Perspectives in Medicine (2012) 1, 198202

Bartels E, Bartels S, Poppert H (Editors):

New Trends in Neurosonology and Cerebral Hemodynamics an Update.
Perspectives in Medicine (2012) 1, 198202

journal homepage: www.elsevier.com/locate/permed

Vertebral artery hypoplasia and the posterior

circulation stroke
Andrea Skultty Szrazov a,, Eva Bartels b, Peter Turcni a

a
University Hospital of Bratislava, 1st Neurological Clinic, Bratislava, Mickiewicziva 13, Slovakia
b
Center for Neurological Vascular Diagnostics, Mnchen, Germany

KEYWORDS Summary The aim of this preliminary study is to evaluate the hypothesis of a possible causal
Posterior circulation link between the anatomical ndings of vertebral artery hypoplasia (VAH) and the incidence
stroke; of posterior circulation stroke. We used full ultrasonographic examination to evaluate patients
Vertebral artery with stroke in the vertebrobasilar circulation territory over a period of 1.5 years. The diam-
hypoplasia (VAH); eter equal or less than 2.5 mm (in V1 and V2 segment of the vertebral artery) was set as a
Ultrasound; feature of vertebral artery hypoplasia. Magnetic resonance imaging and angiography (MRI and
Duplex MRA) or computed tomography and angiography (CT and CTA) were performed to conrm the
ultrasonography; anatomic variation of hypoplasia and the site of the cerebral ischemic territory. In the group
Magnetic resonance of 44 stroke patients, 9 (20%) had a hypoplastic vertebral artery and 35 (80%) were without
angiography (MRA); VAH. Although vertebral artery hypoplasia in previously published literature is seldom shown
Computed as a leading risk factor for stroke in vertebrobasilar (posterior) circulation, its occurrence is
tomography not negligible and in coexistence with known risk factors of stroke may increase the negative
angiography (CTA) clinical impact. Vertebral artery hypoplasia can be diagnosed non-invasively with duplex ultra-
sonography. It is therefore a useful method for detection of this anatomic variation and for
follow-up examination.
2012 Published by Elsevier GmbH. Open access under CC BY-NC-ND license.

Introduction can occur. The intervertebral segment (V2) passes through

The vertebral artery (VA) as a part of the vertebrobasilar
cerebral circulation is one of the main branches of the sub-
clavian artery. The course of the VA is divided into 4 sections
[1,2]. It originates as section V0 from the posteromedial part
of the arc of the subclavian artery and continues cranially. It
is followed by the prevertebral segment (V1), which in 90%
enters into the costotransverse foramen of the sixth cervi-
cal vertebra (C6). Variations as entrance in the C5 or above
the C6 vertebra, coiling or kinking of the vertebral artery
Corresponding author.
E-mail address: aszarazova@gmail.com (A.S. Szrazov).
the costotransverse canal of the cervical vertebrae up to
the C2 vertebra. The atlas loop segment (V3) is created by a
curved course of the artery around the atlas. The intracra-
nial segment V4 is the section of the vertebral artery after
penetrating the atlantooccipital membrane, dura mater and
arachnoidea. At the clivus the right and left vertebral artery
merge to form the basilar artery, which is a part of the
intracranial posterior circulation.
The diameter of vertebral arteries varies from 1.5 to
5.0 mm. Identical width of VA occurs in 25% of the popu-
lation, in 65% the left vertebral artery is wider, whereas in
the remaining 10% the right vertebral artery is larger [3].
Khan et al. found dominance of the left vertebral artery in
50%, and of the right vertebral artery in 25% in regard to the
diameter of the vessel [4].

