Cervical artery dysfunction and manipulation

www.physiotherapy.ca January/February 2010 - Interdivisional Review 23

Cervical artery dissection and manipulation: a review of relevant research with implications for diagnosis and management

Peter A. Huijbregts, PT, MSc, MHSc, DPT, OCS, FAAOMPT, FCAMT

Rob A. B. Oostendorp, PT, MT, PhD

Peter A. Huijbregts, Assistant Professor, University of St. Augustine for Health Sciences, St. Augustine, FLConsultant, Shelbourne Physiotherapy & Massage Clinic, Victoria, BC, Advisory Faculty, North American Institute of Orthopaedic Manual Therapy, Eugene, OR

Rob A. B. Oostendorp. Emeritus Professor of Allied Health Sciences, Scientific Institute for Quality of Healthcare, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands, Emeritus Professor of Manual Therapy, Faculty of Medicine and Pharmacology, Free University of Brussels, Brussels, Belgium

Corresponding author: Peter A. Huijbregts, Shelbourne Physiotherapy & Massage Clinic100B-3200 Shelbourne Street, Victoria V8P 5G8, [email protected]

Orthopaedic Division

IntroductionWhen considering the issue of safety in the context of

orthopaedic physiotherapy we cannot ignore the associ-ation that has been proposed between cervical manipu-lation and stroke due to vertebral and/or internal carotid artery dissection (together called cervical artery dissec-tion or CAD). CAD occurs in about 1-2% of patients, who have sustained blunt trauma including severe facial frac-tures, skull base fractures, and traumatic brain injury. Patients with major thoracic injuries have an increased incidence of carotid artery dissection, whereas cervical spine fractures and spinal cord injury increase the risk of vertebral artery dissection. However, as physiothera-pists we are less concerned with CAD associated with such severe trauma. Most relevant to us is spontaneous CAD defined as dissection associated with minor trauma, including but not limited to sporting activities, whip-lash injury, s tretches, sudden neck movements, severe coughing, and -of interest to this paper- cervical manipu-lation (Debette and Leys 2009).

Epidemiological data indicates that CAD is rare. In a North-American population-based study, Lee et al (2006) estimated incidence at 2.6 (95% CI: 1.86-3.33) per 100,000 per year. Debette and Leys (2009) reported a 1-year in-cidence for carotid artery dissections of 2.9 per 100,000 in Dijon, France. Lee et al (2009) noted that vertebral artery dissection at 0.97 (95% CI: 0.52-1.4) was almost half as common as carotid artery dissection at 1.72 (95% CI: 1.13-2.32) per 100,000 per year. With only up to 20% of CAD progressing to a stroke, this condition is even less common (Blunt and Galton, 1997). So Terrett (2000) made an observation certainly in need of further inquiry when he noted, “... The temporal relationship between young healthy patients without osseous or vascular dis -

ease who attend a spinal manipulative therapy practi-t ioner and then suffer these rare strokes is so well docu-mented as to be beyond reasonable doubt indicating a possible causal relationship...”

Even without consensus on a cause-and-effect rela-tionship between cervical manipulation and CAD, the neck pain, headache, and vertiginous dizziness with which patients with CAD often present (Graziano et al 2007) make the physiotherapist (even one, who does not use thrust manipulation as a clinical intervention) a professional, who at some point may be confronted with this pathology. The goal of this article, therefore, is to provide current best evidence on the association between manipulation and CAD but also to inform the physiotherapist with regard to clinical diagnosis for this pathology.

Research on the association between manipulation and CAD

Evidence linking cervical manipulation to stroke has included multiple narrative reviews of case reports found in the literature (DiFabio 1999, Ernst 2001, Terrett 2000, Triano and Kawchuk 2006). Hurwitz et al (1996) acknowledged the likely high under-reporting bias and noted an estimated risk-adjusted for an only 10% re-porting rate in the literature of 5-10 per 10 million for all complications, 6 in 10 million for serious complications, and 3 in 10 million for the risk of death. Haneline et al (2003) found 13 cases of internal carotid artery dissec-tion temporally associated with cervical manipulation in a 1966-2000 Medline review and estimated the chance of developing CAD in this artery post-manipulation at 1 in 601,145,000.

