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)

We report a patient with meningeal gliomatosis who had signs of meningitis, hypoglycorrhachia, and an intracranial mass. Despite suspicion of a primary intracranial neoplasm, repeated CSF cytologies were not diagnostic and led to a brain biopsy for diagnosis. Immunoperoxidase staining for glial fibrillary acidic protein stained CSF cells that had been thought inflammatory on routine cytology. This case and other reports demonstrate that multiple cytologic examinations may be negative despite extensive gliomatous infiltration of the meninges. Immunoperoxidase staining is useful in cases of suspected meningeal spread of glioma when suspicious cells are seen on routine CSF cytology.
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PMID:Meningeal gliomatosis with "negative" CSF cytology: the value of GFAP staining. 639 Feb 50

A case of cryptococcosis simulating brain tumor was reviewed. A 66-year-old female was admitted to our hospital with chief complaint of vertigo, gait disturbance and dysarthria. These symptoms started about one year before admission and worsened. Vomiting and urinary incontinence appeared. Neurological examination revealed left cerebellar ataxia and dysarthria. In plain CT (computerized tomography) irregular ill-defined low density area was noted in the cerebellar vermis and bilateral cerebellar hemispheres. And slight ventricular dilatation was found. Irregular shape of ring-like enhancement corresponding to capsule and patchy or mottled enhancement inside the tumor were seen. Suboccipital craniectomy was performed and yellowish necrotic tumor with hard capsule was removed. Histological diagnosis was not neoplasm or tuberculoma. Postoperatively liver function progressively worsened. She died due to disseminated intravascular coagulation. Autopsy revealed typical liver cirrhosis without malignant change. 3.0 X 2.5 cm sized, slightly hard, yellowish lesion was found on upper part of cerebellar hemispheres. This had extremely necrotic tissue and a great number of cryptococcus neoformans were found. And other intracranial lesion was not confirmed. Finding of pulmonary cryptococcosis was not gained. Our case is very rare because of solitary cerebellar abscess and absence of meningitic episode or pulmonary cryptococcosis. There are three types of inflammation in cerebral cryptococcosis. The commonest manifestation is the meningitic type, the second mode is granulomatous lesion and the third and the least presentation is intracranial abscess formation. CT reveals various findings according to clinical stage. CT findings are those of meningitis, meningoencephalitis, granuloma and abscess. Cryptococcal granuloma or abscess often simulates brain abscess, glioma and metastatic brain tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of cerebral cryptococcosis, with special reference to computerized tomography findings]. 646 65

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

Gliomas that arise primarily in the leptomeninges are rare. Of the 15 reported cases of primary leptomeningeal glioma, only two diffusely involved the leptomeninges. We report the third case of primary leptomeningeal gliomatosis, this in a 55-year-old man who died three months after the onset of symptoms. The clinical manifestations, CSF findings, and the gross appearance of the brain resembled meningitis rather than neoplasm. Results of cytologic examinations of the CSF were normal and the diagnosis was made at necropsy. The diffuse form of primary leptomeningeal glioma has a shorter clinical course and poorer prognosis than the solitary form. Primary leptomeningeal gliomas are believed to arise from heterotopic neuroglial tissue in the leptomeninges.
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PMID:Primary leptomeningeal gliomatosis: symptoms suggestive of meningitis. 729 14

The nasal encephalocele, the glioma, and the dermoid are the most common of the congenital midline nasal masses. Due to similar embryologic development, each of these lesions may be associated with bony cranial defects and intracranial abnormalities, as well as CSF leakage and the potential for fatal meningitis if not handled properly. Properative manipulation should be avoided. Radiologic studies are instructive only if they are positive. If intracranial attachments are identified radiologically or suspected clinically, neurosurgical consultation should be obtained, and intracranial exploration and resection should be carried out as the initial procedure. Extra-cranial resection of the remaining mass may be performed immediately after intracranial resection, may be postponed, or may become unnecessary.
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PMID:Management of the congenital midline nasal mass: a review. 735 54

Nasal glioma is a developmental abnormality of neurogenic origin with o malignant potential. An intranasal mass requires careful rhinologic and occassionally ophthalmologic, neurologic, and roentgenologic examinations. With a bony defect, pneumoencephalography, angiography, or computerized tomography may be helpful. In such cases, a neurosurgeon should be available at the time of biopsy. Biopsy is necessary for establishing a histopathologic diagnosis. Aspiration of the tumor with a needle or incisional biopsy may yield inconclusive findings and may be associated with CSF rhinorrhea and meningitis, especially if there is an intracranial connection. With adequate initial removal, excisional biopsy usually offers complete cure. A frontal craniotomy approach is preferred for those patients who have nasal glioma with an intracranial connection, CSF rhinorrhea, or recurrent episodes of meningitis. With no evidence of an intracranial connection, a conservative extracranial approach is recommended.
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PMID:Nasal gliomas. 740 59

