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AbstractBackgroundMethodResultsConclusionParkinson’s disease is the second most common neurodegenerative disorder with complex and distributed motor and non-motor symptoms. In this study, cortical gray matter (GM) and cerebral white matter (WM) overall atrophy, and asymmetry of atrophy are investigated in PD with normal cognitive function.Forty-eight male Parkinson’s disease(PD) patients with normal cognitive precede (PD-NC), and thirty matched healthy control (HC) subjects were selected from the Parkinson’s Progression Markers Initiative (PPMI) database. Brain structures volumes were extracted using Freesurfer software based on subject 3 tesla MRI images. The normalized volume of cortical GM and cerebral WM were compared in two study groups, and then the asymmetry index (AI) of GM and WM atrophy was also assessed in two groups. Statistical analysis was constructed using a t-test with p < 0.05 of significance.No significant difference was observed in the volume of cortical GM and cerebral WM in the two study groups. The cortical GM asymmetry index in the PD-NC group was significantly (p = 0.01) higher than the HC group, however, no difference was observed for the cerebral WM asymmetry index.Atrophy in cortical GM and WM was not observed between the PD-NC and the HC group, however, the asymmetry index in GM was significant between the two group. It seems that the brain’s bilateral balance has ruptured in PD. Cortical GM asymmetry in PD-NC can be considered a potent biomarker and should be investigated more in the future. In future studies, construction of a longitudinal study on this issue could be useful. [ABSTRACT FROM AUTHOR]

Alzheimer′s disease (AD) is a neurodegenerative disease in the central nerve system with insidious onset and progressive memory loss, cognitive decline, psychotic and behavioral changes. AD has been mainly considered as a grey matter disorder. Nevertheless, recent evidence suggests that myelin impairment may play an important role in AD pathology. It has also been found that myelin pathology may even precede Aβ and tau pathologies. We summarized the evidence of white matter abnormalities from pathology and imaging studies, the role of myelin in cognition and possible mechanism of myelin damage in AD. Myelin damage combined with other pathological injury contributes to the process of AD. Many factors, such as aging, gene, Aβ-mediated toxicity and tau, ischemic injury also cause myelin breakdown. Therefore, elucidating the exact mechanisms leading to the disruption of myelin in AD may help a better understanding of AD, and thereby its prevention and treatment. [ABSTRACT FROM AUTHOR]

Cerebral white matter lesions (WML) are major risk factors for bipolar disorder (BD). However, studies on the association between cerebral WML volume and BD risk are limited. This study aimed to investigate the relationship between cerebral WML volume and BD incidence. This is a secondary retrospective analysis of patients (N = 146, 72 males, 74 females, mean age = 41.77 years) who have previously undergone magnetic resonance imaging examinations. Information was obtained from the Dryad database. Univariate analysis, piecewise linear regression model, and multivariable logistic regression model were used for statistical analysis. A non-linear relationship was recognized between the cerebral WML volume and BD incidence, in which the inflection point of the WML volume was 6,200 mm3. The effect sizes and confidence intervals on the left and right sides of the emphasis point were 1.0009 (1.0003, 1.0015) and 0.9988 (0.9974, 1.0003), respectively. Subgroup analysis (WML volume < 6,200 mm3) showed that the cerebral WML volume (for 0.1 mm3 increase) was positively related to the BD incidence (OR = 1.11, 95% confidence interval [CI] (1.03, 1.21)). Here we show that the cerebral WML volume is positively and non-linearly correlated to the BD risk. Volumetric analysis of WML provide a better understanding of the association between WML and the BD risk, and thereby the pathophysiological mechanisms of BD. Graphical abstract A non-linear relationship between the volume of cerebral white matter lesions (WML) and bipolar disorder (BD) incidence is shown. The cerebral WML volume is positively and non-linearly correlated to the BD risk. The correlation is stronger when the cerebral WML volume was <6,200 mm3. [ABSTRACT FROM AUTHOR]

