Orthopaedic Division

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, FL
Consultant, 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 Clinic
100B-3200 Shelbourne Street, Victoria V8P 5G8, shelbournephysio@shaw.ca

Introduction ease who attend a spinal manipulative therapy practi-

When 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, stretches, 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-
tioner 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-

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

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 plausible
2. The proposed cause is temporally related to the oc-
currence
3. The relationship is consistent across different sam-
ples and groups
4. There exists a positive correlation between expo-
sure and occurrence
5. 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.
24 January/February 2010 - Interdivisional Review
Clinical diagnosis
With 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 factors
Even 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 list of risk factors identified
but not necessarily validated in the literature.
Trauma
With 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 gender
Although 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).
Arteriopathy
Arteriopathies predisposing the artery to dissection
as a result of pathological weakening of the vessel wall
www.physiotherapy.ca
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 little 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
Car diovas cular r is k factor s pr opos ed as r is k factor s
www.physiotherapy.ca January/February 2010 - Interdivisional Review
for CAD include hyper tens ion, tobacco us e, hyper cho-
les ter olaemia, hyper lipidaemia, diabetes , and at her o-
s cler os is . Mos t r es ear ch into this ar ea has compar ed
pat ient s wit h CAD t o pat ient s wit h is chaemic s t r okes .
Per haps as a r es ult of this under lying differ ence in
pathophys iology mos t car diovas cular r is k factor s
actually s how ORs below 1 indicating a “pr ot ective”
function. Of cour s e, this is likely due to the method-
ology of the r es ear ch compar ing “apples to or anges ”.
In thes e s tudies , hyper tens ion was the only s ignifi-
cant r is k factor with an OR of 1.94 (95% CI: 1.01-3.70).
Although a s eemingly plaus ible r is k factor with a s tiffer
ar ter y mor e s us ceptible to mechanical damage, t he
evidence for ather os cler os is as a r is k factor is bas ed
s olely on cadaver s tudies and the finding that blood
25
Table 2. Classic cardinal signs of vertebrobasilar compro-
mise: Five D's And three N's
flow is pr opor tional to the four th power of vessel diam-
eter (Mitchell 2002).
Infection
There 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 factors
In 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.
History
The 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
26 January/February 2010 - Interdivisional Review
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 symptoms
Although diagnostic utility of these symptoms has
yet to be established, therapists are all familiar with the
ischaemia-related cardinal signs 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 list 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-
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Table 3. Non-ischaemic and ischaemic signs and symptoms of cervical artery dysfunction

case scenario. In their population-based study, Lee et al
(2006) found that 33% of patients with CAD have only
local signs 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 strokes
In 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

