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)

An optic chiasm glioma may cause loss of vision, endocrine disturbances, hydrocephalus and cerebral ischemia due to its proximity to the pituitary, hypothalamus, III ventricle and internal carotids. A 3-month-old infant with optic chiasm glioma developed hypopituitarism and inappropriate secretion of antidiuretic hormone with plasma hypo-osmolality. The cerebrospinal fluid (CSF) protein concentration was markedly elevated. The impairment of fluid absorption via arachnoid villi and peritoneum by the high protein content, and reversed osmotic gradient between protein-rich CSF and hypo-osmolar plasma may have contributed to both nonobstructive hydrocephalus and recurrent ascites following ventriculoperitoneal shunting. Cerebral ischemia from carotid compression may have led to cerebral atrophy.
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PMID:Optic chiasm glioma associated with inappropriate secretion of antidiuretic hormone, cerebral ischemia, nonobstructive hydrocephalus and chronic ascites following ventriculoperitoneal shunting. 179 May 31

We reviewed retrospectively a series of 100 inpatients with onset of epileptic seizure after the age of 60. All of them were investigated by EEG and 96 by CT scan. The most frequent cause of seizure was previous stroke, with 25 cerebral infarcts and 5 hemorrhages. Neoplastic lesions were present in 18 cases, with glioma (high grade), meningioma and metastases in the same proportion. Other etiologies included toxico-metabolic (18 cases), post-traumatic (9 cases), cerebral atrophy (4 cases) and miscellaneous (14 cases). The causes of seizure remained unknown in 7 patients, of whom 6 had focal signs in either clinical examination or EEG. Focal seizures (with or without secondary generalization) accounted for 65% of all cases and generalized seizures for 35%. The EEG was normal in 12 patients and abnormal in 88, with diffuse slowing in 55 patients and focal signs in 70 (some patients had both diffuse slowing and focal signs). Fourteen patients presented status epilepticus. Ten died during hospitalization. We conclude that epileptic seizure with onset after age 60 is nearly always symptomatic, and neuroradiologic investigations are necessary in the search for cerebral lesions. In our study, the prevalence of "idiopathic epilepsy" is lower than previously described.
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PMID:[Initial epileptic crisis after the age of 60: etiology, clinical aspects and EEG]. 234 61

We reviewed the serial CT studies obtained between 1974 and 1986 of 31 patients with malignant glioma who survived for 2 to 11 years after surgical removal of their tumors. In all cases surgery was followed by radiation therapy to the head (6000 rad) and chemotherapy. Patients were divided into two age groups: those under age 40 (n = 13) and those over age 40 (n = 18). By 2 years all patients in the older group developed evidence of leukoencephalopathy characterized by periventricular zones of decreased attenuation. Only 58% of the younger group showed evidence of white matter changes at this point. All patients from both age groups who survived for 4 years developed leukoencephalopathy. The severity of leukoencephalopathy from 6 months after surgery and beyond was always greater in the older group. All patients developed cerebral atrophy as evidenced by sulcal dilatation and ventricular enlargement. Atrophy was progressive beginning with the first postirradiation scan, and was always more severe in the older patients. A significant difference was found in the clinical status of the two age groups as determined by the mental status score and the Karnofsky scale. Despite progressive brain changes, survivors under age 40 maintained a nearly normal mental status and Karnofsky scores until their death, whereas survivors over age 40 showed progressive clinical decline.
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PMID:Longitudinal CT study of parenchymal brain changes in glioma survivors. 313 25

Increasingly vigorous chemotherapy of cancer including primary and metastatic central nervous system disease has resulted in prolonged good-quality survival. However, there has been an associated increase in neurotoxicity from both radiation therapy and chemotherapy. All classes of chemotherapeutic agents contain drugs that are potentially neurotoxic, often only at high doses. Mechlorethamine, the first nitrogen mustard, is not neurotoxic at conventional dosage, but at high doses, it may produce both an acute and a delayed encephalopathy. Methotrexate administered intrathecally often induces reversible aseptic meningitis, but chronic administration, either intrathecally or high-dose intravenously, may produce fatal leukoencephalopathy. 5-Fluorouracil at high dosage may cause cerebellar ataxia, but may also do so at low dosage when combined with thymidine infusions. Cytosine arabinoside at high dosage may also produce cerebellar ataxia. Vincristine produces a peripheral neuropathy, and less commonly causes both autonomic and cranial neuropathy. The enzyme L-asparaginase can produce a dose-related reversible encephalopathy. BCNU, now the mainstay of glioma chemotherapy, may combine with radiation to produce long-term cerebral atrophy. Both intracarotid and high-dose intravenous BCNU administration may cause encephalopathy. Several other chemotherapeutic agents have also been reported to cause neurotoxicity under certain circumstances.
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PMID:Neurological complications of antineoplastic therapy. 638 4

Four cases of subdural effusion following radical surgery for the chiasmal region tumors in childhood were presented in this report. Three out of four cases were craniopharyngioma and the remaining one was optic glioma. The pathogenetic mechanisms of this disorder were explained probably and at least partly by a change from internal to external hydrocephalus or craniocerebral disproportion due to cerebral atrophy in two of the four cases and unclear in the remaining two cases. In all four cases meningitis did not supervene postoperatively. The subdural effusion may be divided into two types according to symptomatology, i.e., "serious type" which presents with severe symptoms and "mild-type" which is virtually asymptomatic. The serious type required immediate surgical procedure, such as continuous subdural drainage and subduroperitoneal shunt, while the mild type should be carefully monitored for the course of subdural effusion by CT scan.
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PMID:[Subdural effusion following radical surgery for chiasmal region tumors in children--report of 4 cases (author's transl)]. 723 33

