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

Continuous all night recordings of epileptiform EEG activities from right frontal scalp and thalamic Centromedian regions and EMG activities from left deltoid muscular region were performed on a child with intractable epilepsia partialis continua, with depth stimulating-recording electrodes used for neuroaugmentive seizure control. In addition, "normal" and "mature" sleep indicators in the same child were simultaneously recorded according to the International Procedures. During wakefulness (W), type B seizures consisted of isolated, high amplitude, negative-positive EEG sharp waves recorded from the right Centromedian region (RCM sharp) correlated with isolated bursts of high amplitude EMG potentials recorded from the left deltoid muscle (LEMG jerks). Type C seizures consisted of clusters of repetitive RCM sharp and LEMG jerks, where individual EEG-EMG activities showed poor correlations. Number and amplitude of type B RCM sharp and LEMG jerks significantly decreased when patient directly shifted from W to slow wave sleep I and II (SWSI and II). Number and amplitude of RCM sharp increased while those of LEMG jerks decreased directly from SWS I and II to slow wave sleep III (SWS III); all forms of EEG-EMG epileptiform type B activities significantly decreased directly or indirectly from W and SWS to paradoxical sleep (PS). Scalp EEG spikes from right frontal and central regions showed almost parallel changes to those of RCM sharp, except during SWS II, when amplitude increased in the former and decreased in the later. Occurrence of type C seizures only decreased during PS and duration decreased directly from SWS I to II and indirectly from SWS I to SWS II and PS; and from W to SWS II and III and PS.
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PMID:Wakefulness-sleep modulation of EEG-EMG epileptiform activities: a quantitative study on a child with intractable epilepsia partialis continua. 212 31

Amplitude and latency changes of early and late components of surface and depth auditory evoked potentials were determined during wakefulness-sleep steady state shifts in epileptic patients, with implanted electrodes used as an electrophysiological procedure for surgical treatment of temporal lobe seizures. Early surface (I and V) and depth (N8 and N15) components of the auditory brainstem potentials and late surface (P2 and N2) and depth (B and C) components of the auditory evoked potentials were produced by either 8/s or single clicks, delivered monoaurally and simultaneously recorded from the vertex and contralateral thalamic (lateral geniculate thalamic nucleus) and frontotemporal (amygdala, hippocampus and orbitofrontal cortex) regions, while patients spontaneously shifted from initial wakefulness (W1) to slow wave sleep (SWS I, II and IV), to paradoxical sleep (PS) and to final wakefulness (W2). Amplitude of late surface (P2 and N2) and depth (B and C) components significantly decreased when patients shifted from SWS IV to PS and increased from PS to W2. Latency of components P2 and B increased while that of components N2 and C decreased from SWS IV to PS. No latency changes in late components were found from PS to W2. In addition, amplitude and latency of P2 and B components significantly decreased while those of N2 and C increased from W1 to SWS IV. Polarity of all late components remained unchangeable during all wakefulness-sleep state shifts, with the exception of that of component C which reversed from W1 to SWS IV. In contrast, early surface (I and V) and depth (N8 and 15) components showed no systematic changes in amplitude and latency during all consecutive wakefulness-sleep shifts, with the exception of a significant increase amplitude but no latency of component V from PS to W1.
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PMID:Wakefulness-sleep modulation of the surface and depth auditory evoked potentials in man. 258 50

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

The effect of repeated Na-penicillin (PCN) microinjections in the temporal lobe amygdala (AM) of free-moving cats was investigated in order to establish if kindling epileptogenesis is possible with this procedure. The cortical propagation of the PCN-induced post-discharge in AM and the sequence of behavioral changes induced by PCN were similar to those of AM electrical kindling. Nevertheless, the epileptogenic effect of PCN had a different evolution from that of electrical kindling, since some PCN habituation was observed after several doses. Repeated microinjections of PCN did not produce lasting alterations in sleep onset and organization. The only mild changes recorded in the 23 h following PCN microinjections were an increased latency of the first rapid eye movement (REM) sleep episode, a SWS II total time and percentage increase, and, with the highest PCN doses, a not very significant diminution of REM sleep total time. Another finding was the occurrence of REM sleep ponto-geniculo-occipital (PGO) waves, coinciding with a depression of the frequency and amplitude of interictal amygdaloid and cortical spikes. The results showed that a microinjection of PCN in the AM produced a reliable model of interictal spikes, paroxysms and generalized convulsive seizures. Nevertheless, long lasting kindling effect was not observed.
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PMID:Repeated penicillin-induced amygdala epileptic focus in freely moving cats. EEG, polysomnographic (23-h recording), and brain mapping study. 877 99

