Attention‐deficit hyperactivity disorder (ADHD) is a neurobehavioural disorder, characterized by symptoms of inattention and/or hyperactivity/impulsivity, in addition to various cognitive deficits, including working memory impairments. This pathology arises from a complex constellation of genetic, structural and neurotransmission abnormalities, which give rise to the aberrant electrophysiological patterns evident in patients with ADHD. Among such, findings have consistently provided support in favour of weaker power across the beta frequency range. Evidence has also emerged that beta rhythmic decrements are linked to working memory encoding. The catecholaminergic modulation of both working memory and beta oscillations may suggest that the link between the two might be rooted at the neurotransmission level. Studies have consistently shown that ADHD involves significant catecholaminergic dysregulation, which is also supported by other clinical studies that demonstrate stimulant‐induced amelioration of ADHD symptomology. In this study, we explore the possible ways that might relate ADHD, working memory, beta rhythms and catecholaminergic signalling altogether by investigating the integrity of encoding‐relevant electroencephalographic beta rhythms in medication‐naïve and stimulant‐medicated adolescent patients. The aberrant parietal and frontal encoding‐related beta rhythm revealed in the ADHD patients together with a working memory (WM) deficit as observed herein was reversed by methylphenidate in the latter case but not with regard to the beta rhythm. This finding per se raises the issue of the role played by beta rhythms in the WM deficits associated with ADHD.
The timing of neural activity is an intriguing way of exposing behaviorally relevant neural activity, as neural populations exploit transient windows of synchronized activations to exchange dynamic communications in the service of various cognitive operations. The link between neural synchrony and working memory (WM) has been supported at the theoretical and empirical level. However, findings have also shown that WM encoding is also related to significant alpha-beta desynchronization. These findings have been primarily recorded during subsequent memory effect paradigms that compare correct with incorrect encoding trials. The dissociable contribution imparted by various processes to WM performance suggests that incorrect performance may not be directly translatable to unsuccessful encoding. Here, we address the relationship between alpha-beta desynchronization and encoding through the use of an alternative paradigm design by contrasting frontal and parietal human scalp electroencephalography activity during the encoding interval of a delayed matching-to-sample task with that recorded during a control task. The additional use of non-verbal/semantic visual stimulation and recruitment of typically developing adolescent subjects has led us to the conclusion that encoding-relevant alpha-beta decrements can be replicated via a non-verbal/semantic delayed matching-to-sample task and these are also evident in typically developing adolescents, in addition to adults, as has been previously demonstrated. The identification of encoding-related alpha-beta decrements in adolescent subjects performing such WM tasks may open new avenues to explore whether such a rhythmic signature may explain WM and electrophysiological deficits that emerge in various adolescent neuropsychiatric disorders such as attention deficit hyperactivity disorder.
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