Clinical Features

Examination of the eyes can be used to evaluate the three cranial nerves that innervate muscles which move the eyeball (CN III, IV, and VI), sensory fibers of the trigeminal (CN VI) and motor fibers of the facial nerve (CN VII) through the blink reflex, the optic nerve (CN II) and parasympathetic fibers of CN III through the pupillary light reflex, and the sympathetic fibers to the head.

Superior oblique Trochlea (pulley)

Superior oblique Trochlea (pulley)

Figure llt-6-16. Muscles of the Eye

Clinical Correlate

All three of the ocular nerves (CN III, IV, and VI) and the ophthalmic division of CN V traverse the cavernous sinus on their way either to or from the superior fissure. All but the abducens nerve course in the lateral wall of the sinus. The abducens nerve courses through the middle of the sinus adjacent to the internal carotid artery, and, as a result, an internal strabismus may precede a complete ophthalmoplegia on the affected side combined with altered sensation in the forehead, scalp, and over the bridge of the nose.

Lesions of the oculomotor nerve (CN III) present most dramatically in a weakness in the ability to adduct the eyeball. The eyeball will be deviated laterally, and it will be abducted and slightly depressed by the unopposed actions of the lateral rectus and superior oblique. Clinically, the lateral deviation of the eye is known as an external strabismus. CN III lesions also cause a ptosis combined with a dilated pupil (mydriasis), a loss of accommodation, and a loss of the motor limb of the pupillary light reflex, resulting in a loss of the ability to constrict the pupil on the affected side. Fibers in the oculomotor nerve are organized so that parasympathetic fibers lie external to those that supply the extraocular muscles. Therefore, compressive lesions (e.g., temporal lobe herniation, aneurysms) tend to involve the parasympathetic fibers first, producing mydriasis and loss of the pupillary light reflex before paralysis of the extraocular muscles. In contrast, vascular disease (e.g., diabetes mellitus) often affects the deeper fibers, causing ptosis and paralysis of the extraocular muscles while sparing the pupil. Common causes of peripheral CN III lesions include berry aneurysms (most often involving the posterior communicating artery) and compression secondary to a subdural or epidural hematoma caused by head trauma and herniation of the temporal lobe under the free edge of tentorium cerebelli.

Lesions of the trochlear nerve produce a diplopia when attempting to depress the adducted eye. The diplopia is most apparent when the patient looks down and away from the lesioned side. Patients complain of difficulty in reading or difficulty in going down stairs. A loss of intorsion may also be important diagnostically in CN IV lesions. Here, the patient tilts his or her head away from the side of the lesioned nerve to counteract the extorsion by the unopposed inferior oblique and inferior rectus muscles. In children, the head tilt might be mistaken for torticollis caused by abnormal contractions of the sternocleidomastoid muscle.

Lesions of the abducens nerve result in a weakness in the ability to abduct the eyeball. CN VI lesions cause the eye to be deviated medially owing to the unopposed action of the medial rectus muscle and other adductors innervated by CN III. Clinically, a medially deviated eye in CN VI lesions is known as an internal strabismus. Patients with internal strabismus may also present with a "pseudoptosis" in. which the patient shuts the eye on the affected side in an attempt to eliminate the diplopia. The abducens nerve may be the first nerve affected in a cavernous sinus lesion.

Clinical Correlate

Argyll Robertson pupils may be seen in patients with tabes dorsalis caused by tertiary neurosyphilis. Tabetic patients present with pain, paresthesias, and polyuria.

Pupillary light and accommodation reflexes

The direct and consensual light reflex causes both pupils to constrict in response to light and uses the sensory fibers of the optic nerve and the parasympathetic fibers of the oculomotor nerve.

Shining a bright light into one eye causes the pupil of that eye to constrict (direct light reflex) and also causes constriction of the pupil in the other eye, which has not been directly stimulated by light (consensual light reflex). The light reflex uses the sensory fibers in the optic nerve (CN II) and the parasympathetic component of the oculomotor nerve (CN III). The reflex has both direct and consensual components. Light stimulating one retina sends impulses into one optic nerve but into both optic tracts through the partial crossing at the optic chiasm. Both optic tracts send impulses to nuclei in the pretectal region of the midbrain, which in turn project back to both Edinger Westphal nuclei, causing both pupils to constrict. By separately testing the effects of light in each eye, localization of a lesion to either the optic or oculomotor nerve can be determined. The accommodation reflex or near response uses both skeletal motor and parasympathetic fibers in the oculomotor nerve. Movement of an object toward the patient results in a bilateral pupillary constriction, a rounding up of the lens (parasympathetic fibers), and convergence (skeletal motor fibers to both medial rectus muscles).

Head and Neck

Pupillary defects

Defects in the response of both pupils to light can be caused by lesions to either the afferent or efferent limbs of the light reflex. An afferent pupillary defect may result from lesions to the optic nerve and can be evaluated using the swinging flashlight test. When light is presented to the normal eye, both pupils will constrict, but when the flashlight is swung to the affected eye, the affected pupil will paradoxically dilate. Lesions to the oculomotor nerve will cause an efferent pupillary defect. Light presented to either eye will cause the pupil on the normal side to constrict, but the affected pupil will not. In Argyll Robertson pupils, there is a bilateral loss of pupillary constriction Ln response to light, but both pupils react normally in accommodation. The location of the lesion resulting in the Argyll Robertson pupils is thought to be inside the midbrain affecting neurons governing the pupillary response but sparing those controlling the near response.

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