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PubMed2007

Lack of correlation between cortical demyelination and white matter pathologic changes in multiple sclerosis.

BACKGROUND: Histopathologic studies have shown that subpial cortical demyelination is extensive in chronic multiple sclerosis (MS). OBJECTIVE: To study whether subpial cortical demyelination in MS is associated with focal or diffuse white matter (WM) pathologic features on magnetic resonance imaging (MR imaging). DESIGN: Comparison of postmortem MR imaging findings with histopathologic findings. SETTING: Brain donations from a general community. PATIENTS: Three patients with MS with extensive cortical demyelination and 3 patients with minor cortical demyelination were selected from an MS autopsy data set. The postmortem MR imaging and histopathologic data of the patients were compared. MAIN OUTCOME MEASURES: Two observers blinded to the results of each other assessed the presence, extent, and distribution of focal and diffuse pathologic changes in WM by MR imaging and by histopathology. RESULTS: Extensive subpial demyelination was not associated with a significant increase in the area of focal and diffuse WM pathologic changes as assessed by Luxol fast blue histochemistry or by MR imaging or with the presence or extent of juxtacortical abnormalities on MR imaging. CONCLUSIONS: The lack of association of MS gray matter demyelination with diffuse or focal WM changes indicates that gray matter demyelination in MS occurs largely independent of WM pathologic changes. The extent or distribution of WM abnormalities cannot be used to identify extensive cortical demyelination in the clinical setting.

Aged↗
PubMed1999

Reduced gray matter volume in schizophrenia.

BACKGROUND: There is emerging evidence that gray matter (GM) is reduced in patients with schizophrenia. Information on the extent of global differences in the 3 principal supertentorial compartments is necessary for interpretation of regional effects. The relation of GM reduction to clinical status and neurocognition also requires examination. METHODS: Magnetic resonance imaging, neurocognitive measures, and clinical assessment of symptoms and functioning were obtained for 130 patients (51 neuroleptic naive, 79 previously treated) and 130 healthy controls (75 men, 55 women in each group). RESULTS: Overall GM volume was reduced in patients compared with controls. This was evident in men (6% reduction) and women (2% reduction) and was already evident at the first presentation of neuroleptic-naive patients. The reduction sustained correction for age and total intracranial volume. Compartmental volumes did not correlate with the severity of positive (r, -0.08 to 0.23) or negative (r, -0.01 to -0.07) symptoms, but GM volume was associated with better premorbid functioning in women (r, 0.36-0.51). Small but significant correlations (r, 0.19-0.44) were observed between GM volume and performance in 6 neurocognitive domains. These correlations varied by diagnosis, most higher in patients, and were moderated by sex. CONCLUSIONS: Gray matter volume reduction in schizophrenia is already evident in men and women at first presentation. While this reduction is not correlated with symptom severity, it is associated with cognitive performance. Since GM development accelerates in the later part of gestation, while white matter growth is primarily postnatal, the results may support the hypothesis that neurodevelopmental processes relate to GM deficit.

Adult↗
PubMed2000

Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder.

BACKGROUND: Major damage to gray and white matter in the prefrontal cortex and autonomic deficits have been found to result in pseudopsychopathic personality in patients with neurological disorders, but it is not known whether people with antisocial personality disorder (APD) in the community who do not have discernable brain trauma also have subtle prefrontal deficits. METHODS: Prefrontal gray and white matter volumes were assessed using structural magnetic resonance imaging in 21 community volunteers with APD (APD group) and in 2 control groups, comprising 34 healthy subjects (control group), 26 subjects with substance dependence (substance-dependent group), and 21 psychiatric controls. Autonomic activity (skin conductance and heart rate) was also assessed during a social stressor in which participants gave a videotaped speech on their faults. RESULTS: The APD group showed an 11.0% reduction in prefrontal gray matter volume in the absence of ostensible brain lesions and reduced autonomic activity during the stressor. These deficits predicted group membership independent of psychosocial risk factors. CONCLUSIONS: To our knowledge, these findings provide the first evidence for a structural brain deficit in APD. This prefrontal structural deficit may underlie the low arousal, poor fear conditioning, lack of conscience, and decision-making deficits that have been found to characterize antisocial, psychopathic behavior.

