Schizotypality and neurological soft signs in patients with obsessive–compulsive disorder

OBJECTIVES: The broad description of schizotypy includes cognitive, sensitive, and information processing deficits connected with thought disorder symptoms. Recently, the term of schizotypy has started to be researched, not only in schizophrenia patients and their relatives but also in other psychiatric populations. Neurological soft signs (NSS) are known as abnormal motor or sensorial findings in the absence of a localized neurological disorder. There are some studies referring to the association between obsessive–compulsive disorder (OCD) and NSS, and vice versa. In this study, we aimed to examine the differences between OCD patients and healthy control groups in terms of schizotypality and NSS. We also aimed to predict risk factors affecting OCD patients with schizotypal features. METHODS: Overall, 92 OCD patients and 91 healthy controls were included in this study. Chapman’s Scales (Physical and Social Anhedonia Scales, Perceptual Aberration Scale, and Magical Ideation Scale) and Schizotypal Personality Questionnaire (SPQ) were administered to patient group. Symptom severity of OCD was recorded using the Yale-Brown Obsessive Compulsive Scale. The neurological portion of the Physical and Neurological Examination for Soft Signs (PANESS) and a Brief Psychiatric Rating Scale were administered to patient and control groups. RESULTS: The patient group had higher scores on total PANESS scale (p < .001) and synergie (p = .012), graphestesia (p < .001), posture (p < .001), topognosia (p < .001), and repetitive movement (p < .001) subscales. There were no statistically significant differences in terms of stereognosis (p = .056) or continuity of movement (p = .79) subscales. We found that the sexual, religious, and order–symmetry obsessions and pathological doubt effects of schizotypality were independent risk factors for schizotypality in OCD. CONCLUSIONS: Both the schizotypal features and NSS worsen the course of OCD and may point out the neurodevelopmental basis of the disease. We can say that OCD patients with high schizotypality should take a separate place on the schizo-obsessive spectrum

Serum 15-d-PGJ2 and PPARγ levels are reduced in manic episode of bipolar disorder while IL-4 levels are not affected

OBJECTIVES: Bipolar disorder (BD) carries a high rate of morbidity and mortality, and the clarification of its aetiology continues to be an important field of research. In recent studies, the clinical characteristics of BDs have been explained through a number of underlying factors, including cytokines, steroids, neurotrophins, mitochondrial energy generation, oxidative stress, and neurogenesis. In this study, we aimed to investigate potential associations between BDs and inflammatory processes. METHODS: Patients with mania or in remission who attended outpatient clinics of the Department of Psychiatry of the Ankara Numune Training and Research Hospital, and who were diagnosed with BD according to the DSM-V criteria, were included in the study. IBM SPSS Statistics 23 software was used for statistical analyses of the data. The normality of the distribution of continuous and discrete numerical variables was tested with a Shapiro–Wilk Test. RESULTS: In this study, the measurements and statistical analyses revealed significantly lower 15-deoxy delta12, 14-prostaglandin J2 (15d-PGJ2) and Peroxisome Proliferator-Activated Receptor-Gamma (PPARγ) levels in patients with mania in comparison to healthy controls and patients in remission. Group comparisons did not reveal any significant differences between IL-4 levels. CONCLUSIONS: This study was not a longitudinal study evaluating the same patients during both relapse and remission periods; no group of patients in a depressive episode of BD were included in the group comparisons either. Although this evidence is not adequate for a definite conclusion, the available evidence suggests that anti-inflammatory markers such as 15d-PGJ2 and IL-4 and nuclear PPARγ receptors are potential biomarkers to clarify the aetiology of BD, and these markers may be included among the therapeutic targets for future pharmacological modulations. Further studies are required in this area