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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 1  |  Page : 164-165

Transient cortical blindness and amnesia after cerebral angiography

1 Department of Neurology, Taipei Medical University-Shuang-Ho Hospital, New Taipei City, Taipei, Taiwan
2 Department of Neurology, Taipei Medical University-Shuang-Ho Hospital, New Taipei City; Department of Neurology, College of Medicine, Taipei Medical University, Taipei, Taiwan

Date of Web Publication11-Jan-2016

Correspondence Address:
Wei-Ting Chiu
Department of Neurology, Taipei Medical University-Shuang-Ho Hospital, New Taipei City, Taipei
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.173659

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How to cite this article:
Ko TH, Chiu WT, Chao YT, Chan L. Transient cortical blindness and amnesia after cerebral angiography. Neurol India 2016;64:164-5

How to cite this URL:
Ko TH, Chiu WT, Chao YT, Chan L. Transient cortical blindness and amnesia after cerebral angiography. Neurol India [serial online] 2016 [cited 2021 Dec 5];64:164-5. Available from:


Transient cortical blindness (TCB) and transient global amnesia (TGA) are both rare complications after cerebral angiography. We present the case of a 65-year-old woman with a history of left sided amblyopia since childhood, and left vertebral artery (VA) dissection along with left sided pontine infarction 4 months ago. She was admitted to our ward with a right-sided weakness for 1 week. The first contrast enhanced magnetic resonance imaging (MRI) revealed no evidence of acute infarction [Figure 1]a,[Figure 1]b,[Figure 1]c. The diagnostic cerebral angiography showed dissection and total occlusion of the left intradural VA. The contrast medium iohexol (omnipaque), 100 ml, was administered intravenously during the procedure. The blood pressure after the angiographic procedure was 148/82 mmHg. Severe headache, nausea, and vomiting was reported soon after the angiography; 4 hours later, acute blindness with barely light perception in bilateral eyes were noted; and the patient could not recall anything that happened after the angiography. Neurological examination showed a normal light reflex but impaired visual acuity in bilateral eyes. The follow-up MRI revealed no remarkable abnormality [Figure 1]d,[Figure 1]e,[Figure 1]f. The blindness and anterograde amnesia resolved within 24 hours. The subsequent ophthalmic examination revealed normal light reflex, visual acuity, and color perception in the right eye and amblyopia in the left eye. Flash-evoked visual evoked potential (VEP) showed prolonged P100 latency in the right eye [Figure 2]a, which returned to normal 11 days later [Figure 2]b.
Figure 1: (a-c) The MRI before cerebral angiography revealed no remarkable abnormality on diffusion weighted imaging (DWI), aparent diffusion coefficient (ADC), and T1WI (a: DWI, b: ADC, c: T1-weighted axial). (d-f) The MRI during transient cortical blindness revealed no cerebral ischemia (d: DWI, e: ADC, f: T1-weighted axial)

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Figure 2: (a) The flash-evoked VEP following transient cortical blindness revealed prolonged P100 latency (137 ms) in the right eye and absence of the wave in the left eye. (b) The pattern-evoked VEP after 11 days revealed significant improvement of P100 latency (107 ms) in the right eye

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Transient cortical blindness (TCB) is a rare complication after angiography and contrast-enhanced computed tomography (CT), which is possibly due to osmotic disruption of the blood–brain barrier by the contrast medium, especially in the vertebrobasilar circulation, which may penetrate the occipital lobes and lead to TCB or other visuospatial disorders.[1] Hyperosmolar ionic contrast medium is associated with a higher incidence of TCB; however, omnipaque that was used in this case is a nonionic and low-osmolarity contrast medium, but has also been reported to cause TCB.[2] In a previous study, abnormal VEPs were recorded during cortical blindness in 15 of 19 patients, but did not correlate with the severity of visual loss or outcome.[3] The possible etiologies of transient global amnesia (TGA) after cerebral angiography include ischemia due to emboli, arterial spasm, epilepsy, or direct toxicity of the contrast.[4] Our case had both TCB and TGA soon after cerebral angiography. We believe that the etiology was associated with disruption of the blood–brain barrier due to the contrast medium.

To conclude, TCB and TGA can occur due to both ionic or nonionic contrast medium toxicity. The pathophysiology is associated with the disruption of the blood–brain barrier. In addition, our case demonstrates that VEP is helpful in the clinical diagnosis of cortical blindness.

  References Top

Lantos G. Cortical blindness due to osmotic disruption of the blood-brain barrier by angiographic contrast material: CT and MRI studies. Neurology 1989;39:567-71.  Back to cited text no. 1
Shah PR, Yohendran J, Parker GD, McCluskey PJ. Contrast-induced transient cortical blindness. Clin Exp Optom 2013;96:333-5.  Back to cited text no. 2
Aldrich MS, Alessi AG, Beck RW, Gilman S. Cortical blindness: Etiology, diagnosis, and prognosis. Ann Neurol 1987;21:149-58.  Back to cited text no. 3
Roccatagliata L, Taveira-Lopes L, Rossignol MD, Biondi A. Cortical blindness and retrograde amnesia following cerebral angiography studied by early diffusion weighted MR imaging: A case report. Neuroradiol J 2009;22:600-4.  Back to cited text no. 4


  [Figure 1], [Figure 2]

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