Klinik und Poliklinik für Neurologie
Klinik für Neuroradiologie,
Johannes Gutenberg-Universität Mainz,
Mainz, Germany
To the Editor:
Vertebral artery (VA) dissection is a well-known cause of
vertebrobasilar ischemia in young people and may be due to
preceding chiropractic maneuvers, cystic medial necrosis,
mucopolysaccharidosis and reticular fiber diseases,
vasculitis,1 2 or a yet-unknown
arteriopathy.3 Common findings in VA dissection are
unilateral or bilateral neck pain associated with cerebellar and brain
stem (usually medullary) infarctions,2 3 which are rarely
associated with clinical signs of spinal cord lesions.4 5 6
Recently, 1 patient each was described with bilateral spinal cord
infarction7 and Brown-Séquard's
syndrome8 as the sole manifestation of spontaneous
unilateral VA dissection. We add another patient with spontaneous
bilateral VA dissection causing MRI-documented bilateral cervical cord
infarction without clinical,
electrophysiological, or radiological signs
of brain stem or cerebellar lesions.
A 31-year-old, previously healthy woman with a history of an episode of
spontaneous right-sided neck pain 3 weeks before noted sudden onset
bilateral neck pain radiating into both arms. Within some hours, she
developed progressive unsteadiness of gait, weakness of the left arm
and leg, and urinary retention. There was no history of neck trauma,
chiropractic manipulation, or abrupt head movements. On examination,
she had normal cranial nerve functions. There was a severe left-sided
hemiparesis with loss of deep tendon reflexes on the left and weak knee
and ankle jerks on the right side. The plantar responses were flexor.
She had bilateral loss of pain and temperature sense below C5. Touch,
vibration, and position sense were unimpaired. She had urinary
retention and feces incontinence. Vital capacity was reduced to 1100
cm3, but PO2 and
PCO2 were within normal limits.
MRI revealed symmetric infarction of the ventral one third
("snake-eye" conformation) of the spinal cord segments C2 to C5
(Figure
Spinal cord infarction may be the sole manifestation of unilateral or
bilateral VA dissection, followed by clinical signs of bilateral
posterior cervical cord infarction,7
Brown-Séquard's syndrome,8 or left-sided
hemiparesis with bilateral loss of pain and temperature, urinary
retention, and feces incontinence, as in our patient. We attributed the
preceding right-sided neck pain of our patient to an ipsilateral VA
dissection, and interpreted the absence of additional neurological
signs as an indicator of a sufficient perfusion within the
vertebrobasilar system at that time. With dissection of the left VA 3
weeks later, perfusion became insufficient, as the time was too short
to restore perfusion of the right VA. The origin of the main feeders of
the cervical part of the anterior spinal artery is highly variable
but usually is the vertebral arteries on one or both
sides.9 Under such anatomic conditions, occlusion of these
VA branches due to bilateral VA dissection causes hypoperfusion (or
circulatory arrest) in the territory of the anterior spinal artery,
which supplies most of the anterior three quarters of the cervical cord
via sulcal vessels, and is the most probable explanation of bilateral
watershed infarction in the cervical cord in our patient.
References
© 1998 American Heart Association, Inc.
Letters to the Editor
Symmetrical Infarction of the Cervical Spinal Cord Due to Spontaneous Bilateral Vertebral Artery Dissection
). Cerebral angiography showed
bilateral VA dissection with nearly total proximal stenosis and
low blood flow in the basilar artery. MRI of the cerebellum and brain
stem was normal. Direct current electro-oculography, brain stem
auditory evoked potentials, and masseter and blink reflexes were also
within normal limits. The patient was initially treated with
intravenous heparin with clotting time increased to 2 times
to normal and later put on phenprocumon. The clinical course was
favorable, and within 3 weeks only mild urinary retention was still
present.

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Figure 1. Cervical MR scan 1 day after admission. Left, T2-weighted
magnetic resonance axial scan at C3 level showing bilateral cervical
spinal cord hyperintensities ("snake-eye" conformation). Right,
Sagital MR scan visualizes expansion of this lesion from C2 to C5
vertebral levels.
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