Because of aberrant embryologic development, encephalocele, nasal dermoid, and glioma may present as a nasofrontal midline mass in a newborn infant. Though uncommon, vascular malformation or hemangioma in the nasofrontal region may present similarly. The correct diagnosis and early management of a nasofrontal mass is imperative because complications such as brain herniation, hypertelorism, or cerebrospinal fluid rhinorrhea may ensue, resulting in poor facial or visual development, recurrent meningitis, and brain abscess. Nasofrontal encephalocele and midline frontal vascular malformation are rare congenital abnormalities presenting as a midline nasofrontal mass. We report two neonatal cases, one a frontoethmoidal encephalocele and another, a frontal vascular malformation. Both had uncomplicated surgical interventions. The physical findings and clinical review are presented. The diagnostic approach toward midline nasofrontal mass is discussed.
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PMID:Congenital midline nasofrontal mass. Two case reports with a clinical review. 758 21

Recent studies using a rat model of pneumococcal meningitis have shown that nitric oxide synthase (NOS) inhibitors greatly attenuated microvascular changes and brain edema formation. The site of NO production during bacterial meningitis is unknown. In this study we tested whether primary astrocyte cultures from neonatal rat cortex can be induced to release NO upon stimulation with pneumococci. NO production was assessed by measuring nitrite in the cell culture supernatant using the Griess reaction. Stimulation with heat-killed unencapsulated pneumococci (HKP) increased nitrite concentrations in astrocyte culture supernatants in a dose-dependent fashion. Administration of N-nitro-L-arginine (L-NA), aminoguanidine, L-canavanine, cycloheximide, and dexamethasone prevented the increase in nitrite concentrations. Addition of L-arginine, but not of D-arginine, partially reversed the inhibitory effect of L-NA. Administration of SOD increased nitrite accumulation. Moreover, at 72 h after stimulation with heat-killed pneumococci (10(7) cfu/ml) astrocytes showed an inducible NOS-like immunoreactivity. Accumulation of nitrite was also observed when rat cerebellar neurons and microglia were stimulated with HKP, whereas there was only a slight increase of nitrite in media of rat C6 glioma cells, but no increase of nitrite when the human glioblastoma cell line LN-229 was stimulated with HKP. There was a stronger increase in nitrite levels when astrocytes from Lewis rats were used compared to that from Wistar rats. In conclusion, our study indicates that astrocytes, neurons and microglia are inducible for NO production upon stimulation with pneumococci.
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PMID:Production of nitrite by primary rat astrocytes in response to pneumococci. 764 48

The toxicity and therapeutic effect of the ventriculolumber perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl-1-1(2-chloroethyl)-1-nitros our ea hydrochloride (ACNU) against subarachnoid dissemination of gliomas were studied. Twenty-one patients (6 patients with anaplastic glioma, 7 with glioblastoma and 8 with medulloblastoma or PNET) received ventriculolumber perfusion of ACNU when they were diagnosed as having subarachnoid dissemination. The course of perfusion and cumulative dose of ACNU was 10 times and 95 mg on average, respectively. Most of the patients received systemic chemotherapy in combination with perfusion therapy and some patients with radiotherapy. Response rate was 17% and median survival time after the diagnosis of dissemination was 12 months for anaplastic gliomas, 29% and 12 months for glioblastoma, and 88% and over 25 months for medulloblastoma and PNET. The ventriculolumber perfusion of ACNU was performed for prophylactic purpose in 7 patients with high risk at the early postoperative period in combination with conventional adjuvant therapy. The course of perfusion and cumulative dose of ACNU was 2.3 times and 21 mg on average, respectively. One patient developed subarachnoid dissemination and died 22 months after surgery. Other 6 patients survived without dissemination on median over 29 months after surgery. Side effects encountered were headache in 4 patients, nausea and vomiting in 5, a convulsion in 2, right facial weakness in 1, fecal incontinence in 3 and meningitis in 2. They were all temporary except for facial weakness occurred in one patient. These data suggest that the ventriculolumber perfusion of ACNU is a safe and useful in the treatment and prophylaxis against the subarachnoid dissemination of gliomas.
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PMID:Ventriculolumber perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)-methyl]-1-(2-chloroethyl-1-nitrosou rea hydrochloride for subarachnoid dissemination of gliomas. 969 73

The paper describes the most infrequent case of cryptococcal granuloma of the midbrain in a HIV-negative female patient aged 41 years. The patient with midbrain lesion without signs of meningitis was found to have a bulky midbrain opercular formation that was regarded as a nodal glioma. The diagnosis of cryptococcal granuloma was established after removal of the formation (via occipito-transtentorial access with dissection of the lamina tecti) and pathomorphological examination. Microbiological studies verified the diagnosis. Despite the initiation of specific treatment with amphotericin B, the patient died on day 12 following surgery for cryptococcal meningoencephalitis.
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PMID:[A cryptococcal granuloma of the midbrain]. 1042 May 45


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