By Tom Ahern, BVSc, MRCVS
Have you ever had any of the following problems with your horse?
- an instructor or judge tell you your horse is stiff through the shoulders, ewe-necked, not coming through from behind, not bending one way or the other?
- a lameness that seems to be in one front leg one day and the other the next?
- a lameness that doesn't respond to anti-inflammatory medication e.g. bute?
- a horse that suffers from an intermittent undiagnosed (despite lameness work ups / x-rays, scans) forelimb lameness?
- a horse that goes lame in front every time its hooves are trimmed, no matter how carefully/ appropriately?
- a horse that is ‘poll shy', girth shy, cold backed?
- a sensitive to touch, groom, mane-pull horse?
- a ‘Jekyll & Hyde' horse, relaxed and supple one day and uptight and stiff the next?
- a horse that hates trotting?
- a horse that no matter how much care you take still gets laminitis at the drop of a hat?
- a horse that attacks/ bites its own legs or tendons?
- and more?!
If you brought your concerns to the attention of a practitioner, what process would be followed?
Initially there would be a consultation followed by adjunctive tests and treatment if applicable. The first stage of the consultation process involves the collection of a history from you or the rider/ trainer, which could include statements similar to those above.
Next he or she would perform a clinical examination. After this a list of possible or ‘differential diagnoses' would be compiled. Further investigations including laboratory and machine diagnostics may then be recommended to eliminate some of these possibilities so that hopefully a final or definitive diagnosis could be reached. Appropriate treatment if indicated would then be instituted.
When presented with the situations mentioned above, one of the conditions on that list of ‘possible diagnoses' should be Neuropathic Pain (NP). Why? To answer that question we first need to understand how neuropathic pain differs from other forms of pain and how it presents clinically.
What Is Pain?
Pain is of course by definition an uncomfortable and/ or distressing sensation. Why then does it exist? Pain is both an indicator of tissue trauma and also a built-in warning system. For example, a stomach ulcer produces a pain over the stomach so that we stop eating. A sprained wrist leads to pain in the wrist and consequently we are unlikely to lift a water bucket. Pain prevents us from doing more harm to already traumatised tissues. If we elect to treat the pain only, with no concern for the trauma, then we may well be ignoring that ‘warning'.
Somatic pain (SP):
Most of the normal everyday pain that we deal with occurs as a result of trauma to joints, tendons, ligaments, muscles, skin (cuts/ splinters) etc. This normal or somatic pain (SP) is triggered when some of the chemicals that are produced by the body as part of an inflammatory process within the traumatised tissues stimulate local pain receptors. To reduce this pain we can medically block or slow the production of these triggering chemicals whilst natural healing proceeds. This blocking can be achieved by the administration or application of anti-inflammatory medications which may be naturopathic or proprietary. Cortisones or NSAIDs (non-steroidal anti-inflammatory drugs) are the most commonly used proprietary medications.
Two very important characteristics of SP are:
The pain is always perceived locally (within the traumatised tissues).
The pain is most often triggered by ‘inflammation' and therefore should respond to anti-inflammatory medication.
Neuropathic pain (NP):
Then what about NP? NP, like other types of pain, acts as a warning signal. NP however occurs specifically in response to abnormal pressures being applied to neural or nerve tissues. This pressure may be applied laterally (compression) or longitudinally (tension).
Nerves, including our spinal cord, are elastic structures which must be free to stretch and recoil when required. These actions permit the nervous system to adapt to changes in body posture and movement. For our bodies to move or be mobile the nervous system must be able to move with it. If the ability of the nervous system to move is impeded (which is often referred to in terms of reductions in ‘range of movement' or ROM), then accordingly our body's (limbs and torso) ROM will likewise be reduced. If the compression or tension is continuous then the associated NP will also be. If the tension or compression is positional then pain will also be positional and NP will therefore be intermittent according to body position.
Where Does Pain Originate?
