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NEUROPATHIC PAIN: ARE YOU SEEING IT PAIN MANAGEMENT MORE THAN YOU THINK? (YES) Mark Epstein, DVM, DABVP (C/F), CVPP

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NEUROPATHIC PAIN: ARE YOU SEEING IT PAIN MANAGEMENT MORE THAN YOU THINK? (YES) Mark Epstein, DVM, DABVP (C/F), CVPP NEUROPATHIC PAIN: ARE YOU SEEING IT PAIN MANAGEMENT MORE THAN YOU THINK? (YES) Mark Epstein, DVM, DABVP (C/F), CVPP Neuropathic pain occurs when something has gone terribly wrong with the normal, protective mechanisms of nociception and pain signaling. The International Association for the Study of Pain defines neuropathic pain as “pain caused by a lesion or disease of the somatosensory nervous system” (IASP 1994). The easy part of this definition is “lesion,” because it is something that can be identified via a history of trauma, surgery (for example, severing nerve trunks during amputation), or imaging (for example, central nervous system [CNS] tumor or intervertebral disc herniation). The much more difficult part of this definition has to do with “disease,” because central and peripheral hypersensitization characteristics of neuropathic pain involve biochemical and microanatomical changes below the sensitivity of any conventional imaging to detect. Sustained or intense nociception, and damage to peripheral nerves, alters considerably the dynamic of usual pain machinery, moving it from a physiologic, protective nature to a maladaptive one. The constant or exaggerated presence of inflammatory and bioactive mediators at a peripheral site forms a “sensitizing soup” that creates relentless excitation of afferent nociceptors. This construct, and/or direct nerve damage, can effect a tsunami of excitatory neuropeptides in the dorsal horn of the spinal cord. Normally stubborn NMDA calcium channels are thrown wide open, and the resulting calcium influx into postsynaptic interneurons elicits a cascade of signaling mechanisms involving Protein Kinase C (PKC), nitrous oxide (NO), Substance P, and neurokinase (NK-1) receptors (the expression of the NK-1 receptor appears to also contribute to opioid-induced hyperalgesia and tolerance [Louis et al. 2007]), calcitonin gene-related peptide (CGRP), and more. Not only does the interneuron stay depolarized, but a phenotypic change may be induced where it may not reset. Expression of c-fos, c-jun, and Knox-24 genes transcribe new (probably aberrant) proteins that produce permanent microstructural changes of the neuron. Furthermore, the afferent nociceptor can conduct a signal efferently in an antidromic fashion. There, at the peripheral site of original stimulus, further release of inflammatory mediators is elicited, recruiting and activating other previously innocent bystanding nociceptors, further bombarding the dorsal horn with impulses (ibid.). As the feedback loop persists, more and more cells express c-fos and other genes, nerve growth factor is stimulated into production (suspected to be from glial cells), more interconnections are made between types and locations of neurons in the spinal cord (Doubell et al. 1999), and mere touch can now be perceived as pain. These interconnections are not isolated to somatosensory neurons, for they have been shown to newly express adrenoceptors, which are activated by catecholamines. Sympathetic stimulation may then result in nociception (Baron 2000; Ramer et al. 1999) and may in fact be central to the pathophysiology of some of more intense, refractory forms of neuropathic pain known as complex regional pain syndrome. Moreover, neuropathic pain is associated with alterations in receptor location (more places on more axons) and sensitivity to excitatory amino acids (greater) throughout the nervous system (Devor et al. 1993). Glial cells (astrocytes, microglia, oligodendrocytes) in the spinal cord, whose purpose was once thought to be merely structural and macrophage-like in nature (providing synaptic architecture, host defense, and myelin, respectively), are now known to be also highly integrated into the pain process, particularly with regard to chronic and neuropathic pain (Watkins et al. 2001). Recently described is the tetrapartite synapse, which includes an astrocyte, microglial cell, and the pre- and postsynaptic neuronal terminal (De Leo et al. 2006). Glia are the predominate source of nerve growth factor, and a recently isolated chemokine, fractalkine, appears to be a neuron- glial cell signal, activating glially dependent pain (Shan 2007). Indeed, the glia appears to play a primary role with regards to synaptic strength, plasticity, and sensitization in the spinal cord, which exhibits substantial change under the influence of chronic or intense pain (Honore et al. 2000). The result of all this is reduced firing thresholds, upregulation of central neuronal activity, downregulation of inhibitory activity, expansion of the receptive field, peripheral hypersensitivity, and intensified pain