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Petit mal epilepsy is primarily a disorder of childhood. It is a comparatively rare type of seizure and is relatively benign. It rarely causes demonstrable evidence of pathologic cerebral changes, except in patients who have frequent attacks of petit mal status. Patients with petit mal epilepsy are prone to develop major motor (grand mal) seizures. Therefore, concurrent administration of petit mal and major motor anticonvulsants is recommended.
Although petit mal epilepsy is believed to arise from the thalamocortical system, it has been suggested recently that high-voltage spike-and-wave activity (HVS) in mutant mice can cause structural reorganization in the hippocampus, similar to that seen in temporal lobe epilepsy. We tested this assumption in rat strains with low and high incidence of HVS. No relationship was found between mossy fiber sprouting and HVS incidence. Hippocampal neurons were not driven by HVS. These findings suggest that petit mal seizures do not invade the hippocampus and are not causally related to sprouting of the mossy fibers.
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A petit mal seizure detector totally implemented in a 16 bit microcomputer and capable of analyzing on-line at least one channel of EEG data is described. The system uses the repetition period of the wave complexes as the primary parameter for the detection and performs well in clinically significant seizures. Besides characterizing the paroxysms in duration and time of occurrence, the system also evaluates on-line the mean values and variances of the detection parameters, yielding more quantitative information about the seizure data than previously described systems.
The mechanisms of petit mal epilepsy remain a mystery despite successful therapy. Previous workers have proposed that paroxysmal activity of cortical inhibitory systems plays a role in absence seizures. In this study, we have compared the effects of bicuculline, a potent convulsive agent and GABA antagonist, with ethosuximide, a drug used to treat petit mal epilepsy, on the thalamocortical motor system of the cat. Under chloralose anesthesia, sequential pairs of pulses were delivered to ventrolateral thalamus (VL) varying either pulse amplitude or interval. The evoked responses were recorded from sensorimotor cortex, analyzed on-line by computer, and plotted as an excitability curve (mean response amplitude as a function of pulse interval), or a family of threshold curves (mean response amplitude as a function of stimulus amplitude at various fixed intervals). Administration of each drug resulted in increased thalamocortical excitability and decreased threshold to stimulation for short pulse-pair intervals, with diminished duration of the excitability curve. Increased alertness was produced by both drugs. Studies with grand mal anticonvulsants demonstrated entirely different effects. Because GABA is thought to be the primary inhibitory transmitter in VL and cerebral cortex, bicuculline would be expected to result in disinhibition. The similarity of the data for ethosuximide suggests that ethosuximide also suppresses inhibition in the thalamocortical motor system and adds further to the accumulating evidence of the role of inhibitory system in petit mal epilepsy.
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.
Ocular manifestations are prominent in petit mal attacks. The nuclei innervating the extraocular muscles lie in mesencephalic and pontine regions of the brainstem which have been regarded by some as critical areas in the generation of petit mal attacks. Ocular signs and their timing relative to spike-and-wave onset were studied cinematographically in 4 patients with petit mal epilepsy. Each patient showed a consistent pattern of eye deviation or fixation during spike-wave bursts. Neither the activation of oculomotor pathways, as indicated by eye deviation, nor their inactivation, as suggested by interruption of ongoing elicited ocular activity, preceded the appearance of spikewaves. Because ocular manifestations began only after the onset of spike-wave, this study provided no evidence that brainstem oculomotor regions were involved in the initiation of these petit mal attacks.
