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PubMed1988

Absence of white matter changes on magnetic resonance imaging in children treated with CNS prophylaxis therapy for leukemia.

Previous studies have shown that magnetic resonance imaging (MRI) is sensitive to white matter changes in children receiving cranial radiation of 3000 cGy or greater. The current study used MRI to investigate the integrity of white matter in children receiving 1800 to 2400 cGy of cranial radiation. Ten survivors of acute lymphoblastic leukemia (ALL) who received intrathecal methotrexate (MTX) and either 1800 or 2400 cGy of cranial radiation were studied with MRI and neuropsychologic testing. Magnetic resonance (MR) scans were normal in nine of ten patients. One patient had prominent and asymmetrical lateral ventricles and mildly enlarged cortical sulci. White matter tracts were normal in appearance. However, seven of nine children had below average intellectual functioning. Results indicate that children receiving less than 2500 cGy of cranial radiation fail to show white matter changes on MRI, despite evidence of cognitive impairment.

Brain↗
PubMed1992

White matter changes in children treated for acute lymphoblastic leukemia.

BACKGROUND AND METHODS: Twenty-seven children with acute lymphoblastic leukemia (ALL) were studied by magnetic resonance (MR) imaging after central nervous system (CNS) treatment. The children were followed by clinical evaluations and computed tomographic (CT) brain scans. Two CNS treatment techniques were used. Eleven patients received intravenous and intrathecal methotrexate; 16 patients received 18-30 Gy of cranial radiation therapy in addition to systemic chemotherapy. The time interval between the CNS treatment and MR scans varied from 9 months to 4 years 8 months. RESULTS: Four of the 27 children (15%) showed white matter changes on the MR scans attributable to therapy, but only one had hypodensity on CT. Three of the 16 children (19%) receiving radiation therapy in addition to chemotherapy had white matter changes. One of the 11 patients (9%) from the group receiving only chemotherapy did so. The difference between the two treatment groups was not significant. CONCLUSIONS: Radiation therapy or chemotherapy (alone or in combination) may have been responsible for the white matter changes. MR imaging is a sensitive detector of white matter changes in children with ALL, but its value and significance during follow-up should be assessed in well-designed longitudinal research studies.

Adolescent↗
PubMed2000

Do white matter changes contribute to the subsequent development of dementia in patients with mild cognitive impairment? A longitudinal study.

OBJECTIVE: White matter lesions on brain CT or MRI are a frequent finding in patients with Alzheimer's disease. However, little is known about the prognostic significance of these changes in cognitively impaired individuals who are at risk for subsequent development of dementia. This study aims at investigating the potential impact of white matter lucencies (WML) on brain CT on the course of mild cognitive impairment. PATIENTS AND METHODS: Twenty-seven patients (mean age 72, SD 4.03) with mild cognitive impairment (MCI) and no signs of cerebrovascular disease were prospectively examined. At their initial presentation, all patients underwent a structured interview for the diagnosis of dementia (SIDAM) and a brain CT. Linear measures of atrophy and visual ratings of white matter changes were performed. At follow-up (mean interval 29 months), these patients were re-examined with the SIDAM. Eight patients had developed dementia and met clinical criteria for Alzheimer's disease (crossover group). RESULTS: Evaluation of the initial CT scans revealed significantly more frequent and extended white matter abnormalities and a higher degree of temporal lobe atrophy in the crossover group as compared to the cognitively stable group. In the crossover group, high WML severity initially was associated with a lesser degree of temporal lobe atrophy and higher global cognitive performance. CONCLUSION: We conclude that WML play a role in the dementia process and that they might accelerate cognitive decline in individuals with mild cognitive impairment. WML should be included in prospective studies of MCI as potential predictor variables.

Aged↗
PubMed2000

MRI volumetric correlates of white matter lesions in dementia with Lewy bodies and Alzheimer's disease.

