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Biomedical subjects

L Gustafson

Publications and source records attributed to L Gustafson.

124 records · Page 7Linked to original sources
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Blood pressure and drug treatment in clinically diagnosed Lewy body dementia and Alzheimer's disease.

The aim of the study was to investigate arterial blood pressure (BP) and the use of pharmacological treatment in patients with Lewy body dementia (cLBD) and Alzheimer's disease (cAD) diagnosed on clinical grounds. BP and pharmacological treatment was analysed based on the medical records of 200 deceased dementia patients. Forty-eight cases with LBD and 45 AD were diagnosed using clinical criteria. The patients, who died between 1985 and 1994, were part of a prospective longitudinal dementia project. The majority of the cases were examined and cared for at the psychogeriatric and psychiatric departments. BP levels were very similar at an early stage of dementia but there was a marked decrease during the course of dementia in cAD and cLBD. The cLBD cases became hypotensive during the course of dementia to a significantly greater extent and also had a more pronounced drop in systolic BP at orthostatic testing compared to the cAD cases. cLBD and cAD were prescribed neuroleptics and medication potentially associated with hypotension to the same extent. The total number of these drugs was however higher in cLBD than in cAD. Antiparkinsonian treatment was, as expected, more common in cLBD compared to cAD. The findings suggest that insufficient BP regulation and drug treatment could affect the clinical picture of dementia, particularly in cLBD patients.

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Plasma homocysteine is a sensitive marker for tissue deficiency of both cobalamines and folates in a psychogeriatric population.

The concentration of blood folates was decreased and the concentration of plasma homocysteine was increased in a psychogeriatric population, whereas the concentrations of methylmalonic acid or serum cobalamins were not changed compared with healthy subjects. The highest frequency of abnormal values was shown by plasma homocysteine concentration, which was increased in 88 of 168 patients. In 29 of these 88 patients increased concentration of plasma homocysteine could possibly be attributed to tissue cobalamin deficiency. One patient had only a lowered concentration of blood folate. Thirteen patients had elevated concentrations of serum creatinine which could explain increased plasma homocysteine concentration. Even if the remaining patients (n = 45) had normal vitamin levels in circulation, the increased plasma homocysteine concentration in most cases must be attributed to tissue deficiency of cobalamins and/or folates. Thus, many patients with increased plasma homocysteine concentrations need further vitamin supplementation despite their normal vitamin levels in serum and blood. Copyrightz1999S.KargerAG,Basel

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Magnetic resonance imaging and histopathology in dementia, clinically of frontotemporal type.

The magnetic resonance imaging (MRI) and computed tomography findings in 28 patients with the clinical diagnosis of frontotemporal dementia (FTD) were compared with the findings in a control group of 76 individuals without dementia or stroke. A pattern of frontal and temporal atrophy with predominantly frontal white matter changes was found in the FTD patients, and this was significantly different from the radiological findings in the control group. Six of the FTD patients have undergone autopsy. Histopathological evaluation showed a primary cortical degenerative disease (frontal lobe degeneration of non-Alzheimer type) in 3 of them, and primary white matter disorder, mainly frontal, of basically ischemic type (selective incomplete white matter infarction) in 3 of them. MRI could be a helpful tool to support the clinical diagnosis FTD, especially in young patients. MRI may also be helpful for the differentiation of a primary neurodegenerative from a mainly ischemic-vascular type of dementia.

Adult↗
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Frontotemporal dementia can be distinguished from Alzheimer's disease and subcortical white matter dementia by an anterior-to-posterior rCBF-SPET ratio.

