Vertebrobasilar Anatomy and Physiology

This essay is by Jim Meadows, BScPT, MCPA, FCAMPT. It is the second in a series on clinical assessment of vertebrobasilar insufficiency.

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The vertebrobasilar’s anatomy is not very consistent. In fact the likelihood of the classical system as described in anatomy texts actually being present in any individual is probably very low. For example, only 40% of the population have equal sized vertebral arteries — so already “abnormal” is more common than “normal.” Then consider the other anomalies in the system: hypoplasticity, atretism, absence, persistence of fetal arteries (bilateral absence), fibromuscular dysplasia, aneurysm, and variable origins not only of the vertebrals themselves but of the numerous other branches — and you start to get an idea of how complex the system may be.

This essay will discuss the anomalies most significant in their impact on us as manual therapists. But first the “normal” anatomy as described in textbooks — and even here the descriptions vary considerably, so what follows is one description that does not apply to most people but is an idealized or average representation. Points where significant anomalies occur are noted and described in the Major Anomalies section below.

Anatomy

The vertebral artery (VA) arises from the subclavian arteries as they arch laterally^[1] and in front of the 7th cervical vertebra, the osteal or first portion (V1) of the artery begins. It has a fair degree of slack to accommodate large movements of the head. It enters the transverse foramen of C6^[2] and forms the transverse or second portion (V2), ascending the transverse tunnel whose boundaries are:

• The foramen
• Scalenes laterally
• Zygapophyseal joints and their capsules (ligamentum flavum) posteriorly
• Longus colli and longus capitus muscles anteriorly
• The uncovertebral joints and disc medially

V2 enters the transverse foramen of C2 and forms the sub-occipital or third portion (V3) — the most kinked part of the artery. After entering the transverse foramen of C2 it stretches to reach C1’s foramen, then turns 90 degrees medially and runs in a groove behind the articular mass of the zygapophyseal joint^[3],[4], then turns anterior to pierce the posterior sub-occipital membrane and enter the spinal canal. It then turns upward and enters the foramen magnum to form the intracranial or fourth portion (V4).

The basilar artery forms from the joining of the two vertebrals at the lower border of the pons and runs upward to divide into the two posterior cerebral arteries. These divide again into the cortical and thalamic arteries, and the cortical divides again into the temporal and calcerine (optic) arteries^[5]. Also coming off the posterior cerebral artery on each side are the posterior communicating arteries, which join with the middle cerebral arteries — forming a link with the anterior circulation via the circle of Willis so that blood can be shunted backwards and forwards as demand varies.

Branches

The first branches of the artery are the radicular (spinal) arteries — a variable number^[6] — which leave the artery to enter the intervertebral foramen, travel along the spinal nerve, and then split to accompany the anterior and posterior roots to the spinal cord, supplying those parts of the cord together with the dural sheaths, nerves, and meninges.

Osseomuscular branches given off from the sub-occipital portion supply the atlas and axis vertebrae and the posterior sub-occipital muscles. Osseomeningeal branches arise from the intracranial portion and supply the basal meninges and the internal occipital bone.

Just before the arteries join to form the basilar, a branch is given off each side which joins to run down the medulla and spinal cord as the anterior sulcal (spinal) artery, supplying the medulla and anterior spinal cord by anastomosing with the anterior spinal arteries^[7].

Just before the arteries join, the posterior inferior cerebellar artery is given off on each side. It winds around the medulla, supplies it, and then supplies a large part of the cerebellum. Coming off the posterior inferior artery are the two posterior spinal arteries, which run the spinal canal anterior and posterior to the posterior spinal root, supplying it, its dural sleeve, the posterior meninges, and spinal cord.

The basilar gives off multiple pontine branches supplying the pons, and two of particular interest to us: the anterior inferior cerebellar artery and the internal auditory (labyrinthine) artery, which supplies the 8th nerve and the membranous labyrinth.

The temporal artery from the posterior cerebral artery supplies the parietal-temporal region (notably Wernicke’s area), and the calcerine or optical artery supplies the calcerine radiation and the visual cortex in the occipital lobe.

Major Anomalies

Aside from those already mentioned, several anomalies can significantly affect how a patient responds to an injury of this artery.

1. Side to Side Caliber Difference — The average size of the arteries is millimeters, but only about 40% of the population have roughly equal sized arteries. The larger is termed dominant and the smaller minor.
2. Hypoplasticity — In a few percent of the population one artery is significantly smaller than the other. If it is 1 millimeter or less it is termed hypoplastic and is essentially non-functional.
3. Absence — One or both arteries may be absent. Interestingly, unilateral absence is the worse of the two — there is no supply to that side, but bilateral absence is not really absence but fetal artery persistence, where each segment gets its own small artery.
4. Atretism — The vertebral artery fails to form the basilar but instead terminates as the posterior inferior cerebellar artery.

