Effortful Eyelid Opening With Enhanced Mechanoreceptor Stretch in the Superior Tarsal Muscle Accelerates Inferred Microsaccade Frequency and Velocity, Exacerbating Reflexive Frequent Blinking: A Report of Two Cases.

To maintain eyelid opening and arousal without proprioceptive or visual fading, microsaccades of fast-twitch fibers (FTFs) in the levator palpebrae superioris muscle (LPSM) and the global layer of the superior rectus muscle (GLSRM) continually stretch mechanoreceptors in the superior tarsal muscle (STM). This stretch generates proprioceptive signals that induce reflex contractions of LPSM slow-twitch fibers (STFs) and regulate arousal via the mesencephalic trigeminal nucleus (MTN) and locus coeruleus (LC). Concurrently, counteracting microsaccades of FTFs in the global layer of the inferior rectus muscle (GLIRM) stretch putative mechanoreceptors in the inferior tarsal muscle (ITM), inducing reflex contractions of STFs in the palpebral orbicularis oculi muscle (POOM) that anchor the eyelid to the globe and, when excessive, can produce apraxia of eyelid opening. We previously reported a patient with right lower eyelid retractor (LER) disinsertion who had sensitized right ITM mechanoreceptors. She could voluntarily provoke clonic reflex contractions of the right POOM STFs by combining maximal downgaze (effortful GLIRM FTF contractions that enhance ITM stretch) with maximal bilateral upper eyelid opening (effortful LPSM and GLSRM FTF contractions that further enhance STM stretch). This indicated that the contractions resulted from additive overstimulation of STM mechanoreceptors rather than ITM stretch alone. Because the superior colliculus (SC) generates microsaccades via the LC and elevated arousal increases microsaccadic velocity, we hypothesized that enhanced STM mechanoreceptor stretch raises arousal and accelerates the frequency and velocity of microsaccades in LPSM, GLSRM, and GLIRM FTFs via the MTN, LC, and SC. Accelerated microsaccades would continually restretch STM or ITM mechanoreceptors, inducing clonic reflex contractions of LPSM or POOM STFs that manifest as frequent blinking (FB). To test this hypothesis, we examined two patients with bilateral disinsertions of the levator aponeurosis and LER. Their sensitized STM and ITM mechanoreceptors were expected to provoke FB during effortful eyelid opening. We modulated STM and ITM stretch by loading a 3 g weight on the upper eyelid and by digitally elevating or pulling down the lower eyelid, then quantified blink dynamics by video analysis. Preoperatively, digital elevation of the lower eyelid (enhancing ITM stretch) increased reflex POOM STF contractions. These contractions antagonized upper eyelid opening, further stretched the STM, increased reflex LPSM STF contractions, and accelerated FB frequency and velocity in a degree-dependent manner. Adding the 3 g upper eyelid weight further accelerated FB dynamics during effortful opening, whereas pulling down the lower eyelid (slackening the ITM) reduced POOM reflex contractions, slackened the STM, and abolished FB. After surgical aponeurosis reinsertion restored tarsal stability and reduced baseline STM stretch, the combination of upper eyelid weight loading and lower eyelid elevation no longer induced FB at the two-week or six-month follow-up. These clinical observations suggest that enhanced STM mechanoreceptor stretch may accelerate inferred FTF microsaccades across the LPSM, GLSRM, and GLIRM, thereby driving reflex contractions of the antagonistic LPSM and POOM STFs and exacerbating FB.