Background & Objectives: The cerebral small vessel disease (CSVD) manifest as white matter lesion (WML) in magnetic resonance imaging (MRI). The diffusion tensor imaging (DTI) study shows a lower white matter integrity in white matter lesion (WML) and its penumbra region, suggesting cerebral white matter damage. The aim of this study is to establish correlation between the DTI values of white matter with the age related white matter changes (ARWMC) visual rating score and identify predictors of ARWMC score. Methods: 63 brain MRI images of subjects were selected. Relevant clinical information of the subjects which satisfied QRISK2 risk factors were retrieved from the patients' folder. DTI parameters were obtained via postprocessing at OsiriX DTImap workstation. Results: FA frontal (r = -0.36; p = 0.003) and AD frontal (r = -0.26; p = 0.040) had a substantial and negative correlation with the ARWMC score. There was a significant positive correlation shown between the ARWMC score and RD frontal (r = 0.30; p = 0.018). There were positive significant association between the ARWMC score and age (b(95%CI): 0.106 (0.061, 0.151); p<0.001) and QRISK2 score (b(95%CI): 0.235 (0.036, 0.433)). Conclusion: DTI is a good method to study the cerebral white matter integrity. It was found that frontal lobe is the first region affected in relation to ageing, in particular the myelin integrity. Increasing age and higher QRISK2 cardiovascular risk factors were shown to increase the ARWMC score. [ABSTRACT FROM AUTHOR]

Background Myelin loss is a feature of cerebral small vessel disease (cSVD). Although physical activity levels may exert protective effects over cSVD pathology, its specific relationship with myelin content in people living with the cSVD is unknown. Thus, we investigated whether physical activity levels are associated with myelin in community-dwelling older adults with cSVD and mild cognitive impairment. Methods Cross-sectional data from 102 individuals with cSVD and mild cognitive impairment were analyzed (mean age [ SD ] = 74.7 years [5.5], 63.7% female). Myelin was measured using a magnetic resonance gradient and spin echo sequence. Physical activity was estimated using the Physical Activity Scale for the Elderly. Hierarchical regression models adjusting for total intracranial volume, age, sex, body mass index, and education were conducted to determine the associations between myelin content and physical activity. Significant models were further adjusted for white matter hyperintensity volume. Results In adjusted models, greater physical activity was linked to higher myelin content in the whole-brain white matter (R 2change =.04, p =.048). Greater physical activity was also associated with myelin content in the sagittal stratum (R 2change =.08, p =.004), anterior corona radiata (R 2change =.04, p =.049), and genu of the corpus callosum (R 2change =.05, p =.018). Adjusting for white matter hyperintensity volume did not change any of these associations. Conclusions Physical activity may be a strategy to maintain myelin in older adults with cSVD and mild cognitive impairment. Future randomized controlled trials of exercise are needed to determine whether exercise increases myelin content. [ABSTRACT FROM AUTHOR]

Background: Cynical hostility (CH), a specific dimension of hostility that consists of a mistrust of others, has been suggested as a high-risk trait for dementia. However, the influence of CH on the incidence of Alzheimer's disease (AD) remains poorly understood. This study investigated whether late-life CH is associated with AD risk and structural neuroimaging markers of AD. Methods: In community-dwelling older adults from the French ESPRIT cohort (n = 1388), incident dementia rate according to CH level was monitored during an 8-year follow-up and analyzed using Cox proportional hazards regression models. Brain magnetic resonance imaging volumes were measured at baseline (n = 508). Using automated segmentation procedures (Freesurfer 6.0), the authors assessed brain grey and white volumes on all magnetic resonance imaging scans. They also measured white matter hyperintensities volumes using semi-automated procedures. Mean volumes according to the level of CH were compared using ANOVA. Results: Eighty-four participants developed dementia (32 with AD). After controlling for potential confounders, high CH was predictive of AD (HR 2.74; 95% CI 1.10–6.85; p = 0.030) and all dementia types are taken together (HR 2.30; 95% CI 1.10–4.80; p = 0.027). High CH was associated with white matter alterations, particularly smaller anterior corpus callosum volume (p < 0.01) after False Discovery Rate correction, but not with grey matter volumes. Conclusions: High CH in late life is associated with cerebral white matter alterations, designated as early markers of dementia, and higher AD risk. Identifying lifestyle and biological determinants related to CH could provide clues on AD physiopathology and avenues for prevention strategies. [ABSTRACT FROM AUTHOR]

