Tourette’s syndrome (SGT) like many neurological diseases has a genetic component. Although not inherited, there is a genetic predisposition that increases the risk of developing the disease for a patient’s relatives.
Biological mechanisms of Tourette’s syndrome
The precise mechanisms underlying the symptoms of Tourette’s Gilles syndrome are still poorly understood, but the region of the basal ganglia or basal ganglia, the deep structures of our brain, is particularly involved in tics.
Scintigraphy studies showed hypoactivity in the basal ganglia and orbito-frontal cortex, while the lateral premotor cortex showed hyperactivity.
Conversely, in functional Magnetic Resonance Imaging (MRI) performed while the patient controlled and suppressed his tics showed an activation of the prefrontal cortex and anterior cingulate, and a deactivation of the pallidum, putamen and thalamus.
Recently, histological analysis has suggested that these abnormalities may reflect GABAergic neuronal migration disorder, reinforcing the hypothesis of dysfunction of the striatum and the ganglia in general.
The dysfunction of this area may be due to a disruption of neurotransmitters, the chemical molecules essential for the transmission of nerve impulses between neurons.
GABAergic neurons (using GABA as a neurotransmitter) synchronize the firing of neural networks and generate oscillations that are essential for learning and generally for integrating information. An interneuron innervates hundreds of major cells and controls their discharge. GABA plays a key role in the development of coherent adult activities.
At Paris Brain Institute
Work in patients with sudden manifestations of verbal or physical aggression has shown by functional MRI a decrease in connections within the orbito-frontal cortex and a dysfunction in connectivity between the orbito-frontal cortex, amygdala and hippocampus. This study concludes that these explosive “crises” result from ineffective control of actions and dysfunction of emotional regulation and impulsivity.
- In a study published in the journal Brain, Yulia Worbe and her collaborators, “Mov’It: Movement, Investigations, Therapeutics. Experimental pathophysiology and Therapeutics” led by Professor VIDAILHET and Professor LEHERICY) have shown that patients with Tourette’s syndrome develop more habitual behaviours than healthy subjects of the same age.
These results shed new light on the mechanisms underlying the formation and persistence of tics, which could be partly learned actions becoming automatic, and persisting in the same way as bad habits. Alterations in certain neural networks involved in the genesis of habits may explain the exacerbation of these behaviours in patients.
