Neuropathic pain in the horse:

Some observations and clinical presentations which suggest a rationale for the anatomical displacement (referral) of altered sensations.

Tom J. Ahern BVSc


Horses were examined in an attempt to determine the cause of lameness and altered gait. Following a lack of response to testing for joint and other musculoskeletal abnormalities, the subjects were reexamined for evidence of altered neural sensitivity (neuropathic pain). Hoof pain, similar to idiopathic hand or foot pain in humans, was detected. A possible relationship between hoof pain, altered cervicothoracic cutaneous sensitivities, and previously reported episodes of spinal trauma are discussed.



Pain in the human species is described as anything from a chronic irritative feeling to a peracute excruciatingly uncomfortable sensation, perceived by the affected individual, which he or she then reported as such to a clinician who duly recorded type, intensity, location and duration. In the animal species, such as the horse, verbal communication is not possible. Verbalising in the form of deep groans or grunts are normally only observed in cases of major limb fractures , acute abdominal catastrophes or acute pleuritis. Unlike the human situation the clinician is then responsible for both the detection and assessment of pain. This is achieved by utilising diagnostic tools such as palpation, pain exacerbation (joint flexion or applied lesional pressure), response to systemic analgesia or regional anaesthesia and observations of altered gaits or lameness. Diagnostic machinery is then used in an attempt to identify causative lesions particularly in cases of chronic pain.



The author has in recent years encountered numerous cases (equine) of lameness with concurrent altered regional responses to touch and or pressure, where attempts to define a causative lesion, and or treatment using conventional therapies, were unsuccessful. The altered sensations (pain) were then investigated as possibly having a neuropathologic origin. Positive responses to spinal mobilisation therapies with elimination or reduction of lameness and altered sensations, suggested a neurological basis for many of these cases. A single procedure,Cervical Vertebral Mobilisation Under Anaesthesia (CVMUA) was used in all cases.



Typically, cases of forelimb lameness presented with hyperaesthesia and mechano allodynia of the corium ( the sensitive tissue between the hoof wall and third phalynx / pedal bone) in one or both fore feet. In nearly every case there were cutaneous regions of the neck, shoulders and/or thorax where hyperaesthesia and or mechano allodynia could likewise be demonstrated. Histories of horses pulling back whilst tethered, falling head first in races or rearing and falling backwards were typical. Each incident appeared to have resulted in abnormal pressures being applied to a number of cervicospinal joint complexes with resultant associated trauma. Clinical examinations of the animals by the owners own veterinarian immediately after the incidents most often led to the documentation of minor lacerations and bruising with no other structural trauma being reported. Hypersensitivity of the laminar corium and cutaneous regions of the neck and trunk in some cases developed quite soon after the incident whilst in other cases the onset was more insidious. Unfortunately these neurological anomalies were rarely reported as being significant by the attending veterinarian.



Clinical observation of these animals most often revealed altered behaviour aside from altered gait / lameness .There was most often a reduced willingness to exercise which on occasions progressed to almost complete inactivity. A resentment of handling and physical contact , including that with former equine companions, was often apparent. Affected animals were often seen grazing away from the herd. If approached they would turn away and prepare to kick out at the intruder with their hind feet. When the herd was on the move they would be seen as the widest runner and were thus always in a position to avoid inadvertent contact with others.Their reluctance to run between other horses during competition had also infuriated many a racehorse trainer or punter. To best understand these physical and behavioural adaptations one should consider the following!



Where a specific area of trauma and its associated pain were anatomically intimately associated, as would be the case with a traumatised finger caught in the car door, the individual would most often ably immobilise the digit without necessitating any upper limb, trunk or unaffected limb immobilisation. This was because either motion of, or outside contact with these or other unaffected areas of the body was unlikely to have any direct or indirect affect on healing of the digit. The same situation was not however true of centrally occurring trauma involving the neuraxis, spinal or perispinal (e.g. sympathetic trunks) structures where ambulation, lifting and many other limb movements could result in unwanted pressures being applied to traumatised structures. Likewise being bumped, jostled, jerked or the reverse were likely to further exacerbate existing trauma.



It would appear then that the often anatomically displaced pain states associated with centrally occurring neural trauma were in fact strategically placed to induce voluntary immobilisation which then reduced the opportunity for self exacerbation of this trauma. Idiopathic hand and foot/hoof pain were then seen to be expressions of neuropathic pain, which by virtue of their anatomical position reduced the individuals tendency to perform normal daily duties such as lifting objects and ambulating. Others such as shoulder and upper thoracic pain reduced the individuals propensity towards physical contact with other in motion or motionless individuals or objects which could likewise exacerbate existing trauma. One could also view the often anxious, nervous, sensitive and demur disposition of affected individuals as an indication to others to keep their distance. Centrally existing trauma sites were then ably protected whilst healing occurred.



Therapeutic disappointments were most often experienced when treatment regimes were mistakenly entirely directed towards the areas where referred neuropathic pain was being perceived. Even worse situations occurred when, in the absence of a definitive diagnosis, pain states were ignored and exercise of a heavy or competitive nature was continued.Treatments were most effective when therapeutic regimes dealt with demonstrable reduced spinal joint mobility and associated reduced neural mobility together with states of altered sympathetic tone.



Diagnosis and treatment of any condition was invariably made easier as we better understood its pathogenesis and varied presentations. It was hoped that by observing and investigating neuropathic pain in species other than man, where the psychological element was not a factor, would disperse some of the mystique surrounding these syndromes.


FURTHER READING


1) Ahern T.J., Cervical vertebral mobilisation under anaesthetic (CVMUA),

a physical therapy for the treatment of cervico-spinal pain and stiffness.

J. of Equine Vet. Sci. 1994; 14: 540-545.

2) Ahern T.J., Laminar corial hyperaesthesia in chronic forelimb lameness.

J. of Equine Vet. Sci. 1995; 15: 460-463.

3) Ahern T.J., Reflex sympathetic dystrophy syndrome (RSDS), complex

regional pain syndrome-Type 1 (CRPS 1), neuropathic pain: an equine

perspective. J. of Equine Vet. Sci. 1996; 16: 463-468.

4) Ahern T.J., Spinal mobilisation therapy; with particular reference to cervical

vertebral mobilisation under anaesthetic (CVMUA). In: Pain Management of

Dogs and Horses: Some Alternative Therapies . CVE. Western Australia.

Murdoch University, 1997: 43 -49 .