Global Dysrhythmia of Cerebro-Basal Ganglia–Cerebellar Networks Underlies Motor Tics following Striatal Disinhibition

Kevin W. McCairn · Atsushi Iriki · Masaki Isoda

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Obsessive-Compulsive Spectrum Disorders Motor Control and Adaptation Neurological disorders and treatments

Abstract

Motor tics, a cardinal symptom of Tourette syndrome (TS), are hypothesized to arise from abnormalities within cerebro-basal ganglia circuits. Yet noninvasive neuroimaging of TS has previously identified robust activation in the cerebellum. To date, electrophysiological properties of cerebellar activation and its role in basal ganglia-mediated tic expression remain unknown. We performed multisite, multielectrode recordings of single-unit activity and local field potentials from the cerebellum, basal ganglia, and primary motor cortex using a pharmacologic monkey model of motor tics/TS. Following microinjections of bicuculline into the sensorimotor putamen, periodic tics occurred predominantly in the orofacial region, and a sizable number of cerebellar neurons showed phasic changes in activity associated with tic episodes. Specifically, 64% of the recorded cerebellar cortex neurons exhibited increases in activity, and 85% of the dentate nucleus neurons displayed excitatory, inhibitory, or multiphasic responses. Critically, abnormal discharges of cerebellar cortex neurons and excitatory-type dentate neurons mostly preceded behavioral tic onset, indicating their central origins. Latencies of pathological activity in the cerebellum and primary motor cortex substantially overlapped, suggesting that aberrant signals may be traveling along divergent pathways to these structures from the basal ganglia. Furthermore, the occurrence of tic movement was most closely associated with local field potential spikes in the cerebellum and primary motor cortex, implying that these structures may function as a gate to release overt tic movements. These findings indicate that tic-generating networks in basal ganglia mediated tic disorders extend beyond classical cerebro-basal ganglia circuits, leading to global network dysrhythmia including cerebellar circuits.

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References

2005Altered parvalbumin-positive neuron distribution in basal ganglia of individuals with Tourette syndrome 2006Recent advances in Tourette syndrome research 2009Decreased number of parvalbumin and cholinergic interneurons in the striatum of individuals with Tourette syndrome 2006Neural correlates of tic generation in Tourette syndrome: an event-related functional MRI study 2001Basal ganglia dysfunction in Tourette’s syndrome: a new hypothesis 1993Definitions and Classification of Tic Disorders 2012Widespread abnormality of the γ-aminobutyric acid-ergic system in Tourette syndrome 1970Stereotaxic atlas of the brain of Macaca fuscata

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2022A neural network for tics: insights from causal brain lesions and deep brain stimulation 2015Neuroimaging of tic genesis: Present status and future perspectives 2015Corticostriatal interactions in the generation of tic-like behaviors after local striatal disinhibition 2016A Primary Role for Nucleus Accumbens and Related Limbic Network in Vocal Tics 2017Tourette syndrome: a disorder of the social decision-making network

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