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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Correlations between the clinical diagnosis on admission and the aetiological diagnosis revealed by computerized tomography (CT) were studied in 248 cases of acute hemiplegia. In 15% of the cases, hemiplegia was not due to a cerebral vascular accident. This mechanism was overestimated in 9% of the cases and missed in 14%. Ischaemia was overestimated in 15% of the cases and haemorrhage in 45%. With regard to transient deficit, CT scans showed that ischaemia was responsible for only 72% of acute hemiplegias, 28% of them being due to haematoma, tumour or subdural haematoma. In many cases where subdural haematoma or tumour was suspected on clinical grounds, CT confirmed that the suspicion was founded.
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PMID:[Etiological diagnosis errors corrected by x-ray computed tomography in acute hemiplegia]. 294 28

The purpose of this study was to determine if a significant correlation exists between the side of hemiplegia caused by a cerebrovascular accident and side of a subsequent major lower-extremity amputation. We also attempted to determine if a relationship exists between the time from cerebrovascular accident to the amputation, or level of amputation, and any concomitant risk factors including diabetes mellitus, hypertension, heart disease, or cigarette smoking. Forty-seven patients were included in the study; 40 of the 47 had an amputation on the side of the hemiplegia, which represented a statistically significant relationship (chi 2 = 5.00, p less than 0.05). The cause of limb loss was chronic ischemia in all cases; trophic ulcers and pressure necrosis played a significant role in 23 cases. No conclusions could be made between the level of amputation or time between the cerebrovascular accident and amputation in relation to the presence or absence of diabetes mellitus, hypertension, heart disease, or cigarette smoking.
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PMID:Amputation as a consequence of stroke. 318 24

Cerebral ischemia was recorded in 1.9% of 1277 patients with myocardial infarction. In most cases ischemia involved the carotid artery system, usually causing a hemiparesis or hemiplegia. Patients were mostly elderly, and the ischemic episode worsened their prognosis. The pathogenesis was surely often of embolic origin but several facts suggest that other mechanisms were also involved. Anticoagulant therapy, at least in the form in which it was used in these patients, i.e. subcutaneous administration of calcium heparin 5000 I.U. b.i.d. for thrombophlebitis prophylaxis, does not seem to prevent these complications.
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PMID:Cerebrovascular accidents in acute myocardial infarction. 362 75

A case of a acoustic neuroma with a two-stage removal due to severe bleeding is presented. The patient remained drowsy after the second operation and by the 8th day deteriorated quickly with progressive right hemiplegia and aphasia. The cerebrospinal fluid was bloody, vasospasm was shown in the angiograms, and an ischemic area was disclosed in the computed tomography scan. The outcome and the neuroradiologic examinations suggested that blood in the basal cisterns caused the vasospasm and the brain ischemia. A review of the literature disclosed only one similar case.
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PMID:Vasospasm after acoustic neuroma removal. 396 76

Periventricular arteriovenous malformations (AVMs) have often been deemed inoperable because of their location in critical structures. Furthermore, the excision of large lesions may be complicated by the potential for serious brain swelling and hemorrhage due to "autoregulation breakthrough." Nonetheless, the unfavorable natural history of the untreated disease in a symptomatic young patient has induced us to approach these lesions using staged microsurgical excision combined with elective barbiturate coma for maximal cerebral protection. Between 1979 and 1983, six patients (four female, aged 12 to 60 years, and 2 male, aged 14 and 29) who harbored large AVMs in the basal ganglia, thalamic, and hypothalamic areas presented with subarachnoid hemorrhage (2 cases), progressive neural deficits (3 cases), and intractable headache (1 case). Nineteen staged operations were performed for the complete excision of these lesions. Among the first three patients, there was one death due to "autoregulation breakthrough" hemorrhage into the lateral ventricle during the excision of a lesion approached through the sylvian fissure using standard anesthesia techniques. This led to the adoption of the transventricular surgical approach and elective barbiturate coma to facilitate exposure of the lesion and to protect the adjacent vital structures from potential ischemia. Three patients were treated in this fashion uneventfully. Of the five successfully treated patients, two have returned to their preoperative status and one has completely recovered from global hemispheric ischemia and hemiplegia. The hemiparesis in one patient worsened as a result of postoperative hypertensive intraventricular hemorrhage, and one patient developed mild dysphasia and hemiparesis. This experience suggests that this approach offers a valid therapeutic regimen for the treatment of this disease. During the same period, three patients--one man (age 23) and two women (aged 29 and 22)--harboring four intraventricular AVMs presented with intraventricular hemorrhage. After the acute effects of chemical ventriculitis and hydrocephalus were overcome with cerebrospinal fluid diversion, all four lesions were excised microsurgically using the transtemporal approach. One patient demonstrated significant and progressive improvement of her preoperative memory deficit. The remaining two patients have both returned to their preoperative employment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Microsurgical excision of paraventricular arteriovenous malformations. 398 6

