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


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 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.


METHODS
In 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.


RESULTS
Non-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.


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.
Baron
R
R
Department of Neurology, University of California, San Francisco, USA. r.baron@neurologie.uni-kiel.de
Baron
Y
Y
Disbrow
E
E
Roberts
T P
TP
D000328:Adult; D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D002211:Capsaicin / Q000494:pharmacology*; D004558:Electric Stimulation; D005073:Evoked Potentials, Somatosensory; D005260:Female; D005542:Forearm / Q000294:innervation; D006801:Humans; D006930:Hyperalgesia / Q000139:chemically induced / Q000503:physiopathology*; D008280:Magnetics; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D013003:Somatosensory Cortex / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology
D002211:Capsaicin