Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Computerized tomography of the head was carried out on 69 elderly patients who met the DSM-III criteria for delirium and 31 neurological controls in order to evaluate the focal changes and generalized brain atrophy associated with delirium. Neither the difference between the mean ages nor the sex distribution in these groups was statistically significant. The delirious patients differed from the controls significantly in ventricular dilatation and cortical atrophy, and there was a statistically significant correlation between the width of the sylvian fissure and Mini-Mental State Examination score. Focal changes were also statistically more common in the delirious patients, and these changes tended to concentrate in the high-order association areas of the right hemisphere. Results suggest a marked predisposing role for the structural brain diseases (primary degenerative and multi-infarct type dementias, parkinsonism) in the development of delirium in elderly patients.
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PMID:Computed tomography findings in delirium. 270 27

A Japanese male showed gradually progressing dementia with psychiatric symptoms including abnormal behavior, night and day reversal, nocturnal delirium, loud shouting, agitation, resistance to care, and loud soliloquy. The patient had a history of right cerebral embolism due to atrial fibrillation 1 month before the onset of dementia. Head CT revealed widespread cerebral infarction in the right cerebral hemisphere with bilateral lateral ventricular dilatation. The patient died at the age of 83, 10 months after the onset of cerebral embolism. The clinical diagnosis was mixed-type dementia. On autopsy the brain weighed 1,160 g. Widespread cerebral amyloid angiopathy (CAA) was observed, with distribution most severe in the cerebral cortical vessels and slightly milder in the leptomeningial and subarachnoid vessels. The artery, arteriole, and capillary walls were thickened by the deposition of amorphous, eosinophilic and beta-protein immunopositive amyloid. Abeta-deposition was more severe in capillaries and CAA tended to be more severe in the occipital regions. Multiple cortical microinfarcts were found, particularly in the crests of the cerebral gyri of watershed zones. Cerebral white matter, basal ganglia, thalamus, brainstem and spinal cord were relatively preserved from CAA. Infarction was not apparent, except for an embolic lesion in the right cerebral hemisphere and the cortical microinfarcts. We did not observe fibrinoid necrosis, granulomatous angiitis or giant cell reaction associated with CAA-vasculopathies. Rare instances were observed of neurofibrillary tangles and senile plaques corresponding to Braak stages II and A, respectively. We thought the multiple cortical microinfarcts occurred due to chronic hypoperfusion associated with CAA-associated vasculopathies of capillaries in the cerebral cortex. We suspected that the dementia was influenced by the CAA with multiple cortical microinfarcts. Pathologic findings of the patient suggest that CAA without AD-related Abeta-deposition might exist and that capillary Abeta-deposition might be an important factor of hemodynamic perturbation.
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PMID:[An autopsy case of senile dementia suspected to be influenced by cerebral amyloid angiopathy with multiple cortical microinfarcts]. 2096 Sep 31