Refine
Year of publication
- 2021 (14) (remove)
Document Type
- Article (14)
Has Fulltext
- yes (14)
Is part of the Bibliography
- no (14)
Keywords
- Klassifikation (2)
- Sprache (2)
- Sprachstörung (2)
- Sprechen (2)
- Sprechstörung (2)
- classification (2)
- language (2)
- speech (2)
- speech and language disorder (2)
- Affective Misattribution Procedure (1)
- Angststörungen (1)
- Attention-Deficit/Hyperactivity Disorder (ADHD) (1)
- Autism (1)
- Autism spectrum disorder (1)
- Autismus-Spektrum-Störungen (1)
- CCC-2 (1)
- CNV (1)
- Contingent Negative Variation, CNV (1)
- Continuous Performance Test, CPT (1)
- Cue-P3 (1)
- DPPIV (1)
- Dysfunctional social assumptions (1)
- EEG (1)
- Elternurteil (1)
- Epigenetik (1)
- Event related potentials (1)
- Expectation violation (1)
- Human behaviour (1)
- Implicit Processing (1)
- Implicit Association Test (1)
- Intention attribution (1)
- Interpretation Bias (1)
- Kindes- und Jugendalter (1)
- Molecular neuroscience (1)
- Neurofeedback (1)
- Predictive coding (1)
- ROC analyses (1)
- ROC-Analysen (1)
- Randomized Controlled Trial (1)
- Randomized controlled trial (1)
- Response control (1)
- SNV (1)
- Screeningfragebogen (1)
- Slow Cortical Potentials, SCP (1)
- Social Phobia (1)
- Social cognition (1)
- Sustained attention (1)
- Tempo-parietal junction (1)
- Transcranial direct current stimulation (1)
- anxiety (1)
- anxiety disorders (1)
- artifacts (1)
- attention-deficit/hyperactivity disorder (ADHD) (1)
- autism (1)
- autism spectrum disorders (1)
- behavioral inhibition (1)
- biological networks (1)
- biologische Netzwerke (1)
- callous-unemotional traits (1)
- children and adolescents (1)
- conduct disorder (1)
- data quality (1)
- electroencephalography (EEG) (1)
- epigenetics (1)
- genetic variants (1)
- genetische Varianten (1)
- human behaviour (1)
- intellectual disability (1)
- language impairment (1)
- molecular neuroscience (1)
- multicenter study (1)
- mutism (1)
- parent rating (1)
- psychiatric comorbidity (1)
- screening questionnaire (1)
- sex differences (1)
- social anxiety (1)
- social communication (1)
- tDCS (1)
Institute
Abstract: Neurophysiological measures of preparation and attention are often atypical in ADHD. Still, replicated findings that these measures predict which patients improve after Neurofeedback (NF), reveal neurophysiological specificity, and reflect ADHD-severity are limited. Methods: We analyzed children’s preparatory (CNV) and attentional (Cue-P3) brain activity and behavioral performance during a cued Continuous Performance Task (CPT) before and after slow cortical potential (SCP)-NF or semi-active control treatment (electromyogram biofeedback). Mixed-effects models were performed with 103 participants at baseline and 77 were assessed for pre-post comparisons focusing on clinical outcome prediction, specific neurophysiological effects of NF, and associations with ADHD-severity. Results: Attentional and preparatory brain activity and performance were non-specifically reduced after treatment. Preparatory activity in the SCP-NF group increased with clinical improvement. Several performance and brain activity measures predicted non-specific treatment outcome. Conclusion: Specific neurophysiological effects after SCP-NF were limited to increased neural preparation associated with improvement on ADHD-subscales, but several performance and neurophysiological measures of attention predicted treatment outcome and reflected symptom severity in ADHD. The results may help to optimize treatment.
