This article presents a case study of an 8-year-old girl who experienced a right middle cerebral artery stroke after a medical procedure. Imaging revealed a right supraclinoid internal carotid artery occlusion, likely caused by perioperative carotid compression or dissection. Follow-up imaging 20 months later showed that the right carotid canal, which houses the internal carotid artery, had decreased in size to about half that of the left carotid canal. This observation suggests that while carotid canal asymmetry is often congenital, an acquired internal carotid artery lesion can also result in decreased size of the corresponding carotid canal over time. Therefore, the size of the carotid canal alone cannot be used to determine whether an internal carotid artery occlusion is congenital or acquired.

1. Please cite this article in press as: Wyse E, et al. The observation of an ipsilateral carotid canal hypopla-
sia cannot be used to ascertain the congenital nature of a carotid artery occlusion. J Neuroradiol (2015),
http://dx.doi.org/10.1016/j.neurad.2015.02.003
ARTICLE IN PRESS+Model
NEURAD-505; No. of Pages 2
Journal of Neuroradiology (2015) xxx, xxx—xxx
Available online at
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CORRESPONDENCE
The observation of an ipsilateral
carotid canal hypoplasia cannot be
used to ascertain the congenital
nature of a carotid artery occlusion
It is classically accepted that in patients with a hypoplas-
tic or absent internal carotid artery (ICA), the observation
of a similarly hypoplastic or absent carotid canal indicates
the congenital nature of the anomaly [1—3] We present a
case of acquired ICA occlusion with subsequent decrease in
the size of the corresponding carotid canal.
Figure 1 DSA, right common carotid injection, lateral view,
showing a supraclinoid occlusion of the right ICA.
Figure 2 CT, axial images through the horizontal portion of
the carotid canals (top) and at the carotid foramina (bottom).
The right foramen (A, 12.3 mm2
) ipsilateral to the carotid occlu-
sion is smaller that the left one (B, 23.9 mm2
).
The patient was an 8-year-old girl presenting with a
right middle cerebral artery stroke after tonsillectomy
and adenoidectomy. Digital subtraction angiography (DSA)
revealed a right supraclinoid ICA occlusion, suggesting
perioperative carotid compression and/or dissection with
clot formation and distal migration (Fig. 1). The patient was
later diagnosed with activated protein C resistance. While
the cervical segment initially appeared to have a normal
caliber, with subsequent imaging confirming that the right
http://dx.doi.org/10.1016/j.neurad.2015.02.003
0150-9861/© 2015 Elsevier Masson SAS. All rights reserved.

2. Please cite this article in press as: Wyse E, et al. The observation of an ipsilateral carotid canal hypopla-
sia cannot be used to ascertain the congenital nature of a carotid artery occlusion. J Neuroradiol (2015),
http://dx.doi.org/10.1016/j.neurad.2015.02.003
ARTICLE IN PRESS+Model
NEURAD-505; No. of Pages 2
2 Correspondence
ICA was providing both the right ACA and MCA, follow-up
investigations obtained 20 months later showed the right
carotid canal to be about half the size of the left one (12.3
versus 23.9 mm2
) (Fig. 2).
Our observation suggests that, although carotid canal
asymmetry can certainly result from a congenital ICA
anomaly, this radiological sign is not infallible. The hypoplas-
tic canal documented in our patient was associated with an
ICA lesion acquired at the age of 8, even though the ossifi-
cation of the central skull base is believed to be complete
by age 2 [4] This observation may have clinical and legal
implications when the chronology of a carotid injury has to
be determined.
Disclosure of interest
The authors declare that they have no conflicts of interest
concerning this article.
References
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[2] Quint DJ, Silbergleit R, Young WC. Absence of the carotid canals
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[3] Tasar M, Yetiser S, Tasar A, Ugurel S, Gonul E, Saglam M. Con-
genital absence or hypoplasia of the carotid artery: radioclinical
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Emily Wysea
Danielle Eckart Sortea
Lori Jordanb
Philippe Gaillouda,∗
a
Division of Interventional Neuroradiology, The Johns
Hopkins University School of Medicine, Bloomberg 7218,
1800 E Orleans Street, Baltimore, MD 21287, MD, USA
b
Department of Neurology, Vanderbilt University,
Nashville, TN, USA
∗
Corresponding author. Tel.: +410 955 8525;
fax: +410 614 8238.
E-mail address: phg@jhmi.edu (P. Gailloud)