Introduction Vertebral artery dissection (VAD) is a common cause of ischemic stroke in patients younger than 45 yrs of age. VAD is rarely life–threatening but we here present a patient with VAD who developed fatal apnoea.

Case Presentation A 70 year old lady with a history of chronic obstructive pulmonary disease, smoking and diabetes mellitus presented had been lifting in a cramped attic and developed discomfort across the shoulders 2 days previously. The following day she noticed progressive weakness in all four extremities increasing dyspnoea and increasing pain across the shoulders. On examination she was dyspnoeic and was unable to lie supine because of this. She had left sided miosis, gaze evoked nystagmus. She had quadriparesis with pyramidal type weakness in the legs and reduced arm, reflexes. Her plantars were extensor. She had a sensory level to pin prick at about T10. She had post void bladder retention of >200 ml. The vital capacity was 1.3 litres sitting and 0.7L supine. Two hours after admission the patient was found to be apnoeic. A CT pulmonary angiogram showed no pulmonary emboli. The patient required ventilator support and inotropes but she deteriorated she had dexamethasone, spinal drain inserted to help spinal cord edema and died over 48 hours.

MRI of cervical spine showed infarction of the anterior spinal cord from C 2 to T1 which was confluent rostrally and extended into a typical snake eye appearance caudally. The right vertebral artery showed focal narrowing typical of dissection. The brain MRI including medulla were normal.

Discussion This patient had subacute onset of cervical cord infarction. The history and MRI findings were in keeping with cervical dissection. The vertebral artery is most vulnerable as it travels in the vertebral foramen and makes a curvature at C1–2 and dissection at this point usually causing cerebellar infarction and lateral medullary syndrome. A spinal cord infarct may occur if the extra–cranial vertebral artery is involved. Intracranial vertebral arterial dissection has a poor prognosis for neurological recovery but are usually not fatal. Extracranial VAD may cause spinal cord infarction but respiratory failure associated with this has only been reported once previously to our knowledge. Cardio–respiratory decompensation is uncommon with any VAD but rarely occurs as a result of progressive ischaemia of the dorsolateral medulla. We found case reports which associates cardiorespiratory arrest with vertebral artery dissection and central apnea related to VAD. In that case a variability in the anatomy of vertebral arteries and origin of anterior spinal artery appears to have been important. Anticoagulation and thrombolysis are generally contraindicated in intracranial dissections because there may be a co–existing sub arachnoid haemorrhage. In extracranial dissection thrombolytics have been used with good effect in individual cases and should be considered in patients with cervical spinal cord infarction related to dissection.