Vertebral Artery Injury Presenting with
Signs of Middle Cerebral Artery Occlusion
A Case Report

George Sternbach, M.D.
Michael Cohen, M.D.
and David Goldschmid, M.D.
DALY CITY, CALIFORNIA

ABSTRACT

Therapeutic manipulation of the neck has been shown to produce injury to the vertebral
artery. The clinical syndromes produced by this arterial insufficiency generally reflect
dysfunction of the brainstem or cerebellum. The authors present a case of such injury that
presented with clinical findings, namely, hemiparesis and aphasia, suggestive of involvement of the dominant middle cerebral artery. These findings may have been the result of
disruption of flow through the posterior cerebral artery to the thalamus, internal capsule,
and cerebral peduncles.

From the Departments of Emergency Medicine and *Neurology, Seton Medical Center, Daly City,
California.
©1995 Westminster Publications, Inc., 708 Glen Cove Avenue, Glen Head, NY 11545, U.S.A.

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Introduction
Vertebral artery injury caused by therapeutic neck
manipulation is a well-described syndrome. We
recently encountered such a case in which the patient presented with signs suggestive of obstruction of the middle cerebral artery.
Case Report

The patient was a thirty-year-old right-handed
presented to the emergency department with a chief complaint of inability to move
the right side of her body. The patient was
brought to the hospital by paramedics after having experienced the weakness immediately following a chiropractic manipulation of her neck.
Two weeks prior to this presentation, she had
undergone chiropractic manipulation for myofascial neck pain. On that occasion, she had experienced severe neck pain radiating to the back of
the head, vertigo, and a general feeling of weakness during the manipulation. These symptoms
were transient except for the neck pain, lasting a
few minutes after the manipulation was terminated. The persistence of neck pain ultimately
caused her to return to the chiropractor on the
day of presentation. Cervical manipulation performed by that individual resulted in severe dizziness and right-sided weakness.
The patient had no other history of significant prior medical illness or injury. She had
been taking oral contraceptives but was taking
no other medications.
On physical examination the vital signs were
as follows: blood pressure: 121/85 mm Hg;
woman who

pulse: 77/minute; respirations: 24/minute; temperature : 36.8°C. The patient was awake and
alert. Findings from the initial physical examination were entirely normal except for the following findings on neurologic examination: a
dense right hemiparesis involving the upper and
lower extremity equally, aphasia, a left gaze
preference, and ocular nystagmus to the right.
There was no sensory deficit. Deep tendon reflexes were symmetrical throughout, with flexor
plantar responses bilaterally.
Radiographs of the cervical spine and noncontrast computed tomographic (CT) scan of the
brain appeared normal. An echocardiogram and
carotid artery ultrasound examination were also
unremarkable. A selective left vertebral and left
common carotid arteriogram was performed. This

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demonstrated that the distal portion of the left
vertebral artery was irregular, this irregularity beginning at the C2 level and extending into the intracranial portion. There were high-grade
stenoses in the vicinity of the left posterior inferior cerebellar artery origin, with reduced flow into
that vessel (Figure 1). The mid and distal basilar
artery vascular distribution was normal. The left
carotid artery also was normal in appearance.
The patient’s neurologic signs fluctuated dramatically over the following several hours. She
displayed periods of complete resolution of findings, which were followed by recurrence of right
hemiparesis, aphasia, and a right central facial
nerve paralysis. The time frame of appearance
and resolution of neurologic signs was dramatic,
sometimes occurring in the space of several minutes. On one examination, the patient also displayed transient skew deviation of the eyes, upbeating nystagmus with attempts at upward gaze,
and downward gaze paresis.
The patient was admitted to the hospital.
Anticoagulation was instituted, with the initial
intravenous administration of 3,000 units of heparin followed by a continuous intravenous heparin infusion. Her neurologic findings resolved
completely over the following twenty-four
hours. She was subsequently given a regimen of
oral anticoagulation and discharged from the
hospital without neurologic deficit five days
after her admission.

