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Review
. 2022 Feb 10;12(2):242.
doi: 10.3390/brainsci12020242.

Tics and Emotions

Affiliations
Review

Tics and Emotions

Gerry Leisman et al. Brain Sci. .

Abstract

Tics can be associated with neurological disorders and are thought to be the result of dysfunctional basal ganglia pathways. In Tourette Syndrome (TS), excess dopamine in the striatum is thought to excite the thalamo-cortical circuits, producing tics. When external stressors activate the hypothalamic-pituitary-adrenal (HPA) axis, more dopamine is produced, furthering the excitation of tic-producing pathways. Emotional processing structures in the limbic are also activated during tics, providing further evidence of a possible emotional component in motor ticking behaviors. The purpose of this review is to better understand the relationship between emotional states and ticking behavior. We found support for the notion that premonitory sensory phenomena (PSP), sensory stimulation, and other environmental stressors that impact the HPA axis can influence tics through dopaminergic neurotransmission. Dopamine plays a vital role in cognition and motor control and is an important neurotransmitter in the pathophysiology of other disorders such as obsessive-compulsive disorder (OCD) and attention deficit hyperactivity disorder (ADHD), which tend to be comorbid with ticking disorders and are thought to use similar pathways. It is concluded that there is an emotional component to ticking behaviors. Emotions primarily involving anxiety, tension, stress, and frustration have been associated with exacerbated tics, with PSP contributing to these feelings.

Keywords: HPA axis; Tourette syndrome; basal ganglia; dopamine; emotions; premonitory sensory phenomena; tics.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Hypothetical model of the basis for dysfunction in TS. Secondary to the reduction in T regulatory lymphocytes (Tregs), an enhancement of cytokines and reduction in immune tolerance may be facilitated by increased dopamine levels as well as dysgammaglobulinemia, which could possibly facilitate autoimmunity (after Eelamin, I., Edwards, M. J., and Martino, D. (2013). Immune dysfunction in Tourette syndrome. Behavioural neurology, 27(1), 23–32. with permission).
Figure 2
Figure 2
The basal ganglia that clinically includes sub-thalamic nucleus and substantia nigra whose component structures are highly interconnected (after Leisman, G., Braun-Benjamin, O., and Melillo, R. (2014). Cognitive-motor interactions of the basal ganglia in development. Frontiers in systems neuroscience, 8, 16. with permission).
Figure 3
Figure 3
Diagrammatic representation of the association between promontory sensations and ticking behavior. Environmental and contextual triggers intensify PSPs, as well as dopaminergic activity that are hypothesized to increase tic behavior. The tics themselves affect the intensity of PSPs that could in turn potentially create a maladaptive habit as a coping mechanism (after Godar, S. C., and Bortolato, M. (2017). What makes you tic? Translational approaches to study the role of stress and contextual triggers in Tourette syndrome. Neuroscience & Biobehavioral Reviews, 76, 123–133. doi:10.1016/j.neubiorev.2016.10 (2017), with permission).

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