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|Title:||The sensory control of movement in the human hand subsequent to peripheral nerve injury|
|Abstract:||This study presents the first comprehensive study into the recovery of kinaesthesia in man subsequent to peripheral nerve injury (PNI). An AC induction motor was used to apply movement to the models of the thumb carpometacarpal joint, little finger metacarpophalangeal joint and index finger metacarpophalangeal joint for investigating median, ulnar and mixed nerve (ulnar and median) innervation, respectively.;Thumb: High kinaesthetic acuity was present in the thumb following local anaesthesia of the median nerve. Median and radial nerve anaesthesia demonstrated that much of this remaining sensation was due to the contribution of the radial nerve. Kinaesthesia in median PNI subjects was characterised by high movement detection but inconsistent grading of movement.;Little Finger: Ulnar nerve anaesthesia resulted in profound kinaesthetic loss. Some subjects could detect at least some movements but could not grade amplitudes and velocities, sometimes sensing movements in the extension, flexion plane. Subsequent to ulnar PNI, kinaesthetic sensation varied from no sensation to kinaesthetic acuity approaching normal levels. Of the three models, the little finger provided the most complete model for assessing kinaesthetic recovery.;Index: Both ulnar and median nerve anaesthesia had a small but detrimental effect on the ability to sense movement in the index indicating that muscle and skin/joint proprioceptors both contribute to kinaesthesia. Median and ulnar nerve anaesthesia had opposite effects on the ability to grade movements, causing underestimation and overestimation of amplitudes, respectively. Median PNI resulted in variability and in the ability to grade movement, whereas ulnar PNI resulted in consistent exaggeration of amplitude.;The three intrinsic muscles, abductor pollicis brevis, first dorsal interosseus and abductor digiti minimi all generated 8-10 Hz tremor, both in the normal hand, and subsequent to PNI and carpal tunnel syndrome (CTS). These findings provide further evidence for the central origin of 8-10 Hz pulsatile output.|
|Rights:||Copyright © the author. All rights reserved.|
|Appears in Collections:||Theses, College of Medicine, Biological Sciences and Psychology|
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