Summary: Focal cerebral ischemia was induced in rats by occlusion of the middle cerebral artery. By a triple tracer technique, cerebral glucose utilization, glucose content, and blood flow were simultaneously determined. Computer-assisted autoradiography revealed a core of dense ischemia in the lateral two-thirds of the striatum. A border zone of increased 2-deoxy-o-glucose (DG) uptake surrounded the ischemic insult in the acute stage. The lumped constant was increased only moderately in the border zone. Therefore, the enhanced DG uptake re flected increased glucose consumption. CBF was re duced to 20-30% in the cortical border, while minor deClinical imaging of acute stroke requires a reli able indicator of irreversible damage and poten tially viable tissue. The visualization of CBF does not faithfully reflect the severity of ischemic damage. Positron emission tomography (PET) of the acute phase of stroke reveals a wide range of CBF values that change in either direction with time, "lUXury perfusion" being one of the extremes (Lassen, 1966). Several authors have raised the question of whether the changes of CBF are sec ondary to more fundamental changes and thus no more than an epiphenomenon (Ackerman et aI., 1981).Received August 16, 1985; 414pression and in some animals hyperemia were evident in the striate border. Six hours after the insult, the border zones of increased glucose consumption had disappeared in half the animals. In no animals examined after 20 h was glucose consumption enhanced. The study indicated a stable metabolic response to a reproducible focal insult. We conclude that continued enhancement of glucose consumption in marginally perfused areas indicates neuronal damage. Key Words: Autoradiography-Cere bral blood flow-Cerebral ischemia-2-Deoxyglucose method-Lumped constant-Middle cerebral artery oc clusion.Quantitative 2-deoxY-D-glucose (DG) autoradiog raphy has been used in animal models of ischemia and 18F-labeled 2-fluoro-2-deoxY-D-glucose (FDG) in PET of stroke patients. Heterogeneous distur bances including increased, decreased, or normal accumulation of DG and FDG have been reported in the early phase of ischemia (Fieschi et aI. , 1978;Diemer and Siemkowicz, 1980; Wise et aI. , 1983). In experimental focal ischemia, several authors have found foci of greatly suppressed DG uptake surrounded by a rim of increased DG accumulation (Ginsberg et a\. , 1977; Welsh et aI. , 1980; Choki et aI. , 1983). In the method of Sokoloff et al. (1977), local DG accumulation is the basis for estimation of local glucose phosphorylation. However, only in normal tissue can the rate of DG be assumed to be a known fraction of glucose consumption. The "iso tope" correction ratio of DG accumulation to glu cose consumption, the lumped constant (LC), may change in conditions in which the relationship be tween plasma and brain glucose has changed.Therefore, in pathological tissue the magnitude of the LC must be determined separately before it is possible to calculate glucose consumption from the DG accumulatio...

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Quantitation of morphological changes in the nervous system is valuable for demonstrating different regions and cell types involved in a pathological process. Quantitative anatomical studies are numerous, whereas quantitations of pathological conditions are relatively few. This seems to be due partly to technical difficulties arising when comparing normal with pathological brain tissue. Shrinkage of the whole brain or of substructures is important but difficult to determine, and earlier studies are often inaccurate due to lack of precise measurement of this parameter. This review deals with three different technical aspects: (1) measurements at the macroscopical level, (2) the light microscopical morphometry, and (3) the stereological principles which are used primarily in electron microscopical quantitation. The most used techniques and formulas are reviewed in order to give an impression of the possibilities and requirements in quantitative neuropathology. After each of the major areas, macroscopical measurements, determination of nuclear and cell size and nuclear number, vascular network, and stereology, a few practical comments are given as well as references for further information on the topic. The quickly developing electronic image analysis is dealt with in the section on capillary network measurements and in the last, concluding section.

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The nuclei of Purkinje cells and Bergmann astrocytes were counted on sagittal sections from cerebellum and the length of stratum gangliosum was measured in rats with CCl4-induced liver disease, using an electronic image analyzer. After 8 weeks of CCl4-administration a reduction was found in the number of Purkinje cells, many of which showed homogenizating changes. Ten weeks after termination of the administration period the number of Purkinje cells was reduced by 12 percent. The number of Bergmann astrocytes remained significantly increased after 8 weeks of CCl4-administration (max. 20 per cent). The changes of Purkinje cell and Bergmann astrocyte density developed during the period of severe liver necrosis, whereas only minor changes were found in the ensuing period of liver "cirrhosis". In the perfusion fixed specimens, the Bergmann astrocyte nuclei increased in volume up to 65 per cent and immersion fixed brains showed typical Alzheimer type II nuclear changes. The impact of the increased plasma ammonia concentration on the astrocytes is discussed.