Activation of the somatosensory cortex during Aβ-fiber mediated hyperalgesiaa MSI study

R. Baron, Y. Baron, E. Disbrow, T. P L Roberts

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


Objective: To investigate the neural activation in the primary somatosensory cortex (SI) that is induced by capsaicin-evoked secondary Aβ-fiber-mediated hyperalgesia with magnetic source imaging (MSI) in healthy humans. Background: Dynamic 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 Aβ low threshold mechanoreceptive afferents become capable of activating central pain signalling neurons. A similar state of central sensitization can be experimentally produced with capsaicin. Methods: In six individuals the somatosensory evoked magnetic fields (SEFs) induced by non-painful electrical stimulation of Aβ-afferents at the forearm skin were recorded. Capsaicin was injected adjacent to the stimulation site to induce secondary dynamic Aβ-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. Results: Non-painful electrical stimulation of Aβ-afferents induced SEFs in SI at latencies between 20 and 150 ms. Stimulation of Aβ-afferents within the capsaicin-induced secondary hyperalgesic skin induced SEFs at identical latencies and locations as compared with the stimulation of Aβ-afferents within normal skin. The amplitudes, i.e., the magnetic dipole strengths of the SEFs were higher during Aβ-hyperalgesia. Conclusions: Acute 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. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)75-82
Number of pages8
JournalBrain Research
Issue number1
StatePublished - Jul 14 2000


  • Allodynia
  • C-nociceptor
  • Human
  • Magnetic source imaging
  • Neuropathic pain
  • Sensitization

ASJC Scopus subject areas

  • Neuroscience(all)


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