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Query: UMLS:C0014544 (epilepsy)
64,704 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using an ambulatory cassette EEG system (Oxford Medilog 9000), polysomnography was performed in 25 cases of children with epilepsy and 25 normal children. The results revealed decreases in REM sleep and REM density in intractable epilepsy. An increase of slow waves was observed during REM sleep in severe myoclonic epilepsy in infancy or its adjacent group, and this result was more clearly demonstrated by an EEG auto analysis with fast Fourier transform. This above ambulatory cassette EEG system will be utilized more easily for polysomnography, and contribute to the research not only of the pathophysiology of epilepsy but also of the sleep mechanism itself.
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PMID:[Application of ambulatory cassette EEG system to the polysomnography in childhood epilepsy]. 190 57

Electrical status epilepticus during sleep (ESES) is primarily an EEG-defined syndrome in children characterized by the occurrence of continuous spike and slow waves during non-rapid-eye-movement (non-REM) sleep, the paroxysmal abnormalities being substantially less frequent during the awake state and REM sleep. Etiologically, cases can be divided into symptomatic and cryptogenic varieties. Partial motor seizures, frequently nocturnal, precede the emergence of ESES, whereas absence seizures often occur during the phase of ESES. The emergence of ESES is associated with neuropsychological regression. The characteristic electrographic pattern and epilepsy generally disappear during adolescence and are associated with an improvement in neuropsychological function. However, if the cases reported in the literature are representative, then there is a high probability of considerable residual dysfunction. A number of factors, broadly termed ascertainment biases, likely contribute to the paucity of reports from North America and the greater recognition of the syndrome in Europe and Japan. The current information on ESES is critiqued in this review.
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PMID:Electrical status epilepticus during slow-wave sleep: a review. 191 35

Four girls with childhood absence epilepsy with several seizures every day were investigated using an ambulatory cassette EEG. Recordings were started at about 6 pm, and were run continuously for about 22 hours. We studied only the regular and symmetrical 3 Hz spike-wave discharges of at least 5 seconds duration, which are quite similar to or identical with those found in the clinical seizures. Regular spike-wave discharges occurred frequently during wakefulness in 2 cases and during sleep in the other 2 cases: in the latter, they occurred rarely during wakefulness. During wakefulness, we did not find a special time zone in which regular spike-wave discharges were facilitated; during nocturnal sleep, however, they were concentrated in the last third. The rate of regular spike-wave discharges per hour was the highest during stage 1, low during stages 2 and REM, and zero during stage 3 + 4. Average duration of regular spike-wave discharges was the longest during wakefulness in most cases, and shortest during stage 2 in all the cases.
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PMID:Circadian rhythm of regular spike-wave discharges in childhood absence epilepsy. 192 15

It is not in the best interest of persons with epilepsy to deny the possibility that seizures could cause enduring behavioral disturbances. Rather, it is essential to pursue clinical and animal investigations in order to identify any such changes that might occur and to elucidate their mechanisms. Many testable hypotheses can be developed from existing evidence. Antiepileptic medication may produce interictal behavioral disturbances in patients with epilepsy by indirect mechanisms. Some aberrant behaviors could be due to medication-induced systemic disorders, neuroendocrine dysfunction, or REM deficit, whereas depression following successful treatment with drugs, as well as with surgery, may be related more specifically to cessation of seizures. The underlying neuropathological process also induces neurological and mental deficits, but it is not always possible to differentiate those behavioral disturbances due to destructive effects of the lesion from those due to recurrent epileptic seizures. Behavioral disturbances are associated more frequently with epileptogenic lesions in limbic structures than with those elsewhere in the brain, but a relationship between hemispheric lateralization of the epileptogenic lesion and specific interictal behavioral symptoms remains controversial. When considering the effects of seizures per se on interictal behavior, it is important to realize that some "interictal" behavioral disturbances may actually be ictal events. Prolonged affective, autonomic, and psychic disturbances can occur in clear consciousness with unilateral limbic seizures that are not associated with scalp EEG changes. When epilepsy is acquired as a result of cerebral damage, the epileptogenic process takes time to develop before spontaneous seizures appear. It is more reasonable to assume that this progressive process continues than to postulate that it stops completely at the time the first seizure occurs. Epilepsy-induced protective homeostatic mechanisms that act to terminate ictal events, prevent ictal spread, and maintain the interictal state may also disrupt interictal function. Furthermore, seizures could indirectly influence interictal behavior as a result of their effects on neuroendocrine function and sleep. Because of confounding biological factors, it is difficult to document the association of any epilepsy disorder, by itself, with progressive behavioral disturbances in humans. Secondary epileptogenesis, protective homeostatic mechanisms, and epilepsy-induced disturbances in development can be readily demonstrated, however, in experimental animal models. In experimental animals, endogenous opoids are released during seizures and mediate some postictal behaviors. A physiological dependency on high levels of endogenous opioids released during seizures could produce depression as a withdrawal symptom interictally or when seizures no longer occur as a result of successful therapy. Experimental animal models of depression exist to test hypotheses concerning pro- and antidepressant effects of epileptogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurobiological evidence for epilepsy-induced interictal disturbances. 200 26

Polygraphic sleep recordings (EEG, EMG, and EOG) were performed in two groups of epileptic subjects, six with fragile-X syndrome and six with symptomatic epilepsy. Recordings were visually scored for sleep stages and number of spikes/min. Subjects with fragile-X syndrome showed a well defined pattern of production of interictal epileptiform activity with the lowest values during REM sleep; symptomatic epileptic subjects showed less defined and more variable spike/min diagrams. The spectral analysis of the outline of such diagrams confirmed these differences showing shorter periodicities (80-100 min) in the fragile-X group compared to those of the symptomatic group (160-220 min). Finally, a model with multiple feedback circuits is proposed in order to explain the different patterns observed.
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PMID:Modulation of the interictal epileptiform EEG activity during sleep: from oscillations to complex dynamics. 206 67

