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\begin{document}

\title{Transient Cortical Blindness, a Rare Complication During Cerebral
Digital Subtraction Angiography: A Case Report and Literature review}



\author[1]{Benjamin Sarkodie}%
\author[2]{Bashiru Jimah}%
\author[3]{Dorothea Anim}%
\author[4]{Edmund Brakohiapa}%
\author[3]{Emmanuel Jackson}%
\affil[1]{University of Ghana}%
\affil[2]{University of Cape Coast College of Health and Allied Sciences}%
\affil[3]{Korle Bu Teaching Hospital}%
\affil[4]{University of Ghana Medical School}%


\vspace{-1em}



  
  \date{May 17, 2024}


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\selectlanguage{english}
\begin{abstract}
Transient cortical blindness (TCB) is a rare~cerebral angiography
complication with unknown etiology. A patient with a wide-neck cavernous
aneurysm developed TCB. Vision restored spontaneously one hour after
angiography, with no lasting neurological deficit. Three hours after the
incident, MRI indicated no abnormalities.%
\end{abstract}%



\sloppy


\textbf{Introduction}

Transient cortical blindness (TCB) is associated with loss of perceived
vision, normal fundi, normal papillary reflexes, and unaltered
extraocular movements (1,2). It is a rare but a known complication of
cerebral and coronary angiography following administration of contrast
medium with a reported incidence of 0.3-1\% (3). Till et al. reported
recently an incidence of 0.2\% due to the emergence of newer contrast
agent (4). Vertebral angiography has a relative higher incidence (5).
The symptoms may start immediately after contrast medium injection and
resolve within 24hours. We report a case of TCB during DSA and MRI
features.

\textbf{CASE REPORTS}

A 42-years-old male with body mass index of 25kg/m\textsuperscript{2},
presented with two episodes of right retro-orbital pain with loss of
vision in the right eye. No history of headache, nystagmus or
strabismus. No loss of consciousness. He had no history of head injury.
No history of diabetes or increased triglycerides . He was a newly
diagnosed well-controlled essential hypertensive on 5mg amlodipine. His
admission blood pressure was 135/80mmHg. He was on Plavix 75mg and
Aspirin 75mg daily due to the previous intracranial flow diverter. No
family history of aneurysm. Physical examination showed normal
extraocular muscles and no cranial nerve palsy. Pupils were equal and
reactive to light and accommodation. No other neurological deficit was
elicited.

His admission~magnetic resonance cerebral angiography demonstrated a
huge right cavernous saccular aneurysm (Fig 1). 24hours later, 42.5 x
35mm Pipeline Flex embolization device (PED) (Intracranial flow diverter
stent) was deployed across the cavernous internal carotid artery
aneurysmal neck to exclude the aneurysm from the parent artery. No
immediate complication was noted. No contrast medium reaction was
reported for 6months. Patient was discharged after 24hours on prasugrel.
Patient reported improvement in the symptoms with no new symptoms.
Follow up skull radiographs at one and six months showed PED stent
migration.

A follow-up right internal carotid artery and vertebral artery digital
subtraction angiography at 6months was done using a right radial artery
approach with a 5F DAV catheter. 0.5ml/kg of Omnipaque 300 mg/ml
contrast medium diluted to 50\% with normal saline was used for the
angiography. The internal carotid angiogram showed proximally migrated
stent into the sac of the aneurysm (fig 2) with no extravasation of
contrast medium. During the same procedure, when the right vertebral
artery was canulated and contrast medium injected, the patient became
suddenly aggressive, he experienced brief tonic seizure (lasting about
30seconds), followed by horizontal nystagmus, tinnitus, loss of vision
and incoherent speech. Over a period of one hour after the seizure
seized, he became calm, coherent in speech and gradually recovered his
vision in that order. The procedure was aborted. His blood pressure
during and after the procedure were stable between 140/80 -- 145/84mmHg.
His renal function and electrolytes were within normal limits.

