The Egyptian Journal of Radiology and Nuclear Medicine (2016) 47, 891–896

Egyptian Society of Radiology and Nuclear Medicine

The Egyptian Journal of Radiology andNuclearMedicine

www.elsevier.com/locate/ejrnmwww.sciencedirect.com

CASE REPORT

Primitive Hypoglossal Artery: A case report

* Postal address: 27 Ahmad Foad Nour Str., Camp Caesar, Alexan-

dria 21525, Egypt. Tel.: +20 01001948320.

E-mail address: mohamed.shaban@gmail.com.

Peer review under responsibility of The Egyptian Society of Radiology

and Nuclear Medicine.

http://dx.doi.org/10.1016/j.ejrnm.2016.05.0100378-603X � 2016 The Egyptian Society of Radiology and Nuclear Medicine. Production and hosting by Elsevier.This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Mohamed Samir Shaaban *

Diagnostic and Interventional Radiology Department, Faculty of Medicine, Alexandria University, Egypt

Received 5 October 2015; accepted 15 May 2016Available online 2 June 2016

KEYWORDS

Carotid artery anomalies;

Circle of Willis;

Persistent hypoglossal artery;

Basilar artery

Abstract We report a case of a left sided Primitive Hypoglossal Artery detected by multi-detector

CT cerebral angiography, performed for a 47 years old female patient complaining of sudden onset

of drowsiness, who had undergone non-contract CT of the brain which revealed small ischemic

infarcts in the left cerebellar peduncle. On MDCT cerebral angiography, the left internal carotid

artery passes through the left hypoglossal canal, to form the basilar artery, while the left carotid

canal was empty. The left anterior and middle cerebral arteries were formed through patent and

prominent anterior communicating artery.� 2016 The Egyptian Society of Radiology and Nuclear Medicine. Production and hosting by Elsevier.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-

nd/4.0/).

1. History

47 years old female suffered sudden onset of drowsiness andvertigo, with mild headache. Her vital signs and routinelaboratory tests were normal. Upon initial non-contrast CT

of the brain, small hypodense foci were detected in the leftcerebellar peduncle, diagnosed as ischemic infarcts. Dopplerexamination of the carotid arteries was normal. MDCT

angiography of the cerebral circulation was performed by 20-Detectors Siemens SOMATOM Definition AS (Siemens Med-ical Solutions, Malvern, PA), with 20 � 0.6 collimation, 0.5Rotation time, and 1.4 Pitch. Reconstruction was performed

by 0.75 mm slice thickness and 0.5 increment. Images wereprocessed by Syngo CT Workplace VA44A with multiplanarreformatting and Volume Rendering Technique. The patient

was injected with 100 mL of meglumine ioxitalamate350 mg l/ml using a power injector (Medrad, Vistron CT) at

the rate of 5 ml per second through an 18 gauge venous can-

nula in the left antecubital vein.

2. Imaging findings

Upon the initial non-contrast CT of the brain, small hypo-dense ischemic infarcts were detected in the left cerebellarpeduncle and left cerebellar hemisphere, in the territory of

the left superior cerebellar artery (Fig. 1). On CT cerebralAngiography, The upper cervical parts of both internal carotidarteries were normal in course and caliber (Fig. 2). The leftinternal carotid artery deviated postero-medially at the level

of CV1, to enter the skull cavity via the left hypoglossal canal,leaving the left carotid canal empty (Fig. 3). It then curvedupward and then medially to form the basilar artery which

gave origin to the posterior cerebral arteries bilaterally andthe right superior cerebellar artery. The left superior cerebellarartery was markedly attenuated, which explains the left cere-

bellar peduncle infarcts (Fig. 4). The left posterior communi-cating artery was hypoplastic, while the right posteriorcommunicating artery was patent (Figs. 5 and 6). The canalic-

ular, cavernous and supra-clinoid portions of the left internal

Fig. 1 Axial non-contrast CT scan at the level of cerebellum showing ischemic infarct in the left cerebellar peduncle and left cerebellar

hemisphere (yellow arrow).

Fig. 2 Axial CT cerebral angiography scan in arterial phase at the level of CV1–CV2, showing both internal carotid arteries of both sides

at their normal sites (yellow arrows).

