OBJECTIVE: This annotation reviews recent evidence that points to the likely role of aberrant neural oscillations in the pathogenesis of Tourette syndrome (TS). METHODS: The available anatomic and electrophysiological findings in TS are reviewed in the context of an emerging picture of the crucial role that neural oscillations play in maintaining normal central nervous system (CNS) function. RESULTS: Neurons form behavior-dependent oscillating networks of various sizes and frequencies that bias input selection and facilitate synaptic plasticity, mechanisms that cooperatively support temporal representation as well as the transfer and long-term consolidation of information. Coherent network activity is likely to modulate sensorimotor gating as well as focused motor actions. When these networks are dysrhythmic, there may be a loss of control of sensory information and motor action. The known electrophysiological effects of medications and surgical interventions used to treat TS likely have an ameliorative effect on these aberrant oscillations. Similarly, a strong case can be made that successful behavioral treatments involve the willful training regions of the prefrontal cortex to engage in tic suppression and the performance of competing motor responses to unwanted sensory urges such that these prefrontal regions become effective modulators of aberrant thalamocortical rhythms. CONCLUSIONS: A deeper understanding of neural oscillations may illuminate the complex, challenging, enigmatic, internal world that is TS.
OBJECTIVE: This annotation reviews recent evidence that points to the likely role of aberrant neural oscillations in the pathogenesis of Tourette syndrome (TS). METHODS: The available anatomic and electrophysiological findings in TS are reviewed in the context of an emerging picture of the crucial role that neural oscillations play in maintaining normal central nervous system (CNS) function. RESULTS: Neurons form behavior-dependent oscillating networks of various sizes and frequencies that bias input selection and facilitate synaptic plasticity, mechanisms that cooperatively support temporal representation as well as the transfer and long-term consolidation of information. Coherent network activity is likely to modulate sensorimotor gating as well as focused motor actions. When these networks are dysrhythmic, there may be a loss of control of sensory information and motor action. The known electrophysiological effects of medications and surgical interventions used to treat TS likely have an ameliorative effect on these aberrant oscillations. Similarly, a strong case can be made that successful behavioral treatments involve the willful training regions of the prefrontal cortex to engage in tic suppression and the performance of competing motor responses to unwanted sensory urges such that these prefrontal regions become effective modulators of aberrant thalamocortical rhythms. CONCLUSIONS: A deeper understanding of neural oscillations may illuminate the complex, challenging, enigmatic, internal world that is TS.
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