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

This study replicated and extended previous work indicating a reciprocal relationship between persistent sleep disorders and seizure susceptibility in amygdala-kindled cats. Eight kindled cats (experimental group) and six nonkindled cats (control group) were assessed for several sleep and waking state parameters. Seizure susceptibility, indexed by thresholds to generalized afterdischarge and tonic-clonic convulsions, was also evaluated in experimental subjects during each of the following states: alert but quiet wakefulness, slow-wave sleep, transitions from slow-wave to REM sleep, and REM sleep. There were two primary findings: (i) slow-wave sleep and transitions from it to REM sleep were disrupted in amygdala-kindled cats whereas REM sleep was normal when an effective transition had been made; and (ii) disturbed states were also more susceptible to generalized seizures than were stable REM sleep and waking episodes, suggesting that abnormal rather than normal sleep created a predisposition for seizures.
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PMID:State disorders and state-dependent seizures in amygdala-kindled cats. 370 36

Serial polysomnograms were performed on 11 children with primary Lennox-Gastaut syndrome (LGS), 6 control children with other seizure disorders, and 12 who were developmentally normal. Five LGS children had abnormal polysomnograms with either complete absence or marked reduction of REM sleep; the other six LGS children had only a mild reduction of REM sleep. The percentage of REM in LGS children was less than in the controls with other seizure disorders (p less than 0.05) or the normal children (p less than 0.005). The scatter of REM percentages in LGS may imply heterogeneity of the syndrome, perhaps related to the severity of brainstem dysfunction or neurochemical derangement.
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PMID:Sleep patterns in the Lennox-Gastaut syndrome. 374 89

Eighteen EEG long-term recordings were carried out in patients with generalized fits of different etiologies using a mobile 4-channel monitoring system in order to observe individual patterns of epileptic activity. In patients with idiopathic tonic-clonic seizures (A) no connection of frequency of spike-wave bursts with the sleep-wakefulness cycle was observed. In patients suffering from fits of organic nature (B) a peak of paroxysms was obtained in the hours before sleep onset, whereas in patients with absence seizures (C) a maximum was found in the morning hours after awakening. In patients with idiopathic fits (tonic-clonic and absence seizures) the minimum of bursts was observed in REM sleep, whereas stage 0 (tonic-clonic) and stage 1 (absence) were most prone to discharges. Patients with secondary generalized epilepsy had most spike-wave bursts in deep sleep. In the absence seizure group the transitional periods within the light non-REM-sleep stages were more susceptible to paroxysms than the retained stages. In patients with idiopathic grand mal seizures, the highest frequency of paroxysmal discharges was found during time spent awake in the night when retained over a longer period of time. The group including cases with attacks of organic nature did not show any preference to shifting times or preservation episodes of sleep stages.
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PMID:Mobile long-term EEG monitoring in generalized seizure disorders of different etiology. 375 18

Regional cerebral blood flow (r CBF) was measured by the I.V. 133 Xenon method and use of 27 detectors in 91 patients with complex partial epilepsy in interictal periods (at least 48 h over a complex partial seizure). Some were also examined less than 48 h before or after seizures. All were studied with ictal and interictal electroencephalography (EEG), polysomnography, computed tomography (CT), some had nuclear magnetic resonance scans (MR). The blood flow values were compared with a group of a 20 normal subjects matching for age. A significant decrease of r CBF ranged from 15% to 25% was found in the temporal region in three groups of epileptic patients: with repeated normal CT scans and lateralized EEG abnormalities (N = 46); with cortical atrophy in CT scan (N = 12); with neurosurgical focal lesions on CT and or MR scans glioma, arteriovenous malformation) (N = 10). r CBF was normal or decreased by less than 15% in the other regions of the brain. Patients with repeated normal CT scans and bilateral EEG abnormalities either asynchronous or alternatively observed in the right side or left side on waking EEG or during NREM sleep and REM sleep, did not show reduction in r CBF. In a previous study, r CBF distribution was also found normal during interictal phase in patients with primary generalized epilepsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Regional cerebral blood flow in partial complex epilepsy with and without the presence of lesions]. 380 89

