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Disorders of the extraocular muscles and neuromuscular junction can produce a virtually unlimited variety of disordered ocular motility patterns because their clinical manifestations are not limited by the scope of a single cranial nerve or supranuclear process. These disorders are frequently bilateral and often involve the levator palpebrae and orbicularis oculi (but not the pupil), and in some cases can result in total bilateral ophthalmoplegia. Not surprisingly, many of these disorders have systemic manifestations.
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Diseases of the extraocular muscles can produce motility disturbances in two ways: (1) the disease process can affect the muscle's ability to contract and thus cause weakness and, (2) the muscle may be stiffened by disease, causing a restriction of muscle movement by tethering. Occasionally both processes are present to some degree, as weak muscles can become fibrotic and restricted over time. Myasthenia gravis and related disorders cause muscle weakness by affecting transmission at the neuromuscular junction with an otherwise normal nerve and muscle.
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Six extraocular muscles insert on the globe. In the horizontal plane, the lateral rectus muscle abducts and the medial rectus muscle adducts the eye. Vertical movement is more complicated because two muscles (superior rectus and inferior oblique) elevate the eye, and two muscles (inferior rectus and superior oblique) depress the eye. The actions of the oblique muscles on the globe may seem mysterious, but they are easily remembered with a clear understanding of how they insert on the globe and the direction of their action (Figure 8–1). Table 8–1 lists the primary and secondary actions of the extraocular muscles. Note that the vertically acting muscles also tort the eye, but the torsional forces are balanced when both elevators (superior rectus and inferior oblique) or both depressors (inferior rectus and superior oblique) are active.
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