NP is not triggered by inflammation and is therefore not responsive to anti-inflammatory medications. This is one distinct variation from SP, and there is another: NP is also a 'referred' pain. Pains that emanate from the chest and abdominal cavities are classed as referred pains. This means that unlike SP, where the pain is felt within the traumatised tissues, these pains are perceived in areas and tissues other than those directly involved.
For example, cardiac or heart pain is perceived inside the left arm and in the superficial muscles and skin over the area of the heart. For this reason both patients and clinicians can be perplexed as to the origins of the presenting pain. A pain or altered sensation in the sole of the foot can indicate compression at the beginning of the sciatic nerve some 60 cm away. Shoulder pain can result from a compressive lesion in the upper thorax (chest) or neck region. NP is also not transmitted via special pain receptors (nociceptors) as is the case with SP.
Distinguishing Features of NP
NP is perceived when normal pressure/ stretch receptors (mechanoreceptors) become ‘hyperactivated'. Thermal or temperature receptors can also become overreactive. In the areas (e.g. skin, muscles, ligaments, tendons, corial laminae) where these normal receptors have become hyperactive, there will be an accordingly overreactive response to pressure. E.g. when you apply normal saddle / rider pressure to some horses' backs (dorsal thoracic regions) they will over-react/ drop! When you apply pressure to the poll through a halter and lead some horses will pull back violently. This could indicate that some of the normal pressure receptors in these areas have become hyper-reactive. We describe these areas as being ‘hyperaesthetic', not poll shy or cold backed.
Thus three important distinguishing features of NP are:
Pain is always referred. It may be referred to tissues close to the site of compression or tension or to tissues at quite some distance from this site.
NP is not produced as a direct result of an inflammatory process and is therefore unlikely to respond directly to anti-inflammatory medication.
NP presents most commonly as being an area of the animal's body where normal responses to touch and pressure are exaggerated. These are unfortunately not uncommon. Exaggerated thermoreceptor (temperature) responses have been described by human sufferers as searing or burning sensations. Animals cannot of course communicate the latter sensations. It would not seem unreasonable to assume that if these sensations were ‘unrelenting' that the animal may in desperation physically attack or bite at the area involved in an attempt to rid itself of the pain!
Triggers of NP
Most of the NP that we encounter in practise is intermittent. In these instances NP is only perceived whilst the altered receptors are being stimulated in sufficient numbers. Pressure can be applied to these activated receptors in four different ways.
Internal pressures or ‘tension' - When a horse tenses, the pressures created within the tissues will trigger mechanoreceptors. If these mechanoreceptors are hypersensitised then NP can occur. Tension could be due to the anticipation of pain that might occur during an event, in response to first seeing the saddle if a horse is ‘sensitive backed', or in response to a sudden noise or movement. Loud, rough handlers as opposed to quiet, gentle persons are more likely to make the horse tense and trigger NP.
Positional pressures - These are applied when the torso is asked to turn sharply (left or right), to under flex or collect, to lift shoulders and extend. NP horses often work normally and in a relaxed willing manner through their available ROM. However when asked to do a ‘little more', thus attempting to use ROM which is no longer available, positional or ‘proprioceptive' mechanoreceptors that are hypersensitised can be triggered. The horse's response is usually quick and direct, e.g. head tossed in the air or back humped warning of a pending ‘buck' or if asked to jump too high, a ‘refusal'.
External pressures -
(a) Tack - bridles, girths and saddles (including ill-fitting) applied over areas of hyperaesthetic tissues (girth, poll, withers, under saddle and flanks).
(b) People - bumpy/ poor riding. A farrier's knife getting a little close to hyperaesthetic corial tissues. A ‘rough' handler. Mane pulling, grooming.
