Examining extraocular movements

In this video, from our Clinical Neurology Essentials course, you'll learn about the anatomical relationships between cranial nerves III, IV, and VI in order to recognize abnormalities and localize lesions.

Robert Coni, DO EdS
Robert Coni, DO EdS
19th Mar 2019 • 5m read

There are three cranial nerves that control eye movements—but how can you find out which nerve has been compromised and where the lesion is? In this video, from our Clinical Neurology Essentials course, you'll learn how to test and analyze the eye movements controlled by cranial nerves III (oculomotor), IV (trochlear), and VI (abducens). You'll be able to identify commonly encountered abnormalities and follow the breadcrumbs to find out which nerves are affected and how.

Join our Clinical Neurology Essentials course now!

Confidently choose and perform the most appropriate neurologic examination for any patient! With our Clinical Neurology Essentials course, you'll learn and master basic and advanced examination skills, neuroanatomy, and the art of asking the right questions, so that you can interpret examination findings and localize pathologies with ease.

Start the first chapter of our Clinical Neurology Essentials course for free

Video Transcript

[00:00:00] Let us review the muscles of the orbit, their innervation, and the eye movements they control. There are six muscles controlling extraocular movements, these are controlled by three nerves. The oculomotor nerve, cranial nerve III, controls the majority of the muscles, specifically, it controls superior and inferior rectus, medial rectus, and the inferior oblique. The trochlear nerve, cranial nerve IV, controls one muscle,

[00:00:30] superior oblique. The abducens nerve, cranial nerve VI, also controls one muscle, lateral rectus. In this graphic, you can see the major muscles involved in moving each globe through that cardinal field of view. This is presented for study in a handout from this lesson. So how do we assess eye movements? There are nine cardinal planes of view. Instruct your patient to follow your finger with their eyes, move your finger through the cardinal fields stopping

[00:01:00] for one to two seconds at each extreme of gaze before bringing gaze back to the center each time. As you lead the patient's eyes with your finger, observed for conjugate movement, meaning the globe's move the same distance at the same time, and at each gaze endpoint, observed for nystagmus as you hold that point for two seconds. After each field is observed, test convergence by slowly bringing your finger toward the patient's nose and encourage them to follow.

[00:01:30] Look for pupillary constriction or miosis as the eyes adapt for accommodation. More advanced testing can be done at the bedside. The red glass test involves putting a red glass in front of one eye. I use a camera filter for that. By convention, one should use the right eye then shine a light a few inches from the nose and ask if the red light is all that is seen or if there is separation either horizontally or vertically. Then move through all nine fields of gaze asking the same

[00:02:00] thing. Ask which position produces the greatest degree of separation, this indicates the muscle most involved. Now let's take a closer look at the oculomotor nerve, cranial nerve III. The nucleus of cranial nerve III is located in the midbrain. It exits from the midbrain ventrally between the cerebral peduncles, it passes through the cavernous sinus along with cranial nerves IV, V, and VI and then exits into the orbit. Cranial nerve III innervates four of the

[00:02:30] six extraocular muscles, the superior, inferior, and medial rectus, and the inferior oblique, plus the levator palpebrae which raises the lid. The oculomotor nerve also carries parasympathetic fibers from the Edinger-Westphal nucleus which is also in the midbrain providing the efferent pathway for the pupillary reflex. We can test the pupillary reflex by shining a light in front of the patient's eyes. The efferent fibers from cranial

[00:03:00] nerve II carry this sensory information while the afferent parasympathetic fibers from cranial nerve III carry information back to the eye causing constriction of the pupillo-constrictor muscle. These parasympathetic fibers also innervate the ciliary muscle for accommodation which relaxes and allows the lens to thicken for better close vision. Parasympathetic fibers are carried on the outside of the main nerve bulk and thus with compression of cranial nerve III,

[00:03:30] one will see pupil dilation. Diabetes can lead to nerve infarcts through the small vessel disease of the vasa nervorum. Here, the internal fibers are damaged while external parasympathetic fibers are spared. Motor findings predominate, however, the pupil is spared. Patients have ptosis and the eye is abducted. Ocular migraine can also cause this to occur transiently. The posterior communicating artery course brings it in close proximity to cranial nerve

[00:04:00] III. The artery can develop an aneurysm at its intersections which can compress the nerve. When this happens, the parasympathetic fibers on the surface are first affected and will result in pupillary dilation on that side. This is because of unrestricted sympathetic drive to dilate the pupil. If the aneurysm is large enough, you might see some of the muscles activated by cranial nerve III affected and the patient develops diplopia. Cranial nerve III also passes along

[00:04:30] the medial temporal lobe region known as the cerebral temporal uncus. In circumstances of rapid increased intracranial pressure, the uncus may bulge into and between the falx cerebri where it will compress cranial nerve III. This condition is called uncal herniation and leads the pupil dilation, cranial nerve III palsy, and usually coma. There may be plegia ipsilateral or on the same side as the pupillary dilation

[00:05:00] due to compression of the cerebral peduncle or the crus cerebri by the opposite side of the falx cerebri. One would normally expect plegia on the opposite side of the pupil sign and this special unexpected pathology is known as Kernohan's notch. Midbrain stroke will often cause ocular movement issues especially when there is involvement of the medial longitudinal fasciculus provoking diplopia, muscle diseases or myopathies, and disorders of the neuromuscular

[00:05:30] junction affect ocular motility. What about the trochlear nerve, cranial nerve IV? The nucleus of cranial nerve four is in the midbrain. Fibers cross the midbrain before exiting dorsally on the opposite side. It enters the cavernous sinus, traverses it, traveling with cranial there III and VI, and exits into the orbit. It innervates the superior oblique muscle which rotates the eye inward and when abducted, downward. In cranial nerve

[00:06:00] IV dysfunction, the patient has inability to gaze down and in toward the nose. The eyes deviated upward and outward. This creates vertical diplopia. This might provoke the patient to hold their head slightly tilted away from the affected side which corrects the eye misalignment. The fourth nerve has the longest course of all the cranial nerves. This end the fact that these nerves course from the dorsal surface to the ventral

[00:06:30] surface make it vulnerable to trauma, and it is often injured in closed-head injuries. Other pathologies which may affect cranial nerve IV include aneurism, infection, and neoplasm. Let's finish by looking at the abducens nerve, cranial nerve VI. The nucleus of cranial nerve VI is located in the pons. Its course from its dorsal midbrain exit, takes it into the cavernous sinus and then into the orbit. Cranial nerves VII passes

[00:07:00] dorsally around the nucleus of cranial nerve VI. Cranial nerve VI innervates the lateral rectus muscle which moves the eye laterally. Trauma to the orbit, cavernous sinus thrombosis, and tumors in the cerebellopontine angle region might also affect this cranial nerve.