In 24 patients with petit mal-epilepsy 54 all-night polygraphic recordings were registered. In petit mal-epilepsy the epileptic clinical manifestations as well as the electrographic discharges appear with maximal intensity in sleep stage 2. However, these electrical and clinical phenomena are not characteristic of petit mal. Therefore one may surmise that the facilitation of epileptiform phenomena in sleep stage 2 is generally applicable, and does not represent a particular characteristic of petit mal. In sleep stages 1 and REM as well as in the transitional stages well organized characteristic spike-and-wave discharges occur which are identical to those appearing during wakefulness. Sleep stages 1 and the transitional stages are functionally unstable states when bioelectrical discharges as well as clinical absences are activated. In stage REM the spike-and-wave discharges either disappear or persist, however, in comparison to the frequency of discharges during NREM-sleep they are likely to be activated during REM. This feature seems to be characteristic of petit mal and occurs in every patient in an individually set pattern. The appearance of electrographic epileptiform discharges and clinical absences bears an individual character and accordingly the following variations can be distinguished: - petit mal during wakefulness, - petit mal, when falling asleep, - petit mal in awakenings, - petit mal during transitional states, - the intense activating effect of sleep stage 2 on epileptiform patterns, however this is not characteristic of petit mal only. During NREM-sleep epileptiform discharges are easily activated by acoustic stimuli and correspond to epileptiform phenomena which occur spontaneously during the same stage.(ABSTRACT TRUNCATED AT 250 WORDS)
An unusual case of petit mal epilepsy is described. It is of particular interest because of the age of its appearance and the morphological type of the seizures. These two aspects make this case unique in world literature.
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28 children with Petit mal epilepsy were treated with valproic acid either as drug of primary choice or because of resistance to other antiepileptic drugs. Efficacy of treatment was measured by reduction of seizure frequency and EEG-recordings. Serum concentration of valproic acid was measured in all patients. The best clinical efficacy was found in children with absence seizures, who also required the lowest dosages. Side effects of therapy were (in most cases) transitory.
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In this study we investigated the relationship between penicillin-induced hypothermia and petit mal epilepsy induced by this proconvulsant antibiotic. In order to find a possible dose-dependent relationship, we used two doses: 1500.000 and 1000.000 U/kg b.wt., both known as being sufficient to induce absence-like attacks with subsequent spike and wave discharges (SWD) in electrocorticogram (ECoG). Because of experimental data suggesting penicillin binding to benzodiazepine receptor recognition site, we also studied penicillin-induced changes in body temperature after diazepam pretreatment. Results of this study clearly show that penicillin in doses known to induce petit mal-like epilepsy concomitantly induces statistically significant dose-dependent decrease in body temperature. Pretreatment with diazepam completely prevents both penicillin-induced hypothermia and SWDs. On the other hand, both the diazepam and mixed diazepam + penicillin treatments did not significantly alter body temperature. These results suggest, however, that at least some of the penicillin effects described could be assigned to its binding to the benzodiazepine receptor recognition site at GABA(A) ionophore. This may have an important clinical implication because the inhibitory action of penicillin at the benzodiazepine receptor recognition site could account for the mechanism of penicillin-induced unspecific encephalopathies in humans. The relationship between petit mal epilepsy and hypothermia sheds new light on the action mechanisms of penicillin-induced absence seizures.
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d-Amphetamine is effective in controlling seizures in petit mal epilepsy. The flash-evoked afterdis-charge (FEAD) in rats has been proposed as a model of the peit mal seizure. The experiments reported here investigated the dose response relationship for the suppression of FEAD by d-amphetamine, and compared its effects with those of the dopamine-mimetic, apomorphine. Significant suppression of FEAD was observed at doses of d-amphetamine greater than 0.2 mg/kg. A maximum decrease of 60% occurred at 1.2 mg/kg. Higher doses did not result in any further suppression. In contrast, apomorphine and no effect on the FEAD even at doses that induced intense stereotypic behavior. In other experiments, administration of either the dopamine antagonist pimozide or the alpha-adrenergic antagonist phenoxybenzamine exacerbated FEAD and also prevented the suppression of FEAD by d-amphetamine. The results of these experiments support the hypothesis that the FEAD is a valid model of the petit mal seizure. Furthermore, they provide evidence that norepinephrine is necessary for the seizure-suppressant action of d-amphetamine.