Cases reported "Glioblastoma"

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1/52. glioblastoma multiforme in a case of acquired immunodeficiency syndrome: investigation a possible oncogenic influence of human immunodeficiency virus on glial cells. Case report and review of the literature.

    Malignant glioma is the most common primary brain neoplasm, but generally it is not included in the differential diagnosis of enhancing lesions of the central nervous system (CNS) in patients suffering from acquired immunodeficiency syndrome. We report a case of glioblastoma multiforme (GBM) in a 29-year-old man with human immunodeficiency virus (hiv). Primary CNS lymphoma was suspected, making a definitive histological diagnosis crucial. An initial stereotactic biopsy sample was insufficient to establish a diagnosis and a second biopsy of the lesion was obtained. The histopathological investigation confirmed GBM and adjuvant external radiation treatment was given to the patient, who survived for 4 months after the initial biopsy. A decline in the rate of toxoplasma infection and the changing diseases observed in hiv infection indicate the importance of obtaining a biopsy in cases of CNS mass lesions.
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2/52. Right temporal lobe glioblastoma presenting in the left orbit. Case report.

    Dissemination of gliomas outside the central nervous system without preceding neurosurgery is a rare phenomenon. Glial neoplasms presenting as bone lesions are even more rare. A case of glioblastoma multiforme (GBM) with initial presentation in the orbit following a single generalized seizure is described. Signs of intracranial hypertension resulted from subarachnoid tumor invasion. The patient was treated with whole-dose radiation therapy but survived for only 6 months following the initial presentation. An autopsy revealed a right temporal GBM with extensive subarachnoid spread and invasion in the left orbit and skull base. The literature on dissemination of primary tumors of the brain is reviewed.
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3/52. cerebrospinal fluid oligoclonal IgG bands in patients with spinal arteriovenous malformation and structural central nervous system lesions.

    OBJECTIVE: To investigate the incidence and characteristics of patients with structural central nervous system (CNS) lesions and cerebrospinal fluid oligoclonal IgG bands. DESIGN: A retrospective study. METHOD: The medical records of patients with cerebrospinal fluid oligoclonal IgG bands were evaluated for the presence of structural CNS lesions, their location and cause, and for clinical characteristics. SETTING: cerebrospinal fluid oligoclonal IgG bands were examined in the Neuroimmunology Laboratory, Hadassah University Hospital, Jerusalem, israel. patients: Two hundred seventy of 570 patients with positive cerebrospinal fluid oligoclonal IgG bands were available for analysis. Twenty patients had structural CNS lesions. RESULTS: Twenty (7.5%) of the 270 patients had structural CNS lesions: 3 patients had spinal arteriovenous malformation; 5 patients had tumors; 9 patients had compressive cervical myelopathy. Traumatic leukomalacia, arnold-chiari malformation type 1, and CNS hemosiderosis were present in 1 patient each. In 2 patients (1 patient with recurrent meningioma and 1 patient with posttraumatic encephalomalacia) the presence of a structural CNS lesion was followed by the development of multiple sclerosis. In all 3 patients with spinal arteriovenous malformation, oligoclonal IgG identification prolonged the time to diagnosis and therapy, which varied from a few weeks to 3 years. CONCLUSIONS: Structural CNS lesions, responsible for the neurological disorder, were present in 20 patients (7.5%) with cerebrospinal fluid oligoclonal IgG bands. The mechanism underlying oligoclonal IgG presence in spinal arteriovenous malformation and the coexistence of multiple sclerosis and structural CNS lesions is unknown, but may be related to recurrent tissue damage with repeated presentation of CNS antigens to the immune system.
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4/52. Systemic metastasis in glioblastoma may represent the emergence of neoplastic subclones.

