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Spinal sulcal artery syndrome due to spontaneous bilateral vertebral artery dissection
  1. S WEIDAUER,
  2. D CLAUS
  1. Department of Neurology
  2. Institute for Radiology, Klinikum Darmstadt, Teaching Hospital University Frankfurt, Germany
  1. Professor D Claus, Department of Neurology, Klinikum Darmstadt, Teaching Hospital University Frankfurt, Heidelberger Landstrasse 379, 64297 Darmstadt, Germany.
  1. M GARTENSCHLÄGER
  1. Department of Neurology
  2. Institute for Radiology, Klinikum Darmstadt, Teaching Hospital University Frankfurt, Germany
  1. Professor D Claus, Department of Neurology, Klinikum Darmstadt, Teaching Hospital University Frankfurt, Heidelberger Landstrasse 379, 64297 Darmstadt, Germany.

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In young adults vertebral artery dissection (VAD) is an important cause of brain infarction.1 2 A known mechanism is microtraumata due to abrupt head movements— for example, chiropractic manoeuvres. In addition a pathogenetic role of connective tissue diseases, cystic media necrosis, fibromuscular dysplasia, migraine, and inflammatory diseases has been postulated.3In VAD initial neck pain is often reported, which may be slight. Lesions caused by VAD are cerebellar or brainstem infarcts, unilateral or bilateral thalamic infarcts (top of the basilar syndrome), or infarctions in the posterior cerebral artery territory due to intra-arterial embolism or haemodynamic decompensation when collaterals are insufficient.1 Lesions of the cervical spinal cord are rare because of its good collateral supply.4 5 We report on a patient with a syndrome of the spinal sulcal artery (incomplete Brown-Séquard syndrome) caused by spontaneous bilateral VAD.

A 43 year old man with a history of arterial hypertension presented with left sided numbness sparing the face, which had evolved suddenly while he was walking. In addition, he reported on dull right sided neck pain irradiating into the occiput, which had been initiated by a head rotation while he was working at a computer 2 weeks before. The neck pain had spontaneously ceased 6 days later. Neurological examination disclosed dissociated sensation defect on the left with an indistinct level around C4 to C6. Below this level on the left he had a marked hypalgesia and nearly a loss of temperature sense. The right limbs were warmer than the left ones. In addition, we found mild right sided motor system deficits. Cranial nerve function was intact, despite a right sided Horner’s syndrome. According to chest radiography phrenic nerve function was preserved. Routine laboratory findings including CSF analysis were normal. The hemiparesis and the different temperature sensation in the limbs resolved completely within 3 weeks.

Tibial nerve somatosensory evoked potentials (SSEPs) had regular N22 and P40 latencies and amplitudes. Central motor conduction time (CMCT) after transcranial magnetic stimulation was prolonged to the right abductor digiti minimi (9.2 ms) and tibialis anterior (23.1 ms). The CMCT to the left target muscles was normal. Duplex sonography showed increased flow velocity on the level of the cervical vertebrae 3 to 5 with a maximum of 214 cm/s in the right and 197 cm/s in the left vertebral artery. Colour mode showed irregular narrowings of the lumen indicating dissections.

Cervical MRI showed a spinal cord infarction at the level C2 (figure). The circumference and dorsal part of the cord were not affected. In digital subtraction angiography (DSA) both vertebral arteries had string signs in the V1 and V2 segments with collateral flow to the distal V2–4 segments via the thyreocervical trunk (cervical ascendent artery) and the costocervical trunk also. The anterior spinal artery was incompletely contrasted by unilateral spinal branches of the right vertebral artery. They originated at the level of dissection. The intradural origins of the anterior spinal artery from the distal part of the vertebral arteries (V4 segment) were not visible.

Coronal T2 weighted MRI: ventrolateral paramedian right sided medullary infarction.

Bilateral spontaneous VAD is not rare, but often missed. In most cases, microtrauma preceding the dissection can be recalled by the patients. Due to the mild mechanical impact, the action of predisposing factors might be postulated. Among these may be changing in type III collagen, migraine, fibromuscular dysplasia, infections in the near past, and inflammatory vasculopathy.2 Magnetic resonance imaging with typical semilunar mural haematoma and in addition magnetic resonance angiography (MRA) with complementary documentation of an irregular lumen or tapering occlusion have a high sensitivity and specificity in cases of internal carotid artery dissection.1 By contrast, mural haematomas of the VA especially in the V1 and the V3 segments are often not detectable by MRI. In cases of unclear non-invasive findings, DSA is still the method of choice.1

In addition to consecutive brain infarctions, cervical spinal cord infarctions and nerve root compression syndromes may occur in cases of unilateral or bilateral VAD. Probably as a result of the pial collateral network and the dual posterior spinal artery, spinal cord infarction is often located in the anterior spinal artery territory with the grey matter of the anterior horns exhibiting the highest vulnerability to ischaemia.4 5 This mechanism may lead to a typical “snake eye” configuration of medullary infarction.3 Besides the supply via VA spinal branches, which is found in 19% only unilaterally,4 there are branches originating from the ascendant cervical artery (thyreocervical trunk) and the costocervical trunk supplying the spinal cord.

DSA findings in the present case suggest that spinal branches originating from the right V2 segment were dominant feeders of the anterior spinal artery whereas there was no evidence of direct communication between vertebral and spinal arteries from the V4 segment. The dissection involved the V2 segment from which these spinal branches originate. A transient occlusion of these spinal branches is a likely consequence. This unusual type of arterial medullary supply may explain why VAD causes spinal cord infarction. Contrary to Pullicino,5 who described upper limb atrophies due to cervical spinal cord infarction involving the anterior horns, the present case shows a unilateral involvement of commissural, spinothalamic, pyramidal, and vasoconstrictor tracts. To our knowledge sulcal spinal artery syndrome caused by bilateral spontaneous VAD has not yet been described. In conclusion, differential diagnosis of acute spinal symptoms in young adults should include spontaneous unilateral or bilateral VAD with cervical spinal cord ischaemia.

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