The British Journal of Radiology, 84 (2011), e23–e26

CASE REPORT

Recanalisation of the internal carotid artery via the vasa vasorum
after coil occlusion
T MEGURO, MD, K MURAOKA, MD, K TERADA, MD, N HIROTSUNE, MD and S NISHINO, MD
Department of Neurological Surgery, Hiroshima City Hospital, 7-33 Motomachi, Naka-ku, Hiroshima 730-8518, Japan

ABSTRACT. Antegrade recanalisation of a completely occluded internal carotid artery
(ICA) via the vasa vasorum is extremely rare. Here, we report such a case after proximal
endovascular coiling in a case of dissected (i.e. non-atherosclerotic) ICA. A 42-year-old
man presented with thromboembolic stroke of the left frontal lobe owing to pseudoocclusion of the left ICA manifesting as motor aphasia and right hemiparesis. There
were abundant floating thrombi in the petrous portion of the left ICA. Because of good
collateral flow in the left middle cerebral artery territory through the anterior
communicating artery and external carotid artery system, endovascular coil
embolisation of the left ICA was performed for prevention of further thromboembolic
stroke. The patient showed progressive recovery following endovascular treatment,
and was discharged with mild right hemiparesis 1 month later. He maintained a
regimen of aspirin and physical rehabilitation. At follow-up, 38 months later, the
patient was asymptomatic. Angiography demonstrated occlusion of the left ICA and
multiple serpiginous vessels originating from the proximal internal and external carotid
arteries and which filled the ICA distal to the occlusion. This case suggests that an ICA
occluded by proximal coil embolisation—even in a non-atherosclerotic case—might be
recanalised via the vasa vasorum.

The vasa vasorum supply the arterial blood to the
adventitia and outer third of the media in large arteries,
whereas diffusion across the endothelial layer supplies
oxygen and other nutrients to the endothelium and inner
media [1, 2]. Atherosclerotic changes cause an increase in
the vasa vasorum, which form a dense vascular network
within the plaque [3, 4], and vessels originating from the
arterial lumen may develop and communicate with the
vasa vasorum [3, 5]. However, after complete occlusion of
the internal carotid artery (ICA), recanalisation via the vasa
vasorum is rare, with only a few reported cases [5–12].
We describe a case of recanalisation of the ICA
occluded by endovascular coiling. It seems that collateralisation via the vasa vasorum developed in the 3 year
follow-up period.

Case report
A 42-year-old man was admitted to the neurology
department of a local hospital on 17 August 2005. He had
experienced sudden onset of weakness of the right
extremities and speech disturbance. CT and MRI of the
brain revealed left cerebral infarction, and antiplatelet
and anticoagulation therapy (aspirin 100 mg day21 and
argatroban 60 mg day21) was initiated. His neurological
Address correspondence to: Toshinari Meguro, MD, Department of
Neurological Surgery, Hiroshima City Hospital, 7-33 Motomachi,
Naka-ku, Hiroshima 730-8518, Japan. E-mail: tmeguron@
hotmail.com

The British Journal of Radiology, February 2011

Received 1 December 2009
Revised 13 February 2010
Accepted 26 February 2010
DOI: 10.1259/bjr/31383692
’ 2011 The British Institute of
Radiology

symptoms improved satisfactorily but suddenly deteriorated on the third day from onset. Repeat MRI/magnetic
resonance angiography (MRA) suggested an increase in
cerebral infarction because of the left ICA occlusion, and
he was immediately transferred to our department.
On admission, his Glasgow coma scale score was 9
(E3V1M5). He had right hemiplegia and motor aphasia.
Laboratory data revealed no definitive abnormality. A CT
scan showed a low-density area in the left frontal lobe,
so emergency cerebral angiography was performed.
On the left common carotid injection, the ICA appeared occluded 3 cm distal to the carotid bifurcation
(Figure 1a). The suprapetrous portion of the left ICA was
canalised via the external carotid (vidian and inferolateral
trunk arteries), but the petrous and cervical portions of
the ICA were not seen on the early-phase image obtained
within 2 s after injection. The delayed-phase image (after
2.5 s) revealed a slow stream of contrast material
progressing antegrade through the ICA. Floating thrombi
were seen in the petrous ICA on the late-phase image
(Figure 1b). The circulation of the left hemisphere was
mainly derived through collateral vessels from the
anterior communicating artery and external carotid
artery systems.
The patient was diagnosed as having ICA dissection,
and we decided to undertake endovascular occlusion of
the left ICA to prevent further thromboembolism. The left
ICA was occluded with Guglielmi detachable coils (Boston
Scientific/Target Therapeutics, Fremont, CA) (Figure 2).
The patient was neurologically unchanged immediately
e23