The authors report a case of neuronal ceroid lipofuscinosis (Kufs' disease) confirmed by stereotactically obtained brain biopsy findings and initially diagnosed as a butterfly glioma. The presenting symptoms in the 64-year-old patient were mental alterations with progressive dementia, followed by muscular atrophy and myoclonia with distal preponderance. The mild initial disturbances of coordination increased, and the patient developed a markedly ataxic gait. Computerized tomography (CT) scanning and magnetic resonance imaging revealed generalized cerebral atrophy and a bifrontal space-occupying lesion involving the callosum. The original "clearcut" diagnosis of glioblastoma multiforme, based on CT scans, was unexpectedly disproved by examination of stereotactically obtained brain biopsy specimens, which revealed a neuronal ceroid lipofuscinosis (Kufs' disease). To the authors' knowledge, this is the first report of a case presenting with both diffuse brain atrophy and localized accumulation of neuronal lipofuscin, mimicking a mass lesion on radiological studies.
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PMID:Adult neuronal ceroid lipofuscinosis with clinical findings consistent with a butterfly glioma. Case report. 945 42

Abnormalities on CT or MRI and neuropsychological performance in patients with low-grade glioma, with (n = 23) or without (n = 16) prior cerebral radiotherapy, were evaluated. Cerebral atrophy was observed in 14 of 23 patients (61%) treated with prior radiotherapy, and in 1 of 16 patients (6%) without prior radiotherapy. White matter abnormalities were observed in six patients, all of whom were treated with prior radiotherapy. These radiologic cerebral abnormalities correlated with cognitive performance.
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PMID:Radiotherapy-induced cerebral abnormalities in patients with low-grade glioma. 1210

To evaluate the influence of radiation volume and other risk factors for the development of delayed radiation toxicity in patients treated for low-grade glioma, a retrospective analysis of 41 adult patients treated with focal or whole brain radiotherapy (WBRT) was performed. For all patients CT and MRI scans were revised to quantify brain atrophy and white matter lesions. Medical data were reviewed concerning baseline and tumor characteristics, treatment, survival, signs and symptoms of clinical encephalopathy and cardiovascular risk factors. In patients treated with WBRT an increased risk was found for brain atrophy (RR 3.1), white matter lesions (RR 3.8) and clinical encephalopathy (RR 4.2). An increased risk of atrophy (RR 2.2) and white matter lesions (RR 2.9) was also found in patients aged over 40 years. Furthermore, brain atrophy and white matter lesions were more severe in patients treated with WBRT and in older patients. In conclusion, both the incidence and the severity of abnormalities is greater in patients treated with WBRT and in older patients.
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PMID:Delayed radiation toxicity after focal or whole brain radiotherapy for low-grade glioma. 1501 65

Glutaryl-CoA dehydrogenase deficiency or glutaric acidemia type I (GA I) is an inherited neurometabolic disorder biochemically characterized by tissue accumulation of predominantly glutaric (GA) and 3-hydroxyglutaric (3OHGA) acids and clinically by severe neurological symptoms and structural brain abnormalities, manifested as progressive cerebral atrophy and acute striatum degeneration following encephalopathic crises, whose pathophysiology is still in debate. Considering that reactive astrogliosis is a common finding in brain of GA I patients, in the present study we investigated the effects of GA and 3OHGA on glial activity determined by S100B release by rat C6-glioma cells. We also evaluated the effects of these organic acids on some parameters of oxidative stress in these astroglial cells. We observed that GA and 3OHGA significantly increased S100B secretion and thiobarbituric acid-reactive substances (lipid peroxidation), whereas GA markedly decreased reduced glutathione levels in these glioma cells. This is the first report demonstrating that the major metabolites accumulating in GA I activate S100B secretion in astroglial cells, indicating activation of these cells. We also showed that GA and 3OHGA induced oxidative stress in C6 lineage cells, confirming previous findings observed in brain fresh tissue. It is therefore presumed that reactive glial cells and oxidative damage may underlie at least in part the neuropathology of GA I.
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PMID:Induction of S100B secretion in C6 astroglial cells by the major metabolites accumulating in glutaric acidemia type I. 2043 86

Following tumor resection, the majority of high-grade glioma (HGG) patients are treated with a combined modality regimen of radiotherapy and temozolomide. As a result of the tumor itself or as treatment-related neurotoxic side-effects, these patients may experience cognitive deficits. Additionally, radiological abnormalities expressed as white matter hyperintensities (WMH) and cerebral atrophy (CA) can develop. In this study, these functional and morphological parameters are evaluated, and their relation is investigated. After surgery, HGG patients underwent chemo-irradiation for six weeks, followed by six cycles of temozolomide. Assessments were performed before chemo-irradiation, post-concomitantly, after the third and sixth adjuvant cycle, and 3 and 7 months after treatment. Degree of WMH and CA was scored on MRI. Patients' neuropsychological performance was compared to healthy matched controls, yielding six cognitive domain z-scores. Development or progression of pre-existing WMH and CA during follow-up was observed in 36 and 45 % of the patients (n = 39) respectively. Cognitive functioning remained stable or improved in 70 % of the patients and deteriorated in 30 % of the patients (n = 33). Of the cognitive decliners, 80 % had tumor progression within 4 months thereafter. No clear association between cognitive functioning and WMH or CA was found. Central neurotoxic effects of combined modality treatment in HGG patients expressed by radiological abnormalities are encountered in approximately 40 % of patients. However, functional impact as indexed by cognitive functioning was found to be limited. Furthermore, development or progression of pre-existing WMH and CA does not consistently result in functional impairment as measured by cognitive tests.
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PMID:Central neurotoxicity of standard treatment in patients with newly-diagnosed high-grade glioma: a prospective longitudinal study. 2426 31


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