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

Petit mal absences in childhood are often followed by grand mal seizures in adolescence and a coexistence of both types of seizures is not uncommon at all. It is noteworthy, however, that such a coexistence does not imply immediate transition from one type of seizure into the other one. Hence, a grand mal attack may be prepared by all sorts of focal seizures, psychomotor automatisms or bilateral-synchronous myoclonus but immediately preceding petit mal (with generalized spike-wave discharges) is probably extremely rare. The presented case is characterized by unusually late onset of petit mal and grand mal seizures at age 32 and, following a mild head injury, a few episodes of petit mal status (ictal stupor) at age 52. At that time, a series of petit mal absences and eventually a smooth transition from petit mal to grand mal could be recorded. Uncommon frequency characteristics (especially some interspersed spiking at a rate of 9-15/sec) were found at the onset of the ictal spike-wave activity during the petit mal absences. This is regarded as the expression of failing inhibitory mechanisms which generally prevent the immediate development of a grand mal out of a petit mal absence.
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PMID:Immediate transition from a petit mal absence into a grand mal seizure. Case report. 81 90

A study was conducted in 9 children with petit mal epilepsy to compare the plasma levels of ethosuximide after divided daily administration with those after single daily administration. The children received their previously established dose in divided doses for 4 wk, single morning doses for 4 wk, and again in divided doses for 4 wk. None of the children suffered petit mal seizures during the study. Three had grand mal seizures but the frequency did not differ between the dosage regimens. Plasma levels during the single-dose period peaked more rapidly and fell more quickly than during the other periods, but mean levels remained in the therapeutic range. The mean half-life of the drug in these children was 29 hr. For reasons not understood, plasma levels generally were lower in the second divided dose period than in the other two periods. No adverse experiences were reported during the study. The data indicate that ethosuximide is clinically effective when given in a single daily dose. This regimen offers advantages in convenience and possibly in patient compliance.
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PMID:Ethosuximide dosage regimens. 81 88

Types of seizures, age at onset of epilepsy, preoperative duration of epilepsy, and age at operation were studied in the literature and in 74 patients who underwent unilateral temporal lobe resection in 1960-1969 in Denmark. The medical and surgical series were compared. The age at onset was significantly lower in the surgical series. Prognostically favourable factors were: i) preoperative presence of a single type of seizure; ii) duration of epilepsy of less than 4 years, and in grand mal epilepsy of less than 1 year; iii) operation for epilepsy in or before early adulthood. Prognostically unfavourable factors were i) preoperative presence of grand mal; ii) age at onset of epilepsy or of the first grand mal seizure between 5 and 20 years; iii) preoperative duration of psychomotor epilepsy over 10 years.
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PMID:Temporal lobe epilepsy: types of seizures, age, and surgical results. 81 58

Prior to the release of carbamazepine for the treatment of patients with psychomotor and grand mal seizures, primidone was regarded as the drug of choice for these disorders, especially when combined with diphenylhydantoin (DPH). It was, therefore, of interest to compare the effectiveness of carbamazepine against primidone when added to a therapeutic dose of DPH. Forty-five patients completed a 6-month study with each patient serving as his own control. The patients were initially stabilized on therapeutic doses of DPH and one of the test compounds, while all other medications were withdrawn. After 3 months of treatment, they were transferred onto the other drug for a second 3-month period. Extensive laboratory testing, including anticonvulsant levels, electroencephalograms, and neuropsychological evaluations, was performed. For the most part, the patients remained on outpatient status, returning for reports of seizure frequency, side effects, and laboratory studies every 14 days. The study was conducted in a single blind fashion by the treating neurologists; double blind by the electroencephalographer and psychologists. The results indicated that the two drugs did not differ in their effectiveness on seizure control. There were somewhat more side effects--none serious--with carbamazepine than with primidone. The EEG showed increased fast activity with primidone and increased theta activity with carbamazepine. There was no difference in regard to decrease of electroencephalographic seizure discharges. The patients showed more impairment on a repeatable neuropsychological test battery with primidone than with carbamazepine, and they also showed an increase on the psychopathic deviate scale of the Minnesota Multiphasic Inventory. Depressive feelings, when present, lessened while under treatment with carbamazepine. The results suggest that patients with the seizure types under consideration and who do not respond to DPH alone or to a DPH-phenobarbital combination can be placed on either carbamazepine or primidone while phenobarbital is discontinued. A patient who is intellectually and emotionally intact with no past history of behavioral disturbances may do better on primidone than carbamazepine, because this drug gives fewer side effects. On the other hand, those patients who have a past history of emotional and/or intellectual disturbances may profit more from carbamazepine.
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PMID:A comparison of the effectiveness of primidone versus carbamazepine in epileptic outpatients. 81 30