Krabbe Disease (KD) is an autosomal recessive disorder that results from loss-of-function mutations in the GALC gene, which encodes lysosomal enzyme galactosylceramidase (GALC). Functional deficiency of GALC is toxic to myelin-producing cells, which leads to progressive demyelination in both the central and peripheral nervous systems. It is hypothesized that accumulation of psychosine, which can only be degraded by GALC, is a primary initiator of pathologic cascades. Despite the central role of GALC in KD pathomechanism, investigations of GALC deficiency at a protein level are largely absent, due in part, to the lack of sensitive antibodies in the field. Leveraging two custom antibodies that can detect GALC at endogenous levels, we demonstrated that GALC protein is predominantly localized to oligodendrocytes in cerebral white matter of an infant brain, consistent with its functional role in myelination. Mature GALC could also be quantitatively detected as a 26 kDa band by western blotting and correlated to enzyme activity in brain tissues. The p.Ile562Thr polymorphic variant, which is over-represented in the KD population, was associated with reduced mature GALC protein and activity. In three infantile KD cases, homozygous null mutations in GALC lead to deficiency in total GALC protein and activity. Interestingly, although GALC activity was absent, normal levels of total GALC protein were detected by a sandwich ELISA using our custom antibodies in a later-onset KD brain, which suggests that the assay has the potential to differentiate infantile- and later-onset KD cases. Among the infantile KD cases, we quantified a 5-fold increase in psychosine levels, and observed increased levels of acid ceramidase, a key enzyme for psychosine production, and hyperglycosylated lysosomal-associated membrane protein 1, a marker for lysosomal activation, in periventricular white matter, a major pathological brain region, when compared with age-matched normal controls. While near complete demyelination was observed in these cases, we quantified that an early-infantile case (age of death at 10 months) had about 3-fold increases in both globoid cells, a pathological hallmark for KD, and CD8-positive T lymphocytes, a pathological marker for multiple sclerosis, in the white matter when compared with a slower progressing infantile case (age of death at 21 months), which suggests a positive correlation between clinical severity and neuropathology. Taken together, our findings have advanced the understanding of GALC protein biology in the context of normal and KD brain white matter. We also revealed new neuropathological changes that may provide insights to understand KD pathogenesis.

Although the term sulcus is known for almost four centuries, its formal, precise, consistent, constructive, and quantitative definition is practically lacking. As the cerebral sulci (and gyri) are vital in cortical anatomy which, in turn, is central in neuroeducation and neuroimage processing, a new sulcus definition is needed. The contribution of this work is threefold, namely to (1) propose a new, morphology‐based definition of the term sulcus (and consequently that of gyrus), (2) formulate a constructive method for sulcus calculation, and (3) provide a novel way for the presentation of sulci. The sulcus is defined here as a volumetric region on the cortical mantle between adjacent gyri separated from them at the levels of their gyral white matter crest lines. Consequently, the sulcal inner surface is demarcated by the crest lines of the gyral white matter of its adjacent gyri. Correspondingly, the gyrus is defined as a volumetric region on the cortical mantle separated from its adjacent sulci at the level of its gyral white matter crest line. This volumetric sulcus definition is conceptually simple, anatomy‐based, educationally friendly, quantitative, and constructive. Considering the sulcus as a volumetric object is a major differentiation from other works. Based on the introduced sulcus definition, a method for volumetric sulcus construction is proposed in two, conceptually straightforward, steps, namely, sulcal intersection formation followed by its propagation which steps are to be repeated for every sulcal segment. These sulcal and gyral constructions can be automated by applying existing methods and public tools. As a volumetric sulcus forms an imprint into the white matter, this enables prominent sulcus presentation. Since this type of presentation is novel yet unfamiliar to the reader, also a dual surface presentation was proposed here by employing the spatially co‐registered white matter and cortical surfaces. The results were presented as dual surface labeled sulci on eight standard orthogonal views, anterior, left lateral, posterior, right lateral, superior, inferior, medial left, and medial right by using a 3D brain atlas. Moreover, additional 108 labeled images were created with sulcus‐oriented views for 27 individual left and right sulci forming 54 dual white matter‐cortical surface images strengthening in this way the educational value of the proposed approach. These images were included for public use in the NOWinBRAIN neuroimage repository with over 7700 3D images available at www.nowinbrain.org. The results demonstrated the superiority of white matter surface sulci presentation over the standard cortical surface and cross‐sectional presentations in terms of sulcal course, continuity, size, shape, width, depth, side branches, and pattern. To my best knowledge, this is the first work ever presenting the labeling of sulci on all cerebral white matter surfaces as well as on dual white matter‐cortical surfaces. Additionally to neuroeducation, three other applications of the proposed approach were discussed, sulcal reference maps, sulcus quantification in terms of new parameters introduced here (sulcal volume, wall skewness, and the number of white matter basins), and an atlas‐assisted tool for exploration and studying of cerebral sulci and gyri. [ABSTRACT FROM AUTHOR]

