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)

Felbamate (FBM) monotherapy was evaluated in 44 patients with uncontrolled partial onset seizures in a unique, single-center, randomized, double-blind, parallel-group trial. During the 56-day baseline period, patients were required to have at least 8 seizures and to be receiving only one standard antiepileptic drug (AED) at a therapeutic level; a second AED was allowed if at a subtherapeutic level. Patients were randomized to valproate (VPA), 15 mg/kg, or to FBM, 3,600 mg/day. In the treatment phase, previous AEDs were discontinued by study day 28 (by one-third decrements on study days 1, 14, and 28). Study end points were completion of 112 study days or the fulfilling of escape criteria. Criteria for escape relative to baseline were: two-fold increase in monthly seizure frequency, two-fold increase in highest 2-day seizure frequency, single generalized tonic-clonic seizure (GTC) if none occurred during baseline, or significant prolongation of GTCs. The predetermined primary efficacy variable was the number of patients escaping in each treatment group. Nineteen patients on VPA and 3 on FBM met escape criteria (p less than 0.001, chi-square test). When overall seizure frequency among study completers was compared with baseline, the FBM group had a 50 to 65% reduction in seizure frequency. FBM adverse experiences were all mild or moderate in severity, and the incidence of adverse experiences was lower in monotherapy. FBM monotherapy was effective in the treatment of partial onset seizures with or without generalization and demonstrated a favorable safety profile.
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PMID:Felbamate monotherapy: controlled trial in patients with partial onset seizures. 849 49

Benign myoclonic epilepsy in infancy (BME) is characterized by the occurrence of brief myoclonic attacks in normal infants aged 4 months to 3 years. There is no prior personal history, although in some patients 1 or 2 isolated febrile convulsions may occur prior to the onset of myoclonias. A family history of epilepsy or febrile convulsions is present in 30% of cases. Myoclonic attacks are short and mild, they involve mainly the head and upper limbs. The psychomotor development continues normally after the onset of seizures. The EEG shows a normal background activity and generalized spike-wave or polyspike-wave discharges associated with the myoclonias. These abnormalities are activated by drowsiness and during the first stages of sleep. A clinical and EEG photosensitivity is present in one-third of the patients. Myoclonias can be easily controlled by valproate monotherapy. Rare grand mal seizures can occur during adolescence, after withdrawal of drug treatment. The psychomotor evolution is good if treatment is started early. When myoclonias begin during the first year of life, the diagnoses of cryptogenic infantile spasms and of non-epileptic benign infantile myoclonus must be eliminated. In cases with a later onset, the following diagnoses can usually be easily discarded: cryptogenic Lennox-Gastaut syndrome, myoclonic-astatic epilepsy and unclassified epilepsies with the association of myoclonias and other types of seizures.
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PMID:Benign myoclonic epilepsy of infancy: electroclinical symptomatology and differential diagnosis from the other types of generalized epilepsy of infancy. 141 73

Thirty-two patients with juvenile myoclonic epilepsy (JME) were studied to evaluate the seizure prognosis. The response to antiepileptic drugs was excellent in 68%, but the patients, who had much more focal discharges on EEG and were sensitive to neuropsychological EEG activations at the beginning of treatment, had an unfavorable outcome. A combination of absence seizure alone resulted in the excellent prognosis for both absence and myoclonic seizures, and a combination of generalized tonic-clonic seizure on awakening related to rare myoclonic seizures. These findings suggest that the outcome of JME would be predicted by the EEG abnormality and the combination of the other types of seizures, which are probably determined by the pathophysiology at the beginning of treatment.
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PMID:The seizure prognosis of juvenile myoclonic epilepsy. 143 50

