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Assessment and Mechanisms of Mechanical Allodynia Scandinavian Journal of Pain 2 (2011) 7–8 Contents lists available at ScienceDirect Scandinavian Journal of Pain journal homepage: www.ScandinavianJournalPain.com Editorial comment Assessment and mechanisms of mechanical allodynia Maija Haanpää a,b,c,∗ a Department of Neurosurgery, Helsinki University Central Hospital, Postal Box 266, FIN-00029 HUS, Helsinki, Finland b Rehabilitation ORTON, Helsinki, Finland c Etera Mutual Pension Insurance Company, Finland Mechanical allodynia, i.e. pain due to a mechanical stimulus mechanical allodynia. Ten patients had spontaneous ongoing pain, which does not normally provoke pain, is a troublesome compo- whereas two patients had only evoked pain. In the neuropathic nent of neuropathic pain, being present in 20% of neuropathic pain area all patients reported pain from vF1 (force varying individually sufferers across diagnostic entities and in 49% of patients with pos- from 0.03 g to 15.0 g). Only patients with clinically established static therpetic neuralgia [1]. It causes functional impairment and may mechanical allodynia reported sustained pain during the vF10. severely interfere with activity of daily living. Mechanical allody- The main finding was that elevation of vF1 and vF10 occurred nia is divided into dynamic and static subtypes, referring to pain simultaneously and significantly prior to an increase in the ther- caused by light moving stimulus on the skin or sustained pressure mal perception thresholds during the nerve block, which supports against the skin, respectively. The mechanisms of mechanical allo- the role of A-beta fibers as peripheral mediator of both vF1 and dynia are not fully elucidated, and the assessment methods are not vF10. The peripheral receptor organs for vF1 and vF10 are supposed thoroughly evaluated. To improve treatment of neuropathic pain, to be rapidly and slowly adapting mechanoreceptors, respectively. both needs should be better met to systematically evaluate the None of the patients reported an elevation of the perception level effect of different treatments on components of neuropathic pain to warmth at the time of elevation of vF1 or vF10 excluding contri- (including mechanical allodynia). bution of C-fibers. Single patients demonstrated a slight decrease The study of Landerholm and Hansson [2] aimed at examining in cold perception levels at the time of elevation of vF1 and vF10. if short (1 s) or longer lasting (10 s) non-painful von Frey fila- Hence, a possible contribution to mechanical allodynia from A- ment stimulation of the neuropathic skin could be used to assess delta fibers cannot be completely ruled out. perception thresholds to dynamic and static mechanical allody- The finding of A-beta fiber involvement in dynamic mechanical nia, respectively. They used a compression/ischemia-induced nerve allodynia corroborates earlier studies [4,5]. Those studies suggested block in conjunction with repeated quantitative sensory testing static mechanical allodynia to be mediated by C-fibers, whereas (QST) of A-delta and C-fiber function to assess which nerve fiber in the study of Landerholm and Hansson pain provoked by vF10 population contributes to pain at perception threshold level using was mediated by A-beta fibers. In their patients, pain provoked 1 s (vF1) and 10 s (vF10) von Frey filament stimulation of the skin. A vF10 corresponded with the presence of clinically established static brief vertical von Frey stimulation activates A-beta mechanorecep- mechanical allodynia. Whether this is true in other groups of tors, which are activated also in brush-evoked dynamic mechanical patients with peripheral neuropathic pain should be studied fur- allodynia. A sustained light von Frey stimulation of the neuropathic ther. skin is presumed to activate epidermal C- and A-delta nociceptors Use of vF1 and vF10 to assess perception thresholds to dynamic [3]. The QST measurements were performed at the contralateral and static mechanical allodynia is tempting. According to the cur- non-injured area, at the allodynic area, and at the ipsilateral adja- rent study pain provoked by vF1 was in accordance with the cent non-painful area to monitor the progression of the nerve block presence of dynamic mechanical allodynia, and pain was provoked of the painful limb. by vF10 only in patients with static mechanical allodynia. However, The study population consisted of 18 patients with chronic pain the number of patients in this group was relatively small, and all of (pain duration 1–12 years, mean 5 years) due to unilateral partial them had partial peripheral traumatic nerve injury. More studies peripheral traumatic nerve injury in a limb. Detailed information are needed to confirm if these findings can be repeated in other of the type of the nerve trauma was not provided. All patients had patients with painful peripheral neuropathic pain due to partial dynamic mechanical allodynia, and nine patients had also static 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 DOI of refers to article:10.1016/j.sjpain.2010.08.001. ∗ its treatments. The sophisticated and carefully performed study Correspondence address: Department of Neurosurgery, Helsinki University Cen- of Landerholm and Hansson sheds light on the neurophysiological tral Hospital, Postal Box 266, FIN-00029 HUS, Helsinki, Finland. E-mail addresses: maija.haanpaa@orton.fi, maija.haanpaa@hus.fi basis of mechanical allodynia. 1877-8860/$ – see front matter © 2010 Scandinavian Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.sjpain.2010.11.003 8 M. Haanpää / Scandinavian Journal of Pain 2 (2011) 7–8 References [2] Landerholm ÅH, Hansson PT. The perception threshold counterpart to dynamic- and static mechanical allodynia assessed using von Frey filaments in peripheral [1] Maier C, Baron R, Tolle TR, Binder A, Birbaumer N, Birklein F, Gierthmuhlen J, neuropathic pain patients. Scand J Pain 2011;2:9–16. Flor H, Geber C, Huge V, Krumova EK, Landwehrmeyer GB, Magerl W, Maihofner [3] Treede RD, Rolke R, Andrews K, Magerl W. Pain elicited by blunt pressure: neu- C, Richter H, Rolke R, Scherens A, Schwarz A, Sommer C, Tronnier V, Uceyler robiological basis and clinical relevance. Pain 2002;3:235–40. N, Valet M, Wasner G, Treede RD. Quantitative sensory testing in the German [4] Koltzenburg M, Lundberg LE, Torebjork HE. Dynamic and static components of Research Network on Neuropathic Pain (DFNS): somatosensory abnormalities mechanical hyperalgesia in human hairy skin. Pain 1992;2:207–19. in 1236 patients with different neuropathic pain syndromes. Pain 2010;3:439– [5] Ochoa JL, Yarnitsky D. Mechanical hyperalgesias in neuropathic pain patients: 50. dynamic and static subtypes. Ann Neurol 1993;5:465–72..
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