Cerebral blood flow and metabolism during cardiopulmonary bypass: evidence of microembolic encephalopathy.
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Biomedical subjects
Publications and source records attributed to J Kessler.
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The effect of age on regional cerebral metabolic rate of glucose (rCMRGl) was studied in 14 patients with presenile dementia of Alzheimer type (DAT) and 24 patients suffering from senile DAT in comparison to 20 age-matched normal subjects by positron emission tomography (PET) of 2-(18F)-fluoro-2-deoxy-D-glucose (FDG). The metabolic pattern was condensed to a single metabolic ratio. It was calculated as the quotient of rCMRGl in regions typically affected by AD (frontal and temporoparietal cortex) divided by that in regions typically not affected. In normals this ratio was 1.05 +/- 0.04 and did not depend on age. In patients, the metabolic ratio was generally smaller and there was a significant difference between presenile (0.82 +/- 0.1) and senile DAT (0.90 +/- 0.1). This was due to a different metabolic pattern in the two age groups: metabolic impairment was focused on frontal and temporo-parietal cortex in presenile DAT, whereas more global rCMRGl reductions were present in senile DAT. The results suggest a more generalized disorder in senile dementia impairing metabolism globally in addition to the more localized changes that are typical for DAT.
Progression rates of Alzheimer's disease (AD) vary considerably, and they are particularly difficult to predict in patients with mild cognitive impairment. We performed a prospective multicenter cohort study in 186 patients with possible or probable AD, mostly with presenile onset. In a cross-sectional analysis at entry, impairment of glucose metabolism in temporoparietal or frontal association areas measured with positron emission tomography was significantly associated with dementia severity, clinical classification as possible versus probable AD, presence of multiple cognitive deficits and history of progression. A prospective longitudinal analysis showed a significant association between initial metabolic impairment and subsequent clinical deterioration. In patients with mild cognitive deficits at entry, the risk of deterioration was up to 4.7 times higher if the metabolism was severely impaired than with mild or absent metabolic impairment. Copyrightz1999S.KargerAG, Basel
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.
70 patients with probable Alzheimer's disease were randomly allocated to four groups: 17 patients received only social support, 18 cognitive training twice a week, in 17 cognitive training was combined with pyritinol 2 x 600 mg/day and in 18 cognitive training was combined with phosphatidylserine 2 x 200 mg/day. Treatment duration was 6 months. Before and after treatment, the patients underwent neuropsychological testing as well as measurement of the regional cerebral metabolic rate for glucose using positron emission tomography and 18F-2-fluoro-2-deoxy-D-glucose. Before treatment the groups were comparable in respect to resting and activated glucose pattern achieved by a visual recognition task. Electrophysiological changes were assessed as EEG power, globally and in 4 frequency bands. This 6-month study in four groups of patients with Alzheimer's disease indicated that phosphatidylserine treatment has an effect on different measures of brain function. Since neuropsychological improvements were best documented after 8 and 16 weeks and faded towards the end of the treatment period, it must be concluded that this symptomatic therapy is mainly of short-term benefit and was overcome by the progressive pathological changes at the end of the treatment period.
We report about 38 patients aged between 1 and 19 years (36.8% female, 63.2% male; mean age 7.8 years) admitted as inpatients for further neurorehabilitation mostly 4 weeks after severe acquired brain injury (ABI) of different aetiology. Of the patients, 73.7% were in a state of minimal responsiveness (vigilance score < 7 WVS) on admission. We evaluate the course of rehabilitation and the outcome 6 months after the end of the inpatient-period. The average stay of 15.5 weeks is strikingly low. The average intensity of therapy comes to about 16 units per week including strategies of rehabilitative education. The incidence of good rehabilitation was 21%, whereas almost 45% of patients displayed severe impairment. Although further improvements were found in almost 40% of patients 6 months later, these only slightly changed the overall picture of the GOS values. More than 3/4 returned to their families after rehabilitation, often despite great functional impairment. A return to the former environment outside the family (kindergarten, school) was, however, possible in 2/3 of the subjects. The proportion of minimally responsive patients fell from 73.7% to 18.4% during the stationary rehabilitation phase. After a further 6 months (follow up), 36.4% of the originally minimally responsive patients achieved a GOS value of > 5.
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.
Older subjects (institutionalized in a home for the aged and non-institutionalized) were compared in a test battery according to the recommendations of the NINCDS-ADRA. The institutionalized subjects were not distinguishable from the controls when only a small amount of information was to be processed or when the information had to be recalled with no distraction. Possible reasons for the observed differences are discussed.
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BACKGROUND: This investigation was undertaken to gain insight into the validity of the American Medical Association (AMA) Masterfile data. METHODS: Allopathic family physicians were chosen as the study population Omissions were picked up from by comparing the AMA list with the 1990 Ohio Academy of Family Physicians Foundation-Ohio Department of Health (OAFPF-ODH) census. Verification of the 1990 specialty and geographic location of allopathic family physicians not common to both files was achieved by sequentially (1) reviewing the AMA names against 1990 deletions from the 1985 OAFPF-ODH census, (2) contacting physicians directly by telephone, (3) verifying 1990 physician status with county medical personnel, and (4) mailing a brief questionnaire to each physician whose 1990 status remained unverified. RESULTS: The status of specialty and geographic location in 1990 was verified in 91 percent of names not common to both lists. Incorrect omissions (undercounts) and incorrect inclusions (overcounts) offset each other for both lists. Two groups of family physicians contribute to counting biases: family physicians who fulfill short-term goals by part-time practice in several locations, and family physicians who restrict their practice to a limited medical content area. CONCLUSIONS: Because of nearly equal offsetting of overcounting (incorrect inclusions) and under counting (incorrect omissions), the 1990 Ohio family physician AMA Masterfile data is adequate for work-force projections and policy studies when the county data are aggregated at the state level. The overcounting and undercounting for smaller areas or categories must still be studied, however. Application of the AMA Masterfile data of other geographic areas requires a knowledge of the components of undercounts and overcounts of the population being studied.
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