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Cognitive dysfunction in schizophrenia: comparison of treatment with atypical antipsychotic agents and conventional neuroleptic drugs.

Impaired cognitive function is both a feature of schizophrenia and a side effect of conventional neuroleptics. Maze tests were used to determine the effects on cognition of conventional dopamine antagonist neuroleptics (haloperidol and fluphenazine) and the newer serotonin-dopamine antagonist antipsychotics (risperidone and clozapine). Patients on clozapine or risperidone showed better performance on the maze tasks than untreated patients or patients taking conventional neuroleptics. In particular, patients treated with risperidone or clozapine were better able to maintain motor coordination while they focused on the more complex "frontal" maze tasks which required sequencing and planning. In view of the restrictions on the use of clozapine, it is suggested that risperidone should be more widely used in schizophrenia because it preserves cognitive function better than conventional neuroleptics and is therefore likely to allow patients to have better insight into their illness and to have better long-term quality of life expectations.

Clozapine

[Disseminated sclerosis: organic basis for mental disorders and cognitive dysfunction].

The MRI-(magnetic resonance imaging) scanner has improved the knowledge of the organic basis of cognitive defects in multiple sclerosis. Recent studies demonstrated a correlation of MRI-verified single lesions, atrophy of the corpus callosum and cognitive defects; but failed to demonstrate the convincing correlation between psychic symptoms and MRI-verified lesions.

Atrophy

Delayed hypoxic encephalopathy without cognitive dysfunction.

Three days after an episode of hypoxia, a 20-year-old man developed profound motor deficit in the absence of behavioral or cognitive disturbance. Previous reviews of delayed hypoxic encephalopathy have stressed behavioral and cognitive disturbances as the initial symptoms. This patient's pyramidal tract dysfunction in the absence of higher cortical dysfunction serves to illustrate that delayed hypoxic encephalopathy is predominantly a white matter rather than a gray matter disorder.

Adult

The value of Luria's Neuropsychological Investigation for the assessment of cognitive dysfunction in Alzheimer-type dementia.

Items from Luria's Neuropsychological Investigation (LNI) were used to assess cognitive functioning in three groups: patients with Alzheimer-type dementia (ATD), with alcoholic Korsakoff syndrome (KS) and control subjects of comparable age. The LNI was shown to be a sensitive assessment in that it distinguished differences within the ATD group and among the three groups. The validity and usefulness of the LNI in Alzheimer-type dementia are discussed.

Aged

CNNM2 in schizophrenia: multilevel evidence of genetic susceptibility, magnesium homeostasis, neurodevelopment and cognitive dysfunction.

Schizophrenia (SCZ) is a common psychiatric disorder with a complex, genetically and environmentally influenced etiology, but the specific pathogenesis remains unclear. In recent years, the SCZ susceptibility gene CNNM2 (encoding cyclin M2) located at the 10q24.32-33 locus has received widespread attention. The well-validated SCZ risk interval 10q24.32-33 harbors two independent risk variants: rs11191580 in NT5C2 (significantly associated with CNNM2 mRNA and protein levels) and rs7914558 in CNNM2. Results from functional genomic analyses indicate that lower CNNM2 expression is significantly associated with SCZ. Imaging genetics studies have demonstrated that carriers of risk alleles of CNNM2 SNPs exhibit alterations in brain structure. Animal model studies have revealed that Cnnm2 downregulation in mice leads to impairments in sensorimotor gating and cognitive function. As an Mg2+ transporter, CNNM2 primarily maintains systemic Mg2+ homeostasis. According to clinical studies, a proportion of patients with SCZ exhibit reduced Mg2+ concentrations in plasma and cerebrospinal fluid. CNNM2 dysfunction may contribute to the pathology of SCZ by disrupting Mg2+ homeostasis, thereby affecting neurodevelopment and synaptic plasticity. A systematic consolidation of current evidence supporting the involvement of CNNM2 in SCZ pathogenesis provides a direction for further investigation of the pathological mechanisms underlying this disease, and for identification of novel targets for clinical intervention..

Schizophrenia

Cognitive dysfunction in psychiatric consultation subgroups: use of two screening tests.

Elderly patients are highly vulnerable to illness-related and drug-induced cognitive changes, especially during the acute phase of a medical or surgical illness. Using a structured cognitive screening examination enhances the accurate identification of patients with cognitive impairment. We compared the cognitive portion of the Alzheimer's Disease Assessment Scale (ADAS-COG) to the Mini-Mental State Examination (MMSE) in screening for the presence of organic brain dysfunction. Using cutoff scores, the two tests were in agreement in 94.4% of 36 cases, with total scores on the two tests correlated at r = -.90 (P less than .01). Of these 36 patients for whom psychiatric consultations were requested, 14 (38.8%) were found to be cognitively impaired. We discuss the relationship of test scores to the stated reason for the consultation, as well as variables influencing test results. Finally, we demonstrate the usefulness of cognitive testing in patients who refuse treatment.

Adult

Cognitive dysfunction following surgery for intracerebral glioma: influence of histopathology, lesion location, and treatment.

This study examined the relationship between cognitive function, tumor malignancy, adjunctive therapy, and lesion lateralization following surgery for intracerebral glioma. Neuropsychological test battery results showed no difference between patients with highly malignant gliomas and those with less malignant gliomas, but differences were found for tumor lateralization and type of therapy. Scores on a test of graphomotor speed were lowest for patients who had received radiation or a combination of radiation and chemotherapy, regardless of lesion location. Other test results did not differ according to type of prior treatment but were related instead to tumor lateralization. Left hemisphere lesions were associated with lower scores on verbal tests, while right hemisphere lesions were related to lower scores on a test of facial recognition. These findings suggest that neuropsychological tests may be useful for distinguishing between the diffuse side effects of brain tumor therapy and the focal effects of tumors and surgery on brain functions. In addition, it appears that any differences in cognitive function due to tumor malignancy are eliminated or reduced following surgical intervention.

Adult

Cognitive dysfunction in chronic schizophrenia followed prospectively over 10 years and its longitudinal relationship to the emergence of tardive dyskinesia.

Basic cognitive function was assessed at initial and at 5- and 10-year follow-up assessments among 41 primarily middle-aged in-patients manifesting the severest form of schizophrenia; additionally, the presence and severity of tardive dyskinesia was evaluated on each occasion. Overall, there was a modest but significant deterioration in cognitive function over the decade, particularly among older men. Longitudinally, patients with persistent tardive (orofacial) dyskinesia continued to show poorer cognitive function than those consistently without such movement disorder, though within neither group did cognitive function change over the decade. Those patients demonstrating prospectively the emergence of orofacial dyskinesia showed a marked deterioration in their cognitive function over the same time-frame within which their movement disorder emerged, but this decline did not progress further thereafter. There appears to exist some modes, progressive deterioration in cognitive function even late in the chronic phase of severe schizophrenic illness which appears to derive primarily from patients showing de novo emergence of tardive orofacial dyskinesia.

Adult