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)

A 74-year-old right-handed man with multiple cerebral infarction who presented with dementia simulating dementia of Alzheimer type (DAT) is reported. He had been well until April 20, 1987 when he developed transient right hand palsy lasting overnight. Eleven days later, he became confused, disorientated, and amnestic. He was admitted to this hospital on June 8. Physical examination revealed hypertension (170/90mmHg). On neurological examination, his consciousness was clear but he was demented. He showed disorientation, amnesia, and urinary incontinence. His most prominent symptom was disturbance of speech, including fluent aphasia and alexia with agraphia. Additionally, he showed ideomotor apraxia, construction apraxia, right-left agnosia, finger agnosia, and acalculia. On July 9, he had a transient attack of right hemiplegia with confusion. The brain CT scan performed on admission was unremarkable except for cavum septi pellucidum and a small low density area in the right basal ganglia. However, single photon emission computed tomography (SPECT) by 123I-labeled N-isopropyl-p-iodoamphetamine disclosed hypoperfusion of the cerebral blood flow in the border zones of the temporoparietal and frontal lobes on the left. A follow-up brain CT scan taken one month later demonstrated low density in the new areas corresponding to hypoperfusion shown by SPECT. Although the clinical features of the present case resembled those of DAT, dementia in this case was regarded as the result of multiple cerebral infarction since it occurred acutely with mild motor deficits, and brain CT scans and SPECT showed lesions indicating focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multi-infarct dementia clinically simulating dementia of Alzheimer type. A comparison with angular gyrus syndrome]. 278 20

Blood velocity in the middle cerebral artery was measured by transcranial Doppler ultrasonography in 15 patients suffering complete hemiplegia of less than 12 hours' duration, presumed due to cerebral ischemia. Among seven patients in whom blood velocity was greater than 30 cm/sec, five made complete or partial useful recovery of the involved hand and arm. Among eight patients in whom blood velocity was less than 30 cm/sec, one recovered completely while the other seven retained permanent total paralysis of the hand and arm.
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PMID:Prognosis of acute hemiplegia estimated by transcranial Doppler ultrasonography. 328 21

Behavioral changes after occlusion of the left middle cerebral artery (MCA) in rats were investigated for 16 weeks. Impairment of motor coordination and incidence of neurological deficits including hemiplegia and abnormal posture were present for the first 2 and 4 weeks after MCA occlusion, respectively. Learning behavior in one-trial passive avoidance task was disturbed for the entire 16-week period when rats were trained at days 3 after MCA occlusion. Reacquisition was also impaired when rats were retrained on 8 weeks after MCA occlusion. Except for synchronized EEG at days 2 after MCA occlusion, significant changes in spontaneous movement and EEG were not observed in the MCA-occluded group. These results suggest that this rat model of MCA-occlusion is useful for quantitatively measuring functional changes in chronic phase of focal cerebral ischemia.
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PMID:Behavioral changes after focal cerebral ischemia by left middle cerebral artery occlusion in rats. 340 38

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

We describe a 68-year-old patient with cerebral ischaemia who underwent a phlebotomy to lower an elevated haematocrit (0.61 l/l. The procedure was complicated by the development of a total hemiplegia after two hours. CT scanning showed two borderzone infarcts. We conclude that the plasma volume of patients with cerebral ischaemia and a high haematocrit may be contracted to such an extent that venesection is hazardous. The most appropriate treatment in these patients is expansion of the plasma volume.
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PMID:Cerebral borderzone infarcts after phlebotomy. 380 83

