OBJECTIVE: Little is known about the effects of psychodrama group therapy on the level of stress, anxiety and depression of the group members, and the biological markers of stress. The aim of this study test cortisol level as a biological reflection of some mental characteristics gained by the psychodrama method in coping with stress. METHODS: Depressive patients aged between 18 and 65 years, who diagnosed with depression according to DSM-5, without psychiatric comorbidity, who do not use drugs and were available for psychodrama were enrolled into the study. These patients were evaluated using the Perceived Stress Scale, State-Trait Anxiety Inventory and Beck Depression Inventory. In order to observe the circadian rhythm of cortisol, samples were collected from the participants before lunch, before dinner and before going to sleep on the day before psychodrama and on the 0, 15th, and 30th minutes after awakening in the morning of the psychodrama day; as well as just before and after the psychodrama session. Saliva cortisol level just before the initial session of psychodrama group therapy was compared with the saliva cortisol level just after the last psychodrama session at the end of 16 weeks. RESULTS: Statistically significant difference was determined between the scores of perceived stress scale, STAI-1, STAI-2, beck depression inventory and salivary cortisol level before and after psychodrama session. There was significant decrease in both the scale scores and salivary cortisol after vs. before psychodrama. CONCLUSION: This results is important as it shows the biological aspect of clinical improvement. Further studies would provide us with better understanding of the effects of psychodrama group psychotherapy on depressive mood and biological projections by means of short-term and long-term follow-up studies.
Anxiety ; Biomarkers ; Circadian Rhythm ; Comorbidity ; Depression* ; Follow-Up Studies ; Humans ; Hydrocortisone* ; Lunch ; Meals ; Methods ; Psychodrama* ; Psychotherapy, Group ; Saliva*

OBJECTIVE: Multiple sclerosis (MS) is an inflammatory disease characterized by demyelinating plaques in the white matter. Chronic cerebrospinal venous insufficiency (CCSVI) has been proposed as a new hypothesis for the etiopathogenesis of MS disease. MS-CCSVI includes a significant decrease of cerebrospinal fluid (CSF) flow through the cerebral aqueduct secondary to an impaired venous outflow from the central nervous system. This study aimed to determine whether CSF flow dynamics are affected in MS patients and the contributions to differential diagnosis in active and chronic disease using phase-contrast magnetic resonance imaging (PC-MRI). MATERIALS AND METHODS: We studied 16 MS patients with chronic plaques (group 1), 16 MS patients with active plaques-enhanced on MRI (group 2), and 16 healthy controls (group 3). Quantitatively evaluation of the CSF flow was performed from the level of the cerebral aqueduct by PC-MRI. According to heart rates, 14–30 images were obtained in a cardiac cycle. Cardiac triggering was performed prospectively using finger plethysmography. RESULTS: No statistically significant difference was found between the groups regarding average velocity, net forward volume and the average flow (p > 0.05). Compared with the controls, group 1 and group 2, showed a higher peak velocity (5.5 ± 1.4, 4.9 ± 1.0, and 4.3 ± 1.3 cm/sec, respectively; p = 0.040), aqueductal area (5.0 ± 1.3, 4.1 ± 1.5, and 3.1 ± 1.2 mm2, respectively; p = 0.002), forward volume (0.039 ± 0.016, 0.031 ± 0.013, and 0.021 ± 0.010 mL, respectively; p = 0.002) and reverse volume (0.027 ± 0.016, 0.018 ± 0.009, and 0.012 ± 0.006 mL, respectively; p = 0.000). There were no statistical significance between the MS patients with chronic plaques and active plaques except for reverse volume. The MS patients with chronic plaques showed a significantly higher reverse volume (p = 0.000). CONCLUSION: This study indicated that CSF flow is affected in MS patients, contrary to the hypothesis that CCSVI-induced CSF flow decreases in MS patients. These findings may be explained by atrophy-dependent ventricular dilatation, which may occur at every stage of MS.
Central Nervous System ; Cerebral Aqueduct ; Cerebrospinal Fluid ; Chronic Disease ; Diagnosis, Differential ; Dilatation ; Fingers ; Heart Rate ; Humans ; Magnetic Resonance Imaging ; Multiple Sclerosis ; Plethysmography ; Prospective Studies ; Venous Insufficiency ; White Matter