Maladaptive neural compensatory mechanisms in Bell's palsy-induced blepharospasm.

We described four patients with Bell's palsy and blepharospasm and evaluated potential mechanisms that may be responsible for an apparent association between the two disorders. Eyelid movements in spontaneous blinks were studied by the search coil technique in patients with this novel disorder. Kinematic analyses documented bilateral eyelid spasm subsequent to unilateral Bell's palsy. The temporal interval between the onset of palsy and onset of blepharospasm was highly variable (weeks to > 20 years). Changes in the relationship between spontaneous blink peak velocity and amplitude, the main sequence, shared features previously found in uncomplicated Bell's palsy and blepharospasm patients. Furthermore, as in patients with typical Bell's palsy and idiopathic blepharospasm, both normal blinks and spasms were conjugate in spite of interocular differences in blink amplitude/peak velocity. We suggest that there is a correlation between the eyelid palsy and subsequent blepharospasm, and have designated this potentially new disease entity as Bell's palsy-induced blepharospasm. We propose a two-stage model for Bell's palsy-induced blepharospasm in which blink adaptive systems may produce the maladaptive consequence of eyelid spasms.

The role of blink adaptation in the pathophysiology of benign essential blepharospasm.

OBJECTIVE: To investigate eyelid movements in patients with benign essential blepharospasm (BEB), with an emphasis on the characterization of the kinematics of normal and spastic blinks, assessment of interocular differences, and further delineation of the role of adaptive blink mechanisms in eyelid movement disorders. PATIENTS AND METHODS: The electromagnetic search coil technique was used to record the metrics of blinks bilaterally in 5 patients with untreated BEB. Eyelid kinematics and the main-sequence (peak velocity vs amplitude) relationships were analyzed. RESULTS: Patients with BEB exhibited a decrease in blink amplitude and peak velocity. Moreover, the main-sequence slope was decreased bilaterally. Spasms were bilateral and relatively conjugate. There was no change in the coordination of normal blinking across the 2 eyelids. CONCLUSIONS: These data demonstrate the operation of the adaptive regulation of blinking in an eyelid movement disorder. The findings suggest that the adaptive regulation of blink is a bilateral event. Blink-adaptive control systems can act on the blink reflex excitability and main-sequence relationships, changing these either together or independently. The hyperexcitable blink reflex of BEB is met by what is believed to be an adaptive decrease in the main-sequence slope that would decrease the strength of debilitating spasms. Collectively, these data extend the knowledge of the pathophysiology of BEB and, perhaps more important, establish the role of blink system plasticity in eyelid movement disorders.

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.

Bell's Palsy-associated blepharospasm relieved by aiding eyelid closure.

The efficacy of the blink reflex is maintained by adaptive control mechanisms. We describe a 39-year-old woman with the rare complication of blepharospasm-like symptoms appearing contralateral to an eyelid weakened by facial nerve palsy. The hyperexcitable blink reflex may be a maladaptive consequence of adaptive systems but was not accompanied by an expected increase in main sequence slope. Eyelid spasms were eliminated by the implantation of a gold weight to assist closure of the paretic eyelid. We suggest that aiding closure of the weak eyelid in this case caused a reduction in blink system excitability via the same compensatory mechanisms that initially produced the eyelid spasm. Data also suggest that blink-adaptive systems act via changes in reflex excitability and/or main sequence relationships, and that these may be regulated either synergistically or independent of one another.