The aim of this study was to examine the haemodynamic response to seizures in three infants with Sturge-Weber syndrome by measuring regional cerebral blood flow using transcranial Doppler sonography and 99mTc HMPAO SPECT. Time-locked video/digital EEG recording was carried out for ictal studies. MRI was performed in all subjects. SPECT showed hemispheric hypoperfusion interictally in all three patients and also ictally in one of the three; a small region of hyperperfusion was seen on the same ictal scan in the latter, ie. the patient with interictal and ictal hypoperfusion. In the two older children middle cerebral artery velocity (MCAV) was reduced by between 29 and 62% in the middle cerebral artery of the predominantly affected hemisphere compared with the contralateral side. During seizures, increases of 6 to 30% in MCAV were recorded for the clinically seizing hemisphere compared with 24 to 170% for the contralateral side in four of the seizures recorded. In one infant, MCAV fell bilaterally during a seizure that generalized (-18 and -43% in the predominantly affected and contralateral side respectively). Sequential recordings in one infant suggested that, with time, the haemodynamic response to seizures of the unaffected hemisphere may decrease. These findings suggest that the venous malformation in SWS is associated with an impairment of the cerebral haemodynamic response to seizure activity.
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PMID:Sturge-Weber syndrome: cerebral haemodynamics during seizure activity. 1045 32

We have previously shown that IL-6 protein levels are increased in cerebrospinal fluid in humans after recent tonic-clonic seizures with unchanged levels of IL-1beta and TNFalpha. Here we studied the expression of cytokines IL-6, LIF, IL-1beta and TNFalpha and cytokine receptors IL-6R, LIFR and Gp130 in the rat brain after kainic acid-induced status epilepticus using Northern blot analysis and in situ hybridization histochemistry. After seizures, IL-6 mRNA was induced in the hippocampus, cortex, amygdala and meninges, and IL-6R was up-regulated in the hippocampus. LIF was up-regulated in the hippocampus, cortex and meninges after seizures, and LIFR mRNA was induced in the hippocampus and cortex. Gp130 was constitutively expressed in the brain. After seizures, Gp130 transcription was rapidly induced in the meninges. In thalamus, cortex, amygdala and hippocampus Gp130 mRNA was induced in a delayed fashion. IL-1beta transcription was induced in the temporal lobe cortex and thalamus, and TNFalpha in the hippocampus. In general, the cytokine and their receptor mRNA levels were low in intact rat brain, but were induced by seizures. Since IL-6 and LIF transcripts were induced in the meninges after seizures, the protein products of these transcripts may be more readily released in cerebrospinal fluid after seizures. In addition, the activity of IL-6 and LIF signaling pathways may be influenced by increased expression of their receptors after seizures.
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PMID:Expression of cytokines and cytokine receptors in the rat brain after kainic acid-induced seizures. 1259 Nov 61

Although numerous studies have demonstrated the neurotrophic capacity of gp130 cytokines, it remains unclear whether endogenously expressed cytokines actually function in a direct neuromodulatory manner. Therefore, using the lithium-pilocarpine status epilepticus model, we performed a detailed in situ hybridization time-course study of five gp130 cytokines (interleukin [IL]-6, leukemia inhibitory factor [LIF], IL-11, oncostatin-m [OSM], and ciliary neurotrophic factor), gp130, and the receptors of the cytokines we found to be induced (IL-6 receptor [IL-6R], LIF receptor [LIF-R], and IL-11 receptor [IL-11R]). Additionally, to further understand the regulation of these cytokines, we compared their expression with the pattern of neuronal degeneration and microglial activation. Under control conditions, all cytokines, except LIF, exhibited faint to moderate expression in hippocampal principal layers. After seizure, IL-6, LIF, and IL-11 exhibited a rapid, robust, and transient upregulation in non-principal cells. LIF also exhibited a remarkably early and transient induction in the granule cell layer of the dentate gyrus. OSM exhibited only a mild and inconsistent induction. All receptors examined were strongly expressed only in hippocampal principal layers under control conditions. A mild and late induction of the IL-6R, LIF-R, and IL-11R occurred after seizure with a scattered distribution. A progressive and chronic induction of gp130 was observed in cells that appeared to be associated with blood vessels. Degeneration of hilar interneurons and CA1 pyramidal cells was early and progressive. Granule neurons of the dentate gyrus, however, exhibited a delayed and precipitous pattern of degeneration, specifically in the lateral portion of the superior blade. Microglial activation was maximal 24-48 h post-seizure. We speculate that gp130 cytokines play a paracrine, neuromodulatory role in the hippocampus since both before and after seizure, principal cells appear to be the major cell type expressing the receptors for these cytokines. Furthermore, we suggest that activity-dependent mechanisms may be involved in the regulation of cytokines expressed early, and that relatively late occurring cytokine expression may be elicited by injury-related stimuli.
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PMID:Spatiotemporal distribution of gp130 cytokines and their receptors after status epilepticus: comparison with neuronal degeneration and microglial activation. 1461