responses to further stimulation (Giordano 2006). In short, it is a neurologic natural disaster. Eventually, as the process of pain has become located centrally (in the spinal cord) rather than at the site of the original stimulus, the pain is said to be “neuropathic” in origin. Once neural pathways are thus sensitized, the physiologic (and physical) responses to pain may persist, even when the peripheral nerves themselves are blocked (or even transected) (Lascelles et al. 1998). Clearly, at this point, pain has become a disease itself: Pain is created either without the presence of a noxious stimulation, or far out of proportion to it. Be aware: The progression to neuropathic pain does not necessarily result from chronic pain conditions. In some cases, a patient can move toward a neuropathic state within a matter of minutes to hours of experiencing tissue damage. How do we know if a patient has neuropathic pain? It is not easy. Two main clinical features are hyperalgesia, when a noxious stimulus is more painful that it should be, and allodynia, when a normally nonnoxious stimulus (e.g., touch) is painful. In humans, patients are considered to have neuropathic pain if they fulfill five of the following eight criteria (Geber et al. 2009; Treede et al. 2008): 1. History consistent with nerve injury 2. Pain in the absence of ongoing tissue damage 3. Pain plus sensory deficit 4. Pain characterized as burning, pulsing, shooting, or stabbing 5. Paroxysmal or spontaneous pain 6. Associated dysthesias (e.g., tingling) 7. Allodynia, hyperpathia, hyperalgesia 8. Associated autonomic features (edema, vasodilation/constriction) In humans, these criteria are divined through history, physical examination, and semiquantitative dynamic testing (feather brushing, von Frey devices, touching with hot or cold objects), necessarily involving patient self-reporting as well as observer evaluation. Two scoring systems in common use are the Neuropathic Pain Scale (NPS) and the Leeds Assessment of Neuropathic Signs and Systems (LANSS). In veterinary medicine, in the obvious absence of self-reporting, we can rely only upon observer evaluation. Adapting from the human scheme, Karol Mathews proposed in her excellent review paper of neuropathic pain the following qualitative criteria in animals (Mathews 2008): For hyperalgesia, stimuli that would be uncomfortable for normal patients is observably painful in a neuropathic state. It is suggested that a “normal” area be tested in the affected patient, against which testing the suspected neuropathic region can be compared (clipping hair may be required). For allodynia, stimuli that a normal animal would sense but not consider painful at all is observably painful. Hyperalgesia Allodynia Manual pinprick Manual light pressure or sharpened wooden stick Light pressure Stroking w/ brush, gauze, cotton applicator Thermal cold (acetone, cold metal 0°C) Thermal cold (objects at 20°C) Thermal heat (object at 46°C) Thermal warm (objects at 40°C) Two studies have looked at the prevalence of pain and neuropathic pain in veterinary patients, one in an outpatient population and one in an emergency / critical-care setting. For outpatient dogs and cats, pain was present in 20% and 14% of patients, respectively, and neuropathic pain was present in 7% to 8% of both species (Muir et al. 2004). In the emergency setting, pain was present in over 50% of both patient populations, and neuropathic pain was present in 9% of dogs and 3% of cats (Wiese et al. 2005). Human medicine has identified a number of quintessentially neuropathic pain syndromes. In animals, it is axiomatic that any trauma or surgery can result in the creation of neuropathic pain, with the possibility increasing proportionate to the degree of tissue and especially nerve damage. Examination of the literature supports neuropathic pain in the following conditions in animals: • Postamputation: While postamputation pain is very common in humans, only one case report exists in a cat (O’Hagan 2006). Yet most clinicians with experience in onchyectomy can probably report the occasional patient (especially in years past when regrettably little thought was given to perioperative pain management) who continues to be lame many months postsurgically; these can be suspected to be cases of postamputation neuropathic pain. Postamputation neuropathic pain is an area ripe for investigation in veterinary medicine. • Spinal cord lesions: Syringomyelia, an inherited defect of the CNS common to the Cavalier King Charles Spaniel, is described with classic neuropathic pain (Rusbridge and Jeffery 2008). It is well established in humans that the far more common CNS lesions, such as intervertebral disc disease, lumbosacral stenosis, fibrocartilagenous emboli, tumors, and so on, elicit neuropathic pain, but the literature is currently lacking in animals. This makes it another area ripe for investigation in veterinary medicine.
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