A 56-year-old male patient with a history of stage IV non-Hodgkin’s lymphoma presented with neurologic symptoms. Originally diagnosed in 1987, he experienced failure with multiple regimens, including cytoxan, fludarabine, mitoxantrone, and rituxan. He was referred to Dana-Farber Cancer Institute (Boston, MA) in 2003 where he underwent a nonmyeloablative peripheral blood stemcell transplantation. On day 135, he developed mild chronic skin changes of graft-versus-host disease (GVHD), which responded to topical steroids. However, by 9 months, he was diagnosed with extensive chronic GVHD of oropharynx, eyes, skin, and liver. He was given oral prednisone with good results. Three years after transplantation, the GVHD appeared to be in remission, and his low-dose prednisone was discontinued. However, after 3 months, he had desquamation of more than 70% of his body-surface area and was readministered high-dose steroids and mycophenolate mofetil. Just before the prednisone was discontinued, the patient began complaining of weakness, nausea, and vomiting. He had episodes of dizziness and tinnitus, and was thought to have positional vertigo. After a fall, a magnetic resonanceimagingofthebrainwasperformed, whichshowedanexpansile lesion of the corpus callosum with a broad differential diagnosis including infection, inflammation, and neoplasia. The patient began to lose weight and was received sertraline for depression. Subsequently, he developed difficulty rising from chairs due to proximal weakness. Rapamycin was initiated out of concern for muscle GVHD. On physical examination, the patient described a sensation of lightheadedness and impending loss of consciousness. These episodes were sometimes accompanied by nausea, vomiting, and diaphoresis. The patient stated that his legs were becoming progressively weaker, and that he had numbness extending from his feet up to his thighs. Laboratory evaluation showed that thyroid-stimulating hormone, vitamin B12, glycosylated hemoglobin, cytokeratin, and erythrocyte sedimentation rate were normal. In addition, rapid plasma reagin, hepatitis B, and hepatitis C titers were negative. The patient became more depressed and moody, despite an initial response to sertraline. Examination at that time was remarkable for inattention and irritability. He had minimal weakness of intrinsic hand muscles, and four times proximal left lower extremity weakness, in addition to the chronic right foot weakness. Reflexes and sensation were stable. Rapamycin was discontinued, and the patient continued on prednisone. After another fall at home, a repeat brain magnetic resonance imaging demonstrated worsening of the corpus callosum lesions; these lesions were hypodense and expansile on T1 sequences and showed no enhancement after gadolinium administration (Figs 1A and 1D). There was T2 prolongation on