Catatonia: Immunological Aspect (on the Model of Motor Symptom Complexes in the Clinic of Schizophrenia and Schizophrenic Spectrum Disorders)

Abstract

Introduction: the clinical heterogeneity of catatonic disorders, as well as the involvement of various mechanisms (GABAergic and glutamate systems, and neuroendocrine dysfunctions of the hypothalamic-pituitary-adrenal axis (HPA) disorders in the immune system) in the pathogenesis of these conditions served as a basis for the consideration of catatonia from a position of the modern clinical and biological model of schizophrenia, which considers the formation of psychopathological symptoms in this disease in the conjunction with inflammation. The aim: to establish relationships between immunological processes of sterile inflammation and psychopathological characteristics of catatonic disorders formed on their basis. Patients: 41 patients with schizophrenia (F20) and schizophrenic spectrum disorders (F21, F25) were examined, among them 26 patients with motor disorders belonging to the category of “non-psychotic” catatonia (12 patients with stereotypic catatonia and 14 patients with parakinetic catatonia), and 15 patients with schizophrenic spectrum disorders without symptoms of catatonia. A control group consisted of 17 healthy people. Methods: the activity of leukocyte elastase (LE) and α1-proteinase inhibitor (α1-PI), S-100B and myelin basic protein (MBP) antibody levels in plasma, and leukocyte inhibitor index (LII) were determined. Results: in all groups, a significant increase in the activity of LE and α1-PI was revealed in comparison with the control (p< 0.05). LE activity and LII value were significantly higher in patients with stereotypic catatonia and schizophrenic spectrum disorders compared to patients with parakinetic catatonia (p< 0.05; p< 0.01). Cluster analysis revealed two immunological clusters in the general group of patients: the 1st cluster was characterized by pro-inflammatory status with high proteolytic activity, which corresponded to physiological inflammation. This status was typical for most patients with stereotypic catatonia, as well as for patients with schizophrenic spectrum disorders (75% and 98.3%). The 2nd cluster was characterized by a pro-inflammatory status with low proteolytic system activity, which was a sign of inflammation imbalance presumably associated with functional depletion of neutrophils. This status was predominantly in patients with parakinetic catatonia (66.7%). Conclusion: the study confirmed the role of inflammation in the forming of non-psychotic catatonic disorders in schizophrenia and schizophrenic spectrum disorders 18 and revealed their immunological heterogeneity, as well as the relationship between the clinical features of catatonia and the features of the proteolytic system of inflammation.