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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases are described who developed epileptic seizures whilst taking maprotiline hydrochloride in therapeutic dosage. In both cases the electroencephalogram was normal and the fits stopped on withdrawal of the drug.
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PMID:Epileptiform seizures with maprotiline hydrochloride. 53 62

Effects of cocaine on the spread of epileptiform discharges within the limbic system were studied in cats prepared with bilateral arrays of indwelling electrodes. Low frequency focal electrical stimulation at threshold intensity was employed to initiate after-discharges in the hippocampus and amygdala. Latencies for the propagation of epileptiform activity to distant limbic sites were determined. Saline and drug tests were alternated, with 96-hr intervals between cocaine administrations. Three subconvulsant doses (1--10 mg/kg cocaine hydrochloride, injected intramuscularly) were tested in a counterbalanced order. Cocaine administration significantly increased the speed at which epileptiform discharges spread to the amygdala and to the hippocampus. This effect was dose-related, it followed both hippocampal and amygdalar stimulation and was evident in ipsilateral as well as contralateral projection sites. These changes were found when limbic seizure patterns were localized and also after fully developed motor convulsions were evoked. In addition, cocaine decreased the duration of the propagated discharges. These results suggest that subconvulsive doses of cocaine have an excitatory effect on the hippocampus and amygdala, increasing their sensitivity to repetitive discharges originating in distant sites. A concurrent inhibitory effect is suggested by the decreased duration of the propagated discharges.
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PMID:Effects of cocaine on propagation of limbic seizure activity. 53 57

This study compares the effects of various so-called trimix mixtures (10, 20, and 40% N2 in He-O2) on the convulsion threshold pressure (Pc) and EEG activity in 60 adult male Wistar rats with chronically implanted electrodes with those in 20 rats in He-O2 only. Restrained animals were individually compressed with trimix mixtures at 80 or 160 atm per hour to a simulated depth of 138 ATA; colonic temperature was maintained at normal levels. Pc was defined as the initial occurrence of overt sustained generalized tonic-clonic seizures, accompanied by typical "spike and wave" patterns in all EEG leads. As in man, in rats trimix increased the depth of the onset of HPNS tremors and myoclonic jerks in all six groups of rats. However, the Pc of the trimix groups was no different from the Pc of the helium-oxygen group (113 ATA), and at 40% N2, rats showed EEG seizures but no overt convulsions. These results are discussed in relation to those of other studies showing the extension of Pc in mice and monkeys attained by adding narcotics to heliox; the paper also considers the relevance of method of compression, addition of nitrogen, core temperature, and species differences, as well as the need for EEG measurements and direct observation of overt convulsions as indicators of an effective antagonism of HPNS.
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PMID:Effect of helium/nitrogen/oxygen mixtures on HPNS convulsion threshold in euthermic rats. 53 65

The causes and short-term prognoses of neonatal convulsions in infants less than four weeks of age were studied in 77 full-term infants born in Stockholm in 1970--1976. In half of the infants (48%), hypoxia was considered to be the probable main etiology, while infection and metabolic disease including hypoglycemia and hypocalcemia were the next commonest cause, 12% for each condition. The etiology was unknown in 29% of the infants although 15 of those 22 included in this group had other additional diagnoses. The total mortality was 13%. At one year of age, 19 of the surviving 64 infants (30%) had severe psychomotor retardation. Of 11 infants with normal mental development at 12 months of age 6 had cerebral palsy and 5 epileptic seizures. Thirty-four (53%) of the infants still had no signs of sequelae. The poorest prognosis was found in the group with hypoxia as the main probable etiology. The incidence of neonatal convulsions was 1.5 per 1 000 full-ferm deliveries. In a similar study from Gothenburg which was performed 10 years earlier the incidence was 3.7 per 1 000. Corresponding figures for perinatal mortality rate were 13.5 and 23.8.
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PMID:Neonatal convulsions. Incidence and causes in the Stockholm area. 53 4