Twenty-nine children with childhood epilepsy characterized by frequent grand mal (generalized tonic-clonic) seizures in spite of maximal doses of antiepileptic drugs and by an early onset of seizures (before 1 year of age) were followed up for more than 5 years. The children were divided into 3 groups: severe myoclonic epilepsy in infancy (SME), no SME, and intractable childhood epilepsy with generalized tonic-clonic seizures (GTC). In all the 3 groups, the grand mal seizures persisted, whereas the other types of seizures tended to disappear as the patients aged, and the prognosis for mental development was poor. In the majority of cases in all the 3 groups, the waking grand mal seizures altered to sleep grand mal seizures with aging. Two pairs of monozygotic twins with SME suggested that genetic factors play a role in this epileptic syndrome. Intractable childhood epilepsy with GTC is distinguished by the absence of other types of generalized seizures. It cannot be regarded as an epileptic syndrome, but its pathogenesis and treatment require further studies.
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PMID:Long-term course of childhood epilepsy with intractable grand mal seizures. 143 51

All-night polygraphic EEG recordings were carried out in 20 epileptic patients who are characterized as follows; 1) clinical attacks took the form of generalized tonic-clonic seizure (GTCS), which occurred only or at least 90% during sleep without other seizure types in awakening, 2) no epileptic discharges were revealed in routine EEG examinations, also including sphenoidal electrode deriving during daytime, 3) recognizable organic brain damage in these patients had been excluded by neurological examinations and CT-scan. Interictal records showed epileptiform abnormalities in 5 of the 20 patients, which were all related with NREM sleep. Four patients exhibited bilateral synchronous paroxysms of 3-3.5 Hz spike-wave short burst and only one patient had temporal-localized discharges. The results of this study demonstrated that although there was a difference compared with other reports, the most characteristic features seen in our patients diagnosed as idiopathic generalized epilepsy (IGE) were as follows: 1) less frequent SGM seizures within a year, 2) SZ onset around teen age, 3) seizures were easily evoked by some precipitating factors and 4) no recognizable organic lesions. As a conclusion, patients with an uncertain or unknown type of epilepsy should always be examined with sleep recordings and all-night sleep recordings if necessary.
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PMID:Sleep grand mal--all-night polygraphic EEG recordings in 20 cases. 143 66

Generalized tonic-clonic seizures are the most common type of convulsive disorders in children. They are always a sign of an epileptogenic cerebral dysfunction and present either acutely, predominantly as a single event with detectable origin, or chronically, recurring as an epileptic syndrome. In view of the etiology and classification of convulsions it is important to differentiate between primarily and secondarily generalized seizures. This distinction is first of all based on an exact description of the very beginning and of the course of the seizures, on the EEG findings and on any connection between the seizures and a particular time of day. Primarily generalized tonic-clonic seizures with and without associated petit mal seizures are manifestations of an idiopathic epilepsy and are most probably genetically determined, secondarily generalized seizures on the other hand are often signs of a central nervous lesion or of another symptomatic form of epilepsy. Benign idiopathic partial seizures, however, take the from of secondarily generalized convulsions during the morning sleep. Prolonged tonic-clonic seizures of any origin require vigorous treatment with anticonvulsants, if necessary in an intensive care unit. Recurrent seizures are treated with long-term anticonvulsant medication. The first-line treatment is valproic acid or phenobarbitone (or if necessary, a bromide) in primarily generalized seizures and carbamazepine or phenytoin in secondarily generalized convulsions. The recommended duration of this therapy and the risk of recurrence of seizures vary widely with the underlying etiology and the type of epilepsy.
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PMID:[Grand mal epilepsy in childhood]. 143 12

Kindled seizures evoked by electrical stimulation of limbic pathways in the rat induce sprouting and synaptic reorganization of the mossy fiber pathway in the dentate gyrus (DG). To investigate whether seizures evoked by different methods also induce reorganization of this pathway, the distribution of mossy fiber terminals in the DG was examined with Timm histochemistry after systemic administration of pentylenetetrazol, a chemoconvulsant that reduces Cl- mediated GABAergic inhibition. Myoclonic seizures evoked by subconvulsant doses of pentylenetetrazol (24 mg/kg i.p.) were not accompanied by electrographic seizures in the DG, and did not induce mossy fiber sprouting. Generalized tonic-clonic seizures evoked by repeated administration of PTZ (24 mg/kg i.p.) were consistently accompanied by electrographic seizure activity in the DG, and induced sprouting and synaptic reorganization of the mossy fiber pathway. The results demonstrated that repeated generalized tonic-clonic seizures evoked by pentylenetetrazol induced mossy fiber synaptic reorganization when ictal electrographic discharges activated the circuitry of the DG.
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PMID:Activation of the dentate gyrus by pentylenetetrazol evoked seizures induces mossy fiber synaptic reorganization. 145 Sep 33

