Neuropathic pain : somatosensory functions related to spontaneous ongoing pain, mechanical allodynia and pain relief
Abstract: Introduction and aim: Patients with neuropathic pain suffer from spontaneous ongoing pain and from abnormal stimulus-evoked pain, e.g., allodynia. Dynamic mechanical allodynia (DMA) is evoked by a normally innocuous light moving mechanical stimulus on the skin and static mechanical allodynia (SMA) by a sustained, normally innocuous pressure against the skin. Some patients report variable intensity of DMA which at times is only unpleasant, i.e., dynamic mechanical dysesthesia (DMD). The aim was to probe for common denominators of sensory disturbances linked to mechanisms underlying development of or protection against pain after a traumatic peripheral nerve injury (Study I). Also, we aimed at examining if short or longer lasting non-painful von Frey filament stimulation of the neuropathic skin could be used to assess perception thresholds to DMA and SMA (Study II). Further, we investigated if DMA is the hyperbole of DMD both mediated by Abeta fibres in the periphery (Study III). Finally, we explored the modulatory effect of spinal cord stimulation (SCS) on somatosensory functions within the painful area (Study IV). Methods: Using methods of quantitative sensory testing a detailed analysis of somatosensory functions was performed in patients with and without pain after a traumatic peripheral nerve injury (Study I) and in patients reporting a sustained pain relieving effect of at least 30 % following SCS (Study IV). A compression/ischemia-induced (differential) nerve block in conjunction with repeated quantitative sensory testing of A-delta and C-fibre function was used to assess which nerve fibre population that contributes to pain at perception threshold level using 1 s (vF1) and 10 s (vF10) von Frey filament stimulation of the skin (Study II). The same approach was used to study which part of the peripheral fibre spectrum that contributes to DMA and DMD (Study III). Results: Pain patients reported allodynia to cold and pressure in conjunction with an increase in the perception threshold to non-painful warmth on the injured side compared to the uninjured side. Painfree patients reported hypoesthesia to light touch, cold and warmth on the injured side. No significant difference could be demonstrated comparing side-to-side differences between patients with and without pain. During the nerve block elevation of vF1 and vF10 occurred simultaneously and significantly prior to an increase in the perception level to cold or warmth. During the nerve block there was a transition of DMA to DMD in all patients with peripheral neuropathic pain and in 3/7 patients with central post stroke pain. Remaining patients lost DMA without transition. The transition/loss of DMA occurred early and concurrently in time in all patients paralleled by a continuous impairment of mainly A-beta fibre function. Following SCS decreased perception threshold to light touch and increased perception threshold to pressure pain were found in the neuropathic area when comparing with pre-stimulation values. Compared to the contralateral side these perception thresholds changed towards normalisation also including a significant normalisation of the perception threshold to non painful cold. SCS did not alter sensitivity to noxious temperature stimulation. Conclusions: Increased pain sensitivity to cold and pressure was found on the injured side in pain patients, pointing to hyperexcitability in the pain system, not verified by a more challenging analysis of side-to side differences between patients with and without pain. A-beta fibres are the peripheral mediators of both vF1 and vF10 although different receptor organs may be involved, i.e., rapidly (RA) and slowly (SA-I) adapting mechanoreceptors, respectively. We suggest DMA to be the hyperbole of DMD, the difference being the number of mechanoreceptive fibres having access to the nociceptive system. Sensory alterations following SCS indicate a possible link to the release of a functional block on somatosensory function induced by activity in the nociceptive system. No significant correlation could be demonstrated between the degree of threshold alterations versus the degree of SCS-induced pain relief.
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