2211-968X 2012 Published by Elsevier GmbH. Open access under CC BY-NC-ND license.
doi:10.1016/j.permed.2012.02.063
The posterior circulation stroke
The following congenital anatomic variations of the ver-
tebral artery are described in the literature: vertebral artery
aplasia and vertebral artery hypoplasia (VAH). Aplasia of VA
occurs in about 1% of the population [5].
Vertebral artery hypoplasia (VAH) is classied as a ves-
sel with a diameter in the entire course of less than 2 mm
[6], respectively less than 3 mm [7], or with a side dif-
ference equal or greater than 1:1.7 [8]. Additionally to
the vessel diameter, another criterion contains reduced
blood ow velocity and increased resistance index values in
the ultrasonographic ndings [1,9]. There is a tendency of
compensatory increase in the vessel diameter of the con-
tralateral vertebral artery of more than 5 mm [1]. These
various denitions of the incidence of VAH are based on
subsequent characteristics: a diameter of less than 2 mm
was observed by the method of duplex ultrasonography by
the authors Delcker and Diener in 1.9% of the population
[6], a diameter of less than 3 mm was described by Touboul
et al. in 6% of the population [7]. Trattnig et al. set a
side asymmetry in the ratio 1:1.7 for more than 10% of
patients examined by ultrasonography [8]. Frequency of VAH
(diameter equal or less than 2 mm) in the general popula-
tion is 26.5% in unilateral and 1.6% in bilateral hypoplasia
of the vertebral artery [10]. In terms of side difference,
the right hypoplastic vertebral artery occurs in 6.2% of the
population, while left vertebral hypoplasia is present less
frequently in 4.5% [2]. Visualization of vertebral artery is
possible by ultrasonographic examination, by invasive or
non-invasive angiography (MRA, CTA), and also by autopsy
ndings. As mentioned previously, a more narrow vessel
lumen is present in the ultrasonographic image in vertebral
artery hypoplasia, and additionally, blood ow parameters
are dened by a reduced diastolic ow velocity associated
with higher peripheral resistance. The resistance index (RI)
is equal to or greater than 0.75. The peak systolic velocity
(PSV) is usually less than 40 cm/s [1,5].
In the literature, morphological variations of the verte-
bral artery are described as being associated with different
clinical symptoms. Nevertheless, vertebral hypoplasia as a
possible risk factor for pathology, particularly of stroke in
the vertebrobasilar circulation territory, was little empha-
sized yet.
The aim of this preliminary study is to evaluate a
hypothesis of a possible causal link between the anatomical
ndings of VAH and the incidence of posterior circulation
stroke. For this purpose, we assessed the relative fre-
quencies of posterior circulation strokes in patients with
VAH as compared to patients without VAH, and also the
relative frequencies of the conventional vascular risk fac-
tors (hypertension, diabetes, hyperlipidemia and smoking).
Additionally, we determined the possible mechanism of
stroke in our patients.
Materials and methods
A group of 44 patients (30 men, 14 women; mean age 67
years [range 4488]) with acute ischemia in the verte-
brobasilar territory had a full ultrasonographic examination
of the extra- and intracranial arteries between September
2009 and February 2011.
199
The location of the acute ischemic infarct was judged
clinically and conrmed by CT scan or MRI.
We excluded patients with transient ischemic attacks
(TIA), patients with other vertebral artery ndings (such
as atheromatosis, stenosis or occlusion) or other cerebral
lesions, as well as those in whom a full ultrasono-
graphic examination of the vertebral arteries was not
possible.
We used a 7.5-MHz linear array transducer for the
duplex ultrasonographic examination of the vertebral arter-
ies (B-mode and color-coded duplex ow imaging). In the
V1 (prevertebral) and V2 (intervertebral) segments of the
extracranial vertebral artery the distance between the
internal layers of the parallel walls of the vessel (caliber
of VA) and the hemodynamic characteristics of blood ow
were measured.
The diameter equal or less than 2.5 mm, respectively the
side difference equal or greater than 1:1.7 were set as a
feature of vertebral artery hypoplasia. Additionally, reduced
ow velocities as compared to the contralateral side, and
higher peripheral resistance ipsilaterally (RI equal or greater
than 0.75) were considered.
MRA, CTA or conventional angiography was performed to
conrm the presence or absence of the anatomic variation
of hypoplasia.
We also investigated the occurrence of other concomi-
tant vascular risk factors such as hypertension, diabetes,
hyperlipidemia and smoking.
Results
In the group of 44 posterior circulation stroke patients, 9
(20%) had a hypoplastic vertebral artery and 35 (80%) were
without VAH (Fig. 1A). There was more frequent right-sided
VAH in 7 (78%), as compared to left-sided VAH in 2 (22%)
cases (Fig. 1B). One patient had bilateral VAH (both ver-
tebral arteries had a diameter of less than 2.5 mm), more
signicant on the right side. None of the patients had basilar
artery hypoplasia. In the group of non-VAH patients were 22
men and 13 women, in the VAH group 8 men and 1 woman
(Fig. 1C). There was a slight difference for age between the
non-VAH (mean age 68.3 years) and VAH group (mean age
62.3 years).
The distribution of other vascular risk factors in both
groups was represented as follows (Fig. 1D): hypertension
(n = 40 patients), diabetes mellitus (n = 19), hyperlipidemia
(n = 17) and smoking (n = 16).
The frequency of the presence of these risk factors
(hypertension: p = 0.99; diabetes mellitus: p = 0.26 and
smoking: p = 0.45) in patients with posterior circulation
strokes with or without VAH did not differ.
We found that in the group of patients without VAH hyper-
lipidemia occurred more often than in the VAH group (16:1).
There was a statistically signicant relationship between
nding of non-VAH and hyperlipidemia (p = 0.027).
Possible mechanism of stroke were embolism, especially
cardioembolism (n = 10), atherosclerotic changes of vessels
(small vessel disease n = 16, or large vessel disease n = 25). In
6 cases, the mechanism of stroke was cryptogenic (unknown
mechanism n = 6) (Fig. 1E).
200 A.S. Szrazov et al.

Figure 1 Descriptive statistics of the study data. (A) Percentage of the presence and absence of VAH (vertebral artery hypoplasia)
in patients with posterior circulation stroke. (B) Percentage of vertebral artery hypoplasia location in patients with posterior
circulation stroke. (C) The presence and absence of VAH (vertebral artery hypoplasia) by gender in the study group in absolute
numbers. (D) The presence of risk factors (in absolute numbers) by patients with posterior circulation stroke in the study group
(patients with more than one risk factor were present). (E) The representation of stroke etiology (in absolute numbers) by patients
with posterior circulation stroke in the study group (a combination of different stroke mechanisms occurred).

