In a previous study, Caccia et al. (1973) described the reflex responses of hand muscles to stimulation of the digital nerves of different fingers in man. In this study, we have found that reflex cutaneomuscular responsiveness to stimulation of the digital nerves of the little finger is altered in subjects with carpal tunnel syndrome, a chronic partial median nerve entrapment at the wrist (CPNE).

Recordings were obtained from the preferred hand of 17 adult subjects with CPNE and 12 healthy subjects. CPNE subjects were diagnosed using nerve conduction studies. With ethical approval and informed consent, surface EMG was recorded from first dorsal interosseous (1DI) muscle and the sensory nerve action potential (SNAP) recorded from the ulnar nerve whilst electrically stimulating the digital nerves of the little finger (2.5 X sensory threshold, 100 µS, 5 Hz). Subjects performed a sustained weak abduction of the index finger against resistance. EMG was rectified. EMG and SNAP were averaged time-locked to the stimulus for 256 sweeps.

Three reflex components may be identified: a short latency spinal component E1, followed by I1 and E2 components (Jenner & Stephens, 1982). In the present study, the size of each reflex component was expressed as % EMG modulation (mean values shown in brackets). The E2 reflex component recorded from 1DI following stimulation of the digital nerves of the little finger was present in 70 % of CPNE compared with 16 % of control subjects. The size of the E2 component recorded from the CPNE (6.9 %) and control subjects (1.4 %) was significantly different (Mann-Whitney test, P < 0.05). In contrast, the size of the E1, I1 components recorded from the CPNE (2.9 %, 3.7 %) and control subjects (5.1 %, 4.2 %) were not significantly different (Mann-Whitney, P > 0.05). There was no significant difference in SNAP size recorded from the ulnar nerve in healthy and CPNE subjects (Mann-Whitney, P > 0.05).

We conclude that the E2 component associated with distant digital nerve stimulation of the little finger seen in subjects with CPNE reflects ‘reorganisation’ within the CNS, resulting from interruption of afferent input to the primary sensory cortex following median nerve entrapment.