Neurophysiology of dystonia: The role of inhibition
TLDR
The pathophysiology of dystonia has been best studied in patients with focal hand dySTONia, and a possible hypothesis is that there is a genetic loss of inhibitory interneurons in Dystonia and that this deficit is a substrate on which other factors can act to produce dystonIA.About:
This article is published in Neurobiology of Disease.The article was published on 2011-05-01 and is currently open access. It has received 306 citations till now. The article focuses on the topics: Dystonia.read more
Citations
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Emerging concepts in the physiological basis of dystonia
Angelo Quartarone,Mark Hallett +1 more
TL;DR: It is speculated that during motor learning this abnormal plasticity may lead to an abnormal sensorimotor integration, leading to consolidation of abnormal motor engrams, which might explain the delayed clinical effects of deep brain stimulation (DBS) in patients with generalized dystonia.
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The non-motor syndrome of primary dystonia: clinical and pathophysiological implications.
TL;DR: Growing evidence indicates an important non-motor component to primary dystonia, including abnormalities in sensory and perceptual functions, as well as neuropsychiatric, cognitive and sleep domains, is indicated.
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Transcranial focused ultrasound neuromodulation of the human primary motor cortex
TL;DR: This is the first report of the effect of ultrasound on human motor cortical excitability and motor behavior and confirms previous results in the somatosensory cortex that ultrasound results in effective neuronal inhibition that confers a performance advantage.
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Primary dystonia and dystonia-plus syndromes: clinical characteristics, diagnosis, and pathogenesis
TL;DR: The dystonias are a heterogeneous group of hyperkinetic movement disorders characterised by involuntary sustained muscle contractions that lead to abnormal postures and repetitive movements and a greater understanding of the causes of dystonic movements from the study of genetics, neurophysiology, and functional imaging is gained.
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Network localization of cervical dystonia based on causal brain lesions.
Daniel T. Corp,Daniel T. Corp,Juho Joutsa,R. Ryan Darby,R. Ryan Darby,Cathérine C.S. Delnooz,Bart P.C. van de Warrenburg,Danielle Cooke,Cecília N. Prudente,Jianxun Ren,Martin M. Reich,Martin M. Reich,Amit Batla,Kailash P. Bhatia,Hyder A. Jinnah,Hesheng Liu,Michael D. Fox,Michael D. Fox +17 more
TL;DR: A technique termed 'lesion network mapping', which uses connectome data from a large cohort of healthy subjects to test whether lesion locations causing cervical dystonia map to a common brain network, lends insight into the causal neuroanatomical substrate of cervical Dystonia and demonstrates convergence across idiopathic and acquired dySTONia.
References
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The basal ganglia: focused selection and inhibition of competing motor programs.
TL;DR: The hypothesis states that the basal ganglia do not generate movements, and when voluntary movement is generated by cerebral cortical and cerebellar mechanisms, the basal Ganglia act broadly to inhibit competing motor mechanisms that would otherwise interfere with the desired movement.
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Transcranial Magnetic Stimulation: A Primer
TL;DR: Transcranial magnetic stimulation is a technique for noninvasive stimulation of the human brain that can influence brain function if delivered repetitively, and is being developed for various therapeutic purposes.
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TL;DR: It is suggested that subthreshold transcranial magnetic stimulation is capable of activating separate populations of excitatory and inhibitory interneurones in the motor cortex.
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Differential effects on motorcortical inhibition induced by blockade of GABA uptake in humans
TL;DR: In vivo evidence of differential modulation of cortical inhibition by blockade of GABA uptake is provided, suggesting that presynaptic GABA autoreceptors may be involved in modulating cortical inhibition in the human motor cortex.
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Human motor evoked responses to paired transcranial magnetic stimuli.
TL;DR: The early facilitation observed at high intensities seems to be a consequence of a rise in cortical excitability induced by the conditioning stimulus, causing an increase in the number or size, or both, of descending volleys from the test stimulus.