Review of the angiograms did not show any vascular occlusion or spasm in
the vertebrobasilar and internal carotid artery territories. Brain
Magnetic Resonance Imaging was arranged within two hours after
angiography and demonstrated nonspecific patchy T1- weighted
hypo-intensities and T2-weighted hyper-intensities in the
periventricular areas. No restricted diffusion was seen on diffusion
weighted images and apparent diffusion coefficient (Fig. 3). Gadolinium
was not used since the non-contrast images were non-specific. Computed
Tomography scan of the brain was not done because, the authors were of
the opinion that T2 weighted MRI images were more sensitive to fluid
related abnormalities and to reduce the radiation to the patient.
Patient was discharged after 24hours of observation. Three months follow
after discharged was unremarkable.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Fig 1 : Magnetic resonance angiography (a) image showing right cavernous
aneurysm.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Fig 2: Digital subtraction angiography of the right internal cerebral
artery showing (a) a huge cavernous aneurysm (b) migrated PED stent into
the aneurysm sac\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

Fig 3: (a) FLAIR (b) DWI (c) images showing patching right parietal lobe
hyperintensities

\textbf{Discussion}

Transient cortical blindness is a dramatic complication of coronary and
cerebral angiography. It is rare and this is the first case in our
institution with 61 cerebral angiograms over a period of 2 years (0.02).
This is consistent with recent reports attributable to newer contrast
agents (4).

The symptoms of TCB may start immediately after contrast agent injection
and upto 24hours (5). Bilateral visual loss has been reported in a
number of case reports as noted in the current case (6-8).The index case
experienced in addition, tonic seizure, tinnitus, horizontal nystagmus
and incoherent speech. The recovery of normal vision and symptoms may
range from few hours, as in the index case of one hour to about 5days
(7,9,10).

A rare complication of cerebral angiography is embolism which may lead
to cortical ischaemia, often unilateral. Bilateral cortical blindness in
the clinical context of angiography is unlikely to be bilateral embolic
infarction. However, it is essential to rule out hemorrhagic or embolic
infarction with CT and /or MRI, which were absent in the current case.

Two main speculative highly debatable hypotheses have been postulated
for TCB following cerebral angiography. Most authors believe that the
neurotoxic effect of the contrast agent causes osmotic disruption of the
blood brain barrier (BBB) (11).The susceptibility of the different
sympathetic innervation of the posterior circulation to blood brain
barrier disruption appears to support this hypothesis (12). When
contrast agent such as Omnipaque is not diluted, it becomes hyperosmotic
to blood and may worsen the BBB disruption. It is believed that higher
dose of contrast medium may prolong the exposure time of the
cerebrovascular endothelium to the agent by increasing the exposure
time, thus resulting in BBB malfunction, which would further increase
the transfer of contrast material (13). Table 1 shows previous
literature on the type of contrast medium and clinical presentation of
patients with TCB during carotid and vertebral angiography.

Table 1 \textbf{Contrast encephalopathy following arteriography with
adverse clinical outcomes: demographics, contrast agents, presentation,
CT findings and clinical outcome.}\selectlanguage{english}
\begin{longtable}[]{@{}lllllllllll@{}}
\toprule
\textbf{Reference} & \textbf{Age/Sex} & \textbf{Arteriography} &
\textbf{Indication} & \textbf{Possible risk factor} & \textbf{Previous
angiography} & \textbf{Contrast agent/Volume} & \textbf{Presentation} &
\textbf{CT/MRI involved} & \textbf{Clinical resolution} & \textbf{CT/MRI
resolution}\tabularnewline
\midrule
\endhead
Sarkodie et al. (2021) & 42/M & Carotid artery & Post flow diverted
insertion follow up & Hypertension & Yes & Iohexol injection/40ml
diluted to 80ml & Cortical blindness, Horizontal nystagmus, brief motor
seizure & MRI -Periventricular T1 hypo and T2 hyper-intensities & Within
one hour & N/A\tabularnewline
Guimaraens et al. (2009)(14) & 51/M & Carotid artery & Right ICA
aneurysm coiling & Hypertension & No & Iopromide /300ml & Gerstmann's;
left visual field deficit,hemiparesis & MRI - Right fronto-
parietal-occipital & 2days & 5days\tabularnewline
Fang et al. (2009)(15) & 80/M & Carotid artery Coronary artery &
Coronary and carotid stenting & Hypertension & No & Iohexol /250ml &
Right hemiparesis & left fronto- parietal- occipital & 2days &
4days\tabularnewline
Niimi et al. (2008)(16) & 54/F & Vertebral artery & Coiling basilar apex
aneurysm & Non reported & No & Non-ionic/62ml & Vision loss to light
perception & occipital lobe & 30days & N/A\tabularnewline
Saigal et al. (2004)(17) & 74/F & Carotid artery Vertebral artery &
Coiling basilar tip aneurysm & Hypertension & No & Iohexol /Not stated &
Complete bilateral blindness; confusion & left parieto-occipital & 1day
& N/A\tabularnewline
Dangas et al. (2001)(18) & 82/M & Carotid artery & Carotid artery
stenting & Hypertension & Yes & Ioxaglate/50ml & Confusion; left
hemiparesis & Right fronto-parietal & 2days & 2days\tabularnewline
\bottomrule
\end{longtable}

Posterior reversible leukoencephalopathy syndrome (PRES) is the second
hypothesis (13). It is a neurotoxic state that occurs secondary to the
inability of the posterior circulation to autoregulate in response to
acute changes in blood pressure. Hyperperfusion occurs with resultant
disruption of the BBB and vasogenic edema in the periventricular and
perivascular spaces, without infarction, most commonly in the
parieto-occipital regions (19).

