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R Mielke

Publications and source records attributed to R Mielke.

62 records · Page 4Linked to original sources

Differences of regional cerebral glucose metabolism between presenile and senile dementia of Alzheimer type.

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.

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[Schizencephaly].

Schizencephaly is a developmental disorder of the human brain caused by a defect of neuronal migration. We observed a 7 month old african boy suffering from nystagmus and hemiparesis. The neuroimaging reveals a large cleft in cortical and subcortical structures and typical changes of polymicrogyria. In the differential-diagnosis encephaloclastic porencephaly should be considered.

Agenesis of Corpus Callosum↗

[Neonatal spasms--a review of symptoms, etiology, therapy and prognosis].

Seizures in the newborn are a distinctive sign of underlying disease. Different convulsive patterns are described. The most common neurologic syndrome consists of subtle seizures. The most important cause is ischemic encephalopathy. Hypocalcemia is the main metabolic disease. Hypoglycemia seems not to be of special relevance for pathogenesis of newborn seizures. Other episodic symptoms of non-epileptic origin should be considered in the differential diagnosis. It is critical to diagnose the cause and to treat it, since the prognosis depends on the underlying disturbance. Phenobarbital is the anticonvulsive drug of first choice. Duration of treatment is determinated of an preexisting brain damage. Newborns with normal neurological evaluation don't need any longer anticonvulsive treatment after cessation of seizures. The EEG is an important prognostic tool.

Anticonvulsants↗

Impairment of neocortical metabolism predicts progression in Alzheimer's disease.

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

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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↗

Long-term effects of phosphatidylserine, pyritinol, and cognitive training in Alzheimer's disease. A neuropsychological, EEG, and PET investigation.

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.

Aged↗

Cytogenetic investigations from lymphocyte cultures of patients with probable Alzheimer's disease.

Chromosome investigations were carried out on lymphocyte cultures of 21 patients with probable Alzheimer's disease in comparison to an age-matched control group of 11 healthy subjects. Different cytogenetic parameters were analyzed: sister chromatid exchanges, polyploid mitoses, mitotic activity and secondary chromosomal aberrations such as gaps, breaks and exchanges. Only the average rate of sister chromatic exchanges was slightly decreased in patients (8.4 +/- 1.7; control group: 10.4 +/- 2.1). There were interindividual differences of values for each of the cytogenetic parameters analyzed, but these were not related to the onset, duration or severity of dementia.

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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↗