Reflex behavior and programming in Parkinson's disease.
Several aspects of characteristically impaired postural adjustments indicate a defective central programming of the respective EMG patterns in PD. This may be due to deficits in the supraspinal control of spinal interneuronal circuits. This impairment obviously contributes to the difficulty of these patients in performing two motor acts simultaneously. In addition, parkinsonian patients exhibit a reduced sensitivity of polysynaptic reflexes in the leg extensor muscles which correlates with their postural instability. The activity of monosynaptic reflexes is negligible, as in healthy subjects. The impairment of proprioceptive reflex function may be partially compensated for by changes of intrinsic muscle stiffness. Discrepancies in the literature about the behavior of the polysynaptic EMG responses in parkinsonian patients may in part arise from the fact that it depends on both the particular muscle under study and the actual motor task investigated.
Dietz
V
V
Department of Clinical Neurology and Neurophysiology, University of Freiburg, Germany.
D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D000818:Animals; D004576:Electromyography; D000882:Haplorhini; D006801:Humans; D009127:Muscle Rigidity / Q000503:physiopathology; D009129:Muscle Tonus / Q000502:physiology; D009132:Muscles / Q000294:innervation; D010300:Parkinson Disease / Q000503:physiopathology*; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000503:physiopathology; D004856:Postural Balance / Q000502:physiology*; D011187:Posture / Q000502:physiology; D011434:Proprioception / Q000502:physiology; D012018:Reflex / Q000502:physiology*
D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine