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Unilateral Upper Cervical Posterior Spinal Artery Syndrome Following Sneezing

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Unilateral Upper Cervical Posterior Spinal Artery Syndrome Following Sneezing Journal of Neurology, Neurosurgery, and Psychiatry 1992;55:841-843 841 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.9.841 on 1 September 1992. Downloaded from SHORT REPORT Unilateral upper cervical posterior spinal artery syndrome following sneezing N J Gutowski, R P Murphy, D J Beale Abstract settled to 120/80 mmHg. He had a left Hor- A 35 year old man experienced severe ner's syndrome with ipsilateral, trapezius transitory neck pain following a violent weakness, reduced facial sensation to pain and sneeze. This was followed by neurological temperature, C2 anaesthesia, posterior column symptoms and signs indicating a left sided loss and hemiparesis. There was right sided upper cervical cord lesion. MRI showed spinothalamic loss below T4. At presentation an infarct at this site in the territory ofthe he had a flaccid left sided weakness with a left posterior spinal artery. This discrete global reduction in power to 1/5 in the arm and infarct was probably due to partial left 2/5 in the leg and reduced reflexes. After 5 days vertebral artery dissection secondary to there was left sided increased tone, pyramidal sneezing. weakness with 2/5 power in the arm and 3/5 in the leg, brisk reflexes and an extensor plantar (J Neurol Neurosurg Psychiatry 1992;55:841-843) response. Normal investigations included CT head Infarction in the area supplied by the posterior scan, full myelogram and CSF examination. A spinal artery is rarely recognised clinically. We full vascular screen was normal except verte- report a discrete upper cervical posterior spinal bral dopplers which showed slower flow on the artery syndrome following a violent sneeze. left side. The MRI 7 days after admission revealed the presence of abnormal increased signal from C1 to C3 on the left side of the Case report cord on T2 and proton density weighted After a violent sneeze, a previously healthy 35 images. Axial Ti images before contrast year old man had severe left sided neck pain showed no evidence of increased signal or cord lasting 10 minutes. An hour later he developed expansion. After intravenous Gadolinium a left hemiparesis and hemisensory loss over 30 DTPA there was peripheral enhancement cor- minutes. These symptoms persisted. The next responding to the area of increased signal in day paraesthesiae ascended from the right foot keeping with acute infarction (fig 1). The left to the mid-trunk over half an hour and he also vertebral artery at this level was considerably developed urinary retention. There was no smaller than the right. No intracranial abnor- diplopia or dysphagia. He had not smoked for mality was seen. There was no evidence of http://jnnp.bmj.com/ seven years. hind-brain herniation, or of a cervical syrinx. On examination he was initially hypertensive Vertebral angiography was not felt to be at 160/120 mmHg, but after 12 hours this clinically justified. Neurology Department, North Staffordshire Royal on October 1, 2021 by guest. Protected copyright. Infirmary, Princes Road, Hartshill, Stoke-on-Trent, ST4 7LN, UK N J Gutowski R P Murphy X-Ray Department, Walsgrave Hospital, Walsgrave, Coventry, UK D J Beale Correspondence to: Dr Gutowski, Ludwig Institute for Cancer Research, (Middlesex Hospital/University College Branch), Courtauld Building, 91 Riding House Street, London WIP 8BT, UK MR Scan seven admission. Axial Ti SE 510/25 intravenous Received 6 August 1991 Figure I (OST) days after weighted image after and in revised form gadolinium contrast showing peripheral enhancement in the left postero-lateral aspect of the cord at C2 (left). Coronal Tl 2 December 1991. weighted post-contrast SE 320/25 image showing enhancement on the left lateral aspect of the cord between Cl and C3 Accepted 9 December 1991 (right). 842 Gutowski, Murphy, Beale overlapping but discrete (fig 2). The former J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.9.841 on 1 September 1992. Downloaded from was supplied entirely by the anterior spinal artery and the latter received supplies from both the anterior and posterior spinal arteries via the pial plexus. The lesion predicted anatomically corre- sponded both to the area supplied by the left posterior spinal artery,2 that is, the left postero- lateral rim ofthe cord (fig 2), and to the area of infarction seen on MRI (fig 1). Firstly, this demonstrates that cord infarction can be vis- ualised by MRI when myelography is normal. Secondly, that the lesion causing the neuro- logical signs was an infarct in the region Anteric Lateral S-,pinotharmic r vt a rtervB supplied by the left posterior spinal artery at c'. - Cervical -i- -- Thoracic the level of C1-3. L Lumbar S Sacral Posterior spinal artery syndrome is rarely recognised clinically though there are a few Figure 2 Cervical cord cross-section at C2. On the left