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

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

Male Wistar rats were subjected to daily sessions of electrical amygdala kindling until a generalized seizure was observed on five consecutive days. Bilateral microinjections (0.5 microliter) of ethosuximide (ETX) (10 pg/microliters) or saline were then administered through guide cannulas into the substantia nigra (pars reticulata). No significant difference was observed between the ETX (N = 8) and saline (N = 8) groups in duration of afterdischarge or in the latency for stage 5 generalized seizures. Our results indicate that ETX applied to the substantia nigra is not effective in suppressing amygdala-kindled seizures.
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PMID:Bilateral microinjection of ethosuximide into the substantia nigra does not prevent amygdala-kindled seizures. 213 21

Electrical stimulation of the noradrenergic locus coeruleus (LC) delays the generalization of partial seizures during amygdaloid kindling by increasing the time spent in the earliest stages of seizure development. To determine whether noradrenergic axons projecting to the midbrain and forebrain are involved in this antikindling effect, we examined the effects of lesions of the dorsal noradrenergic bundle, induced by intracerebral infusions of 6-hydroxydopamine (6-OHDA), on kindling and the antikindling action of stimulation of the LC. Stimulation of the LC during amygdaloid kindling increased the number of afterdischarges (ADs) spent in the early stages of partial seizure and decreased the number of ADs spent in later stages of generalized seizure, as has been described previously. LC-stimulated rats also displayed longer durations of AD during early stages of kindling. The antikindling effect of LC stimulation was blocked by lesions of the dorsal bundle, whereas the facilitatory effects of LC stimulation on generalization and on the duration of AD were unaffected by the lesions. These results suggest that the antikindling action of LC stimulation is mediated by the ascending projections of noradrenergic neurons, presumably through enhanced release of noradrenaline. On the other hand, the facilitatory effects of LC stimulation on the development of later stages of seizure and on the duration of AD appear to be independent of the ascending dorsal bundle.
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PMID:Antikindling effects of locus coeruleus stimulation: mediation by ascending noradrenergic projections. 215 8

Functional brain imaging by either single photon emission computed tomography (SPECT) or positron emission tomography (PET) is now a well-established technique in the diagnosis and evaluation of the epilepsies. Perhaps only in stroke have these emerging technologies proven of greater significance. Scalp, cortical, or depth electroencephalographic (EEG) data previously have been the gold standards for the localization and subcharacterization of epileptic activity in the human brain. Yet, they are fraught with difficult interpretations, technical difficulties, and limitations in sampling accuracy. Both SPECT and PET have localizing power approaching that of combined scalp and depth EEG. In the following discussion, a brief overview of the results of PET investigations in epilepsy is presented as background and comparative material for the concurrent and, more recently, dominant role of SPECT in evaluating patients with seizure activity. SPECT results in the interictal state in partial and generalized seizure activity are reviewed followed by an analysis of the role of ictal SPECT imaging in epilepsy. Next, relationships among interictal hypoperfusion (or hypometabolism) and computed tomography, magnetic resonance imaging, neuropathology, clinical severity, and cognitive function are discussed. The role of perfusion or metabolism imaging in the management of antiepileptic pharmacotherapy is also discussed, and the potential for receptor imaging in the evaluation of the epilepsies is examined. Finally, application in pediatric epilepsy are presented.
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PMID:Single photon emission computed tomography in epilepsy. 223 51

We describe a model of 'sleep epilepsy' after amygdala kindling in kittens. Seizure activity was evaluated at different times in the sleep-wake cycle. Susceptibility was documented by thresholds for evoked convulsions in kittens without spontaneous seizures (n = 5) and by polygraphic or split-screen video recordings in kittens with spontaneous seizures (n = 6). There were 3 main findings: (1) subconvulsive seizures occurred randomly in waking and slow-wave-sleep (SWS); (2) convulsive seizure activity peaked during SWS, especially during the transition from SWS into rapid-eye-movement (REM) sleep; (3) generalized seizure activity was suppressed during stable REM sleep. Seizure patterns thus resemble clinical data designating convulsive temporal lobe epilepsy (TLE) the prototypic pure sleep epilepsy, whereas complex-partial TLE can occur at any time. Prominent secondary TLE generalization during the REM transition suggested involvement of brainstem regions which generate REM onset and innervate the temporal lobe. Adrenergic cells of the locus ceruleus discharge at progressively reduced rates during the transition into REM. Decreased norepinephrine release at this time might disinhibit epileptic neurons in the kindled focus, thus encouraging seizure propagation during the REM transition.
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PMID:Spontaneous sleep epilepsy in amygdala-kindled kittens: a preliminary report. 229 22

This study demonstrates that the central medial intralaminar nucleus (CeM) controls generalized seizure threshold and expression, and that these functions are under gamma-aminobutyric acid (GABA)ergic control, with significant differences between receptor subtypes. Injections of the GABAA-agonist piperidine-4-sulfonic acid and the GABAB-agonist (-)baclofen in the CeM markedly facilitated myoclonic and clonic seizures, but had different effects on tonic seizures. These results are best explained by the concept that the CeM is not a site of seizure origin or spread but rather regulates other structures involved in seizures.
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PMID:The central medial nucleus: thalamic site of seizure regulation. 230 21