Background: To examine structural connectivity of white matter tracts in patients with Pantothenate Kinase-Associated Neurodegeneration (PKAN) dystonia and identify those ones which correlate negatively to severity of symptoms.Methods: In a group of 41 patients suffering from PKAN dystonia and an age- and gender-matched control group, white matter tractography was carried out, based on diffusion tensor imaging magnetic resonance data. Postprocessing included assessment of Quantitative Anisotropy (QA) using q-space diffeomorphic reconstruction in order to reduce influence of iron accumulation in globus pallidus of patients.Results: Whole brain tractography presented significantly reduced QA values in patients (0.282 ± 0.056, as compared to controls (0.325 ± 0.046, p < 0.001). 9 fiber clusters of tracts correlated negatively to the dystonia score of patients: the middle cerebellar peduncle and the tracts of both cerebellar hemispheres as well as corpus callosum, forceps minor, the superior cortico-striate tracts and the superior thalamic radiations of both cerebral hemispheres (False Discovery Rate FDR = 0.041).Conclusion: The finding of a reduced global structural connectivity within the white matter and of negative correlation of motor system-related tracts, mainly those between the basal ganglia, cortical areas and the cerebellum, fits well to the concept of a general functional disturbance of the motor system in PKAN. [ABSTRACT FROM AUTHOR]

Depression is a common co-morbidity in asthma, worsening asthma control and impairing quality of life. Previous studies have reported a higher risk of cognitive deficit in depression, yet little research has focused on the level of cognition in asthmatic patients with depression. Evidence shows that inflammation may play an important role in both asthma and depression. Cerebral white matter injury, possibly induced by inflammation, has been associated with depression. This study assesses cognitive function in patients with asthma and a depression comorbidity, compared to patients with asthma only or depression only. Four groups were studied: Asthma comorbid Depression group (A + D, n = 26), Depression group (D, n = 25), Asthma group (A, n = 33) and Normal controls (N, n = 28). Cognitive function was evaluated using Montreal Cognitive Assessment (MoCA). Inflammatory cytokines were measured, including interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), high-mobility group box 1(HMGB1) and Netrin-1. Cerebral white matter injury was assessed by serum myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG), and their correlations with cognitive performance were calculated. A + D group showed the highest incidence of cognitive deficit, with the cognitive domain particularly affected. Compared to N group, serum levels of IL-6, HMGB1, Netrin-1, MBP and MOG were significantly elevated in A + D group. MOG level negatively correlated with the MoCA score. Patients with comorbidities presented with more severe cognitive deficits and higher levels of inflammatory cytokines. Cerebral white matter injury may account for the cognitive deficit in patients and MOG could be a potential biomarker for this process. [ABSTRACT FROM AUTHOR]

Objective: Psychosis spectrum disorders are associated with cerebral changes, but the prognostic value and clinical utility of these findings are unclear. Here, we applied a multivariate statistical model to examine the predictive accuracy of global white matter fractional anisotropy (FA) for transition to psychosis in individuals at ultra‐high risk for psychosis (UHR). Methods: 110 UHR individuals underwent 3 Tesla diffusion‐weighted imaging and clinical assessments at baseline, and after 6 and 12 months. Using logistic regression, we examined the reliability of global FA at baseline as a predictor for psychosis transition after 12 months. We tested the predictive accuracy, sensitivity and specificity of global FA in a multivariate prediction model accounting for potential confounders to FA (head motion in scanner, age, gender, antipsychotic medication, parental socioeconomic status and activity level). In secondary analyses, we tested FA as a predictor of clinical symptoms and functional level using multivariate linear regression. Results: Ten UHR individuals had transitioned to psychosis after 12 months (9%). The model reliably predicted transition at 12 months (χ2 = 17.595, p = 0.040), accounted for 15–33% of the variance in transition outcome with a sensitivity of 0.70, a specificity of 0.88 and AUC of 0.87. Global FA predicted level of UHR symptoms (R2 = 0.055, F = 6.084, p = 0.016) and functional level (R2 = 0.040, F = 4.57, p = 0.036) at 6 months, but not at 12 months. Conclusion: Global FA provided prognostic information on clinical outcome and symptom course of UHR individuals. Our findings suggest that the application of prediction models including neuroimaging data can inform clinical management on risk for psychosis transition. [ABSTRACT FROM AUTHOR]

