“OBJECTIVE: Disturbances in the maturation of neural systems that mediate self-regulatory processes may contribute to
the development of Tourette's syndrome by releasing motor and vocal tics from regulatory control. The purpose of this
study was to examine the age correlates of functional activity in neural circuits that sub serve self-regulatory control
in children and adults with Tourette's syndrome. METHOD: The participants were 136 children and adults, which included
66 Tourette's syndrome patients and 70 healthy comparison subjects. During performance of the Stroop interference task,
the authors compared the functional magnetic resonance imaging (fMRI) blood-oxygen-level dependent response in patients
with Tourette's syndrome with that of healthy comparison subjects. General linear modelling of Stroop-related activations
was used to compare the differential effects of age and behavioural performance on changes in self-regulatory control between
the two diagnostic groups. RESULTS: Although the correlations of age with behavioral performance on the Stroop task were similar
between patients with Tourette's syndrome and healthy comparison subjects, the two groups differed significantly in their
correlations of age with the magnitude of regional brain activation during the task. Interactions of age with diagnosis
were detected in the ventral prefrontal (Brodmann's areas 10 and 24) and posterior cingulate cortices (Brodmann's area 31),
and post hoc analyses indicated that subjects with Tourette's syndrome deactivated these regions less with advancing age.
Greater activation of bilateral frontostriatal regions (Brodmann's areas 9/46, 45/46; lenticular nucleus; and thalamus)
accompanied poorer performance in the patient group, which-in the presence of normal behavioural performance on the Stroop
task-suggests that greater activation of the frontostriatal systems helps to maintain task performance in individuals with
Tourette's syndrome. CONCLUSIONS: Normative developmental correlates of activity in frontostriatal circuits that sub serve
self-regulatory control are disturbed in persons with Tourette's syndrome. These aberrant developmental correlates are
likely a consequence of greater anatomical and functional disturbances in these circuits in adults with Tourette's
syndrome, which leads to impaired regulation of tic behaviours. Reduced default-mode processing in ventral prefrontal
and posterior cingulate cortices in adults with Tourette's syndrome suggests the presence of greater difficulty in
engaging mental processes that become active when freed from the demands of more challenging cognitive tasks. However,
individuals with Tourette's syndrome appear to co-opt normal developmental processes in circuits that sub serve age-related
improvement in self-regulatory control while presumably struggling to maintain adequate task performance.”
As I would understand this text persons with Tourette has some problems with some circuits wich would cause electrical
charges (electrical charges are normal in any ones brain as that’s what leads your thoughts) to jump where they are not
supposed to be and therefore causing involuntary tics.
“There is considerable evidence that Gilles de la Tourette syndrome (TS) is due to frontal-striatal dysfunction.
Here we determine whether adaptive cortical changes occur that might ameliorate the effects of this dysfunction.
Specifically we test the hypothesis that increased interactions between selected cortical areas may help compensate
through strengthened inhibition of inappropriate motor responses. To this end we recorded EEG in nine unmedicated patients
with TS and nine age-matched healthy subjects during a variety of behavioural tasks related to motor inhibition. Functional
connectivity between cortical areas was assessed by means of EEG coherence in the alpha frequency band (8-12 Hz). Elevated
coherence was found between sensorimotor areas and the prefrontal and mesial frontal cortex during the acute voluntary
suppression of tics. The same frontomesial network was overactive in TS patients compared with healthy subjects even when
suppression of voluntary movement rather than tics was required during a Go-NoGo task. Behavioural performance in the Go-NoGo
task was not different between patients and controls, confirming that the elevated frontomesial coherence in TS was likely to
be adaptive rather than functionally disruptive. It is concluded that the gain in inhibitory frontomesial cortical networks is
adaptively heightened in TS, and that the same network can also be engaged in the voluntary suppression of tics.”
This would mean that TS is treatable as the body can adept to compensate for the problems with some help of training and/or medical procedure.