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Excerpt
Neuropathic pain is defined as ‘pain initiated or caused by a primary lesion or dysfunction in the nervous system’ [1]. It can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease (e.g. diabetes mellitus, herpes zoster, HIV) or due to neuroma formation (amputation, nerve transaction, trauma) or nerve compression (e.g. tumours, entrapment, nerve crush) [2]. Central pain syndromes, on the other hand, result from damage to different regions of the brain or the spinal cord. Despite these disparate causes, the symptoms of neuropathic pain, although broad, invariably include spontaneous pain, tactile allodynia, hyperalgesia and sensory deficits.
Spontaneous pain can be either continuous or paroxysmal and is often characterized as a persistent ongoing pain localized within the innervation area of the lesioned nerve/nerve root. It is often described as 'cramping, burning or stabbing' (continuous) or as a 'shooting electric pulse-like' pain (paroxysmal).
Allodynia is the perception of pain to a stimulus, which, under normal conditions, does not provoke pain. Since allodynia is largely mediated by the peripheral activation of large diameter, low threshold Aβ fibres, gentle brushing of the skin or even contact with clothes can evoke intense pain in these patients. Hyperalgesia, on the other hand, is a term used to describe an exaggerated response to a noxious stimulus, far beyond that of a normal response. Hyperalgesia therefore reflects an increased pain sensitivity to suprathreshold stimulation. Thus, hyperalgesia represents a mere quantitative change, whilst allodynia represents a qualitative change in the perception of pain.
Rather paradoxically, another feature of neuropathic pain states is sensory deficit, which results from a partial or complete loss of afferent inputs. Hence patients can often suffer sensory loss, whilst at the same time exhibit certain hyperphenomena such as allodynia or hyperalgesia in a neighboring region. Neuropathic pain syndromes differ extensively between individuals and the symptoms outlined above can occur either singly, or in various combinations. Furthermore, the quality of the neuropathic pain sensation may also differ from that of a normal pain sensation. The existence of multiple kinds of abnormal pain sensations in neuropathic patients suggests that more than one mechanism underlies this clinical condition.
Earlier models of neuropathic pain involved total hindpaw denervation including dorsal rhizotomy (section of dorsal roots), total nerve section and crush. More recently, models of partial denervation based on restricted sciatic nerve injury have become increasingly employed. Unlike models of total denervation, these models preserve at least some of the sensory information passing into the spinal cord. The three models which are widely used are the chronic constriction injury (CCI) model [3], partial sciatic tight ligation (PSTL) model [4] and the selective spinal nerve ligation (SNL) model [5]. Additionally, neuropathy models which involve systemic treatments have also been described (e.g. streptozocin-induced diabetic neuropathy).
Here we review some examples of plasticity in peripheral sensory nerves that may be key mechanisms in the origins of neuropathic pain.
