Oculomotor nerve

The superior branch of the oculomotor nerve or the superior division, the smaller, passes medially over the optic nerve. It supplies the superior rectus and levator palpebrae superioris.

The inferior branch of the oculomotor nerve or the inferior division, the larger, divides into three branches.

• One passes beneath the optic nerve to the medial rectus.
• Another, to the inferior rectus.
• The third and longest runs forward between the inferior recti and lateralis to the inferior oblique.
• From the third one, a short thick branch is given off to the lower part of the ciliary ganglion, and forms its short root.

All these branches enter the muscles on their ocular surfaces, with the exception of the nerve to the inferior oblique, which enters the muscle at its posterior border.

The oculomotor nerve (CN III) arises from the anterior aspect of the mesencephalon (midbrain). There are two nuclei for the oculomotor nerve:

• The oculomotor nucleus originates at the level of the superior colliculus. The muscles it controls are the striated muscle in levator palpebrae superioris and other extraocular muscles except for the superior oblique muscle and the lateral rectus muscle.
• The Edinger-Westphal nucleus supplies parasympathetic fibers to the eye via the ciliary ganglion, and thus controls the sphincter pupillae muscle (affecting pupil constriction) and the ciliary muscle (affecting accommodation).

Sympathetic postganglionic fibres also join the nerve from the plexus on the internal carotid artery in the wall of the cavernous sinus and are distributed through the nerve, e.g., to the smooth muscle of superior tarsal (Mueller's) muscle.

Paralysis of the oculomotor nerve, i.e., oculomotor nerve palsy, can arise due to:

• direct trauma,
• demyelinating diseases (e.g., multiple sclerosis),
• increased intracranial pressure (leading to uncal herniation)
  • due to a space-occupying lesion (e.g., brain cancer) or a
  • spontaneous subarachnoid haemorrhage (e.g., berry aneurysm), and
• microvascular disease, e.g., diabetes.

In people with diabetes and older than 50 years of age, an oculomotor nerve palsy, in the classical sense, occurs with sparing (or preservation) of the pupillary reflex. This is thought to arise due to the anatomical arrangement of the nerve fibers in the oculomotor nerve; fibers controlling the pupillary function are superficial and spared from ischemic injuries typical of diabetes. On the converse, an aneurysm which leads to compression of the oculomotor nerve affects the superficial fibers and manifests as a third nerve palsy with loss of the pupillary reflex (in fact, this third nerve finding is considered to represent an aneurysm—until proven otherwise—and should be investigated).[3]

Cranial nerves III, IV, and VI are usually tested together as part of the cranial nerve examination. The examiner typically instructs the patient to hold his head still and follow only with the eyes a finger or penlight that circumscribes a large "H" in front of the patient. By observing the eye movement and eyelids, the examiner is able to obtain more information about the extraocular muscles, the levator palpebrae superioris muscle, and cranial nerves III, IV, and VI. Loss of function of any of the eye muscles results in ophthalmoparesis.

Since the oculomotor nerve controls most of the eye muscles, it may be easier to detect damage to it. Damage to this nerve, termed oculomotor nerve palsy, is known by its down and out symptoms, because of the position of the affected eye (lateral, downward deviation of gaze).

The oculomotor nerve also controls the constriction of the pupils and thickening of the lens of the eye. This can be tested in two main ways. By moving a finger toward a person's face to induce accommodation, their pupils should constrict.

Shining a light into one eye should result in equal constriction of the other eye. Fibers from the optic nerves cross over in the optic chiasm with some fibers passing to the contralateral optic nerve tract. This is the basis of the "swinging-flashlight test".

Loss of accommodation and continued pupillary dilation can indicate the presence of a lesion on the oculomotor nerve.