The cases of the Lennox syndrome which began at the age between 14 and 16, namely in puberty, were reported. The first case, a 22-year-old woman, was attacked with grand mal seizure at the age of 15, and one year later "Juchzer" (ref. Doose) appeared. This continued for two years, and then astatic seizures appeared. The second case, a 20-year-old woman, was attacked with grand mal seizure at the age of 14, and soon after astatic seizure appeared. Thus both are closely related with grand mal seizures. The first case is idiopathic, and the intelligence developed normally till the onset of the Lennox syndrome. but after that it became disturbed. The second case is residual state of arsenic toxicosis, and so the intelligence was already disturbed before the onset. On EEG both of them at first showed diffuse slow waves of high voltage, and in several years after the appearance of the Lennox syndrome, slow spike-waves were found. On therapy, scarcely no beneficial effects were noted by conventional antiepileptics, and by nitrazepam only the temporal beneficial effect was obtained. The symptoms of our cases are generally similar to the Lennox syndrome in infancy. Though we observed only two cases, we presented our cases as the Lennox syndrome with late onset.
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PMID:On the Lennox syndrome with the onset in puberty. 82 22

In the area of Cesena, Italy, the prevalence of epilepsy was about 3/1,000 among the 13,000 children of school age, 6-14 years. Only half the epileptic pupils had a normal scholastic record. One-third were in special classes, nearly all because of mental retardation due either to birth injury or to damage in infancy. The others (17%) were behind by one or more classes, mainly because of a depressive reaction owing (in half of the intelligent epileptics) mainly to classmates' fear of seizures and to the hostility of classmates' parents after the pupil had a grand mal seizure in school. Teachers had usually not learned how to manage either seizures in the classroom or the problems of pupils with epilepsy.
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PMID:Record in grade school of pupils with epilepsy: an epidemiological study. 82 93

Ontogenetic studies of epileptogenic process were carried out in albino rats ranging in age from birth to 45 days. Experimental epilepsy was produced by two different procedures and the results were compared with each other. Tungstic acid gel was applied to the motor area of the left side of the cortex, and the following results were obtained. The latency of the seizure appearance was long during 10 days after birth, became progressively short thereafter and reached the minimum in about 20 days of age, and gradually returned to the adult level again by 45 days of age. No abvvious seizure was exhibited until five days of age. Seizure patterns developed from tonic or twitch-like jerky convulsion (10 days old) to rhythmic or clonic type of seizure (13 days old), and the seizure patterns similar to those in the adult rat were observed in about 20 days of age. Cortical seizure activity was initially observed in about 10-day-old rats; single high amplitude slow wave appeared and small spikes became superimposed on it in the course of maturation. Atypical spike and wave complexes were observed after 20 days of age. Electrical stimulation was applied to the left cortical motor area by constant current stimulator, and the following seizure patterns were observed: No obvious seizure could be elicited in newborn rat, whereas from three days of age, tonic seizure of the whole body, and from seven days old twitch-like convulsion of extremities were observed. In ages from 10 to 20 days, seizure induced by electrical stimulation was mainly tonic in pattern; extension of forelimbs and flexion of hindlimbs in most cases were observed before 13 days old, but both fore-and hindlimbs were extended therafter. Tonic-clonic seizure patterns were exhibited after 20 days of age. From these results, it was considered that tonic convulsions and high voltage slow cortical seizure activites were produced from the activites of the local cortical neuronal connections, and rhythmic and/or clonic seizure patterns and spike and wave seizure activities were elicited from the more complex, i.e. cortico-subcortical neuronal circuits. Possible contributing factors for the determination of seizure susceptibility in immautre rats were also discussed.
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PMID:Ontogenetic studies of seizure patterns and seizure activities induced by cortical focus. 99 11

The products from nonflaming combustion of wood and a trimethylol-propane-based rigid-urethane foam that was not fire-retarded produced elevated carboxyhemoglobin levels but no abnormal neurological effects. However, when this type of foam contained a reactive phosphate fire retardant, the combustion products caused grand mal seizures and death in rats. The toxic combustion product responsible for the seizures has been identified as 4-ethyl-1-phospha-2,6,7-trioxabicyclo(2.2.2.)octane-1-oxide.
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PMID:Extreme toxicity from combustion products of a fire-retarded polyurethane foam. 111 19

