Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the relationship between middle cerebral artery (MCA) trunk lesions and the etiology of Binswanger type (B type) infarction, which was demonstrated as a diffuse subcortical low density area/high intensity area by CT/MRI, patients with both MCA lesions and B type infarction were studied clinically. Eighteen patients with B type infarction were diagnosed among 224 patients with MCA occlusion/stenosis on angiography accounting for 8%. The incidence was as high as 25% in M2 stenosis. The mean age of B type infarction patients was 64 years and 16 of them were men. Chronologically stepwize/slowly-progressive deterioration of clinical manifestations were observed in 14. All patients had hemiplegia, though half of them were mild or moderate in severity. Furthermore, aphasia, Gerstmann syndrome and dementia were present in 10, 1 and 2 patients, respectively. Twelve had a history of hypertension, while 11 showed transient decreases with marked changes (more than 31 mmHg in mean arterial blood pressure) in arterial blood pressure during their clinical course. Out of 9 patients in whom cerebral blood flow (CBF) was measured by 133Xe injection method/inhalation method, 7 demonstrated mild to moderate decreases in mean CBF (more than 30 ml/100 g/min) with no relation to the severity of MCA lesions. These findings suggested that hemodynamic mechanisms associated with hypoperfusion due to marked fluctuations in blood pressure are accelerating factors of B type infarction and MCA lesions, even though ischemia in the subcortical area due to leptomeningeal anastomosis may be mild or moderate.
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PMID:[Clinical study on the relationship between middle cerebral artery lesions and Binswanger type infarction]. 260 75

The term lacuna or lacunar cavity defines the pathological lesion while the clinical pictures due to lacuna or lacunes are referred to as 'lacunar syndromes'. The lacunar syndromes include: (1) the typical lacunar syndromes or lacunar syndromes proper--pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis including dysarthria and clumsy hand, sensorimotor stroke and abnormal movement syndromes, (2) reversible ischemic attacks (TIA and/or PTIA or RIND), (3) other clinical syndromes which may be due to lacunar lesions such as suprabulbar palsy; lacunar dementia, or subacute arteriosclerotic encephalopathy (or Binswanger's disease). The different clinical pictures are reviewed, some mechanisms underlying the lacunar lesion are briefly discussed and the old label 'small vessel diseases' in cases with lacunes is reconsidered.
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PMID:The lacunar syndromes. 269 95

An 80-year-old hypertensive woman developed right hemiplegia and died 24 hours after admission. Neuropathologic examination revealed multiple cerebral infarcts of various ages and diffuse subcortical arteriosclerotic encephalopathy. Clusters of asymptomatic "expanding" lacunes, due to dilatation of the perivascular spaces, were found in both dentate nuclei. These cavities, which presented as space-occupying lesions, were surrounded by a single layer of flattened cells and contained 1 or more sections of normal-looking arterioles. Such a topographic grouping of lacunes in the dentate nucleus has not been described previously. The mechanism of widening of the perivascular compartment remains unclear; its occurrence in a hypertensive patient and its association with typical Binswanger's subcortical arteriosclerotic encephalopathy and severe atherosclerosis with multiple infarcts suggest a common pathophysiologic mechanism possibly including an alteration of the blood-brain barrier.
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PMID:Expanding cerebellar lacunes due to dilatation of the perivascular space associated with Binswanger's subcortical arteriosclerotic encephalopathy. 368 82

A clinicopathologic study was made of 45 elderly persons whose autopsied brains showed the pathologic changes of progressive subcortical vascular encephalopathy (Binswanger type). Progressive subcortical vascular encephalopathy (PSVE) was observed in 3.8 per cent of all autopsied brains of elderly persons and in 6.7 per cent of the brains of those with cerebrovascular diseases. White matter lesions were graded from I to III (slight to severe). Small infarcts in the basal ganglia, thalamus, and pons were common, but the cerebral cortex was usually preserved. Neuropsychiatric symptoms included dementia, urinary incontinence, hemiplegia, pseudobulbar palsy, psychosis, parkinsonism, and mutism. In thge Grade III group there was a high incidence of pseudobulbar palsy, parkinsonism, and mutism. Pathologic study showed marked cerebral arteriosclerosis in almost all cases. Angionecrosis was observed in 60 to 80 per cent. Fibrotic and stenotic changes of the blood vessels in the deep white matter were also noted, particularly in 90 per cent of the Grade III cases. A suggested explanation for the pathogenesis of PSVE is based on the effects of various complications such as hypertension, cardiac disease and malnutrition which may play an important role in PSVE when they occur in elderly persons with a history of long-standing hypertension, marked cerebral arteriosclerosis, and arteriolar changes in the cerebral white matter.
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PMID:Clinicopathologic study of progressive subcortical vascular encephalopathy (Binswanger type) in the elderly. 709 54