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

Milacemide, 2-N-pentylaminoacetamide, a glycine prodrug, which readily crosses the blood-brain barrier, has been tested for antiepileptic efficacy and tolerability in 30 patients compared in a double-blind design with 30 patients treated with placebo. All patients continued to receive, without alteration, their previous partly effective medication. All patients presented an average of at least 10 seizures a month during the 6 months preceding the trial with no more than 50% fluctuation. The ratio of seizure frequency in the trial period over the seizure frequency in the baseline period (RSF) was calculated. In the milacemide group, 9 of 29 patients had an RSF less than 0.7 as opposed to 2 of 29 in the placebo group. Although no firm proof of therapeutic efficacy, this and the dramatic improvement of a patient with myoclonus epilepsy indicates that further studies are warranted. This opinion is strengthened if one considers the subgroup of patients aged less than or equal to 25 years in which a statistically significant reduction in seizure frequency was observed with milacemide treatment. The drug was well tolerated.
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PMID:Double-blind study of milacemide in hospitalized therapy-resistant patients with epilepsy. 351 69

In kindled rats, the administration of cysteamine (CSH, 200 mg/kg, i.p.) 4 h prior to a kindled seizure leads to long-term (up to 10 days) inhibition of kindled seizures. CSH (200 mg/kg, i.p.) also induces myoclonic seizures in kindled rats. We suggest that the long-term inhibition of kindled seizures might be the result of the myoclonus, not the somatostatin depletion as previously suggested. Prior administration of the short-acting benzodiazepine midazolam (5 mg/kg, i.p.) eliminated the CSH-induced myoclonus and prevented the long-term inhibition of kindled seizures. These results suggest that the CSH-induced long-term inhibition of kindled seizures is the result of an interaction between the myoclonic seizure and a subsequent kindled seizure.
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PMID:Prevention of cysteamine-induced myoclonus blocks the long-term inhibition of kindled seizures. 360 50

Three Asian patients, since adolescence, had myoclonic jerks and tonic-clonic seizures during card games, draughts, and a local game "punchi." Interictal EEG showed generalized bisynchronous atypical 3-Hz spike and wave discharges. Test procedures evoked EEG dysrhythmia and clinical seizures in two patients. These patients and previously reported cases have the seizure disorder juvenile myoclonic epilepsy (impulsive petit mal), which seems particularly sensitive to provocation by cognitive functions, especially decision making. Myoclonic epilepsy is considered resistant to antiepileptic drugs other than clonazepam and valproate, but two of our patients responded well to clobazam.
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PMID:Epileptic seizures evoked by card games, draughts, and similar games. 362 11

A strain of Wistar rats was inbred in our laboratory for its susceptibility to sound. The seizures are characterized by one or two wild running fits which terminate in a tonic dorsiflexion with open mouth, followed by a catatonic state. During the tonic phase of the seizure, the cortical EEG is flattened for 2 to 3 s. Then, a slow and regular low-voltage (9-12 c/s) activity is observed during 40 to 60 s. When these animals are submitted to daily sound-stimulations, the behavioral as well as the EEG manifestations of the audiogenic seizures change progressively. After 5 to 30 exposures, the wild running becomes disorganized by occurrence of myoclonic jerks of the limbs and the body. In some animals, the tonic extension disappears and a myoclonic seizure develops progressively with facial and forelimb clonus, rearing and falling. In other animals, the tonic phase still occurs and is followed by a generalized clonic phase. During both the myoclonic and the tonicoclonic seizures, rhythmic spikes, polyspikes and spike and waves of high amplitude (1-10 c/s) during 40 to 120 s are observed on EEG recordings. These EEG modifications often outlast the sound stimulation. The pharmacological reactivity in rats exposed to single or repeated audiogenic seizures is similar: phenytoin and carbamazepine suppress both kinds of seizures at low doses whereas ethosuximide is efficacious only at high doses. In order to know whether the repeated exposure to sound or the repetition of seizures are responsible of the observed changes in audiogenic seizures, animals susceptible to sound were exposed daily to the seizure-inducing sound after previous injection of Diazepam, which prevented them from convulsing. On the other hand, sound susceptible animals were injected daily with a dose of PTZ inducing one or several convulsions without exposure to sound. None of these treatments ever facilitated the development of kindled audiogenic seizures. The progressive modification of behavioral and EEG modifications occurring when audiogenic seizures are repeated suggests that kindling has developed, the seizure extending from the brainstem to forebrain structures.
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PMID:Kindling of audiogenic seizures in the rat. 366 6

Prolactin secretion after tonic-clonic seizures (10 patients), complex partial seizures (five) and non-epileptic attacks (three) was studied in a group of children aged between 0.3 and 14 years. Seven patients with other subcategories of seizure disorders were also studied. Eight children with tonic-clonic seizures exhibited post ictal concentrations of prolactin greater than 500 mU/l. One of the children, who responded on one occasion, did not do so on another. Three children with complex partial seizures had post ictal prolactin concentrations greater than 500 mU/l, while in two the increased values were more modest (390 mU/l and 420 mU/l). The timing of the peak post ictal prolactin concentration varied from less than 20 minutes to a prolonged plateau for three hours. Other seizure types--simple partial with motor signs (2), absence seizure (1), myoclonic seizure (1), minor epileptic status (3) (with one exception), and non-epileptic attacks (3) were not associated with post ictal concentrations greater than 500 mU/l.
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PMID:Prolactin and seizure activity. 393 64

