|
| ||
|
|
||
Cerebral White Matter (cerebral + white_matter)
Terms modified by Cerebral White Matter Selected AbstractsDevelopment of cortical and subcortical brain structures in childhood and adolescence: a structural MRI studyDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 1 2002Elizabeth R Sowell PhD The purpose of the present study was to describe in greater anatomical detail the changes in brain structure that occur during maturation between childhood and adolescence. High-resolution MRI, tissue classification, and anatomical segmentation of cortical and subcortical regions were used in a sample of 35 normally developing children and adolescents between 7 and 16 years of age (mean age 11 years; 20 males, 15 females). Each cortical and subcortical measure was examined for age and sex effects on raw volumes and on the measures as proportions of total supratentorial cranial volume. Results indicate age-related increases in total supratentorial cranial volume and raw and proportional increases in total cerebral white matter. Gray-matter volume reductions were only observed once variance in total brain size was proportionally controlled. The change in total cerebral white-matter proportion was significantly greater than the change in total cerebral gray-matter proportion over this age range, suggesting that the relative gray-matter reduction is probably due to significant increases in white matter. Total raw cerebral CSF volume increases were also observed. Within the cerebrum, regional patterns varied depending on the tissue (or CSF) assessed. Only frontal and parietal cortices showed changes in gray matter, white matter, and CSF measures. Once the approximately 7% larger brain volume in males was controlled, only mesial temporal cortex, caudate, thalamus, and basomesial diencephalic structures showed sex effects with the females having greater relative volumes in these regions than the males. Overall, these results are consistent with earlier reports and describe in greater detail the regional pattern of age-related differences in gray and white matter in normally developing children and adolescents. [source] Neuroimaging of cortical development and brain connectivity in human newborns and animal modelsJOURNAL OF ANATOMY, Issue 4 2010Gregory A. Lodygensky Abstract Significant human brain growth occurs during the third trimester, with a doubling of whole brain volume and a fourfold increase of cortical gray matter volume. This is also the time period during which cortical folding and gyrification take place. Conditions such as intrauterine growth restriction, prematurity and cerebral white matter injury have been shown to affect brain growth including specific structures such as the hippocampus, with subsequent potentially permanent functional consequences. The use of 3D magnetic resonance imaging (MRI) and dedicated postprocessing tools to measure brain tissue volumes (cerebral cortical gray matter, white matter), surface and sulcation index can elucidate phenotypes associated with early behavior development. The use of diffusion tensor imaging can further help in assessing microstructural changes within the cerebral white matter and the establishment of brain connectivity. Finally, the use of functional MRI and resting-state functional MRI connectivity allows exploration of the impact of adverse conditions on functional brain connectivity in vivo. Results from studies using these methods have for the first time illustrated the structural impact of antenatal conditions and neonatal intensive care on the functional brain deficits observed after premature birth. In order to study the pathophysiology of these adverse conditions, MRI has also been used in conjunction with histology in animal models of injury in the immature brain. Understanding the histological substrate of brain injury seen on MRI provides new insights into the immature brain, mechanisms of injury and their imaging phenotype. [source] Reversible Cytotoxic Edema in a Cirrhotic Patient Following TIPSJOURNAL OF NEUROIMAGING, Issue 4 2009James R. Babington MD ABSTRACT The authors report the magnetic resonance imaging (MRI) findings in a 52-year-old man with cirrhosis from chronic hepatitis C who developed episodic acute hepatic encephalopathy Type C following placement of transjugular intrahepatic portosystemic shunt (TIPS). Brain MRI revealed hyperintense T2 signal and restricted diffusion distributed through the cerebral cortex. The patient's mentation improved with treatment of his hyperammonemia. Brain MRI performed 5 months later revealed diffuse cerebral atrophy and new areas of hyperintense T2 signal in the cerebral white matter. The cortical signal abnormalities and low apparent diffusion coefficient values on the initial MRI resolved with exception of a mild amount of hyperintense FLAIR signal in the cingulate cortex. Acute hepatic encephalopathy following portosystemic shunting,either from placement of TIPS or from development of spontaneous shunts,is a widely recognized complication of portal hypertension and cirrhosis. We report MRI findings of reversible cytotoxic edema in a patient with acute hepatic encephalopathy following placement of TIPS. [source] Gene Expression in Human Alcoholism: Microarray Analysis of Frontal CortexALCOHOLISM, Issue 12 2000Joanne M. Lewohl Background: Changes in brain gene expression are thought to be responsible for the tolerance, dependence, and neurotoxicity produced by chronic alcohol abuse, but there has been no large scale study of gene expression in human alcoholism. Methods: RNA was extracted from postmortem samples of superior frontal cortex of alcoholics and nonalcoholics. Relative levels of RNA were determined by array techniques. We used both cDNA and oligonucleotide microarrays to provide coverage of a large number of genes and to allow cross-validation for those genes represented on both types of arrays. Results: Expression levels were determined for over 4000 genes and 163 of these were found to differ by 40% or more between alcoholics and nonalcoholics. Analysis of these changes revealed a selective reprogramming of gene expression in this brain region, particularly for myelin-related genes which were down-regulated in the alcoholic samples. In addition, cell cycle genes and several neuronal genes were changed in expression. Conclusions: These gene expression changes suggest a mechanism for the loss of cerebral white matter in alcoholics as well as alterations that may lead to the neurotoxic actions of ethanol. [source] Chromium(VI) as a novel MRI contrast agent for cerebral white matter: Preliminary results in mouse brain in vivoMAGNETIC RESONANCE IN MEDICINE, Issue 1 2006Takashi Watanabe Abstract This work demonstrates that intraventricular microinjections of a low dose of potassium dichromate (0.4 ,L of 10 mM solution) yield a specific contrast enhancement of white matter (WM) tracts in T1 -weighted 3D MRI of mouse brain in vivo. Pronounced and persistent signal increases (40,100% at 24 hr after injection) were observed in the corpus callosum, anterior commissure, fornix, and stria medullaris, as well as in the mammillothalamic tract and fasciculus retroflexus. These results suggest that the extracellular diffusion of diamagnetic chromium(VI) (Cr(VI)) after injection is followed by a tissue-specific reduction to paramagnetic Cr(V) and (III), which relies predominantly on the oxidation of myelin lipids. Because Cr(VI)-induced contrast leads to only a mild unspecific enhancement (10,20%) of gray matter (GM) structures, such as the hippocampal formation, the method reveals novel information that differs from that obtainable using other paramagnetic ions, such as manganese. Magn Reson Med, 2006. © 2006 Wiley-Liss, Inc. [source] Methotrexate-related leukoencephalopathy without radiation therapy: Distribution of brain lesions and pathological heterogeneity on two autopsy casesNEUROPATHOLOGY, Issue 2 2009Jun Matsubayashi This report concerns two rare autopsy cases of methotrexate (MTX)-related leukoencephalopathy without radiation therapy. In the first case, there were widespread necrotic foci with prominent spheroids, that is, disseminated necrotizing leukoencephalopathy (DNL), mainly in the cerebral white matter. In contrast, in the second case, there were widespread demyelinated foci without significant axonal changes, which we would like to name disseminated demyelinating leukoencephalopathy (DDL), mainly in the cerebral white matter. We emphasize that the pathology of pure MTX-related leukoencephalopathy is not uniform, and may show at least two kinds of histologic change. Furthermore, both cases did not develop significant vascular changes, which are usually induced by radiation therapy. The distribution of the lesions in two cases was examined by large specimens, including hemisphere specimens. The distribution of the lesions in the brain of our cases was also different. In the first case, the DNL lesions were predominantly distributed in the frontal and temporal lobes. In the second case, the DDL lesions were prominently localized in the occipital lobe. To our knowledge, this is