Loss of tendon organ inhibition in Parkinson's disease.
Electrical stimulation via skin electrodes placed over human tendons results in a reflex inhibition of voluntary activity in the stimulated muscle, probably due to activation of Golgi tendon organ afferents. The characteristics of this response in the extensor digitorum communis (EDC) muscles of subjects with Parkinson's disease were compared with those in age-matched controls. The threshold of the inhibitory response was significantly increased in the patient population compared with controls (159 +/- 34 V for tremulous patients; 134 +/- 10 V for rigid patients, 90 +/- 5.5 V for age-matched controls and 70 +/- 16 V for all normals). The latency of the inhibitory wave was increased (onset latency was 68.01 +/- 5.5 ms in patients was 51.5 +/- 4.9 ms in controls). The duration of I was also increased in patients (60 +/- 20.8 ms) relative to controls (46 +/- 11.8 ms). This was associated with slow development of the inhibition with the result that maximal inhibition was delayed by approximately 20 ms. Other features of the patient response were its oscillatory character whereby the initial inhibitory and excitatory components were followed by further prominent peaks and troughs which gave the appearance of continuing response cycles. Such behaviour was not seen in normal records. Also electrical stimulation of the extensor muscle tendon produced concurrent records in the forearm flexor muscle, which resembled those from the stimulated muscle. This was in contrast to normal records which showed no response in the flexor. The possible contribution of a disorder of tendon organ reflexes to the rigidity and tremor of Parkinson's disease is discussed.
Burne
J A
JA
Department of Biomedical Science, University of Sydney, Australia.
Lippold
O C
OC
D000368:Aged; D004558:Electric Stimulation; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000503:physiopathology*; D011930:Reaction Time / Q000502:physiology; D013710:Tendons / Q000503:physiopathology*