Research into risk of harm is wrought with method-

24 January/February 2010 - Interdivisional Review www.physiotherapy.ca

ological shortcomings and not only because of the ob-vious ethical concerns with studies that would pro-spectively expose patients to a suspected risk factor (Rubinstein et al 2005). In the context of risk of harm it would seem prudent to consider the epidemiological Bradford-Hill criteria that state that a cause-and-effect relationship becomes likely when the following criteria are all met (Triano and Kawchuk 2006):

1. The proposed relationship is biologically plausible2. The proposed cause is temporally related to the oc-

currence3. The relationship is consistent across different sam-

ples and groups4. There exists a positive correlation between expo-

sure and occurrence5. There exists no other plausible explanation

Although opinions certainly and justifiably differ, case reports and narrative reviews of such case reports pro-vided by authors in diverse geographical locations tem-porally linking possible mechanical trauma of the cer-vical arteries due to manipulation to CAD would seem to qualify as supporting the first three criteria.

Exploring the criterion of a correlation between expo-sure to manipulation and occurrence of CAD, Rothwell et al (2001) compared 582 patients with vertebrobas-ilar accidents over the period 1993-1998 with age- and sex-matched controls from the provincial insurance da-tabase in Ontario, Canada. They also determined expo-sure to chiropractic using this same database. These au-thors found that subjects younger than 45 years were five times more likely (95% CI: 1.31-43.87) to have visited a chiropractor in the month preceding the stroke. This same age group was also five times (95% CI: 1.34-18.57) more likely to have had three or more visits with cer-vical or thoracic spine-related complaints or headache in the month prior to the stroke. No significant associa-tion was noted for subjects older than 45 years.

Cassidy et al (2008) used a very similar study design comparing 818 patients with vertebrobasilar accidents to age- and sex-matched controls from a provincial in-surance database and also found an odds ratio (OR) of 3.13 (95% CI: 0.52-1.32) for having visited a chiropractor in the month before the stroke in those younger than 45 years, whereas the OR was 0.83 (95% CI: 0.52-1.32) for those older than 45 years. However, these researchers also looked at visits to general medical practitioners preceding the stroke and found an OR of 3.57 (95% CI: 2.17-5.86) for those under 45 years and 2.67 (95% CI: 2.25-3.17) for patients having visited their medical doctor in the month preceding the vertebrobasilar accident. These authors suggested that the similar association between chiropractic and medical visits might indicate that patients with an undiagnosed vertebral artery dis -section seek clinical care for headache and neck pain before having a stroke rather than lending credence to an exposure-and-occurrence relationship between ma-nipulation and CAD.

Clinical diagnosisWith the scope of physiotherapy often limited with

regard to ordering and interpreting relevant medical di-agnostic tests , clinical diagnosis based on history taking including an inventory of risk factors and physical exam-ination are the most important tools for the therapists when confronted with a patient with neck pain, head-ache, and dizziness or vertigo.

Risk factorsEven without answering the question on causation it

is plausible that in the case of a pathologically weakened artery mechanical forces such as those induced during thrust and non-thrust manipulation of the cervical spine may cause mechanical or traumatic damage to the vessel wall of the cervical arteries, in particular the vertebral artery. This means that the therapist needs to be able to identify possible risk factors predisposing the artery to CAD whether iatrogenic, i.e. due to manipulation, or due to mechanical events other than manipulation. Table 1 provides the rather large lis t of risk factors identified but not necessarily validated in the literature.

TraumaWith regard to the role of trauma of head and neck,

Beaudry and Spence (2003) attributed 70 of 80 traumat-ically- induced cases of vertebrobasilar ischaemia to motor vehicle accidents. Cogbill et al (1994) reported that 72% of trauma-induced internal CAD in their study was the result of a motor vehicle accident. However, note that many patients after whiplash trauma note diz-ziness and meet criteria for inner ear pathology (Grimm 2002, Oostendorp et al 1999, Wrisley et al 2000).

