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At least 127 records · Page 7Linked to original sources
PubMed1998

Cognitive dysfunction and impaired organization of complex motility in degenerative parkinsonian syndromes.

BACKGROUND: A frontostriatal pattern of cognitive decline, consisting of a frontal lobe-like syndrome without genuine cortical defects such as amnesia, apraxia, aphasia, or agnosia, is well established in basal ganglial diseases. Recent pathological investigations, however, have again noted cortical damage in progressive supranuclear palsy (PSP), suggesting that cortical defects could be present. OBJECTIVES: To delineate the pattern of cognitive impairment and to detect higher-order motor impairments (including ideomotor apraxia) in parkinsonian syndromes. PATIENTS AND METHODS: We assessed ideomotor apraxia, and simple and sequential tapping in patients with Parkinson disease, multiple system atrophy, and PSP with similar disease severity, age range, and education. We also administered a comprehensive battery of neuropsychological tests to examine general intelligence, memory, executive functions, attention, and visuospatial orientation. The results were compared between groups and with a matched normal control group. RESULTS: Sequential tapping and the imitation of sequences of gestures were impaired in all patient groups, with patients with PSP performing worse than the other groups. Based on ideomotor apraxia scores and a qualitative analysis of errors, 3 patients with PSP and 2 with multiple system atrophy were considered apraxic. General intelligence and executive functions were compromised in all patient groups. The impairment of patients with PSP was more pervasive than that of the other groups, and included compromise of visuospatial functions, attention, and memory. Discriminant analysis of all cognitive and motor tests showed that the tapping and ideomotor apraxia tests best identified the patients vs control subjects. CONCLUSIONS: The presence of cortical as well as subcortical damage in patients with PSP and those with multiple system atrophy is indicated by the presence of pervasive cognitive and motor disturbances in the former, substantial motor disorganization in the latter, and the finding of ideomotor apraxia in some patients with these diseases. Furthermore, the discovery that tests of motor and gesture best identified all patients vs control subjects is consistent with the existence of a common motor disorganization in these parkinsonian syndromes, in agreement with the known damage to the corticostriatal pathways in these conditions.

Aged↗
PubMed1991

[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↗
PubMed1975

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↗
PubMed1985

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.

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PubMed2026

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↗
PubMed1987

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↗
PubMed1996

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↗
PubMed1996

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↗
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↗
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↗