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

The time course of delta activity within nonREM (NREM) episodes is measured for 24 healthy subjects with normal REM latencies. The first two NREM episodes in particular, show two very clearly separated peaks for about 35% of the subjects. Another 25% show two less well separated peaks. These double peak patterns are also prevalent in the literature, but there has been a tendency to dismiss them as a skipped REM effect. They are, however, still evident even when the data are averaged over the 24 subjects, indicating a systematic phenomenon. These averaged data are well fitted by an analytic function given by the sum of two consecutive overlapping Gaussian curves. The well-behaved residuals also, are an indication that a biphasic model of this kind is statistically appropriate. The model proposed is simple, with parameters related to physiological phenomena, and it suggests that there may be an underlying process with delta waves emanating from two separate signal sources. Recent neurophysiological findings suggest that delta oscillations are generated both in the thalamus and in the cortex and show that excessive synchronization of slow oscillations may lead to seizures. Hence the speculation that the biphasic process may emanate from cortical and thalamic sources and be protective in the sense that it permits smaller delta amplitudes at each source while retaining the integral delta energy necessary to satisfy sleep pressure. It is significant that the two peaks are most evident in the first two NREM episodes where delta power is high.
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PMID:Evolution of delta activity within the nonREM sleep episode: a biphasic hypothesis. 922 65

The cerebral cortex and thalamus constitute a unified oscillatory machine displaying different spontaneous rhythms that are dependent on the behavioral state of vigilance. In vivo multi-site recordings from a variety of neocortical areas and related thalamic nuclei in cat, including dual simultaneous intracellular recordings, demonstrate that corticofugal volleys are effective in synchronizing fast (20-50 Hz) and low-frequency (< 15 Hz) oscillations in thalamocortical networks, characterizing activated and de-afferented states. (i) Fast spontaneous oscillations depend on the depolarization of thalamic and cortical cells and appear in a sustained manner during waking and REM sleep. Corticothalamic neurons, discharging high-frequency (400 Hz) spike-bursts at 30-40 Hz, are good candidates to synchronize fast oscillations in reentrant thalamocortical loops. Weakly synchronized, fast spontaneous oscillations may be reset and become robustly coherent after relevant sensory stimuli in waking or internal signals during the dreaming state. (ii) During quiescent sleep, the long-range synchronization of brain electrical activity results from synchronous hyperpolarizations in forebrain neurons. The corticothalamic inputs during the depolarizing component of the slow oscillation (< 1 Hz) are effective in grouping the thalamic-generated sleep rhythms (spindles at 7-14 Hz and delta at 1-4 Hz) into complex wave-sequences. These inputs also control the shape of spindles, and favor the long-range synchronization and nearly simultaneous appearance of spindles. (iii) The cortical control of thalamic activity is also demonstrated in spike-wave-seizures developing from sleep patterns. More than half of thalamocortical neurons are silent during spike-wave seizures, being tonically hyperpolarized, and display IPSPs (closely related to the paroxysmal depolarizing shifts of cortical cells) that are determined by the pattern of activities in thalamic reticular cells. All these data congruently show the power of cortical control upon thalamic oscillators.
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PMID:Synchronized activities of coupled oscillators in the cerebral cortex and thalamus at different levels of vigilance. 927 82

REM sleep behaviour disorder (RSBD) is a recently described parasomnia characterised by a history of excessive nocturnal motor activity and absence of muscle atonia during REM sleep. Only limited literature is available on this condition. The exact prevalence is unclear, but recent studies suggest it might not be an uncommon condition. The elderly are more often affected and there is a male preponderance. While transient RSBD can be seen after taking certain drugs or during drug withdrawal, the chronic type is usually idiopathic or associated with an underlying degenerative neurological condition. It can result in considerable distress and/or serious injury to the patients or their bed partners. Differential diagnoses include sleep-walking, night terrors, nightmares, nocturnal seizures, obstructive sleep apnoea, post-traumatic stress disorder, dissociative states and nocturnal confusional states. The dramatic response to clonazepam highlights the importance of recognition and appropriate treatment of this sleep disorder.
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PMID:REM sleep behaviour disorder: an overview. 953 85