Sleep-wake disturbances are common in epilepsy, yet the potential adverse effect of seizures on sleep is not well characterized. Genetically epilepsy-prone rats (GEPRs) are a well-studied model of genetic susceptibility to audiogenic seizures. To assess their suitability for investigating relationships between seizures and disordered sleep, we characterized the sleep, activity, and tempera ture patterns of 2 GEPR strains (designated 3 and 9) and Sprague-Dawley (SD) rats in the basal state, after forced wakefulness, and after exposure to sound-induced seizures at light onset and dark onset. Because of observed differences in rapid-eye-movement sleep (REMS), we also assessed serum levels of prolactin, which is implicated in REMS regulation. The data reveal that under basal conditions, the GEPR3 strain shows less SWS and REMS, higher core temperatures, and higher serum prolactin concentrations than do GEPR9 and SD strains. All 3 strains respond similarly to enforced sleep loss. Seizures induced at light onset delay the onset of SWS in both GEPR strains. Seizures induced at dark onset do not significantly alter sleep. Genotype assessment indicates that although both GEPR strains are inbred (that is, homozygous at 107 genetic markers), they differ from each other at 74 of 107 loci. Differences in basal sleep, temperature, and prolactin between GEPR3 and GEPR9 strains suggest different homeostatic regulation of these functions. Our detection of concurrent alterations in sleep, temperature, and prolactin in these 2 GEPR strains implicates the hypothalamus as a likely site for anatomic or physiologic variation in the control of these homeostatic processes.
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PMID:Sleep, temperature, activity, and prolactin phenotypes of genetically epilepsy-prone rats. 1706 25

The natural history of Sturge-Weber Syndrome is variable where some patients have refractory epilepsy and persistent neurologic deficits while others do well. Also, evolution of MRI abnormalities is largely unknown. This long-term follow-up study tries to address these two issues. This retrospective and later prospective study followed 9 children with confirmed SWS. Clinical details of seizures, stroke-like episodes, neurologic and developmental deficits were ascertained specifically. Patients were divided into those with onset below or after 6 months of age for analysis. Disease was classified as active or inactive and correlations were made with the use of aspirin. All past, as well as prospectively acquired imaging was reviewed by two independent blinded neuroradiologists and the images were analysed as ictal (temporally related to seizure/stroke-like event) or interictal. Degree and extent of leptomeningeal enhancement was specifically looked for. Four boys and five girls were followed up for a mean of 6.1 years. Disease activity subsided in 8/9. Early-onset patients had a severe early course with significant residual deficits while late-onset patients did uniformly well. In 6 patients where aspirin was used, a stable course ensued. There was a significant increase in degree/extent of leptomeningeal enhancement during an ictus which returned to the baseline in the interictal state in all 7 patients where both images were available. Focal cerebral atrophy worsened in early-onset cases. In conclusion, SWS patients with onset of seizures/stroke-like events before 6 months of age seem to do worse with a severe early course and persistent neurologic deficits. However the course stabilizes after 5 years of age in most. Late-onset SWS patients have a benign course. Aspirin use is associated with a stable course though further studies are needed. The leptomeningeal enhancement appears to increase during acute events before returning to baseline suggesting that extent of the disease is probably best judged during the interictal state.
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PMID:Natural history and magnetic resonance imaging follow-up in 9 Sturge-Weber Syndrome patients and clinical correlation. 1762 34

In many experimental designs, animal observation is associated with local field potential (LFP) recordings in order to find correlations between behavior dynamics and neuronal activity. In such cases, relevant behaviors can occur at different times during free-running recordings and should be put together by the time of analysis. Here, we developed a MATLAB semi-automated toolbox to quantitatively analyze the temporal progression of brain oscillatory activity in multiple free-running LFP recordings obtained during spontaneous behaviors. The algorithm works by selecting LFP epochs at user-defined onset times (locked to behavior, drug injection time, etc.), calculates their time-frequency spectra, detects long-lasting oscillatory events and calculates linear coherence between pair of electrodes. As output, it generates several table-like text and tiff image files, besides group descriptive statistics. To test the algorithm, we recorded hippocampus and amygdala LFPs from rats in different behavioral states: awake (AW), sleep (SWS, slow-wave sleep and REMS, rapid-eye movement sleep) and tonic-clonic seizures. The results show that the software reliably detects all oscillatory events present in up to seven user-defined frequency bands including onset/offset time and duration. It also calculates the global spectral composition per epoch from each subject and the linear coherence (with confidence intervals) as a measure of spectral synchronization between brain regions. The output files provide an easy way to do within-subject as well as across-subject analysis. The routines will be freely available for downloading from our website http://www.neuroimago.usp.br/BPT/.
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PMID:A semi-automated algorithm for studying neuronal oscillatory patterns: a wavelet-based time frequency and coherence analysis. 1793 90


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