Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

'Pure motor hemiplegia' is a common stroke syndrome defined by Fisher as paralysis of face, arm, and leg on one side, unaccompanied by sensory signs, visual field defect, aphasia, or apractognosia. It occurs almost exclusively in hypertensive patients and carried a good prognosis. We report a case of a normotensive patient in whom pure motor hemiplegia was the presenting feature, not of a cerebrovascular syndrome, but of a pontine glioblastoma. We note that brain-stem tumours may masquerade as brain-stem strokes.
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PMID:Pure motor hemiplegia secondary to brain-stem tumour. 17 27

Two patients, in whom visual disturbance (Case 1) and sudden hemiparalysis due to a hemorrhagic lesion (Case 2) had led to craniotomy and histological diagnosis of giant cell glioblastoma, each had an unexpectedly long survival period of 7 and 9 years, respectively. Radiologically, the tumours were well demarcated, but without any distinguishing features, by comparison with glioblastomas in general. The tumours, to a great extent, consisted of cells with large, bizarre multiple nuclei. The highly pleomorphic cells displayed strong cytoplasmic GFAP immunopositivity, which suggested an astroglial origin. Thus, these tumours were considered a variant of glioblastoma ("giant cell glioblastoma") with a more favourable prognosis than experienced by most patients with glioblastoma.
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PMID:Giant cell glioblastoma: a work-up of 2 cases with long survival. 271 38

Reversible osmotic blood-brain barrier (BBB) modification was used in 38 patients with glioblastoma to enhance the delivery of chemotherapeutic agents. The patients ranged in age from 14 to 70 years (mean, 43), and all had prior surgery and radiation; 5 had also received systemic chemotherapy. Karnofsky Performance Status (KPS) scores ranged from 60 to 100% (mean, 79) on admission to the treatment program. Barrier modification was achieved by intracarotid or intravertebral artery infusion of mannitol, and a chemotherapy regimen of methotrexate, cytoxan, and procarbazine was given in conjunction with barrier modification. The 38 glioblastoma patients were compared to two control groups of patients with glioblastoma; these encompassed 14 patients treated with surgery and radiation and 8 treated with surgery, radiation, and systemic chemotherapy. Survival analysis using the Cox Proportional Hazards Regression Model (corrected for age, sex, presence or absence of necrosis, and functional status) showed that patients receiving chemotherapy with BBB modification had a statistically significant (P = 0.0006) longer expected survival (17.5 months) than the control groups (12.8 and 11.4 months, respectively). Presently 16 patients of the barrier-enhanced treatment group are alive at 5 to 42 months from diagnosis (median, 20) with KPS scores ranging from 40 to 90% (median, 65). The neurological complications seen included a stroke-like syndrome in 3 patients (1 with decreased motor movement in the hand, 1 with marked hemiparesis, and 1 with hemiplegia), transient exacerbation of preexisting neurological deficits lasting 2 to 3 days, and a 15% incidence of seizures during or within 24 hours of the BBB modification. In 2 of the 38 patients, radiographic documentation of central nervous system tumor regression concurrent with the development of new tumor nodule(s) in portions of the brain distant from the region of osmotic BBB opening was seen. These studies indicate that chemotherapeutic drug delivery to tumors (as well as surrounding brain) can be augmented by osmotic BBB modification and that such therapy can result in a prolongation of survival.
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PMID:Therapeutic efficacy of multiagent chemotherapy with drug delivery enhancement by blood-brain barrier modification in glioblastoma. 309 67

Gliomas are the most common intracranial tumors. In the US, approximately 15,000 patients die with glioblastoma per year (CBTRUS 2002). Despite modern diagnostics and treatments the median survival time does not exceed 15 months. However, it has long been observed that after surgical removal, tumors recur predominantly within 1 cm of the resection cavity. This is mainly due to the fact that at the time of surgery, cells from the bulk tumor have already invaded normal brain tissue. Decades ago Matsukado showed that more than 50% of untreated brain tumors had already reached the contralateral hemisphere (J Neurosurg 18: 636-644, 1961). Therefore one of the most important hallmarks of malignant gliomas is their invasive behavior. Dandy already recognized the highly invasive characteristics of this tumor type and performed hemispherectomy in patients with preoperative hemiplegia (J Am Med Assoc 90: 823-825, 1928). Despite his and others' heroic efforts, recurrence was detected as early as 3 months after surgery (Bell, LJ: J Neurosurg 6: 285-293, 1949), leading to the discontinuation of this radical approach. Diffuse gliomas remain a particularly challenging clinical management problem. Over the last 20 years no significant increase in survival of patients suffering from this disease has been achieved. Even drugs directed against newly identified targets like MMPs or angiogenesis-related targets fail to increase survival duration (Tonn, Goldbrunner: Acta Neurochir Suppl 88: 163-167, 2003) Furthermore, anti-angiogenic drugs have been shown to increase glioma invasiveness, finally leading to gliomatosis cerebri. (Lamszus et al.: Acta Neurochir Suppl 88: 169-177, 2003). In this review we focus on the main features which may underlie the invasive phenotype of human gliomas, and offer a biological basis for optimism towards therapeutic advances to come.
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PMID:Molecular mechanisms of glioma cell migration and invasion. 1567 79

Diagnosis of tuberculoma is difficult because of its tumorlike aspects. This report describes the case of a male who displayed a hemiplegia revealing an intracranial mass. Neuroimaging was consistent with a glioblastoma; however, the definite diagnosis was a tuberculoma. Clinical features of tuberculomas are nonspecific. Even though the neuroimaging features are sensitive, they are much less specific, with variability related to the tuberculoma course. Investigations leading to the diagnosis are histologic analysis showing a granuloma with or without caseating necrosis, and the microbiologic identification of Mycobacterium tuberculosis. Every intracranial tumor with malignant radiologic and clinical appearance must evoke a suspicion for tuberculoma.
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PMID:Pseudotumor presentation of intracerebral tuberculomas. 1589 33