Conduct disorder (CD), a psychiatric disorder characterized by a repetitive pattern of antisocial behaviors, results from a complex interplay between genetic and environmental factors. The clinical presentation of CD varies both according to the individual’s sex and level of callous-unemotional (CU) traits, but it remains unclear how genetic and environmental factors interact at the molecular level to produce these differences. Emerging evidence in males implicates methylation of genes associated with socio-affective processes. Here, we combined an epigenome-wide association study with structural neuroimaging in 51 females with CD and 59 typically developing (TD) females to examine DNA methylation in relation to CD, CU traits, and gray matter volume (GMV). We demonstrate an inverse pattern of correlation between CU traits and methylation of a chromosome 1 region in CD females (positive) as compared to TD females (negative). The identified region spans exon 1 of the SLC25A24 gene, central to energy metabolism due to its role in mitochondrial function. Increased SLC25A24 methylation was also related to lower GMV in multiple brain regions in the overall cohort. These included the superior frontal gyrus, dorsolateral prefrontal cortex, supramarginal gyrus, secondary visual cortex and ventral posterior cingulate cortex, which are regions that have previously been implicated in CD and CU traits. While our findings are preliminary and need to be replicated in larger samples, they provide novel evidence that CU traits in females are associated with methylation levels in a fundamentally different way in CD and TD individuals, which in turn may relate to observable variations in GMV across the brain.
Correction to: Translational Psychiatry https://doi.org/10.1038/s41398-021-01609-y, published online 24 September 2021
Since the publication of the article the authors have noticed mistakes in the text, figures, tables and supplementary materials. The authors apologize for these errors, which have now been corrected in the original article. Please note that these changes do not affect the results of the paper or their interpretation.
Die Ätiologie der Autismus-Spektrum-Störungen (ASS) ist in genetischen Risikofaktoren sowie der Interaktion von genetischen und biologisch wirksamen Umweltrisikofaktoren begründet. ASS werden aufgrund von Verhaltensmerkmalen, nämlich bleibend eingeschränkter sozialer Kommunikation, sowie durch stereotypes Verhalten, sensorische und Sonderinteressen diagnostiziert. Hinsichtlich des genetischen Hintergrundes besteht eine hohe genetische Heterogenität, d. h., die genetischen Ursachen sind vielfältig und individuell oft sehr unterschiedlich ausgeprägt. Allerdings konvergieren diese Ursachen in bestimmten biologischen Mechanismen und überlappenden biologischen Endstrecken, deren Veränderung sehr wahrscheinlich den autismusspezifischen Verhaltensmerkmalen zugrunde liegt. Die vorliegende, selektive Literaturübersicht summiert die genetischen Befunde und fokusiert sich insbesondere auf Mechanismen und Endstrecken, die aufgrund der neueren Forschung immer besser charakterisiert werden. Der Artikel schließt mit Hinweisen zur klinischen Relevanz der aktuellen Befunde sowie offenen Fragen der translationalen Forschung.
Sprach- und Sprechstörungen kommen bei zahlreichen Kindern vor und werden in der ICD-11 analog zur ICD-10 als Entwicklungsstörungen im Kapitel 6 (Psychische, Verhaltens- und Entwicklungsstörungen) klassifiziert. International sind bislang die ICD-10-Kriterien nicht von allen Professionen, die sich mit Sprach- und Sprechstörungen klinisch oder im Rahmen der Forschung beschäftigen, akzeptiert. Sie werden einerseits als zu wenig differenziert hinsichtlich der unterschiedlichen Sprachkomponenten vonseiten der Linguistik, Sprachtherapie oder Logopädie erlebt. Zum anderen wird die unklare Abgrenzung organisch bedingter Sprach- und Sprechprobleme von der Sprachentwicklungsstörung vonseiten der Medizin teilweise kritisch bewertet. In dem vorliegenden Artikel wird deshalb einerseits die Klassifikation von Sprach- und Sprechproblemen und -störungen in der ICD-11 im Vergleich zur ICD-10 vorgenommen. Wesentlich erscheint hier die in der ICD-11 neu eingeführte Differenzierung in „primäre“ und „sekundäre“ Neuroentwicklungsstörungen. Zum anderen erfolgt aber auch eine Auseinandersetzung mit dem DSM-5 sowie anderen Klassifikationsvorschlägen vonseiten der englischsprachigen Sprachtherapie (CATALISE-2) und der deutschsprachigen Pädaudiologie („phonologische Wahrnehmungsstörung“) sowie der Vorschlag einer Ergänzung der aktuellen ICD-11-Klassifikation hinsichtlich konkreter sprachlicher Einschränkungen bei einem Kind mit Sprachentwicklungsstörung, basierend auf einer ausführlichen Diagnostik. Wir hoffen, mit dem Artikel so den Weg für eine berufsübergreifende Klassifikation von Sprach- und Sprechstörungen nach ICD-11 zu bahnen, damit perspektivisch alle Berufsgruppen, die Diagnostik und Therapie der betroffenen Personen anbieten, eine vergleichbare Terminologie verwenden. Diese vergleichbare Terminologie soll sowohl die klinische Versorgung verbessern als auch die unterschiedlichen Forschungsansätze und -richtungen vergleichbarer machen.
