PubMed Health⌕ Search

Biomedical subjects

E Englund

Publications and source records attributed to E Englund.

At least 19 recordsLinked to original sources
PubMed1999

Paragangliomas of the spinal canal.

We report the clinical MRI and histopathological features of five consecutive cases of spinal paraganglioma. Three intradural tumours were found in the typical location (two at the L4, one at the S2 level); one intradural extramedullary tumour arose at an unusual level, from the ventral C2 root, and one extradural tumour growing along the L5 nerve root sheath had an aggressive growth pattern with early, local paraspinal recurrence and, eventually, intradural metastatic spread. This type of growth pattern has not been described previously. Paragangliomas of the spinal canal are more common than previously thought and can be located anywhere along the spine, although the lumbosacral level is the most common. Their appearance on MRI can not distinguish them from other tumours in the spinal canal. Even though paragangliomas in general are benign and slowly growing their growth pattern can vary and be more aggressive, to the point of metastatic spread.

Adult↗
PubMed1999

Neuronal loss in the brainstem and cerebellum--part of the normal aging process? A morphometric study of the vermis cerebelli and inferior olivary nucleus.

Based on the known age-related loss of Purkinje cells (PC) in the cerebellum, this study focuses on whether a marked loss of PC occurs in individuals of very high age. The inferior olive, which is intimately connected with the cerebellum anatomically as well as functionally, was also studied. The study group included 15 nondemented and basically healthy cases aged 32-104 years. Linear neuronal density was expressed as number of PC per millimeter tissue measured in the vermis and as neuronal numbers per square millimeter tissue in the inferior olive. The linear PC density clearly decreased with increasing age, R2 = 0.82 and p < .001. The inferior olive showed a small but insignificant age-related neuronal loss. We conclude that aging results in reduced PC density in the vermis cerebelli, further accentuated in the very late stages of life.

Adult↗
PubMed1999

Molecular genetic characterisation of frontotemporal dementia on chromosome 3.

We have previously localized a locus causing familial nonspecific dementia to the centromeric region of chromosome 3 in a pedigree from the Jutland area of Denmark. This pedigree shows anticipation. Here we present further analysis of these anticipation data which are suggestive of trinucleotide repeat expansion involvement. We also outline our strategies to clone the mutant gene via its putative associated trinucleotide repeat sequence.

Adult↗
PubMed1999

White matter changes in stroke patients. Relationship with stroke subtype and outcome.

White matter changes (WMC), detected by imaging techniques, are frequent in stroke patients. The aim of the study was to determine how WMC relate to stroke subtypes and to stroke outcome. We made a systematic Medline search for articles appearing with two of the following key words: either 'WMC or white matter lesions or leukoencephalopathy or leukoaraiosis' and 'stroke or cerebral infarct or cerebral hemorrhage or cerebrovascular disease or transient ischemic attack (TIA)'. WMC, as defined radiologically, are present in up to 44% of patients with stroke or TIA and in 50% of patients with vascular dementia. WMC are more frequent in patients with lacunar infarcts, deep intracerebral hemorrhages, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy and cerebral amyloid angiopathy. After an acute ischemic stroke, WMC are associated with a higher risk of death or dependency, recurrent stroke of any type, cerebral bleeding under anticoagulation, myocardial infarction, and poststroke dementia. WMC in stroke patients are often associated with small-vessel disease and lead to a higher risk of death, and poor cardiac and neurological outcome. However, several questions remain open and need further investigations.

Age Factors↗
PubMed1999

Tuberculosis control in the Caucasus: successes and constraints in DOTS implementation.

SETTING: The pilot projects for tuberculosis (TB) control, supported by the World Health Organization (WHO) and based on the WHO recommended control strategy, directly-observed treatment, short-course (DOTS) in the Caucasian countries (Armenia, Azerbaijan, Georgia). OBJECTIVE: To evaluate the results 2 years after the implementation of the pilot projects. METHODS: Analysis of data on case detection, sputum conversion and treatment outcome reported quarterly to the WHO from the Ministries of Health in each country. RESULTS: Since the establishment of the project, 1330, 764 and 4866 new cases and relapses, respectively, of TB have been detected in the pilot areas of Armenia, Azerbaijan and Georgia. In Armenia and Azerbaijan, respectively 46% and 57% of all cases were smear positive, whilst in Georgia, the corresponding figure was only 12%. After 3 months' treatment, 93% of new smear-positive patients had become smear-negative. The sputum conversion rate for relapses and other retreatment cases (failure, treatment interrupted) was 85%. In Armenia, 78.1% of new smear-positive patients were treated successfully (cured or completed treatment). The corresponding percentages for Azerbaijan and Georgia were 87.9% and 59.6%. Treatment success rates among retreatment cases was generally low, at respectively 46%, 64%, and 35%, in Armenia, Azerbaijan, and Georgia. CONCLUSION: The results of the implementation of the WHO TB control pilot projects in Armenia, Azerbaijan and Georgia suggest that the DOTS strategy is feasible in emergency situations in general, and in the Caucasus in particular.

