Oculomotor Nerve (Essay Sample)

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Oculomotor Nerve
The cranial nerve implicated is the oculomotor nerve (Cranial nerve III). The nerve leaves the brainstem through the wall of the cavernous sinus (Drake, Vogl, & Mitchell, 2012). It then leaves through the superior orbital fissure of the skull and it enters the eye orbit. As it leaves the superior orbital fissure, the nerve divides into superior and inferior branches. The oculomotor nerve is primarily responsible for movements pertaining to the eye. These movements include papillary reactions (miosis or mydriasis), elevation of the upper eyelid, and other extraocular movements. Therefore, injury to the nerve can result in impaired vision (double vision), drooping of the eyelid of the affected eye (ptosis), and impaired pupillary reactions. Oculomotor nerve innervates the motor nerve fibers of the upper eyelid. The nerve also has a parasympathetic output whose presynaptic and postsynaptic fibers to sphincter and ciliary muscles of the eye synapse in the ciliary ganglion (Drake et al., 2012). The ciliary and sphincter muscles control movements of the pupil in reaction to different lighting situations.
Rectus muscle (superior, middle, and inferior), levator palpebrae superioris, and the inferior oblique muscles are controlled by the oculomotor nerve complex (Miller, Newman, & Walsh, 2007). The superior division of the nerve innervates the levator palpebrae superioris and the superior rectus muscle, while the other muscles are innervated by the inferior division. Injury of the oculomotor nerve would have happened due to an injury to the head when the elderly woman fell. The abduction and depression of the right eye are due to the unopposed action of the lateral rectus muscle. The medial rectus muscle and the lateral rectus muscle have an antagonistic action (Miller et al., 2007). Therefore, injury to the oculomotor nerve will diminish its effect on the medial rectus or cause in its dysfunction, which affects the antagonistic balance of the muscles. Injury of the nerve disrupts parasympathetic output to the ciliary and sphincter muscles of the eye, leaving the action of sympathetic output uninhibited (Dragoi, n.d). This gives the observed mydriasis of the pupil despite changes in lighting. Injury to the oculomo...