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Cervical Artery Dysfunction (CAD):

Implications for Physiotherapy


Diagnosis and Management

Master Class Penticton, BC


September 13, 2010

Peter Huijbregts
Presenter
 Diploma Physiotherapy (1990)
 MSc Manual Therapy (1994)
 MHSc Physical Therapy (1997)
 Doctor of Physical Therapy (2001)
 Fellow Canadian Academy of Manipulative
Therapy, American Academy of Orthopaedic
Manual Therapy
 Board-certified Orthopaedic Specialist
Presenter
 Assistant Professor, University of St.
Augustine for Health Sciences
 Advisory Faculty, NAIOMT
 Editor-in-Chief, Consulting Editor JMMT
 Clinical Consultant, Shelbourne
Physiotherapy Clinic
 Consulting Editor, Jones & Bartlett
Publishers
Objectives

Upon completion of this session participants will


be able to discuss:

 Epidemiology of cervical (vertebral and


internal carotid) artery dysfunction
 Anatomy, pathology, and physiology relevant
to cervical artery dysfunction
Objectives
 Research evidence on the use of manual
therapy interventions
 Research linking cervical manual therapy
interventions to cervical artery dysfunction
 Relevant clinical (differential) diagnosis
 Risk management and emergency
procedures related to cervical artery
dysfunction
High-profile cases in Canada
 Laurie-Jean Mathiason
 20-year old female
 Fell down stairs and hurt her back
 Boyfriend suggested seeing his chiropractor
 Over the next months 189 adjustments in 21
visits including upper cervical
 Note: initial complaint was low back pain…
High-profile cases in Canada
 Rotary neck manipulation resulted in
inability to turn head
 That night she kept walking into things
at work
 Another visit to chiropractor next day
High-profile cases in Canada
 Neck adjustment
 Patient immediately began to cry
 Left eye rolled up, right roamed
randomly
 Convulsions
High-profile cases in Canada
 Turned blue, foaming at the mouth, did
not recognize her mother
 Coma
 Died next day from a traumatic rupture
left vertebral artery

Benedetti P, McPhail W. Spin Doctors 2002


High-profile cases in Canada
 Lana Dale Lewis, age 45, Toronto, ON
 Treated for migraine
 Complained of intense pain after
cervical manipulation
 Stroke few days after visit
 Second fatal stroke again a few days
later on September 12, 1996
High-profile cases in Canada
 Inquest 2002-2004
 Coroner’s jury verdict: Death by
accident
 Linked stroke causally to manipulation

Burdett J. Fatal chiropractic: The Lana Dale Lewis case. Association for Science &
Reason 2007
Laeeque H, Boon H. Print media coverage on the Lana Dale Lewis Inquest verdict:
Exaggerated claims or accurate reporting? Health Law Review 13(1):7-15.
High-profile cases in Canada
 Mrs. Sandy Nette, Edmonton, AB
 Bilateral vertebral artery dissection
 Chiropractic neck manipulation
 $ 500-million class-action lawsuit against
chiropractor, his clinic, Alberta College and
Association of Chiropractors, and AB Ministry
of Health and Wellness

Benedetti P, McPhail W. Twist and Shout. Globe and Mail, June 14, 2008
Relevance to Physiotherapy
 Now wait a minute…
Relevance to Physiotherapy
 Now wait a minute…
 Why would we as physiotherapists be
worried about the association between
manipulation and stroke?
Relevance to Physiotherapy
 Now wait a minute…
 Why would we as physiotherapists be
worried about the association between
manipulation and stroke?
 Isn’t this purely a chiropractic problem?
Clinical Vignette
 63-year old male
 Hypertensive
 Right cerebral infarct five years earlier
 Four months previously vertebrobasilar
infarct
Clinical Vignette
 PHYSIOTHERAPIST applied cervical
manipulation
 Immediate dizziness post-manipulation
 Over the next few hours dysarthria,
dysphagia, and left-sided paralysis
 Medullary infarct
Situation in the Netherlands
 In 2006, patients lodged 18 complaints
with professional association
 Of these 5 pertained to complaints
resulting from manual therapy
interventions to the neck

Vossen H. De Wijer A. Cervicale manipulaties: risico’s, neveneffecten en


prognostische factoren. Waar liggen onze verantwoordelijkheden?
Tijdschr Man Ther 2007;4:36-37.
Epidemiology CAD
 1-2% of patients with blunt, non-penetrating
headtrauma
 Includes facial and skull base fractures and
traumatic brain injury
 Increased incidence of ICA dissection in
patients with thoracic injuries
 Increased incidence of vertebral artery
dissection in patients with cervical fractures
and cord lesions
Debette S, Leys D. Cervical artery dissections: Predisposing factors, diagnosis, and
outcome. Lancet Neurol 2009;8:668-678.
Epidemiology CAD
 North American general population
study: 1-year incidence 2.6 (95% CI
1.86-3.33) per 100,000 for CAD
 Dijon, France: 1-year incidence 2.9 per
100,000 for ICA dissection

Lee VH, Brown RD, Mandrekar JN, Mokri B. Incidence and outcome of cervical
artery dissection: a population-based study. Neurology 2006; 67:1809–1812.
Debette S, Leys D. Cervical artery dissections: Predisposing factors, diagnosis, and
outcome. Lancet Neurol 2009;8:668-678.
Epidemiology CAD
 1-year incidence dissection vertebral
artery 0.97 (95% CI 0.52-1.4)
 Almost half of incidence ICA dissection:
1.72 (95% CI 1.13-2.32) per 100,000

Lee VH, Brown RD, Mandrekar JN, Mokri B. Incidence and outcome of cervical
artery dissection: a population-based study. Neurology 2006; 67:1809–1812.
Epidemiology CAD

 Of all CAD, 20% develop into CVA


 CAD accounts for approximately 20% of
all strokes in young versus 2.5% in
older patients

Blunt SB, Galton C. Cervical carotid or vertebral artery dissection. BMJ


1997;314:243.
Epidemiology CAD
 Note the extremely low incidence of
CAD and even lower incidence of CAD-
associated CVA in the general
population
 Remember this when establishing
pretest probability
Anatomy and physiology
review

Time to review some material?


1. Arterial anatomy
2. Mechanisms of arterial injury
3. Anatomy and physiology of the
cervical arteries
Anatomy: Artery
Three-layer structure
artery

 Intima
 Media
 Adventitia
Anatomy: Artery
INTIMA
 Layer of endothelial cells lining vessel interior
 Rests on basal lamina
 Turnover rate 1% per day
 Sub-endothelial layer: longitudinally arranged
loose connective tissue and some smooth
muscle cells
 In arteries: Internal elastic lamina, fenestrated
elastin allows diffusion to vessel wall
Anatomy: Artery
MEDIA
 Concentric layers of helically arranged
smooth muscle cells
 Variable amounts of elastic fibers and
lamellae, reticular fibers, and
proteoglycans
 In larger arteries: External elastic lamina
separating media from adventitia
Anatomy: Artery
ADVENTITIA
 Longitudinally oriented Type I collagen
and elastic fibers
 Gradually becomes continuous with
enveloping connective tissue

Junqueira LC, et al. Basic Histology. 8th ed (1995)


Mechanisms of Arterial
Trauma
 Subintimal hematoma
 Intimal tear
 Intimal tear with thrombus formation
 Intimal tear with embolic formation
 Vessel wall dissection with subintimal
hematoma
 Vessel wall dissection with pseudo-aneurysm
 False aneurysm
Subintimal Hematoma
 Disruption vasa
vasorum leads to
subintimal bleeding
and occlusion of VA
lumen

 May also cause


vasospasm
Intimal Tear
 Intima is the least
elastic layer and,
therefore, most likely to
tear
 Exposure sub-
endothelial layer causes
thrombosis
 Clot may propagate
proximally or distally
 Vasospasm due to
thrombin release
Intimal Tear with Embolization
 Propagating clot
extends into lumen
and breaks off
 Embolus
 Distal arterial
occlusion and
infarction
Dissection and Subintimal
Hematoma
 Disruption intima and
internal elastic lamina
 Blood dissects these
layers from muscular
media: dissecting
aneurysm
 Compresses lumen
 Exposure sub-
endothelial tissue and
thrombosis
Dissection and Subintimal
Hematoma: Reperfusion
 Hemorrhage may
again rupture
through intima
 Reestablishes
communication with
true lumen
 Recanalization may
occur
Dissection with Pseudo-
Aneurysm
 Disruption of media,
internal elastic lamina,
and intima
 Pseudo-aneurysm
under extending
adventitia
 May propagate distally
 Frequent cause of
occlusion PICA
False Aneurysm
 Disruption total arterial
wall
 Peri-arterial
hemorrhage contained
in fascia
 External compression
lumen
 Turbulence in lumen
may cause thrombus
and embolus formation
Anatomy: Vertebral Artery
V1: Extra-Vertebral Segment
 Branches off the subclavian artery and enters
the transverse foramen of C6 in 89% of
people
 Enters C7 in 3%, C5 in 6%, and C4 in 1% of
population
 Anterior boundary formed by anterior scalene
and longus colli muscles
 Posterior boundary transverse processes C7-
T1 and first rib
V2: Intra-Vertebral Segment
 Runs through transverse foramina C7-
C2
 Bordered anteromedially by
uncovertebral joints
 May be adherent to periosteum of the
uncinate processes
 Many anatomical variants have been
described
V3: Atlanto-Axial Segment
 Transverse foramen of C1 is far lateral as
compared to that of C2
 This causes a dorsolateral routing of the
vertebral artery from the C2 to the C1
transverse foramen
 Tethered at C1 and C2 transverse foramina
and atlanto-axial membrane
 Artery more prone to injury at this segment?
Atlanto-Axial Segment and
Rotation
V3: Atlanto-Axial Segment
 After exiting the C1 transverse foramen the
artery runs medially in a sulcus in the lateral
mass of the atlas
 Anatomical variant: Arcuate foramen and
ponticulus posterior in posterior arch atlas
 Anterior boundary is formed by the C0-C1
joint
 Posterior boundary is formed by the obliquus
capitis superior and rectus capitis posterior
major muscles
V4: Subforaminal and Intra-
Cranial Segment
 Piercesthe posterior atlanto-occipital
membrane and dura and arachnoid
mater
 Courses on intra-cranially in
subarachnoid space
Cervical Branches
 Spinal rami branch off the vertebral artery
and enter the intervertebral foramen where
they split in anterior and posterior radicular
arteries, anterior central artery, and anterior
and posterior vertebral canal arteries
 Radicular arteries supply the anterior and
posterior nerve roots and spinal ganglion
 The other branches supply epidural tissues
Cervical Branches
 Muscular, cutaneous, and articular rami
supply the local joints, intrinsic cervical
muscles, and the skin innervated by the
dorsal ramus of the cervical spinal nerves
 These branches also supply the flaval and
interspinal ligaments
 The ascending axial arteries supply the body
and odontoid process of C2 and the alar,
transverse, and cruciform ligaments
Sub-Foraminal Branches
 Subforaminal branches include the anterior,
posterior, and lateral spinal arteries
 The posterior spinal artery also frequently branches
off from the posterior inferior cerebellar artery
 Below C4 these spinal arteries form anastosmoses
with the spinal rami of the vertebral arteries through
the anterior radicular arteries
 This leaves the upper cervical cord vulnerable to
vascular ischaemia: Implication?
Intra-Cranial Branches
 The posterior inferior cerebellar artery (PICA)
branches off before coalescence of the
vertebral arteries into the basilar artery
 PICA supplies the dorsolateral medulla
oblongata, the cerebellar vermis, and a
number of cerebellar nuclei
 The basilar artery supplies the medulla
oblongata, the pons, the mesencephalon, and
parts of the cerebellum
Intra-Cranial Branches
 The labyrinthine arteries branch off early from
the basilar artery or the anterior inferior
cerebellar arteries, which makes the
vestibular nucleus and the inner ears very
susceptible to ischaemic abnormalities
 The posterior cerebral arteries branch off the
basilar artery and supply the thalamus and
hypothalamus and the occipital and temporal
lobes

