[Gait disorders in Parkinson's disease: and pathophysiological approaches]

Gait disorders and axial symptoms are the main therapeutic challenges in advanced Parkinson's disease (PD). Gait disorders in PD are characterized by spatial and temporal dysfunction. Gait hypokinesia is the first to appear and is responsible for the decrease in velocity. A good sensitivity to the levodopa is well established. Morris et al. [Morris ME, Iansek R, Matyas TA, Summers JJ. Ability to modulate walking cadence remains intact in Parkinson's disease. J Neurol Neurosurg Psychiatry 1994a;57(12):1532-4; Morris ME, Iansek R, Matyas TA, Summers JJ. The pathogenesis of gait hypokinesia in Parkinson's disease. Brain 1994b;117(Pt. 5):1169-81; Morris ME, Iansek R, Matyas TA, Summers JJ. Stride length regulation in Parkinson's disease. Brain 1996;119:551-68] demonstrated that the ability to modulate walking cadence remains intact in PD, and could correspond to a compensatory mechanism. More advanced disease stages of the disease are characterized by abnormal temporal parameters (such as stride length variability, stride time variability and cadence elevation) which are unresponsive to levodopa therapy and may be correlated with the occurrence of falls and freezing of gait (FOG). Lastly, postural instability also results in falls and is poorly responsive to levodopa. A link between gait impairment and frontal disorders has recently been suggested. After a few years of evolution, paradoxical episodic phenomena are described: festination ("hastening gait" with rapid small, short steps) and FOG (involuntary and sudden cessation of gait). Both symptoms are often incapacitating for PD patients, because of their resultant loss of independence and their poor response to levodopa therapy. Kinematical studies of FOG revealed a decrease in velocity, stride length and an exponential increase in cadence, prior to a FOG episode. New approaches (functional MRI, wavelets...) should offer new perspectives concerning these disabling symptoms.