Background: Magnetic resonance imaging of the internal auditory meatus frequently detects incidental white matter hyperintensities. This study investigated the association between these and the risk of stroke and transient ischaemic attack, or myocardial infarction. Methods: The records of patients with incidental white matter hyperintensities were reviewed, and data were collected on: age, sex, cardiovascular risk factors, and incidence of stroke and transient ischaemic attack, or myocardial infarction, five years later. The risk factors associated with vascular events were explored. Results: Of 6978 patients, 309 (4.4 per cent) had incidental white matter hyperintensities. Of these, 20 (6.5 per cent) had a stroke or transient ischaemic attack within five years, and 5 (1.7 per cent) had a myocardial infarction. The number of cardiovascular risk factors was significantly associated with the incidence of stroke and transient ischaemic attack (p = 0.004), and myocardial infarction (p = 0.023). Conclusion: The number of cardiovascular risk factors predicts the likelihood of vascular events; appropriate risk factor management is recommended for patients with incidental white matter hyperintensities of presumed vascular origin. [ABSTRACT FROM AUTHOR]

Aim:Cerebral white matter hyperintensities (WMLs) are known to be observed in migraine patients but there only are a handful of studies focused on WMLs in migraine with aura (MWA). In this study, we aimed to investigate the frequency of WML and demographic and environmental factors associated with WML in patients with MWA.Methods:A total of 112 patients diagnosed with migraine were enrolled. Detailed systemic and neurological examinations, blood pressure, weight and height measurements, presence of hypertension, smoking status, clinical and demographical data and visual analog scale, allodynia symptom checklist (ASC) and migraine disability assessment scale scores were recorded. The migraine groups with and without aura were compared statistically. A logistic regression analysis was performed to analyse the risk factors for the development of WMLs.Results:Supratentorial and periventricular WMLs were more frequent in patients with MWA (p=0.008). Presence of aura and longer disease duration were independent risk factors for the development of WMLs (p=0.0020 and p=0.019, respectively). Migraine attack frequency, and ASC scores were higher in patients with MWA (p=0.005, p=0.015 and p

Purpose of the study. Concussion does not cause any lesions available for visualization using computed tomography and magnetic resonance imaging. However, it can cause changes at the microstructural level, which can be detected by the diffusion-tensor imaging. The purpose of this study is to identify the effect of acute concussion on diffusion parameters in the corpus callosum, corticospinal tract, and thalamus in children.Patients and methods. Fractional anisotropy and the apparent diffusion coefficient were determined in 11 patients with a diagnosis of concussion (41 ± 19 hours from the moment of injury) and in 11 healthy subjects. Philips Achieva dStream 3T magnetic resonance imager was used. Diffusion tensor imaging data were processed in the Philips Intellispace Portal program in the Fibertrack section.Results. Fractional diffusion anisotropy significantly increases and the apparent diffusion coefficient decreases in the thalamus of patients with concussion. In corpus callosum there is a growth trend in fractional anisotropy.Conclusion. The detected changes indicate the initial stage of cell edema in the thalamus caused by concussion. Diffusion-tensor imaging is the only magnetic resonance imaging method which may be sensitive to this pathology.

Background and purpose: Although two white matter hyperintensity (WMH) probability maps of healthy older adults already exist, they have several limitations in representing the distribution of WMH in healthy older adults, especially Asian older adults. We constructed and validated a WMH probability map (WPM) of healthy older Koreans and examined the age-associated differences of WMH. Methods: We constructed WPM using development dataset that consisted of high-resolution 3D fluid-attenuated inversion recovery images of 5 age groups (60–64 years, 65–69 years, 70–74 years, 75–79 years, and 80+ years). Each age group included 30 age-matched men and women each. We tested the validity of the WPM by comparing WMH ages estimated by the WPM and the chronological ages of 30 healthy controls, 30 hypertension patients, and 30 S patients. Results: Older age groups showed a higher volume of WMH in both hemispheres (p