1. Maturation of the excitatory and inhibitory neuromechanisms at various levels of the central nervous system was demonstrated by the convulsogenic activity induced by leptazol in the developing albino rat.2. The somatomotor end points considered (myoclonic jerk, myoclonic seizure, tonic seizure and catalepsy) were not observed in all age groups. Tonic seizure was seen at birth, myoclonic jerks at 2 weeks of age, myoclonic seizure and catalepsy at 3 weeks of age.3. The convulsive sequences described presented three different patterns, defining three age groups: the infant pattern (infant group: newborn-1 week old animals); the transitional pattern (transitional group: 2 week old animals); and the adult pattern (adult group: 3 week old-adult animals).4. Effective doses were determined for the three types of convulsive sequence: MJ50 for the myoclonic major sequence (maximal end point: myoclonic jerk), MS50 for the myoclonic major sequence (maximal end point: myoclonic seizure) and the TS50 for the myoclonic-tonic-clonic sequence (maximal end point: tonic seizure).5. The correlation of the convulsive patterns with the dose and latency variations suggests that: (a) the neuromechanisms responsible for the tonic seizure and clonic seizure, located at brainstem and spinal cord levels, function at birth and reach maturity at 3 weeks of age; (b) the neuromechanisms responsible for the myoclonic manifestations and for catalepsy, located at the striato-thalamocortical level, start functioning at 2-3 weeks of age, indicating the later maturation of the more cephalic structures.
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PMID:Maturation of convulsogenic activity induced by leptazol in the albino rat. 510 3

We report on two patients who have a mitochondrial myopathy, encephalopathy, lactic acidosis, and recurrent cerebral insults that resemble strokes (MELAS). These two and nine other reported patients share the following features: ragged red fibers evident on muscle biopsy, normal early development, short stature, seizures, and hemiparesis, hemianopia, or cortical blindness. Lactic acidemia is a common finding. We believe that MELAS represents a distinctive syndrome and that it can be differentiated from two other clinical disorders that also are associated with mitochondrial myopathy and cerebral disease: Kearns-Sayre syndrome and the myoclonus epilepsy ragged red fiber syndrome. Existing information suggests that MELAS is transmitted by maternal inheritance. The ragged red fibers suggest an abnormality of the electron transport system, but the precise biochemical disorders in these three clinical syndromes remain to be elucidated.
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PMID:Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes: a distinctive clinical syndrome. 609 82

Eleven patients with long-standing progressive myoclonus epilepsy, PME, and age- and sex-matched epileptic controls received L-tryptophan (L-Trp) 100 mg/kg body weight combined with carbidopa in addition to their usual anticonvulsant regimen. During six weeks of the trial an improvement in activities of daily living and a decrease of action myoclonus was noted in the PME patients. The frequency of seizures compared with the past year decreased significantly in the PME patients, but not in the epileptic controls. Changes in the EEGs of the PME patients were scant, but a slight decrease was noted in myoclonic spikes. Both plasma Trp and platelet 5-HT increased significantly and at least as much as in epileptic controls. 5-HIAA and HVA concentrations in the CSF of the PME patients increased significantly during the trial. The results support previous findings concerning Trp treatment in PME, and longer trials with Trp + carbidopa could be of value in this disease.
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PMID:L-tryptophan-carbidopa trial in patients with long-standing progressive myoclonus epilepsy. 617 51

Recent data and concepts concerning the convulsant effects of kynurenines, neuroactive metabolites of tryptophan, in mice, rats, and frogs are reviewed. Myoclonic seizures of the hindlegs are induced in mice by l- and d,l-kynurenine. Both l- and d,l-kynurenine exhibit a selective synergism with strychnine. The convulsant effect of l-kynurenine is selectively antagonized by taurine, less selectively by l-glycine, and not at all by gamma-aminobutyric acid (GABA) or the GABA agonist muscimol. Derivatives of GABA and some standard anticonvulsant drugs alter seizures induced by l-kynurenine and quinolinic acid in different ways. The involvement of brian kynurenines in the genesis of epileptic seizures is suggested.
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PMID:Kynurenines and seizures. 626 4

In 1981, Inanaga et al reported on the efficacy of DN-1417 (a TRH analog) in the treatment of degenerative myoclonus epilepsy and other forms of intractable epilepsy. Following this report, we studied the efficacy and safety of DN-1417 treatment in 10 intractable epileptic children ranging in age from 6 months to 11 years (mean 4 years), including 7 with Lennox syndrome (LS), 2 with West syndrome (WS) and 1 with degenerative myoclonus epilepsy (DME). The daily dose was from 0.02 to 0.05 mg/kg, initially, and then was increased to 0.05 mg/kg. Complete control of seizures was achieved in 2 patients with LS, a 50% or greater decrease in seizure frequency was observed in one patient each with LS and DME and a less than 50% decrease in 1 with LS and 2 with WS. There was no change in 2 LS cases, and 1 LS case became worse. Activation of psychic activities, such as psychomotor activity, facial expression and motivation, was also noted in 7 of the 10 patients. Furthermore, improvement of motor function was noted in 5 patients. Electroencephalographic abnormalities improved in 2 completely seizure free patients with LS in which EEG ameliorated along with clinical seizure control.
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PMID:A pilot study on the anticonvulsive effects of a thyrotropin-releasing hormone analog in intractable epilepsy. 641 1


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