~

991

Vertebral Artery Dissection, Showalter et al.

Vertebral Artery Dissection
William Showalter, MD, Victor Esekogwu, MD, Kim I. Newton, MD, Sean 0. Henderson, MD

I

.ABSTRACT
........................................................................................................................................

Vertebral artery dissections (VADs) following a variety of minor traumatic mechanisms have been previously
reported. This article reports 2 cases of VAD with delayed recognition following motor vehicle collisions
(MVCs). The first VAD patient developed major neurologic abnormalities 28 hours after an MVC. The second
VAD patient presented with 3 weeks of neck and head pain beginning 8 weeks after an MVC and subsequent
chiropractic manipulation. The anatomy and pathophysiology of VAD are reviewed. Early ED recognition
prior to the onset of major neurologic deficits (e.g., paresis, dysarthria, ataxia, or altered mental status) is
emphasized. An algorithm for the ED management of the entity is suggested.
Key words: vertebral artery dissection; stroke; neck trauma: case report.
Acad. Emerg. Med. 1997; 4:991-995.

I Vertebral artery dissection (VAD) following blunt
trauma has been previously described as a rare occur~ e n c e . ’ More
-~
recently, awareness of this potentially catastrophic clinical entity has heightened.‘.’ Case reports
found thus far in the emergency medicine (EM) literature
have focused on making the diagnosis only after disabling
neurologic deficits have occ~rred.’.~.’
In 2 of these cases,’”
the onset of major neurologic findings was delayed and
the diagnosis was made after initial release from the ED.
We report 2 additional cases of delayed clinical presentation. We review the related anatomy and pathophysiology of VAD and propose a diagnostic algorithm when
VAD is suspected.

I ...................................
CASE1
A 32-year-old woman was brought by paramedics to the
ED after a motor vehicle collision (MVC). The patient
had been the restrained driver of a vehicle that was broadsided at an intersection by a van traveling at an unknown
speed. There was no loss of consciousness and the patient
was ambulatory at the scene. Due to the significant passenger space intrusion on the driver’s side of the vehicle,
the patient was positioned with full cervical spine precautions and transported to a Level-1 trauma center.
Upon arrival at the ED, the patient complained of pain
............................................................................
From LAC + USC Medical Center, Los Angeles. CA, Department of
Emergency Medicine (WS. VE, KIN. SOH).
Received: November 7. 1996; revision received: March 19, 1997; second revision: April 2. 1997: accepted: April 3, 1997.
Address for correspondence and reprints: Victor Esekogwu. MD, Department of Emergemy Medicine, LAC+ USC Medical Center, Unit #1,
Room #101I, 1200 North State Srreet, Los Angeles, CA 90033. Fax:
213-226-8044: e-mail: esekogwu@hsc.usc.edu

in the left neck, left lumbar area, and bilateral lower extremities. Physical examination showed the patient to be
awake, alert, oriented, and obese, and to have stable vital
signs. There was no evidence of head trauma, pupils were
equal, round, and reactive t o light, and extraocular movements were intact. On cervical examination, the patient
continued to complain of vague, left-sided neck pain, but
no discrete area of tenderness could be identified. Mild
epigastric tenderness was noted on examination of the abdomen. There was tenderness in the left lumbar area. Ecchymoses were seen in the pretibial areas bilaterally. Sensory and motor examinations were normal. Extremity
reflexes were symmetrical and toes were down-going bilaterally.
Cervical spine, chest, pelvis, lumbar spine, and lowerextremity films were negative. Initial urinalysis following
catheter placement revealed microscopic hematuria with
>50 red blood cells per high power field. Urine pregnancy
test was negative, as was the abdominal CT. Although the
patient had suffered little visible trauma, she was admitted
for observation. Twenty eight hours after arrival, the patient made an attempt to g e t out of bed and fell to the
floor. Upon arrival of her physician, the patient was able
to open her eyes to verbal stimulus, follow commands,
and mumble inappropriate speech [Glasgow Coma Scale
score (GCS) = 121. Within 30 minutes she had become
completely unresponsive with no eye opening and no motor movement (GCS = 3).
Emergency orotracheal intubation was performed, and
a head C T revealed compression of the fourth ventricle.
The patient was then taken emergently to the operating
room for a ventriculostomy. A subsequent angiogram of
the vertebral arteries showed dissection on the left (Fig.
l), which had caused bilateral cerebellar infarcts. These
became visible several days later (Fig. 2). In this case, the
VAD extended intracranially, and subarachnoid blood was

