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E Englund

Publications and source records attributed to E Englund.

32 records · Page 2Linked to original sources
PubMed1987

Frontal lobe degeneration of non-Alzheimer type. IV. White matter changes.

The cerebral white matter in 16 cases of frontal lobe non-Alzheimer degeneration with dementia (FLD), four cases of Pick's disease and five age-matched controls was studied microscopically. All cases of dementia had white matter alterations, consisting of gliosis and loss of myelin, with a regional spread of changes that roughly corresponded with that of the cortical degeneration. The white matter changes were less severe than the cortical alterations, although the relative degree of severity between grey and white matter pathology varied from case to case. The white matter changes were in some respects similar in FLD and Pick's disease. They differed from those of other organic dementias. In FLD, they seem to be part of the histopathologic picture and to be secondary to the cortical degeneration.

Aged↗
PubMed1987

Correlations between histopathologic white matter changes and proton MR relaxation times in dementia.

Our previous studies have shown that incomplete white matter infarctions are common in senile dementia of the Alzheimer type. To visualize and interpret these changes on magnetic resonance imaging (MRI), knowledge of MR relaxation times associated with this histopathology is important. The proton MR relaxation times T1 and T2 were determined in vitro for 3 groups of specimens. Fifty specimens of normal and incompletely infarcted white matter from 21 patients with senile dementia and 38 normal and pathologic white matter specimens from 19 elderly cases with infarcts were analyzed. The specimens were evaluated for infarct type, grade of incomplete infarction, and the proportion of old complete or incomplete infarction versus normal tissue in each sample. The incomplete infarct had longer relaxation times than normal white matter, with prolongation of T1 and T2 being proportional to the severity of the tissue changes. Old complete infarcts had longer relaxation times than both normal white matter and incomplete infarctions. These differences in relaxation times, reflecting various degrees of tissue damage, are important for the interpretation of MR images in vivo. Visualization of incomplete infarctions is essential for an in vivo diagnosis of these frequent and sometimes extensive changes.

Alzheimer Disease↗
PubMed1986

A white matter disorder in dementia of the Alzheimer type: a pathoanatomical study.

In cases of Alzheimer's presenile and senile dementia, Alzheimer's disease (AD) and senile dementia of the Alzheimer type (SDAT), respectively, we have observed, in addition to the gray matter degeneration, a lesion that has the character of an incomplete infarction confined to the white matter. It is encountered in 60% of both groups, with mild changes in two thirds and moderate or severe changes in one third. It involves the deep white matter symmetrically, tapering off toward the cortex. It is characterized by partial loss of myelin, axons, and oligodendroglial cells; mild reactive astrocytic gliosis; and sparsely distributed macrophages as well as stenosis resulting from hyaline fibrosis of arterioles and smaller vessels. No complete or cavitating infarctions and no hypertensive vascular changes were observed. The white matter changes are thought to be due to hypoperfusion of the concerned white matter territories since, in addition to the white matter hyaline vascular stenosis, these cases show signs of cardiovascular disease, usually with hypotension. The white matter disorder also occurs independent of the gray matter process of AD and SDAT and may be seen as the sole brain lesion in non-AD subjects. Its occurrence is thus neither regularly related to the severity nor to the regional appearance and accentuation of the cortical Alzheimer process and is thus not likely to be just the result of a wallerian degeneration. Histologically it is similar in several respects to Binswanger's disease, although with some distinct differences. It is thus related to the cerebrovascular group of disorders in addition to AD and SDAT. In view of its frequency and severity, this white matter lesion is important to define, to diagnose, and ultimately to prevent or cure.

Aged↗
PubMed1986

Brain changes in dementia of Alzheimer's type relevant to new imaging diagnostic methods.

