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Blink reflex recovery in facial weakness

An electrophysiologic study of adaptive changes

From the National Institute of Neurological Disorders and Stroke (Drs. Sandbrink, Schulman, Hallett, and Floeter), National Institutes of Health; the Department of Neurology (Dr. Delgado), National Naval Medical Center, Bethesda, MD; and the Neurology Section (Dr. Syed), The Aga Khan University, Karachi, Pakistan.

Address correspondence and reprint requests to Dr. M.K. Floeter, EMG Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive, MSC 1404, Bethesda, MD 20892–1404.

OBJECTIVE: To study the electrophysiologic effects of unilateral facial weakness on the excitability of the neuronal circuitry underlying blink reflex, and to localize the site of changes in blink reflex excitability that occur after facial weakness.

BACKGROUND: Eyelid kinematic studies suggest that adaptive modification of the blink reflex occurs after facial weakness. Such adaptations generally optimize eye closure. A report of blepharospasm following Bell’s palsy suggests that dysfunctional adaptive changes can also occur.

METHODS: Blink reflex recovery was evaluated with paired stimulation of the supraorbital nerve at different interstimulus intervals. Comparisons were made between normal control subjects and patients with Bell’s palsy who either recovered facial strength or who had persistent weakness.

RESULTS: Blink reflex recovery was enhanced in patients with residual weakness but not in patients who recovered facial strength. Facial muscles on weak and unaffected sides showed enhancement. In patients with residual weakness, earlier blink reflex recovery occurred when stimulating the supraorbital nerve on the weak side. Sensory thresholds were symmetric. Conclusion: Enhancement of blink reflex recovery is dependent on ongoing facial weakness. Faster recovery when stimulating the supraorbital nerve on the paretic side suggests that sensitization may be lateralized, and suggests a role for abnormal afferent input in maintaining sensitization. Interneurons in the blink reflex pathway are the best candidates for the locus of this plasticity.

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