Electroencephalogram prediction of propofol effects on neuromodulation in disorders of consciousness.

Objective: This study aimed to characterize electroencephalogram (EEG) responses to low-dose propofol anesthesia in patients with disorders of consciousness (DoC) of distinct etiologies-traumatic brain injury (TBI), anoxic ischemic encephalopathy (AIE), and cerebrovascular accident (CVA)-and explore their prognostic relevance for recovery after spinal cord stimulation (SCS). Methods: A retrospective cohort of 40 DoC patients (TBI: 15, CVA: 14, AIE: 11) undergoing SCS under propofol anesthesia was analyzed. Pre- and post-anesthesia 19-lead EEG recordings were evaluated for power spectral density (PSD) in δ (0.5-4 Hz), θ (4-8 Hz), α (8-13 Hz), β (13-30 Hz), and γ (30-45 Hz) bands, alongside permutation entropy (PE). Consciousness levels were quantified using the Coma Recovery Scale-Revised (CRS-R) preoperatively and 3 months post-SCS. Etiology-stratified analyses compared neurophysiological and clinical outcomes. Results: Propofol universally suppressed β- (p < 0.001-0.05) and γ-band (p < 0.001-0.05) power across all groups. Etiology-specific EEG patterns emerged: AIE patients displayed reduced frontal α-power (Δ = -0.23, p = 0.03), while TBI/CVA patients showed prefrontal-parietal β/γ suppression (Δβ = -0.41, Δγ = -0.38; p < 0.001). Significant PE reduction (ΔPE = -0.21, p < 0.001) correlated with CRS-R improvement (r = -0.67, p = 0.003) in TBI/CVA subgroups but not in AIE (ΔPE = -0.05, p = 0.12). Three-month outcomes varied by etiology: 20% of TBI patients achieved a minimally conscious state (CRS-R ≥ 10) with enhanced motor (Δ = +0.25, p < 0.01) and visual function (Δ = +0.19, p = 0.03). CVA patients exhibited partial motor (Δ = +0.20, p = 0.007) and arousal gains (Δ = +0.17, p = 0.01), whereas AIE patients showed negligible improvement (mean ΔCRS-R = 0.4 ± 0.3). Conclusion: Propofol-induced EEG modulation reflects etiology-dependent neural network vulnerabilities in DoC. TBI/CVA patients demonstrated entropy reduction linked to clinical recovery, suggesting transient network stabilization that may enhance SCS efficacy. In contrast, AIE-associated static dynamics imply irreversible structural damage. Integrated PSD/PE analysis holds prognostic potential for predicting SCS responsiveness, particularly in TBI/CVA cohorts. These findings advocate etiology-tailored neuromodulation strategies, though multicenter validation is imperative for clinical translation.