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Biomedical subjects

A Brun

Publications and source records attributed to A Brun.

At least 145 records · Page 8Linked to original sources
PubMed1987

Frontal lobe degeneration of non-Alzheimer type. I. Neuropathology.

Among 158 cases of organic dementia in a prospective study concerning both psychiatry and regional cerebral blood flow there were 26 cases with a mainly frontal or fronto-temporal dementia. Careful neuropathological investigation disclosed 20 cases of a mainly frontal or fronto-temporal grey matter degeneration, in four of them compatible with Pick's disease (2.5%) whereas 16 cases (10%) appeared to form a separate group without histological Alzheimer features and therefore named 'frontal lobe degeneration of non-Alzheimer type' (FLD). The remaining group of dementias of a clinically similar type proved to consist of cases of Jakob-Creutzfeldt's and Alzheimer's disease with frontal predominance and also a case of normal frontal cortex with a projected dysfunction caused by bilateral thalamic infarctions. Also other similar conditions are accounted for from the literature. The validity of the pathological changes described here, particularly with regard to their severity and regional distribution as well as their tendency to spare certain areas is attested by the clinical picture including neuropsychiatric symptoms and the regional cerebral blood flow pattern, both consistently producing the picture of a frontal and fronto-temporal disease of a progressive degenerative type. These features are dealt with in the following papers by Gustafson (1987) and Risberg (1987). FLD is in some morphological respects similar to other dementing disorders such as the ALS dementia complex and progressive subcortical gliosis, though with both clinical and clear-cut pathoanatomical differences. For the time being it seems safest to conclude that we are faced with a hitherto not fully recognized if not a new type of dementia caused by 'simple' neuronal degeneration of mainly the frontal or frontal and temporal lobes. It makes up about 10% of organic dementias, a figure that would be higher in purely clinical classifications due to the admixture of other frontal lobe disorders or frontally projected dysfunction clinically simulating FLD of the pathoanatomical type here described.

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↗
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↗
PubMed1986

Effect of selective lesions in the hypothalamic-pituitary region on the development of cerebral vasospasm following an experimental subarachnoid hemorrhage in the rat.

Intracisternal injection of blood in the rat induced an angiographically demonstrable biphasic cerebral vasospasm with a maximal acute spasm at 10 min and a maximal late spasm at 2 days after the subarachnoid hemorrhage. Systemic administration of 6-hydroxydopamine, which destroys catecholamine fibers in the circumventricular areas characterized by the absence of a blood-brain barrier, prevented the development of both the acute and the late spasm. Isolation or removal of one of the circumventricular organs, the pituitary, from the brain via a stalk transection or a hypophysectomy did not affect the degree of vasospasm. Lesion of the median eminence, another region without a blood-brain barrier, prevented the development of both types of spasm. The median eminence receives projections from the A1 and A2 nuclei in the medulla oblongata. It is suggested that the projections of these nuclei to the internal layer of the median eminence underlie the development of spasm.

Animals↗
PubMed1986

A boy with complete triploidy and unusually long survival.

A boy with complete triploidy and extensive external and internal congenital malformations who survived for almost seven months is presented. He was born after 31 weeks of gestation, was utterly small for gestational age and the delivery was induced because of intrauterine asphyxia. The infant had typical features of the complete triploidy syndrome. He did not develop mentally or motorically even to a normal neonatal level. Banding analysis of chromosomes and HLA-antigen typing of the patient and his parents suggested that the abnormal cell division had occurred during the oogenesis. The boy suffered a fatal Pneumocystis carinii infection, suggesting defective cellular immunity. In the vast majority of previously reported cases of complete triploidy the infant has died either before birth or within the first postnatal hours and except for four patients, all reported patients have died before the age of 2 months. Our patient illustrates the fact that with modern neonatal intensive care, infants with severe malformation syndromes can survive for longer periods than previously, but in the case of patients with the complete triploidy syndrome without developing mentally at all. The ethical problem of artificially prolonged survival in severely handicapped children is discussed.

Abnormalities, Multiple↗
PubMed1986

Infantile spasms and neuronal heterotopias. A report on six cases.

Six infants with infantile spasms are presented, three primarily considered idiopathic and three symptomatic. Autopsy unexpectedly revealed heterotopias, cortical dyslamination, and other brain malformations in all six cases. No history of any etiologic moment during the neuronal migratory period of early gestation was found. It is concluded that wide-spread disturbances of CNS morphology should always be considered in cases of infantile spasms.

Abnormalities, Multiple↗
PubMed1986

Nephrosis and disturbances of neuronal migration in male siblings--a new hereditary disorder?

Two male siblings (a boy aged 2 years 10 months at death and a male fetus aborted in gestational week 22) showed similar brain and kidney malformations, comprising paraventricular heterotopias, central canal abnormalities (including hydrocephalus in the boy), and glomerular kidney disease with proteinuria. There were no known hereditary diseases in the families of the parents, and there was one healthy sibling of either sex. The malformations thus seem to be hereditary in an autosomal or possibly X linked recessive fashion.

Cerebral Ventricle Neoplasms↗
PubMed1986

Study of the efficacy of an inactivated virus vaccine against porcine parvovirus.

The efficacy of an inactivated virus vaccine against porcine parvovirus has been studied by immunizing 4 sows during pregnancy. A parvovirus virulent strain has been inoculated to these sows and to two other unvaccinated sows used as controls. The infection was performed between the 52nd and the 57th day of gestation. In the litters born from the vaccinated sows, 82% of the piglets were alive and normal. Neither PPV antibodies nor antigen could be revealed in the stillborn fetuses born from the 4 vaccinated sows. Reversely, only 9.5% of the piglets born from the 2 unvaccinated sows were alive at birth, although they were probably infected during pregnancy. In total, 86% of fetuses in these 2 litters were mummified. A field study allowed to show that the double vaccination antibodies induced, persisted with constant titers for, at least, 13 months. Moreover, the reproductive performance of 413 gilts, vaccinated twice before mating, were not affected by this treatment.

Animals↗
PubMed1985

Transmissible gastroenteritis (TGE) of swine: survivor selection of TGE virus mutants in stomach juice of adult pigs.

Two transmissible gastroenteritis (TGE) virus mutants (188-SG and 152-SG) were obtained from a low-passage virus strain (D-52) by 188 and 152 cycles of stomach juice treatment and multiplication in cell culture. Compared to the high-passage Purdue-115 and the original D-52 strains, these mutants were more stable at pH 2.0, more resistant to pepsin and trypsin, and characterized by a small plaque phenotype. In vivo, the two mutants were not found to be virulent for 4-day-old piglets and sows after oral inoculation. To test induction of lactogenic immunity, the 188-SG mutant was administered orally to pregnant sows (6 or 7 weeks before parturition) followed by one intramuscular booster (1 week before parturition). After challenge with virulent TGE virus, piglet mortality 7 days after exposure was reduced (to 22%) as compared to the death rate in piglets from control sows (91%).

Animals↗