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 70-year-old man was admitted to our hospital because of fever and progressive dyspnea in December 1989. He was already diagnosed as having erythrocytosis secondary to pulmonary fibrosis 4 years previously and the values of his hematocrit (Ht) were maintained between 44.5 and 62.9% by repeated phlebotomy. Immediately after admission, severe diarrhea developed and the Ht value was 61.5%. Around 1:30 a.m. of the 3rd hospital day, he developed disturbance of consciousness. In addition, the serum levels of LDH, CPK, aldolase, and myoglobin of muscle origin increased markedly and the Ht value showed 78.5%. While the level of consciousness was gradually restored by 600 ml phlebotomy and 1,500 ml saline infusion, dysarthria and hemiplegia became evident. The Ht value early in the morning of the 3rd hospital day was reduced to 59.4%. Although cranial CT and MRI performed 74 days and 15 months, respectively, after the onset of the symptoms failed to reveal any abnormal shadow, he was clinically suspected to have cerebral infarction. These findings emphasize that abrupt increase in Ht or blood viscosity is a possible factor triggering cerebral infarction, and adequate control of Ht value is recommended for the prevention of such a condition in the aged.
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PMID:[Cerebral infarction and high serum levels of muscle-derived enzymes associated with abrupt increase in hematocrit in a patient with secondary erythrocytosis]. 175 34

Magnetic resonance images of a case of superior sagittal sinus thrombosis before and after complete recanalization are presented. The patient was a 61-year-old man with two days history of intermittent right hemiconvulsion followed by post-ictal hemiplegia. Mild erythrocytosis was noted on admission. CT scans revealed left frontal hemorrhagic infarction with empty delta sign in the middle portion of the superior sagittal sinus. Left carotid angiogram showed occlusion of two frontal cortical veins and retrograde filling of these veins into the cavernous sinus. Lack of filling of the middle and anterior part of the superior sagittal sinus was noted. These studies led to the diagnosis of superior sagittal sinus thrombosis associated with hemorrhagic infarction. He was treated with intravenous infusion of low molecular dextran and venesection. Neither heparin, urokinase, hyperosmolar solutions nor steroids were used because of the presence of hemorrhagic infarction and of the lack of signs of increased intracranial pressure. He completely recovered neurologically and recanalization of the superior sagittal sinus was confirmed angiographically eight weeks after the onset. Magnetic resonance images were taken with a Siemens 1.5 T Magnetom scanner using spin-echo pulse sequences. A T 1-weighted mid-sagittal magnetic resonance image ten days after the onset showed hyperintensity in the middle part of the superior sagittal sinus which corresponded to the thrombus. Both T 1 and T 2 weighted coronal images revealed a small area of hypointensity indicating the existence of residual blood flow in the superior sagittal sinus in addition to the thrombus both in the sinus and in the cortical vein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sequential magnetic resonance images of a case of cerebral sinus thrombosis--imaging of the thrombosed sinus and its recanalization]. 340 6