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Biomedical subjects

M Grond

Publications and source records attributed to M Grond.

57 records · Page 4Linked to original sources

Incidence of space-occupying brain edema following systemic thrombolysis of acute supratentorial ischemia.

Whether 'malignant' brain edema following ischemic stroke is due to or aggravated by reperfusion and therefore more frequent after thrombolytic therapy of stroke is still under debate. From 3/96 to 1/97, we treated 51 patients with acute supratentorial stroke within 3 h after symptom onset with rt-PA following a protocol similar to the NINDS study. The results of thrombolytic therapy were evaluated by repeated clinical examination and computed tomography (CT) during the first week after ictus. The incidence of space-occupying brain edema following intravenous thrombolytic therapy of acute ischemic stroke was lower than the edema frequency after conventional treatment, but mortality from 'malignant' edema was higher in the patients with thrombolysis. Thus, space-occupying edema after acute ischemic stroke may be aggravated by thrombolytic treatment. Forced reperfusion of already irreversibly damaged tissue increases edema formation and enlarges developing infarcts with a deleterious increase of intracranial pressure.

Adult↗

Clinical deterioration in probable Alzheimer's disease correlates with progressive metabolic impairment of association areas.

Regional cerebral glucose metabolism (rCMRG1) measured by positron emission tomography of 18F-2-fluoro-2-deoxy-D-glucose was studied longitudinally (interval ranging from 6 to 27 months) in 25 patients with probable Alzheimer's disease (AD). A significant decline of rCMRG1 was noted in the whole brain (p = 0.02) which was most pronounced in the temporoparietal (p = 0.002), frontal (p = 0.01), superior parietal (p = 0.01) and occipital (p = 0.03) association cortex. A similar decline was also present in the thalamus (p = 0.04) but not in the primary visual and sensorimotor cortex, basal ganglia, cerebellum and brainstem. The changes of rCMRG1 in the temporoparietal, frontal and occipital association cortex were related to the change of the Mini Mental State Examination score (temporoparietal: r = 0.49, p = 0.01; frontal: r = 0.40, p = 0.05; occipital: r = 0.44, p = 0.03). The rate of clinical and metabolic decline was not related to age at onset, sex, family history or duration of disease. The results suggest that clinical deterioration and metabolic impairment in probable AD are closely related and dependent on progression of pathological changes in cortical association areas.

Aged↗

Frontal lobe tasks do not reflect frontal lobe function in patients with probable Alzheimer's disease.

Thirty-one patients with probable Alzheimer's disease (AD) according to NINCDS-ADRDA criteria were psychometrically tested with various frontal lobe tasks. The results were correlated with regional cerebral glucose metabolism (rCMRG1) as measured by positron emission tomography of 18F-2-fluoro-2-deoxy-D-glucose. RCMRG1 of frontal functional-anatomically defined regions was not linked to the performance seen in frontal lobe testing. The majority of the frontal lobe tasks showed a high correlation to severity of dementia that was related to rCMRG1 of the temporo-parietal cortex. There were high intercorrelations of frontal lobe test scores to other tests. Thus, these tasks seem to measure nonspecific cognitive changes in AD patients.

Aged↗