Discussion
The first instances of cerebrovascular accident associated with manipulation of the cervical spine
were reported in 1927.1 In 1947, 2 cases of death
due to cerebellar necrosis following chiropractic
manipulation were reported.2 In the four decades
that followed, 52 cases, in total, were reported in
which vertebral arterial flow was impaired following therapeutic cervical manipulation.33
Vertebral artery injury has also been described
following neck trauma, athletic injury, yoga, calisthenics, overhead work, and cervical traction.4-8
The common feature of these activities is the application of hyperextension and rotation forces to
the neck. This is also the mechanism considered
to be responsible for vertebral artery injury fol-

lowing therapeutic manipulation.
The vascular injuries described have resulted
in a variety of neurologic deficits. Reported

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Figure 1.

Vertebral

arteriogram revealing
diffuse narrowing and
irregularity of the
vertebral artery.

deficits have included those of Wallenberg’s lateral medullary infarction syndrome (ipsilateral
loss of pain and temperature sensation of the
face, contralateral loss of such sensation on the
body, Horner’s syndrome, paralysis of the soft
palate), &dquo;locked-in&dquo; syndrome (quadriplegia with
preservation of blinking, vertical eye movements,
and respiration), sixth nerve and other gaze
palsies, visual field deficits, Horner’s syndrome,
and quadriplegia.9 Symptoms typically include
vertigo, slurred speech, diplopia, weakness,

paresthesias, tinnitus, or ataxia.
The pathophysiology of the injury has been
variously postulated to involve vascular intimal
tearing, thrombus and intramural hematoma

formation, vasospasm, aneurysmal dissection,
and embolization.9 Where postmortem vascular
evaluation has been performed, this has demonstrated intimal dissection with distal thrombus
propagation.l° The usual site of injury is in the
extracranial portion of the vertebral artery at the
C2 level.
Although the production of various brain
stem syndromes in conjunction with cervical manipulation is well documented, the distinctive aspect of our case was the presentation with signs
suggestive of dominant-hemisphere middle cerebral artery occlusion (aphasia and contralateral
hemiparesis). Although internal carotid artery
dissecting hematoma complicating cervical chiro-

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practic manipulation has been described,&dquo; arteriography demonstrated that this was not the case
here. The carotid circulation was free of lesions,
whereas there was considerable abnormality of
the vertebral system.
Chambers and colleagues described 12 patients with acute stroke whose features were indicative of middle cerebral artery occlusion but
who in fact were demonstrated to have experienced occlusion of the proximal posterior cerebral artery.12 These patients presented with clinical syndromes indicative of infarction of the opposite cerebral hemisphere in the territory of the
middle cerebral artery (hemiparesis, hemisensory

loss, hemianopsia, hemispatial neglect). However, all were subsequently found on CT scan or autopsy to have had infarction of the thalamus, inferomesial temporal lobe, and occipital lobe. The
3 patients who underwent arteriography also
demonstrated severe vertebrobasilar occlusive
disease. The cause of aphasia in dominant-hemisphere lesions was thought to be thalamic infarction, with hemiparesis resulting from infarction
of the cerebral peduncles or the anterior segment
of the posterior limb of the internal capsule.
Chambers’ study illuminated the clinical
overlap existing between posterior and middle
cerebral arterial occlusion, a fact not commonly
recognized. This circulatory overlap may explain

the clinical presentation of our case, in which
there were predominantly signs of middle
cerebral artery territory involvement, even
though it was the vertebral circulation that was
involved. Clinical signs that may provide clues
that a posterior cerebral artery lesion is responsible for findings ordinarily produced by middle
cerebral artery occlusion include the presence of
Horner’s syndrome, oculomotor palsy, or vertical
gaze paresis.

Conclusion

Although the history of cervical manipulation
prior to this patient’s presentation strongly suggested injury to the vertebral circulation, the clinical signs pointed to middle cerebral involvement.
The clinician should suspect involvement of either vascular system under such circumstances.

George Sternbach, M.D.
Department of Emergency Medicine
Seton Medical Center
1900 Sullivan Avenue
Daly City, CA 94025

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