[Gait disorders in Parkinson disease. Clinical description, analysis of posture, initiation of stabilized gait].
A WELL INFORMED DESCRIPTION: The parkinsonian posture is generally described as a stooped one. At the beginning of the disease, the gait troubles remain moderate; gradually the gait is composed of small steps without a wide base; the patient tends to run after his centre of gravity by accelerating the step (festination phenomenon). Difficulties occurs for starting up (delay of gait initiation), for about-turn or for clearing obstacles. Kinetic jammings and standing around (freezing) can last several seconds and be responsible for falls. POSTURAL INSTABILITY, A MAJOR SYMPTOM IN PARKINSON'S DISEASE: This symptom is little improved by therapies and is responsible for serious disability. Postural instability induces a disequilibrium and is partially due to a simultaneous antagonist muscles contraction and to the impossibility of modifying postural responses to changing support conditions. The passive viscoelastic properties of muscles and tendons constitute a first line of defence against the disequilibrium and contribute to postural stability in the case of medium disturbances. Automatic and voluntary postural responses which come into play in the case of major disturbances can also be impaired (delay or defect of the responses). GAIT INITIATION FAILURE ARE FREQUENT: They result from an increase of the postural phase and a decrease of the propulsion forces, depending on a deficit of the postural anticipation mechanisms and also the sequential organization and the integration of two different motor programs, postural and locomotor. They can be controlled partially with sensory stimuli, notably visual inputs. DATA CONCERNING STABILIZED WALKING AND ITS PATHOPHYSIOLOGY REMAINS TO BE CLARIFIED: Spatial and temporal parameters are impaired: speed, step length and swing phase are reduced, while cadence increases to compensate these troubles. These modifications are the consequence of an incapacity to produce internal marks to generate regular steps. When the parkinsonian patient is supplied with external marks, these parameters can be normalized. From a pathophysiological point of view, gait disorders could result from defective central integration of proprioceptive information during movement within the basal ganglia, associated with a visual perceptive deficit linked with a retinal dopaminergic cells dysfunction and finally from an impairment of the proprioceptive feedback of the load receptors in the leg extensor muscles.
Kemoun
G
G
Service de Neurologie et Pathologie du Mouvement, Hôpital Salengro, CHRU F 59037 Lille.
Defebvre
L
L
D000978:Antiparkinson Agents / Q000009:adverse effects / Q000627:therapeutic use; D001479:Basal Ganglia / Q000187:drug effects; D005684:Gait / Q000187:drug effects; D006801:Humans; D007980:Levodopa / Q000009:adverse effects / Q000627:therapeutic use; D010300:Parkinson Disease / Q000175:diagnosis* / Q000188:drug therapy; D004856:Postural Balance / Q000187:drug effects; D011187:Posture; D016138:Walking
D000978:Antiparkinson Agents; D007980:Levodopa