Oculomotor nerve

The oculomotor nerve (n. oculomotorius) is mixed, has motor and autonomic nerve fibers, which are processes of the cells of the corresponding nuclei located in the tegmentum of the midbrain. The oculomotor nerve also contains sensitive proprioceptive fibers from those muscles of the eyeball that this nerve innervates. The oculomotor nerve is separated by 10-15 roots from the medial surface of the cerebral peduncle (in the interpeduncular fossa) at the anterior edge of the bridge. Then the nerve passes in the lateral wall of the cavernous sinus and penetrates into the orbit through the superior orbital fissure. In the orbit or before entering it, the oculomotor nerve divides into upper and lower branches.

The superior branch (r. superior) of the oculomotor nerve runs along the side of the optic nerve, innervating the muscle that lifts the upper eyelid and the superior rectus muscle of the eye.

The inferior branch (r. inferior) is larger and also lies to the side of the optic nerve. It innervates the inferior and medial rectus muscles of the eye, as well as the inferior oblique muscle of the eye. Autonomic fibers extend from the inferior branch of the oculomotor nerve in the form of the oculomotor (parasympathetic) rootlet [radix oculomotoria (parasympathica)]. This rootlet contains preganglionic fibers that go to the ciliary ganglion. The ciliary ganglion has a diameter of about 2 mm and is located on the lateral surface of the optic nerve. The processes of the cells of this ganglion (postganglionic fibers) go to the ciliary muscle of the eye and to the muscle that constricts the pupil.

Nuclear complex of the oculomotor nerve

The nuclear complex of the third pair of cranial nerves (oculomotor) is located in the midbrain at the level of the superior colliculus, ventral to the Sylvian aqueduct. It consists of the following paired and unpaired nuclei.

1. The levator nucleus is an unpaired caudal midbrain structure that innervates both levators. Lesions limited to this region cause bilateral ptosis.
2. The nucleus of the superior rectus muscle is paired and innervates the contralateral superior rectus muscle. Lesions of the nucleus of the third pair of cranial nerves do not affect the ipsilateral, but affect the contralateral superior rectus muscle.
3. The nuclei of the medial rectus, inferior rectus, and inferior oblique muscles are paired and innervate the corresponding ipsilateral muscles. Lesions limited to the nuclear complex are relatively rare. More common lesions are associated with vascular disorders, primary tumors, and metastases. Involvement of the paired nucleus of the medial rectus muscle causes bilateral internuclear ophthalmoplegia with strabismus, characterized by exotropia, impaired convergence, and adduction. Lesions of the entire nucleus are often associated with lesions of the adjacent and caudal nucleus of the fourth pair of cranial nerves.

Oculomotor nerve bundle

The fasciculus consists of efferent fibers that originate from the nucleus of the third cranial nerve through the red nucleus and the medial part of the cerebral peduncle. They then emerge from the midbrain and travel in the interpeduncular space. The causes of nuclear and fasciculus lesions are similar, except that the fasciculus may become demyelinated.

1. Benedikt's syndrome, caused by damage to the fasciculus transversus cerebralis, is characterized by damage to the ipsilateral third cranial nerve and contralateral extrapyramidal symptoms such as hemitremor.
2. Weber syndrome, caused by damage to the bundle passing through the cerebral peduncle, is characterized by damage to the ipsilateral third pair of cranial nerves and contralateral hemiparesis.
3. Nothnagel syndrome with lesions of the cerebellar bundle and superior cerebellar peduncle is characterized by damage to the ipsilateral third pair of cranial nerves and cerebellar ataxia. The main causes are vascular disorders and tumors.
4. Claude syndrome is a combination of Benedikt and Nothnagel syndromes.

Basilar part of the oculomotor nerve

The basilar part begins with a series of "rootlets" that leave the midbrain on the medial surface of the cerebral peduncle, before joining the main trunk. The nerve then runs laterally between the posterior cerebral and superior cerebellar arteries and parallel to the posterior communicating artery. Since the nerve is not accompanied by other cranial nerves as it passes through the base of the skull in the subarachnoid space, isolated lesions of the third pair of cranial nerves are usually basilar. There are 2 main causes:

1. An aneurysm of the posterior communicating artery before its junction with the internal carotid artery usually presents as an acute, painful lesion of the third pair of cranial nerves with pupillary reactions.
2. Head trauma complicated by extradural or subdural hematoma may result in inferior herniation of the temporal lobe through the tentorium cerebelli. Compression of the third pair of cranial nerves, passing over the edge of the tentorium, initially causes irritative miosis followed by mydriasis and complete damage to the third pair of cranial nerves.

Intracavernous part of the oculomotor nerve

The oculomotor nerve enters the cavernous sinus by penetrating the dura mater lateral to the posterior clinoid process. In the cavernous sinus, the oculomotor nerve runs in the lateral wall above the IV cranial nerve. In the anterior part of the cavernous sinus, the nerve divides into superior and inferior branches, which penetrate the orbit through the superior orbital fissure within the circle of Zinn. The main causes of damage to the intracavernous part of the III cranial nerve can be:

1. Diabetes, which can cause vascular damage (in which case the pupil is usually intact).
2. Pituitary apoplexy (hemorrhagic infarction), which can cause damage to the third pair of cranial nerves (for example, after childbirth), if the pituitary gland bulges laterally and is pressed against the cavernous sinus.
3. Intracavernous pathology such as aneurysm, meningioma, carotid-cavernous fistula, and granulomatous inflammation (Tolosa-Hunt syndrome) may be the cause of cranial nerve III lesions. Due to its proximity to other cranial nerves, intracavernous lesions of cranial nerve III are usually associated with lesions of cranial nerves IV and VI, as well as the first branch of the trigeminal nerve.

Intraorbital part of the oculomotor nerve

1. The superior branch innervates the levator and superior rectus muscles.
2. The inferior branch innervates the medial rectus, inferior rectus, and inferior oblique muscles. The branch to the inferior oblique muscle also contains preganglionic parasympathetic fibers from the Edinger-Westphal nucleus that innervate the sphincter pupillae and ciliary muscle. Lesions of the inferior branch are characterized by limited adduction and depression of the eye and a dilated pupil. Lesions of both (superior and inferior) branches are usually traumatic or vascular.

Pupillomotor fibers of the oculomotor nerve

Between the brainstem and the cavernous sinus, the pupillomotor parasympathetic fibers are located superficially in the superomedial part of cranial nerve III. They are supplied by the pial blood vessels, while the main trunk of cranial nerve III is supplied by the vasa nervorum. Pupillary abnormalities are very important signs, often helping to differentiate "surgical" from "therapeutic" lesions. Pupillary abnormalities, like other manifestations of cranial nerve III lesions, are complete or partial, and their regression may have some peculiarities. Thus, moderate mydriasis and areactivity may be clinically significant.

1. "Surgical" lesions (aneurysms, trauma, and hook wedging) cause pupillary abnormalities by compressing the pial vessels and superficial pupillary fibers.
2. "Therapeutic" lesions (hypertension and diabetes) usually spare the pupil. This is explained by the fact that microangiopathy in these cases, affecting the vasa nervorum and causing ischemia of the main nerve trunk, spares the superficial pupillary fibers.

These principles are not infallible, however; pupillary abnormalities may occur with some diabetes-related lesions of the third pair of cranial nerves, while the intactness of the pupil does not always allow one to exclude aneurysm or other compression lesions. Sometimes pupillary abnormalities may be only a sign of a lesion of the third pair of cranial nerves (basal meningitis, herniation of the hook).

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