Tourette syndrome (TS) is a neurodevelopmental disorder of childhood onset characterized by chronic motor and vocal tics. Although its etiology and pathophysiology are still unknown, there is increasing evidence for disruptions in the structure and function of cortico-striatal-thalamic-cortico (CSTC) neural circuitry. This altered functioning of CSTC circuitry including the prefrontal cortex might be associated with general problems of inhibitory control, not only of motor function, but also of cognitive and emotional regulation [1
]. Unfortunately, the large number of neuropsychological studies addressing inhibition in TS could not draw a clear picture (for a review see [1
First, it has to be taken into consideration that there are separable types of inhibition, probably all with different neural substrates [3
]. However, there were inconsistencies between studies in TS even when they used the same task for measuring inhibitory control. For example, a flanker task did not show deficits in response inhibition in adults [4
], but in children with 'pure' TS compared to a control group [5
]. Two studies using another test of response inhibition, an A-X version of the continuous performance task (CPT) revealed divergent findings in children with TS compared to healthy controls. One study found differences [6
], the other not [7
Second, all these inconsistencies might be attributable to several confounders. The uncontrolled psychiatric symptomatology often comorbid to TS like attention-deficit/hyperactivity disorder (ADHD) is thought to contribute mainly to found inhibitory deficits [8
]. Additionally, previous and actual medication as well as short- and long-term compensatory mechanisms due to voluntary tic-suppression might have confounded previous findings on response inhibition performance in TS.
Hence, there is consensus that response inhibition in TS merits a more thorough investigation of less heterogeneous samples to come to firmer conclusions [4
]. Because the a priori exclusion of confounders is the less biased method compared to post hoc statistical adjustment [9
], we chose this approach to have the best ability to detect response inhibition deficits specific for TS per se. We applied a Go/Nogo task as one of the most common neuropsychological paradigms to investigate response inhibition in the motor domain [10
Normal performance in the Go/Nogo task has been found in children with TS without comorbid conditions [12
] as well as in adults with TS (some of them with comorbid ADHD and/or OCD) [13
]. This is surprising as there are quite prominent differences between both versions of the Go/Nogo task applied.
For example in the task of Ozonoff et al. [12
] the ratio of Go to Nogo stimuli is 50:50, whereas it is 83:17 in that of Hershey et al. [13
]. Frequent Go stimuli are needed to ensure a prepotent tendency to respond that must then be inhibited for Nogo stimuli. But relatively rare Nogo stimuli entail the problem that novelty effects of increased arousal and orientation could not be distinguished from inhibitory requirements [14
]. Hence, on the one hand a task with rare Nogo stimuli is needed to ensure that responses are prepotent and response inhibition is difficult, but on the other hand it has to control for the effects of stimulus probability [15
]. This is even more important in TS as patients were found to be impaired on tasks requiring the processing of novel stimuli [16
Hence, we progress the field of inhibitory control in TS in two points. First, we applied a more demanding Go/Nogo task than Ozonoff et al. [12
] to detect inhibitory deficits that could possibly not be detected by their task. Additionally, the present Go/Nogo task controlled for the first time in TS research for the important confounding of novelty. Second, we included only medication naïve boys with 'pure' TS to avoid confounding effects of medication and psychopathology other than TS. To minimize the extent of compensatory mechanisms we included boys with a short history of tics. In accordance with previous studies on inhibitory control we expected impaired performance of the subjects suffering from TS compared to healthy controls in our highly demanding Go/Nogo task.