White Matter Damage In Patients Research Articles

Cerebral white matter injury in haemodialysis patients: a cross-sectional tract-based spatial statistics and fixel-based analysis.

End-stage renal disease (ESRD) patients on maintenance haemodialysis (HD) often have damage to brain white matter (WM) and cognitive impairment. However, whether this damage is caused by maintenance HD or renal dysfunction is unclear. Herein we investigate the natural progression of WM damage in patients with ESRD and the effects of HD on WM using tract-based spatial statistics (TBSS) and fixel-based analysis (FBA). Eighty-one ESRD patients, including 41 with no dialysis (ND) and 40 on HD, and 46 healthy controls (HCs) were enrolled in this study. The differences in WM among the three groups [ESRD patients with HD (ESRD-HD), ESRD patients without HD (ESRD-ND) and HCs] were analysed using TBSS and FBA. Pairwise comparison was then used to compare the differences in WM between two groups. The relationships between WM and neurocognitive assessments/clinical data were analysed in ESRD patients with and without HD. The damage to WM in ESRD-ND and ESRD-HD appeared around the lateral ventricles in TBSS, while FBA reflected that the changes had extended to adjacent WM in the anterior hemisphere, with a larger region in ESRD-HD compared with ESRD-ND and the brainstem was also widely affected in ESRD-HD. The Montreal Cognitive Assessment (MoCA) scores were lower in the ESRD-HD group. RD in the body of the corpus callosum were negatively correlated with MoCA scores in both groups. Fiber density and cross-section (FDC) in the left thalamo-prefrontal projection (T_PREFL) and left and right cingulum (CGL and CGR) were positively correlated with MoCA scores in both groups. Creatinine (Cr) was positively correlated with FDC in some frontal projection fibres in the striatum and thalamus, CG and fronto-pontine tract and was positively correlated with FD mainly in premotor projection fibres in the striatum and thalamus in the ESRD-HD group. Cr was negatively correlated with mean and radial diffusivity in regions of the corona radiata in the ESRD-ND group. FBA is more sensitive in detecting differences between ESRD patients and HCs. When ESRD patients receive maintenance HD, the degree of WM damage may not be aggravated, but the range of damaged WM may be expanded, especially in the anterior hemisphere and brainstem. Some of these changes in the anterior hemisphere may contribute to cognitive decline.

Cerebral white matter damage in patients with end stage kidney disease associates with cognitive impairment

Abstract Background and hypothesis Damages in brain white matter often occurs in individuals with chronic kidney disease, which might be related to their cognitive decline. This study aims to investigate tract specific white matter damage in patients with end stage renal disease by using fixel based analysis. Methods Images of 31 end stage renal disease patients and 16 normal controls (aged: 61.1 ± 10.4 years; 11 men) were acquired from a 1.5 T MR scanner. The patients were subsequently divided into with normal cognition (N = 17, aged: 66.9 ± 7.2 years; 10 men) and cognitive impairment (N = 14, aged: 72.4 ± 9.4 years; 7 men). Cognitive assessment, neurologic, hematologic and biochemical samples were collected. Fixel-based analysis was used to examine the tract-specific damage within white matter. Differences between groups were evaluated through connectivity-based fixel enhancement and non-parametric permutation testing. Correlation with biomarkers was conducted through general linear model. Significance was determined with familywise error-corrected p-value < 0.05. Results Reduced fixel-based metrics were observed in specific tract located the cerebral peduncle, internal capsule, corpus callosum, fornix, and superior corona radiata in patients when compared to normal controls, indicating a reduction in fiber content. The fibers crossing the corpus callosum and the fornix/stria terminalis are particularly vulnerable sites, which can be associated with the decrease in both Mini-Mental State Examination (R2 ranged between 0.420 and 0.556) and Montreal Cognitive Assessment (R2 ranged between 0.425 and 0.509), as well as the plasma concentration of calcium (R2 ranged between 0.207 and 0.322). The plasma concentration of indoxyl sulfate was associated with the descending tracts from right posterior limb of internal capsule to cerebral peduncle (R2 ranged between 0.262 and 0.335). Conclusions Tract specific white matter damage can be noticed in the patients with end stage renal disease, and can be associated with their cognitive decline.