The aim of the study was to examine the relationship between white matter changes on magnetic resonance imaging (MRI), brain atrophy and ventricular dilation in late-life dementias. T(1)-weighted, T(2)-weighted, and proton density MRI scans were acquired in subjects with Alzheimer's disease (AD, N=25) and dementia with Lewy bodies (DLB, N=27). Total brain and ventricular volumes were measured and white matter lesions rated using a semi-quantitative scale. Periventricular hyperintensities (PVH) were found to independently correlate with advancing age and increasing ventricular dilatation in all subjects. In contrast, deep white matter hyperintensities (DWMH) did not correlate with measures of brain atrophy, ventricular dilatation or age, but were associated with a history of hypertension. These findings support the hypothesis that PVH and DWMH are pathologically diverse and that white matter change in AD and DLB may be determined by similar processes. In particular, PVH appear to be linked to atrophic processes involving ventricular enlargement and DWMH to ischaemic risk factors.

Age Factors↗
PubMed2000

Quantitative analysis of short echo time (1)H-MRSI of cerebral gray and white matter.

Quantitative analysis of (1)H-magnetic resonance spectroscopic imaging (MRSI) data was developed using the user-independent spectral analysis routine LCModel. Tissue segmentation was performed using statistical parametric mapping software (SPM 96), and the results were used to correct for cerebrospinal fluid contamination. A correction was developed for the imperfections in the spectroscopic excitation profile in order to improve the uniformity of metabolite images. After validation in phantoms, these techniques were applied to study differences in metabolite concentrations between gray and white matter in normal volunteers (n = 13). A positive correlation was found between concentration and gray matter content for most metabolites studied. The estimated ratios of metabolite concentration in gray vs. white matter were: N-acetyl aspartate + N-acetyl aspartyl glutamate (NAc) = 1.16+/- 0.11; creatine = 1.7+/-0.3; glutamate + glutamine = 2.4+/-0.5; myo-inositol = 1.6+/-0.3; choline = 0.9+/-0.2. The ratio of NAc/Cr was negatively correlated with gray matter content: gray/white = 0.69 +/-0.08. These methods will be useful in the evaluation of metabolite concentrations in MRSI voxels with mixed tissue composition in patient groups.

Adult↗
PubMed2003

White matter tract alterations in fragile X syndrome: preliminary evidence from diffusion tensor imaging.

Fragile X syndrome, the most common form of hereditary mental retardation, causes disruption in the development of dendrites and synapses, the targets for axonal growth in the central nervous system. This disruption could potentially affect the development, wiring, and targeting of axons. The current study utilized diffusion tensor imaging (DTI) to investigate whether white matter tract integrity and connectivity are altered in fragile X syndrome. Ten females with a diagnosis of fragile X syndrome and ten, age matched, female control subjects underwent diffusion weighted MRI scans. A whole brain analysis of fractional anisotropy (FA) values was performed using statistical parametric mapping (SPM). A follow-up, regions-of-interest analysis also was conducted. Relative to controls, females with fragile X exhibited lower FA values in white matter in fronto-striatal pathways, as well as in parietal sensory-motor tracts. This preliminary study suggests that regionally specific alterations of white matter integrity occur in females with fragile X. Aberrant white matter connectivity in these regions is consistent with the profile of cognitive and behavioral features of fragile X syndrome, and potentially provide additional insight into the detrimental effects of suboptimal levels of FMRP in the developing brain.

Adolescent↗
PubMed2004

Genetic disorders affecting white matter in the pediatric age.

