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)

The effect of the opiate antagonist naloxone on both the neurological deficit and regional cortical blood flow after middle cerebral artery occlusion in the cat was investigated. In animals with mild symptoms, naloxone did not consistently produce a significant behavioral effect. In all cats with neurological deficits, including hemiplegia or severe hemiparesis, 2 mg/kg naloxone administered intravenously 4 h after the ischemic lesion produced a reversal of neurological symptoms. This effect began within 2 min following naloxone injection and lasted for approximately 20 min. Animals were then anesthetized and cortical blood flow was measured by the hydrogen clearance method. Average cortical blood flow on the side of the occlusion was 50% that of the control side. Naloxone produced a significant additional decrease of 19.5% in cortical blood flow in the ischemic hemisphere, whereas no effect on blood flow on the control side was noted. Thus, although naloxone appears to temporarily reverse the severe neurological deficits resulting from middle cerebral artery occlusion in the cat, this effect appears to be accompanied by a decrease in local blood flow to the ischemic cortex.
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PMID:Focal cerebral ischemia in the cat: effect of naloxone on cortical blood flow and neurological deficit following middle cerebral artery occlusion. 345 50

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

We studied effects of YM796, a novel muscarinic agonist, on behavioral, histological and regional cerebral blood flow changes in the chronic phase after focal cerebral ischemia in rats. YM796 (0.03, 0.1, 0.3 and 1 mg/kg) was administered orally once a day from the 7th to the 13th day after the permanent occlusion of left middle cerebral artery. On the 7th day, rats were trained in one-trial step-through passive avoidance task 45 min after drug administration. Test trials were carried out on the 8th and 14th days. Neurological deficits, including hemiplegia and abnormal posture, were observed on the 7th and 14th days. After the completion of behavioral studies, the rats were decapitated and cerebral infarction was measured. Regional cerebral blood flow was also measured by the hydrogen clearance technique 7 days after MCA occlusion. YM796 (0.1-1 mg/kg) significantly (P < 0.05) attenuated the impairment of learning behavior in a dose-dependent manner without affecting spontaneous locomotor activity. The ameliorating effect of YM796 (0.3 mg/kg) on the impaired learning behavior was significantly (P < 0.05) suppressed by intracerebroventricular injection of pirenzepine (10 micrograms/rat), an M1 antagonist. No significant difference in either neurological deficits or cerebral infarction was found between the vehicle- and YM796-treated groups. Further, YM796 (0.3 mg/kg) had little effect on the reduced blood flow in the ipsilateral frontal cortex 7 days after occlusion. These results suggest that YM796 improves the impaired learning behavior probably by activating central M1 receptors in a rat model of chronic focal cerebral ischemia.
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PMID:YM796, a novel muscarinic agonist, improves the impairment of learning behavior in a rat model of chronic focal cerebral ischemia. 771 53

Two cases of severe complications due to injection of hydrogen peroxide under pressure into areas of muscular attrition in war wounds are reported. In both cases the administration of hydrogen peroxide was associated with tachypnoea, with major arterial desaturation and a precordial "mill-wheel" murmur was heard. In one case, these symptoms were followed by hemiplegia caused by paradoxical arterial gas embolism, and in the other case by a pulmonary oedema confirmed by computerized tomography. Both patients recovered under hyperbaric oxygen therapy. The release of gaseous oxygen under the effect of tissue catalase and the membrane peroxydasic activity of hydrogen peroxide initiate such complications. The injection of hydrogen peroxide under pressure into a closed or partially closed cavity should therefore be strictly prohibited.
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PMID:[Risks of hydrogen peroxide irrigation in military surgery]. 773 29

We examined a patient with alternating hemiplegia of childhood (AHC) who had over a 23-year history of AHC to investigate the origin of the neurological deterioration with increasing age. Hemiplegic attacks had occurred consistently at a frequency of a few per week since infancy, and he first experienced attacks of cerebellar ataxia at the age of 23 years. Intellectual impairment, dysarthria, dystonic posturing, and a wide-based gait had been slowly progressive, but they had been stable since he turned twenty. The electromyographic response to transcranial magnetic stimulation was normal between attacks and showed reversible alteration during an attack. MRI revealed slight dilatation of the lateral ventricles, and MR angiography showed normal cerebral blood flow. Proton MR spectroscopy between attacks showed normal peak area ratios for N-acetyl groups, choline-containing compounds, and creatine and phosphocreatine, and it also demonstrated no lactic peak. 123I-IMP SPECT between attacks demonstrated diffuse cerebral hypoperfusion despite no evidence of ischemic change in the above MR study. These results suggest that the slowly progressive neurological deficits are due to the primary underlying pathology rather than the secondary neuronal loss as a result of frequent ischemic attacks.
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PMID:Alternating hemiplegia of childhood: report of a case having a long history. 913 95