A random cluster sample survey of approximately 18,000 people in 11 villages was performed in Ulanga, a Tanzanian district with a population of approximately 139,000 people. Well-instructed fourth-year medical students and neurologic and psychiatry nurses identified persons with epilepsy using a screening questionnaire and sent them to a neurologist for detailed evaluation. Identified were 207 subjects (88 male, 119 female) with epilepsy; of these, 185 (89.4%) (80 male, 105 female) had active epilepsy. The prevalence of active epilepsy was 10.2 in 1,000. Prevalence among villages varied, ranging from 5.1 to 37.1 in 1,000 (age-adjusted 5.8-37.0). In a 10-year period (1979-1988) 122 subjects living in the 11 villages developed epilepsy, with an annual incidence of 73.3 in 100,000. Generalized tonic-clonic seizures (GTCS) accounted for 58% and partial seizures accounted for 31.9%, whereas in 10.1% seizures were unclassifiable. Of the partial seizures, secondarily generalized seizures were the most common. Possible etiologic or associated factors were identifiable in only 25.3% of cases. Febrile convulsions were associated in 13.4 of cases. Other associated factors included unspecified encephalitis (4.7%), cerebral malaria (1.9%), birth injury (1.4%), and other (3%). In 38% of the cases, there was a positive family history of epilepsy.
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PMID:Prevalence and incidence of epilepsy in Ulanga, a rural Tanzanian district: a community-based study. 146 63

Kainic acid (KA 4-14 mg/kg) administered intraperitoneally (i.p.) produces automatisms (scratching until third postnatal week, "wet dog" shakes thereafter), and clonic and tonic-clonic seizures in rats aged 7, 12, 18, 25, and 90 days. Administration of carbamazepine (CBZ) i.p. (25 or 50 mg/kg), phenobarbital (PB 20-80 mg/kg), clonazepam (CZP 0.2 or 1 mg/kg), or valproate (VPA 200 mg/kg) influenced neither incidence nor latency of automatisms. Clonic seizures that are regularly observed after the third postnatal week in controls were either abolished or substantially suppressed by any of the aforementioned antiepileptic drugs (AEDs). Tonic-clonic seizures observed in the first 3 postnatal weeks were suppressed only by solvent [including propyleneglycol (PEG), ethanol, and water]; the effect of AEDs on tonic-clonic seizures was proconvulsant instead. The automatisms were most resistant to AED therapy. These results induce some doubts about the adequacy of the KA model for identifying AEDs effective against complex partial seizures, but forthcoming AEDs that suppress automatisms in the KA rat model might also be active against human complex partial seizures.
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PMID:Action of antiepileptic drugs against kainic acid-induced seizures and automatisms during ontogenesis in rats. 146 81

Three consecutive cases of severe aplastic anemia undergoing immunosuppressive therapy with cyclosporin A (CyA) and high-dose methylprednisolone (HDMP) developed grand mal seizures after receiving ketoconazole treatment. All the seizures were reversed after transient discontinuation of those drugs. To our knowledge, it has not been reported as yet that the combination of ketoconazole and HDMP may considerably increase the risk of CyA-induced seizure. We would advise that ketoconazole and HDMP not be taken concomitantly with CyA treatment, and whenever ketoconazole therapy is needed, CyA be started with as small a dose as possible.
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PMID:Ketoconazole and high-dose methylprednisolone predisposing to cyclosporine-induced seizures: report of 3 cases. 146 96


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