Sprach- und Sprechstörungen kommen bei zahlreichen Kindern vor und werden in der ICD-11 analog zur ICD-10 als Entwicklungsstörungen im Kapitel 6 (Psychische, Verhaltens- und Entwicklungsstörungen) klassifiziert. International sind bislang die ICD-10-Kriterien nicht von allen Professionen, die sich mit Sprach- und Sprechstörungen klinisch oder im Rahmen der Forschung beschäftigen, akzeptiert. Sie werden einerseits als zu wenig differenziert hinsichtlich der unterschiedlichen Sprachkomponenten vonseiten der Linguistik, Sprachtherapie oder Logopädie erlebt. Zum anderen wird die unklare Abgrenzung organisch bedingter Sprach- und Sprechprobleme von der Sprachentwicklungsstörung vonseiten der Medizin teilweise kritisch bewertet. In dem vorliegenden Artikel wird deshalb einerseits die Klassifikation von Sprach- und Sprechproblemen und -störungen in der ICD-11 im Vergleich zur ICD-10 vorgenommen. Wesentlich erscheint hier die in der ICD-11 neu eingeführte Differenzierung in „primäre“ und „sekundäre“ Neuroentwicklungsstörungen. Zum anderen erfolgt aber auch eine Auseinandersetzung mit dem DSM-5 sowie anderen Klassifikationsvorschlägen vonseiten der englischsprachigen Sprachtherapie (CATALISE-2) und der deutschsprachigen Pädaudiologie („phonologische Wahrnehmungsstörung“) sowie der Vorschlag einer Ergänzung der aktuellen ICD-11-Klassifikation hinsichtlich konkreter sprachlicher Einschränkungen bei einem Kind mit Sprachentwicklungsstörung, basierend auf einer ausführlichen Diagnostik. Wir hoffen, mit dem Artikel so den Weg für eine berufsübergreifende Klassifikation von Sprach- und Sprechstörungen nach ICD-11 zu bahnen, damit perspektivisch alle Berufsgruppen, die Diagnostik und Therapie der betroffenen Personen anbieten, eine vergleichbare Terminologie verwenden. Diese vergleichbare Terminologie soll sowohl die klinische Versorgung verbessern als auch die unterschiedlichen Forschungsansätze und -richtungen vergleichbarer machen.
Background: Both selective mutism (SM) and social anxiety disorder (SAD) are severe pediatric anxiety disorders with the common trait of behavioral inhibition (BI). The underlying pathophysiology of these disorders remains poorly understood, however converging evidence suggests that alterations in several peripheral molecular pathways might be involved. In a pilot study, we investigated alterations in plasma molecular markers (dipeptidyl peptidase-4 [DPPIV], interleukin-6 [IL-6], tumor necrosis factor-β [TNF-β] and neuropeptide-Y [NPY]) in children with SM, SAD, and healthy controls, as well as the correlation of these markers to symptom severity. Methods: We included 51 children and adolescents (aged 5–18 years; n = 29 girls): n = 20 children in the SM-, n = 16 in the SAD- and n = 15 in the control-group (CG). Peripheral blood samples were analyzed for DPPIV, IL-6, TNF-β, and NPY concentrations. Diverse psychometric measures were used for BI, anxiety, and mutism symptoms. Results: Lower DPPIV-levels were correlated with more anxiety symptoms. However, we could not find a difference in any molecular marker between the patients with SAD and SM in comparison to the CG. Conclusion: DPPIV is proposed as relevant marker for child and adolescent anxiety. Investigating the pathophysiology of SM and SAD focusing on state and trait variables as anxiety or BI might help better understanding the underlying mechanisms of these disorders. Further studies with especially larger cohorts are needed to validate the current pilot-findings.
