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Results for “Cognitive Dysfunction”

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PubMed1997

Cognitive dysfunctions induced by scopolamine are reduced by systemic or intrahippocampal mineralocorticoid receptor blockade.

Central cholinergic blockade with scopolamine (SCOP) produces profound cognitive impairments in human and animal subjects. We hypothesized that cognitive deficits induced by cholinergic blockade originate partly from its ability to enhance reactivity to the environment, an effect that would be ameliorated by prior mineralocorticoid receptor (MR) blockade, because MR antagonists reduce reactivity to novelty. In the present study, we investigated whether or not systemic or intrahippocampal infusions of the MR antagonist spironolactone (SPIRO) would affect SCOP-induced cognitive impairments in a water maze task. Adult male Lister hooded rats (350-450 g) served as subjects. In Experiment 1, rats were administered SPIRO (0 or 100 mg/kg i.p.) followed 10 min later by SCOP (0, 0.5, or 2.0 mg/kg i.p.; n = 10/group). In Experiment 2, groups of rats implanted with hippocampal cannulae received central infusions of SPIRO (50 ng/microliter; 3 microliters in total) 10 min prior to SCOP injection (2.0 mg/kg i.p.; n = 6/group). Behavioural testing started 15 min after SCOP administration and consisted of a simple water maze task in which animals were required to locate a submerged platform using spatial cues. The testing regime consisted of two phases: a) acquisition, and b) retention, 24 h later. Peripheral, but not central, injections of SPIRO enhanced water maze performance during acquisition in SCOP-treated rats, as shown by shorter latencies and shorter distances travelled to locate the hidden platform. Both peripheral and central SPIRO administration reduced the long-term retention deficits in performance in the SCOP-treated animals. These data are in general agreement with a growing body of research suggesting that corticosteroid hormones interact with central cholinergic systems to affect both physiological and behavioural responses. MR blockade may reduce an animal's reactivity to the environment and enable it to selectively filter out extraneous stimuli that it would otherwise react to, thus impairing performance.

Animals↗
PubMed2006

Asymmetric cerebral embolic load and postoperative cognitive dysfunction in cardiac surgery.

BACKGROUND: The aim of the study was to determine the effects of asymmetric cerebral embolic load on cognitive functions. METHODS: Thirty-six open heart surgery (OH) and 26 coronary artery bypass grafting (CABG) patients were evaluated by neuropsychological and transcranial Doppler tests. RESULTS: OH was associated with a significantly larger microembolic load in comparison to CABG. In OH patients, the microembolic load at the left middle cerebral artery correlated with a verbal memory decline, whereas the microembolic load at the right middle cerebral artery correlated with a nonverbal memory deficit. CABG patients also showed a postoperative verbal memory decline which correlated with cardiopulmonary bypass length but not with microembolic load. CONCLUSION: Massive microembolic load during OH induces specific cognitive impairment in accordance to the brain region to which they are delivered. In atherosclerotic patients, the left temporal region is especially prone to perioperative ischemia.

Adolescent↗
PubMed2003

Cognitive dysfunction in cortical cerebellar atrophy correlates with impairment of the inhibitory system.

The aim of the present study was to evaluate the profile of cognitive impairment in patients with cortical cerebellar atrophy (CCA) by measurement of event-related potentials (ERP) and neuropsychological tests. We studied 13 CCA patients and 13 age-, sex- and education-matched normal controls. For ERP recording, we used the conventional auditory oddball task as well as the continuous performance task, which evaluates the attentional performance and ability to control a motor response, i.e., to execute ("Go") or inhibit a motor reaction ("No Go"). Brain electric activity was recorded using 20 scalp electrodes and computed into series of potential distribution maps. For components of ERP, reference-independent measures [global field power (GFP)] were determined, and low-resolution brain electromagnetic tomography (LORETA) was used to compute the three-dimensional intracerebral distribution of electric activity of the P3 component of Go and No Go responses. A comprehensive neuropsychological test battery was also assessed. GFP peak latency was prolonged and GFP peak was attenuated under the No Go condition in patients with CCA, although there were no differences in the auditory oddball task and in the Go condition between the two groups. LORETA showed low activation of frontal source in CCA patients in No Go P3 compared with the controls. However, neuropsychological tests revealed no differences between the two groups. Our results indicate that degeneration of the cerebellum contributes to frontal dysfunction, and suggest this dysfunction is characterized by an impairment of the inhibitory system.

Aged↗
PubMed2000

[The Eppendorf Schizophrenia Inventory (ESI). Development and evaluation of a questionnaire for assessment of characteristic self perception of cognitive dysfunctions by schizophrenic patients].

