The glutamatergic dysfunction hypothesis for schizophrenia

Schizophrenia is a syndrome, undoubtedly with multiple etiologies, that variably exhibits several features including positive and negative symptoms, cognitive deficits, onset in young adulthood, and deterioration from the previous level of function. This review will examine the growing evidence that dysfunction of corticolimbic glutamatergic neurotransmission may contribute to or account for the manifestations of schizophrenia. Glutamatergic neurons represent the primary excitatory afferent and efferent systems innervating the cortex, limbic regions, and striatum. The postsynaptic actions of glutamate are mediated by a family of glutamate-gated ion channels that permit the influx of sodium and calcium, thereby depolarizing (exciting) neurons. One of these receptors, the N-methyl-D-aspartate (NMDA) receptor, is the site of action of psychotomimetics such as phencyclidine and related anesthetics, which can reproduce in normal individuals most of the symptomatic features of schizophrenia. An endogenous antagonist at the NMDA receptor, N-acetyl-aspartyl glutamate, appears to have enhanced activity in the frontal cortex and hippocampal formation in persons with this disorder. Glutamatergic dysfunction may be particularly relevant to those forms of schizophrenia in which negative symptoms, cognitive deficits, and deterioration are prominent features. In support of this inference, clinical studies have shown that drugs that enhance NMDA-receptor function reduce negative symptoms and cognitive deficits in persons with chronic schizophrenia who are receiving neuroleptics. Thus, dysfunction of glutamatergic neurotransmission represents an important organizational focus for research on the complex manifestations of schizophrenia.     

Cognitive abstraction, shifting, and control: Clinical sample comparisons of psychopaths and nonpsychopaths.

Gorenstein (1982) suggested that psychopaths exhibit deficits in cognitive processes commonly associated with frontal lobe functioning, but other investigators reported collecting findings (Hare, 1984; Sutker, Moan, & Allain, 1983). There is also evidence indicating that intellectual level influences performances in measures of frontal lobe integrity and mitigates against expression of cognitive dyscontrol especially among psychopaths. The present study extended previous research by comparing clinical samples of psychopaths and nonpsychopaths identified by object instrument and behavioral self-report data. Dependent measures included test of concept formation, abstraction, flexibility, planning, and control. Compared to men defined as normal controls, male psychopaths showed no greater deficits in abstraction, flexibility, control, or planning. Intelligence significantly influenced performances on dependent measures for both groups. Results suggest that analogies between psychopathy and frontal lobe deficits are premature, if not unsupported. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neural and cognitive plasticity: From maps to minds.

Some species and individuals are able to learn cognitive skills more flexibly than others. Learning experiences and cortical function are known to contribute to such differences, but the specific factors that determine an organism's intellectual capacities remain unclear. Here, an integrative framework is presented suggesting that variability in cognitive plasticity reflects neural constraints on the precision and extent of an organism's stimulus representations. Specifically, it is hypothesized that cognitive plasticity depends on the number and diversity of cortical modules that an organism has available as well as the brain's capacity to flexibly reconfigure and customize networks of these modules. The author relates this framework to past proposals on the neural mechanisms of intelligence, including (a) the relationship between brain size and intellectual capacity; (b) the role of prefrontal cortex in cognitive control and the maintenance of stimulus representations; and (c) the impact of neural plasticity and efficiency on the acquisition and performance of cognitive skills. The proposed framework provides a unified account of variability in cognitive plasticity as a function of species, age, and individual, and it makes specific predictions about how manipulations of cortical structure and function will impact intellectual capacity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of type II diabetes mellitus on cognitive function

BACKGROUND: As people with diabetes mellitus suffer from peripheral and autonomic neuropathy, we thought it possible that deficits in cognitive function might also be found. Our objective was to compare the cognitive function of elderly persons with non-insulin-dependent diabetes mellitus (NIDDM) with a matched sample of persons without NIDDM: METHODS: Ninety outpatients over 50 years of age with NIDDM and 90 matched nondiabetic patients were recruited for the study. The Modified Mini-Mental State (3MS) and the Delayed Word Recall (DWR) test were used to assess cognitive function. RESULTS: On the 3MS test, the mean score of persons with NIDDM was 75.6, and that of nondiabetic persons was 79.5 (two-tailed t = 3.04, P = .013). On the DWR, the mean score of persons with NIDDM was 3.9, and that of persons without NIDDM was 4.7 (two-tailed t = 3.52, P = .012). CONCLUSIONS: Persons with NIDDM had significantly poorer scores on two tests of cognitive function. Physicians should be aware of this association between type II diabetes and a small but definite impairment of cognitive function.     