Disease Notification↗
PubMed1998

A 50-year perspective of a family with chromosome-14-linked Alzheimer's disease.

A Swedish family with two generations suffering from presenile dementia with an unusually severe Alzheimer encephalopathy was first reported in 1946. The hypothesis that the disease was inherited through a dominant gene is strongly supported by the follow-up 50 years later of three additional generations and molecular genetic findings of a novel presenilin-1 gene mutation in the family. The pedigree contains six cases with well-documented dementia in four consecutive generations. The Alzheimer encephalopathy was unusually severe in the three cases studied post-mortem, with a pronounced involvement of the central grey structures, such as the claustrum, the nuclei around the third ventricle, the central thalamic nuclei and the brain stem. There were no vascular lesions and little amyloid angiopathy. All six affected cases showed the typical temporoparietal symptom pattern and other core symptoms of Alzheimer's disease, such as logoclonia, myoclonic twitchings and major motor seizures. Other predominant features were psychomotor slowness, increased muscular tension, a stiff stooped gait and a rapid loss of weight. The symptom pattern is convincingly explained by the consistent and severe involvement of cortical and central grey structures and is probably linked to the presenilin-1 gene mutation.

Alzheimer Disease↗
PubMed1998

Adrenoleukodystrophy--unusual CT and MR findings in two siblings. Case reports.

PURPOSE: To describe the unusual appearance of adrenoleukodystrophy (ALD) in MR imaging. MATERIAL AND METHODS: An analysis was made of MR findings, histopathology and clinical course in the cases of two brothers with ALD. RESULTS: The older brother presented with frontal contrast-enhanced lesions, including a cyst. These were initially misinterpreted as a tumour at both radiology and pathology. The correct diagnosis was made after the discovery of very-long-chain fatty acids in the blood. The younger brother presented initially with involvement of various segments of the corticospinal tract. CONCLUSION: It is important that the radiologist be aware of the variants of ALD in MR imaging so as to avoid diagnostic mistakes.

Adrenoleukodystrophy↗
PubMed1998

Neuropathology of white matter changes in Alzheimer's disease and vascular dementia.

Morphological white matter changes were investigated in clinically and neuropathologically diagnosed cases of Alzheimer's disease (AD; 60 cases) and vascular dementia (VaD; 40 cases). In 33 of 60 AD cases, a white matter disease (WMD) characterized by tissue rarefaction, mild gliosis and a non-amyloid small-vessel sclerosis occurred in the central, preferentially frontal deep white matter. The mean vessel density was significantly lower than in normal control case frontal white matter. The presence of WMD did not parallel the severity of grey matter Alzheimer encephalopathy. In 25 of 60 AD cases, white matter degeneration with signs of both condensation and rarefaction of tissue elements was seen subjacent to advanced cortical degeneration in the temporal lobes. It concurred with WMD in only 13 cases and was judged to be of anterograde, Wallerian type and not related to angiopathy. In VaD, similar changes occurred, accompanied by several types of focal and topographically related lesions. For diffuse white matter pathology of similar appearance in vascular and neurodegenerative disease with dementia, there may be various at least partly contrasting aetiologies, which can be differentiated by the presence of even minor focal lesions in some cases. For the recognition of such subtle variations in the spectrum of WMD, modern imaging techniques are crucial for detailed clinical diagnosis and attempts at therapeutic intervention.

Aged↗
PubMed1997

The apolipoprotein E epsilon4 allele frequency is normal in fronto-temporal dementia, but correlates with age at onset of disease.

The apolipoprotein (apoE) epsilon4 allele was studied in fronto-temporal dementia (FTD), a diagnostic category including the specific disorders Pick's disease and frontal lobe degeneration of non-Alzheimer type (FLD). These dementing diseases have neuronal and synaptic degeneration in common with Alzheimer's disease (AD), for which the presence of the apoE epsilon4 allele is a known risk factor, and lowers the age of onset of disease. Previous studies on the apoE epsilon4 allele frequency in FTD have been inconclusive. The structural hallmarks of AD, allegedly linked to apoE presentation, neuritic plaques (NP), primarily composed of aggregates of beta-amyloid, and neurofibrillary tangles (NFT), primarily composed of hyperphosphorylated tau, are lacking in FTD. However, tau-positive cytoskeletal pathology is found in Pick's disease, but not in FLD. Resolving whether the epsilon4 frequency is increased in FTD or not may thus give clues to the pathogenetic mechanism of apoE in AD. We therefore studied apoE alleles in a well characterized material of FTD patients. The epsilon4 allele frequency was similar in 25 patients with FTD (14.0%) as compared with 26 healthy controls (13.5%). A post-mortem neuropathological examination was performed in 10 cases (nine had FLD and one Pick's disease). Our finding of a normal epsilon4 allele frequency in our group of FTD, principally consisting of FLD cases, support hypotheses involving differential binding of apoE to beta-amyloid and/or tau, in the development of beta-amyloid deposition and NP formation and/or tau hyperphosphorylation and NFT formation, for the pathogenetic role of apoE in AD. The age at onset was significantly lower (P < 0.01) in FTD patients possessing the epsilon4 allele (48.7 +/- 8.0 years) than in patients not possessing this allele (58.9 +/- 7.6 years). We conclude that, although the apoE epsilon4 allele frequency is not increase in FTD, the epsilon4 allele is not an etiological factor, but may rather be an accelerating factor in the degenerative process of FTD, thereby resulting in an earlier presentation of the disorder in individuals predisposed to develop FTD.

