Increased capsaicin-induced secondary hyperalgesia in patients with multiple chemical sensitivity.
Holst H, Arendt-Nielsen L, Mosbech H, Elberling J.
Clin J Pain. 2011 Feb;27(2):156-62.
Source
Danish Research Centre for Chemical Sensitivities, Gentofte Hospital University of Copenhagen.
Source
Danish Research Centre for Chemical Sensitivities, Gentofte Hospital University of Copenhagen.
Abstract
OBJECTIVE:
the underlying cause of pathophysiological mechanisms triggering multiple chemical sensitivity (MCS) remains disputed.Recently, alterations in the central nervous system, for example,central sensitization, similar to various chronic pain disorders, have been suggested. Capsaicin is used in experimental pain models to provoke peripheral and central sensitization. In patients with symptoms elicited by odorous chemicals capsaicin-induced secondary hyperalgesia and temporal summation were assessed as markers for abnormal central nociceptive processing together with neurogenic inflammation (flare).
the underlying cause of pathophysiological mechanisms triggering multiple chemical sensitivity (MCS) remains disputed.Recently, alterations in the central nervous system, for example,central sensitization, similar to various chronic pain disorders, have been suggested. Capsaicin is used in experimental pain models to provoke peripheral and central sensitization. In patients with symptoms elicited by odorous chemicals capsaicin-induced secondary hyperalgesia and temporal summation were assessed as markers for abnormal central nociceptive processing together with neurogenic inflammation (flare).
METHODS:
sixteen patients fulfilling Cullen criteria for MCS and 15 eczema patients with airway symptoms induced by odorous chemicals (EC) were compared with 29 age-matched healthy controls.Participants underwent 2 intradermal injection of capsaicin (3.3 mM and 33 mM). Measurements included pain intensity, flare, pinprick hyperalgesia, temporal summation, and McGill Pain Questionnaire score.
RESULTS:
no difference was found in the flare area between the groups. The capsaicin-evoked pain intensity was higher in MCS patients compared with controls (P<0.01, 33 mM). The area of secondary hyperalgesia was larger in both the patient groups compared with controls (P<0.05) at both capsaicin concentrations. Temporal summation was increased in MCS patients compared with controls(P<0.01). Further, in patients with comorbidity of fibromyalgia, pain and chronic fatigue, pain continued after end stimulation, and the stimulus response function was enhanced compared with patients without comorbidity, and significant to controls (P<0.05).
CONCLUSION:
this is the first study to show facilitated pain processing in MCS and EC patients with the most abnormal responses in MCS.
PMID: 21268302 [PubMed - indexed for MEDLINE]
