Obstructive sleep apnea impairs white matter integrity in vulnerable regions, and this impairment is associated with increased disease severity. The possible interactions between systemic inflammation and central nervous system microstructural damage may represent variant hypoxic patterns and their consequent processes in OSA.

Background. Parkinson’s disease (PD) is a common neurodegenerative disease associated with accumulation of misfolding proteins and increased neuroinflammation, which may further impair the glymphatic system. The purpose of this study was to utilize diffusion tensor image analysis along the perivascular space (DTI-ALPS) to evaluate glymphatic system activity and its relationship with systemic oxidative stress status in PD patients. Methods. Magnetic resonance imaging and neuropsychological tests were conducted on 25 PD patients with normal cognition (PDN), 25 PD patients with mild cognitive impairment (PD-MCI), 38 PD patients with dementia (PDD), and 47 normal controls (NC). Oxidative stress status was assessed by plasma DNA level. Differences in ALPS-index among the subgroups were assessed and further correlated with cognitive functions and plasma DNA levels. Results. The PD-MCI and PDD groups showed significantly lower ALPS-index compared to normal controls. The ALPS-index was inversely correlated with plasma nuclear DNA, mitochondrial DNA levels, and cognitive scores. Conclusions. Lower diffusivity along the perivascular space, represented by lower ALPS-index, indicates impairment of the glymphatic system in PD patients. The correlation between elevated plasma nuclear DNA levels and lower ALPS-index supports the notion that PD patients may exhibit increased oxidative stress associated with glymphatic system microstructural alterations.

BackgroundSystemic inflammation, neurocognitive impairments, and morphologic brain changes are associated with obstructive sleep apnea (OSA). Understanding their longitudinal evolution and interactions after surgical treatment provides clues to the pathogenesis of cognitive impairment and its reversibility. In the present study, we investigate clinical disease severity, systemic inflammation, cognitive deficits, and corresponding gray matter volume (GMV) changes in OSA, and the modifications following surgery.MethodsTwenty-one patients with OSA (apnea-hypopnea index, AHI > 5) and 15 healthy volunteers (AHI < 5) underwent serial evaluation, including polysomnography, flow cytometry for leukocyte apoptosis categorization, cognitive function evaluation, and high-resolution brain scan. Disease severity, leukocyte apoptosis, cognitive function, and imaging data were collected to assess therapeutic efficacy 3 months after surgery.ResultsPre-operatively, patients presented with worse cognitive function, worse polysomnography scores, and higher early leukocyte apoptosis associated with increased insular GMV. There was reduced GMV in the anterior cingulate gyrus before and after surgery in the cases compared to that in controls, suggesting an irreversible structural deficit. Post-operatively, there were significant improvements in different cognitive domains, including attention, executive and visuospatial function, and depression, and in early leukocyte apoptosis. There was also a significant decrease in GMVs after treatment, suggesting recovery from vasogenic edema in the precuneus, insula, and cerebellum. Improvement in early leukocyte apoptosis post-surgery predicted better recovery of precuneus GMV.ConclusionsIn OSA, increased disease severity and systemic inflammation can alter GMV in vulnerable regions. Surgical treatment may improve disease severity and systemic inflammation, with subsequent recovery in brain structures and functions.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-0887-8) contains supplementary material, which is available to authorized users.

Objectives The aim of this study was to evaluate the relationship between cognitive impairment and brain perfusion using arterial spin labelling (ASL) in end-stage renal disease (ESRD) patients undergoing PD. Methods ESRD patients undergoing PD were recruited. Laboratory screening, neuropsychological tests and ASL magnetic resonance imaging (MRI) were conducted prior to and after 6 months of PD. Age- and sex-matched normal subjects without ESRD served as the control group. Comparisons of regional CBF between ESRD patients before or after undergoing PD and normal controls were performed. Correlations between biochemical, neuropsychological and CBF data were also conducted to evaluate the relationships. Results ESRD patients showed poor performance in many of the neuropsychological tests; PD improved cognition in some domains. Pre-PD patients had higher mean CBF than post-PD patients and normal controls, but no significant difference was found between the normal controls and post-PD patients. Negative correlations were observed pre-PD (regional CBF in left hippocampus vs. perseverative responses, r = -0.662, p = 0.014), post-PD (mean CBF vs. haemoglobin level, r = -0.766, p = 0.002), and before and after PD (change in CBF in the left putamen vs. change in haematocrit percentage, r = -0.808, p = 0.001). Conclusion Before PD, ESRD patients had increased cerebral perfusion that was related to poorer executive function, especially in the left hippocampus. Post-PD patients performed better in some cognitive test domains than pre-PD patients. The degree of anaemia, i.e., haemoglobin level or haematocrit percentage, might predict cognitive impairment in PD patients. Key Points • In this study, ESRD patients before PD had cerebral hyperperfusion that was related to poorer executive function. • Post-PD patients performed better in some cognitive test domains than pre-PD patients did. • The degree of anaemia might predict cognitive impairment in PD patients. Electronic supplementary material The online version of this article (10.1007/s00330-018-5675-9) contains supplementary material, which is available to authorized users.

