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Autoradiographic Measurements of [14C]-Iodoantipyrine in Rat Brain Following Central Post-Stroke Pain
Published on: July 18, 2016
Neuroanatomy and lesion networks of central poststroke pain
Hassan A Karoam1,2, Joel Bruss2,3, Katharine Champoux2
1Interdisciplinary Graduate Program in Neuroscience, University of Iowa Graduate College, Iowa City, IA, United States.
Abstract:
Identifying lesion sites associated with central poststroke pain (CPSP) may facilitate targeted screening for early symptoms, possibly even paving the way for preventive measures and earlier treatment initiation. Here, we test the hypothesis that damage to a nociceptive pathway extending from the brainstem to the cerebral cortex, and including white matter tracts, is associated with CPSP. We investigated the lesion locations of 72 patients with CPSP relative to poststroke comparison subjects without pain (n = 123), divided into a discovery and independent validation data set. The study included three main analyses: (1) we compared lesion intersection with our a priori region of interest (ROI) between groups with and without CPSP, (2) we performed lesion-symptom mapping to evaluate whether lesions associated with CPSP localize to the a priori ROI, and (3) we used lesion network mapping to infer the broader structural and functional connectivity patterns associated with CPSP lesions. CPSP lesions overlapped the nociceptive pathway ROI to a greater extent than comparison lesions. Lesion-symptom mapping identified a CPSP-associated region overlapping with the ventrocaudal thalamus and adjacent white matter, which was located mostly within the a priori ROI. Lesion network mapping demonstrated that lesions associated with CPSP disrupt nodes and tracts of the nociceptive pathway ROI. Interestingly, the CPSP lesion network results demonstrated connectivity to intereffector nodes of the primary motor cortex, providing a novel link between CPSP and the somato-cognitive action network. Together, these findings indicate that CPSP can be conceptualized as a lesion-associated network disruption of the nociceptive pathway and somato-cognitive action network.

