Keywords dry eye; blinking; blepharospasm; eyelid movements; blink oscillations; brainstemThe primary purpose of the eyelids is to ensure corneal integrity. An important component of this protective function is maintaining the corneal tear film. Blink characteristics can determine tear film stability. Increasing blink amplitude thickens the lipid layer that overlies the aqueous layer of the tear film. This thickening reduces evaporation of the aqueous layer. Because each blink reforms the tear film, increasing blink frequency reduces tear film breakup. [1][2][3][4] Both innocuous stimuli such as air across the eyelashes, and noxious stimuli such as touching the cornea, elicit trigeminal reflex blinks. If abnormal corneal afferent activity caused by corneal irritation acts as an "error signal" that adjusts the amplitude and frequency of reflex blinks evoked by both innocuous and corneal stimuli, then corneal irritation creates an adaptive blink response regardless of whether a corneal or an innocuous trigeminal stimulus elicits the blink.An investigation of the effects of aging on trigeminal blinks 5 supports the hypothesis that corneal irritation modifies trigeminal reflex blinks evoked by innocuous stimuli. In people over age 40 years, a single innocuous, supraorbital (SO) nerve stimulus frequently evokes a reflex blink and additional blinks that occur at a nearly constant interval relative to the onset of the preceding blink, blink oscillations. Because blink oscillations are more frequent and larger than reflex blinks, this modification increases tear film stability. Peshori and colleagues 5 propose that the development of consistent blink oscillations in many individuals over age 40 years is a blink adaptation that compensates for the subclinical reduction in corneal wetting that accompanies aging. 6 This hypothesis predicts that innocuous SO stimuli should produce more blink oscillations in people with dry eye than in age-matched control subjects. We test this prediction by comparing the SO-evoked blinks of individuals with dry eye with those of age-matched controls. Given the frequent occurrence of dry eye at the onset of benign essential blepharospasm (BEB), 7 blink modifications associated with dry eye may play a role in the origin of BEB. We present a hypothesis that links the adaptive processes initiated by dry eye with the origin of BEB. METHODSMeasurements of eyelid movement and orbicularis oculi electromyographic (OOemg) activity were made on seven subjects, ranging in age from 44 to 72 years of age. Five female subjects had been diagnosed with dry eye at the SUNY Stony Brook Ophthalmology Clinic. The data from these subjects were compared with those from age-matched control subjects in another study. 5 Two normal subjects, a man and a woman, participated in an experimental paradigm described below. Apart from dry eye, no subject had any ocular disorders other than the need for corrective lenses. A previous study 8 detailed measurement of lid movements and OOemg used in the current study. Upper eye...

Neurons located in the border region between the interpolaris and caudalis subdivisions of the spinal trigeminal nucleus (Vi/Vc) are second order neurons of the corneal reflex, receiving corneal afferents and projecting to the lid closing, orbicularis oculi (OO) motoneurons. Recordings of Vi/Vc neurons identified by antidromic activation from stimulation of the facial nucleus and non-identified Vi/Vc neurons reveal two neuron types, phasic and tonic. Corneal stimulation elicits Adelta latency action potentials that occur early enough to initiate OO contraction and C-fiber latency action potentials that can modulate the end of the blink in phasic Vi/Vc neurons. Tonic Vi/Vc neurons exhibit a constant irregular, low frequency discharge as well as the cornea-evoked activity exhibited by phasic neurons. For both phasic and tonic neurons, blink amplitude increases with the total number of spikes evoked by the corneal stimulus. Peak firing frequency predicts peak orbicularis oculi EMG activity. Paradigms that suppress cornea-evoked blinks differentially affect Vi/Vc neurons. Microstimulation of the border region between the spinal trigeminal caudalis subdivision and the C1 spinal cord (Vc/C1) significantly reduces the number of spikes evoked by corneal stimulation and suppresses blink amplitude. In the paired stimulus paradigm, a blink evoked by a corneal stimulus 150 ms after an identical corneal stimulus is significantly smaller than the blink elicited by the first stimulus. Vi/Vc neuron discharge, however, is slightly larger for the second blink. Our data indicate that second-order Vi/Vc neurons do not determine the specific pattern of OO muscle activity; rather Vi/Vc neurons initiate OO motoneuron discharge and program the activity of another circuit that generates the late phase of the blink. The Vc/C1 suppression of Vi/Vc neurons suggests that the Vc/C1 region provides an "internal model" of the intended blink.