Effects of maternal cigarette smoking during pregnancy on long-term physical and cognitive parameters of child development

The negative impact of maternal cigarette smoking during pregnancy on the growth and development of the foetus has been well documented. However, the long-term effects of the subsequent cognitive and physical development of the child are less clearly understood. This article presents a critical review of the literature on this topic. The review shows that the effects of prenatal exposure to smoking on children's physical development are mediated by a dose-response relationship. Although the observed effects are long term, they are small and may have no major functional importance. The evidence on the long-term consequences of intellectual function is still unclear. One reason is that very few studies have looked at the long-term consequences of maternal smoking on both physical and cognitive development. More effort is needed to investigate this important issue.     

Management of primary chest wall tuberculosis

The elderly are persons over age 65, now comprising 12% of our population. The normal elderly function normally both in their self care, and also in their social activities of daily living, which we tabulate. The current terms for the normally functioning elderly who show only mild psychological deficits are age-associated memory impairment and age-related cognitive decline, which we define, criticize and tabulate. The psychological deficits of the elderly consist of mild generalized slowing and inaccuracies compared to normal young persons. These deficits are measured by objective psychological tests which mimic real daily living situations--the name-face test, fire alarm test, two delayed recall tests, misplaced objects test, shopping list test, and digit symbol test, which we describe. A longer early formal education is preventive of mental dulling during normal aging. Treating using overlearning, by cognitive training, is significantly beneficial.     

Attention, learning, and memory performances and intellectual resources in Vietnam veterans: PTSD and no disorder comparisons.

Attention, learning, memory, and estimated intellectual potential were examined in 26 Vietnam veterans diagnosed with posttraumatic stress disorder (PTSD) and in 21 Vietnam veterans without mental disorders. Results revealed PTSD-associated cognitive deficits on tasks of sustained attention, working memory, initial learning, and estimated premorbid intelligence but not on measures of focus of attention, shift of attention, or memory savings. Cognitive task performances adjusted for estimated native intelligence remained negatively correlated with PTSD severity. An intellectual measure adjusted for cognitive task performances was negatively correlated with PTSD severity, even after the authors statistically controlled the level of combat exposure. Results suggested that although intellectual resources may constitute a vulnerability-protective factor for PTSD development, PTSD was associated with cognitive impairment independent of intellectual functioning. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A longitudinal analysis of cognitive dysfunction, coping, and depression in multiple sclerosis.

Using a longitudinal design, the authors examined coping and cognitive functioning in the development of depression in individuals with multiple sclerosis (MS). Coping style was evaluated in 2 conceptually distinct roles: as moderator and mediator of the impact of cognitive dysfunction on depression. Using indices derived from the COPE (C. S. Carver, M. F. Scheier, & J. K. Weintraub, 1989), the authors operationalized coping in 3 ways—as active, avoidant, and an index accounting for relative levels of both. Coping both moderated and partially mediated the relationship between cognitive dysfunction and depression. Moderation results suggest that the relationship between cognitive dysfunction and depression is dependent on coping style—adaptive coping protects individuals from experiencing depression related to their cognitive deficits; however, when individuals use maladaptive coping, cognitive dysfunction puts them at risk for depression. Mediational results suggest that cognitive dysfunction leads to depression partially due to cognitive dysfunction’s effects on coping. That is, cognitive deficits may impair individuals’ ability to use adaptive coping strategies, leaving them more likely to use maladaptive strategies. Clinical and theoretical implications of these findings are discussed. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Obsessive-compulsive disorder associated with brain lesions: clinical phenomenology, cognitive function, and anatomic correlates

We studied the behavioral, cognitive, and neuroimaging characteristics of obsessive-compulsive disorder (OCD) in 13 patients with focal brain lesions (acquired OCD) and compared their clinical features and the severity of obsessive and compulsive (OC) symptoms with patients with idiopathic OCD. Both OCD groups were further compared with matched normal controls on a series of neuropsychological tests. Patients with acquired OCD had a negative familial history and later age at onset of OCD symptoms than patients with idiopathic OCD. The two OCD groups showed relatively similar clinical phenomenology, severity of OC symptoms, and profile of neuropsychological deficits. Compared with normal control subjects, both OCD groups showed cognitive deficits affecting attention, intellectual function, memory, word retrieval, and motor and executive functions. Eight of the 13 patients with acquired OCD had abnormal neurologic examinations, whereas only 3 of the 13 patients with idiopathic OCD had abnormal neurologic examinations. Neuroimaging in the acquired OCD group disclosed a variety of lesions involving exclusively the cerebral cortex (frontal, temporal, or cingulate regions), the basal ganglia, or both. These results suggest that acquired and idiopathic OCDs may share a common pathophysiologic mechanism, and that structural damage to specific frontal-limbic-subcortical circuits plays an important role in the pathogenesis of acquired OCD.     