(c) The working surface. If a horse has NP of the hooves (laminar corial hyperaesthesia) then contact with a hard surface as opposed to soft will be more likely to trigger NP. In contrast, working on very soft slippery surfaces can result in sudden changes of head/ neck/ limb position which can also trigger NP, but this time in upper body positional receptors. A firm/ giving surface is less likely to stimulate either receptors.
Systemic pressures - These can be induced by:
(a) The anticipation of pending discomfort prior to a show or event.
(b) Increases in circulating toxins during periods of ill health. Both these circumstances (stresses) can lead to increases in adrenal output, which include norepinephrine, itself a recognised NP trigger in tissues where altered receptors are present. This means that these events could either trigger or exasperate existing levels of NP. A ‘vicious circle' - anxiety triggering pain, this pain triggering further anxiety, triggering more pain ..... and so on ... can ensue!
When does NP occur?
As with SP, NP occurs initially in response to trauma. However, in the case of NP the trauma involves neural or nerve tissues.
This more often occurs when a horse falls, pulls back, is cast, or suffers other traumatic events when, in particular, spinal joints are strained or damaged. Unfortunately these events have often occurred many years before the horse is presented to a practitioner or therapist, sometimes as a foal or weanling.
Remove the triggers - Rectification of the triggers such as ill-fitting saddle and tack, poor riding/ handling, working conditions, toxins, stressors, etc. should be your first line of treatment.
Medication - A number of drugs are being investigated to ascertain their potential for use in patients where NP is a problem, though it will be some time before these come on the market.
Surgery - There are also some cases where surgical intervention is indicated (intervertebral disc or sympathetic ganglionic procedures).
Physical therapies - Presently most treatments for NP come under the banner of ‘physical therapies'. There are many forms of physical therapies that can be used to treat NP. We will split these into three categories dictated by their general approach and mode of action.
Relaxation techniques - The first and often least invasive are the approaches that seek to relax the horse internally. Touch therapies and owner/ horse relaxation education are examples of these. Some ‘natural medications', aromas and proprietary tranquillisers are also used.
Pain relief techniques - These therapists in most cases attempt to desensitise the areas that are hypersensitive by using different forms of constant stimulation. The basic concept is to fatigue the activated receptors so that they send a lesser or normal rather than exaggerated signal to the brain. Whilst pain is relieved, ROM of affected tissues can be restored either with voluntary movements (active motion therapy) or with the aid of a therapist using natural stretch therapies (passive motion therapy). These stretch therapies include under saddle (rider) relax and stretch training. Acupuncture, trigger point therapy, massage therapy and machine therapies such as magnetic field and TENS are some examples of this approach to treatment.
Mobilisation techniques - The more direct forms of treatment are those that attempt to directly mobilise the structures and tissues that have ‘acquired post injury' reduced ROM (stiffness). The affected nerves are those which course through these tissues. Manipulative and mobilisation procedures are the main forms of treatment. The animal may or may not be sedated during attempts to mobilise or manipulate tissues in the standing animal. In particular circumstances, e.g. long standing lower cervical (neck) stiffness or loss of ROM, treatments under anaesthetic are usually more successful. This procedure is referred to as a CVMUA (Cervical Vertebral Mobilisation Under Anaesthetic).
How do I know if the treatment is helping my horse?
There are three markers which are the best indicators of improvement.
A decrease or elimination of areas of altered sensation - No longer poll shy, cold backed, or objecting to grooming; not biting when girthed; not lame after farrier; etc.
ROM improved or restored - Performance under saddle (e.g. stride length, collection, lateral work) improved, or complete and even.
Horse's general attitude - With NP, horses can be uptight, unpredictable, depressed. Without they are relaxed, bright, willing, and predictable.
Hopefully you are now starting to fit the pieces together and are beginning to understand the fundamentals of NP. Remember a sensitive horse is not necessarily a ‘touchy' horse but may well be a ‘hyperaesthetic' horse. Also be aware that quite often several forms of therapy can be combined to improve your chances of success in reducing or eliminating NP in your horse.