The Etiology of Cervical Artery Dissection
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Friday, April 24, 2015 12:00 AM

The etiology of cervical artery dissection (CAD) is, for the most part, unclear; and what has been proposed as an explanation for its pathogenesis is largely hypothetical. Nevertheless, a number of risk factors have been reported to be associated with the condition, including connective tissue abnormalities, hypertension, recent infection, migraine headache, the use of oral contraceptives, and others. Of special interest to chiropractors is the role cervical spine manipulation (CSM).  

The understanding of CAD is greatly enhanced by having a basic grasp of the relevant anatomy. A pair of vertebral arteries (VAs) and a pair of internal carotid arteries (ICAs) pass through the cervical region to supply the brain with blood. The ICAs and their branches are often referred to as the anterior circulation because they supply blood to the anterior portion of the brain. The vertebral and basilar arteries comprise the vertebrobasilar system, which is referred to as the posterior circulation because it supplies blood to the posterior brain.

The VA typically emerges from the subclavian artery and can be divided into 4 segments. The first segment is the prevertebral segment, also known as V1, which lies between the longus colli and the anterior scalene muscles before entering the transverse foramen of C6.

The second segment, referred to as the cervical segment or V2, passes through the transverse foramina of C6 through C1 to become the atlantal segment or V3 when it exits through the transverse foramen of C1. After exiting the C1 transverse foramen, the atlantal segment abruptly transitions from a vertical pathway to a horizontal orientation. It is as this point where the artery is thought to be most susceptible to injury related to sudden or extreme head movement. The atlantal segment is enclosed in a muscular sheath and passes through a groove behind the C1 articular process before entering the cranium through the atlantooccipital membrane and the dura mater. The VA is fixed to the inner surface of the tunnel formed by the transverse foramina by a continuous layer of collagen.

The final segment is the intracranial segment or V4, which travels upward across the medulla to the pontomedullary junction. At that point, it joins with the opposite VA to become the basilar artery. The basilar artery extends distally to form the posterior inferior and anterior inferior cerebellar arteries, the internal auditory artery, the superior cerebellar artery, the posterior cerebral artery, and numerous medullary and pontine branches. The posterior inferior cerebellar artery frequently develops differently, however, emerging as a branch of the VA before the formation of the basilar artery.

The ICA arises from the common carotid artery at the level it bifurcates into external and internal branches. Like the VA, it is made up of 4 segments. The cervical segment ascends vertically through the neck, situated posterior to the external carotid artery. The cervical portion of the ICA lies below the sternocleidomastoid muscles and is separated from the external carotid artery by the styloglossus and stylopharyngeal muscles. It is located anterior to the longus cervicis muscle and the transverse processes of the upper 3 or 4 cervical vertebrae. After entering the carotid canal at the base of the skull, the ICA is known as the petrous segment until it passes through the skull and becomes the cavernous segment. The artery’s final subdivision is the supraclinoid segment.  The ICA is freely moveable within its cervical pathway, but becomes fixed to the surface of the bone as it enters the carotid canal above the atlas. 

The cervical arteries are made up of 3 layers: the tunica intima, the tunica media, and the tunica adventitia, which is the outermost layer. The tunica intima is the innermost layer of the artery that makes up the vessel lining. It is composed of squamous endothelial cells supported by a thin layer of connective tissue. This layer is thinner and more fragile than the others, making it more susceptible to tearing. Consequently, it is the typical site of an initial defect that forms in a developing dissection.

The tunica media is the middle muscular layer, which is also the thickest layer. Under autonomic control, muscular contractions can alter the diameter of the vessel. These contractions may develop into spasms, which are thought to occur with enough force to block the arterial lumen and interrupt the blood flow.

The tunica adventitia is the outermost layer that mainly consists of longitudinally arranged collagen fibers. This layer merges with bone surfaces at various points along the course of the arteries, which anchors their position. The artery wall itself receives a supply of blood by way of the vasa vasorum, which extends to the outer stratum of the tunica media. 

The cervical arteries are innervated with pain-sensitive nerve fibers that may generate neck pain and headache when provoked. Several studies have shown that pain is typically the first symptom associated with CAD and a recent descriptive study involving 245 CAD patients reported that 8% of them presented with head or neck pain as their only symptom. Pain related to CAD frequently occurs suddenly and is of severe intensity, often described by patients as being different from any previous pain. Accordingly, the clinical manifestations of CAD typically include severe head and neck pain that involves mostly the ipsilateral occipitocervical area when the VA is affected or the periorbital, frontal, and upper cervical region when the ICA is involved.  These symptoms may or may not be followed by ischemic involvement in the brain, cerebellum, or brain stem. The interval of time between the initial pain of CAD and ischemic symptoms is quite variable, however, with reports ranging from almost immediately to several weeks. 