Sleep disorders have an incidence of approximately 65 percent in early childhood. Etiologic there are constitutional and neurotic factors in night terror. Neurophysiologically it occurs at fast arousal out of non-REM-sleep. There are no relations to epilepsy, also not at existence of spike potentials in the EEG. At a cross-sectional examination of 20 children with pavor nocturnus 14 exhibited sharp waves and one SW. The EEG can hint at constitutional factors, retardation of cerebral maturation, but psychological examination is in severe cases more useful for effective therapy.
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PMID:[Significance of EEG findings in pavor nocturnus]. 209 14

The effects of sleep and sleep deprivation on epilepsy are well known, but the effects of seizures and antiepileptic drugs (AEDs) on sleep have been less well studied. We recorded nocturnal sleep in 17 patients receiving antiepileptic monotherapy with ambulatory cassette EEG devices. Twelve patients had complex partial seizures and five had tonic-clonic convulsions. Two patients' seizures were largely nocturnal, and no seizures occurred during sleep recording. Five patients each were taking phenytoin (PHT), carbamazepine (CBZ), and valproate (VPA), and two were taking clonazepam (CZP), all with therapeutic serum levels and no toxic symptoms. Total sleep time was reduced, wakefulness increased, and sleep latency prolonged in partial seizures as compared with generalized epilepsy. REM sleep was reduced and its latency decreased in partial seizure patients. Both groups had decreased slow wave sleep; that of partial seizure patients was decreased more markedly. PHT increased sleep latency and decreased sleep time, and CBZ increased awakening and diminished slow wave and REM sleep. Patients taking VPA had slight reduction in slow wave sleep; those taking CPZ had decreased sleep and REM latencies. Epilepsy may affect nocturnal sleep, and the effects of partial and generalized seizure disorders may be different. AEDs may also have differential effects on nighttime sleep. These may prove important in the long-term management of epileptic patients.
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PMID:Outpatient sleep recording during antiepileptic drug monotherapy. 211 39

A night-time polygraphic sleep recording was performed in 14 patients with late onset partial epilepsy receiving chronic carbamazepine monotherapy. All patients had unstable nocturnal sleep patterns as indicated by significantly altered sleep continuity parameters compared with normal controls. Patients with poor seizure control tended to show greater alterations of sleep stability compared to patients in complete clinical remission but the difference failed to reach statistical significance. Epileptic patients also showed less REM sleep and longer REM latencies compared with normal controls, the most altered REM values being observed in patients with poor seizure control. These data confirm that polygraphic sleep alterations are seen in patients with symptomatic focal epilepsy and indicate that these abnormalities occur irrespective of seizure recurrence.
Epilepsy Res
PMID:Sleep patterns in patients with late onset partial epilepsy receiving chronic carbamazepine (CBZ) therapy. 212 55

The spatial and temporal EEG features of the epileptogenic syndrome induced by cessation of chronic intracortical GABA infusion in normal rats are described. In the initial stages, the paroxysmal discharges (PDs) induced by withdrawal from unilateral GABA application may appear either unilaterally or bilaterally, although with greater amplitude on the infused side. PDs are transitorily accompanied by behavioral signs of distal myoclonus of the body territory corresponding to the infused area (contralateral hindlimb). Later, the paroxysmal activity becomes more localized, circumscribed to the cannula-infused site and with ipsilateral propagation to anterior cortical areas. The amplitude of PDs decreases progressively while their frequency increases, reaching its maximal value at about 4 h after the first PDs have appeared. In the final stages of the syndrome, which may last several days, clinical manifestations are absent and PDs are activated by slow-wave sleep and reduced during REM sleep and waking. Chronic intracortical applications of taurine failed to induce any electroclinical changes on withdrawal and were unable to inhibit the focus elicited by GABA withdrawal, whereas reinstatement of GABA infusion into the epileptogenic area was effective in blocking the paroxysmal activity. Intracortical infusion of baclofen induced the appearance of an epileptogenic focus that waned on withdrawal. The GABA-withdrawal syndrome appears to be a new model of focal status epilepticus; it may be useful as an experimental model of human partial epilepsy to investigate the role of GABAergic neurotransmission.
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PMID:Electroencephalographic study of the GABA-withdrawal syndrome in rats. 236 74

Effects of deprivation of REM sleep on spontaneous occurring spike wave complexes in the WAG/Rij rat strain were studied by means of the pendulum and platform technique. During the deprivation period, which lasted three days, variable results were obtained. While a suppression of the total duration of epileptic activity was found for the pendulum deprived animals, no such evident effect was detected in the platform deprived rats. Probably, instrumental effects are responsible for these differential results. On the other hand, subsequent to deprivation, a prolonged reduction of the total duration of spike wave activity was seen in both deprived groups. While it is known that under normal circumstances absences only occur during low levels of arousal and because there is evidence that deprivation of REM sleep has arousal increasing properties, it is suggested that the reduction in epilepsy is caused by an increase of arousal. This result also implies that, at least in the case of absence epilepsy, REM sleep deprivation is not the crucial factor for the epilepsy provoking effect of total sleep deprivation.
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PMID:Absence epilepsy in rats is reduced by deprivation of REM sleep. 251 89


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