Social anxiety, anxious self-preoccupation, and recall of self-relevant information.

Theoretical and empirical efforts concerning cognitive processes associated with anxiety have typically emphasized either cognitive deficits (i.e., reduced learning, memory, and task performance) or cognitive excesses (i.e., increased self-focused, ruminative thought). Evidence of these 2 types of cognitive processes has primarily been based on different types of sources (performance measures and self-reports), which precludes direct comparisons of the extent to which cognitive deficits and/or excesses characterize anxiety states. The present study attempted to directly compare the cognitive excesses and deficits associated with social anxiety by operationalizing both types of cognitive phenomena with similar performance measures. 97 undergraduates, selected on the basis of high or low scores on the Social Avoidance and Distress Scale, performed a modified self-referent depth-of-processing paradigm under stress or no-stress conditions. Socially anxious Ss in a socially evaluative situation evidenced a specific type of cognitive excess (i.e., concern over evaluations by others) but not cognitive deficits. Results are discussed in terms of person-by-situation models of anxiety and the nature and treatment of social anxiety. (42 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Postmortem studies in schizophrenia

The past decade has seen renewed interest in the neuropathology of schizophrenia. The advent of new postmortem techniques and functional imaging, along with a greater understanding of the neuropsychology of schizophrenia, have provided many new clues to the nature of the underlying brain dysfunction in this disorder. There has also been a greater understanding of the presence of severe cognitive dysfunction among many elderly persons with schizophrenia. In this article, a series of investigations are described that seek to answer basic questions about the neuropathology of schizophrenia, in particular as it pertains to cognitive impairment. The first study describes neuropathological findings in 100 consecutively autopsied persons with schizophrenia, the majority of whom had had detailed antemortem assessments. Results from this first study prompted the conclusion that schizophrenia is not characterized by classical, histologically identifiable neuropathology. Moreover, most cases of dementia in schizophrenia are probably not the result of neuropathologically identifiable dementing illnesses. The next four studies examined chemical markers that are altered in Alzheimer's disease and some other dementing conditions and have also been suggested to be abnormal in schizophrenia: choline acetyltransferase, catecholamines and indolamines, neuropeptides, and synaptic proteins. Schizophrenia cases as a group did not show a cholinergic deficit; nor did they differ from elderly comparison cases with respect to cortical catecholamines and indolamines. Among the schizophrenia cases, however, cognitive impairment was negatively correlated with choline acetyltransferase activity. Those with cognitive impairment showed evidence of cortical noradrenergic and serotonergic deficits. Neuropeptide deficits were also present in schizophrenia, but their pattern differed from that seen in Alzheimer's disease. Increased synaptic protein activity was found in the cingulate cortex of persons with schizophrenia, and this activity was correlated with schizophrenia symptoms. From this second series of studies, it was concluded that some biological measures in schizophrenia may be related to cognitive impairment (e.g., cortical amines), whereas others may be related to diagnosis (e.g., neuropeptide deficits). In addition, synaptic organization may correlate with schizophrenia symptoms.     

Cultural differences and inferences about psychological processes.

Discusses the inadequacy of experimental evidence and logical considerations in current theories of intellectual deficits caused by cultural deprivation. Reports on the presence or absence of competence have been based on noncomparable experimental situations. Deficit interpretations have assumed that absence of performance reflects absence of a particular psychological process. A strategy is proposed which combines usual experimental approaches with ethnographic methods for the study of cognitive processes. (44 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Core neurocognitive functions in children treated for posterior fossa tumors.

Identifying cognitive deficits associated with pediatric brain tumors and their treatment is important in delineating the mechanisms of intellectual decline often associated with these diseases. The authors evaluated sustained attention, information processing speed, working memory, and IQ in 64 patients with posterior fossa tumors, including those treated with either: (a) surgery and cranial radiation (n = 32), and (b) surgery without radiation (n = 32). Ten patients treated for non-CNS solid tumors were included as a comparison group. The authors also examined the impact of relevant demographic and medical variables on neurocognitive outcome. The authors found that neither age at, nor time since, diagnosis predicted cognitive outcome in this sample. Further, sustained attention and working memory were largely intact and there were no differences between groups. Patients treated with cranial radiation demonstrated lowered short-form IQ and slow information processing speed: Patients treated with cranial radiation and who experienced postsurgical complications demonstrated the poorest performance. The authors consider information processing speed to be an excellent candidate mechanism in understanding the impact of cranial radiation on intellectual outcome. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Test anxiety and ineffective test taking: Different names, same construct?

