Visual Loss, Homonymous Hemianopia, and Unilateral Optic Neuropathy as the Presenting Symptoms of Vertebrobasilar Dolichoectasia

Vertebrobasilar dolichoectasia (VBD) is a relatively rare disorder for which unfortunately there is no treatment. Here we describe a case of simultaneous pre- and postchiasmal visual pathway pathology secondary to a space occupying VBD. In addition our patient demonstrates one of the very few cases of VBD compression of the retrochiasmal pathway with no other cranial nerve involvement. 1. Introduction Dolichoectasia refers to a diffuse dilatation of an artery (differentiating it from aneurysms) as well as marked elongation and tortuosity of the vessel. Intracranially, the most commonly affected area is the vertebrobasilar segment with carotid and middle cerebral artery ectasia occurring less often. Although vertebrobasilar dolichoectasia (VBD) is frequently asymptomatic, presenting symptoms vary from being secondary to ischemia, compression, or rarely vascular rupture [1, 2]. VBD has been described to cause ophthalmological symptoms, by direct compression of cranial nerves such as the trigeminal and facial and less frequently the abducens and oculomotor nerves [3, 4]. In addition, rare cases of direct compression by a VBD of the optic tract or the chiasm causing visual loss have also been previously reported [5, 6]. Here, we report a patient with right homonymous hemianopia due to direct compression by the ectatic basilar artery on the left optic track and compressive left optic neuropathy by secondary displacement of the adjacent left internal carotid artery. 2. Case Presentation A 71-year-old man presented with gradual, progressive, and bilateral visual loss and reading difficulties over the last 6 months. His medical history was unremarkable, and he had no other symptoms apart from failing vision. He had no previous ophthalmic history apart from moderate amblyopia on the right eye (RE). The best corrected visual acuities were 20/40 RE and 20/100 left eye (LE), respectively. Automated refraction revealed anisometropic myopia of ？5,25？sph RE and ？3,75？sph LE. On Ishihara colour test the patient identified 15/15 plates on the RE and 13/15 plates on the LE. Pupils were equal and normally reactive to light and near stimuli. There was no sign of a relative afferent pupillary defect (RAPD). Ocular motility and remaining cranial nerve examination was normal. Optic disc evaluation showed normal discs, central cupping of 0.4, with myopic peripapillary chorioretinal atrophy and a slight tilt of the right disc. Humphrey perimetry 30-2 revealed a dense right homonymous hemianopia with constriction of the remaining left hemifield in the LE (Figure 1). Figure 1: