Abnormal intrinsic brain activity patterns in patients with carbon monoxide poisoning associated with neurotransmitter profiles.

Currently, no study has comprehensively evaluated local neuronal activity in the brain following carbon monoxide poisoning (COP). Moreover, the corresponding pathological changes in brain disease are not randomly distributed, and the molecular mechanism underlying the abnormal neuronal activity pattern associated with COP remains unknown. In this study, low-frequency fluctuation amplitude (ALFF) was combined with neurotransmitter maps to initially explore potential brain activity patterns related to COP and their potential neurochemical basis. In COP patients, brain activity in regions of the higher order association network was decreased, while brain activity in regions of the lower order sensorimotor network was increased, and brain activity in these regions was correlated with the severity of clinical symptoms. In addition, abnormal intrinsic brain activity patterns in COP patients were spatially correlated with the density of neurotransmitter receptors and transporters for monoaminergic neurotransmission (i.e., norepinephrine, serotonin, and dopamine), and N-methyl-D-aspartate receptors. These results suggest that ALFF can characterize COP-related intrinsic brain activity abnormalities, which may be driven by specific neurotransmitter signals in the brain, and that low-frequency fluctuation in specific brain regions can be used to explain clinical symptoms and neurocognitive manifestations.