SENSORY DYSFUNCTION IN FIBROMYALGIA PATIENTS WITH IMPLICATIONS FOR PATHOGENIC MECHANISMS

This study, addressing etiologic and pathogenic aspects of fibromyalgi a (FM), aimed at examining whether sensory abnormalities in FM patient s are generalized or confined to areas with spontaneous pain. Ten fema le FM patients and 10 healthy, age matched females participated. The p atients were asked to rate the intensity of ongoing pain using a visua l analogue scale (VAS) at the site of maximal pain, the homologous con tralateral site and two homologous sites with no or minimal pain. Quan titative sensory testing was performed for assessment of perception th resholds in these four sites. Von Frey filaments were used to test low -threshold mechanoreceptive function. Pressure pain sensitivity was as sessed with a pressure algometer and thermal sensitivity with a Thermo test(R). In addition the stimulus-response curve of pain intensity as a function of graded nociceptive heat stimulation was studied at the s ite of maximal pain and at the homologous contralateral site. FM patie nts had increased sensitivity to non-painful warmth (P < 0.01) over pa inful sites and a tendency to increased sensitivity to non-painful col d (P < 0.06) at all sites compared to controls, but there was no diffe rence between groups regarding tactile perception thresholds. Compared to controls, patients demonstrated increased sensitivity to pressure pain (P < 0.001), cold pain (P < 0.001) and heat pain (P < 0.02) over all tested sites. The stimulus-response curve was parallely shifted to the left of the curve obtained from controls (P < 0.003). Intragroup comparisons showed that patients had increased sensitivity to pressure pain (P < 0.01) and light touch (P < 0.05) in the site of maximal pai n compared to the homologous contralateral site. These findings could be explained in terms of sensitization of primary afferent pathways or as a dysfunction of endogenous systems modulating afferent activity. However, the generalized increase in sensitivity found in FM patients was unrelated to spontaneous pain and thus most likely due to a centra l nervous system (CNS) dysfunction. The additional hyperphenomena rela ted to spontaneous pain are probably dependent on disinhibition/facili tation of nociceptive afferent input from normal (or ischemic) muscles .