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Improving our learning abilities is important for numerous aspects of our life. Several studies found beneficial effects of presenting cues (odor or sounds) during learning and during sleep for memory performance. A recent study applying a real-life paradigm indicated that additional odor cueing during a Final Test can further increase this cueing effect. The present online study builds on these findings with the following questions: (1) Can we replicate beneficial memory effects of additional odor cueing during tests? (2) How many odor cueing learning sessions and odor cueing nights of sleep maximize the learning success? (3) Can odor cueing also reduce the amount of forgetting over time? 160 Participants learned 40 German Japanese word pairs in four groups with separate experimental conditions over three days. Group N received no odor during the whole study. Group LS received odor cueing during learning and sleep, group LT during learning and testing and group LST during learning, sleep and testing. Participants performed intermediate tests after each learning session plus three final tests 1, 7 and 28 days after the last learning session. Results: (1) Group LST learned 8.5% more vocabulary words than the other groups overall. (2) This odor cueing effect increased across the three days of cued learning. (3) We found no clear evidence for effects of odor cueing on the forgetting dynamics. Our findings support the notion of a beneficial effect of odor cueing. They further suggest to use at least 3 days and nights of odor cueing. Overall, this study indicates that there is an easy, efficient and economical way to enhance memory performance in daily life. [ABSTRACT FROM AUTHOR]

Symptoms of obsessive–compulsive disorder (OCD) may rarely occur in the context of genetic syndromes. So far, an association between obsessive–compulsive symptoms (OCS) and ACTG1-associated Baraitser-Winter cerebrofrontofacial syndrome has not been described as yet. A thoroughly phenotyped patient with OCS and ACTG1-associated Baraitser-Winter cerebrofrontofacial syndrome is presented. The 25-year-old male patient was admitted to in-patient psychiatric care due to OCD. A whole-exome sequencing analysis was initiated as the patient also showed an autistic personality structure, below average intelligence measures, craniofacial dysmorphia signs, sensorineural hearing loss, and sinus cavernoma as well as subtle cardiac and ophthalmological alterations. The diagnosis of Baraitser-Winter cerebrofrontofacial syndrome type 2 was confirmed by the detection of a heterozygous likely pathogenic variant in the ACTG1 gene [c.1003C > T; p.(Arg335Cys), ACMG class 4]. The automated analysis of magnetic resonance imaging (MRI) revealed changes in the orbitofrontal, parietal, and occipital cortex of both sides and in the right mesiotemporal cortex. Electroencephalography (EEG) revealed intermittent rhythmic delta activity in the occipital and right temporal areas. Right mesiotemporal MRI and EEG alterations could be caused by a small brain parenchymal defect with hemosiderin deposits after a cavernomectomy. This paradigmatic case provides evidence of syndromic OCS in ACTG1-associated Baraitser-Winter cerebrofrontofacial syndrome. The MRI findings are compatible with a dysfunction of the cortico-striato-thalamo-cortical loops involved in OCD. If a common pathophysiology is confirmed in future studies, corresponding patients with Baraitser-Winter cerebrofrontofacial syndrome type 2 should be screened for OCS. The association may also contribute to a better understanding of OCD pathophysiology. [ABSTRACT FROM AUTHOR]

