Int J Clin Pract. 2013 (Sep); 67 (9): 825–833 ~ FULL TEXT
Peter J. Tuchin, GradDipChiro, DipOHS, PhD
Department of Chiropractic,
Faculty of Science,
Sydney, NSW, Australia.
Serious complications following spinal manipulative therapy
(SMT) of the cervical spine, including stroke, are relatively
rare. Estimates vary between 1:400,000 cervical
spine manipulations and 1:5.6 million. [1, 2] However,
there is controversy on how frequent events such as stroke
are, and whether there is a causal relationship with SMT.
Even more controversy can be found specifically relating
to chiropractic SMT and whether this has a higher risk
than other types of SMT. Both sides of the debate appear
to have extremists with a biased perspective. Previous articles
have not provided a comprehensive review of the evidence
for and against chiropractic. A recent article noted
several weaknesses or inconsistencies in some articles discussing
chiropractic treatment and stroke.  A critical
review of a paper previously published in the International
Journal of Clinical Practice has been conducted to provide
evidence for the alternative theories regarding the safety of
chiropractic SMT and whether there is a causal relationship
with the stroke.  A critical review of the current
literature will also help to assess any misconceptions or
distortion of the results of studies on chiropractic and
From the FULL TEXT Article:
Ischaemic stroke is a significant cause of morbidity
and death, even in younger age groups such as
under 45 years of age.  Some studies have estimated
an annual occurrence of 10.8/100,000 (0.01%
of the population), with vertebral artery dissection
(VAD) and carotid artery dissection (CAD) occurring
in 1/100,000–2.6/100,000 cases, respectively. 
The most frequently reported risk factors are dyslipidaemia
(60%), smoking (44%) and hypertension
(39%), but 33% had an undetermined aetiology. In
addition to dyslipidaemia, smoking and hypertension,
other reported risk factors include obesity,
cardiovascular disease, history of transient ischemic
attack (TIA), diabetes mellitus (type 1 & 2), atrial
fibrillation, hormone replacement therapy, migraine,
heavy drinking, recent or acute infection, recent
heavy drinking, oral contraceptive pill (OCP),
obstructive sleep apnoea, illicit drug use, lupus anticoagulant,
active malignancy, gravidity or postpartum
period and other genetic factors. [7–15] VAD
has been reported to occur after hyperextension
movements of the cervical spine
(such as archery or ceiling painting),
minor traumas or falls, and
Some studies have suggested that
chiropractic causes stroke, however,
there are often plausible alternate
explanations which have been overlooked
(Table 1 gives alternative
explanations for cases described by
Ernst in 2010). For example, Johnson
et al. reported a case of VAD
which occurred 15 days after a chiropractic
treatment.  A 44–year-old
man developed acute neck pain
after his first cricket match in over
20 years (whilst bowling). He consulted
a chiropractor who gave SMT
which provided some relief from the
pain. Five days after this treatment,
he developed vertigo which lasted
4 days and then resolved spontaneously.
He suffered another episode
of vertigo (including headache,
vomiting, tinnitus, double vision
and arm weakness) and returned to
the chiropractor who referred him
immediately to the hospital. He was
admitted to hospital, but died some 15 days after the
SMT and 18 days after the cricket game which triggered
the acute neck pain. No details were given on
standard risk factors for dissection or stroke, but
widespread vertebral changes were noted. Obviously,
in a 15–day interval, many other events could have
occurred leading to the VAD.
Another example, reported by Stevinson et al. was
a case of subdural haematoma (SDH) after a chiropractic
treatment.  This was reported in a paper
which was a survey of neurologists recalling potential
cases of VAD over a 12–month period. This article
had three lines of text describing the clinical background
of this case, which makes it more likely that
an important clinical fact was overlooked (such as
trauma causing the SDH). It is also impossible to
imagine what mechanism could cause a SDH after a
neck manipulation. In both these cases, there are
clearly numerous other potential causes of the VAD
or the adverse event (SDH).
A man aged 46 was diagnosed with acute subdural haematoma occurring immediately after chiropractic treatment. A burrhole was required. There was no neurological deficit at one month or six month follow-up.
Some cases of VAD have also occurred prior to the patient receiving the chiropractic SMT they were seeking. [22, 23] This article will assess if a causal relationship exists between chiropractic and stroke.
Testing a causal relationship usually requires an agreement with a number of specific criteria, which
were first described by Hill. 
The nine criteria are:
- Biological gradient or dose–response relationship
- Other explanations
- Experimental confirmation
The first criterion in Hill’s paper relates to the
strength of any association. Hill gives the example of
Percival Pott who identified scrotal cancer in chimney
sweeps as 200 times higher to workers not
exposed to chimney soot.
A study by Smith et al. used a nested case–control
design, to review all those patients under age 60 with
cervical arterial dissection (n = 151) and ischaemic
stroke or TIA between 1995 and 2000 at two academic
stroke centres.  They compared results of
the cases with VAD/TIA (n = 7) to controls (n = 3).