Oostendorp R. Functionele Vertebrobasilaire Insufficientie. PhD Thesis. Nijmegen,


The Netherlands: Katholieke Universiteit Nijmegen, 1988.
Anatomy: Internal carotid
Fig 2
artery

C1 (atlas)

Vertebral Artery
Internal Carotid Artery

C6
Anatomy: ICA
 Provides 80% of blood flow to the brain
versus 20% supplied by the
vertebrobasilar system
 Traverses sternocleidomastoid, longus
capitis, stylohyoid, omohyoid, and
digastric muscles
Anatomy: ICA
 Fixed to the anterior aspect of the C1
vertebral body and in the carotid canal
in the petrous bone
 Sustained rotation and extension-
rotation tests have also been proposed
as tests of ICA function
Relevance to Physiotherapy?
Physiotherapists routinely use cervical manual
therapy in patients with:
 Neck pain
 Headache: Cervicogenic, tension-type,
migraine
 Dizziness: Cervicogenic
 TMD
 Subacromial impingement
 Lateral epicondylalgia
Do these patients make up a
big portion of our day-to-day
clinical practice?
Epidemiology Neck Pain
• Point prevalence neck pain: 9%
• 6-month prevalence: 54%
• Lifetime prevalence: 66%
• Point prevalence chronic neck pain (>6
months): 18%

Douglass AB, Bope ET. Evaluation and treatment of posterior neck pain in
family practice. J Am Board Fam Pract 2004;17:S13-S22.
Guez M, et al. Chronic neck pain of traumatic and non-traumatic origin.
Acta Orthop Scand 2003;74:576-579
Epidemiology Headache
 Cervicogenic headache: 0.4-2.5% in the
general population and up to 15-20% in those
with chronic headaches
 Tension-type headache: Two-thirds of males
and over 80% of females in developed
countries
 Migraine headache: 1-year prevalence 6-8%
in males and 15-18% of females in Europe
and US
World Health Organization. Headache Fact Sheet. 2008.
Haldeman S, Dagenais S. Cervicogenic headaches: A critical review.
Spine J 2001;1:31-46
Epidemiology Dizziness
 Dizziness accounts for 7% of physician visits
for patients over the age of 45
 For adults over 65, it is the number one
reason to visit a physician
 Approximately 15 to 30% of people
experiencing dizziness will seek medical
attention

Huijbregts P, Vidal P. Dizziness in orthopaedic physical therapy practice:


Classification and pathophysiology. J Man Manip Ther 2004; 12: 196-211
Epidemiology impingement
 Point-prevalence in the Dutch general
population of 20.9%
 1-year incidence of 11.2 per 1,000 patients in
Dutch general medical practice
 41% of the patients seeking care for
shoulder complaints diagnosed with
impingement

Picavet HSJ, Van Gils HWV, Schouten JSAG. Klachten van het bewegingsapparaat in de
Nederlandse bevolking: Prevalenties, consequenties en risicogroepen. Centraal Bureau
voor Statistiek, Bilthoven: 2000
Van der Windt DA, Koes BW, De Jong BA, Bouter LM. Shoulder disorders in general
practice: Incidence, patient characteristics and management. Ann Rheum Dis 1995;54:959-
964
Epidemiology lateral
epicondylalgia

 Affects 1-2% of general population

Allander E. Prevalence, incidence, and remission rates of some common rheumatic


diseases and syndromes. Scand J Rheumatol 1974;3(3):145-153.
Relevance to Physiotherapy?
 Cervical spine diagnoses were the reason for
referral in 16% of 1,258 outpatient PT
patients, second only to lumbar spine-related
diagnoses
 Headache reported as co-morbidity in 22% of
2,433 patients presenting for outpatient
PT/OT

Boissonnault WG. Prevalence of comorbid conditions, surgeries,


and medication use in a physical therapy outpatient population:
A multi-centered study. J Orthop Sports Phys Ther 1999;29:506-
519
Relevance to Physiotherapy?
 11% of 1,258 PT patients indicated the
shoulder as their chief area of
complaints
 Boissonnault WG. Prevalence of comorbid conditions, surgeries, and
medications in a physical therapy outpatient population: A multi-centered study.
J Orthop Sports Phys Ther 1999;29:506-525
Relevance to Physiotherapy?
 Allmember organizations IFOMT teach
cervical segmental examination,
manipulation, and mobilization
techniques
 19/20 member organizations teach
upper cervical manipulation
Rivett D, Carlesso L. Safe Manipulative Practice in the Cervical Spine (2008)
So why use manual therapy?
 Evidence-based practice
 The process of integrating the best
research evidence available with both
clinical expertise and patients’ values

Sackett DL, et al. Evidence-Based Medicine. How to Practice & Teach EBM. New
York, NY: Churchill Livingstone, 1997.
So why use manual therapy?
 Evidence-informed not evidence-driven
practice
 The clinician takes the evidence from
research into account when making clinical
decisions with regard to patient management
but evidence does not dictate these decisions
Bohart A. Evidence-based psychotherapy means evidence-informed, not evidence-
driven. Journal of Contemporary Psychotherapy 2005;35:39-53.
Research evidence
Systematic reviews on the effectiveness of
manual therapy for patients with mechanical
neck pain have indicated positive outcomes
on pain and function for (non) thrust
interventions but only when combined with
exercise and only in subacute and chronic
conditions

Gross AR, Hoving JLK, Haines TA, et al: A Cochrane Review of manipulation and
mobilization for mechanical neck disorders. Spine 29:1541,2004.
Sarigiovannis P, Hollins B: Effectiveness of manual therapy in the treatment of
non-specific neck pain: A review. Phys Ther Rev 10:35,2005.
Research evidence
Hoving et al reported no significant between-group
differences for pain, perceived recovery, and function
in patients with neck pain managed by their family
physician, exercise and stretching, or non-thrust
techniques and stabilization exercises at 1 year

But indicating relevant short-term effectiveness they


noted significantly better results for the manual
therapy group at 7 weeks
Hoving JL, De Vet HCW, Koes BW, et al: Manual therapy, physical therapy, or
continued care by the general practitioner for patients with neck pain: Long-term
results from a pragmatic randomized controlled clinical trial. Clin J Pain
22:370,2006.
Research evidence
Further indicating the cost-effectiveness of
manual therapy management for patients with
mechanical neck pain, an economic
evaluation alongside this randomized trial
(RCT) also showed significantly lower cost for
the manual therapy intervention as compared
to both others

 Korthals-De Bos IBC, Hoving JL, Van Tulder MW: Cost effectiveness of
physiotherapy, manual therapy, and general practitioner care for neck pain:
Economic evaluation alongside a randomised controlled trial. BMJ
326:911,2003.
Research evidence
 Multi-center RCT on patients with cervical
radiculopathy
 True versus sham mechanical traction for
cervical radiculopathy
 Both groups also received cervical and
thoracic non-thrust techniques, thoracic thrust
techniques, postural education, and cervical
mobility and cervical and scapulothoracic
strengthening exercises
Research evidence
 No between-group differences
 Within-group statistically and clinically
significant improvements in pain and
function

Young IA, Michener LA, Cleland JA, Aguilera AJ, Snyder AR: Manual
therapy, exercise, and traction for patients with cervical radiculopathy:
A randomized clinical trial. Phys Ther 89:632,2009.
Research evidence
A systematic review of randomized and
(non) controlled clinical trials found
consistent significant improvements with
soft tissue, non-thrust, and thrust
interventions for patients with
cervicogenic dizziness

