Year : 2021 Month : February Volume : 10 Issue : 7 Page : 454-457

A Rare Case of Internal Carotid Artery Aneurysm Presenting as Total Ophthalmoplegia

 

Sapan Jaiswal1, Neha Bajpayee2, Abhishek G.U.3

1, 2, 3 Department of Ophthalmology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Medical Sciences (Deemed to Be University), Sawangi (Meghe), Wardha, Maharashtra, India.

CORRESPONDING AUTHOR

Dr. Sapan Jaiswal, Meghdoot Apartments, Datta Meghe Institute of Medical Sciences, Sawangi, Wardha, Maharashtra, India.
Email : sapanjaiswal554@gmail.com

INTRODUCTION

Cerebral aneurysms are pathological focal dilatations of cerebral vasculature that are prone to rupture1. Pathogenesis involves aberrations of cerebral vasculature resulting in compromised integrity of internal elastic lamina with associated defects in adjacent media and adventia.1

Apart from posterior communicating artery aneurysm, internal carotid artery aneurysms account for 4 % of all cerebral aneurysms.2 Paraclinoid aneurysms are defined as those originating from the ICA between the infra clinoid portion (C3) and proximal of the posterior communicating artery. Their classification is given by Al Rodhan3 is as follows:

Type Ia – superior hypophyseal, type Ib – ventral paraclinoid, type II – true ophthalmic, type III – carotid cave, type IV – transitional, type V – intra cavernous.

In literature many cases of cerebral aneurysms presenting with visual symptoms have been reported 4 in which, aneurysms were located on internal carotid artery near ophthalmic artery called as paraclinoid aneurysms.

The unruptured cerebral aneurysms cause mass effect hence producing symptoms of nausea, vomiting and severe headache and later on by compressing surrounding cranial nerves produce ocular symptoms like ophthalmoplegia and ptosis.  The aneurysms may rupture and result in intracranial bleed which again by mass effect can produce the above told symptoms.

We report a case of unruptured intracranial aneurysm presenting with total ophthalmoplegia with visual deficit as the primary symptom.

PRESENTATION OF CASE

 A 27-year-old male patient presented to ophthalmology OPD with complaints of diminution of vision in left eye and drooping of left upper eye lid for 1 week. Patient gives a history of acute onset of symptoms which progressed over a period of 1 week. There was no history of trauma, hypertension, diabetes mellitus or any other cardiovascular abnormalities.

 

 

 

 

 

On Examination

 

Right Eye

Best corrected visual acuity recorded was 6 / 6 in right eye. Anterior segment examination: within normal limits. Ocular movements: free and full in all directions of gaze.  Intraocular pressure was 14 mm hg by applanation tonometry. Fundus examination: clear media, normal disc, normal blood vessels and macula on with bright foveal reflex.

 

Left Eye

Best corrected visual acuity recorded was counting fingers 1 metre in left eye. Anterior segment examination: left upper lid showed severe / grade 3 ptosis. Pupil was dilated and not reacting to light. Ocular movements: were restricted in all directions of gaze in left eye. Intraocular pressure was 16 mm hg by applanation tonometry. Fundus examination: clear media, normal disc, normal vessels and macula was on with bright foveal reflex and a haemorrhagic spot of about half disc diameter noted on peripheral temporal retina.

 

Contrast enhanced CT was advised which revealed a giant internal carotid artery aneurysm in the cavernous region on left side (Figure 4). Left superior ophthalmic vein dilatation. There was no evident bleeding visible in CT. This large aneurysm was pressing on 3rd, 4th and 6th cranial nerves on left side resulting in ophthalmoplegia on left side. Patient was further referred for interventional radiology opinion where he was advised for digital subtraction angiography. Further digital subtraction angiography was done to confirm the diagnosis which showed contrast opacification in the region indicating unruptured internal carotid artery aneurysm in left paraclinoid region measuring approximately 8 mm (Figure 5). Patient’s laboratory results including complete blood count, kidney function test, liver function test and coagulation profile were within normal limits.

 

 

DISCUSSION OF MANAGEMENT

Patient underwent endovascular embolisation by left internal carotid artery aneurysm coiling procedure under local anaesthesia. Cerebral angiogram done post procedure (Figure 6) showed coil noted in situ in paraclinoid region on left side with surrounding metal artefact – indicating successful embolisation and exclusion of aneurysm.