Sixteen patients with frontotemporal dementia (FTD), 27 with early-onset Alzheimer's disease, 25 with late-onset Alzheimer's disease, 19 with subcortical white matter dementia (SWD) and 28 normal controls underwent semiquantitative regional cerebral blood flow measurement (rCBF) using single-photon emission tomography (SPET; (99m)Tc-HMPAO) and either computerized tomography (CT) or magnetic resonance imaging (MRI) of the brain. An anterior-to-posterior rCBF-SPET ratio (mesial superior frontal gyrus/medial temporal lobes) was calculated, which significantly separated the FTD group from the other dementia groups and controls with a sensitivity of 87.5% and a specificity of at least 78.6%. CT/MRI was found to be helpful in the differential diagnosis between FTD and SWD. In FTD patients, the mesial superior frontal gyrus, near the polus frontalis, was found to be the region with the most reduced rCBF values.

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Regional cerebral blood flow measurements in the clinical evaluation of demented patients.

The clinical usefulness of two-dimensional measurements of regional cerebral blood flow (rCBF) for diagnosis of dementia is discussed on the basis of data from 150 patients with autopsy-based diagnosis. The specificity of Alzheimer's disease is found to be very good but the sensitivity only in the order of 75-80%, the majority of the mislabelled cases having selective incomplete white matter infarcts in addition to their Alzheimer pathology. Frontal lobe dementia is recognized by rCBF with high sensitivity but fairly low specificity due to the fact that frontal flow decreases are shared with several other disorders. Regarding cerebrovascular dementia the sensitivity is rather good (95%) while specificity is somewhat lower (70-75%). It is argued that rCBF should be interpreted diagnostically only when clear-cut findings are made preferably in a series of measurements. The noninvasiveness, repeatability, low radiation dose and low cost makes the present method an excellent tool for research as well as for clinical routine use.

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Somatostatin and neuropeptide Y in cerebrospinal fluid: correlations with severity of disease and clinical signs in Alzheimer's disease and frontotemporal dementia.

Alzheimer's disease (AD) and frontotemporal dementia (FTD) are the most common types of progressive neurodegenerative disorder in our catchment area. The distribution of cortical degeneration in FTD is mainly the reverse of that in AD, while there are both differences and similarities in the clinical characteristics. Somatostatin and neuropeptide Y (NPY) are neuropeptides with a widespread distribution in the human cerebral cortex. Somatostatin is involved in the regulation of hormone release from the anterior pituitary and may act as a neurotransmitter-modulator. NPY is a potent anxiolytic neuropeptide. Somatostatin and NPY coexist in the cerebral cortex, basal ganglia and in amygdaloid complexes. The present study of AD (n = 34) and FTD (n = 22) analyses the cerebrospinal-fluid (CSF) levels of somatostatin-like immunoreactivity and NPY-like immunoreactivity and correlates their levels to 54 different clinical items, such as restlessness, anxiety, irritability and depression. The CSF levels of the two neuropeptides somatostatin and NPY were significantly correlated in FTD (p < 0.02), but not in AD. Several significant correlations to the clinical signs were found: in AD disorientation and dyspraxia, and in FTD agitation, irritability and restlessness. Somatostatin showed a significant negative correlation with severity of dementia in AD (p < 0.013).

Adult↗
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Apolipoprotein-E genotyping in Alzheimer's disease and frontotemporal dementia.

Alzheimer's disease (AD) and frontotemporal dementia (FTD) are characterized by progressive neuronal loss and microvacuolization, although with different distributions of cortical involvement. In contrast to AD there is no amyloid, senile plaques or tangles in FTD. The involvement of chromosome 19 in AD has been associated with apoliprotein E (ApoE) and the epsilon 4 gene frequency has been related to increased risk and early onset of AD. Our analysis of frequency of the ApoE alleles in 38 patients with AD, 21 patients with FTD and 29 normal controls indicates an association of both AD and FTD with an increased frequency of the epsilon 4 allele and in AD also with homozygosity for epsilon 4. Our results might indicate that ApoE epsilon 4 is an important aggravating and pathoplastic factor in the presence of genetic and other determinants for the development of AD or FTD. A significantly higher epsilon 2 frequency in our FTD material compared to AD and normals might also indicate a connection with the distribution of cortical degeneration.