Age and genderAlthough age of 30-45 years and female gender have

been proposed as risk factors for manipulation-associ-ated CAD, Terrett (2000) indicated that the overall dis -tribution of patients with regard to gender and age at-tending for chiropractic care closely matches the gender and age distribution of those with serious adverse events thereby discounting these proposed risk factors. Kawchuk et al (2008) also found no association for age and gender and the incidence of CAD post-manipulation. Relevant to the clinical diagnosis of spontaneous if not manipulation-induced CAD is that Lee et al (2006) re-ported a mean age of 45.8 years for North American pa-tients. In Europe, Touzé et al (2003) reported a mean age of 44.0 and Arnold et al (2006) noted a mean age of 45.3 years. In three large studies (Beletsky et al 2003, Lee et al 2006, Schievink et al 1994) 50-52% of patients with CAD were women, whereas in two European studies (Arnold et al 2006, Touzé et al 2003) 53-57% were men. Carotid artery dissection seems to be more common in men and at an older age (47.0 versus 43.4 years) than is vertebral artery dissection (Dziewas et al 2003, Lee et al 2006).

ArteriopathyArteriopathies predisposing the artery to dissection

as a result of pathological weakening of the vessel wall


Table 1. Proposed risk factors cervical artery dysfunction

include Ehlers -Danlos syndrome, fibromuscular dys-plasia, cystic medial necrosis , and autosomal dominant polycystic kidney disease. Alpha-1-antitrypsin deficiency initially showed highly elevated ORs but this association currently finds litt le support in the literature (Triano and Kawchuk 2006). Although associated with collagen tissue abnormalities and arteriopathy, evidence for Marfan syndrome and osteogenesis imperfecta as a risk factor for CAD is absent (Debette and Leys 2009). In all, these risk factors can, at best, be suspected based on physical examination but would seem relevant if noted in the medical history. Research evidence for these arte-riopathies in the etiology of CAD, however, is limited.Cardiovascular risk factors

Cardiovascular r isk factors proposed as r isk factors

for CAD include hypertens ion, tobacco use, hypercho-les terolaemia, hyper lipidaemia, diabetes , and athero-scleros is . Mos t research into this area has compared pat ients with CAD to pat ients with ischaemic s t rokes . Perhaps as a result of this under lying difference in pathophys iology most cardiovascular r isk factors actually show ORs below 1 indicat ing a “protect ive” funct ion. Of course, this is likely due to the method-ology of the research comparing “apples to oranges”. In these s tudies , hypertens ion was the only s ignifi-cant r isk factor with an OR of 1.94 (95% CI: 1.01-3.70). Although a seemingly plaus ible r isk factor with a s t iffer ar tery more susceptible to mechanical damage, the evidence for atheroscleros is as a r isk factor is based solely on cadaver s tudies and the finding that blood


flow is proport ional to the four th power of vessel diam-eter (Mitchell 2002).

InfectionThere is a noted seasonal variation in the incidence

of CAD with significantly more cases occurring in winter as compared to other seasons (Paciaroni et al 2006). Perhaps explaining this seasonal variation, a prospec-tive study showed an adjusted OR of 3.1 (95% CI: 1.1-9.2) for an acute infection in the four weeks preceding a cer-vical artery incident (Guillon et al 2003).

Other risk factorsIn a systematic review Rubinstein et al (2005) noted

as clinically relevant risk factors migraine (OR 3.6; 95% CI: 1.5-8.6), recent infection (OR 1.6; 95% CI: 0.67-3.80), and trivial trauma including cervical manipulation (OR 3.8; 95% CI: 1.3-11). Triano & Kawchuk (2006) reported an OR of 1.6 (95% CI: 0.67-3.80) for coughing, sneezing, or vomiting; vascular risk factors and a current smoking habit had ORs of 0.14 (95% CI: 0.34-0.65) and 0.49 (95% CI: 0.18-1.05), respectively. Although earlier research im-plicated oral contraceptive use as a risk factor, Haneline and Lewkovich (2006) indicated that currently no con-sensus exists on relevance of this proposed risk factor. In all, this inventory of risk factors would seem to indi-cate no shortage of possible alternative explanations for CAD.