We present a 43-year-old patient who has had up to 15 frontal lobe seizures nightly for 12 years. The patient had no complaints apart from excessive daytime sleepiness. Neurological and psychiatric examination as well as cerebral computed tomograph and magnetic resonance imaging were normal. After sleep deprivation an interictal electroencephalogram demonstrated a recurrent excess of theta activity over the right frontal and frontopolar area. A cerebral PET study showed diminished glucose metabolism of the right cingular and frontomesial region. The sleep structure was extremely fragmented. There was an excessive reduction of slow-wave sleep and REM sleep. Carbamazepine therapy produced complete seizure control lasting a few weeks, followed by return of up to 8 seizures per night. Vigabatrin as add on therapy diminished the noctural seizures to 1 to 3 per night.
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PMID:[Day time fatigue in frontal lobe epilepsy with primarily sleep-related seizures. A case report]. 955 63

We report a case of a 43-year old woman with Lennox-Gastaut syndrome who exhibited atypical absence seizures, atonic seizures and generalized toniclonic seizures which were not controlled by antiepileptic drug (AED) treatment. Because of this, felbamate (FBM) (1800 mg per day) was progressively added to the pre-existent therapy. The patient underwent a 24-hour-video-EEG monitoring before and after 4 months of FBM therapy. Analysis of the video-EEG signal recorded during wakefulness revealed the presence of ictal activity represented by repetitive, bilateral, slow spike and wave bursts underlying atypical absence seizures; the ictal activity occurring during non-REM sleep was characterized by runs of bilateral, rapid, high-voltage spikes followed by slow spike and wave complexes corresponding to brief tonic seizures. FBM therapy induced disappearance of the EEG ictal slow, spike and wave complexes leaving rather unaffected the runs of spikes. Computerized analysis of both the EEG background activity and the sleep structure displayed a better organization of the global cerebral rhythms under FBM treatment. Our findings suggest a selective effect of FBM on the ictal atypical spike and wave pattern. The differential effect of FBM on ictal patterns may be a reflection of a different action on the excitatory and inhibitory systems.
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PMID:Changes of the EEG paroxysmal pattern during felbamate therapy in Lennox-Gastaut syndrome: a case report. 977 42

The facilitating effect of awakening and sleep deprivation on seizure production and EEG abnormalities is characteristic of idiopathic generalized epilepsies (IGE). This effect is particularly patent in awakening epilepsy. Paroxysmal events occurring in non-REM sleep, related to spindle production during transitional periods or awakening are characteristic of IGE. Because IGEs are particularly sensitive to sleep, sleep deprivation, and awakening, the association of these three conditions is particularly helpful in exploration protocols, especially when no wakefulness abnormalities are seen on the EEG. These observations in IGE suggest a dysfunction of awakening control systems. Awakening epilepsies may be differentiated from sleep-induced seizures observed in other IGE and in partial epilepsies.
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PMID:[Effect of awakening and sleep deprivation in triggering idiopathic generalized epilepsy]. 1022 16

Our objective was to determine, in three separate studies, the effects of controlled-release carbamazepine (CBZ-CR), lamotrigine (LTG), and gabapentin (GBP) on nocturnal sleep in epilepsy. Antiepileptic drugs (AEDs) control seizures and also modify hypnic structure. Despite widespread clinical use, their effects on sleep are not well known. PSG was performed in all three studies as follows: CBZ-CR: at baseline, after initial administration of CBZ-CR 400 mg, and after 1 month of CBZ-CR treatment (400 mg BID) in a sample of seven temporal lobe epileptic (TLE) patients. Results were compared with those of nine healthy volunteers; LTG: at baseline, after 3 months of stable treatment with LTG (300 mg/day); GBP: at baseline, after 3 months of stable treatment with GBP (1800 mg/day). Significant findings are as follows for each study. The acute administration of CBZ-CR increased number of stage shifts, reduced REM sleep, and increased REM sleep fragmentation. In the TLE group, these effects were almost completely reversed after chronic treatment. LTG increased REM sleep, reduced number of entries into REM sleep, decreased number of phase shifts, and decreased percentage of slow-wave sleep. GBP increased REM sleep percentage, increased mean duration of REM periods, reduced number of awakenings, and reduced stage 1 sleep percentage. We conclude that CBZ-CR disrupts REM sleep, but only during acute administration. LTG and GBP improve sleep stability while reducing seizures.
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PMID:Effect of anticonvulsants on nocturnal sleep in epilepsy. 1071 81

