On the night he finished a 105-mile bicycle tour in late September 2003, a 68-year-old man noticed blurred vision whenever he looked to his left. One week later, he noted horizontal diplopia for distant objects in primary gaze. An ophthalmologist (KC) eliminated diplopia from a small-angle esotropia with a low-power Fresnel prism. Three weeks later, eliminating the diplopia required a stronger prism. He denied any constitutional symptoms or other ophthalmic or neurologic symptoms. Medical history included hypertension, benign prostatic hypertrophy, and Dukes A colon cancer treated with hemicolectomy in 1988. With a presumptive diagnosis of ischemic left sixth cranial nerve palsy, no brain imaging was performed.
On examination in January 2004, 4 months after onset of diplopia, visual acuity, color vision, pupil size and reactivity, and ophthalmoscopy were normal. He had no ptosis, lid twitch or fluttering eye movements, or lid fatigue after sustained upgaze. Ductions were normal OD, but he had only 50% abduction OS. Measured with Maddox rod and fixation at distance, he had 35 prism-diopters of esodeviation in primary gaze, increasing to more than 40 prism-diopters in left gaze and decreasing to 20 prism-diopters in right gaze.
Two days later he underwent brain imaging with a 3-Tesla magnetic resonance imaging and magnetic resonance angiography that demonstrated a dolichoectatic left vertebral artery compressing the left sixth cranial nerve against the pons at the nerve's root exit zone (Fig. 1). Erythrocyte sedimentation rate, C-reactive protein, glycosylated hemoglobin, and cardiac echography were normal. Follow-up examination in September 2004, 12 months after the onset of diplopia, still showed OS abduction limited to 50% and a 25 prism-diopter esodeviation in primary gaze at distance.
Later in September 2004, he underwent left medial rectus recession of 5.5 mm without transposition. Examination in December 2004 demonstrated orthophoria in primary gaze. He was free of diplopia in all gaze positions without need for prism.
Dolichoectasia refers an unusually dilated and tortuous artery. Most often, dolichoectasia is associated with brain stem stroke, but it may also cause compressive cranial nerve palsy (3). Dolichoectasia commonly affects the basilar or carotid arteries (1,2). Our case unusually involved the vertebral artery. We believe this to be the first reported case to show in detail the anatomic relationship between the sixth cranial nerve root exit zone in the pons and a compressing dolichoectatic artery. Given that the palsy occurred after a strenuous aerobic exercise, we wonder if increased flow through this dilated vessel provoked the palsy (4).
1. Goldenberg-Cohen N, Miller NR. Noninvasive neuroimaging of basilar artery dolichoectasia in a patient with an isolated abducens nerve paresis. Am J Ophthalmol
2. Ohtsuka K, Sone A, Igarashi Y, Akiba H, Sakata M. Vascular compressive abducens nerve palsy disclosed by magnetic resonance imaging. Am J Ophthalmol
3. Rautenberg W, Aulich A, Rother J, Wentz KU, Hennerici M. Stroke and dolichoectatic intracranial arteries. Neurol Res
4. Rush, JA, Younge BR. Paralysis of cranial nerves III, IV, and VI: cause and prognosis in 1,000 cases. Arch Ophthalmol