Abnormalities of Hippocampal Subfields in Individuals With Acute Carbon Monoxide Poisoning.

OBJECTIVE

To investigate alterations in hippocampal subfields in patients with acute carbon monoxide poisoning (ACMP) and explore their relationship with neurocognitive function.

MATERIALS AND METHODS

Forty-seven ACMP patients and 29 age- and sex-matched healthy controls (HCs) were recruited. All ACMP patients underwent carboxyhemoglobin (COHb) assessment at admission and acquired MRI scans within 3 days post-exposure. Cognitive functions were assessed using the mini-mental state examination (MMSE) and Montreal Cognitive Assessment (MoCA), and activities of daily living were evaluated using the Functional Independence Measure (FIM) and Barthel Index (BI). Differences in hippocampal volume between groups were analyzed using Analysis of Covariance (ANCOVA), and correlations with cognitive and functional scores were evaluated.

RESULTS

After follow-up, 27.66% (13/47) of ACMP patients developed Delayed Encephalopathy After Carbon Monoxide Poisoning (DEACMP). The COHb concentration was significantly higher in the DEACMP group (median 17.70% vs. 11.95%, z = -2.225, p = 0.026) compared to the Recovery group. The cognitive function scores, delayed memory-related sub-items scores derived from cognitive assessments, and activities of daily living scores in the DEACMP group were lower than those in the Recovery group (all p < 0.05). The ACMP group showed significant volume reduction in the bilateral whole hippocampus, cornu ammonis (CA) cornu ammonis 3, CA4, GC.ML.DG, Moleculat_layer, and right subiculum compared to HCs. The right subiculum and right CA4 volumes were smaller in the DEACMP group than in the Recovery group. The ROC curve analysis indicated that the combination of COHb concentration, MoCA, and FIM scores had good predictive value for DEACMP(the area under the ROC curve = 0.887, p < 0001). Correlation analysis showed that MoCA-delayed recall was positively associated with the volume of the left CA1 subfield (r = 0.357, p = 0.020), and MMSE-delayed recall was positively associated with the volume of the left presubiculum (r = 0.323, p = 0.037).

CONCLUSION

This study is the first to report specific hippocampal subfield alterations in ACMP patients, suggesting their potential as non-invasive markers of hippocampal injury. The hippocampal subfields may contribute to the development of DEACMP by modulating cognitive processes. These findings may improve understanding of the neurological impact of hypoxic injuries in human subject research.