Investigated the relative contributions of test anxiety and exam-taking skills to information-processing deficits in a dual-task paradigm. Under stress instructions, 64 high- and low-test-anxious college students with either good or poor exam-taking skills alternately performed a primary task (Raven Advanced Progressive Matrices) separately and concurrently with a secondary task (a backward digit span test). Results indicate that exam-skilled, high-anxious Ss performed comparably with skilled, low-anxious peers on the primary Raven task, yet significantly worse on the concurrent backward digit span task. Conversely, high-anxious, unskilled Ss were exceeded by low-anxious, unskilled peers on both tasks. Findings suggest that test anxiety and exam-taking ability independently influence cognitive problem solving in the evaluative setting. It is suggested that although good exam skills can compensate for anxiety-induced deficits in working-memory capacity by refocusing attention toward the task, processing deficits still emerge as task demands increase. Measures of state anxiety and cognitive interference further suggest that a negative internal focus, not arousal, underlies such deficits. (43 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cognitive performance in very old diabetic persons: The impact of semantic structure, preclinical dementia, and impending death.

The authors examined the associations of diabetes mellitus with cognitive performance in a population-based sample of nondemented and nondepressed very old persons. Diabetic participants (n = 31) were compared with nondiabetic controls (n = 307), adjusting for age, educational level, and related vascular diseases and signs. Results showed that diabetic persons performed significantly worse on tests of verbal fluency and episodic memory but that the effects on both types of abilities were less pronounced in tasks involving higher degrees of semantic structure. Follow-up analyses further revealed that preclinical dementia and impending death accounted for much of the observed associations. The results suggest that cognitive deficits among very old diabetics are most likely detected by tasks that draw less on semantic structures and that the most robust effects may be found in letter fluency performance (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Neuropsychological aspects of multiple sclerosis

Twenty-six persons (five males and 21 females) with the neurological diagnosis of multiple sclerosis, and an equal number of control subjects matched on age, sex, and education were given a battery of tests designed to assess motor and intellectual functioning. Subjects in the multiple sclerosis group displayed marked deficits on all tests of motor skill except grip strength. Although verbal intelligence was not impaired in subjects with multiple sclerosis, these subjects performed more poorly than control subjects on two different tests of memory even though these tasks required minimal motor responsivity. Correlational analyses on the several motor and cognitive tasks revealed that correlations between motor and memory performance were consistently higher in persons with multiple sclerosis than in controls. These results suggest that whereas multiple sclerosis may not have mch effect on the utilization of stored verbal information, the processing and storage of new verbal material are disrupted by the disease to a degree that is paralleled by the extent of motor impairment. This finding is consistent with the view that the memory impairments observed are secondary to the primary motor deficit, but the alternative explanation that memory functions, like motor functions, are especially vulnerable to the demylination process of multiple sclerosis is equally viable at present.     

Cognitive deficits and psychiatric rehabilitation outcomes in schizophrenia

Many patients with schizophrenia are characterized by cognitive deficits that limit their ability to benefit from psychiatric rehabilitation interventions. While this suggests that cognitive rehabilitation is important, more needs to be known about which cognitive deficits interfere with which aspects of outcome and functioning before effective interventions are developed. We report data on cognitive predictors of three types of outcome: acquisition and performance of skills in a skills training group; aspects of daily ward functioning; and ability to be discharged from a state hospital. Our data indicate that poorer outcomes in each of these areas are associated with different, but somewhat overlapping, profiles of cognitive deficits. These data are relevant for designing both ward-based and individualized interventions. Integrating traditional psychiatric rehabilitation approaches with targeted cognitive interventions is necessary to maximize the impact of psychiatric rehabilitation services on individuals with chronic schizophrenia.     

Intellectual disabilities and depression: How to adapt psychological assessment and intervention.

Persons with intellectual disabilities (ID) are at higher risk of developing a depressive disorder than are members of the general population. This article attempts to answer the question of how best to adapt psychological assessment and intervention for depressive disorder to the needs of adults with ID. Current knowledge suggests that a diagnostic assessment conducted by a multidisciplinary team is the best way to evaluate the influence of biological and psychosocial factors that may contribute to the development of depressive symptoms, and identify potential differential diagnoses. The greater the person's communication and cognitive deficits are, the greater the clinician's difficulties are in assessing and treating depressive disorder in persons with ID. Family and caregivers of such persons are therefore essential partners in assessment and therapeutic process. The recommended interventions are education, skill development, environment modification, and cognitive and behavioural therapy. All of these must, however, be adapted to the person's level of functioning. While the use of antidepressants may prove necessary, side effects must be carefully monitored. (PsycINFO Database Record (c) 2010 APA, all rights reserved)