992

ACADEMIC EMERGENCY MEDICINE

OCT 1997

VOL 4/NO 10

seen in an ED at that time complaining of neck pain, had
normal cervical spine films, and had been released home
with the diagnosis of cervical strain.
Based on this information, magnetic resonance angiography (MRA) of the head and neck was obtained and
the patient was found to have a dissection of the right
vertebral artery (Fig. 3). Emergency neuroIogic consultation was then obtained and the patient was subsequently
anticoagulated. Eight weeks after the diagnosis, he was
doing well taking warfarin sodium.

I

I FIGURE 1. Angiograrn showing irregular stenosis of the left vertebral artery extending into the basilar artery representing the internal
lumen of the dissecting artery.

DISCUSSION
........................

Epidemiology: The exact incidence of VAD is unknown. In a search of the literature between 1978 and
1988, > l o 0 reported cases of VAD were identified.4 Mas
et al. cited an audience poll conducted at a meeting of the
Stroke Council of the American Heart Association in
1988, which found 250 additional unreported cases.'
Generally, VAD occurs in middle-aged adults with an
average age of 38 years and a range of 3-63 years.'.' Most
often patients are healthy and without predisposing risk
factors for
Failure to make the diagnosis and
institute appropriate therapy can result in serious longterm neurologic sequelae or death.5 Clinically, VAD results in posterior circulation transient ischemic attack,
stroke, and less frequently, SAH.4 The initiating factor is

detected. Due to the subarachnoid hemorrhage (SAH) and
the fear of further hemorrhage, the patient was given aspirin therapy rather than heparin. Over the course of the
next few weeks, despite an improvement in mental status,
the patient continued to have significant weakness and
loss of motor control in all 4 extremities as well as a left
gaze palsy. Four weeks following admission, she was
transferred to a regional rehabilitation center to undergo
therapy for her persistent neurologic deficits.

I

CASE2
..............................................................................

A 36-year-old man presented to a community hospital ED
complaining of a severe right-sided neck, occipital, frontal, and retro-orbital pain of 3 weeks' duration. The patient
had been seen by several physicians prior to this and had
been told he had a migraine headache. Although he had
been taking the medications prescribed and had also been
to see a chiropractor several times, he was unable to obtain any relief of his symptoms. His only other complaint
was of intermittent blurred vision in the right eye when
the pain was most severe. He had no other neurologic
complaints.
Physical examination revealed only a slight decrease
in light touch and pinprick on the right face and body.
During the examination the patient stated that he had been
in an MVC 8 weeks prior to presentation. He had been

I FIGURE 2. Head CT scan with bilateral cerebellar infarcts and hydrocephalus.

993

Vertebral Artery Dissection, Showalter et al.

a tear in the arterial intima with subsequent hemorrhage
into the wall of the blood vessel and the formation of a
clot. The injury may involve only the arterial intima, but
most often extends into the tunica media. Occasionally,
the adventitial layer is perforated and bleeding occurs outside of the wall of the vessel.’
Spontaneous dissections are rare. Most are anecdotal
cases related to underlying pathologic conditions such as
cystic medial necrosis,I0 BehGet’s disease,” rheumatoid
arthritis,12 giant cell arteriti~,’~
osteogenesis imperfe~ta,’~
and fibromuscular dysplasia.* Cases of VAD secondary to
trauma are much more commonly reported, often in the
presence of major cervical trauma with accompanying
cervical spine fracture or dislocation.l“’16However, most
recognized cases of VAD occur following a seemingly
trivial traumatic event such as sneezing, coughing, or doing yoga exercises. Perhaps the most frequently reported
cases are those observed following chiropractic manipuIation.’.’.”