Reid SA, Rivett DA: Manual therapy treatment of cervicogenic dizziness: A


systematic review. Man Ther 10:4,2005
Research evidence
 RCT in patients with cervicogenic dizziness
treated with a Mulligan cervical SNAG
intervention showed clinically and statistically
significant reduced dizziness, neck pain, and
dizziness-related disability over the group
treated with detuned laser

Reid SA, Rivett DA, Katekar MG, Callister R: Sustained natural apophyseal glides
are an effective treatment for cervicogenic dizziness. Man Ther 13:357,2008
Research evidence
A systematic review noted moderate
evidence for short-term efficacy of
spinal manipulation similar to
Amitryptiline in patients with migraine
and chronic tension-type headache
 No added benefit if manipulation was
added to massage in patients with
episodic tension-type headache
Research evidence
 Moderate evidence that spinal
manipulation was more efficacious for
cervicogenic headache than massage

Bronfort G, Assendelft WJJ, Evenas R, Haas M, Bouter L: Efficacy of


spinal manipulation for chronic headache: A systematic review. J
Manipulative Physiol Ther 24:457,2001
Research evidence
A systematic review yielded two RCTs
that showed significant effects of spinal
thrust interventions on headache
intensity and duration and medication
intake in patients with cervicogenic
headache
Fernández-de-las-Peñas C, Alonso-Blanco C, Cuadrado ML, Pareja JA:
Spinal manipulative therapy in the management of cervicogenic
headache. Headache 45:1260,2005
Research evidence
 RCT showed that twice weekly 45-minute
massage and trigger point release sessions
resulted in significant decreases in headache
frequency, intensity, and duration and
headache-related disability in patients with
tension-type headache with these effects
lasting into the 3-week follow-up period
Moraska A, Chandler C: Changes in clinical parameters in patients with
tension-type headache following massage therapy: A pilot study. J Man
Manip Ther 16:106,2008
Research evidence
 Prospective cohort study in patients with migraine
showed significant improvements in headache
frequency, intensity, duration, and disability after 2
months of thrust interventions as deemed indicated
by the clinician to the whole spine
 At 12 months there were still significant
improvements as compared to baseline for headache
frequency, intensity, and duration and medication use

Tuchin PJ: A twelve month clinical trial of chiropractic spinal manipulative therapy for
migraine. Aust Chiro Ost 8:61,1999
Research evidence
 RCT comparing spinal manipulation to
interferential current in patients with migraine
 Significant between-group differences
favoring manipulation for headache
frequency, duration, disability, and medication
use during the 2-month post-intervention
follow-up
Tuchin PJ, Pollard H, Bonello R: A randomized controlled trial of
chiropractic spinal manipulative therapy for migraine. J Manipulative
Physiol Ther 23:91,2000
Research evidence
 Kalamir et al reported that cervical
manipulation might be beneficial for
patients with temporomandibular
disorders, although this
recommendation was based solely on
case studies
Kalamir A, Pollard H, Vitiello AL, Bonello R: Manual therapy for
temporomandibular disorders: A review of the literature. J Bodywork
Movement Ther 11:84,2007
Research evidence
 Cohort studies on patients with subacromial
impingement
 Medium and long-term (up to one year) benefits of
thrust and non-thrust interventions to the cervical and
thoracic spine, ribs, shoulder, and shoulder girdle
 Over or in addition to exercise, medical care, and
steroid infiltration

Bang MD, Deyle GD: 2000 Comparison of supervised exercise with and without manual physical
therapy for patients with shoulder impingement syndrome. J Orthop Sports Phys Ther
30:126,2000
Bergman GJD, Winters JC, Groenier KH, Pool JJM, Meyboom-De Jong B, Postema K, Van der
Heijden GJMG: Manipulative therapy in addition to usual medical care for patients with
shoulder dysfunction and pain. Ann Int Med 141:432,2004
Research evidence
 Vicenzino et al have provided preliminary
suggestions for a treatment-based classification
system for patients with lateral epicondylalgia
 Perhaps patients presenting with greater pressure
pain threshold deficits relative to pain-free grip force
deficits should first be treated with manipulative
therapy techniques directed at the cervical spine

Vicenzino B, Cleland JA, Bisset L: Joint manipulation in the management of lateral


epicondylalgia: A clinical commentary. J Man Manip Ther 15:50,2007
Clinical decision-making

 Evidence for effectiveness


 Evidence for risk of harm
 Risk-benefit analysis
Risk of harm research
 Standardization of terminology only just
beginning
 Minor adverse events: relatively short
duration, less severe, occur immediately
after treatment or with short latency
period, minimal effect on function, fully
reversible, require no adaptation of
current treatment or additional treatment
Risk of harm research
 Major adverse events: moderate to long
duration, moderate to severe and
unacceptable, require additional intervention

 Carlesso L, MacDermid JC, Santaguida PL. Standardization of adverse event


terminology and reporting in orthopaedic physical therapy: application to the
cervical spine. J Orthop Sports Phys Ther 2010;40:455-463.
 Carnes D, Mullinger B, Underwood M. Defining adverse events in manual
therapies: A modified Delphi consensus study. Man Ther 2010;15:2-6.
Risk of harm research
 Research into risk of harm is wrought with
methodological shortcomings
 Obvious ethical concerns with studies that
would prospectively expose patients to a
suspected risk factor
 Non-standardized terminology
 Non-adherence to CONSORT guideline
 Mostly based on case reports and case
series
 Emphasizes serious adverse events
Minor adverse events
 Survey South-African physiotherapists
 Mostly dizziness and headache
 Also nystagmus, vision disturbances, nausea
and vomiting, acute wry neck, increased arm
pain +/- neurological deficit, syncope
 Average duration 6.3 days
 1 minor event per 3,020 manipulations
Michaeli A. Reported occurrence and nature of complications following manipulative
physiotherapy in South Africa. Aust J Physiother 1993;39:309-315.
Minor adverse events
 Survey Irish manual physiotherapists
 26% respondents reported adverse events
after cervical manipulation/mobilization in
preceding 2 years
 Mostly dizziness, nausea, and temporary
increase in complaints
 1 case each of drop attack, syncope, and TIA
post-mobilization
Sweeney A, Doody C. Manual therapy for the cervical spine and reported adverse
effects: A survey of Irish manipulative physiotherapists. Man Ther 2010;15:32-
36.
Minor adverse events
 Prospective study physiotherapists, osteopaths,
chiropractors
 60.9% of 283 patiënten reported at least one post-
manipulation minor event
 Headache (19.8%), stiiffness (19.5%), local
discomfort (15.2%), radiating discomfort (12.1%), and
fatigue (12.1%)
 Muscle tension (5.8%), dizziness (4.3%) en nausea
(2.7%)
 Majority of complaints occurred within 4 hours and
had resolved fully within 24 hours
Cagnie B, Vinck E, Beernaert A, Cambier D. How frequent are side effects of spinal
manipulation and can these side effects be predicted? Man Ther 2004;9:151-6.
Minor adverse events
 RCT comparing chiropractic cervical
manipulation to mobilization
 85 of 280 patients reported advesre
event
 Manipulation group: 48 patients with
120 complaints
 Mobilization group: 37 patients with 92
complaints
Minor adverse events
 25% increased neck pain and stiffness
 Headache (15.7%), fatigue (10%), radiating pain
(6.1%)
 Dizziness, extremity weakness, tinnitus, depression
or anxiety, nausea and vomiting, vision disturbances,
confusion, or disorientation (1%)
 Majority occurred within 24 hours and fully resolved
within 24 hours of onset
 Headache, dizziness, fatigue, and nausea in up to
75% general population in preceding three days

Hurwitz EL, Morgenstern H, Vassilaki M, Chiang LM. frequency and clinical predictors of adverse
reactions to chiropractic care in the UCLA Neck Pain study. Spine 2005; 30:1477-1484.
Minor adverse events
 Systematic review
 No increase in neck pain for cervical manipulation as
compared to cervical mobilization (combined with
thoracic manipulation): relative risk (RR) =1.25, 95%
CI 0.84-1.87; P > 0.05)
 Small increase in incidence of mild neurological
symptoms: RR = 1.96, 95% CI 1.09-3.54, P < 0.05).

Carlesso LC, Gross AR, Santaguida PL, Burnie S, Voth S, Sadie J. Adverse events associated
with the use of cervical manipulation and mobilization for the treatment of neck pain in
adults: A systematic review. Man Ther 2010;15(5):434-444.
Major adverse events

“…The temporal relationship between young


healthy patients without osseous or vascular
disease who attend an SMT practitioner and
then suffer these rare strokes is so well
documented as to be beyond reasonable
doubt indicating a possible causal
relationship…”

Terrett AGJ. Vertebrobasilar stroke following spinal manipulation therapy.


