Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unlike neurological deficits resulting from intracranial hemorrhage in patients with cerebral arteriovenous malformation (AVM), which have well defined etiology, the pathogenesis and treatment of progressive and/or fluctuating non-hemorrhagic neurological and psychological deficits require clarification. Values for local cerebral blood flow (LCBF) and local partition coefficients (L lambda) were measured by the method using stable xenon (Xe)-computerized tomography (CT-CBF) scanning, and were compared to 133Xe inhalation values using external probes in 16 patients with cerebral AVM's. Values were measured by both methods before and after total excision of AVM's in five cases. Neurological and mental status assessments were compared with LCBF results. Clinical improvement was most evident after total excision of AVM's. Other procedures, such as clipping of vessels, partial excision, and ventriculoperitoneal shunting for hydrocephalus, were associated with frequent complications. Embolization carried risks of cerebral infarction and was not efficacious unless combined with excision. Medical treatment resulted in poor or unsuccessful seizure control, with neurological deterioration despite anticonvulsant therapy. Compared with age-matched normal individuals, LCBF values in patients with AVM's were significantly reduced, particularly adjacent to the AVM's. Mean L lambda values for gray and white matter were normal. After excision, LCBF values in gray and white matter increased significantly up to normal. Due to overestimation of CBF by shunt flow with the 133Xe method of measurement, no correlation was found with results of the CT-CBF method before AVM excision, but significant correlation of the two methods resulted after excision. If accurate LCBF values are obtained by high resolution, direct measurement of tracer clearance from brain tissue, progressive and/or fluctuating neuropsychological deficits correlate with the degree of cerebral steal.
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PMID:Xenon-enhanced CT CBF measurements in cerebral AVM's before and after excision. Contribution to pathogenesis and treatment. 686 79

Lactic acid concentration has been determined in the cerebrospinal fluid (CSF) of 715 patients suffering from various neurological diseases. It was found to be most often elevated in cases of ischemic cerebral infarction, cerebral contusion, arteriosclerotic dementia, metastatic encephalitis, bacterial meningitis, menigiosis carcinomatosa and after epileptic seizures. In fewer cases lactate levels were increased with brain tumors, encephalitis, viral meningitis and radiculitis. Diagnostic relevance of CSF lactic acid determination is discussed with regard to ischemic cerebral disorders, differential diagnosis of viral and bacterial meningitis and for the confirmation of epileptic seizures.
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PMID:[Importance of cerebrospinal fluid lactate determination in neurological diseases]. 686 67

Sudden cerebrovascular insults occurred during or immediately following remission induction therapy in 4 children with acute lymphoblastic leukemia. In 3, cerebral infarction was due to thrombosis. In the fourth, an intracerebral hematoma developed representing either frank hemorrhaging or a hemorrhagic infarction. None of the patients had central nervous system leukemia or extreme leukocytosis at the time of diagnosis. Symptoms were obtundation, hemiparesis, seizures, and headache. The induction chemotherapy included L-asparaginase which causes deficiencies of antithrombin, plasminogen, fibrinogen, and factors IX and XI. These hemostatic abnormalities may explain the thromboses and bleeding observed in these children.
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PMID:Thrombotic and hemorrhagic strokes complicating early therapy for childhood acute lymphoblastic leukemia. 693 53

Central nervous system disorders are not uncommon in patients with hyperparathyroidism and hypercalcaemia. Usually these consist of neuropsychiatric disturbances but acute encephalopathies and seizures may occur. A rare manifestation is cerebral infarction. A patient is presented with neuroradiological evidence of infarction caused by cerebral arterial spasm which appears related to hypercalcaemia due to hypervitaminosis D. Arterial spasm is suggested as a possible aetiological factor in focal neurological lesions associated with hypercalcaemia.
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PMID:Hypercalcaemia associated with cerebral vasospasm causing infarction. 696 41

We add two cases of neoplastic angioendotheliosis to the previous 13 with central nervous system manifestations. This unusual neoplastic phenomenon is thought to represent a diffuse malignant proliferation of endothelial cells. A man aged 58 first had transient ischemic attacks followed by a subacute profound dementia with psychomotor retardation. Remission followed steroid therapy. Abulia recurred along with a gradually progressive paraplegia leading to death 16 months after onset of symptoms. Pathologic examination showed tumor masses in the basal ganglia and widespread patchy cerebral infarction. The spinal cord below the midthoracic level was destroyed. Microscopically small mononuclear tumor cells were widespread within and largely confined to the lumens of small cerebral blood vessels which showed varying degrees of occlusion and recanalization. Factor 8 antigen, a specific endothelial cell marker, was not present on the surface of the malignant cells. Another man aged 61 developed subacute dementia with frontal lobe signs, dysphasia and impairment of memory. Computerized tomography showed multiple infarcts. A brief respite followed steroid therapy but progressive deterioration led to death in 15 weeks. Frontal lobe biopsy revealed the same neoplastic vascular process. The hallmark of the illness is a progressive subacute lobar dementia. Transient spells may occur. Hemiparesis is unusual and seizures do not occur except terminally. Angiography is normal.
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PMID:Neoplastic angioendotheliosis. 703 26

