Summary: While motor tics have long been linked to malfunctions in the brain’s motor cortex, the emotional and sensory aspects of Tourette syndrome remained a mystery. A team has now mapped a vital bridge between the “body” and “mind” centers of the brain.
The study identifies a pathway traveling from the motor cortex through a thalamic relay to the insular cortex. This circuit explains how a motor dysfunction spreads to influence emotional processing and internal awareness, offering a biological explanation for the complex mix of tics, sensory urges, and psychiatric conditions seen in Tourette’s.
Key Facts
- The Insular Connection: Researchers discovered a specific neuronal pathway linking the motor cortex (responsible for movement) to the insular cortex (responsible for emotions and internal awareness) via a thalamic relay station.
- Reducing Tic Intensity: By inhibiting this newly identified pathway in mice, the team was able to significantly reduce the strength of motor tics, even though the frequency of the tics remained unchanged.
- Explaining Co-occurrence: This “bridge” between movement and emotion centers explains why Tourette syndrome is frequently accompanied by obsessive-compulsive disorder (OCD), ADHD, and the sensory “premonitory urge” patients feel.
- Future Non-Invasive Therapy: The discovery identifies a specific target for safer, less invasive treatments like ultrasound neuromodulation, potentially replacing the need for invasive deep brain stimulation.
Source: Kobe University
Tic disorders, such as Tourette syndrome, are among the most common neuropsychiatric conditions and have a significant impact on children’s lives. However, their underlying neuronal mechanisms remain poorly understood,” says Kobe University neurophysiologist TACHIBANA Yoshihisa.
Researchers of the field have come to understand that there is a circuit in the brain’s motor cortex that causes the motor tics when malfunctioning.
However, a hallmark of Tourette’s is the “premonitory urge” felt by people with the condition, and the condition is often accompanied by others such as obsessive-compulsive disorder, attention deficit and hyperactivity disorder or autism spectrum disorder, which hints at an involvement of other brain regions.
Tachibana explains, “Indeed, brain imaging studies of people with tic disorders have reported abnormal activity in the insular cortex, which is responsible for emotional processing and internal awareness, but there has been very little research on the relationship between tic disorders and this region.”
Tachibana, who specializes on the connection between “the body” and “the mind,” has previously published that two thirds of Tourette’s patients wearing a dental mouthguard showed marked improvements of motor and vocal tics.
They traced the neurons responsible for perceiving muscle movements and found that they connected to the insular cortex, suggesting that tics can be ameliorated by changing the way this region is connected to the brain’s motor cortex.
To test that hypothesis, the researchers now set out to elucidate how these regions are connected and how manipulating the connection changes tics in a study that involved mice in which tics were artificially induced.
In the journal Cell Reports, they report their discovery of a neuronal connection from the motor cortex via an intermediary thalamic relay station to the insular cortex. This relay station is relevant, too, because it has been used as the target for a therapy of Tourette’s using deep brain stimulation, even though it wasn’t clear why it works. In addition, they showed that by inhibiting this connecting pathway, they could markedly reduce the strength of tics, albeit not their frequency.
“We believe that the neuronal circuit we found plays a crucial role as a bridge connecting brain regions that were previously thought to act independently from each other,” comments Tachibana.
In their study, the researchers further explain that they still think that the motor tics are possibly generated by the aberrant function of the brain’s motor cortex, but the connection they found probably explains how this dysfunction spreads to other regions. This may therefore not only explain where the emotional and cognitive symptoms of Tourette’s come from, but also why the condition is so often accompanied by other neuropsychiatric disorders.
At the same time, the connection also suggests a new avenue for research on a treatment. Tachibana says: “The currently used deep brain stimulation is invasive and comes with a risk of complications. On the other hand, targeted intervention of the neuronal processing in the circuit we identified, such as ultrasound neuromodulation, may be options for the development of less invasive and safer treatment methods.”
Funding: This research was funded by the Japan Society for the Promotion of Science (grants 18K06852, 22K19732, 24H00422, 24K02339, 24H00620), the Taiju Life Social Welfare Foundation, and the Japan Agency for Medical Research and Development (grant JP23wm0625001). It was conducted in collaboration with researchers from the National Institute for Physiological Sciences and the Graduate University for Advanced Studies, SOKENDAI.
Key Questions Answered:
A: Muscle and jaw movements send sensory signals to the brain. This research suggests those signals travel to the insular cortex. By wearing a mouthguard, the input to this circuit changes, essentially “rewiring” the feedback loop between the mouth and the emotion-processing centers of the brain.
A: Not exactly. The researchers believe the motor cortex still generates the tics, but the insular cortex is what gives them their “strength” and causes the emotional/cognitive symptoms. The insular cortex is like an amplifier that determines how intense the tic feels and how much it affects the person’s awareness.
A: Now that the specific “relay station” has been identified, researchers can begin human trials to see if targeted sound waves can calm the circuit. This is a top priority because it would be far safer than the brain surgery required for current deep brain stimulation.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this AI and auditory neuroscience research news
Author: Daniel Schenz
Source: Kobe University
Contact: Daniel Schenz – Kobe University
Image: The image is credited to H. Kuno et al., Cell Reports
Original Research: Open access.
“Intralaminar thalamus relays basal ganglia output to the insular cortex to drive tic generation” by Hiroto Kuno, Natsumi Tsuji, Kenta Kobayashi, Toru Takumi, and Yoshihisa Tachibana. Cell Reports
DOI:10.1016/j.celrep.2026.117272
Abstract
Intralaminar thalamus relays basal ganglia output to the insular cortex to drive tic generation
Motor and vocal tics accompanied by premonitory urges are hallmark symptoms of Tourette syndrome (TS), yet the underlying neuronal mechanisms remain incompletely understood.
Here, we establish a mouse model of tic-like movements by unilateral striatal injection of a GABAA receptor antagonist. This model induces c-Fos activation in both motor and limbic structures, including the insular cortex (IC).
Fiber photometry reveals tic-associated activity in IC as well as the primary motor cortex (M1). Viral tracing demonstrates that basal ganglia outputs from the substantia nigra pars reticulata are transmitted to IC via the intralaminar thalamic nuclei (ITN).
Chemogenetic inhibition of IC or the thalamo-insular pathway suppresses tic-like behaviors and reduces tic-associated cortical activity. These findings identify IC as a candidate node involved in tic generation and highlight ITN as relay stations linking motor and limbic circuits.
Aberrant thalamo-insular signaling may contribute to tic-related pathophysiology and represents a potential circuit-level therapeutic target.
