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Management of neuropathic pain
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The International Association for the Study of Pain [IASP] states that neuropathic pain is “pain caused by a lesion or disease of the somatosensory system” and it may be further categorized as central or peripheral. A Neuropathic pain is a descriptive term, and a diagnosis requires that a lesion in the somatosensory nervous system can be demonstrated (e.g., Magnetic resonance imaging [MRI], neurophysiologic testing, histologic methods post-mortem). Neuropathic pain is termed maladaptive as it serves no biologic function (i.e., it neither protects nor supports healing and repair). People describe the pain related to nerve damages as shooting, burning, tingling or prickling. It is also characterized by hypersensitivity to stimuli (hyperalgesia) and abnormal responses to normally non-noxious stimuli (allodynia). Neuropathic pain is difficult to diagnose in animals because they cannot self-report and is often assumed to be present by a process of elimination (e.g., inflammatory pain) and based on behaviours, response to stimuli including touch and electrodiagnostic (sensory nerve action and somatosensory evoked potential testing).1 In some cases, non-response to traditional analgesics raises the possibility of an underlying neuropathic cause.
Neuropathic pain is implicated in several equine conditions including head shaking (trigeminal nerve involvement),1,2 dangerous behaviours secondary to ganglioneuritis,3 post-operative neuropathy,4 laminitis, navicular disease5 and osteoarthritis.6
Treating neuropathic pain is challenging in all species including humans. The most common drugs used include antiepileptic drugs (e.g., gabapentin, pregabalin, phenobarbital, carbamazepine), nonsteroidal anti-inflammatory drugs, corticosteroids, N-methyl-D-aspartate [NMDA] receptor antagonists (e.g., amantadine, ketamine, magnesium sulphate), sodium and calcium channel blockers, tricyclic antidepressants and drugs that alter serotonin release or uptake.
In horses with naturally occurring laminitis, tramadol provided limited pain relief, but the addition of ketamine at sub-anaesthetic doses significantly improved objective measures of pain such as forelimb loading.7 Gabapentin was used successfully to treat pain associated with post-anaesthetic neuropathy in a mare4 and in a horse with temporohyoid osteoarthropathy.8 Some horses with “headshaking” showed a positive response to carbamazepine but several dosing regimens may need to be tested before a response is observed.9 Magnesium sulphate acts at NMDA receptors and was successful in decreasing headshaking behaviours in a small clinical study.10
Neuropathic pain is likely underdiagnosed in horses, involves complex changes in the somatosensory nervous system and has a negative impact on quality of life. Treatment options are limited and there are no authorized equine specific drugs. Treatment responses are variable, and “trial and error” may be required to find a drug that an individual horse will respond to. In the face of treatment failure, euthanasia is often chosen. There is a clear need for more studies into neuropathic pain in horses and reliable treatment options.
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