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Vertebrobasilar Anatomy and Physiology

The vertebrobasilar’s anatomy is not very consistent, in fact the likelihood of the classical system as described by anatomy texts actually being present in any individual is probably very very low. For example, only 40% of the population have equal sized vertebral arteries so already “abnormal” is more common than “normal”. Then considered the other anomalies in the system such as hypoplasticity, atretism, absence, persistence of fetal arteries (bilateral absence), fibromuscular dysplasia, aneurysm, 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 which are most significant in their impact on us as manual therapists. But first the “normal” anatomy as described in text books, but even here the descriptions vary considerably so I’ll give you one description but just remember that it does not apply to most people but is an idealized or perhaps average representation. I will mark each point where there is a significant anomaly and describe these later.

Anatomy

The vertebral artery (VA) arises from the subclavian arteries as they arch laterally1 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 it so that it can accommodate large movements of the head. It enters the transverse foramen of C62 and forms the transverse or second portion (V2) and ascends 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) and this is the most kinked part of the artery. After entering the transverse foramen of C2 it has to stretch a little to reach C1’s foramen and then it turns 90 degrees medially and runs in a grove behind the articular mass of the zygapophyseal joint3,4, then turns anterior to pierce the posterior sub-occipital membrane and enter the spinal canal. It then turns upwards and enters the foramen magnum to form the intracranial or fourth portion (V2).

The basilar artery forms from the joining of the two vertebrals at the lower border of the pons and then runs upwards and divides to form the two posterior cerebral arteries. These divide again into the cortical and thalamic arteries and the cortical divides again into the temporal and calcerine or optic arteries5.

Also coming off of the posterior cerebral artery on each side are the posterior communicating arteries which join with the middle cerebral arteries.

This is the VB system in outline and via the posterior communicating arteries it forms a link with the anterior circulation via the circle of Willis so that blood can be shunted backwards and forwards as demand requirement vary.

Branches

The first branches of the artery are the radicular (spinal) arteries there are a variable number of these6 and they 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 where the supply those parts of the cord together with the dural sheathes, the nerves and the meninges.

There are osseomuscular branches given off from the sub-occipital portion that supply the atlas and axis vertebrae and the posterior sub-occipital muscles. The osseomeningeal branches arise from the intracranial portion and supply the basal meninges and the internal occipital bone.

Just before the arteries join together to form the basilar a branch is given off of each which joins with the other to run down the medulla and spinal cord as the anterior sulcal (spinal) artery to supply the medulla and anterior spinal cord by anastomosing with the anterior spinal arteries.

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

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

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

As previously stated the posterior communicating artery comes off of the posterior cerebral artery and connects with the middle cerebral artery to form the circle of Willis.

Major Anomalies

Aside from those already mentioned there are a few that can really affect how the 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 and if it is 1 millimeter or less then it is termed hypoplastic and it useless.
  3. Absence
    One or both arteries may be absent; interestingly a unilateral absence is the worse of the two as 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
    This is where 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 no supply of blood to that side (in the case of the atretic artery no supply from the osseomeningeal arteries up). Of course 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, internal and external penetrating and blunt trauma. The result of all of these is either bleeding or thrombus formation or both.

Intramural tears are dissections, that is 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. There a couple of things that can happen here, the blood can be diverted and flow on the outside of the intima in which case oxygen is not absorbed and ischemia occurs or in addition the media is stripped away from the adventitia by the blood flow and the adventitia balloons out to form a pseudoaneurysm which can rupture with minimal force (sneezing, movement etc.) or “spontaneously”. The artery can also be cut across its length as a transection and it can be complete or partial. The vertebral vein does not exist along the extracranial extent of the artery but is replaced by a plexus of veinlets that surround the artery and if both blood vessels are transected the blood from the artery can flow into the tear in the vein and cause it to become engorged and choke down on the artery closing it, this is termed a collar hematoma.

All of these injuries will cause a thrombus to form and 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 causing a stroke. How serious is the stroke depends on which artery is blocked. Vasospasm is another consequence of a torn artery and this 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 are vascularized 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 although, as seen in table 2, there are structures more commonly affected 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 the neck to the apices of the scapula, and 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, 7, 8, 9, 10, 11, 12th nuclei Locked in syndrome (everything paralytic and spastic due to ischemia above
Anterior inferior cerebellar Cerebellum Ataxia, drop attacks, dysphasia
Internal auditory (labyrinthine) 8th nerve and membranous labyrinth Vertigo, disequilibrium, nystagmus, tinnitus and hypacusia

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

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 ambigus Dysphagia

Other structures and symptoms include:

Lateral spinothalamic tract hemilateral paresthesia
Atlas, axis, suboccipital mm and basal meninges posterior headache
Centromedian part of the trigeminothalamic tract perioral paresthesia

There is a good deal of anomalous arterial structure in this system and other syndromes and symptoms do occur but less frequently than those listed but any central nervous sign or symptom must be taken seriously and investigated. It is our job to recognize these signs and symptoms to find out as much about them as we can safely and refer them and any other found information appropriately.

Next time; The common and perhaps the only presenting symptoms; dizziness and headache.


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 also more superficial make it vulnerable to blunt or penetrating trauma.

4 Another variation is that while the artery does run in the groove on the backside of the articular mass of C1 the ligament that usually restrains it is replaced by a bony bridge and this seems to cause stenosis.

5 Intracranially there are many anomalies as far as additional or missing arteries or where each branch arises but these are completely not our concern.

6 Rarely is there one at level and 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 oozing through it from both directions, this is called the watershed.

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