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Does Dolichoectasia of the Carotid Artery Cause Optic Neuropathy?

Dolichoectatic intracranial vessels have abnormal configuration with tortuosity and distension. Symptomatic vascular compression by dolichoectatic arterial vessels is a well-known phenomenon that may cause variable symptoms and signs such as hemifacial spasm, downbeat nystagmus, lateral medullary syndrome with the ocular tilt reaction, and sixth nerve palsy (1). Auditory and vestibular findings have been reported with involvement of the vertebrobasilar (V-B) vessels. The main focus of this discussion will be dolichoectasia of the internal carotid artery (ICA) and other surrounding vessels causing compression of the anterior visual pathways. In 1997, Jacobson et al (2) reported that among 100 patients, anatomic contact between the optic nerve and ICA was common (70%). Anatomic compression, however, was rare (12% bilateral and 5% unilateral). Freeman and Newman (3) described a case of presumed vascular compressive optic neuropathy that deteriorated after surgical decompression and slowly improved with subsequent steroid treatment. Jacobson (4) argued that this might have been due to ischemia of the compressed optic nerve with slow recovery. He proposed that the mechanism of optic neuropathy with vascular compression included direct compressive injury and chronic ischemia due to compromised regional perfusion. The characteristics of a dolichoectatic ICA are not well defined. Jacobson et al (2,4) found that increased diameter of the ICA correlated with degree of anatomic compression of the optic nerve. The mean diameter of the artery in his symptomatic patients was significantly greater at 5.1 vs 3.8 mm in asymptomatic patients. On neuroimaging, the dolichoectatic ICA often was in contact with the anterior visual pathway with asymmetric displacement and compression. Golnik et al (5) reported further magnetic resonance imaging (MRI) characteristics in patients with unexplained optic neuropathy. Patients were excluded if they had symptoms or findings of other identifiable etiologies, age was less than 46 years at onset of symptoms, or if there was a history of optic disc cupping. Extensive workup to evaluate for other causes of optic neuropathy was performed. Among the 20 patients evaluated, the distance between the optic nerve and ICA flow void on digitized coronal magnetic resonance images was significantly less on the atrophic side (mean 0.42 mm) compared with the normal side (mean 1.04 mm) and control group (mean 0.96 mm). Men and women were equally affected and average age was 63 years. Visual loss was slowly progressive in most of the patients and median visual acuity was 20/30 (range: 20/20–4/200). Contrary to Jacobson’s study, Golnik et al found that the affected ICA flow void diameter was not significantly different from the normal side or control group (mean 3.75 mm on the atrophic side, 4.03 on the normal side, and 4.20 in controls). One limitation of the study, however, was that flow void measurement did not include arterial wall thickness, which could also theoretically contribute to compression of the optic nerve. The study by Golnik et al (5) highlighted that a normalappearing ICA can potentially cause symptomatic compression of the optic nerve if the anatomic distance is significantly less than 1 mm. This anatomic relationship is best seen on T1-weighted coronal images with a slice thickness of 3 mm and gap of 0.3 mm (4). I find the thin-section coronal T2 steady-state free procession sequence to be especially helpful in visualizing the vascular-nerve anatomic contact (Fig. 1). Unless alerted to the possibility of compressive optic neuropathy, neuroradiologists may not mention this asymmetric anatomic variation in their report. In most of the reported cases of dolichoectatic arterial compression of the anterior visual pathways, visual loss progressed slowly over several years and rarely required surgical intervention (5–9). Jacobson (4) reported the largest series to date with 18 patients and 24 affected eyes, and Department of Ophthalmology (VIE), SUNY Downstate Medical Center. Brooklyn, New York; and Midwest Eye Institute (VAP), Indianapolis, Indiana.