Tourette Syndrome (TS) is a neurodevelopmental condition defined by the presence of chronic, involuntary motor and vocal tics. These sudden, repetitive movements and sounds represent a failure of the brain’s natural ability to inhibit unwanted actions. Neuroimaging techniques allow researchers to look inside the living brain to identify physical and activity-based deviations from neurotypical brains. Comparing Tourette’s brain scans to those of healthy controls reveals consistent differences in structure, function, and chemical environment.
How Scientists View the Tourette’s Brain
Scientists use several advanced tools to visualize the brain and understand the basis of tics. Structural imaging, primarily Magnetic Resonance Imaging (MRI), provides high-resolution pictures of the brain’s anatomy, allowing measurement of volume, shape, and tissue density. This method helps determine if the physical architecture of specific brain regions is altered in individuals with TS.
Functional imaging, such as functional MRI (fMRI), measures brain activity by tracking blood flow, revealing which regions are working and how they communicate with each other. This is used to map the brain’s communication pathways and identify differences in neural circuit activity. Molecular imaging, including Positron Emission Tomography (PET) and Single-Photon Emission Computed Tomography (SPECT), visualizes the brain’s chemical environment. These scans use specialized tracers to track neurotransmitters or their receptors, providing insight into the chemical imbalances associated with the disorder.
Structural Differences: Volume and Anatomy
One of the most consistently reported anatomical findings in TS brains involves the basal ganglia, a group of deep brain structures involved in movement control and habit formation. Studies frequently suggest a volume reduction in the caudate nucleus, a component of the striatum, which is a primary input center of the basal ganglia. This reduction is often estimated to be around 5% compared to neurotypical controls.
The physical size of other basal ganglia components, such as the putamen and globus pallidus, can also be smaller, particularly in adults with persistent symptoms. These volumetric differences imply a deviation in the development or maturation of the subcortical motor control system.
Cortical regions, the brain’s outer layer, also show anatomical variations in TS. The thickness of the cortex, particularly in the motor and prefrontal areas, can be altered. Children with TS often show larger volumes in the dorsal prefrontal cortex, a region linked to executive function and inhibitory control. This enlargement is hypothesized to be a neuroplastic adaptation, helping the brain attempt to suppress tics.
The corpus callosum, the large bundle of white matter fibers connecting the two brain hemispheres, also exhibits differences. The overall cross-sectional area of the corpus callosum is sometimes smaller in individuals with TS, which suggests altered interhemispheric communication.
Functional Differences: Circuitry and Connectivity
The core of the functional difference lies in the Cortico-Striato-Thalamo-Cortical (CSTC) loop, which is the network responsible for selecting and executing movements while suppressing unwanted ones. In TS, the function of this loop is atypical, leading to a failure of movement selection and the appearance of tics. The standard brain uses this circuitry like a gate, opening it for intended movements and keeping it closed for actions that should be inhibited.
Functional imaging studies consistently show a state of hyper-excitability or disinhibition in this circuit in TS brains. Activity in the basal ganglia, specifically the putamen and thalamus, is often increased during rest or prior to a tic, which correlates with tic severity. This increased activity suggests that the “gate” that normally suppresses irrelevant movements is leaky or opens too easily.
Connectivity analysis further details this functional dysregulation by measuring the communication between regions. Individuals with TS exhibit stronger functional connectivity within subcortical nodes, such as the striatum and thalamus, compared to control subjects. This enhanced internal communication may reflect aberrant activity propagation within the movement initiation centers.
Conversely, there is often reduced functional connectivity found in brain areas responsible for inhibitory control, such as the prefrontal cortex, and its connections to the striatum. This imbalance is thought to underpin the generation of tics. The atypical firing patterns are especially pronounced in the supplementary motor area, which is highly active just before a tic is expressed.
The Neurochemical Environment
The functional dysregulation in the CSTC loop is heavily modulated by an atypical neurochemical environment, primarily involving the neurotransmitter dopamine. Dopamine is a chemical messenger that plays a significant role in movement, reward, and motivation, and it powerfully modulates the basal ganglia’s function. The effectiveness of dopamine-blocking medications in treating tics strongly supports its involvement.
Molecular imaging studies using PET scans have provided specific details about dopamine signaling. Research suggests that while the total number of dopamine D2 receptors may be unchanged or slightly increased, the release of dopamine is significantly altered. Specifically, individuals with TS appear to have an increase in phasic dopamine release, which is the rapid, spike-like release that occurs in response to stimuli. This heightened sensitivity or availability of dopamine in the striatum can enhance the excitability of motor pathways.
This altered dopamine dynamic is hypothesized to lower the threshold for movement initiation, making it easier for tics to be expressed. Other neurotransmitter systems also show differences, although the findings are less consistent than those for dopamine.
Some studies suggest a reduction in GABAergic interneurons in the striatum, which would further contribute to the disinhibition of the motor system. Furthermore, atypical binding of serotonin transporter and 5-HT2A receptors has been observed, suggesting that the serotonin system interacts with and influences the primary dopamine-driven pathology.