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 12-year-old girl with serologically-proved Mycoplasma pneumoniae infection developed right-sided hemiparalysis 10 days after the onset of the disease. Cerebral infarction was documented by cranial computed tomography; cerebral angiography revealed left carotid artery occlusion. Cerebrospinal fluid examination was normal. Cerebral infarction is a rare central nervous system complication of M. pneumoniae infection; however, occlusion of the internal carotid artery near the bifurcation has never been demonstrated; therefore, this patient with central nervous system complication of M. pneumoniae infection is unique.
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PMID:Internal carotid artery occlusion associated with Mycoplasma pneumoniae infection. 162 26

Two different techniques were utilized to identify the infiltration of polymorphonuclear leukocytes (PMN) into cerebral tissue following focal ischemia: histologic analysis and a modified myeloperoxidase (MPO) activity assay. Twenty-four hours after producing permanent cortical ischemia by occluding and severing the middle cerebral artery of male spontaneously hypertensive rats, contralateral hemiparalysis and sensory-motor deficits were observed due to cerebral infarction of the frontal and parietal cortex. In hematoxylin-and-eosin-stained histologic sections, PMN, predominantly neutrophils, were identified at various stages of diapedesis from deep cerebral and meningeal vessels at the periphery of the infarct, into brain parenchyma. When MPO activity in normal brain tissue was studied initially, it could not be demonstrated in normal tissues extracted from non-washed homogenates. However, if tissue was homogenized in phosphate buffer (i.e., washed), MPO activity was expressed upon extraction. Utilizing this modified assay, MPO activity was significantly increased only in the infarcted cortex compared to other normal areas of the brain. This was observed in non-perfused animals and after perfusion with isotonic saline to remove blood constituents from the vasculature prior to brain removal. The increased PMN infiltration and MPO activity were not observed in forebrain tissue of sham-operated control rats. Also, MPO activity was not increased in the ischemic cortex of MCAO rats perfused immediately after middle cerebral artery occlusion, indicating that blood was not trapped in the ischemic area. By using a leukocyte histochemical staining assay, activity of peroxidases was identified within vascular-adhering/infiltrating PMN in the infarcted cortex 24 hr after focal ischemia. An evaluation of several blood components indicated that increased MPO activity was selective for PMN. The observed increase of approximately 0.3 U MPO/g wet weight ischemic tissue vs. nonischemic cerebral tissues probably reflects the increased vascular adherance/infiltration of approximately 600,000 PMN/g wet weight infarcted cortex 24 hr after focal ischemia. This combined biochemical and histological study strongly suggests that PMN adhere within blood vessels and infiltrate into brain tissue injured by focal ischemia and that the associated inflammatory response might contribute to delayed progressive tissue damage in focal stroke. This modified MPO assay is a useful, quantitative index of PMN that can be utilized to elucidate the potential deleterious consequences of neutrophils infiltrating into the central nervous system after cerebral ischemia, trauma, or other pro-inflammatory stimuli.
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PMID:Polymorphonuclear leukocyte infiltration into cerebral focal ischemic tissue: myeloperoxidase activity assay and histologic verification. 165 59

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

The mechanism of periodic lateralized epileptiform discharges (PLEDs) still remains unclear, although it has been the subject of a number of theories. We investigated the relationship between the level consciousness and PLEDs in order to clarify both the clinical significance and the mechanism of PLEDs. We studied two neonates and two infants with acute organic lesions of the brain (cerebral infarction, meningoencephalitis, cerebral hemorrhage, acute infantile hemiplegia), of whom all showing PLEDs in EEG. In each case, we analyzed sequential EEG records and the level of consciousness, and measured the periodicity, voltage and duration of PLEDs by a computer controlled digitizer. In each case, the periodicity and voltage of the discharges were related to the level of consciousness. The appearance rate of PLEDs was relatively high at the level of consciousness from III-100 to III-200. The inverse correlation between the frequency (1/periodicity) and the voltage of PLEDs was significant in 53% of the total records of PLEDs; it was also frequently observed at the level of consciousness between III-100 and III-200. From above findings we concluded that an appropriate degree of damage to produce PLEDs is required in both the cerebral cortex and subcortical white matter corresponding to the level of consciousness from III-100 to III-200.
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PMID:[Clinicoencephalographic study of periodic lateralized epileptiform discharges in infants]. 176 Feb 5

A 67-year-old female suddenly developed a speech disturbance and right hemiplegia. She was diagnosed as having cerebral infarction. Then 2 months later, she had a fever and disturbance of consciousness. She died of respiratory insufficiency. The brain CT showed multiple high density areas with niveau. The autopsy revealed primary pulmonary artery sarcoma and multiple metastasis to the brain, the small intestine, etc. Primary pulmonary artery sarcoma is a very rare tumor which can occur in the pulmonary trunk of a person from any age groups. This case is a very rare one with cerebral metastasis.
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PMID:[Primary pulmonary artery sarcoma showing multiple HDA on the brain CT--an autopsy case report]. 176 64

