Search

Mitochondria are complex endosymbionts that evolved from primordial purple nonsulfur bacteria. The incorporation of bacteria-derived mitochondria facilitates a more efficient and effective production of energy than what could be achieved based on previous processes alone. In this case, endosymbiosis has resulted in the seamless coupling of cytochrome c oxidase and F-ATPase to maximize energy production. However, this mechanism also results in the generation of reactive oxygen species (ROS), a phenomenon that can have both positive and negative ramifications on the host. Recent studies have revealed that neuropsychiatric disorders have a pro-inflammatory component in which ROS is capable of initiating damage and cognitive malfunction. Our current understanding of cognition suggests that it is the product of a neuronal network that consumes a substantial amount of energy. Thus, alterations or perturbations of mitochondrial function may alter not only brain energy supply and metabolite generation, but also thought processes and behavior. Mitochondrial abnormalities and oxidative stress have been implicated in several well-known psychiatric disorders, including schizophrenia (SCZ) and bipolar disorder (BPD). As cognition is highly energy-dependent, we propose that the neuronal pathways underlying maladaptive cognitive processing and psychiatric symptoms are most likely dependent on mitochondrial function, and thus involve brain energy translocation and the accumulation of the byproducts of oxidative stress. We also hypothesize that neuropsychiatric symptoms (e.g., disrupted emotional processing) may represent the vestiges of an ancient masked evolutionary response that can be used by both hosts and pathogens to promote self-repair and proliferation via parasitic and/or symbiotic pathways.

Pascal Büttiker,1 George B Stefano,1 Simon Weissenberger,2 Radek Ptacek,1 Martin Anders,1 Jiri Raboch,1 Richard M Kream1 1Department of Psychiatry, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic; 2Department of Psychology, University of New York in Prague, Prague, Czech RepublicCorrespondence: Pascal Büttiker, Altenbach 26, Vaduz, 9490, Liechtenstein, Tel +41 78 653 8442, Email pascal_buettiker@hotmail.comAbstract: Long COVID, in which disease-related symptoms persist for months after recovery, has led to a revival of the discussion of whether neuropsychiatric long-term symptoms after viral infections indeed result from virulent activity or are purely psychological phenomena. In this review, we demonstrate that, despite showing differences in structure and targeting, many viruses have highly similar neuropsychiatric effects on the host. Herein, we compare severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), human immunodeficiency virus 1 (HIV-1), Ebola virus disease (EVD), and herpes simplex virus 1 (HSV-1). We provide evidence that the mutual symptoms of acute and long-term anxiety, depression and post-traumatic stress among these viral infections are likely to result from primary viral activity, thus suggesting that these viruses share neuroinvasive strategies in common. Moreover, it appears that secondary induced environmental stress can lead to the emergence of psychopathologies and increased susceptibility to viral (re)infection in infected individuals. We hypothesize that a positive feedback loop of virus-environment-reinforced systemic responses exists. It is surmised that this cycle of primary virulent activity and secondary stress-induced reactivation, may be detrimental to infected individuals by maintaining and reinforcing the host’s immunocompromised state of chronic inflammation, immunological strain, and maladaptive central-nervous-system activity. We propose that this state can lead to perturbed cognitive processing and promote aversive learning, which may manifest as acute, long-term neuropsychiatric illness.Keywords: HIV-1, SARS virus, virus latency, neuropsychiatry, interoception

Objective: Cognitive and motor disintegration and other functional disturbances in various neuropsychiatric disorders may be related to inhibitory deficits that may manifest as a persistence or re-expression of primitive reflexes and few recent data suggest that these deficits may occur in Attention Deficit and Hyperactivity Disorder (ADHD). Methods: We have tested a hypothesis to which extent ADHD symptoms and balance deficits are related to persisting primitive reflexes, such as Asymmetric Tonic Neck Reflex (ATNR) and Symmetric Tonic Neck Reflex (STNR) in 80 medication-naïve children with ADHD (40 boys and 40 girls) in the school age (8–11 years) and compared these data with a control group of 60 children (30 boys and 30 girls). Results: These data show new finding that ADHD symptoms and balance deficits are strongly and specifically associated with persistent ATNR in girls and STNR in boys. Conclusions: These results provide first evidence in medical literature that ADHD in girls and boys is specifically related to distinguished neurological developmental mechanisms related to disinhibition of primitive reflexes.