the first report describing not only the pathological findings of MTX-related leukoencephalopathy without irradiation but also the precise distributions of the lesions. [source] Oxidative stress in developmental brain disordersNEUROPATHOLOGY, Issue 1 2009Masaharu Hayashi Oxidative stress is one of the predisposing factors in adult neurological disorders. We have examined the involvement of oxidative stress in child-onset neurodegenerative disorders, and here we review the findings from our analysis. In cases of Cockayne syndrome, the oxidative products of lipids and proteins were increased in the globus pallidus; however, oxidative nucleotide damage that coincided with reduced copper/zinc superoxide dismutase (Cu/ZnSOD) expression was observed in cases of xeroderma pigmentosum, and these patients also presented increased oxidative stress markers in urine samples. In spinal muscular atrophy, lipid peroxidation in conjunction with oxidative DNA damage was observed in motor neurons. Cases of subacute sclerosing panencephalitis presented oxidative nucleoside damage in cerebral cortical neurons at early disease stages, which were subsequently replaced by lipid peroxidation in glial cells of cerebral white matter. In relation to progressive myoclonic epilepsy, oxidative damage to DNA, proteins, and lipids appeared to coincide with cerebral and cerebellar cortical lesions of neuronal ceroid-lipofuscinosis. Patients with Lafora disease also presented an increase in oxidative stress markers for DNA and/or lipids in the brain and urine. These findings imply involvement of oxidative stress in developmental brain disorders; antioxidant agents could prove to be useful for treating patients with those disorders. [source] Corticobasal degeneration as cause of progressive non-fluent aphasia: Clinical, radiological and pathological study of an autopsy caseNEUROPATHOLOGY, Issue 6 2006Masaki Takao A Japanese male developed gradual loss of spontaneous speech at age 60. Three years later meaningful speech had deteriorated to the point that it had become restricted to monotonous utterances. Neuropsychological examination at age 62 showed that he had severe non-fluent aphasia. A brain MRI demonstrated mild cortical atrophy with ischemic lesions in the cerebral white matter. He was diagnosed as having primary progressive aphasia. At age 63, he was admitted to the hospital to reevaluate the neurological condition. Neurologic examination showed severe non-fluent aphasia, hyperreflexia, snout and sucking reflexes. No alien hand was observed. He was able to walk, dress, wash himself and use chopsticks as well as name real objects. At age 65, 99mTc-hexamethylpropyleneamine oxime single photon emission computed tomography (HMPAO-SPECT) revealed diffuse cerebral hypoperfusion that was particularly prominent in the left frontal lobe. An MRI showed progressive cortical atrophy with the definite atrophy of the left paracentral gyrus. The hippocampal formation and putamen were also atrophic. He died of pneumonia at age 67. The brain weighed 810 g with atrophy of the frontal lobe, globus pallidus, enlargement of the lateral ventricles and depigmentation of the substantia nigra. Microscopic examination showed severe neuronal loss and gliosis in the cerebral cortex, globus pallidus interna and substantia nigra. Ballooned neurons were observed in the cerebral cortex. Gallyas-Braak method revealed numerous astrocytic plaques and argentophilic threads in the cerebrum. Clinical diagnosis of corticobasal degeneration sometimes is difficult in individuals with atypical clinical presentations. More exact clinical and radiological criteria may warrant a diagnosis of corticobasal degeneration. [source] Pathological changes in the cerebral medullary arteries of five autopsy cases of malignant nephrosclerosis: Observation by morphometry and reconstruction of serial sectionsNEUROPATHOLOGY, Issue 3 2003Riki Okeda Hypertension (HT) is a serious risk factor of not only cerebral infarction and bleeding, but also Binswanger's encephalopathy (BE). In BE especially, severe stiffening of the cerebral medullary arteries because of hypertensive changes with loss of medial smooth muscle cells (SMC) occurs, which induces diffuse atrophy of the cerebral white matter. But, it is not yet ascertained whether HT is particularly severe in BE. Therefore, a spectrum of the pathological changes of the cerebral arteries were investigated by reconstruction of serial sections and morphometry of the medial thickness in five autopsied patients with malignant nephrosclerosis (MN) of