However, the number of cases that Smith assessed is
a number too small to not be questioned. In addition,
the time period was up to 30 days after the
SMT which is inconsistent with all other studies.
Furthermore, Smith included cases of TIA which is
also inconsistent with all the other studies (TIA is a
benign condition and often asymptomatic in
patients). If only two cases from the VAD/TIA group
are altered because of the 30–day measure or because
of TIA, then the results are not statistically significant.
(The Johnson paper discussed above highlights
the possibility of other factors causing the VAD in
the 30–day period.)
A review of the methodology of the Smith study
revealed many other flaws and the results section
demonstrated that the two groups were significantly
different in many areas.  For example, 10 cases
were excluded (i.e. more than cases included)
because of iatrogenic cause of the VAD. A total of 21
cases were excluded from the dissection group, which
is three times the size of the included cases.
An important point of Smith’s paper ‘... patients
with dissection were more likely ... to have had neck
or head pain preceding stroke or TIA’ confirms the
2008 Cassidy study (discussed later), which concluded
that patients present to either a chiropractor
or GP with neck pain because of their stroke already
being present.  In the Smith study, 76% of people
with VAD had neck pain prior to the stroke vs.
40% of the controls (p < 0.001) and 39% of the control
group had previously had SMT without any
VAD. A total of seven people had a VAD or TIA
within 30 days of SMT over a 5–year period at two
academic stroke units from a total of 1,107 patients.
There was no discussion about what activities or
other treatment these seven patients had in that 30–day period.
Smith’s paper states that ‘Information about location,
duration and quality of neck pain and head pain
was incomplete due to limited patient recall’. But they
also concluded ‘... that spinal manipulation is independently
associated with vertebral arterial dissection,
even after controlling for neck pain’. Also, Smith stated
‘two of the dissection patients had VAD within
seconds of receiving SMT’. This would suggest that
the VAD must have been present before the SMT, as it
seems impossible for a thrombus to instantly form,
dislodge, travel to the cerebral cortex to cause a stroke
‘... within seconds of receiving SMT’.
Saaed et al. reported that headache and/or neck
pain was the prominent feature in 88% of patients in
their study, and was a warning sign in 53%, preceding
onset of stroke by up to 14 days.  This study
identified three patients in a 10–year period who
were reported to have chiropractic SMT that triggered
the stroke. However, there is no evidence to
show that these patients did not have the VAD prior
to any SMT because of some other more common
cause (e.g. minor neck trauma).
Rothwell et al. studied hospitalization records to identify vertebrobasilar accidents (VBAs) in Ont., Canada, during 1993–1998.  They matched 582 cases for age and sex to four controls from the Ontario population with no history of stroke at the event date. Public health insurance billing records were used to document the use of chiropractic services before the event date. The Rothwell study compared results of cases with VAD (n = 5, i.e. 1% of cases) to controls (n = 4), which are again numbers too small to be reliable. Using the Rothwell data, one could argue that the control group for the < 45 years were nine times as likely to have a chiropractic treatment in the previous month than the VAD group. However, the major weakness with the Rothwell study was the lack of any clinical data associated with the VAD cases. That is, what were the events/symptoms that lead the patient to consult the chiropractor.
Some authors have expressed concerns of ‘several hundred cases of vascular accidents after spinal manipulation’ as evidence. However, many of these cases of SMT were not delivered by a qualified chiropractor, and most did not describe any well documented risk factors for stroke.
For example, Hufnagel et al.:
... analyzed the clinical course and neuroradiological findings of ten patients aged 27–46 years, with ischemic stroke secondary to vertebral artery dissection (VAD; n = 8) or internal carotid artery dissection
(CAD; n = 2), all following chiropractic manipulation of the cervical spine. 
However, none of the ten cases above described by Hufnagel, had a chiropractor perform the SMT. That is, seven cases had the SMT from an orthopaedic specialist and three from a physiotherapist.
Further examples include Chen et al. who reported a 72–year-old man who developed a haematoma in the ligamentum flavum.  The paper states ‘... following traditional massage therapy’. Also, Morandi et al. reported a 49–year-old female who developed a caudal spinal cord ischaemia after a lumbar SMT.  The paper states ‘Three weeks into the episode, a physician performed lumbar vertebral manipulation’. Both these papers use chiropractic as a key word and as a consequence, falsely increase the perceived association of chiropractic with stroke.
Other cases of the stroke have been reported as spontaneous or related to trivial trauma, such as sport, turning the neck whilst driving or reversing, yoga and coughing. These events may have preceded the chiropractic treatment or have occurred at a similar time to the chiropractic treatment, but are often unreported. In fact, the event that triggered the stroke may have also produced neck pain, for which the patients sought treatment from a chiropractor. Marx et al. evaluated cases of arterial dissection in Germany from 1996 to 2005.  In the seven cases of ICAD and the nine cases of VAD, a causal link to SMT could not be made. In addition, in five of the seven cases of ICAD and seven of the nine cases of VAD, there was a clear evidence that the dissection was present prior to the SMT.
