Intelligence moderates impulsivity and attention in ADHD children: an ERP study using a go/nogo paradigm.

OBJECTIVES: If the cardinal symptoms of ADHD - hyperactivity, impulsivity and inattention - are combined with a learning disability (70 ≥ IQ < 85), the question arises whether a child shows hyperkinetic behaviour because of intellectual overload in a challenging situation, for example at school. Perhaps, this behaviour is not a primary attention deficit disorder but an impulse control disorder, determined by the primarily intelligence level. It raised the question whether attention deficit and impulse control regarded as behavioural inhibition deficit may depend on intelligence and therefore should be separated into distinct clinical entities. METHODS: A total of 45 children (15 with ADHD, 15 with learning disabilities (LD), 15 with ADHD and learning disabilities) were compared in a matched-pair design with 42 control children using a go/no go paradigm (visual continuous performance test, CPT). The dependent variable was the target P3 amplitude, averaged from a 10-20 EEG measurements under distinct trigger conditions. For statistical analysis, a three-factor analysis of variance (MANOVA) with repeated measurements was used. In a subsequent regression analysis with residuals, the influence of intelligence (IQ) was calculated and a "parallel analysis of variance" was conducted. RESULTS: No differences in the P3 amplitudes in the comparison ADHD-control group were found. Reduced P3 amplitudes as main effects in the LD group compared with controls were found and a significant group-dependent interaction on reduced P3 amplitudes comparing ADHD + LD versus control group. Using residuals (IQ), this interaction was not longer verifiable. CONCLUSION: Impulsivity and attention deficit as the cardinal symptoms of ADHD, regarded as behavioural inhibition deficit, are essentially moderated by the primary intelligence, rather than by an attention deficit. The lower the IQ, the more ADHD surfaces as a disturbed impulsivity and lesser as an attention deficit.

Effects of methylphenidate on motor system excitability in a response inhibition task.

BACKGROUND: Motor system excitability is based on a complex interaction of excitatory and inhibitory processes, which in turn are modulated by internal (e.g., volitional inhibition) and external (e.g., drugs) factors. A well proven tool to investigate motor system excitability in vivo is the transcranial magnetic stimulation (TMS). In this study, we used TMS to investigate the effects of methylphenidate (MPH) on the temporal dynamics of motor system excitability during a go/nogo task. METHODS: Using a double-blind, placebo-controlled, crossover design, 14 healthy adults (8 male, 6 female; aged 20-40 yrs) performed a spatial go/nogo task (S1-S2 paradigm) either under dl-methylphenidate (MPH, 20 mg) or placebo. TMS single and double-pulses (interstimulus interval: 3 ms) were delivered either at 120, 230 or 350 ms after the S2 stimulus (control, go and nogo trials). RESULTS: At the performance level, faster reaction times and a trend towards less impulsivity errors under MPH vs. placebo were observed.In nogo trials, i.e., when a prepared response had to be inhibited, motor evoked potentials (MEPs) had a smaller amplitude at an interval of 230 ms compared to 120 and 350 ms. The short-interval intracortical inhibition (SICI) increased over time.Under MPH, SICI in nogo trials was larger compared to placebo. With the interval between S2 and the TMS-pulse increasing, MEP amplitudes increased under MPH in nogo trials but an early inhibitory effect (at 120 ms) could also be observed. CONCLUSION: Our results show a distinct pattern of excitatory and inhibitory phenomena in a go/nogo task. MPH appears to significantly alter the dynamics of motor system excitability. Our findings suggest that a single dose of 20 mg MPH provides some fine-tuning of the motor system in healthy adults.

Intracortical motor inhibition and facilitation in adults with attention deficit/hyperactivity disorder.

Using transcranial magnetic stimulation (TMS), disturbed facilitatory and inhibitory motor functions were recently found to correlate with motor hyperactivity in children with ADHD. Since hyperactivity seems to become reduced in ADHD during the transition to adulthood, a normalization of motor cortical excitability might be assumed. Therefore, we investigated the same inhibitory and facilitatory TMS paradigms in ADHD adults as we had previously examined in children. Motor cortical excitability was tested with TMS paired-pulse protocols in 21 ADHD adults and 21 age- and gender-matched healthy controls. In contrast to our results in ADHD children, no group-specific differences in amplitude changes of motor evoked potentials for inhibitory inter-stimulus intervals (ISI) (3, 100, 200 and 300 ms) or for facilitatory ISIs (13, 50 ms) could be detected. In ADHD adults, disturbed facilitatory and inhibitory motor circuits as found in ADHD children could not be shown, probably due to a development-dependent normalization of motor cortical excitability.

Impaired transcallosally mediated motor inhibition in adults with attention-deficit/hyperactivity disorder is modulated by methylphenidate.

Using transcranial magnetic stimulation (TMS) in children with ADHD, an impaired transcallosally mediated motor inhibition (ipsilateral silent period, iSP) was found, and its restoration was correlated with improvement of hyperactivity under medication with methylphenidate (MPH). Hyperactivity has been reported to decrease during transition into adulthood, although some motor dysfunction might persist. As one underlying neurophysiological process, a development-dependent normalization of motor cortical excitability might be postulated. In order to test this hypothesis, we measured the iSP in 21 adult ADHD patients and twenty-one sex- and age-matched healthy controls. In 16 of these patients, a second TMS was performed under treatment with MPH. Our results indicate a persistence of impaired transcallosally mediated motor cortical inhibition (shortened duration) in ADHD adults, which was correlated with clinical characteristics of hyperactivity and restlessness, and was restored by MPH. In contrast to ADHD in childhood, the iSP latency was not impaired, suggesting a partial development-dependent normalization of motor cortical excitability in ADHD adults. ISP duration appears to be a sensitive parameter for the assessment of disturbed intercortical inhibition in adults with ADHD.

Restoration of disturbed intracortical motor inhibition and facilitation in attention deficit hyperactivity disorder children by methylphenidate.

BACKGROUND: Previous investigations using transcranial magnetic stimulation (TMS) have shown that neural inhibitory motor circuits are disturbed in ADHD children. We sought to investigate the influence of methylphenidate (MPH) on inhibitory and facilitatory motor circuits of ADHD children with TMS paired pulse protocols using surplus long interval inter-stimulus intervals (ISI) not investigated so far. METHODS: Motorcortical modulation was tested with TMS paired pulse protocols employing ISI of 3, 13, 50, 100, 200, and 300 msec in 18 ADHD children before and on treatment with MPH. Clinical improvement by MPH was measured by the Conners score. RESULTS: Analysis of variance (ANOVA) revealed a significant three-way interaction "Group x Amplitude x ISI," p = .001. Subsequent two-factorial ANOVAs and t-tests showed group specific differences of motor evoked potential (MEP) amplitudes for inhibitory ISIs of 3 and 100 msec, and for facilitatory ISIs of 13 and 50 msec. Compared to controls, an adjustment of these parameters by MPH could be shown. On MPH, a significant bivariate correlation was found between the Conners score reduction and averaged MEP amplitude changes only for inhibitory ISIs (3 and 100 msec). CONCLUSIONS: In ADHD children, MPH modulates disturbed facilitatory and inhibitory motor circuits, which for the latter is associated with clinical improvement.