Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumors of the central nervous system are an unusual cause of sudden death. This report describes the sudden death of a presumed healthy 28-year-old woman from primary diffuse leptomeningeal gliomatosis. She presented to an emergency room with headache and vomiting, subsequently became unresponsive and was pronounced dead 14 h later. Autopsy revealed a diffuse extensive infiltrate of well-differentiated astrocytoma in the leptomeninges of the brain and spinal cord without an underlying parenchymal tumor. Primary diffuse leptomeningeal gliomatosis is a rare tumor that arises within the leptomeninges from small neuroglial heterotopic rests that undergo neoplastic transformation. Grossly. this tumor can mimic leptomeningeal carcinomatosis, pachymeningitis, tuberculosis, sarcoidosis, and fungal infections. However, the histologic features of primary diffuse leptomeningeal gliomatosis should allow it to be readily distinguished from grossly similar conditions. The mechanism of death in this case is most likely tumor obstruction of cerebrospinal fluid outflow resulting in the usual complications seen with increased intracranial pressure. Although this tumor is aggressive and is associated with a rapidly progressive fatal course, it has not been previously associated with sudden death.
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PMID:Sudden death due to primary diffuse leptomeningeal gliomatosis. 1130 49

The authors present an unusual complication of a recurrent chiasmal/hypothalamic pilocytic astrocytoma. From his second year of life onwards, the patient was repeatedly operated on and also underwent external radiation therapy (54 Gy total dose) 1 month after the first subtotal tumor resection. Nine years after irradiation, the patient was referred to our center with a sudden onset of severe headache, vomiting and neck stiffness. Computed tomography, magnetic resonance imaging, and cerebral angiography demonstrated an intratumoral, intraventricular, and subarachnoidal hemorrhage from an anterior communicating artery aneurysm encased in the pilocytic astrocytoma. The aneurysm was clipped and the patient recovered nicely from the hemorrhage. Three years later, the patient suddenly died of cardiac failure. Autopsy disclosed vessel wall changes compatible with radiation-induced vasculopathy. In light of this finding, the importance of radiation therapy and intracranial neoplasms for aneurysm formation is discussed.
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PMID:Intracranial hemorrhage from an aneurysm encased in a pilocytic astrocytoma--case report and review of the literature. 1130 72

Pilocytic astrocytomas are usually present as solitary posterior cranial fossa tumours. An unusual case of pilocytic astrocytoma in a 3 year and 8 month old boy is presented. The patient presented over the course of 10 months with intermittent headaches, vomiting, gait ataxia and drowsiness. After extensive investigations magnetic resonance imaging (MRI) revealed widespread lesions throughout the central nervous system, including multiple cystic cerebral grey matter lesions. A brain biopsy was performed and pathological studies revealed pilocytic astrocytoma. The literature pertaining to neuraxis dissemination of pilocytic astrocytomas in the paediatric population is reviewed. There are only a very limited number of reports of pilocytic astrocytoma ca using multiple brain lesions, with no publications of multiple cystic brain lesions. We believe this to be a unique case of pilocytic astrocytoma presenting with widespread cystic lesions throughout the brain.
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PMID:Multiple cystic brain lesions in a patient with pilocytic astrocytoma. 1143 82

(1) Temozolomide, a cytotoxic agent, was recently licensed in France for treating patients with anaplastic astrocytoma who are in relapse or progression after standard therapy. (2) The clinical dossier contains only one non comparative trial. (3) In this trial, 111 patients with anaplastic astrocytoma or oligoanaplastic astrocytoma had not all had the standard treatment with surgery, radiotherapy and chemotherapy based on nitrosourea plus procarbazine. In the subgroup of 54 patients who met these criteria, median global survival on temozolomide was 16 months, or 31 months from the start of initial treatment, which was no better than survival before the introduction of temozolomide. (4) The adverse effects of temozolomide include gastrointestinal disorders (nausea, vomiting, constipation), headache, and haematological disorders.
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PMID:Temozolomide and anaplastic astrocytoma: new indication. No clear proof of efficacy. 1147 93

