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)

In order to clarify the mechanism of the effect of sodium valproate (VPA) on absence seizures, we performed sleep polygraph recordings in 10 patients with typical absence. VPA was effective in six cases (group A), partially effective in two (group B), and ineffective in two (group C). In 5 of 9 cases, the tonic sleep components were abnormal. In 4 cases, the percentage of slow wave sleep increased before administration of VPA, and did not change remarkably by its administration. In group A and B, twitch movements (TM), one of the phasic sleep components detected in the mentalis muscle on surface EMG, decreased or were unchanged after administration of VPA, especially during the REM period. In contrast, TM increased in group C. We speculate that the changes of TM (especially in the REM periods) after administration of VPA are well related to its effectiveness. Since TMs are thought to be controlled by the nigrostriatal dopaminergic pathway, the different response of basal ganglia to VPA among cases with absence epilepsy would have some relation to the different effectiveness of VPA in controlling seizures.
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PMID:[Polygraphical sleep study on typical absence: relationship between the effect of sodium valproate and nigrostriatal function]. 818 77

Seizure patients often complain of sleepiness or disturbed sleep. Although susceptible of medication effect, the multiple sleep latency test (MSLT) may quantify daytime sleepiness and help to establish whether qualitative sleep disturbance accompanies epilepsy. In order to measure daytime sleepiness in epilepsy patients, 30 patients with newly diagnosed or presently untreated complex partial seizures had MSLT after an overnight sleep EEG that showed no sleep deprivation or nocturnal seizures. Four 20-minute naps were undertaken at 09:00, 11:00, 13:00, and 15:00, and sleep latency was recorded along with 8 channels of EEG. Twenty of 30 seizure patients reported subjective sleepiness. Eight patients had average sleep latencies less than 8 minutes, and 3 had latencies less than 5 minutes. No sleep onset REM or respiratory disturbance was noted. Twenty-five patients had EEG abnormalities but none had ictal seizures. Right temporal epileptiform activity correlated with sleepiness. MSLT may quantify sleepiness in epilepsy patients, which is common but may be subjective or psychophysiological. Some patients with partial seizures have persistent daytime sleepiness independent of medication, possibly related to residual medication effects or non-specific effect of their epileptogenic foci.
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PMID:Multiple sleep latency tests in epilepsy. 819 89

The mechanism of death following exposure to anticholinesterases, such as the highly toxic nerve agents soman and VX, and other organophosphate anticholinesterases such as the insecticide parathion, remains unclear, although evidence from nerve agent research suggests that death occurs by an atropine blockable respiratory failure mediated through mechanisms involving the central nervous system. It is proposed that REM sleep pathways, which can be triggered by acetylcholine accumulation in the pontomedullar reticular field, mediate respiratory failure through the inhibition of respiratory muscles. Cholinergic activation of REM sleep activities may also account for other physiological and behavioural effects that follow exposure to nerve agents. These include forebrain activation, which is associated with EEG desynchronization and seizures, locomotor depression with concomitant loss of righting reflex, and limb jerks and extensions. Pharmacologic evidence for atropine and clonidine protection against soman intoxication effects is entirely consistent with a scenario of cholinergic receptor activation in the pontomedullar reticular field.
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PMID:REM sleep pathways and anticholinesterase intoxication: a mechanism for nerve agent-induced, central respiratory failure. 823 94

