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)

From 1969-1974 1000 unselected enucleated globes have been examined histopathologically. 277 derive from the University Eye Hospital in Hamburg, 723 from various Eye Hospitals in northern and southern Germany. They originate from 589 men and 408 women, three times the sex was unknown. 86 globes had to be removed from children less than 15 years old. 6 groups of etiologies have been distinguished: trauma (308), histologically confirmed neoplastic disease (281), ocular manifestations of systemic diseases (diabetes mellitus, occlusions of central retinal vessels presumably following generalized vascular disease etc.: 128), "operative ocular disease" (164), primary inflammatory disease (71), miscellaneous (malformations, high myopia, pseudo-glioma and pseudo-melanoma: 48). The etiology "operative ocular disease" consists of 67 primary glaucomas (57 adults, 10 buphthalmus), 41 idiopathic cataracts (7 of these congenital) and 3 primary corneal dystrophies, as well as 53 cases of primary retinal detachment. Among the 281 neoplastic diseases, there are 238 primary intraocular malignant melanomas of the uvea, 18 retinoblastomas, 4 primary reticulumcellsarcomas of the retina, 2 choroidal nevi, 10 intraocular metastases and 9 orbital tumors. 16 enucleations among the 1000 enucleations have been performed for pseudo-gliomas (5 x Coats disease, 5 x persistent primary hyperplastic vitreous, 2 x retrolental fibroplasia, others 4 x). The manifestations of systemic disease are consisting of 68 central retinal vein-occlusions, 30 complications of diabetes mellitus and 10 central retinal artery occlusions as well as 20 other generalized diseases. A primary inflammatory disease led to enucleation 50 times due to an intraocular process, 5 times due to scleritis and 18 times as a consequence of keratitis (including 13 times herpes simplex). As the final clinical cause for enucleation the following categories have been elaborated: secondary glaucomas (416), clinical diagnosis of "tumor" (275), atrophy and phthisis bulbi (118), inflammation (112), acute trauma to 4 weeks after the accident (72), others (7). In conclusion the central role of rubeosis iridis leading to secondary angle closure glaucoma is emphasized. This process presents a challenge to ophthalmologic research. Finally the significance of early surgery for primary angle closure glaucomas and for complete restoration of the anterior chamber after trauma and any intraocular procedure is stressed.
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PMID:[Etiology and final clinical cause for 1000 enucleations. (A clinico-pathologic study) (author's transl)]. 95 59

To determine the frequency and nature of MRI lesions in children with neurofibromatosis type I (NF1), 50 patients aged 8 to 16 years were evaluated prospectively with cranial MRI. Forty-one children were asymptomatic with respect to central nervous system pathology, and 50% were macrocephalic. Sixteen patients (32%) had normal MRI examinations. Thirty-two patients (64%) had high intensity lesions on T2-weighted images and 16 patients (32%) had hyperintense lesions on T1-weighted images. Seven patients (14%) had ventricular dilatation (associated with increased intracranial pressure in 2) and 11 patients (22%) had optic pathway lesions (optic glioma in 7). MRI was superior to CT in differentiating optic sheath thickening and optic nerve tortuosity from optic glioma in four patients. An intracranial tumour (ependymoma) and sphenoid wing dysplasia were evident in individual patients. Findings previously unreported in NF1 included an aqueductal web resulting in hydrocephalus, intraocular neurofibroma resulting in retinal detachment, and asymptomatic enlargement of the septum pellucidum. T1 and T2 signal abnormalities in isolation were not associated with neurological deficits or the occurrence of macrocephaly, and all lesions that required intervention were suspected clinically. Macrocephaly in the absence of increased intracranial pressure or accelerated head growth is not an indication for neuroimaging in children with NF1. However, the majority of children (68%) had disease-specific abnormalities and thus MRI may provide a useful adjunct to clinical evaluation in the diagnosis of equivocal cases.
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PMID:MRI findings in children with neurofibromatosis type 1: a prospective study. 866 66

Retinal glial tumors and pseudotumors can be classified into astrocytic hamartoma, acquired retinal astrocytoma, massive gliosis, and focal nodular gliosis. Each has different clinical manifestations. Astrocytic hamartoma is usually seen patients who have some manifestations of tuberous sclerosis complex (TSC). It can occur as a noncalcified or calcified variety, and often a combination of the two, and has fairly typical features with fluorescein angiography, ultrasonography, and optical coherence tomography. Although it is generally a stationary lesion, an aggressive variant seen in very young children with TSC can lead to exudative retinopathy, retinal detachment, and neovascular glaucoma. Acquired astrocytoma general occurs in somewhat older individuals who do not have TSC. Like the aggressive form of astrocytic hamartoma it can lead to exudative retinopathy and exudative retinal detachment. Pseudoneoplastic diffuse retinal gliosis can occur as massive glial proliferation in eyes with prior trauma, Coats disease, retinal angiomatosis and other conditions and often occurs in blind eyes. Pseudoneoplastic focal retinal gliosis is characterized by a very superficial, white, noncalcified lesion in otherwise normal eye in somewhat older individuals. Recognition of these glial lesions is important because they can resemble malignant tumors and have different clinical courses and complications.
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PMID:Glial tumors of the retina. The 2009 King Khaled Memorial Lecture. 2396 Aug 60