Retrospective analysis of 27 patients of thalamic glioma including adults and children treated over a period of 7 years from 1991-1997 was done. The study group included 19 males and 8 females; 9 patients were less than 15 years and 18 patients more than 15 years of age at the time of diagnosis. The commonest symptoms were headache and vomiting. 12 patients underwent VP shunt as an initial procedure and 7 underwent total or partial surgical resection. Confirmed histopathological examination was possible in 16 patients; while 12 had low grade astrocytoma, 4 cases had high grade histology. All patients were treated with radiotherapy to a total dose of 50-60 Gy in 25-30 fractions. Median follow up was 9.63 months. The disease free survival in these patients was 28% at 2 years. Prognostic factors which included age, sex, duration of symptoms, surgical procedures, histology and radiotherapy dose were evaluated for significance. A subtotal resection conferred a better prognosis.
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PMID:Prognostic factors influencing the outcome of thalamic glioma. 1196 Jan 49

We report on two children with bilateral thalamic astrocytomas. The first patient developed psychomotor regression at the age of 20 months followed by rapidly progressive ataxia, intention tremor, slurred speech, and bouts of drowsiness. Magnetic resonance imaging (MRI) of the brain showed swelling and high signal intensity in both thalami accompanied by supratentorial hydrocephalus. The second patient presented with progressive cerebellar ataxia, headache, and vomiting at the age of 11 years. MRI of the brain revealed symmetrical, hyperintense and sharply delineated swelling of both thalami. Additional lesions were seen in the cerebellum and the right temporal lobe. In both cases proton magnetic resonance spectroscopy (MRS) of the lesions showed a striking decrease of the neuronal marker N-acetylaspartate, an increase of choline-containing compounds, and a minimal lactate peak. Stereotactic biopsies from the thalamus of the first patient and from a cerebellar lesion of the second patient finally revealed glial tumors, namely a diffuse astrocytoma of World Health Organization (WHO) grade II in the first patient and an anaplastic astrocytoma of WHO grade III in the second patient. We conclude that the clinical manifestations and MRI patterns of bilateral thalamic astrocytomas are very similar to those of encephalitis and neurometabolic disorders and should therefore be included in the differential diagnosis of these encephalopathies.
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PMID:Diagnostic difficulties in childhood bilateral thalamic astrocytomas. 1257 91

Multiple metastatic brain tumors and multifocal primary brain tumors of a single histological type are well described in the literature. The concurrent presence of multiple primary brain tumors with different histological characteristics, however, is very rare. The authors describe the first known case in which an oligodendroglioma and a juvenile pilocytic astrocytoma (JPA) presented as synchronous primary brain tumors in the same patient. This 43-year-old man presented with a 2-month history of progressive headaches, nausea, and vomiting. Magnetic resonance imaging demonstrated an enhancing heterogeneous right medial cerebellar lesion and a larger calcified, nonenhancing, heterogeneous right frontal lesion with surrounding edema and a mass effect. The results of a metastatic workup were unremarkable. The patient underwent an initial right frontotemporal craniotomy and a subsequent suboccipital craniectomy 2 years later for resection of the posterior fossa lesion. Histological examination revealed the frontal and cerebellar lesions to be an oligodendroglioma and JPA, respectively. A molecular analysis detected a deletion of chromosome 1p36 in the oligodendroglioma, but not in the JPA. After the initial operation, the patient received follow-up care for his oligodendroglioma, but eventually required temozolomide for tumor progression. His condition remains stable both neurologically and according to imaging studies. The authors describe the first known case in which a low-grade oligodendroglioma and a JPA presented as synchronous primary brain tumors. They review the literature on multiple primary brain tumors with different histological characteristics and discuss potential mechanisms for the development of these lesions.
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PMID:Oligodendroglioma and juvenile pilocytic astrocytoma presenting as synchronous primary brain tumors. Case report with histological and molecular differentiation of the tumors and review of the literature. 1507 Jan 26