Adult↗
PubMed1997

Radical endarterectomy of severely calcified ascending aorta prevents stroke during open-heart surgery.

In ten patients (7 women), mean age 73 years, with severely calcified ascending aorta, aortic valve and coronary artery disease were surgically treated after radical endarterectomy of the ascending aorta during cardiopulmonary bypass and with or without deep hypothermic total circulatory arrest. One patient died 10 days and one 11 months postoperatively of complications which neither directly nor indirectly could be attributed to the aortic endarterectomy. The eight surviving patients are doing well after follow-up averaging 16 months. CT scans 1 year postoperatively showed no aneurysmal dilation of the ascending aorta or aortic dissection distal to the endarterectomy site. Radical endarterectomy of calcified ascending aorta thus can be performed with relatively low mortality and stroke risk and may be considered in patients undergoing valve replacement and/or coronary artery bypass grafting.

Aged↗
PubMed1996

Fundamental pathological lesions in vascular dementia.

This review concerns the fundamental cerebral lesions in cases of vascular dementia. Extracerebral vascular alterations are dominated by atherosclerosis with or without thrombosis. In addition, occlusion of extracerebral arteries can be induced by thrombo-embolism and in rare cases by other vascular diseases, chiefly arteritis. Intracerebral microangiopathies are usually of arteriolosclerotic or hyalinotic types in which there is degeneration of smooth muscle cells of the media and deposition of components of extracellular matrix, chiefly collagens. Ageing, chronic hypertension, hyperlipidemias and diabetes are important factors inducing vascular lesions. The vascular lesions, often combined with systemic factors, may produce various ischemic and edematous alterations of the brain parenchyma. Occlusion and obliteration of arteries (macroangiopathy) are associated with large infarcts, whereas microangiopathy may cause lacunar infarcts and some forms of white matter degeneration. Cases of vascular dementia usually present many types of lesions in the brain parenchyma and its arterial supply. The extent and location of the injuries differ considerably from case to case. Location of the lesions, volume of destroyed tissue, multiplicity and bilateral occurrence are most important parameters underlying the clinical manifestations in vascular dementia. A strategic location of a small injury is in some cases of particular importance.

Aged↗
PubMed1990

White matter changes in dementia of Alzheimer's type: the difference in vulnerability between cell compartments.

Structural white matter changes were found to be common in dementia of Alzheimer's type. A neuropathological investigation was undertaken in order to characterize and quantify these white matter changes. The tissue changes were compared with those in white matter in normal control cases and in complete white matter infarcts. Our results support the hypothesis that the white matter lesion seen in dementia of Alzheimer's type is due to incomplete infarction involving both axons and myelin and is a result of mild ischaemia. In mild ischaemia, the myelin compartment appears to be the most vulnerable. We have termed the lesion selective incomplete white matter infarction.

Aged↗
PubMed1988

White matter changes in dementia of Alzheimer's type. Biochemical and neuropathological correlates.

A correlative neuropathological-biochemical study was undertaken in order to characterize the selective incomplete white matter infarctions (SIWI) frequently found in dementia of Alzheimer's type. The brain tissue analysed represented white matter with incomplete infarction, complete infarcts and with histologically normal tissue, in cases with dementia, mainly of Alzheimer and multi-infarct type, in nondemented subjects with cerebral infarcts and in age-matched control cases. The biochemical results verify the existence of the white matter changes and agree on their regional distribution as they appear in the morphological analyses. The increasing severity of SIWI as assessed histologically was reflected in a proportional reduction of several biochemically quantified white matter components. The histological difference between incomplete and complete infarction was also expressed biochemically. Incomplete white matter infarction with and without associated complete infarcts were biochemically similar. The aetiological significance of the loss of different white matter components is discussed. The biochemical data support the concept of SIWI as being an independent white matter disorder of cerebrovascular, hypoperfusional/hypoxic origin.

Aged↗
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↗