HistoryThe most common complaints with which patients

with CAD in progress might present for therapy in-clude neck pain, headache, and vertiginous dizziness (Graziano et al 2007). Terrett (2000) provided data on the presenting complaints of 137 chiropractic patients, who

Table 2. Classic cardinal signs of vertebrobasilar compro-mise: Five D's And three N's

subsequently had a manipulation-associated stroke:

* 47.4% noted neck pain and stiffness

* 19.7% noted neck pain, stiffness, and headache

* 16.8% had torticollis

Of course, these predominant symptoms help little in the way of distinguishing those patients with mechanical neck problems that might benefit from physiotherapy management perhaps including manipulation and those that are in the process of having a CAD.

Non-ischaemic and ischaemic symptomsAlthough diagnostic utility of these symptoms has

yet to be established, therapists are all familiar with the ischaemia-related cardinal s igns and symptoms indica-tive of vertebrobasilar circulatory compromise (Table 2). However, it is important to realize that with CAD isch-aemic symptoms are not the only symptoms that occur. Non-ischaemic symptoms usually develop first and are likely the result of stimulation of free nerve endings and subsequent substance P-mediated neurogenic inflam-mation of the tunica adventitia of the affected artery and direct compression on local somatic structures in-cluding cervical nerve roots, cranial nerve nuclei, and the cervical sympathetic chain (Kerry and Taylor 2006). In fact, these non-ischaemic symptoms occur hours to days and even a few weeks prior, although usually less than a month prior to the ischaemic findings (Blunt and Galton 1997, Debette and Leys 2009). Ischaemic findings develop in 30-80% of all dissections and as noted above up to 20% progress to a full cerebrovascular accident (Blunt and Galton, 1997).

Additional symptoms other than those in Table 2 have been described for CAD. Table 3 provides a lis t of ischaemic and non-ischaemic signs and symptoms asso-ciated with CAD (Blunt and Galton 1997, Haneline and Lewkovich 2004, Kerry and Taylor 2006, Kerry et al 2008). Although in a large hospital-based series described in only 7% of patients with CAD (Debette and Leys 2009), when present cranial nerve palsies are relevant to the di-agnosis of CAD. Due to their close anatomical association with the internal carotid artery, dissection of this artery and the associated increase in its girth mainly causes dysfunction of the cranial nerves IX-XII with the hypo-glossal nerve (XII) initially affected and then the other three nerves; eventually all cranial nerves except the ol-factory (I) can be affected. Whereas cranial nerve dys-function has a non-ischaemic etiology in internal carotid artery dissection, it is part of the ischaemic presentation of a vertebral artery dissection. Nerve root impairment at the C5-C6 level can result from compression by an enlarged vertebral artery (Debette and Leys 2009). The pathognomonic “thunderclap headache” with CAD is a referred pain due to stimulation of vascular nociceptive nerve endings as a result of the ongoing dissection and inflammation of the artery (Triano and Kawchuk 2006).

With our physiotherapy training inducing a healthy dose of vigilance with regard to CAD, physiotherapists often are unaware that not all CAD will lead to a worst-


case scenario. In their population-based study, Lee et al (2006) found that 33% of patients with CAD have only local s igns and symptoms with no retinal or cerebral ischaemia and that 6% of patients are asymptomatic. Symptoms are often limited and benign and include tran-sient headache, neck pain, Horner syndrome, and cranial nerve palsies that may vary based on the artery involved and the extent of the causative pathology. Although Debette and Leys (2009) noted that in such statistics socio-professional effects are insufficiently captured, in the Lee et al (2006) study, for example, 92% of patients had a good outcome. Still, in the context of diagnosis therapists need to be familiar with the two types of ver-tebral artery-related strokes (Terrett 2000). We assume

here that presentation of a stroke in the internal carotid distribution is more common knowledge among physio-therapists .

