Acupuncture for Tourette's Syndrome (TS): Neurotransmitters, the Vagus nerve, and a Patient's Recovery Story

Discover how acupuncture supports Tourette’s Syndrome by regulating dopamine, GABA, and Vagus nerve tone – with science explained and a real case study shared.

My Story

I am passionate about treating Tourette's Syndrome and tic disorders in general. It isn’t simply because of the amazing transformations I’ve seen acupuncture produce – the shackles of fear and a sense of the body’s betrayal dropping away. It also comes from my own past. I grew up a lisping, stuttering runt with a neck tic, being the go-to for the schools’ bullies. Every day carried the same sharp fear; that my body would betray me, showing the world the stress I felt inside. My stuttering and nervous tic became a signal to others – a dinner bell for tormentors, my own body seeming more on their side than mine.

It was a long road to heal those parts of me. That journey is why, when I see someone else’s burden lift, it feels like a gift to me. To have them see that this disorder is not a definition of themselves but rather a stage with an end where they come out of it with the strength of lions from the road they’ve walked. That is the gift. That is why I refine my techniques so carefully – to help each person find their way back to themselves, and to make that recovery come just a little faster.

Tourette’s Syndrome at the Circuit Level: The Science

When we think of TS, most people picture the tics – sudden head jerks, eye blinks, or vocal outbursts that seem to come from nowhere. But beneath those outward signs lies a remarkably intricate story of brain circuits and chemical messengers. The brain isn’t just “firing wrong.” It’s more like the traffic lights at a busy intersection flickering out of sync – green in two directions at once, leaving chaos to spill onto the road.

A tic can feel a bit like a sneeze that builds pressure until it bursts through. You can delay it for a moment, but the release feels almost inevitable. That same mix of tension and relief is what many people with Tourette’s Syndrome describe when they talk about the “urge” before a tic.

Back then, I had no language for what was happening in my own brain. Today, neuroscience gives us a clearer picture of why the body moves against our will – and why treatment needs to start with restoring balance in these deeper circuits.

Let’s look at these circuits more closely – the basal ganglia and its neurotransmitters – to see how each one contributes to the pattern we call Tourette’s Syndrome.

Mechanistic Overview (Clinician-Facing)

1. Neuroanatomical Pathways: CSTC Circuits

• Direct Pathway (faciliatory): Cortex → Striatum → GPi/SNr → Thalamus → Cortex.

  • Function: facilitates intended motor activity.

• Indirect Pathway (inhibitory): Cortex → Striatum → GPe → STN → GPi/SNr → Thalamus → Cortex.

  • Function: suppresses competing or unwanted movements.

• In TS: Excessive facilitation (overactive direct pathway) combined with reduced inhibition (weakened indirect pathway) produces disinhibition of motor programs and tic expression.

  
  

2. Neurotransmitter Systems by Functional Role

• Dopamine (DA):

  • Hyperdopaminergic activity in the striatum is a central finding.

  • Evidence of D2 receptor supersensitivity and increased phasic DA release.

  • PET imaging shows elevated intrasynaptic DA in TS patients (Singer et al., Arch Gen Psychiatry, 2002).

  • Clinical correlation: efficacy of D2 receptor antagonists (haloperidol, risperidone).

• GABA:

  • Striatal GABAergic interneurons normally suppress medium spiny neurons (MSNs).

  • Reduced GABA concentrations detected via MRS in TS (Peterson et al., Arch Gen Psychiatry, 2001).

  • Result: diminished inhibition, leading to hyperexcitable CSTC loops.

• Glutamate:

  • Major excitatory drive in CSTC circuits.

  • Altered thalamocortical glutamatergic transmission linked to tic expression.

  • NMDA receptor modulation alters tic-like behaviors in preclinical models (Yager et al., Neuropsychopharmacology, 2015).

• Norepinephrine (NE):

  • Modulates attention and arousal; dysfunction exacerbates tic severity and ADHD comorbidity.

  • α2-adrenergic agonists (clonidine, guanfacine) reduce symptoms, especially in ADHD+TS cases.

• Serotonin (5-HT):

  • Primarily implicated in comorbid OCD/anxiety.

  • Dysfunction in orbitofrontal-striatal circuits parallels OCD traits seen in TS patients.

  • SSRIs used clinically for OCD features.

• Acetylcholine (ACh):

  • Striatal cholinergic interneurons are key regulators of motor inhibition.

  • Dysfunction contributes to tic generation, though less studied than DA/GABA.

    
    

3. Neurodevelopmental Trajectory

• Childhood: Striatal inhibitory circuits immature; DA hyperactivity evident early.

