Case Report A Case of Complete Recovery of Fluctuating Monocular Blindness Following Endovascular Treatment in Internal Carotid Artery Dissection Ki-Tae Kim, MD,* Seung Guk Baik, MD, PhD,† Kyung-Pil Park, DM, PhD,* and Min-Gyu Park, MD* Background: Monocular blindness may appear as the first symptom of internal carotid artery dissection (ICAD). However, there have been no reports that monocular visual loss repeatedly occurs and disappears in response to postural change in ICAD. Methods: A 33-year-old woman presented with transient monocular blindness (TMB) following acute-onset headache. TMB repeatedly occurred in response to postural change. Two days later, she experienced transient dysarthria and right hemiparesis in upright position. Pupil size and light reflex were normal, but a relative afferent pupillary defect was positive in the left eye. Diffusion-weighted imaging showed no acute lesion, but perfusion-weighted imaging showed perfusion delay in the left ICA territory. Digital subtraction angiography demonstrated a false lumen and an intraluminal filling defect in proximal segment of the left ICA. Results: Carotid stenting was performed urgently. After carotid stenting, left relative afferent pupillary defect disappeared and TMB was not provoked anymore by upright posture. At discharge, left visual acuity was completely normalized. Conclusions: Because fluctuating visual symptoms in the ICAD may be associated with hemodynamically unstable status, assessment of the perfusion status should be done quickly. Carotid stenting may be helpful to improve the fluctuating visual symptoms and hemodynamically unstable status in selected patient with the ICAD. Key Words: Transient monocular blindness—internal carotid artery— dissection—stenting. Ó 2015 by National Stroke Association Various visual symptoms and signs, such as Horner syndrome, scintillations, transient monocular blindness (TMB), permanent visual loss, and ischemic ocular syndrome, can be caused by internal carotid artery dissec- tion (ICAD).1,2 TMB has been reported in 6% to 38% of patients with ICAD.1 However, to the best of our knowledge, there have been no reports that TMB caused by ICAD waxes and wanes in response to postural change. From the *Department of Neurology, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan; and †Department of Radiology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, Yangsan, Republic of Korea. Received April 22, 2015; revision received June 11, 2015; accepted June 18, 2015. This work was supported by 2014 clinical research funding from Pusan National University Yangsan Hospital. The authors report no conflicts of interest. Address correspondence to Min-Gyu Park, MD, Department of Neurology, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Pusan National University School of Medicine, 20 Geumo-ro, Mulgeum, Yangsan 626-770, Republic of Korea. E-mail: umbilicus2@gmail.com. 1052-3057/$ - see front matter Ó 2015 by National Stroke Association http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2015.06.029 Journal of Stroke and Cerebrovascular Diseases, Vol. 24, No. 9 (September), 2015: pp e283-e286 e283 K.-T. KIM ET AL. e284 We report a case showing a complete recovery of fluctuating TMB following endovascular treatment in patient with ICAD. Our institutional review board approved this case report: patients’ informed consent was not required because this case report was retrospective. Case Report A 33-year-old woman presented with TMB in left eye following acute-onset headache. Monocular blindness developed episodically only in the upright position and was relieved quickly by lying down. Two days later, transient dysarthria and right hemiparesis occurred in upright position and were alleviated by lying down. She was transferred to our emergency center for further evaluation. She denied any trauma and medical history. Her vital signs were stable. Snellen chart revealed a reduced visual acuity of the left eye (OS 20/30 and OD 20/17) in a supine position. Pupil size and light reflex were normal, but there was a relative afferent pupillary defect (RAPD) in the left eye. Photostress recovery test showed a prolonged recovery time in the left eye. Fundoscopic examination was normal bilaterally. In a supine position, she did not show any focal neurologic deficits including monocular visual loss. Diffusion-weighted imaging (DWI) showed no diffusion restriction (Fig 1, A), but perfusion-weighted imaging (PWI) showed a perfusion delay in the left ICA territory. Time-to-peak map showed a delayed time to peak more than 4 seconds in the left hemisphere compared to those in the right (Fig 1, B). Especially, left border-zone area showed a mean transit time delay more than 6 seconds (Fig 1, C). Susceptibility-weighted imaging (SWI) showed prominent multiple hypointense vessels in the left hemisphere (Fig 1, D). Contrastenhanced magnetic resonance (MR) angiography showed a focal stenosis of the left proximal ICA (Fig 1, E). Time-offlight MR angiography showed a faint flow through the left middle cerebral artery and ICA and numerous cortical branches of the left posterior cerebral artery compared to those of the right (Fig 1, F). Digital subtraction angiography (DSA) demonstrated an intraluminal filling defect and a false lumen in the proximal segment of the left extracranial ICA, which was consistent ICAD (Fig 1, G). DSA showed collateral blood flow via anterior communicating artery and left ophthalmic artery. The patient was medicated with 75 mg of clopidogrel and 100 mg of aspirin in another hospital for 2 days before