Systemic adverse effects, therefore, are problematic when pharmacologically managing NeP via the oral route. The success, however, of oral medications in NeP has been limited by systemic side effects. The International Association for the Study of Pain also published evidence-based recommendations for the pharmacologic management of NeP: first-line recommendations are tricyclic antidepressants, gabapentin and pregabalin, and topical lidocaine, while opioid analgesics, tramadol, certain antiepileptics, and topical capsaicin are chosen based on individual patient tolerability and comorbidities. The Canadian Pain Society published evidence-based guidelines for the pharmacologic management of NeP. Little evidence for these management options has been published in the literature. Nonpharmacologic management includes: exercise, transcutaneous electrical nerve stimulation (TENS), percutaneous electrical nerve stimulation (PENS), graded motor imagery, cognitive behavioural therapy, and supportive psychotherapy. Complex regional pain syndrome is also an example of NeP.ĭevelopment of effective therapies is in its infancy. Polyneuropathies include diabetic and HIV neuropathies. Peripheral mononeuropathies include postherpetic neuralgia, radiculopathy, and carpal tunnel syndrome. Central neuropathic pain includes poststroke pain, below-level pain after spinal cord injury, pain in multiple sclerosis and phantom limb pain. The underlying causes of NeP may also be divided into central and peripheral causes. NMDA receptors are involved in sensory input at the level of the spinal cord, thalamus, limbic system, and cerebral cortex. Thirdly, activation of N-methyl-D-aspartate (NMDA) receptors lowers the threshold for nerve transduction, as well as facilitates synaptic transmissions. In addition, descending pathways are ‘disinhibited’ by lower levels of inhibitory transmitters, such as GABA and glycine, in spinal cord dorsal horn neurons. For example, molecular changes in central neurons enhance the response in pain transmission neurons. Īt the central level, sensitization of dorsal horn neurons can be induced by amplified and facilitated activity from peripheral nociceptors. Gene transcription is altered in dorsal root ganglia, sodium channels are upregulated and calcium channels are altered to produce allodynia. In addition, neuromas form on adjacent, uninjured nerves, leading to mechanosensitivity and expanded receptive fields. Other receptors and release of neurotransmitters, such as substance P, are also altered post-inflammation. Abnormally expressed sodium channels in C fibre nociceptors result in spontaneous ectopic activity. Īt the peripheral level, hypersensitivity is postulated to be secondary to post-nerve injury and inflammation results in the sensitization of nociceptors through alteration of sodium channel distribution and function. NeP can develop from dysfunction at any one or more of these levels. The pain pathway involves the peripheral nerves, spinal cord, and the brain. The pathophysiology of NeP is incompletely understood, however, many mechanisms have been put forth in the literature. In addition, NeP impairs partici-pants’ mood, quality of life, activities of daily living, and performance at work. Symptoms are usually quite severe and may become chronic. And the tendency is the prevalence of NeP will increase with the aging of population, because several NeP syndromes such as painful diabetic neuropathy are more common in the elderly.Ĭlinical features of NeP include allodynia, hyperalgesia, numbness, weakness, and spontaneous pain that is burning, shooting, or shock-like. The Canadian Pain Society (CPS) has suggested that up to one million Canadians may have NeP. An estimate of the prevalence of chronic NeP in the general population is 8.2%. NeP, therefore, is a possible outcome from a wide variety of central and peripheral nerve disorders. Accessed April15, 2021.Neuropathic pain (NeP), as defined by the International Association for the Study of Pain (IASP), is a result of a primary lesion or dysfunction of the nervous system. UK: National Institute for Health and Care Excellence 2013. Neuropathic pain: the pharmacological management of neuropathic pain in adults in non-specialist settings. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Recommendations for the pharmacological management of neuropathic pain: an overview and literature update. Neuropathic pain: mechanisms and their clinical implications. The effect of opioid therapy on endocrine function.
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