This study explored characteristic subjective experiences of schizophrenia. A questionnaire for self-assessment of disturbances in several cognitive and perceptual areas (the Eppendorf Schizophrenia Inventory, or ESI) was constructed and administered to first-episode schizophrenics (SCHe, n = 45), negative syndrome schizophrenics (SCHn, n = 45), remitted schizophrenics (SCHr, n = 24), depressives (DEP, n = 43), alcoholics (ALK, n = 48), obsessive-compulsive patients (ZWA, n = 46), and healthy controls (KON, n = 57). Comparisons between the SCHe, SCHn, DEP, ALK, and ZWA groups and a subsequent factor analysis revealed four schizophrenia-specific dimensions: attention and speech impairment (AS), ideas of reference (IR), auditory uncertainty (AU), and deviant perception (DP). Further analyses suggested that the AS syndrome may represent a mediating vulnerability factor while IR, AU, and DP probably are reversible episode indicators. The results may contribute to refinements in the measurement of specific prepsychotic signs, thus facilitating the development of early intervention approaches.

Adult↗
PubMed1996

Cardinal features of cognitive dysfunction in Alzheimer's disease: a factor-analytic study of the Alzheimer's Disease Assessment Scale.

Factor analysis methodology applied to Alzheimer's Disease Assessment Scale (ADAS) subtest profiles for patients in two large-scale clinical trials of the antidementia drug tacrine yielded three oblique factors interpreted as dysfunctions in memory, language, and praxis. The factor structures confirmed reliable assessment of primary dimensions of cognitive impairment in Alzheimer's disease that the original authors of the ADAS proposed to measure and that correspond well to that of the only previously reported factor analysis of the ADAS-COG. The presence of a strong general factor, supported by stable correlations among the oblique primary factors, justifies the recommendation to continue reliance on the ADAS-COG total score as a primary outcome measure in clinical trials, whereas the factor scores are recommended for evaluation of differential treatment effects on more specific aspects of the general cognitive decline. The stability of correlations across time appears to satisfy a primary requirement for application of repeated measures ANOVA to ADAS-COG total score and factor scores in longitudinal clinical trials.

Aged↗
PubMed2006

Cognitive dysfunction in NF1 knock-out mice may result from altered vesicular trafficking of APP/DRD3 complex.

BACKGROUND: It has been estimated that more than 50% of patients with Neurofibromatosis type 1 (NF1) have neurobehavioral impairments which include attention deficit/hyperactivity disorder, visual/spatial learning disabilities, and a myriad of other cognitive developmental problems. The biological mechanisms by which NF1 gene mutations lead to such cognitive deficits are not well understood, although excessive Ras signaling and increased GABA mediated inhibition have been implicated. It is proposed that the cognitive deficits in NF1 are the result of dysfunctional cellular trafficking and localization of molecules downstream of the primary gene defect. RESULTS: To elucidate genes involved in the pathogenic process, gene expression analysis was performed comparing the expression profiles in various brain regions for control and Nf1+/- heterozygous mice. Gene expression analysis was performed for hippocampal samples dissected from postnatal day 10, 15, and 20 mice utilizing the Affymetrix Mouse Genome chip (Murine 430 2.0). Analysis of expression profiles between Nf1+/- and wild-type animals was focused on the hippocampus because of previous studies demonstrating alterations in hippocampal LTP in the Nf1+/- mice, and the region's importance in visual/spatial learning. Network analysis identified links between neurofibromin and kinesin genes, which were down regulated in the Nf1+/- mice at postnatal days 15 and 20. CONCLUSION: Through this analysis, it is proposed that neurofibromin forms a binding complex with amyloid precursor protein (APP) and through filamin proteins interacts with a dopamine receptor (Drd3). Though the effects of these interactions are not yet known, this information may provide novel ideas about the pathogenesis of cognitive defects in NF1 and may facilitate the development of novel targeted therapeutic interventions.

Amyloid beta-Protein Precursor↗
PubMed1998

[The mini-mental state examination in screening of cognitive dysfunction and dementia].

The mini-mental state examination (MMSE) is one of the most widely used screening instruments for the detection of cognitive impairments, used primarily in connection with screening for dementia. The intent of this review is to describe the original purpose of the MMSE and how it is currently used in clinical practice and in research. Advantages and limitations of the MMSE in providing a valid diagnosis of cognitive impairments (dementia) are discussed including sensitivity and specificity, the issues of the relationship of the MMSE scores to sociodemographic variables and examinations of factor structures of the MMSE. It is concluded that the MMSE provides a valid diagnosis of cognitive impairments among people with moderate and severe dementia in general populations. However, MMSE is not recommended as a screening instrument for the detection of early stages of dementia. Studies are needed to extend the present knowledge about how or whether the MMSE can be used in the clinical diagnostic evaluation of dementia and how demented patients treated with medications should be monitored.

Cognition Disorders↗