Faculty Bibliography

On 11 March 2011, a devastating earthquake struck off the coast of Japan, causing blustering tsunami that swept over the northeast coast of the country. Many struggled to evacuate from their homes, schools, and workplaces as 8- to 9-m-tall tsunami rapidly reached the coast within half an hour after the earthquake (Emergency Disaster Response Headquarters). The officials reported a record-breaking magnitude of 9.0 Mw, which made this earthquake the most devastating earthquake in the Japan's history. It had not been long since the previous massive earthquake had hit Kobe in 1995, killing 6,434 people (Japan Meteorological Agency). The author presents the outline of the initial mental-health-care responses at various levels. It has focused on the comprehensive strategies and policies that were intended to cover all the affected areas but has not described the individual countermeasures and reactions in each prefecture and city. The psychological effects of the atomic plant accident in Fukushima has not been mentioned in detail, because the scope of the physiological effect of the accident has not been settled yet and the society is not necessarily ready to deal with the accident as a psychological matter rather than a sociopolitical one. A number of psychiatric professionals are deeply concerned with the psychological and prolonged impact of the accident, including those who are in the Fukushima prefecture and conducting heroic efforts to care for the residents.

BACKGROUND: Incidence proportion of post-traumatic stress disorder (PTSD) after motor vehicle accidents (MVA) vary considerably across countries, and whether heart rate (HR) and respiratory rate (RR) immediately after MVA predict subsequent PTSD remains controversial. This study examined the incidence proportion of PTSD at 6 months after MVA in Japan, and the predictors of PTSD in MVA survivors. METHOD: Patients with MVA-related injuries consecutively admitted to the intensive care unit of a teaching hospital in Tokyo were recruited. Six months after MVA, PTSD was diagnosed using the Clinician Administered Post-traumatic Stress Disorder Scale (CAPS). RESULTS: Of the 300 participants, 106 completed the assessments at 6 months after MVA and PTSD was diagnosed in 7.5% of the patients. Eight of the 300 participants (2.7%) were regarded as having PTSD after imputing their CAPS score at follow-up assessment for participants who dropped out. In multivariate regression analysis, no variables were shown to be independent predictors for PTSD. HR and RR did not predict PTSD in the analysis. DISCUSSION: The results suggested that the incidence proportion of PTSD following MVA in Japan was lower than that in most developed countries, and HR and RR might not be accurate screening tools despite their importance in a fear-conditioning model of the genesis of PTSD.

We recently developed new disaster mental health guidelines in Japan through the Delphi process, a method for building consensus among experts, using as a reference the guidelines developed by The European Network for Traumatic Stress (TENTS) in Europe. We included in our survey 30 items used in the TENTS survey, 20 of which achieved positive consensus in that survey. Here we report on the extent of agreement of 95 Japanese experts on each of these 30 items and examine the reasons for disagreements with the TENTS survey results based on the comments obtained from the participants of our survey. Of the 20 items, 12 also gained consensus in our survey and 1 additional item achieved consensus that did not achieve it in the TENTS survey. Items that did not gain consensus in our survey, but did in the TENTS survey, were recommendations for close collaboration with the media, screening volunteers for their suitability, and withholding formal screening of the affected population. The need for specialist care for specific populations was endorsed in our survey, but not in the TENTS survey. Overall, the opinion of Japanese experts was congruent with that of Western experts, but some guideline amendments would be beneficial.

The effectiveness of D-cycloserine (DCS), an N-methyl-D-aspartate glutamate receptor partial agonist, and valproic acid (VPA), a histone deacetylase inhibitor, in facilitating the extinction of fear-conditioned memory has been explored in humans and animals. Here, we confirmed whether DCS (100 mg) and VPA (400 mg) act in off-line learning processes during sleep or waking, for further clinical application to anxiety disorders and posttraumatic stress disorder (PTSD). We performed a randomized, blind, placebo-controlled clinical trial in 90 healthy adults. Visual cues and electric shocks were used as the conditioned stimulus (CS) and unconditioned stimulus (US), respectively. The extinction effect was observed not in simple recall after the extinction of coupled CS-US, but was observed in the post-re-exposure phase after unexpected re-exposure to reinstatement CS-US coupling. Newly acquired conditioned fear was also eliminated or habituated by DCS and VPA administration, in line with previous findings. Furthermore, VPA facilitated the off-line learning process of conditioned fear extinction and habituation during sleep, while DCS facilitated this process during waking. These novel findings suggest that DCS and VPA might enhance exposure-based cognitive therapy for anxiety disorders and PTSD by reducing the vulnerability to reinstatement and preventing relapses of fear-conditioned responses, and provide evidence for a peculiarity of the sleep-dependent off-line learning process for conditioned fear extinction. This article is part of a Special Issue entitled 'Cognitive Enhancers'.