The aim of the article is to correlate grey and white matter changes and their topography to the results of modern methods for brain imaging such as CT, rCBF, PET, SPECT and NMR in Alzheimer's type of dementia. The findings are based on the study of a large material investigated thoroughly patho-anatomically. The findings are correlated with psychiatric and neurophysiologic follow-up studies. The degenerative grey matter process shows a regionally varying accent according to a pattern which is consistent and typical for the disease. This corresponds to metabolic changes on rCBF, PET and SPECT and thereby becomes of diagnostic value. This pattern is largely symmetric. Metabolic asymmetries have however been reported on PET scans. In this context individual variations of the topographic degenerative brain pattern and normal anatomical brain asymmetries are of interest. The white matter however also frequently shows changes, in particular loss of myelin and axons and a mild gliosis, slight in 1/3 of the cases and severe in an additional 1/3. These changes cause a decrease of density in the centrum semiovale correlating to lipid depletion. They may also influence the ventricular shape and size, of interest in CT or NMR studies. Also here variations in ventricular shape, normal and such due to pathological processes unrelated to the Alzheimer disease, may cause confusion, regarding degree of atrophy and even type of brain process. Such factors should be considered in the interpretation of non-invasive brain studies.

Aging↗
PubMed1981

Regional pattern of degeneration in Alzheimer's disease: neuronal loss and histopathological grading.

The various structural components of the cortical degeneration of Alzheimer's disease were defined and graded. The severity of the degenerative process was thus mapped in different cortical areas where neuronal numbers and cortical width were also measured and compared with controls. Contrary to the general opinion that the degenerative process is rather uniformly diffuse, though accentuated in the medial temporal and frontal cortex, we found a consistent and more elaborate pattern with clearcut regional differences. Thus the degeneration involved, besides basal medial temporal limbic areas, the posterior cingulate gyrus and superior parietal lobule particularly, with somewhat less marked changes in the inferior parietal lobule and inferior temporal gyri. The sensorimotor, calcarine and anterior cingulate areas of the cortex were notably spared until very late stages. This regionally variable severity of the degeneration was also paralleled by a regionally varying reduction in neuronal numbers and cortical width, and agrees with our previously published results of a regional pattern which closely correlates with clinical parameters, including symptom pattern and regional cerebral blood flow alterations.

Aged↗
PubMedDate not supplied

Vascular dementia: the role of cerebral infarcts.

Although vascular dementia (VaD) is the second most frequent cause of dementia after Alzheimer disease (AD), the concept remains controversial in terms of delineation. The objective of this review is to investigate, from available literature, the role of cerebral infarcts in the pathogenesis of VaD and to identify areas of interest that need further evaluation and research. The incidence of new onset dementia is increased after stroke. Stroke subtypes, total volume of cerebral infarction and functional tissue loss, and location of the lesions are probably the major determinants of VaD. Any cause of stroke can lead to VaD. In some circumstances the causal relation between stroke and dementia is clear: (1) in young patients who are unlikely to have associated Alzheimer pathology; (2) when the cognitive functioning was normal before stroke, impaired immediately after, and does not worsen over time; (3) when the lesions are located in strategic areas; and (4) when a well-defined vasculopathy known to cause dementia is proven. However, several issues remain unsolved in VaD: lack of specificity of the diagnostic criteria; influence of white matter changes and associated Alzheimer pathology; influence of preexisting cognitive status; possibility of having VaD without stroke and the clinical relevance of silent infarcts to VaD; and best therapeutic strategy to be used to prevent VaD and to prevent stroke in patients with VaD. These questions form the basis for proposals for future research.

Cerebral Infarction↗
PubMedDate not supplied

Reduced number of caudate nucleus dopamine uptake sites in vascular dementia.

The dopamine (DA) uptake sites in the caudate nucleus were studied in patients with vascular dementia (VAD) and in a control group using the presynaptic DA uptake site marker [3H][2beta-carbomethoxy-3beta-(4-fluorophenyl) tropane] as radioligand. There was a significant decrease in the number of DA uptake sites in the VAD group, while the binding affinity was unchanged. The present results indicate that in the patients investigated, the cerebrovascular disease process involves dopaminergic neuron terminals in the caudate nucleus. Our findings are discussed in relation to the reductions in number of DA uptake sites that have previously been revealed in Alzheimer's and Parkinson's diseases.

Aged↗
PubMedDate not supplied

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↗
PubMedDate not supplied

Alzheimer's disease and the cerebellum: a morphologic study on neuronal and glial changes.

