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PubMedDate not supplied

[Myoclonias and epilepsy].

INTRODUCTION: The myoclonias and epilepsies may be closely related as in the so-called myoclonic epilepsies. The myoclonic epilepsies form a heterogeneous group of epilepsies in which myoclonias and myoclonic seizures are the most relevant symptom. DEVELOPMENT: Following the classification of epileptic disorders into syndromes, we consider the most relevant electroclinical characteristics of the different epilepsies seen from the first year of life to old age. Regarding the idiopathic focal epilepsies we consider epilepsy with Rolandic paroxysms in which, in some patients, negative myoclonus and a myoclonic variant of reading epilepsy may occur. Negative epilepsy and continuous partial epilepsy are considered with the cryptogenic and symptomatic focal epilepsies. In the idiopathic generalized epilepsies we consider the benign myoclonic epilepsy of infancy and its reflex variant, juvenile myoclonic epilepsy and palpebral myoclonias with absences. In the group of cryptogenic and symptomatic generalized epilepsies we analyze epilepsy with myoclonic absences, myoclonic-static epilepsies, the myoclonic variant of the Lennox-Gastaut syndrome, progressive myoclonic epilepsies, adult familial myoclonic epilepsies and the myoclonic epilepsies of the elderly. Finally, among the unclassified group of epilepsies, we briefly consider severe myoclonic epilepsy of infancy and the myoclonic epilepsies associated with static encephalopathy.

Epilepsies, Myoclonic↗
PubMed2004

Clinical investigation of genetic contributions to childhood-onset epilepsies and epileptic syndromes.

Although there have been major advances in the understanding of the molecular bases of certain inherited epilepsy syndromes, clinical studies are still needed to verify the possible genetic contributions to common epilepsies. We examined the proportions of positive family histories of epilepsy (within second-degree relatives) and consanguinity (within first-degree relatives) in 311 probands with childhood-onset epilepsy, and found that they had high family history rates of epilepsy (19.3%) and consanguinity (6.1%). A positive family history of epilepsy was found more in probands with generalized epilepsy than in ones with localization-related epilepsy, and more in probands with idiopathic/cryptogenic epilepsy than in ones with symptomatic epilepsy. However, on analysis after the symptomatic epilepsies had been divided into two categories, probands with pre- or perinatal symptomatic generalized epilepsy and ones with postnatal symptomatic localization-related epilepsy showed high positive family history rates, similar to ones with idiopathic/cryptogenic epilepsy. On the other hand, a positive family history of consanguinity was noted more in probands with generalized epilepsy than in ones with localization-related epilepsy, but there was no significant difference between probands with idiopathic/cryptogenic epilepsy and ones with symptomatic epilepsy. These findings suggest that in addition to the hereditary effect on idiopathic/cryptogenic epilepsy, a genetic susceptibility may contribute to the development of pre- or perinatal symptomatic generalized epilepsy, and to that of postnatal symptomatic localization-related epilepsy. Furthermore, a genetic predisposition seems to have an influence through consanguinity on the etiologies of both idiopathic/cryptogenic and symptomatic generalized epilepsies.

Adolescent↗
PubMed1998

The syndromic classification of the International League Against Epilepsy: a hospital-based study from South India.

