Brain activation changes before and after XXXX treatment in @entity27 .

@entity1 @entity73 @entity27 @entity2786
STUDY OBJECTIVES: @entity27 ( @entity27 ) is associated with @entity73 , most of which are corrected after positive airway pressure ( @entity2786 ) treatment. Previous studies investigating the neural underpinnings of @entity27 failed to provide consistent results both on the cerebral substrates underlying @entity73 and on the effect of treatment on these anomalies. The aims of the study were a) to investigate whether never-treated OSA @entity1 demonstrated differences in brain activation compared to healthy controls during a cognitive task; and b) to investigate whether any improvements in cognitive functioning found in OSA @entity1 after treatment reflected a change in the underlying cerebral activity. DESIGN: OSA @entity1 and healthy controls underwent functional magnetic resonance imaging (fMRI) scanning. They were compared on performance and brain activation during a 2-back working-memory task. @entity1 were also re-evaluated after 3 months treatment with @entity2786 . Cognitive functions were evaluated using neurocognitive tests. Sleepiness (ESS), mood (Beck Depression Inventory) and, quality-of-life (SF-36) were also assessed. SETTING: The Sleep Disorders Center and CERMAC at the Vita-Salute San Raffaele University. @entity1 OR @entity1 : 17 OSA @entity1 and 15 age- and education-matched healthy controls. INTERVENTIONS: @entity2786 treatment for 3 months. MEASUREMENTS AND RESULTS: Compared to controls, never-treated OSA @entity1 showed increased activations in the left frontal cortex, medial precuneus, and hippocampus, and decreased activations in the caudal pons. OSA @entity1 showed decreases in activation with treatment in the left inferior frontal gyrus and anterior cingulate cortex, and bilaterally in the hippocampus. Most neurocognitive domains, impaired at baseline, showed significant improvement after treatment. CONCLUSIONS: OSA @entity1 showed an overrecruitment of brain regions compared to controls, in the presence of the same level of performance on a working-memory task. Decreases of activation in prefrontal and hippocampal structures were observed after treatment in comparison to baseline. These findings may reflect a neural compensation mechanism in never-treated @entity1 , which is reduced by effective treatment.