showing the areas supplied by the clinico-pathological reports of mainly bilateral peripheral and central arterial systems. On the right showing the main tracts, and the cases.34 The cardinal feature is posterior col- grey tone area indicating the projected lesion in the present case. umn involvement. In the presence of damage to the posterior horns there is suspended global anaesthesia. This posterior spinal artery syndrome cannot occur in a pure form since A diagnosis of upper cervical infarction in the posterior spinal arteries do not supply an the region supplied by the left posterior spinal area with clear cut boundaries and the pyra- artery was made, probably secondary to partial midal and antero-lateral tracts are often left vertebral artery dissection. involved.5 The cause of posterior spinal artery He was treated with aspirin and physio- occlusion is rarely ascertained. In early cases therapy. He recovered continence after a fort- syphilitic arteritis was suspected. In single night. By 9 weeks the left hemiparesis had cases indirect trauma, atheromatous embolisa- virtually resolved and dorsal column sensation tion and intrathecal phenol have been the had returned in the left arm. cause.3 Considerable neurological improve- At 14 weeks the MRI showed some resolu- ment can occur after infarction, as in the tion of the signal change and a lack of post- present case, if the patient survives the initial contrast enhancement, this was consistent with period of swelling and oedema. a previous episode of infarction. The inequality It is probable that this unusual left posterior in size of the vertebral arteries remained. spinal artery syndrome was due to partial left vertebral artery dissection secondary to sneez- ing. Vertebral artery dissection would have Discussion occluded a posterior radicular artery arising The combination of neurological signs could from it at the upper cervical level, in turn only be explained anatomically by a single infarcting the area supplied by the posterior lesion on the periphery of the left side of the spinal artery.2 MRI showed the left vertebral http://jnnp.bmj.com/ cord postero-laterally between Cl and C3. At artery to be smaller than the right, and this level the left dorsal column and pyramidal although this may be a normal variant it was tracts were affected below their decussations in felt to be compatible with a dissection, though the lower medulla. In addition at the postero- the definitive investigation of angiography was lateral aspect of the cord, the left C2 sensory not thought to be clinically justified. As our root and the descending tract and nucleus ofV patient started to improve before a definitive were damaged. The most caudal part of the diagnosis was made, he was treated with nucleus and tract ofV extends to C3. aspirin and was not anticoagulated. on October 1, 2021 by guest. Protected copyright. Twenty four hours after the first neurological Most cases of vertebral artery dissection signs he developed right sided spinothalamic have been triggered by cervical manipulation.6 loss to a level of T5 and a left Horner's Abnormal neck movements during other activ- syndrome due to involvement of the posterior ities -l0 including nose blowing," can cause two-thirds of the left lateral spinothalamic dissection of the cervicocerebral arteries. We tract,' (fig 2). Left trapezius weakness was propose that in this case, neck movement caused by damage to the motor axons of the during sneezing caused vertebral dissection. spinal accessory nerve and anterior cervical Two cases of left upper cervical cord infarc- roots coursing through the left antero-lateral tion associated with left sided medullary part of the cord, which also contained the infarction, secondary to left vertebral artery posterior two thirds of the left lateral spino- dissection documented on angiography, have thalamic tract. been reported.78 In neither case was the The history of abrupt onset of signs follow- infarct visualised. ing a violent sneeze suggested a vascular cause. It is unlikely that the cause of this unusual Turnbull et al2 in a detailed microangiographic left posterior spinal artery syndrome was a study of the cervical cord blood supply showed fibrocartilaginous embolus to the spinal arter- that the cord itself was supplied by two arterial ies for the following reasons. In fibrocartilagi- systems, central and peripheral, which were nous embolism most of the emboli are found Unilateral upper cervical posterior spinal artery syndrome following sneezing 843 5 Lazorthes G. Pathology, classification and clinical aspects of J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.9.841 on 1 September 1992. Downloaded from in vessels in the anterior part of the sub- vascular diseases of the spinal cord. In: Vinken PJ, Bruyn arachnoid space, usually in the distribution GW, eds. Handbook of clinical neurology. Oxford: North- Holland, 1972;12:492-506. of the anterior spinal artery.'2 13 Also, the 6 Sherman DG, Hart RG, Easton JD.
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