Annet Bluschke

ADHD patients fail to maintain task goals in face of subliminally and consciously induced cognitive conflicts

BACKGROUND Attention deficit hyperactivity disorder (ADHD) patients have been reported to display deficits in action control processes. While it is known that subliminally and consciously induced conflicts interact and conjointly modulate action control in healthy subjects, this has never been investigated for ADHD. METHOD We investigated the (potential) interaction of subliminally and consciously triggered response conflicts in children with ADHD and matched healthy controls using neuropsychological methods (event-related potentials; ERPs) to identify the involved cognitive sub-processes. RESULTS Unlike healthy controls, ADHD patients showed no interaction of subliminally and consciously triggered response conflicts. Instead, they only showed additive effects as their behavioural performance (accuracy) was equally impaired by each conflict and they showed no signs of task-goal shielding even in cases of low conflict load. Of note, this difference between ADHD and controls was not rooted in early bottom-up attentional stimulus processing as reflected by the P1 and N1 ERPs. Instead, ADHD showed either no or reversed modulations of conflict-related processes and response selection as reflected by the N2 and P3 ERPs. CONCLUSION There are fundamental differences in the architecture of cognitive control which might be of use for future diagnostic procedures. Unlike healthy controls, ADHD patients do not seem to be endowed with a threshold which allows them to maintain high behavioural performance in the face of low conflict load. ADHD patients seem to lack sufficient top-down attentional resources to maintain correct response selection in the face of conflicts by shielding the response selection process from response tendencies evoked by any kind of distractor.

Specific cognitive-neurophysiological processes predict impulsivity in the childhood attention-deficit/hyperactivity disorder combined subtype.

BACKGROUND Attention-deficit/hyperactivity disorder (ADHD) is one of the most prevalent neuropsychiatric disorders in childhood. Besides inattention and hyperactivity, impulsivity is the third core symptom leading to diverse and serious problems. However, the neuronal mechanisms underlying impulsivity in ADHD are still not fully understood. This is all the more the case when patients with the ADHD combined subtype (ADHD-C) are considered who are characterized by both symptoms of inattention and hyperactivity/impulsivity. METHOD Combining high-density electroencephalography (EEG) recordings with source localization analyses, we examined what information processing stages are dysfunctional in ADHD-C (n = 20) compared with controls (n = 18). RESULTS Patients with ADHD-C made more impulsive errors in a Go/No-go task than healthy controls. Neurophysiologically, different subprocesses from perceptual gating to attentional selection, resource allocation and response selection processes are altered in this patient group. Perceptual gating, stimulus-driven attention selection and resource allocation processes were more pronounced in ADHD-C, are related to activation differences in parieto-occipital networks and suggest attentional filtering deficits. However, only response selection processes, associated with medial prefrontal networks, predicted impulsive errors in ADHD-C. CONCLUSIONS Although the clinical picture of ADHD-C is complex and a multitude of processing steps are altered, only a subset of processes seems to directly modulate impulsive behaviour. The present findings improve the understanding of mechanisms underlying impulsivity in patients with ADHD-C and might help to refine treatment algorithms focusing on impulsivity.

The neuronal mechanisms underlying improvement of impulsivity in ADHD by theta/beta neurofeedback

Neurofeedback is increasingly recognized as an intervention to treat core symptoms of attention deficit hyperactivity disorder (ADHD). Despite the large number of studies having been carried out to evaluate its effectiveness, it is widely elusive what neuronal mechanisms related to the core symptoms of ADHD are modulated by neurofeedback. 19 children with ADHD undergoing 8 weeks of theta/beta neurofeedback and 17 waiting list controls performed a Go/Nogo task in a pre-post design. We used neurophysiological measures combining high-density EEG recording with source localization analyses using sLORETA. Compared to the waiting list ADHD control group, impulsive behaviour measured was reduced after neurofeedback treatment. The effects of neurofeedback were very specific for situations requiring inhibitory control over responses. The neurophysiological data shows that processes of perceptual gating, attentional selection and resource allocation processes were not affected by neurofeedback. Rather, neurofeedback effects seem to be based on the modulation of response inhibition processes in medial frontal cortices. The study shows that specific neuronal mechanisms underlying impulsivity are modulated by theta/beta neurofeedback in ADHD. The applied neurofeedback protocol could be particularly suitable to address inhibitory control. The study validates assumed functional neuroanatomical target regions of an established neurofeedback protocol on a neurophysiological level.

