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Results for “Epilepsy, Generalized”

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PubMed2001

Neuropsychology of epilepsy.

PURPOSE: The neuropsychological approach to epilepsy is indispensable for assessment of cognitive function in an interictal period including pre- and postsurgical evaluation, and for disclosing the semiology of nonconvulsive status epilepticus. Another use of the neuropsychological approach is to identify a seizure-precipitating factor by loading systematic cognitive tasking, termed "neuropsychological EEG activation" (NPA), during standard EEG recordings. METHODS: In this study, NPA tasks consisted of reading, speaking, writing, written arithmetic calculation, mental arithmetic calculation, and spatial construction. RESULTS: The NPA tasks provoked epileptic discharges in 7.9% of the 480 epileptic patients and were often accompanied by myoclonic seizures. Among the cognitive tasks, mental activities mainly associated with use of the hands [i.e., writing (68.4%), written calculation (55.3%), and spatial construction (63.2%)] provoked the most discharges. Seizure-precipitating mental activities were found to be almost exclusively related to idiopathic generalized epilepsies (IGEs). CONCLUSIONS: These results suggest that NPA is a useful tool for examining the relationship between cognitive function and epileptic seizures, and that the IGE patients with myoclonic seizures are vulnerable to higher mental activity.

Brain Mapping↗

PubMed1977

[Initial EEG findings and the prognosis of epilepsy with generalized convulsive seizures].

Correlation between the initial EEG's and the prognosis of generalized convulsive seizures without other seizures was investigated. The subjects of this study was 437 epileptics with the period of the follow-up over 3 years. They were devided into 2 groups from view point of prognosis: "good prognosis" group, in which their seizures were completely controlled, the "poor prognosis", not well controlled. Most of the EEG findings appear to be not of value in predicting the prognosis. Exceptionally, however, the localized seizure discharged in the areas of T3,4, C3, 4 and P3,4 and 14--6 Hz positive spikes related closely to good prognosis, in the group of 7 to 12 years of the age.

Adolescent↗

PubMed2003

Schizoid neurochemical pathology-induced membrane Na(+)-K+ ATPase inhibition in relation to neurological disorders.

Psychiatric abnormalities have been described in primary neurological disorders like multiple sclerosis, primary generalized epilepsy, Parkinson's disease, subacute sclerosing panencephalitis (SSPE), central nervous system glioma, and syndrome X with vascular dementia. It was therefore considered pertinent to compare monoamine neurotransmitter pattern in schizophrenia with those in the disorders described above. The end result of neurotransmission is changes in membrane Na(+)-K+ ATPase activity. Membrane Na(+)-K+ ATPase inhibition can lead to magnesium depletion, which can lead to an upregulated isoprenoid pathway. The isoprenoid pathway produces three important metabolites--digoxin, an endogenous membrane Na(+) -K+ ATPase inhibitor; ubiquinone, a membrane antioxidant and component of mitochondrial electron transport chain; and dolichol, important in N-glycosylation of protein. The serum/plasma levels of digoxin, dolichol, ubiquinone, magnesium, HMG CoA reductase activity, and RBC Na(+)-K+ ATPase activity were estimated in all these disorders. The result showed that the concentration of serum tryptophan and serotonin was high and serum tyrosine, dopamine, adrenaline, and noradrenaline low in all the disorders studied. The plasma HMG CoA reductase activity, serum digoxin, and serum dolichol levels were high and serum ubiquinone levels, serum magnesium, and RBC Na(+)-K+ ATPase activity were low in all the disorders studied. The significance of these changes in the pathogenesis of syndrome X, multiple sclerosis, primary generalized epilepsy, schizophrenia, SSPE, and Parkinson's disease is discussed in the setting of the interrelationship between these disorders documented in literature.

Adult↗

PubMed1990

Dopamine D1 receptor modulation of pilocarpine-induced convulsions.

