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(Stroke. 1998;29:1742.)
© 1998 American Heart Association, Inc.


Letters to the Editor

Symmetrical Infarction of the Cervical Spinal Cord Due to Spontaneous Bilateral Vertebral Artery Dissection

Thomas Hundsberger, MD; Frank Thömke, MD; Hanns Christian Hopf, MD

Klinik und Poliklinik für Neurologie

Clemens Fitzek, MD

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 (FigureDown). 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.

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

  1. Leys D, Lesoin F, Pruvo JP, Gozet G, Jomin M, Petit H. Bilateral spontaneous dissection of extracranial vertebral arteries. J Neurol.. 1987;234:237–240.[Medline] [Order article via Infotrieve]
  2. Mokri B, Houser OW, Sandok BA, Piepgras DG. Spontaneous dissections of the vertebral arteries. Neurology.. 1988;38:880–885.[Abstract/Free Full Text]
  3. Hinse P, Thie A, Lachenmayer L. Dissection of the extracranial vertebral artery: report of four cases and review of the literature. J Neurol Neurosurg Psychiatry.. 1991;54:863–869.[Abstract]
  4. Pryse-Phillips W. Infarction of the medulla and cervical cord after fitness exercises. Stroke.. 1989;20:292–294.[Abstract/Free Full Text]
  5. Gutowski NJ, Murphy RP, Beale DJ. Unilateral upper cervical posterior spinal artery syndrome following sneezing. J Neurol Neurosurg Psychiatry.. 1992;55:841–843.[Abstract]
  6. Pullicino P. Bilateral distal upper limb amyotrophy and watershed infarcts from vertebral dissection. Stroke.. 1994;25:1870–1872.[Abstract]
  7. Bergqvist CAG, Goldberg HI, Thorarensen O, Bird SJ. Posterior cervical spinal cord infarction following vertebral artery dissection. Neurology.. 1997;48:1112–1115.[Abstract]
  8. Goldsmith P, Rowe D, Jäger R, Kapoor R. Focal vertebral artery dissection causing Brown-Séquard's syndrome. J Neurol Neurosurg Psychiatry.. 1998;64:415–416.[Free Full Text]
  9. Lasjaunias P, Berenstein A. Surgical Neuroangiography. Vol 3: Functional Ananomy of Brain, Spinal Cord and Spine. Berlin, Germany: Springer; 1990.



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