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At least 1,531 records · Page 85Linked to original sources
PubMed2002

Mapping cortical gray matter asymmetry patterns in adolescents with heavy prenatal alcohol exposure.

Here we report on detailed three-dimensional quantitative maps of brain surface and gray matter density asymmetry patterns during normal adolescent development and show how these anatomical features of the brain are disrupted as a result of prenatal exposure to large quantities of alcohol. We studied two independent samples of normally developing children, adolescents, and young adults, totaling 83 subjects from two different research groups, and compared them to 21 individuals with heavy prenatal alcohol exposure. Surface-based image analysis techniques allowed us to match cortical anatomy across subjects and between hemispheres based on manually delineated sulcal landmarks. Quantitative maps of brain surface asymmetry reveal prominent peri-Sylvian hemispheric differences in which the superior temporal and inferior parietal cortices are shifted backward in the left relative to the right hemisphere in both normal and alcohol-exposed subjects. Cortical surface gray matter asymmetry, mapped here in adolescent populations, is most prominent in the posterior inferior temporal lobes (right greater than left), and this effect does not differ between groups of normally developing children, adolescents, or young adults. Alcohol-exposed individuals show a significant reduction in this asymmetry, whether studied with surface-based or more traditional volumetric region of interest analyses. This region of cortex, near the junction of Brodmann's areas 21, 22, and 37, primarily subserves language functions that are known to be impaired on average in the alcohol-exposed subjects. Our findings elucidate regional patterns of brain surface and gray matter asymmetry during normal development and may contribute to a more comprehensive understanding of the neural substrates of cognitive dysfunction after heavy prenatal alcohol exposure.

Adolescent↗
PubMed2002

What's wrong with the National Ambient Air Quality Standard (NAAQS) for fine particulate matter (PM(2.5))?

Associations between airborne concentrations of fine particulate matter (PM(2.5)) and mortality rates have been investigated primarily by ecologic or semiecologic epidemiology studies. Many investigators and regulatory agencies have inferred that the weak, positive association often observed is causal, that it applies to all forms of airborne PM(2.5), and that current ambient levels of PM(2.5) require reduction. Before implementing stringent regulations of ambient PM(2.5), analysts should pause to consider whether the accumulated evidence is sufficient, and sufficiently detailed, to support the PM(2.5) National Ambient Air Quality Standard. We take two tacks. First, we analyze the toxicologic evidence, finding it inconsistent with the notion that current ambient concentrations of all forms of fine particulate matter should affect pulmonary, cardiac, or all-cause mortality rates. More generally, we note that the thousands of forms of PM(2.5) are remarkably diverse, yet the PM(2.5) NAAQS presumes them to be identical toxicologically, and presumes that reducing ambient concentrations of any form of PM(2.5) will improve public health. Second, we examine the epidemiologic evidence in light of two related examples of semiecologic associations, examples that both inform the PM-mortality association and have been called into question by individual-level data. Taken together, the toxicologic evidence and lessons learned from analogous epidemiologic associations should encourage further investigation of the association between particulate matter and mortality rates before additional regulation is implemented, and certainly before the association is characterized as causal and applicable to all PM(2.5).

Air Pollutants↗
PubMed2000

Longitudinal change of white matter abnormalities.

A three year follow-up of 273 participants (mean age 60+/-6.1 years) of the Austrian Stroke Prevention Study provides first information on the rate, clinical predictors, and cognitive consequences of MRI white matter hyperintensity in elderly individuals without neuropsychiatric disease. Lesion progression was found in a total of 49 (17.9%) individuals. It was minor in 27 (9.9%) and marked in 22 (8.1%) participants. Diastolic blood pressure (odds ratio 1.07/mmHg) and early confluent or confluent white matter hyperintensities at baseline (odds ratio 2.62) were the only significant predictors of white matter hyperintensity progression. Lesion progression had no influence on the course of neuropsychologic test performance over the observational period.

Aged↗
PubMed1996

Anaplastic (malignant) ganglioglioma arising from heterotopic grey matter nodules.

Anaplastic ganglioglioma is a rare malignant neoplasm. The short clinical course and the anaplastic histological features are characteristics of malignant ganglioglioma. Immunohistochemistry is necessary for the final diagnosis. The MRI appearances are described here for the first time in literature. Nodular grey matter heterotopias had been demonstrated and the patient developed an anaplastic ganglioglioma two years later, on the same place where the grey matter heteropias had been seen. This finding supports the hypothesis that these tumours may arise from grey matter nodules.

Adult↗
PubMed1996

Layer VII and the gray matter trajectories of corticocortical axons in rats.

The trajectory of long distance intrahemispheric corticocortical axons has been investigated using the anterograde fluorescent axonal tracer fluororuby. Most axons of this kind were found to travel through the gray matter of layers VI and VII rather than in the white matter. The cell-sparse zone immediately superficial to layer VII contains a dense aggregate of longitudinally directed axons. Corticocortical axons traveling in the mediolateral plane also utilize the deep gray matter predominately. Layer VII neurons are persistent remnants of the subplate in rats. Based on our retrograde labeling results, they are involved in long distance as well as local corticocortical connections. Layer VII neurons are often labeled in a more continuous pattern after cortical injections of retrograde tracers than neurons of layers II, III and V, which are labeled in a patchy manner.

Animals↗
PubMed1996

A light- and electron-microscopic study of GluR4-positive cells in cerebral cortex, subcortical white matter and corpus callosum of neonatal, immature and adult rats.

The distribution of the [3H]alpha-amino-3-hydroxy-5-methylisoxzalepropionic acid (AMPA) receptor subunit GluR4 was studied in frontal, parietal and temporal cerebral cortex, subcortical white matter and corpus callosum of neonatal, immature and mature rats. In 1- to 2-day-old rats, a few oligodendrocyte progenitors and amoeboid microglia in the supraventricular part of the corpus callosum were immunolabelled for GluR4. At 7 to 10 days, the number of amoeboid microglia and oligodendrocyte progenitors in white matter increased; many neurons in cortex, including pyramidal neurons, were also moderately labelled for GluR4. The pattern of GluR4 immunostaining in 14-day-old rats was different from that in 7- to 10-day-old rats, but similar to the adult, in that there was no immunoreactivity in microglia and oligodendrocyte progenitors in subcortical white matter. A proportion of non-pyramidal neurons in cortex were moderately labelled, while some pyramidal neurons were lightly labelled. A population of small glial cells with features of oligodendrocyte progenitors were densely labelled in cortex.

Animals↗
PubMed1995

White matter amyloid in Alzheimer's disease brain.

Amyloid beta-protein (A beta) deposits in the white matter were investigated by the double immunohistochemical staining for A beta and neuritic, glial or vascular components. Reactive astroglia and neurite abnormality were absent around A beta deposits in the white matter (w-A beta) even those with a core. The association of w-A beta with blood vessels was not consistent. Aggregates of activated microglia were found to be the sole but a consistent accompaniment of A beta deposits even in the absence of other components such as neuron, synapse, neurite abnormality and reactive astroglia, as observed in the white matter. This suggests that the aggregates of activated microglia most likely represent one of the factors promoting the process of A beta deposition.

Alzheimer Disease↗
PubMed1995

White matter microglia produce membrane-type matrix metalloprotease, an activator of gelatinase A, in human brain tissues.

Membrane-type matrix metalloprotease (MT-MMP) is an activator of gelatinase A (MMP-2), which has previously been found in carcinoma cells. We examined non-neurological and Alzheimer's disease brain tissues for MT-MMP by immunohistochemistry and in situ hybridization. The anti-MT-MMP antibodies gave positive staining of brain microglial cells in all the brain tissues. Positively stained microglia were found only in the white matter. The cells producing MT-MMP protein were also shown to be white matter microglia. These results provide further evidence that activated gelatinase A, which may be a processing enzyme for degradation of beta-amyloid protein, may be produced in white matter microglia.

Aged↗
PubMed1990

Prominent white matter lesions develop in Mongolian gerbils treated with 100% normobaric oxygen after global brain ischemia.

Carotid arteries were occluded bilaterally for 15 min in two groups of Mongolian gerbils. The first group received 100% oxygen during the first 3 h of reperfusion. During that period, room air was given to the second group. After 3 h, both groups received room air. Brains of gerbils that died within 14 days after occlusion were removed, fixed in formalin and embedded in paraffin. Gerbils that survived 15-28 days were perfused with formalin before their brains were removed and embedded in paraffin. Adjacent, serially cut sections were stained with luxol fast blue (LFB)-H&E, cresyl violet, according to the Bodian method, or immunocytochemically with antisera raised against myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP). In brain sections of gerbils receiving 3 h of 100% oxygen, there were circumscribed white matter lesions in the corpus striatum, lateral thalamus, mesencephalon and posterior limb of the internal capsule. Myelin sheaths were swollen, fragmented and were less intensely stained by MBP antiserum. MBP and LFB-stained myelin fragments were present extracellularly and in macrophages. Many axons in these areas appeared undamaged. Previously described ischemic changes were found in gray matter and some areas of white matter in both groups. However, neurons in the deeper laminae of the cerebral cortex appeared to be better preserved in gerbils given oxygen. The results suggest that hyperoxia, if present immediately after transient brain ischemia, may damage myelin more severely than other cellular elements.

Animals↗
PubMed1989

White matter ultrastructural pathology of experimental Creutzfeldt-Jakob disease in mice.

