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Biomedical subjects

C Weiller

Publications and source records attributed to C Weiller.

123 records · Page 7Linked to original sources

[Anticoagulation in acute cerebral infarct. Benefits, risks, therapeutic failures].

We studied 2 groups of ischemic stroke patients who received therapeutic heparinization during the acute phase in order to prevent thromboembolic reinfarction. 530 patients were studied retrospectively (Group B) and 127 prospectively (Group A). Doses of 24,000-38,000 IE/24 h of heparin were given i.v., resulting in a partial thromboplastin time 2-3 times that of normal controls. Three patients from Group A suffered a massive intracranial hemorrhage. All of them had a large infarction (greater than 5 cm in diameter). They had been given anticoagulants within the first 12 h. Two of them presented with uncontrollable hypertension (systolic BP up to 240 mm Hg). Ischemic reinfarction during the first two weeks occurred in 2.3% and 2.4% of subgroups, respectively. This was less than would have been expected from the literature (approx. 14-15%). Features of these patients were 1.) insufficient heparin dosage, 2.) progression of hemodynamically relevant internal carotid artery lesions leading to critical low-flow or 3.) embolization of a floating thrombus from the internal carotid artery in the middle cerebral artery. It appears that therapeutic heparinization reduces the rate of reinfarction within the acute phase of ischemic strokes. This type of treatment should, however, be confined to patients with an embolic stroke mechanism. Careful surveillance of blood pressure and PTT are prerequisites. Anticoagulation should be avoided in patients with massive infarctions (greater than 5 cm in diameter) or uncontrollable hypertension.

Cerebral Infarction↗

The large striatocapsular infarct. A clinical and pathophysiological entity.

We examined 29 patients with strictly subcortical large striatocapsular infarctions. Eight of them had aphasia or neglect. All patients underwent transcranial Doppler ultrasonography or selective carotid angiography, magnetic resonance imaging, and single photon emission tomography for assessment of cerebral blood flow, blood volume, and cerebral perfusion reserve. The signs were compatible with cortical territorial infarctions rather than lacunes. On both magnetic resonance imaging and computed tomographic scans, the lesions corresponded to the territories of the medial and lateral group of the lenticulostriate arteries, Heubner's artery, or the anterior choroidal artery. The infarctions were either due to cerebral embolization into the M1 segment of the middle cerebral artery or due to stenosis at the same site, ie, lesions that acutely and simultaneously occluded the orifices of the lenticulostriate or neighboring arteries. Persistent occlusion of the middle cerebral arteries and a decrease of cortical regional cerebral blood flow were only found in patients with aphasia or neglect. All patients without aphasia or neglect showed a rapid recanalization of the middle cerebral artery occlusion or a stenosis of the M1 segment and no cortical regional cerebral blood flow decrease. Large striatocapsular infarctions occur due to occlusive disease of the middle cerebral artery (large-vessel disease) and not due to a disseminated in situ occlusion of the long penetrating arteries (small-vessel disease), as in lacunes. Neuropsychological deficits can be explained by decreased cortical blood flow due to a persistent occlusive lesion of the middle cerebral artery.

Adult↗

[Reproducibility of ultrasound criteria for characterizing carotid artery stenoses].

Comparisons with intraoperative findings suggest that Duplex scanning may be of value in predicting the morphology of carotid artery stenoses. Such studies, however, are based on the results obtained by experienced investigators. To clarify whether sonographic criteria can be standardized, 6 investigators from different hospitals each documented 30 carotid artery stenoses of greater than or equal to 40% diameter reduction which could be imaged in at least 2 planes. Three sonographic criteria (plaque surface, echo density, echo structure), each with 8 categories, were assessed from the image documentations by the 6 as well as by 2 independent further investigators. Depending on the experience and on the device used 29-81% of all stenoses greater than or equal to 40% examined in the different laboratories could be included in the study. The +/- 1 category concordance between the different investigators averaged 50-60% for all sonographic criteria independent from the degree of stenosis and from the image quality. Because of lack of sufficient reproducibility the subjective assessment of sonographic criteria is found to be not suitable for use in multicentre studies.

