Oculomotor nerve

Damage within the midbrain nuclei

Within the brainstem, organization of the oculomotor and Edinger-Westphal nuclei in the midbrain can mean quite specific localization of damage. More anterior lesions within the oculomotor nucleus would tend to damage motor supply to the ipsilateral inferior rectus, and the sphincter pupillae and ciliary muscles (Edinger-Westphal nucleus). Lesions occurring more posteriorly and laterally would affect the nerve supply to the ipsilateral medial rectus and inferior oblique muscles, whereas as more medially located lesions might affect the supply to the contralateral superior rectus muscle. The nerve supply to the superior rectus is the only case in which the input comes from the contralateral side of the oculomotor nucleus.

Damage within the brainstem

Injury within the midbrain at the level of the oculomotor nucleus can result in two different syndromes:

• Moritz Benedikt syndrome - Is a lesion of the oculomotor nerve fibers as they pass through the red nucleus. A lesion here will result in a contralateral tremor, due to damage to the superior rectus input, and the typical oculomotor nerve lesion symptoms:
  • Deviation of the ipsilateral eye downward and outward (due to action of the intact superior oblique and lateral rectus muscles)
  • A drooping of the ipsilateral eyelid (ptosis) due to a lack of levator palpabrae superioris action
  • Diplopia (double vision)
  • Ipsilateral loss of accommodation and light reflexes due to lack of sphincter pupillae and ciliary muscles
  • Dilation of ipsilateral pupil (unopposed due to lack of sphincter pupillae action)
• Weber syndrome - This syndrome results due to damage located more anteriorly than in Moritz Benedikt syndrome, just before the nerve fibers exit the brainstem. In this case, the typical oculomotor nerve lesion symptoms are present but the contralateral tremor progresses to a contralateral upper motor neuron paralysis affecting the superior rectus.

Damage outside the brainstem

Damage to the oculomotor nerve after it leaves the brainstem results in a collection of symptoms known as oculomotor nerve palsy. Symptoms include:

• Deviation of the ipsilateral eye out downward and outward
• Ptosis
• Double vision
• Ipsilateral pupil dilation
• Unresponsive light and accommodation reflexes in the ipsilateral eye

Recall that as the oculomotor nerve fibers exit the brainstem they pass between the posterior cerebral and superior cerebellar arteries. This makes the oculomotor nerve susceptible to aneurysms that may press on the nerve, or aneurysm rupture, which will manifest as a sudden headache and symptoms of an oculomotor nerve lesion.

Interestingly, the distribution of visceral and somatic motor fibers, within the oculomotor nerve outside of the brainstem, can also be important clinically. The parasympathetic visceral motor fibers associated with the pupillary light reflex, tend to run superifically within the nerve. Thus they are more susceptible to compression from aneurysms in the posterior cerebral or posterior communicating arteries, as these arteries lie superior to the nerve as it exits the brainstem. On the other hand, in vascular ischemic disease, such as in diabetes, the more centrally located somatic motor fibers tend to be adversely affected. This is because the blood supply to the oculomotor nerve runs deep in the nerve, and interruptions to that blood supply will spare the more superficially located fibers related to the pupillary light reflex.

These details regarding the location of both the somatic motor and visceral motor components of the oculomotor nerve can be of great importance when assessing functioning of the nerve in patients. Oculomotor nerve lesion symptoms associated with visceral motor dysfunction accompanied by head pain would be indicative of an aneurysm. Painless dysfunction of the somatic motor functions of the nerve however, would be indicative of vascular ischemic disease, perhaps as a complication of diabetes.

Nerve testing

Testing the proper functioning of the oculomotor nerve can be quite simple, but it is incredibly important to test both the somatic and visceral motor functioning of the nerve. In addition, testing must be combined with an understanding of the symptoms that would occur from damage to the oculomotor nerve structures within different regions of the brainstem, and also outside of the brainstem.

Somatic motor testing

As we know, the somatic motor function of the nerve supplies input to the majority of the muscles that move the eye. Often the proper functioning of these muscles is tested by getting the patient to follow an object, such as a pen, with their eyes in an ‘H’ pattern. For oculomotor nerve functioning, the practitioner needs to pay special attention to adduction, elevation, and depression of the eye to see if these movements occur. Also he or she must observe the eyelid to see if it is drooping or not.

Visceral motor testing

Testing of two functions needs to occur here: accommodation and the pupillary light reflex. However, testing the pupillary light reflex is perhaps more helpful in terms of isolating oculomotor nerve involvement.

To test accommodation, the practitioner typically has the patient follow the tip of their finger or a pen, as they move it from a distance to close to the patient’s face. Two things should happen: the eyes should both rotate medially and the pupils will constrict. Unfortunately, a lack of medial rotation could be due to damage to the somatic motor input to the medial rectus, and a lack of pupil constriction in both eyes might indicate damage to the optic nerve (CNII) rather than the oculomotor nerve. It is difficult to determine whether there has been damage to the input to the ciliary muscle that changes the shape of the lens with this type of testing.

However, also testing the pupillary light reflex will give a more complete picture of oculomotor nerve involvement. This is normally accomplished by shining a bright light into one eye and watching for pupil constriction in the eye being stimulated with light, and also the contralateral eye. Information that is coming into the brain from the eyes travels via the optic nerve (CNII). This information is sent to both the right and left Edinger-Westphal (EW) nuclei, regardless of which eye is being tested. If the practitioner shines a light in one eye and both pupils constrict, this indicates that both the optic and oculomotor nerves are intact. If the light is shone in one eye and neither pupil constricts, an absence of both the direct and consensual light reflexes, this indicates a lesion to the optic nerve in that eye. In this case the information doesn’t reach the EW nucleus to be passed to the oculomotor nerve in either eye.

If the light is shone is one eye and the pupil in that eye fails to constrict (an absence of the direct light reflex), this indicates an oculomotor nerve lesion to that eye. In this case the information has reached both EW nuclei because the optic nerve is intact, but the oculomotor nerve, to the tested eye, is lesioned, preventing pupil constriction.