Correlation study between brain damage and anxiety, depression, and cognitive impairment in patients with moderate to severe obstructive sleep apnea hypopnea syndrome using diffusional kurtosis imaging

Objective: To explore the brain white matter damage in patients with moderate to severe obstructive sleep apnea hypopnea syndrome(OSAHS) using diffusional kurtosis imaging(DKI), and to analyze its relationship with anxiety, depression and cognitive impairment in patients. Methods: This was a retrospective case-control study. Fifty confirmed cases (47 males and 3 females) of moderate to severe OSAHS diagnosed by polysomnography(PSG) from November 2017 to December 2022 were selected as OSAHS group(age range from 22 to 65 years old, with median age of 40 years old), and 32 healthy controls(27 males and 5 females) of non-OSAHS diagnosed by PSG were selected as control group(age range from 19 to 56 years old, with median age of 34 years old). DKI scanning, Beck Anxiety Inventory(BAI), Beck Depression Inventory-Ⅱ(BDI-Ⅱ), and Montreal cognitive assessment(MoCA) scores were performed in all subjects. Differences in kurtosis fractional anisotropy(KFA) of various brain regions were compared between the two groups to identify differential brain regions. Correlations were analyzed between KFA reduction and anxiety, depression, and cognitive impairment in OSAHS patients. To study the correlation between brain injury and anxiety, depressive mood, and cognitive dysfunction, statistical methods such as non-parametric tests for two independent samples, chi-square tests, and partial correlation analysis, were used to analyze the evaluation indicators of the two groups. Results: The KFA values in right external capsule, left anterior corona radiata, right anterior corona radiata, left posterior corona radiata, right posterior corona radiata, left superior corona radiata, right superior corona radiata, left superior longitudinal fasciculus, right superior longitudinal fasciculus, genu of corpus callosum, splenium of corpus callosum, body of corpus callosum, posterior cingulate gyrus of moderate to severe OSAHS group were all lower than those in the control group(t=-2.247, -3.028, -3.955, -4.871, -2.632, -2.594, -2.121, -2.167, -3.129, -2.015, -2.317, -2.313, -2.152,P<0.05). For the moderate to severe OSAHS group, the correlation between AHI and KFA values of right posterior corona radiata, right superior corona radiata, left anterior corona radiata, left posterior corona radiata, left superior corona radiata, left superior longitudinal fasciculus, genu of corpus callosum, body of corpus callosum, splenium of corpus callosum were all negative(r=-0.378, -0.307, -0.337, -0.343, -0.341, -0.613, -0.390, -0.384, -0.396, P<0.05). The correlation between LSO2 and KFA values of right anterior corona radiata, right posterior corona radiata, right superior corona radiata, right superior longitudinal fasciculus, left anterior corona radiata, left posterior corona radiata, left superior corona radiata, left superior longitudinal fasciculus, genu of corpus callosum, body of corpus callosum, splenium of corpus callosum, posterior cingulate gyrus were all positive(r=0.330, 0.338, 0.425, 0.312, 0.433, 0.358, 0.410, 0.459, 0.473, 0.659, 0.489, 0.356, P<0.05). The correlation between BAI scores and KFA values of right external capsule, right anterior corona radiata, left posterior corona radiata, left superior corona radiata, body of corpus callosum, splenium of corpus callosum were all negative(r=-0.306, -0.372, -0.296, -0.346, -0.318, -0.386, P<0.05). The correlation between BDI-Ⅱ scores and KFA values of right superior corona radiata, right superior longitudinal fasciculus, left anterior corona radiata, genu of corpus callosum, body of corpus callosum, splenium of corpus callosum were all negative(r=-0.334, -0.289, -0.309, -0.310, -0.503, -0.469, P<0.05). The correlation between MoCA scores and KFA values of right posterior corona radiata, right superior longitudinal fasciculus, left anterior corona radiata, left superior corona radiata, left superior longitudinal fasciculus, genu of corpus callosum, body of corpus callosum, splenium of corpus callosum were all positive(r=0.368, 0.431, 0.324, 0.410, 0.469, 0.384, 0.369, 0.309, P<0.05). Conclusions: With the aggravation of OSAHS, the damage to some brain regions becomes more pronounced in moderate to severe OSAHS patients. These damage brain functional areas are closely related to the anxiety, depression, and cognitive impairment of patients.