In 30 patients with petit mal-epilepsy 37 telemetric and allnight polygraphic recordings were registered. The electrical paroxysms have been according to their morphological characteristics and to the background activity into the following groups distributed: regular 3/s spike and wave paroxysms usually of 10-20 s duration, appearing in a normal background activity (10 patients-13 records). 2-4/s polyspike and wave patterns of 10-20 s duration, appearing in a disorganized, slow background activity (8 patients-10 records), short paroxysms of 1-4 s duration, appearing, as a rule, in a normal background activity (12 patients-14 records). The clinical seizures and their electrical patterns eventually accompanying the absences were also characterized. During the petit mal paroxysms the degree of the disturbance of consciousness exhibited a large scale variation. There are considerable intra-, but also inter-individual differences. The sometimes very slight biological changes, occurring in connection with the electrical paroxysms, can be exactly measured by psychophysiological tests, thus the precise clinical registration of the absences is possible. The "hypersynchron alpha-state" produces the significant increase of the petit mal paroxysms in comparison with the paroxysm value of the telemetric record of wakefulness (p less than 0,01). According to our results, the petit mal paroxysms in REM do not show a significant reduction in comparison with the waking period. In cases of petit mal epilepsy in the different vigilance levels one may distinguish in the cerebral electrical activity stable "non-epileptogenic" and unstable "epileptogenic" epochs changing each other under the influence of the ultradian regulatory mechanisms.
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PMID:[Circadian phenomena in petit mal epilepsy]. 392 35

Total sleep deprivation in a treadmill, and REM sleep and partial slow-wave sleep deprivation by the platform technique led to reduced seizure threshold in kindled rats. After treadmill deprivation there was also a reduction in seizure duration. Arousing aspects of the sleep deprivation procedures counteracted the sleep deprivation effect. In the treadmill experiment this led to an increase in seizure threshold in the control group. In the platform experiment the reduction in seizure threshold was delayed for 24 h after the deprivation because of these short-acting processes. Seizure thresholds remained low for at least 72 h.
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PMID:Sleep deprivation and kindled seizures. 395 52

Sleeping-waking is a basic biological rhythm. A study of sleep in epilepsy established that changes in the EEG vary with different sleep phases. Activation of epileptic electroencephalographic phenomena was observed more frequently during NREM (non-rapid eye movement) phases; the REM, or paradoxical, sleep phase seemed to inhibit such phenomena. On this basis some authors are attempting far-reaching conclusions concerning a connection between separate sleep phases and the development of epileptic seizures. To a certain degree, a similar interpretation is focusing on the problem of the relationship of seizures and their frequency to the sleeping-waking rhythm. In this connection, it must be noted that in themselves EEG changes and epilepsy, a disease in which convulsive episodes play a substantial role, are not identical. Horyd and Baransia-Teruszak found no reliable correlation between EEG changes and type of seizure. There was a correlation between frequency of seizures and the electroencephalographic picture in only 30% of the cases. The authors believe that in the remaining 70% the connection between EEG shifts and clinical manifestations of epilepsy is more complex. On the other hand, as N. N. Bemin et al. indicated, based on hypotheses developed by N. P. Bekhtereva on "flexible" and "rigid" connection, sleep is one of the processes that is regulated by flexible connections and for this reason the sequence and duration of sleep phases is exceptionally variable and depends on most various external and internal factors.
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PMID:Sleeping-waking rhythm and frequency of seizures in epilepsy without psychoses and with chronic psychoses. 409 75