A healthy boy who had showed no evidence of cerebral lesions developed epileptic seizures resembling grand mal during nocturnal sleep at the age of 9 years and 2 months. Interictal EEG showed diffuse sharp waves that were maximal in the right centroparietal area and recurred at short intervals. Polysomnography for one night was performed when the patient was 9 years and 11 months old. The values of sleep variables (percentage of sleep period time for each sleep stage, sleep latency, REM density) were within normal limits. Interictal sharp waves appeared most frequently in the stages 3 and 4, and least in the stages REM and W. Partial seizure of the left face occurred with impaired consciousness in the stage 2 at around 5 a.m. On the ictal EEG, a low-voltage fast discharge was initiated in the right frontal area, followed by a diffuse rhythmic discharge of high voltage at 5-6 Hz, which was associated with a clinical seizure. The seizures completely ceased within one month after the polysomnography. Interictal sharp waves that migrated to the centrotemporal or midtemporal area disappeared at the age of 15 years and 9 months. The patient is now 19 years and 5 months of age. Although his interictal EEG and clinical seizures were atypical, we diagnose his disease as benign childhood epilepsy with centrotemporal spike based on the polysomnographic findings and the clinical and EEG follow-up.
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PMID:[A case of benign childhood epilepsy with centrotemporal spike diagnosed by a seizure during polysomnography and clinical and EEG follow-up]. 826 Feb 12

The case of a healthy 2-year-old girl with repeated nocturnal tongue biting as a result of rhythmic movements of the jaw associated with body rocking in non-REM sleep is described. Parasomnias manifesting with rhythmic, stereotyped movements of the head, trunk and extremities are well described in healthy children. The term rhythmic movement disorders (RMD) was introduced for these repetive movements in sleep which may appear as head banging (jactatio capitis), body rocking or leg rolling. Severe injuries including fractures, subdural effusions and eye injures are reported. Repeated tongue injuries have not been described as a consequence of RMD. The differential diagnosis from nocturnal seizures is crucial to avoid overtreatment of this benign albeit dramatically presenting condition.
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PMID:Parasomnia with rhythmic movements manifesting as nocturnal tongue biting. 835 23

The possibility that REM sleep deprivation (REMD) induced increased susceptibility of rats to the convulsive effects of metaphit was investigated. Metaphit-induced audiogenic seizures were studied in three groups of animals: 1) caged controls; 2) large platform animals; and 3) small platform, REMD animals. After 48 h of confinement to their environments the rats from all three groups were injected with metaphit (10 mg kg-1, IP) and the procedures continued for the next 24 h. Immediately after removal from platforms and at 3-h intervals thereafter all rats were individually subjected to intense sound stimulation. Convulsive responses were recorded and analyzed with respect to incidence, intensity, and duration. The REMD rats were found to be more sensitive to the convulsive effects of metaphit compared to nondeprived rats. This was manifested in significantly shorter latencies to seizures, and significantly higher incidence, severity, and duration of seizures, especially of the most severe seizure component-tonic extensor convulsion. Inducing rats to convulse while they were being REM sleep deprived eliminated the REM sleep rebound observed in REMD rats that did not convulse. The occurrence of spontaneous EEG seizures during the undisturbed recovery period reduced REM sleep rebound. The results demonstrate a reciprocal relation between seizure behavior and REM sleep.
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PMID:Potentiation of metaphit-induced audiogenic seizures by REM sleep deprivation in rats. 837 29

Trisomy 17 has never been reported in a live birth. We present a case of mosaic trisomy 17 in a male presenting with mental retardation, seizures, attention deficit hyperactivity and autistic disorders, hearing loss, growth retardation, microcephaly, and minor anomalies. Although peripheral blood lymphocyte chromosomes were normal, trisomy 17 was present in the skin fibroblasts. The percentage of abnormal cells appears to have increased from 18% in an initial skin biopsy at age 3 years 8 months to 80% at age 8 years 8 months. Molecular analysis using 13 highly polymorphic markers spanning the length of chromosome 17 demonstrated the extra chromosome 17 in the skin to be of paternal origin. Three alleles were never seen in the trisomic cell line, suggesting that the extra chromosome arose through a mitotic duplication error after conception. Uniparental disomy was excluded in the euploid blood sample. Although Smith-Magenis syndrome involves a deletion of proximal 17p, some of the clinical features of this mosaic trisomy 17 patient, such as decreased REM sleep and increased tolerance to pain, are suggestive of phenotypic features observed in Smith-Magenis syndrome. We speculate that there are dosage-sensitive genes located in 17p11.2 that produce these phenotypes for either deficiencies or over-expression of their gene products.
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PMID:A clinical and molecular study of mosaicism for trisomy 17. 855 63

