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.
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.
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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