Pediatric white matter disorders can be distinguished into well-defined leukoencephalopathies, and undefined leukoencephalopathies. The first category may be subdivided into: (a) hypomyelinating disorders; (b) dysmyelinating disorders; (c) leukodystrophies; (d) disorders related to cystic degeneration of myelin; and (e) disorders secondary to axonal damage. The second category, representing up to 50% of leukoencephalopathies in childhood, requires a multidisciplinar approach in order to define novel homogeneous subgroups of patients, possibly representing "new genetic disorders" (such as megalencephalic leukoencepahlopathy with subcortical cysts and vanishing white matter disease that have recently been identified). In the majority of cases, pediatric white matter disorders are inherited diseases. An integrated description of the clinical, neuroimaging and pathophysiological features is crucial for categorizing myelin disorders and better understanding their genetic basis. A review of the genetic disorders affecting white matter in the pediatric age, including some novel entities, is provided.

Brain Diseases↗
PubMed2002

Melatoninergic neuroprotection of the murine periventricular white matter against neonatal excitotoxic challenge.

Periventricular leukomalacia is one of the main causes of cerebral palsy. Perinatal white matter lesions associated with cerebral palsy appears to involve glutamate excitotoxicity and excess free radical production. When injected intracerebrally into newborn mice, the glutamatergic analog ibotenate induces white matter cysts mimicking human periventricular leukomalacia. Melatonin acts on specific receptors. It also exhibits intrinsic free radical scavenging properties. The goal of the present study is to determine whether melatonin can protect against excitotoxic lesions induced by ibotenate in newborn mice. Mice that received intraperitoneal melatonin had an 82% reduction in size of ibotenate-induced white matter cysts when compared with controls. Although melatonin did not prevent the initial appearance of white matter lesions, it did promote secondary lesion repair. Axonal markers supported the hypothesis that melatonin induced axonal regrowth or sprouting. The protective effects of melatonin were suppressed by coadministration of luzindole, a melatonin receptor antagonist. Forskolin, an adenylate cyclase activator, prevented the protective effects of melatonin; inhibitors of protein kinase C and mitogen-associated protein kinase had no detectable effect. Melatonin and derivatives that block cAMP production through activation of melatonin receptors could represent new avenues for treating human periventricular leukomalacia.

Animals↗
PubMed2001

Adult-onset Leukoencephalopathy with vanishing white matter presenting with dementia.

We report on a case of dementia and extensive cerebral white matter abnormalities seen on magnetic resonance-images which meet the criteria for leukoencephalopathy with vanishing white matter. This is an inherited condition that was first thought to occur only in children. Our patient shows that vanishing white matter should be considered in adult patients with early-onset dementia and extensive white matter changes seen on magnetic resonance images.

Adult↗
PubMed1988

Toluene abuse causes diffuse central nervous system white matter changes.

We describe the findings of magnetic resonance imaging (MRI) of the brain in 6 chronic toluene vapor abusers and the neuropathological findings in 1 abuser not studied by MRI. MRI in 6 chronic toluene abusers revealed the following abnormalities: (1) diffuse cerebral, cerebellar, and brainstem atrophy; (2) loss of differentiation between the gray and white matter throughout the central nervous system; and (3) increased periventricular white matter signal intensity on T2-weighted images. Another chronic toluene abuser (MRI not performed) died as a result of acute toluene overdose. The brain displayed diffuse, ill-defined myelin pallor, maximal in cerebellar, periventricular, and deep cerebral white matter. Neurons were preserved throughout, axonal swelling or beading was not seen, gliosis was minimal, and occasional, scant perivascular macrophage collections were seen. Taken in concert, these findings suggest that the pathological and MRI abnormalities are due to either increased water content of the white matter or subtle toluene-induced metabolic changes in myelin.

Brain↗
PubMed1979

The morphology of extrachoroidal ependyma overlying gray and white matter in the rabbit lateral ventricle.

