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Deep White Matter (deep + white_matter)
Terms modified by Deep White Matter Selected AbstractsNeuropathological evidence for ischemia in the white matter of the dorsolateral prefrontal cortex in late-life depressionINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 1 2003Alan J. Thomas Abstract 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. Copyright © 2002 John Wiley & Sons, Ltd. [source] Subacute sclerosing panencephalitis: Relationship between clinical stage and diffusion-weighted imaging findingsJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 3 2006Alpay Alkan MD Abstract Purpose To investigate the relationship between clinical stages and apparent diffusion coefficient (ADC) changes in the brain of patients with subacute sclerosing panencephalitis (SSPE). Materials and Methods A total of 18 patients with stage II (N = 11) and III (N = 7) SSPE and 11 age-matched controls underwent routine MRI and diffusion-weighted imaging (DWI). The ADC values were automatically calculated. Seven distinct neuroanatomic structures (frontal, parieto-occipital, and cerebellar white matter; deep white matter; thalamus; basal ganglia; and brainstem) were selected for analysis in the patient and control groups. Results Hyperintensities in the periventricular and subcortical white matters on T2-weighted images and ADC maps were detected in 63.6% of patients with stage II and in all patients with stage III. There were significant differences between stage II and III patients and also between patients and control group in ADC values that obtained from all locations. The highest mean ADC values were calculated in stage III patients. Although MRI and DWI findings were normal in four patients with stage II disease, ADC values were significantly increased when compared with controls. Conclusion The stage of disorder may be independent of DWI appearance during the early stage (stages I and II), even though the brain is affected. Therefore, DWI and ADC values supplemental to routine MRI should also be utilized for lesion detection and definition to enhance diagnostic accuracy in patients with SSPE. J. Magn. Reson. Imaging 2006. © 2006 Wiley-Liss, Inc. [source] An autopsy case of Fabry disease with neuropathological investigation of the pathogenesis of associated dementiaNEUROPATHOLOGY, Issue 5 2008Riki Okeda The pathogenesis of dementia associated with Fabry disease was examined neuropathologically in an autopsy case. The patient was a 47-year-old computer programmer who developed renal failure at the age of 36, necessitating peritoneal dialysis, and thereafter suffered in succession episodic pulmonary congestion, bradyacusia, heart failure, and dementia, before dying of acute myocardial infarction. MRI of the brain demonstrated leuko-araiosis. The CNS parenchyma showed widespread segmental hydropic swelling of axons in the bilateral cerebral and cerebellar deep white matter in addition to neuronal ballooning due to glycolipid storage in a few restricted nuclei and multiple tiny lacunae. Hydropic axonal swelling was also sparsely distributed in the pyramidal tract, pedunculus cerebellaris superior and brachium colliculi inferioris, but wallerian degeneration of these tracts was absent. Additional features included angiopathy of the subarachnoidal arteries due to Fabry disease, such as medial thickening resulting from glycolipid deposition in smooth muscle cells (SMCs) and adventitial fibrosis with lymphocytic infiltration, together with widespread subtotal or total replacement of medial SMCs by fibrosis, associated with prominent intimal fibrous thickening and undulation of the internal elastic membrane of medium-sized (1000,100 ,m diameter) arteries. The findings in this case suggest that axonopathic leukoencephalopathy due to multisegmental hydropic swelling of axons in the bilateral cerebral deep white matter is responsible for the dementia associated with Fabry disease, and may be caused by ischemia resulting from widespread narrowing and stiffening of medium-sized subarachnoidal arteries and progressive heart failure. [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] Methodological aspects of 3D and automated 2D analyses of white matter neuronal density in temporal lobe epilepsyNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 3 2006S. H. Eriksson White matter neuronal density has been correlated with clinical outcome after temporal lobectomy for refractory epilepsy. Both morphometric 2D (two-dimensional) and stereological 3D (three-dimensional) analyses of neuronal density have been performed. 