Neuronal Intra-Individual Variability Masks Response Selection Differences between ADHD Subtypes—A Need to Change Perspectives

Due to the high intra-individual variability in attention deficit/hyperactivity disorder (ADHD), there may be considerable bias in knowledge about altered neurophysiological processes underlying executive dysfunctions in patients with different ADHD subtypes. When aiming to establish dimensional cognitive-neurophysiological constructs representing symptoms of ADHD as suggested by the initiative for Research Domain Criteria, it is crucial to consider such processes independent of variability. We examined patients with the predominantly inattentive subtype (attention deficit disorder, ADD) and the combined subtype of ADHD (ADHD-C) in a flanker task measuring conflict control. Groups were matched for task performance. Besides using classic event-related potential (ERP) techniques and source localization, neurophysiological data was also analyzed using residue iteration decomposition (RIDE) to statistically account for intra-individual variability and S-LORETA to estimate the sources of the activations. The analysis of classic ERPs related to conflict monitoring revealed no differences between patients with ADD and ADHD-C. When individual variability was accounted for, clear differences became apparent in the RIDE C-cluster (analog to the P3 ERP-component). While patients with ADD distinguished between compatible and incompatible flanker trials early on, patients with ADHD-C seemed to employ more cognitive resources overall. These differences are reflected in inferior parietal areas. The study demonstrates differences in neuronal mechanisms related to response selection processes between ADD and ADHD-C which, according to source localization, arise from the inferior parietal cortex. Importantly, these differences could only be detected when accounting for intra-individual variability. The results imply that it is very likely that differences in neurophysiological processes between ADHD subtypes are underestimated and have not been recognized because intra-individual variability in neurophysiological data has not sufficiently been taken into account.

Neurofeedback and its possible relevance for the treatment of Tourette syndrome

Neurofeedback is an increasingly recognized therapeutic option in various neuropsychiatric disorders to treat dysfunctions in cognitive control as well as disorder-specific symptoms. In this review we propose that neurofeedback may also reflect a valuable therapeutic option to treat executive control functions in Gilles-de-la-Tourette syndrome (GTS). Deficits in executive control functions when ADHD symptoms appear in GTS likely reflect pathophysiological processes in cortico-thalamic-striatal circuits and may also underlie the motor symptoms in GTS. Such executive control deficits evident in comorbid GTS/ADHD depend on neurophysiological processes well-known to be modifiable by neurofeedback. However, so far efforts to use neurofeedback to treat cognitive dysfunctions are scarce. We outline why neurofeedback should be considered a promising treatment option, what forms of neurofeedback may prove to be most effective and how neurofeedback may be implemented in existing intervention strategies to treat comorbid GTS/ADHD and associated dysfunctions in cognitive control. As cognitive control deficits in GTS mostly appear in comorbid GTS/ADHD, neurofeedback may be most useful in this frequent combination of disorders.

Conflict processing in juvenile patients with neurofibromatosis type 1 (NF1) and healthy controls – Two pathways to success

Neurofibromatosis Type 1 (NF1) is a monogenetic autosomal-dominant disorder with a broad spectrum of clinical symptoms and is commonly associated with cognitive deficits. Patients with NF1 frequently exhibit cognitive impairments like attention problems, working memory deficits and dysfunctional inhibitory control. The latter is also relevant for the resolution of cognitive conflicts. However, it is unclear how conflict monitoring processes are modulated in NF1. To examine this question in more detail, we used a system neurophysiological approach combining high-density ERP recordings with source localisation analyses in juvenile patients with NF1 and controls during a flanker task. Behaviourally, patients with NF1 perform significantly slower than controls. Specifically on trials with incompatible flanker-target pairings, however, the patients with NF1 made significantly fewer errors than healthy controls. Yet, importantly, this overall successful conflict resolution was reached via two different routes in the two groups. The healthy controls seem to arrive at a successful conflict monitoring performance through a developing conflict recognition via the N2 accompanied by a selectively enhanced N450 activation in the case of perceived flanker-target conflicts. The presumed dopamine deficiency in the patients with NF1 seems to result in a reduced ability to process conflicts via the N2. However, NF1 patients show an increased N450 irrespective of cognitive conflict. Activation differences in the orbitofrontal cortex (BA11) and anterior cingulate cortex (BA24) underlie these modulations. Taken together, juvenile patients with NF1 and juvenile healthy controls seem to accomplish conflict monitoring via two different cognitive neurophysiological pathways.