Electroencephalography (EEG) represents a widely established method for assessing altered and typically developing brain function. However, systematic studies on EEG data quality, its correlates, and consequences are scarce. To address this research gap, the current study focused on the percentage of artifact-free segments after standard EEG pre-processing as a data quality index. We analyzed participant-related and methodological influences, and validity by replicating landmark EEG effects. Further, effects of data quality on spectral power analyses beyond participant-related characteristics were explored. EEG data from a multicenter ADHD-cohort (age range 6 to 45 years), and a non-ADHD school-age control group were analyzed (ntotal = 305). Resting-state data during eyes open, and eyes closed conditions, and task-related data during a cued Continuous Performance Task (CPT) were collected. After pre-processing, general linear models, and stepwise regression models were fitted to the data. We found that EEG data quality was strongly related to demographic characteristics, but not to methodological factors. We were able to replicate maturational, task, and ADHD effects reported in the EEG literature, establishing a link with EEG-landmark effects. Furthermore, we showed that poor data quality significantly increases spectral power beyond effects of maturation and symptom severity. Taken together, the current results indicate that with a careful design and systematic quality control, informative large-scale multicenter trials characterizing neurophysiological mechanisms in neurodevelopmental disorders across the lifespan are feasible. Nevertheless, results are restricted to the limitations reported. Future work will clarify predictive value.
Sex differences in psychiatric comorbidity and clinical presentation in youths with conduct disorder
(2021)
Background: Conduct disorder (CD) rarely occurs alone but is typically accompanied by comorbid psychiatric disorders, which complicates the clinical presentation and treatment of affected youths. The aim of this study was to investigate sex differences in comorbidity pattern in CD and to systematically explore the ‘gender paradox’ and ‘delayed-onset pathway’ hypotheses of female CD.
Methods: As part of the FemNAT-CD multisite study, semistructured clinical interviews and rating scales were used to perform a comprehensive phenotypic characterization of 454 girls and 295 boys with CD (9–18 years), compared to 864 sex- and age-matched typically developing controls.
Results: Girls with CD exhibited higher rates of current major depression, anxiety disorders, post-traumatic stress disorder and borderline personality disorder, whereas boys with CD had higher rates of current attention-deficit/hyperactivity disorder. In line with the ‘gender paradox’ hypothesis, relative to boys, girls with CD showed significantly more lifetime psychiatric comorbidities (incl. Alcohol Use Disorder), which were accompanied by more severe CD symptoms. Female and male youths with CD also differed significantly in their CD symptom profiles and distribution of age-of-onset subtypes of CD (i.e. fewer girls with childhood-onset CD). In line with the ‘delayed-onset pathway’ hypothesis, girls with adolescent-onset CD showed similar levels of dimensional psychopathology like boys with childhood-onset CD, while boys with adolescent-onset CD had the lowest levels of internalizing psychopathology.
Conclusions: Within the largest study of CD in girls performed to date, we found compelling evidence for sex differences in comorbidity patterns and clinical presentation of CD. Our findings further support aspects of the ‘gender paradox’ and ‘delayed-onset pathway’ hypotheses by showing that girls with CD had higher rates of comorbid lifetime mental disorders and functional impairments, and they usually developed CD during adolescence. These novel data on sex-specific clinical profiles of CD will be critical in informing intervention and prevention programmes.
Interpretation bias and dysfunctional social assumptions are proposed to play a pivotal role in the development and maintenance of social phobia (SP), especially in youth. In this study, we aimed to investigate disorder-specific implicit assumptions of rejection and implicit interpretation bias in youth with severe, chronic SP and healthy controls (CG). Twenty-seven youth with SP in inpatient/day-care treatment (M age = 15.6 years, 74% female) and 24 healthy controls (M age = 15.7 years, 54% female) were included. The Implicit Association Test (IAT) and the Affect Misattribution Procedure (AMP) were completed to assess implicit assumptions and interpretation bias related to the processing of social and affective stimuli. No group differences were observed for the IAT controlling for depressive symptoms in the analyses. However, group differences were found regarding interpretation bias (p = .017, η2p = .137). Correlations between implicit scores and explicit questionnaire results were medium to large in the SP group (r =|.28| to |.54|, pall ≤ .05), but lower in the control group (r =|.04| to |.46|, pall ≤ .05). Our results confirm the finding of an interpretation bias in youth SP, especially regarding the implicit processing of faces, whereas implicit dysfunctional social assumptions of being rejected do not seem to be specific for SP. Future research should investigate the causal relationship of assumptions/interpretation bias and SP.