Neuro ophthalmic manifestations of intracranial aneurysms: A case series

Abstract

To report the various neuro-ophthalmic manifestations of patients with intracranial aneurysms at a tertiary eye care center in Southern India. This is a retrospective case series of patients in a single center between January 2017 and January 2018. We present a series of five cases of intracranial aneurysms in the age group of 13 to 66 years comprising four women and one boy. The patients had varied presentations on the initial examination. It is extremely rare that a patient visits a hospital due to visual symptoms caused by an aneurysmal compression of the optic nerve. An intracranial aneurysm needs to be ruled in cases of unexplained unilateral vision loss or nerve palsy. Early diagnosis and prompt treatment can save the patient from complete vision loss or other complications due to an aneurysm.

INTRODUCTION

Intracranial aneurysms occur principally at arterial bifurcations of the circle of Willis at the base of the brain, accounting for 80% to 90% of all aneurysms.^[1] Aneurysms of the anterior communicating artery or the anterior cerebral artery at its junction with the anterior communicating artery usually rupturing before becoming large enough to compress the visual pathways. Visual impairment is usually caused by subarachnoid hemorrhages due to aneurysmal rupture. An aneurysm from the bifurcation of the internal carotid artery presenting with features of ipsilateral optic nerve compression without oculomotor involvement is very rare.^[2] The purpose of this article is to describe the various neuro-ophthalmic manifestations in patients with intracranial aneurysms.

MATERIALS AND METHODS

This is a hospital-based retrospective review of case records of patients seen in our neuro-ophthalmology department between January 2017 to January 2018. All patients with a diagnosis of intracranial aneurysms were included in the analysis. A detailed ocular and systemic history were taken. A complete ocular examination including best-corrected visual acuity and anterior segment examination was done with slit-lamp biomicroscopy and posterior segment examination was done with +90D and indirect ophthalmoscopy. Magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), computerized tomography (CT), and digital subtraction angiography (DSA) had been advised for these patients. After confirmation of diagnosis, they were referred to a neurosurgeon for further management. The study got approved from the Institutional Humans Ethics Committee on 08-April-2022.

RESULTS

Table 1 is a summary of the clinical presentation and treatment of the five patients with intracranial aneurysms seen in our hospital between January 2017 to January 2018. The mean age of presentation was 34.8 years. Four patients were women and one patient was a boy. All patients had unilateral ocular findings on clinical presentation. Three of the five patients were diagnosed to have pupil sparing 3^rd cranial nerve (CN) palsy and the remaining two were diagnosed to have compressive optic neuropathy.

Table 1: Clinical profile of patients

CASE SERIES

The clinical presentation and treatment protocols of five patients who were diagnosed to have intracranial aneurysms and their treatment protocols are tabulated as shown in Table 1. MRI with MRA -giant aneurysm originating from left internal carotid artery bifurcation [Figure 1].

Figure 1: Magnetic resonance imaging (MRI) and Magnetic resonance angiography (MRA): Brain and Orbit without Intravenous contrast revealed a giant aneurysm measuring 2.1*1.9*1.8 cm originating from left internal carotid artery bifurcation with vasospasm and reduction signals in M1, M2, M3, and M4 signals of left middle cerebral artery and ischemic optic neuropathy changes in left optic nerve

DISCUSSION

An aneurysm may originate from any of the intracranial arteries. About 85% of all intracranial aneurysms originate from ICA or one of its branches. About 25% to 40% of all intracranial aneurysms arise from the main trunk of this vessel, usually at the origin of the posterior communicating artery, but also its terminal bifurcation, at the origin of the ophthalmic artery or within the cavernous sinus.^[2]

Most of the unruptured intracranial aneurysms (UIAs) remain asymptomatic. But some patients with UIAs may present with CN palsy. The 3^rd CN palsy is a well-known symptom associated with an intracranial aneurysm commonly co-existing with posterior communicating artery (P-Com) aneurysm. The most common cause of 3^rd CN palsy is diabetic neuropathy and another common cause is compression of the nerve by an intracranial aneurysm. The incidence of 3^rd CN palsy associated with the intracranial aneurysm is reported to be about 13.8%. The possible mechanism of 3^rd CN palsy secondary to intracranial aneurysm are as follows: (1) Direct compression of 3^rd CN by an aneurysmal mass, (2) Pulsating effect of the aneurysm, and (3) Irritation by subarachnoid hemorrhage.^[3]

Oculomotor CN palsy can be classified as complete or incomplete palsy. Complete 3^rd CN palsy is the presence of ptosis, Diplopia, ophthalmoplegia, and pupillary involvement. Incomplete 3^rd CN palsy is partial impairment of extraocular movements with pupillary sparing.

Intracranial aneurysms also cause 6^th CN palsy. They are typically fusiform and arise from the intracavernous carotid artery or vertebrobasilar system. Fusiform aneurysms cause 6^th CN palsy mostly by compression or ischemia of adjacent structures.^[4]

Carotid bifurcation aneurysms account for 4.4% of all single intracranial aneurysms. They occur more frequently in women than in men. Most carotid bifurcation aneurysms become symptomatic only when they bleed. Bifurcation aneurysms may become quite large without rupturing and such aneurysms often produce visual symptoms and signs. Aneurysms of the internal carotid artery are usually detected after the first subarachnoid hemorrhage associated with CN signs. Sudden vision loss is due to acute expansion of the pre-existing asymptomatic aneurysm kinking the optic nerve. Aneurysmal enlargement occurs due to thinning of the wall from episodes of bleeding.

Aneurysms that cause visual deficits due to anterior optic pathway compression can arise in any portion of the circle of willis. The ophthalmic segment of the ICA is located just below the optic nerve and optic chiasma. Unruptured intracranial aneurysms that arise from this location may induce mass effects on the optic pathway.

ICA aneurysms usually compress the ipsilateral optic nerve or chiasma leading to unilateral vision loss or bitemporal hemianopia. When the compression is more anterior, a junctional scotoma may be present with ipsilateral paracentral scotoma progressing to complete visual loss and contralateral temporal quadrantanopia or hemianopia.^[5]

Headache and orbital pain are common and dementia or personality changes are also reported in some cases.^[6] Cervical carotid artery ligation with or without bypass procedure remains a safe and valid treatment. Early diagnosis, no misdiagnosis, and immediate referral to a neurosurgeon have prevented subsequent neurological damage.^[7]

CONCLUSION

In cases of unexplained unilateral or bilateral vision loss or pupil sparing 3^rd CN palsy and 6^th CN palsy, an intracranial aneurysm needs to be ruled out. MRI Brain with MRA is essential and prompt treatment is crucial in preventing morbidity and mortality.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published, and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.