Adult↗
PubMed2000

Reduced dorsal and orbital prefrontal gray matter volumes in schizophrenia.

BACKGROUND: Converging neuroanatomic, neurophysiological, and neurobehavioral evidence implicate prefrontal subregions in schizophrenia. Neuroanatomic studies with magnetic resonance (MR) imaging enable regional volume parcellation. Inconsistent reports may relate to variable methods and small samples. We attempted to resolve volume differences within sectors of the prefrontal lobe in a large sample, relating volumes to clinical and neurocognitive features. METHODS: Magnetic resonance imaging was performed in 70 patients with schizophrenia (40 men and 30 women; 29 neuroleptic naive and 41 previously treated) and 81 healthy controls (34 men and 47 women). Gray and white matter volumes of the dorsolateral, dorsomedial, orbitolateral, and orbitomedial prefrontal cortex were quantified. Symptoms, functioning, and neurocognition were assessed concurrently. RESULTS: Reduced prefrontal gray matter volume was observed in patients. The reduction was evident for the dorsolateral area in men (9%) and women (11%), for the dorsomedial area only in men (9%), and for orbital regions only in women (23% and 10% for lateral and medial, respectively). The reduction of orbital volume in women was associated with poorer premorbid functioning, more severe negative symptoms, and depression. Volume of dorsal cortex was positively associated with better performance on abstraction and attention tasks across all groups. CONCLUSIONS: Schizophrenia is associated with reduced gray matter volume in prefrontal cortex, which affects men and women in the dorsolateral sector. The effects are moderated by sex for dorsomedial and orbital regions and are related to symptom severity and cognitive function. This is not a by-product of treatment, since the differences are evident in neuroleptic-naive patients.

Adult↗
PubMed2003

Gray and white matter brain abnormalities in first-episode schizophrenia inferred from magnetization transfer imaging.

BACKGROUND: Neuroimaging studies suggest that schizophrenia is associated with gray and possibly white matter changes. It is unclear whether these changes are present at illness onset or which brain structures are selectively affected. New imaging methods such as magnetization transfer imaging may be more sensitive than conventional volumetric imaging to the subtle structural brain changes in schizophrenia. METHODS: High-resolution volumetric T1-weighted images and magnetization transfer images were acquired from 30 patients (29 with first-episode schizophrenia and 1 with schizophreniform psychoses) and 30 control subjects. Images were processed using voxel-based morphometry, which allows whole-brain analysis. RESULTS: Compared with controls, the magnetization transfer ratio (an index of signal loss derived from magnetization transfer imaging) was reduced bilaterally in the medial prefrontal cortex (right greater than left), insula (left greater than right), and white matter incorporating the fasciculus uncinatus (left greater than right) in the patient group. Analysis of the T1-weighted images did not reveal significant volumetric differences between patients and controls. CONCLUSIONS: Gray and white matter abnormalities are present in schizophrenia at illness onset. The magnetization transfer ratio is sensitive to these abnormalities, which cannot be explained by detectable atrophy in our patient group.

Adolescent↗
PubMed2000

Aberrant dendrite growth in central nervous system white matter induced by a mutant proteolipid protein transgene.

Transgenic mice were produced that carry a construct encoding a mutant form of the DM20 isoform of myelin proteolipid protein. The transgene is under the direction of the human Plp gene promoter, which has previously been shown to direct tissue-specific expression of transgenes. Two lines of mice were generated with this construct, both of which express the transgene at extremely low levels. Central nervous system myelination proceeds normally in the transgenic mice. However, in aged transgenic mice, areas of dendrite processes synapsed with axonal termini were observed within the white matter of the spinal cord. This phenotype was accompanied by focal areas of astrocytic hypertrophy and an increase in apoptotic cell death in white matter but not gray matter. One interpretation of these findings is that expression of the mutant DM20 alters signaling between oligodendrocytes and neurons, producing abnormal neurite outgrowth.

Age Factors↗
PubMed1997

Atypical location of cannabinoid receptors in white matter areas during rat brain development.

