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[Cognitive dysfunction and emotional disturbances in children with neurofibromatosis type one (Recklinghausen's disease). Review of the literature].

Neurofibromatosis type 1 (NF1) is a genetic disorder associated with a high risk of the neuropsychological, emotional and psychosocial disturbances in children with NF1. In this research the results of the psychological and neuropsychological studies in children with NF1 were presented. According to data of current research, the most common cognitive deficits are connected with visual-spatial impairment, however verbal, working memory and executive function deficits associated with prefrontal cortex dysfunction are also important. The results indicate that the neuropsychological deficits may increase during the course of the illness.

Affective Symptoms↗
PubMed2006

Central nicotinic cholinergic systems: a role in the cognitive dysfunction in attention-deficit/hyperactivity disorder?

Theories of the neurobiological basis of Attention-Deficit/Hyperactivity Disorder (ADHD) have largely focused on dysregulation of central dopaminergic function. However, other neurotransmitter systems may be implicated in specific cognitive deficits in ADHD. Interest in the potential involvement of nicotinic cholinergic systems in ADHD has arisen in part from the observation that adolescents and adults with ADHD smoke cigarettes at significantly higher rates than people without this disorder. In addition, several studies report that nicotine alleviates ADHD symptoms, and recent neuro-genetics studies indicate that cholinergic systems may be altered in persons with ADHD. In this review, we describe the evidence for a role of central nicotinic cholinergic systems in cognitive deficits in ADHD. We also propose mechanisms by which alterations in cholinergic function may contribute directly and/or indirectly to these deficits. Finally, we identify specific paradigms and models to guide future investigations into the specific involvement of nicotinic cholinergic systems in ADHD, possibly leading to the development of more effective pharmacotherapies for ADHD.

Animals↗
PubMed1997

Effect of nimodipine on the cognitive dysfunction induced by phenytoin and valproate in rats.

Anticonvulsant effects of phenytoin (PHT) and valproate (VPA) were studied alone and in combination with nimodipine (NMD) against maximal electroshock (MES)-induced seizures in rats. PHT and VPA induce cognitive deficit in terms of long-term memory loss. The effect of NMD on the cognitive deficit induced by PHT and VPA was studied through the step-through passive avoidance test (PAT). It was seen that there was a potentiation of antielectroshock effect of PHT and VPA when NMD at a dose of 4 mg/kg was combined with PHT or VPA. NMD reversed the long-term memory loss induced by PHT and VPA in the PAT.

Animals↗
PubMed1983

Cognitive dysfunction and tardive dyskinesia.

From a prospective study of tardive dyskinesia (TD), psychiatric patients with neuroleptically-induced "persistent" TD were contrasted with controls on a neuropsychological measure of abstracting ability. A significant association is demonstrated between impaired cognitive performance and TD, even when the neuropsychological measure was obtained in advance of TD onset.

Aged↗
PubMed1995

Radiation-induced cognitive dysfunction: an experimental model in the old rat.

PURPOSE: To develop a model of radiation-induced behavioral dysfunction. METHODS AND MATERIALS: A course of whole brain radiation therapy (30 Gy/10 fractions/12 days) was administered to 26 Wistar rats ages 16-27 months, while 26 control rats received sham irradiation. Sequential behavioral studies including one-way avoidance, two-way avoidance, and a standard operant conditioning method (press-lever avoidance) were undertaken. In addition, rats were studied in a water maze 7 months postradiation therapy. RESULTS: Prior to radiation therapy, both groups were similar. No difference was found 1 and 3 months postradiation therapy. At 6-7 months postradiation therapy, irradiated rats had a much lower percentage of avoidance than controls for one-way avoidance (23% vs. 55%, p < or = 0.001) and two-way avoidance (18% vs. 40%, p < or = 0.01). Seven months postradiation therapy the reaction time was increased (press-lever avoidance, 11.20 s vs. 8.43 s, p < or = 0.05) and the percentage of correct response was lower (water maze, 53% vs. 82%) in irradiated rats compared with controls. Pathological examination did not demonstrate abnormalities of the irradiated brains at the light microscopic level. CONCLUSION: Behavioral dysfunction affecting mainly memory can be demonstrated following conventional radiation therapy in old rats. This model can be used to study the pathogenesis of radiation-induced cognitive changes.

Aging↗
PubMed2006

Is depth of anesthesia, as assessed by the Bispectral Index, related to postoperative cognitive dysfunction and recovery?

