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A previously healthy 28-year-old Caucasian woman experienced a syncope and was referred to our emergency department. On admission, the patient was neurologically normal and alert. Electrocardiogram (ECG) was normal. Peripheral blood count and blood chemistry, including C-reactive protein and cardiac troponin T, were within normal limits. The patient revealed no history of drug or alcohol abuse. Testing for opiates, benzodiazepines, tricyclic antidepressants and metamphetamine in urine was negative. During the initial clinical assessment, the patient suddenly developed dysarthria, nystagmus on bilateral gaze, left hypoglossal paresis and left arm weakness. Head CT and intracranial CT angiography were performed immediately and revealed no pathology. Following the CT scan, the patient developed acute dyspnoea and hypoxia, and required immediate intubation. ECG now showed high T-waves in precordial leads and cardiac troponin T was measured as 0.93 ng/ml (normal range below 0.03 ng/ml). Transthoracic echocardiography revealed a highly reduced left ventricular ejection fraction of 15–20%. Within 2 hours, the ejection fraction recovered to 40–45% with persisted basal hypokinesia. Brain MRI 4 hours following the onset of brain-stem symptoms revealed acute ischaemic lesions in both cerebellar hemispheres (fig 1A) and in the left dorsolateral medulla oblongata. Magnetic resonance angiography showed multifocal narrowing of both vertebral …
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