Accelerated Echo Planer J-resolved Spectroscopic Imaging of Putamen and Thalamus in Obstructive Sleep Apnea

Obstructive sleep apnea syndrome (OSAS) leads to neurocognitive and autonomic deficits that are partially mediated by thalamic and putamen pathology. We examined the underlying neurochemistry of those structures using compressed sensing-based 4D echo-planar J-resolved spectroscopic imaging (JRESI), and quantified values with prior knowledge fitting. Bilaterally increased thalamic mI/Cr, putamen Glx/Cr, and Glu/Cr, and bilaterally decreased thalamic and putamen tCho/Cr and GABA/Cr occurred in OSAS vs healthy subjects (p < 0.05). Increased right thalamic Glx/Cr, Glu/Cr, Gln/Cr, Asc/Cr, and decreased GPC/Cr and decreased left thalamic tNAA/Cr, NAA/Cr were detected. The right putamen showed increased mI/Cr and decreased tCho/Cr, and the left, decreased PE/Cr ratio. ROC curve analyses demonstrated 60–100% sensitivity and specificity for the metabolite ratios in differentiating OSAS vs. controls. Positive correlations were found between: left thalamus mI/Cr and baseline oxygen saturation (SaO(2)); right putamen tCho/Cr and apnea hypopnea index; right putamen GABA/Cr and baseline SaO(2); left putamen PE/Cr and baseline SaO(2); and left putamen NAA/Cr and SaO(2) nadir (all p < 0.05). Negative correlations were found between left putamen PE/Cr and SaO(2) nadir. These findings suggest underlying inflammation or glial activation, with greater alterations accompanying lower oxygen saturation. These metabolite levels may provide biomarkers for future neurochemical interventions by pharmacologic or other means

Obstructive Sleep Apnoea and Hypertension: the Role of the Central Nervous System

Purpose of review Obstructive sleep apnoea (OSA) is associated with both nocturnal and daytime hypertensions which increase cardiovascular morbidity and mortality. It is thought that the repeated episodes of hypoxia and hypercapnia during nocturnal airway obstructions that characterise OSA result in increased sympathetic drive that persists during wakefulness. Although the underlying mechanisms responsible for this hypertension remain to be elucidated, several neural and humoral mechanisms have been proposed and recent evidence suggesting changes in the central nervous system may play a significant role. The purpose of this review is to explore recent evidence of central changes associated with elevated sympathetic drive in individuals with OSA. Recent findings Recent human brain imaging investigations and, in particular, combined microneurography recording of resting sympathetic activity with high-resolution functional magnetic resonance imaging have provided some important insights into changes in brain function and anatomy associated with resting sympathetic activity. Functional and anatomical changes occur in OSA, including in regions of the brainstem circuitry known to be responsible for setting resting sympathetic activity. Furthermore, these changes are reversed following continuous positive airway treatment in concert with reductions in resting sympathetic drive. Summary These resent findings suggest that the central changes may contribute significantly to the hypertension associated with OSA

Hippocampal hypertrophy and sleep apnea: A role for the ischemic preconditioning?

The full impact of multisystem disease such as obstructive sleep apnoea (OSA) on regions of the central nervous system is debated, as the subsequent neurocognitive sequelae are unclear. Several preclinical studies suggest that its purported major culprits, intermittent hypoxia and sleep fragmentation, can differentially affect adult hippocampal neurogenesis. Although the prospective biphasic nature of chronic intermittent hypoxia in animal models of OSA has been acknowledged, so far the evidence for increased 'compensatory' neurogenesis in humans is uncertain. In a cross-sectional study of 32 patients with mixed severity OSA and 32 non-apnoeic matched controls inferential analysis showed bilateral enlargement of hippocampi in the OSA group. Conversely, a trend for smaller thalami in the OSA group was noted. Furthermore, aberrant connectivity between the hippocampus and the cerebellum in the OSA group was also suggested by the correlation analysis. The role for the ischemia/hypoxia preconditioning in the neuropathology of OSA is herein indicated, with possible further reaching clinical implications. © 2013 Rosenzweig et al