Microstructural alterations in white matter and related neurobiology based on the new clinical subtypes of Parkinson's disease.

The advent of new clinical subtyping systems for Parkinson's disease (PD) has led to the classification of patients into distinct groups: mild motor predominant (PD-MMP), intermediate (PD-IM), and diffuse malignant (PD-DM). Our goal was to evaluate the efficacy of diffusion tensor imaging (DTI) in the early diagnosis, assessment of clinical progression, and prediction of prognosis of these PD subtypes. Additionally, we attempted to understand the pathological mechanisms behind white matter damage using single-photon emission computed tomography (SPECT) and cerebrospinal fluid (CSF) analyses. We classified 135 de novo PD patients based on new clinical criteria and followed them up after 1 year, along with 45 healthy controls (HCs). We utilized tract-based spatial statistics to assess the microstructural changes of white matter at baseline and employed multiple linear regression to examine the associations between DTI metrics and clinical data at baseline and after follow-up. Compared to HCs, patients with the PD-DM subtype demonstrated reduced fractional anisotropy (FA), increased axial diffusivity (AD), and elevated radial diffusivity (RD) at baseline. The FA and RD values correlated with the severity of motor symptoms, with RD also linked to cognitive performance. Changes in FA over time were found to be in sync with changes in motor scores and global composite outcome measures. Furthermore, baseline AD values and their rate of change were related to alterations in semantic verbal fluency. We also discovered the relationship between FA values and the levels of α-synuclein and β-amyloid. Reduced dopamine transporter uptake in the left putamen correlated with RD values in superficial white matter, motor symptoms, and autonomic dysfunction at baseline as well as cognitive impairments after 1 year. The PD-DM subtype is characterized by severe clinical symptoms and a faster progression when compared to the other subtypes. DTI, a well-established technique, facilitates the early identification of white matter damage, elucidates the pathophysiological mechanisms of disease progression, and predicts cognitively related outcomes. The results of SPECT and CSF analyses can be used to explain the specific pattern of white matter damage in patients with the PD-DM subtype.

Diffusion tensor imaging techniques show that parkin gene S/N167 polymorphism is responsible for extensive brain white matter damage in patients with Parkinson's disease