Three cases of peripapillary choroidal filling defects demonstrated by fluorescein angiography are presented. In two cases the defect was interpreted as an occlusion of a posterior ciliary artery. One of these patients had neovascularization of the iris and ischemia of the upper half of the retina. Later a contralateral hemiplegia developed. The other patient had no other known vascular disease of the eye except occlusion of the posterior ciliary artery by giant cell arteritis. One patient had underfilling of the peripapillary choroid which was interpreted as insufficiency of the ciliary circulation; he had neovascularization of the iris, a nonperfused area in the retina and extensive microangiopathy due to arterial hypertension. It was concluded that ciliary hypoxia is the cause of iris and papillary neovascularization. Occlusion of one posterior ciliary artery is not enough to decompensate anterior segment circulation, unless other high risk factors such as carotid insufficiency or arterial hypertension are present.
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PMID:[The significance of ciliary circulation in the development of iris neovascularisation (author's transl)]. 616 Dec 69

We documented the anatomic basis for hemiplegia occurring on the same side of the body as the lateral medullary infarction. Extension of the zone of ischemia into the rostral spinal cord involves corticospinal fibers after they cross from the opposite side.
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PMID:Ipsilateral hemiplegia and the Wallenberg syndrome. 669 20

Sequential computed tomography (CT) scans were performed for up to 7 months on patients who presented with clinical evidence of lacunar infarction or ischemia. Sixty-nine percent of the patients showed lacunar infarction, and a negative scan did not suggest a better prognosis in stroke patients. Of patients with transient ischemic attacks (TIA) (lacunar), those with repeated bursts of hemiplegia (capsular warning syndrome) were more likely to be CT-positive (p less than 0.01). The clinical features of patients with lacunar infarction were examined and correlated with the features of infarction. Partial syndromes were found in 32% of the cases and included examples of monoparesis and dysarthria alone.
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PMID:A prospective study of lacunar infarction using computerized tomography. 719 33

An awake-primate model has been developed which permits reversible middle cerebral artery (MCA) occlusion during physiological monitoring. This method eliminates the ischemia-modifying effects of anesthesia, and permits correlation of neurological function with cerebral blood flow (CBF) and neuropathology. The model was used to assess the brain's tolerance to focal cerebral ischemia. The MCA was occluded for 15 or 30 minutes, 2 to 3 hours, or permanently. Serial monitoring evaluated neurological function, local CBF (hydrogen clearance), and other physiological parameters (blood pressure, blood gases, and intracranial pressure). After 2 weeks, neuropathological evaluation identified infarcts and their relation to blood flow recording sites. Middle cerebral artery occlusion usually caused substantial decreases in local CBF. Variable reduction in flow correlated directly with the variable severity of deficit. Release of occlusion at up to 3 hours led to clinical improvement. Pathological examination showed microscopic foci of infarction after 15 to 30 minutes of ischemia, moderate to large infarcts after 2 to 3 hours of ischemia, and in most cases large infarcts after permanent MCA occlusion. Local CBF appeared to define thresholds for paralysis and infarction. When local flow dropped below about 23 cc/100 gm/min, reversible paralysis occurred. When local flow fell below 10 to 12 cc/100 gm/min for 2 to 3 hours or below 17 to 18 cc/100 gm/min during permanent occlusion, irreversible local damage was observed. These studies imply that some cases of acute hemiplegia, with blood flow in the paralysis range, might be improved by surgical revascularization. Studies of local CBF might help identify suitable cases for emergency revascularization.
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PMID:Thresholds of focal cerebral ischemia in awake monkeys. 724 Nov 87

A mother and son suffer from hemiplegic migraine with onset in childhood. Both have nystagmus which has not changed for many years, but the date of onset is uncertain. They have an asymmetrical tremor, clinically indistinguishable from essential tremor. Neuroophthalmological examination revealed inability to produce smooth pursuit, gaze-paretic nystagmus, rebound nystagmus, failure of fixation suppression of the vestibuloocular reflex both horizontally and vertically, and low gain of the optokinetic system. These abnormalities, confirmed by electrooculography, are commonly seen in disease of the cerebellum and brainstem. Treatment with propranolol and pizotyline lessened the number of episodes of hemiplegia and improved the tremor. Hemiplegic migraine has been reported in association with nystagmus, retinal degeneration, deafness, and ataxia in varying combinations in three other families with autosomal dominant inheritance. These associated neurological manifestations likely represent system degenerations rather than the effect of repeated ischemia imputable to the migraine itself. The syndrome of hemiplegic migraine, tremor, and ocular smooth pursuit system disorder seen in this family appears to be inherited as a single autosomal dominant trait, although more than one autosomal dominant gene may be involved.
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PMID:An autosomal dominant syndrome of hemiplegic migraine, nystagmus, and tremor. 743 78


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