Vertebral artery-related strokesIn Wallenberg syndrome or dorsolateral medullary

syndrome of Wallenberg occlusion of the posterior infe-rior cerebellar artery, frequently due to distal extension of a vertebral artery dissection, leads to destruction of the nuclei and pathways in the dorsolateral medulla oblongata. Another cause may be the occlusion of the parent vertebral artery, in which case the syndrome is called syndrome of Babinski-Nageotte. Ischaemia of the inferior cerebellar peduncle leads to ipsilateral ataxia

Table 3. Non-ischaemic and ischaemic signs and symptoms of cervical artery dysfunction


and hypotonia. Destruction of the descending spinal tract and the trigeminal nucleus (located from the midbrain to the medulla) causes a loss of pain and temperature sen-sation on the ipsilateral face in addition to loss of the ipsilateral corneal reflex. Destruction of the ascending lateral spinothalamic tract causes loss of pain and tem-perature sensation in the contralateral trunk, which to-gether with the sensory loss in the ipsilateral face results in a pathognomonic presentation of alternating anal-gesia. Ischaemia of the descending sympathetic tract as it courses downward in the medulla oblongata and cer-vical spinal cord causes Horner syndrome, damage to the vestibular nuclei causes nystagmus, vertigo, nausea, and vomiting, and ischaemia in the nucleus ambiguous of the glossopharyngeal nerve can cause hoarseness, dysphagia, or intractable hiccups (Terrett, 2000).

Locked-in syndrome or cerebromedullospinal discon-nection syndrome occurs due to occlusion of the mid-basilar artery. This effectively transects the brain stem at the mid-pons level. Because the reticular formation and the ventral pons are unaffected the patient retains consciousness but decerebrate rigidity develops due to the cerebrospinal tracts having been destroyed. The nuclei for the cranial nerves V-XII are destroyed but cra-nial nerve IV is spared leaving only eye convergence and upward gaze for the patient to communicate with his environment. Skin sensation remains grossly intact be-cause the lateral spinothalamic tract is usually spared and the patient can still hear because the auditory nerves ascend in the brainstem lateral to the infarction area (Terrett 2000).

Physical examination

Cranial nerve examination, observation, and auscultationIf the history reveals symptoms that would suggest

CAD (Tables 2 and 3), targeted neurological and other tests are carried out that do not put the patient at undue risk. In this context we should think of cranial nerve ex-amination and observation of the miosis (inability to dilate a pupil), ptosis (droopy upper eye lid), enoph-thalmus (deeper seated eye), and anhydrosis (decreased sweating ipsilateral head and shoulders) consistent with Horner syndrome. Auscultation for a carotid bruit may be indicated. Magyar et al (2002) noted 56% sensitivity and 91% specificity for detection of a 70-99% carotid ste-nosis when compared to Doppler duplex ultrasound.

Sustained extension-rotation and rotation testsIn 1927, De Kleyn and Nieuwenhuyse reported de-

creased and absent vertebral artery blood flow based on cadaver perfusion studies in various head and neck po-sitions. Based on these early perfusion studies, the sus-tained extension-rotation and sustained rotation tests have been proposed and widely instructed and clini-cally used as tests to determine the presence of verte-brobasilar artery circulatory compromise. In fact, 17 of 20 member organizations of IFOMT still teach these tests (Rivett and Carlesso 2008).

Extension-rotation as a clinical test has been exten-sively studied with equivocal results . Some authors have reported significant decreases in blood flow (Rivett et al 1999, Yi-Kai et al 1999), whereas other studies have found no changes (Arnold et al 2004, Licht et al 2000). Case reports have noted false negative results (Rivett et al 1998, Westaway et al 2003), and case series have re-ported 75-100% false positive results (Arnold et al 2004, Haynes 2002). Research findings for the sustained cer-vical rotation test are equally equivocal with significant decreases (Arnold et al 2004, Mitchell 2003, Nakamura et al 1998, Rivett et al 1999, Yi-Kai et al 1999) or no effect noted on vertebral artery blood flow or volume (Haynes et al 2002, Licht et al 1999). A recent meta-analysis of Doppler studies of vertebral artery blood flow velocities during cervical rotation found that blood flow was com-promised more in patients than in asymptomatic sub-jects, on contralateral rotation, in sitting more than lying, and intracranial more than cervical (Mitchell 2009).

