Dan Milea MD, PhD Department of Ophthalmology Pitié-Salpêtrière Hospital 83 Boulevard de l'Hôpital 75013 Paris France Tel: + 33 1 42 16 32 14 Fax: +33 1 42 16 32 45 Email: firstname.lastname@example.org
Purpose: The vast majority of ruptured aneurysms of the anterior communicating artery typically present with subarachnoid haemorrhage. Isolated visual complaints are very uncommon in this setting. We present an unusual case of a patient with an acute retrobulbar optic neuropathy, secondary to a ruptured anterior communicating artery aneurysm.
Design: Observational case report.
Methods: A 29-year-old woman was assessed for an acute, isolated unilateral optic neuropathy of unknown origin. Although an initial encephalic MRI was believed to be normal, an underlying ruptured anterior communicating artery aneurysm was eventually diagnosed when the patient became stuporous because of intracranial bleeding.
Conclusions: Occurrence of an acute retrobulbar optic neuropathy may be the initial isolated sign related to a ruptured anterior communicating artery aneurysm, prompting an appropriate neuroradiological assessment.
The vast majority of ruptured aneurysms of the anterior communicating artery typically present with subarachnoid haemorrhage; isolated visual complaints are very uncommon in this setting (Chan et al. 1997). A possible explanation is that an anterior communicating artery aneurysm usually ruptures before becoming large enough to compress the visual pathways (Kasner et al. 1997). In this report, we describe an unusual case of a patient presenting with an acute isolated retrobulbar optic neuropathy, secondary to a ruptured anterior communicating artery aneurysm.
A 29-year-old woman complained of acute, unilateral left vision loss, occurring several hours after the onset of diffuse mild, transient, isolated headache, believed to be secondary to a migraine attack. Her past medical history was unremarkable, except for a similar isolated episode of headache 1 month earlier.
At admission, examination of the left eye revealed 20/40 best corrected vision and unilateral dyschromatopsia. There was a left relative afferent pupillary defect, but no pain on eye movements and no headache. The remainder of the ocular examination was normal, including both ocular fundi. A kinetic perimetry disclosed a left superior altitudinal hemianopia (Fig. 1) and the patient was diagnosed with left retrobulbar optic neuropathy. Both an initial CT scan and MRI with gadolinium injection were considered normal, although not centred on the anterior visual pathways.
Three days later, the headache relapsed and as the patient became progressively stuporous, a spinal tap was performed, disclosing 30 000/mm3 red cells. A new cerebral CT scan confirmed subarachnoid haemorrhage. A cerebral digitalized subtracted angiography (Fig. 2) showed an aneurysm arising from the right part of the anterior communicating artery. The sack extended to the left, thus explaining the involvement of the left subarachnoid cisterns by the haemorrhage. The aneurysm was treated successfully by embolization using detachable platinum coils. One year postoperatively, vision had improved to 20/25 in the affected eye, although left superior hemianopia was still present, associated with pallor of the left optic disc. A follow-up MRI (Fig. 3) allowed us to confirm the anatomical relationship between the optic nerves and the sack filled with the coils. The left optic nerve was displaced and compressed at its inferior level.
Occurrence of monocular visual loss as the initial focal sign after haemorrhage from an anterior communicating aneurysm is a very uncommon event (Chan et al. 1997; Craenen et al. 2004). In a series of six patients collected over 37 years, the affected eye was most often blind, and only one patient was initially found to have a remaining inferotemporal quadrant of vision in the affected eye (Chan et al. 1997). The acute onset of a hemianopic altitudinal visual field loss while the fundus has a normal appearance is suggestive of a posterior ischaemic optic neuropathy, which is classically not associated with a ruptured aneurysm (Sadda et al. 2001). The occurrence of ischaemic optic neuropathy has been already described after anterior communicating artery rupture (Hara et al. 2003), the atrophy of the optic nerve being attributed to an initial optic disc oedema.
Retrospectively, in our case, the review of the initial MRI, considered as ‘normal’, revealed a small parachiasmal hypersignal, which could have initially indicated a neuro vascular imaging procedure.
Previous pathologic specimens after anterior communicating artery ruptured aneurysms showed direct bleeding into the optic nerve (Chan et al. 1997), but vasospasm was also described as a possible explanation (Hara et al. 2003). In our case, postembolization MRI (Fig. 3) suggests that direct inferior compression of the left optic nerve is compatible with the topography of the unilateral superior hemianopia at the initial presentation, but ischaemia in the territory of the arteries distributed in the posterior part of the optic nerve cannot be ruled out.
In conclusion, our case suggests that acute retrobulbar optic neuropathy may be the first visual sign of an anterior communicating artery aneurysm rupture, particularly if associated with headache, prompting an appropriate neuroradiological assessment.