Neuropathic pain

Abstract

Neuropathic pain is caused by a lesion or disease of the somatosensory system, including peripheral fibres (Aβ, Aδ and C fibres) and central neurons, and affects 7–10% of the general population. Multiple causes of neuropathic pain have been described and its incidence is likely to increase owing to the ageing global population, increased incidence of diabetes mellitus and improved survival from cancer after chemotherapy. Indeed, imbalances between excitatory and inhibitory somatosensory signalling, alterations in ion channels and variability in the way that pain messages are modulated in the central nervous system all have been implicated in neuropathic pain. The burden of chronic neuropathic pain seems to be related to the complexity of neuropathic symptoms, poor outcomes and difficult treatment decisions. Importantly, quality of life is impaired in patients with neuropathic pain owing to increased drug prescriptions and visits to health care providers, as well as the morbidity from the pain itself and the inciting disease. Despite challenges, progress in the understanding of the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, which emphasize the need for a multidisciplinary approach to the management of neuropathic pain.

An update and systematic review on drug therapies for the treatment of refractory chronic cough

“…The overall prevalence of CC is 9.6% [58] which is similar to the prevalence of neuropathic pain in Australia (8.5%) [59] and in Europe (7–8%) [60]. There are, however, wide regional variations ranging from a high of 18.1% in Oceania down to 2.3% in Africa for CC [58].…”

Selective neuronal silencing using synthetic botulinum molecules alleviates chronic pain in mice

“…Differences between animal behavioural tests and human chronic pain features, particularly the assessment of both sensory and affective features of the pain state, as well as measurements of long-term efficacy and species variability may have been confounding factors (6). Nevertheless the successful translation of the substance Psaporin treatment from rats to companion dogs with bone cancer pain suggests (11,14) there is potential for the introduction of botulinum-based silencing approaches for the control of pain without cytotoxicity or recourse to repeated treatment of analgesics that can produce adverse behavioural effects.…”

“…Persistent pain is highly prevalent and extremely difficult to treat (6,7) with widely prescribed drugs such as opioids having significant unwanted side effects (7)(8)(9). While research into developing new analgesic drug therapies has been intense, translating knowledge from preclinical observations in animal models to new therapies in the clinic has been challenging (6). Research into the control of chronic pain states has however identified pathways connecting the spinal cord and brain that are key to the regulation of on-going pain states (10)(11)(12)(13).…”

“…In some cases ongoing disease or the failure of potentiated pain signaling networks to return to pre-injury levels leads to persistent or chronic pain conditions (5). Persistent pain is highly prevalent and extremely difficult to treat (6,7) with widely prescribed drugs such as opioids having significant unwanted side effects (7)(8)(9). While research into developing new analgesic drug therapies has been intense, translating knowledge from preclinical observations in animal models to new therapies in the clinic has been challenging (6).…”

Temporal Kinetics of Microgliosis in the Spinal Dorsal Horn after Peripheral Nerve Injury in Rodents

“…One of the hallmark symptoms is mechanical allodynia (non-nociceptive mechanical stimuli elicit pain), and neuropathic pain is often resistant to currently available therapies. 1) Injury to peripheral nerves of rodents, which are frequently used as models of neuropathic pain, produces mechanical pain hypersensitivity and alterations at molecular and cellular levels that result in multiple forms of neuronal plasticity and structural reorganization, not only in the affected sensory ganglion cell body, but also in the spinal dorsal horn (SDH). 2,3) The peripheral nerve injury (PNI)-induced alterations in the SDH are observed not only in neurons, but also in glial cells, especially microglia, which are known as resident immune cells in the central nervous system (CNS).…”