Our literature review identified ANS dysfunction in individuals with ADHD , more often in the direction of hypo-arousal than hyper-arousal , particularly at rest and during tasks requiring response regulation and sustained attention .
Stimulant medications  increased ANS activity and , in some studies , reinforcers and rewards produced a similar effect , suggesting that ANS function can be modified in ADHD .
Although arousal mechanisms have frequently been found to be atypical in ADHD , these findings usually emerged from indirect behavioural measures which give only a limited underst and ing of arousal dysregulation in this condition .
Timing of caffeine's impact on autonomic and central nervous system measures: Clarification of arousal effects
The timing of  caffeine  effects on arousal levels  was examined . From previous work in our laboratory , an increase in skin conductance level ( SCL ) was used as the marker of arousal increase , and we sought to identify the timing of this and related effects following caffeine ingestion . A single oral dose of caffeine ( 250 mg ) was used in a r and omised double-blind placebo-controlled repeated- measures cross-over study . Eyes-closed resting electroencephalogram ( EEG ) and autonomic data ( SCL , heart rate , respiration rate , and systolic and diastolic blood pressure ) during 2 min epochs that commenced every 4 min after ingestion , were analysed . The SCL placebo data were used to identify potential arousal measures prior to examining caffeine effects . Caffeine was associated with increased SCL , increased respiratory rate and a global reduction in alpha power . There were no significant cardiovascular effects of caffeine-induced arousal . These caffeine results are consistent with our recent electrodermal and EEG studies of arousal , and confirm the potential use of caffeine as a simple means of experimentally modifying arousal levels without task-related confounds
Our literature review identified ANS dysfunction in individuals with ADHD , more often in the direction of hypo-arousal than hyper-arousal , particularly at rest and during tasks requiring response regulation and sustained attention .
Stimulant medications  increased ANS activity and , in some studies , reinforcers and rewards produced a similar effect , suggesting that ANS function can be modified in ADHD .
Although arousal mechanisms have frequently been found to be atypical in ADHD , these findings usually emerged from indirect behavioural measures which give only a limited underst and ing of arousal dysregulation in this condition .