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Keywords:

  • horse;
  • MUP analysis;
  • muscle;
  • nerve;
  • equine dysautonomia;
  • electrophysiology

Summary

Reasons for performing the study: Clinical evidence of motor neuron involvement in equine grass sickness (EGS) has not been reported.

Hypothesis: Quantitative electromyography (EMG) analysis can elucidate subtle changes of the lower motor neuron system present in horses with EGS, performed ante mortem.

Methods: Fourteen horses diagnosed clinically with acute, subacute or chronic EGS were examined and quantitative EMG performed. Previously published data on healthy horses and horses with proven lower motor neuron disease (LMND) were used as controls. In 8 horses post mortem examination was performed, and in 7 muscle biopsies of the lateral vastus muscle underwent histopathology and morphometry.

Results: Clinical electrophysiological evidence of neuropathy was present in 12 horses. Analysis of data from the first 4 horses resulted in 95% confidence intervals (CI) of nontransformed data for motor unit action potential (MUP) duration in subclavian, triceps and lateral vastus muscle of 11.0–13.7, 14.8–20.3 and 12.2–17.2 msecs, respectively, and for MUP amplitude 291–453, 1026–1892 and 957–1736 μ V, respectively. For number of phases the 95% CI was 3.6–4.4, 2.9–3.6 and 2.9–3.4, respectively, and for number of turns 5.0–6.5, 4.3–5.3 and 3.7–4.6, respectively. No changes in duration of insertional activity were measured. Pathological spontaneous activity was observed in all horses. EGS as evidenced by degenerative changes in the autonomic ganglia in combination with minor degenerative changes of the spinal lower motor neurons was observed on post mortem examination in all 8 available autopsies. In muscle biopsies of 4 out of 7 horses changes consistent with slight neurogenic atrophy were found.

Conclusions and potential relevance: EMG results demonstrated the presence of a neuropathy of skeletal muscles in all horses suspected to have EGS. The combination of clinical and electrophysiological evidence may aid differential diagnosis of neurogenic disease in cases of weight loss and colic.