In PD patients, which represent a model of basal ganglia system dysfunction, length and velocity of the first step during gait initiation are known to be reduced and improved by dopaminergic therapy whereas postural instability is less sensitive to the treatment suggesting the involvement of other brain structures dysfunction and/or lesion. One way to evaluate the postural control during the gait initiation process is to measure the vertical velocity of the centre of gravity by using a force platform. In healthy adults, during the single support phase, a forward fall of the centre of gravity occurs and is actively reversed by the stance leg soleus muscle activation prior foot contact. In parkinsonian patients with postural instability, this phenomenon, called active braking, is altered. It is assumed that this postural instability results from additional lesions and/or dysfunction in the basal ganglia output structures, especially in the midbrain, containing the pedunculopontine nucleus and the mesencephalic locomotor region, two structures known to participate to the control of locomotion and posture in animals.