Brain Stimul
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Controlled Clinical Trial
Deep Brain Stimulation Influences Brain Structure in Alzheimer's Disease.
Deep Brain Stimulation (DBS) is thought to improve the symptoms of selected neurological disorders by modulating activity within dysfunctional brain circuits. To date, there is no evidence that DBS counteracts progressive neurodegeneration in any particular disorder. ⋯ We present the first in-human evidence that, in addition to modulating neural circuit activity, DBS may influence the natural course of brain atrophy in a neurodegenerative disease.
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Slow Wave Activity (SWA), the low frequency (<4 Hz) oscillations that characterize Slow Wave Sleep (SWS) are thought to relate causally to declarative memory consolidation during nocturnal sleep. Evidence is conflicting relating SWA to memory consolidation during nap however. ⋯ These results provide preliminary evidence suggesting a causal and specific role of SWA in declarative memory consolidation during nap.
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Transcranial static magnetic field stimulation (tSMS) in humans reduces cortical excitability. ⋯ Our data indicate that the application of tSMS is safe in healthy human subjects, at least within these parameters.
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Individuals with communication disorders, such as aphasia, exhibit weak auditory cortex responses to speech sounds and language impairments. Previous studies have demonstrated that pairing vagus nerve stimulation (VNS) with tones or tone trains can enhance both the spectral and temporal processing of sounds in auditory cortex, and can be used to reverse pathological primary auditory cortex (A1) plasticity in a rodent model of chronic tinnitus. ⋯ VNS speech sound pairing provides a novel method to enhance speech sound processing in the central auditory system. Delivery of VNS during speech therapy could improve outcomes in individuals with receptive language deficits.
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Periodic stimulation of occipital areas using transcranial alternating current stimulation (tACS) at alpha (α) frequency (8-12 Hz) enhances electroencephalographic (EEG) α-oscillation long after tACS-offset. Two mechanisms have been suggested to underlie these changes in oscillatory EEG activity: tACS-induced entrainment of brain oscillations and/or tACS-induced changes in oscillatory circuits by spike-timing dependent plasticity. ⋯ Our results indicate that plasticity mechanisms are sufficient to explain α-aftereffects in response to α-tACS, and inform models of tACS-induced plasticity in oscillatory circuits. Modifying brain oscillations with tACS holds promise for clinical applications in disorders involving abnormal neural synchrony.