SAEM Clinical Images Series: A Man with Blurry Vision

cranial nerve

A middle-aged man with a past medical history of hypertension and tobacco use disorder presented to the Emergency Department after evaluation by an ophthalmologist.  He complained of ten days of a right-sided headache and three days of diplopia. He denied eye pain, pain with eye movements, photophobia, and vision loss.

Vitals: Temp 98.4 °F (36.9 °C); BP 122/72; Pulse 90; Resp 16; SpO2 100%

Neuro: Ptosis, “down and out” deviation and pupil dilation of the right eye were noted. Extraocular movements were intact and pupils were reactive to light bilaterally. No other neurologic deficits were observed.


This patient has a partial cranial nerve (CN) III (oculomotor nerve) palsy. CN III is composed of: (a) internal somatic motor fibers that innervate the levator palpebrae superioris (which elevates the upper eyelid) and the medial recti, superior recti, inferior recti, and inferior oblique extraocular muscles, and (b) external parasympathetic fibers innervating the ciliary muscles (involved in accommodation) and sphincter pupillae (involved in pupillary constriction). The presentation of complete isolated CN III palsy generally involves ipsilateral ptosis (due to levator palpebrae paralysis) and “down and out” ocular deviation (due to preservation of superior oblique and lateral rectus function).

The most common etiology of CN III palsy is ischemia of the nerve fibers secondary to diabetes mellitus or hypertension, which preferentially affects the internal somatic fibers that surround the blood supply. This etiology classically results in a pupil-sparing palsy due to preserved function of the external parasympathetic fibers. However, the most feared etiology is an intracranial aneurysm, most commonly a posterior communicating artery aneurysm. This source of external compression classically affects both the internal somatic motor fibers and external parasympathetic fibers, resulting in asymmetric pupil dilation.

Take-Home Points

  • CN III palsy etiologies include ischemia secondary to diabetes mellitus or hypertension, and structural causes, most commonly a posterior communicating artery aneurysm.
  • On exam, complete CN III palsies will present with ipsilateral ptosis, “down and out” ocular deviation, and pupillary dilation. Partial CN III palsies may have a more subtle presentation.
  • New-onset CN III palsy should be evaluated with a CTA to rule out an aneurysm.

  • Biousse V, Newman NJ. Third nerve palsies. Semin Neurol. 2000;20(1):55-74. doi: 10.1055/s-2000-6833. PMID: 10874777. 2. Singh A, Bahuguna C, Nagpal R, Kumar B. Surgical management of third nerve palsy. Oman J Ophthalmol. 2016 May-Aug;9(2):80-6. doi: 10.4103/0974-620X.184509. PMID: 27433033; PMCID: PMC4932800.

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2021 SAEM Annual Meeting | Copyrighted by SAEM 2021 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.