Right insular atrophy in neurocardiogenic syncope: a volumetric MRI study

• Published in: American journal of neuroradiology : AJNR 2014-01, Vol.35 (1), p.113-118
• Main Authors: Kim, J B, Suh, S-i, Seo, W-K, Koh, S-B, Kim, J H
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Atrophy - pathology; Brain; Cerebral Cortex - pathology; Child; Female; Humans; Image Interpretation, Computer-Assisted - methods; Imaging, Three-Dimensional - methods; Magnetic Resonance Imaging - methods; Male; Neurons - pathology; Reproducibility of Results; Sensitivity and Specificity; Syncope, Vasovagal - pathology; Young Adult
• ISSN: 0195-6108; 1936-959X
• DOI: 10.3174/ajnr.A3611

Alterations in the central autonomic network are hypothesized to play a role in the pathophysiologic mechanism underlying neurocardiogenic syncope; however, few data are available regarding the structural changes of the brain in this condition. We used voxel-based morphometry and regional volumetry to identify possible neuroanatomic correlates. We prospectively studied 32 patients with neurocardiogenic syncope with a positive response to the head-up tilt test and 32 controls who had no history of syncope. We used voxel-based morphometry to compare GM volumes between patients and controls. In addition, regional volumes of structures known to be included in the central autonomic network were measured and compared between the groups. Correlation analyses were also performed between clinical variables and anatomic data. Voxel-based morphometry showed a significant GM volume reduction in the right insular cortex in patients with neurocardiogenic syncope compared with controls (corrected P = .033). Regional volumetry showed a significant reduction of right insular volumes in patients compared with controls (P = .002, MANCOVA). Smaller right insular volumes in patients with neurocardiogenic syncope were related to larger drops in systolic (P = .020) and diastolic (P = .003) blood pressures during the head-up tilt test. We observed a novel finding of right insular atrophy in patients with neurocardiogenic syncope with a positive response to the head-up tilt test, implicating the role of right insular dysfunction in the pathophysiologic mechanism underlying neurocardiogenic syncope. Our findings further support the hypothesis that right insular dysfunction may cause a decrease in sympathetic activity and a reciprocal increase in parasympathetic activity, leading to syncope.