Abstract

Equine trigeminal-mediated headshaking (TMHS) is the most frequent chronic idiopathic craniofacial pain syndrome of the horse. While a reduced trigeminal activation threshold is well documented, the upstream driver has remained elusive, and no single pathomechanism explains the characteristic features of the syndrome: predominance in geldings, middle-age onset, marked exacerbation under ridden work, and triggering by light, wind, pollen or tack. We propose an integrated three-mechanism model: (1) trapezius-driven central sensitisation of the trigeminocervical complex (TCC; subnucleus caudalis, Vc, and upper cervical dorsal horns C1–C3), in which chronic myofascial overload of the trapezius generates a persistent nociceptive barrage via the accessory nerve and cervical dorsal rami that induces microglial activation and p38 MAPK-dependent signalling in Vc; (2) ganglionar amplification through upregulation of voltage-gated sodium channels Nav1.7 and Nav1.8, sustained by satellite glial cell coupling via connexin-43 gap junctions; and (3) peripheral Piezo2-mediated mechanotransduction as a sensitisation-dependent depolarisation mechanism in V2 afferents. Kiyomoto and colleagues showed that unilateral trapezius inflammation induces microglial activation, p38 phosphorylation, WDR neuron hyperexcitability and ectopic facial allodynia in the rat Vc, all reversed by the p38 inhibitor SB203580, supplying the mechanistic keystone. Six independently falsifiable hypotheses are stated. Together these mechanisms form a self-reinforcing cascade in which a peripheral myofascial driver primes a central amplifier sustained at ganglionar and peripheral transducer levels. The framework explains observations that single-pathway accounts cannot, generates testable predictions, and opens rational routes to prevention, phenotyping and disease-modifying treatment.

Key words: Central sensitisation; Headshaking; Horse; Trapezius; Trigeminocervical complex.