There is no standard of care for elderly patients with glioblastoma (GBM) and poor performance status. A 79-year-old woman with GBM, aphasia, and hemiplegia achieved a complete response after only one cycle of temozolomide (TMZ) (150mg/m2/day over 5 days). Genomic profiling of the tumor demonstrated loss of chromosome 10 and MDM2 amplification, which are predictive of poor outcome. The MGMT promoter was methylated, and it is likely that this at least partially explains the exquisite chemosensitivity in our patient. This unusual case report suggests that TMZ warrants further investigation in elderly patients with poor performance status.
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PMID:Complete response after one cycle of temozolomide in an elderly patient with glioblastoma and poor performance status. 1831 94

Bevacizumab is expected to constitute a new treatment modality for radiation necrosis. In the present cases, we observed a recurrence of radiation necrosis after temporary improvement by bevacizumab treatment. Re-treatment with bevacizumab controlled the necrosis again. A 39-year-old male and a 57-year-old female were diagnosed with glioblastoma and lung cancer metastasis, respectively. The former patient underwent partial resection of the glioblastoma, followed by boron neutron capture therapy (BNCT) and 30 Gy of fractionated X-ray radiotherapy. Eleven months after BNCT, he suffered from left hemiparesis and convulsions with enlargement of a perifocal edema. The latter patient underwent stereotactic radiosurgery twice for the same tumor. Three months after the second radiosurgery, she had an uncontrollable convulsion and right hemiplegia with a massive perifocal edema. Both lesions were suggested to be radiation necroses by positron emission tomography using amino acids as a tracer. Neither patient responded to corticosteroids, anticoagulants, or vitamin E. They underwent treatment with 5 mg/kg bevacizumab biweekly, for a total of 6 cycles. The size of the perifocal edema was clearly reduced in response to the treatments. The neurological status of the patients improved concomitant with therapy. However, the clinical status of both patients was aggravated several months after the bevacizumab was stopped, and the perifocal edemas enlarged again. The patients underwent a second treatment with bevacizumab, and the perifocal edemas again decreased. Although radiation necrosis may recur several months after bevacizumab treatment, repeated bevacizumab treatments also appear to be effective.
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PMID:Repeated treatments with bevacizumab for recurrent radiation necrosis in patients with malignant brain tumors: a report of 2 cases. 2069 73

Nivolumab is an immune checkpoint inhibitor (ICI) currently undergoing Phase III clinical trials for the treatment of glioblastoma. The authors present the case of a 10-year-old girl with glioblastoma treated with nivolumab under compassionate-use guidelines. After the first dose of nivolumab the patient developed hemiparesis, cerebral edema, and significant midline shift due to severe tumor necrosis. She was managed using intravenous dexamethasone and discharged on a dexamethasone taper. The patient's condition rapidly deteriorated after the second dose of nivolumab, demonstrating hemiplegia, seizures, and eventually unresponsiveness with a fixed and dilated left pupil. Computed tomography of her brain revealed malignant cerebral edema requiring emergency decompressive hemicraniectomy. Repeat imaging demonstrated increased size of the lesion, reflecting immune-mediated inflammation and tumor necrosis. The patient remained densely hemiplegic, but became progressively more interactive and was ultimately extubated. She resumed nivolumab several weeks later, but again her condition deteriorated with headache, vomiting, swelling at the craniectomy site, and limited right-sided facial movement following the sixth dose. MRI demonstrated severe midline shift and uncal herniation despite her craniectomy. Her condition gradually declined, and she died several days later under "do not resuscitate/do not intubate" orders. To the authors' knowledge, this represents the first case of malignant cerebral edema requiring operative intervention following nivolumab treatment for glioblastoma in a pediatric patient.
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PMID:Severe cerebral edema following nivolumab treatment for pediatric glioblastoma: case report. 2785 78

We report a case of glioblastoma due to putaminal hemorrhage. Notably, the glioblastoma was located at some distance from the hematoma. A 42-year-old right-handed man presented with a sudden-onset headache, motor aphasia, and right hemiplegia. CT showed left putaminal hemorrhage and a mass lesion with a slightly high density in the midbrain away from the hematoma. Conservative treatment was initiated for the patient. Initially, we suspected a benign tumor-like cavernous malformation based on the CT findings. However, MRI showed ring enhancement of the mass lesion on contrast-enhanced MRI and hyperintensity on arterial spin labeling(ASL). A part of the wall of the putaminal hemorrhage also exhibited hyperintensity on ASL. Since we suspected a malignant brainstem tumor and a secondary intracerebral hemorrhage caused by this tumor, we performed a stereotactic brain biopsy. Histological examination revealed that the tumor was a wild-type <i>IDH-1</i> glioblastoma. In the acute phase, the intracerebral hemorrhage presented as a hyperintensity on T1-weighted imaging. Therefore, it was difficult to distinguish hemorrhagic glioblastoma from an intracerebral hemorrhage. Even if an intracerebral hemorrhage is observed at common sites, it is important to consider the possibility of a malignant brain tumor and complete a prompt examination. In addition, ASL imaging may be useful in detecting hemorrhagic malignant brain tumors.
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PMID:[A Case of Putaminal Hemorrhage Caused by Underlying Tectal Glioblastoma]. 3307 Dec 28