Case Report
Unilateral Contrast Neurotoxicity as a Stroke Mimic After Cerebral
Angiogram
Diogo C. Haussen, MD, Royya Modir, MD, Dileep R. Yavagal, MD
From the Miller School of Medicine/University of Miami Hospital and Jackson Memorial Hospital, Miami, FL.

ABSTRACT
Contrast neurotoxicity (CN) following exposure to iodinated contrast is uncommon, and
usually presents as cortical blindness due to bilateral occipital lobe involvement. Unilateral cortical dysfunction due to CN could mimic an acute stroke and has been rarely
described. We report the case of an 89-year-old female who developed a transient
dense/complete left homonymous-hemianopsia and left-sided tactile extinction after
undergoing a right internal carotid (ICA) artery rotational angiogram with a standard
high-volume iodinated contrast injection for 3D visualization a 6×4-mm right posterior
communicating artery aneurysm with a fetal posterior cerebral artery (PCA) incorporated
in the neck. This was associated with transient fullness and loss of gray-white matter
differentiation in the right occipital and parietal lobes. The potential mechanism of CN
in our case was the injection of a high volume of contrast in the ICA for the rotational
angiogram. The presence of a right fetal PCA possibly allowed the contrast to reach the
right occipital lobe. CN manifesting as an acute focal neurologic syndrome should be
considered in the setting of recent iodinated contrast exposure.

Acceptance: Received February 20,
2011, and in revised form July 28, 2011.
Accepted for publication July 29, 2011.
Correspondence: Address correspondence to Dileep Yavagal, MD, 1095 NW
14th Terrace, Lois Pope Life Center – 2nd
Floor, Miami, FL 33136, E-mail: dyavagal
@med.miami.edu.
Individual contributions: Diogo C.
Haussen: drafting the manuscript; Royya
Modir: revising the manuscript; and
Dileep R. Yavagal: conceptualizing and
revising the manuscript.
Funding: None.
Disclosures: Diogo C. Haussen and
Royya Modir report no disclosures.
Dileep R. Yavagal serves as a consultant to Boston Scientific, Micrus, Abbott Vascular, and Coaxia. He has received research support from a University
of Miami intramural grant: Interdepartmental Research Development Initiative
(IRDI) grant 2009–2010, Department of
Neurology, University of Miami and the
Anderson Family Gift Fund to Division
of Interventional Neurology. He has received travel support from Abbott Vascular, Inc.
J Neuroimaging 2011;XX:1–3.
DOI: 10.1111/j.1552-6569.2011.00655.x

Introduction
The occurrence of contrast neurotoxicity (CN) leading to transient neurological symptoms following exposure to iodinated
contrast is uncommon but well reported, ranging between
0.3% and 2.9%.1-3 Although it is most commonly seen after
cerebral angiograms, it has been also described after contrastenhanced computed-tomography (CT), cardiac and peripheral
angiograms.1-4 The vast majority of cases of CN present with
cortical blindness due to bilateral occipital lobe involvement.
The symptoms might develop within minutes or hours of contrast exposure (including cases where deficits are noticed immediately at the end of the procedure) and resolve over hours to
days.2,5-8 Unilateral cortical involvement due to CN has been
rarely reported.2,5,8 Such unilateral dysfunction could mimic
an acute stroke, posing an urgent diagnostic challenge. We

report a case of unilateral occipitoparietal CN after an internal carotid artery angiogram.

Case Report
An 89-year-old female with a history of hypertension, stage-I
chronic renal disease, and bradycardia status-postpacemaker
insertion was admitted with worsening right eye pain, diplopia
and ptosis. On exam, she was found to have a right cranial
nerve III palsy. A computed-tomography angiogram (CTA) of
the brain demonstrated a posterior communicating aneurysm
(PcomA). Bilateral internal carotid artery (ICA) and left vertebral artery catheter cerebral angiograms were performed. A
right ICA rotational angiogram with a standard high-volume
iodinated contrast injection (18 cc at 2.5 cc/second) was

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Copyright C 2011 by the American Society of Neuroimaging

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homonymous-hemianopsia, and left-sided tactile extinction.
The use of conscious sedation during the procedure might
have delayed the symptom recognition. Immediate CT demonstrated fullness in the sulci over the right occipital and parietal
lobes, with loss of gray-white matter differentiation (Figs 1B, C).
MRI was contraindicated due to presence of a pacemaker. Vigorous hydration was started for possible CN. At 24 hours, the
visual field deficit improved to a left lower homonymous
quadrantanopsia, the sensory abnormality was minimal, and a
follow-up brain CT demonstrated resolution of the above findings (Figs 1D, E). At 36 hours, the neurological deficits were
completely resolved.