Adult↗
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Tacrine treatment modifies cerebrospinal fluid neuropeptide levels in Alzheimer's disease.

Biochemical and histochemical studies have demonstrated a widespread deficit in the activity of acetylcholinesterase (AChE) in the brains of patients with Alzheimer's disease (DAT). Multiple disturbances in several transmitter systems have been found. The most consistent neurochemical changes in DAT are reductions in the cholinergic system. The major pharmacological approach today in DAT is based on the cholinergic theory assuming that acetylcholine has a major cortical impact on cognitive processes. Tetrahydroaminoacridine (THA, tacrine) is a centrally active reversible acetylcholinesterase inhibitor. A large number of trials have been performed in patients with DAT. This article was to evaluate whether THA treatment induced neuropeptide alteration in DAT before and after 1 year on oral THA treatment.

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Long-term effects of tacrine on regional cerebral blood flow changes in Alzheimer's disease.

UNLABELLED: Regional cerebral blood flow (rCBF) was studied in patients with Alzheimer's disease (AD) before and after 14 months of tacrine treatment. The treated group was compared with an identical reference group of untreated AD patients. At baseline the two groups showed an identical rCBF and mean hemispheric blood flow. After 14 months the tacrine-treated patients showed a stable rCBF level and a significant increase in rCBF in the central-parietal regions, compared to the untreated reference group, who showed typical AD reductions in rCBF in these regions. CLINICAL OUTCOME: 7 of 9 patients in the tacrine group were clinically unchanged or slightly improved during the study time. In the untreated group 8 of 11 patients had deteriorated in clinical assessments and none had improved. Long-term tacrine treatment in Alzheimer's disease may delay the progression of symptoms.

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Oral tetrahydroaminoacridine treatment of Alzheimer's disease evaluated clinically and by regional cerebral blood flow and EEG.

Neurochemical evidence indicates that cognitive impairment in dementia of Alzheimer type (DAT) is related to degeneration of cholinergic neurons in the brain. A pharmacological approach is treatment with a cholinesterase inhibitor such as tetrahydroaminoacridine (THA). THA treatment of 17 patients with DAT was studied with a double-blind crossover design with three types of treatment, THA + lecithin, THA + placebo and placebo + placebo. Each treatment period was 6 weeks with wash out periods of 2 weeks. The treatment was evaluated with clinical ratings, psychometric testing, EEG and regional cerebral blood flow (rCBF) measurements. No significant clinical differences between treatment periods were found in the total sample, but marked individual differences were observed. The patients were subdivided into three outcome groups based on four clinical measures: 6 patients improved (responders), 5 patients were mainly unchanged, and 6 patients showed further deterioration during the trial period of 26 weeks. Pretreatment rCBF in responders differed significantly from that of the deteriorated patients. EEG showed more high frequency activity among responders. Hepatotoxic side effects were observed in several cases. Three subjects showed marked increases of liver enzymes, with normalization following dose reduction. The majority of patients who improved or remained unchanged during the study chose to continue THA treatment in an open trial.

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Multichannel EEG frequency analysis and somatosensory-evoked potentials in patients with different types of organic dementia.

Thirty-five patients with organic dementia were investigated with multichannel FFT analysis of EEG. In 21 of them, somatosensory-evoked potentials (SEPs) with stimulation of the median nerves were also recorded. Based on clinical and psychometric data and regional cerebral blood flow measurements, the patients were subdivided into Alzheimer-type dementia (DAT) of moderate (n = 10) and severe (n = 11) degree, multi-infarct dementia (MID) (n = 7), and frontotemporal degeneration (FTD) (n = 7). The FTD patients showed mild EEG abnormality and the MID patients showed increases of low frequency activity in combination with a well-preserved posterior dominant activity. The DAT patients showed the most pronounced abnormalities with deterioration of the posterior activity combined with a large increase of low frequency activity. The SEPs of the DAT group showed an amplitude enhancement of the parietal response components. The FTD group showed only a moderate delay of the precentral N30 component. The MID group showed individually varying abnormalities, including a delay of the primary cortical response. It is concluded that the different distributions of pathology in the different organic dementia disorders are reflected in the quantified EEG and SEPs as studied with multichannel technique.

