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© Copyright © 2019 Andrillon, Windt, Silk, Drummond, Bellgrove and Tsuchiya. Sleep has been classically described as an all-or-nothing global phenomenon. However, recent research strongly suggests that this view requires tempering. Invasive and non-invasive recordings in animals and humans show that neural activity typically associated with sleep can locally occur during wakefulness. Although local sleep is defined neuronally, it has been associated with impaired performance during cognitive tasks. Comparatively, the phenomenology of local sleep (i.e., what it feels like when your brain is partially asleep) has been less explored. Taking into account the literature on the neuronal and behavioral profile of local sleep intrusions in wakefulness, we propose that occurrences of local sleep could represent the neural mechanism underlying many attentional lapses. In particular, we argue that a unique physiological event such as local sleep could account for a diversity of behavioral outcomes from sluggish to impulsive responses. We further propose that local sleep intrusions could impact individuals’ subjective experience. Specifically, we propose that the timing and anatomical sources of local sleep intrusions could be responsible for both the behavioral consequences and subjective content of attentional lapses and may underlie the difference between subjective experiences such as mind wandering and mind blanking. Our framework aims to build a parallel between spontaneous experiences in sleep and wakefulness by integrating evidence across neuronal, behavioral and experiential levels. We use the example of attention deficit hyperactivity disorder (ADHD) to illustrate how local sleep could explain complex cognitive profiles which include inattention, impulsivity, mind-wandering and mind-blanking.

Dopaminergic neurotransmission was attenuated in 28 healthy male participants by using 2 mg haloperidol. A repeated-measures placebo-controlled crossover design was implemented, and performance indices of attention and inhibition were assessed in the visual spatial cueing task (VSC) and stop signal task (SST). Additionally, the effect of haloperidol on motoric parameters was assessed. It was expected that haloperidol as contrasted to placebo would result in a reduction of the "validity effect," the benefit of valid cueing as opposed to invalid cueing of a target in terms of reaction time. Furthermore, an increase in stop signal reaction time (SSRT) in the SST was expected.Results partially confirmed the hypothesis. Haloperidol negatively affected inhibitory motor control in the SST as indexed by SSRT, but there were no indications that haloperidol affected bias or disengagement in the VSC task as indicated by a lack of an effect on RTs. Pertaining to secondary parameters, motor activity increased significantly under haloperidol. Haloperidol negatively affected reaction time variability and errors in both tasks, as well as omissions in the SST, indicating a decreased sustained attention, an increase in premature responses, and an increase in lapses of attention, respectively.

Dopaminergic neurotransmission was attenuated in 28 healthy male participants by using 2 mg haloperidol. A repeated-measures placebo-controlled crossover design was implemented, and performance indices of attention and inhibition were assessed in the visual spatial cueing task (VSC) and stop signal task (SST). Additionally, the effect of haloperidol on motoric parameters was assessed. It was expected that haloperidol as contrasted to placebo would result in a reduction of the "validity effect," the benefit of valid cueing as opposed to invalid cueing of a target in terms of reaction time. Furthermore, an increase in stop signal reaction time (SSRT) in the SST was expected.Results partially confirmed the hypothesis. Haloperidol negatively affected inhibitory motor control in the SST as indexed by SSRT, but there were no indications that haloperidol affected bias or disengagement in the VSC task as indicated by a lack of an effect on RTs. Pertaining to secondary parameters, motor activity increased significantly under haloperidol. Haloperidol negatively affected reaction time variability and errors in both tasks, as well as omissions in the SST, indicating a decreased sustained attention, an increase in premature responses, and an increase in lapses of attention, respectively.

Fragile X syndrome (FXS) is the most common cause of inherited intellectual disability and a variant of autism spectrum disorder (ASD). The FXS population is quite heterogeneous with respect to comorbidities, which implies the need for a personalized medicine approach, relying on biomarkers or endophenotypes to guide treatment. There is evidence that quantitative electroencephalography (EEG) endophenotype-guided treatments can support increased clinical benefit by considering the patient's neurophysiological profile. We describe a case series of 11 children diagnosed with FXS, aged one to 14 years, mean 4.6 years. Case data are based on longitudinal clinically-observed reports by attending physicians for comorbid symptoms including awake and asleep EEG profiles. We tabulate the comorbid EEG symptoms in this case series, and relate them to the literature on EEG endophenotypes and associated treatment options. The two most common endophenotypes in the data were diffuse slow oscillations and epileptiform EEG, which have been associated with attention and epilepsy respectively. This observation agrees with reported prevalence of comorbid behavioral symptoms for FXS. In this sample of FXS children, attention problems were found in 37% (4 of 11), and epileptic seizures in 45% (5 of 11). Attention problems were found to associate with the epilepsy endophenotype. From the synthesis of this case series and literature review, we argue that the evidence-based personalized treatment approach, exemplified by neurofeedback, could benefit FXS children by focusing on observable, specific characteristics of comorbid disease symptoms.

