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)

Circling seizures (CS) have been described in association with focal lesions as well as with generalized EEG discharges. We report 1 patient with juvenile myoclonic epilepsy (JME) who developed CS. There were no focal findings on clinical examination, EEG, or imaging studies. We propose that CS in this patient may represent a profound asymmetry in expression of an idiopathic generalized epilepsy rather than a partial condition.
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PMID:Circling seizures in a case of juvenile myoclonic epilepsy. 815 50

Circling, turning, rotating, spinning, wheeling, and cursive hyperkinesia are all synonymous terms used to describe the active movement of an animal in a circular direction. Circling behavior can be evoked by unilateral electrical and chemical stimulation or lesions of various brain sites, but can also occur after systemic drug administration or spontaneously in normal animals or mutant rodents. In humans, stereotypic body rotation can occur as a distinctive entity of generalized and focal epilepsy, and may be due to involvement of the striatum. We have previously described a Lewis rat mutant (ci2) with a behavioral phenotype characterized by lateralized circling, hyperactivity, opisthotonus, and ataxia. In these rats, circling occurs in phases or bursts either spontaneously or in response to stress. Neurochemical data indicate that the circling behavior of the ci2 mutants is related to an abnormal asymmetry in dopaminergic activity in the striatum. Because of the similarities to rotational epilepsy, we used video and electroencephalographic recordings to study whether the rotational behavior of the ci2 mutant rat is a result of a partial or generalized epilepsy. Epileptic WAG/Rij rats were used for comparison. Video monitoring of ci2 rats in the absence of any stress or disturbance showed that circling occurs in paroxysmal bursts during active wakefulness, but not during passive wakefulness or sleep. Circling was not preceded or followed by any convulsive motor seizures and was not associated with epileptiform abnormalities in the electroencephalogram, whereas WAG/Rij rats exhibited myoclonic seizures and epileptic spike-wave discharges during passive wakefulness and sleep. As a result of the association of circling with active wakefulness, ci2 rats exhibited many more rotations during the dark (active) phase compared with the light (rest) period. Increase in active wakefulness during the light phase by transfer of the rats to a new environment induced or intensified circling behavior. Most ci2 rats showed a consistent lateral preference during circling, but some rats changed their preference from one session to another. The data indicate that spontaneous paroxysmal circling behavior in the ci2 rat is not a consequence of epilepsy but reflects a hyperkinetic movement disorder with abnormal lateralization of brain function.
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PMID:Spontaneous paroxysmal circling behavior in the ci2 rat mutant: epilepsy with rotational seizures or hyperkinetic movement disorder? 1171 68

A dextromethorphan (3-methoxy-17-methylmorphinan) analog, dimemorfan (3-methyl-N-methylmorphinan) that is not metabolized to dextrorphan [3-hydroxy-17-methylmorphinan, which induces phencyclidine (PCP)-like behavioral effects], attenuates maximal electroshock seizures. However, the pharmacological mechanism of action of dimemorfan remains to be determined. In this study, we assessed the locomotor activity mediated by these morphinans. Circling behavior was pronounced in mice treated with PCP or dextrorphan, while animals treated with dextromethorphan exhibited moderate behaviors. Dimemorfan did not show any significant behavioral effects. We used BAY k-8644 (an L-type Ca2+ channel agonist in the dihydropyridine class) to explore the effects of dextromethorphan and dimemorfan on the convulsant activity regulated by calcium channels. Intracerebroventricular injection of BAY k-8644 (37.5 microg) significantly induced seizures in mice. As with dextromethorphan (6.25 or 12.5 mg/kg), dimemorfan (6.25 or 12.5 mg/kg) pretreatment significantly attenuated BAY k-8644-induced seizures in a dose-dependent manner. BAY k-8644-induced seizure activity paralleled increased expression of c-fos and c-jun, AP-1 DNA binding activity, and fos-related antigen immunoreactivity. Pretreatment with dextromethorphan or dimemorfan significantly attenuated the expression induced by BAY k-8644. Therefore, our results suggest that the anticonvulsant effects of dextromethorphan and dimemorfan are mediated, at least in part, via L-type calcium channel, and that dimemorfan is equipotent to dextromethorphan in preventing BAY k-8644-induced seizures, while it lacks behavioral side effects related to psychotomimetic reactions.
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PMID:Dimemorfan prevents seizures induced by the L-type calcium channel activator BAY k-8644 in mice. 1508 42