A morphologic investigation of ependyma over gray matter (caudate nucleus) and over periventricular white matter (tapetum) of the rabbit lateral ventricle was undertaken prior to evaluation of morphological changes which occur with experimental hydrocephalus. Ependymal cells over the caudate nucleus are cuboidal and heavily ciliated. Numerous microvilli cover the cell surface. The lateral margins are straight and interdigitations between adjacent ependymal cells are absent. Ependymal cells over white matter are squamous. Nonciliated as well as ciliated cells contribute to the epithelial lining. Microvilli are present at the cell surface but tend to aggregate near the cellular borders. The lateral margins are convoluted and complex interdigitations are present between adjacent cells. Morphologic differences between ependymal cells over the caudate nucleus and those over periventricular white matter may help to explain the differential response to hydrocephalus observed in these two regions of the lateral ventricle.

Animals↗
PubMed2006

Smaller white-matter volumes are associated with larger deficits in attention and learning among long-term survivors of acute lymphoblastic leukemia.

BACKGROUND: The primary objective of this study was to test the hypothesis that survivors of childhood acute lymphoblastic leukemia (ALL) have deficits in neurocognitive performance, and smaller white-matter volumes are associated with these deficits. METHODS: The patients studied included 112 ALL survivors (84 patients who had received chemotherapy only, 28 patients who had received chemotherapy and irradiation; 63 males, 49 females; mean age +/- standard deviation, 4.1 yrs +/- 2.6 yrs at diagnosis; mean +/- standard deviation yrs since diagnosis, 6.0 +/- 3.5 yrs), and 33 healthy siblings who participated as a control group. Neurocognitive tests of attention, intelligence, and academic achievement were performed; and magnetic resonance images were obtained and subsequently were segmented to yield tissue volume measurements. Comparisons of neurocognitive measures and tissue volumes between groups were performed, and the correlations between volumes and neurocognitive performance measures were assessed. RESULTS: Most performance measures demonstrated statistically significant differences from the normative test scores, but only attention measures exceeded 1.0 standard deviation from normal. Patients who had received chemotherapy alone had significantly larger volumes of white matter than patients who had received treatment that also included cranial irradiation, but their volumes remained significantly smaller than the volumes in the control group. Smaller white-matter volumes were associated significantly with larger deficits in attention, intelligence, and academic achievement. CONCLUSIONS: Survivors of childhood ALL had significant deficits in attention and smaller white-matter volumes that were associated directly with impaired neurocognitive performance. Cranial irradiation exacerbated these deficits.

Adolescent↗
PubMed2007

Smaller regional volumes of brain gray and white matter demonstrated in breast cancer survivors exposed to adjuvant chemotherapy.

BACKGROUND: Previous studies have shown cognitive impairment in breast cancer survivors who were exposed to adjuvant chemotherapy. Neural damage by chemotherapy might have played some part in these findings. The current study explored the regional brain volume difference between breast cancer survivors exposed to adjuvant chemotherapy (C+) and those unexposed (C-). METHODS: High-resolution 1.5-tesla brain magnetic resonance imaging (MRI) databases of breast cancer survivors and healthy controls were used. Brain images were preprocessed for optimal voxel-based morphometry. Comparisons of gray matter and white matter were performed between the C+ and the C- groups, by using MRI scans from within 1 year (the 1-year study, n = 51 and n = 55, respectively) or 3 years after their cancer surgery (the 3-year study, n = 73 and n = 59, respectively). As exploratory analyses, correlation analyses were performed between indices of the Wechsler Memory Scale-Revised and regional brain volume where the volume were significantly smaller. As a reference, MRI scans of cancer survivors were compared with those of healthy controls (n = 55 for the 1-year study and n = 37 for the 3-year study). RESULTS: The C+ patients had smaller gray matter and white matter including prefrontal, parahippocampal, and cingulate gyrus, and precuneus in the 1-year study. However, no difference was observed in the 3-year study. The volumes of the prefrontal, parahippocampal gyrus, and precuneus were significantly correlated with indices of attention/concentration and/or visual memory. Comparisons with healthy controls did not show any significant differences. CONCLUSIONS: Adjuvant chemotherapy might have an influence on brain structure, which may account for previously observed cognitive impairments.

