Differential pain modulation properties in central neuropathic pain after spinal cord injury

Abstract

It seems that central neuropathic pain (CNP) is associated with altered abilities to modulate pain; whereas dysfunction in descending pain inhibition is associated with the extent of chronic pain distribution, enhanced pain excitation is associated with the intensity of chronic pain. We investigated the hypothesis that CNP is associated with decreased descending pain inhibition along with increased neuronal excitability and that both traits are associated with spinothalamic tract (STT) damage. Chronic spinal cord injury subjects with CNP (n = 27) and without CNP (n = 23) and healthy controls (n = 20) underwent the measurement of pain adaptation, conditioned pain modulation (CPM), tonic suprathreshold pain (TSP), and spatial summation of pain above injury level. Central neuropathic pain subjects also underwent at and below-lesion STT evaluation and completed the questionnaires. Central neuropathic pain subjects showed decreased CPM and increased enhancement of TSP compared with controls. Among CNP subjects, the dysfunction of CPM and pain adaptation correlated positively with the number of painful body regions. The magnitude of TSP and spatial summation of pain correlated positively with CNP intensity. STT scores correlated with CNP intensity and with TSP, so that the more affected the STT below injury level, the greater the CNP and TSP magnitude. It seems that CNP is associated with altered abilities to modulate pain, whereas dysfunction in descending pain inhibition is associated with the extent of chronic pain distribution and enhanced pain excitation is associated with the intensity of chronic pain. Thus, top-down processes may determine the spread of CNP, whereas bottom-up processes may determine CNP intensity. It also seems that the mechanisms of CNP may involve STT-induced hyperexcitability. Future, longitudinal studies may investigate the timeline of this scenario.

Assessment and manifestation of central sensitisation across different chronic pain conditions

“…Patients with neuropathic pain after a spinal cord injury showed a dysfunction of CPM which correlated positively with the number of painful body regions (Gruener et al, 2016).…”

“…The CPM deficit has been shown to correlate with the severity in patients with spinal cord injury neuropathic pain (Albu et al, 2015) where the CPM deficit correlates positively with the number of painful body regions (Gruener et al, 2016), painful chemotherapy-induced polyneuropathy (NahmanAverbuch et al, 2011), complex-regional pain syndrome (Seifert et al, 2009), postherpetic neuralgia (Pickering et al, 2014), and traumatic peripheral nerve injury (Bouhassira et al, 2003).…”

Chronic pain in pachyonychia congenita: evidence for neuropathic origin

“…However, the patients did have reduced CPM compared with controls, which is indicative of dysfunctional pain inhibition capacity. Such a dysfunction is common in patients with chronic pain of various aetiologies, including neuropathic pain . It is not clear whether deficient CPM preceded the development of the chronic pain in PC (and thus contributed to its emergence) or resulted from it.…”

“…Sensory detection thresholds were measured to evaluate the sensitivity of the nervous system to innocuous stimuli and to evaluate conduction in C fibres (warmth threshold), A‐delta fibres (cold threshold) and A‐beta fibres (touch threshold) . Warm and cold detection thresholds were measured using the computerized thermal stimulator . The mechanical detection threshold was measured using the Semmes–Weinstein monofilaments .…”

“…Pain thresholds were measured in order to evaluate the sensitivity of the nervous system to noxious stimuli and to evaluate conduction in nociceptive C fibres and A‐delta fibres. Heat pain threshold (HPT) was measured using the computerized thermal stimulator . Pressure pain threshold (PPT) was measured using the pressure algometer .…”