www.physiotherapy.ca January/February 2010 - Interdivisional Review 27

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 auscultation
If 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 tests
In 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).
28 January/February 2010 - Interdivisional Review
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
www.physiotherapy.ca
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.
Conclusion
There 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.
References
Arnold C, Bourassa R, Langer T and Stoneham G (2004): Doppler
studies evaluating the effect of a physical therapy screening protocol on
vertebral artery blood flow. Man Ther 9:13-21.
Arnold M, Kappeler L, Georgiadis D, et al (2006): Gender differences in
spontaneous cervical artery dissection. Neurol 67:1050-1052.
www.physiotherapy.ca January/February 2010 - Interdivisional Review
Beaudry M and Spence JD (2003): Motor vehicle accidents: The most
common cause of traumatic vertebrobasilar ischaemia. Can J Neurol Sci
30:320-325.
Beletsky V, Nadareishvili Z, Lynch J, Shuaib A, Woolfenden A and Norris
JW (2003): Cervical arterial dissection: Time for a therapeutic trial?
Stroke 34:2856-2860.
Blunt SB and Galton C (1997): Cervical carotid or vertebral artery dissec-
tion. BMJ 314:243.
Cassidy JD, et al. (2008): Risk of vertebrobasilar stroke and chiropractic
care. Spine 33:S176-S183.
Cogbill TH, Moore EE, Meissner M, et al (1994): The spectrum of blunt
injury to the carotid artery: A multi-center perspective. J Trauma 37:473-
479.
Côté P, et al (1996): The validity of the extension-rotation test as a clin-
ical screening procedure before neck manipulation: A secondary anal-
ysis. J Manipulative Physiol Ther 19:159-164.
Debette S and Leys D (2009): Cervical artery dissections: Predisposing
factors, diagnosis, and outcome. Lancet Neurol 8:668-678.
De Kleyn A and Nieuwenhuyse AC (1927): Schwindelanfälle bei einer
bestimmten Stellung des Kopfes. Acta Otolaryngologica 11:155-157.
DiFabio RP (1999): Manipulation of the cervical spine: Risks and ben-
efits. Phys Ther 79:50-65.
Dziewas R, Konrad C, Drager B, et al (2003): Cervical artery dissection:
Clinical features, risk factors, therapy and outcome in 126 patients. J
Neurol 250:1179-1184.
Ernst E (2002): Manipulation of the cervical spine: A systematic review of
case reports of serious adverse events, 1995-2001. Med J Aust 176:376-
380.
Graziano DL, Nitsch W andHuijbregts PA (2007): Positive cervical artery
testing in a patient with chronic whiplash syndrome: Clinical decision
making in the presence of diagnostic uncertainty. J Manual Manipulative
Ther 15:E45-E63.
Grimm RJ. (2002): Inner ear injuries in whiplash. J Whiplash Rel Disord
1:65-75.
Guillon B, et al (2003): Infection and the risk of spontaneous cervical
artery dissection. Stroke 34:e79-e81.
Haldeman S, et al (2002): Unpredictability of cerebrovascular ischaemia
with cervical spine manipulation therapy: A review of sixty-four cases
after cervical spine manipulation. Spine 27:49-55.
Haneline MT, Croft AC and Frishberg BM (2003): Association of internal
carotid artery dissection and chiropractic manipulation. The Neurologist
9:35-44.
Haneline MT and Lewkovich (2004): Identification of internal carotid
artery dissection in chiropractic practice. J Can Chiropr Assoc 48:206-
210.
Haneline M and Triano J (2005): Cervical artery dissection: A compar-
ison of highly dynamic mechanisms: Manipulation versus motor vehicle
collision. J Manipulative Physiol Ther 28:57-63.
Haynes MJ (2002): Vertebral arteries and cervical movement: Doppler
ultrasound velocimetry for screening before manipulation. J Manipulative
Physiol Ther 25:556-567.
Haynes MJ, Cala LA, Melsom A, Mastaglia FL, Milne N and McGeachie
JK (2002): Vertebral arteries and cervical rotation: Modeling and mag-
netic resonance angiography studies. J Manipulative Physiol Ther
25:370-383.
Kawchuk GN, et al (2008): The relationship between the spatial distribu-
tion of vertebral artery compromise and exposure to cervical manipula-
tion. J Neurol 255:371-377.
Kerry R and Taylor AJ (2006): Cervical arterial dysfunction assessment
and manual therapy. Man Ther 11:243-253.