PURPOSE: To determine the distribution of various epilepsies and epileptic syndromes in the epileptic population treated in a university hospital in a developing country. METHODS: Data concerning 2,531 patients with epilepsy seen between January 1989 and June 1994 were analyzed using the International League Against Epilepsy (ILAE) classification. RESULTS: Of 2,531 cases, 48% fell into ILAE categories 1.3, 3.2, or 4.1 (cryptogenic, without unequivocal generalized or focal seizures; or situation-related seizures, respectively). Localization-related epilepsies (LREs) and epileptic syndromes (1.1, 1.2, 1.3) were found in 1,591 (62.9%) patients; of these patients, symptomatic localization-related epilepsies totaled 62.7%. and idiopathic localization-related epilepsies accounted for only 0.7%. Juvenile myoclonic epilepsy was the most common type of idiopathic generalized epilepsy (IGE), comprising 4.9% of the total study population and 7.7% of patients registered in the epilepsy clinic. A combination of childhood and juvenile absence epilepsies were found in only 0.4% of the total study population. Single computed tomography (CT) enhancing lesion (SCTEL) and focal cerebral calcification (FCC) accounted for 22% of the etiologic factors for localization-related epilepsies. Neurologic deficits were found in 9.5% of patients with SCTEL; none were found with FCC. None of the patients with these lesions had any history of antecedent events that suggested CNS involvement. In patients with localization-related epilepsies with unremarkable clinical data, the proportion of CT scans showing SCTELs was 39 (95% confidence interval [CI], 0.35-0.43) and 0.18 (95% CI, 15-0.21) for FCCs. The proportion for both lesions together was 0.57 (95% CI, 0.53-0.61). Seizures did not recur once the lesion resolved in patients with SCTELs. In patients with FCCs, seizure remission was 71.5% (95% CI, 53.7-85.4) at 3 years. CONCLUSIONS: This study illustrates the rarity in one patient population of some of the syndromes and categories described in the ILAE classification. Childhood and juvenile absence epilepsies together formed a small proportion. SCTEL and FCC were important etiologic factors for localization related epilepsies. The epilepsy associated with SCTEL was a form of benign epilepsy; epilepsy associated with FCC had remission rates similar to other remote symptomatic epilepsies. Without neuroimaging evidence, these 2 lesions would have been missed and the patients might have been grouped under cryptogenic localization related epilepsy. For this reason, we emphasize the need for neuroimaging in patients with localization related epilepsies with unremarkable clinical findings, before classification into the cryptogenic category. In the absence of neuroimaging, such patients should be classified as "probably cryptogenic."

Adolescent↗
PubMedDate not supplied

[Eponyms and epilepsy (history of Eastern civilizations)].

The history of eponyms for epilepsy in the lands of the Eastern globe present the portrait of the attitudes of both the laymen and skilled people towards the disease and patient, as well as to the Nature itself. As opposed to the West which during the Middle ages changed its concepts of epilepsy as the organic brain disease for the sublime 'alchemic' position, the people of the East were more prone to consider from the beginning of their civilization till the XIX century that epilepsy is the consequence of the evanescent spiritual and extracorporal forces which by themselves were out of their reach. As compared to the western civilization, the historical resources are, often as a consequence of a linguistic barriers, more scarce-as consequently is the number of eponyms, but are nevertheless picturesque. The medical science from Babylonian period presumed that epileptic manifestations are the consequence of the demonic or ill spiritual actions. There existed an attitude that at the beginning of an epileptic attack the patient was possessed by a demon (the Akkadic, i.e., Babylonian verb "sibtu" denoting epilepsy, had the meaning "to seize" or "to be obsessed"); at the end of the clonic phase the demon departed from the body. Different demons were responsible for different forms of epilepsy such as nocturnal and children epilepsy, absence epilepsy and pure convulsions, simple and complex automatisms, and gelastic epilepsy. Thus, the doctors from the period of Babylon aside from making primordial classification of epilepsies, knew about their clinical picture (prodromal symptoms and aura, Jackson's epilepsy. Todd's paralysis), postictal phenomena and intericatl emotional instability; provocative factors were also known (sleep deprivation, emotions, as well as alcohol, albeit in a negative sense-as a cure for epilepsy). There is no doubt than in the period of Babylon the clinical picture of serial fits and its progress to status epilepticus were clearly recognized and considered as life threatening events. Persian history of epilepsy, except from the 6th century Zoroastrian "Avesta" document, lacks the written or spoken medical heritage untill the 7th century A.D. and the Arabic conquest of the entire Moslem world. On the other hand, Islamic medicine should be freed from the simple prejudice that the Moslem authors were only the translators of Greek medicine; contrary to such a view, their work contains a high degree of individuality. Although Mohammed introduced a lot of novelty into medicine, Khoran and the Sayings do not explicitly refer to epilepsy. Of importance is to notice that Moslem medicine did not have demons in the "repertoire" of direct causes of epilepsy. The causes and the cures of epilepsy were more magic-mystical and occult in nature, which is reminiscent of the European, as well as Serbian Middle age attitudes. Avicenna recognized difference between children and adult epilepsy. He considered insomnia and afternoon siesta as well as intensive sounds and light to be a provocative factors, whereby we see that at least empirically he knew of sleep (deprivation), startle and reflex epilepsy. The XIII century invasion of Mongols brought about the recession in Moslem Medicine; it recovered only in the XVIII century under the strong influence of European medicine handed over to us through Jewish doctors of various nationalities. The story of the China history of epilepsy has its debut approximately in the 8th century B. C. Medical texts from this period name epilepsy "Dian" and "Xian" which meant "the falling sickness" and "convulsions", respectively. Chinese medical terminology often interchangeably used the words "mania", "madness" and "psychosis" for "epilepsy" which, aside from a prominent language barrier, brings additional confusion. Although Chinese documents gave the first description of the grand mal epileptic attack already in the 8th century B. C. (ABSTRACT TRUNCATED)

China↗
PubMed2005

Genetics of idiopathic epilepsies.

