Assessment and mechanisms of mechanical allodynia

Mechanical allodynia, i.e. pain due to a mechanical stimulus which does not normally provoke pain, is a troublesome component of neuropathic pain, being present in 20% of neuropathic pain sufferers across diagnostic entities and in 49% of patients with postherpetic neuralgia [1]. It causes functional impairment and may severely interfere with activity of daily living. Mechanical allodynia is divided into dynamic and static subtypes, referring to pain caused by light moving stimulus on the skin or sustained pressure against the skin, respectively. The mechanisms of mechanical allodynia are not fully elucidated, and the assessment methods are not thoroughly evaluated. To improve treatment of neuropathic pain, both needs should be better met to systematically evaluate the effect of different treatments on components of neuropathic pain (including mechanical allodynia).

The study of Landerholm and Hansson [2] aimed at examining if short (1 s) or longer lasting (10 s) non-painful von Frey filament stimulation of the neuropathic skin could be used to assess perception thresholds to dynamic and static mechanical allodynia, respectively. They used a compression/ischemia-induced nerve block in conjunction with repeated quantitative sensory testing (QST) of A-delta and C-fiber function to assess which nerve fiber population contributes to pain at perception threshold level using 1 s (vF1) and 10 s (vF10) von Frey filament stimulation of the skin. A brief vertical von Frey stimulation activates A-beta mechanoreceptors, which are activated also in brush-evoked dynamic mechanical allodynia. A sustained light von Frey stimulation of the neuropathic skin is presumed to activate epidermal C- and A-delta nociceptors [3]. The QST measurements were performed at the contralateral non-injured area, at the allodynic area, and at the ipsilateral adjacent non-painful area to monitor the progression of the nerve block of the painful limb.

The study population consisted of 18 patients with chronic pain (pain duration 1–12 years, mean 5 years) due to unilateral partial peripheral traumatic nerve injury in a limb. Detailed information of the type of the nerve trauma was not provided. All patients had dynamic mechanical allodynia, and nine patients had also static mechanical allodynia. Ten patients had spontaneous ongoing pain, whereas two patients had only evoked pain. In the neuropathic area all patients reported pain from vF1 (force varying individually from 0.03 g to 15.0 g). Only patients with clinically established static mechanical allodynia reported sustained pain during the vF10.

The main finding was that elevation of vF1 and vF10 occurred simultaneously and significantly prior to an increase in the thermal perception thresholds during the nerve block, which supports the role of A-beta fibers as peripheral mediator of both vF1 and vF10. The peripheral receptor organs for vF1 and vF10 are supposed to be rapidly and slowly adapting mechanoreceptors, respectively. None of the patients reported an elevation of the perception level to warmth at the time of elevation of vF1 or vF10 excluding contribution of C-fibers. Single patients demonstrated a slight decrease in cold perception levels at the time of elevation of vF1 and vF10. Hence, a possible contribution to mechanical allodynia from Adelta fibers cannot be completely ruled out.

The finding of A-beta fiber involvement in dynamic mechanical allodynia corroborates earlier studies [4,5]. Those studies suggested static mechanical allodynia to be mediated by C-fibers, whereas in the study of Landerholm and Hansson pain provoked by vF10 was mediated by A-beta fibers. In their patients, pain provoked vF10 corresponded with the presence of clinically established static mechanical allodynia. Whether this is true in other groups of patients with peripheral neuropathic pain should be studied further.

Use of vF1 and vF10 to assess perception thresholds to dynamic and static mechanical allodynia is tempting. According to the current study pain provoked by vF1 was in accordance with the presence of dynamic mechanical allodynia, and pain was provoked by vF10 only in patients with static mechanical allodynia. However, the number of patients in this group was relatively small, and all of them had partial peripheral traumatic nerve injury. More studies are needed to confirm if these findings can be repeated in other patients with painful peripheral neuropathic pain due to partial nerve trauma, polyneuropathy or neuritis.

Developments of the assessment methods are welcome in the field. Systematic wide-range studies using relevant methods are needed to better understand mechanisms of neuropathic pain and its treatments. The sophisticated and carefully performed study of Landerholm and Hansson sheds light on the neurophysiological basis of mechanical allodynia.