Arterial dissection is an uncommon vascular wall condition that typically involves a tear at some point in the artery’s lining and the formation of an intimal flap, which allows blood to penetrate into the muscular portion of the vessel wall. Blood flowing between the layers of the torn blood vessel may cause the layers to separate from each other, resulting in arterial narrowing or even complete obstruction of the lumen. Moreover, pulsatile pressure damages the muscular layer, resulting in a splitting or dissection of the intimal and medial layers that may extend along the artery variable distances, usually in the direction of blood flow. Another way for dissection to occur involves a primary intramural hemorrhage of the vasa vasorum, which builds pressure between the intimal and medial layers and may eventually rupture into the vessel’s true lumen.  Occasionally, a double lumen (also known as false lumen) is formed when the subintimal hemorrhage ruptures back into the arterial lumen distally. 


The underlying cause of intimal tears is uncertain, although some experts maintain that because tearing occurs, previous trauma was necessarily involved. On the other hand, intimal tears are common in cases of spontaneous CAD in which no known trauma occurred before the dissection. A number of risk factors that instigate structural abnormalities of the arterial wall may increase its susceptibility to mechanical stress and predispose these patients to dissection.


Subintimal hematoma develops after the intimal lining separates from the media and blood begins to accumulate in the vessel wall. The accrued blood soon develops into a thrombus and deforms the intima into the arterial lumen. Blood flow in the cervical arteries can be obstructed directly by the subintimal hematoma or emboli may detach from a thrombus and travel distally to obstruct the progressively smaller vessels in the brain, resulting in a stroke. Indeed, it is the release of emboli that most commonly causes brain ischemia secondary to CAD. 

Subadventitial hematoma occurs when a dissection penetrates through the tunica media into the subadventitial plane, resulting in the accumulation of blood between these layers. Instead of deforming the arterial lumen, as in subintimal dissection, the vessel’s outer wall expands outward and a pseudoaneurysm develops. This deformity is observed regularly in CAD patients. In fact, a recent study involving 71 CAD patients reported that 35 (49.3%) of them had pseudoaneurysms. Interestingly, none of these 35 patients had transient ischemic attack, stroke, aneurysmal rupture, or clinical symptoms suggestive of vessel compression.

Internal carotid artery dissections occur about 3 to 5 times more frequently than those involving the VA, although VA dissections are more likely to be associated with rapid head movements.  The male-to-female ratio for the incidence of CAD is roughly equivalent, and the mean age of CAD patients is 46.3 years. The reported incidence is 2.6 to 2.9 per 100,000 for ICA dissection and 1 to 1.5 per 100 000 for VA dissection. Cervical dissections represent the underlying etiology in approximately 20% of ischemic strokes that occur in patients 30 to 45 years age, compared with 2% or 2.5% in older patients. Given that the earliest symptoms of CAD often include headache and neck pain, some of these patients will undoubtedly present to chiropractic offices for treatment before a stroke is recognizable. Cervical spine manipulation performed at this point may be blamed for causing the full manifestation of the stroke, whether or not a causative relationship truly existed.

The cervical arteries are susceptible to dissection in association with a variety of trivial events. This association is confusing, however, because people normally encounter innumerable trivial events during their lifetime without ever experiencing dissection. Moreover, patients do not live in a vacuum and are typically exposed to other potentially contributory incidents before and after an event that is suspected of causing a particular CAD. For instance, they turn their heads to back up cars, have their hair washed at a beauty shop, practice yoga, sleep on their stomachs, get angry, or experience some other event that could have been the true cause of the dissection. Furthermore, because most CADs develop in the absence of any discernible mechanical event, it is very difficult to indict a particular incident or factor as the cause of a particular stroke.

A number of pathophysiological risk factors have been described in the literature that are thought to contribute to the development of CAD. Like trivial events, not all risk factors are present in every patient; and some patients experience CAD without any of them. The most compelling risk factors have to do with connective tissue abnormalities, which may contribute to a weakening of the vascular wall, making it more susceptible to tearing. Indeed, many researchers think that an underlying arterial abnormality must be present for dissection to occur. Included in this line of reasoning is the fact that elevated homocysteine levels, linked to arterial weaknesses both in vitro and in vivo, are known to activate proteolytic enzymes and interfere with the cross-linking of the collagen. Both these phenomena compromise the integrity of the arterial wall. Nonetheless, the exact pathogenesis of CAD is uncertain. Its etiology is probably multifactorial and related to a variety of arteriopathies that are produced by an assortment of genetic and environmental factors. Despite the many risk factors that have been proposed as possible causes of CAD, it is still unknown which of them definitely predispose patients to CAD after CSM. Thus, it is not possible at this time to accurately identify patients at risk of CAD before CSM.