Surgical decompression for optic neuropathy from carotid artery ectasia: case report with technical considerations.

Abstract

Symptomatic compression of the optic nerve (ON) through its intracranial course or within the orbit may occur at several locations by abnormalities of adjacent soft tissue, bony, or vascular structures. Compressive optic neuropathy secondary to vascular ectasia is a rare phenomenon. An adult male patient presented with a several month history of monocular visual loss. Imaging demonstrated compression of the ipsilateral ON by an ectatic carotid artery. Magnetic resonance imaging, ophthalmologic examination, and cerebral angiography did not demonstrate an alternative etiology of his visual loss. Conservative management was recommended; however, the patient's vision deteriorated further and pterional craniotomy was offered. Intraoperative examination demonstrated a distal origin of the ophthalmic artery that was bulging into, and pulsating against, the adjacent ON. Anterior clinoidectomy, falciform ligament transection, and sponge padding of the ON were then performed. The patient's visual loss improved rapidly postoperatively and at 1 month follow-up the patient exhibited normal visual fields on ophthalmologic testing. We present a patient with severe monocular visual loss and significant anatomic displacement of the ON by an ectatic internal carotid artery-ophthalmic artery complex with dramatic and rapid visual improvement after surgical decompression. Complete untethering of the nerve and total cessation of transmitted pulsatility may not be necessary for symptomatic improvement. Optic nerve contact or displacement by the ipsilateral carotid artery is common in asymptomatic patients, therefore ruling out other etiologies of monocular visual loss before surgical decompression is paramount.