Abstract
<strong>Background:</strong> Anatomically, cortical-basal ganglia-thalamo-cortical (CBGTC) circuits have an essential role in the expression of tics. At the biochemical level, the proper conveyance of messages through these circuits requires several functionally integrated neurotransmitter systems. In this manuscript, evidence supporting proposed pathophysiological abnormalities, both anatomical and chemical is reviewed. In addition, the results of standard and emerging tic-suppressing therapies affecting nine separate neurotransmitter systems are discussed. The goal of this review is to integrate our current understanding of the pathophysiology of Tourette syndrome (TS) with present and proposed pharmacotherapies for tic suppression. <strong>Methods:</strong> For this manuscript, literature searches were conducted for both current basic science and clinical information in PubMed, Google-Scholar, and other scholarly journals to September 2018. <strong>Results:</strong> The precise primary site of abnormality for tics remains undetermined. Although many pathophysiologic hypotheses favor a specific abnormality of the cortex, striatum, or globus pallidus, others recognize essential influences from regions such as the thalamus, cerebellum, brainstem, and ventral striatum. Some prefer an alteration within direct and indirect pathways, whereas others believe this fails to recognize the multiple interactions within and between CBGTC circuits. Although research and clinical evidence supports involvement of the dopaminergic system, additional data emphasizes the potential roles for several other neurotransmitter systems. <strong>Discussion:</strong> A greater understanding of the primary neurochemical defect in TS would be extremely valuable for the development of new tic-suppressing therapies. Nevertheless, recognizing the varied and complex interactions that exist in a multi-neurotransmitter system, successful therapy may not require direct targeting of the primary abnormality.
Highlights
Tourette syndrome (TS) is a neuropsychiatric disorder whose primary symptoms include motor and vocal tics
We review the proposed anatomical pathways, and the hypothesized alterations of neurotransmitter systems located within these circuits
Within each specific transmitter system, we review the mechanism of action and efficacy of standard and emerging pharmacotherapeutic agents used for tic suppression
Summary
Tourette syndrome (TS) is a neuropsychiatric disorder whose primary symptoms include motor and vocal tics. Tics are common in the pediatric population, with estimates of their presence in about 20% of children.[1] For the diagnosis of TS, an individual must have multiple motor and at least one vocal tic, a waxing and waning course, and a duration of tics for greater than 1 year. The efficacy of current pharmacotherapeutic agents and future therapies for tics should be understood in the context of the pathophysiologic model underlying this movement abnormality. The goal of this review is to integrate our current understanding of the pathophysiology of TS with present and proposed pharmacotherapies for tic suppression. Within each specific transmitter system, we review the mechanism of action and efficacy of standard and emerging pharmacotherapeutic agents used for tic suppression. Our hope is that integrating the biochemical alteration(s) underlying tics with knowledge of the mechanism of drug action will lead to better treatment
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