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)

Three single CSF proteins with different molecular size (albumin, immunoglobulin G, and alpha2-macroglobulin) were determined by the method of electroimmunoassay in 61 children with febrile convulsions (FC) in order to evaluate the permeability of the blood-CSF barrier (B-CSF-B). Forty-two children with acute extracerebral infection served as controls. In contrast to a group of 22 children who suffered from acute meningoencephalitis or encephalitis, the CSF values of 48 children with FC were within normal limits. Thus even a very mild form of inflammatory encephalopathy-undetectable with conventional CSF investigation-was excluded in the majority of the children with FC. In 11 patients, however, CSF concentrations of albumin and alpha2-macroglobulin were abnormally raised, indicating a B-CSF-B distrubance. Elevated albumin values were found most frequently. In several children with FC lasting more than 20-30 min, B-CSF-B damage was probably caused by prolonged seizure activity since there is a linear correlation between albumin concentration and duration of convulsions. Several other factors known to raise the children's risk of developing epilepsy in later life were associated with the protein pattern of B-CSF-B disturbance in some of the children. In these cases, the cause of abnormal permeability of B-CSF-B is unknown and the condition might have existed prior to the occurrence of seizures.
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PMID:Febrile convulsions and blood-cerebrospinal fluid barrier. 7 3

Five patients experienced severe encephalopathy within hours of receiving their initial dose of cranial irradiation for the treatment of central-nervous-system leukaemia. Neurological findings included cranial-nerve palsies, seizures, ataxia, depressed consciousness, increased intracranial pressure, and signs of herniation. Symptoms developed within 3-30 hours of the first radiation treatment of 50-200 rad. Each patient had also received one or more injections of intrathecal chemotherapy before encephalopathy developed. The aetiology of this syndrome is uncertain but may involve transient cerebral oedema and/or an altered blood-brain barrier produced by the combination of intrathecal chemotherapy and cranial irradiation.
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PMID:Acute encephalopathy after initiation of cranial irradiation for meningeal leukaemia. 7 11

EEG patterns recorded in the waking state and during sleep were studied in 6 rhesus monkeys inoculated with a strain of Kuru previously passaged in rhesus monkey (ENAGE strain, rhesus L6 56). The onset of the disease was confirmed by the appearance of various clinical signs in 4 monkeys 15 months after inoculation. At the 16th month, the first EEG modifications appeared during sleep, which became lighter. The waking EEG was abnormal during the mature phase of the disease; it was characterized by slow anomalies and scattered spikes. The sleep EEG still presented 3 stages of Slow Wave Sleep which, however, were totally unlike the physiological stages. REM sleep rapidly disappeared, as did the cyclic organization pattern. Irritative phenomena became very significant and, in particular, very frequent 'tonic seizures' were observed. Experimental Kuru thus appears, in the rhesus monkey, as an epileptogenic encephalopathy, which is differentiated from both the human disease and the experimental disease in the chimpanzee.
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PMID:Experimental kuru in the rhesus monkey: a study of EEG modifications in the waking state and during sleep. 8 63

Four cases on a combination of lithium and thioridazine developed severe neurotoxic symptoms, e.g., delirium, seizures, encephalopathy and grossly abnormal EEG's. All patients had been on lithium without thioridazine prior to and after the neurotoxic episode with no complications or EEG changes. The possible risk of combining lithium and neuroleptics (thioridazine) is discussed and repeated EEGs are recommended as a preventive measure.
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PMID:Neurotoxicity with combined use of lithium and thioridazine. 10 47

Clinical and Neuropathological data on sixteen cases of progressive myoclonic encephalopathy are reported. This neurological syndrome appears after an average duration of thirty two months of haemodialysis and leads to death in four and a half months, and is characterized by myoclonus, speech disorder, epileptic seizures, and mental-status changes. At first, clinical signs and symptoms are related to haemodialysis, later they become permanent. An early diagnosis is based on EEG which is the only useful laboratory test, demonstrating bisynchronous slow-wave bursts. The caracteristic histopathologic findings are neuronal depopulation, lipofuscin accumulation, and appearance of Neurofibrillary degeneration, especially in Motor cortex, red nucleus and dentato-olivary systems. It seems to be justified to attribute P.M.D.E. to aluminium chronic poisonning; the source of the aluminium intoxication is not aluminium containing phosphate-binding gels but intravenously administreted tape-water. The intracellular binding of aluminium is shown from a histochemical study employing fluorescent stain Morin.
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PMID:[Progressive myoclonic encephalopathy in dialysis patients. Clinical, electroencephalographic and neuropathological study. Pathogenetic discussion]. 10 55

