Many neurophysiological abnormalities have been described in the primary motor cortex of patients with
Parkinson's disease. However, it is unclear whether there is any relationship between them and
bradykinesia, one of the cardinal motor features of the condition. In the present study we aimed to investigate whether objective measures of
bradykinesia in
Parkinson's disease have any relationship with neurophysiological measures in primary motor cortex as assessed by means of
transcranial magnetic stimulation techniques. Twenty-two patients with
Parkinson's disease and 18 healthy subjects were enrolled. Objective measurements of repetitive finger tapping (amplitude, speed and decrement) were obtained using a motion analysis system. The excitability of primary motor cortex was assessed by recording the input/output curve of the motor-evoked potentials and using a conditioning-test paradigm for the assessment of short-interval intracortical inhibition and facilitation. Plasticity-like mechanisms in primary motor cortex were indexed according to the amplitude changes in motor-evoked potentials after the paired associative stimulation protocol. Patients were assessed in two sessions, i.e. OFF and ON medication. A canonical correlation analysis was used to test for relationships between the kinematic and neurophysiological variables. Patients with
Parkinson's disease tapped more slowly and with smaller amplitude than normal, and displayed decrement as tapping progressed. They also had steeper input/output curves, reduced short-interval intracortical inhibition and a reduced response to the paired associative stimulation protocol. Within the patient group,
bradykinesia features correlated with the slope of the input/output curve and the after-effects of the paired associative stimulation protocol. Although dopaminergic
therapy improved movement kinematics as well as neurophysiological measures, there was no relationship between them. In conclusion, neurophysiological changes in primary motor cortex relate to
bradykinesia in patients with
Parkinson's disease, although other mechanisms sensitive to
dopamine levels must also play a role.