The laryngeal adductor response (LAR) is a protective reflex that prevents aspiration and can be elicited either by electrical stimulation of afferents in the superior laryngeal nerve (SLN) or by deflection of mechanoreceptors in the laryngeal mucosa. We hypothesized that because this reflex is life-sustaining, laryngeal muscle responses to sensory stimuli would not be suppressed during volitional laryngeal tasks when compared to quiet respiration. Unilateral electrical superior laryngeal nerve stimulation was used to elicit early (R1) and late (R2) responses in the ipsilateral thyroarytenoid muscle in 10 healthy subjects. The baseline levels of muscle activity before stimulation, R1 and R2 response occurrence and the integrals of responses were measured during each task: quiet inspiration, prolonged vowels, humming, forced inhalation and effort closure. We tested whether R1 response integrals during tasks were equal to either: (1) baseline muscle activity during the task added to the response integral at rest; (2) the response integral at rest minus the baseline muscle activity during the task; or (3) the response integral at rest. R1 response occurrence was not altered by task from rest while fewer R2 responses occurred only during effort closure and humming compared to rest. Because the R1 response integrals did not change from rest, task increases in motor neuron firing did not alter the LAR. These findings demonstrate that laryngeal motor neuron responses to sensory inputs are not gated during volitional tasks confirming the robust life-sustaining protective mechanisms provided by this airway reflex.

In this study we used microstimulation to investigate the influence of the superior colliculus on the trigeminal blink reflex. We report that stimulation in the intermediate to deep layers of the tectum produced inhibition of reflex blinks at a latency of approximately 26 ms. We considered the hypothesis that the blink inhibition was mediated via the omnipause neurons (OPNs) of the eye movement control system in the brainstem. Our results show that the least effective sites for suppression were in the rostral colliculus. This is inconsistent with the prediction that OPNs should be maximally recruited from the rostral tectum near the "fixation zone." From these points and other considerations, we conclude that the reflex blink suppression from the superior colliculus is not directly mediated by the OPNs or the saccadic eye movement circuits.

Hypophonia is an early symptom in Parkinson's disease (PD) that involves an increase in laryngeal muscle activity, interfering with voice production. Our aim was to use an animal model to better understand the role of different dopamine receptor subtypes in the control of laryngeal neurophysiology. First, we evaluated the combined effects of SCH23390-a D(1) receptor antagonist with a D(2) receptor antagonist (eticlopride) on laryngeal neurophysiology, and then tested the separate effects of selective receptor antagonists. Thyroarytenoid (TA) and gastrocnemius (GN) muscle activity was measured at rest and while stimulating the internal branch of superior laryngeal nerve to elicit the laryngeal adductor response (LAR) in alpha-chloralose-anesthetized rats. Paired stimuli at different interstimulus intervals between 250 and 5,000 ms measured central conditioning of the LAR. Changes in resting muscle activity, response latency, amplitude, and LAR conditioning after each drug were compared with the saline control. SCH23390 alone increased the resting TA muscle activity (P < 0.05). With the combined SCH23390 + eticlopride or SCH23390 alone, response latency decreased (P < 0.01), amplitude increased (P < 0.01), and the test LAR was reduced at 2,000-ms ISI (P < 0.01). No LAR changes occurred when eticlopride was administered alone at a low dose and only a tendency to suppress responses was found at a high dose. No changes in GN muscle activity occurred in any of the groups. The results suggest that a loss of stimulation of D(1) receptors plays a significant role in laryngeal pathophysiology in PD.