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Clinical and Experimental Emergency Medicine logoLink to Clinical and Experimental Emergency Medicine
. 2014 Sep 30;1(1):65–66. doi: 10.15441/ceem.14.002

Third cranial nerve palsy and posterior communicating artery aneurysm

Joon-young Kim 1, Sang-Cheon Choi 1,
PMCID: PMC5052823  PMID: 27752555

A 64-year-old woman with a history of diabetes mellitus and smoking was admitted to the emergency department because of headache, vomiting, binocular diplopia and right-sided ptosis. Five days earlier, she had a sudden headache of a stabbing nature in the right frontal area, which recurred every 5 hours. The visual analogue scale (VAS) score for pain was 8. Three days later, she noticed binocular diplopia and right-sided ptosis (Fig. 1A, B). Neurologic examination revealed right-sided third cranial nerve palsy with ipsilateral pupil dilation and no other definite focal neurologic deficits. Computed tomography (CT) scan and CT 3-D angiography revealed a 1-cm saccular aneurysm with lobulated contour in the right posterior communicating artery (Fig. 2A, B). On neurosurgical consultation, coil embolization of the aneurysm was performed successfully. The initial symptoms improved after 2 weeks and completely resolved after a 3-month follow-up in the outpatient department.

Fig. 1.

Fig. 1.

Right-sided third cranial nerve palsy with ipsilateral pupil dilation was shown in images.

Fig. 2.

Fig. 2.

A 1-cm saccular aneurysm with lobulated contour in the right posterior communicating artery was shown in computed tomography (CT) scan and three-dimensional CT angiography.

Unless proven otherwise, acute third cranial nerve palsy with ipsilateral pupillary dilatation is caused by a posterior communicating artery aneurysm [1]. Concomitant headache is a frequent symptom [1,2]. Expansion of such aneurysm may cause compression of the outer fibers of third cranial nerve palsy [1,2]. The pupillomotor fibers are located in the outer portion of this nerve; therefore, the pupil becomes dilated on the affected side. The posterior communicating artery can rupture spontaneously [3,4]. Treatment involves emergent blood pressure reduction if hypertensive, and neuroimaging and neurosurgical intervention [5].

Footnotes

No potential conflict of interest relevant to this article was reported.

REFERENCES

  • 1.Newman SA. Aneurysms. In: Miller NR, Newman NJ, editors. Walsh and Hoyt’s clinical neuro-ophthalmology. 5th ed. Baltimore, MD: Williams & Wilkins; 1998. pp. 3075–83. [Google Scholar]
  • 2.Soni SR. Aneurysms of the posterior communicating artery and oculomotor paresis. J Neurol Neurosurg Psychiatry. 1974;37:475–84. doi: 10.1136/jnnp.37.4.475. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.De la Monte SM, Moore GW, Monk MA, Hutchins GM. Risk factors for the development and rupture of intracranial berry aneurysms. Am J Med. 1985;78(6 Pt 1):957–64. doi: 10.1016/0002-9343(85)90218-9. [DOI] [PubMed] [Google Scholar]
  • 4.Okawara SH. Warning signs prior to rupture of an intracranial aneurysm. J Neurosurg. 1973;38:575–80. doi: 10.3171/jns.1973.38.5.0575. [DOI] [PubMed] [Google Scholar]
  • 5.Nelson PK, Levy D, Masters LT, Bose A. Neuroendovascular management of intracranial aneurysms. Neuroimaging Clin N Am. 1997;7:739–62. [PubMed] [Google Scholar]

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