Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0494475 (tonic-clonic seizure)
 1,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this report 52 patients meeting the criteria of centrencephalic myoclonic-astatic petit mal (10) at the beginning of petit mal are included. The results of clinical and encephalographic follow-up examinations are as follows: 1) The type reported here apparently has a petit mal course with peculiar characteristics, it therefore must be separated from Lennox syndrome: centrencephalic myoclonicastatic petit mal, pyknolepsia, bilateral myoclonus (impulsive petit mal). It should file under generalized primary petit mal epilepsy. 2) It is primarily defined by its EEG marker: "centrencephalic" EEG pattern (irregular and/or regular spike-wave groups, photosensibility and abnormal theta- and/or delta-rhythm). Rarely (33%) minor cerebral organic lesions as additional pathogenetic factors are uncovered by clinical and electroencephalographic examinations. 3) The clinical picture is characterized, aside from myoclonic and/or astatic seizures, by frequent absences (80%), rare tonic seizures (6%), petit mal status (25%) and mostly generalized grand mal seizures (62%). 4) There are changes of the course of the disease to Lennox syndrome (N = 6) in in children suffering from marked cerebral organic lesions at the onset of petit mal and in development of severe epilepsy. 5) Least favorite markers with respect to prognosis are concomitant grand mal seizures (p = 0,05), petit mal status (p = 0.008), additional 2/sec spike wave-pattern (spike wave Variant) in the EEG (p = 0.002) and previous seizures with focal signs. Favourite outcome of epilepsy are frequently connected to missing cerebral organic lesions (p = 0.05).
 ...
PMID:[Centrencephalic myoclonic-astatic petit mal. Clinical and electroencephalographic long-term follow-up study in 52 patients (author's transl)]. 9 76

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.
 ...
PMID:On the Lennox syndrome with the onset in puberty. 82 22

Free amino acid patterns of cerebrospinal fluid in infants and children with various types of convulsive disorders were compared with those in age-matched normal subjects. The total free amino levels in Lennox syndrome were higher than the normal values, and those in infantile spasms controlled by ACTH were higher than those in uncontrolled infantile spasms. Although the levels of only one or two amino acids in tonic-clonic seizure, focal seizure and febrile seizure were higher or lower than those of the controls, the levels of 8 amino acids in infantile spasms were lower and those of 10 amino acids in Lennox syndrome were generally higher compared to the controls. Among amino acids in CSF of children with tonic-clonic seizure, infantile spasms or Lennox syndrome, only the ornithine level was commonly lower than that of the controls. After the treatment, in tonic-clonic seizure, the levels of taurine, asparagine and glycine were increased, and in infantile spasms, those of asparagine, glutamine, glycine, alanine, phenylalanine, lysine and arginine were increased while that of taurine was decreased. These results suggest that each type of convulsive disorder shows the specific amino acid pattern, and the effects of anticonvulsants may be partially understood through the changes of the free amino acid patterns in the brain.
 ...
PMID:Amino acid metabolism in the brain with convulsive disorders. Part 3: Free amino acid patterns in cerebrospinal fluid in infants and children with convulsive disorders. 632 17