the procedure. DSA was performed with a 6Fr, guiding catheter (Flexor Shuttle Select; Cook Medical, Bloomington, IN). A distal protection device (Filter wire EZ embolic protection device; Boston scientific, Fremont, MA) was placed under roadmap guidance into the distal cervical ICA. Prestenting ballooning was performed using the 5 mm 3 40 mm, Sterling Monorail Balloon (burst pressure of 6 atm, Boston scientific, Fremont, MA), but the dissec- tion lesion was not improved. The Carotid WALLSTENT (7 mm 3 50 mm, Boston scientific, Fremont, MA) was placed across the dissection segment of left ICA. Poststenting ballooning was performed using the 3 mm 3 20 mm, Catheter PTCA Balloon Ryujin (burst pressure of 14 atm, Terumo, Tokyo, Japan). Poststenting angiography demonstrated good apposition of the stent throughout the dissection segment of the left ICA with no residual stenosis (Fig 1, H). Restoration of normal flow through the ICA and the intracranial vessels were identified on the final angiographic runs (Fig 1, I). After the procedure, the left RAPD disappeared immediately. A day after the procedure, the decreased visual acuity of the left eye was normalized. Also, TMB did not develop in upright posture. The patient was maintained on a daily regimen of aspirin (100 mg) and clopidogrel (75 mg) for 6 months. Discussion TMB is not an uncommon manifestation in ICAD, but fluctuating TMB in response to postural change has not been reported previously in ICAD.1,2 There are 2 possible mechanisms for explaining the TMB in ICAD: 1) embolic mechanism and 2) hypoperfusion mechanism.1,3,4 In our case, the ophthalmoscope examination showed no occlusion of the retinal arteries by embolus: therefore, the embolic mechanism could be ruled out. The hypoperfusion mechanism in our case could be backed by neurologic and MR findings. The monocular blindness was not developed in supine position, but the RAPD of the left eye was observed, which suggested that retina or optic nerve may be affected by a decreased ocular blood flow due to ICAD even in supine position. MR imaging findings also support the hypoperfusion mechanism. DWI showed no diffusion restriction, but PWI showed a marked perfusion delay in the left ICA territory; it is often called as ‘‘a total DWI/PWI mismatch.’’5 Especially, perfusion delay was significant in the left border-zone area, which could explain why right hemiparesis developed in upright posture and disappeared in supine position. SWI showed the prominent multiple hypointense vessels in the left hemisphere compared to the right hemisphere; it means an increased ratio of deoxyhemoglobin/ oxyhemoglobin by increased oxygen demand in the left hypoperfused hemisphere.6 Therefore, the patient was considered to be in hemodynamically unstable condition even in supine position and have a high risk of neurologic deterioration. The changing position from supine to upright posture may aggravate a cerebral hypoperfusion caused by ICA occlusion. The collateral flow may be helpful to overcome the hypoperfusion and prevent ischemic symptoms of the left hemisphere in upright posture. But, considering the left positive RAPD even in supine position, the left ocular hypoperfusion may be more severe FLUCTUATING MONOCULAR BLINDNESS IN INTERNAL CAROTID ARTERY DISSECTION e285 Figure 1. Diffusion-weighted imaging shows no lesion of diffusion restriction (A). Time-to-peak map shows a perfusion delay in territory of the left ICA (B). Mean transit time map shows a mean transit time delay more than 6 seconds in the left border-zone area (C, arrow, gray-colored area). Susceptibility-weighted imaging shows prominent multiple hypointense vessels (dashed circle) in the left hemisphere (D). Enhanced MRA reveals a focal stenosis (arrow) of the left proximal ICA (E). Time-of-flight MRA shows a faint flow of the left middle cerebral artery (arrow) and numerous distal branches (arrowheads) of the left posterior cerebral artery (F). Digital subtraction angiography shows an intraluminal filling defect and a false lumen (arrow) in the proximal segment of the left ICA (G). After carotid stenting, the dissection lesion is restored to normal anatomy of the ICA and restoration of intracranial flow through the left is identified on the final angiography (H, I). Abbreviations: ICA, internal carotid artery; MRA, magnetic resonance angiography. than left hemispheric hypoperfusion, which would explain why the fluctuating monocular blindness was frequently developed without ischemic symptoms of the left hemisphere in upright posture. The safety and efficacy of endovascular stenting in ICAD is still unclear because of lack of randomized controlled trials. But several studies suggested that endovascular stenting is safe and effective in selected patients: (1) patients with recurrent symptoms despite medical therapy, (2) patients with hemodynamic instability, (3) patients with impending rupture of pseudoaneurysm, and (4) contraindication to anticoagulation because of intracranial or systemic hemorrhage.7-9 Our case fulfilled the first 2 of the 4 indications for endovascular stenting mentioned above. In our case, because the dissection lesion was located in the proximal straight segment of extracranial ICA, we used the closed-cell stent to preserve the original anatomy of ICA.10 Carotid stenting was successfully performed without any procedure-related complications using embolic protection device.10 After successful recanalization, TMB and other neurologic symptoms were not developed in response to postural change. 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