As a consequence, the strength of any association for stroke with chiropractic SMT appears negligible.
Hill’s second criterion relates to consistency. An
association is consistent if results are confirmed in
different settings and with different types of investigations.
The association between SMT and stroke is
controversial, with some studies (usually case
reports) reporting a relationship, but other studies
(such as case–controlled studies) reporting only an
Cassidy et al. assessed cases of VBA strokes admitted to Ontario hospitals from 1 April 1993 to 31 March 2002.  Four controls were age and gender matched to each case. Case and control exposures to chiropractors and PCPs were determined from health billing records in the year before the stroke date. In the case-crossover analysis, cases acted as their own controls. Their study found 818 VBA strokes hospitalised in a population of more than 100 million person-years. In those aged < 45 years, cases were about three times more likely to see a chiropractor or a PCP before their stroke than controls. Results were similar in the case–control and case-crossover analyses. There was no increased association between chiropractic visits and VBA stroke in those older than 45 years. Positive associations were found between PCP visits and VBA stroke in all the age groups. Practitioner visits billed for headache and neck complaints were highly associated with subsequent VBA stroke.
Cassidy concluded VBA stroke is a very rare event in the population. The increased risks of VBA stroke associated with chiropractic and PCP visits is likely because of patients with headache and neck pain from VBA dissection seeking care before their stroke. The study found no evidence of excess risk of VBA stroke associated with chiropractic care compared with primary care.
Some studies have reported ‘trivial trauma’ of the neck, which included sports activities and SMT, could precipitate stroke.  Haldeman et al. concluded stroke is a potential consequence of any neck movement.  Therefore, there appears to be consistency with neck movement causing stroke, but not with SMT.
Some authors have also expressed opinions about a
dose–response relationship with chiropractic and
stroke. For example, Ernst reported that a dose–response relationship can be detected because of
more chiropractors causing vascular accidents than
osteopaths.  Ernst believes this is because of osteopaths
tendency to prefer soft tissue techniques
(mobilisation) and employ SMT techniques less frequently.
If this had been reported in any published
studies, a dose–response relationship comparison
may be possible, but there is no evidence to support
this theory. Also, one could argue that it is a comparison
of the safety of different techniques and not
dose–response. For example, one would also need to
consider the relative size of each profession and the
utilization rates of the public for each profession.
Ernst highlighted in his 2010 paper ‘Vascular accidents
are associated much more commonly with
chiropractors than with osteopaths’.  However,
Table 2 demonstrates that most cases are not a chiropractor
delivering the SMT (see Table 2). That is,
from the 17 references that Ernst cited, 5 were probably
qualified chiropractors, 5 were stated as not chiropractors,
6 were from countries with no legislation for
chiropractic, and one the paper was not attainable.
Other studies have also noted patients can have
had many sessions of chiropractic SMT without
experiencing CVA, and then suddenly a VAD occurs.  A 26–year-old woman had experienced a mild
headache, cough and low-grade fever for 4 days and
was given antibiotics. The patient had received over
20–chiropractic manipulations over the previous 2
years and was taking oral contraceptives. The symptoms
of bilateral stroke began 36 h after the chiropractic
SMT. This suggests that a new situation
occurred which caused the VAD and not as a consequence
There is also a previously reported situation,
where chiropractic is reported as the profession of
the person giving the SMT, when this has been
incorrectly documented.  In another example,
Reuter describes 36 cases of VAD after chiropractic
SMT, where 18 (50%) the SMT was delivered by an
orthopaedic surgeon, 5 (14%) by a physiotherapist,
2 (6%) by a GP, 1 (3%) by a neurologist, 1 (3%)
by a homoeopath and 3 (9%) by an unknown person.  This leaves four cases (11%) where the
SMT was delivered by a chiropractor (i.e. 89% the
SMT was delivered by a non-chiropractor). The
cases were collected by a retrospective survey over a
3–year period. Importantly, there was no table
describing risk factors for any of the patients,
including the chiropractic patients, and this article
was also from a country where chiropractic practice
is not regulated (i.e. there are no standards for education). 
Therefore, a dose–response relationship does not appear to exist.
Temporality states that the exposure must always
precede the outcome. Often with the cases of chiropractic
and stroke, a clear time-line between the
onset of initial symptoms and the stroke has not
been established. For example, Jeret described a case
of a 51–year-old man who had chiropractic manipulation
of his neck and presented to the hospital
5 days later.  The patient was reported to have
had intermittent slurred speech, left facial droop and
mild left hand weakness for 2–3 days. There was no
description for the onset of the presenting symptom
to the chiropractor and no description of any known
risk factors for CVA previously reported. Interestingly,
the initial symptoms were all related to a left
side infarct and 2 weeks after admission to a hospital,
the patient had a right sided infarct. It is plausible
this man had stroke because of risk factors other
In addition, other events which immediately preceded
the stroke have often not been documented in
case reports. For example, Jeret described a second
case of a 64–year-old man who had chiropractic
manipulation from his daughter.
