急性一酸化炭素中毒による亜急性遅発性脳症における臨床的回復と関連する皮質微細構造の変化：症例報告

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) causes disabling cognitive-behavioral symptoms. While cortical atrophy is recognized as a correlate of long-term outcome, links between intracortical microstructural dynamics and clinical presentation remain largely unexplored. We followed a 51-year-old man with new-onset DEACMP for 5 months, using serial MRI combining cortical thickness with T1-weighted/T2-weighted (T1w/T2w) mapping as a proxy for intracortical microstructure. Despite progressive cortical thinning, T1w/T2w signals showed heterogeneous, region-specific trajectories. In the frontal networks, increases within premotor and dorsolateral prefrontal cortices aligned with improvements in executive function, whereas limited change in orbitofrontal/ventrolateral cortices was consistent with behavioral disinhibition. Overall, the clinical picture tracked more closely with intracortical signals than with morphometric atrophy. By combining T1w/T2w mapping with morphometry, this case provides the first longitudinal evidence of divergent cortical trajectories in subacute DEACMP-progressive thinning versus early intracortical improvement; confirmation in larger cohorts is warranted.