Staff attitudes and perceptions towards the use of coercive measures in psychiatric patients.

The failure of efforts to significantly reduce the use of physical coercive measures (PCMs) in psychiatric hospitals remains a global concern. There is a gap in the understanding of staff's characteristics that may affect their attitudes and perceptions towards PCMs. This study used a cross-sectional design to examine the attitudes and perceptions of staff working at a mental health centre in Israel regarding the use of PCMs and to explore whether staff attitudes differed depending on their professional and demographic background. This study also sought to explore staff willingness to accept a policy of reducing the use of PCMs. The data were collected from 149 staff members (nurses, physicians, and auxiliary staff) working at mental health centre, using a questionnaire developed for this study. The findings indicate a low degree of support for use of PCMs among participants who were older, female, more qualified psychiatric nurses, with longer duration of employment, and those who have not participated in coercive intervention in the past year. The majority of the sample reported a low willingness to reduce the use of PCMs, and a lack of institutional support after participating in a coercive event. High hospital occupancy and insufficient staffing were perceived as contributing factors to coercive incidents. Therefore, availability of trained and experienced staff, elimination of organizational barriers, along with creating and maintaining a safe clinical environment should be a priority. Alternative non-coercive interventions should further be taught and used for managing aggressive and violent behaviour in the psychiatric clinical settings.

Mild Cognitive Impairment and Neurofeedback: A Randomized Controlled Trial.

Background and Objectives: Mild cognitive impairment (MCI) is often a precursor of dementia, and in particular of Alzheimer's Disease (AD) which is the most common cause of dementia. Individuals with amnestic MCI are several-fold more likely to develop AD than the general population. Therefore, MCI comprises a well-detectable, early stage time-point for therapeutic intervention and strategic prevention. Based on common electroencephalographical (EEG) pattern changes seen in individuals with MCI, we postulated that EEG-based neurofeedback could help improve the memory performance of patients with MCI. Memory performance is of particular importance in these patients, since memory decline is the most prominent symptom in most patients with MCI, and is the most predictive symptom for cognitive deterioration and the development of AD. Methods: In order to improve the memory performance of patients with MCI we used a system of EEG-based neurofeedback in an attempt to reverse alterations of the EEG that are known to be common in patients with MCI. Our protocol comprised the provision of positive feedback in order to enhance the activity level of the upper alpha band. Participants were divided to two groups receiving either neurofeedback training to enhance the upper alpha frequency (Experimental group) or random feedbacks (Sham group) Results: We witnessed a significant improvement in memory performance in subjects in the experimental group compared to those in the sham group. This improvement was maintained for at least 1 month. Conclusions: Neurofeedback may be a promising and affordable novel approach for treating the decline in memory witnessed in patients with MCI.

Significance of the orexinergic system in modulating stress-related responses in an animal model of post-traumatic stress disorder.

Converging evidence indicates that orexins (ORXs), the regulatory neuropeptides, are implicated in anxiety- and depression-related behaviors via the modulation of neuroendocrine, serotonergic, and noradrenergic systems. This study evaluated the role of the orexinergic system in stress-associated physiological responses in a controlled prospective animal model. The pattern and time course of activation of hypothalamic ORX neurons in response to predator-scent stress (PSS) were examined using c-Fos as a marker for neuronal activity. The relationship between the behavioral response pattern 7 days post-exposure and expressions of ORXs was evaluated. We also investigated the effects of intracerebroventricular microinfusion of ORX-A or almorexant (ORX-A/B receptor antagonist) on behavioral responses 7 days following PSS exposure. Hypothalamic levels of ORX-A, neuropeptide Y (NPY), and brain-derived neurotrophic factor (BDNF) were assessed. Compared with rats whose behaviors were extremely disrupted (post-traumatic stress disorder [PTSD]-phenotype), those whose behaviors were minimally selectively disrupted displayed significantly upregulated ORX-A and ORX-B levels in the hypothalamic nuclei. Intracerebroventricular microinfusion of ORX-A before PSS reduced the prevalence of the PTSD phenotype compared with that of artificial cerebrospinal fluid or almorexant, and rats treated with almorexant displayed a higher prevalence of the PTSD phenotype than did untreated rats. Activated ORX neurons led to upregulated expressions of BDNF and NPY, which might provide an additional regulatory mechanism for the modulation of adaptive stress responses. The study indicates that the activated ORX system might promote adaptive responses to PSS probably via stimulation of BDNF and NPY secretion, and early intervention with ORX-A reduces the prevalence of the PTSD phenotype and increases the prevalence of adaptive phenotypes. The findings provide some insights into the mechanisms underlying the involvement of the ORX system in stress-related disorders.

