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Anatomy clinical correlates: Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves

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Anatomy clinical correlates: Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves

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A 32-year-old woman comes to the emergency department complaining of a one-week history of eye pain and double vision. The patient also noticed swelling that started around her right eye but is now around both eyes. She says she feels “warm” but does not have a thermometer at home to take her temperature. Before her symptoms started, she had a toothache, for which she tried ibuprofen. She did not see a dentist. She has no significant past medical or surgical history. Temperature is 38.5°C (101.3°F), pulse is 80/min, respirations are 15/min, and blood pressure is 130/80 mmHg. Physical examination reveals proptosis of both eyes with periorbital edema. In addition, abduction of the right eye is impaired. All other eye movements are normal, and both pupils are 3 mm in diameter and reactive to light. Which of the following is the most likely diagnosis?

Transcript

In order to move our eyes and see the world around us, like watching this osmosis video, we rely on the control of our extraocular muscles which are primarily innervated by three cranial nerves; cranial nerve III, or the oculomotor nerve, cranial nerve IV or the trochlear nerve, and cranial nerve VI or the abducens nerve. These cranial nerves allow us to move our eyes in various directions, and also help to govern certain reflexes of the eyes. Injury to these cranial nerves can lead to a number of problems involving the eye, so understanding their anatomy can help us better understand the clinical consequences of these conditions!

First up, let’s discuss damage to the oculomotor nerve, also called oculomotor nerve palsy. The oculomotor nerve carries both motor and parasympathetic fibers which can be injured either individually or together. When looking at the anatomy of the oculomotor nerve, the parasympathetic fibers are found in the peripheral or superficial portion of the nerve, and the motor fibers are found in the central or deep portion of the nerve. This is significant as more external compression may only affect the parasympathetic fibers, where lesions of central nerve fibers might only affect the motor fibers. Remember, Motor is Middle, and Parasympathetic is Peripheral.

Now, if the motor fibers of the oculomotor nerve are damaged, that results in ophthalmoplegia, meaning impaired function of the four extraocular muscles innervated by the oculomotor, which are the superior, medial and inferior rectus, and the inferior oblique muscles. When these four muscles are impaired, that leaves the two other extrinsic eye muscles unaffected, so their actions are now left unopposed. This means the lateral rectus pulls the eye laterally, and the superior oblique pulls it inferiorly and laterally. Individuals with this type of injury present with the ipsilateral eye in a characteristic ‘down and out’ position. When the individual tries to look in any other direction, they will complain of double vision, or diplopia. Furthermore, there is also paralysis of the levator palpebrae superioris muscle that leads to ptosis, or drooping of the upper eyelid.

On the other hand, damage can occur to the parasympathetic fibers of the oculomotor nerve, which affects the function of the smooth muscle of the sphincter pupillae, that normally constricts the pupil; and to the ciliary body, where parasympathetic stimulation causes a sphincter like contraction of the ciliary body to relax and thicken the lens for near vision accommodation. Impaired parasympathetic innervation of the sphincter pupillae results in mydriasis, a dilated and fixed pupil, due to unopposed action of the dilator pupillae, and this is often referred to as a “blown pupil”. An impaired ciliary muscle results in cycloplegia, which is the inability to accommodate the lens,

Let’s look into the causes of oculomotor nerve injury and their symptom patterns. First up, there’s vascular compromise, such as a midbrain stroke, which can injure the oculomotor nerve before it even leaves the midbrain. This results in damage to the motor fibers of the oculomotor nerve and the typical “down and out” appearance. Additionally, the individual can also develop contralateral hemiparesis if the descending motor tracts which travel through the midbrain are also damaged. This combination of symptoms should raise suspicion for a midbrain stroke.

Remember that the oculomotor nerve leaves the midbrain between the cerebral peduncles and crosses the tentorial notch.