More recently studies have also looked at the effects of these tests on perfusion in the internal carotid artery (ICA). Refshauge (1994) noted an increase in right ICA blood flow velocity with sustained contralateral rotation in healthy volunteers. In contrast, Licht et al (2002) found no change in peak flow or time-averaged mean flow ve-locity during sustained extension-rotation test. Clinically relevant is that the patients in that study nonetheless ex-perienced symptoms (including vertigo, visual blurring, nausea, hemicranial paraesthesiae) classically consid-ered a positive response on this test. Rivett et al (1999) reported an increase in ICA blood flow velocity with cer-vical extension and attributed this to narrowing in the ICA. In contrast to the other two studies, they noted a decrease in peak systolic and end-diastolic blood flow velocity in both ICA during sustained rotation. Again rel-evant with regard to the clinical interpretation is the fact that these authors found no between-group differences for subjects that were positive or negative on this test.

Richter and Reinking (2005) calculated diagnostic ac-curacy statistics for the De Kleyn-Nieuwenhuyse test based on studies by Côté et al (1996) and Sakaguchi et al (2003) by comparing ultrasound flow study findings to clinical symptoms thought indicative of vertebral artery compression. Sensitivity for the both vertebral arteries in the Côté et al (1996) study was 0% and specificity for the right vertebral artery was 86%, whereas the left ver-tebral artery scored 67%. Note that a positive test was defined as the occurrence on a 30-second hold of ver-tigo, nausea, tinnitus, lightheadedness, visual problems, and numbness of the face or on one side of the body, nystagmus, vomiting, or loss of consciousness.

Diagnostic accuracy data calculated from the Sakaguchi et al (2003) study included sensitivity of 9.3% (95% CI: 4-19.9%), specificity of 97.8% (95% CI: 96.7-98.5%), a posi-tive likelihood ratio (LR) of 4.243 (95% CI: 1.678-10.729), and a negative LR of 0.928 (95% CI: 0.851-1.011). In light of the very low incidence of CAD discussed in the intro-duction, the effect of a positive test finding on post-test


probability despite a moderately high positive LR is very limited. Most relevant, however, is that the very low sen-sitivity and negative LR indicate that this test is useless for its intended purpose of screening for cervical artery circulatory compromise.

In addition, Thiel and Rix (2005) rightfully question the ability of positional testing in a still patent vessel to produce clinically useful information with regard to the risk of adverse effects with manipulative interven-tion. They also noted that the test itself might put the pa-tient at risk in case of a pathologically weakened vessel, especially since cadaver studies have shown greater strain values with the test as compared to manipulation. Haldeman et al (2002) also questioned the predictive va-lidity of the test: In their retrospective review of 64 med-icolegal cases where manipulation was associated with stroke, in 27 patients the test was documented with neg-ative results in all cases. In summary, the test lacks di-agnostic and prognostic validity and may put patients at risk for cervical artery circulatory compromise, espe-cially if the history indicates the possibility of such dys-function leading us to recommend discarding this test and its variants altogether.

ConclusionThere is little doubt that there is a biologically plau-

sible mechanism for the observed temporal association of CAD and manipulation that appears consistent across diverse geographical areas. However, evidence on the relation between exposure to manipulation and the oc-currence of CAD is equivocal and a variety of risk factors have been identified that offer alternative explanations for the occurrence of CAD. It would seem that manipula-tion is one possible factor in the multi-factorial etiology of CAD.

Although various risk factors have been identified in the etiology of CAD, with research evidence for these risk factors absent or at best limited, accurate identifi-cation of a patient population at risk for CAD with ma-nipulation is not a viable option as of yet. Current best evidence would indicate refraining from manipulation if risk factors are identified.

Considering the current level of evidence perhaps more important is that the therapist is able to recog-nize the signs and symptoms of CAD that may have been the patient or perhaps even a referring physician as an indication for physiotherapy management. In this con-text information from the history seems more relevant than physical examination findings. In fact we suggest discarding the sustained (extension) rotation tests alto-gether due to their lack of diagnostic and prognostic ac-curacy and the potential for harm to the patient.

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Cervical artery dysfunction and manipulation

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