No abstract

No abstract

No abstract

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.

Sirs: Lumbar puncture is not a completely innocuous procedure. Severe neurological complications including meningitis, cranial nerve or nerve root involvement, brain stem herniation, subdural hematoma, subarachnoid hemorrhage and cerebral venous thrombosis occur in less than 0.5 % of the cases [8]. We report a patient who developed an isolated cortical venous thrombosis after a lumbar puncture.A right-handed, 35-year-old woman, taking oral contraceptives, presented with chronic paresthesias and weakness of the left hand for 4 years. She was also complaining of recurrent buccal aphthosis. The clinical examination revealed a tetrapyramidal syndrome with left predominance and a mild paresis of the left upper and lower limbs with no facial involvement. Cervical magnetic resonance imaging (MRI) showed a left chronic myelitic lesion in the 3 first cervical segments (Fig. 1). The auditory brain-stem, the visual monocular pattern, and the median and the posterior tibial nerve evoked potentials were normal. The motor evoked potentials (MEPs) were elicited by transcranial and cervical magnetic stimulations and recorded from the abductor pollicis brevi (APB) muscles. The left APBMEPs were delayed after transcranial stimulations but normal after cervical stimulations. These findings suggested an involvement of the pyramidal pathways originating from the right motor cortex either at a right supramedullary level or a left cervical spinal level. A lumbar puncture was performed in the sitting position, using a non atraumatic needle (22G). The cerebrospinal fluid (CSF) was acellular with a normal total protein content. Oligoclonal bands of IgG, specific for the CSF, were found. Serum antinuclear antibody, anti-borrelia and anti-viral (including HIV, EBV, CMV, Hepatitis B and C, herpes zoster and simplex) serologies were negative.Two days after the lumbar puncture, the patient developed a positional post-dural-puncture headache which rapidly progressed to an intense and continuous headache complicated by confusion and left motor partial epileptic seizures with worsening and extension of the left hemiparesis to the face. The EEG showed focal slow waves and spikes in the right fronto-parietal derivations. Cranial computed tomography (CT) revealed focal edema with hemorrhagic effusions over the right fronto-parietal cortex. Brain MRI (Figs. 2 and 3) showed right frontal and fronto-parietal cortical venous thrombosis with no dural sinus involvement. High signal intensity lesions on T2 and FLAIR were also found in the periventricular white matter. Blood studies showed a neutrophilic leukocytosis (15.300 WBC/mm 3 , 89 % neutrophils) and an inflammatory reaction (C reactive protein at 56 mg/L, N < 10). Coagulation tests were unremarkable including protein C, protein S and antithrombin III levels. No mutations of coagulation factors II and V were found and anticardiolipin antibodies were absent.A mild hyperhomocystinemia was found (20.4mMol/L, N < 15).Angiotensin converting enzyme level was normal. She was given valproate (600 mg/day), fo...