Association of brain lymphoma and WHO grade II oligodendroglioma in a same immunocompetent patient.

A 59-year-old man with no previous medical history presented with generalized seizures in December 2006. Brain magnetic resonance imaging (MRI) revealed a unique nonenhancing T1 hypointense and fluid-attenuated inversion-recovery (FLAIR) hyperintense lesion, involving the left frontal lobe (Fig 1). Awake surgery with intraoperative language mapping was performed, with a complete resection verified on postoperative MRI. The neuropathologic examination demonstrated a WHO grade 2 oligodendroglioma (Fig 2). There was a codeletion 1p19q. The patient had no postoperative deficit and returned to a normal life. Neither radiotherapy nor chemotherapy was administrated. Corticosteroid therapy with prednisolone was stopped 6 weeks after surgery. Follow-up cerebral MRIs conducted at 3 months and 9 months revealed no signs of tumor recurrence. The patient had no seizures under levetiracetam treatment at 2 g/d during 15 months. The patient was rehospitalized in March 2008 for complex partial status epilepticus with slowness of initiation and a persistent motor aphasia. He was afebrile with normal laboratory results. Brain MRI showed multiple lesions, involving the right temporal, frontal, and central regions, with a hypersignal on T2 FLAIR and contrast uptake on injected T1 (Fig 3A). Sudden occurrence of multifocal enhanced contrahemispheric lesions after more than 1 year of complete stabilization was very atypical for a WHO grade 2 glioma. Immunologic evaluation as well as lumbar puncture were normal, with normal cytochemistry, lactate dehydrogense, and Beta 2 microglobulin assays. HIV, EpsteinBarr virus, Herpes virus, and cytomegalovirus serologies were negative. The ophthalmologic examination was also normal, especially with no uveitis. Epilepsy was controlled under fosphenytoin. Corticosteroid therapy with prednisolone at 1 mg/kg was administrated, with neurologic improvement. A new MRI performed 1 month later revealed a total disappearance of the right hemispheric lesion (Fig 3B). Such history was not compatible with anaplastic transformation of a WHO grade 2 glioma. Corticosteroid therapy was progressively decreased in 5 months. At this moment, the patient again presented with repeated partial epileptic seizures, with reoccurrence of language disorders combined to a right hemiparesis. A new cerebral MRI revealed the appearance of several nodular contrast uptakes involving both hemispheres as well as the corpus callosum, and associated with a left frontoinsular hyperintensity on FLAIR-weighted MRI (Fig 4). A cerebral biopsy was thus performed, with no corticosteroid therapy. The neuropathologic study described lesions demonstrating a diffuse large B-cell lymphoma, polymorphic centroblastic type (revised European-American lymphoma REAL classification). On immunocytochemistry, the CD20 and the MUM1 were strongly positive (Fig 5). The pelvic-abdominal-thoracic scanner as well as the positron emission tomography scan did not reveal any abnormalities. It was, therefore, a primitive non-Hodgkin’s cerebral lymphoma. It is worth noting that the samples from the first surgery 18 months before were re-examined, with confirmation of the diagnosis of WHO grade 2 oligodendroglioma. Chemotherapy was instituted with an RMVBP Fig 1. Fig 2. JOURNAL OF CLINICAL ONCOLOGY D I A G N O S I S I N O N C O L O G Y