1. Experiments were performed to investigate the effects of cortical lesions on convulsive behaviour. Rats were lesioned in the left motor or sensory cortex by aspirating cortical tissue 2 to 3 months prior to the elicitation of convulsions. Convulsions were induced in the awake rats by the GABA antagonist Na-penicillin (Na-PCN) which was applied into the superficial layer of the foreleg field of their right motor cortex. Convulsive activity was recorded by means of the EEG. 2. The time courses of convulsive cortical activity were similar in the animals without or with a cortical lesion. Generalized seizures belonged to the tonic-clonic type in both intact and lesioned rats. 3. The early period of convulsive activity was described by the time to the onset (latency) of the first convulsive potential, jerk and seizure, and by the mean repetition rate of jerks during the first ten minutes, and the duration of the first generalized seizure. None of these parameters was significantly affected by a cortical lesion. 4. The median duration of the convulsive activity in intact animals was 162 min. In rats with a lesion in the sensory cortex it raised to more than 540 min while a lesion of the motor cortex increased the median duration to more than 273 min. The differences between intact and lesioned rats were significant (p less than 0.01 and p = 0.05, respectively). 5. The median time to the onset of the last generalized seizure in intact rats corresponded to 92 min with respect to the time of Na-PCN application. In rats with a lesion of the sensory cortex the last seizure was generated 433 min and in animals with a lesion of the motor cortex 167 min after Na-PCN treatment of the motor cortex of one side. This increase of latency of the last seizure was significant for the rats with a lesioned sensory area (p less than 0.02) or motor area (p = 0.05) compared to that of the intact rats. Additionally, the number of generalized seizures was significantly (p less than 0.01) increased by both groups of rats with a lesion of the motor or sensory cortex. 6. It is suggested that a substantial lesion of the cortex decreases predominantly the intrinsic cortical inhibition thus destabilizing brain function. This destabilizing effect becomes pronounced under the condition of superimposed suppression of the GABAergic cortical component. It is concluded that the intrinsic cortical inhibitory mechanism which in the intact brain acts against hyperexcitation and prevents the development of neuronal synchronization, i.e. the formation of seizures, becomes less effective in performing this task once an abnormal brain activation has developed.
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PMID:The influence of cortical lesions on penicillin induced convulsive activity in the awake rat. 233 Dec 5

Among 630 patients with human immunodeficiency virus infection, 70 patients with new-onset seizures were studied. Generalized seizures occurred in 66 patients (94%): they occurred as the initial seizure in 56 patients (80%) and during follow-up in another 10 patients (14%). Partial seizures (18 patients), status epilepticus (10 patients), and recurrent seizures (38 patients) were also noted. Identified processes included cerebral toxoplasmosis in 11 patients, cerebral lymphoma in 8, metabolic derangement in 8, cryptococcal meningitis in 7, and vascular infarction in 4. In 32 patients (46%) seizures were not associated with identifiable brain lesions and were believed to result from human immunodeficiency virus cerebral infection. Phenytoin treatment was associated with adverse drug reactions in 16 of 62 patients who received it. Our results suggest that the majority of patients with human immunodeficiency virus and seizures do not have secondary focal brain lesions as the cause of the seizures and that human immunodeficiency virus infection alone can, and often does, cause seizures.
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PMID:Seizures in human immunodeficiency virus infection. 234 90

Pyrethroid insecticides have recently been purported to possess strong proconvulsant potential. The seizure-inducing properties of two pyrethroids were assessed by pentylenetetrazol (PTZ) seizure models (repeated ip, suprathreshold ip, and iv), and electrical kindling of the amygdala. The efficacy of po versus ip routes of deltamethrin administration was compared using iv-PTZ administration and tests of locomotor activity in a figure-eight maze. Both po and ip deltamethrin produced comparable decreases in motor activity indicating the effectiveness of both of these exposure routes on biological activity. The Type I pyrethroid, cismethrin (15 mg/kg, po), produced a 17% reduction in the threshold dosage of ip-PTZ required to induce a seizure, while delaying the onset of generalized seizure activity. The Type II pyrethroid, deltamethrin (10 mg/kg, po), failed to alter threshold or latency to seizure onset, but did increase seizure duration. No differences were revealed between po (0, 10, 15 mg/kg) or ip (0, 1, 10 mg/kg) administered deltamethrin on seizure thresholds or durations following iv-PTZ. Seizure severity, however, was enhanced by pyrethroids administered po in the iv-PTZ and suprathreshold-ip PTZ tests, ip deltamethrin was without effect. Cismethrin (0, 8, 15 mg/kg) and deltamethrin (0, 6, 10 mg/kg) administered po daily, 2 hours prior to electrical kindling stimulation facilitated amygdala kindling to a minimal but equivalent degree at the highest dosage. This dosage also evoked strong behavioral signs of toxicity. Deltamethrin also induced spontaneous seizures in partially kindled animals in the absence of stimulation. Thus strong evidence of proconvulsant activity of pyrethroids was not evident. The primary effects were limited to an enhancement of seizure severity in response to PTZ (tonic seizures) and the provocation of spontaneous seizures in partially kindled animals.
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PMID:An examination of the proconvulsant actions of pyrethroid insecticides using pentylenetetrazol and amygdala kindling seizure models. 237 58

To determine the role of Alzheimer's disease as a causative factor for late-onset epilepsy, 44 subjects with mild senile dementia of the Alzheimer type and 58 healthy control subjects were examined over a 90-month period for the development of focal or generalized seizure activity (excluding myoclonus). At entry, all subjects were free of prior seizures and other neurologic, medical, and psychiatric disorders with the potential to impair cognition. Although no control subject developed seizures during the study period, 7 subjects with senile dementia of the Alzheimer type had at least one documented seizure. All 7 subjects had progressed to the severe stage of dementia by the time of the first seizure. Seizures were generalized tonic-clonic in type and were unassociated with clinical or (in 3 subjects) neuropathologic evidence for epileptogenic factors other than Alzheimer's disease. We conclude that advanced Alzheimer's disease alone may be an important risk factor for new-onset seizures in older adults.
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PMID:Advanced Alzheimer's disease is a risk factor for late-onset seizures. 237 89


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