Hemispheric modulatory influences on skin resistance response latency: Unilateral stimulation, bilateral recording

Esen F., Esen H.

International Journal of Neuroscience, vol.112, no.12, pp.1397-1406, 2002 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 112 Issue: 12
  • Publication Date: 2002
  • Doi Number: 10.1080/00207450290158313
  • Journal Name: International Journal of Neuroscience
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.1397-1406
  • Keywords: Evoked bilateral EDA, Hemispheric asymmetry, Latency
  • Eskisehir Osmangazi University Affiliated: Yes


In order to evaluate the bilateral asymmetries in evoked electrodermal activity (EDA) and the use of EDA parameters as indices of relative hemispheric activations, skin resistance level (SRL), skin resistance response (SRR), and the SRR latency (L) were examined in 25 right-handed male subjects. We used bilateral recording with a unilateral stimulation (auditory click/patellar tendon tap) to assess the asymmetries of EDA variables related to the side of stimulation and to handedness. Although no significant asymmetry in C = SRR max/SRL ratio was found, significant differences in latency were observed. Ipsilateral responses were 100 ms faster than contralateral responses for auditory stimulus, a result that can be explained in terms of contralateral delay of neuronal communication on EDA-l pathway. Response latency to reflex-motor activation was 60-100 ms shorter in the dominant hand, regardless of the stimulation site used. This result indicates that the reaction time of the EDA-2 pathway of the left hemisphere was shorter than the right for right-handed subjects. It is concluded that there is hemispheric asymmetry on EDA-2 pathway and that this asymmetry appears to be dependent on the preferred dexterity. These results have implications for the influence of both central and peripheral factors on EDA laterality and principally on laterality of response amplitude. Further, there is no single cortical mechanism modulating the asymmetries in the latency of this response.