Objective: To explore the clinical and electrophysiological characteristics of sensory neuron disease (SND).
Methods: The clinical and electrophysiological characteristics were analyzed from November 2007 to November 2012 in 57 patients with sensory neuron disease and another 95 with sensory polyneuropathy. Nerve conduction studies of median nerve, ulnar nerve, tibial nerve, peroneal nerve and sural nerve and electromyogram (EMG) of bulbar, cervical, thoracic and lumbosacral region, somatosensory evoked potential (SEP) and contact heat evoked potential (CHEP) were performed.
Results: The amplitude of sensory nerve action potential (SNAP) decreased in 50 SND patients and disappeared in another 7. The parameters of SEP and CHEP were abnormal. The amplitude of SNAP was lower in median and ulnar nerve than in sural nerve ((0.6 ± 0.2) µV, (0.7 ± 0.2) µV vs (1.5 ± 0.5) µV; t = 2.42, 2.38; P < 0.05). The latencies of SEPs were longer in SND patients than in those with sensory polyneuropathy (t = 1.99, 1.99, 2.00, 2.07, 1.99; 1.98, 1.99, 2.02, 1.98, 1.99; P < 0.05).Comparing with those with sensory polyneuropathy, the latencies of CHEP were longer in SND patients when the stimuli was applied at hand dorsum, proximal volar forearm and anticus tibialis (t = 2.01, 2.00, 2.02; P < 0.05). No difference existed in latencies between 2 groups when the stimuli was at the levels of C7 and T12 (t = 0.97, 0.68; P > 0.05).
Conclusion: Sensory neuron diseases usually present with sensory symptoms and ataxia. The amplitude of SNAP decreases or disappears especially in upper extremities. Both SEP and CHEP are abnormal.
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