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Dopamine, Basal Ganglia, and Tics: The Neurobiological Background of Tourette Syndrome

Tourette syndrome (TS) is a neurodevelopmental disorder characterized by uncontrollable, recurring movements (motor tics) and vocalizations (vocal tics). The first symptoms usually appear in childhood, often between the ages of four and six. Initially, motor tics such as blinking or head jerking are common before vocal tics develop, which are often mistaken for harmless habits like throat clearing or coughing. In most cases, symptoms increase until the age of ten to twelve before gradually declining in adulthood. However, in about 10 to 20 percent of affected individuals, symptoms persist or even worsen. Tics can be temporarily suppressed, but this often leads to an intensified release of symptoms. Factors such as stress, emotional strain, or fatigue exacerbate tics, while focused activities can temporarily reduce them. Additional psychiatric comorbidities frequently occur, including attention deficit hyperactivity disorder (ADHD) and obsessive-compulsive disorder (OCD). While ADHD is often diagnosed before the first tics appear, OCD typically develops during adolescence and often persists longer than the tics.

The symptoms of Tourette syndrome can be explained by alterations in specific brain networks. The basal ganglia, a brain region essential for controlling and inhibiting movements, play a crucial role. Normally, inhibitory circuits in the basal ganglia suppress unwanted movements, but this inhibition appears to be impaired in Tourette syndrome. Another key factor is the dysregulation of the dopamine system. Excessive dopamine release in the basal ganglia enhances motor tics. Dopamine is a central neurotransmitter in movement control and influences the reward system. Increased dopamine release contributes to the manifestation of tics as automated movement habits, which are associated with a temporary relief of tension. Additionally, the sensorimotor network plays a crucial role. Affected individuals show increased neuronal activity in the insular cortex, a region responsible for the perception of internal bodily sensations. This explains the characteristic premonitory urge that many individuals experience immediately before a tic. Furthermore, the anterior cingulate cortex, responsible for impulse control, and the centromedian thalamus, which regulates motor sequences, are involved in this complex process.

Neurophysiological studies have shown that during deep brain stimulation (a potential therapy), certain brain regions exhibit increased low-frequency activity (1–10 Hz). Such activity patterns are particularly measurable in the centromedian thalamus and anterior pallidum. It is suspected that these low-frequency signals are associated with the internal urge to perform tics.

The diagnosis of Tourette syndrome is made clinically based on a comprehensive medical history and neurological examination, as there are no specific laboratory or imaging tests available. The hallmark of TS is the simultaneous occurrence of motor and vocal tics, which change over time. These tics are categorized into simple (e.g., blinking, shoulder shrugging, throat clearing) and complex tics (e.g., sequences of movements or repeating words). The severity of tics is often assessed using the Yale Global Tic Severity Scale (YGTSS). Diagnosis follows the DSM-5 criteria, which require that symptoms begin before the age of 18, persist for at least one year, and include both motor and vocal tics. Other conditions such as myoclonus, epilepsy, or OCD must be ruled out. Notably, during the COVID-19 pandemic, an increase in tic-like symptoms was observed in adolescents that did not correspond to classical Tourette syndrome. Thus, distinguishing TS from other movement disorders is crucial.

The treatment of Tourette syndrome depends on symptom severity and individual distress levels. Mild tics often require no therapy, whereas more severe symptoms may be managed with behavioral therapy, medications, or neuromodulation techniques. Behavioral therapy, particularly Habit Reversal Training (HRT) and Comprehensive Behavioral Intervention for Tics (CBIT), has proven especially effective. These therapies help individuals become aware of their tics and develop alternative movement patterns. If behavioral therapy is insufficient, dopamine antagonists (e.g., tiapride, aripiprazole) can be used, though they may cause side effects such as fatigue or weight gain. Another treatment option for TS is botulinum toxin injections, which block acetylcholine release at the neuromuscular junction, leading to targeted muscle relaxation and tic reduction. This therapy is particularly effective for localized tics, such as those affecting the face, neck, or eyelids. However, excessive muscle weakening is a potential risk, making precise injection techniques and dosages crucial.

Given the significant side effects of conventional TS medications, interest in alternative and complementary therapies is growing. Herbal preparations such as Ningdong granules (NDG), Choudongning capsules, and 5-Ling granules (5-LGr) have shown significant tic reduction. Acupuncture has also been described as a potentially effective treatment.

Various dietary supplements are under investigation. Taurine, which acts on GABA receptors, has been shown to reduce tics in combination with tiapride without notable side effects. The role of vitamin D remains unclear. An unconventional approach is the use of a specialized oral splint device, which may influence tic intensity through sensory stimuli.

Currently, numerous studies are exploring new treatment options for TS. For example, the drug atomoxetine, a norepinephrine reuptake inhibitor, is being tested for its ability to improve impulse control in TS patients. Additionally, serotonin modulators like pimavanserin are being evaluated, particularly for patients with co-occurring depression or anxiety disorders.

A novel research approach focuses on the gut-brain axis. Probiotics such as Lactobacillus plantarum PS128, which modulate neurotransmitters, are being investigated for their potential to reduce tics. Initial studies have shown promising effects in autistic children, prompting ongoing clinical trials for TS. Another experimental approach involves fecal transplants: in a small study, four out of five patients experienced significant symptom improvement.

In severe cases, deep brain stimulation (DBS) can be used to target specific brain regions. This method directly intervenes in the disrupted networks of the basal ganglia and reduces tic frequency. Digital therapy options, including online platforms and apps, also offer valuable support and have demonstrated efficacy comparable to traditional behavioral therapies.

Overall, the treatment of Tourette syndrome must be individually tailored. Behavioral therapy remains the first-line treatment, while medications and neuromodulation techniques can be beneficial in more severe cases. Advancing our understanding of the neural basis of the disorder paves the way for new therapeutic approaches. Future research may enable more precise interventions in the disrupted neuronal networks, ultimately improving the lives of affected individuals.

 

Sources: 

Frey, J., & Malaty, I. A. (2022). Tourette Syndrome Treatment Updates: A Review and Discussion of the Current and Upcoming Literature. Current Neurology and Neuroscience Reports, 22(2), 123–142. Source

Johnson, K. A., Worbe, Y., Foote, K. D., Butson, C. R., Gunduz, A., & Okun, M. S. (2023). Tourette Syndrome: Clinical Features, Pathophysiology, and Treatment. The Lancet. Neurology, 22(2), 147–158. Source

Jones, K. S., Saylam, E., & Ramphul, K. (2025). Tourette Syndrome and Other Tic Disorders. In StatPearls. StatPearls Publishing. Source

Müller-Vahl, K. (2019). Behandlung des Tourette-Syndroms. Tourette-Gesellschaft Deutschland e.V. Source

Novotny, M., Valis, M., & Klimova, B. (2018). Tourette Syndrome: A Mini-Review. Frontiers in Neurology, 9. Source