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

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

Among progressive myoclonus epilepsies (PME), the nosography of the Ramsay Hunt syndrome (RHS) has been much debated. The authors report on a homogeneous group of 43 patients originating from around the western Mediterranean, with a large number of northern African subjects, who were followed up for a mean period of 11.6 years. Onset is between 6 and 17 years (mean: 11.2) and the transmission appears to be recessive. The clinical features include: action myoclonus, generalized epileptic seizures, mild cerebellar signs and lack of dementia. EEG features include normal background activity, spontaneous fast generalized spike-wave discharges, photosensitivity, lack of activation during nREM sleep and vertex/rolandic spikes during REM sleep. The prognosis is variable, even within families, but the progression seems to be slow in a majority of patients. This condition can be distinguished from mitochondrial encephalomyopathy and is less severe than Baltic myoclonus. The authors propose that this form of PME, formerly reported as RHS, be more properly described as Mediterranean myoclonus.
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PMID:The Ramsay Hunt syndrome revisited: Mediterranean myoclonus versus mitochondrial encephalomyopathy with ragged-red fibers and Baltic myoclonus. 210 22

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.
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PMID:Sleep patterns in patients with late onset partial epilepsy receiving chronic carbamazepine (CBZ) therapy. 212 55

The epileptic or nonepileptic origin of nocturnal paroxysmal dystonia (NPD) has been debated. We studied three patients with frequent attacks during non-REM sleep. During prolonged video-EEG monitoring, two patients had a convulsive seizure after a typical NPD episode and on these occasions EEG showed epileptiform discharge. In the three patients, attacks occurred repeatedly with different intensity, representing "fragments" of the same seizure. These fragments of the attack could occur periodically every 20-40 s. We postulate that short NPD attacks are actually epileptic seizures originating from the frontal lobes. The rhythmicity of the episodes may be due to rhythmic oscillation of cortical function during non-REM sleep.
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PMID:Nocturnal paroxysmal dystonia with short-lasting attacks: three cases with evidence for an epileptic frontal lobe origin of seizures. 240 Dec 46

REM sleep is the most antiepileptic state in the sleep-wake cycle for human generalized epilepsy, yet the neural mechanism is unknown. This study verified the antiepileptic properties of REM sleep in feline generalized epilepsy and also isolated the responsible factors. Conclusions are based on 20 cats evaluated for generalized EEG and motor seizure susceptibility before and after dissociation of specific REM sleep components. Bilateral electrolytic lesions of the medial-lateral pontine tegmentum created a syndrome of REM sleep without atonia. Systemic atropine created a syndrome of REM sleep without thalamocortical EEG desynchronization. Identical results were obtained in two seizure models, systemic penicillin epilepsy and electroconvulsive shock. (1) Normal REM sleep retarded the spread of EEG seizure discharges and had even more potent anticonvulsant effects. (2) Selective loss of 'sleep paralysis' (skeletal muscle atonia) during REM abolished REM sleep protection against myoclonus and convulsions without affecting generalized EEG paroxysms. (3) Conversely, selective loss of thalamocortical EEG desychronization abolished REM sleep protection against generalized EEG seizures without affecting clinical motor accompaniment. These results suggest that the descending brainstem pathways which mediate lower motor neuron inhibition also protect against generalized motor seizures during REM sleep. Protection against spread of EEG paroxysms is governed by a separate mechanism, presumably the ascending brainstem pathways mediating intense thalamocortical EEG desynchronization during REM sleep.
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PMID:Mechanisms of seizure suppression during rapid-eye-movement (REM) sleep in cats. 259 45

Piperidine (Pip) is a normal constituent in mammalian brain, affects synaptic mechanism in the CNS, and influences neural mechanisms governing regulation of emotional behavior and extrapyramidal function. In addition, there are enzyme systems within the brain that synthesize and metabolize Pip, and uptake and storage mechanisms for Pip are found in the nerve endings. Pip is highly concentrated in the pituitary and pineal glands, hippocampus and caudate nucleus among the regions of the brain. Levels of Pip in the brain show physiological variations associated with environmental changes. The levels increase significantly under deep anesthesia. The study on the time relations of the change in brain levels of Pip and the anesthetic activity demonstrates that the level increases prior to the loss of the righting reflex and that the elevated level declines prior to the reappearance of the reflex. Furthermore, Pip levels in the lower brainstem reticular formation show sleep-related changes during REM sleep deprivation and REM sleep rebound that followed. Direct administration of Pip into the hippocampus and amygdala of cats with chronically implanted electrodes and a cannula caused resting and calmness in small doses, and seizure discharge accompanied by hyperemotionality in large doses. Administration into the pontine reticular formation induced REM and NREM sleep. Iontophoretic application produced the excitation and inhibition of single neuron activities in the cerebral cortex, hippocampus, caudate nucleus, cerebellum, and pituitary in anesthetized rats. With no anesthesia, Pip caused the inhibitory action in a higher percentage of the neurons studied, compared with the result obtained under anesthesia. Pip-induced excitation and inhibiton were blocked by tetramethylammonium but little affected by scopolamine. The kinetic study of Pip-induced Cl- current in internally perfused neurons of Aplysia, by using the 'concentration camp' and voltage clamp techniques, revealed that Pip acted on at least two components of nicotinic receptor-Cl- channel complex, and further that Pip could discriminate between the transient and the persistent components of ACh-induced Cl- current. These findings suggest that Pip may have close connections with neuroendocrine as well as neuronal functions, and further, with the mechanisms underlying sleep-consciousness and emotional function. Because of piperidine's multiplex pharmacological activities, the study of piperidine may provide a clue to the discovery of new active drugs and to the elucidation of causes of pathological states relating to the brain function.
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PMID:[Piperidine in the brain: its neurobiological significance]. 269 May 41

Thirteen patients with dyssynergia cerebellaris myoclonica (Ramsay Hunt syndrome) had full clinical and neurophysiological study as well as muscle biopsy. The patients had action myoclonus, generalised epileptic seizures, and mild cerebellar syndrome. The disease was inherited in an autosomal recessive pattern in five patients, and occurred as isolated cases in the remaining eight patients. The age at onset of symptoms ranged from 6 to 15 years (mean, 10.4 years). The EEG and polygraphic findings included normal background activity in most patients, spontaneous fast generalised spike-and-wave discharges, photosensitivity, no activation during slow sleep, and vertex and rolandic spikes in REM sleep. Results of muscle biopsy, performed an average of 14 years after onset of the disease, were normal and showed no mitochondrial abnormalities. These findings suggest that Ramsay Hunt syndrome is a condition with distinctive clinical and neurophysiological features and unrelated to mitochondrial encephalomyopathies.
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PMID:Dyssynergia cerebellaris myoclonica (Ramsay Hunt syndrome): a condition unrelated to mitochondrial encephalomyopathies. 210 13

A 16-year-old patient presenting with complex partial seizures occurring in the transition from a REM period to wakefulness is described. His baseline EEG showed generalized and symmetrical slow spike and wave complexes, on a normal background activity, activated by NREM sleep. Polygraphic and videotape recordings, carried out for several nights, showed that after nearly each REM period, he would wake up briefly, presenting eye blinking followed by a burst of generalized hypersynchronous theta to start his seizures. These were characterized by moaning and autoaggressive behaviour, the ictal EEG showing generalized slow spike and wave complexes in the midst of several movement artifacts. At the end of each fit he fell back to REM sleep. Carbamazepine treatment completely resolved his symptoms, with full normalization of EEG activity.
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PMID:Nocturnal complex partial seizures precipitated by REM sleep. A case report. 278 40


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