Adolescent↗
PubMed2006

Developmental regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit expression in forebrain and relationship to regional susceptibility to hypoxic/ischemic injury. I. Rodent cerebral white matter and cortex.

This is the first part of a two-part study to investigate the cellular distribution and temporal regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) subunits in the developing white matter and cortex in rat (part I) and human (part II). Western blot and immunocytochemistry were used to evaluate the differential expression of AMPAR subunits on glial and neuronal subtypes during the first 3 postnatal weeks in the Long Evans and Sprague Dawley rat strains. In Long Evans rats during the first postnatal week, GluR2-lacking AMPARs were expressed predominantly on white matter cells, including radial glia, premyelinating oligodendrocytes, and subplate neurons, whereas, during the second postnatal week, these AMPARs were highly expressed on cortical neurons, coincident with decreased expression on white matter cells. Immunocytochemical analysis revealed that cell-specific developmental changes in AMPAR expression occurred 2-3 days earlier by chronological age in Sprague Dawley rats compared with Long Evans rats, despite overall similar temporal sequencing. In both white and gray matter, the periods of high GluR2 deficiency correspond to those of regional susceptibility to hypoxic/ischemic injury in each of the two rat strains, supporting prior studies suggesting a critical role for Ca2+-permeable AMPARs in excitotoxic cellular injury and epileptogenesis. The developmental regulation of these receptor subunits strongly suggests that Ca2+ influx through GluR2-lacking AMPARs may play an important role in neuronal and glial development and injury in the immature brain. Moreover, as demonstrated in part II, there are striking similarities between rat and human in the regional and temporal maturational regulation of neuronal and glial AMPAR expression.

Age Factors↗
PubMed1980

Gliogenesis of astrocytes and oligodendrocytes in the neocortical grey and white matter of the adult rat: electron microscopic analysis of light radioautographs.

The identification of newly formed glial cells in the normal adult cerebral cortex is unresolved, since the identification of cells incorporating [H3] thymidine has not been demonstrated in the adult by electron microscopy. In the present study, this problem has been studied by combining the resolution of the electron microscope with radioautography of 1-micrometer sections. Four normal male rats were injected at 90 days of age with [H3] thymidine and allowed to survive for 30 days. Labeled cells were found in 1-micrometer sections of the visual cortex of these adult rats, and electron micrographs of selected cells from these same sections demonstrated clearly two types of cells labeled, astrocytes and oligodendrocytes, in both grey and white matter. The few cells that were tentatively identified as labeled microglia in the light microscope proved to resemble oligodendrocytes when examined in the electron microscope. In 1-micrometer sections of the cortical grey matter, heavily labeled astrocytes (13 or more silver grains over the nucleus) represent about 0.08% of the total astrocytic population, and heavily labeled oligodendrocytes also were about 0.08% of their population. In the cortical white matter, about 0.03% heavily labeled astrocytes were observed, compared to about 0.07% heavily labeled oligodendrocytes. For all neuroglial cells in both white and grey matter, the average percent heavily labeled cells was 0.066%, a value large enough to suggest a slow turnover of neuroglial cells during the lifespan of the rats.

Animals↗
PubMed1988

Ion channel expression by white matter glia: I. Type 2 astrocytes and oligodendrocytes.

