THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES

Pure Motor Stroke Due to Vertebral
Artery Dissection
Stephen J. Phillips, William J. Maloney and Jean Gray

ABSTRACT: A 39-year-old man presented with a pure motor stroke 9 days after cervical chiropractic manipulation.
Computerised tomographic scanning showed a pontine infarct. Cerebral angiography showed changes consistent with
the diagnosis of bilateral vertebral artery dissection. It is postulated that the infarct resulted from artery-to-artery
embolism.
RESUME: Ictus moteur pur du a la dissection des arteres vertebrales Un homme age de 39 ans s'est presente
avec un ictus moteur pur survenu 9 jours apres des manipulations cerviales chiropractiques. Le CT scan a montre un
infarctus au niveau du pont. Une angiographic cerebrale a montre des changements compatibles avec un diagnostic de
dissection bilaterale des arteres vertebrales. Nous postulons que l'infarctus est le resultat d'une embolie d'artere-aartere.
Can. J. Neurol. Sci. 1989; 16: 348-351

Fisher has described more than 20 clinical syndromes of
lacunar infarction, 1 i.e. small deep cerebral infarcts due to
hypertension-associated arteriolar disease. However, it has
become increasingly apparent that clinical findings do not reliably indicate the site of the underlying brain lesion or its pathogenesis. Pure motor stroke 1 2 (hemiparesis without associated
sensory deficit, homonymous hemianopia, aphasia, or agnosia)
— one of the commonest lacunar syndromes — has been
described in association with: lacunar infarcts in the internal
capsule or basis pontis; 2 infarction of the cerebral cortex, centrum semiovale, medullary pyramid, and cerebral pedunc | e; 3.4,5,6 small hemorrhages involving the internal capsule,
putamen, and basis pontis; 7 saccular basilar artery aneurysm;8
brain abscess; 9 cysticercosis; 10 and primary or metastatic brain
tumour." A recently reported study of a new model of stroke in
the rat suggests that small deep infarcts may be produced by
platelet emboli from the cervical carotid artery. 12 Here we
report a patient who had a pure motor stroke due to a pontine
infarct caused by a presumed embolus from a vertebral artery
dissection.
CASE REPORT

A 39-year-old man experienced the sudden onset of dizziness,
speech disturbance, and left-sided weakness while hurrying to work on
April 15, 1988. He was transferred from his local hospital to Camp Hill
Hospital on April 19.
Nine days before the onset of these symptoms he completed a 10day "course" of chiropractic treatment for a painful, stiff neck which he
had had for about 6 weeks. Otherwise, he had been fit and well. There
was no past history of migraine, neurological symptoms, cardiovascular
disease, hypertension, diabetes, alcohol abuse, or use of tobacco,

Figure 1 — Unenhanced CT scan showing an
infarct in the right side of the pons.

From the Department of Medicine, Camp Hill Hospital (J.G., S.J.P.), and Department of Radiology, Victoria General Hospital (W.J.M.), and
Dalhousie University, Halifax
Received November 17, 1988. Accepted in final form April 24, 1989
Reprint requests to: Dr. S. Phillips, Department of Medicine, Camp Hill Hospital, 1763 Robie Street, Halifax, Nova Scotia, Canada B3H 3G2

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LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES

cocaine or other sympathomimetic drugs. Family history was negative
for premature vascular disease. He was not taking medications.
At the time of admission to our hospital, the general medical examination was unremarkable. Features of Marfan's syndrome were absent.
While in hospital, his systolic blood pressure ranged between 110-140
mm Hg, and the diastolic between 70-80 mm Hg. No cardiac abnormalities were detected, and there were no bruits over the head and neck.
Neurological examination showed a left hemiparesis involving face,
arm, and leg. No other cranial nerve signs were detected. Speech and
language were normal. There were no cerebellar or sensory signs. His
neurological deficit was moderately severe; he could not walk, and had
no useful function in the left upper extremity, i.e. grade 6 on the Stroke
Severity Scale.13
The following investigations were normal or negative: hemoglobin,
hematocrit, platelet count, ESR, serum proteins, serum protein electrophoresis, VDRL, chest X-ray, and ECG. Plain films of the cervical
spine showed no evidence of congenital anomaly, subluxation, arthritic
or degenerative changes. An echocardiogram showed prolapse of the
anterior leaflet of the mitral valve.
A computerised tomographic (CT) scan done 6 days after stroke
onset was normal. A CT scan done 18 days after stroke onset showed a
right-sided mid-pontine infarct (Figure 1).
Four-vessel cerebral angiography was performed 13 days after
stroke onset. The extracranial carotid arteries and the intracranial circulation were normal. Both posterior cerebral arteries filled from the
carotid system. The left vertebral artery tapered to an occlusion in the
foramen transversarium at the level of C6 (Figure 2). There was collateral flow to the distal left vertebral artery via branches of the left occipital artery. The right vertebral artery was irregularly stenosed throughout much of its course in the foramen transversarium (Figure 3). The
distal right vertebral artery and the basilar artery appeared normal. The
angiographic appearances were considered indicative of bilateral vertebral artery dissection.