Two epileptic patients developed an acute toxic encephalopathy consisting of altered behavior, deteriorating seizure control, and confusion while taking sodium valproate alone. Serum valproate levels were greater than 100 microgram/ml in both. Toxic symptoms resolved when the dose of valproate was reduced, with a consequent fall in serum concentration of the drug.
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PMID:Acute intoxication with sodium valproate. 11 82

EEG findings and the course of epileptic seizures in two patients with neuronal ceroid lipofuscinosis (Batten Spielmeyer Vogt syndrome) are presented. Both patients, during the course of disease, developed therapy resistant epileptic reactions with myoclonicastatic seizures. These seizures in connection with diffuse encephalopathy and EEG pattern with 2.5 to 3.5/sec slow-spike-wave meet the criteria of the Lennox syndrome. Pathogenetic questions regarding possible additional genetic predisposition for epileptic seizures are discussed. Since therapeutic effect of different medications is uncertain hormonal therapy may be considered.
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PMID:[Myoclonic-astatic seizures (Lennox syndrome) in the course of juvenile neuronal ceroid-lipofuscinosis (M. Batten-Spielmeyer-Vogt) (author's transl)]. 21 38

A comparative study of five observations of a r (20) syndrome characterized by facial dysmorphism, the absence of severe malformations, and rather late onset of encephalopathy and seizures.
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PMID:[Ring-20 chromosome: a new syndrome]. 30 53

Diseases of the central nervous system (CNS) occurring during treatment of acute lymphoblastic leukemia (ALL) may be of leukemic or nonleukemic origin. Well known examples for CNS disease of nonleukemic origin are somnolence following prophylactic CNS irradiation, methotrexate-induced encephalopathy and acute infections caused by bacteria, viruses and toxoplasma gondii. Less known is the fact that also subacute CNS infections may occur in patients undergoing cytostatic therapy. Progressive multifocal leukoencephalopathy and subacute sclerosing panencephalitis (SSPE) are examples of this category of disease. Up to now 11 well documented cases of SSPE were reported occurring during treatment of ALL. Main clinical features were disorders of behaviour, consciousness and speach, seizures, paresis and inappropriate secretion of ADH. Several authors were able to demonstrate a deficiency of cellular immunity in patients with SSPE. In some cases this deficiency was consistent with reduced reactivity of T-lymphocytes against measles antigen only. The presence of inhibiting factors may be responsible for this phenomenon. Other authors found a normal or increased function of cellular immunity in SSPE; In hamsters occurrence of SSPE is induced by the simultaneous injection of hamster-adapted SSPE virus and antihamster lymphocyte serum. We, therefore, conclude that also in humans SSPE appearing during treatment of ALL is due to immunosuppression.
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PMID:[Non-leukemic disease of the central nervous system in children with acute lymphoblastic leukemia. III. Subacute sclerosing panencephalitis (author's transl)]. 36 90

Medical and psychological status of 166 patients previously treated for lead poisoning and of 22 sibling controls were evaluated. Maximum blood lead levels ranged from 40 to 471 microgram/dL. Eighteen patients had definite symptoms, 32 had questionable symptoms, and 116 were asymptomatic. No patients developed seizures, other neurological sequelae, or abnormal nerve conduction velocity. No statistically significant relationship was found between blood lead concentration (PbB) and subsequent intellectual function. The mean IQ of the patient cohort was 87, approximately at the 50th percentile for inner-city schoolchildren in Chicago. Detection prior to encephalopathy and prompt detoxification were effective in preventing or minimizing sequelae despite high PbBs.
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PMID:Lead poisoning without encephalopathy. Effect of early diagnosis on neurologic and psychologic salvage. 46 33


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