Bipolar disorder (BD) is a severe and lifelong condition. Primary endogenic polygenetic forms are common. Secondary organic forms have received increasing interest recently due to the detection of immunological encephalopathies that mimic various psychiatric syndromes, including BD. However, only limited data about routine findings of cerebrospinal fluid (CSF) analyses in BD are available. Therefore, we investigated the frequency of alterations in the CSF in patients with BD and the association with autoantibodies, cerebral magnetic resonance imaging, and electroencephalography findings. CSF samples of patients with BD collected from January 1998 until December 2015 were analyzed retrospectively. Patients with preexisting causes for alterations in the CSF (e.g., patients with obvious past or current neurological disorders) were excluded. In total, 63 patients with BD fulfilled the inclusion criteria for the study. In 1.6% of the patients with BD, an increased white blood cell count was found in the CSF. Increased albumin quotients were found in 12.9% of the patients, oligoclonal bands (OCBs) in 1.6%, and increased immunoglobulin (Ig) G indices in 3.2% (OCBs were not measured in case of increased IgG indices). No significant differences in CSF findings were found between patients with manic and depressive episodes. The main findings of this open uncontrolled study are that alterations in the CSF may be found in a small, but potentially relevant, subgroup of patients with BD. These findings are discussed in light of the new concepts of mild encephalitis and immunological encephalopathy. The detection of patients with possibly secondary organic bipolar syndromes could open up new causal treatment options with immunomodulatory medication.

Autism spectrum disorder (ASD) is characterized by impaired social interaction and communication skills, repetitive behaviors, restricted interests, and specific sensory processing. Particularly, adults with high-functioning ASD often remain unrecognized, presumably due to their high compensatory skills, but at the cost of high stress, which is often linked to anxiety and depression. This may further explain the significantly high suicide rates and reduced life expectancy among individuals with ASD. Thus, providing support to high-functioning autistic adults in managing core symptoms, as well as co-occurring anxiety and depression, appears essential. To date, only a limited number of evidence-based psychosocial therapeutic options are available, and very few of them have undergone rigorous evaluation in a clinical context. To obtain a comprehensive understanding, a systematic literature search was conducted according to the PRISMA checklist, and only studies demonstrating robust methodological quality were included and discussed in this review article. Although promising initial key factors and methods have been identified, additional evidence-based studies are imperative to ascertain the optimal treatment and evaluate the long-term outcomes for adults with high-functioning ASD.

Objective: Autism spectrum (ASD) and attention-deficit/hyperactivity disorder (ADHD) are neurodevelopmental disorders with a high rate of comorbidity. To date, diagnosis is based on clinical presentation and distinct reliable biomarkers have been identified neither for ASD nor ADHD. Most previous neuroimaging studies investigated ASD and ADHD separately. Method: To address the question of structural brain differences between ASD and ADHD, we performed FreeSurfer analysis in a sample of children with ADHD (n = 30), with high-functioning ASD (n = 14), with comorbid high-functioning ASD and ADHD (n = 15), and of typically developed controls (TD; n = 36). With FreeSurfer, an automated brain imaging processing and analyzing suite, we reconstructed the cerebral cortex and calculated gray matter volumes as well as cortical surface parameters in terms of cortical thickness and mean curvature. Results: A significant main effect of the factor ADHD was detected for the left inferior frontal gyrus (Pars orbitalis) volume, with the ADHD group exhibiting smaller Pars orbitalis volumes. Dimensional measures of autism (SRS total raw score) and ADHD (DISYPS-II FBB-ADHD score) had no significant influence on the left Pars orbitalis volume. Both, ASD and ADHD tended to have an effect on cortical thickness or mean curvature, which did not survive correction for multiple comparisons. Conclusion: Our results underline that ADHD rather than ASD is associated with volume loss in the left inferior frontal gyrus (Pars orbitalis). This area might play a relevant role in modulating symptoms of inattention and/or impulsivity in ADHD. The effect of comorbid ADHD in ASD samples and vice versa, on cortical thickness and mean curvature, requires further investigation in larger samples.

Objective: Severe malnutrition in patients with anorexia nervosa (AN) as well as possible trait-related aberrations lead to pronounced structural brain changes whose reversibility after recovery is currently unclear. Previous diffusion tensor imaging (DTI) studies investigating white matter (WM) microstructure alterations in AN are inconsistent. Methods: In this so far largest DTI study in adults, we investigated 33 AN patients, 20 recovered (REC), and 33 healthy women. DTI data were processed using the "DTI and Fiber tools," and the Computational Anatomy Toolbox. WM integrity, both in terms of fractional anisotropy (FA) and mean diffusivity (MD), was assessed. Results: We found a significant FA decrease in the corpus callosum (body) and an MD decrease in the posterior thalamic radiation in the AN group. The REC group displayed FA decrease in the corpus callosum in comparison to HC, whereas there were no MD differences between the REC and HC groups. Conclusion: Despite prolonged restoration of weight in the REC group, no significant regeneration of WM integrity in terms of FA could be observed. Transient changes in MD likely represent a reversible consequence of the acute state of starvation or result from dehydration. Reduction of FA either may be due to WM damage resulting from malnutrition or may be considered a pre-morbid marker.

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.

Vitamin D has many immunomodulatory, anti-inflammatory, and neuroprotective functions, and previous studies have demonstrated an association between vitamin D deficiency and neuropsychiatric disease. The aim of our study was to analyze the prevalence of vitamin D deficiency in a 1-year cohort of adult inpatients with schizophreniform and autism spectrum syndromes in a naturalistic inpatient setting in Germany.