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Electromyographic (EMG) activity of abnormal involuntary movements and their modifications after Piribedil, a dopaminergic agonist, were analysed in patients presenting with tremor or tardive dyskinesia induced by treatment with neuroleptics. Quantitative analysis of EMG bursts and of their phase relationships with bursts of antagonist muscles revealed differences between tremor and tardive dyskinesia; three separate EMG types of the latter were found. In tremor, EMG activity was coordinated between agonists and antagonists. Length and frequency of bursts are characteristic. In tardive dyskinesia, phase histograms of antagonist muscle bursts showed an absence of reciprocal organisation of EMG activity. This activity was made up of either rhythmical bursts (type I and II according to the frequency) or irregular discharges (type III). Piribedil decreased tremor but facilitated EMG activity in tardive dyskinesia. These results give an objective measurement or classification of tremor and tardive dyskinesia induced by neuroleptics. [ABSTRACT FROM AUTHOR]

The effects of a muscle twitch on the tremor of the extensor indicis muscle and of the tibial anterior muscle have been recorded in 14 patients with essential tremor and in 10 patients with Parkinson's disease. The muscle twitch evoked by the electrical stimulation of the motor nerve inhibits the tremor and synchronises it. The mean duration of the inhibition is 92.1 +/- 6.8 ms for essential tremor and 183.0 +/- 16.8 ms for Parkinsonian tremor. This inhibitory phase lasts longer when the muscle twitch is induced during the second half of the Parkinsonian tremor cycle. The effects of voluntary contraction and of unloading suggest that inhibition and resetting of the tremor can be attributed to the autogenic mechanism induced by Ib fibres discharges. The presence of a rhythmic inhibition in the cycle of Parkinsonian tremor accounts for the longer duration of the inhibitory phase. In practice, these techniques aid the diagnosis of tremor in these two conditions, for example they assist the identification of low frequency essential tremor and of postural tremor in Parkinson's disease. [ABSTRACT FROM AUTHOR]

A reciprocal continuous inhibition by flexor on extensor muscles was proved during Parkinsonian rigidity. Extensor motoneurone excitability was tested by Hoffmann's reflex and flexor activity was altered by lidocaine anaesthesia of the peroneal nerve (PN). During PN anaesthetic block, a gradual increase of Hoffmann's reflex was noted. It was statistically significant at the 15th minute after lidocaine injection, and was maximum at the 30th minute. The reciprocal inhibition was considerable in 16 patients with Parkinsonism, as recorded before treatment. In normal subjects, it was small and non-significant. After one month's treatment with L-dopa at the usual therapeutic dose, this reciprocal inhibition greatly decreased in the same patients. The origin of this reciprocal continuous inhibition is discussed. [ABSTRACT FROM AUTHOR]

Biological causes provoking dystonia can not be systematized, with the exception of the small group of levodopa-responsive dystonia. Therefore the pathophysiology of the dystonic syndrome can be approached by considering the site of the lesions. In 40 cases of uni or bilateral symptomatic dystonias, this site could be identified with CT Scan or MRI. Twenty-one were located in the striatum, six in the pallidum, seven in the thalamus, six in the midbrain. Each group is characterized by etiologic and clinical criteria, sometimes associated with abnormal movements. In the striatal group, the most important, dystonia was often associated by athetosis or choreoathetoid abnormal movements. In some cases, in children, lesions were vascular due to impairment of lenticulo-striatal arteries, often following cranial trauma. The pallidal lesions were usually provoked by metabolic or infectious agents. Most thalamic dystonias were of vascular origin, sometimes accompanied by myoclonia. Midbrain lesions were usually vascular with tremor. Athetosis occurred after striatal rarely after pallidal lesions. It is advisable not to assimilate dystonia and athetosis as both are simultaneously observed if the lesions are located in the striatum, rarely in the the pallidum but not in the midbrain.