Cranial Nerve III (Oculomotor) Palsy
The clinical presentation of CN III palsy is as follows:
- Classic = down and out eye
- CN III supplies majority of muscles controlling eye movements
- LR6, SO4 (lateral rectus = CN VI, superior oblique = CN IV, everything else = CN III)
- In addition, CN III supplies the levator palpebrae and sphincter pupillae (responsible for pupil constrictions)
- May have difficulty with conjugate gaze leading to strabismus and diplopia
If a CN III palsy is present, evaluation of the pupil is a crucial step. The parasympathetic fibers that control pupil constriction run on the outside of CN III. Thus, if the pupil is affected it is most likely due to external compression. Thus, if the pupil is not affected it is usually a result of paralysis of the nerve from ischemia most commonly secondary to diabetes or hypertension. The vasculature runs within the nerve itself and thus does not affect the pupil.
- CN III + pupillary involvement = concern for external compression by aneurysm, mass
- CN III + no pupillary involvement = concern for ischemia secondary to diabetes or hypertension
Bottom Line: If a cranial nerve III palsy is present on your exam, ensure that you have a thorough evaluation of the pupil to help narrow the differential.
Evaluation of Ptosis
When patient’s present with ptosis, it is important to think about three clinical diagnoses associated with ptosis:
- CN III palsy (see notes above)
- Horner’s syndrome
- Myasthenia gravis
Pearls on Horner’s Syndrome:
- Classic Presentation
- Partial ptosis – due to paralysis of Muller’s muscle
- Enophthalmos – backward displacement of eyeball into the orbit
- If concerning for Horner’s and considering imaging for lesion, must consider advanced imaging that includes brain, neck, and chest given that carotid sympathetic plexus and superior cervical ganglion travel down into thoracic region and Horner’s can result from carotid dissection.
Pearls on Myasthenia Gravis (MG):
We discussed the role of ice packs in the diagnosis of MG. Lowering temperature produces improvement in myasthenic muscle function, thought to be from inhibiting acetylcholinesterase function. Ice is applied to the eyelid for 2-10 minutes (intervals of 2, 5, and 10 minutes have been studied).
In MG, there will be an improvement in their ptosis which was measured in studies by measuring the width of the palpebral fissure.
The pros of this are its safety, speed, and ease of administration. The sensitivity has been estimated as 76.9% (CI 49.2%–92.5%) for the 5-minute application and the specificity was 98.3% (CI 90.3%–99.9%) in a recent study evaluating the diagnostic value of the ice test (Chatzistefanou et al. The ice pack test in the differential diagnosis of myasthenic diplopia. Ophthalmo