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Biomedical subjects

H Traupe

Publications and source records attributed to H Traupe.

138 records · Page 8Linked to original sources

CT-visualization of an intraspinal osteoma-like mass in Paget's disease.

Neuroradiological examination in a case of polyostotic Morbus Paget with compression of the thoracic spinal cord was extended to spinal computed tomography. The use of radiography, myelography, and skeletal scintigraphy as regards diagnostic information is compared to CT. Obviously the use of CT provides a valuable completion for the evaluation of extradural space-occupying spinal lesions. Undisturbed by overlying structures of CT has the potential to differentiate various types of tissues. CT clearly depicts the lesion and aids in the recognition of the type of the compressing foreign body, which in this case was an osteoma-like protrusion.

Diagnosis, Differential↗

Hyperperfusion and enhancement in dynamic computed tomography of ischemic stroke patients.

The passage of contrast medium was observed using serial computed tomography (CT) in 24 stroke patients. Density--time profiles of various brain regions were plotted. In normal brain tissue, X-ray attenuation showed a maximum increase during the arterial phase (16.4 +/- 11.0%) and was 2.8 +/- 2.2% above control during stable distribution. In hypoperfusion, increase in attenuation was always below 10% in the arterial phase, while hyperperfusion was characterized by an attenuation increase of 25 to 70%. Enhancement was defined by a density increase of 16.8 +/- 14.8% and a tissue/blood ratio between 7 and 60%. An attempt was made to establish a relationship between the serial CT pattern and the prognosis. Enhancement tended to indicate severe morphological changes followed by permanent neurological deficit, whereas hyperperfusion was generally an indicator of probably recovery.

Adult↗

Comparison between hydrogen clearance and microsphere technique for rCBF measurement.

Regional cerebral blood flow was measured repeatedly in anesthetized and immobilized cats under various experimental conditions by recording the clearance of inhaled hydrogen with inserted platinum electrodes and by recording the distribution of 15 mu microspheres labeled with 3 different radioisotopes. The values for both methods in normal cortical tissue were comparable (75.7 +/- 23.5 ml/100 g min for H2-clearance; 67.6 +/- 26.2 ml/100 g min for microsphere technique), but were below those recorded in awake cats. With both methods the values could be reliably reproduced (correlation coefficient between measurements: 0.903 for H2-clearance, 0.754 for microsphere technique). During ischemia induced by temporary occlusion of the middle cerebral artery the microsphere technique usually yielded higher flow values than the H2-clearance, and did not indicate severe ischemia in 6 out of 20 instances. After restoration of flow, hyperperfusion was observed by the microsphere technique in 2 cases only while H2-clearance indicated hyperemia in 6 instances. This limited comparability between the 2 methods was also expressed in a low correlation coefficient (0.486) calculated from 139 flow values obtained simultaneously with both methods. The discrepancy between the methods under pathological conditions might be due mainly to the different recording volumes: while Pt-electrodes record H2-clearance from a few mm3 or less, tissue samples of 300-700 mg were necessary for the microsphere technique and inhomogeneities of flow may thereby escape detection. The technique for measuring cerebral blood flow in an experimental setup should be selected according to the requirements of the study and according to the limitations of the various methods.

Animals↗

Reperfusion of focal ischemia of varying duration: postischemic hyper- and hypo-perfusion.

Reperfusion into focal ischemia was studied in 25 cats after middle cerebral artery (mca) occlusion of 15 min to 2 hours duration. Changes in cerebral blood flow (CBF) were followed with the hydrogen clearance method in the center and periphery of the ischemic lesion expected. Postischemic hyperperfusion was found often after 15 and 30 min ischemia and regularly after 60 min mca occlusion. It was followed by normal flow after 15 and 30 min occlusion and by postischemic hypoperfusion after 1 hour ischemia. After 2 hours occlusion hypoperfusion generally was not preceded by hyperperfusion. After 60 min ischemia hyperperfusion could not prevent the development of severe hypoperfusion, but often was accompanied by a marked flow reduction in the periphery of the mca territory. The data indicate that hyperperfusion after ischemic periods lasting 60 min and more induces hypoperfusion in the area itself and in neighbouring regions by affecting perfusion pressure and thereby may enlarge ischemic damage.

Animals↗

Flow and neuronal density in tissue surrounding chronic infarction.

In 6 cats, cerebral infarction was produced by transorbital occlusion of the left middle cerebral artery (MCA). Five animals developed typical cortical infarcts. Eight weeks later, cerebral blood flow (CBF) was determined by 14C-iodoantipyrine autoradiography and the number of intact neurons was counted histologically. Two non-operated cats served as controls. Cortical blood flow in the infarcted hemisphere was reduced by 24.6-74.4% when compared to the flow in the contralateral cortex and in controls. Averaged white matter flow was decreased by 39.1%. Regional cortical flow was gradually reduced from parasagittal regions towards the infarct. In the surrounding of the infarct, cortical perfusion was decreased to 24.8 +/- 9.7 ml/100 g/min, i.e. 19.7% of contralateral flow. Although the infarcts were sharply demarcated macroscopically, the number of cortical neurons decreased gradually from the midline to the peri-infarct zone. A significant linear correlation was found between absolute CBF-values and the number of neurons in areas of the infarcted hemisphere. The homolateral gyrus lateralis had normal neuronal density but flow was reduced by 20%. These findings suggest that the blood flow reduction in tissue surrounding chronic infarcts is due to neuronal cell loss and to functional inactivation caused by damage of afferent fibers.

Animals↗