Since the acute revascularization was adopted as a probable means of surgical treatment for the acute cerebral ischemia, it became essential to discuss how the initial symptom at onset can predict the subsequent development of severe or mild cerebral infarction. In the 2 past years, 207 cases of cerebral ischemic lesion were admitted non-selectively and mostly in the early stage after the attack. Excluding 40 cases of surgical treatment, 167 cases were classified into 30 cases of TIA, 13 cases of RIND, 94 cases of minor completed stroke and 30 cases of major completed stroke. In 30 cases of major completed stroke, 21 cases developed severe motor hemiplegia from the onset and the rest 9 cases initially mild hemiparesis which gradually developed to severe hemiplegia thereafter. The cases of minor completed stroke showed mild or moderate hemiparesis initially and did not worsen thereafter. In the group of TIA and RIND, no case had developed severe hemiplegia in any stage of clinical course. The disturbance of consciousness were noted in 5 cases out of 94 cases of minor completed stroke (5%) and 12 cases out of 30 cases of major completed stroke (40%) in the following time course. More than half of the cases of major completed stroke were considered to be cerebral embolism including the retrospective review.
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PMID:[Assessment of major stroke at onset in cerebral ischemia. In consideration of acute revascularization]. 399 Aug 98

The effects of an opiate agonist (morphine) and antagonist (naloxone) on neurologic function in conditions of acute and subacute focal cerebral ischemia were tested in a baboon model. Fourteen baboons (Papio papio) underwent unilateral transorbital microsurgical occlusion of the middle cerebral artery (MCA). Blood pressure, heart rate and core temperature were monitored continuously; frequent arterial blood gas measurements were made. Cardiac output, cardiac filling pressures, and regional cerebral blood cross-flow were measured in selected baboons. Naloxone administered intravenously consistently reversed hemiparesis and hemiplegia in all baboons for as long as they lived (4 h to 8 days postocclusion). Morphine administered intravenously converted hemiparesis to hemiplegia; this effect was naloxone-reversible. There were no significant changes in any parameter measured after the administration of either drug. Phenylephrine (used to elevate mean arterial pressure to 20 mm higher than the highest pressure measured after naloxone administration) and isoproterenol (used to elevate cardiac output to 1 l/min higher than the highest value measured after naloxone administration) produced no change in neurologic function. It appears that naloxone can reverse, and morphine exacerbate, focal ischemic neurologic deficits produced in baboons by MCA occlusion. The observed changes in neurologic function are not associated with or mediated by alterations in core temperature or cardiopulmonary functions.
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PMID:Naloxone reversal and morphine exacerbation of neurologic deficits secondary to focal cerebral ischemia in baboons. 669 45

Stroke induced by a carotid occlusion in gerbils was reversed by intraperitoneal (i.p.) injection of naloxone (1 mg/kg) for up to 30 min. Placebo-treated stroked gerbils died in 48 hr; 40% of gerbils implanted with 10 mg naloxone pellets survived over 2 weeks without neurologic deficit. Intravenous (i.v.) injection of naloxone produced the same transient reversal of hemiplegia in 2 patients with neurologic deficit from cerebral ischemia. These findings suggest the involvement of endorphins and opiate receptors in the pathophysiology of stroke, and suggest the possible clinical use of opiate antagonists in humans in the acute phase of stroke.
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PMID:Reversal of neurological deficits by opiate antagonist naloxone after cerebral ischemia in animals and humans. 708 9

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

Blunt carotid artery trauma is uncommon but has been associated with severe, permanent neurologic deficits in 42% and mortality in 30% of 96 patients previously reported in the English literature. Since neurologic symptoms characteristically develop only after a latent interval and since physical evidence of significant cervical trauma often is absent, diagnosis of nonpenetrating carotid injuries with the use of arteriography usually is delayed until the appearance of obvious, frequently irreversible neurologic complications. Carotid injuries should be suspected in patients who develop monoplegia or hemiplegia following blunt craniocervical trauma, particularly if computerized tomography excludes the presence of intracranial hemorrhage. The cumulative results of a collected series of 96 patients suggest that early surgical correction of blunt carotid injuries is appropriate for patients with transient episodes of cerebral ischemia, strokes in evolution, or mild completed neurologic deficits.
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PMID:Blunt carotid artery trauma: report of two cases and review of the literature. 736


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