A consideration of oculomotor disorders would be incomplete without reference to the eyelids and blinking. In the normal individual, the eyelids on both sides are at the same level with respect to the limbus of the cornea and there is a variable prominence of the eyes, depending on the width of the palpebral fissure. The function of the lids is to protect the delicate corneal surfaces against injury and the retinae against glare; this is done by blinking and lacrimation. Eyelid movement is normally coordinated with ocular movement—the upper lids elevate when looking up and descend when looking down. Turning the eyes quickly to the side is sometimes attended by a single blink, which is necessarily brief so as not to interfere with vision. When the blink duration is prolonged, it is indicative of an abnormally intense effort required to initiate the saccade; usually this is because of frontal lobe or basal ganglionic disease.
Closure and opening of the eyelids is accomplished through the reciprocal actions of the levator palpebrae and orbicularis oculi muscles. Relaxation of the levator and contraction of the orbicularis effect closure; the reverse action of these muscles effects opening of the closed eyelids. Opening of the lids is aided by the superior tarsal (Müller) muscle, which is tonically innervated by sympathetic fibers. The levator is innervated by the oculomotor nerve, and the orbicularis by the facial nerve. The trigeminal nerves provide sensation to the eyelids and are also the afferent limbs of corneal and palpebral reflexes. Central mechanisms for the control of blinking, in addition to the reflexive brainstem connections between the third, fifth, and seventh nerve nuclei, include polysynaptic circuits of the cerebrum, basal ganglia, and hypothalamus. Voluntary lid closure is initiated through frontobasal ganglionic connections.
The eyelids are kept open by the tonic contraction of the levator muscles, which overcomes the elastic properties of the periorbital muscles. The eyelids close during sleep and certain altered states of consciousness as a result of relaxation of the levator muscles. Facial paralysis causes the closure to be incomplete.
Normal blinking is always bilateral and occurs irregularly at a rate of 12 to 20 times a minute, the frequency varying with the state of concentration and with emotion. The natural stimuli for the blink reflex are corneal contact, a tap on the brow or around the eye, visual threat, an unexpected loud sound, and, as indicated above, turning of the eyes to one side. There is normally a rapid adaptation of blinking in response to visual and auditory stimuli but not to corneal stimulation.
Electromyography of the orbicularis oculi reveals two components of the blink response, an early and late one; these features are difficult to appreciate by clinical observation alone. The early monosynaptic response consists of only a slight movement of the upper lids; the immediately following polysynaptic response is more forceful and approximates the upper and lower lids. Whereas the early part of the blink reflex is beyond volitional control, the second part may be inhibited voluntarily.
Blepharospasm, an excessive and forceful closure of the lids with increased frequency, is a common disorder that is seen in isolation or as part of a number of dyskinesias and drug-induced movement disorders. Extremes of this condition may result in functional blindness. Treatment for dry eye syndrome is often attempted by ineffective; periodic injections with botulinum toxin can alleviate symptoms. The combination of blepharospasm with dystonic grimacing movements of the lower face is termed Meige syndrome.
The opposite sign, reduced frequency of blinking (< 10/min), is characteristic of Parkinson disease and progressive supranuclear palsy. In these cases, there is reduced adaptation to repeated supraorbital tapping at a rate of about 1/s; therefore, the patient continues to blink with each tap on the forehead or glabella, referred to as the glabellar, or Myerson sign.