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Cervical Artery Dysfunction

and Manipulation: A Cause-


and-Effect Relationship?

Orthopaedic Speaker Series


Royal Jubilee Hospital
Victoria, BC
April 14th, 2009
Dr. Peter Huijbregts, PT, DPT
Objectives
 Discuss epidemiology of cervical (vertebrobasilar
and internal carotid) artery dysfunction
 Discuss anatomy and physiology relevant to
cervical arterial dysfunction
 Discuss research linking cervical manipulation to
artery dysfunction
 Discuss relevant clinical (differential) diagnosis
Discuss risk management and emergency
procedures with regard to cervical artery
dysfunction
 Note: absence of risk-benefit discussion
Timely?
 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
Clinical Vignette # 1
 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…
Clinical Vignette # 1
 Rotary neck manipulation resulted in
inability to turn head
 That night she kept walking into things at
work
 Another visit to chiropractor next day
Clinical Vignette # 1
 Neck adjustment
 Patient immediately began to cry
 Left eye rolled up, right roamed randomly
 Convulsions
Clinical Vignette # 1
 Turned blue, foaming at the mouth, did not
recognize her mother
 Coma
 Died next day from a traumatic rupture left
vertebral artery
Relevance to Physiotherapy?
With research evidence supporting its efficacy
physiotherapists routinely use cervical
manipulation in patients with:
 Neck pain
 Headache: Cervicogenic, tension-type, migraine
 Dizziness: Cervicogenic

19/20 member organizations IFOMT teach upper


cervical manipulation
Rivett D, Carlesso L. Safe Manipulative Practice in the Cervical Spine (2008)
Do these patients make up a
big portion of our day-to-day
clinical practice?
In other words:

What is the risk a


physiotherapist might
inadvertently cause a stroke
with cervical manipulation?
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 Manual Manipulative Ther
2004; 12: 196-211
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
 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 # 2
 63-year old male
 Hypertensive
 Right cerebral infarct five years earlier
 Four months previously vertebrobasilar
infarct
Clinical Vignette # 2
 PHYSIOTHERAPIST applied cervical
manipulation
 Immediate dizziness post-manipulation
 Over the next few hours dysarthria,
dysphagia, and left-sided paralysis
 Medullary infarct
Relevance to Physiotherapy?

“…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)
Relevance to Physiotherapy?
 Rare strokes?
 Read: Dissection of the vertebral and/or
internal carotid arteries (ICA)
Epidemiology Cervical Artery
Dissection
 Cervical artery dissection accounts for
approximately 20% of all strokes in young versus
2.5% in older patients
 Incidence general population: 2.6 per 100,000
 Note the low incidence!

Graziano DL, Nitsch W, Huijbregts PA. Positive cervical artery testing in a patient
with chronic whiplash syndrome. J Manual Manipulative Ther 2007;15:E45-
E63
Manipulation, Dissection, and
Stroke?

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
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)
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
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
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
Evidence Linking Manipulation
to Stroke
 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
Evidence Linking Manipulation
to Stroke
 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
Evidence Linking Manipulation
to Stroke?
 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
Evidence Linking Manipulation
to Stroke?
 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)
Evidence Linking Manipulation
to Stroke?
 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)
Evidence Linking Manipulation
to Stroke?
“… [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.
First Relevant Question

How do we identify patients at risk


for cervical artery dysfunction?
Second Relevant Question

How do we identify patients with cervical


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

 Major presenting 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)
What about Risk Factors?
Atherosclerosis Direct vessel trauma
Hypertension Autosomal polycystic kidney
Hypercholesterolaemia 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?
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 ration in chiropractic
office: 40.7-59.3% or 44.8-55.2%?
Arteriopathies
 Marfan syndrome
 Ehlers-Danlos syndrome
 Fibromuscular dysplasia
 Cystic medial necrosis
 Osteogenesis imperfecta
 Alpha-1-antitrypsin deficiency
 Autosomal dominant polycystic kidney disease
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
 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
Cardiovascular Risk Factors
 Hypertension
 Tobacco use
 Hypercholesterolaemia
 Diabetes
 Atherosclerosis
Hypertension
 Frequency of tobacco use, hypertension,
diabetes, and hypercholesterolaemia
 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

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?
 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 # 3
 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)
Systematic Review of Risk
Factors CAD
 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)
 Most studies major sources of bias

Rubinstein SM, et al. A systematic review of the risk factors for cervical
artery dissection. Stroke 2005;36:1575-1580
So Where Does This Leave
Us?
 Presenting complaint provides no relevant
information
 Clinically relevant risk factors: Previous
medical history of treatment with cervical
manual therapy interventions, hypertension,
previous infection, and migraine headache
 Questionable risk factors: Atherosclerosis,
thyroid disease, and arteriopathies…
Physical Examination?
De Kleyn-Nieuwenhuyse Test
 In 1927, 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?
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?
 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?

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

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
Diagnosis

 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
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

 Manipulation or 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
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
 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
I would like to thank Deborah
Cracknell for inviting me to do
this presentation for you all
this afternoon.

Any questions?

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