BackgroundChronic neuropsychological sequelae may occur in patients with tuberculous meningitis (TBM). The impact of structural abnormalities on the clinical performance of patients with TBM is unknown. This study applied the Diffeomorphic Anatomical Registration Through Exponentiated Lie Algebra (DARTEL) voxel-based morphometry (VBM) to determine if gray matter deficits in TBM are associated with acute presentations and chronic cognitive impairment.MethodsSeventeen patients with TBM who discontinued their anti-TB therapy for more than six months, and 17 age-, sex-, and education-matched healthy subjects were enrolled. Differences in gray matter volume (GMV) between patients and healthy controls were investigated using DARTEL-VBM to determine structural abnormalities. Disease severity during the acute stage was scored by clinical profiles and conventional imaging findings. Correlations among chronic structural deficits, cognitive impairment, and initial disease severity were assessed.ResultsThe patients with TBM had worse neuropsychological subtest performances than the healthy controls. Compared to the controls, the patients showed smaller GMVs in the right thalamus, right caudate nucleus, right superior and middle temporal gyrus, right precuneus, and left putamen (p < 0.001). The smaller GMVs in the right thalamus, right superior temporal gyrus, right precuneus, left putamen, and right caudate nucleus (p < 0.05) were further associated with worse cognitive function. More severe initial disease also correlated with smaller GMVs in the right caudate nucleus (p < 0.05).ConclusionMultiple domain cognitive impairment may persist in patients with chronic TBM even after appropriate treatment. Worse initial disease severity may contribute to the vulnerability of brain tissue to damage, with subsequent neuropsychological consequences.

Background: Sarcopenia is critically associated with morbidity and mortality in the progression of Parkinson's disease (PD). However, analyses of clinical severity and brain changes, such as white matter (WM) alterations in PD patients with sarcopenia are limited. Further understanding of the factors associated with sarcopenia may provide a focused screen and potential for early intervention in PD patients. Methods: 52 PD patients and 19 healthy participants accepted dual-energy X-ray absorptiometry to measure the body composition. Using diffusion tensor imaging, the difference of WM integrity was measured between PD patients with sarcopenia (PDSa) and without sarcopenia (PDNSa). Multivariate analysis was performed to explore the relationships between clinical factors, WM integrity, and sarcopenia in PD patients. Results: 21 PD patients (40.4%) had sarcopenia. PDSa had a higher Unified Parkinson's Disease Rating Scale (UPDRS III) score, lower body mass index (BMI) and lower fat weight compared with the PDNSa. Additionally, PDSa patients exhibited lower fractional anisotropy accompanied by higher radial diffusivity and/or higher mean diffusivity in the fronto-striato-thalamic circuits, including bilateral cingulum, left superior longitudinal fasciculus, left genu of corpus callosum, and right anterior thalamic radiation, which participate in the executive function. In addition, decreased muscle mass was associated with worse WM integrity in these regions. Multiple linear regression analysis revealed that WM integrity in the left cingulum, right anterior thalamic radiation, together with gender (male) significantly predicted muscle mass in PD patients. Conclusions: WM alterations in the executive network, such as the fronto-striato-thalamic circuits, may indicate a risk factor for ongoing sarcopenia in PD patients. The effectiveness of using executive function to serve as a prodromal marker of sarcopenia in PD patients should be evaluated in future studies.

Parkinson's disease (PD) is a neurodegenerative disorder associated with the striatum. Previous studies indicated that subdivisions of the striatum with distinct functional connectivity profiles contribute to different pathogeneses in PD. Segregated structural covariance (SC) pattern between the striatum and neocortex observed in healthy subjects, however, remain unknown in PD. The purpose of this study is to map and compare the subregional striatal SC network organization between 30 healthy controls and 48 PD patients and to investigate their association with the disease severity. The striatal SC network was statistically inferred by correlating the mean gray matter (GM) volume of six striatal subdivisions (including the bilateral dorsal caudate, superior ventral striatum, inferior ventral striatum, dorsal caudal putamen, dorsal rostral putamen, and ventral rostral putamen) with the entire neocortical GM volume in voxel-wise manner. The PD patients revealed marked atrophy in the striatum, cerebellum, and extra-striatum neocortices. As predicted, segregated striatal SC network patterns were observed in both groups. This suggests that in PD, pathological processes occurring in the striatum affect the same striato-cortical networks that covary with the striatum in healthy brains. The PD patients further demonstrated atypical striatal SC patterns between the caudate, parahippocampus temporal cortices, and cerebellum, which corresponded to dopaminergic associated network. The areas with significant group differences in SC were further associated with disease severity. Our findings support previous studies indicating that PD is associated with altered striato-cortical networks, and suggest that structural changes in the striatum may result in a cascade of alterations in multiple neocortices.

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