Tourette syndrome (TS), like many neurological diseases, has a genetic component. Although not hereditary, there is a genetic predisposition that increases the risk of a patient's relatives developing the disease.
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The precise mechanisms behind the symptoms of Tourette syndrome are still poorly understood, but the region of the basal ganglia or basal ganglia, deep structures in our brain, is particularly implicated in tics.

Scintigraphic studies show that the basal ganglia and orbitofrontal cortex are hypoactive, while the lateral premotor cortex is hyperactive.

cause et mécanisme biologique gilles de la tourette

Conversely, functional Magnetic Resonance Imaging (MRI) performed while the patient was controlling and suppressing his tics showed activation of the prefrontal and anterior cingulate cortices, and deactivation of the pallidum, putamen and thalamus.

Recently, histological analysis has suggested that these abnormalities may reflect a disorder in the migration of GABAergic neurons, reinforcing the hypothesis of a dysfunction of the striatum and the grey nuclei in general.

Dysfunction in this area could be due to a disturbance in neurotransmitters, the chemical molecules essential for transmitting nerve impulses between neurons.

GABAergic neurons (using GABA as a neurotransmitter) synchronise the discharge of neuronal networks and generate oscillations that are essential for learning and, in general, for the integration of information. An interneuron innervates hundreds of main cells and controls their discharge. In adults, GABA plays a key role in the generation of coherent activities.


At the Paris Brain Institute

Research on patients presenting with sudden outbursts of verbal or physical aggression has revealed, using functional MRI, a reduction in connections within the orbitofrontal cortex and a dysfunction in connectivity between the orbitofrontal cortex, the amygdala and the hippocampus. The study concludes that these explosive ‘seizures’ result from ineffective control of actions and dysfunction of emotional regulation and impulsivity.

These results shed new light on the mechanisms underlying the formation and persistence of tics, which could in part be learned actions that become automatic and persist in the same way as bad habits. Alterations in certain neuronal networks involved in the generation of habits could explain the exacerbation of these behaviours in patients.

Further information: https://institutducerveau-icm.org/en/actualite/tourettes-syndrome-tics-a-bad-habit/