Our patient was a 62-year-old retired accountant of previous good health. He was not taking any medications and had no family history of neurological disease. He was involved in a minor road traffic accident in which his car was shunted from behind. No immediate injuries were sustained; however, he presented to his general practitioner 4 days later with lumbar spine discomfort. He was prescribed a codeineeparacetamol combination pill and diclofenac. Immediately after taking the first dose of these medications he developed severe dizziness and marked vomiting, which culminated in mild haematemesis, indicative of a MalloryeWeiss tear. Subsequently he discovered that he was dyspnoeic lying flat. He presented to his local emergency department with symptoms including marked orthopnoea, and dyspnoea on water immersion past his costal margin and on bending forward. Physical examination showed gross paradoxical abdominal motion and mild breathlessness when recumbent. Respiratory system, some left basal crackles; cardiovascular system, normal; abdomen, normal; neurology, normal. Arterial blood gas measurements showed a PaO2 of 11.1 kPa and a PaCO2 of 5.1 kPa. A chest radiograph showed an elevated left hemidiaphragm with some atelectasis above it. A CT pulmonary angiogram excluded any diaphragmatic rupture or pulmonary embolus as an underlying cause of orthopnoea. His sniff nasal inspiratory pressure (SNIP) was measured at 22 cm H2O. Detailed testing showed no response to bilateral anterior magnetic phrenic nerve stimulation or to right unilateral phrenic nerve stimulation, with a greatly reduced response to left-sided stimulation (twitch transdiaphragmatic pressure 1.3 cm H2O; normal >8 cm H2O). Pulmonary function tests (performed in the erect position) were consistent with diaphragm paralysis, showing a restrictive pattern with mildly reduced carbon monoxide gas transfer (TLCO 82% predicted) which became supernormal when corrected for alveolar volume (KCO 116% predicted). Forced vital capacity (FVC) was 64% predicted, with a forced expiratory volume in 1 s (FEV1)/FVC ratio of 81% and stable over the course of 7 months follow-up. Clinic FVC testing in the erect position was 2.8 and 1.5 litres when supine (54% reduction). Upright cervical spine MRI revealed minor degenerative changes at C5/6 only. Nerve conduction studies (arms and legs) and needle electromyograph (EMG) examination of the upper limbs were normal.