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      Resting-State Neurophysiological Activity Patterns in Young People with ASD, ADHD, and ASD + ADHD

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          Abstract

          Altered power of resting-state neurophysiological activity has been associated with autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), which commonly co-occur. We compared resting-state neurophysiological power in children with ASD, ADHD, co-occurring ASD + ADHD, and typically developing controls. Children with ASD (ASD/ASD + ADHD) showed reduced theta and alpha power compared to children without ASD (controls/ADHD). Children with ADHD (ADHD/ASD + ADHD) displayed decreased delta power compared to children without ADHD (ASD/controls). Children with ASD + ADHD largely presented as an additive co-occurrence with deficits of both disorders, although reduced theta compared to ADHD-only and reduced delta compared to controls suggested some unique markers. Identifying specific neurophysiological profiles in ASD and ADHD may assist in characterising more homogeneous subgroups to inform treatment approaches and aetiological investigations.

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          EEG alpha and theta oscillations reflect cognitive and memory performance: a review and analysis.

          Evidence is presented that EEG oscillations in the alpha and theta band reflect cognitive and memory performance in particular. Good performance is related to two types of EEG phenomena (i) a tonic increase in alpha but a decrease in theta power, and (ii) a large phasic (event-related) decrease in alpha but increase in theta, depending on the type of memory demands. Because alpha frequency shows large interindividual differences which are related to age and memory performance, this double dissociation between alpha vs. theta and tonic vs. phasic changes can be observed only if fixed frequency bands are abandoned. It is suggested to adjust the frequency windows of alpha and theta for each subject by using individual alpha frequency as an anchor point. Based on this procedure, a consistent interpretation of a variety of findings is made possible. As an example, in a similar way as brain volume does, upper alpha power increases (but theta power decreases) from early childhood to adulthood, whereas the opposite holds true for the late part of the lifespan. Alpha power is lowered and theta power enhanced in subjects with a variety of different neurological disorders. Furthermore, after sustained wakefulness and during the transition from waking to sleeping when the ability to respond to external stimuli ceases, upper alpha power decreases, whereas theta increases. Event-related changes indicate that the extent of upper alpha desynchronization is positively correlated with (semantic) long-term memory performance, whereas theta synchronization is positively correlated with the ability to encode new information. The reviewed findings are interpreted on the basis of brain oscillations. It is suggested that the encoding of new information is reflected by theta oscillations in hippocampo-cortical feedback loops, whereas search and retrieval processes in (semantic) long-term memory are reflected by upper alpha oscillations in thalamo-cortical feedback loops. Copyright 1999 Elsevier Science B.V.
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            Motivation, emotion, and their inhibitory control mirrored in brain oscillations.

            Recent studies suggest brain oscillations as a mechanism for cerebral integration. Such integration can exist across a number of functional domains, with different frequency rhythms associated with each domain. Here, evidence is summarized which shows that delta oscillations depend on activity of motivational systems and participate in salience detection. Theta oscillations are involved in memory and emotional regulation. Alpha oscillations participate in inhibitory processes which contribute to a variety of cognitive operations such as attention and memory. The importance of inhibitory functions associated with alpha oscillations increases during the course of evolution. In ontogenesis, these functions develop later and may be more sensitive to a variety of detrimental environmental influences. In a number of developmental stages and pathological conditions, a deficient alpha and/or increased slow-wave activity are associated with cognitive deficits and a lack of inhibitory control. It is shown that slow-wave and alpha oscillations are reciprocally related to each other. This reciprocal relationship may reflect an inhibitory control over motivational and emotional drives which is implemented by the prefrontal cortex.
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              A dynamic developmental theory of attention-deficit/hyperactivity disorder (ADHD) predominantly hyperactive/impulsive and combined subtypes.

              Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive/behavioral developmental disorder where all clinical criteria are behavioral. Inattentiveness, overactivity, and impulsiveness are presently regarded as the main clinical symptoms. The dynamic developmental behavioral theory is based on the hypothesis that altered dopaminergic function plays a pivotal role by failing to modulate nondopaminergic (primarily glutamate and GABA) signal transmission appropriately. A hypofunctioning mesolimbic dopamine branch produces altered reinforcement of behavior and deficient extinction of previously reinforced behavior. This gives rise to delay aversion, development of hyperactivity in novel situations, impulsiveness, deficient sustained attention, increased behavioral variability, and failure to "inhibit" responses ("disinhibition"). A hypofunctioning mesocortical dopamine branch will cause attention response deficiencies (deficient orienting responses, impaired saccadic eye movements, and poorer attention responses toward a target) and poor behavioral planning (poor executive functions). A hypofunctioning nigrostriatal dopamine branch will cause impaired modulation of motor functions and deficient nondeclarative habit learning and memory. These impairments will give rise to apparent developmental delay, clumsiness, neurological "soft signs," and a "failure to inhibit" responses when quick reactions are required. Hypofunctioning dopamine branches represent the main individual predispositions in the present theory. The theory predicts that behavior and symptoms in ADHD result from the interplay between individual predispositions and the surroundings. The exact ADHD symptoms at a particular time in life will vary and be influenced by factors having positive or negative effects on symptom development. Altered or deficient learning and motor functions will produce special needs for optimal parenting and societal styles. Medication will to some degree normalize the underlying dopamine dysfunction and reduce the special needs of these children. The theory describes how individual predispositions interact with these conditions to produce behavioral, emotional, and cognitive effects that can turn into relatively stable behavioral patterns.
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                Author and article information

                Contributors
                +44 (0)207 848 5272 , elizabeth.1.shephard@kcl.ac.uk
                +44 (0)207 848 5272 , charlotte.tye@kcl.ac.uk
                Journal
                J Autism Dev Disord
                J Autism Dev Disord
                Journal of Autism and Developmental Disorders
                Springer US (New York )
                0162-3257
                1573-3432
                13 September 2017
                13 September 2017
                2018
                : 48
                : 1
                : 110-122
                Affiliations
                [1 ]ISNI 0000 0001 2322 6764, GRID grid.13097.3c, MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology, and Neuroscience, , King’s College London, ; De Crespigny Park, London, SE5 8AF UK
                [2 ]ISNI 0000 0001 2322 6764, GRID grid.13097.3c, Department of Child and Adolescent Psychiatry, Institute of Psychiatry, Psychology, and Neuroscience, , King’s College London, ; De Crespigny Park, London, SE5 8AF UK
                [3 ]ISNI 0000 0001 2322 6764, GRID grid.13097.3c, Present Address: Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology, and Neuroscience, , King’s College London, ; De Crespigny Park, London, UK
                Article
                3300
                10.1007/s10803-017-3300-4
                5760605
                28900800
                a34d6022-67e7-4ead-94cc-9a51435cb41b
                © The Author(s) 2017

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100000317, Action Medical Research;
                Award ID: GN2301
                Award Recipient :
                Funded by: The Waterloo Foundation
                Award ID: G686984
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100000272, National Institute for Health Research;
                Funded by: Steele Charitable Trust
                Award ID: G38575208
                Award Recipient :
                Categories
                Original Paper
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2018

                Neurology
                asd,adhd,co-occurring asd + adhd,resting-state,eeg,spectral power
                Neurology
                asd, adhd, co-occurring asd + adhd, resting-state, eeg, spectral power

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