Over the last few years, awareness of autism spectrum disorder (ASD) in adults has increased. The precise etiology of ASD is still unresolved. Animal research, genetic and postmortem studies suggest that the glutamate (Glu) system has an important role, possibly related to a cybernetic imbalance between neuronal excitation and inhibition. To clarify the possible disruption of Glu metabolism in adults with high-functioning autism, we performed a magnetic resonance spectroscopy (MRS) study investigating the anterior cingulate cortex (ACC) and the cerebellum in adults with high-functioning ASD. Twenty-nine adult patients with high-functioning ASD and 29 carefully matched healthy volunteers underwent MRS scanning of the pregenual ACC and the left cerebellar hemisphere. Metabolic data were compared between groups and were correlated with psychometric measures of autistic features. We found a significant decrease in the cingulate N-acetyl-aspartate (NAA) and the combined Glu and glutamine (Glx) signals in adults with ASD, whereas we did not find other metabolic abnormalities in the ACC or the cerebellum. The Glx signal correlated significantly with psychometric measures of autism, particularly with communication deficits. Our data support the hypothesis that there is a link between disturbances of the cingulate NAA and Glx metabolism, and autism. The findings are discussed in the context of the hypothesis of excitatory/inhibitory imbalance in autism. Further research should clarify the specificity and dynamics of these findings regarding other neuropsychiatric disorders and other brain areas.

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MRS is a promising tool for the non-invasive in vivo assessment of the cerebral neurochemistry in ADHD. More regions of interest (ROI) like amygdala, hippocampus, thalamus and cerebellum should be assessed in future studies. Further methodological improvements of MRS are desirable in order to assess the absolute metabolite concentration of several ROIs at the same time. Such developments will open novel perspectives in spectroscopic investigations of ADHD.

AN is accompanied by severe loss of brain volume and cortical thickness as assessed by complementary investigation tools. However, these changes seem to be largely reversible, which should be encouraging for therapists and patients. The underlying neurobiological mechanisms remain unclear and should be assessed in further studies.

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The central role played by cerebrospinal-fluid (CSF) examinations including antineuronal autoantibody (Ab) testing is increasingly recognized in psychiatry. The rationale of this study was to present a multimodally investigated group of patients. In total, 992 patients were analyzed for CSF alterations: 456 patients with schizophreniform and 536 with affective syndromes. Ab measurement included testing for established antineuronal IgG-Abs against intracellular antigens in serum (Yo/Hu/Ri/cv2[CRMP5]/Ma1/Ma2/SOX1/TR[DNER]/Zic4/amphiphysin/GAD65) and for cell surface antigens in the CSF (NMDAR/AMPA-1/2-R/GABA-B-R/LGI1/CASPR2/DPPX). In 30 patients with “red flags” for autoimmune psychosis, “tissue tests” were performed. Additional diagnostics included MRI and EEG analyses. CSF white-blood-cell counts were increased in 4% and IgG indices in 2%; CSF-specific oligoclonal bands were detected in 4%; overall, 8% displayed signs of neuroinflammation. In addition, 18% revealed increased albumin quotients. Antineuronal Abs against intracellular antigens were detected in serum in 0.6%. Antineuronal Abs against established cell surface antigens were detected in serum of 1% and in the CSF of 0.3% (CSF samples were only questionably positive). Abnormal IgG binding in “tissue tests” was detected in serum of 23% and in CSF of 27%. In total, 92% of the Ab-positive patients demonstrated at least one sign of brain involvement in additional diagnostics using CSF, MRI, EEG, and FDG-PET. In summary, CSF basic analyses revealed signs of blood–brain-barrier dysfunction and neuroinflammation in relevant subgroups of patients. Established antineuronal IgG-Abs were rare in serum and even rarer in the CSF. “Tissue tests” revealed frequent occurrences of Ab-binding; therefore, novel antineuronal Abs could play a relevant role in psychiatry.

Prolonged amygdala response and a functional disconnection between ventral and dorsal mPFC regions may be part of the neural mechanisms underlying emotional dysregulation in BPD patients.

Background: Links between eating disorders (EDs) [e.g., anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED)] and the major neurodevelopmental disorders of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) have been repeatedly highlighted. In both ASD and ADHD, these links range from an elevated risk for EDs to common symptomatic overlaps and etiological commonalities with EDs. Methods: We performed a systematic literature search (through July 2019) with Medline via Ovid for epidemiological data on EDs (AN, BN, and BED) in combination with both ASD and ADHD. Results: The reviewed studies showed that, on average, 4.7% of patients with certain ED diagnoses (AN, BN, or BED) received an ASD diagnosis. Reliable data on the prevalence of EDs in ASD samples are still scarce. Comorbid ASD is most commonly diagnosed in patients with AN. The prevalence of ADHD in EDs ranged between 1.6% and 18%. Comorbid ADHD was more often reported in the AN-binge eating/purging subtype and BN than in the AN restrictive subtype. The prevalence of EDs in ADHD ranged between no association and a lifetime prevalence of 21.8% of developing an ED in women with ADHD. Conclusions: Studies on the prevalence rates of EDs in ADHD and ASD and vice versa are heterogeneous, but they indicate frequent association. While there is growing evidence of clinical overlaps between the three disorders, it remains difficult to determine whether overlapping characteristics (e.g., social withdrawal) are due to common comorbidities (e.g., depression) or are instead primarily associated with EDs and neurodevelopmental disorders. Furthermore, prospective studies are required to better understand how these disorders are related and whether ADHD and ASD could be either specific or nonspecific predisposing factors for the development of EDs.