Brain Ischemia↗

[Determination of regional cerebrovascular perfusion reserve (rCPR) using quantitative flow/volume (F/V)-SPECT. Results in patients with subcortical ischemic brain lesions with or without neuropsychological symptoms].

NPS (aphasia or neglect) are a regular concomitant symptom of cortical, and, occasionally, subcortical ischemic lesions. In 19 patients with subcortical lesions (eight with NPS, 11 without NPS), F/V-SPECT was employed to search for changes in rCPR in both, lesions and ipsilateral cortex. Results were correlated with NPS and MRI findings. Compared to the unaffected hemisphere, all subcortical lesions showed reduced regional cerebral blood flow (rCBF) (-16 to -23%), increased regional cerebral blood volume (rCBV) (+34 to +62%), and decreased or missing rCPR (-27 to -28%). Compared to MRI, there was no difference in lesion size in the thromboembolic lesions. Hemodynamic low-flow infarcts, however, were greater with SPECT than in MRI. In patients without NPS, the adjacent cortex was normal in SPECT and MRI. In addition, patients with NPS revealed reduced rCBF (-18%), increased rCBV (+19%), and decreased rCPR (-22%) in the adjacent cortex. MRI was normal in the same cortical area. These results indicate that NPS in subcortical lesions may be caused by a hemodynamic mechanism causing reduction of rCPR in the adjacent cortex.

Adult↗

[Pattern of cerebral infarct in computerized tomography. Pathophysiologic concepts, validation and clinical relevance].

Our pathogenetically oriented classification system of hemispheric brain infarctions is reviewed. New data are presented to validate this classification from various points of view. A retrospective analysis of 73 patients with large striato-capsular infarcts demonstrated that two-thirds of them had a source of embolism either in the carotid bifurcation or in the heart. SPECT-imaging in patients with hemispheric brain infarctions of various origin revealed that the area of exhausted cerebral perfusion reserve largely exceeds the area of the infarct visible on CT if a hemodynamically caused low-flow infarction is present. This is not the case in the territorial type. Measurement of the hemispheric vasomotor reactivity to capnic stimuli confirmed this finding by demonstrating a severely reduced VMR in low-flow infarctions, but not in thrombo-embolically caused territorial infarctions. Lacunar infarctions due to occlusion of single long penetrating arteries should be judged as either "unequivocal", "probable" or "possible lacunae" and should be differentiated from small lacunar-like infarctions in the cortex ("non-lacunae") which represent small territorial infarctions due to thromboembolism of small pial arteries. Infarctions in the temporo-parieto-occipital watershed area are difficult to distinguish from territorial infarctions within the posterior part of the middle cerebral artery distribution. For research purposes, such patients should be excluded in order to keep the subgroups homogeneous. Consequences of this classification system for diagnostic and therapeutic strategies in stroke patients are discussed.

Blood Flow Velocity↗

Combined SPECT imaging of regional cerebral blood flow (99mTc-hexamethyl-propyleneamine oxime, HMPAO) and blood volume (99mTc-RBC) to assess regional cerebral perfusion reserve in patients with cerebrovascular disease.

In 53 patients with cerebrovascular disease (CVD), regional cerebral blood flow (CBF) and blood volume (CBV) were imaged by SPECT within one session. Slice division (CBF: CBV) yielded distribution of regional cerebral perfusion reserve (CPR). Semiquantitative evaluation was obtained from manually set ROIs by interhemispherical ratios (for CBF, CBV and CPR), using 2 SD from a normal group (n = 10) as a threshold. Sensitivities were 59% for CBF, 94% for CBV and 83% for CPR. Combined sensitivity was 98%. Establishing three constellations for CBF, CBV and CPR, regionally normal CBFs but quantitatively increased CBVs (+69%) and decreased CPRs (-31%) were found in relatively early stages of CVD. Very advanced cases showed decreased CBFs (-65%), CBVs (-40%), CPRs (-49%) and a surrounding penumbra. In 87% (46/53 patients), such rheologically postulated constellations could be demonstrated. We conclude that combined CBF and CBV SPECT, assisted by CPR images, is a promising tool to detect CVD and to assess its individual regional severity.