The effectiveness and safety of a very low molecular weight heparin fraction were evaluated in the prevention of deep-vein thrombosis in patients confined to bed due to hemiplegia consecutive to a recent cerebral infarction. CY 222 was administered within 48 hours of the stroke by one single daily subcutaneous injection of 0.6 ml (= 15,000 U AXa IC) during 14 days. This randomized pilot study involved 30 patients. The effects of CY 222 were assessed in a group of 15 patients compared with a control group of 15 untreated patients. No deep-vein thrombosis was detected by the labelled fibrinogen test in the treated group, as against 12 patients in the control group. Six patients (3 in each group) died during the study. One case of lethal pulmonary embolism was observed and confirmed at autopsy in the control group. In the remaining 5 patients, no systematic autopsy which would have asserted the absence of pulmonary embolism or drug-induced haemorrhage was performed. Numerous standard laboratory tests confirmed that CY 222 was well tolerated.
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PMID:[Prevention of deep venous thrombosis of the leg by a very low molecular weight heparin fraction (CY 222) in patients with hemiplegia following cerebral infarction: a randomized pilot study (30 patients)]. 215 40

A 38-year-old man had a left lower lobectomy for pulmonary carcinoid. Following the operation, torsion of the left residual upper lobe occurred. Re-explosive thoracotomy was performed on the second postoperative day. The left upper lobe showed a clockwise 180-degree rotation. Pneumonectomy was not done. After the re-thoracotomy, the patient developed right hemiplegia. Head CT showed a cerebral infarction due to the thrombus of pulmonary vein that was released after the repair of the torsion.
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PMID:[Torsion after left lower lobectomy and cerebral infarction following the re-exploratory thoracotomy: a case report]. 223 92

We report 2 cases (n. 1 and 2) of cerebral infarction caused by a left atrial myxoma, and 1 case (n. 3). of dementia associated with a large left atrial myxoma. Cerebral emboli and neurological symptoms which can occur prior to cardiac obstructive and/or systemic signs require echocardiography. The cardiac post-operative condition was dramatically improved in cases revealed by an hemiplegia.
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PMID:[Neurological disorders disclosing auricular myxoma: 3 cases]. 223 96

We reported an autopsy case of thrombotic occlusion of the superior cerebral vein with hemorrhagic laminar necrosis of the right parietal cortex. A 68-year-old woman was admitted to our hospital because of a severe headache and left hemiplegia of acute onset. There was a past history of hypertension, fever of unknown origin, leukocytopenia and nasal dermatitis. Magnetic resonance images (MRI) disclosed thrombosis of the superior sagittal sinus and of the right parietal cortical vein as well as right parieto-occipital cerebral infarction. Although she improved with mild sequelae, the subsequent MRI showed a recurrent thrombosis of the superior sagittal sinus. Ten months after the onset she died suddenly, presumably due to acute myocardial infarction. Pathologically, thrombotic occlusion of the right parietal cortical vein, recurrent thrombosis of the superior sagittal sinus and old hemorrhagic cortical laminar necrosis of the right parietal region were revealed. Moreover, intracranial arteritis and phlebitis were observed, as well as arteriolitis in the peripheral nerves. In our case, MRI was useful for the diagnosis and following the course of cerebral venous thrombosis. Cerebral noninfective vasculitis may well have caused the venous thrombosis.
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PMID:[Thrombosis of the superior cerebral vein with hemorrhagic cerebral infarction--serial MRI and pathological study of a case]. 225 22

Cerebrovascular involvement is rare in progeria syndrome (Hutchinson-Gilford syndrome). A patient with progeria syndrome, who developed cerebral infarction, was reported. At 7 years of age, she suffered from right hemiplegia and transient ischemic attacks. X-ray CT showed multiple low density lesions in left frontal and parieto-occipital areas, which were enhanced with a contrast medium. Cerebral angiography demonstrated complete occlusion of left carotid artery and narrowing of vertebral artery. Brain imaging using 123I-N-isopropyl-p-iodoamphetamine (123I-IMP SPECT), which expressed regional cerebral blood flow, showed extensive perfusion defect over the left cerebral hemisphere in early scans, and redistribution phenomena in late scans. The symptoms improved gradually, which correlated well with 123I IMP-SPECT findings. This method will be useful to determine the prognosis as well as to understand changeable hemodynamic pathophysiology. A slowing of back ground on EEG also correlated well with clinical symptoms. It was necessary to examine the possibility of cerebrovascular involvement in progeria.
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PMID:[A case of progeria syndrome with cerebral infarction]. 229 53


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