[Clinical neurophysiology in the evaluation and physiopathology of Parkinson's disease].
Clinical Neurophysiology brings about 2 major contributions in the study of Parkinson's disease: on the one hand, it makes it possible to measure the motor troubles; on the other, it enables their pathophysiological analysis. The 3 classical signs must be studied separately. Tremor can easily be recorded by electromyography. Moreover, its parkinsonian nature can be specified by studying the resetting of EMG bursts following electrical stimulation of the motor nerve. A pace maker has been demonstrated in the thalamus from where rhythmic messages are first sent to motor cortex and thereafter reverberated to spinal motoneurons. Rigidity can be assessed by sophisticated but not generalized methods. It is easier to evaluate it by long-loop responses evoked by proprioceptive or exteroceptive stimulations. These responses reflect activity in pathways relaying in supraspinal structures. Contrary to spasticity, rigidity is not basically due to dysfunctions in segmentary spinal circuits. It is more likely that it depends on hyperactive and hyperexcitable long loop pathways. This hypothesis is in agreement with well established facts showing that parkinsonian hypertonia vanishes after dorsal root section. Akinesia is complex semeiologically. It is made of various components some of which can be measured. Reaction times and movement times provide interesting data which however are not strictly correlated with the motor handicap. Motor programmes are assembled in normal delays but they are not "called upon" correctly, reflecting a disturbance in the motor planning. A lack of "energetization" of the motor cortex and the pyramidal tract is likely. A functional disconnection between the motor program/plan side and the execution side can be hypothesized to explain the 3 major signs; on the one hand, neural messages are not correctly transferred to the pyramidal system, on the other, spinoencephalospinal loops on the execution side become more active as they escape from the control normally exerted by the plan/program side where basal ganglia play a prominent role.
D000818:Animals; D001479:Basal Ganglia / Q000378:metabolism / Q000503:physiopathology; D001767:Blinking; D001921:Brain / Q000503:physiopathology; D004576:Electromyography; D006801:Humans; D009046:Motor Neurons / Q000502:physiology; D009069:Movement Disorders / Q000209:etiology; D009127:Muscle Rigidity / Q000209:etiology; D009482:Neurophysiology; D010300:Parkinson Disease / Q000175:diagnosis / Q000503:physiopathology*; D011930:Reaction Time; D012021:Reflex, Abnormal / Q000209:etiology; D013116:Spinal Cord / Q000503:physiopathology; D014202:Tremor / Q000209:etiology
Apport de la neurophysiologie clinique à l'évaluation et à la physiopathologie de la maladie de Parkinson.