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Recent studies have suggested that maternal obesity during pregnancy is associated with differences in neurodevelopmental outcomes in children. In this study, we aimed to investigate the relationships between maternal obesity during pregnancy and neonatal brain cortical development.MATERIALS AND METHODS:
Forty-four healthy women (28 normal-weight, 16 obese) were prospectively recruited at <10 weeks’ gestation, and their healthy full-term neonates (23 boys, 21 girls) underwent brain MR imaging. All pregnant women had their body composition (fat mass percentage) measured at ~12 weeks of pregnancy. All neonates were scanned at ~2 weeks of age during natural sleep without sedation, and their 3D T1-weighted images were postprocessed by the new iBEAT2.0 software. Brain MR imaging segmentation and cortical surface reconstruction and parcellation were completed using age-appropriate templates. Mean cortical thickness for 34 regions in each brain hemisphere defined by the UNC Neonatal Cortical Surface Atlas was measured, compared between groups, and correlated with maternal body fat mass percentage, controlled for neonate sex and race, postmenstrual age at MR imaging, maternal age at pregnancy, and the maternal intelligence quotient and education.RESULTS:
Neonates born to obese mothers showed significantly lower (P ≤ .05, false discovery rate–corrected) cortical thickness in the left pars opercularis gyrus, left pars triangularis gyrus, and left rostral middle frontal gyrus. Mean cortical thickness in these frontal lobe regions negatively correlated (R = –0.34, P = .04; R = –0.50, P = .001; and R = –0.42, P = .01; respectively) with the maternal body fat mass percentage measured at early pregnancy.CONCLUSIONS:
Maternal obesity during pregnancy is associated with lower neonate brain cortical thickness in several frontal lobe regions important for language and executive functions.
Small vessel disease, a disorder of cerebral microvessels, is an expanding epidemic and a common cause of stroke and dementia. Despite being almost ubiquitous in brain imaging, the clinicoradiologic association of small vessel disease is weak, and the underlying pathogenesis is poorly understood. The STandards for ReportIng Vascular changes on nEuroimaging (STRIVE) criteria have standardized the nomenclature. These include white matter hyperintensities of presumed vascular origin, recent small subcortical infarcts, lacunes of presumed vascular origin, prominent perivascular spaces, cerebral microbleeds, superficial siderosis, cortical microinfarcts, and brain atrophy. Recently, the rigid categories among cognitive impairment, vascular dementia, stroke, and small vessel disease have become outdated, with a greater emphasis on brain health. Conventional and advanced small vessel disease imaging markers allow a comprehensive assessment of global brain heath. In this review, we discuss the pathophysiology of small vessel disease neuroimaging nomenclature by means of the STRIVE criteria, clinical implications, the role of advanced imaging, and future directions.
In this second of 3 review articles on the endovascular management of intracranial dural AVFs, we discuss transarterial treatment approaches. The treatment goal is to occlude the fistulous point, including the most distal portion of the arterial supply together with the most proximal portion of the draining vein (ie, the "foot" of the vein), which can be accomplished with liquid embolic agents via transarterial access. Anatomic factors to consider when assessing the safety and efficacy of a transarterial approach using liquid embolic agents include location, angioarchitecture, and proximity of arterial feeders to both the vasa nervosum of adjacent cranial nerves and the external carotid–internal carotid/vertebral artery anastomoses. Anatomic locations typically favorable for transarterial approaches include but are not limited to the transverse/sigmoid sinus, cerebral convexity, and superior sagittal sinus. In this review article, we discuss the technical approaches, outcomes, potential complications, and complication avoidance strategies for transarterial embolization.
Arterial sclerosis resulting from hypertension slows CSF transportation in the perivascular spaces, showing the intrinsic relationship between the CSF and the blood vasculature. However, the exact effect of hypertension on human CSF flow dynamics remains unclear. The present study aimed to evaluate CSF flow dynamics in treatment-naive patients with essential hypertension using phase-contrast cine MR imaging.MATERIALS AND METHODS:
The study included 60 never-treated patients with essential hypertension and 60 subjects without symptomatic atherosclerosis. CSF flow parameters, such as forward flow volume, forward peak velocity, reverse flow volume, reverse peak velocity, average flow, and net flow volume, were measured with phase-contrast cine MR imaging. Differences between the 2 groups were assessed to determine the independent determinants of these CSF flow parameters.RESULTS:
Forward flow volume, forward peak velocity, reverse flow volume, reverse peak velocity, and average flow in the patients with hypertension significantly decreased (all, P < .05). Increasing systolic blood pressure was significantly associated with lower forward flow volume (β = –0.44 mL/mL/mm Hg; 95% CI, –0.83 to –0.06 mL/mL/mm Hg), forward peak velocity (β = –0.50 cm/s/mm Hg; 95% CI, –0.88 to –0.12 cm/s/mm Hg), reverse flow volume (β = –0.61 mL/mL/mm Hg; 95% CI, –0.97 to –0.26 mL/mL/mm Hg), reverse peak velocity (β = –0.55 cm/s/mm Hg; 95% CI, –0.91–0.18 cm/s/mm Hg), and average flow (β = –0.50 mL/min/mm Hg; 95% CI, –0.93 to –0.08 mL/min/mm Hg).CONCLUSIONS:
The CSF flow dynamics in patients with hypertension are decreased, and increasing systolic blood pressure is strongly associated with lower CSF flow dynamics.