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The effect of gamma-hydroxybutyrate (GHB) in relatively low doses (12.5--200 mg/kg) on sleep stages, electrocorticogram (ECoG) patterns and behavior was investigated in the rat. 50-100 mg/kg GHB induced slow wave sleep but, in contrast to the cat, not paradoxical sleep. 200 mg/kg induced a hypersynchronous, bilaterally symmetrical ECoG pattern, which was different in amplitude and frequency distribution from normally occurring high amplitude patterns. When the hypersynchrony occurred in bursts, the rats displayed a sudden arrest of motor behavior. Convulsions were not induced. The results, together with the finding of others that GHB is a natural constituent of mammalian brain and our previous observation that the GHB-induced hypersynchrony can be antagonized by anti-absence (anti-petit mal) drugs are discussed in view of the possibility that GHB might play a role in the etiology of absence epilepsy in man.
Ethosuximide, clonazepam and valproic acid differ in their chemical structures and properties. They appear to be well absorbed when given by mouth, but their patterns of distribution within the body are different. If these 3 drugs have a common mode of action, the virtual restriction of valproate to extracellular water suggests that this common mode of action is likely to involve receptors on the neuronal cell surface. Even if there is no common mode of action the apparent volume of distribution of valproate is consistent with its known effects on enzymes of the GABA shunt, and in particular on those shunt enzymes which are involved in the transmitter GABA pool in the region of synapses. The 3 drugs also show differences in elimination rate, which make it desirable to give valproate 3 times a day and clonazepam twice a day, whereas ethosuximide could reasonably be given once daily without undesirably wide fluctuations in plasma drug level over the dosage interval. Further studies of the pharmacokinetics of ethosuximide, clonazepam and valproate are still needed, but sufficient data are already available to provide some basis for rational use of these drugs in treating petit mal 'absence' epilepsy.
According to electroencephalographical studies on the pathogenesis of epilepsy a hereditary predisposition plays a greater role than believed before. It is far more frequent than the manifest disease. The phenomenon of cerebral excitability is influenced by different genetically determined, differently age- and sexdependent but amongst each other independent factors. When defining the risk of epilepsy for siblings and descendents in practice, one is forced to proceed from the statistical empirical value with all its uncertainty. During the past few years, the figures have become more exact for special types of epilepsy as absence-epilepsy, myoclonic astatic Petit mal, and Impulsiv-Petit mal. Details of these results and their consequences for genetic advice are discussed.
An attempt is made to clarify the confusion over the classification of the myoclonic epilepsies of childhood. Six types of seizure are described, the classification being based on clinical and electroencephalographic findings. The types of myoclonic epilepsy are infantile spasms, myoclonic astatic epilepsy, myoclonic absence, myoclonic epilepsy of childhood, myoclonic epilepsy of adolescence and photomyoclonic epilepsy, the last being subdivided into myoclonic jerks and eyelid myoclonia. Synonyms are given for all types, based on the major papers in the literature over the last 16 years. The similarity of infantile spasms and myoclonic astatic epilepsy is discussed, as are the so-called 'Lennox' and 'Lennox-Gastaut' syndromes.
203 epileptic children (127 boys, 76 girls), who had demonstrated at least once focal sharp waves in the EEG during the course were investigated regarding clinical and historical data as well as familial morbidity for seizures. Expectedly, the seizure symptomatology was multiform: focal seizures of different type, especially secondarily generalized, grand mal, psychomotor fits, infantile spasms etc. Organic brain lesions play an important role. In 23% of cases a familial seizure affliction can be registered. The morbidity (close family) is significantly lower than in families of patients with spike wave absences (2.5 and 4.4% resp., Doose et al. 1973). Like in spike wave absence epilepsies mothers and mothers' siblings are more often affected than fathers and fathers' siblings. Among the affected relatives grand mal epilepsies predominate. The increase of febrile convulsions and spike wave absences observed in the families of absence epileptics is not present. In probands with onset of epilepsy during early childhood a significantly increased familial affliction can be observed. A more extensive discussion of the results will follow in a second paper deeling with EEG findings in probands and siblings.
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Valproic acid is a new antiepileptic drug. It has a marked effect on generalized spike-wave discharges. The exact mechanism of action is uncertain; however, some evidence suggests an effect on the metabolism of gamma-aminobutyric acid. It is rapidly absorbed from the gastrointestinal (GI) tract. Concurrent administration with phenobarbital may result in elevated phenobarbital plasma concentrations. Administration with phenytoin sodium may transiently result in lower total phenytoin plasma levels. Side effects are generally mild and include fatigue, GI disturbances, weight gain, a fine postural and resting tremor, mild thrombocytopenia, and an increase in hepatic enzymes. Platelet counts and liver function monitoring should be done during valproic acid therapy. Drowsiness may be seen in patients receiving other antiepileptic drugs concurrently.
