Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A metastasizing glioma in a 4-year-old boxer bitch is described. Clinical symptoms included ataxia, blindness, and increased cervical pain sensation. The tumor metastasized to an extraordinary extent via the cerebrospinal fluid. Tumor masses surrounded the whole spinal cord including the cauda equina. Histological examination revealed a variable morphology of the glioma. Immunohistochemical investigations showed some tumor cells reacting with antibodies specific to GFAP and S-100 protein. In contrast, NSE, 200 kd NF, vimentin, and desmin could not be demonstrated within tumor cells. The results are discussed in detail.
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PMID:[Metastasizing glioma in a Boxer]. 194 88

The case notes of 29 children ranging in age between 6 months and 17 years were reviewed for the period 1978-88. This study was done to determine if there were any differences when compared with other series in the developed countries. In addition, the distribution, tumour type, clinical presentations, and outcome were reviewed. Of the 29 tumours, 15 tumours were confined to the posterior fossa (52 per cent), and tumours were located supratentorially (48 per cent). Of the 15 tumours in the posterior fossa, five were medulloblastomas, four brain stem astrocytomas, and six cerebellar astrocytomas. The supra-tentorial tumours included, five astrocytomas, two pituitary tumours, two cranio-pharyngiomas, one hypothalamic glioma, and four intraventricular tumours. Clinical presentation was confined to symptoms and signs related to raised intracranial pressure, ataxia, seizures, and cranial nerve involvement. All the tumours were resected surgically except for the brain stem tumours, which were treated in most cases with radiation therapy. The overall mortality was 48 per cent (14 patients died). We were unable to comment on long-term survival except for a 100 per cent survival in patients with pituitary and cerebral tumours, and 67 per cent in patients with cerebellar astrocytomas.
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PMID:Primary pediatric brain tumours in Barbados: 10-year analysis (1978-1988). 202 66

we report a patient with Wallenberg's syndrome caused by glioma of the lateral medulla oblongata, and review the literature for Wallenberg's syndrome associated with neoplastic disease. A 46-year-old man was admitted because of progressive dysphagia and vertigo. Neurological examination revealed atypical symptoms and signs of Wallenberg's syndrome on the right side, hypalgesia on the second and third divisions of the left trigeminal nerve, paresis of the right palate and uvula, and ataxia of the right extremities. Although CT showed no abnormality in the posterior fossa, MRI demonstrated a mass with abnormal signal intensities in the right dorsolateral portion of the medulla. Biopsy specimens showed astrocytoma (grade III). Based on the present case and a review of 10 previously reported cases of Wallenberg's syndrome caused by neoplastic disease, the clinical features of this syndrome are characterized by gradual development and steady progression of symptoms, non-classical or atypical symptomatology, numerous additional symptoms and signs depending on the site and size of tumors, and poor prognosis.
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PMID:[Wallenberg's syndrome caused by a brain tumor--a case report and literature review]. 216 89

The nitrosourea-induced rat glioma clone RG2 was tested for its capacity to form multicellular tumor spheroids (MTS's). Resulting spheroids were investigated by light and electron microscopy with regard to their proliferation patterns and morphological features. Using microsurgical techniques and avoiding mechanical injury of the brain tissue, the authors successfully transplanted avascular MTS's under the dura of the cerebellum, above the vermis, in 43 adult syngeneic Fischer CD rats. The rate of tumor establishment was 93%, and the tumors that were solid and spheroid in shape grew exponentially. Neovascularization could be observed at 3 days after implantation, and invasion of the cerebellum occurred by 3 to 5 days. Neurological deterioration, including ataxia, impairment of walking, and apathy, could be observed after 10 days. The mean survival time was approximately 16 days. The subdural cerebellar tumors were studied by histological techniques, and two morphometric methods were applied to check the growth of implanted spheroids. All tumors were deeply stained with the Evans blue dye-albumin complex, demonstrating disturbance of the blood-brain barrier. The easy accessibility of the cerebellar vermis in rats, the microsurgical implantation of glioma spheroids under the dura avoiding nerve tissue disruption, and the high percentage of reproducible establishment of tumors favor this experimental brain-tumor model. This should be an excellent model for study of experimental therapies.
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PMID:RG2 glioma growth in rat cerebellum after subdural implantation. 242 62

A 41 year old male presented with headache, lethargy, and ataxia and found to have a left temporal lobe mass and a leukoerythroblastic peripheral blood smear. The latter prompted an iliac crest bone marrow biopsy on which a diagnosis of metastatic glioma was made and verified by immunohistologic characterization. The patient was treated with cranial irradiation and simultaneous systemic BCNU (bis-dichloroethylnitrosurea) with complete response. This case with diffuse bone marrow involvement demonstrates that a glioblastoma is capable of extracranial metastases without previous intervention. From a review of reported cases of gliomas of extraneural metastasis, it is concluded that untreated gliomas are capable of vascular spread although less frequently than previously manipulated tumors.
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PMID:Intracranial astrocytoma with diffuse bone marrow metastasis: a case report and review of the literature. 329 52

