Advance information and movement sequencing in Gilles de la Tourette's syndrome.

Abstract

Tourette's syndrome is a chronic neurological disorder manifested by involuntary motor tics and vocalisations. Because the basal ganglia have been implicated in the pathology underlying Tourette's syndrome, the present two procedures, both involving sequential movements, sought to determine the extent to which patients with Tourette's syndrome were reliant on, and could utilise different levels of advance information. Patients with Tourette's syndrome were found to be more reliant than controls on external visual cues to execute rather than to initiate a motor programme. When there was a high level of reduction in advance information--that is, a visual pathway to be followed was extinguished well in advance of each successive movement--executions progressively slowed as the sequence was traversed. Similarly, if no advance information was provided before each move, movement execution was slower than that of controls. The movement initiation times of patients with Tourette's syndrome were, however, similar to those of controls, as were their movement execution times when advance visual information was available. It seems that patients with Tourette's syndrome, like parkinsonian patients who are known to have a basal ganglia disorder, require external sensory cues to sequence a motor programme effectively. The present study found evidence consistent with the hypothesis that patients with Tourette's syndrome, like patients with Parkinson's disease, may be dysfunctional in internal switching mechanisms. Alternatively, with limited visual guidance, patients with Tourette's syndrome, regardless of medication or depression state, may require more time to plan and programme each next submovement, and under such conditions may require external visual cues to direct attention effectively to given targets. Although the underlying pathogenesis is still speculative, it is concluded that there is much to support the notion that Tourette's syndrome may stem from abnormalities of the major pathways between the basal ganglia and the frontal lobes.