exacerbated form. Each presented clinically acute progression of long-standing HT at the terminal stage and pathologically typical renal changes. The heartweight was 380,900 g. Morphometry of the medial thickness of the arachnoid arteries presented significant medial hypertrophy in four cases of MN, but in the medullary arteries it presented in only two cases with marked cardiomegaly of 700 g and 900 g. In four cases of MN, only a few medullary arteries showed slight pathological changes. However, in another case with cardiomegaly of 900 g, all 10 medullary arteries showed multiple segments of atheroma, medial SMC loss, and prominent dilatation; edematous concentric intimal fibrosis with luminal obstruction and atrophy of the white matter were absent. In conclusion, only one case of MN showing marked cardiomegaly of 900 g presented severe pathological changes of the cerebral medullary arteries comparable with those of BE, although other MN-cases showing severe cardiac hypertrophy presented only trivial arterial changes. Therefore, the cerebral medullary artery seems to be protected from HT, yet it is involved in a case of severe and long-standing HT inducing an extreme cardiomegaly. [source] Microvasculature of the human cerebral white matter: Arteries of the deep white matterNEUROPATHOLOGY, Issue 2 2003Hiroko Nonaka The vascular architecture of the human cerebral deep white matter was studied using soft X-ray and diaphanized specimens, achieved by intra-arterial injection of barium and vascular stain respectively, and also by electron microscopic examination of the corrosion cast of arteries in normal adult brains. The deep white matter arteries passed through the cerebral cortex with a few branches to the cortex and ran straight through the white matter. The arteries concentrated ventriculopetally to the white matter around the lateral ventricle. Anastomoses were noted around the ventricular wall at the terminals of the deep white matter arteries. No centrifugal branches irrigating the periventricular white matter from the lenticulo-striate arteries were observed in the present study. The presence of anastomoses among the terminal branches of deep white matter arteries protects against ischemic change or infarction in this area from an occlusion of a single deep white matter artery. This may lead to development of terminal zone infarction from ischemia or vascular diseases, affecting multiple deep white matter arteries. The subcortical and deep white matter arteries had thick adventitial sheaths and large adventitial spaces in the white matter but not in the cortex. The presence or absence of the adventitial space is regarded as another characteristic difference between the arteries in the white matter and cortex. This difference may influence pathological changes in vascular lesions in these respective areas. [source] Minocycline treatment following hypoxic/ischaemic injury attenuates white matter injury in a rodent model of periventricular leucomalaciaNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2008M. Lechpammer Aims: Periventricular white matter injury in premature infants occurs following hypoxia/ischaemia and systemic infection, and results in hypomyelination, as well as neuromotor and cognitive deficits later in life. Inflammatory infiltrates are seen within human cerebral white matter from periventricular leucomalacia (PVL) cases. Methods: In this study, we examine the time course of CD-68+ microglial cell responses relative to cell death within white matter following hypoxia/ischaemia in a rat model of PVL. We also tested the efficacy of the minocycline, an agent that suppresses microglial activation, in this model when administered as a post-insult treatment. Results: We show that preoligodendrocyte injury in the post-natal day 6 begins within 24 h and continues for 48,96 h after hypoxia/ischaemia, and that microglial responses occur primarily over the first 96 h following hypoxia/ischaemia. Minocycline treatment over this 96 h time window following the insult resulted in significant protection against white matter injury, and this effect was concomitant with a reduction in CD-68+ microglial cell numbers. Conclusions: These results suggest that anti-inflammatory treatments may represent a useful strategy in the treatment of PVL, where clinical conditions would favour a post-insult treatment strategy. [source] Relaxation times of choline, creatine and N -acetyl aspartate in human cerebral white matter at 1.5 TNMR IN BIOMEDICINE, Issue 3 2002D. R. Rutgers Abstract Several studies have