Sleep deprivation immediately following an aversive event reduces fear by preventing memory consolidation during homeostatic sleep. This suggests that acute insomnia might act prophylactically against the development of posttraumatic stress disorder (PTSD) even though it is also a possible risk factor for PTSD. We examined total sleep deprivation and memory suppression to evaluate the effects of these interventions on subsequent aversive memory formation and fear conditioning. Active suppression of aversive memory impaired retention of event memory. However, although the remembered fear was more reduced in sleep-deprived than sleep-control subjects, suppressed fear increased, and seemed to abandon the sleep-dependent plasticity of fear. Active memory suppression, which provides a psychological model for Freud's ego defense mechanism, enhances fear and casts doubt on the potential of acute insomnia as a prophylactic measure against PTSD. Our findings bring into question the role of sleep in aversive-memory consolidation in clinical PTSD pathophysiology.

BACKGROUND: This prospective cohort study investigated the serum levels of brain-derived neurotrophic factor (BDNF), which mediates synaptic plasticity crucial for fear memory extinction, in patients severely injured in motor vehicle accidents (MVAs). METHOD: A nested, case-controlled study was conducted with 103 MVA survivors: 8 medication-naive patients who met the criteria for full diagnosis of posttraumatic stress disorder (PTSD) at 6 months after MVA, 10 medication-naive patients with partial PTSD and 85 patients with no PTSD. PTSD was evaluated by the Clinician-Administered PTSD Scale (CAPS). Serum BDNF levels were measured shortly after the MVA (baseline) and at 6-month follow-up. RESULTS: Posttrauma serum BDNF levels differed between the 3 groups after controlling for age and sex (F = 3.41, p = 0.04), with unexpectedly higher serum BDNF levels seen in the full-PTSD group compared with the no-PTSD group. Additional analysis of patients with serum samples taken at baseline and at 6 months revealed the full-PTSD group had significantly higher serum BDNF levels over the 6 months than the no-PTSD group after controlling for age and sex (F = 6.44, p < 0.01). A positive correlation was seen between changes in serum BDNF levels over 6 months and the CAPS score at 6 months (r = 0.26, p = 0.014). CONCLUSIONS: The findings of this study, the first to report longitudinal serum BDNF levels in MVA survivors, suggest that elevated serum BDNF levels could be a biomarker of PTSD after a traumatic event.

At the 13th meeting of the European Society for Traumatic Stress Studies in 2013, a symposium was held that brought together international researchers and clinicians who were involved in psychosocial responses to disaster. A total of six disasters that occurred in five countries were presented and discussed. Lessons learned from these disasters included the need to: (1) tailor the psychosocial response to the specific disaster, (2) provide multi-dimensional psychosocial care, (3) target at-risk population groups, (4) proactively address barriers in access to care, (5) recognise the social dimensions and sources of resilience, (6) extend the roles for mental health professionals, (7) efficiently coordinate and integrate disaster response services, and (8) integrate research and evaluation into disaster response planning.

INTRODUCTION: Critically injured patients are at risk of developing posttraumatic stress disorder (PTSD). Propofol was recently reported to enhance fear memory consolidation retrospectively. Thus, we investigated here whether administration of propofol within 72 h of a motor vehicle accident (MVA) affects the subsequent development of PTSD symptoms. METHODS: We examined data obtained from a prospective cohort study of MVA-related injured patients, admitted to the intensive care unit of a general hospital. We investigated the effect of propofol administration within 72 h of MVA on outcome. Primary outcome was diagnosis of full or partial PTSD as determined by the Clinician-Administered PTSD Scale (CAPS) at 6 months. Secondary outcomes were diagnosis of full or partial PTSD at 1 month and CAPS score indicating PTSD at 1 and 6 months. Multivariate analysis was conducted adjusting for being female, age, injury severity score (ISS), and administration of ketamine or midazolam within 72 h of MVA. RESULTS: Among 300 patients recruited (mean ISS, 8.0; median Glasgow Coma Scale (GCS) score, 15.0; age, 18 to 69 years), propofol administration showed a higher risk for full or partial PTSD as determined by CAPS at 6 months (odds ratio = 6.13, 95% confidence interval (CI): 1.57 to 23.85, P = 0.009) and at 1 month (odds ratio = 1.31, 95% CI: 0.41 to 4.23, P = 0.647) in the multivariate logistic regression. Multivariate regression analysis showed a trend toward adverse effects of propofol on PTSD symptom development at 6 months after MVA (beta = 4.08, 95% CI: -0.49 to 8.64, P = 0.080), but not at 1 month after MVA (beta = -0.42, 95% CI: -6.34 to 5.51, P = 0.890). CONCLUSIONS: These findings suggest that using propofol in the acute phase after MVA might be associated with the development of PTSD symptoms 6 months later. However, since the design of this study was retrospective, these findings should be interpreted cautiously and further study is warranted.