Folic acid was administered intravenously during constant EEG monitoring to eight epileptic subjects who had received diphenylhydantoin therapy for more than 1 year. Six of the subjects displayed low folate levels by Lactobacillus casei assay in plasma and/or whole blood. Six patients received 75 mg of folate intravenously over a 30-min period without clinical effect of EEG change. One patient exhibited an increase in spike discharges on the EEG in comparison to the baseline pattern, but no clinical change or seizure while receiveing 150 mg of folate in a 30-min period. One patient displayed a 2-sec burst of spike and slow wave activity on the EEG after receiveing 7.2 mg of folate in a 3-min period. A tonic-clonic seizure occured after the infusion of 14.4 mg of folate, and again after infusion of 19.2 mg of folate. There appear to be wide variation in the ability of drug-treated epileptic subjects to tolerate infusions of folic acid. These variations help explain conflicting reports in the literature concerning the effect of folic acid administration on seizure control. Megadoses of folic acid should be employed with great caution in all subjects, but particularly among epileptics. Information is lacking as to whether folate might induce seizures in certain ostensibly normal individuals. It is postulated that folic acid exerts a direct effect among sensitive subjects on existing pathways concerned with the metabolism of folate, histidine, or other important brain metabolites. The mechanism of the anticonvulsant action of diphenylhdantoin remains unknown, but there is considerable evidence to suggest that it interferes with the deamination of histidine.
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PMID:Harmful effect of megadoses of vitamins: electroencephalogram abnormalities and seizures induced by intravenous folate in drug-treated epileptics. 111 18

1. An attempt was made to evaluate the pathophysiology of symptoms of hyponatremia as related to changes in brain water and electrolytes. Studies were carried out in 66 hyponatremic patients and 5 groups of experimental animals. 2. In hyponatremic patients, symptoms (depression of sensorium, seizures) correlated well with plasma Na+ (r = 0.64, p less than .001), but there was substantial overlap. In patients with acute hyponatremia, all were symptomatic and 50% died. Among patients with hyponatremia of at least 3 days duration, sympatomatic patients had plasma Na+ (115 +/- 1 mEq/L) which was significantly less (p less than .001) than that of asymptomatic patients (plasma Na+ = 122 +/- 1 mEq/L). Among symptomatic patients, mortality was 12% and 8% had seizures, while none of the asymptomatic patients died or had seizures. 3. Among 14 patients with acute (less than 12 hrs) hyponatremia, the mean plasma Na+ was 112 +/- 2 mEq/L. All such patients had some depression of sensorium and four had grand male seizures. Seven of these patients were treated with hypertonic (862 mM) NaCl, while four were treated only with fluid restriction. Of the seven patients treated with hypertonic NaCl, five survived, while three of four patients treated with fluid restriction died. There was no evidence of circulatory congestion or cerebral damage in the patients treated with hypertonic NaCl. 4. Among rabbits with acute (2-3 hours) hyponatremia (plasma Na+ = 119 +/- 1 mEq/L), all had grand mal seizures and 86% died. All such animals had cerebral edema (brain H2O content 17% above control value) but brain content of Na+, K+ and Cl- was normal. 5. Rabbits with 3 1/2 days of hyponatremia (plasma Na+ = 122 +/- 2 mEq/L) appeared to be asymptomatic, even though brain water content was 7% above normal (p less than .01). 6. Rabbits with 16 days of more severe hyponatremia (plasma Na+ = 99 +/- 3 mEq/L) were weak, anorexic, lethargic and unable to walk. Brain water content was 7% above normal, although brain osmolality (218 +/- 12 mOsm/kg H2O) was similar to plasma (215 +/- 8 mOsm/kg). Brain content of Na+, K+, Cl- and osmoles was 17 to 37% less than normal values, so that the brain established osmotic equilibrium with plasma primarily by means of a loss of electrolytes. 7. These studies suggest that in patients with hyponatremia, symptoms and morbidity are only grossly correlated with either magnitude or duration of hyponatremia. Symptoms appear to correlate best with the interplay between a net increase in brain water versus a loss oof brain electrolytes. However, even asymptomatic animals have subclinical brain edema when plasma Na+ is below 125 mEq/L, and such edema may cause permanent brain damage. Thus, many patients with similar levels of plasma Na+, particularly when they are symptomatic, should probably be treated with hypertonic NaCl infusions.
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PMID:Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. 125 11


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