    Glioblastomas only rarely metastasize to sites outside the central nervous system, for reasons that are poorly understood. We report the clinicopathological and molecular genetic findings in 6 patients with metastatic glioblastoma. Four patients were under the age of 32 and all but 1 patient died within 2 yr of diagnosis. The number of metastases ranged from 1 to 3. At the time of death, 3 patients had apparent tumor control at their primary site. We evaluated DNA from both primary and metastatic glioblastomas for genetic alterations commonly found in glioblastomas: TP53 mutations, CDKN2A/p16 deletions, EGFR amplification, and allelic loss of chromosomes 1p, 10q and 19q. Four of 6 cases had TP53 mutations and only single cases had EGFR amplification, CDKN2A/p16 deletions, or allelic loss of 1p, 10q and 19q; 2 cases had no detectable genetic alterations. In 2 cases, the primary and metastatic tumors had identical genotypes. Remarkably, however, 2 cases had different TP53 alterations in the primary and metastatic lesions, or among the metastatic tumors, which suggests that some metastatic deposits may represent emergence of subclones that were not necessarily dominant in the primary tumor. The present observations and a review of the recent literature demonstrate that metastatic glioblastomas tend to occur in younger adults who do not follow long clinical courses, and may be characterized by TP53 mutations and differential clonal selection.
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5/52. Rhabdoid glioblastoma.

    Rhabdoid phenotypic change has been described in a number of different neoplasms from diverse organ sites. These tumors share common light and electron-microscopic features, display a polyphenotypic immunohistochemical profile and often show cytogenetic abnormalities of chromosome 22. In the central nervous system (CNS), most rhabdoid tumors occur in the posterior fossa of very young children and are associated with a primitive neuroectodermal tumor (PNET) component and are designated atypical teratoid/rhabdoid tumors. Infrequently, other rhabdoid tumors of the CNS have been described, including rhabdoid meningiomas and malignant rhabdoid tumors of uncertain histogenesis. Several examples of conventional gliomas displaying significant areas with rhabdoid morphology were also presented in an abstract by Kepes and Moral [1991], although never published in final manuscript form. We now detail the case of an 18-year-old male with an aggressive, supratentorial CNS rhabdoid tumor that was associated with an epithelioid glioblastoma and apparently arose from areas of low-grade glioma. The rhabdoid tumor component was present in the original tumor but became more predominant with each of 3 successive resections. No areas of PNET were identified. Electron microscopy and immunohistochemistry showed features classic for rhabdoid tumors and cytogenetic studies demonstrated multiple tumor clones with monosomy 22. This case documents progressive rhabdoid transformation of a glioma, expands the spectrum of CNS tumor types that can display a rhabdoid phenotype and highlights the diagnostic and therapeutic challenges with this type of tumor.
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6/52. glioblastoma multiforme of the brain stem in a patient with acquired immunodeficiency syndrome.

    glioblastoma of the brain stem is rare and there is no description of such a lesion in patients suffering from acquired immunodeficiency syndrome. The majority of intracerebral mass lesions are due either to toxoplasmosis or primary central nervous system lymphomas so that it is usually not included in the differential diagnosis of enhancing lesions of the central nervous system in these patients. A 31-year-old human immunodeficiency virus (hiv) infected man presented with a four months history of slowly progressive deterioration of brainstem associated symptoms despite antitoxoplasmic therapy. magnetic resonance imaging revealed a large ring enhancing lesion in the brainstem. Clinical and neuroradiological data could not establish a proper diagnosis and a stereotactic serial biopsy was undertaken. Histological examination of the specimen showed a glioblastoma multiforme (GBM) as the first reported case of GBM located in the brainstem in an acquired immunodeficiency syndrome (AIDS) patient. Patient management and effectiveness of stereotactic serial biopsy are discussed.
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7/52. Metastatic epithelioid sarcoma to the brain: palisaded necrosis mimicking glioblastoma multiforme.

    Epithelioid sarcomas are rare, morphologically distinct tumors that have a propensity to arise in the extremities. Brain metastasis from epithelioid sarcoma are a relatively rare occurrence. We report a case of brain metastasis in a 50-year-old man who was previously diagnosed with an epithelioid sarcoma arising in the elbow. Before the diagnosis of brain metastasis, he had developed an axillary lymph node metastasis. He presented with neurologic symptoms of progressively worsening headache and loss of vision on the right side. He underwent gross total resection of an occipital lobe mass. Histologically, the tumor was focally characterized by prominent perinecrotic pseudopalisading and demonstrated immunoreactivity with antibodies to cytokeratin AE1/3 and CAM5.2; the tumor did not stain with glial fibrillary acidic protein antibody. The literature is reviewed and the morphologic distinction between metastatic epithelioid sarcoma and other central nervous system neoplasms is discussed.
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8/52. Leukemic dissemination within a glioblastoma in a patient with chronic lymphoid leukemia.