investigated the T1 and T2 relaxation time of choline, creatine and N -acetyl aspartate in cerebral white matter in normal human subjects. However, these studies demonstrate a large variation in T1 and T2 values. In the present study, relaxation times of choline, creatine and N -acetyl aspartate were determined in cerebral white matter in 15 control subjects (age 21,±,2 y, mean,±,SD) at 1.5 T. Using PRESS, seven or eight data points were obtained to fit the T1 and T2 relaxation curves to, respectively. The mean voxel size was 14,cm3. The T1 relaxation times of choline, creatine and N -acetyl aspartate were 1091,±,132 (mean,±,SD), 1363,±,137 and 1276,±,132,ms. The T2 relaxation times were 352,±,52, 219,±,29 and 336,±,46,ms, respectively. Copyright © 2002 John Wiley & Sons, Ltd. [source] Megalencephalic leukoencephalopathy with cysts without MLC1 defectANNALS OF NEUROLOGY, Issue 6 2010Marjo S. van der Knaap MD Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is an autosomal recessive disease characterized by early infantile macrocephaly and delayed motor and cognitive deterioration. Magnetic resonance imaging (MRI) shows diffusely abnormal and swollen cerebral white matter and subcortical cysts. On follow-up, atrophy ensues. Approximately 80% of MLC patients have mutations in MLC1. We report 16 MLC patients without MLC1 mutations. Eight retained the classical clinical and MRI phenotype. The other 8 showed major MRI improvement. They lacked motor decline. Five had normal intelligence; 3 displayed cognitive deficiency. In conclusion, 2 phenotypes can be distinguished among the non- MLC1 mutated MLC patients: a classical and a benign phenotype. ANN NEUROL 2010;67:834,837 [source] White matter changes in extremely preterm infants, a population-based diffusion tensor imaging studyACTA PAEDIATRICA, Issue 6 2010Béatrice Skiöld Abstract Aim:, To investigate cerebral white matter (WM) abnormalities (J Pediatr 2003; 143: 171) and diffuse and excessive high signal intensities (DEHSI), (J Pediatr 1999; 135: 351) in a cohort of extremely preterm infants born in Stockholm during a 3-year period, using magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI). Methods:, MRI at term-equivalent age was performed in 109 infants and DTI data were acquired in 54 infants. Survival rate in the entire cohort was 67%. Sixteen term-born healthy control infants were scanned for comparison. Results:, No or mild WM abnormalities were seen in 86% of infants and 14% had moderate or severe WM abnormalities. DEHSI were seen in infants with all grades of white matter abnormalities and were present in 56% of infants. In the WM at the level of centrum semiovale, infants with any WM abnormalities or DEHSI had lower Fractional Anisotropy and higher Apparent Diffusion Coefficient compared with control infants. No significant differences in diffusion were seen in infants without DEHSI compared with the controls in this region. Compared with controls, the preterm infants had significantly altered diffusion in the corpus callosum. Conclusion:, Only 14% of the extremely preterm infants had moderate or severe WM abnormalities on MRI. However, the incidence of DEHSI was high. In the DEHSI regions, changes in diffusion parameters were detected, indicating altered WM organization. [source] Treatment of X-linked childhood cerebral adrenoleukodystrophy by the use of an allogeneic stem cell transplantation with reduced intensity conditioning regimenCLINICAL TRANSPLANTATION, Issue 6 2005Igor B Resnick Abstract:, Childhood cerebral form of X-linked adrenoleukodystrophy (X-ALD) is a rapidly progressive demyelinating condition affecting the cerebral white matter, which rapidly leads to total disability and death. The only known curative treatment for this condition is allogeneic hematopoietic stem cell transplantation (HSCT). Procedure-related toxicity is assumed to be the cause of death of patients with X-ALD. Three cases of ALD successfully transplanted with the use of non-myeloablative fludarabine based conditioning are described. Patients showed smooth peri-bone marrow transplantation course with fast and stable engraftment. In the 3- to 5 yr follow-up period, patients showed no deterioration in their clinical and neurological condition. Levels of very long chain fatty acids were very variable and had a tendency to decrease in at least one of the three patients. In another patient, an improvement of magnetic resonance imaging changes was found. Non-myeloablative HSCT should be considered as an early treatment for X-ALD. [source] | ||||||||||||||||||||||