A 29-year-old immunocompetent woman was admitted in 2006 with ataxia, limb weakness, generalized dystonia, and vertical diplopia that developed after a febrile episode. Brain magnetic resonance imaging (MRI) revealed the presence of extensive periventricular white matter lesions that did not enhance after gadolinium injection. As low titers of cytomegalovirus-IgM antibodies were found in the serum, a presumed diagnosis of postviral acute disseminated encephalomyelitis (ADEM) was made, and the patient received a 5-day course of 1 g methylprednisolone. The clinical and radiological outcome was very rapidly favorable, and subsequent brain MRIs in 2007 and 2008 were normal. In March 2011, the patient was readmitted with the complaints of abnormal fatigue, imbalance, and speech disorder. The neurological examination showed fluctuating spatiotemporal disorientation with dyscalculia, verbal deafness, gait ataxia, right hemianopia, and pyramidal signs in the four limbs. The brain MRI demonstrated extensive T₂ hyperintense white matter lesions predominating in the left temporal and parieto-occipital lobes, with a pseudotumoral aspect enhancing with gadolinium contrast. A clinical improvement was transiently noted after pulse steroid therapy, but after relapse and radiological worsening, the diagnosis of recurrent ADEM was challenged. The brain biopsy confirmed the presence of primary central nervous system lymphoma (PCNSL) under the variant form of lymphomatosis cerebri. Despite a partial response to chemotherapy, the patient died 8 months after the diagnosis. We discuss the role of sentinel lesions that may precede PCNSL for several years and insist on the importance to consider early brain biopsy in the presence of extensive, non-enhancing white matter lesions, even in a young and immunocompetent patient.

Pregabalin, used for treating partial epilepsy and neuropathic pain, is usually well tolerated. Patients with impaired renal function are at risk to develop more serious adverse events. A 64-year-old woman was admitted in the Emergency Department for altered consciousness and abnormal movements. She recently started to take pregabalin (150 mg/day) for neuropathic pain. The drug was withdrawn 36 h before hospitalization following worsening of neurological symptoms. At physical examination, myoclonus was noted as main finding in the limbs and head, with encephalopathy. Laboratory investigations revealed acute renal failure with serum creatinine at 451.3 μmol/l. Urine output was preserved. After supportive care alone, myoclonus resolved after 24 h and consciousness was normal after 48 h. Renal function was also recovered. At the time of admission, the concentration of plasma pregabalin was 3.42 μg/ml, within therapeutic range. The calculated terminal elimination half-life was 11.5 h. Pregabalin-induced myoclonus may not be strictly related to drug accumulation in acute renal failure, with the possibility of a threshold phenomenon.