Study Objectives: Sleep spindles, defining electroencephalographic oscillations of nonrapid eye movement (NREM) stage 2 sleep (N2), mediate sleep-dependent memory consolidation (SDMC). Spindles are also thought to protect sleep continuity by suppressing thalamocortical sensory relay. Schizophrenia is characterized by spindle deficits and a correlated reduction of SDMC.
View Article and Find Full Text PDFBackground And Objectives: Rolandic epilepsy (RE), the most common childhood focal epilepsy syndrome, is characterized by a transient period of sleep-activated epileptiform activity in the centrotemporal regions and variable cognitive deficits. Sleep spindles are prominent thalamocortical brain oscillations during sleep that have been mechanistically linked to sleep-dependent memory consolidation in animal models and healthy controls. Sleep spindles are decreased in RE and related sleep-activated epileptic encephalopathies.
View Article and Find Full Text PDFSleep spindles mediate sleep-dependent memory consolidation, particularly when coupled to neocortical slow oscillations (SOs). Schizophrenia is characterized by a deficit in sleep spindles that correlates with reduced overnight memory consolidation. Here, we examined sleep spindle activity, SO-spindle coupling, and both motor procedural and verbal declarative memory consolidation in early course, minimally medicated psychosis patients and non-psychotic first-degree relatives.
View Article and Find Full Text PDFBackground And Objectives: Sleep spindles are prominent thalamocortical brain oscillations during sleep that have been mechanistically linked to sleep-dependent memory consolidation in animal models and healthy controls. Sleep spindles are decreased in Rolandic epilepsy and related sleep-activated epileptic encephalopathies. We investigate the relationship between sleep spindle deficits and deficient sleep dependent memory consolidation in children with Rolandic epilepsy.
View Article and Find Full Text PDFIn severe epileptic encephalopathies, epileptic activity contributes to progressive cognitive dysfunction. Epileptic encephalopathies share the trait of spike-wave activation during non-REM sleep (EE-SWAS), a sleep stage dominated by sleep spindles, which are brain oscillations known to coordinate offline memory consolidation. Epileptic activity has been proposed to hijack the circuits driving these thalamocortical oscillations, thereby contributing to cognitive impairment.
View Article and Find Full Text PDFEnlarged lateral ventricle (LV) volume and decreased volume in the corpus callosum (CC) are hallmarks of schizophrenia (SZ). We previously showed an inverse correlation between LV and CC volumes in SZ, with global functioning decreasing with increased LV volume. This study investigates the relationship between LV volume, CC abnormalities, and the microRNA MIR137 and its regulated genes in SZ, because of MIR137's essential role in neurodevelopment.
View Article and Find Full Text PDFResearch on the role of the hippocampus in memory acquisition has generally focused on active learning. But to understand memory, it is at least as important to understand processes that happen offline, during both wake and sleep. In a study of patients with amnesia, we previously demonstrated that although a functional hippocampus is not necessary for the acquisition of procedural motor memory during training session, it is required for its offline consolidation during sleep.
View Article and Find Full Text PDFBackground: Multiple facets of sleep neurophysiology, including electroencephalography (EEG) metrics such as non-rapid eye movement (NREM) spindles and slow oscillations (SO), are altered in individuals with schizophrenia (SCZ). However, beyond group-level analyses which treat all patients as a unitary set, the extent to which NREM deficits vary among patients is unclear, as are their relationships to other sources of heterogeneity including clinical factors, illness duration and ageing, cognitive profiles and medication regimens. Using newly collected high density sleep EEG data on 103 individuals with SCZ and 68 controls, we first sought to replicate our previously reported (Kozhemiako et.
View Article and Find Full Text PDFSleep spindles are believed to mediate sleep-dependent memory consolidation, particularly when coupled to neocortical slow oscillations. Schizophrenia is characterized by a deficit in sleep spindles that correlates with reduced overnight memory consolidation. Here, we examined sleep spindle activity, slow oscillation-spindle coupling, and both motor procedural and verbal declarative memory consolidation in early course, minimally medicated psychosis patients and non-psychotic first-degree relatives.
