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

Twenty mature horses with typical headshaking of 2 week-7 year duration wer e studied. Clinical examinations included radiography of the head and nasop haryngeal endoscopy. All were assessed at rest and at exercise, both before and after fitting an occlusive nasal mask, application of tinted contact l enses and the perineural anaesthesia of the infraorbital and posterior ethm oidal branches of the trigeminal nerve. Infraorbital anaesthesia had no eff ect in 6/7 cases but 11/17 (65%) cases showed a 90-100% improvement followi ng posterior ethmoidal nerve anaesthesia. Tinted contact lenses had no appa rent long-term benefit, although 2 cases showed a transient improvement. We found no other evidence to suggest a photic aetiology in the current serie s of cases. Treatment regimens based on the results of the diagnostic inves tigative methods included sclerosis of the posterior ethmoidal branch of th e trigeminal nerve. This was effective in some cases but the benefits were temporary. Cyproheptadine alone was ineffective but the addition of carbama zepine 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 clin ical features is consistent with involvement of the trigeminal nerve, parti cularly 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, f uture studies will include a more detailed investigation of dosages, durati on of effectiveness (in some cases it appears short-lived) and other effect s. In practice there is a realistic possibility of controlling but not curi ng headshaking with carbamazepine therapy at the present time. Other future investigations will include details of the functional anatomy of the trige minal nerve and the role of the P2 myelin protein in headshaking and other neurological disease.