ObjectiveTo explore the influence of disease and genetic factors on the white matter microstructure in patients with PD. The white matter microstructural changes in the substantia nigra-striatum system were detected by diffusion tensor imaging (DTI) using the region of interest (ROI) and diffusion tensor tracer (DTT) methods. MethodsPatients with primary Parkinson's disease (PD) without a family history of PD were selected and divided into PD-G/G and PD-G/A groups according to their parkin S/N167 polymorphism. Control groups matched for age, sex, and gene type (G/G and G/A) were also included. Three-dimensional brain volume imaging (3D-BRAVO) and DTI were performed. The microstructural changes in the substantia nigra-striatum system were evaluated by the ROI and DTT methods. The Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Hoehn-Yahr (H–Y) staging, and the third part of the Unified Parkinson's Disease Rating (UPDRS-III) scales evaluated the cognitive and motor function impairment in patients with PD. Independent samples t-test compared normally-distributed data, and the Wilcoxon rank sum test compared measurement or categorical non-normally distributed data. Multiple regression analysis was used to analyze the correlation between various DTI indicators and the MMSE, MoCA, UPDRS-III, and H–Y scores in the PD-G/G and PD-G/A groups. P < 0.05 was considered statistically significant. ResultsThe white matter microstructural changes in the nigrostriatal pathway differed significantly between the PD or PD-G/A and the control group (P < 0.05)The ROI method showed that the left globus pallidus radial diffusivity (RD) value was negatively correlated with the MMSE score (r = −0.404, P = 0.040), and the left substantia nigra (LSN) fractional anisotropy (FA) value was positively correlated with the MoCA score (r = 0.405, P = 0.040) and negatively with the H–Y stage (r = −0.479, P = 0.013).The DTT method showed that the MMSE score was positively correlated with the right substantia nigra (RSN) FA value (r = 0.592, P = 0.001) and negatively with its RD value (r = −0.439, P = 0.025). The H–Y grade was negatively correlated with the number of fibers in the RSN (r = −0.406, P = 0.040). The UPDRS-Ⅲ score was positively correlated with the mean diffusivity (r = 0.420, P = 0.033) and RD (r = 0.396, P = 0.045) values of the LSN, and the AD value of the RSN (r = 0.439, P = 0.025). ConclusionThe DTI technique detected extensive white matter fiber damage in patients with PD, primarily in those with the G/A genotype, that led to motor and cognitivesymptoms.

An investigation of the association between focal damage and global network properties in cognitively impaired and cognitively preserved patients with multiple sclerosis.

The presence of focal cortical and white matter damage in patients with multiple sclerosis (pwMS) might lead to specific alterations in brain networks that are associated with cognitive impairment. We applied microstructure-weighted connectomes to investigate (i) the relationship between global network metrics and information processing speed in pwMS, and (ii) whether the disruption provoked by focal lesions on global network metrics is associated to patients' information processing speed. Sixty-eight pwMS and 92 healthy controls (HC) underwent neuropsychological examination and 3T brain MRI including multishell diffusion (dMRI), 3D FLAIR, and MP2RAGE. Whole-brain deterministic tractography and connectometry were performed on dMRI. Connectomes were obtained using the Spherical Mean Technique and were weighted for the intracellular fraction. We identified white matter lesions and cortical lesions on 3D FLAIR and MP2RAGE images, respectively. PwMS were subdivided into cognitively preserved (CPMS) and cognitively impaired (CIMS) using the Symbol Digit Modalities Test (SDMT) z-score at cut-off value of -1.5 standard deviations. Statistical analyses were performed using robust linear models with age, gender, and years of education as covariates, followed by correction for multiple testing. Out of 68 pwMS, 18 were CIMS and 50 were CPMS. We found significant changes in all global network metrics in pwMS vs HC (p < 0.05), except for modularity. All global network metrics were positively correlated with SDMT, except for modularity which showed an inverse correlation. Cortical, leukocortical, and periventricular lesion volumes significantly influenced the relationship between (i) network density and information processing speed and (ii) modularity and information processing speed in pwMS. Interestingly, this was not the case, when an exploratory analysis was performed in the subgroup of CIMS patients. Our study showed that cortical (especially leukocortical) and periventricular lesions affect the relationship between global network metrics and information processing speed in pwMS. Our data also suggest that in CIMS patients increased focal cortical and periventricular damage does not linearly affect the relationship between network properties and SDMT, suggesting that other mechanisms (e.g. disruption of local networks, loss of compensatory processes) might be responsible for the development of processing speed deficits.

Morphology and pathogenesis of white matter changes in chronic cerebrovascular disease

This review contains up-to-date information on the fundamentals and clinical aspects of white matter disease in chronic progressive cerebrovascular disease with cognitive impairment, the leading risk factors for which are hypertension and cerebral atherosclerosis. Highly informative methods of neuroimaging have contributed significantly to the study of this problem, confirming the important role of white matter changes in the development and progression of cognitive impairment. The full range of the morphological changes in white matter, typical of vascular encephalopathy and cognitive dysfunction, is presented. Chronic hypoperfusion and white matter ischaemia play a leading role in the pathogenesis of white matter changes in vascular dementia development, but alternative hypotheses are also emerging. Further fundamental morphological and clinical studies will help to determine the leading mechanisms of white matter damage in patients with vascular and other age-related forms of dementia. This is necessary for the development of effective methods of treatment and prevention.

