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