Findings of genetic overlap between Schizophrenia, Attention-Deficit/Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD) contributed to a renewed conceptualization of these disorders as laying on a continuum based on aetiological, pathophysiological and neurodevelopmental features. Given that cognitive impairments are core to their pathophysiology, we compared patients with schizophrenia, ADHD, ASD, and controls on ocular-motor and manual-motor tasks, challenging crucial cognitive processes. Group comparisons revealed inhibition deficits common to all disorders, increased intra-subject variability in schizophrenia and, to a lesser extent, ADHD as well as slowed processing in schizophrenia. Patterns of deviancies from controls exhibited strong correlations, along with differences that posited schizophrenia as the most impaired group, followed by ASD and ADHD. While vector correlations point towards a common neurodevelopmental continuum of impairment, vector levels suggest differences in the severity of such impairment. These findings argue towards a dimensional approach to Neurodevelopmental Disorders' pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Disorders with neurodevelopmental aetiology such as Attention-Deficit/Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD) and Schizophrenia share commonalities at many levels of investigation despite phenotypic differences. Evidence of genetic overlap has led to the concept of a continuum of neurodevelopmental impairment along which these disorders can be positioned in aetiological, pathophysiological and developmental features. This concept requires their simultaneous comparison at different levels, which has not been accomplished so far. Given that cognitive impairments are core to the pathophysiology of these disorders, we provide for the first time differentiated head-to-head comparisons in a complex cognitive function, visual search, decomposing the task with eye movement-based process analyses. N = 103 late-adolescents with schizophrenia, ADHD, ASD and healthy controls took a serial visual search task, while their eye movements were recorded. Patients with schizophrenia presented the greatest level of impairment across different phases of search, followed by patients with ADHD, who shared with patients with schizophrenia elevated intra-subject variability in the pre-search stage. ASD was the least impaired group, but similar to schizophrenia in post-search processes and to schizophrenia and ADHD in pre-search processes and fixation duration while scanning the items. Importantly, the profiles of deviancy from controls were highly correlated between all three clinical groups, in line with the continuum idea. Findings suggest the existence of one common neurodevelopmental continuum of performance for the three disorders, while quantitative differences appear in the level of impairment. Given the relevance of cognitive impairments in these three disorders, we argue in favour of overlapping pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Primary schizophreniform psychoses are thought to be caused by complex gene–environment interactions. Secondary forms are based on a clearly identifiable organic cause, in terms of either an etiological or a relevant pathogenetic factor. The secondary or "symptomatic" forms of psychosis have reentered the focus stimulated by the discovery of autoantibody (Ab)-associated autoimmune encephalitides (AEs), such as anti-NMDA-R encephalitis, which can at least initially mimic variants of primary psychosis. These newly described secondary, immune-mediated schizophreniform psychoses typically present with the acute onset of polymorphic psychotic symptoms. Over the course of the disease, other neurological phenomena, such as epileptic seizures, movement disorders, or reduced levels of consciousness, usually arise. Typical clinical signs for AEs are the acute onset of paranoid hallucinatory symptoms, atypical polymorphic presentation, psychotic episodes in the context of previous AE, and additional neurological and medical symptoms such as catatonia, seizure, dyskinesia, and autonomic instability. Predominant psychotic courses of AEs have also been described casuistically. The term autoimmune psychosis (AP) was recently suggested for these patients. Paraclinical alterations that can be observed in patients with AE/AP are inflammatory cerebrospinal fluid (CSF) pathologies, focal or generalized electroencephalographic slowing or epileptic activity, and/or suspicious "encephalitic" imaging findings. The antibody analyses in these patients include the testing of the most frequently found Abs against cell surface antigens (NMDA-R, CASPR2, LGI1, AMPA-R, GABAB-R), intracellular antigens (Hu, Ri, Yo, CV2/CRMP5, Ma2 [Ta], amphiphysin, GAD65), thyroid antigens (TG, TPO), and antinuclear Abs (ANA). Less frequent antineuronal Abs (e.g., against DPPX, GABAA-R, glycine-R, IgLON5) can be investigated in the second step when first step screening is negative and/or some specific clinical factors prevail. Beyond, tissue-based assays on brain slices of rodents may detect previously unknown antineuronal Abs in some cases. The detection of clinical and/or paraclinical pathologies (e.g., pleocytosis in CSF) in combination with antineuronal Abs and the exclusion of alternative causes may lead to the diagnosis of AE/AP and enable more causal therapeutic immunomodulatory opportunities. [ABSTRACT FROM AUTHOR]

The amygdala reveals enhanced reactivity to fearful eye whites, even when they are backwardly masked by a neutral face and therefore processed with limited visual awareness. In our fMRI study, we investigated whether this effect is indeed associated with fear detection within the eyes of the neutral face mask, or more generally, with reactivity to any salient increase in eye white area. In addition, we examined whether a single dose of intranasal oxytocin would modulate amygdala responses to masked fearful eye whites via a double-blind, placebo-controlled pharmacological protocol. We found that increased amygdala responses to salient changes within a face's eye region occurred specifically for masked fearful eyes but not for similar increases in white area as induced by nonsocial control stimuli. Administration of oxytocin attenuated amygdala responses to masked fearful eye whites. Our results suggest that the amygdala is particularly tuned to potential threat signals from the eye region. The dampening effects of oxytocin on early amygdala reactivity may reflect reduced vigilance for facial threat cues at a preconscious level. Future studies may investigate whether this early modulation accounts for the beneficial effects of oxytocin on social cognition in anxiety-related disorders, as suggested by previous studies. [ABSTRACT FROM AUTHOR]

