• Brain research · Jul 2000

    Activation of the somatosensory cortex during Abeta-fiber mediated hyperalgesia. A MSI study.

    • R Baron, Y Baron, E Disbrow, and T P Roberts.
    • Department of Neurology, University of California, San Francisco, USA. r.baron@neurologie.uni-kiel.de
    • Brain Res. 2000 Jul 14;871(1):75-82.

    ObjectiveTo investigate the neural activation in the primary somatosensory cortex (SI) that is induced by capsaicin-evoked secondary Abeta-fiber-mediated hyperalgesia with magnetic source imaging (MSI) in healthy humans.BackgroundDynamic mechanical hyperalgesia, i.e. pain to innocuous light touching, is a symptom of painful neuropathies. Animal experiments suggest that alterations in central pain processing occur so that tactile stimuli conveyed in Abeta low threshold mechanoreceptive afferents become capable of activating central pain signalling neurons. A similar state of central sensitization can be experimentally produced with capsaicin.MethodsIn six individuals the somatosensory evoked magnetic fields (SEFs) induced by non-painful electrical stimulation of Abeta-afferents at the forearm skin were recorded. Capsaicin was injected adjacent to the stimulation site to induce secondary dynamic Abeta-hyperalgesia. Thereafter, the SEFs induced by the identical electrical stimulus applied within the secondary hyperalgesic skin were analyzed. The electrical stimulus was subsequently perceived as painful without changing the stimulus intensity and location. Latencies, anatomical source location and amplitudes of SEFs during both conditions were compared.ResultsNon-painful electrical stimulation of Abeta-afferents induced SEFs in SI at latencies between 20 and 150 ms. Stimulation of Abeta-afferents within the capsaicin-induced secondary hyperalgesic skin induced SEFs at identical latencies and locations as compared with the stimulation of Abeta-afferents within normal skin. The amplitudes, i.e., the magnetic dipole strengths of the SEFs were higher during Abeta-hyperalgesia.ConclusionsAcute application of capsaicin produces an increase in the excitability of central neurons, e.g., in SI. This might be due to sensitization of central neurons so that normally innocuous stimuli activate pain signalling neurons or cortical neurons might increase their receptive fields.

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