BACKGROUND The early days of a given experience are associated with typically what might be characterized as an idealized enthusiasm. Conversely burnout syndrome experienced later in the given experience is associated with disillusionment, disappointment, and symptoms which resemble a depression. This very common propensity is a parallel to the concept of "splitting" described by Kernberg with a pronounced "black and white" perceptual dichotomy between the early idealization and later disillusionment. This study intends examination of relationships between burnout syndrome, depression, and Kernberg's concept of splitting. MATERIAL AND METHODS In this present study, we assessed 132 female health care professionals working with a population of diabetic patients utilizing Burnout Measure (BM) Splitting Index (SI), Beck Depression Inventory II (BDI-II), and additional psychometric instruments, the Toronto Alexithymia Scale and the Trauma Symptoms Checklist. RESULTS The study results indicated significant Spearman correlations between burnout syndrome as measured by BM and depression (BDI-II) (R=0.62, P0.01), and burnout syndrome as measured by BM and splitting (SI) (R=0.45, P0.01). These findings may have implications for prevention and treatment of burnout syndrome. CONCLUSIONS The current study findings provide implications that the defensive mechanism of splitting may allow for the prediction of burnout symptoms which in turn may allow for the prediction of burnout syndrome. This dynamics may potentially be of use in both the potential detection and prevention of burnout syndrome.

BACKGROUND Burnout is a state of vital exhaustion that is manifested on physical, cognitive, and emotional levels. Teachers work in a field where they are exposed daily to high job-related stressors, which can result in job change, a higher rate of unhappiness, and even earlier retirement. This study explored the relationship between job stressors, lifestyle, and burnout. MATERIAL AND METHODS Descriptive statistics were used to explore the burnout levels, together with t tests to compare between men and women, and regression analysis was performed to explore the relationship between the rates of burnout and lifestyle. RESULTS The overall sample size was 2394 teachers from primary schools. While males had higher emotional burnout, females reported higher physical burnout rates. We found that higher income was associated with less burnout, and a healthier lifestyle is associated with lower burnout rates. Teachers who take time for family and personal interests have significantly lower rates of burnout than those that do not. CONCLUSIONS Based on our results, we propose that teachers should be informed about the risk of burnout. We found that some teachers reported they do not know what burnout syndrome is. The primary aim should be to increase awareness. In fact, burnout is a major threat to those who are perfectionists and who tend to work overtime.

Attention deficit hyperactivity disorder (ADHD) is a lifelong neurodevelopmental disorder that can affect many areas of the daily life of individuals and is associated with poor health outcomes and with debilitating deficits in executive function. Recently, increasing numbers of research studies have begun to investigate the associations between neural and behavioral manifestations of ADHD. This review summarizes recent research on the perception of time in ADHD and proposes that this symptom is a possible diagnostic characteristic. Controlled studies on time perception have compared individuals with ADHD with typically developing controls (TDCs) and have used methods that include the Zimbardo Time Perspective Inventory (ZTPI). Practical approaches to time perception and its evaluation have shown that individuals with ADHD have difficulties in time estimation and discrimination activities as well as having the feeling that time is passing by without them being able to complete tasks accurately and well. Although ADHD has been associated with neurologic abnormalities in the mesolimbic and dopaminergic systems, recent studies have found that when individuals with ADHD are treated medically, their perception of time tends to normalize. The relationship between ADHD and the perception of time requires greater attention. Further studies on time perception in ADHD with other abnormalities, including executive function, might be approaches that refine the classification and diagnosis of ADHD and should include studies on its varied presentation in different age groups.

The relationship between tDCS (transcranial direct current stimulation) and its influence on glycemia has been the aim of limited research efforts. Usually, the focus has been set on lowering the blood sugar level or interference with insulin resistance, but also the treatment of diabetic polyneuropathy and pain management. In this case report, we outline the development of hyperglycemia and the following onset of type I diabetes during a series of tDCS in a 24-year old Caucasian female patient treated with our research protocol (10 sessions; 2 mA; 30 min; the anode over F3; the cathode over Fp2) for anorexia nervosa.