So if there’s a tumor or an intracranial hemorrhage, those can increase the intracranial pressure and cause a transtentorial herniation. One type is an uncal herniation, during which the medial part of the temporal lobe called the uncus is forced through the tentorial notch, which can compress or stretch the oculomotor nerve due to its close proximity. Since the parasympathetic fibers are more superficial, early compression can initially present with a blown pupil. As compression continues, the motor fibers will be affected as well leading to extraocular muscle dysfunction and a “down and out” position of the ipsilateral eye. If pressure continues to increase, the uncus can also compress the contralateral oculomotor nerve, as well as the midbrain, leading to coma.

The oculomotor nerve also courses alongside the posterior communicating artery, as it exits the brain. So if a posterior communicating artery aneurysm occurs, that can compress the oculomotor nerve. Similar to uncal herniations, posterior communicating artery aneurysms can initially present with a blown pupil, with progressive compression leading to motor fiber compression and extraocular muscle dysfunction.

Aneurysms are typically asymptomatic, but with rapidly developing oculomotor palsy together with a sudden onset of severe headache, rupture of a posterior communicating artery aneurysm should be suspected.

Finally, microvascular injury can also cause damage to the oculomotor nerve. One major cause of microvascular injury is diabetes mellitus, as chronically elevated blood glucose levels damage the endothelial cells of blood vessels resulting in ischemia. This process typically affects smaller blood vessels for example as the vasa vasorum, which are small arterial vessels that supply the deep central portion of the oculomotor nerve and can be damaged in diabetic vascular disease. Because the vasa vasorum supplies the central portion of the oculomotor nerve, the motor fibers will become damaged first leading to motor deficits of the oculomotor nerve. However, the parasympathetic nerves may be spared as their blood supply comes from the blood vessels that supply the overlying pia mater of the nerve. So with diabetes mellitus, oculomotor palsy typically spares the pupil, and the light and accommodation reflexes are preserved. Remember our memory trick before where the M in Motor stands for Medial, you can also use the M in diabetes Mellitus to remember Medial as well!

Speaking of the light and accommodation reflexes, let’s discuss a characteristic pupil finding called an Argyll Robertson pupil. This refers to a pupil that does not constrict when exposed to light, but still has a functioning accommodation reflex. The Argyll Robertson pupil is most commonly associated with late stage neurosyphilis.

Now, parts of the light and accommodation reflex share the same pathway. By following and comparing their pathways, we can see the possible sites where a lesion may occur to result in an Argyll Robinson pupil, where one pathway is damaged and the other is preserved. So, both reflex pathways travel together from the retina to the optic tract. From here, the accommodation pathway travels to the lateral geniculate body of the thalamus, to the visual cortex, and eventually back to the superior colliculus of the midbrain and then the Edinger-Westphal nuclei.

The light reflex pathway, on the other hand, differs from the optic tract and goes straight to the pretectal nuclei of the midbrain and then to the Edinger Westphal nuclei. Once both of these pathways travel through the Edinger Westphal nuclei, they both travel with the oculomotor nerve to the eye.

Based on these two different pathways we can see three possible sites of a lesion which may result in preservation of the accommodation reflex, and loss of the pupillary light reflex. First, there may be a lesion of the fibers along their pathway from the optic tract to the midbrain only affecting the pupillary light pathway; second, there may be a lesion of the pretectal nuclei where only the pupillary light reflex synapses; and third, the part of the Edinger Westphal nuclei that only receives input from the pretectal nuclei, not the superior colliculus fibers of the accommodation reflex, may be damaged. It is thought that neurosyphilis affects one of these areas resulting in an Argyll Robertson Pupil.

Let’s take a short break and see if you can recall the clinical features of oculomotor nerve palsy.

Great! Let’s switch gears and look at the trochlear nerve, or CN IV, that innervates the superior oblique muscle. The main role of this muscle is to internally rotate the eye, but remember that it can also depress the eye when it’s adducted.

During trochlear nerve palsy, the individual is unable to turn the eye inferomedially, so the eye deviates superiorly and laterally, resulting in impaired downward gaze and the eye being forced into external rotation. Individuals typically present with vertical diplopia, especially when trying to look down and inwards, especially when reading a book or walking down stairs.