Oculomotor nerve palsies, or third nerve palsies, can be complex cases to manage due to varying etiology and clinical presentations. In this course, learn about the treatment options in order to feel more confident when managing these patients in your practice!
Oculomotor nerve palsies can have various aetiologies and clinical presentations, often making it a complex case to manage. This course will summarize the pathway of the oculomotor nerve and the numerous causes of nerve dysfunction, clinical features for complete and incomplete palsies, and treatment options in order to feel more confident with your clinical management.
Early diagnosis of the etiology is essential for determining additional work-up and management care. Keep the following aetiologies in mind when asking case history questions and performing clinical tests1,2,3:
The oculomotor nerve nuclei are located in the midbrain at the level of the superior colliculus. From there, the nerve fibers travel between the posterior and superior cerebral arteries, and along the posterior communicating artery. The nerve pierces the dura mater and enters the cavernous sinus, and leaves through the superior orbital fissure.4
At this point the nerve divides into superior and inferior divisions. The superior branch innervates the levator palpebrae superioris and superior rectus muscle, with sympathetic innervation to the superior tarsal muscle. The inferior branch innervates the inferior rectus, inferior oblique, and medial rectus muscles, with parasympathetic innervation to the ciliary ganglion for pupil constriction and accommodation.
The oculomotor nerve travels a long path from the midbrain to the EOM muscles. The manifestations of the palsy may depend on the location of the lesion along the pathway.5
Patients presenting with an oculomotor nerve palsy will likely complain of diplopia and the ptosis at the time of onset, with or without ocular pain. Additional neurological manifestations that can be associated with the palsy include hemiplegia, involuntary muscle movements, and an altered mental status.
The nerve palsies can present as incomplete or complete depending on where it is affected in the pathway. Incomplete oculomotor nerve palsies can take on various appearances depending on which extraocular muscles are affected:
A complete unilateral palsy has the classic appearance of a full ptosis, the eye positioned down and outward, and a dilated pupil. The eye is unable to adduct, infraduct, or supraduct, and the pupil has a sluggish reaction to light.6
Figure 1. Versions testing on a patient with a complete unilateral left oculomotor nerve palsy.
Versions and ductions are helpful tests when evaluating an incomplete palsy. Versions in nine fields of gaze will identify the affected muscles, while monocular ductions will confirm that the muscle restrictions are neurological if the results are negative.
Pupil testing is crucial for all oculomotor nerve palsies to confirm any pupillary involvement that may be caused by an aneurysm at the posterior communicating artery.
A fixed, dilated (or even partially dilated), poorly reactive pupil suggests that the palsy is pupil-involving. Additional tests to consider include visual fields and exophthalmometry for any visual field defects or proptosis, respectively.
The most important etiology to rule out for all oculomotor nerve palsies is an aneurysm compressing the internal carotid or posterior communicating artery as a ruptured aneurysm has a mortality of up to 50%.7
It is strongly recommended to obtain neuroimaging for all oculomotor nerve palsies immediately, as 14% of patients with an aneurysm demonstrate normal pupillary function at the time of onset.7
Here’s a quick summary of the mode of imaging recommended for these patients:
Ordering any of these three imaging modes is acceptable for the evaluation of an aneurysm, however, CTA is highly recommended as it offers the shortest scan time and can be performed in patients with implanted metal objects.7 If an aneurysm is found, or the results are conflicting with the palsy presentation, then MRA or DSA are often recommended as the secondary test to confirm results.
Once an aneurysm or any other compressive lesion has been ruled out, further testing is required to evaluate the true etiology. Consider a comprehensive work-up for ischemic and inflammatory processes, including8 (Wills eye manual pg 238-240):
Treatment options and follow-up intervals will vary depending on the underlying neurological or systemic condition that is causing the palsy. The initial treatment should focus on addressing the underlying abnormality. It’s important to co-manage this condition along with other health care professionals including primary care physicians, and neurologists. If the palsy is causing diplopia, consider an occlusion patch or Fresnel prism for temporary relief.9
If the palsy is secondary to an ischemic or inflammatory process, patients should have some or full improvement within three to six months. If there is residual diplopia past six months, consider ground-in prism lenses or strabismus surgery for long-term management. For a residual ptosis, consider a referral to oculoplastics for blepharoptosis surgery.
For all patients presenting with a new oculomotor nerve palsy, be concerned for compressive aneurysms by the internal carotid or posterior communicating arteries as the mortality rate, if ruptured, is quite high. For all other aetiologies, collaborate with the appropriate health care professionals to provide the best management.