ADHD is now increasingly recognized as developmental impairment of executive functions (EFs), the brain’s cognitive management system. Executive function (EF) is a set of self-regulatory mechanisms for planning, organizing, directing, and managing cognitive processes and emotional responses. Children with ADHD have serious difficulties with EF in so many areas that some psychiatrists and psychologists have proposed renaming this disorder as EF disorder or EF deficit disorder. Many of the executive dysfunctions described earlier are found in children with ADHD including difficulties with priority and time management, planning and organization, initiating and completing tasks in a timely manner, difficulty shifting cognitive set, a high level of procrastination, forgetfulness and poor working memory. Barkley proposed the hypothesis that attention-deficit/ hyperactivity disorder (ADHD) symptoms may be due to EF deficits. In a meta-analysis of 83 studies, children and adolescents with ADHD exhibited significant deficits compared to those without ADHD in neuropsychological measures of EF; the EF domains that showed impairments included planning, spatial and verbal working memory, response inhibition, and vigilance. The ES is mediated by various networks in the frontal, parietal and occipital cortices, the thalamus and the cerebellum. It is linked through a series of circuits connecting every region of the central nervous system. The circuits originate in the dorsolateral prefrontal cortex (PFC) / orbitofrontal cortex (OFC), project through the striatum, synapse at the level of the globus pallidus, substantia nigra and the thalamus and finally return to the PFC forming closed loops. Each circuit regulates specific functions. The circuit that is most responsible for coordinating EF is located primarily in the frontal lobe. Functional imaging studies have implicated the PFC as the primary site of cortical activation during tasks involving EF. There is not yet full agreement regarding exactly which functions should be classified as EFs. But there is a general agreement that there were three core EFs: 1) inhibition [inhibitory control, including self-control (behavioral inhibition) and interference control (selective attention and cognitive inhibition)], 2) working memory (WM), and 3) cognitive şexibility (also called set shifting, mental şexibility, or mental set shifting and closely linked to creativity). From these, higher order EFs are built such as reasoning, problem solving, and planning. The therapeutic effect of the stimulants in ADHD is associated with their effects on the catecholamine system. Impaired neurotransmission causing executive dysfunction occurs because of abnormalities of the dopamine transporter. All currently approved pharmacotherapies for ADHD, both stimulants and non-stimulants, work by potentiating neurotransmission in the PFC. In ADHD subjects, single doses of the non-stimulant atomoxetine produced selective effects on response inhibition in the absence of effects on attention and memory. Although a norepinephrine reuptake inhibitor, atomoxetine acts primarily via presynaptic norepinephrine transporter blockade and elevates dopamine in selective cerebral regions.