T Meguro, K Muraoka, K Terada et al

(a)

(b)

Figure 1. Left common carotid angiograms, lateral view. (a) Early-phase image shows the left internal carotid artery (ICA)
occlusion 3 cm distal to the carotid bifurcation. (b) Later-phase image shows a slow stream of contrast material progressing
antegrade through the ICA. Floating thrombi were seen in the petrous ICA.

(a)

(b)

Figure 2. Left common carotid angiograms after endovascular occlusion of the internal carotid artery (ICA) with coils. (a) No
subtraction. (b) The cervical ICA was completely occluded by the coil.
e24

The British Journal of Radiology, February 2011

Case report: Internal carotid artery recanalisation via vasa vasorum

after the treatment but gradually improved. He underwent
anticoagulant therapy (argatroban 60 mg day21) for
7 days and took aspirin (100 mg day21) from then on.
He was transferred to a local rehabilitation centre 2 weeks
later. His neurological symptoms gradually improved. He
had mild right hemiparesis, and 3 months later his score
on the modified Rankin scale was Grade 1.
A follow-up angiography was performed 38 months
after treatment. The left common carotid injection demonstrated that the left ICA had recanalised with
multiple small vascular channels. The multiple small
vascular channels arose from the proximal left ICA and
the left external carotid artery ran outside the expected
lumen of the left ICA, then filled the native lumen distal
to the petrous portion of the ICA (Figure 3).

Discussion
The authors suppose that the cause of ICA pseudoocclusion in this case was ICA dissection, according to
the initial angiographic findings. Spontaneous dissection
of the ICA is a frequent cause of stroke in young to
middle-aged patients, accounting for approximately 20%
of stroke in patients ,45 years of age [13]. Conservative
management with anticoagulation and/or antiplatelet
medications is the primary treatment for symptomatic
carotid dissection. Thromboembolism, not haemodynamic infarction, is the essential stroke mechanism in ICA
dissection, and ICA dissection has the potential for
pseudoaneurysm formation in its dissecting part that
may be causing a mass effect and thrombus formation

(a)

within the pseudosac with subsequent embolisation.
Prevention of arterioarterial embolism is the main
therapeutic goal in ICA dissection [14]. Because most
dissections of the carotid artery heal spontaneously,
surgical or endovascular treatment should be attempted
if symptoms progress despite the conservative treatment
[13, 15].
It has been recognised that the vasa vasorum in the
cervical carotid artery originate from the external carotid
artery and internal carotid artery near the carotid
bifurcation [3, 5]; however, recanalisation of an occluded
cervical internal carotid artery via the vasa vasorum is
very rare. There have been only a few reported cases
[5–12]. Among most of the reported cases, the cause of
internal carotid artery occlusion was atherosclerosis. Bo
et al [3] reported that the vasa vasorum are prominent in
areas of marked atherosclerosis. The proliferation of vasa
vasorum into atherosclerotic plaques is related to
angiogenic factors in the atherosclerotic plaques and
subsequent neovascularisation.
Except for the vasa vasorum that developed, the
possible mechanisms of the antegrade recanalisation of
the occluded ICA in our patient were neovascularisation
in the embolised coil mass and thrombus, and recanalisation of the pseudolumen of the carotid dissection.
These mechanisms might be partially involved in this
case. However, the most characteristic angiographic
finding of recanalised vessels via the vasa vasorum is
the location of vascular channels outside the expected
carotid artery lumen that provide collateral flow from
the proximal external and internal carotid arteries to the

(b)

Figure 3. Left common carotid angiograms 38 months after treatment. Frontal (a) and lateral (b) views. Multiple small vascular
channels arising from the proximal internal carotid artery (ICA) and the external carotid artery project over the expected course
of the ICA with antegrade filling of the distal ICA.

