Multimodal magnetic resonance imaging (MRI) quantification of hippocampal injury in acute carbon monoxide poisoning: reduced hippocampal volume as a sensitive biomarker linked to cognitive impairment and prognosis.

Background: Acute carbon monoxide poisoning (ACMP) can cause hippocampal injury and cognitive impairment, and some patients develop delayed encephalopathy after ACMP. However, hippocampal abnormalities in the acute stage have not been sufficiently characterized with multimodal magnetic resonance imaging (MRI). This study aimed to evaluate acute-stage hippocampal structural and perfusion-related changes and their associations with cognitive function and later neurological outcomes. Methods: In this prospective cohort study, 57 patients with ACMP who underwent baseline MRI within 3 days after poisoning and 57 healthy controls (HC) matched for sex, age, and education were included. During more than 3 months of clinical follow-up, 15 patients developed delayed encephalopathy after ACMP and 42 achieved full recovery. All participants underwent T2 fluid-attenuated inversion recovery (T2 FLAIR), three-dimensional (3D) T1-weighted structural imaging, and 3D pseudocontinuous arterial spin labeling (3D PCASL). Hippocampal volume, normalized T2 FLAIR signal intensity, and cerebral blood flow (CBF) were quantified. Group differences were analyzed using analysis of covariance (ANCOVA), and associations between hippocampal indices and Montreal Cognitive Assessment (MoCA) scores were evaluated using partial correlation analysis with false discovery rate (FDR) correction. Results: Significant group differences were found in the left hippocampal body volume (F=3.769, P=0.028), right whole hippocampal volume (F=6.374, P=0.003), right hippocampal head volume (F=3.945, P=0.024), and right hippocampal body volume (F=12.586, P<0.001). Post hoc analyses showed that, compared with HC, both the non-delayed encephalopathy and delayed encephalopathy groups had lower left hippocampal body volume (P=0.038 and P=0.040, respectively), lower right whole hippocampal volume (P=0.011 and P=0.004), and lower right hippocampal body volume (both P<0.001). In addition, the delayed encephalopathy group had lower right hippocampal body volume than the non-delayed encephalopathy group (P=0.044). Right whole, head, and body hippocampal volumes were positively correlated with delayed recall scores (all FDR-corrected P≤0.003). In addition, bilateral whole hippocampal volume and bilateral hippocampal body volume were positively correlated with orientation scores (FDR-corrected P=0.013, 0.026, and 0.039 for bilateral whole, right body, and left body volumes, respectively). No significant between-group differences were found in hippocampal T2 FLAIR signal intensity or CBF (all P>0.05). Conclusions: Hippocampal volume reduction is detectable on MRI in the acute stage of carbon monoxide (CO) poisoning, with the right hippocampal body showing the most prominent association with cognitive impairment and subsequent delayed encephalopathy. Acute-stage reduction in right hippocampal body volume may serve as a sensitive imaging marker for early risk stratification in these patients.