A 63-year-old woman with a history of multiple sclerosis and chronic musculoskeletal pain was found unresponsive in bed by her husband at about 1100 h. A year prior, the patient had been prescribed fentanyl patches for postoperative pain, which she did not use. Her usual daily medications included hydromorphone 9 mg 3 times per day, zopiclone 7.5 mg every night at bedtime and pregabalin 75 mg twice per day, all of which had been taken at the same dose at which they had been used for the last year, except for the hydromorphone. In the weeks before her presentation to hospital, the patient had not been taking her hydromorphone as prescribed because of adverse effects. At about 2300 h the evening before her arrival in the emergency department, the patient had reported increasing pain and applied three 12 µg fentanyl patches, doubling her daily morphine equivalent dose by the time she was found unresponsive 12 hours later. Her husband performed 10 minutes of cardiopulmonary resuscitation without checking for a pulse. When paramedics arrived, the patient had a pulse of 91 beats/min and was in normal sinus rhythm, with a blood pressure reading of 94/57 mm Hg and oxygen saturation of 84%. She awoke after naloxone infusion in the emergency department. Toxicology screening was positive for opiates only. Routine serology testing showed mild transient elevation in transaminase, troponin and creatine kinase levels. Over the following days, the patient showed profound anterograde amnesia and was unable to recall daily autobiographical details, despite meticulously recording them in a journal (Figure 1).Neurologic examination identified anisocoria and mild spastic paraparesis, which were unchanged from a previously documented examination 3 years earlier. Her Montreal Cognitive Assessment score was 19/30: she lost 3 points for date, month and day; 5 points on delayed recall despite intact immediate recall; and 1 point on each of trails, cube and repetition. No prior cognitive testing was available for comparison. Gadolinium-enhanced magnetic resonance imaging (MRI) of the head performed on day 7 showed striking bilateral gyriform hippocampal hyperintensity on T 2 -weighted imaging with corresponding restricted diffusivity on diffusion-weighted imaging (Figure 2), in addition to white-matter lesions compatible with multiple sclerosis that were stable on comparison with previous imaging. Electroencephalography done the same day showed no epileptiform activity. The patient's cerebrospinal fluid profile was unremarkable, and results of polymerase chain reaction testing for herpes simplex virus were negative. Results of testing for arbovirus and syphilis, and a routine paraneoplastic antibody panel were also negative.Magnetic resonance imaging of the head on day 12 showed complete resolution of the previously seen hippocampal diffusion PRACTICE | CASES VULNERABLE POPULATIONS CPD