In a group of 400 epileptic inpatients of the Neurological Clinic of Parma, 82 were over 60 years of age. Only 59 of them presented fits for the first time after the 60th year of age and in 78% of these, a definite anatomical damage could be demonstrated (neuroradiological investigations). One half of the epileptic syndromes with known etiology were thought to be related to cerebrovascular disease, but only few cases followed a stroke with persistent neurological symptoms. Intracranial space-occupying lesions were found to be the cause of epilepsy in 17% of cases. Partial epileptic seizures, secondarily generalized seizures, clinical signs of neurological damage, slow focal changes in the E.E.G. were the main features of this group of patients. In 22% of cases, miscellaneous causes were found: head injuries, exogenous intoxications due to accidental or iatrogenic ingestion, or alcoholic abuse. Relatively frequent were the seizures appearing in the course of degenerative or slow viruses induced encephalopathies. In 22% no demonstrable cause was found. Adequate follow-up may help us to discover etiological factors which at present are not obvious, but some form of idiopathic epilepsy with onset in this age range cannot be definitively ruled out. Only in 15% of cases interictal E.E.G. changes consisted in specific generalized or focal paroxysmal discharges (spikes, polyspikes, polyspike-and-wave). In about half of the cases the interictal E.E.G. failed to provide valuable informations, but an ictal E.E.G. could be obtained in 13 cases out of 59.
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PMID:[Epilepsy in the third age: seizures presenting after the age of 60 years (author's transl)]. 54 18

A 4-year-old girl who developed convulsions after an accidental ingestion of excessive dosage (50 mg/kg) of nalidixic acid, while treated with the drug (50 mg/kg/day) over 30 days for a urinary tract infection, was reported. Thirty minutes after ingestion, vomiting, tonic-clonic seizures, and abnormal movements were supervened. After ninety minutes, the serum levels of nalidixic acid and hydroxynalidixic acid were 146.1 and 48.9 microgram/ml, respectively. In controls, the mean levels of nalidixic acid and hydroxynalidixic acid were 7.8 +/- 6.8 (SD) and 3.02 +/- 2.6 microgram/ml, respectively.
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PMID:Convulsions from excessive dosage of nalidixic acid: a case report. 55 53

Two groups of female cats (6 each) were used: (1) a seizure group which received a minimum convulsive dose (MCD) of cocaine i.v., and (2) a subseizure group which received a subconvulsive dose of cocaine i.v., for 13 successive days. Determination of the MCD across 13 days in the seizure group and on Day 14 in the subseizure group revealed significant tolerance to cocaine-induced convulsions. However, reverse tolerance to cocaine-induced abnormal behavior developed as dystonic posture and speed of stereotyped movement increased during the 13-day treatment period in the subseizure group. These data are discussed in terms of local anesthetic and catecholaminergic effects of cocaine, as well as possible differential effects of various routes of administration.
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PMID:Tolerance to cocaine-induced convulsions in the cat. 56 34

A cohort of 666 children who had convulsions with fever were followed to determine the risks of subsequent epilepsy. High risks were found in children with preexisting cerebral palsy or mental retardation. Other major risk factors were atypical features of the febrile convulsions (such as focal seizures) and duration of febrile seizures for 10 minuts or more. The risk of developing epilepsy by age 20 was about 6 percent for all children who had experienced febrile convulsions. However, this risk figure consisted of a combination of 2.5 percent of children without prior neurologic disorder or atypical or prolonged seizures, and 17 percent of those with such complications.
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PMID:The risk of epilepsy following febrile convulsions. 57 73

A series of newly synthesized N-phenyl-substituted derivatives of succinimide were screened for anticonvulsant activity. Addition of a sulfonamide group in the p-position was of great consequence for the anticonvulsant effect. Substitution of a halogen in the m- or o-position improved activity against electroshock induced seizures. Pentylenetetrazole convulsions could only be prevented by few of these substances in smaller than 200 mg/kg oral doses. Activity could be further enhanced by adding more aliphatic or aromatic groups to the succinimide ring. The lethal doses of most of the active succinimides were higher than 5000 mg/kg p.o. With sublethal doses mice sometimes become drowsy and had myoclonic seizures and/or diarrhoea. At therapeutic dose levels kinetic disturbances, potentiation of pentobarbitone hypnosis or analgesia were rarely observed.
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PMID:[Anticovulsant activity of N-(p-sulfamoyl-phenyl)-succinimide derivatives (author's transl)]. 57 5

A male neonate presented with very frequent seizures, from the second day of life until the age of two weeks. Subsequently, convulsions did not recur. The patient, 7 years of age at present, has developed normally. Family history revealed transient neonatal convulsions in 8 other family members. The condition is inherited as an autosomal dominant trait.
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PMID:Benign familial neonatal convulsions. 58 Dec 20


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