Disynaptic Ia reciprocal inhibition acts, at the spinal level, by actively inhibiting antagonist motor neurons and reducing the inhibition of agonist motor neurons. The deactivation of this pathway in Parkinson's disease is still debated. Disynaptic reciprocal inhibition of H reflexes in the forearm flexor muscles was examined in 15 control subjects and 16 treated parkinsonian patients at rest and at the onset of a voluntary wrist flexion. Two patients were reassessed 18 h after withdrawal of antiparkinsonian medication. At rest, the level of Ia reciprocal inhibition between the wrist antagonist muscles was not significantly different between patients and controls. In contrast, clear abnormalities of this inhibition were revealed by voluntary movements in the patients. In normal subjects, at the onset of a wrist flexion, Ia reciprocal inhibition showed a large decrease, and we argue that this decrease is supraspinal in origin. On the less affected sides of the patients the descending modulation was still present but lower than in controls; on the more affected sides this modulation had vanished almost completely. These movement-induced abnormalities of disynaptic Ia reciprocal inhibition were closely associated with Parkinson's disease but were probably not dependent on L-dopa. They could play a role in the disturbances of precise voluntary movements observed in Parkinson's disease.

A potent heteronymous excitation of quadriceps motoneurones via common peroneal group II afferents has recently been demonstrated in normal subjects. The aim of this study was to investigate whether this group II excitation contributes to rigidity in Parkinson's disease. The early and late facilitations of the quadriceps H reflex elicited by a conditioning volley to the common peroneal nerve (CPN) at twice motor threshold, attributed to non-monosynaptic group I and group II excitations, respectively, were investigated. The comparison was drawn between results obtained in 20 "de novo" patients with Parkinson's disease (hemiparkinsonian, 17; bilateral, three) and 20 age-matched normal subjects. There was no statistically significant effect of "group" (patients/controls), "duration", "global severity" [Unified Parkinson's Disease Rating Scale (UPDRS)] or "side" (unilaterally versus bilaterally affected) factors on either group I or group II facilitations. To further the analysis, the factors of status (affected or non-affected limb), akinesia (lower limb akinesia score) and rigidity (lower limb rigidity score) were entered in a general linear model to explain the variations of the quadriceps H reflex facilitation. Rigidity was the only factor useful in predicting the value of the group II facilitation of the quadriceps H reflex (P < 0.007). Group I and group II facilitation was then compared between the rigid, non-rigid and control lower limbs [multivariate analysis of variance (MANOVA)]. Results are represented as mean +/- SEM (standard error of the mean). Group II facilitation was enhanced in the rigid lower limb of unilaterally affected patients (153.2 +/- 7% of control H reflex) compared with non-rigid lower limbs (124 +/- 4% of control H reflex; P < 0.007) or control lower limbs (126.1 +/- 4.1%; P < 0.01). There was no difference between the non-rigid lower limbs of the unilaterally affected patients and the control lower limbs, but a difference was observed between the rigid lower limbs of unilaterally less affected and bilaterally more affected patients (153.2 +/- 7% and 123.8 +/- 7.5% of control H reflex, respectively; P < 0.04). These results suggest a facilitation of the transmission in the interneuronal pathway activated by group II afferents in rigid lower limb of de novo hemiparkinsonian patients, probably resulting from a change in their descending monoaminergic inhibitory control.

The possibility was investigated that human handedness is associated with an asymmetrical cortical and/or peripheral control of the cervical premotoneurones (PreMNs) that have been shown to mediate part of the descending command to motoneurones of forearm muscles. Heteronymous facilitation evoked in the ongoing voluntary extensor carpi radialis (ECR) electromyographic activity (EMG) by weak (0.8 times motor threshold) stimulation of the musculo-cutaneous (MC) nerve was assessed during tonic co-contraction of biceps and ECR. Suppression evoked by stimulation of a cutaneous nerve (superficial radial, SR) at 4 times perception threshold in both the voluntary EMG and in the motor evoked potential (MEP) elicited in ECR by transcranial magnetic stimulation (TMS) was investigated during isolated ECR contraction. Measurements were performed within time windows or at interstimulus intervals where peripheral and cortical inputs may interact at the level of PreMNs. Results obtained on both sides were compared in consistent right- and left-handers. MC-induced facilitation of the voluntary ECR EMG was significantly larger on the preferred side, whereas there was no asymmetry in the SR-evoked depression of the ongoing ECR EMG. In addition, the suppression of the ECR MEP by the same SR stimulation was more pronounced on the dominant side during unilateral, but not during bilateral, ECR contraction. It is argued that (1) asymmetry in MC-induced facilitation of the voluntary EMG reflects a greater efficiency of the peripheral heteronymous volley in facilitating PreMNs on the dominant side; (2) asymmetry in SR-induced suppression of the MEP during unilateral ECR contraction, which is not paralleled by a similar asymmetry of voluntary EMG suppression, reflects a higher excitability of cortical neurones controlling inhibitory spinal pathways to cervical PreMNs on the preferred side.

Objectives-Cortical command to upper limb motor neurons is transmitted, in humans, not only through the monosynaptic corticomotor neuronal pathway, but also through cervical premotor neurons. Whether activity in this nonmonosynaptic corticospinal pathway is modified in Parkinson's disease was explored. Methods-Ongoing EMG activity recorded in wrist extensors during tonic extension of the wrist is suppressed by a volley evoked by stimulating the superficial radial nerve. It has been shown that this cutaneous induced suppression is due to inhibition of transmission of the cortical command at a premotor neuronal level. By comparing the cutaneous induced EMG depression between 45 de novo parkinsonian patients and 23 age matched controls it has been possible to appreciate if and to what extent the "nonmonosynaptic" part of the cortical command is modified in these patients. Results-At the early stage of the illness the EMG depression, reflecting the "nonmonosynaptic" part of the cortical command, was bilaterally increased despite very asymmetric clinical status. When the duration of the disease was more than 36 months, EMG depression returned to its control level. No correlation was found between the amount of the EMG depression and parkinsonian symptoms before and after levodopa treatment. Conclusion-Increase of the relative "non-monosynaptic" part of the cortical command could reflect a compensatory motor mechanism elaborated upstream from the motor cortex (J Neurol Neurosurg Psychiatry 1998;64:166-171)

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