This report is a follow-up to a previous paper which described seizure rate changes with central cortical EEG feedback training in 8 poorly controlled epileptic subjects. Data examined here include associated training compliance and performance, sleep EEG spectra, clinical EEG and anticonvulsant blood levels. The study employed a double-cross-over, single blind ABA design applied to two subgroups of epileptic patients. Both groups had in common two training periods (A1, A2) in which either 12--15 c/sec (subgroup I, n = 4) or 18--23 c/sec (subgroup II, n = 4) was reinforced in the absence of 6--9 c/sec, movement or epileptiform discharge, and one training period (B) in which 6--9 c/sec was reinforced in the absence of 12--15 or 18--23 c/sec as well as movement and epileptiform discharge. Training periods occurred primarily in the home and lasted 3 months. Compliance with training instructions and response acquisition were demonstrated. Overall anticonvulsant blood levels were low and unrelated to EEG or seizure changes. Clinical EEG findings corresponded to sleep EEG and seizure rate outcomes. Power spectral analysis of sampled non-REM sleep from all-night EEG recordings obtained after each training phase indicated contingency specific changes which were limited to sensorimotor recordings in subgroup I and corresponded to the pattern of seizure rate changes in this group. EEG changes were also limited to sensorimotor cortex in subgroup II, but were linear and paralleled a progressive decrease in seizure rate. Both groups, however, showed the same pattern of EEG changes with seizure reductions; low and high frequencies were reduced and intermediate, rhythmic frequencies increased. Correlational analysis confirmed this relationship. The pattern, duration and topographic specificity of these changes suggested a normalization of sensorimotor EEG substrates related to the EEG feedback traning.
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PMID:Quantitative analysis of training, sleep EEG and clinical response to EEG operant conditioning in epileptics. 615 36

Cerebral electrical activity was recorded through chronic stereotactically implanted electrodes in 19 epileptic patients suffering from different types of severe and medically refractory partial seizures and who were considered for surgical treatment. 213 brain sites, in all cerebral lobes, in neocortical as well as in archicortical structures, were explored. The behaviour of the interictal spiking across wakefulness and nocturnal physiological sleep was analysed, using automatic elaboration. (i) Spike rate is affected by the occurrence of sleep and by the passage from one sleep phase to another. The degree and direction of the phenomenon differ remarkably in the various patients and, in the same patient, in the different cerebral sites explored. Generally, interictal spiking increases at the beginning of sleep, reaches its maximum during the deep non-REM phases and returns to a level slightly lower than that in wakefulness during REM. (ii) The nocturnal spike rate is hardly influenced by spike location. In most cases, however, the variations recorded during sleep are more significant in the frontal regions than elsewhere. (iii) Spike rate across wakefulness and sleep is affected by the local level of epileptogenicity: spiking variations are less in the most epileptogenic cerebral zone (identified by the origin of the seizure discharges and by the disappearance of seizures following its surgical removal) than elsewhere. The physio-pathological meaning and the diagnostic value of these findings, and particularly of the peculiar stability or autonomy of the electrical epileptic activity of the most epileptogenic cerebral zone, is discussed.
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PMID:Interictal epileptic activity during sleep: a stereo-EEG study in patients with partial epilepsy. 620 46

Sleep deprivation enhances seizure susceptibility in experimental and human epilepsies. Because sleep abnormalities are also common in these populations, a possible explanation for this close association is that sleep deprivation activates seizures by enhancing existing sleep disturbances. The present experiment examined this hypothesis by comparing sleep-waking state percentages and the number of after-discharge-eliciting stimulations required to induce generalized tonic-clonic convulsions with the amygdala kindling model of epilepsy in 3 groups of cats (n = 5 each). One group consisted of experimental subjects who received bilateral lesions of the basal forebrain, a preoptic area long implicated in the generation of normal sleep state characteristics. A second group sustained unilateral lesions of the basal forebrain area. Since only bilateral destruction of this region produces sleep-waking cycle abnormalities, this group provided a lesion control. Finally, a third group had no lesion and provided a control which allowed normative assessment of sleep state patterns and seizure susceptibility in otherwise unmanipulated cats. The results were: cats without lesions showed a parallel development of seizure and sleep disorders, the latter indexed by progressive SWS and REM sleep deficits; cats with unilateral lesions showed identical trends in the development of sleep and seizure anomalies; and cats with bilateral lesions of basal forebrain displayed similar but more severe sleep disturbances than those evidenced by control subjects and also required fewer after-discharge stimulations to establish kindled convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep disruption with basal forebrain lesions decreases latency to amygdala kindling in cats. 620 6


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