Clinical Commentary Electrical nerve stimulation for the management of equine trigeminal mediated headshaking K. J. Pickles Chine House Veterinary Hospital, Sileby, Leicestershire, UK. Corresponding author email: kpickles@chinehousevets.co.uk Keywords: horse; headshaking; idiopathic; trigeminal; neurology Previously termed idiopathic headshaking, it is now widely accepted that trigeminal-mediated headshaking (TMHS) is a more accurate term with clinical signs of TMHS considered to reflect trigeminal neuropathic pain (Pickles et al. 2014; Roberts 2014). Although involvement of the trigeminal nerve had long been suspected in the aetiology of TMHS due to the presenting clinical signs (Williams 1897, 1899), a reduced threshold of activation of the maxillary branch of the trigeminal nerve in headshaking horses compared with control horses has only been recently definitively confirmed (Aleman et al. 2013, 2014). These elegant nerve conduction studies, the seasonality of clinical signs in many headshaking horses and absence of gross or histopathological lesions in the trigeminal nerves and ganglia from headshaking horses (Newton 2001; Aleman et al. 2013; Roberts et al. 2017) are suggestive of a functional rather than structural nerve disorder, although this requires further validation. In further support of this hypothesis is the finding that the activation threshold of the trigeminal nerve in a horse with seasonal TMHS tested during a time of remission showed a threshold for activation similar to control horses (Aleman et al. 2014). Unfortunately this horse was not tested during seasonal exacerbation of headshaking signs, which would appear to be the next logical step in elucidating any seasonal malleability of the activation threshold of the trigeminal nerve. The cause of the aberrant trigeminal nerve activity (‘hypersensitivity’) in equine TMHS remains frustratingly elusive. Despite its predilection for latency in the trigeminal ganglion, equine herpesvirus-1 does not appear to be involved in the pathogenesis of TMHS (Aleman et al. 2012). Some clinical similarities appear to exist between TMHS and human trigeminal neuralgia (HTN), a debilitating cause of facial pain in people, which is described by sufferers as intermittent or continuous burning, itching, tingling, or electric-like pain in an area innervated by the trigeminal nerve (Nurmikko and Eldridge 2001). These same descriptions are often used by owners when recounting their horse’s headshaking behaviour. However, the majority of HTN patients have unilateral focal compression and demyelination of the trigeminal nerve root entry zone (Devor et al. 2002) with resultant ipsilateral (only) clinical signs (Nurmikko and Eldridge 2001). Neither demyelination injury (Newton 2001; Aleman et al. 2013; Roberts et al. 2017), nor the reduced conduction velocity (Aleman et al. 2014) which would be caused by such lesions, have been found in trigeminal nerve studies of headshaking horses. How or why some horses enter spontaneous remission of TMHS, which may last from weeks to years, is unknown. Long-term remission appears uncommon with only 5% of 109 headshaking horses reported to cease TMHS for more than one year (Madigan and Bell 2001). As headshaking horses can go into spontaneous remission (albeit rarely), some after many years of TMHS, it suggests reversibility of the trigeminal nerve hypersensitivity is possible. This offers the tantalising prospect of manipulation of the threshold activation as the Holy Grail of a true treatment, rather than just a management strategy, for TMHS. Electrical nerve stimulation is the therapeutic alteration of activity in the central, peripheral, or autonomic nervous systems by transcutaneous or implanted electrical devices. Two such therapies, percutaneous electrical nerve stimulation (PENS) and electroacupuncture, have recently been reported as successful in the management of TMHS in some horses (Roberts et al. 2016; Devereux 2017). These are a welcome addition to the armoury of TMHS treatments and appear to offer a more rational approach than prior mechanical or pharmacological treatments which did not address the underlying aberrant neurophysiology. Whilst these therapies do appear to show promise, cited remission times post-treatment of horses with seasonal TMHS such as those by Devereux (2017) should be interpreted with caution when they overlap with times of year when the horse would be expected to enter seasonal remission. Therapeutic application of electricity for pain dates back thousands of years since ancient Egyptians utilised electric fish to provide pain relief (Heidland et al. 2013). Following widespread use in the 19th Century, electrotherapy fell out of favour until publication of the gate control theory of pain by Melzack and Wall (1965) led to a resurgence of interest in neurostimulation. This gate control theory is also the science that underpins the common parental response of rubbing a sore area on a child. Melzack and Wall (1965) reported that the substantia gelatinosa in the dorsal horn of the spinal cord acts as a gate control system, which modulates the synaptic transmission of nerve impulses from peripheral fibres to the central nervous system. Small nociceptive A-d and C fibres hold the ‘gate’ in an open position, while stimulation of large mechanoreceptive A-b fibres by touch, pressure or vibration close the ‘gate’ and inhibit pain transmission to the brain. Small nociceptive fibres have a higher activation threshold than larger mechanoreceptive fibres such that selective low level stimulation of mechanoreceptors can prevent or reduce pain transmission. Activation of these large A-b fibres recruits inhibitory interneurons within the substantia gelatinosa of the spinal cord which exert their inhibitory action on both large and small diameter fibres synapsing higher up the spinal cord. Additionally, activation of the descending inhibitory pathway, © 2017 EVJ Ltd 1 EQUINE VETERINARY EDUCATION Equine vet. Educ. (2017)  () - doi: 10.1111/eve.12800