Summary: For years, motor tics were primarily associated with dysfunction in the brain’s motor cortex, but the emotional and sensory features of Tourette syndrome remained poorly explained. A research team has now mapped a critical pathway linking movement regions to centers that process emotion and internal awareness, offering a biological explanation for the mix of tics, premonitory sensations, and psychiatric comorbidities seen in Tourette’s.
The study identifies a circuit that carries signals from the primary motor cortex through an intralaminar thalamic relay to the insular cortex. This connection clarifies how a motor system malfunction can influence emotional processing and bodily awareness, and it points to a precise neural target for developing less invasive therapies.
Key Facts
- Insular connection: The team mapped a neuronal pathway linking the motor cortex (movement control) to the insular cortex (emotion and interoception) via a thalamic relay.
- Reducing tic strength: In mice, inhibiting this pathway significantly reduced the intensity of motor tics while leaving tic frequency largely unchanged.
- Explaining co-occurrence: This bridge between motor and limbic regions helps explain why Tourette syndrome is commonly accompanied by OCD, ADHD, and the sensory “premonitory urge.”
- Potential non-invasive treatment: The identified circuit offers a concrete target for emerging approaches such as ultrasound neuromodulation, which could reduce reliance on invasive deep brain stimulation.
Source: Kobe University
TACHIBANA Yoshihisa, neurophysiologist at Kobe University, notes: “Tic disorders like Tourette syndrome are among the most common neuropsychiatric conditions affecting children, yet their neuronal basis remains incompletely understood.”
Previous work established that abnormal activity in a motor cortex circuit can generate motor tics. However, many patients also experience strong internal urges before a tic and frequently have other psychiatric diagnoses, suggesting involvement of additional brain regions beyond motor areas.
Clinical imaging studies have reported abnormal insular cortex activity in people with tic disorders, but the relationship between the insula and tic generation had not been clearly defined. Tachibana, who studies connections between bodily sensation and mental state, previously observed that a dental mouthguard improved motor and vocal tics in many patients, suggesting peripheral sensory input can modulate tic expression.
Following that observation, the researchers traced neurons that convey muscle and jaw movement signals and found projections to the insular cortex. This raised the hypothesis that altering insular input could change how motor tics affect emotional and interoceptive processing.
To probe that hypothesis, the team used a mouse model in which tics were induced by localized disruption of inhibitory signaling in the striatum. Using viral tracing, fiber photometry, and chemogenetic tools, they mapped the pathway from basal ganglia output through intralaminar thalamic nuclei to the insular cortex and monitored activity during tic-like movements.
Their results, published in Cell Reports, show tic-associated activity not only in the primary motor cortex but also in the insular cortex. Importantly, inhibitory manipulation of the insular cortex or of the thalamo-insular route substantially reduced the strength of tic-like behaviors and the cortical activity associated with them, even though the number of tics did not change appreciably.
“We propose that this circuit functions as a bridge connecting motor areas with limbic and interoceptive regions that were previously considered separate,” Tachibana explains. The motor cortex may still generate the abnormal signals that produce tics, but the thalamo-insular pathway appears to propagate and amplify those signals into the emotional and sensory domain, shaping the subjective intensity and accompanying psychiatric symptoms.
Beyond clarifying mechanisms, the study points to a concrete therapeutic opportunity: targeting the identified relay and its insular projections could suppress tic intensity without brain surgery. Tachibana suggests that focused interventions, such as ultrasound neuromodulation directed at the relay or insular targets, might deliver safer, less invasive alternatives to deep brain stimulation.
Funding: This research was supported 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). The work involved collaboration with the National Institute for Physiological Sciences and the Graduate University for Advanced Studies, SOKENDAI.
Key Questions Answered:
A: Jaw and facial muscle movements produce sensory feedback that travels to the brain. The study suggests these signals reach the insular cortex. By altering peripheral input with a mouthguard, the feedback loop into the insula is modified, which can reduce the perceived intensity of tics.
A: The evidence indicates the motor cortex still initiates tic-like activity. The insular cortex appears to act as an amplifier and integrator that shapes tic strength and the accompanying emotional and interoceptive experience, rather than being the primary generator.
A: Identifying a specific relay and cortical target makes clinical translation more feasible, and the authors note this pathway is a high priority for further investigation. Human trials will be needed to evaluate safety and effectiveness before ultrasound neuromodulation can be recommended clinically.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- The journal paper was reviewed in full.
- Additional context was added by staff.
About this AI and auditory neuroscience research news
Author: Daniel Schenz
Source: Kobe University
Contact: Daniel Schenz – Kobe University
Image credit: 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. 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 core features of Tourette syndrome, yet the neuronal mechanisms that drive these behaviors remain incompletely characterized. The authors developed a mouse model of tic-like movements by unilateral striatal injection of a GABAA receptor antagonist, which produced c-Fos activation in motor and limbic structures, including the insular cortex (IC).
Fiber photometry recorded tic-related activity in both IC and primary motor cortex (M1). Viral tracing showed that basal ganglia outputs from the substantia nigra pars reticulata reach IC through intralaminar thalamic nuclei (ITN). Chemogenetic inhibition of IC or the thalamo-insular pathway suppressed tic-like behaviors and reduced associated cortical activity.
These findings position the insular cortex as a candidate node in tic generation and highlight intralaminar thalamic nuclei as relays that connect motor and limbic circuits. Aberrant thalamo-insular signaling may therefore contribute to tic-related pathology and offers a circuit-level target for future therapeutic development.