White matter damage in patients with mild cognitive impairment in Parkinson's disease.

This study investigates the correlation between white matter structural damage and cognitive impairment in patients with Parkinson's disease (PD) and mild cognitive impairment (MCI). A total of 40 patients with PD were divided into two groups, i.e., a mild cognitive impairment (PD-MCI) and a normal cognitive (PDN) group, and 20 healthy patients were enrolled as the control group. Changes in the white matter structure of patients with PD were evaluated using diffusion tensor imaging (DTI), and cognitive function was evaluated using the Montreal Cognitive Assessment (MoCA) scale and Mini-Mental State Examination (MMSE). Finally, the correlations between the two groups were analyzed. The Unified Parkinson's Disease Rating Scale score was significantly higher in the PD-MCI than in the PDN group (P=0.008). The total MoCA and MMSE scores in the PD-MCI group were significantly lower than in the PDN and control groups (P<0.01). Patients in PDMCI group were tested by MMSE scale, and the abnormal score rate was 60.0%. Among them, 8 PD patients with normal MMSE total score were found to have mild cognitive impairment by MoCA evaluation. When compared with the PDN and control groups, the MoCA scores for visual space, which is assessed as part of the MoCA scale and generally represents bilateral parietal function; naming; memory; and attention were significantly lower in the PD-MCI group (P<0.001). When compared with the PDN group, the fractional anisotropy (FA) values for the right parietal and left occipital lobes were significantly lower in the PD-MCI group (P=0.005; P=0.018). The relationship between MoCA value and right parietal white matter and left occipital white matter was 0.555, 0.474, respectively. A Pearson's correlation test was conducted to compare the FA values and MoCA scores of the various brain areas in the PD-MCI group and revealed a significant positive correlation between the MoCA score and the white matter of the right parietal and left occipital lobes (P<0.01). Patients with PD experience early cognitive impairment, and the MoCA scale can be used for early screening. In addition, the DTI of white matter can highlight early white matter damage. In the current study, the damaged brain areas displayed by DTI were consistent with areas showing decreased MoCA scores and were positively correlated with the severity of PD.

Correlation Analysis Between Local Cerebral Blood Flow and Severity of Vascular Cognitive Dysfunction

Research methods: This paper analyses the correlation between cerebral blood flow perfusion caused by cerebral vascular stenosis and the reduction of patients with cognitive dysfunction and white matter damage. A total of 118 patients with reduced cerebral blood flow perfusion due to cerebrovascular stenosis were selected to be included in the disease group, and 118 patients with no cerebrovascular stenosis and no neurological disease were included in the control group. The cerebral blood flow perfusion index and cognitive function index were compared between the two groups of patients. The correlation between each index and the degree of brain white matter damage was analysed. Results: The scores of brain white matter damage in patients with disease group were higher than those in control group, and cCBV, cCBF, TTP, MTT, MoCA, MMSE, ADL, and WMS were lower than those in control group, and the difference was statistically significant (P &lt; 0.05). cCBV, cCBF, TTP, MTT, and white matter damage scores were highly correlated with MoCA, MMSE, ADL, and WMS (P &lt; 0.05). There is a clear correlation between cerebral vascular perfusion, cognitive dysfunction, and white matter damage in patients with cerebrovascular stenosis. The more severe the perfusion of cerebral blood flow, the more severe the cognitive dysfunction and the white matter damage.