In: Murphy R. Conservative Management of Cervical Spine Syndromes
(2000)
Serious Manipulation-Related
Adverse Events

Two types of vertebral artery


stroke:
1. Wallenberg syndrome
2. Locked-in syndrome
Wallenberg Syndrome
 Dorsolateral medullary syndrome of
Wallenberg
 Occlusion PICA
 Other cause: Occlusion parent vertebral
artery, a.k.a. syndrome of Babinski
Nageotte
 Due to destruction nuclei and pathways
in dorsolateral medulla oblongata
Wallenberg Syndrome
 Inferior cerebellar peduncle: ipsilateral ataxia
and hypotonia
 Descending spinal tract and nucleus CN V:
loss of pain and temperature sensation
ipsilateral face and loss corneal reflex
 Ascending lateral spinothalamic tract: loss of
pain and temperature sensation contralateral
trunk and limbs (alternating analgesia)
Wallenberg Syndrome
 Descending sympathetic tract:
Ipsilateral Horner’s syndrome
 Lower vestibular nuclei: Nystagmus,
vertigo, nausea, and vomiting
 Nucleus ambiguous of
glossopharyngeal and vagus nerves:
Hoarseness, dysphagia, or intractable
hiccups
Locked-In Syndrome
 Cerebromedullospinal disconnection
syndrome
 Occlusion mid-basilar artery
 Bilateral ventral pontine infraction
 Effectively transects brain stem at mid-
pons region
 Patients are “conscious, paralyzed
mutes”
Locked-In Syndrome
 Consciousness retained because
reticular formation midbrain and rostral
pons is unaffected
 Cerebrospinal tracts destroyed:
Decerebrate rigidity
 Nuclei CN V-XII destroyed: Also affects
oculomotor nerve (CN III) due to
descending neuronal connections
Locked-In Syndrome
 Cutaneous sensation may be grossly intact
because lateral spinothalamic tract located
laterally in brain stem is spared
 Auditory nerves ascend brainstem lateral to
infarct area: Patient still can hear
 CN IV spared: Eye convergence and upward
gaze intact
Establishing causality
 Retrospectively establishing cause-and-
effect relationships?
 In clinical medicine we cannot establish
causal relationship beyond any doubt
 But we can increase or decrease
conviction of a causal effect
 Bradford-Hill criteria: Sir Austin Bradford
Hill (1965)
Bradford-Hill Criteria for
Causation
 Biologically plausible
 Proposed cause temporally related to
occurrence
 Consistent across different samples and
groups
 Positive correlation exposure and
occurrence
 No other explanation
Bradford-Hill Criterion # 1:
Biological Plausibility

It is certainly biologically plausible that


excessive mechanical force imparted to
the artery could cause arterial wall
damage especially in case of
pathologically weakened artery
Bradford-Hill Criterion # 1:
Biological Plausibility
 Cadaver study: 5 cadavers 80-99 y.o.
 SMT contralateral C1-C2, C3-C4, C6-
C7
 AROM and extension-rotation testing
 6.2% +/-1.3% to the distal (C0-C1) loop
of the VA and a 2.1% +/-0.4% strain to
the proximal (C6-subclavian artery) loop
Bradford-Hill Criterion # 1:
Biological Plausibility
 Strain range AROM tests: 1.2+/-0.6% -
12.5+/-10.1%
 Strain range extension-rotation tests: 3.2+/-
2.4% - 11.8+/-8.6%
 Failure testing: 139% to 162%
 Single thrust unlikely to mechanically disrupt
VA

Symons B, Leonard TR, Herzog W. Internal forces sustained by the vertebral artery
during spinal manipulative therapy. J Manipulative Physiol Ther 2002;25:504-10.
Bradford-Hill Criterion # 1:
Biological Plausibility
 24 test specimens from cadaveric rabbit
ascending aorta
 Specimens were exposed to 1000 strain
cycles of 0.06 and 0.30 of their in situ length
 Control and 0.06 strain tissues were
statistically the same (P = .406)
 0.30 strain group showed micro-structural
damage beyond that seen in the control
group (P = .024)
Bradford-Hill Criterion # 1:
Biological Plausibility
 Cadaveric rabbit arterial tissue similar in size
and mechanical properties of that of the
human VA can withstand repeat strains of
magnitudes and rates similar to those
measured in the cadaveric VA during cervical
SMT without incurring micro-structural
damage beyond control levels
Austin N, DiFrancesco LM, Herzog W. Micro-structural damage in arterial tissue
exposed to repeated tensile strains. J Manipulative Physiol Ther 2010;33:14-19
Bradford-Hill Criterion # 1:
Biological Plausibility
 Eight piezoelectric ultrasound crystals of 0.5-
mm diameter were sutured into the lumen of
the left and right VA of one cadaver
 Strains calculated during cervical spinal
range of motion testing, chiropractic cervical
spinal manipulation adjustments, and
vertebrobasilar insufficiency testing
 Lateral flexion + rotation and lateral flexion
SMT at C2-C3 and C4-C5 bilaterally
Bradford-Hill Criterion # 1:
Biological Plausibility
 Complex and non-intuitive strain patterns of
the VA within the cervical transverse foramina
 Strains for cervical spinal manipulations were
consistently lower than those obtained for
cervical rotation
 Neck manipulations impart stretches on the
VA that are well within the normal physiologic
range of neck motion
Wuest S, Symons B, Leonard T, Herzog W. Preliminary report: biomechanics of
vertebral artery segments C1-C6 during cervical spinal manipulation. J
Manipulative Physiol Ther 2010;33:273-278.
Bradford-Hill Criteria #2 - #3

 Proposed cause temporally related to


occurrence
 Consistent across different samples and
groups
Evidence Linking Manipulation
to Stroke

 Terrett(1995): Narrative review of


English, French, German,
Scandinavian, and Asian literature
1934-2000: 185 cases reported, death
in 30 cases
Evidence Linking Manipulation
to Stroke

 Updated in 2001: 236 cases reported


 Triano and Kawchuk (2006) updated
this review and found reports of 80
additional cases of post-manipulation
complications

Triano JJ, Kawchuk G. Current Concepts in Spinal


Manipulation and Cervical Arterial Incidents (2006)
Evidence Linking Manipulation
to Stroke
 DiFabio (1999): systematic review over
period 1925-1997
 177 cases with mostly arterial dissection or
spasm, brain stem lesion, and Wallenberg
syndrome
 Death resulted in 18% (n=32)
 Also visual defects, hearing loss, balance
deficits, and phrenic nerve damage
Evidence Linking Manipulation
to Stroke

 Cervical manipulation NOT a new treatment


in 41% of patients
 When described rotational thrust seemed
most injurious (23%)
 However, technique described in only 54%

DiFabio RP. Manipulation of the cervical spine: Risks and benefits.


Phys Ther 1999;79:50-65
Evidence Linking Manipulation
to Stroke
 Ernst (2002): Systematic review over 1995-
2001 period
 42 cases with serious adverse events: Mainly
arterial dissection
 Also long thoracic nerve palsy, disk
herniations, myelopathy, epidural hematoma
Evidence Linking Manipulation
to Stroke
 Insufficient data on type of manipulation used
 Underreporting bias?

Ernst E. Manipulation of the cervical spine: A systematic


review of case reports of serious adverse events,
1995-2001. Med J Aust 2002;176:376-380
Evidence Linking Manipulation
to Stroke
 True risk remains unknown
 Estimated risks adjusted assuming a
reporting rate of only 10% in literature
 All complications: 5-10 per 10 million
 Serious complications: 6 in 10 million
 Risk of death: 3 in 10 million

Hurwitz EL, et al. Manipulation and mobilization of the cervical


spine: A systematic review of the literature. Spine
1996;21:1746-1759
Current Emphasis on ICA:
Let’s Put This in Perspective

Terrett only found five cases (2.7%) of


185 reported cervical artery injuries
associated with SMT involving the ICA

Terrett AGJ. Current Concepts: Vertebrobasilar Complications


following Spinal Manipulation (2001)
Current Emphasis on ICA:
Let’s Put This in Perspective

 Systematic review Medline 1966-2000


 13 reports of dissection ICA temporally
associated with neck manipulation
 Risk of ICA dissection with manipulation
estimated at less than 1 in 601 million
Haneline MT, Croft AC, Frishberg BM. Association of internal carotid artery
dissection and chiropractic manipulation. The Neurologist 2003;9:35-44
Bradford Hill criterion #4: Positive
correlation exposure and occurrence

 582 cases of vertebrobasilar accidents (VBA)


in ON, 1993-1998
 Age and sex-matched controls from provincial
insurance database
 Exposure to chiropractic using provincial
insurance data
 VBA< 45 years old 5 times more likely (95%
CI 1.31-43.87) to have visited a chiropractor
within 1 week before VBA
Bradford Hill criterion #4: Positive
correlation exposure and occurrence

 Also, in younger age group 5 times as likely


to have had ≥ 3 visits with cervical diagnosis
in month before VBA (95% CI 1.34-18.57)
 No significant associations for those over 45
years old
 Further prospective study indicated; sources
of bias acknowledged

Rothwell DM, Bondy SJ, Williams JI. Chiropractic manipulation and


stroke: A population-based case control study. Stroke
2001;32:1054-1060
Bradford Hill criterion #4: Positive
correlation exposure and occurrence

 Population-based study over period 1993-


2001
 818 subjects with VBA stroke
 Case crossover portion: 4 control periods
randomly chosen from the year before the
stroke
 Case control portion: 4 age and sex-matched
controls from provincial insurance database
Bradford Hill criterion #4: Positive
correlation exposure and occurrence

 Case control study


 Visiting chiropractor in month before
stroke
 > 45: OR 0.83 (95% CI: 0.52-1.32)
 < 45: OR 3.13 (95% CI: 1.48-6.63)
Bradford Hill criterion #4: Positive
correlation exposure and occurrence

 However,…
 Case control study
 Visiting GP in month before stroke
 > 45: OR 2.67 (95% CI: 2.25-3.17)
 < 45: OR 3.57 (95% CI: 2.17-5.86)
Bradford Hill criterion #4: Positive
correlation exposure and occurrence

“… [A similar association between chiropractic


and GP visits in the month before the stroke
event] suggests that patients with
undiagnosed VA dissection are seeking
clinical care for headache and neck pain
before having a VBA stroke…”

Cassidy JD, et al. Risk of vertebrobasilar stroke and chiropractic


care. Spine 2008;33:S176-S183.
Bradford Hill criterion #5: No other
explanation

 Are there other plausible causes or


pathologies that might lead to CAD?
 Risk factor identification: Role in clinical
diagnosis
Risk Factors
Atherosclerosis Direct vessel trauma
Hypertension Autosomal polycystic
Hypercholesterolaemia kidney disease
Hyperlipidaemia Iatrogenic causes
Hyperhomocysteinaemia Endothelial inflammatory
Diabetes mellitus disease (e.g., temporal
arteriitis)
Genetic clotting disorders
Arteriopathies
Infections
Age
Smoking
Female gender
Free radicals
Thyroid disease
Upper cervical instability
Oral contraceptive use
Migraine
Direct Vessel Trauma:

