Headshaking in horses: possible aetiopathogenesis suggested by the results of diagnostic tests and several treatment regimes used in 20 cases.

Twenty mature horses with typical headshaking of 2 week-7 year duration were studied. Clinical examinations included radiography of the head and nasopharyngeal endoscopy. All were assessed at rest and at exercise, both before and after fitting an occlusive nasal mask, application of tinted contact lenses and the perineural anaesthesia of the infraorbital and posterior ethmoidal branches of the trigeminal nerve. Infraorbital anaesthesia had no effect in 6/7 cases but 11/17 (65%) cases showed a 90-100% improvement following posterior ethmoidal nerve anaesthesia. Tinted contact lenses had no apparent long-term benefit, although 2 cases showed a transient improvement. We found no other evidence to suggest a photic aetiology in the current series of cases. Treatment regimens based on the results of the diagnostic investigative methods included sclerosis of the posterior ethmoidal branch of the trigeminal nerve. This was effective in some cases but the benefits were temporary. Cyproheptadine alone was ineffective but the addition of carbamazepine resulted in 80-100% improvement in 80% of cases. Carbemazepine alone was effective in 88% of cases but results were unpredictable at predefined dose rates. The positive response to carbamazepine, combined with the clinical features is consistent with involvement of the trigeminal nerve, particularly the more proximal branches such as the posterior ethmoidal nerve. Headshaking has some clinical features in common with trigeminal neuralgia in humans. As a result of the findings detailed in this paper, we conclude that a trigeminal neuritis or neuralgia may be the basis of the underlying aetiopathology of equine headshaking. Initial observations of the positive response of headshakers to carbamazepine therapy is encouraging. However, future studies will include a more detailed investigation of dosages, duration of effectiveness (in some cases it appears short-lived) and other effects. In practice there is a realistic possibility of controlling but not curing headshaking with carbamazepine therapy at the present time. Other future investigations will include details of the functional anatomy of the trigeminal nerve and the role of the P2 myelin protein in headshaking and other neurological disease.