A 25-year-old woman with recently diagnosed systemic lupus erythematosus and class IV lupus nephritis confirmed with biopsy and treated with mycophenolate mofetil presented with a 2-day history of progressively worsening edema of her face and lower extremities. She had no antecedent infection or vaccination. She was admitted to the hospital and treated with methylprednisolone, furosemide, and C1 esterase inhibitor. On hospital day 2, she experienced a witnessed generalized tonic-clonic seizure. At that time, she became hypoxic and was intubated for airway protection. Her laboratory study results preceding the seizure were remarkable for hyponatremia, with a blood sodium level of 122 mEq/L (122 mmol/L) (normal range, 135–145 mEq/L [134–145 mmol/L]), which was corrected to 137 mEq/L (137 mmol/L) over 48 hours. Same-day cerebrospinal fluid analysis was unremarkable, and unenhanced head CT findings (not shown) were normal, with no evidence of intracranial hemorrhage or edema. Her subsequent hospital course was complicated by renal failure requiring continuous renal replacement therapy, hypertension (systolic blood pressure ranging from 140 mm Hg to 190 mm Hg), anemia requiring blood transfusions, thrombocytopenia, and pneumonia. She remained intubated with a limited neurologic examination due to sedative medications until hospital day 10. After extubation, she was noted to have a right gaze preference. She was able to speak in short phrases and follow simple commands. Neurologic examination was notable for drowsiness, right gaze deviation, direction-changing torsional nystagmus, horizontal ophthalmoplegia, and generalized symmetric weakness without upper motor neuron signs. The following day (hospital day 11), unenhanced MRI of the brain was performed (Fig 1) along with MR angiography of the brain (Fig 2). Biopsy of the temporal artery was normal, without evidence of inflammation.Axial diffusion-weighted images (Fig 1a, 1d) showed symmetric areas of bilateral paramedian thalamic and pontine hyperintensity that had corresponding hypointensity on the apparent diffusion coefficient map (not shown); this was compatible with diffusion restriction and was thought to represent cytotoxic edema. Axial T2 fluid-attenuated inversion recovery images (Fig 1b, 1e) showed more extensive confluent T2 hyperintensity with swelling involving the bilateral thalami, brainstem, and middle cerebellar peduncles, compatible with vasogenic edema. Within the areas of diffusion restriction, the susceptibility-weighted images (Fig 1c, 1f ) showed punctate hypointensity within the areas of restricted diffusion in the bilateral thalami and pons, compatible with microhemorrhages. Meanwhile, MR angiography of the circle of Willis (Fig 2) showed no stenosis of the basilar artery. There were subtle short segment stenoses involving bilateral external carotid arteries, the right V4 segment, and the right P2 segment. This was confirmed with diagnostic catheter angiography (not shown). However, biopsy of an affected narrowed temporal artery revealed no evidence of vasculitis. At 1-month follow-up in the setting of improved symptoms and treatment of hypertension, axial diffusion-weighted images (Fig 3a, 3d) showed reso- lution of the prior diffusion restriction involving the paramedian thalami and pons. In addition, axial T2 fluid-attenuated inversion recovery imaging (Fig 3b, 3e) showed resolution of the prior extensive confluent T2 hyperintensity and associated swelling involving the bilateral thalami, pons, and middle cerebellar peduncles. Meanwhile, axial susceptibility-weighted imaging (Fig 3c, 3f ) showed persistent punctate microhemorrhages in the bilateral thalami and pons. What is your diagnosis?