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MORPHOLOGICAL VARIANTS OF THE CIRCLE OF WILLIS
AND THEIR ROLE IN ISCHEMIC STROKE RISK
Davronov U.T.
Assistant of the Department of Anatomy and Clinical Anatomy,
Bukhara State Medical Institute named after Abu Ali ibn Sina
Abstract:
The Circle of Willis is a crucial arterial anastomosis located at the base
of the brain. It ensures redundancy in cerebral circulation, maintaining perfusion in
case of vascular occlusion. However, only a minority of individuals have a complete
and symmetric Circle of Willis. The high prevalence of morphological variants—such
as hypoplasia or absence of component arteries—may compromise cerebral collateral
capacity. This article reviews the anatomical configurations of the Circle of Willis,
evaluates their embryological origins, and explores their implications in ischemic
stroke vulnerability.
1. Introduction
The Circle of Willis (CW), also known as circulus arteriosus cerebri, forms the
primary collateral pathway between the anterior and posterior circulations of the brain.
It connects the internal carotid system to the vertebrobasilar system through the anterior
and posterior communicating arteries (ACoA and PCoA). This arterial circle is ideally
positioned to compensate for occlusions or stenoses, making it a focal point in
cerebrovascular pathology.
However, anatomical studies reveal that only about 20–30% of people have a
‘complete’ CW. Morphological variants may range from mild asymmetries to
significant absence or hypoplasia of key segments, potentially leading to poor
redistribution of blood during ischemic events. The significance of these variants
becomes more pronounced in the context of ischemic stroke, which remains a leading
cause of disability and death worldwide.
2. Materials and Methods
This study is based on a systematic review of anatomical, radiological, and
clinical literature. The search included:
• Databases: PubMed, Scopus, Google Scholar
• Keywords: “Circle of Willis,” “anatomical variation,” “ischemic stroke,”
“collateral circulation,” “PCoA hypoplasia,” “cerebral angiography”
• Inclusion criteria: Studies between 2000–2024, sample size > 100, angiographic
or autopsy-based morphology studies, human subjects
• Exclusion criteria: Animal models, incomplete datasets, pediatric-only studies
Morphological variants were categorized based on established templates (e.g.,
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Krabbe-Hartkamp classification). Stroke risk associations were evaluated using meta-
analytical and cohort data where available.
3. Results
3.1 Prevalence of Variants
Based on pooled data from over 12,000 subjects in 20 studies:
• Complete Circle: 21–28%
• Hypoplastic/absent PCoA: 50–60%
• Absent or fenestrated ACoA: 10–20%
• Fetal-type PCA (fPCA): 11–29%
• Unilateral CW completeness: Present in ~65%
• Bilateral incompleteness: 20–30% of cases
3.2 Stroke Risk Correlation
• Incomplete CW is significantly associated with increased ischemic stroke risk
(Odds Ratio ~1.7–2.2).
• Individuals with bilateral PCoA hypoplasia or fPCA variants have higher infarct
size and poorer recovery outcomes.
• The absence of ACoA is a critical factor in anterior cerebral infarction,
particularly in cases of unilateral carotid occlusion.
3.3 Imaging Insights
Modern imaging such as 3D TOF-MRA, CT angiography, and DSA offers high-
resolution visualizations of CW anatomy. Functional assessments using perfusion MRI
also show how collateral circulation responds during occlusive events.
4. Discussion
4.1 Embryological Basis of Variants
The formation of the CW begins in the fifth gestational week. Disruptions in fetal
vasculogenesis can result in persistent fetal-type PCA or regressions in PCoAs. The
prevalence of variants suggests that embryologic factors and genetic influences play a
major role.
4.2 Collateral Compensation
A complete CW provides dynamic compensation during arterial occlusions. In
individuals with incomplete circles, this ability is impaired, leading to rapid ischemic
progression. In particular, posterior circulation strokes often show poor outcomes when
PCoAs are missing or hypoplastic.
4.3 Clinical Relevance
Understanding CW variants is critical for:
• Surgical planning: e.g.
, carotid endarterectomy, aneurysm clipping
• Endovascular therapy: Predicting collateral flow response
• Risk stratification: In patients with TIA or asymptomatic stenosis
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• Stroke rehabilitation prognosis
Recent findings suggest that including CW configuration into stroke risk scoring
models enhances predictive accuracy.
5. Conclusion
The Circle of Willis is often anatomically incomplete, and its morphological
variations can substantially influence the outcome of cerebral ischemic events. Routine
non-invasive evaluation of CW anatomy can inform both risk assessment and treatment
planning. Further research into genetic and developmental contributors to CW variants
may open up preventive strategies.
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