Summary:  Although the causes of cognitive impairment in patients with epilepsy have not been completely elucidated, three factors are clearly involved: the underlying etiology of epilepsy, the effects of seizures themselves, and the central nervous system effects of antiepileptic drugs (AEDs). All commonly used AEDS have some effect on cognitive function, and the effect may be substantial when crucial functions are involved, such as learning in children or driving ability in adults, or when already‐vulnerable functions are involved, such as memory in elderly patients. The available evidence is insufficient to support definite conclusions about the cognitive effects of three of the newer AEDs, tiagabine, gabapentin, and levetiracetam. Better evidence is available for lamotrigine (LTG), topiramate (TPM), and, to a lesser degree, oxcarbazepine (OXC). OXC appears not to affect cognitive function in healthy volunteers or adults with newly diagnosed epilepsy, but its cognitive effects in children and adolescents have not been systematically studied. A relatively large number of studies are available for LTG, which has demonstrated a favorable cognitive profile overall, both in volunteers and in patients with epilepsy. Although dose and titration speed may be confounding factors in some of the studies of TPM, there is clear evidence that this agent does affect cognitive function, with specific effects on attention and verbal function. For LTG, attempts have been made to correlate cognitive effects with what is known of the drug's mechanism of action; this is an area of research that deserves further exploration with regard to other AEDs as well, especially TPM.

Summary:  Purpose: This study addressed whether cognitive impairment in children with epilepsy is caused by disease‐related stable factors, such as the type of epilepsy, or by acute effects of paroxysmal epileptic activity such as epileptic EEG discharges. We studied a nonselected group with short nonconvulsive seizures, as these seizures may elude detection and may therefore persist over a longer period. In this group, the diagnostic issue is to differentiate between the combined effects of several epilepsy‐related factors on cognition. Methods: All children were assessed with 32‐channel EEG, synchronized with a computerized cognitive test system and a video‐monitoring system. Recording time was 2 h. The primary inclusion criteria were unclear seizures and fluctuations in cognitive performance and/or frequent epileptic EEG discharges in a recent EEG. Results: One hundred fifty‐two patients met the inclusion criteria; 31 patients appeared not to have a diagnosis of epilepsy and were used as a nonepilepsy control group. Our results show that type of epilepsy has an impact on stable cognitive functions, such as educational achievement. Paroxysmal epileptic activity (acute effects of seizures and epileptic EEG discharges) affects primarily transient mechanistic cognitive processes (alertness, mental speed). Conclusions: These results suggest that the effects of paroxysmal epileptic activity on transient cognitive mechanisms may accumulate over time and consequently affect the more stable aspects of cognitive function such as educational achievement. The clinical relevance is that early detection of the cognitive impact of seizure‐related activity and subsequent treatment may prevent its detrimental impact on cognitive and educational development.

Working memory is a temporary storage system under attentional control. It is believed to play a central role in online processing of complex cognitive information and may also play a role in social cognition and interpersonal interactions. Adolescents with a disorder on the autism spectrum display problems in precisely these domains. Social impairments, communication difficulties, and repetitive interests and activities are core domains of autism spectrum disorders (ASD), and executive function problems are often seen throughout the spectrum. As the main cognitive theories of ASD, including the theory of mind deficit hypotheses, weak central coherence account, and the executive dysfunction theory, still fail to explain the broad spectrum of symptoms, a new perspective on the etiology of ASD is needed. Deficits in working memory are central to many theories of psychopathology, and are generally linked to frontal-lobe dysfunction. This article will review neuropsychological and (functional) brain imaging studies on working memory in adolescents with ASD. Although still disputed, it is concluded that within the working memory system specific problems of spatial working memory are often seen in adolescents with ASD. These problems increase when information is more complex and greater demands on working memory are made. Neuroimaging studies indicate a more global working memory processing or connectivity deficiency, rather than a focused deficit in the prefrontal cortex. More research is needed to relate these working memory difficulties and neuroimaging results in ASD to the behavioral difficulties as seen in individuals with a disorder on the autism spectrum.