View Article and Find Full Text PDFBackground: Effective biomarkers of cognitive behavioral therapy (CBT) response provide information beyond available behavioral or self-report measures and may optimize treatment selection for patients based on likelihood of benefit. No single biomarker reliably predicts CBT response. In this study, we evaluated patterns of brain connectivity associated with self-focused attention (SFA) as biomarkers of CBT response for anxiety and obsessive-compulsive disorders.
View Article and Find Full Text PDFStudy Objectives: Healthy aging and many disorders show reduced sleep-dependent memory consolidation and corresponding alterations in non-rapid eye movement sleep oscillations. Yet sleep physiology remains a relatively neglected target for improving memory. We evaluated the effects of closed-loop auditory stimulation during sleep (CLASS) on slow oscillations (SOs), sleep spindles, and their coupling, all in relation to motor procedural memory consolidation.
View Article and Find Full Text PDFStudy Objective: Sleep spindles are present from birth and reflect cognitive functions across the lifespan, but normative values for this cognitive biomarker across development are lacking. This study aims to establish normative spindle features over development.
Methods: All available normal 19-channel electroencephalograms from developmentally normal children between February 2002 and June 2021 in the MGH EEG lab were analyzed.
There is converging evidence that abnormal thalamocortical interactions contribute to attention deficits and sensory sensitivities in autism spectrum disorder (ASD). However, previous functional MRI studies of thalamocortical connectivity in ASD have produced inconsistent findings in terms of both the direction (hyper vs. hypoconnectivity) and location of group differences.
View Article and Find Full Text PDFADHD has been associated with cortico-striatal dysfunction that may lead to procedural memory abnormalities. Sleep plays a critical role in consolidating procedural memories, and sleep problems are an integral part of the psychopathology of ADHD. This raises the possibility that altered sleep processes characterizing those with ADHD could contribute to their skill-learning impairments.
View Article and Find Full Text PDFPsychon Bull Rev
February 2023
Statistical learning (SL), the ability to pick up patterns in sensory input, serves as one of the building blocks of language acquisition. Although SL has been studied extensively in developmental dyslexia (DD), much less is known about the way SL evolves over time. The handful of studies examining this question were all limited to the acquisition of motor sequential knowledge or highly learned segmented linguistic units.
View Article and Find Full Text PDFTransient oscillatory events in the sleep electroencephalogram represent short-term coordinated network activity. Of particular importance, sleep spindles are transient oscillatory events associated with memory consolidation, which are altered in aging and in several psychiatric and neurodegenerative disorders. Spindle identification, however, currently contains implicit assumptions derived from what waveforms were historically easiest to discern by eye, and has recently been shown to select only a high-amplitude subset of transient events.
View Article and Find Full Text PDFSleep spindles, defining oscillations of stage II non-rapid eye movement sleep (N2), mediate sleep-dependent memory consolidation. Spindles are disrupted in several neurodevelopmental, neuropsychiatric, and neurodegenerative disorders characterized by cognitive impairment. Increasing spindles can improve memory suggesting spindles as a promising physiological target for the development of cognitive enhancing therapies.
View Article and Find Full Text PDFBackground: Communication difficulties are a core deficit in many people with autism spectrum disorder (ASD). The current study evaluated neural activation in participants with ASD and neurotypical (NT) controls during a speech production task.
Methods: Neural activities of participants with ASD (N = 15, = 16.
Rolandic epilepsy is the most common form of epileptic encephalopathy, characterized by sleep-potentiated inferior Rolandic epileptiform spikes, seizures, and cognitive deficits in school-age children that spontaneously resolve by adolescence. We recently identified a paucity of sleep spindles, physiological thalamocortical rhythms associated with sleep-dependent learning, in the Rolandic cortex during the active phase of this disease. Because spindles are generated in the thalamus and amplified through regional thalamocortical circuits, we hypothesized that: 1) deficits in spindle rate would involve but extend beyond the inferior Rolandic cortex in active epilepsy and 2) regional spindle deficits would better predict cognitive function than inferior Rolandic spindle deficits alone.
View Article and Find Full Text PDFClinical populations have memory deficits linked to sleep oscillations that can potentially be treated with sleep medications. Eszopiclone and zolpidem (two non-benzodiazepine hypnotics) both enhance sleep spindles. Zolpidem improved sleep-dependent memory consolidation in humans, but eszopiclone did not.
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