• NeuroImage · Jan 2007

    Human intracranially-recorded cortical responses evoked by painful electrical stimulation of the sural nerve.

    • R Dowman, T Darcey, H Barkan, V Thadani, and D Roberts.
    • Department of Psychology, Clarkson University, Potsdam, NY 13699-5825, USA. rdowman@clarkson.edu
    • Neuroimage. 2007 Jan 15; 34 (2): 743-63.

    AbstractIntracranial recordings were obtained from 5 epilepsy patients to help identify the generators of the scalp somatosensory evoked potential (SEP) components that appear to be involved in orienting attention towards a potentially threatening, painful sural nerve electrical stimulus. The intracranial recording data support, for the most part, the generators suggested by our scalp SEP studies. The generators of the central negativity at 70-110 ms post-stimulus and the contralateral temporal negativity at 100-180 ms are located in the somatosensory association areas in the medial wall of the parietal cortex and in the parietal operculum and insula, respectively. The negative potential at 130-200 ms recorded from over the fronto-central scalp appears to be generated in the medial prefrontal cortex and primary somatosensory cortex foot area. The intracranial recording data suggest that the positive scalp potential at 280-320 ms, which corresponds to the pain-related P2, has multiple generators, including the anterior cingulate cortex, inferior parietal cortex, and possibly the somatosensory association areas in the medial wall of the parietal cortex. Finally, the positive scalp potential at 320-400 ms has generators in brain areas that others have shown to generate the P3a, including the dorsolateral and medial prefrontal cortices, temporal parietal junction, and the posterior hippocampus, which supports our hypothesis that this potential is a pain-evoked P3a. The putative functional roles of the brain areas generating these components and the response properties of the intracranial peaks recorded from these brain areas are in most cases consistent with the attention- and pain-related properties of their corresponding scalp SEP components. The intracranial recordings also demonstrate that the source configuration underlying the SEP components are often more complex than was suggested from the scalp studies. This complexity implies that the dipole source localization analysis of these components will at best provide only a very crude estimate of source location and activity, and that caution must be used when interpreting a change in the scalp component amplitude.

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