Anatomy and Pathophysiology: Anatomically, the vertebral arteries are divided into 4 segments: the first part
originates from the subclavian artery and traverses to the
transverse foramen of C6; the second part passes through
the transverse foramina of C6 to C2; the third part exits
the transverse foramen of C2, winds around C1 posteriorly
in a tortuous manner, and enters the dura at the foramen
magnum; the fourth part begins at the foramen magnum
and ends where it joins the opposite vertebral artery at the
basilar artery.”
In the majority of cases of traumatic VAD, the initial
injury begins in the third part of the vertebral artery. Most
authors concur that the most likely reason for this is that,
with neck movement, 50% of rotation occurs at the atlantoaxial joint before any rotation begins in the cervical
spine.5.’ Rotation of the head stretches and compresses the
vertebral artery at this most mobile cervical joint, an action that has been demonstrated angiographically in normal volunteer^.'^
Several mechanisms have been proposed for the resultant neurologic sequelae. Severe stenosis or occlusion
may result in brain stem or spinal cord ischemia if there
is a concomitant dissection of the contralateral vertebral
artery that limits collateral flow. In some cases one vertebral artery may end distally in the posterior inferior cerebellar artery (PICA), resulting in minimal flow to the
basilar artery distally. In such cases, a lesion of the opposite vertebral artery may result in brain stem and pontine ischemia. A second mechanism involves the formation of an intraluminal clot, which can break off,
embolize, and occlude branches anywhere in the posterior
circulation distal to the source. Finally, the dissection itself may ascend in a cephalic direction extending intracranially into the basilar artery, occluding branches that
supply the upper spinal cord, brain stem, pons, or cere-

I FIGURE 3. Angiogram showing dissection of the right vertebral artery (open arrow).Normal round lumen of left vertebral artery identified
for comparison (closed arrow).

bellum. There is also the added danger of dissection
through the entire wall of the blood vessel, resulting in
SAH. The intracranial portion of the vertebral artery is
more susceptible to rupture than the extracranial section
because the artery walls thin as they cross the dura.

Clinical Findings: These multiple mechanisms, along
with the complexity of the neuronal structures supplied by
the posterior circulation and the variability of the posterior
circulation itself, account for the wide variety of neurologic deficits seen in patients with VAD. The most classic
finding is the lateral medullary or Wallenberg’s syndrome
characterized by dysarthria, dysmetria, ataxia, dysphagia,
vertigo, nystagmus, ipsilateral Homer’s syndrome, and
crossed sensory deficits, i.e., loss of pain and temperature
sensation on the ipsilateral face and contralateral extremities. When present, Wallenberg’s syndrome is due to occlusion of the PICA that supplies the lateral medulla.
However, as this area is most commonly supplied by
branches from the vertebral artery, the lateral medullary
syndrome is not commonly seen in its entirety.
The most common initial symptoms in VAD are neck
pain and occipital headache, which may precede the onset
of neurologic symptoms from seconds to weeks.’.”’.’ It is
thought that this pain is d u e to the initial injury to the

994

ACADEMIC EMERGENCY MEDICINE OCT 1997

Major Neurologic Findings

most of the patients (9/14), there was a history of some
sort of minor trauma that heralded the onset of the pain.

1

1

Angiograrn

MRA or TCD

ADMIT

Immediately
Available?

Positive

-

1

Anticoagulation
ADMIT

1
1

No

1

MRAlTCD

1

Negative

/ 1

Yes

Head CT f LP

1

Neaative

Positive

Yes

VOL 4/NO 10

Evidence

/

Anticoagulate
and Obtain MRA
or TCD ASAP

1 J

NO Anticoagulation

ADMIT

/ i

MRAITCD

Treatment: A VAD is a dynamic lesion, with neurologic
symptoms most often progressing in a stuttering fashion
over the course of hours to days. The progression is
thought to result from propagation of the thrombus or
from distal embolization? This is the rationale for the use
of anticoagulation in the treatment of extracranial VADs.
Tramo et a1.” and Mas et al.” report the use of antiplatelet
agents (aspirin or dipyridamole) in patients with VAD. In
their cases the patients’ symptoms had not changed in the
24 hours prior to admission. Although no randomized
clinical trial has been done to date studying the benefits
of anticoagulation for VAD, anecdotal experience using
heparin for the acute treatment of extracranial VAD has
resulted in the arrest of the progression of the neurologic
deficits in most case^.'.^-'.'^
The treatment of intracranial VAD remains controver~ i a lAnticoagulant
.~
therapy is contraindicated in those patients at risk for hemorrhagic infarcts or SAH. In general,
if the VAD is intracranial a n d o r there is a suspicion of
SAH, the patient should be given only antiplatelet agents
such as aspirin or dipyridamole.

