Cortical Morphology in Patients with Orthostatic Intolerance

Abstract

Background: We evaluated the cortical morphology in patients with orthostatic intolerance. Methods: Thirty patients with orthostatic intolerance, as well as age- and sex-matched normal controls, were enrolled in this study. We divided the patients into orthostatic hypotension (n = 22) and postural tachycardia syndrome (n = 8) groups based on their response to a head-up tilt table test. We analyzed whole-brain T1-weighted MRI images using FreeSurfer 5.1. The measures of cortical morphology were compared between the groups. Results: The cortical thickness in the right hemisphere, including the medial orbitofrontal, peri-calcarine, post-central, inferior temporal, and lateral occipital cortex, and in the peri-calcarine cortex of the left hemisphere was thinned in patients with orthostatic hypotension compared to normal controls. The other measures of cortical morphology, including the surface area, volume, and curvatures, did not differ between patients with orthostatic hypotension and normal controls. However, none of the measures of cortical morphology differed between patients with postural tachycardia syndrome and normal controls. Conclusions: We demonstrated that the cortical morphology significantly changed in patients with orthostatic hypotension but not in patients with postural tachycardia syndrome compared to normal controls. These findings support the hypothesis that orthostatic intolerance is a heterogeneous syndrome.

Alterations of brain network hubs in reflex syncope: Evidence from a graph theoretical analysis based on DTI

“…Another study observed right insular atrophy in patients with neuro‐cardiogenic syncope with positive response to the head‐up tilt test, implicating the role of right insular dysfunction in the pathophysiologic mechanism underlying neuro‐cardiogenic syncope (Kim et al., ). In addition, we previously demonstrated that the cortical thickness of orbitofrontal, pericalcarine, postcentral, inferior temporal, and lateral occipital cortex significantly changed in patients with orthostatic hypotension but not in patients with postural tachycardia syndrome (Shin et al., ). These discrepancies could be caused by the different subjects and imaging methods used, or produced by the different vulnerable brain structures to hypo‐perfusion according to various subjects.…”

“…Second, postural tachycardia syndrome is a form of dysautonomia. A study using voxel‐based morphometry revealed diminished gray matter volume within the frontal gyrus in patients with postural tachycardia syndrome (Shin et al., ). Third, chronic complex regional pain syndrome is a debilitating pain condition accompanied by autonomic abnormalities.…”

“…Although the pathophysiologic mechanism of reflex syncope is not well understood, especially the afferent part of the reflex, the efferent part of the reflex seem to be elucidated with the rapid decrease in heart rate and blood pressure by change of autonomic nervous system control (Alboni & Alboni, 2017 (Shin et al, 2015). Third, chronic complex regional pain syndrome is a debilitating pain condition accompanied by autonomic abnormalities.…”

“…Intermittent and sudden disruptions in the activity of the autonomic nervous system can occur, causing a sudden drop in blood pressure, heart rate, and brain perfusion (Malamud‐Kessler et al., ). Some evidence suggests that brain abnormalities are associated with reflex syncope, highlighting the fact that specific brain regions modulate the cardiovascular autonomic nervous system (Beacher, Gray, Mathias, & Critchley, ; Kim, Suh, Seo, Koh, & Kim, ; Shin et al., ).…”

Is postural orthostatic tachycardia syndrome (POTS) a central nervous system disorder?

“…In a study of 22 patients with orthostatic hypotension, defined as a sustained reduction in blood pressure greater than 20 mm HG systolic or greater than 10 mm HG diastolic within 3 min of standing or a tilt table test [ 2 ], and 8 patients with POTS using T1-weighted MRI, the cortical thickness in the right hemisphere, including the medial orbitofrontal, peri-calcarine, post-central, inferior temporal, and lateral occipital cortex, and in the peri-calcarine cortex of the left hemisphere was thinned in patients with orthostatic hypotension, but not POTS, compared to normal controls [ 23 ].…”