Some patients ultimately diagnosed with primary CNS lymphoma (PCNSL) have transient symptomatic contrast enhancing lesions. These "sentinel lesions" of PCNSL recede spontaneously or with corticosteroid treatment and present an important diagnostic dilemma because they show variable, but non-diagnostic histopathological features.Four previously healthy, immunocompetent patients aged 49 to 58 years had contrast enhancing intraparenchymal brain lesions. Before biopsy, three of the four were treated with corticosteroids. Initial biopsies showed demyelination with axonal sparing in two, non-specific inflammation in one, and normal brain in one. Infiltrating lymphocytes predominantly expressed T cell markers with rare B cells. All four patients recovered within two to four weeks after the initial biopsy and imaging studies showed resolution of the lesions. The CSF was normal in three of the four patients tested; oligoclonal bands were absent in both of the two tested.After seven to 11 months, each patient developed new symptomatic lesions in a different region of the brain, biopsy of which showed a B cell PCNSL. The mechanism of spontaneous involution of sentinal lesions is not understood, but may represent host immunity against the tumour. Sentinel lesions of PCNSL should be considered in patients with contrast Seven months later she again noted fatigue, disorientation, left sided weakness, and visual impairment. Brain CT showed enhancing lesions in the septum pellucidum, head of the right caudate, splenium of the corpus callosum, and at multiple sites in the periventricular white matter. The prior biopsy site in the hypothalamus appeared as a small lucency without enhancement. A stereotactic biopsy of the right caudate lesion in July 1990 showed a B cell lymphoma of the diffuse large cell subtype.

Background: Clinically useful tumor markers have yet to be identified for malignant glioma. We report on two potential novel tumor markers, vascular endothelial growth factor (VEGF) and recoverin (protein A)

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INTRODUCTION: Bevacizumab has been reported to be an effective treatment for symptomatic radiation necrosis and to decrease focal edema around areas of radiation necrosis. We report our preliminary results and ongoing clinical trial of bevacizumab treatment for radiation necrosis. METHODS: Thirteen patients with symptomatic radiation necrosis were treated with bevacizumab. Radiation necrosis was diagnosed according to the patients' clinical courses, magnetic resonance images, and fluoridelabeled boronophenylalanine-positron emission tomography (F-BPA-PET). Lesion/normal (L/N) ratios less than 2.0 and 2.5 on F-BPA-PET were defined as absolute and relative indications for bevacizumab treatment, respectively. The patients were treated with bevacizumab at a dose of 5 mg/ kg every 2 weeks, 6 cycles in total. RESULTS: Two patients were excluded from analysis because of adverse events. Eleven patients underwent 3 to 6 cycles of bevacizumab treatment. The median rate of the reduction in peri-lesional edema was 65.5% (range: 2.0% to 81.0%). The Karnofsky performance status (KPS) improved in 6 patients after bevacizumab treatment, and in 5 patients the status did not change. The L/N ratio on F-BPA-PET (P ¼ 0.0084) and the improvement of KPS after bevacizumab (P ¼ 0.0228) were significantly associated with the reduction rate of peri-lesional edema after bevacizumab treatment. CONCLUSION: Bevacizumab is a very effective treatment for radiation necrosis, irrespective of the original tumor histology. F-BPA-PET could be useful for diagnosing radiation necrosis and for making the decision as to whether or not to treat symptomatic radiation necrosis with bevacizumab. The clinical trial "Intra-venous administration of bevacizumab for the treatment of radiation necrosis in the brain" has been approved as Investigational Medical Care System by the Japanese Ministry of Health, Labour and Welfare. This trial has been ongoing since April, 2011.

The increased potency and greater stability of CPT analogs hold promise for more effective local antitumor treatments against malignant intracranial brain tumors. The greater cytotoxicity of 10,11-MD CPTs in comparison with other CPT analogs as well as CPT, BCNU, or Na-CPT, may present an ideal candidate drug class for development against both primary and metastatic brain tumors.

The inferolateral trunk arises from the internal carotid artery at C-4 and provides vascular supply to cranial nerves III to VI. We report a patient who developed neuropathies of cranial nerves III, V1-3, and VI, 48 hours after infusion of cisplatin into the right internal carotid artery for an anaplastic oligoastrocytoma. The clinical and radiographic findings implicated direct toxicity to nerves in the distribution of the inferolateral trunk. We found additional cases by review of published brain tumor chemotherapy trials, thus identifying a novel, toxic neurovascular mechanism for injury to cranial nerves III to VI.