• Adolescence: Tics peak (ages 10–12) with pubertal DA surges; stress sensitivity magnifies symptoms.

• Adulthood: Up to 50% improve due to strengthening of frontal suppression networks; persistent cases correlate with enduring CSTC abnormalities.

  
  

4. Integrative Model: Disinhibition Hypothesis - Tourette’s Syndrome can be conceptualized as a disorder of failed inhibition within CSTC circuits:

• Excess dopaminergic input.

• Impaired GABAergic function.

• Abnormal sensory-motor gating linking premonitory urges to motor release.

This aligns with the clinical observation that many patients describe a mounting “urge” relieved only by performing the tic.

References (selected):

• Singer HS et al. Elevated intrasynaptic dopamine release in Tourette’s syndrome measured by PET. Arch Gen Psychiatry. 2002;59(12):1151-1160. http://doi.org/10.1001/archpsyc.59.12.1151

• Peterson BS et al. A functional magnetic resonance imaging study of tic suppression in Tourette syndrome. Arch Gen Psychiatry. 2001;58(12):1140–1147. http://doi.org/10.1001/archpsyc.58.12.1140

• Albin RL, Mink JW. Recent advances in Tourette syndrome research. Trends Neurosci. 2006;29(3):175-182. http://doi.org/10.1016/j.tins.2006.01.001

• Yager LM et al. NMDA receptor involvement in tic-like behaviors. Neuropsychopharmacology. 2015;40(5):1332–1342. http://doi.org/10.1038/npp.2014.315

  
  

Case Study: Melody’s Story

To see how the syndrome's mechanisms translate into real life, I want to share the story of Melody, a 19-year-old college student who came to me at her aunt’s urging. She had lived with TS for as long as she could remember. Her most visible symptom was a sharp, involuntary jerk of her head back and to the right. It wasn’t just embarrassing – it left her with chronic neck pain that weighed on her daily life.

Her tics were set off by familiar triggers: lack of sleep, irregular meals, junk food, and stress. Aerobic exercise helped – when she was running, the tics eased. But if she overdid it, fatigue would spark them again. It was a fine line to walk, and as school demands increased, she was losing her footing. Stress mounted with finals approaching and internship applications pending. Her only other coping mechanism was binge-watching TV, which helped her escape but didn’t calm her nervous system for long.

That cycle of stress and shame was closing in. The tics caused embarrassment, which triggered more stress, which fed back into the tics. She described it as a loop she couldn’t break.

The Treatment Approach

At intake, I observed her tic firsthand – it surprised both of us when it surfaced mid-conversation. Her pulse showed excess activity in the vagal pattern I often see with neurological conditions. Tender points at the diaphragm and along the liver and gallbladder meridians stood out. These findings pointed toward starting with a Ren/Yin Qiao protocol – a treatment that regulates parasympathetic tone through vagal afferents.

Alongside acupuncture, I gave her a non-negotiable daily assignment: Loving-kindness meditation, directed not outward but inward. She was to picture herself as a little girl with uncontrollable tics and generate compassion for that child. Twice a day, fifteen minutes, every day. This practice became the emotional anchor for her care.

The Arc of Recovery

• By the 3rd treatment (two weeks in): frequency of tics dropped by 50%, and severity by about 25%.

• By the 6th treatment: after switching to the Dai/Yang Wei protocol (based on pulse changes), her progress accelerated – 75% fewer tics, 50% less severe, and neck pain nearly gone.

• By the 12th treatment: visits were spaced to once every 3-4 weeks. Her tics had become rare and faint shadows of their former intensity. Neck pain no longer lingered, except for brief tension after stress.

  
  

Over the following 18 months, she returned occasionally before high-stress events like exams or interviews. By then, she had built a reliable routine of swimming and trail running for stress relief, with loving-kindness meditation as her emotional safeguard.

Reflection

What struck me most was how much her recovery hinged on regulating the Vagus nerve first. The Ren/Yin Qiao pathway, essentially the parasympathetic foundation, had to be stabilized before other patterns could be addressed. Once that groundwork was laid, her resilience took over.

Melody’s story is one of learning to rewrite the body’s loop - from shame and stress fueling tics, to compassion and regulation loosening their grip. Watching her step into that freedom reminded me of why I do this work.

Living with Tourette’s Syndrome or tic disorders can feel isolating. My concierge neurological acupuncture practice brings care directly to patients across New Hampshire – in their homes or offices – so support is always within reach.

Call Paul at (603) 630-9430 or Email: paul@neuroacupuncturenh.com to schedule a complimentary consultation.