What the last three of these anomalies have in common is that they result in reduced or absent blood supply to that side. Collateral arteries form and there is supply from the anterior circulation and the other side — but there is no real back-up if the contralateral artery is injured.

Pathology

Traumatic pathology can come from over-stretching, internal and external tearing, kinking, choking, and internal and external penetrating or blunt trauma. The result is either bleeding, thrombus formation, or both.

Intramural tears are dissections — longitudinal separations of either the intima from the media, or the intima and media from the adventitia. The cause is usually over-stretching (e.g. a front-end collision). Two outcomes are possible: blood can be diverted to flow outside the intima, in which case oxygen is not absorbed and ischemia occurs; or the media is stripped away from the adventitia by blood flow and the adventitia balloons out to form a pseudoaneurysm, which can rupture with minimal force (sneezing, movement) or apparently spontaneously.

The artery can also be cut across its length as a transection — complete or partial. The vertebral vein does not exist along the extracranial extent of the artery but is replaced by a plexus of veinlets surrounding the artery. If both blood vessels are transected, blood from the artery can flow into the tear in the vein, causing it to become engorged and choke down on the artery — termed a collar hematoma.

All of these injuries will cause thrombus formation. If the thrombus is large enough it can block the artery, but more serious is the release of thrombus material as an embolus, which depending on its size will block a large or small branch and cause a stroke. How serious the stroke is depends on which artery is blocked. Vasospasm is another consequence of a torn artery and may well be the source of the transient signs and symptoms seen in these patients.

Application

By understanding the anatomy of the artery — which structures it vascularizes and in turn which functions those structures serve — the clinician can make a first approximation at a diagnosis. The following structures may all potentially be affected, though some are more commonly involved than others in the most common form of the condition.

Artery / Branch	Structure	Sign / Symptom
Vertebral	Everything	All
Radicular (spinal)	Multisegmental spinal nerve and roots, dural sheath, anterior meninges, spinal cord	Multisegmental radiculopathy, dural pain, upper motor signs
Anterior sulcal (spinal)	Anterior meninges and spinal cord	Short cape syndrome (paresthesia from neck to apices of scapula, upper motor signs)
Posterior inferior cerebellar	Cerebellum and medulla	Ataxia, dysphasia, dysarthria, dysphonia
Posterior spinal	Posterior meninges, spinal cord, dural sheath, spinal nerve roots	Sensory radiculopathy, dural pain, upper motor signs
Osseomuscular	Posterior sub-occipital muscles, axis and atlas	Sub-occipital headache
Osseomeningeal	Basal meninges, internal occipital bone	Occipital headache
Basilar	Pons, CN 7–12 nuclei	Locked-in syndrome
Anterior inferior cerebellar	Cerebellum	Ataxia, drop attacks, dysphasia
Internal auditory (labyrinthine)	8th nerve and membranous labyrinth	Vertigo, disequilibrium, nystagmus, tinnitus, hypacusia

VBI most commonly causes lateral medullary syndrome (Wallenberg’s syndrome), which has a reasonably consistent pattern of signs and symptoms when symptoms are present:

Structure	Sign / Symptom
CN 12	Dysarthria
CN 10	Dysphonia
CN 8	Dizziness and blurred vision
CN 5	Facial paresthesia
Cerebellum	Ataxia, dysarthria
Descending sympathetic tracts	Horner’s syndrome
Nucleus ambiguus	Dysphagia
Lateral spinothalamic tract	Hemilateral paresthesia
Atlas, axis, suboccipital muscles and basal meninges	Posterior headache
Centromedian trigeminothalamic tract	Perioral paresthesia

There is a good deal of anomalous arterial structure in this system and other syndromes do occur, but less frequently than those listed. Any central nervous system sign or symptom must be taken seriously and investigated. It is our job to recognize these signs and symptoms, assess them as safely as possible, and refer appropriately.

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Footnotes

1. Variation: the left arising directly from the aorta. This will result in increased pressures within that artery, which may be a problem with thrombus formation and embolism.
2. 98% of the time this is true, but it can enter at C7 or C5 (most common variations) and as high as C2 (very uncommon).
3. The pro-atlanteal variation has it running along the transverse process, bringing it further from the axis of rotation with increased torque and making it more superficial and vulnerable to blunt or penetrating trauma.
4. Another variation: while the artery does run in the groove on the back side of the articular mass of C1, the ligament that usually restrains it may be replaced by a bony bridge, causing stenosis.
5. Intracranially there are many anomalies regarding additional or missing arteries, or where each branch arises — these are outside our clinical concern.
6. Rarely is there one at each level; often one artery serves two segments.
7. The anterior sulcal and the anterior and posterior spinal arteries supply the cord directly, except for a small transverse portion that relies on blood from both directions — called the watershed.

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VBI Series

1. VBI Screening: Why the 5 Ds Fail Physical Therapists
2. Vertebrobasilar Anatomy for Physical Therapists (this article)
3. VBI and Dizziness: Clinical Classification for Physical Therapists