Previous evidence suggests that the endogenous cannabinoid system could emerge and be operative early during brain development. In the present study, we have explored the distribution of specific binding for cannabinoid receptors in rat brain at gestational day 21 (GD21), postnatal days 5 (PND5) and 30 (PND30), and at adult age (> 70 days after birth) by using autoradiography with [3H]CP-55,940. Our results indicated that specific binding for cannabinoid receptors can be detected in the brain of rat fetuses at GD21 in the classic areas that contain these receptors in adulthood-in particular, in the cerebellum and the hippocampus and, to a lesser extent, in the basal ganglia, several limbic structures, and cerebral cortex. The density of cannabinoid receptors in all these structures increased progressively at all postnatal ages studied until reaching the classical adult values in 70-day-old animals. Interestingly, cannabinoid receptor binding can also be detected at GD21 in regions, in which they are scarcely distributed or not located in the adult brain and that have the particularity of all being enriched in neuronal fibers. Among these were the corpus callosum, anterior commissure, stria terminalis, fornix, white matter areas of brainstem, and others. This atypical location was quantitatively high at GD21, tended to wane at PND5, and practically disappeared at PND30 and in adulthood, with the only exception being the anterior commissure, which exhibited a moderate density for cannabinoid receptors. Moreover, the binding of [3H]CP-55,940 to cannabinoid receptors in the white matter regions at GD21 seems to be functional and involves a GTP-binding protein-mediated mechanism. Thus, the activation of these receptors with an agonist such as WIN-55,212-2 increased the binding of [35S]-guanylyl-5'-O-(gamma-thio)-triphosphate, measured by autoradiography, in the corpus callosum and white matter areas of brainstem of fetuses at GD21. This increase was reversed by coincubation of WIN-55,212-2 with SR141716, a cannabinoid receptor antagonist. As this antagonist is specific for the cerebral cannabinoid receptor subtype, called CB1, we can assert that the signal found for cannabinoid receptor binding in the fetal and early postnatal brain likely corresponds to this receptor subtype. Collectively, all these data suggest the existence of a transient period of the brain development in the rat, around the last days of the fetal period and the first days of postnatal life, in which CB1 receptors appear located in neuronal fiber-enriched areas. During this period, CB1 receptors would be already functional acting through a GTP-binding protein-mediated mechanism. After this transient period, they progressively acquire the pattern of adult distribution. All this accounts for a specific role of the endogenous cannabinoid system in brain development.

Animals↗
PubMed1999

Quantitative analysis of magnetization transfer images of the brain: effect of closed head injury, age and sex on white matter.

Magnetization transfer (MT) imaging has an application in quantitative assessment of cerebral white matter. Previously published postprocessing methods have inherent problems, and therefore a new analysis technique is presented. This technique was found to be more sensitive for white matter changes in patients with a postconcussional syndrome, compared to other methods previously described. Because of the potential application of this technique in longitudinal and group studies, age and sex dependence of the MT ratio (MTR) of white matter were studied. In a group of 51 healthy subjects, a decrease in the mean MTR as well as an increasing distribution width of the MTR was found with increasing age. The mean MTR in males was higher than in females. These results stress the need to take age and sex into account when interpreting MTR data. Magn Reson Med 42:803-806, 1999.

Adult↗
PubMed2000

Prolonged corticosterone treatment of adult rats inhibits the proliferation of oligodendrocyte progenitors present throughout white and gray matter regions of the brain.

It is well established that glucocorticoids inhibit the proliferation of progenitor cells that occurs in the hippocampal dentate gyrus of adult mammals. Active cell proliferation also occurs in the subventricular zone (SVZ) of the lateral ventricle and, to a lesser extent, throughout white and gray matter regions of the adult brain. The aim of the present study was to determine whether extrahippocampal cell proliferation is also affected by glucocorticoids. The cell proliferation marker bromodeoxyuridine (BrdU) was administered to control rats, to adrenalectomized rats, and to rats treated with a daily injection of corticosterone (10 mg/kg) for a period of 15 days. In control and adrenalectomized rats, high to low numerical densities of BrdU-labeled nuclei were detected within the different forebrain regions examined. In rats treated with corticosterone, a dramatic decrease of cell proliferation was detected in the dentate gyrus, but also throughout all white and gray matter regions examined, except for the SVZ of the lateral ventricle. Double-labeling experiments indicated that throughout the different white and gray forebrain regions examined, except for the SVZ, BrdU-labeled nuclei were essentially associated with cells immunostained for the marker of oligodendrocyte progenitors NG2. These data indicate that glucocorticoids inhibit the proliferation of oligodendrocyte precursors located throughout the white and gray matter regions of the adult rat brain. Since the proliferation of oligodendrocyte precursors plays a major role in the processes of remyelination, these data raise the question of possible detrimental effects of therapeutic treatments of CNS trauma based on the administration of glucocorticoids.