The contribution of dopaminergic mechanisms to the generalization of epileptic activity was studied in rats given pilocarpine after pretreatment with selective dopamine agonists. At the dose of 200 mg/kg, pilocarpine produced limbic stereotypes but not convulsions or seizure-related brain damage. Pilocarpine, 200 mg/kg, following pretreatment with the D1 agonist (RS)-2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3 benzazepine, but not its (S)-enantiomer, induced convulsive activity as revealed by behavioral, electroencephalographic alterations and widespread brain damage. These features were identical to those produced by a higher, convulsant dose of pilocarpine (400 mg/kg). On the other hand, pretreatment with the D2 agonist 4,4a,5,6,7,8,8a,9-octahydro-5-n-propyl-2H-pyrazolo-3,4-g-quinoline failed to induce convulsions. Furthermore, the D1 receptor antagonist (R)-(+)-8-chloro-2,3,4,5-n-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine -7-ol prevented the convulsive activity induced by both 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3 benzazepine plus pilocarpine (200 mg/kg) and pilocarpine (400 mg/kg), given alone. However, neither dopamine agonists nor antagonists altered the limbic stereotypes induced by pilocarpine, suggesting a dopamine system involvement primarily in the mechanisms of epilepsy generalization. The results suggest that pharmacological manipulation of dopaminergic transmission may provide an alternative approach to therapy of secondarily generalized epilepsy.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed2002

Partial epilepsy manifesting atonic seizure: report of two cases.

PURPOSE: Atonic seizures are commonly seen in patients with generalized epilepsy but only infrequently in patients with partial epilepsy. Clinically generalized atonic seizures as a partial epilepsy have not been studied in detail with video/EEG monitoring. Here we describe the clinical and physiologic characteristics of atonic seizures due to partial epilepsy and discuss the underlying mechanism. METHODS: Two patients with partial epilepsy manifesting atonic seizures, one with frontal lobe epilepsy (FLE) and the other with parietal lobe epilepsy (PLE), were reported. The long-term video/EEG monitoring, magnetic resonance imaging (MRI), and interictal fluorodeoxyglucose-positron emission tomography (FDG-PET) were investigated in each patient. RESULTS: Paroxysmal diminution of muscle tone mainly involved the axial muscles in both patients. In contrast with the abrupt falls seen in patients with Lennox-Gastaut syndrome, the falls in these patients were slow, taking 2-5 s to fall down. Ictal EEG records showed low-voltage fast activity in the frontocentral area followed by repetitive spikes at the midline frontocentral area in the patient with FLE, and rhythmic spikes in the left central area in the patient with PLE. Interictal FDG-PET disclosed hypometabolic regions consistent with the clinical and EEG findings. CONCLUSIONS: Slow falls might be a feature of atonic seizures in partial epilepsy. Long-lasting atonia in partial epilepsy could be due to either one of the following two possible mechanisms: (a) epileptic activities arising from the negative motor area, of which 50-Hz electric stimulation causes motor inhibition, or (b) sustained atonia with successive electromyogram (EMG) silent periods caused by epileptic discharges arising from the inhibitory area of the primary sensorimotor area.

Adult↗

PubMed2000

Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults.

BACKGROUND: There is controversy regarding the precise mechanism by which epilepsy results after traumatic brain injury (TBI). Previous reports have suggested that mesial temporal lobe epilepsy may result from TBI only in young children, while neocortical epilepsy arises from TBI in later life. These conclusions were based on surgical series and may be biased because of patient selection. OBJECTIVE: To determine the frequency of mesial temporal lobe as opposed to neocortical epilepsy in patients with intractable epilepsy resulting from TBI after the age of 10 years. PATIENTS AND METHODS: We identified 23 patients with intractable epilepsy who had TBI after the age of 10 years, preceding the onset of epilepsy. Patients were studied by simultaneous videotape and scalp electroencephalographic recording of typical seizures; magnetic resonance imaging; neuropsychologic studies; and, when appropriate, intracarotid amobarbital testing. Two patients underwent anterior temporal lobectomies. RESULTS: Of the 23 patients, 8 (35%) had mesial temporal lobe epilepsy, based on the finding of hippocampal sclerosis on a magnetic resonance imaging scan, consistent interictal and ictal electroencephalographic recordings, evidence of temporal lobe dysfunction on neuropsychologic testing, and characteristic seizure semiology. Two of these patients underwent anterior temporal lobectomies with clinical benefit, and hippocampal sclerosis was confirmed pathologically. In 2 cases, patients were not treated surgically because of bilateral temporal lobe dysfunction noted on intracarotid amobarbital testing. Eleven patients had neocortical epilepsy; 1 had primary generalized epilepsy; and, in 3, the site of seizure onset was not localized. CONCLUSIONS: Mesial temporal lobe epilepsy can result from TBI in adolescents and adults as well as in children, and can often be bilateral and associated with multifocal injury. This information may be useful in developing prophylactic therapy for posttraumatic epilepsy.

