Very early expression of vascular endothelial growth factor in brain oedema tissue associated with brain contusion.

BACKGROUND: Brain oedema associated with cerebral contusion can be life-threatening. Mechanisms of the development of brain oedema are still unclear. METHOD: We investigated the expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2 (KDR/Flk-1) in the contusional brain tissue obtained during neurosurgery from 5 patients. FINDINGS: VEGF is expressed in some but not all the astrocytes, and KDR/Flk-1 is expressed in vascular endothelial cells in the con-tusional tissue as early as 3 hours after onset. CONCLUSION: The results suggested that the VEGF is induced in the contusional tissue in the very early period after onset, and that it increases capillary permeability via KDR/Flk-1 resulting in vasogenic type brain oedema.

Tissue reconstruction process in the area of peri-tumoural oedema caused by glioblastoma--immunohistochemical and graphical analysis using brain obtained at autopsy.

BACKGROUND: In the area of peri-tumoural oedema, proteolytic agents derived from the tumour cause tissue degradation, which promotes tumour cell invasion. METHOD: We investigated the biological processes in the area of peri-tumoural oedema, using a brain obtained at autopsy from a patient who died from glioblastoma. Immunohistochemistry was performed to detect vascular endothelial growth factor (VEGF), c-myc, p53, paternally expressed gene-3 (PEG-3), transforming growth factor beta (TGFB), and tumour necrosis factor alpha (TNFA). The data were translated into colour graphics and the localization of these proteins was analyzed. FINDINGS: In the area of peri-tumoural oedema, Ki-67 and p53 positive cells were observed with TGFB expression. Moreover, c-myc, PEG-3, VEGF, and TNFA were also expressed strongly in the glial cells or extra-cellular spaces in the area of peri-tumoural oedema. INTERPRETATION: These data suggest that in the area of peri-tumoural oedema, tissue reconstruction processes take place with concomitant anti-tumour activities. The expression of c-myc, VEGF, and TNFA in the area of peri-tumoural oedema may indicate that these proteins are not utilized for tumour growth, but may be used to guard the brain against tumour invasion. Peri-tumoural oedema does not only indicate the tissue damage caused by tumour, but many tissue reconstruction processes take place in these areas against tumour cell invasion.

Magnetic resonance imaging findings in cerebral fat embolism: correlation with clinical manifestations.

OBJECTIVES: Cerebral fat embolism (CFE) is a serious complication after fracture of long bones. The mortality rate of CFE may be high. However, recent progress in treatment may decrease the mortality. We studied the validity of magnetic resonance imaging (MRI) to detect and grade severity of CFE in 11 patients with CFE. METHODS: Glasgow Coma Scale score, PaO2, PaCO2 at the onset, and minimal hemoglobin and platelet levels were monitored, and phagocytes in bronchoalveolar lavage fluid were counted. Brain computed tomographic and MRI scans were performed serially. MRI findings were graded into four categories according to the severity of T2-weighted images. RESULTS: High-intensity T2 signals were identified in the various brain regions as early as 4 hours after onset of CFE. The maximum MRI grade significantly correlated with Glasgow Coma Scale score at the onset of CFE (p < 0.01). High-intensity T2 signal lesions fused and enlarged with time. In most cases, they diminished within 2 weeks. Three patients had persistent morbidity. CONCLUSION: MRI-T2-weighted imaging seems to be the most sensitive imaging technique for diagnosing CFE, and correlates well with the clinical severity of brain Injury. With the aid of proper treatment for pulmonary fat embolism, CFE is a potentially reversible disease that can have a good outcome.

[Empty sella as an intrasellar herniation of the third ventricle secondary to spontaneous degeneration of a prolactinoma].

A case of a large empty sella was reported, which was intrasellar herniation of the third ventricle associated with a prolactinoma. The patient was a 46-year-old female admitted due to consciousness disturbance with pyrexia and vomiting. She had amenorrhea, galactorrhea and sterility in her past history. On admission, physical and neurological examinations revealed severe dehydration, systemic edema, systemic hypotension, nuchal rigidity, papilloedema and goiter. A spinal tap was performed and revealed an increase in CSF pressure. Laboratory data indicated CSF lymphocytosis, an increase in CSF protein content, high titers of serum microsome test, a low concentration of anterior pituitary hormones in serum except for PRL, and an unusually high concentration of PRL in serum and CSF (4680 and 222ng/ml, respectively). Plain films of the skull showed destructive enlargement of the sella turcica. The patient was diagnosed as having non-bacterial meningitis, chronic thyroiditis and a prolactinoma with hypopituitarism and was then admitted to our department. Except for amenorrhea she was asymptomatic under the administration of levothyroxine, hydrocortisone and bromocriptine. CT scan, MRI, pneumoencephalography and CT cisternography as further examinations disclosed the intrasellar herniation of cisterns and the third ventricle, which were surrounded by an intrasellar parenchymal layer. This layer was thought to be still viable prolactinoma tissue. We supposed the third ventricle entered the enlarged sellar cavity following the spontaneous degeneration of the large prolactinoma. Although we could find some documented reports of similar cases, the complete herniation of the third ventricle secondary to degeneration of an adenoma might be rare.(ABSTRACT TRUNCATED AT 250 WORDS)