PURPOSE: To search for clues to molecular genetics of common idiopathic epilepsy syndromes. Genetic defects have been identified recently in certain inherited epilepsy syndromes in which the phenotypes are similar to those of common idiopathic epilepsies. METHODS: Mutations identified as the causes of inherited idiopathic epilepsies were reviewed. RESULTS: Mutations of the genes encoding two subunits of the neuronal nicotinic acetylcholine receptor were found in autosomal dominant nocturnal frontal lobe epilepsy. Mutations of two K(+)-channel genes were identified in benign familial neonatal convulsions. Mutations of the genes encoding several subunits of the voltage-gated Na(+)-channel and gamma-aminobutyric acid (GABA)(A) receptor also were identified as the underlying causes of various epilepsy syndromes, such as autosomal dominant epilepsy with febrile seizures plus, benign familial neonatal infantile seizures, and autosomal dominant juvenile myoclonic epilepsy. Mutations within the same gene may result in different epilepsy phenotypes. Thus, the Na(+) channel, GABA(A) receptor, and their auxiliaries may be involved in the pathogenesis of various types of epilepsy. Some forms of juvenile myoclonic epilepsy, idiopathic generalized epilepsy, and absence epilepsy may result from mutations of Ca(2+) channels. Mutations of the Cl(-) channel have been recently found to be associated with a certain type of epilepsy. The recent discovery that mutations of LGI1, a gene encoding a nonchannel molecule, are associated with autosomal partial epilepsy with auditory features may provide a new insight into our understanding of the genetics of idiopathic epilepsy. CONCLUSIONS: These findings suggest the involvement of brain channelopathies in the pathogenesis of certain types of idiopathic epilepsy.

Codon, Nonsense↗
PubMed1987

[Animal models of epilepsy and experimental seizures].

Animal models of epilepsy are essential for the search of new effective antiepileptic drugs. Moreover they may lead to the discovery of the basic neuronal dysfunction(s) which underlies human epilepsies. Animal epilepsies as well as experimental seizures are usually considered as valid models of human epilepsies when, and only when, the drugs which are effective in human epilepsies prevent seizures in animals. This, however, precludes finding new drugs for resistant epilepsies. Animal models of epilepsy can be classified as follows: (i) experimental seizures induced by convulsant drugs or by an electrical stimulation; (ii) reflex epilepsies; (iii) idiopathic epilepsies. Examples of animal models of epilepsy taken from each of these three classes are briefly reviewed. Seizures induced by convulsant drugs or by an electroshock are widely used as simple and rapid screening systems for new anticonvulsant compounds. Moreover, the use of chemical convulsants can lead to new hypotheses concerning the mechanisms underlying human epilepsies. Thus, one of the main arguments in favor of the GABAergic hypothesis of epilepsy is that GABA antagonists induce seizures which are readily counteracted by most antiepileptic drugs. Among the other models of experimentally induced seizures, the kindling model is usually considered, on the basis of its pharmacological characteristics, as a Grand Mal type epilepsy model. Thirty years after this model was first described, the exact modifications induced in the brain by the kindling procedure remain unknown. Various animal species exhibit reflex epilepsies. Myoclonic seizures can be induced by photic stimulation in Papio-papio baboons; tonic-clonic seizures can be induced by various auditory stimuli in certain strains of mice and rats; myoclonic and tonic-clonic seizures can be induced by a variety of environmental stimuli in the mongolian gerbil; photosensitive and febrile seizures have been described in fowl. Most antiepileptic drugs are effective in these reflex epilepsies. Alterations in several neurotransmitter systems have been reported in susceptible strains as compared to resistant strains, such as modifications in noradrenergic, serotoninergic, GABAergic or glutamatergic transmissions, but no single abnormal parameter can unequivocally be correlated to seizure susceptibility. Idiopathic epilepsy is not uncommon in dogs and the prevalence of the disease appears to be comparable to that observed in man. Grand Mal type epilepsy appears to be the most frequent type of epilepsy in dogs; little work has been devoted to the study of the neurochemical alterations which may underly the disease.

Acoustic Stimulation↗