Vascular endothelial growth factor (VEGF), a potent angiogenic and vascular permeability factor, may be important as a mediator of brain tumour progression. However, it is still not clear whether VEGF plays a causative role in the early stage of glioma development. We investigated the relationship between VEGF protein expression (as assayed by immunohistochemistry) and different morphological parameters reflecting tumour progression (tumour diameter, vascular density and vascular diameter) in tumours at various stages. As a tumour model, ethylnitrosourea (ENU)-induced rat malignant astrocytoma was used. Tumours were classified by size and level of vascularity estimated by the von Willebrand factor (vWF) staining. Tumours less than 10 mm in diameter were designated early stage neoplastic lesions. All 34 early astroglial tumours were found to be VEGF positive. Increase in the VEGF immunopositive rate of tumour cells correlated significantly with increase in vascular density and vascular diameter. We suggest that VEGF induces angiogenesis and growth of microvessels, promoting growth of the early stage malignant astrocytoma.

Dural arteriovenous fistula (AVF) of the anterior cranial fossa is associated usually with cerebral hemorrhage or subarachnoid hemorrhage, while an association with transient global amnesia has not been reported previously. A case presenting the latter unusual symptom is described and the surgical treatment of AVF is discussed. A 64-year-old woman was hospitalized complaining of transient memory impairment. Magnetic resonance (MR) imaging demonstrated a flow void in the left frontal lobe and temporal pole. Cerebral angiography revealed an AVF in the anterior cranial fossa, which was fed bilaterally by the ethmoidal arteries and by branches of the external carotid arteries. The AVF drained into the superior sagittal sinus and the superficial sylvian vein via large varices. Following transfemoral embolization, surgical treatment was carried out. Postoperative angiography revealed complete obliteration of the anomaly. There were no further episodes of amnesia. In our presented case, there is an association between the presenting symptoms and the AVF. The combination of ischemia and congestion in the frontal and temporal lobes may have caused transient memory impairment. From our surgical experience, the excision of the vascular connection between the dura and the frontal lobe following the coagulation of the dura mater of the anterior part of the base of the skull without extensive excision seems to be recommended.

The three-dimensional structure of the collagen fibers in the outer membrane of recurrent chronic sub dural hematoma was studied by scanning electron microscopy (SEM). Specimens obtained at surgery were treated with NaOH at room temperature to digest away all cellular components and expose the collagen fibers. SEM observation of the dural side of the outer membrane showed the collagen fibers were woven into a compact feltwork with a dense arrangement.The fiber bundles had a honeycomb structure framed by the collagen fibers. Observation of the hematoma side found the collagen bundles had a sparse wavy appearance.The arrangement of the collagen fibers on the dural side is different from that on the hematoma side. The thick outer membrane may be formed by granulation resulting from inflammatory reaction. Collagen fibrillar networks are not fragile, and may reinforce the outer membrane of the recurrent hematoma.

: The most important factors in determining the outcomes of patients with traumatic brain injury TBI is the degree of severity and types of primary brain damage, and the secondary damage to the brain such as low-oxygen and low-blood pressure et al. For severe TBI patients, prompt and appropriate decompression to reduce intracranial pressure ICP and ICU management are commonly required. The second edition of Guidelines for the Management of Severe Head Injury was published by the Japan Society of Neurotraumatology JSNT in 2006. These guidelines include a wide range of topics in the management for severe TBI, from prehospital care, primary care, ICU management and surgical treatment. The essence of extended decompression and neuroprotection for TBI is also focused in the JNST Guidelines. The pathophysiological event in the acute stage of severe TBI is quite variable ; therefore, an appropriate individual based approach in ICU management is necessary under experienced medical teams. Jpn J Rehabil Med .