Creutzfeldt-Jakob disease (CJD), previously regarded as a neurodegenerative disorder strictly of the gray matter, occasionally occurs as a panencephalopathic form which is characterized by severe white matter damage. An ultrastructural study of the white matter pathology in mice experimentally infected with the Fujisaki strain of CJD virus revealed: (1) vacuoles within myelin sheaths, formed by splitting either at the major dense or intraperiod lines, or within axons; (2) macrophages filled with numerous myelin figures, lipid droplets and paracrystalline inclusions; (3) astrocytes actively digesting myelin debris; (4) unusual wrapping of several axons by a common myelin sheath; (5) vesicular degeneration of myelin sheaths; (6) close contact between numerous coated pits and outer myelin lamellae; and (7) proliferation of inner mesaxons. Our data indicate that the damage to myelinated axons in the panencephalopathic type of CJD is accomplished primarily by active degradation of myelin by macrophages and astrocytes and by formation of intra-axonal and intra-myelin vacuoles. The myelin vacuolation is most consistent with that produced by leukolysins released from activated macrophages and astrocytes.

Animals↗
PubMed1995

Selective localization of gelatinase A, an enzyme degrading beta-amyloid protein, in white matter microglia and in Schwann cells.

Gelatinase A is an enzyme capable of cleaving soluble beta-amyloid protein (beta AP), and may function as an alpha-secretase to produce secretory forms of amyloid precursor protein. We examined gelatinase A immunoreactivity in the brains and posterior roots of neurologically normal, lacunar stroke, Alzheimer disease (AD), amyotrophic lateral sclerosis, progressive supranuclear palsy and myasthenia gravis cases. The gelatinase A antibody stained only microglial cells in the white matter in all the brain tissues. In AD brain, the reactive microglia located in the center of classical senile plaques, as well as in other microglial cells in the gray matter, showed no immunoreactivity. Gelatinase A in white matter microglial cells may play a role in preventing local deposition of beta AP. In the posterior root, Schwann cells had positive immunoreactivity. As with other metalloproteases, gelatinase A in Schwann cells may play an antiproliferative role.

Aged↗
PubMed1983

Creutzfeldt-Jakob disease: a case with extensive white matter degeneration and optic atrophy.

A 52-year-old woman is described, whose clinical features were typical of Creutzfeldt-Jakob disease except for the presence of optic atrophy. Serial CT scans showed rapid development of brain atrophy early in the course. Postmortem examination revealed extensive degeneration of the cerebral and cerebellar white matter and of the optic nerves in addition to the classic findings of Creutzfeldt-Jakob disease. It is suggested that both the grey and white matter may undergo a severe destructive process early in the course of the disease, and the possibility is discussed that the white matter involvement is not a result of neuronal loss.

Brain↗
PubMed1988

Cerebral amyloid angiopathy with attenuation of the white matter on CT scans: subcortical arteriosclerotic encephalopathy (Binswanger) in a normotensive patient.

Subcortical arteriosclerotic encephalopathy was diagnosed in a 56-year-old female normotensive patient with gradually progressing dementia, pseudobulbar palsy and motor deficits. CT scan showed white matter low attenuation in the frontal and parietal lobes. Neuropathological examination revealed degeneration of the white matter. Amyloid was found in walls of small cortical vessels. The walls of small vessels in the white matter showed severe thickening, fibrosis and hyalinization but not amyloid. Cerebral amyloid angiopathy may be responsible for subcortical arteriosclerotic encephalopathy.

Amyloid↗
PubMed1991

Pattern recognition in magnetic resonance imaging of white matter disorders in children and young adults.

Magnetic resonance imaging (MRI) is considered to be a highly sensitive modality for visualizing white matter abnormalities. Estimations of its specificity are far less positive. However, diagnostic specificity depends upon both the inherent qualities of MRI and on the quality of image interpretation. Systematic and detailed analysis of many image elements, and substantial prior experience improve the quality of image interpretation and thus improve diagnostic specificity. The present study has been set up to develop a pattern recognition system which combines sensitivity and specificity, systematic analysis of image elements and prior experience. This pattern recognition is based on the data of 277 patients with white matter disorders referred for MRI. The information was stored in a data base and computer analyzed. Twenty-two MRI patterns were discerned in as many disease categories. The frequency of occurrence of each MRI abnormality was assessed per disease category to establish the pattern of abnormalities characteristic for each separate disease category. The pattern recognition program was also written so that: (a) when fed data about MRI abnormalities observed in a new case, the computer produces a differential diagnosis with probabilities and 95% confidence intervals for each differential diagnosis; (b) specific data on the MRI findings of new cases could be added to the data base to improve the experience and accuracy of the program. This program for pattern recognition of abnormalities in the MR images of white matter disorders enhances the specificity of image interpretation and provides a wonderful aid for teaching purposes.

Adolescent↗
PubMed1995

1H and 31P magnetic resonance spectroscopic imaging of white matter signal hyperintensity areas in elderly subjects.