Early Recognition: Since it is possible to stop the progression of further neurologic sequelae in patients already
Positive
Negative
presenting with major neurologic deficits (e.g., paresis,
ataxia, dysarthria, altered mental status), it would be preADMIT
Stop Anticoagulation
ferred to diagnose VAD before major neurologic findings
develop. The characteristic pain of VAD is a unilateral
headache andor neck pain, abrupt in onset and different
HOME
from prior episodes of discomfort. There should be a hisI FIGURE 4. Suggested workup of patients presenting with neck pain
tory of flexion, extension, or rotation of the neck. Together
that is suggestive of vertebral artery dissection after trauma. Major neuthese
should lead to a suspicion of VAD even in the face
rologic findings = paresis, ataxia, dysarthria, altered mental status, or
similar major dysfunction. MRA = magnetic resonance angiogram; of trivial trauma.
TCD = transcutaneous Doppler study; R/O = to rule out; SAH = subIn such cases, noninvasive diagnostic techniques such
arachnoid hemorrhage; CT = computed tomography of head; LP = lumas transcutaneous Doppler (TCD) studies or MRA may be
bar puncture: ASAP = as soon as possible.
used to establish the diagnosis. Patients found to have
VADs may then be given anticoagulant therapy with the
blood vessel because most often the cervical or occipital hope of preventing major neurologic sequelae.’
It is interesting to note that in at least 2 of the 3 cases
pain is lateralized to the side overlying the injured vessel5
and the vessels of the neck are known to be pain-sensi- of VAD reported in the EM literature, the patients had
tive.20
neck pain prior to the onset of neurologic symptoms. In
In 1993, Sturzenegger studied the characteristics of the the third case, the patient initially presented to the ED
pain associated with VAD. In 10 of 14 patients, the cer- following an MVC, and although neck pain was not spevical pain was ipsilateral and posterior. Eleven of 14 pa- cifically mentioned, the patient presumably also was comtients experienced occipital headache. In most patients the plaining of neck pain since she was referred to an orthopain was of acute onset, sharp or dull, and moderate to pedist and prescribed a soft cervical collar. Seven days
severe. The pain occasionally radiated to the ipsilateral after the MVC, she presented to the ED again, this time
temporal area, frontal area, eye, or ear. In 11 of 14 pa- with cranial nerve palsies and truncal ataxia.’ Both our
tients, similar pain had not been previously experienced. patients also complained of headache and neck pain. In
It was also found that none of the 14 patients had cervical these scenarios, MRA, as used in the second case. or TCD
tenderness or restriction of neck movement, but most (9/ may have helped make the diagnosis prior to the onset of
14) had exacerbation of pain with head m ~ v e m e n t For
.~
major neurologic deficits.

1

1
1

995

Vertebral Artery Dissection, Showalter et al.

Rother et a1.22reported that MRA has a sensitivity of
97% and a specificity of 99% for diagnosing VAD. The
more invasive vertebral angiography should be reserved
for cases where MRA or ultrasonographic (duplex and
TCD) imaging is nondiagnostic. Ultrasonography can be
used to measure flow velocity, direction, and pulse contour in middle, anterior, and posterior cerebral arteries as
well as the vertebral and basilar arteries. Unfortunately,
this modality is less specific and less sensitive than MRA
and demands a highly skilled operator.20
Hoffman et a1.20propose the use of MRNultrasonography in place of the invasive angiography as the modality of choice for VAD. Despite the recommendations of
Hoffman et al., vertebral angiography remains the current
standard for the diagnosis of VAD although its findings
are not always diagnostic. When specific radiographic
signs such as pseudoaneurysm or intraluminal clot are
found, the diagnosis is usually assured. More often, irregular stenoses or incomplete occlusions are found, which
are less specific for VAD and may be seen in atherosclerotic or partially recanalized embolic occlusions of the
vertebral artery. These findings must be interpreted in conjunction with the clinical p r e ~ e n t a t i o n . ~ . ” . ~ ~
We suggest a workup approach as shown in Fig. 4.
Patients with an appropriate history and major neurologic
findings should have a head CT scan to rule out a mass
lesion, and a vertebral angiography. For the patient without major neurologic findings, a head CT scan and lumbar
puncture are warranted to rule out SAH when MRA or
TCD is not immediately available. If there is no evidence
of SAH, anticoagulation can be initiated pending MRA or
TCD.

I

CONCLUSIONS

............................................

