Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain tissue damage in congenital hydrocephalic rat (LEW/Jms) was studied in the aspects of the hydrocephalic brain edema and the changes of the vascular apparatus. The characteristic findings in this study were the changes of the small blood vessels and the intracerebral cavity formation. In the acute stage of hydrocephalus (2 to 5 days after birth), spongy appearance and necrosis of the brain edema were observed in the periventricular white matter. The stenotic or obstructive vascular changes were located in connection with the hydrocephalic brain tissue. In this stage, the intracerebral cavity was formed particularly in the periventricular edematous white matter resulting in a thinning of the occipital lobes. In the late stage of hydrocephalus (9 to 15 days after birth), the lateral ventricles were severely dilated, and a markedly dilatated intracerebral cavity was observed in the periventricular white matter. The edematous area was observed adjacent to the dilated lateral ventricles or the intracerebral cavity. In the late stage, the number of small vessels filled with carbon black decreased in the area of the CSF edema when compared to the acute stage, and many obstructive blood vessels were observed in the same area. Moreover, dilatated blood vessels without carbon black were observed in the border zone between the normal and the edematous area adjacent to the intracerebral cavity. These vascular changes may occur by the accumulation of the CSF as well as the mechanical compression, and consequently lead to the microcirculatory disturbance. These microcirculatory disturbances may contribute to the intracerebral cavity formation with the accumulation of the CSF in the extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain tissue damage in congenital hydrocephalus of the inbred rat, LEW/Jms--intracerebral cavity formation]. 387 51

A 54-year-old woman was hospitalized because of paraparesis, sensory disturbance of the lower extremities, and dysuria. Laboratory data included an erythrocyte sedimentation rate (ESR) of 16 mm/h and lactate dehydrogenase (LDH) level of 459 IU/l. Myelogram showed an enlarged spinal cord at the L1 level, and spinal MRI revealed a high signal area on T2-weighted images. Spinal cord biopsy by thoraco-lumbar laminectomy showed thickening of the pia mater and neovascularization, but no malignant cells. Immediately after the operation, the patient displayed progressive mental deterioration. Cranial MRI showed widespread high signal areas in the cerebral white matter on T2-weighted images which resembled those of leukoencephalopathy. Steroid therapy was tried but was ineffective. Ten months after the onset of symptoms, a brief period of regression of both clinical symptoms and MRI appearances occurred following the administration of Inosiplex, subsequent progressive deterioration led to death 14 months after the onset of symptoms. LDH, C-reactive protein (CRP), and cerebrospinal fluid (CSF) protein were all elevated during the deterioration of her general status. Postmortem examination revealed a large tumor mass of the left adrenal gland which extended to the Th12, L1, and L2 vertebrae and remarkable brain edema. Microscopic mononuclear tumor cells were widespread but confined to the lumens of small vessels of the brain, spinal cord, spinal root and right adrenal gland, almost as if they were occluded. Cerebral white matter presented widespread multiple small infarcts and extensive myelin thinning. In addition to the left adrenal gland, interstitial invasions of tumor cells were discovered in the kidneys, iliopsoas muscles, oviducts, myocardium, lymph nodes, and thyroid gland.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsied case of intravascular malignant lymphomatosis with paraparesis, that presented a leukoencephalopathy-like image after spinal cord biopsy]. 836 55

A 15-year-old boy presented with an anaplastic supratentorial ependymoma causing massive intratumoral calcification, without contributory medical and family history, and manifesting as persistent headache for 2 months. Physical examination found no neurological deficit except for visual defect in the right lower quadrant, with intact visual acuity. Blood examination showed no abnormalities. Cranial computed tomography revealed a huge calcified mass in the left parietooccipital lobe, with extensive perilesional brain edema. Cranial radiography showed diffuse and symmetrical thinning of the calvarial bone. Magnetic resonance imaging confirmed the tumor as an assembly of medullated masses with extraventricular location, 7 x 6.5 x 6.5 cm in diameter, and appearing as heterogeneous intensity on both T(1)- and T(2)-weighted images with inhomogeneous enhancement except for the central cores. The patient underwent tumor resection. Intraoperative findings revealed that the cortical veins overlying the tumor were reddish and moderately engorged. The hypervascular tumor, entirely extraventricular in location, was totally resected without neurological deterioration. Histological examination revealed that the tumor was highly cellular with hyperchromatic nuclei and cell atypia. Necrosis, mitotic figures, and perivascular pseudorosette formations were frequently seen. Immunohistochemical study showed positive staining for glial fibrillary acidic protein, S-100 protein, vimentin, and epithelial membrane antigen, but negative for synaptophysin. The MIB-1 labeling index was 26.5%. The findings were compatible with anaplastic ependymoma (World Health Organization classification grade 3). Ependymoma should be included in the differential diagnosis of a supratentorially located, extraventricular mass with massive intratumoral calcification.
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PMID:Huge supratentorial extraventricular anaplastic ependymoma presenting with massive calcification--case report. 2018 83