The worldwide fascination of da Vinci's Mona Lisa has been dedicated to the emotional ambiguity of her face expression. In the present study we manipulated Mona Lisa's mouth curvature as one potential source of ambiguity and studied how a range of happier and sadder face variants influences perception. In two experimental conditions we presented different stimulus ranges with different step sizes between stimuli along the happy-sad axis of emotional face expressions. Stimuli were presented in random order and participants indicated the perceived emotional face expression (first task) and the confidence of their response (second task). The probability of responding 'happy' to the original Mona Lisa was close to 100%. Furthermore, in both conditions the perceived happiness of Mona Lisa variants described sigmoidal functions of the mouth curvature. Participants' confidence was weakest around the sigmoidal inflection points. Remarkably, the sigmoidal functions, as well as confidence values and reaction times, differed significantly between experimental conditions. Finally, participants responded generally faster to happy than to sad faces. Overall, the original Mona Lisa seems to be less ambiguous than expected. However, perception of and reaction to the emotional face content is relative and strongly depends on the used stimulus range. [ABSTRACT FROM AUTHOR]

Presents a case of extremely high elevated serum creatine kinase (CK) levels induced by olanzapine therapy. Case report of a 33-year-old white German man with schizoaffective disorder according to ICD-10 criteria who had been treated with olanzapine for seven weeks when he suddenly developed extremely high elevated serum CK concentrations; Suggestion that dramatic elevations in serum CK and myoglobin levels seem to be a rare but possibly dangerous complication of olanzapine therapy.

Adult ADHD is a risk factor for co-occurring disorders and negative psychosocial consequences. Given this background there is a need for effective psychotherapeutic treatments for adults with ADHD. Due to overlapping clinical features in adult ADHD and borderline personality disorder our treatment is mainly based on the principles of dialectical behavioral treatment. Cognitive behavioral treatment strategies are mainly integrated to modify maladaptive thoughts interfering with therapy. The structured program is applied in weekly session to adult ADHD outpatients in a group setting. As shown in our pilot study and feasibility multicenter trial, the DBT-based program resulted in good outcomes. ADHD severity, depression and personal health status were significantly improved. Patients regarded the program topics ‘‘behavioural analyses’’, ‘‘mindfulness’’ and ‘‘emotion regulation’’ as the most helpful. However, so far, randomized placebo- controlled studies comparing the effects of medical management, disorder-oriented psychotherapy, and the combination of both are still lacking. Therefore, the University Freiburg has initiated a multicenter trial at eight university sites which is funded by the German Federal Ministry of Research and Education (01GV0606). Preliminary data of this study will be presented. [ABSTRACT FROM AUTHOR]

The Ritvo Autism Asperger Diagnostic Scale-Revised (RAADS-R) demonstrated excellent results in its original study, with a sensitivity of 97% and a specificity of 100% (Ritvo et al. in J Autism Dev Disord 41:1076–1089, 2011). As a result, it was included in the National Institute for Health and Care Excellence (NICE) guidelines (Recommendations | Autism spectrum disorder in adults: diagnosis and management | Guidance | NICE, 2022). The questionnaire includes 80 questions across four subcategories (language, social relatedness, circumscribed interests, sensory motor). So far, the subcategory sensory motor has not been addressed in most available instruments, despite being part of the diagnostic criteria specified in DSM-5 (Falkai et al., in Diagnostisches Und Statistisches Manual Psychischer Störungen DSM-5. Hogrefe, 2015) and ICD-11 (ICD-11 for Mortality and Morbidity Statistics, 2022). In our validation study, we tested a translated German version of the questionnaire in 299 individuals (110 persons with ASD according to ICD-10 F84.0, F84.5, 64 persons with an primary mental disorders (PMD), 125 persons with no disorders). To enhance the practical use of the instrument in clinical everyday practice, the questionnaire was completed by the participants without the presence of a clinician—unlike the original study. Psychiatric diagnoses were established following the highest standards, and psychometric properties were calculated using established protocols. The German version of the RADS-R yielded very good results, with a high sensitivity of 92.5% and a high specificity of 93.6%. The area under the curve (AUC = 0.976), indicates a high quality and discriminatory power of RADS-R. Furthermore, the ROC curve analysis showed that the optimal threshold to distinguish between the ASD and non-ASD groups in the German version of the RAADS-R is a score of 81. In comparison to the RADS-R, the co-administered instruments Social Responsiveness Scale (SRS), Autism Spectrum Quotient (AQ), and Empathy Quotient (EQ) each showed slightly better specificity but worse sensitivity in this sample.The study included individuals already diagnosed with ASD according to ICD-10 (F84.0, F84.5), with or without an primary mental disorders, preventing us from identifying the influence of comorbidities on the RADS-R results. In addition, a self-report questionnaire has generally only limited objectivity and may allow for false representation of the symptoms. The RADS-R compares well with other questionnaires and can provide valuable additional information. It could turn out to be a helpful diagnostic tool for patients in Germany. We propose naming the German version RADS-R (Ritvo Autism Diagnostic Scale – rRevised) to reflect the change in terminology. [ABSTRACT FROM AUTHOR]