Cerebral infarction was produced in rats by internal carotid injection of 35 mu plastic microspheres. Electroencephalograms were recorded through the scalp and from the thalamus. Regional concentration of endogenous brain ATP was studied by the histochemical bioluminescent method. Following embolization, a specific pattern of seizure propagation is noted. Spike activity appears first in the contralateral hemisphere, then the contralateral thalamus, infarcted thalamus, and finally the cortex. The results of these present experiments suggest that seizure activity following an evolving focal ischemic injury in the brain appears in the face of lowered ATP content.
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PMID:Seizure propagation and ATP depletion in the rat stroke model. 735 65

The clinical and laboratory features of 24 patients with proven mitral valve prolapse (MVP) and brain dysfunction are reported. The age range of affected patients was between 20 and 63 years (average of 43) and 70 percent were women. MVP was documented prior to the brain illness in only 4 patients. The majority of patients experienced bland cerebral infarction. Disorders also included transient ischemic attacks, cerebellar infarctions, parencymatous and subarachnoid hemorrhage, seizures and retinal artery occlusion. Significant risk factors for stroke other than MVP were lacking in the patient group. Cerebral angiograms occasionally showed distal occlusions of small arteries suggesting embolic brain lesions. Our study suggests that MVP is a risk factor for stroke. We recommend echocardiography in patients with cerebral ischemia who lack clear, recognized risk factors for stroke. We believe the basis for this brain disorder to be emboli from damaged mitral valve leaflets.
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PMID:Brain events associated with mitral valve prolapse. 742 82

Twenty-three patients with epileptic type moyamoya disease are reviewed among 200 moyamoya disease patients. Ten boys and 13 girls aged 5 months to 12 years were followed over 6 months to 17.3 years. Six had generalized seizure and 17 had focal seizure. Operations were performed within 1 year in eight patients, within 1-3 years in five, and more than 3 years after onset in 10. Nineteen patients improved and suffered no seizure without receiving antiepileptic drugs, but four patients developed true epilepsy and three of these suffered cerebral infarction. Multivariate analyses showed that toddlers aged less than 1 year and mild or severe abnormal computed tomographic (CT) findings correlated with a bad outcome. This study showed that epileptic type moyamoya disease has the same clinical features as transient ischemic attack or infarction type. Age under 1 year and CT abnormalities indicate a poor prognosis and necessity for early reconstructive surgery.
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PMID:Long-term follow-up study of "epileptic type" moyamoya disease in children. 750 1

A cohort of 8 patients with myxoma of the left atria and neurological manifestations is reported. Cerebral ischaemia, sometimes responsible for epileptic seizures, led to the discover of the myxoma (5 cases) or recurrence after exeresis (1 case) with imaging evidence of cerebral infarction in 5 cases. The first manifestation was a retinal embolism and temporary ischaemia in 1 case and pulmonary embolism with regressive cerebral ischaemia in another case with bilateral myxoma. Some clinical particularities should be underlined including exercise-induced neurological defect (3 cases), systemic embolism associated with cerebral infarction (3 cases), migraine headache as the initial manifestation (1 case) preceding by a pseudolupic syndrome suggesting the possibility of cerebral vasculitis or infectious endocarditis (1 case). The prognosis depends on the risk of recurrent atrial tumour formation (1 case). Metastases are rare. Multiple cerebral aneurysms (3 cases) did not lead to haemorrhagic complications.
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PMID:[Myxoma of the left atrium with neurologic manifestations: 8 cases]. 759 71

Patients infected with the human immunodeficiency virus (HIV) appear to have a high risk of ischaemic cerebral events. We observed two cases of cerebral infarction in patients with acquired immune deficiency syndrome (AIDS). In the first case, a 38-year-old homosexual with no cardiovascular risk other than smoking presented with rapidly progressive hemiparesia. Brain CT-scan visualized two infarcts in the territory of the right sylvian artery and the arteriography an occlusion of the internal carotid artery. In the second, a 37-year-old homosexual, hospitalization was required for a left-sided pure sensitive epilepsy seizure. There was no cardiovascular risk other than smoking. Magnetic resonance imaging showed parietal ischaemia and thrombus in the left atrium without atrial hypertrophy was seen at transoesophageal echocardiography. In both cases, there was no evidence of endocarditis, dissection of the neck vessels or disseminated intravascular coagulation nor of associated viral or bacterial infectious complication of AIDS. Angiographic findings eliminated cerebral vascularitis. Among the perturbed haemostasis factors previously reported in HIV+ patients, we observed free proteins S deficiency (68 and 43%) and heparin cofactor II deficiency (54 and 40%). Serum albumin was 33 and 32 g/l respectively. Outcome was favourable in both cases with anticoagulant therapy. These coagulation anomalies would not appear sufficient to explain cerebral infarction. Other mechanisms including immune complexed deposition, direct HIV toxicity for endothelial cells or the effect of cytokines on smooth muscles fibres and fibroblasts are probably more important causal factors.
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PMID:[Cerebral infarction in human immunodeficiency virus infection]. 763 44


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