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Focal vertebral artery dissection causing Brown-Séquard’s syndrome
  1. P GOLDSMITH,
  2. D ROWE
  1. Department of Neurology
  2. Department of Neuroradiology,
  3. Department of Neurology
  4. National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
  1. Dr R Kapoor, Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.
  1. R JÄGER
  1. Department of Neurology
  2. Department of Neuroradiology,
  3. Department of Neurology
  4. National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
  1. Dr R Kapoor, Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.
  1. R KAPOOR
  1. Department of Neurology
  2. Department of Neuroradiology,
  3. Department of Neurology
  4. National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK
  1. Dr R Kapoor, Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.

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Vertebral artery dissection typically causes an ischaemic brain stem stroke. We report a man who presented with left sided neck pain and Brown-Séquard’s syndrome localised to C1, and in whom a focal C1 ischaemic cord lesion secondary to a localised vertebral artery dissection was found using MRI.

A 47 year old machine operator was admitted as an emergency with neck pain, headache, and gait disturbance. Three weeks before admission he developed minor stiffness of his upper cervical region while decorating his home, which was relieved by ibuprofen. There was no history of neck manipulation or trauma. Two days before admission he awoke with a severe left sided pounding headache and neck ache with an associated cold sensation on the left side of his neck. He was nauseated but did not vomit. His symptoms again resolved within an hour with ibuprofen, but two hours later there followed a tingling sensation in his left index finger, thumb, and forearm spreading up to his elbow. He slept for a few hours but awoke with more generalised paraesthesiae in the left arm which spread over the next 36 hours to involve the left trunk and leg. He noticed minor gait disturbance as well as left eye pain described as “like an ice cream headache”. The remainder of the history was non-contributory.

Apart from xanthelasma the general examination was entirely normal. His blood pressure was 120/80. There was minor limitation of movement of his cervical spine. Cranial nerve examination was normal. Slight spasticity was evident in the left arm and leg. Both plantars were extensor. There was decreased sensation in the distribution of C2 on the left and decreased sensation to pinprick and temperature on the right and to vibration and joint position sense on the left below this. Thus the examination was consistent with Brown-Séquard’s syndrome on the left at the level of C1–2.

Biochemical, haematological, and immunological investigations were normal. Fasting cholesterol was 8 mmol/l, triglycerides 3.80 mmol/l. ECG was normal. CSF protein was 0.63 g/l, glucose 3.1 mmol/l (blood 4.3 mmol/l). There was no xanthochromia. There were three white cells and 57 red cells and no oligoclonal bands. Visual and auditory evoked potentials were normal but there were abnormal somatosensory evoked potentials from the left upper limb. A sagittal T2 weighted MRI showed an area of high signal, consistent with an ischaemic lesion, in the posterior aspect of the cervical cord at the level of C1 (figure). This was shown to involve the left posterior column and left corticospinal tract on corresponding axial cuts. T1 weighted spin echo images through the C1 region showed the typical features of an arterial dissection1 with an eccentric rim of high signal adjacent to a residual flow void in the left vertebral artery. This periarterial collar was distinguished from adjacent fat tissue by a fat suppression sequence. He was anticoagulated with heparin and then warfarin and started on lipid lowering agents. Three months later his original symptoms and signs had resolved completely.

Figure (A) Sagittal T2 weighted fast spin echo sequence (TR/TE 5000/130 ms) through the cervical cord showing an area of high signal (arrow) in the posterior aspect of the cord at C1 level not associated with cord swelling. (B) Axial fat saturated T1 weighted spin echo (TR/TE 480/14 ms) through C1 shows a crescentic high signal rim (arrow) lateral to the narrowed residual lumen of the left vertebral artery as it runs though the C1 transverse foramen.

Vertebral artery dissection has generally been associated with head and neck pain and brain stem stroke. There have, however, been some case reports of vertebral dissection with symptoms initially suggesting cervical involvement. Giroud et al 2 described a woman who had intermittent pain in her right arm for five days before presenting with sudden onset cerebellar dysarthria and diplopia. A few cases seem to remain localised to the cervical cord. Dubardet al 3 described a cervical myelopathy secondary to a vertebral artery dissection. This may have resulted from direct compression by the dissected vertebral artery or from occlusion of a radiculomedullary artery originating from the vertebral artery. There has, however, been only one previous clinical report of vertebral artery dissection associated clearly with a lesion of the cervical cord. Gutowski et al 4 described a man presenting with an ipsilateral Horner’s syndrome, C2 and facial anaesthesia, and posterior column loss, contralateral spinothalamic loss below T4, trapezius weakness, and hemiparesis. The cord was diffusely involved from C1 to C3. This is the level where mechanical torsion and stretch is maximal and where many dissections seem to concentrate, the dissection then spreading proximally or distally. In the present case the high signal intensity lesion within the spinal cord is consistent with an ischaemic lesion in the left posterior spinal artery territory. The posterior spinal arteries supply the posterior columns and adjacent peripheral mantle of white matter. Involvement of the posterior columns is therefore the hallmark of a posterior spinal artery infarct. It is, however, rare in its pure form and more extensive lesions with involvement of the corticospinal tracts, as in our case, are commonly seen and are due to the frequent variations in arterial supply and a complex collateral network.5 We hypothesise that our patient had more extensive involvement or some cord swelling not seen on imaging to explain the bilateral upgoing plantars. The patient’s prior decorating activities may have had an aetiological role: an association with minor and trivial neck trauma is often cited, although the true role of such everyday occurrences is hard to judge. For example, when related to chiropractic manipulation the onset of symptoms is delayed for hours or days. The evolution of symptoms in a stuttering fashion over hours or days is also typical. The nature of his retrobulbar pain is consistent with the hypothesis of referred pain being mediated by the trigeminothalamic tract in migraine and trigeminal autonomic cephalgias.

In conclusion, we draw attention to vertebral artery dissection as a cause of spinal cord ischaemia and Brown-Séquard’s syndrome.

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