The frequency of the presence of the stroke mechanisms
(cardioembolism: p = 0.69; atherosclerotic changes of large
vessels: p = 0.14) in non-VAH and VAH groups did not differ.
There was a non-signicant tendency (p = 0.053) for
atherosclerotic changes of small vessels to be more frequent
in posterior circulation strokes with VAH than in non-VAH
group (6:10).
We found no recurrent strokes of the posterior circulation
over the 1.5-year period of this still ongoing study.
Discussion
Ischemic stroke localized in the vertebrobasilar circulation
territory accounts for about a quarter of all ischemic strokes
[11,12]. Mumenthaler describes the presence of ischemia
in this localization in 15% of strokes [13]. The clinical sig-
nicance of vertebral artery hypoplasia is currently not
sufciently recognized. Perren et al. carried out a study
which examined 725 patients with established diagnosis
of rst ever stroke. Two thirds of ischemic events were
localized in the carotid circulation and 247 patients had
ischemia in the posterior fossa. Vertebral artery hypopla-
sia was observed in 13% of ischemic strokes in the posterior
fossa, in the other localizations the presence of VAH was
4.6%. Based on these results, the authors conclude that
the hypoplastic vertebral artery on one side (predominantly
right in the study group in 70%) is more frequently a pos-
sible risk factor for vertebrobasilar ischemia, as compared
to other localizations of stroke. According to this, vertebral
artery hypoplasia was considered as a risk factor, equiva-
lent to other conventional risk factors such as hypertension,
diabetes, smoking and hyperlipidemia [14]. In the article
Arterial occlusion depending on the size (diameter) of
blood vessels? Caplan declared essential importance of
baseline vessel diameter before subsequent obstruction of
any etiology occurs [15]. He stated that a restricted artery
(in the paired arteries) is more prone to closure, especially
when other vascular risk factors are present. It is assumed
that if this claim is true for carotid circulation territory [16],
it is also highly likely in the vertebrobasilar localization. He
based this argument on ndings in the New England Medical
Center Posterior Circulation Registry from 2004 [17], which
proved the occurrence of ischemia in the area supplied by
the vertebral artery (brainstem and posteriorinferior ter-
ritory of cerebellum) located ipsilaterally to the narrower
vertebral artery.
The posterior circulation stroke 201

Figure 2 Findings in a 48 years old female patient of our study with a left-sided VAH and an ipsilateral cerebellar ischemia. (A)
Ultrasonographic view of a V2 segment of a hypoplastic vertebral artery on the left side with a diameter of 2.5 mm and reduced blood
ow velocity (max. syst. velocity 16.5 cm/s). (B) Ultrasonographic view of diameter (4.3 mm) and hemodynamic characteristics of
a non-hypoplastic vertebral artery on the right side by the same patient. (C) Magnetic resonance angiography image of vertebral
artery hypoplasia (black arrows) on the left side. The black arrows show an inadequate circulation. (D) Magnetic resonance view of
ischemic focus in the left cerebellum (black arrow) in a patient with VAH (vertebral artery hypoplasia) on the left side.

Similar to Caplans ndings our results show that poste-
rior circulation strokes occur more often ipsilateral to the
VAH (Fig. 2A). The pathomechanism of ischemia in the pres-
ence of VAH has not yet been determined precisely. The
clinical severity of VAH depends on how well the collateral
supply functions, especially via the circle of Willis, and the
sufciency of the anterior circulation and of the cervical
collaterals. The compensatory hyperplasia of the contralat-
eral artery plays also an important role in maintaining an
adequate blood supply to the brain, particularly in the pos-
terior fossa. However, if the supplemental system fails, the
compensatory mechanisms are exhausted and that can lead
to stroke [1,5].
In our study we found that the distribution of vascular
risk factors, except hyperlipidemia, was equal between the
group with and without VAH. Therefore, we assume that VAH
contributes as an additional risk factor to ischemic events in
the posterior circulation, presumably due to hemodynamic
reasons. Nevertheless, the relatively small sample size as a
limitation to this study should be considered, when evalu-
ating our results. In summary, the current data on this topic
show that there is a tendency of coincidence of posterior cir-
culation stroke and the presence of VAH. Further evidence
regarding these ndings and profound comprehension of the
pathomechanism is needed.
Conclusions
As a result from our study we emphasize the need for
increased attention that should be directed to hypoplastic
vertebral arteries. It is not negligible, that the vertebral
artery hypoplasia in coexistence with known risk factors for
stroke may increase their negative clinical impact. Duplex
sonography as an important diagnostic method may con-
tribute to detect vertebral artery hypoplasia non-invasively.
Acknowledgments
This work was supported by the Framework Programme for
Research and Technology Development, Project: Building
of Centre of Excellency for Sudden Cerebral Vascu-
lar Events, Comenius University Faculty of Medicine in
Bratislava (ITMS:26240120023), conanced by European
Regional Development Fund.
202
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