A patient presented with disorders of saccadic and pursuit movements a wandering gaze, the impossibility to maintain fixation, a concentric shortening of visual attention mainly of the right side, an incomplete right homonymous hemianopia (respecting 10 to 20 degrees), and optical and auditory ataxia predominantly affecting the right hand. Pathology showed a large left parietal glioma in the white matter in the superior and inferior parietal lobes, with microscopic evidence of parietal cortex invasion. A hematoma on the right side was situated entirely parasagitally in the precuneus, approaching the cortex at this level. The two lesions were independent and the splenium was intact. The frontal lobes were normal. A review of nearly 30 cases of bilateral syndrome of the parieto-occipital junction showed that anomalies of visually guided ocular movements were always present. These cases require differentiation from those, such as the present case, which involve mainly a visuomotor coordination disorder and from those with predominant visual disorientation.
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PMID:[Bilateral parietal syndrome approximating a Balint syndrome]. 608 35

In this paper we present a case of glioma which was located in the cerebellopontine angle. The patient, a 3-year-old male, experienced difficulty with gait for one month before admission. He was admitted to Toyota Memorial Hospital on February 2, 1991, suffering from severe headache and vomiting. Neurological examination upon admission revealed horizontal nystagmus and ataxia. MRI revealed a mass in the cerebellopontine angle. Craniotomy was performed on February 4, 1991, and a tumor was revealed in the cerebellopontine angle. The tumor was clearly demarcated and encapsulated; the cerebellum and brainstem were compressed without damage. Most of the tumor was removed. A histopathological summary of the tumor follows. The tumor appeared as exophytic lesions on the pons, extending into the cerebellopontine angle. Tumor cells contained small round nuclei and acidophilic cytoplasm. The oncocyte, which was growing endomorphically, revealed a short-cell projection, suggesting a tendency to penetrate blood vessels. Intercellular microcystic degeneration was observed clearly, with some parts of the oncocyte forming a myxoid matrix. Immunohistochemically, most of the tumor cells reacted positively to Vimentin, but negatively to S-100 protein and GFAP. Given the pathological information, the tumor was interpreted as anaplastic astrocytoma. Postoperative radiation therapy was performed, but the patient died four months later because the tumor had spread to the brainstem. In this paper we discuss the differential diagnosis of the cerebellopontine angle tumor and the appearance of anaplastic astrocytoma as exophytic lesions on the pons and the spread of the tumor into the cerebellopontine angle.
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PMID:Anaplastic astrocytoma in the cerebellopontine angle. 822 Jul 82

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

Tectal glioma is a topographical diagnosis including tumors of different histology, mainly low-grade astrocytomas. Clinical symptoms are usually associated with increased intracranial pressure. This report discusses the management of this rare tumor in children. Clinical charts of 12 children with tectal glioma treated in our department between 1976 and 2001 were retrospectively reviewed. The mean age at the time of diagnosis was 6.75 years (range, 4 weeks to 16 years). The duration between first symptoms and the diagnosis of tectal glioma was in the range of 2 days to 9 years. Ten patients presented with symptoms associated with increased intracranial pressure, one patient presented with ataxia, and in one case tectal glioma was an incidental finding. First-line therapy was endoscopic third ventriculostomy in 5 cases (42%), ventriculoperitoneal shunting in 6 cases (50%), and combined partial tumor resection and shunting in one case. Histology was obtained in 5 cases (low-grade astrocytoma, n = 4; ependymoma, n = 1). All patients had good neurologic function at the end of follow-up. Tectal glioma represents a distinct subgroup of brainstem tumors associated with a good (or favorable) prognosis. Effective treatment for hydrocephalus is essential; the tumor should be monitored by regular clinical examination and magnetic resonance imaging. Biopsy is warranted in cases with tumor progression.
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PMID:Management of tectal glioma in childhood. 1587 19

Children with pontine glioma usually present classically with ataxia, motor deficits and cranial nerve palsies. The pons has generally not been regarded as a structure that mediates complex affective behaviour. However, we report nine children who either at the time of presentation or progression demonstrated marked behavioural changes manifesting as either "pathological laughter" or separation anxiety in the form of school refusal. A mechanism of how pontine lesions can cause such complex affective and cognitive behaviour has been suggested to consist of the disruption of a network of cerebro-ponto-cerebellar pathways and the evidence for this mechanism is discussed.
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PMID:Pathological laughter and behavioural change in childhood pontine glioma. 1631 50


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