Norrie disease (ND) is an X-linked recessive disorder causing ocular atrophy, mental retardation, deafness, and dysmorphic features. Virtually absent monoamine oxidase (MAO) type-A and -B activity has been found in some boys with chromosome deletions. We report the coexistence of cataplexy and abnormal REM sleep organization with ND. Three related boys, referred for treatment of medically refractory atonic spells and apneas, underwent extended EEG-video-polysomnographic monitoring. They demonstrated attacks of cataplexy and inappropriate periods of REM sleep during which they were unarousable. One boy also had generalized tonic-clonic seizures. Previous testing revealed that all three have complete ND gene deletions. In all subjects, platelet MAO-B activity was absent, serum serotonin levels were markedly increased, and plasma catecholamine levels were normal. Data from the canine narcolepsy syndrome model implicate abnormal catecholaminergic and cholinergic activities in the pathogenesis of cataplexy. Our findings suggest that abnormal MAO activity or an imbalance between serotonin and other neurotransmitter levels may be involved in the pathogenesis of human cataplexy.
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PMID:Cataplexy and monoamine oxidase deficiency in Norrie disease. 862 63

The main interest in the association between sleep and temporal lobe dysfunction is based on the activation of ictal and interictal epileptic phenomena. The clinical semiology of NREM and REM parasomnias may resemble complex partial seizures. The differentiation between epilepsy and dissociated states of wakefulness and sleep is of high diagnostic and therapeutic importance. Systems within temporal lobe structures are also responsible for disturbed sleep or dyssomnia. The limbic brain is connected with different nodal points in the network underlying sleep organisation and participates in both sleepinducing and arousal mechanisms. Experimental amygdala kindling, an animal epilepsy model involving temporal structures, induces disturbed sleep patterns favouring waking and light sleep. In epilepsy unstable disrupted and superficial sleep patterns prevail without overt seizures. Sleep-fragmentation and deprivation may impair daytime functioning and cognitive performance by lowering the seizure-threshold. The recognition of dyssomnia and of excessive sleepfragmentation and sleepiness has obvious implications for behavioural and drug treatment.
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PMID:Sleep and the temporal lobe. 866 24

Some periods in the sleep-waking cycle are more seizure prone than others. In absence epilepsy, transition periods between nonrapid-eye-movement (nonREM) sleep and waking or REM sleep can be more seizure prone that stable states. One feature of transition periods that is hypothesized to promote seizure activity is the presence of coincident activity in ascending brainstem reticular formation (RF) arousal systems with synchronized thalamo-cortical activity. To evaluate this hypothesis we examined the state-dependent effects of low intensity RF stimulation on thalamic single unit activity in control conditions and following systemic penicillin-G administration to adult cats. In control conditions, RF stimulation during waking and REM sleep typically evoked a short-latency action potential in thalamic neurons. The same stimulation during nonREM sleep commonly evoked a high frequency burst of action potentials followed by a period of suppressed discharge. In 16/26 neurons, a second rebound burst of action potentials followed the period of discharge suppression. The average interval between the initial and rebound bursts was 75.1 +/- 6.0 ms, which was similar to the interburst interval recorded in these same cells during spontaneous EEG spindles. Following administration of penicillin-G, RF stimulation during nonREM sleep evoked high frequency burst firing, followed by 1-2 rebound bursts in 21/22 thalamic neurons. The average evoked interburst interval was 152.5 +/- 7.3 ms, a value comparable to the interburst interval displayed by these same cells during spontaneous spike-wave seizure activity (157.8 +/- 8.7 ms). RF-evoked rhythmic discharges were dependent upon the presence of thalamocortical synchronization, as responses evoked during waking and REM sleep in penicillin treated cats were similar to those observed in control conditions.
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PMID:Brainstem stimulation during sleep evokes abnormal rhythmic activity in thalamic neurons in feline penicillin epilepsy. 872 98


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