Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

C- and Aδ-fiber components of heat-evoked cerebral potentials in healthy human subjects

Magerl, Waltera; Ali, Zahid1,b; Ellrich, Jens2,a; Meyer, Richard A.b; Treede, Rolf-Detlefa,*

doi: 10.1016/S0304-3959(99)00061-5
Research Papers
Buy

Feedback-controlled laser heat was used to stimulate the hairy skin of the hand dorsum and forearm, and heat-evoked cerebral potentials were recorded at midline (Fz, Cz, Pz) and temporal (T3, T4) scalp positions. Based on data from primary afferent electrophysiology a stimulus level (40°C) was chosen, which is above C-fiber heat threshold, but clearly below Aδ-nociceptor heat threshold in order to excite selectively C-fibers without concomitant excitation of Aδ-fibers. Feedback-controlled stepped heat stimuli to 40°C elicited ultralate laser evoked potentials (LEPs) at the vertex in a high proportion of experiments (90%). Estimates of conduction velocity calculated from latency shifts between the hand and forearm sites of ultralate LEPs (2.4 m/s) and of reaction times (2.8 m/s) confirmed mediation of ultralate potentials by unmyelinated nerve fibers (nociceptors and/or warm fibers). The ultralate LEP could be differentiated from resolution of contingent negative variation (CNV), an endogenous potential related to expectation and response preparation, by its scalp topography. Strong heat stimuli of 48°C, which is suprathreshold for most Aδ- and C-fiber nociceptors, elicited the well-known late LEPs mediated by nociceptive Aδ-fibers confirming previous studies. The LEP waveform to strong heat stimuli also contained an ultralate component reminiscent of an ultralate LEP following the late LEP. Ultralate and late LEP had identical scalp topography. In conclusion, the method of temperature-controlled laser heat stimuli allows the selective and reliable examination of Aδ- and C-fiber-mediated afferent pathways and the related cortical processing without the complication of dissociating A-fiber nerve blocks.

aInstitute of Physiology and Pathophysiology, Johannes-Gutenberg-University, Saarstr. 21, D-55099 Mainz, Germany

bDepartment of Neurosurgery, Johns Hopkins-University, 600 N. Wolfe St., Meyer 5-109, Baltimore, MD 21287-7509, USA

* Corresponding author. Tel.: +49-6131-395715; fax: +49-6131-395902

E-mail address:treede@mzdmza.zdv.uni-mainz.de

1 Present address: Merck, Sharpe and Dohme, Neuroscience Research Centre, Terlings Park, Harlow CM20 2QR, Essex, UK.

2Present address: Institute of Physiology and Experimental Pathophysiology, Friedrich-Alexander University, Universitätsstr. 17, D-91054 Erlangen, Germany.

Received July 28, 1998; received in revised form January 12, 1999; accepted February 10, 1999

© 1999 Lippincott Williams & Wilkins, Inc.
You currently do not have access to this article

To access this article:

Note: If your society membership provides full-access, you may need to login on your society website