Gray matter atrophy cannot be fully explained by white matter damage in patients with MS

Background: Source-based morphometry (SBM) was recently used for non-random “patterns” of gray matter (GM) atrophy or white matter (WM) microstructural damage. Objective: To assess whether and to what extent such patterns may be inter-related in MS. Methods: SBM was applied to images of GM concentration and fractional anisotropy (FA) in MS patients (n = 41, median EDSS = 1) and normal controls (NC, n = 28). The same procedure was repeated on an independent and similar data set (39 MS patients and 13 NC). Results: We found in MS patterns of GM atrophy and reduced FA (p < 0.05, corrected). Deep GM atrophy was mostly (70%) explained by lesion load in projection tracts and lower FA in posterior corona radiata and thalamic radiation. By contrast, sensorimotor and posterior cortex atrophy was less (50%) dependent from WM damage. All patterns correlated with EDSS (r from −0.33 to −0.56, p < 0.03) while the only cognition-related correlation was between posterior GM atrophy pattern and processing speed (r = 0.45, p = 0.014). Reliability analysis showed similar results. Conclusion: In relatively early MS, we found a close link between deep GM atrophy pattern and WM damage while sensorimotor and posterior cortex patterns were partially independent from WM damage and perhaps related to primary mechanisms. Patterns were clinically relevant.

Microstructural damage of white-matter tracts connecting large-scale networks is related to impaired executive profile in alcohol use disorder.

Alcohol Use Disorders (AUD) is associated with negative consequences on global functioning, likely reflecting chronic changes in brain morphology and connectivity. Previous attempts to characterize cognitive impairment in AUD addressed patients' performance in single domains, without considering their cognitive profile as a whole. While altered cognitive performance likely reflects abnormal white-matter microstructural properties, to date no study has directly addressed the relationship between a proxy of patients' cognitive profile and microstructural damage. To fill this gap we aimed to characterize the microstructural damage pattern, and its relationship with cognitive profile, in treatment-seeking AUD patients. Twenty-two AUD patients and 18 healthy controls underwent a multimodal MRI protocol including diffusion tensor imaging (DTI), alongside a comprehensive neurocognitive assessment. We used a principal component analysis (PCA) to identify superordinate components maximally explaining variability in cognitive performance, and whole-brain voxelwise analyses to unveil the neural correlates of AUD patients' cognitive impairment in terms of different white-matter microstructural features, i.e. fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD) and radial diffusivity (RD). PCA revealed a basic executive component, significantly impaired in AUD patients, associated with tasks tapping visuo-motor processing speed, attention and working-memory. Within a widespread pattern of white-matter damage in patients, we found diverse types of relationship linking WM microstructure and executive performance: (i) in the whole sample, we observed a linear relationship involving MD/RD metrics within both 'superficial' white-matter systems mediating connectivity within large-scale brain networks, and deeper systems modulating their reciprocal connections; (ii) in AUD patients vs. controls, a performance-by-group interaction highlighted a MD/AD pattern involving two frontal white-matter systems, including the genu of corpus callosum and cingulum bundle, mediating structural connectivity among central executive, salience and default mode networks. Alterations of prefrontal white-matter pathways are suggestive of abnormal structural connectivity in AUD, whereby a defective interplay among large-scale networks underpins patients' executive dysfunction. These findings highlight different directions for future basic and translational research aiming to tailor novel rehabilitation strategies and assess their functional outcomes.

Analysis of White Matter Damage in Patients with Multiple Sclerosis via a Novel In Vivo MR Method for Measuring Myelin, Axons, and G-Ratio [Proceedings of the 2017 Young Investigator Award

Analysis of White Matter Damage in Patients with Multiple Sclerosis via a Novel In Vivo MR Method for Measuring Myelin, Axons, and G-Ratio [Proceedings of the 2017 Young Investigator Award

Markers of early target-organ brain damage in essential arterial hypertension: the search continues. Possibilities of diffusion tensor magnetic resonance imaging

The article touches upon the issue of brain as an end-organ target of essential arterial hypertension (AH). The article gives current information about the possibilities and potential clinical application of diffusion-tensor magnetic resonance imaging for the earliest assessment of white matter damage in patients with essential AH. Dataare presented upon the reduction of fractional anisotropy in hypertensive patients and its correlation with blood pressure level.

