Age-related changes in human blinks. Passive and active changes in eyelid kinematics.

PURPOSE: The authors analyzed eyelid kinematics in normal aging subjects to test the hypothesis that eyelid movements exhibit age-related changes and that blink disorders prevalent among the elderly, in turn, represent an outcome of normal aging processes. METHODS: The electromagnetic search coil technique was used to study blinks in normal human subjects for each decade from 40 to 89 years. Blink metrics (amplitude, peak velocity, and duration), main sequence relationships, and conjugacy were assessed. RESULTS: Mean amplitude and peak velocity of blinks decreased with age for spontaneous blinks and, to a lesser extent, for voluntary blinks. Some but not all, of this decline could be attributed to a peripheral phenomenon, narrowed palpebral fissure width. The spontaneous blink down phase main sequence slope also declined with age. By contrast, blink rate and the coordination of movements of the two eyelids--blink conjugacy--exhibited no change. CONCLUSIONS: These data demonstrate that disorders of blink systems typically seen in persons 50 years of age or older occur on a background of normal age-dependent changes in eyelid kinematics. Alterations in main sequence slope imply the operation of central adaptive systems during aging. Reduction in main sequence slope is interpreted as a reduction in aggregate orbicularis oculi motoneuron activity. Such a central neurologic adjustment in the motor output of blink systems may serve to compensate for an age-related increase in blink reflex excitability. Compensatory reduction in the main sequence relationship may offset a potentially hyperexcitable blink reflex, thereby reducing the likelihood of disorders such as blepharospasm. The authors conclude that although there are changes in the kinematics of blinking with age, such changes do not necessarily predispose an aging population to eyelid motility disorders.

Kinematic analysis of eyelid movements in patients recovering from unilateral facial nerve palsy.

We assessed eyelid function by subjective clinical examination and quantitative means in patients recovering from facial nerve palsy. Electromagnetic search coil techniques were used to record the concurrent movements of the two eyelids to study alterations in blink main sequence (peak velocity versus amplitude) relationships and interocular differences in eyelid kinematics. After onset of unilateral palsy, the paresis of eyelid closure showed varying degrees of recovery. Adaptive increases in blink main sequence slope contributed to maximizing closure of the paretic eyelid. However, blink adaptation mechanisms must operate bilaterally, as there also was evidence of altered main sequence slope in the nonparetic eyelid. In general, main sequence slope was inversely related to the level of eyelid paresis. The highest indices of blink adaptation were in those patients with moderate paresis, and main sequence slope was decreased in those patients with increasing degrees of recovery. The assessment of eyelid function with search coil techniques provides a sensitive means of monitoring disease and treatment course. Data also aid understanding of adaptive gain control in the neural control of blink in health and disease.

Aberrant reinnervation of facial musculature in a subhuman primate: a correlative analysis of eyelid kinematics, muscle synkinesis, and motoneuron localization.

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 zygomaticus 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.

Conjugacy of spontaneous blinks in man: eyelid kinematics exhibit bilateral symmetry.

PURPOSE: To provide a quantitative description of the conjugacy of human eyelid movements during spontaneous blinks. METHODS: Eyelid movements occurring during spontaneous blinks were recorded bilaterally using a modification of the electromagnetic search coil technique. In off-line analyses, covariation of amplitude, peak velocity, and duration of blink down phases were determined for the two eyelids. Interocular differences in the timing of blink onset and offset, and time to peak velocity, also were evaluated. RESULTS: Human blink motor control systems act to link tightly the spatial and temporal characteristics of movements of the two eyelids. Data show that human spontaneous blinks are conjugate. Analysis of interocular covariation of blink amplitude, peak velocity, and duration yielded linear functions with high correlation coefficients. Interocular comparison of eyelid movement durations during blinks showed a particularly high correlation. There were negligible interocular differences in blink down-phase onset time, termination time, and time to peak velocity. A small percentage of blinks exhibited interocular differences in amplitude and peak velocity of > 20%; however, even in these cases, blink duration remained tightly linked. CONCLUSION: Spatial and temporal properties of eyelid movements occurring during spontaneous blinks are conjugate. These data support the hypothesis that a bilateral gating mechanism regulates blink duration. Elements downstream from the gate may differentially and unilaterally alter blink amplitude and peak velocity, but the duration of blinks remains time-locked for the two eyelids.

Quantitative analysis of eyelid movement metrics reveals the highly stereotyped nature of monkey blinks.

Blink movement metrics were studied in three alert cynomolgus monkeys using electromagnetic search coils attached to the eyelids bilaterally. Monkey blinks averaged approximately 24 degrees. Down-phase peak velocities were approximately twice those of the corresponding up phases. Most blinks were symmetrical with close temporal linkage of onset and offset between the two eyelids. Monkey blinks exhibited higher peak velocities and shorter durations than have been previously described for similar amplitude movements in humans. Peak velocity vs. amplitude plots were linear and non-saturating within a 45 degrees range for both up and down phases. The relationship between blink peak velocity and average velocity was linear with a slope of approximately 2.0. These values were very similar to those obtained by others, not only for blinks, but also for saccadic eye and ballistic limb movements. Down-phase amplitude-duration behavior could be best described by a linear function with slope < 0.7, while amplitude-duration slope of up phases was best described by a second-order polynomial. Unlike saccadic eye movements, larger amplitude blinks are obtained primarily via increases in peak velocity rather than through extension of blink duration. These data provide mathematical descriptions of monkey blink behavior that indicate the stereotypical nature of blinks. This will serve as a normative data base with which to better understand the neural processing that goes into blinks and will allow the assessment of eyelid movement disorders and evaluation of potential treatments of these disorders.

Types and time course of the alterations induced in monkey blink movements by botulinum toxin.

The alterations induced in eyelid movement metrics subsequent to unilateral injections of botulinum toxin type A into the orbicularis oculi muscle were studied in chronic alert monkeys using the search coil technique. Botulinum toxin caused rapid paralysis of blinks in the treated eyelid. The amplitude and peak velocity of blinks generated by this eyelid remained at or below 20% of that of the fellow, untreated eyelid for 10-20 days. Blink amplitude gain increased linearly thereafter, attaining control values by 40-60 days after injection. Recovery of blink peak velocity was slower. The adaptive alterations in blink duration that were observed during the acute phase of toxin paralysis suggest that the mechanisms responsible for blink reflex plasticity may produce bilateral adjustments in eyelid function. Taken together, these data establish a quantitative data base that can be exploited in order to: (1) better understand the neural adaptive mechanisms that operate during eyelid movements and (2) allow quantitative comparisons between current treatment protocols that employ botulinum toxin and protocols that may lead to improvements in the treatment of chronic eyelid spasm (blepharospasm).