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Departments of Ophthalmology (Drs. Baker, Huffman, and Porter, and M.W. Stava), Neurology (Drs. Baker and Nelson), and Anatomy and Neurobiology (Dr. Porter), University of Kentucky Medical Center, Lexington, KY; and the Departments of Anatomy and Neurology (Dr. May), University of Mississippi Medical Center, Jackson, MS.
A macaque monkey with a preexisting facial nerve injury showed a synkinesis of perioral muscles with blinking and thus provided a serendipitous model for a multiphasic analysis of this common neurologic syndrome. The amplitude of the paretic eyelid in spontaneous and air-puff-induced blinks was about one-third that of the normal eyelid. Despite the blink hypometria, induced blink durations remained matched for the two lids. EMG confirmed co-contraction of the zygomaticus and orbicularis oculi muscles on the affected side during blinking, with silence of the zy-gomaticus on the normal side. Neuroanatomic investigation showed that, on the affected side, some zygomaticus motoneurons were in the somatotopically correct nuclear subdivisions but that the majority were in the dorsal subdivision, which normally innervates the orbicularis oculi. This study supports the contention that some orbicularis oculi motoneurons are incorrectly rerouted to supply the perioral musculature following recovery from a peripheral seventh-nerve injury. This same pattern of relative weakness in eyelid muscles and the stereotyped co-contraction of lid and perioral muscles with blinking occurs in humans, suggesting that aberrant reinnervation may be the mechanism for this clinical phenomenon.
Address correspondence and reprint requests to Dr. Robert S. Baker, Department of Ophthalmology, E304 Kentucky Clinic, University of Kentucky Medical Center, Lexington, KY 40536-0284.
Supported by grants from Research to Prevent Blindness, Inc., the Benign Essential Blepharospasm Research Foundation, and the National Institutes of Health (EY09762, EY09834, and EY10760).
Received March 4,1994. Accepted in final form April 28,1994.
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