Age Factors↗
PubMed2000

Automated segmentation and measurement of global white matter lesion volume in patients with multiple sclerosis.

A fully automated magnetic resonance (MR) segmentation method for identification and volume measurement of demyelinated white matter has been developed. Spin-echo MR brain scans were performed in 38 patients with multiple sclerosis (MS) and in 46 healthy subjects. Segmentation of normal tissues and white matter lesions (WML) was obtained, based on their relaxation rates and proton density maps. For WML identification, additional criteria included three-dimensional (3D) lesion shape and surrounding tissue composition. Segmented images were generated, and normal brain tissues and WML volumes were obtained. Sensitivity, specificity, and reproducibility of the method were calculated, using the WML identified by two neuroradiologists as the gold standard. The average volume of "abnormal" white matter in normal subjects (false positive) was 0.11 ml (range 0-0.59 ml). In MS patients the average WML volume was 31.0 ml (range 1.1-132.5 ml), with a sensitivity of 87.3%. In the reproducibility study, the mean SD of WML volumes was 2.9 ml. The procedure appears suitable for monitoring disease changes over time. J. Magn. Reson. Imaging 2000;12:799-807.

Adult↗
PubMed2000

Magnetic resonance diffusion tensor imaging for characterizing diffuse and focal white matter abnormalities in multiple sclerosis.

High-resolution diffusion tensor imaging (DTI) was performed in 14 patients with clinically definite multiple sclerosis (MS) and the trace of the diffusion tensor ( ) and the fractional anisotropy (FA) were determined in normal appearing white matter (NAWM) and in different types of focal MS lesions. A small but significant increase of the in NAWM compared to control white matter ((840 +/- 85) x 10(-6) mm(2)/sec vs. (812 +/- 59) x 10(-6) mm(2)/sec; P < 0.01) was found. In addition, there was a significant decrease in the FA of normal-appearing regions containing well-defined white matter tracts, such as the genu of the internal capsule. In non-acute lesions, the of T(1)-hypointense areas was significantly higher than that of T(1)-isointense lesions ((1198 +/- 248) x 10(-6) mm(2)/sec vs. (1006 +/- 142) x 10(-6) mm(2)/sec; P < 0. 001), and there was a corresponding inverse relation of FA. Diffusion characteristics of active lesions with different enhancement patterns were also significantly different. DTI with a phase navigated interleaved echo planar imaging technique may be used to detect abnormalities of isotropic and anisotropic diffusion in the NAWM and selected fiber tracts of patients with MS throughout the entire brain, and it demonstrates substantial differences between various types of focal lesions.

Adult↗
PubMed2001

Quantitative (31)P spectroscopic imaging of human brain at 4 Tesla: assessment of gray and white matter differences of phosphocreatine and ATP.

This report describes the implementation and application of a multicompartment analysis of (31)P spectroscopic imaging data to determine the tissue-specific heterogeneities in metabolite content in the human brain and surrounding tissue. Using this information and a multicompartment regression analysis the phosphocreatine and ATP content of "pure" cerebral gray and white matter, the cerebellum, and skeletal muscle was determined in a group of 10 healthy volunteers. The data were converted to mM units using previously reported values for the T(1)s of phosphocreatine and ATP at 4 T, the water content of human brain, and an external reference for absolute quantification. The phosphocreatine concentration in cerebral gray and white matter, the cerebellum, and skeletal muscle was 3.53 +/- 0.33, 3.33 +/- 0.37, 3.75 +/- 0.66, and 25.8 +/- 2.3 mM, respectively. The ATP concentration in cerebral gray and white matter, the cerebellum, and skeletal muscle was 2.19 +/- 0.33, 3.41 +/- 0.33, 1.75 +/- 0.58, and 8.5 +/- 1.9 mM, respectively. Magn Reson Med 45:46-52, 2001.

Adenosine Triphosphate↗
PubMed2007

Autosomal-recessive syndrome with alopecia, hypogonadism, progressive extra-pyramidal disorder, white matter disease, sensory neural deafness, diabetes mellitus, and low IGF1.

