Unilateral Oculomotor Nerve Palsy Secondary to Internal Carotid Artery Aneurysm Without Pupil involvement: A Case Report

Acquired oculomotor palsies (OMP) can result from numerous factors. The most common causes are presumed microvascular, trauma, compressive neoplasm, postneurosurgery and compression from aneurysm.1,2 ONP caused by internal carotid artery (ICA) aneurysm is a common clinical manifestation suggesting impending rupture or re-rupture of the aneurysm.3 Classically, OMP is associated with a complete or incomplete involvement of the levator palpebrae superioris (causing ptosis) and a "down and out" appearance of the ipsilateral eye. This particular eye duction reflects the actions of depression (by the superior oblique muscle innervated by the fourth cranial nerve) and abduction (by the lateral rectus muscle innervated by the sixth cranial nerve of the globe.4 The pupil involvement is seen in the vast majority of patients with compressive third nerve palsies.2 This case report will present a patient with unilateral acquired oculomotor nerve palsy secondary to an incidental left-sided cavernous ICA aneurysm without pupil involvement.

Danilo A Paulo1, Lt Col Richard Blanch,2 1. Birmingham Neuro-Ophthalmology, University Hospitals Birmingham NHS Foundation Trust, B15 2TH, UK. 2. Birmingham Neuro-Ophthalmology, University Hospitals Birmingham NHS Foundation Trust, B15 2TH, UK. Corresponding Author: Mr Richard Blanch, [e-mail] ORCID ID DAP 0000-0002-3217-0026 RJB 0000-0002-6142-3280 Statements and Declarations Funding No funds were used in the preparation of this manuscript. Competing interests DP reports no conflicts. RJB reports no conflicts. Unilateral oculomotor nerve palsy secondary to internal carotid artery aneurysm without pupil involvement: a case report. Danilo Andriatti Paulo, Richard J Blanch. 1) Introduction Acquired oculomotor palsies (OMP) can result from numerous factors. The most common causes are presumed microvascular, trauma, compressive neoplasm, post neurosurgery and compression from aneurysm.1,2 OMP are typically more frequently observed in posterior communicating aneurysms; however, they can also be caused by internal carotid artery (ICA) aneurysms, which often present as clinical manifestations indicating an impending rupture or re-rupture of the aneurysm.3 Classically, OMP is associated with a complete or incomplete involvement of the levator palpebrae superioris (causing ptosis) and a “down and out” appearance of the ipsilateral eye. This particular eye duction reflects the actions of depression (by the superior oblique muscle innervated by the fourth cranial nerve) and abduction (by the lateral rectus muscle innervated by the sixth cranial nerve of the globe.4 The pupil involvement is seen in the vast majority of patients with compressive third nerve palsies.2 This case report will present a patient with unilateral acquired oculomotor nerve palsy secondary to an incidental left-sided cavernous ICA aneurysm without pupil involvement. 2) Case presentation A 77-year-old female patient with type-2 diabetes and essential hypertension complained of progressive trigeminal neuralgia followed by a MRI head reported as the incidental diagnosis of a cavernous ICA aneurysm (Fig 1, 2 and 3). Initially the patient was treated conservatively. 3 months after the diagnosis, she developed sudden onset left-sided ptosis and binocular vertical diplopia. Ophthalmic examination revealed left-sided incomplete ptosis (1mm) and limited extraocular movement with partially impaired adduction and infraduction. Pupil size was symmetric with both pupils equally reactive to light. Her best-corrected visual acuity, colour vision and intraocular pressure were normal in both eyes. Cranial nerves 4-8 were also normal on examination with normal corneal and facial sensation. There was no chemosis, proptosis, conjunctival injection, swollen eyelids, or ocular bruits. Given the acute-onset third nerve palsy, a repeat MRI head with contrast and MRA were performed, revealing suggestive thrombosis due to the absence of flow void on T2-weighted imaging. This finding may account for an increased size of the existing aneurysm compared to the previous image, which previously measured 12.3 x 13.7 x 17.5 mm and currently measures 16.4 x 12.4 x 19.6 mm. As a result, the patient has been referred for neurovascular intervention.. Figure 1 – MRI head scans – arrows in red showing the cavernous ICA aneurysm in different sequences: axial T1, axial T2 and coronal T2 respectively. Figure 2 – axial MRA head scan – arrows in red showing the cavernous ICA aneurysm. 