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

To determine the role of Alzheimer's disease as a causative factor for late-onset epilepsy, 44 subjects with mild senile dementia of the Alzheimer type and 58 healthy control subjects were examined over a 90-month period for the development of focal or generalized seizure activity (excluding myoclonus). At entry, all subjects were free of prior seizures and other neurologic, medical, and psychiatric disorders with the potential to impair cognition. Although no control subject developed seizures during the study period, 7 subjects with senile dementia of the Alzheimer type had at least one documented seizure. All 7 subjects had progressed to the severe stage of dementia by the time of the first seizure. Seizures were generalized tonic-clonic in type and were unassociated with clinical or (in 3 subjects) neuropathologic evidence for epileptogenic factors other than Alzheimer's disease. We conclude that advanced Alzheimer's disease alone may be an important risk factor for new-onset seizures in older adults.
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PMID:Advanced Alzheimer's disease is a risk factor for late-onset seizures. 237 89

Nine patients had reflex activation of seizures by calculation, card and board games, or spatial tasks. The common denominator for these and the 16 others reported in the literature appears to be activity related to function of the parietal lobe. The clinical and EEG findings in all 25 patients support the diagnosis of primary generalized epilepsy. Seizures usually start during adolescence and consist of myoclonus, absences, and generalized convulsions. Specific inquiry about reflex activation should be carried out in patients with generalized epilepsy since this is rarely provided spontaneously. Attacks could be controlled satisfactorily in 89% of our patients. The genetic features are those of a primary generalized epileptic disorder without evidence for a specific inheritance of reflex sensitivity. Neuropsychological analysis of the stimuli points to parietal cortical dysfunction. These stimuli lead to activation of a generalized epileptic process analogous to the occipital cortical participation in the activation of generalized epileptic abnormality occurring in patients with photosensitive epilepsy.
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PMID:Reflex seizures induced by calculation, card or board games, and spatial tasks: a review of 25 patients and delineation of the epileptic syndrome. 238 24

The effects of dextromethorphan (DM), a nonopioid antitussive and a functional N-methyl-D-aspartate (NMDA) antagonist, on expression and development of amygdaloid kindled seizures were examined. The maximum anticonvulsant effect of DM (30 mg/kg) on fully kindled seizures appeared within 30 min of administration and lasted for at least 2 h. DM decreased, in a dose-dependent manner [10-70 mg/kg, intraperitoneally (i.p.)], the severity of kindled seizures 30 min after injection, but the estimated ED50 was 3 times higher than the previously reported value for maximal electroshock convulsions. Furthermore, the high dose (70 mg/kg), while suppressing kindled seizures, produced myoclonus which coincided with EEG spike activity in the amygdala and the cortex. When tested on the development of kindling, 30 mg/kg DM retarded the growth of afterdischarge in the amygdala and the cortex, but had no effect on the development of behavioral seizures. DM 60 mg/kg accelerated development of kindling and produced spontaneous seizures. These results indicate that DM, unlike other NMDA antagonists, has a narrow therapeutic window as an anticonvulsant on kindled seizures and that higher doses may potentiate the kindling process.
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PMID:Effects of dextromethorphan, a nonopioid antitussive, on development and expression of amygdaloid kindled seizures. 240 Dec 41

Previous studies by our laboratory have shown that exposures to either lindane or dieldrin enhanced the rate of acquisition of the fully kindled amygdaloid seizure in the rat. To examine whether this enhancement generalizes to all groups of chlorinated hydrocarbon pesticides, the effect of dichlorodiphenyltrichloroethane (DDT) or chlordecone (kepone) was examined on the acquisition rate of the kindled amygdaloid seizure in the rat. Daily DDT exposure (5, 10 or 20 mg/kg, PO) failed to modify the rate of acquisition of the kindled amygdaloid seizure despite resulting in tremors in many of the rats in the high dose group. A single high dose of kepone (50 mg/kg) which resulted in up to 9 days of tremors and weight loss in the treated animals, also failed to modify the rate of kindling acquisition. These data demonstrate that not all CNS active chlorinated hydrocarbon pesticide exposures result in enhancement of kindling acquisition. The kindled amygdaloid seizure model of epilepsy appears to differentiate between the neurotoxic consequences of chlorinated hydrocarbon pesticides that cause myoclonus and seizures (e.g., lindane and dieldrin) and those that primarily cause tremors (DDT and kepone).
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PMID:Chlorinated hydrocarbon pesticides and amygdaloid kindling. 241 43

Cortical and subcortical multiunitary activities (MUA) and EEG were simultaneously recorded in baboons made photosensitive by a subconvulsant dose of DL-allylglycine. Intermittent light stimulation (ILS) trains induced in these animals fronto-rolandic (FR) paroxysmal discharges (PDs, constituted as spikes and waves) and grand mal seizures. During the induction of FR PDs by ILS trains, the visual structures (occipital cortex, colliculi superioris, pulvinar) showed a significant MUA increase which was not related to the PD spike or wave but correlated with the flashes. The first structure showing bursts of MUA that frequently preceded the PD appearance was the FR cortex. When PDs appeared, the bursts were related to the spikes of PDs and were followed by an inhibition during the slow wave. The pontine and mesencephalic reticular formations and the facial nuclei were activated in bursts after the FR PDs had reached a certain amplitude. The thalamic nuclei ventralis lateralis, centrum medianum and lateralis posterior were activated only later, when the FR PDs had reached an even greater amplitude. It is suggested that the activation of visual structures is necessary for FR PD appearance. The secondary pontine and mesencephalic activation could reinforce that of the FR cortex and then the thalamus, and could determine the myoclonus observed in unparalysed animals. When the ILS is continued, grand mal seizures appear. The onset of the seizures could be linked to the loss of FR cortical control of the subcortical structures. The resulting reticular activation would be responsible for the vasomotor modifications which constitute the first clinical signs of a seizure.
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PMID:Multiunitary activity analysis of cortical and subcortical structures in paroxysmal discharges and grand mal seizures in photosensitive baboons. 242 96