 Manipulation
 Whiplash
Direct Vessel Trauma:
Whiplash
In a retrospective analysis, Beaudry and
Spence attributed 70 of 80 traumatically
induced cases of vertebrobasilar
ischaemia to motor-vehicle accidents

Beaudry M, Spence JD. Motor vehicle accidents: The most


common cause of traumatic vertebrobasilar ischaemia. Can J
Neurol Sci 2003;30:320-325
Whiplash and Dizziness
Dizziness, vertigo, and dysequilibrium are
symptoms in 20-58% of individuals that
have sustained a whiplash-type injury of
the cervical spine or a closed head
injury

Wrisley DM, et al. Cervicogenic dizziness: A review of


diagnosis and treatment. J Orthop Sports Phys Ther
2000;30:755-766
Whiplash and Dizziness
 Damaged peripheral labyrinth or cochlea in 90% and
both in 69% of 227 post-whiplash patients at
neurology evaluation
 92% met the diagnostic criteria for inner ear
contusion
 Of this subgroup, 63% was diagnosed with BPPV,
64% with secondary endolymphatic hydrops, and
21% with unilateral or bilateral perilymphatic fistulae
 25% prevalence of BPPV in 273 consecutive patients
with rear-end impact whiplash injury without head
injury
 Grimm RJ. Inner ear injuries in whiplash. J Whiplash Rel Disord 2002:1:65-75;
Oostendorp RAB, et al. Dizziness following whiplash injury: A neuro-otological
study in manual therapy practice and therapeutic implication. J Manual
Manipulative Ther 1999;7:123-130
Not all Dizziness Implies CAD

 Benign Paroxysmal Positional Vertigo


 Cervicogenic dizziness
 Vertebrobasilar insufficiency
Dizziness type Nystagmus and dizziness Associated signs and
characteristics symptoms
Cervicogenic Positioning-type  No latency period  Nystagmus
dizziness  Brief duration  Neck pain
 Fatigable with  Suboccipital
repeated motion headaches
 Cervical motion
abnormality on
examination
BPPV Positioning-type  Short latency: 1-5  Nystagmus
seconds
 Brief duration: <30
seconds
 Fatigable with
repeated motion
Cervical Positional-type  Long latency: 55+/- Ischaemic and
artery 18 seconds (depending on etiology)
dysfunction  Increasing possibly non-ischaemic
symptoms and signs signs and symptoms as
with maintained described in Table 10
head position
 Not fatigable with
repeated motion
Hallpike-Dix Maneuver
 Positional
nystagmus on this
test has been shown
to identify patients
with posterior SCC
BPPV with 78%
sensitivity
 Specificity as high
as 88% has been
reported
Age: 30-45 year old?
Age
 Relevant to the clinical diagnosis of
spontaneous if not manipulation-
induced CAD is that Lee et al (2006)
reported a mean age of 45.8 years for
North-American patients

Lee VH, Brown RD, Mandrekar JN, Mokri B. Incidence and outcome of
cervical artery dissection: a population-based study. Neurology 2006;
67:1809–1812
Age
 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
for patients diagnosed with CAD
Touzé E, Gauvrit JY, Moulin T, Meder JF, Bracard S, Mas JL. Risk of
stroke and recurrent dissection after a cervical artery dissection: a
multi-center study. Neurol 2003;61:1347–1351.
Arnold M, Kappeler L, Georgiadis D, et al. Gender differences in
spontaneous cervical artery dissection. Neurol 2006; 67:1050–1052.
Gender: Female
Predisposition?
 Terrett (1995) literature review of 185 patients
with severe CSMT complications
 Gender known for 180
 77 males (42.8%) of whom 13 died (16.9%)
 103 females (57.2%) of whom 17 died
(16.5%)
 Reflects of male-female ratio in chiropractic
office: 40.7-59.3% or 44.8-55.2%?
Gender
 In three large studies (Beletsky et al
2003, Lee et al 2006, Schievink et al
1994) 50-52% of patients with CAD
were women
 In two European studies (Arnold et al
2006, Touzé et al 2003) 53-57% were
men
Gender
 ICA dissection seems to be more common in
men and at an older age (47.0 versus 43.4
years) than is VA dissection (Dziewas et al
2003, Lee et al 2006)
Beletsky V, Nadareishvili Z, Lynch J, Shuaib A, Woolfenden A, Norris JW. Cervical
arterial dissection: Time for a therapeutic trial? Stroke 2003;34:2856-2860.
Schievink WI, Mokri B, O’Fallon WM. Recurrent spontaneous cervical-artery
dissection. N Engl J Med 1994;330:393–397.
Dziewas R, Konrad C, Drager B, et al. Cervical artery dissection: Clinical features,
risk factors, therapy and outcome in 126 patients. J Neurol 2003;250:1179-1184.
Arteriopathies
 Marfan syndrome
 Ehlers-Danlos syndrome
 Fibromuscular dysplasia
 Cystic medial necrosis
 Osteogenesis imperfecta
 Alpha-1-antitrypsin deficiency
 Autosomal dominant polycystic kidney
disease
 Previous CAD
Marfan Syndrome
 Higher reported incidence of CAD
 Typically show signs of impaired skeletal
integrity resulting in joint hypermobility
 Extremely arched palate with crowded teeth
 Long limbs, spider-like fingers:
Arachnodactyly
 Chest abnormalities: Pectus excavatum
 Kyphoscoliosis
 Sometimes only vascular defects with
minimal or no outward clinical manifestations
Ehlers-Danlos Syndrome
 Higher reported incidence of CAD
 Vascular Type IV variant may play a role in
familial CAD
 History of easy bruising
 Thin skin with visible veins
 Characteristic facial features: Protruding
eyes, small chin, thin nose and lips, and
sunken cheeks

Martin JJ, et al. Familial cervical artery dissections: Clinical,


morphologic, and genetic studies. Stroke 2006;37:2924-2929
Hypermobility: Beighton Score
Hypermobility: Brighton Criteria
Fibromuscular Dysplasia
 Rare non-atherosclerotic and non-
inflammatory vascular condition
 Primarily affects medium-sized arteries,
in particular the ICA and renal arteries
 Present in females 3 to 4 times more
frequently than in males
 Bilateral in 65% of patients
Fibromuscular Dysplasia
 May be related to mechanical stress to the
arterial wall, ischaemia within the vessel due
to disturbance of the vasa vasorum, or
hormonal activity that negatively affects the
muscular wall
 Present in up to 23% of patients with ICA
dissection
 Presenting complaint may vary from TIA to
headache and dizziness
Cystic Medial Necrosis
 Focal degeneration of the elastic tissue
and muscle of the tunica media, with the
development of mucoid material
 Associated with a variety of systemic
disorders
 Typically occurs in patients > 40
 Male: female ratio = 2:1
Cystic Medial Necrosis
 Typically affects large arteries, chiefly
the aorta
 Sometimes associated with the cervical
arteries
 Breakdown of collagen, elastin, and
smooth muscle, along with an increase
in the artery’s ground substance
 Ehlers-Danlos and Marfan syndrome
Osteogenesis Imperfecta
 Bone fragility
 Also blue sclerae, diminished hearing,
thinness of the skin, and joint
hypermobility
 Type 1 associated with CAD:
Decreased or structurally defective type
I collagen produced
Alpha-1-Antitrypsin Deficiency
• Circulating serine proteinase inhibitor of
proteolytic enzymes that contributes to
maintenance of integrity of connective tissues
• Deficiency provides insufficient protection
against effect collagenase and elastase and
may damage vessel wall
• Genetic systemic disorder with lung and liver
disease
Alpha-1-Antitrypsin Deficiency
• 22 consecutive patients with SCAD and 113
controls with non-CAD stroke
• Significantly lower levels in CAD (P=0.01)
• OR 17.7 (95% CI: 2.9-105.6) for A1-AT levels
< 90 mg/dl
Alpha-1-Antitrypsin Deficiency
 Findings were refuted by a more recent and
methodologically sound study
 Another small study consisting of 12 spontaneous
CAD patients found 3 cases with a deficiency of
alpha-1-antitrypsin
 Overall, there is little evidence in support of this
relationship

Vila N, et al. Levels of α1-antitrypsin in plasma and risk of spontaneous


cervical artery dissections. Stroke 2003;34:e168-169
Haneline M, Lewkovich GN. A narrative review of pathophysiological
mechanisms associated with cervical artery dissection. J Can Chiropr
Assoc 2007; 51(3):146–157
Autosomal Dominant
Polycystic Kidney Disease
 Common heritable condition: Prevalence rate
of 1 in 400 to 1 in 1000
 Affecting the renal system
 May also lead to extra-renal complications,
including connective tissues disorders

Haneline M, Lewkovich GN. A narrative review of


pathophysiological mechanisms associated with cervical artery
dissection. J Can Chiropr Assoc 2007; 51(3):146–157
Previous CAD
 Incidence of new CAD in first year post-CAD:
1.7% (95% CI 0.3-3.6%)
 Cumulative 1-year incidence of 10.7% (95%
CI 6.5-14.9%) and 3-year incidence of 14.0%
(95% CI 8.9-19.1%) for new CVA post initial
CAD diagnosis
Weimar C, Kraywinkel K, Hagemeister C, Haass A, Katsarava Z, Brunner F, et al.
Recurrent stroke after cervical artery dissection. J Neurol Neurosurg Psychiatry
2010;81:869-873.
Cardiovascular Risk Factors
 Hypertension
 Tobacco use
 Hypercholesterolaemia
 Diabetes
 Atherosclerosis
Hypertension
 Risk factors studied: tobacco use,
hypertension, diabetes, and
hypercholesterolaemia
 Compared a group of 153 consecutive
patients with CAD, a group of patients
with ischaemic stroke unrelated to CAD,
and a group of controls
Hypertension
 Hypertension was the only one of 4
variables significantly associated with
CAD, but only in the subgroup of CAD
patients who developed cerebral
infarction
 Overall OR 1.94 (95% CI: 1.01-3.70)
 For VA dissection OR 2.69 (95%
CI:1.20-6.04)
Atherosclerosis
 362 cadaver vertebral arteries
 Grade 0 (0% occlusion) to grade 5 (75%
occlusion) atherosclerosis
 Highest incidence of grade of atherosclerosis:
Grade 3
 Mainly in atlanto-occipital portion of VA: 4.0%
 Also in intra-cranial portion of VA: 35.2%
Atherosclerosis
 Blood flow proportional to fourth power
of diameter
 Population at risk for developing VBI?
 Note: Only basic science extrapolation!