    Metastasis from an extracranial tumor to a primary central nervous system tumor is a rare event, and most reported cases concern metastases to meningiomas. The authors describe the first case of leukemic cell dissemination within a glioblastoma. The patient likely presented a genetic predisposition to multiple neoplasms, and the unusual localization of leukemic cells might be partly related to the characteristic microvascular proliferation in glioblastoma.
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9/52. Radiological response and histological changes in malignant astrocytic tumors after stereotactic radiosurgery.

    Stereotactic radiosurgery is an encouraging approach to deliver higher doses of radiation boost for malignant gliomas safely and precisely. The purpose of this study was to investigate the radiation response and histological changes of malignant astrocytic tumors after stereotactic linac radiosurgery (SLRS). We studied an autopsy case of recurrent glioblastoma multiforme (GBM) and two surgical cases with gross total removal of recurrent GBM and anaplastic astrocytoma transformed from fibrillary astrocytoma treated with SLRS. Destructive changes, such as the disappearance of viable cells, coagulation necrosis, and fibrinoid degeneration of vascular walls, were observed in the center of the target of SLRS, which showed histologically similar radiobiological reactions to well-known delayed central nervous system radiation necrosis caused by conventional radiotherapy. The region showing such radiation necrosis was within the area irradiated with approximately 15-20Gy or more by SLRS; however, dense viable tumor cells remained in the periphery that was irradiated with less than 15Gy. In a comparative immunohistochemical study of the tumors before and after SLRS, neither MIB-1 and p53 labeling indices nor immunoreactivity for GFAP represented any persistent tendencies. There were very few TUNEL-positive cells in either tumor before and after SLRS. These results showed that radiosurgery for malignant gliomas leads to earlier radiation necrosis than conventional radiation and that it is useful in eradicating tumor cells in the center of the target. However, some viable tumor cells may remain in the periphery irradiated with an insufficient dose for cell death and may be partly transformed in character by dna damage due to radiation. Proton magnetic resonance spectroscopy (MRS) was suggested to characterize the radiation response in radiosurgery tumor targets for correlation with histological findings.
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10/52. Fluctuation of serum phenytoin concentrations during autologous bone marrow transplant for primary central nervous system tumors.

    We reviewed our experience for adult patients receiving oral anticonvulsant therapy during high-dose chemotherapy and autologous bone marrow re-infusion for primary malignant tumors of the central nervous system. Nineteen patients received either iv carmustine (BCNU) 900-1050 mg/m2 and 6120 cGy cranial irradiation (N = 10), iv carmustine 900-1050 mg/m2 and iv cisplatin 200 mg/m2 (N = 8), or iv carmustine 600 mg/m2, iv cisplatin 200 mg/m2, and iv etoposide 2400 mg/m2 (N = 1). Anticonvulsant therapy consisted of phenytoin alone (N = 8), phenobarbital alone (N = 4), carbamazepine alone (N = 2), phenytoin and carbamazepine (N = 2), carbamazepine and phenobarbital (N = 1), and no anticonvulsant therapy (N = 2). serum anticonvulsant concentrations were monitored frequently and doses adjusted to keep values in the therapeutic range. While phenobarbital and carbamazepine doses remained relatively stable, all patients required increased doses of phenytoin anticonvulsant therapy after beginning chemotherapy (mean onset 3.7 days after initiation of chemotherapy). The increase in phenytoin dose ranged from 50% to 300% above baseline (mean 134%). By the time of discharge from the hospital (approximately 3-4 weeks after the start of chemotherapy) anticonvulsant dose was decreased to near pre-therapy levels. These swings coincided with the initiation of dexamethasone therapy for antiemetic effect and were more pronounced in patients also receiving cisplatin therapy. Due to close monitoring of serum phenytoin concentrations, no instances of toxicity due to excessive drug concentration, or seizures due to subtherapeutic doses, were noted in patients with primary CNS malignancies. serum phenytoin concentrations fluctuate markedly during high-dose chemotherapy and must be analyzed frequently during the course of therapy.
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