Sleep medicine
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Review Comparative Study
A review of neurocognitive function and obstructive sleep apnea with or without daytime sleepiness.
Excessive daytime sleepiness (EDS) and neurocognitive dysfunction are commonly observed in patients with obstructive sleep apnea (OSA), and these daytime functional deficits can be reversed partly or completely with treatment such as continuous positive airway pressure (CPAP). Although daytime sleepiness is a possible etiology for neurocognitive dysfunction in OSA patients, EDS is not universally present in all patients with OSA. The objective of this review is to summarize the relationship between neurocognitive function and EDS in OSA, as well as the difference in cognitive domains, improvement, and application of CPAP therapy between patients with and without EDS. ⋯ CPAP failed to improve cognitive dysfunction in OSA patients without EDS after short-term therapy. The evidence suggests that daytime sleepiness possibly relates to the domain and extent of cognitive impairments in OSA, and CPAP therapy has little effect on the improvement of cognitive deficits in OSA patients without EDS. We recommend that additional prospective studies be performed to further quantify the relationship between neurocognitive function in OSA patients with and without EDS.
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Altered brain iron homeostasis with regional iron deficiency has been previously reported in several studies of restless legs syndrome (RLS) patients. Inconsistencies still exist, however, in the reported iron changes in different brain regions and different RLS phenotypes. The purpose of this study was to assess differences in brain iron concentrations between RLS patients and healthy controls and their relation to severity of disease and periodic limb movement during sleep (PLMS). ⋯ Using quantitative magnetic susceptibility as an in vivo indicator of brain iron content, the present study supports the general hypothesis of brain iron deficiency in RLS and indicates its possible link to PLMS.
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Comparative Study
Cognition, temperament, and cerebral blood flow velocity in toddlers and preschool children with sleep-disordered breathing or behavioral insomnia of childhood.
Cognitive decrements, problematic behaviors, and increased cerebral blood flow velocities (CBFVs) have been reported in children aged 3-7 years with sleep-disordered breathing (SDB). Whether similar impairments exist in younger children or those with behavioral insomnia of childhood (BIC) remains unclear. This study aimed to compare cognition and temperament in children aged 1-5 years with SDB or BIC to healthy control children, and to investigate whether cognitive or behavioral deficits associated with sleep problems are related to changes in CBFV. ⋯ During early childhood, problematic temperaments, cognitive deficits, and altered cerebrovascular functioning are associated with SDB but not BIC. CBFV does not appear to mediate these daytime deficits and instead may be an independent outcome of SDB. The findings support the need for an early intervention in pediatric SDB.
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A Task Force was established by the International Restless Legs Syndrome Study Group (IRLSSG) in conjunction with the European Restless Legs Syndrome Study Group (EURLSSG) and the RLS Foundation (RLS-F) to develop evidence-based and consensus-based recommendations for the prevention and treatment of long-term pharmacologic treatment of dopaminergic-induced augmentation in restless legs syndrome/Willis-Ekbom disease (RLS/WED). The Task Force made the following prevention and treatment recommendations: As a means to prevent augmentation, medications such as α2δ ligands may be considered for initial RLS/WED treatment; these drugs are effective and have little risk of augmentation. Alternatively, if dopaminergic drugs are elected as initial treatment, then the daily dose should be as low as possible and not exceed that recommended for RLS/WED treatment. ⋯ Alternatively, the patient can be switched to an α2δ ligand or rotigotine. For severe augmentation the patient can be switched either to an α2δ ligand or rotigotine, noting that rotigotine may also produce augmentation at higher doses with long-term use. In more severe cases of augmentation an opioid may be considered, bypassing α2δ ligands and rotigotine.