generate barcode in c# Disorders of the Eyelids and Blinking in Microsoft Office

Creator QR-Code in Microsoft Office Disorders of the Eyelids and Blinking

Disorders of the Eyelids and Blinking
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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
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to the limbus of the cornea and there is a variable prominence of the eyes, depending on the width of the palpebral ssure The function of the eyelids 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 usually attended by a single blink, which is necessarily brief so as not to interfere with vision When the blink duration is prolonged in this context, it is indicative of an abnormally intense effort required to initiate the saccade; usually this is due to frontal lobe or basal ganglionic disease Closure and opening of the eyelids is accomplished through the reciprocal action 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 tonic sympathetic innervation of Muller s muscles, which is innervated by sympathetic bers 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 re exes Central mechanisms for the control of blinking, in addition to the re exive brainstem connections between the third, fth, and seventh nerve nuclei, include the cerebrum, basal ganglia, and hypothalamus Voluntary 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 due to relaxation of the levator muscles Facial paralysis causes the closure to be incomplete Blinking 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 re ex (blinking is always bilateral) are corneal contact (corneal re ex), 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 blink 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, a feature that is readily corroborated by clinical observation The early response consists of only a slight movement of the upper lids; the immediately following response is more forceful and approximates the upper and lower lids Whereas the early part of the blink re ex is beyond volitional control, the second part can be inhibited voluntarily Blepharospasm, an excessive and forceful closure of the lids, which is described on page 93, is a common disorder that occurs in isolation or as part of a number of dyskinesias and druginduced movement disorders Increased blink frequency occurs with corneal irritation, with sensitization of trigeminal nerve endings, and in oculofacial dyskinetic syndromes, such as blepharospasm A reduced frequency of blinking ( 10 per minute) is characteristic of progressive supranuclear palsy and Parkinson disease In these cases, adaptation to repeated supraorbital tapping at a rate of about 1 per second is impaired; therefore the patient continues to blink with each tap on the forehead or glabella The failure to inhibit this response is referred to as the glabellar or Myerson sign A lesion of the oculomotor nerve, by paralyzing the levator
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muscle, causes ptosis, ie, drooping of the upper eyelid A lesion of the facial nerve, as in Bell s palsy, results in an inability to close the eyelids due to weakness of orbicularis oculi, a slight retraction of the upper lid (due to the unopposed action of the levator), and loss of the blink re ex on the affected side In some instances of Bell s palsy, even after nearly full recovery of facial movements, the blink frequency may be reduced on the previously paralyzed side Of neurologic importance is the fact that a trigeminal nerve lesion on one side, by reducing corneal sensation, interferes with the blink re ex on both sides, while a Bell s palsy does not abolish the contralateral blink Aberrant regeneration of the third nerve after an injury may result in a condition wherein the upper lid retracts on lateral or downward gaze (pseudo von Graefe sign) Aberrant regeneration of the facial nerve after Bell s palsy has an opposite effect closure of the lid with jaw movements or speaking The Gunn jaw-winking phenomenon is a synkinesis that may also occur after aberrant regeneration of the facial nerve but is otherwise a congenital and sometimes hereditary anomaly in which a ptotic eyelid retracts momentarily when the mouth is opened or the jaw is moved to one side In other cases, inhibition of the levator muscle and ptosis occurs with opening of the mouth ( inverse Marcus Gunn phenomenon, or Marin Amat syndrome) A useful clinical rule is that a combined paralysis of the levator and orbicularis oculi muscles (ie, the muscles that open and close the lids) nearly always indicates a myopathic disease such as myasthenia gravis or myotonic dystrophy This is because the third and seventh cranial nerves are rarely affected together in peripheral nerve or brainstem disease An infrequent but overlooked cause of unilateral ptosis is a dehiscence of the tarsal muscle attachment; it can be identi ed by the loss of the upper lid fold just below the brow Bilateral ptosis is a characteristic feature of certain muscular dystrophies and myasthenia gravis; congenital ptosis and progressive sagging of the upper lids in the elderly are other common forms An effective way of demonstrating that mild ptosis is in fact bilateral is to lift one side and observe that the opposite lid promptly droops This re ects the enhanced effort required to maintain patency of the lids The combination of bilateral ptosis and mild weakness of lid closure is particularly characteristic of myasthenia Unilateral ptosis is a notable feature of third nerve lesions (see above) and of sympathetic paralysis, as in the Horner syndrome It may be accompanied by an overaction (compensation) of the frontalis and the contralateral levator palpebrae muscles In patients with myasthenia, Cogan has described a lid twitch phenomenon, in which there is a transient retraction of the upper lid when the patient moves visual xation from the down position to straight ahead Brief uttering of the lid margins upon moving the eyes vertically is also characteristic of myasthenia The opposite of ptosis, ie, retraction of the upper lids, often with a staring expression, is observed with orbital tumors and in thyroid disease, the latter being most common causes of unilateral and bilateral proptosis A staring appearance alone is observed in Parkinson disease, progressive supranuclear palsy, and hydrocephalus, in which there may be downturning of the eyes ( sunset sign ) and paralysis of upward gaze The sunset sign is found mostly in children with hydrocephalus Retraction of the eyelids (Collier sign), when part of a dorsal midbrain syndrome, is accompanied by a light-near pupillary dissociation; it is not accompanied by a lid lag (von Graefe sign) on downward gaze, in distinction to what is observed in thyroid ophthalmopathy Slight lid retraction has been observed in a few patients with hepatic cirrhosis, Cushing
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