BASILAR ARTERY ENLARGEMENT IN AN ELDERLY FEMALE CADAVER
BASILAR ARTERY ENLARGEMENT IN AN ELDERLY FEMALE CADAVER
RESEARCH ARTICLE
Zoe M. Rushetsky, Caleb M. Findley, Grace E. Lynch, Victoria Pfennig, Lynn M. Waters and Diana C.
Peterson
"© 2025 by the Author(s). Published by IJAR under CC BY 4.0. Unrestricted use allowed
with credit to the author."
……………………………………………………………………………………………………....
Introduction:-
The ventral surface of the pons is covered by the basilar artery, which results from the convergence of two vertebral
arteries and provides blood to the brainstem and cerebellum [1]. Dilatation of the basilar artery can be caused by
vertebrobasilar dolichoectasia (VBD) or compensatory changes in atherosclerosis. VBD is associated with
degeneration of the internal elastic lamina and thinning of the arterial media [9], which may pose a significant
clinical risk in the form of ischemic strokes, aneurysm formation, or fatal hemorrhage [13]. The natural history of
VBD is progressive, with worsening arterial dilation and increased risk of adverse events over time [7]. A 5-year
prognosis is favorable in patients who are asymptomatic at time of diagnosis. The 2021 American Heart
Association/American Stroke Association practice guidelines suggest patients be treated medically, with strict blood
pressure control and use of antithrombotic agents [5]. Surgical and endovascular interventions are rarely performed
and lack clinical efficacy [16]. We report a case of an enlargement of the basilar artery found during anatomic
dissection.
Case Report
A 76-year-old female cadaver with an enlarged basilar artery was discovered during a routine educational dissection
in the gross anatomy laboratory at Philadelphia College of Osteopathic Medicine. The cause of death, malignant
neoplasm of the lung, was not related to the vascular finding. The family of the female as well as the body donation
program granted permission to allow the case to be published. The basilar artery measured 33.1 mm in length over
the ventral aspect of the pons. The central segment showed a maximum diameter of 8.5 mm, the rostral segment
measured 3.9 mm, and the caudal segment measured 4.4 mm (Figure1A).
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Corresponding Author:-Zoe M. Rushetsky
Address:-Philadelphia College of Osteopathic Medicine Suwanee, GA, USA.
ISSN:(O) 2320-5407, ISSN(P) 3107-4928 Int. J. Adv. Res. 13(11), November-2025, 880-883
Dissection revealed no evidence of intraluminal plaque (Figure 1B). The arterial wall appeared uniform in thickness
across rostral, central, and caudal segments, with no signs of dissection or wall separation. Branches of the basilar
artery, (i.e., pontine, anterior inferior cerebellar artery, superior cerebellar artery) were normal in caliber and
morphology. No evidence of infarction or ischemia were observed in the adjacent pons or cerebellum.
Figure 1. 1A shows an enlarged basilar artery (line) with normal rostral (a) and caudal (b) diameters. Figure
1B highlights that the wall of the enlargement is uniform in thickness (arrow). Labels: a. rostral basilar
artery, b. caudal basilar artery, c. vertebral arteries.
Discussion:-
The average basilar artery width is 3.6–3.9 mm [15]. In this case, the basilar artery measured 8.5 mm along the
central aspect of the pons, indicating pathologic distension. There are numerous modifiable risk factors that
contribute to the development of vascular pathology: diabetes, smoking, hypertension, hyperlipidemia, and obesity
[8]. Many patients have many of these risk factors. Nicotine use, for instance, is closely linked to hypertension and
is frequently accompanied by concurrent alcohol consumption. Similarly, obesity and hypercholesterolemia are
commonly observed together, further compromising vascular integrity [8]. Both hypertension and smoking
significantly alter intracranial blood flow patterns and are strongly associated with aneurysm development [11].
Damage to the arterial wall is a key contributor to arterial enlargement, which can ultimately lead to aneurysm
formation.
