Loss of reflex inhibition following muscle tendon stimulation in essential tremor

Electrical stimulation of human upper limb muscle tendons produces a reflex inhibition (I1) in the same muscles. This inhibition is reduced in Parkinson's disease (PD), prompting a similar study of essential tremor (ET). In essential tremor, two of eight subjects had no discernible inhibition,...

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Bibliographic Details
Published in:Muscle & nerve 2002-01, Vol.25 (1), p.58-64
Main Authors: Burne, John A., Blanche, Timothy, Morris, John G.L.
Format: Article
Language:English
Subjects:
Biological and medical sciences
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Electric Stimulation
Electromyography
essential tremor
Humans
Medical sciences
movement disorders
muscle tendon
Muscle, Skeletal - physiopathology
Neural Inhibition
Neurology
Parkinson's disease
Reaction Time
Reference Values
Reflex - physiology
tendon inhibition
Tendons - physiopathology
tremor
Tremor - physiopathology
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Summary:Electrical stimulation of human upper limb muscle tendons produces a reflex inhibition (I1) in the same muscles. This inhibition is reduced in Parkinson's disease (PD), prompting a similar study of essential tremor (ET). In essential tremor, two of eight subjects had no discernible inhibition, even following supramaximal stimulation (< 80 mA) of the tendons from extensor digitorum communis and extensor pollicis brevis. In the remaining six subjects, the mean thresholds for I1 in these muscles were increased by 270 and 320%, respectively, relative to controls. The maximal amplitude of the inhibition was significantly reduced in the ET group, as was the following excitation (E1). The latency and duration of I1 were not different in ET subjects and controls. The maximal duration of I1 was correlated with tremor frequency in individuals, and tendon stimulation was effective in initiating ongoing tremor cycles. These results disclose a peripheral reflex abnormality in ET that is mediated by tendon afferents and can be linked to the coexistent tremor. The response in ET was distinguished from that in PD by its different time‐course and by failure of the response to appear in the antagonist muscle. The abnormality may prove a useful marker for ET, which currently lacks a definitive pathological or neurophysiological marker to support objective clinical diagnosis. © 2002 John Wiley & Sons, Inc. Muscle Nerve 25: 58–64, 2002
ISSN:0148-639X
1097-4598
DOI:10.1002/mus.10003