Kerry R, Taylor AJ, Mitchell J, McCarthy C and Brew J (2008): Manual
therapy and cervical arterial dysfunction, directions for the future: A clin-
ical perspective. J Manual Manipulative Ther 16:39-48.
29
Lee VH, Brown RD, Mandrekar JN and Mokri B (2006): Incidence and out-
come of cervical artery dissection: a population-based study. Neurology
67: 1809-12.
Licht PB, Christensen HW and Høilund-Carlsen PF (1999): Vertebral
artery volume flow in human beings. J Manipulative Physiol Ther 22:363-
367.
Licht PB, Christensen HW, and Høilund-Carlsen PF (2000): Is there a role
for premanipulative testing before cervical manipulation? J Manipulative
Physiol Ther 23:175-179.
Licht PB, Christensen HW and Høilund-Carlsen PF (2002): Carotid artery
blood flow during premanipulative testing. J Manipulative Physiol Ther
25:568-572.
Mitchell JA (2002): Vertebral artery atherosclerosis: A risk factor in the
use of manipulative therapy. Physiother Res Int 7:122-130.
Mitchell JA (2003): Changes in vertebral artery blood flow following
normal rotation of the cervical spine. J Manipulative Physiol Ther 26:347-
351.
Mitchell JA (2009): Vertebral artery blood flow velocity changes with cer-
vical spine rotation: A meta-analysis of the evidence with implications for
professional practice. J Manual Manipulative Ther 17:46-57.
Nakamura K, Saku Y, Torigoe R, Ibayashi S and Fujishima M (1998):
Sonographic detection of haemodynamic changes in a case of vertebro-
basilar insufficiency. Neuroradiology 40:164-166.
Oostendorp RAB, et al. (1999): Dizziness following whiplash injury: A
neuro-otological study in manual therapy practice and therapeutic impli-
cations. J Manual Manipulative Ther 7:123-130.
Paciaroni M, et al (2006): Seasonal variability in spontaneous cervical
artery dissection. J Neurol Neurosurg Psychiatry 77:677-679.
Refshauge KM (1994): Rotation: A valid premanipulative dizziness test?
Does it predict safe manipulation? J Manipulative Physiol Ther 17:413-
414.
Richter RR and Reinking MF (2005): Evidence in practice. Phys Ther
85:589-599.
Rivett DA and Carlesso L (2008): Safe Manipulative Practice in the
Cervical Spine: Towards and International Standard. Presented at:
IFOMT Conference, Rotterdam.
30 January/February 2010 - Interdivisional Review
Rivett DA, Milburn PD and Chapple C (1998): Negative premanipulative
vertebral artery testing despite complete occlusion: A case of false nega-
tivity. Man Ther 3:102-107.
Rivett DA, Sharpless KJ and Milburn PD (1999): Effect of premanipula-
tive tests on vertebral artery and internal carotid artery blood flow: A pilot
study. J Manipulative Physiol Ther 22:368-375.
Rothwell DM, Bondy SJ and Williams JI (2001): Chiropractic manipula-
tion and stroke: A population-based case control study. Stroke 32:1054-
1060.
Rubinstein SM, et al (2005): A systematic review of the risk factors for
cervical artery dissection. Stroke 36:1575-1580.
Sakaguchi M, et al (2003): Mechanical compression of the extracranial
vertebral artery during neck rotation. Neurol 61:845-847.
Schievink WI, Mokri B and O'Fallon WM (1994): Recurrent spontaneous
cervical-artery dissection. N Engl J Med 330:393-397.
Terrett AGJ (2000): Vertebrobasilar stroke following spinal manipulation
therapy. In; Murphy DR. Conservative Management of Cervical Spine
Syndromes. New York, NY: McGraw-Hill, 553-578.
Thiel H, and Rix G (2005): Is it time to stop functional pre-manipulation
testing of the cervical spine. Man Ther 10:154-158.
Touzé E, Gauvrit JY, Moulin T, Meder JF, Bracard S and Mas JL (2003):
Risk of stroke and recurrent dissection after a cervical artery dissection:
a multicenter study. Neurol 61:1347-1351.
Triano JJ and Kawchuk G (2006): Current Concepts: Spinal Manipulation
and Cervical Arterial Incidents. Clive, IO: NCMIC.
Westaway MD, Stratford P and Symons B (2003): False negative exten-
sion/rotation pre-manipulative screening test on a patient with an atretic
and hypoplastic vertebral artery. Man Ther 8:120-127.
Yi-Kai L, Yun-Kun Z, Cai-Mo L and Shi-Zhen Z (1999): Changes and im-
plications of blood flow velocity of the vertebral artery during rotation and
extension of the head. J Manipulative Physiol Ther 22:91-95.
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