Early gray matter atrophy and neurological deficits in patients with carbon monoxide poisoning.

Abstract

To investigate early neurological deficits-related change patterns in gray matter (GM) volume in patients with carbon monoxide poisoning (COP) and GM volume differences between patients with and without delayed neurological sequelae (DNS) and those with and without T2 hyperintense lesions after COP. Forty-one COP patients (24 patients with DNS) and 36 sex- and age-matched healthy controls (HC) were enrolled in this study. The neurological assessments were administered within 24h after MRI scans. Voxel-based morphometry analysis was used to detect regional GM volume change. The COP group had statistically significant GM atrophy in the bilateral prefrontal and temporal lobes, anterior cingulate (ACC), thalamus, posterior cerebellum, and right hippocampus compared to the HC group. Atrophy in the left medial orbital superior frontal gyrus (SFG), bilateral ACC, and bilateral thalamus were related to lower Mini-Mental State Examination (MMSE) scores and higher Unified Parkinson's Disease Rating Scale subsection III and neuro-psychiatric inventory scores. Atrophy in the hippocampus and posterior cerebellum were also related to decrease MMSE scores. The DNS subgroup had greater GM atrophy in the limbic system than the non-DNS subgroup. Compared to the subgroup without T2 hyperintense lesions, greater GM atrophy in the limbic system, motor and visual cortex, and default network was observed in the subgroup with T2 hyperintense lesions. GM atrophy in the medial orbital SFG, ACC, thalamus, hippocampus, and posterior cerebellum is associated with early neurological deficits in patients with COP. Greater atrophy occurred in patients with DNS and those with T2 hyperintense lesions.