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Clinical picture of frontal lobe degeneration of non-Alzheimer type.

Frontal lobe degeneration of non-Alzheimer type (FLD) is the second most common primary degenerative dementia in southern Sweden. Clinical findings in 30 FLD cases with postmortem-verified diagnoses are described. FLD starts in the presenium with a mean disease duration of 7.5 years (range 3-17 years). Clinical onset is insidious and slow and the early stage is dominated by personality changes with lack of insight and judgement and signs of disinhibition. A typical feature is progressive loss of expressive speech with stereotyped phrases, late mutism and amimia. Restlessness, changes of oral/dietary behavior and utilization behavior are prevalent as also psychotic features. Temporal and spatial orientation are usually preserved for a long time in contrast to Alzheimer's disease. Dementia in FLD is similar to that of Pick's disease and ALS with dementia. Early recognition of FLD seems possible based on standardized clinical evaluation supported by neuropsychological tests, measurement of regional cerebral blood flow and other types of brain imaging. The etiology of FLD is unknown but a positive heredity was reported in 60%.

Adult↗
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Spectrum of frontal lobe dementia in a Swedish family.

The etiology of frontal lobe dementia of non-Alzheimer type (FLD) is still unknown. There is strong evidence of genetic factors with positive heredity. In this paper, a Swedish family, with several generations affected by FLD is described. In 3 patients typical FLD was confirmed postmortem. The clinical and neuropathological similarities between the patients are impressive.

Adult↗
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Neuropeptides in cerebrospinal fluid of patients with Alzheimer's disease and dementia with frontotemporal lobe degeneration.

The two major primary degenerative dementias, dementia of Alzheimer type (DAT) and frontal lobe degeneration of non-Alzheimer type (FLD) have several clinical features in common but also many symptoms that differ. In a clinical material of 80 patients with either of the two forms of dementia (DAT = 39, FLD = 41) we have studied the levels of neuropeptides in the cerebrospinal fluid (CSF) in order to find biochemical markers for CNS affection. The dementia forms were evaluated by careful clinical analysis, psychometric testing and measurement of regional cerebral blood flow. Approximately one third of the subjects died during the completion of the study and neuropathology was performed, confirming the diagnoses. We observed reductions in the CSF levels of antidiuretic hormone and somatostatin in both DAT and FLD. A strong tendency to reduction was noted for neuropeptide Y (NPY). There was a correlation with the duration of disease demonstrating a significant reduction in NPY levels in subjects with DAT. Most notably there was a strong reduction in the levels of delta sleep inducing peptide (DSIP) in DAT cases only. The levels of DSIP in FLD were the same as in controls. The reverse was found for corticotropin releasing factor (CRF) which had a significant reduction in FLD patients but not in those with DAT. The present study indicates a difference in the CSF levels of neuropeptides, observations that these may serve as biochemical markers which differentiate DAT and FLD.

Adult↗
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Regional cerebral blood flow in frontal lobe dementia of non-Alzheimer type.

Twenty-five out of 26 cases of autopsy-verified frontal lobe degeneration of non-Alzheimer type (FLD) were found to have focal frontal or frontotemporal blood flow reductions involving both hemispheres. The deviant case had an asymmetric frontal pathology only apparent on the right side. Focal reduction of blood flow in the frontal lobes is, however, a common and unspecific flow abnormality found in e.g. Pick's disease. Creutzfeldt-Jakob's disease, and in some cases of Alzheimer's disease. Low frontal flow has also been reported in schizophrenia and in toxic encephalopathy. Since a characteristic feature of FLD is a steady progress of the pathology, serial flow measurements extending over several years are especially informative.

Cerebrovascular Circulation↗