We randomized 74 patients to either a lower Bispectral Index (BIS) regimen (median BIS, 38.9) or a higher BIS regimen (mean BIS, 50.7) during the surgical procedure. Preoperatively and 4-6 wk after surgery, the patients' cognitive status was assessed with a cognitive test battery consisting of processing speed index, working memory index, and verbal memory index. Processing speed index was 113.7 +/- 1.5 (mean +/- se) in the lower BIS group versus 107.9 +/- 1.4 in the higher BIS group (P = 0.006). No difference was observed in the other two test battery components. Somewhat deeper levels of anesthesia were therefore associated with better cognitive function 4-6 wk postoperatively, particularly with respect to the ability to process information.

Adjuvants, Anesthesia↗
PubMed1997

A pivotal role for glutamate in the pathogenesis of schizophrenia, and its cognitive dysfunction.

There is mounting evidence of a glutamate dysfunction in schizophrenia, as suggested by the fact that schizophrenia and phencyclidine psychosis are similar and phencyclidine is known to block the N-methyl-D-aspartate (NMDA) subtypes of glutamate. Both occur mainly after puberty, suggesting they may share similar underlying developmental processes. Direct evidence is now accumulating from the study of messenger RNA that glutamate receptor deficiencies occur in schizophrenia and are regionally and specifically distributed. These results find support from studies of memory, electrophysiological findings, clinical treatment, and pharmacological studies in mammals and humans. Our recent findings of: a) a marked decrease in pyramidal cell dendritic spines in layer III of the frontal and temporal cortex, and b) a greater than 0.90 correlation between decrease in mRNA for the NMDA glutamate receptor and cognitive deterioration in elderly schizophrenics, present the strongest evidence to date that glutamate dysfunction plays an important role in schizophrenia.

Animals↗
PubMed1981

Cognitive dysfunction in schizophrenia, affective disorder and organic brain disease.

We used the Wechsler Adult Intelligence Scale (WAIS) to study a sample of patients with affective disorder (N = 52), schizophrenia (N = 17) and organic brain disease (N = 8). Schizophrenic patients had lower verbal, performance and full-scale IQs than patients with affective disorder, but were no different from those with organic brain disease. An individual WAIS subscale analysis showed that, compared with affectives, schizophrenics had relatively poorer performance on language than non-language tasks. These differences were independent of age, sex, handedness, educational level or drug administration and are consistent with a variety of studies demonstrating significant cerebral dysfunction in carefully diagnosed schizophrenic patients.

Adult↗
PubMed2002

Serum concentration of S-100 protein in assessment of cognitive dysfunction after general anesthesia in different types of surgery.

BACKGROUND: S-100 protein serum concentration (S-100) serves as a marker of cerebral ischemia in cardiac surgery, head injury and stroke. In these circumstances S-100 corresponds well with the results of neuropsychological tests. The aim of the present study was to investigate the value of S-100 and neuron specific enolase (NSE) in reflecting postoperative cognitive deficit (POCD) after general surgical procedures. METHODS: One hundred and twenty patients undergoing vascular, trauma, urological or abdominal surgery were investigated. Serum values of S-100 and NSE were determined preoperatively and 0.5, 4, 18 and 36 h postoperatively. Neuropsychological tests for detecting POCD were performed preoperatively and on day 1, 3, and 6 after the operation. A decline of more than 10% in neuropsychological test results was regarded as POCD. Furthermore, we retrospectively compared the S-100 in patients with and without POCD in different types of surgery. RESULTS: According to our definition, forty-eight patients had POCD (95% confidence interval: 37.5-58.5). These patients showed higher serum concentrations of S-100 (median 024 ng/ml; range 0.01-3.3 ng/ml) compared with those without POCD (n=69; median 0.14 ng/ml; range 0-1.34 ng/ml) 30 min postoperatively (P=0.01). Neuron specific enolase was unchanged during the course of the study. Differences of S-100 in patients with and without POCD were found in abdominal and vascular surgery but not in urological surgery. CONCLUSION: When all patients are pooled, S-100 appears to be suitable in the assessment of incidence, course and outcome of cognitive deficits. We suspect that in some surgical procedures, such as urological surgery, S-100 appears to be of limited value in detecting POCD. Neuron specific enolase did not reflect neuropsychological dysfunction after noncardiac surgery.

