Perifocal abnormal signal intensity area in magnetic resonance imaging in meningiomas.
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Biomedical subjects
Publications and source records attributed to T Nariai.
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To evaluate the effect of encephalo-duro-arterio-synangiosis, (EDAS), we obtained follow-up angiograms and measured regional cerebral blood flow in 21 young patients with Moyamoya disease. Carotid fork stenosis continued to progress after EDAS, although angiography demonstrated a marked increase in the number of middle cerebral artery branches via implanted arteries. Preoperative cortical blood flow was lower than normal. The post-EDAS increases in hemispheric and cortical flow were significant in patients with transient ischemic attacks, but not in patients with infarction. The increase in cortical flow at the site of EDAS was first noted 2 weeks after EDAS.
To investigate the perifocal abnormal signal intensity area in MRI in meningiomas, we have analysed MRI in 10 cases among 73 meningiomas which were diagnosed by X-ray CT and verified by operation and pathology. The MRI scanners used in this study were Siemens Magnetom and Toshiba MRT 15A. Ten meningiomas diagnosed by MRI were as follows; one free convexity, one pyramidal, three falx and parasagittal, one sphenoid ridge, one olfactory groove, one cerebellopontine angle, two ventricular meningiomas. Perifocal abnormal signal intensity area was diagnosed as vasogenic edema in 4 cases. This area was shown as high signal intensity in T2-weighted MRI and was confined to the white matter. In proton density-weighted MRI, it was shown as high signal intensity and usually clearly distinguished from rather iso- or hypointensity tumor area. In T1-weighted MRI, this area was shown as slightly low signal intensity, which could be readily differentiated from the remarkably low intensity ventricular CSF. In one case a thin semi-lunar abnormal intensity area bordering the tumor was verified in MRI, but no abnormal area was shown in CT. In the remaining 6 cases, namely one free convexity, one pyramidal and two ventricular meningiomas, one cerebello-pontine and one sphenoid ridge meningioma, in which CSF abutted the tumor, abnormal signal intensity area was diagnosed as entrapped CSF space. The perifocal abnormal signal intensity area in MRI should be regarded as vasogenic edema or entrapped CSF space, and these two should be differentiated by the signal intensity, the distribution of the area and CT-cisternography.(ABSTRACT TRUNCATED AT 250 WORDS)
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Positron emitting dl-erythro-9,10[18F]difluoropalmitate, [18F]DFPA, was synthesized for the in vivo imaging of brain tumors in rats. Male Fischer 344 rats were intracerebrally implanted with Walker 256 carcinosarcoma tumor cells (1 x 10(6) in 5 microliters tissue culture media) and 7 days later were infused with [18F]DFPA (500-1000 mCi/mmol) i.v. for 5 min. Rats were killed after 20 min. Brains were removed and either prepared for autoradiography, or brain and tumor were separated and their radioactivity quantified by gamma spectroscopy. Brain tumors were well demarcated from surrounding and normal brain in autoradiographs, and closely paralleled tumor growth in histological sections. The mean optical density of tumor was significantly greater, by 318 +/- 68 per cent (P less than 0.025, n = 3), than normal brain in autoradiographs, and that of edematous brain surrounding a large tumor was intermediately increased. [18F]DFPA proved of value to image and circumscribe intracerebral tumors in awake rats, and studies are continuing to facilitate its clinical application in brain tumor patients.
An experimental method and its associated mathematical model are described to quantitate in vivo incorporation rates into and turnovers of fatty acids (FAs) within stable brain metabolic compartments, particularly phospholipids. A radiolabeled FA is injected i.v. in a rat, and arterial plasma unacylated FA radioactivities and unlabeled concentrations are sampled until the animal is killed after 15 min, when the brain is analyzed biochemically or with quantitative autoradiography. Unbound unacylated label in blood easily crosses the blood-brain barrier; rapidly equilibrates in the unacylated FA, acyl-CoA and phosphatidate-diacylglycerol brain pools; then is incorporated into phospholipids and other stable metabolic compartments. Uptake and incorporation of labeled FAs are independent of cerebral blood flow at constant brain blood volume. Different labeled FAs enter specific sn positions of different brain phospholipids, suggesting that a combination of probes can be used to investigate metabolism of these phospholipids. Thus, [9,10-3-H]palmitate preferentially labels the sn1 position of phosphatidylcholine; [1-14C]arachidonate the sn2 positions of phosphatidylinositol and phosphatidylcholine; and [1-14C]docosahexaenoate the sn2 positions of phosphatidylethanolamine and phosphatidylcholine. The FA model provides an operational equation for rates of incorporation of FAs into brain phospholipids, taking into account intracerebral recycling and de novo synthesis of the FA, as well as entry into brain of FA from acylated blood sources. The equation is essentially independent of specific details of the proposed model, and can be used to calculate turnovers and half-lives of FAs within different phospholipid classes. For the model to be most applicable, experiments should satisfy conditions for pulse-labeling of the phospholipids, with brain sampling times short enough to minimize exchange of label between stable metabolic compartments. A 15-20 min sampling time satisfies these criteria. The FA method has been used to elucidate the dynamics of brain phospholipids metabolism in relation to brain development, brain tumor, chronically reduced auditory input, transient ischemic insult, axotomy with and without nerve regeneration, and cholinergic stimulation in animals with or without a chronic unilateral lesion of the nucleus basalis magnocellularis.