Day 1 :
Keynote Forum
Clare Henn-Haase
National University of New York Medical Center, USA / National University of Singapore, Singapore
Keynote: PTSD assessment discrepancies between the PCL screener and the gold standard caps IV/V using DSM-5 and ICD-11 diagnostic criteria in a sample of treatment seeking women in the public sector
Time : 10:20-11:00
Biography:
Clare Henn-Haase has obtained her PsyD in Clinical Psychology from the Illinois School of Professional Psychology, USA. She has worked in the field of trauma for over 15 years. Prior joining NUS, she was involved in clinical research and academia as well as clinical practice where she worked as an Assistant Professor at the University of California, USA and the San Francisco Veterans Affairs for over 10 years and then as Assistant Professor and Clinical Director of the PTSD Research Program at New York University Medical Center, USA for four years. She is a licensed Clinical Psychologist in USA and is certified in several types of trauma treatment including dialectical behavior therapy, cognitive behavior therapy, cognitive processing therapy and prolonged exposure for the treatment of PTSD. She is an active Member of the International Society of Traumatic Stress Studies (ISTSS) and the American Psychological Association. Her research interests include randomized controlled treatment trials for PTSD using evidence based CBT treatment, epidemiological and neuropsychological studies of Post-traumatic Stress Disorder, evidence based treatment trials using cognitive behavioral therapy for the treatment of PTSD and ASD, particularly with women survivors of interpersonal violence, veterans and police officers. She has over 26 peer reviewed publications.
Abstract:
This presentation reports on prevalence rates of DSM-5 and ICD-11 PTSD in a treatment seeking sample of women (n=162) enrolled in an NIMH-funded RCT. Analyses also compared discrepancies between CAPS and PCL ratings. PTSD prevalence and symptom endorsement were measured using clinician ratings (CAPS IV/V) and patient self-report (PCL-IV/V). Although the CAPS is the gold standard for measuring PTSD, the well validated PCL is often used as a comparable measure to screen for or diagnose PTSD. While the CAPS and PCL are highly correlated, there are often discrepancies in reported PTSD symptoms between these measures. In this study, of the patients with DSM-IV PTSD using the CAPS, 96.3% met criteria for DSM-5 and 87.7% met ICD-11 PTSD. Comparing rates of PTSD based on the PCL versus the CAPS, the rate of DSM-5 PTSD was lower on the PCL than the CAPS (78.4% vs. 96.3%) as was that for ICD-11 PTSD (71.0% vs. 87.7%). As expected, the rate of CAPS-based PTSD was lower in ICD-11 than DSM-5. However, there were notable discrepancies between the self-reported and clinician administered measures. Item endorsements indicated that patients self-reported more re-experiencing and fewer symptoms of avoidance of thoughts/feelings, negative emotions, detachment and restricted affect. Implications for measurement development will be discussed.
Keynote Forum
Hesham A El-Beshbishy
Taibah University, Saudi Arabia
Keynote: Targeting synaptic mitochondria and mitochondrial biogenesis for treatment of psychiatric disorders in rat brains
Time : 11:10-11:40
Biography:
Hesham A El-Beshbishy has obtained his PhD in 2001 in the field of Medical Biochemistry and Molecular Biology from Manchester University, UK. He works in the Center for Genetics and Inherited Diseases, Taibah University, Madinah, Saudi Arabia. He is also a Professor in Faculty of Pharmacy at Al-Azhar University, Cairo, Egypt. Previously, he was the Supervisor of the Medical Laboratories Technology Department, Faculty of Applied Medical Sciences at Taibah University in Saudi Arabia. He has published more than 48 papers in reputed journals and has been serving as an Editorial Board Member of several international journals.
Abstract:
Mitochondria play role in depression pathogenesis through mitochondrial dynamin-related protein (Drp-1), fission 1 protein (Fis-1) and brain derived neurotrophic factor (BDNF) through tyrosine kinase B (Trk-B) receptor activation. The precise role of neurotrophins-mitochondrial interaction in depression is unclear. We aimed to study role of mitochondria in pathogenesis and treatment of depression using three different antidepressants. We established animal model of stress-induced depressive behavior named learned helplessness (LH) model. Rats with LH model were treated with fluoxetine FLX (20 mg/kg), imipramine IMP (20 mg/kg) or citalopram CTL (20 mg/kg), i.p. for 2 weeks. The order of decreasing number of LH rats was as follows: CTL>IMP>FLX. Mitochondrial enzymes of brain SDH, MDH, IDH, MAO and SOD enzymes, total antioxidant status, ATP production, BDNF, Drp-1, Trk-B and Fis-1 of depressed (DEP) rats elicited significant declines. Brain lipid peroxides was highly elevated in DEP rats. All these levels were back to normalcy after intake of antidepressants and the protein expression levels of BDNF, Drp-1, Trk-B (full length not truncated) and Fis-1 were enhanced either in prefrontal cortex (PFC) or hippocampus. Electron microscopy of DEP rats exhibited cristae disarrangement, mitochondria with dense matrix surrounded with degenerated cells, mitochondria with increased thickness and remarkably electron dense cristae in degenerated cells. Intake of FLX, CTL or IMP improved mitochondrial damage in brain as well as PFC and hippocampus. We concluded that, use of FLX, IMP and CTL improved depression induced in rats via antioxidant mechanism and through modulation of neurotrophins family in brain PFC and hippocampus.