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Research Review By Dr. Michael Haneline©


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Date Posted:

October 2016

Study Title:

Cervical arterial dissection: An overview and implications for manipulative therapy practice


Thomas L

Author's Affiliations:

School of Health and Rehabilitation Sciences, University of Queensland, Australia.

Publication Information:

Manual Therapy 2016; 21: 2-9.


Cervical artery dissection (CAD) is the underlying pathology in up to 25% of ischemic strokes in younger people (i.e. those under 55 years of age), although CAD is linked to only about 2% of all ischemic strokes in the general population.


Dissections of the cervical arteries (the vertebral artery [VA] and internal carotid artery [ICA]) typically develop from a tear of the artery’s inner wall (called the tunica intima). A tear of the intimal layer can enlarge due to pressure from flowing blood, which enters the tear and dissects the intimal layer away from the medial layer, forming an intramural hematoma.

Blood flow to the brain can be disrupted (i.e. stroke) by CAD as a result of an intramural hematoma blocking blood flow or by embolism from a displaced thrombus. Debette (1) reported that ischemic stroke or transient ischemic attack (TIA) occurs in 67% to 77% of CAD cases. Nonetheless, many CAD cases are asymptomatic or cause minor symptoms that do not prompt the patient to seek care. Such cases may heal spontaneously and may not be reported; thus, the true incidence CAD is unknown, though it is thought to be quite rare.

Estimates place the annual incidence of internal carotid dissection (ICAD) at 2.5-3 per 100,000 and for vertebral artery dissection (VAD) at 1-1.5 per 100,000.

CAD following cervical spine manipulation (CSM) is very rare, with estimates that range from 1 in 100,000 to 1 in 6,000,000 manipulations.


CAD may occur subsequent to a minor or seemingly trivial trauma, yet most of the time it occurs spontaneously (2), even though an initial tear of the artery lining is usually present. The reason the arterial lining can tear absent injury is thought to be related to a pre-existing intrinsic susceptibility (i.e. arteriopathy) that predisposes the artery to damage.

A cervical artery may be susceptible to a variety of extrinsic factors that weaken its inner lining, including infection or pro-inflammatory state. Such a weakness can render the arterial lining temporarily vulnerable to damage. Minor trauma (e.g. CSM, sporting or recreational activities, and sustained or jerky head movements) is thought to be capable of triggering CAD in a susceptible artery.

Rotation has also been implicated as being culpable in producing CAD because most VA dissections occur at the level of C1-2, which is where most cervical rotation occurs, and many patients have reported that they experienced head rotation prior to CAD.

CAD and Manipulative Therapy Practice:

Although the relationship between CSM and CAD has been widely publicized, there is uncertainty about whether CSM can cause a dissection, or whether CAD was actually present prior to CSM and the diagnosis was missed. Given that CAD is typically very difficult to detect in a patient, the second assumption is tenable, at least in some circumstances.

Symptoms of CAD often begin with neck pain or headache, leading most clinicians to suspect a musculoskeletal disorder or migraine. Neurological signs and symptoms may not be present until the dissection or resulting dislodged thrombus interferes with the flow of blood to the brain.

A clinician who treats a patient with neck pain and/or headache that is actually due to CAD may be blamed incorrectly for causing the CAD because of the temporal relationship of CSM with the CAD diagnosis (3). Thus, early recognition and proper management of a CAD in progress is essential.

Can Cervical Spinal Manipulation Cause CAD?

Besides temporal relationship and the anatomical proximity of the cervical arteries to the cervical vertebrae, there are several reasons why CSM is thought to be a cause of CAD. Four mechanisms have been proposed as possible etiologic factors, including:
  1. CSM causing damage to the arterial wall;
  2. CSM of a patient with a dissection in progress that dislodges a thrombus, which results in embolic material being released toward the brain;
  3. alteration of cervical blood flow from unusual neck positions assumed during CSM; and
  4. temporary vasospasm of an artery that interrupts blood flow to the brain.
There are limitations to these hypotheses, however, because animal and cadaver studies have not been able to produce arterial damage after typical manipulative thrusts and there is no real evidence that temporary vasospasm can occur as a result of CSM.

Blood flow can be affected by placing the head and neck in various positions, especially rotation and extension, but the circulatory effects vary widely between individuals. Furthermore, when there is marked blood flow reduction in the cervical arteries, signs of brain ischemia do not develop as long as the Circle of Willis is intact because the body can compensate (4). However, if more than one artery is compromised or the Circle of Willis is inadequate, compensation may not be possible and the risk may increase. These patients can often be identified with provocative physical testing.

Can those at risk be recognized?

The probability that a clinician will encounter a patient with a dissection in progress is fairly small, and CAD occurring following CSM in a clinician's career is even smaller. Nonetheless, given that hundreds of millions of cervical spine manipulations are performed annually, catastrophic, related CAD events will continue to occur.