Superficial white matter damage in anti-NMDA receptor encephalitis

BackgroundClinical brain MRI is normal in the majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. However, extensive deep white matter damage wasrecently identifiedin these patients using diffusion weighted imaging. Here,...

Analysis of White Matter Damage in Patients with Multiple Sclerosis via a Novel In Vivo MR Method for Measuring Myelin, Axons, and G-Ratio.

Myelin and axon volume fractions can now be estimated via MR imaging in vivo, as can the g-ratio, which equals the ratio of the inner to the outer diameter of a nerve fiber. The purpose of this study was to evaluate WM damage in patients with MS via this novel MR imaging technique. Twenty patients with relapsing-remitting MS with a combined total of 149 chronic plaques were analyzed. Myelin volume fraction was calculated based on simultaneous tissue relaxometry. Intracellular and CSF compartment volume fractions were quantified via neurite orientation dispersion and density imaging. Axon volume fraction and g-ratio were calculated by combining these measurements. Myelin and axon volume fractions and g-ratio were measured in plaques, periplaque WM, and normal-appearing WM. All metrics differed significantly across the 3 groups (P < .001, except P = .027 for g-ratio between periplaque WM and normal-appearing WM). Those in plaques differed most from those in normal-appearing WM. The percentage changes in plaque and periplaque WM metrics relative to normal-appearing WM were significantly larger in absolute value for myelin volume fraction than for axon volume fraction and g-ratio (P < .001, except P = .033 in periplaque WM relative to normal-appearing WM for comparison between myelin and axon volume fraction). In this in vivo MR imaging study, the myelin of WM was more damaged than axons in plaques and periplaque WM of patients with MS. Myelin and axon volume fractions and g-ratio may potentially be useful for evaluating WM damage in patients with MS.

Relation between brain temperature and white matter damage in subacute carbon monoxide poisoning.

In the previous studies, carbon monoxide (CO) poisoning showed an imbalance between cerebral perfusion and metabolism in the acute phase and the brain temperature (BT) in these patients remained abnormally high from the acute to the subacute phase. As observed in chronic ischemic patients, BT can continuously remain high depending on impairments of cerebral blood flow and metabolism; this is because heat removal and production system in the brain may mainly be maintained by the balance of these two factors; thus, cerebral white matter damage (WMD) affecting normal metabolism may affect the BT in patients with CO poisoning. Here, we investigated whether the BT correlates with the degree of WMD in patients with subacute CO-poisoning. In 16 patients with subacute CO-poisoning, the BT and degree of WMD were quantitatively measured by using magnetic resonance spectroscopy and the fractional anisotropy (FA) value from diffusion tensor imaging dataset. Consequently, the BT significantly correlated with the degree of WMD. In particular, BT observed in patients with delayed neuropsychiatric sequelae, a crucial symptom with sudden-onset in the chronic phase after CO exposure, might indicate cerebral hypo-metabolism and abnormal hemodynamics like “matched perfusion,” in which the reduced perfusion matches the reduced metabolism.

Injury to white matter tracts in relapsing-remitting multiple sclerosis: A possible therapeutic window within the first 5years from onset using diffusion-tensor imaging tract-based spatial statistics.

