Abstract
with somatoform pain disorders and with depression. We hypothesized that patients with fibromyalgia syndrome have disturbed processing of painful stimuli in the peripheral as well as in the central nervous system. Using near infrared spectroscopy (NIRS) we investigated cerebral activation upon painful stimuli. The main finding was that in spite of lower pressure pain thresholds FMS patients had increased bilateral cortical activation compared to controls. They also had a stronger contralateral activity over the dorsolateral prefrontal cortex in comparison with depressive patients. In a second study [2], we investigated the peripheral nervous system and afferent fiber tracts using three methods: quantitative sensory testing (QST), A-delta fiber evoked potentials, and intraepidermal nerve fiber density in skin biopsies. Patients with FMS but not patients with depression had impaired small fiber function in QST. A-delta evoked potentials had increased N1 latencies upon stimulation at the feet and reduced amplitudes upon stimulation at face, hands, and feet in fibromyalgia patients compared to patients with depression and to controls, indicating abnormalities of small fibers or their central afferents. In skin biopsies intraepidermal nerve fibers at the leg were reduced in patients with fibromyalgia syndrome. All three methods used support the concept of impaired small fiber function in patients with FMS, pointing towards a neuropathic component of their pain that may dynamically evoke and maintain central sensitization.
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