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Query: UMLS:C0494475 (tonic-clonic seizure)
 1,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Forty patients ingesting tricyclic antidepressant (TAD) overdoses were studied as a pharmacologic model to determine whether total tricyclic antidepressant plasma levels correlated with major adverse effects and electrocardiographic findings. Maximum TAD plasma levels were higher in patients who died (p less than 0.025) or had cardiac arrest (p less than 0.02), needed respiratory support (p less than 0.005), were unconscious (p less than 0.02), had grand mal seizures (p less than 0.001), ventricular rate larger than or equal to 120/min (p less than 0.01), cardiac arrhythmia (p less than 0.05), QRS duration larger than or equal to 100 msec (p less than 0.001), or bundle branch block (p less than 0.05). TAD plasma levels correlated with the dose ingested by history (N = 29, r = 0.58, p less than 0.001). Measurement of total TAD (free and protein-bound) appears to correlate well with biologic response.
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PMID:Tricyclic antidepressant plasma levels and adverse effects after overdose. 83 48

A case of giant cell tumour of the sphenoid bone is reported. Besides the familiar presentation with headaches, ocular manifestations, and upper cranial nerve lesions, this case showed previously undescribed features such as grand mal seizures, hemiparesis with facial palsy, and dural extension. The reported high incidence in females is questioned. The tumour histologically showed some cartilage.
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PMID:Giant cell tumour of the sphenoid bone with dural extension. 92

Certain aminothiols rapidly deplete cultured cystinotic skin fibroblasts of their abnormally high free (nonprotein) cystine pool. The free cystine content of these cells if reduced by over 90% in 1 h with 0.1 mM cysteamine. This is more rapid than previously known methods of removing free cystine from cystinotic fibroblasts. The disulfide, cystamine, is also able to deplete cystinotic cells of free cystine. A patient with nephropathic cystinosis and end-stage renal disease was treated with cysteamine, both intravenously and orally. Both methods of administration rapidly lowered the free cystine content of the patient's peripheral leukocytes. Study of the patient's urinary sulfur excretion did not conclusively determine the effect of this therapy on the total body cystine pool. Her renal status remained at end stage after 1 mo of oral cysteamine, when an episode of grand mal seizures prompted cessation of the study. Determination of the proper place of aminothiol therapy in this disease will depend upon further clinical trial with patients whose kidney function has not deteriorated to the point of irreversible change, accompanied by careful monitoring of plasma aminothiol levels.
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PMID:Cystinosis. Intracellular cystine depletion by aminothiols in vitro and in vivo. 93 5

A 3-year-old Latin female is reported with a terminal deletion of the No. 1 chromosome, karyotype formula 46, XX, del(1) (q43). Principle clinical features include: Anatomic - microcephaly; bilateral, convergent strabismus; epicanthus; brachycephaly; bulbar nose; sparse hair; partial soft tissue syndactylism between 2nd and 3rd fingers which are slightly tapered; whorls on all 10 fingers; mild prognathism; solitary kidney; vaginal stenosis; vesicoureteral reflux; asymmetric feet; and subluxation of peroneal tendons around the fibula with severe pronation and heal valgus deformity. Neurologic - moderate motor and mental retardation; high-pitched, shrill cry; absent pincer grasp at 3 years; and grand mal seizures documented from 9 months of age.
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PMID:Terminal (1)(q43) long-arm deletion of chromosome no. 1 in a three-year-old female. 95 13

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

Sodium valproate has been used, in combination with a variety of standard anticonvulsant drugs, to treat 24 children with intractable epilepsy. A reduction of fit frequency greater than 90 percent was obtained in six patients, and a reduction of over 50 per cent in another six, with an improvement in alertness and school performance in the majority of cases. Grand mal, myoclonic and petit mal epilepsy gave the best response, while infantile spasms responded least well. No serious side-effects were encountered.
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PMID:Sodium valproate in the treatment of intractable childhood epilepsy. 109 15

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


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