Hemodynamic stress is a crucial factor in the development of an aneurysm and its subsequent dilation. According to
Laplace’s law, wall tension is directly proportional to vessel radius and blood pressure [3]. Risk factors such as
hypertension promote turbulent flow, characterized by irregular motion that impose abnormal shear stress on the
vascular endothelium. Such damage can initiate a cascade of plaque deposition and narrowing of the lumen [11].
Thinning of the wall and/or increased intracranial pressure would weaken the blood vessel wall, lead to further
expansion, and increase the likelihood of rupture (aneurysm) [4].
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ISSN:(O) 2320-5407, ISSN(P) 3107-4928 Int. J. Adv. Res. 13(11), November-2025, 880-883
A basilar artery with a diameter greater than 4.5 mm or a length exceeding 29.5 mm is classified as VBD [12]. This
condition involves elongation and tortuosity of basilar or vertebral arteries due to degeneration of the tunica media
[14]. VBD affects roughly 1.3% of the population [17] and often results from smooth muscle atrophy, or the
dysregulation of antiproteases and matrix metalloproteinases, which disrupt the normal remodeling of arterial
collagen and elastin [4]. This disease typically manifests as an enlarged, tortuous artery. Either the enlargement or
tortuous nature of VBD can put pressure on cranial nerves and thus leads to a wide array of symptoms (e.g.,
dizziness, unilateral central facial palsy, and sensorineural symptoms like vertigo and hearing loss) [6, 17].
Another pathology that can cause increased external diameter of the basilar artery is stenosis. In this arterial
pathology, the narrowing of the lumen secondary to plaque deposition causes an alteration of blood flow which puts
stress on the vessel wall. This stress leads to compensatory outward remodeling of the tunica media [14]. To
preserve the inner diameter of the vessel, the wall bulges outward. This happens through the proliferation of vascular
smooth muscle, causing the deposition of collagen and degradation of elastin, leading to calcification [4].
The basilar artery, a central component of the posterior circulation within the brain, has been shown to have a
greater likelihood of outward remodeling. The basilar artery may be more susceptible to remodeling due to an
increased responsiveness to sympathetic activity within the basilar artery versus other cerebral vessels [18]. There
are a few cases of basilar artery stenosis that have been documented. It is difficult to quantify numbers within the
population because asymptomatic cases are rarely documented.
Timely diagnosis of arterial enlargements is important clinically, because they pose a significantly greater risk for
rupture and stroke. If an enlargement swells to greater than 1.5× its normal diameter, it is diagnosed as an aneurysm.
Unruptured cerebral aneurysms can lead to subarachnoid hemorrhages, accounting for approximately 85% of such
events, while the remainder typically result from trauma [20]. Aneurysms in the basilar artery pose a unique risk, as
they may compress vital brainstem structures, particularly the pontine and cardiac centers, which regulate respiration
and cardiac output [20].
Fusiform aneurysms, defined by diffuse circumferential dilation of a vessel segment, are rare findings most
frequently in the vertebrobasilar system. They carry a worse prognosis than saccular aneurysms due to their
association with thrombosis, infarction, or mass effect associated with brainstem compression [2]. Saccular
aneurysms are characteristic of a unilateral focal outpouching with a narrow base. In the current case, the diffuse
dilation without focal outpouching suggests a fusiform morphology. The absence of occlusion indicates that blood
flow was maintained despite the abnormal vessel shape.
Conclusion:-
This case describes an asymptomatic enlargement of the basilar artery. Although not the cause of death in this
individual, such vascular changes are clinically significant due to their association with ischemic events, aneurysm
formation, and brainstem compression. Early identification, coupled with management of modifiable risk factors
such as hypertension and smoking, may reduce morbidity and mortality associated with posterior circulation
vascular disease.
Author contributions:-
All authors contributed to writing the manuscript draft and reviewed and edited final drafts of the manuscript. All
authors reviewed and approved the final manuscript.
Funding None:-
Data availability No sets of data were created or analyzed.
Declarations:-
Conflict of interest None:-
Consent to publish by the PCOM body donation program.
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ISSN:(O) 2320-5407, ISSN(P) 3107-4928 Int. J. Adv. Res. 13(11), November-2025, 880-883
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