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