The effect of two drugs upon multifocal myoclonic jerks was evaluated. The drugs influence the central cholinergic system in opposite ways. Eight patients with progressive and nonprogressive myoclonic epilepsy were tested. The single blind test was used. The number of myoclonic jerks after intravenous physostigmine (mean dose 0.02 mg/kg) and that after atropine (0.04 mg/kg) was compared to number of myoclonic jerks in the drug-free periods and with placebo. Placebo was without an effect. Physostigmine slightly increased the number of jerks. Atropine decreased the number significantly. In most patients the results were not striking. It is suggested that the cholinergic system may participate in the physiopathology of the studied myoclonus in a rather indirect, perhaps modulating way.
The goal of the present study was to investigate the reliability of clinical and electroencephalographic (EEG) criteria for the classification of localization-related epileptic syndromes as listed in the Proposals of Revised Classification of Epilepsies and Epileptic Syndromes 1989 (ICE). ICE distinguishes between multiple syndromes within epilepsies of a given lobe. Intracranial recordings were the main element in the development of the revised ICE. Considering that most epilepsy centers have no access to such invasive techniques for precise anatomic localization, it was of interest to assess how accurately the seizure origin could be determined from the scalp EEG and clinical data as reported in ICE. In this retrospective study, we compared the accuracy of the topographic diagnosis made by two groups of physicians evaluating the same patients-one group with and the other without access to results of stereo-EEG (SEEG). Medical files of 87 patients with intractable localization-related epilepsy were analyzed: 38 with frontal, 37 with temporal, 10 with parietal, and 2 with occipital lobe epilepsy were included in the study. All patients underwent previous SEEG and successful cortectomy. Minimum follow-up was 5 years. In most cases, noninvasive techniques and criteria suggested by ICE allowed topographic diagnosis of focal epilepsies according to brain lobe involvement. More detailed diagnosis, localizing the origin of critical activity within a lobe, was often unreliable. Further data are required for a definition of the epileptogenic zone. A spatiotemporal evaluation of critical events, including the intracranial EEG recording, remains the best method for topographic diagnosis of localization-related epilepsy.
Neurophysiological studies were performed on four Papio papio baboons presenting with nonepileptic myoclonus (a startle response resembling stimulus-sensitive jerk). Investigations of the EEG, back-averaged EEG, and somatosensory evoked potentials revealed the absence of cortical correlates preceding the jerks, and exclusion of cerebral cortex involvement. No long-latency reflexes could be recorded in these animals. The jerks were symmetric when evoked by unilateral stimulation in normal baboons as well as in a split-brain animal. Polymyographic records showed that the first muscle involved during the jerk was the trapezius; other muscles were involved with latencies increasing in both cranial and caudal directions. From these data, nonepileptic myoclonus of baboons can be classified as a reticular reflex myoclonus. The involvement of cranial nerves did not follow the layout of the nuclei in the brainstem, indicating that the jerk is most likely generated as a complete movement. The generating structure is probably under cholinergic control. Finally, the Papio papio baboon, which was already known as a model for cortical myoclonus elicited by intermittent photic stimulation in predisposed animals, can also be considered a model for the study of the reticular reflex myoclonus.
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