Figure 3 — Cerebral angiogram. Right subclavian injection showing a
long ribbon-like narrowing of the right vertebral artery (between
arrowheads).
During a 16-day stay in hospital he received daily occupational
therapy and physiotherapy. At the time of discharge he still had a grade
6 neurological deficit on the Stroke Severity Scale,13 but his level of
functioning had improved. He was able to walk with the assistance of a
drop-foot splint and a cane, and opposition movements had begun to
return in the left hand.
DISCUSSION

Figure 2 — Cerebral angiogram. Left subclavian injection showing a
tapering stenosis (lower arrowhead), and occlusion (upper arrowhead) of the proximal left vertebral artery.

Volume 16, No. 3 — August 1989
https://doi.org/10.1017/S0317167100029218 Published online by Cambridge University Press

Head and neck trauma is an important cause of cerebral
infarction in young adults. 1415 Cervical chiropractic manipulation has been linked with dissections of the cervico-cerebral
arteries, particularly the extracranial vertebral artery. 16 " 19
Vertebral artery dissections are typically bilateral in symptomatic cases. They can occur at any point in the course of the vertebral artery, but are most frequent at the C1-C2 and C6 levels,
presumably because the artery is most subject to mechanical
stress at these points. 19 Nucho-occipital pain and the lateral
medullary syndrome are the commonest clinical
manifestations. 18,20,21 The "locked-in" syndrome,18-22 and fatal
brainstem infarction 17 have also been reported in association

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THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES

with vertebral artery dissections. Subarachnoid hemorrhage can
result from dissection of the intracranial vertebral artery
because this type of dissection tends to occur in the subadventitial plane. 2324
We believe that our patient had bilateral vertebral artery dissections induced by cervical chiropractic manipulation.
Atypical features were the absence of neck pain at the onset of
neurological symptoms, and the 9-day delay between the last
chiropractic treatment and the stroke. However, these features
do not cast serious doubt on the diagnosis because painless dissections are known to occur, and the interval between trauma
and stroke may vary from hours to several days. 16 Angiographic
diagnosis of vertebral artery dissection is presumptive, unless a
pseudoaneurysm or double-lumen is demonstrated. 19 These
abnormalties are most likely to be demonstrated by early
angiography; our patient was studied 13 days after stroke-onset.
The long ribbon-like narrowing of the right vertebral artery, and
the tapering stenosis and occlusion of the left vertebral artery
were considered diagnostic of dissection in this patient because
of his age, the history of neck trauma, and the absence of any
other cause for the angiographic findings. Echocardiography
demonstrated the presence of mitral valve prolapse but an
embolus from this source would not produce the persistent,
marked, bilateral arteriopathic changes documented here.
To our knowledge, this is the first time a pure motor stroke
has been associated with vertebral artery dissection. We think
that the pontine infarct was probably caused by artery-to-artery
embolism. This is a recognized mechanism of brainstem infarction, 2526 and our investigations failed to provide a viable alternative explanation.
In his description of the "top of the basilar" syndrome,
Caplan 27 commented that since the basilar artery is widest at its
origin and tapers distally, an embolus small enough to traverse
the vertebral artery would ordinarily not block the basilar artery
except distally. However, the present case and recent experimental evidence 12 suggest that small-diameter penetrating cerebral arteries can be embolized by platelet thrombi from lesions
situated in more proximal segments of the arterial tree. We
admit that the evidence on which our conclusions are based is
circumstantial, but direct proof of such a stroke-mechanism
would be difficult or impossible to obtain, even at autopsy.
Recognition of this mechanism of stroke is important both
from the clinical and scientific points of view.28 Infarcts in the
territory of end-arteries are not always due to small-vessel disease. 29 - 30 The absence of pre-existing hypertension should
prompt investigation for an alternative explanation, as it does in
the normotensive patient who has a spontaneous intracerebral
hemorrhage. 3132 Precise definition of the mechanism of stroke
is necessary for rational therapy,33 and is especially important in
young patients and individuals who have mild strokes. In
research studies it is desirable to categorize strokes according to
mechanism of causation; patients who have small deep cerebral
infarcts do not form a pathogenetically homogeneous group.
The management of dissections is c o n t r o v e r s i a l . 1 6
Antiplatelet agents or anticoagulants are often used, provided
that intracranial vertebral artery dissection and subarachnoid
hemorrhage have been excluded, but it is not known whether
these drugs influence outcome. We did not treat our patient with
these drugs because 4 days had elapsed between stroke onset

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and admission to Camp Hill Hospital, his neurological deficit
had already started to improve, the vertebral artery injury was
caused by an avoidable form of trauma, and there was no evidence of an underlying arteriopathy that could predispose to
recurrent dissection.
ACKNOWLEDGEMENT

Dr. Phillips receives support from the W. Garfield Weston
Foundation of Toronto, and the Nova Scotia Heart Foundation.
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