Computation of power spectra from averaged brief epochs of spike free scalp EEG coincident with the subcortical spike has revealed a distinctive spectral configuration characterized by smooth monotonic decline in power from lowest to highest frequencies. Nine out of 10 patients with epilepsy display similar patterns preceeding long latency responses to a verbal motor reaction time task. Although subcortical spike activity has been recorded from the parasental region of patients with schizophrenia by several investigators half of our patients with schizophrenia displayed a different pattern which resembles a "white noise" spectrum during the delayed reaction time of incorrect response trials. Power spectra derived from 24-hour telemetered scalp EEGs from patients with epilepsy and schizophrenia are also sharply differentiated by similar criteria. These non-invasive methods for analysis of the scalp EEG in relation to careful and controlled behaviour observations may give useful information regarding subcortical activity when intracranial electrodes cannot be utilized.
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A total of 228 children suffering from seizure disorders were investigated by means of cranial computerized tomography (CT). Their age ranged from 3 weeks to 15 years. Structural abnormalities were assessed in 63% of these cases. The greatest incidence of organic abnormalities occurred in children with major epilepsy (83%) and with focal seizures (71%). Clinical data and the course of illness may require additional angiographic and repeated CT investigations.
Eight severely epileptic patients, four males and four females, ranging in age from 10 to 29 years, were trained to increase 12-14 Hzeta EEG activity from the regions overlying the Rolandic area. This activity, the sensorimotor rhythm (SMR), has been hypothesized to be related to motor inhibitory processes (Sterman, 1974). The patients represented a cross-section of several different types of epilepsy, including grand mal, myoclonic, akinetic, focal, and psychomotor types. Three of them had varying degrees of mental retardation. SMR was detected by a combination of an analog filtering system and digital processing. Feedback, both auditory and/or visual, was provided whenever one-half second of 12-14-Hz activity was detected in the EEG. Patients were provided with additional feedback keyed by the output of a 4-7-Hz filter which indicated the presence of epileptiform spike activity, slow waves, or movement. Feedback for SMR was inhibited whenever slow-wave activity spikes or movement was also present. During the treatment period most of the patients showed varying degrees of improvement. Two of the patients who had been severely epileptic, having multiple seizures per week, have been seizure free for periods of up to 1 month. Other patients have developed the ability to block many of their seizures. Seizure intensity and duration have also decreased. Furthermore, the successful patients demonstrated an increase in the amount of SMR and an increase in amplitude of SMR during the training period. Spectral analyses for the EEGs were performed periodically. The effectiveness of SMR conditioning for the control of epileptic seizures is evaluated in terms of patient characteristics and type of seizures.
Motor incoordination, euphoria and hallucinations are symptoms reported for humans voluntarily intoxicated by industrial solvents. An epileptic-like consciousness impairment has also been noted. The present paper describes a technique used for the experimental study of solvent intoxication in which toluene and benzene can be applied directly into the trachea of freely moving cats with chronically implanted electrodes. This technique permits the control of solvent dose and time of exposure. Results showed a 3 Hz spike-wave activity in the gyrus cinguli recording with both toluene or benzene intoxication. Furthermore, benzene inhalation produced generalized tonic-clonic seizures. These effects were dose-related. However, a sensitization period was essential for the development of such alterations, and effects showed a tendency to shortening through chronic exposures. These alterations were correlated with behavioral disturbances such as nodding, twitching and apparent hallucinations. Results are discussed regarding the sensitization period, the optimal peak of effects, and the period of tolerance development relevant to an earlier found amygdalar activation that could be correlated with other methods inducing experimental seizures, such as repetitive stimulation of the brain (kindling).
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Biofeedback training of the sensorimotor rhythm (SMR) was carried out in three male and three female adolescent epileptics and in two normal controls. The patients represented a cross-section of epilepsies including grand mal, myoclonic, afocal and psychomotor types. Three of the cases were mentally retarded. 12-14 Hz (SMR) activity was detected by a combination of sharp analog filtering and digital processing. The patients were provided with feedback whenever they produced 0.5 sec of 12-14 Hz activity of a specified amplitude. Additional feedback was provided for epileptiform activity slow waves or movement. Furthermore, feedback for SMR production was inhibited by digital logic circuitry when movement, slow waves or spikes were present. Seizure reduction was obtained in five of the six epileptics. Several patients showed increased percentage of SMR when feedback was provided and varying degrees of normalization in their EEG as demonstrated by fast Fourier, crossed power spectral density and coherence analyses.
Median reaction times and intra-individual variability were studied in epileptic (N = 63), brain-damaged (non-epileptic) (N = 25) and control patients (N = 25) using a six and one half minute visual, continuous reaction time task. Epileptic and brain-damaged groups were significantly slower than control patients on median reaction times at the 10th, 50th, and 90th percentiles and on the differences between the 10th and 90th percentiles. Thus both general slowing and greater intra-individual variability were found in the epileptic and brain-damaged patients. Reaction times were not related to presence, type and severity of EEG abnormality or to age of onset of epilepsy. Grand mal patients did have significantly greater variability than other types of seizure patients. Epileptic and brain-damaged patients did not differ significantly on any reaction time variables. Both groups were discriminated significantly from the controls on all reaction time measures, especially on the intra-individual variability measure.
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