[Parkinsonian rigidity: clinical and physiopathologic aspects]

Neurophysiologic mechanisms responsible for parkinsonian rigidity are poorly understood. In any case, they have to fit all the clinical data which are first reviewed before discussing 2 theories which are proposed to interpret rigidity. The first theory postulates that increased resistance to mobilization is due to hyperactivity in a long loop reflex pathway which originates at the neuromuscular spindles and relays in the motor cortex. This theory is based on the largely accepted finding that, in parkinsonian patients, M2 response is increased when a voluntary movement is abruptly stopped. Although popular this hypothesis is far from explaining all the clinical facts, namely that rigidity is equal in extensor and flexor, proximal and distal muscles. Based on a reflex set by primary afferent discharges, it is incompatible with the lack of rigidity reinforcement after faster passive mobilization. The second theory rests on data obtained from electrophysiological studies of some spinal interneurones. Both IA and IB inhibitory interneurones are functionally modified but not in the same direction. While the IA inhibitory interneurone is facilitated, the IB inhibitory interneurone is less active. Disappearance of autogenic inhibition can explain rigidity at rest and the tonic stretch reflex. In addition, interneurones intervening in the flexor reflex disclose a modified excitability. It is possible to interpret these facts by postulating an abnormal influence transmitted through descending reticulospinal pathways. This abnormal influence would result from modified activation of reticular nuclei by afferents projecting from the basal ganglia. Such a hypothesis is open to experimental testing through the startle reaction. The latter facilitates the H reflex by the reticulospinal pathways, the influence of cortex--if any--being negligible.(ABSTRACT TRUNCATED AT 250 WORDS)