We explored the manifestations of an autosomal-recessive multisystemic disorder in several Saudi families. Recognized causes of progressive extra-pyramidal disorder and white matter disease were excluded and the neurological, imaging, endocrine, and skin manifestations of this syndrome described. The onset of these symptoms in these patients began in early adolescence and progressed more rapidly in males. All affected patients had total or partial alopecia, clinical and chemical evidence of hypogonadism (low levels of estradiol and testosterone); females had clear evidence of hypogonadism (streak or absent ovaries), and some patients had diabetes mellitus and/or sensorineural deafness. The constant biochemical abnormality was the low IGF-1. The neurological manifestations included moderate to severe intellectual decline and abnormality of muscle tone and posture with choreo-athetoid and dystonic movements resulting in gait difficulty, dysarthria, difficulty swallowing, and scoliosis. The MRI of brain demonstrated white matter involving cerebellum, brain stem, and cerebral structures, as well as abnormal decreased signal intensity in the basal ganglia with involvement of the substantia nigra. We conclude that the association of hypogonadism, alopecia, and persistent low IGF-1 is a significant autosomal recessive syndrome; it is prevalent in Saudi Arabia. We also demonstrate that the progressive extra-pyramidal disorder, white matter disease, and abnormal signals of the basal ganglia are common features of this syndrome. Sensorineural deafness and diabetes mellitus were recognized features.

Adolescent↗
PubMed2002

N-acetylaspartate is an axon-specific marker of mature white matter in vivo: a biochemical and immunohistochemical study on the rat optic nerve.

Axonal pathology is a major cause of neurological disability in multiple sclerosis. Axonal transection begins at disease onset but remains clinically silent because of compensatory brain mechanisms. Noninvasive surrogate markers for axonal injury are therefore essential to monitor cumulative disease burden in vivo. The neuronal compound N-acetylaspartate, as measured by magnetic resonance spectroscopy, is currently the best and most specific noninvasive marker of axonal pathology in multiple sclerosis. The possibility has been raised, however, that N-acetylaspartate is expressed also by oligodendroglial lineage cells. In order to investigate N-acetylaspartate specificity for white matter axons, transected rat optic nerves were analyzed by high-performance liquid chromatography and immunohistochemistry. In transected adult nerves, N-acetylaspartate and N-acetyl aspartylglutamate decreased in concordance with axonal degeneration and were undetectable 24 days posttransection. Nonproliferating oligodendrocyte progenitor cells, oligodendrocytes, and myelin were abundant in these axon-free nerves. At 24 days posttransection, N-acetylaspartate was increased (42%; p = 0.02) in nontransected contralateral nerves. After transection at postnatal day 4, total N-acetylaspartate decreased by 80% (P14; p = 0.002) and 94% (P20; p = 0.003). In these developing axon-free nerves, 25 to 33% of oligodendrocyte progenitor cells were proliferating. These data validate magnetic resonance spectroscopy measurements of N-acetylaspartate as an axon-specific monitor of central nervous system white matter in vivo. In addition, the results indicate that neuronal adaptation can increase N-acetylaspartate levels, and that 5 to 20% of the N-acetylaspartate in developing white matter is synthesized by proliferating oligodendrocyte progenitor cells.

Age Factors↗
PubMed2002

Sporadic Pick's disease: a tauopathy characterized by a spectrum of pathological tau isoforms in gray and white matter.

Pick's disease is characterized neuropathologically by distinct tau-immunoreactive intraneuronal inclusions known as Pick bodies and by insoluble tau proteins with predominantly three microtubule-binding repeat tau isoforms. However, recent immunohistochemical studies showed that the antibody specific for exon 10, which encodes the fourth microtubule-binding repeat, detected other tau lesions in Pick's disease. To better define the spectrum of tau pathology in Pick's disease, we used biochemical, immunohistochemical, and ultrastructural techniques to analyze the tau isoform composition in 14 Pick's disease brains. Western blot analysis showed that both three and four microtubule-binding repeat pathological tau isoforms are present in gray and white matter of various brain regions. Using phosphorylation-dependent anti-tau antibodies, we show that major tau phosphoepitopes are present in sarcosyl-insoluble gray and white matter regions of Pick's disease brains. Also, for the first time to our knowledge, we demonstrated that isoforms with four microtubule-binding repeat tau isoforms are present in Pick bodies from selected brains. Isolated tau filaments were straight or twisted and formed by three microtubule-binding repeat or four microtubule-binding repeat tau isoforms. Major tau phosphorylation-dependent and exon 10-specific epitopes were present in filaments. Therefore, Pick's disease is characterized by an accumulations of Pick bodies in the hippocampal region and cortex as well as the presence of three and four microtubule-binding repeat tau pathology in both cortical gray and white matter that distinguish this tauopathy from other neurodegenerative disorders.

