For Patients With Sequelae From Bell's Palsy, Electrical Stimulation May Cause Increased Synkinesis When Aggressively Applied in the Acute Phase of Recovery.

OBJECTIVES: To investigate the phase-specific impact of cumulative nonselective electrical stimulation (ES) on long-term functional sequelae and subsequent botulinum toxin (BoNT) therapeutic durability in patients with severe Bell's palsy. METHODS: In this retrospective cohort study, 317 patients with severe unilateral Bell's palsy (predominantly ≥ 90% ENoG degeneration, all ≥ 80%) who developed clinically confirmed facial synkinesis were analyzed. Patients were stratified based on ES onset timing (acute < 1 month, subacute 1-6 months, and chronic > 6 months) and cumulative duration. Outcomes were assessed using the Sunnybrook Facial Grading System, Synkinesis Assessment Questionnaire (SAQ), and BoNT durability (duration of effect). Age-adjusted analysis (ANCOVA) and machine-learning-based decision tree regression were employed to identify prognostic thresholds. RESULTS: ES exposure was significantly associated with increased synkinesis (9.32 vs. 8.27, p = 0.007) and reduced BoNT durability (3.15 vs. 4.51 months, p < 0.001) compared to the non-ES group. A critical safety threshold for cumulative ES was identified at 4.64 h, beyond which synkinesis scores deteriorated by 35.7% and BoNT durability decreased by 23.8%. Notably, ES showed a strict phase-dependent dichotomy: acute-phase ES correlated with the highest synkinesis (p < 0.001), whereas chronic-phase ES was associated with significantly lower synkinesis (6.11 ± 2.05) and superior functional recovery compared to both acute-phase and non-ES cohorts (p = 0.015). CONCLUSIONS: The impact of ES on facial nerve recovery is highly phase-specific. While chronic-phase application offers therapeutic potential, excessive acute-phase ES correlates with exacerbated synkinesis and reduced BoNT durability. Our data suggest a cumulative safety threshold of 4.64 h, emphasizing the need for a judicious, time-dependent approach to ES during the acute phase of nerve regeneration.