Aged↗

[Dependence of the risk of brain infarct on the degree of severity of occlusive internal carotid artery lesions].

This retrospective study was performed in order to evaluate the relationship between the risk of brain infarction and the severity of 274 internal carotid artery (ICA) stenoses in 218 patients. Clinical, vascular and brain-morphological findings were compared. Of 106 occluded ICAs, 59% had induced a completed stroke with visible hemispheric infarction in 77%, most of them of the territorial type (35%). 32% of 85 high-grade stenoses had led to completed strokes, with territorial, low-flow and microangiopathic patterns of infarction occurring equally frequent. CT was normal in two-thirds of 83 low-grade ICA-stenoses, whereas 14% showed microangiopathic brain lesions. We conclude that (1) asymptomatic ICA stenoses should not be operated on, as long as they are not of very high degree and (2) even symptomatic ICA stenoses should not undergo endarterectomy, if the patient's stroke was due to lacunar infarctions of typical site and size.

Carotid Artery Diseases↗

[Dialysis encephalopathy and aluminum poisoning? Correlated clinical, pathologic-anatomic and spectrometric findings].

A case of severe dialysis encephalopathy is reported, in which the autopsy finding of an extensive spongiform change in areas of the cortex directly corresponded to high aluminium-concentration in these areas, supporting the theory of an aetiological role for aluminium. A therapeutic approach combining low aluminium intake and removal of aluminium by a chelating agent (desferrioxamine) is promising, but more precise guidelines are needed.

Aluminum↗

[Surface gastritis. Immunoglobulins and lysozyme. The border zone between physiology and pathology].

We examined the infiltration in chronic superficial gastritis immunohistochemically on the contents of IgA-, IgG- and IgM-containing plasma cells and on lysozyme and compared the results on the one hand with those of histologically normal gastric mucosa and on the other side with those of the inflammation at the ulcus border. Not as immunology-related reactions of the gut, one can see the chronic superficial gastritis as a stronger and topographically different variant of the normal reaction of the stomach. It shows the flowing threshold between physiological and accentuated defense and pathological exaggeration.

Chronic Disease↗

Acute stroke evaluated by time-to-peak mapping during initial and early follow-up perfusion CT studies.

BACKGROUND AND PURPOSE: Early diagnosis of perfusion deficits in patients with acute stroke could guide treatment decisions and improve prognosis. We investigated the sensitivity of perfusion CT studies using parametric time-to-peak maps to assess ischemic brain tissue with respect to early infarct signs on native CT scans. METHODS: First-pass, single-section perfusion CT was performed in 20 patients who presented with symptoms of acute stroke within 6 hours of onset. Initial CT perfusion studies were compared with follow-up studies within 30 hours in 10 patients. A manual, region of interest (ROI)-based, local evaluation procedure was performed to determine delayed time-to-peak values and diminished peak amplitudes. In addition, time-to-peak parameter maps were processed off-line from the dynamic CT data sets to identify areas of perfusion deficits, which were expressed as hemispheric lesion areas (HLAs). Evolution of the ischemic regions was assessed by comparing the HLA on the initial and follow-up studies as well as on the native CT scan of the follow-up studies. RESULTS: Diagnostic time-to-peak maps were generated in 19 of 20 initial and in nine of 10 follow-up perfusion CT studies. The initial time-to-peak map showed perfusion deficits in 14 of 20 patients. Hemispheric territorial infarcts were diagnosed with a sensitivity of 93%. Perfusion deficits in two patients with brain stem infarctions and three patients with lacunar strokes were missed. Follow-up time-to-peak maps showed the extent of reperfusion after various therapeutic strategies. CONCLUSION: Perfusion CT is potentially useful for detecting cerebral perfusion deficits in acute ischemic stroke before morphologic changes are observable on native CT scans. Compared with a locally restricted ROI-based evaluation, time-to-peak maps provide sensitive, global indications of malperfused brain areas, facilitate lesion localization, and allow assessment of the evolution of the infarction during follow-up.

Acute Disease↗