Transient cortical blindness

Clinical History

A 30-year-old patient, whithout hypertension, suffered acute headache after coitus. The diagnosis of aneurysmal subarachnoid haemorrhage was made. Selective intra-arterial angiography disclosed 2 intracerebral aneurysms, which were treated with coiling. Approximately 150ml of nonionic contrast material (520mOsm/kg) were used. Within minutes after the procedure the patient developed acute cortical blindness.

Imaging Findings

CT examination, which was performed 3,5 hours after angiography, showed bilateral gyriform occipital hyperattenuation.

MRI, which was performed 5 hours after angiography, showed subtle FLAIR hyperintensities in the occipital cortices. There was no haemorrhage on T2-GE weighted images, and no restricted diffusion.

Discussion

Transient Cortical Blindness (TCB) is a rare but reversible complication of angiography in which intra-arterial contrast material apparently penetrates the blood-brain barrier by opening tight capillary junctions or enhancing endothelial pinocytosis. It then enters the cerebral cortex and adversely affects neuronal membranes. This type of neurotoxicity seems to be related to the chemical or ionic properties of the contrast medium as well as its hyperosmolarity, lipid solubility, and viscosity. The toxicity is predominantly localised to the occipital lobes, because the posterior cerebral circulation is known to be more sensitive to such injuries because of different sympathetic innervation.
TCB due to intra-arterial contrast media appears to be related with a syndrome known as posterior reversible leukoencephalopathy (PRLE), which in turn is related to cyclosporin neurotoxicity, renal insufficiency, and hypertension. Endothelin is a possible common factor in the pathogenesis of TCB and PRLE. Reversible oedema, localised mainly to the occipital lobes, is a prominent feature.
The use of ionic contrast media, or contrast media with high osmolarity (higher than that of blood - 300mOsm/kg), increase the risk of developing TCB. Prolonged contact time, large total dose, hypotension during angiography, chronic hypertension, and renal impairment are factors that may increase susceptibility to osmotic disruption of the blood-brain barrier. Selective vertebral angiography carries the highest risk of neurological complication.
TCB is a partial or complete transient loss of perceived vision; the period of blindness might last from a few hours to a few days. The onset of TCB occurs from minutes up to 12 hours after angiography. Ophthalmologic examination shows normal fundi, normal papillary reflexes, and unaltered extra-ocular movements. Associated symptoms include severe headache, vomiting, loss of coordination or limb weakness, aphasia, confusion, and mental state changes. The incidence of this complication is 0.3-1% when nonionic contrast agents are used, but can be as high as 4% in case of hyperosmolar iodinated contrast agents.
CT imaging shows loss of sulci and hyperattenuated gyri, mainly in occipital and posterior parietal cortices, caused by contrast extravasation due to disruption of the blood-brain barrier. MRI imaging can show transient T2 and FLAIR hyperintensity of the occipital lobes, due to oedema caused by hyponatriema and cytotoxic contrast media. No findings of ischaemia (diffusion is not restricted) or bleeding (no abnormalities on T2-GE) were observed.
Because TCB is self-limiting and benign, no treatment is necessary. Sometimes steroids are given because they might stabilise the blood-brain barrier (and thus reduce vasogenic oedema).

Differential Diagnosis List

Final Diagnosis

Transient cortical blindness after angiography.

URL:	https://www.eurorad.org/case/9186
DOI:	10.1594/EURORAD/CASE.9186
ISSN:	1563-4086