Abstract Background and aims Delirium is a common complication of ischemic stroke (IS). Its neurophysiological mechanisms remain poorly understood. Ischemic lesions are associated with glutamate-mediated excitotoxicity, and balanced neuronal excitation and inhibition (E/I balance) is crucial for effective neural communication and cognition. We hypothesize that disruption of E/I balance contributes to post-stroke delirium (PSD). Recent computational EEG methods allow non-invasive estimation of E/I balance via the spectral slope of neuronal activity, quantified by the aperiodic exponent (EXP). Methods We analyzed a previously published cohort of 514 patients with IS, of whom 39% developed PSD diagnosed by chart review according to DSM-5 criteria. High-quality EEG recordings and stroke localization were available for 185 patients (50 with PSD, 135 without). Patients were case–control matched for stroke location, admission NIHSS, and age, resulting in 80 patients (40 with PSD, 40 without). For each subject, the first eight artifact-poor 8-second EEG epochs were selected. Aperiodic fitting was performed in the 0.5–40 Hz range, and mean EXP and aperiodic offset (OS) were calculated across all channels excluding Fp1 and Fp2. In a subgroup with middle cerebral artery (MCA) infarction (n=74), EXP and OS were analyzed in ipsi- and contralateral derivations. Group differences were assessed using Welch’s t-test. Results Mean EXP and OS were higher in patients with PSD (Figure 1). In MCA infarction, EXP was increased in both ipsi- and contralateral derivations (Table 1). Conclusions PSD is associated with increased aperiodic exponent, suggesting altered E/I balance as a potential neurophysiological mechanism. Conflict of interest Fenne Vandervorst: nothing to disclose Figure 1 - belongs to Results Figure 2 - belongs to Conclusions
Vandervorst et al. (Fri,) studied this question.