Chronic hypertension could weaken the cerebral arterioles and eventually
lead to underperfusion, resulting in brain ischemia and in due course
vasogenic edema (20). Li et al. showed that the rate of hypertension and
diabetes were higher in the patients with TCB even though the
association does not reach statistical significance (20). They also
showed using logistic regression analysis, patients with low weight who
receive higher doses of contrast medium and those with posterior
circulation injection have a higher risk of developing TCB than those
with lower doses and anterior circulation injection (20). The index case
has a 5-year history of chronic hypertension and TCB occurred during
vertebral injection. Yazici et al (21) and Frantz (22) reviewed a total
of 33 patients who had transient cortical blindness following coronary
angiography and showed that 17 patients had bypass graft and nine
patients had chronic arterial hypertension, strengthening the argument
of hypertension and bypass graft as risk factors.

About 50\% of the patients with TCB have normal CT scan features. Tong
et al showed after reviewing 12 cases that half of the patients
presented with extravasation of contrast medium into the subarachnoid
spaces and predominantly occipital lobe white matter changes, either
unilateral or bilaterally (23). MRI is more sensitive especially FLAIR
(fluid-attenuated inversion recovery) and DWI (diffusion weighted
imaging) images and these include high signals in the parieto-occipital
white matter and sometimes patchy contrast enhancement. These findings
are similar in posterior reversible leukoencephalopathy syndrome (7).
The MRI of the brain performed for the index case within two hours of
the incidence showed patchy periventricular T2-high signal intensities.

The condition is self-limiting, and often no treatment is required. The
condition is diagnosed by exclusion, hence some authors advocate the use
of steroids, anticoagulation and hydration prior to the recovery of the
vision loss (23). Steroids will reduce the vasogenic oedema and
stabilize the BBB. Our patient did not receive any specific treatment,
however, we ensured that the airway was patent, blood pressure and pulse
were normal and his random blood sugar was 8mmol/L. He complained of
headache for which 1g paracetamol was administered orally.

\textbf{Conclusion}

TCB is a diagnosis of exclusion. It is dramatic and rare complication of
cerebral and coronary angiography. Though controversial, neurotoxicity
of contrast medium and PRES have been suggested as the possible causes.
Independent risk factors include chronic hypertension, large dosage of
contrast medium and vertebral angiography. The condition shows complete
recovery within hours to days with no residual neurological deficit. It
requires supportive therapy; no evidence is available for the use of
steroids. Embolic infarction as a complication of angiography should be
ruled out with computed tomography, magnetic resonance and angiography
immediately. Due to the dramatic presentation of the index case,
radiologists and radiographers must be aware of TCB to avoid inutile
measures.

\textbf{CONFLICT OF INTEREST}

The authors declare no competing interest.

\textbf{DATA AVAILABILITY STATEMENT}

Data sharing is not applicable to this article as no new data were
created or analyzed in this study.

\textbf{CONSENT}

A consent form was signed by the patient to publish this report in
accordance with the journal's patient consent policy.

\textbf{Acknowledgements}

Authors acknowledge staff of Euracare Advanced Diagnostic and Heart
Center for their dedicated service in the management of the patient.

\textbf{AUTHOR CONTRIBUTIONS}

B Sarkodie and E Jackson performed, the digital subtraction angiography.
B Jimah and D Anim reviewed the MRI. E. Brakohiapa critically reviewed
and revised the manuscript. All authors read and approved the final
version of the manuscript.

\textbf{Reference}

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Figure Captions

Fig 1 : Magnetic resonance angiography (a) image showing right cavernous
aneurysm.

Fig 2: Digital subtraction angiography of the right internal cerebral
artery showing (a) a huge cavernous aneurysm (b) migrated PED stent into
the aneurysm sac

Fig 3: (a) FLAIR (b) DWI (c) images showing patching right parietal lobe
hyperintensities\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Fig-1/Fig-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Fig-2/Fig-2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Fig-3/Fig-3}

\end{center}
\end{figure}

\selectlanguage{english}
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\end{document}