White matter is a compact structure consisting primarily of neuronal axons and glial cells. As in other parts of the nervous system, the function of glial cells in white matter is poorly understood. We have explored the electrophysiological properties of two types of glial cells found predominantly in white matter: type 2 astrocytes and oligodendrocytes. Whole-cells and single-channel patch-clamp techniques were used to study these cell types in postnatal rat optic nerve cultures prepared according to the procedures of Raff et al. (Nature, 303:390-396, 1983b). Type 2 astrocytes in culture exhibit a "neuronal" channel phenotype, expressing at least six distinct ion channel types. With whole-cell recording we observed three inward currents: a voltage-sensitive sodium current qualitatively similar to that found in neurons and both transient and sustained calcium currents. In addition, type 2 astrocytes had two components of outward current: a delayed potassium current which activated at 0 mV and an inactivating calcium-dependent potassium current which activated at -30 mV. Type 2 astrocytes in culture could be induced to fire single regenerative potentials in response to injections of depolarizing current. Single-channel recording demonstrated the presence of an outwardly rectifying chloride channel in both type 2 astrocytes and oligodendrocytes, but this channel could only be observed in excised patches. Oligodendrocytes expressed only one other current: an inwardly rectifying potassium current that is mediated by 30- and 120-pS channels. Because these channels preferentially conduct potassium from outside to inside the cell, and because they are open at the resting potential of the cell, they would be appropriate for removing potassium from the extracellular space; thus it is proposed that oligodendrocytes, besides myelinating axons, play an important role in potassium regulation in white matter. The conductances present in oligodendrocytes suggest a "modulated Boyle and Conway mechanism" of potassium accumulation.

Animals↗
PubMed2005

Decreasing myelin density reflected increasing white matter pathology in Alzheimer's disease--a neuropathological study.

BACKGROUND: White matter disease (WMD) is frequently seen in Alzheimer's disease (AD) at neuropathological examination. It is defined as a subtotal tissue loss with a reduction of myelin, axons and oligodendrocytes as well as astrocytosis. Studies quantitatively defining the myelin loss in AD are scarce. The aim was to develop a method that could provide numerical values of myelin density in AD. The purpose was to compare the myelin contents in increasing grades of pathology of WMD, with age and cortical AD pathology as well as in different regions of the brain in AD. MATERIAL AND METHODS: Sixteen cases with AD and concomitant WMD were investigated with an in-house developed image analysis technique to determine the myelin attenuation with optical density (OD) in frontoparietal, parietal, temporal and occipital white matter on whole brain coronal sections stained for myelin with Luxol Fast Blue (LFB). The OD values in LFB were compared grouped according to Haematoxylin/Eosin (HE) evaluated mild, moderate and severe WMD or normal tissue. The OD values were also correlated with age and cortical AD pathology and compared between the different studied white matter regions. RESULTS: Increasing severity of WMD was associated with a statistically significant OD reduction. No correlation was seen between age and OD or overall cortical AD pathology. The OD values were significantly lower in frontoparietal-compared to occipital white matter. CONCLUSIONS: Myelin loss in AD with WMD is a marked morphologic component of the disease and it is possible to determine the reduction objectively in neuropathological specimens with quantitative measures. This may be of use for clinical diagnostics including brain imaging.

Age Factors↗
PubMed2003

Neuropathological evidence for ischemia in the white matter of the dorsolateral prefrontal cortex in late-life depression.

BACKGROUND: Signal hyperintensities on magnetic resonance imaging in late-life depression are associated with treatment resistance and poor outcome. These lesions are probably vascular in origin and proposed sites for vascular damage include the dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC). METHODS: We therefore examined white matter in these areas for microvascular disease and evidence of ischemia using intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1). We obtained postmortem tissue from elderly depressed (n = 20) and control (n = 20) subjects and blindly rated microvascular disease and ICAM-1 and VCAM-1 amount using quantitative image analysis in sections of the DLPFC, ACC and occipital cortex (OC; control area). RESULTS: We found a significant increase in ICAM-1 in the deep white matter of the DLPFC in the depressed group (p = 0.01) and a trend towards an increase for VCAM-1 (p = 0.10). In the gyral white matter there was a trend towards significance for both molecules (p = 0.07 and 0.10). No differences were found in the ACC or OC or for microvascular disease in any area. CONCLUSIONS: These findings are consistent with white matter ischemia in the DLPFC and lend support to the 'vascular depression' hypothesis. They implicate the DLPFC as an important site in the pathogenesis of late-life depression and have major implications for the understanding and management of late-life depression and raise the possibility of novel treatments being introduced in the future.

Aged↗