Mitchell J. Vertebral artery atherosclerosis: A risk factor in the use


of manipulative therapy? Physiother Res Int 2002;7:122-13
Hypercholesterolaemia
 Prospective study on infection as risk factor
for CAD
 47 consecutive patients with spontaneous
CAD and 52 with ischemic stroke
 Significantly higher hypercholesterolaemia in
controls (42.6%) versus subjects (12.9%)

Guillon B, et al. Infection and the risk of spontaneous cervical artery


dissection. Stroke 2003;34:e79-e81
Hypercholesterolaemia
 72 CAD patients compared with 72 non-
CAD stroke control patients
 Diabetes, current smoking,
hypercholesterolaemia, and oral
contraceptive use not associated with
CAD

Pezzini A, et al. History of migraine and the risk of spontaneous


cervical artery dissection. Cephalagia 2005;25:575-580
Hypercholesterolaemia
 So: Hypercholesterolaemia is
protective?
 Comparing apples and oranges…
 Hypercholesterolaemia more frequent in
subgroup of CAD patients with
ischaemic events

Arnold M, et al. Vertebral artery dissection: Presenting findings and


predictors of outcome. Stroke 2006;37:2499-2503
Thyroid disease
 Case-control study involving 58 subjects
 Present in 31.0% of CAD patients (9/29),
compared with 6.9% of non-CAD stroke
patients (2/29) (P=0.041)
 Immunologic mechanisms contributing to the
vascular damage?
 Reports of ICA dissection in patients with
Graves disease: Effects of thyroid hormones
on the smooth muscle cells and endothelium
of the vascular system
Clinical Vignette
 39-year old male
 Felt dizzy and clammy
 Consulted osteopath and received
traction manipulation
 Semi-comatose state and vomiting
 Died in hospital 19 hours later
 Cerebellopontine infarction following
bilateral vertebral artery dissection
Infection
 Seasonal variation incidence of CAD: related
to the higher incidence of upper respiratory
infections during the winter?
 31.3% (95% CI: 26.5-36.4) of cohort of 352
CAD patients developed dissection in the
winter
 Statistically significantly more than in the
spring, 25.5% (95% CI: 21.1-30.3), the
summer 23.5% (95% CI: 19.3-28.3), and the
autumn 19.7% (95% CI: 15.7-24.1)

Paciaroni M, et al. Seasonal variability in spontaneous cervical artery dissection. J


Neurol Neurosurg Psychiatry 2006;77:677-679
Infection
• Prospective study on infection as risk factor for CAD
• 47 consecutive patients with spontaneous CAD and
52 with ischemic stroke
• Acute infection present within 4 weeks preceding
vascular event more common in SCAD (31.9%) than
control subjects (13.5%)
• Crude OR 3.0 (95% CI: 1.1-8.2, P= 0.032)
• Adjusted OR 3.1 (95% CI: 1.1-9.2)

Guillon B, et al. Infection and the risk of spontaneous cervical artery


dissection. Stroke 2003;34:e79-e81
Oral Contraceptive Use
 One retrospective case-control study
(17subjects, 24 controls) investigating
CAD risk factors generated statistically
significant findings
 Current (but not past) use of oral
contraceptives associated with CAD
Oral Contraceptive Use
 Another case-control study that explored CAD
risk factors found that 58.3% of CAD cases
were using oral contraceptives (27 of 47), as
compared with 40.0% of the controls who had
ischemic stroke from another cause (21 of
52): non-significant difference
 No consensus

Haneline M, Lewkovich GN. A narrative review of


pathophysiological mechanisms associated with cervical artery
dissection. J Can Chiropr Assoc 2007; 51(3):146–157
Other Risk Factors
 Mechanical stress of coughing, sneezing, or
vomiting: OR 1.6 (95% CI: 0.67-3.80)
 Vascular risk factors OR 0.14 (95% CI: 0.34-
0.65)
 Current smoking habit OR 0.49 (95% CI:
0.18-1.05)

Triano JJ, Kawchuk G. Current Concepts in Spinal Manipulation


and Cervical Arterial Incidents (2006)
Systematic Review of Risk
Factors CAD

 Systematic review risk factors cervical


artery dissection
 Two computerized databases, 1966-
2005
 31 case control studies
Systematic Review of Risk
Factors CAD

 Aortic root diameter > 34 (mm):


OR=14.2 (95% CI: 3.2-63.6)
 Homocysteine levels (may cause
endothelial damage): OR=1.3 (95% CI:
1.05-1.52)
 Little relevance to PT clinical practice…
Systematic Review of Risk
Factors CAD
More relevant to PT clinical practice:
 Migraine: OR=3.6 (95% CI: 1.5-8.6)
 Trivial trauma (neck manipulation): OR=3.8
(95% CI: 1.3-11)
 Recent infection: OR=1.6 (95% CI: 0.67-3.80)

However, most studies had major sources of


bias
Rubinstein SM, et al. A systematic review of the risk factors for cervical artery
dissection. Stroke 2005;36:1575-1580
Bradford Hill criteria
 Although opinions certainly and justifiably
differ, case reports and narrative reviews of
such case reports provided by authors in
diverse geographical locations temporally
linking possible mechanical trauma of the
cervical arteries due to manipulation to CAD
would seem to qualify as supporting the first
three criteria
 However, we can argue criteria 4 and 5 are
not satisfied…
Clinical Diagnosis
 Two relevant questions…
First Relevant Question

How do we identify patients at risk


for cervical artery dysfunction?
Identify patients at risk for
CAD
 Clinically relevant risk factors: Previous
medical history of treatment with cervical
manual therapy interventions, hypertension,
previous infection, previous CAD, and
migraine headache
 Questionable risk factors: Atherosclerosis,
thyroid disease, and arteriopathies…
Second Relevant Question

How do we identify patients with cervical


artery dysfunction in progress?
They are not all this easy…
Presenting Complaint?

 Majorpresenting complaint of 137


patients who subsequently had an SMT-
induced vertebrobasilar vascular
incident
Presenting Complaint
 47.4%: Neck pain and stiffness
 19.7%: Neck pain, stiffness, and headache
 16.8%: Torticollis
 2.2%: Low back pain
 2.2%: Abdominal complaint
 1.5%: (Kypho) scoliosis
 1.5%: Head cold
 1.5%: Upper thoracic pain
 0.7%: Upper limb numbness
 0.7%: Hay fever

Terrett AGJ. Vertebrobasilar stroke following spinal manipulation therapy. In: Murphy R.
Conservative Management of Cervical Spine Syndromes (2000)
So Where Does This Leave
Us?

 Presenting complaint provides no


relevant information
Physical Examination?
De Kleyn-Nieuwenhuyse Test
 In1927, De Kleyn and Nieuwenhuyse
reported decreased or even absent
vertebral artery blood flow based on
cadaver perfusion studies in different
head and neck positions
De Kleyn-Nieuwenhuyse Test
 Based on these anatomical observations and
these early perfusion studies, the sustained
extension-rotation and the sustained rotation
tests have been proposed and widely
instructed and used as tests to determine the
presence of vertebrobasilar artery dysfunction

De Kleyn A, Nieuwenhuyse AC. Schwindelanfälle und Nystagmus


bei einer bestimmten Stellung des Kopfes. Acta
Otolaryngologica 1927;11:155-157
Sustained Extension-Rotation
Test and VA
 Extensively studied with equivocal results
 Some authors have reported significant
decreases in VA blood flow, whereas other
studies found no changes
 Case reports have noted false negative
results
 Case series have reported 75-100% false
positive results
Sustained Rotation Test and
VA
 Research findings for the sustained
cervical rotation test are equally
equivocal
 Significant decreases or no effect noted
on vertebral artery blood flow or volume
Sustained Extension-Rotation
Test and VA
 Meta-analysis of Doppler studies of VA blood
flow velocity
 Effect size: Cohen’s d
 VA blood flow velocity compromised more in
patients than asymptomatic subjects, on
contralateral rotation, in sitting more than
lying, intra-cranial more than cervical
Mitchell J. Vertebral artery blood flow velocity changes with cervical spine rotation: A meta-
analysis of the evidence with implications for professional practice. J Manual Manipulative
Ther 2009;17:46-57.
Sustained (Extension)
Rotation Test and ICA

 Refshauge noted an increase in right


ICA blood flow velocity with sustained
contralateral rotation in healthy
volunteers
Sustained (Extension)
Rotation Test and ICA
 In contrast, Licht et al found no change in
peak flow or time-averaged mean flow
velocity in the ICA during sustained
extension-rotation test
 Patients nonetheless experienced symptoms
(vertigo, visual blurring, nausea, hemicranial
paraesthesiae) classically considered a
positive response on this test

 Licht PB, Christensen HW, Høilund-Carlsen PF. Carotid artery


blood flow during premanipulative testing. J Manipulative
Physiol Ther 2002;25:568-572.
Sustained (Extension)
Rotation Test and ICA
 Rivett et al reported increase in ICA blood
flow velocity with cervical extension due to
narrowing in the ICA?
 Decrease in peak systolic and end-diastolic
blood flow velocity in both ICA during
sustained rotation
 Found no between-group differences for
subjects that were positive or negative on this
test