A 64–year-old man presented to the hospital 4 days after ‘gentle’ manipulation of his neck by his daughter,
a chiropractor. He awoke at 2 a.m. feeling that his right arm was strange and that, in fact, it was
not a part of his body.
In this case, other events which immediately preceded
the stroke have not been documented. It is
also plausible this man had stroke because of risk
factors other than chiropractic. For example, during
sleep his neck may have been in an extended and
rotated posture for a prolonged time, which then
caused the compromise to the blood flow in the vertebral
Therefore, a clear temporal relationship of chiropractic
and stroke is not established.
Some authors have postulated that hyperextension
and/or rotation of the upper spine, beyond the physiological
range puts a strain on the VA which, in predisposed
individuals, may result in an intimal
tearing. However, if this were the case then many
more CVA’s would be reported as neck SMT is performed
millions of times each week. Also, other
studies have reported that the force exerted on the
VA during SMT is not enough to produce any tearing
of the VA.  Herzog et al. concluded that VA
strains obtained during SMT are significantly smaller
than those obtained during diagnostic and range of
motion testing, and were much smaller than failure
strains. They concluded that cervical SMT performed
by trained clinicians did not appear to place undue
strain on VA, and thus does not seem to be a factor
in vertebro-basilar injuries.
Mitchell conducted a study on 60 male subjects
and 60 female subjects (240 VAs), using transcranial
Doppler sonography to measure intracranial VA
blood flow, with the cervical spine in neutral and
then rotated maximally to the left and later to the
right.  There was a significant decrease
(p = 0.001) in intracranial VA blood flow following
cervical spine rotation, irrespective of side, but
greater on the contralateral side, in the total sample
and in male subjects. Female subjects had a significantly
higher blood flow than male subjects, and
although they showed a significant decrease in contralateral
rotation, there was no significant difference
in blood flow on the ipsilateral side. The results of
this study suggest that full neck movement may
affect VA blood flow, but this appears less than SMT.  Modern chiropractic SMT procedures do not
require full cervical spine rotation or extension.
Many case reports of stroke after SMT do not discuss
other plausible reasons for the VAD to have had
occurred other than just SMT. Sedat et al. described
a case of dissection of the postero-inferior cerebellar
artery (PICA) after cervical manipulation.  A 42–year-old woman had a cerebellar syndrome related to
an infarct in the area supplied by the PICA, confirmed
by computed tomography (CT) of the brain.
A cervical extradural origin of PICA and a dissection
of it was detected in the CT scan. Anatomical variations
of the vertebral arteries and their branches are
not infrequent and may be another plausible reason
for stroke unrelated to the SMT. The author
acknowledged the anatomical variance had played a
vital role in the patient’s complications to manipulative
As discussed above, arterial dissection can occur
spontaneously, therefore, an alternative explanation
to SMT causing the VAD usually does exist.
For example, a case of a 26–year-old woman who
received ‘chiropractic SMT’ is described by Soper
et al.  The patient had received numerous neck
manipulations for neck stiffness which had been
present for 1 month. In one treatment, she received
an injection of lidocaine and betamethasone, which
was followed by a forcible, bilateral rotation of her
neck (given by a medical practitioner). She developed
pronounced neurological signs and was taken
to the hospital where CT scans of the neck identified
bilateral VAD. A subsequent MRA revealed that the
VAD dissection extended from T1 to C2 on the left
and complete occlusion on the right, with a small
traumatic pseudoaneurysm present.
Galtes et al. presented the case of a 40–year-old
woman cyclist who was struck by a car (while wearing
a helmet), and was neurologically near normal
at presentation to the Emergency Department. 
She was again presented 48 h later with acute right
hemiparesis, decreasing level of consciousness and
unsteadiness. CT revealed massive cerebellar infarction,
but CT angiography was normal. The patient
died in coma 7 days after injury and autopsy
revealed bilateral edematous cerebellar infarction
and bilateral VAD. They concluded the possible
influence of trauma may be further underestimated
if longer intervals between vessel dissection and
Sepelyak et al. described three cases of paediatric
arterial ischaemic stroke which occurred after trivial
head or neck trauma sustained during a sports activity.  One case involved a 10–year-old boy developing
hemiparesis after a collision during a soccer
match. Another case involved a 12–year-old boy
developing parathesias and headaches after a lacrosse
match. The third case involved a 7–year-old boy
developing numbness 3 h after a karate practice. All
recovered to have no or minimal residual deficits
Had any of the previously discussed patients presented
to a chiropractor, then this may have
appeared that chiropractic SMT caused their condition.
