Electrophysiological Evidence of Cognitive Dysfunction After tSAH: An ERP Study Based on Three Different Stimulation Paradigms

Objectives: This study aims to investigate the characteristics of event-related potentials (ERP) in patients with traumatic subarachnoid hemorrhage (tSAH) during the clinical stable phase, with the aim of obtaining neuroelectrophysiological indicators that can objectively assess cognitive dysfunction caused by this injury. Methods: A total of 16 healthy volunteers and 33 tSAH patients in the stable phase were recruited. Demographic and clinical data were collected, MMSE assessments were completed, and EEG data for P300, mismatch negativity (MMN), and contingent negative variation (CNV) were recorded using a 32-lead ERP system. ERP analysis was performed by comparing the tSAH group with the healthy control (HC) group and by further dividing the tSAH group into a cognitive impairment subgroup (CI, n = 18) and a normal cognition subgroup (NC, n = 15) based on MMSE scores, with a focus on the mean amplitude and peak latency within specific time windows and their correlation with cognitive behavioral measures. Results: The results showed no significant differences in demographic characteristics between the two groups, while the MMSE scores of the tSAH group were significantly lower than those of the HC group. Compared with HC, the mean amplitude of P300 in response to the target stimuli was significantly reduced in multiple brain regions in the tSAH group and attenuated the negativity of mean CNV amplitudes across multiple brain regions, while no significant differences in mean MMN amplitudes were detected across electrodes and no significant differences were observed in peak latencies of P300 and MMN. The CI group was slightly older than the NC group; after controlling for the effect of age, the Mini-Mental State Examination (MMSE) scores of the CI group were significantly lower than those of the NC group, but no significant differences were found between the two groups in mean amplitudes and peak latencies of P300 and MMN or in mean CNV amplitudes. Conclusions: This study indicates that tSAH may be one of the relevant risk factors for post-traumatic cognitive dysfunction. ERP findings suggest that the allocation of relevant cognitive resources is attenuated in this population, but no differences were detected in the temporal sequence of neural processing. No significant abnormalities were observed during auditory deviance detection corresponding to the MMN time window, and no significant differences in ERP characteristics were found among the subgroups. This study found that tSAH can cause selective cognitive electrophysiological impairment, but ERP electrophysiological changes do not fully match cognitive impairment classified based on clinical scales.