Central nervous system lesions and segmental activity

Study of activity in segmental pathways can help in understanding the pathophysiology of clinical disorders due to basal ganglia damage. Disynaptic Ia reciprocal inhibition (DI) acts by actively inhibiting antagonistic motoneurones and reducing the inhibition of agonist ones. During movement, activity of interneurones mediating DI is significantly modulated by descending inputs. In Parkinsonian patients, this descending modulation almost completely vanished. Lack of modulation was not dependent on L-DOPA as it occurred in treated patients and was not modified when patients were off medication. A potent heteronymous group II excitation of quadriceps MNs has been recently demonstrated in normal subjects after stimulation of the common peroneal nerve. This group II excitation was significantly enhanced in the rigid lower limb of Parkinsonian patients. We propose that enhanced group II excitation could contribute to rigidity in PD and result from a change in a tonic noradrenergic descending inhibitory control from locus coeruleus.