Posterior reversible encephalopathy syndrome (PRES) is a rare clinicoradiographic entity manifesting as headache, confusion, seizure and/or visual disturbance with cerebral oedema demonstrated in the posterior portions of the cerebral hemispheres on computer tomography (CT)/magnetic resonance imaging (MRI) [1, 7]. It has been reported in association with a number of conditions including acute hypertension, eclampsia, immunosuppressive medication, infection and autoimmune disease [2, 9]. To our knowledge, only two cases of PRES have been previously reported following liquorice ingestion [3, 8]. A previously well 65-year-old woman presented with sudden onset confusion and disorientation. On questioning, she denied any history of neurological disease or taking prescription/recreational drugs. Physical examination revealed slurred speech but no focal neurological signs. Her blood pressure (BP) was 160 9 95 mmHg, pulse rate 88 bpm and temperature 36.4 C. Initial investigations including standard blood tests, toxicology screens, lumbar puncture, CT-head and EEG demonstrated no acute abnormalities. Four days after admission for observation the patient complained of severe occipital headache and loss of vision. She was noted to have reduced visual acuity and bilateral fine resting tremor in her upper limbs exacerbated by purposeful movements. Her systolic BP had risen to above 220 mmHg and repeat blood tests showed plasma sodium of 144 mmol/L, potassium of 3.5 mmol/L and creatinine of 284 lmol/L. A second CT-head revealed hypodensities in the cortical and subcortical regions of the occipital, parietal and posterior frontal lobes with no signs of intracranial haemorrhage or infarction (Fig. 1). An MRI-brain next demonstrated hyperintensities within the same distribution (Fig. 2). A diagnosis of PRES with severe hypertension was made. The patient was transferred to the intensive care unit (ICU) and treated with labetalol and supplementary metoprolol and amlodipine. An arterial blood gas in the ICU showed plasma sodium of 148 mmol/L, potassium of 2.6 mmol/L, bicarbonate of 40 mmol/L, and pH of 7.51. Evaluation for secondary causes of hypertension demonstrated recumbent plasma renin activity of less than 0.08 ng/L/s (normal 0.08–0.64 ng/L/s), recumbent plasma aldosterone activity of less than 70 pmol/L (normal 110–620 pmol/L) and renal artery stenosis following CT-angiography. Her serum cortisol, thyroid stimulating hormone and thyroxine levels were normal and urinary catecholamines unremarkable. The patient’s daughter subsequently revealed that the patient had binged on black liquorice in the immediate days prior to admission. After two further days in intensive care the patient became normotensive, her antihypertensive therapy was withdrawn, and, she developed a marked diuresis (urine output greater than 200 mL/h for 14 hours). The patient spent a further R. D. Morgan (&) Department of Medicine, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK e-mail: robert.morgan@doctors.org.uk