3D analyses are thought to be more accurate than 2D counts, but more time-consuming. We compared 3D and automated 2D measurements in the same specimens. Adjacent 20-µm (for 3D analyses) and 5-µm (for 2D analyses) sections from 10 temporal lobectomies were stained for NeuN immunohistochemistry. Analysis of 100% of a region of interest (ROI) in deep white matter was performed using an image analysis system (Histometrix, Kinetic Imaging, UK). 3D analyses were undertaken using ×,63 magnification (6 h/case). Automated 2D analyses were undertaken using automatic neuronal identification at ×,10 magnification with three to four repeats (1.5 h/case). The range of neuronal densities for 3D measurements was 2120,4910 neurones/mm3, and for automated 2D measurements 17.4,47.1 neurones/mm2. There was a linear correlation between the two methods with an r2 of 0.58. The limits of agreement for the two methods were 1718 to ,2234 neurones/mm3. Count,recount variability was 1.4,9.9% for the 3D and 5.1,36.6% for the automated 2D measurements. We found a wide range of white matter neuronal densities using either analysis. The low agreement between methods, and the high count,recount variability for the automated 2D analyses, indicate that despite being more time-consuming, rigorous 3D stereological analyses have to be performed to obtain reliable results. These findings have implications for studies requiring neuronal counts in normal and disease states. [source] White matter diffusion is higher in Binswanger disease than in idiopathic normal pressure hydrocephalusACTA NEUROLOGICA SCANDINAVICA, Issue 4 2009M. Tullberg Objectives,,, To explore diagnostic differences in periventricular white matter (PWM) and deep white matter (DWM) diffusion patterns in patients diagnosed with Binswanger disease (BD) and in patients diagnosed with probable idiopathic normal pressure hydrocephalus (INPH) using diffusion-weighted imaging (DWI). Materials and methods,,, Apparent diffusion coefficient (ADC) values were calculated in the PWM and DWM in patients with INPH (n = 14) and BD (n = 9) and in controls (n = 10) using an spin echo echo planar imaging single-shot diffusion sequence and region of interest (ROI) analysis. Results,,, Patients with BD had higher ADC values than patients with INPH in the PWM and DWM in the frontal and occipital regions (P < 0.05) and higher values than controls in the frontal PWM and DWM (P < 0.01). After shunt surgery, ADC values were reduced in the frontal PWM in patients with INPH (P < 0.05). Conclusions,,, Increased diffusion in the PWM and DWM in patients with BD may reflect irreversible breakdown of axonal integrity caused by the subcortical ischaemic vascular disease. By contrast, the normal white matter diffusion in patients with INPH indicates structurally intact axons, compatible with the reversibility of this disorder. DWI may be an important non-invasive diagnostic tool for differentiating between INPH and BD and identifying shunt responders and reversible brain damage in patients with INPH. However, the overlap between patients with INPH and BD in this study restricts the predictive value of the method. [source] Brain magnetic resonance imaging abnormalities in neuromyelitis opticaACTA NEUROLOGICA SCANDINAVICA, Issue 4 2008Y. Li Objective,,, Brain abnormalities in neuromyelitis optica (NMO) attracted much attention. Our study was to identify the brain magnetic resonance imaging (MRI) abnormalities in Chinese NMO patients. Methods,,, Patients who fulfilled the latest diagnostic criteria of NMO proposed by Wingerchuk et al. [Neurology 66 (2006) 1485] and whose brain MRI did not meet the multiple sclerosis (MS) criteria of McDonald et al. [Ann Neurol 50 (2001) 121] were selected to perform MRI scanning of the brain, spinal cord and optic nerves. Results,,, Twenty-eight of 33 patients (84.8%) had abnormal MRI findings. Twenty-two patients (66.7%) presented with well-defined brain parenchymal lesions and the other six patients (18.2%) with macroscopic symmetrical diffuse hyperintensities in deep white matter. Fifteen of 22 patients had more than one lesion (,2 lesions) and the other seven patients had single lesion. In the supratentorium, most lesions were punctate or small round dot and non-specific in juxtacortical, subcortical and deep white matter regions, a few were patchy atypical confluent lesions. Brainstem was easily involved (14/33, 42.4%) especially in medulla (7/33, 21.2%). Conclusions,,, This study demonstrates the characteristics of brain MRI abnormalities in Chinese NMO patients, which are helpful to the revision of diagnostic criteria for NMO. [source] | ||||||||||