4.4 Article

EEG analysis reveals widespread directed functional interactions related to a painful cutaneous laser stimulus

Journal

JOURNAL OF NEUROPHYSIOLOGY
Volume 110, Issue 10, Pages 2440-2449

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00246.2013

Keywords

attention; human; pain; cortex; network; event-related causality

Funding

  1. National Institutes of Health National Institute of Neurological Disorders and Stroke [NS-38493-11]
  2. Johns Hopkins Neurosurgery Pain Research Institute

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During attention to a painful cutaneous laser stimulus, event-related causality (ERC) has been detected in recordings from subdural electrodes implanted directly over cortical modules for the treatment of epilepsy. However, these studies afforded limited sampling of modules and did not examine interactions with a nonpainful stimulus as a control. We now sample scalp EEG to test the hypothesis that attention to the laser stimulus is associated with poststimulus ERC interactions that are different from those with attention to a nonpainful stimulus. Subjects attended to (counted) either a painful laser stimulus (laser attention task) or a nonpainful electrical cutaneous stimulus that produced distraction from the laser (laser distraction task). Both of these stimuli were presented in random order in a single train. The intensities of both stimuli were adjusted to produce similar baseline salience and sensations in the same cutaneous territory. The results demonstrated that EEG channels with poststimulus ERC interactions were consistently different during the laser stimulus versus the electric stimulus. Poststimulus ERC interactions for the laser attention task were different from the laser distraction task. Furthermore, scalp EEG frontal channels play a driver role while parietal temporal channels play a receiver role during both tasks, although this does not prove that these channels are connected. Sites at which large numbers of ERC interactions were found for both laser attention and distraction tasks (critical sites) were located at Cz, Pz, and C3. Stimulation leading to disruption of sites of these pain-related interactions may produce analgesia for acute pain.

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