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    Asymmetry of Blinking

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    PURPOSE. Too investigate asymmetry in eyelid movements with blinking, the stability of the asymmetry, and its modifiability in normal humans. METHODS. Differences in the start time and amplitude between the two eyelids were assessed for voluntary blinks and reflex blinks evoked by supraorbital trigeminal nerve stimulation. These variables were also measured before and up to 18 months after 2 hours of unilateral upper lid restraint. RESULTS. With voluntary blinks, one eyelid consistently began to close earlier and made a larger eyelid movement than the other eyelid. Stimulation of the supraorbital branch of the trigeminal nerve evoked relatively larger amplitude blinks in one eyelid that correlated with the asymmetries of voluntary blinks. There was a continuum of eyelid asymmetry across all subjects that was stable and independent of other biological asymmetries, such as handedness. Briefly reducing eyelid mobility created a long-lasting change in eyelid asymmetry with blinking. CONCLUSIONS. Eyelid asymmetry results from differences in the excitability of motoneurons in the left and right facial motor nuclei and does not appear to involve asymmetries in cortical inputs to the brain stem. Because adaptive processes modify the motoneuron excitability that creates eyelid asymmetry, these processes may underlie changes in blinking associated with facial palsy and may play a role in the development of disorders that affect one side of the face, such as hemifacial spasm. (Invest Ophthalmol Vis Sci. 2006;47:195-201) DOI: 10.1167/iovs.04-1279 H umans exhibit several motor, sensory, and functional asymmetries in which one side of the body is dominant or more responsive than the other. The most evident motor asymmetry is handedness, with people typically being either right or left handed. In addition to this well-known asymmetry, human facial expressions of happiness and sadness produce larger movements of the left than the right side of the face. 1,2 The accepted explanation of this facial motor asymmetry is specialization of the right cerebral hemisphere for emotional expression. Clinical studies suggest that differences in excitability between motoneurons in the left and right facial motor nuclei may create asymmetries for reflex blinking. Facial palsy patients exhibit increased motoneuron excitability in the facial nucleus on the affected relative to the unaffected side of the face. 4 -6 One explanation for this increased excitability in Bell's palsy is changes in the motoneuron membrane properties caused by axotomy. It is also possible that the increased excitability involves an adaptive increase in excitatory presynaptic drive to facial motoneurons, 7 to compensate for muscle weakness. Consistent with this explanation, mimicking facial palsy with unilateral eyelid restraint in normal humans appears to increase motoneuron excitability in the restrained eyelid in the absence of axotomy. 8 Our study determined whether eyelid asymmetry exists in normal individuals and investigated whether eyelid asymmetries result from cortical or brain stem mechanisms. Assessing the timing and amplitude of left and right eyelid movement with cortically controlled voluntary blinks and brain stemgenerated trigeminal reflex blinks demonstrates the presence of functional eyelid asymmetry. Comparison of the eyelid asymmetry present in voluntary and reflex blinks showed that a difference in motoneuron excitability is the primary source of eyelid asymmetry in both voluntary and reflex blinks. We also showed that eyelid asymmetry is a modifiable property of the eyelid motor system. METHODS Subjects All experiments adhered to the tenets of the Declaration of Helsinki. Informed consent from the participants and prior institutional review board approval were obtained. The 18 subjects, 10 men and 8 women, ranging from 22 to 59 (mean, 29 Ï® 10) years of age, did not have any history of medications or neurologic, eye, or eyelid disorders that would affect blinking. Procedures Upper eyelid position was monitored bilaterally with the magnetic search coil technique using a 30-turn, 2-mm diameter coil attached to the middle of the upper eyelid as close as possible to its margin. 9 Unilateral electrical stimulation of the supraorbital branch of the trigeminal nerve (SO) evoked bilateral trigeminal reflex blinks. To elicit these reflex blinks, a pair of 9-mm diameter gold-plated electrodes (Grass-Telefactor, West Warwick, RI) was placed over both the left and right SO. One electrode of the pair was placed directly over the supraorbital notch and the second approximately 2.5 cm above the first. The SO stimulus was a 170-s constant current delivered at twice the threshold current (2T) necessary to evoke a blink consistently when stimuli occurred with at least a 20-second interstimulus interval. Across all subjects, 2T current intensity ranged from 2.8 to 8 mA. In four of the eighteen subjects, the effect of changing SO stimulus intensity on eyelid asymmetry was also tested. For these subjects, the perception threshold (PT), the lowest SO stimulus intensity at which the subject consistently reported perceiving SO stimulation, was determined. The subjects then received SO stimuli ranging from twice to six times perception threshold (2PT-6PT). Four times perception threshold is roughly equivalent to the twice blink threshold stimulus intensity used for all the other subjects

    Animal Models for Investigating Benign Essential Blepharospasm

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    An Evoked Potential Determination of the Cat

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    (Statement of Responsibility) by L. Craig Evinger(Thesis) Thesis (B.A.) -- New College of Florida, 1973(Electronic Access) RESTRICTED TO NCF STUDENTS, STAFF, FACULTY, AND ON-CAMPUS USE(Bibliography) Includes bibliographical references.(Source of Description) This bibliographic record is available under the Creative Commons CC0 public domain dedication. The New College of Florida, as creator of this bibliographic record, has waived all rights to it worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law.(Local) Faculty Sponsor: Gorfein, Davi
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