Adult↗

PubMed2004

Sleep and arousal mechanisms in experimental epilepsy: epileptic components of NREM and antiepileptic components of REM sleep.

Neural generators related to different sleep components have different effects on seizure discharge. These sleep-related systems can provoke seizure discharge propagation during nonrapid eye movement (NREM) sleep and can suppress propagation during REM sleep. Experimental manipulations of discrete physiological components were conducted in feline epilepsy models, mostly in the systemic penicillin epilepsy model of primary generalized epilepsy and the amygdala kindling model of the localization-related seizure disorder, temporal lobe epilepsy. The sleep-wake state distribution of seizures was quantified before and after discrete lesions, systemic and localized drug administration, and/or photic stimulation, as well as in relation to microdialysis of norepinephrine. We found that (1) neural generators of synchronous EEG oscillations--including tonic background slow waves and phasic "arousal" events (sleep EEG transients such as sleep spindles and k-complexes)--combine to promote electrographic seizure propagation during NREM and drowsiness, and antigravity muscle tone permits seizure-related movement; (2) neural generators of asynchronous neuronal discharge patterns reduce electrographic seizures during alert waking and REM sleep, and skeletal motor paralysis blocks seizure-related movement during REM; (3) there are a number of similarities between amygdala-kindled kittens and children with Landau-Kleffner Syndrome (LKS) that suggest a link among seizures, sleep disorders, and behavioral abnormalities/regression.

Amygdala↗

PubMed1992

Mapping of cerebral energy metabolism in rats with genetic generalized nonconvulsive epilepsy.

The quantitative 2-[14C]deoxyglucose autoradiographic method was applied to measure local cerebral metabolic rates of glucose (LCMRglc) in a model of genetic petit-mal-like seizures in a strain of Wistar rats. During the experimental period, epileptic rats exhibited synchronous spike-and-wave discharges, whereas the EEG pattern of control animals was normal. Overall, LCMRglc was consistently higher in epileptic rats than in the non-epileptic controls. The increase in LCMRglc was widespread and concerned all cerebral functional systems studied, whether they exhibit spike-and-wave discharges (neocortex and thalamus), or not (limbic system). These results are in good accordance with positron-emission tomography measurements in humans with typical childhood absence epilepsy. There appears to be a lack of anatomical correlation between areas demonstrating hypermetabolism and areas where spike-and-wave discharges are recorded. The administration of 200 mg/kg ethosuximide completely suppressed spike-and-wave discharges in epileptic rats and did not change the EEG pattern in controls. However, LCMRglc were increased to the same extent over control values in epileptic rats whether they were injected with ethosuximide or untreated. By contrast, when epileptic rats were given 2 mg/kg haloperidol, the frequency and the length of spike-and-wave discharges increased, inducing almost a permanent petit-mal status epilepticus. Haloperidol did not change EEG pattern in controls. In haloperidol-treated epileptic rats, LCMRglc decreased to levels comparable to those measured in untreated control rats. In the presence of haloperidol, LCMRglc were similar in both control and epileptic rats. Thus, the diffuse increase in cerebral energy metabolism in epileptic rats as compared to controls is not directly related to the occurrence of spike-and-wave discharges, and may rather be associated with inhibitory mechanisms involved in their termination and suppression, as well as their spread to limbic and motor structures.

Animals↗

PubMed1992

GABA receptors in rats with spontaneous generalized nonconvulsive epilepsy.

We have used the technique of autoradiography to study the binding of [3H]-GABA to GABAA and GABAB receptors in brains taken from rats that are genetically predisposed to petit mal type seizures. A range of concentrations of [3H]-GABA were employed to test the hypothesis that this predisposition was due to regional changes in either the number of GABAA or GABAB receptors, or affinity of GABA for these receptors. We found no statistical difference in the levels of radioligand binding to GABAA and GABAB receptors in animals susceptible to seizures compared to control animals in any of the brain regions studied over the concentration range 25 nM to 400 nM. This indicated that there was no change in either the Kd (affinity) or Bmax (receptor number) in these animals and that the pharmacological basis for the efficacy of GABAB antagonists in this seizure condition probably lies elsewhere.

Animals↗

PubMed1982