The authors report a case of a 13-year-old boy with juvenile pilocytic astrocytoma (JPA) presenting with subarachnoid hemorrhage (SAH). The patient experienced sudden onset of headache, vomiting, and loss of consciousness. Cranial computerized tomography scanning revealed blood within basal cisterns and the third ventricle. Angiography demonstrated normal cerebral vasculature and upward displacement of the bilateral A, segments of the anterior cerebral artery. Magnetic resonance (MR) imaging revealed a chiasmatic/hypothalamic mass with evidence of hemorrhage. The mass was surgically decompressed. Histopathological examination showed evidence of JPA. In all cases of SAH in which there is blood around the third ventricle and a raised A1 segment on angiography, MR imaging should be performed. The presence of a normal sella turcica, as well as indistinct margins between the tumor and the opticochiasmatic apparatus should raise suspicion about the lesion.
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PMID:Juvenile pilocytic astrocytoma presenting with subarachnoid hemorrhage. Case report and review of the literature. 1528 67

A 3-year-old boy presented with headaches, vomiting, lethargy and papilledema. Communicating hydrocephalus along with transependymal fluid absorption and meningeal contrast enhancement was identified on CT. The enhancement was initially thought to be the result of a partially treated meningitis (child was previously on oral antibiotics for a presumed mycoplasma pneumonia). A right ventricular-peritoneal shunt was placed. CSF studies procured during the procedure were all normal. In contrast, CSF from a lumbar puncture contained a high protein, and cytology was highly suspicious for malignancy. Spine MRI showed diffuse leptomeningeal enhancement and a 1.5-cm intramedullary lesion at T12-L1 associated with minimal edema. The lesion was subtotally resected (70%) and diagnosed as an astrocytoma (mostly Kernohan grade 2 but with areas of grade 3). Chemotherapy was administered and follow-up spine MRI at 2 months did not reveal any residual tumor, however, the leptomeningeal enhancement persisted. Sixteen months later, at the completion of the chemotherapy and radiation therapy, the spine MRI remained unchanged. Neurological examination has always been normal. This case illustrates how a spinal cord astrocytoma can metastasize via spinocranial dispersion and present early with hydrocephalus rather than myelopathy.
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PMID:Hydrocephalus as the initial presentation of a spinal cord astrocytoma associated with leptomeningeal spread. 1588 10

The prognosis for patients with diffuse pontine gliomas (DPG) remains poor. New aggressive innovative treatments are necessary to treat this disease. From 1984 to 1998, eight patients (4M/4F), median age 11 years, with DPG were treated with monthly osmotic blood-brain barrier disruption (BBBD) chemotherapy using intraarterial carboplatin or methotrexate and intravenous cytoxan and etoposide. Patients presented for a median duration of 6 weeks with increased intracranial pressure, long tract signs, diplopia, ataxia, and nausea/vomiting. DPG was demonstrated on magnetic resonance (MR) imaging in seven patients and on CT in one. Two patients had biopsies that showed an astrocytoma and an anaplastic astrocytoma. Three tumors enhanced on MR imaging after contrast administration. Three patients had radiation therapy before BBBD chemotherapy and four afterwards. Two patients had chemotherapy (tamoxifen, topotecan) before BBBD chemotherapy and two afterwards. In general, patients were evaluated with MR imaging every 3 months to monitor for a response to treatment. The median number of chemotherapy cycles that were administered by BBBD was 10, mean 10. Three patients also received one, two, or three cycles of intraarterial chemotherapy without BBBD. One patient that was started on carboplatin was converted to methotrexate, and five that were started on the methotrexate protocol were later converted over to carboplatin. One patient received monthly methotrexate followed by 14 days of procarbazine and one patient started on methotrexate was switched to navelbine. MR imaging demonstrated two partial responses, five patients with stable disease, and one with disease progression. The median time to tumor progression was 15 months with the range from <1 to 40 months. The median survival from the time of diagnosis was 27 months, ranging from 7 to 80 months. The median survival time from the first BBBD or intraarterial treatment was 16.5 months, ranging from 5 to 69 months. One patient was lost to follow-up with an unknown date of death. Although the sample size is small, the TTP and survival times are longer than those previously reported in other DPG series. In addition, the ability to demonstrate stable disease or partial responses in DPG on MR imaging argues for the therapeutic benefit of BBBD chemotherapy. The enhanced delivery of chemotherapy afforded by osmotic BBBD supports the further examination of this treatment modality for patients with DPG.
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PMID:Osmotic blood-brain barrier disruption chemotherapy for diffuse pontine gliomas. 1631 49


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