Activation of the somatosensory cortex during A beta-fiber mediated hyperalgesia - a MSI study

Objective: To investigate the neural activation in the primary somatosensor y cortex (SI) that is induced by capsaicin-evoked secondary A beta-fiber-me diated hyperalgesia with magnetic source imaging (MSI) in healthy humans. B ackground: Dynamic mechanical hyperalgesia, i.e. pain to innocuous light to uching, is a symptom of painful neuropathies. Animal experiments suggest th at alterations in central pain processing occur so that tactile stimuli con veyed in A beta low threshold mechanoreceptive afferents become capable of activating central pain signalling neurons. A similar state of central sens itization can be experimentally produced with capsaicin. Methods: In six in dividuals the somatosensory evoked magnetic fields (SEFs) induced by non-pa inful electrical stimulation of A beta-afferents at the forearm skin were r ecorded. Capsaicin was injected adjacent to the stimulation site to induce secondary dynamic A beta-hyperalgesia. Thereafter, the SEFs induced by the identical electrical stimulus applied within the secondary hyperalgesic ski n were analyzed. The electrical stimulus was subsequently perceived as pain ful without changing the stimulus intensity and location. Latencies, anatom ical source location and amplitudes of SEFs during both conditions were com pared. Results: Non-painful electrical stimulation of A beta-afferents indu ced SEFs in SI at latencies between 20 and 150 ms. Stimulation of A beta-af ferents within the capsaicin-induced secondary hyperalgesic skin induced SE Fs at identical latencies and locations as compared with the stimulation of A beta-afferents within normal skin. The amplitudes, i.e., the magnetic di pole strengths of the SEFs were higher during A beta-hyperalgesia. Conclusi ons: Acute application of capsaicin produces an increase in the excitabilit y of central neurons, e.g., in SI. This might be due to sensitization of ce ntral neurons so that normally innocuous stimuli activate pain signalling n eurons or cortical neurons might increase their receptive fields. (C) 2000 Elsevier Science B.V. All rights reserved.