892 M.S. Shaaban

Fig. 3 Axial CT cerebral angiography scan in thin MIP reformatting at the level of skull base showing the left internal carotid artery

passing into the left hypoglossal canal (yellow arrow).

Fig. 4 Coronal CT cerebral angiography scan thin MIP reformatted in arterial phase (a) showing the left internal carotid artery

emerging from the left hypoglossal canal to form the basilar artery (yellow arrow). The left superior cerebellar artery is markedly

attenuated (white arrow), while the right is patent (red arrow). (b) The corresponding thin VRT scan. Both vertebral arteries are

hypoplastic.

Primitive Hypoglossal Artery 893

Fig. 5 CT cerebral angiography scan thin MIP reformatted in arterial phase, axial in the levels of carotid canals (a) and cavernous

sinuses (b), and coronal in the level of cavernous sinuses (c), showing absent canalicular (yellow arrow) and cavernous (red arrow) portions

of the left internal carotid artery.

894 M.S. Shaaban

carotid artery were absent till the bifurcation into the left ante-rior and middle cerebral arteries, supplied via the patent ante-

rior communicating artery. Both vertebral arteries werehypoplastic (Fig. 4).

3. Discussion

Multidetector computed tomographic (CT) angiography hasbeen considered as the first line technique to assess the cerebral

circulation in the cases of acute stroke and subarachnoid hem-orrhage (1,2). Variations of the cerebral circulation, in partic-ular of the circle of Willis, are common, and it is important to

understand the appearance of these normal variants, theirprevalence, and their clinical relevance, as they might be mis-taken for arterial occlusions in cases of hypoplastic or aplasticarteries, and as some of these variants are associated with

aneurysm formation (3,4). The sensitivity and specificity ofmultidetector CT angiography for detection of intracranial

vascular anomalies are reported to be up to 81 to 90% and93%, respectively (3).

Variants of the cerebral circulation can be classified into

fenestrations/duplications, circle of Willis variants, persistentanastomoses between the carotid and basilar arteries, andothers (5–7). Persistent carotid–basilar anastomoses originatedue to faulty development of the internal carotid arteries with

faulty anastomosis at three major sites with the paired longitu-dinal neural arteries that constitute the primitive vertebrobasi-lar system (8). These arteries are named the trigeminal, otic,

and hypoglossal arteries. There are seven transversely orientedarteries in the cervical region. The most cephalic of these arter-ies is the proatlantal intersegmental artery (8,9). Failure of

these vessels to regress during embryonic development results

Fig. 6 CT cerebral angiography scan in VRT reformatting for the circle of Willis, showing patent anterior communicating artery (white

arrow), patent right posterior communicating artery (red arrow), and hypoplastic left posterior communicating artery. Note the left

internal carotid artery as it emerges from the left hypoglossal canal (yellow arrow) to form the basilar artery.

Primitive Hypoglossal Artery 895

in various persistent carotid–vertebrobasilar anastomoses,

including Persistent Trigeminal Artery, Primitive HypoglossalArtery, Proatlantal Intersegmental Artery, Persistent OticArtery, Persistent Dorsal Ophthalmic Artery, and PersistentPrimitive Olfactory Artery (3). The persistent hypoglossal

artery is the second most common carotid–vertebrobasilarartery anastomosis, following the persistent trigeminal artery,with a prevalence of 0.02–0.10% (4,10). It originates from

the internal carotid artery at the levels of the upper cervicalspines, courses through the hypoglossal canal, and anasto-moses with the basilar artery (11,12). In 79% of cases, the pos-

terior communicating arteries are hypoplastic, and in 78% ofcases, the vertebral arteries are hypoplastic (3).

In our case, the facts that the anomalous artery arises fromthe level of C1-3, then passes through the hypoglossal canal to

form the basilar artery which is filled only distal to the point ofjunction, and that the ipsilateral posterior communicatingartery is severely hypoplastic, all meet the ‘‘Lie criteria” used

to diagnose a Primitive Hypoglossal Artery (13,14).

Conflict of interest

The author declares that they have no conflict of interest.

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