Of all the cranial nerve (CN) palsies that affect the eye, the third (oculomotor) nerve palsy (TNP) requires the most urgent evaluation.1 Third nerve dysfunction may signal an underlying neurologic emergency, such as ruptured cerebral aneurysm or giant cell arteritis. Early recognition and prompt treatment choices are key to reversing clinical and visual defects. The classic presentation of isolated TNP is a “down and out eye” deviation and ptosis with or without pupillary involvement.1
Recognize varying clinical presentations. TNPs, isolated or not, may be partial or complete, congenital or acquired, pupil involving or pupil sparing. In many cases, patients may have additional constitutional, ocular, or neurologic symptoms or signs, such as ataxia or hemiplegia.2 Recognition of these clinical findings, which at times can be subtle, is crucial. Appropriate clinical diagnosis and management rely on distinguishing isolated TNP from TNP that involves other CNs.2
Further clues to underlying pathology. Disruption of the third nerve can occur anywhere along its course from the oculomotor nucleus in the brain to its terminus at the extraocular muscles in the orbit.2 TNP’s effect on the pupil can often aid in diagnosis.3 Pupil-sparing TNP is usually due to microvascular ischemia, as may occur with diabetes or hypertension. Pupil involvement, though, may be the first sign of a compressive lesion.
Influence of age. Among individuals older than 60 years, the annual incidence of isolated TNP has been shown to be 12.5 per 100,000, compared with 1.7 per 100,000 in those younger than 60 years.4 In those older than 50 years, microvascular ischemia tends to be the dominant cause.4 Other possible causes include aneurysm, trauma, and neoplasm, particularly pituitary adenoma and metastatic tumor. In childhood and young adulthood, the most common cause of TNP is trauma.5
Use of vascular imaging is influenced by an individual’s age and clinical risk for an aneurysm. Isolated partial TNP or TNP with pupil involvement suggest compression of the third nerve and the need for immediate imaging. Given the dire implications of intracranial aneurysm, most physicians will focus their initial evaluation on vascular imaging, if available.2 If clinical findings instead suggest underlying microvascular ischemia, a delay of imaging may be possible.
In the text that follows, we present 4 patient cases describing the clinical investigative process and treatment determinations based on an individual’s history, clinical presentation, and neurologic findings.
Herpes zoster ophthalmicus
An 84-year-old man with no known medical illness presented to the emergency department (ED) with vesicular skin lesions that had appeared 4 days earlier over his scalp, right forehead, and periorbital region. The vesicles followed the distribution of the ophthalmic division of the trigeminal nerve (FIGURE 1). The patient was given a diagnosis of shingles. The only notable ocular features were the swollen right upper eyelid, injected conjunctiva, and reduced corneal sensation with otherwise normal right eye vision at 6/6. For right eye herpes zoster ophthalmicus (HZO), he was prescribed oral acyclovir 800 mg 5 times per day for 2 weeks.
Continue to: Two days later...