#Źródło: Parnas J et al. EASE: examination of anomalous self-experience. Psychopathology, 2005, 38.5: 236-258.S. Użycie skali EASE w badaniach naukowych wymaga pisemnej zgody autora skali (Josef Parnas, e-mail: jpa@cfs.ku.dk) StreszczenieSkala EASE jest listą objawów do częściowo ustrukturalizowanego fenomenologicznego badania subiektywnych lub empirycznych nieprawidłowości (anomalii), które można uznać za zaburzenia podstawowej, "minimalnej" samoświadomości. EASE opracowana została na podstawie samoopisów otrzymanych od pacjentów chorujących na zaburzenia ze spektrum schizofrenii. Skala ma duże znaczenie dla opisu, diagnozy oraz diagnozy różnicowej zaburzeń ze spektrum schizofrenii. Prezentowana wersja zawiera istotne szczegó-łowe kwestie dotyczące zbierania wywiadu oraz opisy objawów psychopatologicznych (Podręcznik), arkusz wyników (Aneks A), listę pozostałych pozycji Skali stosowanych w czasie wywiadu (Aneks B) oraz porównawczą listę pozycji EASE/BSABS (Bonner Skala für die Beurteilung von Basissymptomen, Bońska Skala do Oceny Objawów Podstawowych) (Aneks C).Słowa kluczowe: schizofrenia, fenomenologia, zaburzenia Ja, Badanie Nieprawidłowego Doświadczania Siebie, EASE WstępTerminy i pojęcia wyjaśnione są w każdej pozycji Skali. Cele i opis populacji będącej przedmiotem badaniaSkala EASE skupia się na anomaliach subiektywnego doświadczenia, które wydają się odzwierciedlać zaburzenia samoświadomości.Skala ta zawiera opis fenomenologiczny, głównie o charakterze jakościowym i dąży do szczegółowego opisu zjawisk, które łączy zdeformowane w jakiś sposób poczucie perspektywy pierwszoosobowej, tj.: zaburzenie lub upośledzenie dotyczące poczucia bycia podmiotem, ośrodkiem, w którym automatycznie zbiegają się działa-nie, myśl i doświadczenie. Istnieje także możliwość oceny częstości i nasilenia tych doświadczeń.Skala ta opracowana została głównie dla zaburzeń ze spektrum schizofrenii, nie może jednak być stosowana jako jedyne narzędzie diagnostyczne (zaburzenia struktury Ja nie są wymieniane przez DSM-V czy ICD-10 jako kluczowe diagnostyczne lub nawet jako ważne cechy schizofrenii; derealizacja i depersonalizacja wspomniane są jako nieistotne cechy schizotypii). EASE nie obejmuje wszystkich możliwych nieprawidłowości doświadczenia siebie, skupia się jedynie na zaburzeniach stanów Ja (w przeciwieństwie do BSABS [1], nie są badane np. zaburzenia postrzegania).

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There is an increasing amount of evidence which links the pathogenesis of irritable bowel syndrome (IBS) with food IgG hyperreactivity. Some authors have suggested that food IgG hyperreactivity could be also involved in the pathophysiology of major depressive disorder (MDD). The aim of this study was to compare levels of serum IgG against 39 selected food antigens between three groups of participants: patients with MDD (MDD group), patients with IBS (IBS group) and healthy controls (HC group). The study included 65 participants (22 in the MDD group, 22 in the IBS group and 21 in the HC group). Serum IgG levels were examined using enzyme-linked immunosorbent assay (ELISA). Medical records, clinical data and laboratory results were collected for the analysis. IgG food hyperreactivity (interpreted as an average of levels of IgG antibodies above 7.5 µg/mL) was detected in 28 (43%) participants, including 14 (64%) from the MDD group, ten (46%) from the IBS group and four (19%) from the HC group. We found differences between extreme IgG levels in MDD versus HC groups and in IBS versus HC groups. Patients with MDD had significantly higher serum levels of total IgG antibodies and IgG against celery, garlic and gluten compared with healthy controls. The MDD group also had higher serum IgG levels against gluten compared with the IBS group. Our results suggest dissimilarity in immune responses against food proteins between the examined groups, with the highest immunoreactivity in the MDD group. Further studies are needed to repeat and confirm these results in bigger cohorts and also examine clinical utility of IgG-based elimination diet in patients with MDD and IBS.

Depressive episodes are associated not only with changes in neurotransmission in the central nervous system, but also may lead to structural changes in the brain through neuroendocrine, inflammatory, and immunological mechanisms. The aim of this article is to present a new hypothesis connecting the inflammatory theory of depression with IgG food hypersensitivity and leaky gut syndrome. This new potential pathway that may mediate the pathogenesis of depression implies the existence of subsequent developmental stages. Overproduction of zonulin triggered, for example, by gliadin through activation of the epidermal growth factor receptor and protease-activated receptor causes loosening of the tight junction barrier and an increase in permeability of the gut wall ('leaky gut'). This results in a process allowing larger molecules that would normally stay in the gut to cross into the bloodstream and in the induction of IgG-dependent food sensitivity. This condition causes an increased immune response and consequently induces the release of proinflammatory cytokines, which in turn may lead to the development of depressive symptoms. It seems advisable to assess the intestinal permeability using as a marker, for example, zonulin and specific IgG concentrations against selected nutritional components in patients with depression. In the case of increased IgG concentrations, the implementation of an elimination-rotation diet may prove to be an effective method of reducing inflammation. This new paradigm in the pathogenesis of depressive disorders linking leaky gut, IgG-dependent food sensitivity, inflammation, and depression is promising, but still needs further studies to confirm this theory.

Although schizophrenia and anorexia nervosa are seemingly very distinct psychiatric disorders, their symptoms are connected by various types of relationships. The present article reviews the literature and recapitulates the views of various authors on the links between these two disorders. Symptoms of anorexia may 1) precede the onset of psychosis; 2) evolve in its active phase or more rarely manifest in remission; and, conversely, 3) psychotic symptoms may occur transiently in the course of anorexia nervosa. When anorexia precedes the manifestation of psychosis, symptoms of anorexia can be treated as a component of the prodromal phase of schizophrenia. Another possibility of co-existence of a psychosis (e.g., schizophrenia) with anorexia is when the eating disorder syndrome manifests at the same time as the full-blown psychotic syndrome. In such cases, when the symptoms of the two disorders occur simultaneously, it is often difficult to say whether the patient is suffering from schizophrenia, in the course of which anorexia has arisen secondary to psychotic symptoms or whether he/she is suffering from anorexia during which he/she has developed psychotic symptoms, usually thematically associated with eating. Studies published so far, mainly case reports, point to the complex nature of the interrelationships between schizophrenia and anorexia nervosa. Further research is needed to conclusively explain the relationships between psychotic disorders and anorexia nervosa, which would allow physicians to use more effective methods of treatment in this group of patients.