Previous research documented a robust link between difficulties in self-regulation and development of externalizing problems (i.e., aggression and delinquency). In this study, we examined the longitudinal additive and interactive genetic and environmental covariation underlying this well-established link using a twin design. The sample included 131 pairs of monozygotic twins and 173 pairs of same-sex dizygotic twins who participated in three waves of annual assessment. Mothers and fathers provided reports of externalizing problems. Teacher report and observer rating were used to assess twin's attention regulation. The etiology underlying the link between externalizing problems and attention regulation shifted from a common genetic mechanism to a common environmental mechanism in the transition across middle childhood. Household chaos moderated the genetic variance of and covariance between externalizing problems and attention regulation. The genetic influence on individual differences in both externalizing problems and attention regulation was stronger in more, chaotic households. However, higher levels of household chaos attenuated the genetic link between externalizing problems and attention regulation.

Previous research documented a robust link between difficulties in self-regulation and development of externalizing problems (i.e., aggression and delinquency). In this study, we examined the longitudinal additive and interactive genetic and environmental covariation underlying this well-established link using a twin design. The sample included 131 pairs of monozygotic twins and 173 pairs of same-sex dizygotic twins who participated in three waves of annual assessment. Mothers and fathers provided reports of externalizing problems. Teacher report and observer rating were used to assess twin's attention regulation. The etiology underlying the link between externalizing problems and attention regulation shifted from a common genetic mechanism to a common environmental mechanism in the transition across middle childhood. Household chaos moderated the genetic variance of and covariance between externalizing problems and attention regulation. The genetic influence on individual differences in both externalizing problems and attention regulation was stronger in more, chaotic households. However, higher levels of household chaos attenuated the genetic link between externalizing problems and attention regulation.

Objective: The main aim of the study was to examine blood oxygen level dependent response during task switching in adults with attention-deficit/hyperactivity disorder (ADHD). Method: Fifteen male adults with ADHD and 14 controls participated and performed a task-switching paradigm. Results: Behaviorally, no specific executive control problems were observed in the ADHD participants, although they did display more errors in general. The neuroimaging data did show remarkable differences between the ADHD and control adults: Adults with ADHD engaged more strongly the dorsal anterior cingulate cortex, middle temporal gyrus, precuneus, lingual gyms, precentral gyrus, and insula than did the healthy controls during task switching. Controls displayed more task-related activity in the putamen, posterior cingulate gyrus, medial frontal gyrus, thalamus, orbitofrontal cortex, and postcentral gyrus. Conclusions: ADHD adults did not display specific executive control problems at a behavioral level, but did engage different brain areas during task switching compared with healthy controls. The results are discussed in the framework of the executive frontostriatal circuitry, conflict detection, and Intentional networks.

Objective: The main aim of the study was to examine blood oxygen level dependent response during task switching in adults with attention-deficit/hyperactivity disorder (ADHD). Method: Fifteen male adults with ADHD and 14 controls participated and performed a task-switching paradigm. Results: Behaviorally, no specific executive control problems were observed in the ADHD participants, although they did display more errors in general. The neuroimaging data did show remarkable differences between the ADHD and control adults: Adults with ADHD engaged more strongly the dorsal anterior cingulate cortex, middle temporal gyrus, precuneus, lingual gyms, precentral gyrus, and insula than did the healthy controls during task switching. Controls displayed more task-related activity in the putamen, posterior cingulate gyrus, medial frontal gyrus, thalamus, orbitofrontal cortex, and postcentral gyrus. Conclusions: ADHD adults did not display specific executive control problems at a behavioral level, but did engage different brain areas during task switching compared with healthy controls. The results are discussed in the framework of the executive frontostriatal circuitry, conflict detection, and Intentional networks.

Attention deficit hyperactivity disorder (ADHD) and autism are two neurodevelopmental disorders associated with prominent executive dysfunction, which may be underpinned by disruption within fronto-striatal and fronto-parietal circuits. We probed executive function in these disorders using a sustained attention task with a validated brain-behaviour basis. Twenty-three children with ADHD, 21 children with high-functioning autism (HFA) and 18 control children were tested on the Sustained Attention to Response Task (SART). In a fixed sequence version of the task, children were required to withhold their response to a predictably occurring no-go target (3) in a 1-9 digit sequence; in the random version the sequence was unpredictable. The ADHD group showed clear deficits in response inhibition and sustained attention, through higher errors of commission and omission on both SART versions. The HFA group showed no sustained attention deficits, through a normal number of omission errors on both SART versions. The HFA group showed dissociation in response inhibition performance, as indexed by commission errors. On the Fixed SART, a normal number of errors was made, however when the stimuli were randomised, the HFA group made as many commission errors as the ADHD group. Greater slow-frequency variability in response time and a slowing in mean response time by the ADHD group suggested impaired arousal processes. The ADHD group showed greater fast-frequency variability in response time, indicative of impaired top-down control, relative to the HFA and control groups. These data imply involvement of fronto-parietal attentional networks and sub-cortical arousal systems in the pathology of ADHD and prefrontal cortex dysfunction in children with HFA. © 2007 Elsevier Ltd. All rights reserved.