WHAT YOU'LL LEARN
Understand the pathway and function of the oculomotor nerve and the manifestations of third nerve palsies
Become more confident in the work-up and management of third nerve palsies
Introduction
Introduction
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.
Etiology
Etiology
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:
Vasculopathic or ischemic process
- Diabetes mellitus
- Hypertension
- Hypercholesterolemia
- Coronary artery disease
- Vasculitis
- Giant cell arteritis
Compression
- Aneurysm of the internal carotid or posterior communicating artery
- Raised intracranial pressure
- Pituitary tumor
- Cavernous sinus fistula or thrombosis
Trauma
- Painful ophthalmoplegia
Infectious or inflammatory diseases of the central nervous system or obit
- Multiple sclerosis
- Myasthenia gravis
- Painful ophthalmoplegia
- Grave’s ophthalmopathy
Toxicity
Review of Pathway and Function
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.
Manifestations Based on Pathway Lesion
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
- Lesions within the midbrain: Often produces bilateral results. This is because the oculomotor nerve has multiple subnuclei, and some of those innervate the contralateral eye:
- Central subnucleus innervates bilateral levator palpebrae superioris muscles.
- Medial subnuclei innervates contralateral SR muscle.
- Lateral subnuclei innervates ipsilateral IR, IO, and MR muscles.
- Lesions within the oculomotor nerve fascicles: This can produce several manifestations, including isolated dysfunction of the superior or inferior division only.
- Lesions within the subarachnoid space: This is the highest area of interest as these lesions can produce pupillary involvement. The subarachnoid space is often imaged to rule out a compressive aneurysm near the posterior communicating artery.
- Lesions within the cavernous sinus, superior orbital fissure, or the orbit: These areas can produce an isolated palsy, but they most commonly involve other cranial nerve dysfunctions, proptosis, and/or visual loss.
Clinical Presentation and Work-Up
Clinical Presentation
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:
- Superior division palsy: Mild or full ptosis and inability to look up.
- Inferior division palsy: Inability to look nasal or down.
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.
Work-Up
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:
Digital Subtraction Angiography (DSA)
- Considered the gold standard method.
- Uses iodine-based intra-arterial contrast material to make blood vessels more visible than bone.
- 1-2% risk of complications including stroke, therefore not used as often.
Computed Tomography Angiography (CTA)
- Uses iodine-based intra-venous contrast material reducing risk of complications.
- Shortest scan time.
- Better resolution than MRA, but aneurysms can be obscured by bony artifacts.
- Can be used for patients with implanted metal objects.
- 95% specificity and 95% sensitivity.
MR Angiography (MRA)
- Does not use ionizing radiation or contrast dye, eliminating risk of radiation exposure.
- Lower specificity than CTA.
- Can be used in conjunction with gadolinium-enhanced brain MRI scans.
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):
- Vital signs (blood pressure)
- Fasting blood sugar and hemoglobin A1c
- Complete blood count (CBC) with differential
- Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
- Comprehensive metabolic panel (CMP)
- Platelet count
Treatment and Management
Treatment options and follow-up
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.
Conclusion and References
Conclusion
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.