In addition, many other case reports describe
patients who have had multiple SMT sessions, and
then suddenly they have an adverse reaction. [60, 63–67] It appears apparent that something had changed
in the patient immediately before the last SMT which
caused a (transient) arteriopathy, allowing a VAD to
occur. Therefore, there are alternative explanations
for VAD other than just SMT.
As the VA becomes the basilar artery entering the
base of the skull, it bends sharply from a vertical to
a horizontal path. This should be the site where any
VAD because of SMT would occur. But many cases
of VAD after SMT have occurred at most sites all
along the VA, including intracranial.  This
appears to support the theory that the VA has been
weakened by some other factor or event which preceded
Saeed et al. conducted a retrospective analysis of
hospital records in a tertiary academic centre for the
period 1989–1999 and identified 26 patients with
VAD (13 men and 13 women).  They reported
possible precipitating factors were identified in 14
patients (53%), with sporting activity (golf, soccer,
running and baseball) and chiropractic manipulations
being the most common (15% and 11%,
respectively). However, seven patients (26%) had
minor neck trauma, which was reported to be up to
3 years before the VAD. In addition, headache and/or neck pain was the prominent feature in 88% of
patients and was a warning sign in 53%, preceding
onset of stroke by up to 14 days. This supports the
premise that patients may present to a chiropractor
with neck pain after a trivial event that caused the
VAD and not the SMT.
There are numerous possible causes for arterial dissections
other than neck manipulations. [10, 12, 18, 69, 70] Vascular accidents have reported
after many types of neck movement, neck injury or
sporting activities. Millions of SMT procedures are
given every year, yet very few cases of VAD after
SMT are reported.  This should also be viewed in
the context that 1/100,000 of population have VAD
each year. Therefore, when chiropractors see 1 million
patients in a year, 10 will have a VAD, but this
does not mean that the SMT caused the VAD.
In cases were there has been a VAD or stroke,
other causes are overlooked. For example, Albuquerque
et al. reviewed 13 cases of artery dissection and
chiropractic SMT, and concluded ‘... a significant
percentage (31%, 4/13) of patients were left permanently
disabled or died as a result of their arterial
However, if this article is critically reviewed, we
find the case where a person died was a 73–year-old
female, with no other clinical details given. For
example, did she have any history of dyslipidaemia,
smoking and hypertension, obesity, cardiovascular
disease, history of TIA, diabetes mellitus (type 1 &
2), atrial fibrillation, hormone replacement therapy,
migraine, heavy drinking, recent or acute infection,
recent heavy drinking, OCP, obstructive sleep
apnoea, illicit drug use, lupus anticoagulant, active
malignancy, gravidity or postpartum period and
other genetic factors. Stroke in a geriatric patient is a
very common occurrence, especially if any of the
above risk factors were present.
In addition, only one of the 13 cases had the
VAD at the V3 segment (where it wraps around the
C1 vertebrae) as a single site. One could argue that
if SMT was the cause of the VAD, then why are
not more found at the V3 segment. Nine of the 13
cases had multiple sites for VAD and ICAD, with
some even intracranial or bilateral. Also, four of the
13 had timelines of more than 7 days for the stroke
to occur after the chiropractic SMT. The paper
reported that four patients were left permanently
disabled or died as a result of their arterial injuries;
however, only one case has any clinical information.
This case was a 30–year-old male who had dissections
of V3, V4 and the basilar artery. It was
reported he had significant complications after
surgery to repair the dissections (thrombosis of
the stents) which possibly caused the permanent
Therefore, VAD specifically because of chiropractic is not established.
Coherence describes the need for any causal association
to be compatible with the existing theory and
knowledge. It had been previously accepted that
manipulation can cause a vascular accident and thus
did not contradict an accepted theory. As previously
discussed, this was often based on poorly written
case studies.  However, considering the bulk of
new arguments, the criterion of coherence does not
seem to be fulfilled.
Stevinson et al. conducted a survey of neurologists
to assess VAD after SMT.  Stevinson
acknowledged that their study had many weaknesses
including recall bias. In addition, they acknowledge
that they have very limited case details regarding
previous neurological symptoms, who delivered the
SMT, and why the patient received SMT. ‘Only
rarely was it possible to check the patient file or
the case notes’. Yet from this, other authors state
that the number of cases on VAD after chiropractic
is grossly underestimated.  It is just as possible
that the number of cases on VAD after chiropractic
is overestimated as the neurologists have overlooked
other possible causes of the VAD and assumed it
was only because of SMT. In addition, one of the
few cases discussed highlights the limited case information
and also notes the SMT was from an osteopath. 
