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

## TL;DR

This study shows that acute carbon monoxide poisoning causes specific changes in brain structures linked to memory and cognitive decline.

## Contribution

The first study to identify specific hippocampal subfield volume reductions in acute carbon monoxide poisoning patients.

## Key findings

- ACMP patients showed reduced volumes in bilateral hippocampal subfields like CA3, CA4, and subiculum.
- DEACMP patients had smaller right CA4 and subiculum volumes compared to those who recovered.
- Hippocampal subfield volumes correlated with cognitive test scores, suggesting a role in cognitive impairment.

## Abstract

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

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.

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).

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.

This study investigated the relationship between hippocampal subfield volumes and cognitive impairments in patients with ACMP. We found significant volume reductions in the bilateral CA3, CA4, GC.ML.DG, Moleculat_layer, and right subiculum in ACMP patients. Among ACMP patients, patients who developed DEACMP had smaller volumes in the right CA4 and right subiculum. Specific hippocampal subfields may be involved in the development of DEACMP by potentially modulating cognitive processes.