Tactile evoked spikes (TES) are a well known EEG feature in children. We reviewed our previous studies concerning this phenomenon, with special reference to the influence of sleep and stimulation rate, the relation with middle-long latency somatosensory evoked potentials (MLSEP) and the relation between TES and spontaneous spikes in the same individual. New data were obtained by re-evaluating 566 children with TES, by assessing MLSEP from each finger, in 15 subjects with TES, and by studying MLSEP following posterior tibial nerve stimulation in 12 children with TES. TES appear to be enlarged components of MLSEP which are present in some children aged 4 to 14 years; they tend to increase during NREM sleep and to decrease during REM sleep; Their amplitude decreases at stimulation rates above 3 Hz. TES are associated with an increased risk of epileptic seizures, which usually have a benign prognosis. The possible neurophysiological mechanisms underlying this phenomenon are discussed.
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PMID:Tactile evoked spikes in children. 1093 41

Awakening epilepsy (AE) is an age related syndrome of idiopathic generalized epilepsy (IGE) characterized by generalized tonic clonic seizures (GTCS) occurring predominantly on awakening (independent of the time of day) or at leisure time (almost at evening). The GTCS can be the only symptom or they can be combined with the other subsyndromes of IGE in childhood or adolescence. The EEG shows the characteristics of IGE (generalized spike wave frequent, foca1 abnormalities rare, photosensitivity increased). The common denominator of external seizures precipitating influences is lack of sleep. The sleep habits of patients with AE who could roughly be characterized as late sleepers and late risers may dispose them to a chronic sleep deficit. Polygraphic studies indicated that their sleep is more unstable and subject to external influences. Microstructural sleep analysis confirms the presence of a disturbance of sleep stability in patients with IGE. Furthermore, it clearly shows that in the prototype of AE, the juvenile myoclonic epilepsy, the epileptiform activity during non-REM sleep is correlated with the arousal phase of the so called cyclic alternating pattern indicating that even in the smallest sleep-waking oscillations awakening is the most sensitive part.
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PMID:Epilepsy with grand mal on awakening and sleep-waking cycle. 1099 62

A review of the literature shows that nap recordings make a significant contribution to epilepsy studies, providing evidence of specific EEG findings in patients suspected of having epilepsy. In addition, sleep deprivation can cause paroxysmal EEG activity and clinical seizures. We studied retrospectively 686 patients, 51.8% males and 48.2% females, who had experienced at least one episode classified from the clinical point of view as epileptic in origin. They were divided into six age groups. Patients underwent a two-hour (1 P.M.-3 P.M.) nap-video-polygraphic recording (EEG 13 channels using the standard 10-20 system, EOG, ECG, EMG and respiration), following a partial sleep deprivation (1 to 3 h) the night before. A second recording was made in 40 patients. In 35.3% of patients, a complete sleep cycle was obtained; in 64.6% sufficient light and deep NREM sleep was obtained, but not REM stage; in 9.3%, we only observed drowsiness and stage 1 of sleep, and this group was excluded from the analysis. Interictal and/or ictal epileptic discharges were observed during the first nap recording in 245 patients (40.4% of the sample). In addition, in 40 patients (11%) with normal or inconclusive first nap EEG, a second recording was able to demonstrate epileptic abnormalities in 35% of cases. Because of its good cost/benefit ratio and availability in most western laboratories, we consider the 'nap plus partial sleep deprivation' method as advantageous over other activation procedures.
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PMID:Nap polygraphic recordings after partial sleep deprivation in patients with suspected epileptic seizures. 1128 Oct 68


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