Aim: Cerebral white matter hyperintensities (WMLs) are known to be observed in migraine patients but there only are a handful of studies focused on WMLs in migraine with aura (MWA). In this study, we aimed to investigate the frequency of WML and demographic and environmental factors associated with WML in patients with MWA. Methods: A total of 112 patients diagnosed with migraine were enrolled. Detailed systemic and neurological examinations, blood pressure, weight and height measurements, presence of hypertension, smoking status, clinical and demographical data and visual analog scale, allodynia symptom checklist (ASC) and migraine disability assessment scale scores were recorded. The migraine groups with and without aura were compared statistically. A logistic regression analysis was performed to analyse the risk factors for the development of WMLs. Results: Supratentorial and periventricular WMLs were more frequent in patients with MWA (p=0.008). Presence of aura and longer disease duration were independent risk factors for the development of WMLs (p=0.0020 and p=0.019, respectively). Migraine attack frequency, and ASC scores were higher in patients with MWA (p=0.005, p=0.015 and p<0.001, respectively). Conclusion: Our results show a significant increase in nonspecific WMLs in patients with MWA. A longer disease duration and presence of aura are significant risk factors for development of these lesions. Our findings warrant further research to validate our result. [ABSTRACT FROM AUTHOR]

Hypomyelination is defined by the evidence of an unchanged pattern of deficient myelination on two MRIs performed at least 6 months apart in a child older than 1 year. When the temporal criteria are not fulfilled, and the follow-up MRI shows a progression of the myelination even if still not adequate for age, hypomyelination is excluded and the pattern is instead consistent with delayed myelination. This can be mild and nonspecific in some cases, while in other cases there is a severe delay that in the first disease stages could be difficult to differentiate from hypomyelination. In hypomyelinating leukodystrophies, hypomyelination is due to a primary impairment of myelin deposition, such as in Pelizaeus Merzabcher disease. Conversely, myelin lack is secondary, often to primary neuronal disorders, in delayed myelination and some condition with hypomyelination. Overall, the group of inherited white matter disorders with abnormal myelination has expanded significantly during the past 20 years. Many of these disorders have only recently been described, for many of them only a few patients have been reported and this contributes to make challenging the diagnostic process and the interpretation of Next Generation Sequencing results. In this chapter, we review the clinical and radiologic features of rare and lesser known forms of hypomyelination and delayed myelination not mentioned in other chapters of this handbook., (Copyright © 2024 Elsevier B.V. All rights are reserved, including those for text and data mining, AI training, and similar technologies.)

Abstract Sleep complaints and brain changes co-occur in older adulthood, but the temporal relation between these processes is poorly understood. Poor sleep may destabilize axonal integrity and deteriorate white matter, but white matter pathology can also precede sleep complaints. Our objective was to explore a prospective, possibly bi-directional association between subjective sleep complaints and micro- and macro-structural properties of cerebral white matter. We assessed sleep complaints and brain magnetic resonance imaging at two time-points (2006–2008 and 2011–2014) in a population-based cohort including 2529 participants (56 ± 6 years old, 55% women). Sleep complaints were assessed with the Pittsburgh Sleep Quality Index. White matter lesion (WML) volume was assessed from fluid-attenuated inversion recovery images and global and tract-specific white matter microstructural integrity with diffusion tensor imaging. Sleep complaints at baseline were not associated with changes in WML volume or global white matter microstructure. In tract-specific analyses, however, sleep complaints were associated with reduced microstructural integrity in two white matter tracts projecting to the brainstem, but only when uncorrected for multiple testing. Likewise, we found no evidence for the reverse association; micro- or macro-structural properties of white matter were not related to changes in sleep complaints over time. This study provides evidence against the hypothesis that sleep complaints lead to white matter changes in the aging brain, and shows that white matter properties do not underlie sleep complaints in older persons. As subjective sleep complaints increase in later life, it is important to demonstrate that these are not etiologically related to cerebral white matter pathology. Highlights • Hypotheses that poor sleep disturbs white matter are based on cross-sectional data. • This prospective bidirectional study in 2529 older adults provides evidence against this hypothesis. • Sleep complaints are no antecedent or sequel of white matter changes in the aging brain. • The increase in sleep complaints and brain changes with aging may be unrelated processes. [ABSTRACT FROM AUTHOR]