Structural manifestations of Alzheimer's disease (AD) including neuronal loss were investigated in 12 cases of AD and in 10 healthy age-matched controls, with focus on the cerebellum. Linear Purkinje cell (PC) density was measured in the vermis and cerebellar hemispheres. Neurons were also counted in the inferior olivary nucleus. In vermis of the AD cases, the mean PC number was significantly lower (p = 0.019) than in the controls. The neurons in the inferior olive were similarly fewer, though not significantly (p = 0.13). Molecular layer gliosis and atrophy in the vermis was clearly severer in AD than in the controls. Features typical of cerebral Alzheimer encephalopathy (plaques, tangles and microvacuolization) were inconspicious. The structural cerebellar changes in the AD cases were thus neuronal loss, atrophy and gliosis, judged to represent the disease process, and with a main involvement in the vermis. This may be reflected in some of the symptoms and signs seen in AD, signs that are generally overlooked or judged to be of noncerebellar origin.

Aged↗
PubMedDate not supplied

Neuropathological brain mapping.

Neuropathological brain mapping is enabled by extensive semiserial sectioning with whole brain coronal microscopical sections prepared from every 5 to 15 mm. By this method not only type of change but also distribution and regional severity can be assessed, which is fundamental for a correct neuropathological diagnosis. This has proved to be of vital importance for the correlation and validation of the clinical symptoms and brain imaging findings in cases of organic dementia, and vice versa for the interpretation of the neuropathological findings. Different patterns for the distribution and types of changes have been revealed for Alzheimer's disease and frontal lobe degeneration, as well as in vascular dementia where pure subgroups could be identified. In the very aged, the mapping of several types of mild lesions have been shown to cooperate to cause a summational dementia.

Alzheimer Disease↗
PubMedDate not supplied

Proton magnetic resonance relaxation times T1 and T2 related to postmortem interval. An investigation on porcine brain tissue.

In order to establish the validity of in vitro determination of the proton magnetic resonance (MR) relaxation times T1 and T2 in brain tissue at increasing time delay after death or operative excision, 81 brain tissue samples from 23 pigs were analyzed repeatedly. These samples, representing cortex, caudate nucleus and white matter, were studied microscopically after MR measurements. The T1 values exhibited no time dependence and the T2 values decreased slightly during the interval 2 to 90 hours after death. The samples were stored at +8 degrees C between the measurements. These results indicate that reliable in vitro measurements can be obtained in autopsy or surgical brain tissue specimens within 90 hours after death or excision, if handled properly.

Animals↗
PubMedDate not supplied

Regional differences in the proton magnetic resonance relaxation times T1 and T2 within the normal human brain.

The proton magnetic resonance (MR) relaxation times T1 and T2 were determined in autopsy specimens from 13 different regions of normal human brains. One hundred and seventy-four tissue samples from 25 brains were examined in a pulsed MR analyzer of 0.25 T and were then also studied histologically. There were regional differences in T1 and T2 within the cerebral gray matter but not within the white matter. These regional differences might reflect the different composition and cytoarchitectonic structure of the cortical regions and should be taken into consideration in the interpretation of cortical lesions on MR images.

Aged↗
PubMedDate not supplied

Tumours of the central nervous system. Proton magnetic resonance relaxation times T1 and T2 and histopathologic correlates.

Proton MR relaxation times T1 and T2 were determined in vitro in 136 small specimens of astrocytomas grades I-IV, of oligodendrogliomas, metastases of adenocarcinomas, meningiomas and acoustic neuromas. In addition, 7 samples of peritumoural white matter were analysed. The analysed specimens were studied microscopically in their entirety regarding tumour type and occurrence of necrosis and non-tumour tissue admixture, such as fibrosis and haemorrhage. Most of the gliomas had longer relaxation times than normal white matter and T2 was significantly longer than in the other three tumour groups. The metastases had longer T1 than normal white matter, while T2 varied. The astrocytomas tended to show shorter relaxation times with increasing degree of malignancy, and shortening of T1 and T2 correlating with the proportion of tissue necrosis. Similarly, the metastases with tissue necrosis had shorter T1 and T2 than non-necrotic samples. The meningiomas had T1 values comparable with normal cortex, while the T2 values varied. Tumours containing a large proportion of fibrous tissue had shorter relaxation times than the others. Acoustic neuromas had only slightly longer T1 than normal white matter, while T2 was not prolonged. Both T1 and T2 were significantly shorter than in all other tumours studied. Peritumoural white matter had prolonged relaxation times compared with normal white matter, correlating to increased water content. These in vitro differences regarding relaxation times in various types of tumours of the central nervous system, dependent on various types of tissue alterations, should be of interest for the interpretation of in vivo images.

Adenocarcinoma↗