An alternative theory could be that a situation
arose where a patient had a VAD commencing,
because of other factors such as minor trauma,
sports, sustained neck positions or excessive neck
movements. This was predisposed by an arteriopathy
(possibly transient) because of hypertension, hyperlipidaemia,
hyperhomocysteinaemia, recent infection,
smoking, diabetes, migraine, or other combinations
of factors. Once the VAD had commenced, the
patient would complain of neck pain or headache,
for which they then sought treatment, possibly from
a chiropractor, or another healthcare practitioner. If
this healthcare practitioner did not take a thorough
clinical history, then they may overlook these above
factors and perform an SMT when it may have been
contra-indicated. Therefore, an existing VAD is exacerbated,
the thrombus is dislodged and creates the stroke.
There is lack of compelling evidence that SMT is
causally associated with stroke. Physical triggers,
including SMT, can serve as plausible final link
between the underlying disease and stroke (for
instance, in case of arterial dissection with existing
connective tissue weakness). It appears few of Hill’s
criteria for causality appear connected with VAD and
chiropractic. There may be some links or association
with SMT and VAD in untrained practitioners, but
this has not been established with chiropractors. The
quality of evidence suggesting causation between chiropractic
and VAD is mostly weak. Therefore, causality
between chiropractic and vascular accidents has
not been determined.
It is possible that healthcare practitioners are not taking a thorough history to determine the cause of the VAD after SMT. Healthcare practitioners are probably missing many clinical facts, because they now only record the patient having SMT. They should enquire about other possible causes or circumstances for VAD.
This may include minor neck trauma, a change in chronic neck pain or headache, recent infection or other predisposing lifestyle factors such as smoking, hyperlipidaemia, hypertension, and hyperhomocysteinaemia.
Therefore, it is important that healthcare practitioners take a thorough clinical history to determine the cause of VAD.
Systematic prospective studies are needed to assess the safety of cervical spine SMT with regards to cerebrovascular events. Such studies should also account for the education of the practitioner.
Lee KP, Carlini WG, McCormick GF, Albers GW.
Neurological complications following chiropractic manipulation: a survey of California neurologists.
Neurology 1995; 45: 1213–5.
Haldeman S, Carey P, Townsend M, Papadopoulos C.
Arterial Dissections Following Cervical Manipulation: The Chiropractic Experience
Canadian Medical Association Journal (CMAJ) 2001 2001 (Oct 2); 165: 905–906
A Replication of the (Ernst) Study
“Adverse Effects of Spinal Manipulation:
A Systematic Review”
Chiropractic & Manual Therapies 2012 (Sep 21); 20: 30.
Vascular accidents after neck manipulation: cause or coincidence?
Int J Clin Pract 2010; 64: 673–7.
Yaghi S, Maalouf N, Keyrouz SG.
Cervical artery dissection: risk factors, treatment, and outcome; a 5-year experience from a tertiary care centre.
Int J Neurosci 2012; 122: 40–4.
Lleva P, Ahluwalia BS, Marks S et al.
Traumatic and spontaneous carotid and vertebral artery dissection in a level 1 trauma centre.
J Clin Neurosci 2012; 19: 1112–4.
Micheli S, Paciaroni M, Corea F et al.
Cervical artery dissection: emerging risk factors.
Open Neurol J 2010; 4: 50–5.
Divjak I, Slankamenac P, Jovicevic M et al.
Diagnosis and outcome of cervical artery dissection.
Med Pregl 2011; 64: 392–6.
Putaala J, Curtze S, Hiltunen S et al.
Causes of death and predictors of 5-year mortality in young adults after first-ever ischaemic stroke: the Helsinki Young Stroke Registry.
Stroke 2009; 40: 2698–703.
Putaala J, Metso AJ, Metso TM et al.
Analysis of 1008 consecutive patients aged 15 to 49 with first-ever ischaemic stroke: the Helsinki young stroke registry.
Stroke 2009; 40: 1195–203.
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: 1179–84.
Chandra A, Suliman A, Angle N.
Spontaneous dissection of the carotid and vertebral arteries: the 10-year UCSD experience.
Ann Vasc Surg 2007; 21: 178–85.
Debette S, Leys D.
Cervical-artery dissections: predisposing factors, diagnosis, and outcome.
Lancet Neurol 2009; 8: 668–78.
Brandt T, Hausser I, Orberk E et al.
Ultrastructural connective tissue abnormalities in patients with spontaneous cervicocerebral artery dissections.
Ann Neurol 1998; 44: 281–5.
Grau AJ, Brandt T, Buggle F et al.
Association of cervical artery dissection with recent infection.
Arch Neurol 1999; 56: 851–6.
Vertebral Artery Dissection Causing Stroke in Sport
J Clin Neurosci 2000 (Jul); 7 (4): 298–300
Rubinstein S, Cote P.
Mild mechanical traumas are possible risk factors for cervical artery dissection.
Cerebrovasc Dis 2007; 24: 319.
Nyberg J, Olsson T, Malm J.
