Oculomotor nerve
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The oculomotorius nerve (n. Oculomotorius) is mixed, has motor and autonomic nervous fibers, which are the processes of the cells of the corresponding nuclei located in the midbrain. In the oculomotor nerve, there are also sensitive proprioceptive fibers from those muscles of the eyeball that innervate this nerve. The oculomotor nerve of 10-15 roots is separated from the medial surface of the brain stem (in the intercostal fossa) at the anterior edge of the bridge. Then the nerve passes in the lateral wall of the cavernous sinus and through the upper orbital slot penetrates into the orbit. In the orbit or in front of it, the oculomotor nerve is divided into the upper and lower branches.
The upper branch (r. Superior) of the oculomotor nerve goes sideways from the optic nerve, innervates the muscle lifting the upper eyelid, and the upper rectus muscle of the eye.
The lower branch (r. Inferior) is larger, lying also on the side of the optic nerve. It innervates the inferior and medial rectus muscles of the eye, as well as the lower oblique muscle of the eye. Vegetative fibers depart from the lower branch of the oculomotor nerve in the form of the oculomotor (parasympathetic) root [radix oculomotoria (parasympathica)]. This spine contains preganglionic fibers reaching the ciliary node. The cervical node has a diameter of about 2 mm, located on the lateral surface of the optic nerve. The processes of cells of this node (postganglionic fibers) go to the ciliary muscle of the eye and to the muscle that narrows the pupil.
Nuclear complex of the oculomotor nerve
The nuclear complex of the third pair of cranial nerves (oculomotor) is located in the middle brain at the level of the upper hillock, ventral to the Sylvian aqueduct. It consists of the following paired and unpaired nuclei.
- The core of the leftist is the unpaired caudal structure of the midbrain, innervating both levators. Defeats bounded by this area cause bilateral ptosis.
- The core of the upper rectus muscle is paired, innervating the contralateral superior rectus muscle. The defeat of the nucleus of the third pair of cranial nerves does not affect the ipsilateral nerves, but affects the contralateral superior rectus muscle.
- The nuclei of the medial straight line, the lower line and the lower oblique muscle are paired and innervate the corresponding ipsilateral muscles. Defeats confined to the nuclear complex are relatively rare. More often lesions are associated with vascular disorders, primary tumors and metastases. Involvement of the paired nucleus of the medial rectus muscle causes two-sided internuclear ophthalmoplegia with strabismus, characterized by exotrophy, a violation of convergence and reduction. The defeat of the entire nucleus is often combined with the defeat of the adjacent and caudal nucleus of the IV pair of cranial nerves.
Oculomotor nerve bundle
The bundle consists of efferent fibers coming from the nucleus of the third pair of cranial nerves through the red nucleus and the medial part of the brain stem. Then they get out of the midbrain and go in the interleukinous space. The causes of nuclear and beam damage are similar, except that the beam can demyelinate.
- Benedikt syndrome with damage to the bundle passing through the red nucleus is characterized by damage to the ipsilateral III pair of cranial nerves and contralateral extrapyramidal symptoms, such as hemitremor.
- Weber syndrome with damage to the bundle passing through the brain stem is characterized by the damage to the ipsilateral III pair of cranial nerves and contralateral hemiparesis.
- Nothnagel syndrome with lesion of the fascicle and the upper leg of the cerebellum is characterized by the defeat of the ipsilateral III pair of cranial nerves and cerebellar ataxia. The main causes are vascular disorders and tumors.
- Claude syndrome is a combination of the syndromes of Benedikt and Nothnagel.
Basilar part of the oculomotor nerve
The basilar part begins next to the "roots" that leave the middle brain on the medial surface of the brain stem, before merging into the main trunk. Further, the nerve passes laterally between the posterior cerebral and upper cerebellar arteries and parallel to the posterior connective artery. Since the nerve, passing the base of the skull in the subarachnoid space, is not accompanied by other cranial nerves, the isolated lesion of the third pair of cranial nerves, as a rule, is basilar. There are 2 main reasons:
- An aneurysm of the posterior connective artery before its connection with the internal carotid artery usually manifests itself as an acute, painful lesion of the third pair of cranial nerves with pupillary reactions.
- Head trauma, complicated by extradural or subdural hematoma, can lead to a lower incidence of the temporal lobe through the nerve of the cerebellum. The compression of the third pair of cranial nerves passing over the margin of the outset first causes an irritic miosis followed by mydriasis and complete defeat of the third pair of cranial nerves.
Intracavernous part of the oculomotor nerve
The oculomotor nerve enters the cavernous sinus, perforating the dura mater lateral to the posterior oblique process. In the cavernous sinus, the oculomotor nerve runs in the lateral wall over the IV pair of cranial nerves. In the anterior part of the cavernous sinus, the nerve divides into the upper and lower branches, which penetrate into the orbit through the upper orbital fissure inside the Zinn circle. The main causes of damage to the intracavernous part of the third pair of cranial nerves can be:
- Diabetes, which can cause vascular lesions (with the pupil usually intact).
- Apoplexy of the pituitary (hemorrhagic infarction), which can cause damage to the third pair of cranial nerves (for example, after childbirth), if the pituitary gland extends laterally and is pressed against the cavernous sinus.
- An intracavernous pathology, such as an aneurysm, meningioma, carotid cavernous anastomosis and granulomatous inflammation (Tolosa-Hunt syndrome), can cause damage to the third pair of cranial nerves. Due to its proximity to other cranial nerves, intracavernous lesions of the third pair of cranial nerves usually combine with the defeat of IV and VI pairs of cranial nerves, as well as the first branch of the trigeminal nerve.
Ingriorbital part of the oculomotor nerve
- The upper branch innervates the levator and the upper rectus muscle.
- The lower branch innervates the medial line, the lower line and the lower oblique muscle. The branch to the lower oblique muscle also contains preganglionic parasympathetic fibers from the Edinger-Westphal nucleus, innervating the sphincter of the pupil and the ciliary muscle. The lesions of the lower branch are characterized by the limitation of bringing and lowering the eye and dilated pupils. The lesions of both (upper and lower) branches are usually traumatic or vascular.
Oculomotor fibers of the oculomotor nerve
Between the brain stem and the cavernous sinus, the papillomotor parasympathetic fibers are superficially located in the upper medial part of the third pair of cranial nerves. They are supplied with blood vessels, while the main trunk of the third pair of cranial nerves is through vasa nervorum. Pupillary disorders are very important signs, often helping to differentiate the "surgical" lesion from the "therapeutic" one. Pupillary disorders like other manifestations of defeat of the third pair of cranial nerves are complete or partial, and their reverse development may have some peculiarities. Thus, moderate mydriasis and areactivity may be clinically significant.
- "Surgical" lesions (aneurysms, trauma and wedging of the hook) cause pupillary dysfunction, squeezing the pial vessels and superficially located pupillary fibers.
- "Therapeutic" lesions (hypertension and diabetes) usually spare the pupil. This is because microangiopathy in these cases, affecting the vasa nervorum and causing ischemia of the main nerve trunk, spares the surface pupillary fibers.
These principles, however, are not infallible; pupillary disorders can occur with certain lesions of the third pair of cranial nerves. Associated with diabetes, while the intact pupil does not allow in all cases to exclude aneurysm or other compression lesions. Sometimes pupillary disorders can only be a sign of the defeat of the third pair of cranial nerves (basal meningitis, wedging of the hook).
What do need to examine?
How to examine?