The author emphasized the importance of a comprehensive history that looks for clinical features and risk factors for CAD. Clinicians should recognize:
  1. that CSM may cause CAD in a susceptible patient;
  2. a patient presenting with CAD in progress; and
  3. patients with abnormal/altered blood flow in whom CSM should be used with caution.
Commonly, the initial symptoms of CAD include unilateral neck pain and headache – symptoms that are also common presenting complaints of patients seeking CSM. Unfortunately, unless neurological signs are present and detected by the clinician, it may be difficult or impossible to distinguish early symptoms of dissection from neck pain of musculoskeletal origin and more common types of headache.

Patients with CAD often report pain that is different from anything they have experienced before, which may be an important clue in making the diagnosis.

Neurological signs and symptoms of CAD, often including visual disturbance, dizziness and imbalance, may be present for days or even weeks before a dissection.

The neurological features of CAD are variable, depending on the area of the brain that is supplied by the involved artery. If the VA is implicated, patients may present with balance disturbance, ataxia, syncope, drop attacks, dysphagia, dysarthria, dizziness, and visual deficits, such as diplopia. ICA dissection may lead to a partial Horner's syndrome (ptosis and miosis – eyelid drooping or pupillary constriction), facial palsy, or lower cranial nerve palsy (rare). If an ICA dissection progresses to an ischemic stroke, the anterior cerebral circulation may be compromised resulting in more typical signs and symptoms of stroke (e.g. limb weakness, paresthesia, speech disturbance).

There are some risk factors for CAD that clinicians should be aware of and correlate with a patient’s history and examination, including:
  • recent minor head and neck trauma,
  • recent infection or viral illness, and
  • valsalva type activities (e.g., intensive/heavy gym work).
Cardiovascular risk factors are probably not important in the pathogenesis of CAD.

Screening for CAD:

The patient’s history is the most important factor in identifying a CAD in progress. Look for features that do not conform to a typical musculoskeletal pattern, especially any associated neurological signs or symptoms that suggest blood flow disturbance to the brain.

Tests that involve sustained rotation and extension of the head and neck to induce dizziness, pre-syncope or nystagmus have questionable validity in screening for CSM related CAD. These tests are general and actually assess the adequacy of collateral flow to the brain, rather than the function of one artery. On the other hand, physical tests may be helpful in identifying the few individuals with insufficient collateral circulation compensation.

Actions to take if CAD is suspected:

If a CAD is suspected, the patient should immediately be referred to the nearest emergency department, by emergency transport in some cases. Since emergency department personnel sometimes fail to diagnose CAD, even though it is present, clinicians must convey their concerns about the possibility of CAD and point out relevant features of the patient’s history and exam that led to the suspicion of CAD. Do not provide CSM to these patients!

Clinical Application & Conclusions:

The author reported that neither the force of the manipulative thrust nor the position of the head during manipulation would likely cause dissection in a patient with normal cervical arteries. If an artery is abnormal, however, it may be susceptible to injury and there is a possibility that CSM or trivial neck strain may cause/trigger dissection, worsen an existing CAD or propagate an embolus.

Identifying which patients will develop CAD following CSM is difficult, if not impossible. Nonetheless, it is critical for clinicians to be aware of, search for, and recognize the signs and symptoms of CAD. If a patient presents with a dissection in progress, CSM should absolutely be avoided.

Effective history taking appears to be the best way to screen patients prior to CSM. In patients with any signs or symptoms of ischemia, even if temporary and subtle, look for a history of:
  • an acute onset of unusual neck pain or headache,
  • recent exposure to minor trauma, or
  • recent infection.
CAD following CSM is very rare and over-stating the risk should be avoided; otherwise, patients might be denied treatment that has been shown to be useful in the treatment of conditions such as neck pain, cervicogenic headache and cervicogenic vertigo.

The author suggests that clinicians should attempt to identify patients who have inadequate collateral brain circulation and then consider alternatives to high velocity manipulation and extreme neck positions.

Study Strengths / Weaknesses

This article represents a fairly well done narrative review. However, the reader should be aware that narrative reviews are highly susceptible to bias (e.g. reporting bias and/or selection bias) and have a number of inherent methodological deficiencies. Accordingly, the conclusions that are presented in a narrative review are more likely to reflect the pre-established opinions of the authors than conclusions found in systematic reviews.

Additional References:

  1. Debette S. Pathophysiology and risk factors of cervical artery dissection: what have we learnt from large hospital-based cohorts? Curr Opin Neurology 2014; 27: 20-8.
  2. Haneline MT, Lewkovich GN. An analysis of the etiology of cervical artery dissection: 1994 to 2003. J Manip Physiol Ther 2005; 28:617-22.
  3. Cassidy D, Boyle E, Cote P, He Y, Hogg-Johnson S, Silver FL, et al. Risk of vertebrobasilar stroke and Chiropractic Care. Results of a population-based case-control and case-crossover study. Spine 2008; 33: S176-83.
  4. Thomas L, Rivett D, Bateman GA, Stanwell P, Levi C. Effect of selected manual therapy interventions for mechanical neck pain on vertebral and internal carotid arterial blood flow and cerebral inflow. Phys Ther 2013; 93: 1563-74.

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