Two hundred and thirty-six adult epileptic outpatients were classified twice: firstly according to the time of seizures reported by the patient or his family in diurnal, nocturnal, awaking and diffuse epilepsies (Es) and secondly according to the sensitivity to sleep or waking of the interictal paroxysmal activities (PA) observed during a polysomnographic night session with a sleep PA increase, with a waking PA increase, with PA indifferent to sleep and waking or with few or no PA. The stability of the sensitivity of the PA to sleep and waking was 84%. Patients with diurnal epilepsy have more frequently myoclonic attacks and a lower seizure frequency. Patients with a sleep PA increase have less frequently generalized motor seizures, more frequently partial complex seizures, a higher seizure frequency, higher total night PA density and more frequently the appearance of new PA during sleep. Patients with a waking PA increase had more frequently massive myoclonus, rarely the appearance of new PA during sleep and a high total night PA density. There is no significant relationship between the two classifications. Neither classification succeeds in discriminating the electro-clinical type of the epilepsies.
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PMID:Two distinct classifications of adult epilepsies: by time of seizures and by sensitivity of the interictal paroxysmal activities to sleep and waking. 243 4

Pathologically enhanced somatosensory evoked potentials (giant SEPs) were recorded in 10 patients with cortical myoclonus of various origins. With non-cephalic reference electrodes a giant frontal negativity corresponding to normal N30 was found over the contra- and ipsilateral hemispheres which was not simply a phase reversal of the well-known enhanced parietal P25. The preceding far-field P14, parietal N20 and frontal P22 were of normal size. A similar result was found when SEPs were studied during the action of etomidate, an ultrashort-acting non-barbiturate hypnotic which produced a marked increase of the parietal P25 and frontal N30 after intravenous administration. These increased components, on the other hand, were abolished when recording was repeated immediately after application of electroconvulsive shock whereas P14, N20, and P22 remained more or less unchanged in both conditions. Our results indicate that there are neuronal elements in the sensorimotor cortex which are more resistant to influences such as narcotic drugs and seizure activity than others, being highly modifiable by these alterations. It is speculated whether these highly modifiable cortical systems are those in which giant SEPs, as well as pharmacologically increased SEP components, arise.
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PMID:Frontal and parietal components of enhanced somatosensory evoked potentials: a comparison between pathological and pharmacologically induced conditions. 245 99

The Lafora type of progressive myoclonus epilepsy is a rare and fatal familial disease characterized by seizures, myoclonus, and dementia. This diagnosis was confirmed in 2 patients by demonstrating the presence of intracytoplasmic polyglucosan bodies, or Lafora bodies, in the peripheral portion of the eccrine sweat gland duct. Exclusive use of the periodic acid-Schiff stain is recommended for demonstrating these diagnostic inclusions. Electron microscopy reveals fine pale-staining filaments, fine dark-staining granules, and dark-rimmed vacuoles within these non-membrane-bound inclusions. Skin biopsy is the preferred method of confirming the diagnosis of Lafora disease.
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PMID:Diagnosis of Lafora disease by skin biopsy. 245 16

It has been hypothesized that the Long-Sleep and Short-Sleep mouse lines were bidirectionally selected for high and low brain excitability, and further, that these differences are mediated by the benzodiazepine/gamma-aminobutyric acid (GABA) receptor-chloride channel complex. Hence, mice from both lines were administered seven convulsants (bicuculline, pentylenetetrazol, 3-carbomethoxy-beta-carboline, picrotoxin, caffeine, flurothyl and strychnine) and myoclonic and clonic seizure latencies recorded. Supporting the original hypothesis, the results show that the two lines were differentiated by all of the convulsants and that in response to the drugs, three distinct convulsive patterns were found. Nevertheless, a simple genetic model accounting for these results was not evident. To further clarify these susceptibility patterns, a convulsant representing each of these patterns (bicuculline, pentylenetetrazol or caffeine) was administered in conjunction with the anticonvulsant-barbiturate phenobarbital or the benzodiazepine antagonist Ro 15-1788. Irrespective of the convulsant given, phenobarbital attenuated both myoclonus and clonus subsequent to all convulsants, while Ro 15-1788 had a more discrete anticonvulsant profile.
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PMID:Patterns of convulsive susceptibility in the long-sleep and short-sleep selected mouse lines. 250 42

The convulsant potency of bicuculline, a GABA antagonist, was shown to be greater in Short-Sleep (SS) mice than in Long-Sleep (LS) mice. LS mice, selectively bred for lengthy ethanol-induced narcosis, had longer latencies to myoclonus and clonus following administration of bicuculline and picrotoxin than did ethanol-resistant SS mice. SS mice were also more susceptible to pentylenetetrazol-induced myoclonus, but not clonus. F1 hybrids showed bicuculline seizure sensitivity intermediate to the two parent lines. Ethanol weakly inhibited bicuculline-induced myoclonus in both LS and SS mice. Clonus was clearly antagonized by ethanol in both lines, but to a similar degree. These data provide evidence for a GABAergic role in genotype-dependent sensitivity to ethanol.
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PMID:Convulsant properties of GABA antagonists and anticonvulsant properties of ethanol in selectively bred long- and short-sleep mice. 250 97


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