Discrimination of brain abscess and cystic tumor by in vivo proton magnetic resonance spectroscopy.

Proton magnetic resonance (MR) spectroscopy was evaluated for the differentiation of brain abscesses and cystic brain tumors. Proton MR spectroscopy was performed in vivo in two patients with brain abscess and eight patients with various cystic brain tumors (anaplastic astrocytoma, glioblastoma, and metastatic brain tumor). MR imaging with contrast medium demonstrated ring-like enhanced mass lesions in all patients. The various resonance peaks in proton MR spectra were assigned to metabolites according to chemical shifts. Treatment of the cystic brain lesions was based on the information from proton MR spectroscopy. Aspirated pus from one patient with brain abscess was examined using ex vivo proton MR spectroscopy. The in vivo spectra of brain abscess contained resonance peaks attributed to acetate, lactate, alanine, amino acids, and lipids in both cases, and an additional peak of succinate in one case. In vivo spectra of the neoplasms contained resonance peaks corresponding to lactate, lipids, choline, creatine, and N-acetyl aspartate. Proton MR spectroscopy is useful for discriminating brain abscess from cystic tumors with similar neuroimaging appearance, which is very important for determining the treatment strategy.

Subdural hemorrhage caused by de novo aneurysm complicating extracranial-intracranial bypass surgery: case report.

A case of a de novo aneurysm leading to subdural hemorrhage after right extracranial-intracranial bypass surgery is described. After an uneventful 2-month postoperative course, the patient experienced sudden onset of occipital headache with vomiting. Radiological study disclosed an acute subdural hematoma in the right temporo-occipital region and a newly formed aneurysm at the site of patent superficial temporal artery-middle cerebral artery anastomosis. The anastomotic portion with the ruptured aneurysm was resected en bloc after alternative occipital artery-middle cerebral artery bypass, and the cut end of the superficial temporal artery was successfully used for end-to-side reanastomosis to the other middle cerebral artery branch. The histological examination of the ruptured aneurysm revealed the features of a true aneurysm.

Origins of nitric oxide synthase-containing nerve fibers in the rat basilar artery with reference to the fine structure of the nerve fibers.

The origins of nitric oxide synthase (NOS)-containing nerve fibers in the rat basilar artery were studied by a combination of Fluoro-Gold retrograde tracing and immunohistochemistry. After application of Fluoro-Gold onto the middle part of the basilar artery, the dye accumulated in the sphenopalatine, otic, trigeminal, superior cervical, nodose ganglia and in the spinal ganglia at level C2 and C3. Nerve cells with NOS-like immunoreactivity were detected in the above ganglia, except for the superior cervical ganglion. Neurons that showed both NOS-like immunoreactivity and Fluoro-Gold fluorescence were numerous in the sphenopalatine and otic ganglia, and less numerous in the trigeminal, nodose and spinal ganglia. Under electron microscopy, a number of unmyelinated nerve terminals with neuronal NOS-like immunoreactivity was seen in proximity to smooth muscle cells in the tunica media of the basilar artery. These findings provide morphological evidence that NOS-containing nerve fibers in the rat basilar artery have multiple origins, and suggest that the control of posterior cerebral circulation by the parasympathetic and sensory ganglia are more complex than previously considered.

Role of basic fibroblast growth factor in the regulation of rat basilar artery tone in vivo.

Using the cranial window method, we investigated the effect of basic fibroblast growth factor (bFGF) on the diameter of the rat basilar artery in vivo. bFGF (5-200 ng/ml) caused significant vasodilation in a dose-dependent manner with the maximal effect (119% of baseline diameter) at 200 ng/ml. Vasodilation was not observed when the basilar artery was treated with heat-inactivated bFGF or bFGF preincubated with bFGF-neutralizing monoclonal antibody. Moreover, bFGF-induced vasodilation was suppressed significantly by coadministration of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). In contrast, NG-nitro-D-arginine methyl ester (D-NAME), which is the isomer of L-NAME, exerted no influence on bFGF-induced vasodilation. These findings suggest that the dilatation by bFGF of the rat basilar artery is mediated by NO, and that bFGF plays an important role in the regulation not only of the anterior circulation as previously described but also of the posterior circulation in the brain.

Large cystic cavernous angioma of the cerebellum--case report.

A 40-year-old female presented with gait disturbance and dysarthria. Computed tomography revealed a large cystic tumor in the cerebellar vermis with a mural nodule located in the deepest portion of the cyst. The magnetic resonance (MR) imaging appearance suggested cavernous angioma. The solid nodule was completely removed through the suboccipital approach. The cyst was filled with transparent yellowish fluid which showed positive Froin's sign. The histological diagnosis of the mural nodule was cavernous angioma. The cyst wall consisted of gliosis and contained no angiomatous tissues. Postoperative MR imaging demonstrated that the nodule was totally removed and the cyst size was reduced. The neurological deficits improved postoperatively. The mechanism of formation of the large cyst was assumed to be repeated peritumoral hemorrhage.

Basic fibroblast growth factor-like immunoreactivity in the rat basilar artery with reference to co-localization with NADPH-diaphorase in the trigeminal ganglion.

The location of basic fibroblast growth factor (bFGF)-like immunoreactivity and nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase (neuronal nitric oxide synthase) activity in the rat basilar artery and in the trigeminal, sphenopalatine and superior cervical ganglia was investigated. bFGF immunoreactivity was seen mainly in adventitial nerve fibers of the rat basilar artery, but not in the endothelium. Electron microscopy of the tunica media showed a number of immunoreactive nerve endings in the vicinity of local smooth muscle cells. Among the cranial ganglia that innervate the basilar artery, only the trigeminal ganglion had bFGF-immunoreactivity neurons. Nerve cells and fibers with NADPH-diaphorase activity were detected in the basilar artery and in the sphenopalatine and trigeminal ganglia, and the co-localization of bFGF and NADPH-diaphorase was noted only in the trigeminal ganglion. Furthermore, Fluro-gold tracing in combination with bFGF immunohistochemistry demonstrated that bFGF-containing nerve fibers in the wall of the basilar artery arise from the trigeminal ganglion. These findings provide a morphological basis for the nitric oxide-mediated dilatation of cerebral arteries by bFGF.

Transient increase in endogenous basic fibroblast growth factor in neurons of ischemic rat brains.

An antiserum against basic fibroblast growth factor (bFGF) was shown to recognize an 18-kDa protein (possibly bFGF) in crude neocortical extracts by immunoblot and used to investigate the changes of bFGF immunoreactivity in neurons and astrocytes of the cerebral cortex of rats 1-21 days after unilateral occlusion of the middle cerebral artery (MCA). The mildly ischemic neocortex exhibited no signs of cell loss or degeneration in Nissl-stained sections 1-14 days after MCA occlusion, but it contained pyramidal cell bodies and processes with more intense bFGF immunoreactivity than did the control neocortex. bFGF immunoreactivity in the ischemic hemisphere gradually declined in intensity and by 21 days after MCA occlusion, it had reached the control level. On the other hand, there were many bFGF immunoreactive astrocytes in the primary olfactory cortex on the side of infarction. These findings suggest that MCA occlusion causes an increase in bFGF content not only in astrocytes but also in neurons, depending on the severity of the ischemic insult in individual cortical regions. The transient augmentation of bFGF expression or accumulation in mildly ischemic pyramidal neurons but not in astrocytes is in line with previous studies suggesting the neurotrophism of exogenously applied bFGF.