Adolescent↗
PubMed2002

Assessing cognitive dysfunction in breast cancer: what are the tools?

The goal of adjuvant chemotherapy in the treatment of breast cancer is to reduce recurrence and mortality. With respect to quality of life and morbidity, however, such treatments come at a cost. Decreased cognitive functioning, development of fatigue, and mood alterations are common during chemotherapy and persist after its conclusion as evidenced by subjective self-reports and objective neurocognitive performance records. Few efforts, however, have used standardized neuropsychological measures, and no study has empirically selected those measures that best distinguish women in active chemotherapy from those who have previously completed it. Perhaps the most glaring deficit in the literature is that no study has used baseline data to track individual neurocognitive changes across treatment phases and after completion. This article provides an overview of the field of neuropsychology and the cognitive domains theorized to be affected by chemotherapy and the measures typically used, including validated computerized tests, which are tools for future studies; briefly summarizes existing research on the cognitive effects that chemotherapy has on breast cancer patients; compares data resulting from an ongoing pilot study of the cognitive performance of women actively undergoing anthracycline-containing chemotherapy with that of women 6-12 months post chemotherapy completion; and provides a preliminary analysis of the relationship between cognitive and emotional functioning. Future uses of these data to refine the ideal tools that efficiently, accurately, and validly detect short-term and persistent chemotherapy effects are proposed.

Adult↗
PubMed1989

Dysfunctional cognitions, attributional style, and depression in bulimia.

A group of 44 bulimic women (DSM-III) as well as 38 women with no indication of an eating disorder, comparable with respect to age, weight and height, were studied by means of the Beck Depression Inventory (BDI), the Dysfunctional Attitude Scale (DAS), the Attributional Style Questionnaire (ASQ), and an Eating Disorder Questionnaire (EDQ). Bulimics showed significantly higher BDI, DAS and ASQ (bad events) scores, respectively. In both groups BDI scores were significantly correlated with DAS and ASQ (bad events) results. BDI was highly predictive of severity of bulimia while no significant prediction was obtained from either DAS or ASQ (bad events) scores. The findings provide first evidence that dysfunctional attitudes and depressive attributional style are predominant in bulimic women but at the same time are not necessarily predictive of the severity of the disorder.

Adult↗
PubMed1996

Pharmacological treatment of cognitive dysfunction in dementia disorders.

Dementia represents a complex heterogeneity of disorders. For Alzheimer's disease great progress in the understanding of underlying genetical, neuropathological and neurochemical mechanisms of the disease has been made during recent years. A variety of therapeutic approaches with cognitive enhancing drugs have been tested in Alzheimer patients. Presently, four main treatment strategies prevail, namely transmitter replacement therapy, growth factors, anti-inflammatory drugs and drugs affecting amyloid processing in the brain. The transmitter therapy is so far the most explored and fruitful strategy. The cholinesterase inhibitor tacrine is in clinical use in many countries. Other cholinergic treatment strategies than cholinesterase inhibitors in development are selective muscarinic receptor agonists and nicotine receptor agonists. The selective 5HT re-uptake blockers might be complementary to drugs with more specific effect on cognition. Although treatment with growth factor therapy e.g. nerve growth factor in Alzheimer patients has given some promising results, further research is needed. Development of drugs affecting amyloid processing is still mainly on a preclinical level.

Aged↗
PubMed1999

Cognitive dysfunction in NIDDM: P3 event related evoked potential study.

P3 component of the endogenous cerebral evoked response is a sophisticated, objective and quantitative approach to assess higher functions of the brain. This test was employed using auditory 'odd ball' paradigm to assess cognitive functions in thirty non insulin dependent diabetic patients (NIDDM) aged 43.6 +/- 9 yrs with poor blood glucose control. (HbAlc. 9.9 +/- 1.0%). The peak latencies of N2, P3 components of event related evoked potentials obtained in these patients were compared with 30 age and sex matched non diabetic healthy controls. Latencies of these potentials were: N2 = 248.0 +/- 36.3, P3 = 391.6 +/- 49.9 msec in NIDDM as compared to 220.6 +/- 26.4, 326.2 +/- 26.8 msec in controls and were highly significant (P < 0.001). The duration of disease, blood glucose level or the physical parameters of height, weight and blood pressure did not show any correlation with N2 or P3 latencies or amplitude. These findings provide an electrophysiological evidence of delayed cognition in poorly controlled NIDDM cases.

Adult↗