3) Discussion Pupil size and reactivity were historically recognized as clinical factors differentiating the aetiologies of third nerve palsy; particularly compressive lesions from microvascular nerve infarction.5 In the presented case, the patient possessed risk factors for third nerve palsy: early stage diabetes mellitus, essential hypertension and ICA aneurysm. Ischemic microvascular lesions are usually related to diabetes and hypertension, often have intact pupillary function and spontaneously resolve within 3 months. In contrast, intracranial aneurysms and other compressive lesions usually cause compressive stress on superficial parasympathetic fibres, resulting in pupillary motor dysfunction and mydriasis.6 However, pupillary involvement up to 2mm has also been observed in a few cases of microvascular third nerve palsy.7,8 Pupil-sparing third nerve palsies have also been reported in compressive lesions, nevertheless, this is very infrequent.9 Kissel at al published that 12 (14.2%) of their 84 patients with aneurysms at or near the junction of the internal carotid and posterior communicating arteries had OMP with no pupils involvement and in only 4 of these patients pupillary involvement developed within 5 days.9 Previously Rucker at al10, Cogan and Mount at al11 and Dailey at al12 published that less than 4% of their patients with OMP secondary to aneurysms had their pupils spared. More recently, a few case reports can be spotted on the literature highlighting the infrequence of isocoric pupils in compressive oculomotor nerve paresis; Fard MA at al13 reported a pupil-sparing third nerve palsy in a 72-year-old patient with a malignant peripheral nerve sheath tumour, and Motoyama at al14 described pupil-sparing oculomotor nerve palsy caused by upward compression of a large posterior communicating artery aneurysm. In this presented case, it was clear that the increase of the ICA aneurysm was responsible for the OMP ipsilaterally; however, no pupil defects were noted, underlining the importance of neurovascular imaging in all cases of acute third nerve palsy. 1) Modi P, Arsiwalla T. Cranial Nerve III Palsy. [Updated 2022 Jul 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. 2) Fang C, Leavitt JA, Hodge DO, Holmes JM, Mohney BG, Chen JJ. Incidence and Etiologies of Acquired Third Nerve Palsy Using a Population-Based Method. JAMA Ophthalmol. 2017 Jan 1;135(1):23-28. doi: 10.1001/jamaophthalmol.2016.4456. PMID: 27893002; PMCID: PMC5462106. 3) Mino M, Yoshida M, Morita T, Tominaga T. Outcomes of Oculomotor Nerve Palsy Caused by Internal Carotid Artery Aneurysm: Comparison between Microsurgical Clipping and Endovascular Coiling. Neurol Med Chir (Tokyo). 2015;55(12):885-90. doi: 10.2176/nmc.oa.2014-0434. Epub 2015 Sep 11. PMID: 26369721; PMCID: PMC4686451. 4) Costello, Fiona. Third Nerve Palsy (Oculomotor Nerve Palsy). Medscape article review. https://emedicine.medscape.com/article/1198462-overview 5) Trobe JD. Third nerve palsy and the pupil. Footnotes to the rule. Arch Ophthalmol. 1988;106(5):601–2. pmid:3358724. 6) Lin, Hsin-Le MD; Hu, Tzu-Te MD∗. Isolated third nerve palsy with pupillary involvement resulting from carotid-cavernous sinus fistula: A case report. Medicine: February 2019 Volume 98 - Issue 6 - p e14472 doi: 10.1097/MD.0000000000014472 7) Goldstein JE, Cogan DG. Diabetic ophthalmoplegia with special reference to the pupil. Arch Ophthalmol. 1960;64:592–600. pmid:13706649. 8) Galtrey CM, Schon F, Nitkunan A. Microvascular Non-Arteritic Ocular Motor Nerve PalsiesWhat We Know and How Should We Treat? Neuroophthalmology. 2014 Nov 21;39(1):1-11. doi: 10.3109/01658107.2014.963252. PMID: 27928323; PMCID: PMC5123092. 9) Kissel JT, Burde RM, Klingele TG, Zeiger HE. Pupil-sparing oculomotor palsies with internal carotid-posterior communicating artery aneurysms. Ann Neurol. 1983;13(2):149–54. pmid:6830174. 10) Rucker CW: Paralysis of the third, fourth, and sixth cranial nerves. Am J Ophthalmol46:787794, 1958 11) Cogan D, Mount HTJ: Intracranial aneurysms causing ophthalmoplegia. Arch Ophrhalmol 70:757-771, 196 12) Dailey EJ, Holloway J, Murto R, Schlezinger N: Evaluation of ocular signs and symptoms in cerebral aneurysm. Arch Ophthalmol 71:463-474, 1964 13) Fard MA, Montgomery E, Miller NR. Complete, Pupil-Sparing Third Nerve Palsy in a Patient With a Malignant Peripheral Nerve Sheath Tumor. Arch Ophthalmol. 2011;129(6):805–820. doi:10.1001/archophthalmol.2011.122 14) Motoyama Y, Nonaka J, Hironaka Y, Park YS, Nakase H. Pupil-sparing oculomotor nerve palsy caused by upward compression of a large posterior communicating artery aneurysm. Case report. Neurol Med Chir (Tokyo). 2012;52(4):202-5. doi: 10.2176/nmc.52.202. PMID: 22522330.