Abstract Background Studies of white matter connectivity in children with disruptive behavior have yielded inconsistent results, possibly owing to the trait's heterogeneity, which comprises diverse symptoms like physical aggression, irritability, and delinquency. This study examined associations of global and specific white matter connectivity with childhood disruptive behavior problems, while accounting for their complex multidimensionality. Methods In a large cross-sectional population-based study of 10-year-old preadolescents (n = 2567), we assessed four previously described empirically derived dimensions of disruptive behavior problems using the Child Behavior Checklist: physical aggression, irritability, disobedient behavior, and delinquent behavior. Global and specific white matter microstructure was assessed by diffusion tensor imaging. Results Global fractional anisotropy and mean diffusivity were not associated with broad measures of disruptive behavior, e.g., Child Behavior Checklist externalizing problems scale. Global fractional anisotropy was negatively associated with delinquent behavior (β = −.123, p false discovery rate adjusted =.028) and global mean diffusivity was positively associated with delinquent behavior (β =.205, p false discovery rate adjusted < 0.001), suggesting reduced white matter microstructure in preadolescents with higher levels of delinquent behavior. Lower white matter microstructure in the inferior longitudinal fasciculus, superior longitudinal fasciculus, cingulum, and uncinate underlie these associations. Global white matter microstructure was not associated with physical aggression, irritability, or disobedient behavior. Conclusions Delinquent behavior, a severe manifestation of childhood disruptive behavior, was associated with lower white matter microstructure in tracts connecting frontal and temporal lobes. These brain regions are involved in decision making, reward processing, and emotion regulation. This study demonstrated that incorporating the multidimensional nature of childhood disruptive behavior traits shows promise in advancing the search for elucidating neurobiological correlates of disruptive behavior. [ABSTRACT FROM AUTHOR]

Background: Mutations in AIMP1, which plays an important role in the development and maintenance of axon-cytoskeleton integrity and regulating neurofilaments, cause neurodegeneration of variable severity and white matter abnormalities.Methods: From the patient records we analyzed the clinical evaluation, molecular genetics, neurodiagnostic, and neuroradiological investigations.Results: We describe six members of a large consanguineous family with a phenotype of severe neurodegeneration in the form of developmental delays, progressive microcephaly, epilepsy, and failure to thrive. MRI showed callosal atrophy and T2 hyperintensity in the superficial white matter. The periventricular and deep white matter structures were, however, preserved. MR spectroscopy demonstrated N-acetylaspartate preservation without evidence of neuroinflammation. Exome sequencing showed a novel homozygous mutation of the AIMP1 gene in all individuals: c.917A>G (p.(Asp306Gly)).Conclusions: This novel homozygous mutation of the AIMP1 gene is characterized by preserved development of the periventricular and deep white matter structures as demonstrated by MRI and MR spectroscopy correlation. [ABSTRACT FROM AUTHOR]

Oxycodone-induced leukoencephalopathy is a rare diagnosis that should be considered in unconscious patients with appropriate history. We describe a case of a 57-year-old unconscious woman who required intubation and did not respond to naloxone infusion. The unconsciousness was initially thought to be due to hypoxic brain injury. However, a further review of brain imaging showed characteristic features of oxycodone-induced leukoencephalopathy. We describe the pathological and radiological features of this condition, and provide a concise review of the limited literature on this condition. Accurate diagnosis of this condition will be valuable to clinicians and patients in terms of their medium-term and long-term prognosis, and potential for rehabilitation. [ABSTRACT FROM AUTHOR]

Leukoaraiosis is a pathological appearance of the brain white matter, which has long been believed to be caused by perfusion disturbances within the arterioles perforating through the deep brain structures. Due to its complex etiopathogenesis and clinical relevance, leukoaroisosis has been investigated in a multitude of studies. As regards the clinical implications of leukoaraiosis, this neuroimaging finding is strongly related to ischaemic stroke, unfavourable course of ischaemic stroke in the acute phase, worse long-term outcomes, and cognitive disturbances. The morphological changes in the deep white matter that are collectively described as leukoaraiosis, despite a seemingly homogenous appearance, probably resulting from various causes, such as atherosclerosis, neurotoxic factors including radiation therapy and chemotherapy, and neuroinfections. Based on our experience and recent literature, we present the symptomatology of leukoaroisosis and similar radiological abnormalities of the cerebral white matter. [ABSTRACT FROM AUTHOR]