These cases illustrate the importance of maintaining a
high index of suspicion for vascular injury in any young
to middle-aged person presenting with persistent unilateral
head or neck pain after even minor trauma. In cases of
posterior circulation symptoms with antecedent trauma,
one’s index of suspicion should be even higher. Evaluation of such cases with urgent MRA, TCD, or vertebral
angiography should be undertaken. Anticoagulation represents the primary therapy for this condition.

2. Pryse-Phillips W. Infarction of the medulla and cervical cord following fitness exercises. Stroke. 1989; 20:292-4.
3. Rae-Grant AD, Lin F, Yaeger BA, et al. Post traumatic extracranial
vertebral artery dissection with locked in syndrome: a case with MRI
documentation and unusually favorable outcome. Neurol Neurosurg
Psychiatry. 1989; 52:1191-3.
4. Hart RG. Vertebral artery dissection. Neurology. 1988: 38:987-9.
5. Sturzenegger M. Headache and neck pain: the warning symptoms of
vertebral artery dissection. Headache. 1994; 34:187-93.
6. DeBehnke DJ. Brady W. Vertebral artery dissection due to minor
neck trauma. J Emerg Med. 1994; 12:27-31.
7. Glauser J, Hastings OM, Mervart M, et al. Dissection of the vertebral
arteries: case report and discussion. J Emerg Med. 1994; 12:307- 15.
8. Mas JL, Henin D, Bousser MG, Chain F. Hauw JJ. Dissecting aneurysm of the vertebral artery and cervical manipulation: a case report
with autopsy. Neurology. 1989; 39:5 12-5.
9. Horowitz IN, Niparko NA. Vertebral artery dissection with bilateral
hemiparesis. Pediatr Neurol. 1994: 11:252-4.
10. Chang CM. Ng HK, h u n g S Y , Fong KY, Yu YL. Fatal bilateral
vertebral artery dissection in a patient with cystic medial necrosis. Clin
Neurol Neurosurg. 1991; 93:309- 11.
11. Bahar S, Coban 0, Gurvit IH, Akmandemir G, Gokyigit A. Spontaneous dissection of the extracranial vertebral artery with spinal subarachnoid hemorrhage in a patient with Behpt’s disease. Neuroradiology. 1993; 35:352-4.
12. Loeb M, Bookman A, Mikulis D. Rheumatoid arthritis and vertebral artery occlusion: a case report with angiographic and magnetic
resonance demonstration. J Rheumatol. 1993; 20: 1402-5.
13. Sheehan MM. Keohane C, Twomey C. Fatal vertebral giant cell
arteritis. J Clin Pathol. 1993: 46: 1129-31.
14. Schievink W1. Michels VV. Peipgras DG. Neurovascular manifestations of heritable connective tissue disorders: a review. Stroke. 1994;
25:889 - 903.
15. Willis BK, Greiner F, Orrison WW, Benzel EC. The incidence of
vertebral artery injury after midcervical spine fracture or subluxation.
Neurosurgery. 1994; 34:435-41.
16. Tulapronchote R, Selhorst JB. Malkoff MD, Gomez R. Delayed
sequelae of vertebral artery dissection and occult cervical spine fractures. Neurology. 1994; 44:1397-9.
17. Mas JL, Bousser MG, Hasboun D. Laplane D. Extracranial vertebral artery dissections: a review of 13 cases. Stroke. 1987; 18:103747.
18. Sherman DG, Hart RG, Easton JD. Abrupt change in head position
and cerebral infarction. Stroke. 1981; 12:2-6.
19. Fans AA, Poser CM, Wilmore DW. Agnew CH: Radiologic visualization of neck vessels in healthy men. Neurology. 1963: 13:386-96.
20. Hoffman M. Sacco RL, Chan S, Mohr JP. Noninvasive detection
of vertebral artery dissection. Stroke. 1993; 24:815-9.
21. Tramo MI, Hainline B, Petito F. Lee B, Cavonna J. Vertebral artery
injury and cerebellar stroke while swimming: case report. Stroke. 1985:
16: 1039-42.
22. Rother J, Wentz KU, Rautenberg W, Schwartz A. Hennerici M.
Magnetic resonance angiography in vertebrobasilar ischemia. Stroke
1993: 24: 1310-5.

IREFERENCES
1. Herr H, Call G. Banks D. Vertebral artery dissection during paroxysmal coughing: case report. Ann Emerg Med. 1992; 21:88-90.

......................