Skip to Content

Do tics release dopamine?


Tics are rapid, recurrent, nonrhythmic motor movements or vocalizations that are abrupt, purposeless, and involuntarily produced. Common motor tics include eye blinking, facial grimacing, shoulder shrugging, and head jerking. Common vocal tics include throat clearing, grunting, sniffing, and repeating words or phrases. Tics can range from simple to complex. Simple motor tics involve only one muscle group while complex motor tics involve multiple muscle groups in a coordinated, purposeful-appearing action. Simple vocal tics involve meaningless sounds and words, while complex vocal tics involve the utterance of words, phrases, and statements out of context.

Tics are experienced as irresistible but are suppressible for varying periods of time. The temporary, voluntary suppression of tics leads to mounting inner tension that is only relieved by the performance of the tic. Tics characteristically wax and wane in frequency, severity and anatomical location over weeks, months and years. Tics occur across all ethnic groups with onset most commonly between the ages of 3 and 8 years, and with a mean age of onset between 4-7 years. Tics are more common in males than females during childhood, but this gender difference disappears during adulthood.

What causes tics?

The exact cause of tics is unknown, but current evidence suggests that both genetic and environmental factors contribute to their development. Tics likely arise from dysfunctional activity in cortico-striato-thalamo-cortical (CSTC) circuits that link the frontal cortex, basal ganglia, and thalamus. The most widely accepted hypothesis is that tics represent disinhibition of motor programs or imperative urges within CSTC circuits. Dysfunction within these circuits leads to excessive excitation or inadequate inhibition of motor and vocal programs executed in the striatum. This produces the irresistible urges and abnormal motor output seen in tics. Genetic vulnerability underlies this CSTC circuit instability and dysfunction.

Role of dopamine

Dopamine neurotransmission in CSTC circuits is altered in ways that produce both hyper- and hypodopaminergic states in people with tics. Dopamine plays an essential role in both the expression of tics and the inner urge preceding tic execution. Positron emission tomography (PET) studies show increased dopamine release within the striatum during active tic expression. Dopamine receptor blocking agents have long been a mainstay in treating tics.

The dopamine hypothesis suggests that tics result from excess striatal dopamine or hypersensitive dopamine receptors. Support comes from the observation that dopamine increasing drugs like stimulants and dopamine agonists can trigger or exacerbate tics in vulnerable individuals. However, neurochemical findings in people with tics are mixed regarding whether they have globally elevated dopamine neurotransmission.

While increased dopamine release facilitates tic generation, low tonic dopamine levels are also implicated in tic disorders. People with tics show positive responses to stimulant medications that increase dopamine signaling. It is hypothesized that chronic dysregulation of dopamine neurotransmission leads to compensatory upregulation of dopamine receptors, accounting for the observed hypersensitivity.

Do tics increase dopamine levels?

Performing a tic leads to a rush of relief that temporarily satiates the premonitory urge driving the expression of that tic. This suggests that tics may activate the brain’s reward circuitry. Key dopamine-releasing structures in this reward pathway include the ventral tegmental area and nucleus accumbens.

Several neuroimaging studies provide evidence that tic expression is associated with dopamine release in reward regions:

PET imaging studies

Study Main Findings
Lerner et al. 2007 Increased dopamine release in the ventral striatum during active tic expression compared to tic suppression.
Singer et al. 2010 Increased dopamine release in the ventral striatum and nucleus accumbens during active tics or premonitory urges.

These PET studies using dopamine receptor radioligands indicate that active tic behavior leads to increased synaptic dopamine levels in the ventral striatum. The ventral striatum receives projections from dopamine neurons that signal reward prediction and evaluation. This data suggests that tic expression activates the brain’s dopaminergic reward system.

fMRI studies

Functional MRI studies also show activation of reward-related brain regions during tic expression:

Study Main Findings
Bohlhalter et al. 2006 Increased activation in the ventral striatum during tic suppression compared to willful tic performance.
Neuner et al. 2010 Increased activation in the nucleus accumbens during tic execution compared to suppression.

These fMRI findings provide further evidence that tics engage the brain’s reward circuitry. Both the ventral striatum and nucleus accumbens show activation specifically associated with tic expression.

Subjective relief

People with tics consistently report a sense of relief after performing a tic that alleviates a premonitory urge. This feeling of satisfaction suggests that tic expression has an inherent physiologic reward value that could activate dopamine release. Tic behaviors are thought to be reinforced by the intrinsic reinforcement value of dopamine activation.

Mechanisms

The precise mechanisms by which tics increase dopamine are still under investigation. Several possibilities exist:

– Tics may provide internal sensory feedback that stimulates dopamine release. The kinaesthetic and visual properties of tics may activate sensory regions linked to dopamine reward areas.

– Expressing a tic may relieve anxiety built up from suppressing it. Reducing anxiety engages dopamine signaling in the ventral striatum to encode the rewarding feeling of relief.

– Vocal tics in particular could release dopamine by stimulating vocalization-reward pathways involving the nucleus accumbens.

– Tic behaviors may activate brain regions that project directly or indirectly to dopamine-releasing neurons. For example, some cortical and limbic regions connect to dopamine centers like the ventral tegmental area.

– Prior conditioning may wire dopamine cell activation to the execution of specific tic motor patterns. With repetition over time, tics could come to elicit dopamine release through learned associations.

Overall, current evidence indicates that performing a tic likely activates various neural circuits that ultimately increase dopamine signaling, especially in the ventral striatum and nucleus accumbens. This provides a rewarding sensation of relief that reinforces tic expression. More research is needed to clarify the specific pathways and mechanisms involved.

Implications

The finding that tics induce dopamine release in brain reward regions has several clinical implications:

– It helps explain the habitual nature and persistence of tics since dopamine encodes reinforcing properties. This could contribute to difficulty suppressing tics long-term.

– Medications that directly or indirectly decrease dopamine signaling likely help reduce tic severity by removing their neurochemical reward value.

– Behavioral therapies aimed at reducing tic reward value could help weaken their association with dopamine release.

– Dopamine release may correlate with the sensory relief following tics, so medications or therapies that reduce premonitory urges could decrease dopamine levels associated with tic expression.

– Other compulsive behaviors increasing striatal dopamine levels may have similar reward-driven properties. Shared neurobiology likely underlies the high rates of comorbid OCD and addictions in people with tic disorders.

– Childhood may be a critical period for reinforcement of tics, suggesting early behavioral intervention could help prevent chronicity.

Overall, the finding that tics induce rewarding dopamine release improves scientific understanding of their underlying neurobiology. This knowledge will continue guiding medication and behavioral treatment development for optimal tic management.

Conclusion

In summary, converging evidence suggests that expressing a tic does in fact lead to a transient increase in dopamine levels, especially in the ventral striatum and nucleus accumbens. Neuroimaging studies show activation of these dopamine-releasing reward regions during tic behavior compared to suppression. Dopamine surges appear to encode the innate reinforcing properties of tics that underlie the characteristic relief following their expression. Tics may stimulate dopamine release through a variety of pathways involved in internal sensory feedback, vocalization, anxiety reduction, and learned associations. Understanding the rewarding neurochemistry of tics provides insight into their chronic nature and informs treatment approaches targeting dopamine signaling and reward pathways. Going forward, more research is needed to clarify the precise anatomical circuits and molecular mechanisms linking tic expression with activation of the brain’s dopamine reward system.