Discussion

Fig 1. Conventional angiogram depicting the aneurysm and CTs
demonstrating the edema and its resolution after 24 hours. (A) Conventional angiogram depicting right posterior communicating artery
aneurysm (lateral view). (B and C) CT brain without contrast at 6
hours after the procedure revealing fullness of the sulci in the right
occipital lobe. (D and E) Repeat CT at 24 hours demonstrating resolution of the abnormalities.

done for 3D visualization of the aneurysm. A right PcomA
aneurysm (6 mm × 4 mm) with a fetal PCA incorporated
in the neck was noted (Fig 1A). No thromboembolic occlusions were noted on angiography and the patient was neurologically intact after the procedure. Six hours after angiogram,
although the patient remained asymptomatic, a routine neuroophthalmological examination showed a dense/complete left

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Journal of Neuroimaging Vol XX No X 2011

Despite the advancement of non-invasive cerebrovascular
imaging techniques, catheter angiography remains the goldstandard and a common procedure for imaging of cerebral
aneurysms and other intracranial vascular disorders. In patients
who develop a stroke syndrome postangiography, urgent accurate diagnosis is paramount. The non-recognition of CN presenting as a stroke mimic might lead to unnecessary repeat
angiography for endovascular therapy. We report a rare case
of unilateral reversible dysfunction of the occipital and parietal
lobes due to CN after cerebral angiography that mimicked an
acute stroke syndrome.
Although uncommon, CN is a striking clinical condition
most often presenting as transient cortical blindness due to bilateral occipital cortex involvement. Postangiogram unilateral
CN presenting as a stroke mimic was previously reported in one
patient that developed encephalopathy and hemiparesis. However, the brain imaging in this case was not compatible with
stroke as the entire right hemisphere was affected, not respecting vascular territories.5 Another subject was found drowsy,
globally aphasic and with worsening of a prior hemiparesis.
Nevertheless, this case had clear abnormal cortical high density (probably related to contrast hangout) involving the entire
right hemisphere.8 Unilateral involvement was also described
in a case where the initial presentation was cortical blindness related to bilateral occipital lobe toxicity and the hemianopsia was
only noted during the recovery phase.2 In another case, hemianopsia related to CN was postulated but multiple small-artery
occlusions were also observed and treated with intraarterial abciximab during the angiogram.2
In our patient, the clinical presentation raised a strong suspicion for cerebral thromboembolism postangiography. However, no evidence for arterial occlusion in the right parietal or
occipital lobes was seen on the angiogram. CN is usually associated with imaging findings of persistent presence of contrast in
the cortex (gyriform hyperattenuation) and vasogenic edema.
In this case, the sole CT finding of effacement of sulci in the right
parietal and occipital lobes was atypical, but felt to be consistent
with CN. The complete resolution of the clinical syndrome and
CT findings within 36 hours confirmed the diagnosis of CN.
The potential mechanism of CN in our case was the injection
of a high volume of contrast in the ICA for the rotational angiogram. The presence of a right fetal posterior cerebral artery
(PCA; Fig 1A) possibly allowed the contrast to reach the right

occipital lobe. The previously noted risk factors for CN present
in our case included renal insufficiency, long duration of the
procedure, and high infusion rate of contrast.2,6,7
In conclusion, CN manifesting as an acute focal neurologic
syndrome should be considered in the setting of recent iodinated contrast exposure.

References
1. Wishart DL. Complications in vertebral angiography as compared
to non-vertebral cerebral angiography in 447 studies. Am J Roentgenol
Radium Ther Nucl Med 1971;113:527-537.
2. Niimi Y, Kupersmith MJ, Ahmad S, et al. Cortical blindness,
transient and otherwise, associated with detachable coil embolization of intracranial aneurysms. AJNR Am J Neuroradiol 2008;29:
603-607.

3. Mani RL, Eisenberg RL. Complications of catheter cerebral arteriography: analysis of 5,000 procedures. III. Assessment of arteries
injected, contrast medium used, duration of procedure, and age of
patient. AJR Am J Roentgenol 1978;131:871-874.
4. Mentzel HJ, Blume J, Malich A, et al. Cortical blindness after
contrast-enhanced CT: complication in a patient with diabetes insipidus. AJNR Am J Neuroradiol 2003;24:1114-1116.
5. Guimaraens L, Vivas E, Fonnegra A, et al. Transient encephalopathy
from angiographic contrast: A rare complication in neurointerventional procedures. Cardiovasc Intervent Radiol 2010;33:383-388.
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2002;57:47-49.
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8. Kim DH, Choi CH, Lee JH, Lee JI. Transient global aphasia with
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Haussen et al: Unilateral Contrast Neurotoxicity Presenting

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