Carotid and vertebral artery dissection a common cause of stroke among younger persons. Minor trauma a precipitating factor in more than fifty percent according to a retrospective study.
Lakartidningen 2007; 104: 24–8.
Dittrich R, Rohsbach D, Heidbreder A et al.
Mild mechanical traumas are possible risk factors for cervical artery dissection.
Cerebrovasc Dis 2007; 23: 275–81.
Johnson CP, Lawler W, Burns J.
Use of histomorphometry in the assessment of fatal vertebral artery dissection.
J Clin Pathol 1993; 46: 1000–3.
Stevinson C, Honan W, Cooke B, Ernst E.
Neurological complications of cervical spine manipulation.
J R Soc Med 2001; 94: 107–10.
Kier AL, McCarthy PW.
Cerebrovascular Accident Without Chiropractic Manipulation: A Case Report
J Manipulative Physiol Ther 2006 (May); 29 (4): 330–335
How really dangerous is spinal manipulation?
Lakartidningen 2000; 97: 9–61.
The environment and disease: association or causation.
Proc Royal Soc Med 1965; 58: 294–300.
Smith WS, Johnston SC, Skalabrin EJ et al.
Spinal manipulative therapy is an independent risk factor for vertebral artery dissection.
Neurology 2003; 60: 1424–8.
Flaws in a recent vertebral artery dissection study by Smith et al..
J Manipulative Physiol Ther 2004; 27: 526–32.
Cassidy JD, Boyle E, Cote P, et al.
Risk of Vertebrobasilar Stroke and Chiropractic Care:
Results of a Population-based Case-control
and Case-crossover Study
Spine (Phila Pa 1976) 2008 (Feb 15); 33 (4 Suppl): S176–183
Bin Saeed A, Shuaib A, Al Sulaiti G, Emery D.
Vertebral Artery Dissection: Warning Symptoms, Clinical Features and Prognosis in 26 Patients
Canadian Journal of Neurological Sciences 2000 (Nov); 27 (4): 292–296
Rothwell DM, Bondy SJ, Williams JI.
Chiropractic Manipulation and Stroke:
A Population-based Case-control Study
Stroke 2001 (May); 32 (5): 1054-1060
Hufnagel A, Hammers A, Schonle PW et al.
Stroke following chiropractic manipulation of the cervical spine.
J Neurol 1999; 246: 683–8.
Chen H-C, Hsu P-W, Lin C-Y, Tzaan W-C.
Symptomatic hematoma of cervical ligamentum flavum: case report.
Spine 2005; 30: E489–91.
Morandi X, Riffaud L, Houedakor J et al.
Caudal spinal cord ischemia after lumbar vertebral manipulation.
Joint Bone Spine 2004; 71: 334–7.
Lipper MH, Goldstein JH, Do HM.
Brown-Sequard syndrome of the cervical spinal cord after chiropractic manipulation.
AJNR Am J Neuroradiol 1998; 19: 1349–52.
MRI confirmed cervical cord injury caused by spinal manipulation in a Chinese patient.
Spinal Cord 2002; 40: 196–9.
Tseng S-H, Chen Y, Lin S-M, Wang C-H.
Cervical epidural hematoma after spinal manipulation therapy: case report.
J Trauma 2002; 52: 585–6.
Segal DH, Lidov MW, Camins MB.
Cervical epidural hematoma after chiropractic manipulation in a healthy young woman: case report.
Neurosurgery 1996; 39: 1043–5.
Tolge C, Iyer V, McConnell J.
Phrenic nerve palsy accompanying chiropractic manipulation of the neck.
South Med J 1993; 86: 688–90.
Schram D, Vosik W.
Diaphragmatic paralysis following cervical chiropractic manipulation: case report and review.
CHEST 2001; 119: 638–40.
Padua L, Padua R, LoMonaco M, Tonali PA.
Radiculomedullary complications of cervical spinal manipulation.
Spinal Cord 1996; 34: 488–92.
Schmitz A, Lutterbey G, von Engelhardt L et al.
Pathological cervical fracture after spinal manipulation in a pregnant patient.
J Manipulative Physiol Ther 2005; 28: 633–6.
Tome F, Barriga A, Espejo L.
Multiple disc herniation after chiropractic manipulation.
Rev Med Univ Navarra 2004; 48: 39–41.
Marx P, Puschmann H, Haferkamp G et al.
Manipulative treatment of the cervical spine and stroke.
Fortschr Neurol Psychiatr 2009; 77: 83–90.
Haldeman S, Kohlbeck FJ, McGregor M.
Stroke, Cerebral Artery Dissection, and
Cervical Spine Manipulation Therapy
J Neurology 2002 (Jul); 249 (8): 1098–1104
Vascular accidents after chiropractic spinal manipulation: myth or reality?
Perfusion 2010; 23: 73–4.
Donzis PB, Factor JS.