 Rivett DA, Sharpless KJ, Milburn PD. Effect of premanipulative tests on


vertebral artery and internal carotid artery blood flow: A pilot study. J
Manipulative Physiol Ther 1999;22:368-375.
Psychometric Data
 Duplex Doppler ultrasonography
 Measured blood flow and vessel diameter
 Subjects 1,108 consecutive subjects referred
for neurovascular evaluation
 136 (12.3%) had unexplained vertebrobasilar
distribution symptoms
 Extension-rotation position held for at least 10
seconds
Sakaguchi M, et al. Mechanical compression of the extracranial
vertebral artery during neck rotation. Neurol 2003;61:845-847
Psychometric Data
 Richter and Reinking calculated
diagnostic accuracy statistics
 Comparing signs and symptoms with
extension rotation as clinical test and
US findings as reference test

Richter RR, Reinking MF. Evidence in Practice. Phys Ther


2005;85:589-599
Psychometric Data
Psychometric Data
 Sensitivity 9.3% (95% CI: 4-19.9%)
 Specificity 97.8% (95% CI: 96.7-98.5%)
 LR+ 4.243 (95% CI: 1.678-10.729)
 LR- 0.928 (95% CI: 0.851-1.011)
 Interpretation in light of extremely low
pretest probability?
Psychometric Data
 12 experimental and 30 control subjects
recruited from chiropractic clinics
 Experimental group had history of symptoms
related to head and neck movement and
positive Wallenberg test (head and neck
extension-rotation for 30 seconds)
 Non-vascular causes excluded by
radiography and neurologist examination

Côté P, et al. The validity of the extension-rotation test as a clinical screening


procedure before neck manipulation: A secondary analysis. J Manipulative
Physiol Ther 1996;19:159-164
Psychometric Data
 Extension-rotation test held for 30 seconds
 Doppler ultrasound at C3-C5: Systolic peak
velocity to end-diastolic minimum velocity
 Positive index test: Vertigo, nausea, tinnitus,
lightheadedness, visual problems, numbness
of the face or one side of the body,
nystagmus, vomiting, or loss of
consciousness
Psychometric Data
Predictive Validity

 How can positional testing of


haemodynamics in a still patent vessel
be expected to produce clinically useful
information regarding the risk of injury
with manipulative interventions?
Predictive Validity
 With an already pathologically weakened
vessel wall, performing the test itself might
put the patient at greater risk due to the
potential stretching forces exerted
 At least in cadaver studies, strain values
produced during the test exceeded those
produced with manipulation

Thiel H, Rix G. Is it time to stop functional pre-manipulation testing


of the cervical spine? Man Ther 2005;10:154-158
Predictive Validity
 Haldeman et al did a retrospective analysis of
64 medicolegal records describing
cerebrovascular ischaemia after cervical SMT
 The clinicians involved described doing the
sustained extension-rotation test in 27 cases
 None of these patients had adverse
responses
Haldeman S, et al. Unpredictability of cerebrovascular ischaemia associated with
cervical spine manipulation therapy: A review of sixty-four cases after cervical
spine manipulation. Spine 2002;27:49-55
Again, Where Does This
Leave Us?
We talked about the limited value of:
 Presenting complaint
 Clinically relevant risk factors
 Questionable risk factors

Sustained extension-rotation test would at


the very most only seem relevant when
positive
Teaching Provocative Tests
 17/20 member organizations IFOMT
teach provocative tests involving
rotation +/- extension
 In March 2004, clinic directors of all US
chiropractic colleges agreed to abandon
teaching provocative tests

Rivett D, Carlesso L. Safe Manipulative Practice in the Cervical Spine (2008)


Clum G. Cervical Spine Adjusting and the Vertebral Artery (2006)
Remember the Two Relevant
Questions?

Goals of history and examination


 Screen patients at risk for adverse
effect with intervention
 Identify patients with cervical artery
dysfunction in progress?
Five Ds And Three Ns
 Dizziness
 Drop attacks
 Diplopia (including amaurosis fugax and corneal
reflux)
 Dysarthria
 Dysphagia (including hoarseness and hiccups)
 Ataxia of gait
 Nausea
 Numbness (in ipsilateral face and/or contralateral
body)
 Nystagmus
Nystagmus
 Repetitive, back-and-forth, involuntary
eye movements initiated by slow drifts
away from the visual target
 Pendular nystagmus consists of slow
sinusoidal oscillations
 Jerk nystagmus is characterized by an
alternating slow drift and a quick
corrective phase
Nystagmus
 Spontaneous nystagmus may imply an
acute peripheral vestibular lesion and
may occur in the symptom-free interval
in patients with vestibular migraine
 Jerk nystagmus with the quick phase
indicating the unaffected side
Nystagmus
 Purely vertical (upbeat or downbeat) or
torsional spontaneous nystagmus is
indicative of a central vestibular lesion
 Nystagmus due to a central lesion
usually cannot be suppressed with
visual fixation
Nystagmus
 Positional
downbeat vertical or skew
nystagmus: Posterior fossa lesions
(Arnold-Chiari malformation or another
compressive lesion at the foramen
magnum)
Nystagmus

 Pendular nystagmus occurs most


commonly in patients with multiple
sclerosis and brain stem stroke
Cervical Artery Dysfunction
 Non-ischaemic signs and symptoms
 Ischaemic signs and symptoms
 Vertebrobasilar system
 Internal carotid artery
Non-Ischaemic Signs and
Symptoms VA
 Ipsilateral posterior neck pain
 Ipsilateral occipital headache
 Sudden-onset and severe
 Described as stabbing, pulsating, aching,
“thunderclap”, sharp, or of an unusual
character
 “A headache unlike any ever experienced
before…”
 Rarely C5-C6 nerve root impairment due to
local neural ischaemia
Ischaemic Signs and
Symptoms VA
 Five Ds And 3 Ns
 Vomiting
 Loss of short-term memory
 Vagueness
 Hypotonia and limb weakness affecting arm
or leg
 Anhydrosis: lack of facial sweating
 Hearing disturbances
 Horner syndrome
Ischaemic Signs and
Symptoms VA
 Malaise
 Perioral dysaesthesia
 Photophobia
 Clumsiness
 Agitation
 Cranial nerve palsies
 Hindbrain stroke: Wallenberg or locked-in
syndrome
Non-Ischaemic Signs and
Symptoms ICA
 Ipsilateral upper and mid-cervical pain
 Ipsilateral fronto-temporal or peri-orbital
headache
 Sudden onset, severe, uncommon
character
 Horner syndrome
 Pulsatile tinnitus
 Cranial nerve palsies
Non-Ischaemic Signs and
Symptoms ICA

 Ipsilateral
carotid bruit
 Neck swelling
 Scalp tenderness
 Anhydrosis face
Ischaemic Signs and
Symptoms ICA
 TIA
 Middle cerebral artery distribution stroke
 Retinal infarction
 Amaurosis fugax: Temporary blindness
 Local patchy blurring of vision: Scintillating
scotomata
 Weakness extra-ocular muscles
 Protrusion eye
 Swelling eye or conjunctiva
 Horner syndrome
Carotid Bruit
 56% sensitivity and 91% specificity for
detection of a 70-99% carotid stenosis when
compared with color duplex ultrasound
 Implication: Maybe this is a test we need to
do more often when the index of suspicion is
raised?

Magyar MT, et al. Carotid artery auscultation:


Anachronism or useful screening procedure? Neurol
Res 2002;24:705-708
Cranial Nerve Palsies
 Relevant to the physical examination are the
cranial nerve palsies that may occur with
cervical artery dissection
 Dissection of the ICA mainly causes CN IX-
XII dysfunction with the hypoglossal nerve
initially affected and then the other three
nerves; eventually all cranial nerves except
the olfactory can be affected
 Cranial nerve palsies are part of the
ischaemic presentation of a vertebral artery
dissection
Cranial Nerve Palsies
 Large study of hospitalized patients
with CAD
 Only 7% had cranial nerve palsies

Debette S, Leys D. Cervical artery dissections: Predisposing factors, diagnosis, and


outcome. Lancet Neurol 2009;8:668-678.
Cranial Nerve Palsies

Cranial nerve Test L/R


I. Olfactory Identify different odors + -
II. Optic Test visual fields (Confrontation method) + -
III. Oculomotor Upward, downward, and medial gaze + -
IV. Trochlear Downward and lateral gaze + -
V. Trigeminal Corneal reflex, face sensation, clench teeth + -
VI. Abducens Lateral gaze + -
VII. Facial Close eyes tight, smile, whistle, puff cheeks + -
VIII. Vestibulo-cochlear Hear watch ticking, hearing tests, balance tests + -
IX. Glossopharyngeal Gag reflex, ability to swallow + -
X. Vagus Gag reflex, ability to swallow, say “Ahhh” + -
XI. Accessory Resisted shoulder shrug + -
XII. Hypoglossal Tongue protrusion (Observe for deviation) + -
Horner Syndrome
 Four physical signs: miosis, ptosis,
enophthalmos, and anhydrosis
 Miosis or inability to dilate a pupil
 Paralysis of the dilatator pupillae muscle
Horner Syndrome
 Incomplete ptosis or droopy upper eyelid
 Weakness tarsalis superior muscle
 Ptosis can occur due to weakness in the
levator palpebrae, a voluntary muscle
innervated by the oculomotor nerve or as a
result of weakness in the sympathetically
innervated tarsalis superior muscle
 Ptosis can also occur congenitally, and it can
occur as a familial condition, with increasing
age, fatigue, depression, and drowsiness
Horner Syndrome
 Enophthalmus or deeper-seated eye
 Weakness orbitalis muscle
 Anhydrosis or decreased sweating
 Affects ipsilateral head and shoulders
 Syndrome often incomplete
 Especially the enophthalmus and the
anhydrosis are frequently absent
 Miosis is often only noticeable in a dark
environment when the unaffected pupil
dilates and the affected pupil does not
Horner Syndrome
Horner Syndrome
Three possible locations for the lesion:
 The central neuron runs from the
hypothalamus to the ciliospinal center and is
located in the cervical spinal cord (C8-T2)
 This may occur as a result of ischaemic
processes affecting the medulla (i.e.,
vertebrobasilar ischaemia) or as a result of
insult to the spinal cord
Horner Syndrome
 The secondary neurons run from the
ciliospinal center by way of the nerve
roots C8-T2 to the sympathetic ganglia
and through these ganglia to the
superior cervical or stellate ganglion
 This may occur as a result of, e.g.,
syringomyelia or a tumor of the apex of
the lung
Horner Syndrome
 The tertiary neuron runs from the stellate
ganglion to the dilatator pupillae and the
vascular supply to the iris
 This may occur due to carotid ischaemia
 Clinical implications?
 Note: A congenital form of Horner’s syndrome
exists and can be recognized by unequal
coloring of both irises
Thunderclap Headache
Headache: Differential
Diagnostic Options