White matter signal hyperintensities (WMSH) are commonly seen on MRI of elderly subjects. The purpose of this study was to characterize metabolic changes in the white matter of elderly subjects with extensive WMSH. We used water-suppressed proton (1H) magnetic resonance spectroscopic imaging (MRSI) to compare six subjects with extensive WMSH with eight age-matched elderly subjects with minimal or absent WMSH, and phosphorus (31P) MRSI to compare nine subjects with extensive WMSH and seven age-matched elderly subjects without extensive WMSH. Relative to region-matched tissue in elderly controls, extensive WMSH were associated with increased signal from choline-containing metabolites, no significant change of signal from N-acetylaspartate, and a trend to a decreased phosphomonoester (PME) resonance. These findings suggest that WMSH may be associated with an alteration of brain myclin phospholipids in the absence of axonal damage. There were no differences in energy phosphates, consistent with lack of ongoing brain ischemia. Within the group with extensive WMSH, PME resonance measures were significantly lower in WMSH than in contralateral normal-appearing white matter. These results provide information on pathophysiology of WMSH and a basis for comparison with WMSH in Alzheimer's disease, vascular dementia, multiple sclerosis, and other diseases.

Aged↗
PubMed1975

[Malignant granular-cell tumor of the cerebral white matter: morphological, cytophotometrical and neurochemical studies (author's transl)].

This is a report of the second known case of a primary malignant granular-cell tumor of the cerebral hemispherical white matter. Two cell types may be distinguished apparently representing different developmental stages of otherwise identical tumor cells. Quantitative histochemical and biochemical studies have shown that tumor cells were containing markedly elevated levels of DNA and RNA. Only few ribosomes and polysomes could be detected, however, by electron microscopy. While cytophotometry disclosed only slightly elevated cytoplasmic proteins, there was a distinct increase in total protein concentration of tumor tissue per unit weight, as measured by conventional techniques. It is suggested that this increase is mainly attributable to structural proteins of cellular and subcellular elements of multiplicating malignant cells. A ratio of RNA to DNA in excess of 1 was found for white matter derived from the central tumor, while the ratios of control tissue were lowered to values far below one due to postmortem changes greatly reducing tissue concentrations of RNA. No detailed characterization of RNA was attempted. The nuclear DNA content of tumor cells reached values equivalent to chromosomal hexadekaploidy. This was in sharp contrast to control data from an Abrikossoff tumor of the oral cavity and from a neurohypophyseal tumorette ("choristoma"), respectively, displaying diploidy only associated with a much lesser increase of cytoplasmic RNA and proteins. Qualitative lipid studies were consistent with a marked active demyelination of the tumor centre as indicated by a severe reduction of cerebrosides and sulfatides and the presence of cholesterol esters. In addition there was a striking loss of phosphatidylethanolamine and a lesser one of sphingomyelin of white matter of both the tumor-stricken and the contralateral unaffected hemispherical regions, possibly suggesting a generally disturbed metabolism of myelin. It is not clear whether these general changes were resulting from the presence of the unilateral tumor or from precocious cerebral involution.

Brain Neoplasms↗
PubMed1980

Creutzfeldt-Jakob disease with extensive degeneration of white matter.

Degeneration of the white matter is uncommon is Creutzfeldt-Jakob disease (CJD), and when it occurs is usually mild, and limited in distribution. In the case of 77-year-old woman with CJD lasting 1 year, there was extensive degeneration of cerebral white matter in addition to severe loss of neurons and hypertrophic astrogliosis in cortex and striatum. The extent and severity of white matter lesions makes the case unusual.

Aged↗
PubMed1993

Inborn errors and demyelination: MRI and the diagnosis of white matter disease.

The progress and extent of myelination can be assessed using magnetic resonance imaging (MRI). Myelination is delayed or diminished in several inherited metabolic abnormalities presenting in early life. Only minimal myelination of the CNS occurs in Pelizaeus-Merzbacher disease. Dysmyelination tends to produce fairly symmetrical lesions affecting white matter. In many mitochondrial enzyme and some lysosomal defects, the grey matter is also involved. The appearances and in particular the distribution on MRI and/or CT are characteristic in some conditions and the diagnosis is limited in others. Demyelination due to inflammatory disorders typically causes multifocal white matter lesions, recurrent in multiple sclerosis, monophasic in acute disseminated encephalomyelitis, extending in progressive multifocal leukoencephalopathy and classically involving the pons or corpus callosum in myelinolysis. Hypoxic ischaemic lesions may be metabolically induced and simulate primary demyelinating disorders. Mitochondrial enzyme defects in particular may present with stroke-like appearances. In many of these conditions, diagnosis is biochemical, but imaging has a significant role in suggesting the diagnosis, and documenting progression, response to therapy or complications.

Basal Ganglia↗