DTI studies in multiple sclerosis (MS) reveal white matter (WM) injury that occurs with disease progression. In the present study we aimed to elucidate the relationship of microstructural WM damage in patients with varying periods of disease duration. DTI scans were acquired from 90 MS patients and 25 healthy controls. Patients were grouped to short (<1 year), moderate (1 up to 6 years) and long (6–10 years) disease duration periods. Statistical analyses of the fractional anisotropy (FA) data were performed using tract-based spatial statistics (TBSS). Whole-brain skeletal FA measurements showed a significant decrease between healthy controls and the short MS disease duration group, as well as between moderate disease duration and long disease duration groups, but failed to show a significant difference between short and moderate disease duration groups.Voxelwise analysis revealed clusters of diffuse FA reductions in 40 WM tracts when comparing healthy controls and MS short disease duration group, with the point of maximal significant difference located in the left inferior longitudinal fasciculus.Comparing short with long disease duration groups, progressive FA reduction was demonstrated across 30 WM tracts, with the point of maximal significant difference migrating to the body of the corpus callosum. A non-linear pattern of WM microstructure disruption occurs in RRMS. Alterations are seen early in the disease course within 1 year from onset, reach a plateau within the next 5 years, and only later additional WM changes are detected. An important period of a possible therapeutic window therefore exists within the early disease stage.

Early Detection of Brain White Matter Damage in Patients with Severe OSA

Objectives: Obstructive sleep apnea (OSA) is commonly associated with neuropsychological sequelae, presumably induced by brain injury resulting from intermittent hypoxia. Newer magnetic resonance imaging modalities allow a more accurate examination of fiber integrity of the brain microstructure. Diffusion tensor imaging (DTI) is sensitive to the microstructure of brain tissue. This study is to evaluate the integrity of white matter in OSA patients with DTI. Methods: The subjects underwent a polysomnography study to determine the severity of OSA and DTI scans to detect fiber integrity. Fractional anisotropy (FA), a measure of fiber integrity, was derived from the diffusion tensor, resulting in a whole brain FA map. The FA maps were compared using voxel-based statistics to determine differences between severe OSA and control groups, with age and sex as a covariate. The correlation between FA value and clinical severity was performed. Results: Twenty patients with severe OSA (apnea/hypopnea index, AHI &gt;30/h) and 14 sex- and age-matched healthy volunteers (AHI &lt;5/h) were recruited. The exploratory group-wise comparison showed that severe OSA patients exhibited reduced FA values in several brain clusters, including the white matter underlying amygdala, superior temporal gyrus, inferior parietal lobule, precuneus, postcentral gyrus, anterior cingulate gyrus, claustrum, insula, basal ganglia, tapetum, and cerebral peduncle compared with controls. The FA values were negatively correlated with clinical disease severity. Conclusions: This study indicates that OSA patients have impaired white matter integrity in vulnerable regions, associated with increased disease severity. The findings likely represent the pathological process of the brain in OSA patients.

Alteration of fractional anisotropy and mean diffusivity in glaucoma: novel results of a meta-analysis of diffusion tensor imaging studies.

ObjectivesWe hypothesized that a meta-analysis of existing studies may help to reveal significant changes on diffusion tensor imaging (DTI) in patients with glaucoma. Therefore, a meta-analysis was utilized to investigate the possibility that DTI can detect white matter damage in patients with glaucoma.MethodsThe study design and report adhered to the PRISMA Statement guidelines. DTI studies that compared glaucoma patients and controls were surveyed using PubMed, Web of Science and EMBASE (January 2008 to September 2013). Stata was used to analyze the decrease in fractional anisotropy (FA) and increase in mean diffusivity (MD) in the optic nerve and optic radiation in patients with glaucoma.ResultsEleven DTI studies were identified through a comprehensive literature search, and 10 independent DTI studies of glaucoma patients were eligible for the meta-analysis. A random effects model revealed a significant FA reduction in the optic nerve and optic radiation, as well as a significant MD increase in the tracts. A heterogeneity analysis suggested that FA may be related to glaucoma severity.ConclusionsOur findings revealed that the optic nerve and optic radiation were vulnerable regions in patients with glaucoma and that FA may be correlated with glaucoma severity and age. Furthermore, this study suggests that magnetic resonance imaging in patients with glaucoma may help to provide objective evidence to aid in the diagnosis and management of glaucoma.

Mapping Regional Grey and White Matter Damage in Patients with Progressive Supranuclear Palsy Syndrome (S57.007)

Mapping Regional Grey and White Matter Damage in Patients with Progressive Supranuclear Palsy Syndrome (S57.007)