The British Journal of Radiology, February 2011

e25

T Meguro, K Muraoka, K Terada et al

more distal cervical carotid artery beyond the occlusion
site. In the present case, angiography confirmed these
findings.
We present the first case of antegrade recanalisation via
the vasa vasorum of an ICA completely occluded by
endovascular coiling. Only one case of recanalisation via
the vasa vasorum after proximal embolisation of the ICA
has been reported [6]. Numagami et al [6] occluded the
ICA with a detachable balloon for treatment of a giant
intracavernous aneurysm; however, the ICA was found to
be recanalised via the vasa vasorum at the follow-up
6 months after treatment. They hypothesised that recanalisation of the ICA via the vasa vasorum was induced by
marginal cerebral blood flow in the ipsilateral hemisphere. We could not determine a relationship between
the development of the vasa vasorum and cerebral blood
flow in the ipsilateral hemisphere, because a detailed
quantitative analysis of cerebral blood flow was not
performed in the presented case.
In conclusion, although antegrade recanalisation via
the vasa vasorum after parent artery occlusion by
endovascular coiling is very rare, it is important to
recognise this phenomenon and it is necessary to check
for it in the imaging follow-up of the parent vessel.

References
1. Werber AH, Heistad DD. Diffusional support of arteries.
Am J Physiol 1985;248:H901–6.
2. Williams JK, Orgren KI, Armstrong ML, Heistad DD. Vasa
vasorum in the carotid sinus of atherosclerotic monkeys:
implications for baroreceptor function. Atherosclerosis
1989;78:25–32.
3. Bo WJ, McKinney WM, Bowden RL. The origin and
distribution of vasa vasorum at the bifurcation of the common
carotid artery with atherosclerosis. Stroke 1989;20:1484–7.
4. Yoshida K, Inoue K, Chin M, Narumi O, Yamagata S.
Occlusive thrombosis with neovascularization of the internal

e26

carotid artery: two case reports. Neurol Med Chir (Tokyo)
2008;48:447–50.
5. Shimizu H, Tominaga T, Ezura M, Yoshimoto T. Bypass
surgery for occluded internal carotid artery revascularized
by vasa vasorum: case report. Neurol Med Chir (Tokyo)
2002;42:57–61.
6. Numagami Y, Ezura M, Takahashi A, Yoshimoto T.
Antegrade recanalization of completely embolized internal carotid artery after treatment of a giant intracavernous aneurysm: a case report. Surg Neurol 1999;52:
611–16.
7. Bradac G, Oberson R. Angiography in cerebro-arterial
occlusive disease. New York: Springer-Verlag, 1979: 69.
8. Colon GP, Deveikis JP, Dickinson LD. Revascularization of
occluded internal carotid arteries by hypertrophied vasa
vasorum: report of four cases. Neurosurgery 1999;45:
634–7.
9. Kasner SE, Liebeskind DS, Cucchiara BL, McGarvey ML,
Detre JA, Sinson G, et al. Internal carotid artery ‘‘spring
sign’’. Neurology 2002;58:1099.
10. Kemeny V, Droste DW, Nabavi DG, Schulte-Altedorneburg
G, Schuierer G, Ringelstein EB. Collateralization of an
occluded internal carotid artery via a vas vasorum. Stroke
1998;29:521–3.
11. Martin MA, Marotta TR. Vasa vasorum: another cause of
the carotid string sign. AJNR Am J Neuroradiol 1999;
20:259–62.
12. Newton T, Potts D. Angiography in radiology of the skull
and the brain. St. Louis: Mosby, 1974: 1214–15.
13. Kadkhodayan Y, Jeck DT, Moran CJ, Derdeyn CP, Cross
DT, 3rd. Angioplasty and stenting in carotid dissection with
or without associated pseudoaneurysm. AJNR Am J
Neuroradiol 2005;26:2328–35.
14. Benninger DH, Georgiadis D, Kremer C, Studer A, Nedeltchev K, Baumgartner RW. Mechanism of ischemic infarct
in spontaneous carotid dissection. Stroke 2004;35:482–5.
15. Schievink WI, Piepgras DG, McCaffrey TV, Mokri B.
Surgical treatment of extracranial internal carotid artery dissecting aneurysms. Neurosurgery 1994;35:809–15;
discussion 815–16.

The British Journal of Radiology, February 2011