Abstract
Peripheral facial nerve palsy (PFP) is characterized by reduced motor performance on one side of face. The electrophysiological findings show smaller or delayed motor and facial reflex responses. It leads to a cortical reorganization and an imbalance in sensorimotor gating is also likely since sensory pathways innervating facial structures are intact and sensory inputs to face are transmitted smoothly. Herein, we aimed to analyze the alterations in sensorimotor gating at the level of brainstem after PFP. To examine sensorimotor gating, we used prepulse modulation (PPM) of blink reflex (BR). We also recorded recovery (RC) of BR to identify excitability changes in the facial nucleus. We included 33 patients with PFP and 39 recordings in those patients. Six patients had serial recordings. Control group was composed of 16 healthy subjects with similar age and gender to the patient group (Table). Baseline BR, BR recovery at ISI of 300 ms and BR-PPM at ISI of 100 ms were performed on the right sides of healthy subjects and on both sides of patients. Severity of PFP was assessed according to clinical findings by House-Brackman scale and using electrophysiological methods. Patients with BR, facial motor response or electromyography findings indicating axon loss more than 85% were considered to have severe axon loss. Time lapse from the onset was categorized as early (<15 days), middle (12–45 days) and late (>45 days). R1, R2 and R2c components of BR on symptomatic side were absent in 17, 9 and 13 recordings, respectively. When they were recorded, latencies were longer and magnitude was lower over symptomatic sides of patients compared to healthy subjects or asymptomatic sides of patients. Multivariate ANOVA showed significance at group level, at prepulse level and group x prepulse level. Mean magnitude of R1 was increased whereas mean R2 and R2c magnitude were reduced in all groups after prepulse stimulation (prepulse inhibition, PPI). Interestingly, suppression of R2 or R2c was lower on both sides of patient group compared to healthy subjects. There was no association between PPM% and categories according to time lapse or HBs. PPM% did not correlate with time lapse, either. Although R2-RC and R2C-RC were lower in healthy subjects compared to both sides of patients, the difference was not significant. When we conducted a multivariate analysis between BR-RC with fixed factor time lapse and HB, recovery rates were significantly lower in patients with lower HB scores. Prepulse inhibition of R2 BR is reduced in patients with PFP. Filtering of facial sensory input at brainstem level is decreased leading to an increased transfer of trigeminal sensory inputs through brainstem. Although increased BR-RC correlated with disease severity, there was no correlation between reduced PPI-BR. Thus, reduced PPI is presumably related to monitor and to choose correct sequence of facial movements.
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