Aged↗
PubMed2003

Homocysteine, white matter hyperintensities, and cognition in healthy elderly people.

Hyperhomocysteinemia is associated with an increased risk of vascular disease, and recent results suggest that it also could increase the risk of dementia. We examined the relationship between homocysteine and cognitive decline in 1,241 subjects aged 61 to 73 years, followed up over 4 years. Plasma homocysteine levels were determined in all participants as well as cardiovascular risk factors, apolipoprotein E genotype, plasma levels of folate, and vitamin B12. Cognitive performances were assessed repeatedly by using Mini-Mental State Examination, Trail Making Test, Digit Symbol Substitution Test, and Finger Tapping Test. At 2-year follow-up, 841 subjects underwent cerebral magnetic resonance imaging, and white matter hyperintensities were rated visually. Analyses were adjusted for all cardiovascular risk factors. Cross-sectional analyses showed that higher concentrations of homocysteine were significantly related to poorer performances at all neuropsychological tests. Longitudinal analyses confirmed this finding. The odds of cognitive decline was 2.8-fold (p < 0.05) higher in subjects with homocysteine levels above 15 micromol/L compared with those with homocysteine levels below 10 micromol/L. In participants who underwent magnetic resonance imaging, the relationship between homocysteine and cognition was unchanged after taking into account white matter hyperintensities suggesting that white matter hyperintensities do not mediate the association between homocysteine and cognition.

Aged↗
PubMed2005

Selective vulnerability of preterm white matter to oxidative damage defined by F2-isoprostanes.

Periventricular white matter injury (PWMI) is the leading cause of cerebral palsy and chronic neurological disability in survivors of prematurity. Despite the large number of affected children, the pathogenetic mechanisms related to PWMI remain controversial. Through studies of 33 human autopsy brains, we determined that early PWMI was related to oxidative damage that particularly targeted the oligodendrocyte lineage, whereas other neuronal and glial cell types were markedly more resistant. F(2)-isoprostanes, an arachidinate metabolite/lipid peroxidation marker of oxidative damage, were significantly increased in early PWMI lesions but not in cerebral cortex. That deleterious lipid peroxidation accompanied early PWMI was supported by similar increases in F(2)-isoprostanes levels in the cerebral cortex from term infants with hypoxic-ischemic cortical injury. Detection of F(4)-neuroprostanes, a neuronal-specific oxidative damage marker, confirmed that neuroaxonal elements were resistant to injury in cerebral cortex and white matter. Significant protein nitration was not detected in PWMI lesions by 3-nitrotyrosine staining. Significant cellular degeneration was confirmed in early PWMI lesions by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling and a marked depletion of oligodendrocyte progenitors of 71 +/- 8%. Hence, the predilection of preterm infants for PWMI is related to selective lipid peroxidation-mediated injury of cerebral white matter and targeted death of oligodendrocyte progenitors.

Apoptosis↗
PubMed2005

Dominant form of vanishing white matter-like leukoencephalopathy.

Leukoencephalopathy with vanishing white matter syndrome (childhood ataxia with central nervous system hypomyelination/vanishing white matter disease) is an autosomal recessive disorder characterized by the occurrence of acute episodes of deterioration after minor head trauma or infection, and symmetrical demyelination on magnetic resonance with cavitation aspects. Mutations in each of the five subunits of eIF2B have been identified. We report in an affected man and his mother an adult-onset form of childhood ataxia with central nervous system hypomyelination/vanishing white matter disease-like disorder with no mutations in the EIF2B genes and normal guanine nucleotide exchange factor eIF2B activity, suggesting a new dominant inheritance of this syndrome that may involve other genes.

Adult↗