 Cervicogenic headache
 Tension-type headache
 Migraine headache
Cervicogenic Headache
Pain, referred from a source in the neck and
perceived in one or more regions of the
head and/or face, fulfilling criteria C and D
Clinical, laboratory and/or imaging evidence of
a disorder or lesion within the cervical spine
or soft tissues of the neck known to be, or
generally accepted as, a valid cause of
headache
Cervicogenic Headache
Evidence that the pain can be attributed to the
neck disorder or lesion based on at least
one of the following:
1. Demonstration of clinical signs that
implicate a source of pain in the neck
2. Abolition of headache following diagnostic
blockade of a cervical structure or its nerve
supply using placebo- or other adequate
controls
Pain resolves within 3 months after successful
treatment of the causative disorder or lesion
Referral Pattern Upper
Trapezius Muscle
Referral Pattern Levator
Scapulae Muscle
Referral Pattern
Sternocleidomastoid Muscle
Referral Pattern Temporalis
Muscle
Referral Patterns Splenius Capitis
(Left) and Cervicis (Right) Muscles
Referral Patterns Semispinalis
Cervicis (Left) and Capitis (Right)
Muscles
Tension-Type Headache
 Hypothesized to be related to myofascial
trigger points
 Prolonged nociceptive input may lead to
central sensitization
 Amplification of receptiveness of central pain-
signaling neurons to input from low-threshold
mechanoreceptors
 Clinically characterized by the presence of
hyperalgesia and/or allodynia
Tension-Type Headache
Headache has at least two of the following
characteristics:
1. Bilateral location
2. Pressing/tightening (non-pulsating) quality
3. Mild to moderate intensity
4. Not aggravated by routine physical activity such as
walking or climbing stairs
Both of the following:
1. No more than one of photophobia, phonophobia or
mild nausea
2. Neither moderate or severe nausea nor vomiting
Not attributed to another disorder
Migraine with Aura
 At least 2 attacks fulfilling criteria 2-4
 Aura consisting of at least one of the following, but no
motor weakness:
 1. Fully reversible visual symptoms including
positive features (e.g., flickering lights, spots or lines)
and/or negative features (i.e., loss of vision)
 2. Fully reversible sensory symptoms including
positive features (i.e., pins and needles, peri-oral
paraesthesiae) and/or negative features (i.e.,
numbness)
 3. Fully reversible dysphasic speech disturbance
Migraine with Aura
 At least two of the following:
 1. Homonymous visual symptoms and/or unilateral
sensory symptoms
 2. At least one aura symptom develops gradually
over ≥5 minutes and/or different aura symptoms
occur in succession over ≥5 minutes
 3. Each symptom lasts ≥5 and ≤60 minutes
 Headache fulfilling criteria Migraine without aura
begins during the aura or follows aura within 60
minutes
Not attributed to another disorder
CPR Migraine Headache
Diagnosis
Five questions:
1. Is it a pulsating headache
2. Does it last between 4 and 72 hours
without medication?
3. Is it unilateral?
4. Is there nausea
5. Is the headache disabling (disrupting
daily activities)?
CPR Migraine Headache
Diagnosis
 ≥ 4 questions yes: LR+ 24 (95% CI: 1.5-388)
 3 questions yes: LR+ 3.5 (95% CI: 1.3-9.2)
 1 or 2 questions yes: LR+ 0.41 (95% CI: 0.32-
0.52)
 Mnemonic POUNDing: Pulsating, Duration of
4-72 hours, Unilateral, Nausea, Disabling
 But note similarity to neurological deficits
noted in cervical artery dysfunction!
Relevance thunderclap
headache
In 27 cases of non-CSMT VAD this headache
preceded the neurological symptoms:
 By less than 1 day in < 30% of cases
 By 1-3 days in 15%
 By 1-2 weeks in 30%
 By > 3 weeks in 25%

Terrett AGJ. Vertebrobasilar stroke following spinal manipulation therapy.


In: Murphy R. Conservative Management of Cervical Spine Syndromes
(2000)
Risk Management

 Manipulationor mobilization
 Type of manipulative technique
 Upper versus lower cervical techniques
Mobilization or Manipulation?
 Michaeli (1993): Questionnaire sent to
manipulative physiotherapists in South
Africa
 228,050 procedures
 Only minor adverse effects reported for
manipulation
 29 patients receiving cervical spinal
manipulation reported 52 complications
Mobilization or Manipulation?
 However:
 58 patients receiving spinal mobilization to
the cervical spine reported 129 complications
 One mobilization patient suffered a CVA
 Implication for risk reduction?

Michaeli A. Reported occurrence and nature of complications


following manipulative physiotherapy in South Africa. Aust J
Physiother 1993;39:309-315
Mobilization or Manipulation?
 Survey Irish manual physiotherapists
 Only three major adverse events all
associated with cervical manipulation
 Drop attack, syncope, TIA

Sweeney A, Doody C. Manual therapy for the cervical spine and reported
adverse effects: A survey of Irish manipulative physiotherapists. Man
Ther 2010;15:32-36.
Manipulation: Effect of
Technique?
 Rotation appears to place the greatest stress
on arterial structures, especially in the upper
cervical spine
 However, Haldeman et al (2002): review 64
medicolegal reports
 Strokes noted after any type of manipulation
 Including rotation, extension, side bending,
non-force, and neutral position manipulation

Haldeman S, et al. Stroke, cervical artery dissection, and cervical


spine manipulation therapy. J Neurol 2002;249:1098-1104
Manipulation: Effect of Level?
 Most reported site of VA damage is at
C1-C2
 Includes traumatic and spontaneous
dissections

Mas JL, et al. Extracranial vertebral artery dissections: A review of 13 cases. Stroke
1987;18:1037-1047
Mokri B, et al. Spontaneous dissections of the vertebral arteries. Neurology
1988;38:880-885
Saeed AB, et al. Vertebral artery dissection: Warning symptoms, clinical features,
and prognosis in 26 patients. Can J Neurol Sci 2000;27:292-296.
Manipulation: Effect of Level?
 Cervical manipulation definable event with
evidence of a mechanical effect
 Provided and recorded by third parties unlike
etiologic mechanisms such as shoulder
checking, hair washing, etc.
 “Not to say less recordable mechanical
events are less related to dissection”

Kawchuk GN, et al. The relationship between the spatial distribution of vertebral
artery compromise and exposure to cervical manipulation. J Neurol
2008;255:371-377.
Manipulation: Effect of Level?
 Populations studied
 5-year retrospective review yielding a cohort
of 25 patients with VA dissection not related
to major trauma or CSMT from Foothills
Hospital, Calgary, AB
 26 of 64 cases reported by Haldeman et al
from retrospective case review article
associated with manipulation
 Diagnostic imaging or reports had to be
available to determine location of VA
dissection
Manipulation: Effect of Level?
 V3 segment most commonly dissected
 Prevalence ratio (PR) V3 versus V1
prevalence in CSMT group = 8.46
(95% CI: 3.53-20.24)
 PR V3 versus V1 in non-CSMT group =
4.00 (95% CI: 1.43-11.15)
Manipulation: Effect of Level?
 Note: Higher prevalence irrespective of
exposure to CSMT
 “Demonstrates the impact of everyday
movements and postures [on this
mechanically more vulnerable segment]”
 Age and gender not found to be significant
factors
 But: V3 vulnerability augmented by CSMT
exposure
Manipulation: Effect of Level?
 However, multiple site lesions also
significantly more common in both
groups
 CSMT: PR = 2.67 (95% CI: 1.98-3.58)
 No CSMT: PR = 2.44 (95% CI: 1.81-
3.29)
 Interpretation?
Manipulation: Effect of Level?
 Report of compression at C6
secondary to osteophyte arising
from superior facet C6

Citow JS, Macdonald RL. Posterior decompression of the vertebral


artery narrowed by cervical osteophyte: Case report. Surg
Neurol 1999;51:495-498.
Emergency Procedures: What
if the Unthinkable Happens…?
Onset of symptoms indicated in 138 of 185
cases:
 69%: during CSMT
 3%: within minutes of CSMT
 8.5%: within 1 hour of CSMT
 8.5%: 1-6 hours post-CSMT
 5%: 7-24 hours post-CSMT
 6%: >24 hours post-CSMT
Emergency Procedures: What
if the Unthinkable happens…?
 Do not re-manipulate the patient’s neck
 Observe the patient: Transient signs
and symptoms or cervicogenic
proprioceptive dizziness?
 Refer the patient: rescue and recovery
position, do not give the patient
anything to eat or drink (dysphagia),
note the time, call 911
Conclusion
 Manipulation is but one factor in the
multi-factorial etiology of CAD
 There may be no dangerous techniques
but rather dangerous patients
 Identification of risk factors or signs and
symptoms indicating CAD in progress
clearly pose contraindication to manual
therapy
Any questions?

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