TY - JOUR
T1 - Contrast-associated transient cortical blindness
T2 - three cases with MRI and electrophysiology findings
AU - Baguma, Marius
AU - Younan, Nadia
AU - London, Frédéric
AU - Ossemann, Michel
AU - Vandermeeren, Yves
N1 - Publisher Copyright:
© 2016, Belgian Neurological Society.
PY - 2017/3/1
Y1 - 2017/3/1
N2 - Transient cortical blindness (TCB) is a rare but striking complication following contrast agent injection. TCB might be secondary to a direct toxicity of the contrast agent, leading to an osmotic disruption of the blood–brain barrier (BBB), with a preferential involvement of the posterior circulation and occipital cortex. We report a series of three patients with contrast medium-associated TCB (intra-arterial injection of non-ionic contrast agent during diagnostic cerebral angiography for two of them and coronary angioplasty for the other one). In two patients, the magnetic resonance imaging (MRI) was unremarkable; in the other patient, typical MRI findings were observed, with FLAIR hyperintensities in the right occipital cortex and decreased apparent diffusions coefficient (ADC). Interestingly, this patient also presented posterior rhythmic epileptiform activities on electroencephalogram during the first 36 h. Visual evoked potentials (VEPs) showed normal retinal potential, but a massive destructuration of the later potentials of the cortical origin. To our knowledge, this is the first time that VEPs acquired during TCB are reported. We discuss these findings with respect to the pathophysiology of TCB.
AB - Transient cortical blindness (TCB) is a rare but striking complication following contrast agent injection. TCB might be secondary to a direct toxicity of the contrast agent, leading to an osmotic disruption of the blood–brain barrier (BBB), with a preferential involvement of the posterior circulation and occipital cortex. We report a series of three patients with contrast medium-associated TCB (intra-arterial injection of non-ionic contrast agent during diagnostic cerebral angiography for two of them and coronary angioplasty for the other one). In two patients, the magnetic resonance imaging (MRI) was unremarkable; in the other patient, typical MRI findings were observed, with FLAIR hyperintensities in the right occipital cortex and decreased apparent diffusions coefficient (ADC). Interestingly, this patient also presented posterior rhythmic epileptiform activities on electroencephalogram during the first 36 h. Visual evoked potentials (VEPs) showed normal retinal potential, but a massive destructuration of the later potentials of the cortical origin. To our knowledge, this is the first time that VEPs acquired during TCB are reported. We discuss these findings with respect to the pathophysiology of TCB.
KW - Angiography
KW - Contrast agent
KW - Cortical blindness
KW - Electrophysiology
UR - http://www.scopus.com/inward/record.url?scp=84991336340&partnerID=8YFLogxK
U2 - 10.1007/s13760-016-0696-0
DO - 10.1007/s13760-016-0696-0
M3 - Article
C2 - 27670442
AN - SCOPUS:84991336340
SN - 0300-9009
VL - 117
SP - 195
EP - 199
JO - Acta Neurologica Belgica
JF - Acta Neurologica Belgica
IS - 1
ER -