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Abnormalities of Hippocampal Subfields in Individuals With Acute Carbon Monoxide Poisoning
Mengyue Tang1, Ting Li1, Yan Deng1
1Sichuan Key Laboratory of Medical Imaging, Department of Radiology, Nanchong, Sichuan, PR China.
Insights
Acute carbon monoxide poisoning (ACMP) can cause delayed encephalopathy (DEACMP), characterized by hippocampal subfield volume reductions. These alterations correlate with cognitive deficits, offering potential biomarkers for DEACMP.
Area of Science:
- Neuroscience
- Radiology
- Toxicology
Background:
- Acute carbon monoxide poisoning (ACMP) is a significant cause of acquired brain injury.
- Delayed Encephalopathy After Carbon Monoxide Poisoning (DEACMP) presents with neurological and cognitive deficits.
- The hippocampus is crucial for memory and is vulnerable to hypoxic injury.
Purpose of the Study:
- To investigate alterations in hippocampal subfields in ACMP patients.
- To explore the relationship between these structural changes and neurocognitive function.
- To identify potential imaging biomarkers for DEACMP.
Main Methods:
- Recruited 47 ACMP patients and 29 healthy controls (HCs).
- Assessed carboxyhemoglobin (COHb) levels and performed MRI scans within 3 days of exposure.
- Evaluated cognitive function (MMSE, MoCA) and daily living activities (FIM, BI).
Main Results:
- 27.66% of ACMP patients developed DEACMP.
- DEACMP patients had higher COHb levels and lower cognitive/functional scores.
- Significant hippocampal subfield volume reductions were observed in ACMP patients, particularly in the right subiculum and right CA4 in DEACMP patients.
- COHb, MoCA, and FIM scores predicted DEACMP with high accuracy (AUC=0.887).
- Hippocampal subfield volumes (left CA1, left presubiculum) correlated with delayed recall scores.
Conclusions:
- This study identifies specific hippocampal subfield alterations in ACMP patients.
- These alterations may serve as non-invasive markers of hippocampal injury.
- Hippocampal subfield changes potentially contribute to DEACMP development by affecting cognitive processes.
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.
