Differential involvement of A-delta and A-beta fibres in neuropathic pain related to carpal tunnel syndrome

Abstract

Carpal tunnel syndrome (CTS), a common entrapment neuropathy involving the median nerve at the wrist, frequently manifests with neuropathic pain. We sought information on pain mechanisms in CTS. We studied 70 patients with a diagnosis of CTS (117 CTS hands). We used the DN4 questionnaire to select patients with neuropathic pain, and the Neuropathic Pain Symptom Inventory (NPSI) to assess the intensity of the various qualities of neuropathic pain. All patients underwent a standard nerve conduction study (NCS) to assess the function of non-nociceptive Abeta-fibres, and the cutaneous silent period (CSP) after stimulation of the IIIrd and Vth digits, to assess the function of nociceptive Adelta-fibres. In 40 patients (75 CTS hands) we also recorded laser-evoked potentials (LEPs) in response to stimuli delivered to the median nerve territory and mediated by nociceptive Adelta-fibres. We sought possible correlations between neurophysiological data and the various qualities of neuropathic pain as assessed by the NPSI. We found that the median nerve sensory conduction velocity correlated with paroxysmal pain and abnormal sensations, whereas LEP amplitude correlated with spontaneous constant pain. Our findings suggest that whereas paroxysmal pain and abnormal sensations reflect demyelination of non-nociceptive Abeta-fibres, spontaneous constant pain arises from damage to nociceptive Adelta-fibres.

e association of neuropathic pain and disease activity, functional level, and quality of life in patients with ankylosing spondylitis: a cross-sectional study

“…It was proposed by Pollard et al that arthritic joints expand their total receptive field to the surrounding noninflamed tissue, called peripheral sensitization (29). Another peripheral mechanism in the development of neuropathic pain in AS patients could be the focal demyelination of nonnociceptive, large myelinated fibers in those patients (30).…”

Characteristics of neuropathic pain and its relationship with quality of life in 72 patients with spinal cord injury

“…This agrees with a previous report that the prevalence of dysesthesia after SCI is~80%. 18 Likewise, studies using the NPSI questionnaire report that paresthesia/dysesthesia is the most frequent and intense type of neuropathic pain in patients with carpal tunnel syndrome 12 and postoperative intramedullary spinal cord tumor. 13 In contrast, the predominant type of neuropathic pain associated with herpes zoster is burning spontaneous pain.…”

“…These qualities make the NPSI useful for specifying and quantifying subjective pain in daily clinical practice. The NPSI has been validated in reports assessing neuropathic pain after herpes, 11 carpal tunnel syndrome 12 and spinal cord tumor. 13 Its application to neuropathic pain after SCI has not been reported, although a recent study strongly recommended using the NPSI to evaluate this pain.…”

Abnormal muscle afferent function in a model of Taxol chemotherapy-induced painful neuropathy

“…Although in the setting of hypersensitivity states, one might expect to observe an increase in conduction velocity, as a reflection of a change in ionic conductance in the axon (Hodgkin 1975;Waxman et al 1999), in the setting of inflammatory pain, conduction velocity has generally been unchanged (Baba et al 1999;Nakatsuka et al 1999), whereas in peripheral neuropathies, even those associated with pain, changes when observed have in general been in the form of a slowing in conduction velocity (Elliott et al 2009;Meyer et al 2010;Nakatsuka et al 1999). These paradoxical findings may be due, in part, to the fact that clinically, in patients with peripheral neuropathies (Nardone and Schieppati 2004;Shefner et al 1991;Truini et al 2009), and in animal models of neuropathic pain (Authier et al 2000;Brussee et al 2008;Cermenati et al 2010;Jolivalt et al 2009;Meyer et al 2010), conduction velocity is generally measured in myelinated, nonnociceptive afferents. However, there are also studies in which slowing of C-fiber conduction velocity in neuropathic pain models [e.g., ddC (Chen and Levine 2007)] and in clinical studies on cutaneous unmyelinated fibers pa- Fig.…”