Sensory dysfunction in fibromyalgia (FM) patients with implications for pathogenic mechanisms

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This study, addressing etiologic and pathogenic aspects of

fibromyalgia (FM), aimed at examining whether sensory

abnormalities in FM patients are generalized or confined to

areas with spontaneous pain.

Ten female FM patients and 10

healthy, age-matched females participated. The patients were

asked to rate the intensity of ongoing pain using a visual

analogue scale (VAS) at the site of maximal pain, the

homologous contralateral site and two homologous sites with no

or minimal pain. Quantitative sensory testing was performed

for assessment of perception thresholds in these four sites.

Von Frey filaments were used to test low-threshold

mechanoreceptive function. Pressure pain sensitivity was

assessed with a pressure algometer and thermal sensitivity

with a Thermotest. In addition the stimulus-response curve of

pain intensity as a function of graded nociceptive heat

stimulation was studied at the site of maximal pain and at the

homologous contralateral site.

FM patients had increased

sensitivity to non-painful warmth (P < 0.01) over painful

sites and a tendency to increased sensitivity to non-painful

cold (P < 0.06) at all sites compared to controls, but there

was no difference 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 pain 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 central nervous system (CNS) dysfunction. The additional

hyperphenomena related to spontaneous pain are probably

dependent on disinhibition/facilitation of nociceptive

afferent input from normal (or ischemic) muscles.

Kosek E, Ekholm J, Hansson P

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