The effect of comorbid ADHD on oculomotor abnormalities in boys with Tourette syndrome (TS) was determined using three saccade tasks to examine the planning and execution of eye movements in a study at the Kennedy Krieger Institute and Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD. Subjects in 3 groups, ages ranging from 7.8-14.6 years (means 10-11 yrs) included 14 with TS-only, 11 with TS+ADHD, and 10 controls. Eye movements were recorded by electro-oculography, and maximum saccadic velocities, amplitudes, and latencies were computer analysed.

Latency of prosaccades (measuring ability to initiate saccades to an unpredictable peripheral visual stimulus) was prolonged in both patient groups (TS-only and TS+ADHD) compared to controls, which indicates that TS is associated with delay in initiation of oculomotor responses. Response inhibition errors on aritisaccade (ability to inhibit a prosaccade) tasks (directional errors) and memory-guided saccade task (anticipatory errors) were increased in boys with TS+ADHD compared to the TS-only group, suggesting that comorbid ADHD is associated with deficits in response inhibition and excessive variability in motor response to a visual stimulus. Accuracy of memory guided saccades was not significantly different in the three group. [1]

COMMENT. This is the first report of the impact of comorbid ADHD on the execution of eye movements. Whereas TS results in slowed oculomotor responses to a visual stimulus, ADHD is associated with an increased variability of response. This finding is consistent with excessive variability in reaction time demonstrated by continuous performance tasks in children with ADHD. The authors emphasize the importance of treating comorbid conditions, especially ADHD, in children with tic disorders. ADHD is reported to occur in more than 50% of patients with TS. See Ped Neur Briefs Nov 2001 for article on increased risk of cognitive deficits and behavioral disturbance in children with tic disorders complicated by ADHD.

In a previous report of the control of volitional and reflexive saccades in 10 subjects with Tourette’s syndrome and 10 controls [2] from Queen’s University, Kingston, Ontario, Canada, saccadic reaction times were longer, saccadic amplitudes were smaller, but the occurrence of direction errors was normal in the immediate antisaccade task. The ability to inhibit reflexive saccades towards novel stimuli was not impaired in TS. Timing errors were significantly greater in TS compared to controls, indicating that the ability to inhibit planned motor programs is significantly impaired. Altered cortical-basal ganglia circuitry leading to reduced cortical inhibition may explain the inability of TS subjects to delay execution of motor responses. Four of the 10 patients in the Canadian study had co-morbidities, 2 with ADHD, but results were analysed separately and comorbidy was not considered responsible for the findings. A medication effect, possibly involved in 6 patients, was also excluded. It is noteworthy that direction errors, normal in this TS study, were only abnormal in the TS+ADHD group of the Hopkins study and not in the TS-only group.

Deficient inhibition as a marker for familial ADHD subgroup has been proposed at the Hospital for Sick Children, Toronto [3]. Family history of ADHD and risk factors were compared in 54 ADHD children having poor or good inhibition (based on stop-signal paradigm performance) and 26 healthy controls. ADHD was significantly more prevalent in families of ADHD children exhibiting poor inhibition (48%) than in those with good inhibition (18.5%) or in controls (7.7%). Neurobiological and psychosocial risk factors were not different in the 3 groups. Cognitive measures of inhibition may act as phenotype markers for genetic analyses of ADHD. Latent-class subtypes of ADHD (Neuman RJ et al. 1999) are independently transmitted in families and should be more appropriate targets than DSM-IV subtypes for molecular genetic studies of ADHD, according to Todd RD et al. [4]