Visual field loss resulting from cervical chiropractic manipulation.
Am J Ophthalmol 1997; 123: 851–2.
Jones MR, Waggoner R, Hoyt WF.
Cerebral polyopia with extrastriate quadrantanopia: report of a case with magnetic resonance documentation of
V2/V3 cortical infarction.
J Neuroophthalmol 1999; 19: 1–6.
Hillier CE, Gross ML.
Sudden onset vomiting and vertigo following chiropractic neck manipulation.
Postgrad Med J 1998; 74: 567–8.
Garner LP, Case WF.
Chiropractic manipulation and atherosclerotic emboli to the eye.
Am Fam Physician 1996; 53, , 90–1.
Vibert D, Rohr-Le Floch J, Gauthier G.
Vertigo as manifestation of vertebral artery dissection after chiropractic neck manipulations.
ORL J Otorhinolaryngol Relat Spec 1993; 55: 140–2.
Yokota J-I, Amakusa Y, Tomita Y, Takahashi S-I.
The medial medullary infarction (Dejerine syndrome) following chiropractic neck manipulation.
No to Shinkei 2003; 55: 121–5.
Jay WM, Shah MI, Schneck MJ.
Bilateral occipitalparietal hemorrhagic infarctions following chiropractic cervical manipulation.
Semin Ophthalmol 2003; 18: 205–9.
Misuse of the Literature by Medical Authors in Discussing Spinal Manipulative Therapy Injury
J Manipulative Physiol Ther 1995 (May); 18 (4): 203–210
Reuter U, Hamling M, Kavuk I et al.
Vertebral Artery Dissections After Chiropractic Neck Manipulation
in Germany Over Three Years
J Neurol 2006; 253: 724–30.
The regulation of chiropractic practice in Europe.
Med Law 2001; 20: 167–75.
More complications of spinal manipulation.
Stroke 2001; 32: 1936–7.
Herzog, W., Leonard, T. R., Symons, B., Tang, C., & Wuest, S.
Vertebral Artery Strains During High-speed,
Low amplitude Cervical Spinal Manipulation
J Electromyography and Kinesiology 2012 (Oct); 22 (5): 740–746
Changes in Vertebral Artery Blood Flow Following
Various Head Positions and Cervical Spine Manipulation
J Manipulative Physiol Ther. 2014 (Jan); 37 (1): 22–31
Symons, B., Leonard, T.R., Herzog, W., 2002.
Internal Forces Sustained by the Vertebral Artery
During Spinal Manipulative Therapy
J Manipulative Physiol Ther 2002 (Oct); 25 (8): 504–510
Sedat J, Dib M, Mahagne MH et al.
Stroke after chiropractic manipulation as a result of extracranial postero-inferior cerebellar artery dissection.
J Manipulative Physiol Ther 2002; 25: 588–90.
Soper JR, Parker GD, Hallinan JM.
Vertebral artery dissection diagnosed with CT.
AJNR Am J Neuroradiol 1995; 16: 952–4.
Galtes I, Borondo JC, Cos M et al.
Traumatic bilateral vertebral artery dissection.
Forensic Sci Int 2012; 214: e12–5.
Sepelyak K, Gailloud P, Jordan LC.
Athletics, minor trauma, and pediatric arterial ischaemic stroke.
Eur J Pediatr 2010; 169: 557–62.
Tinel D, Bliznakova E, Juhel C et al.
Vertebrobasilar ischaemia after cervical spine manipulation: a case report.
Ann Readapt Med Phys 2008; 51: 403–14.
Chen WL, Chern CH, Wu YL, Lee CH.
Vertebral artery dissection and cerebellar infarction following chiropractic manipulation.
Emerg Med J 2006; 23: e1.
Nadgir RN, Loevner LA, Ahmed T et al.
Simultaneous bilateral internal carotid and vertebral artery dissection following chiropractic manipulation: case report and review of the literature.
Neuroradiology 2003; 45: 311–4.
The neuro-ophthalmologic complications of cervical manipulation.
J Neuroophthalmol 2000; 20: 236–9.
Showalter W, Esekogwu V, Newton KI, Henderson SO.
Vertebral artery dissection.
Acad Emerg Med 1997; 4: 991–5.
Albuquerque FC, Hu YC, Dashti SR et al.
Craniocervical arterial dissections as sequelae of chiropractic manipulation: patterns of injury and
J Neurosurg 2011; 115: 1197–205.
Haneline MT, Lewkovich GN.
An analysis of the aetiology of cervical artery dissections: 1994 to 2003.
J Manipulative Physiol Ther 2005; 28: 617–22.
Campos CR, Evaristo EF, Yamamoto FI et al.
Spontaneous cervical carotid and vertebral arteries dissection: study of 48 patients.
Arq Neuropsiquiatr 2004; 62: 492–8.
Return to STROKE AND CHIROPRACTIC