Editorial Perspective: How to optimise frequency band neurofeedback for ADHD.

Attention deficit/hyperactivity disorder (ADHD) is one of the most prevalent paediatric neuropsychiatric disorders and is characterised by hyperactivity, inattention and increased impulsivity. Children with ADHD are often also characterised by deficits in a variety of cognitive domains, including problems in working memory, a generally slower and more variable style of information processing and deficits in temporal processing, inhibitory functions and delay processing. Overarching executive functions like information updating, response inhibition and mental set shifting are also impaired in many, but not all, children with ADHD, demonstrating the neuropsychological heterogeneity characterising this disorder. Deficits in executive functions can persist into adulthood and have a substantial negative impact on everyday life. A variety of approaches are commonly considered for the treatment of ADHD (including pharmacological interventions, patient-centred cognitive-behavioural therapy approaches and specific teacher/parent training programmes). More recently, adding to this multimodal treatment approach, neurofeedback has grown in popularity as an intervention option for patients with ADHD. This article considers this intervention approach and the opportunities for optimising treatment for executive control dysfunctions in ADHD using theta/beta neurofeedback.

Intact Context-Dependent Modulation of Conflict Monitoring in Childhood ADHD:

Objective: Conflict monitoring is well known to be modulated by context. This is known as the Gratton effect, meaning that the degree of interference is smaller when a stimulus–response conflict had been encountered previously. It is unclear to what extent these processes are changed in ADHD. Method: Children with ADHD (combined subtype) and healthy controls performed a modified version of the sequence flanker task. Results: Patients with ADHD made significantly more errors than healthy controls, indicating general performance deficits. However, there were no differences regarding reaction times, indicating an intact Gratton effect in ADHD. These results were supported by Bayesian statistics. Conclusion: The results suggest that the ability to take contextual information into account during conflict monitoring is preserved in patients with ADHD despite this disorder being associated with changes in executive control functions overall. These findings are discussed in light of different theoretical accounts on contextual modulations of conflict monitoring.

Auditory post-processing in a passive listening task is deficient in Alzheimer’s disease

OBJECTIVE To investigate whether automatic auditory post-processing is deficient in patients with Alzheimers disease and is related to sensory gating. METHODS Event-related potentials were recorded during a passive listening task to examine the automatic transient storage of auditory information (short click pairs). Patients with Alzheimers disease were compared to a healthy age-matched control group. A young healthy control group was included to assess effects of physiological aging. RESULTS A bilateral frontal negativity in combination with deep temporal positivity occurring 500 ms after stimulus offset was reduced in patients with Alzheimers disease, but was unaffected by physiological aging. Its amplitude correlated with short-term memory capacity, but was independent of sensory gating in healthy elderly controls. Source analysis revealed a dipole pair in the anterior temporal lobes. CONCLUSION Results suggest that auditory post-processing is deficient in Alzheimers disease, but is not typically related to sensory gating. The deficit could neither be explained by physiological aging nor by problems in earlier stages of auditory perception. Correlations with short-term memory capacity and executive control tasks suggested an association with memory encoding and/or overall cognitive control deficits. SIGNIFICANCE An auditory late negative wave could represent a marker of auditory working memory encoding deficits in Alzheimers disease.

Cortical post-movement and sensory processing disentangled by temporary deafferentation.

Motor system calibration depends crucially on the adjustment to the consequences of a movement, which often occur when the movement itself is already completed. The mechanisms by which reafferent feedback information is compared to the programmed movement remain unclear. In the current study, the hypothesis of a short term memory trace in the motor cortex which outlasts quick movements and is generated independently from reafferent feedback was challenged by temporal deafferentation. Post-movement cortical potentials were recorded by high-resolution EEG during a reaction time task which required speeded unilateral right-hand or left-hand button presses. We analysed lateralized motor N700 (motor post-imperative negative variation), a post-movement component, under temporary deafferentation achieved through application of a blood pressure tourniquet in ten healthy adult subjects. Motor N700 persisted under deafferentation in the absence of reafferent tactile and proprioceptive feedback input into the sensorimotor cortex, which was abolished under deafferentation. Source analysis pointed towards continuing activation in the pre-/primary motor cortex. Thus, motor post-processing can be dissociated from reafferent sensory feedback. Motor cortex activation outlasts quick movements for about a second also in the absence of a reafferent signal. Continuing motor cortex activation could act as an internal motor model in motor learning and allow better adjustment of movements according to the evaluation of their consequences.