IntroductionAttention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in children whose symptoms were first described by Heinrich Hoffmann in 1863. 1 It is characterized by disruption of inattention, conduct disorder, poor social communication, and hyperactivity/impulsivity. Inattention causes an inability to remain focused on schoolwork, seeming not to listen, and losing things at school more frequently than what is consistent with the child's developmental level. Hyperactivity and impulsivity, on the other hand, result in excess activity, fidgeting, trouble remaining seated, disturbing others' activities, and trouble waiting for one's turn. 2,3 ADHD tends to overlap with other common externalizing disorders in children, such as oppositional disorder and conduct disorder. 4,5 If the condition persists until adulthood, it often leads to social performance deficit as well as educational and professional dysfunctions. 6 Although hyperactivity subsides with age, attention deficit increases in most patients. 7 In most cultures, demographic surveys report a prevalence of nearly 5% and 2.5% in children and adults, respectively. 8 Overall, the disorder affects boys more than girls, with 1.2% and 1.6% higher occurrence during childhood and adulthood, respectively. However, girls are more prone to displaying inattention symptoms. 9 Evidence from various studies in neuropsychology, 10 pathophysiology, 11 genetics, 12 and phenotypes, 13 suggest that several factors with varying levels of intensity manifest clinically as attention deficit and hyperactivity. Since the 1970s, numerous studies have identified impairments in executive functioning as the core cause of ADHD in adolescents. 14 These impairments lead to deficits in essential cognitive abilities for complex goaloriented behaviors and adjusting to a range of changes and environmental demands. 9 several authors 15,16 believed that some, but not all, children with ADHD suffer from significant impairments in several areas of executive functioning; however, other authors such as Brown 17 discussed that ADHD is fundamentally a developmental disorder that affects executive functions (EFs) in all cases. Thus, this paper focuses exclusively on this issue. The aim of this study is to review existing research on cognitive impairments in children with ADHD with a focus on EFs.

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Purpose: Sodium Valproate (VPA) is one of the first-generation Antiepileptic Drugs (AEDs) which mediates epileptic activities by releasing stimulators of Gamma-Aminobutyric Acid (GABA) and is greatly used to treat partial and generalized seizures. Lamotrigine )LTG( is commonly used as AEDs that are widely utilized in first-line monotherapy or in combination with other AEDs. Our specific goal was to compare these two AEDs with different molecular mechanisms on both cortical and subcortical brain structures, along with cognitive performance and dysfunctions. Materials and Methods: We conducted a retrospective study comparing LTG with sodium VPA, both administrated as monotherapy. Twenty patients with a confirmed generalized-epilepsy tonic-clonic seizure who had been treated at least 6 months with LTG (n=8) and Sodium VPA (n=12) were retrospectively recruited. We also included 12 age, gender, and education-matched Healthy Controls (HC). We evaluated cognitive performances. All participants underwent a Magnetic Resonance Imaging (MRI) scanner and T1-weighted MR images were acquired. Voxel-based morphometric alterations in the brain cortex, as well as subcortical structures, were inspected using Statistical Parametric Mapping (SPM) software. Results: The cognitive performance was revealed inferior in patients on Sodium VPA. Poor performance was associated with significant volume reduction in insula bilaterally, and subcortical structures of thalamus, cerebellum, and hippocampus compared to the HC. Comparing patients on LTG to HC revealed significant volume reduction in the anterior cingulate cortex in concordance with slight cognitive dysfunctions. Conclusion: These findings suggested that different molecular mechanisms of Antiepileptic Drugs (AEDs) may affect brain structures and cognition with different severity levels, presumably with more adverse effects induced by GABA mediations from sodium VPA.