Abstract

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 non-monosynaptic 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 “non-monosynaptic” part of the cortical command is modified in these patients.

RESULTS At the early stage of the illness the EMG depression, reflecting the “non-monosynaptic” 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