Neurofeedback Improves Memory and Peak Alpha Frequency in Individuals with Mild Cognitive Impairment.

Mild cognitive impairment (MCI) is a syndrome characterized by a decrease in cognitive abilities, while daily function is maintained. This condition, which is associated with an increased risk for the development of Alzheimer's disease, has no known definitive treatment at present. In this open-label pilot study we explored the possible benefits of neurofeedback for subjects with MCI. Eleven participants diagnosed with MCI were trained to increase the power of their individual upper alpha band of the electroencephalogram (EEG) signal over the central parietal region. This was achieved using an EEG-based neurofeedback training protocol. Training comprised ten 30-min sessions delivered over 5 weeks. Cognitive and electroencephalographic assessments were conducted before and after training and at 30 days following the last training session. A dose-dependent increase in peak alpha frequency was observed throughout the period of training. Memory performance also improved significantly following training, and this improvement was maintained at 30-day follow-up, while peak alpha frequency returned to baseline at this evaluation. Our findings suggest that neurofeedback may improve memory performance in subjects with mild cognitive impairment, and this benefit may be maintained beyond the training period.

Role of Endogenous and Exogenous Corticosterone on Behavioral and Cognitive Responses to Low-Pressure Blast Wave Exposure.

The complex interactions and overlapping symptoms of comorbid post-traumatic stress disorder (PTSD) and mild traumatic brain injury (mTBI) induced by an explosive blast wave have become a focus of attention in recent years, making clinical distinction and effective intervention difficult. Because dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is thought to underlie trauma-related (psycho)pathology, we evaluated both the endogenous corticosterone response and the efficacy of exogenous hydrocortisone treatment provided shortly after blast exposure. We employed a controlled experimental blast-wave paradigm in which unanesthetized animals were exposed to visual, auditory, olfactory, and tactile effects of an explosive blast wave produced by exploding a thin copper wire. Endogenous corticosterone concentrations were evaluated at different time points (before, and 3 h, 5 h and 17 days) after blast exposure. Subsequently, the efficacy of exogenous hydrocortisone (25 mg/kg-1 or 125 mg/kg-1) injected intraperitoneally 1 h after exposure was compared with that of a similarly timed saline injection. Validated cognitive and behavioral tests were used to assess both PTSD and mTBI phenotypes on days 7-14 following the blast. Retrospective analysis revealed that animals demonstrating the PTSD phenotype exhibited a significantly blunted endogenous corticosterone response to the blast compared with all other groups. Moreover, a single 125 mg/kg-1 dose of hydrocortisone administered 1 h after exposure significantly reduced the occurrence of the PTSD phenotype. Hydrocortisone treatment did not have a similar effect on the mTBI phenotype. Results of this study indicate that an inadequate corticosteroid response following blast exposure increases risk for PTSD phenotype, and corticosteroid treatment is a potential clinical intervention for attenuating PTSD. The differences in patterns of physiological and therapeutic response between PTSD and mTBI phenotypes lend credence to the retrospective behavioral and cognitive classification criteria we designed, and is in keeping with the assumption that mTBI and PTSD phenotypes may reflect distinct underlying biological and clinical profiles.

Biological and Behavioral Patterns of Post-Stroke Depression in Rats.

BACKGROUND: Post-stroke depression (PSD) is the most frequent psychiatric complication following ischemic stroke. It affects up to 60% of all patients and is associated with increased morbidity and mortality following ischemic stroke. The pathophysiology of PSD remains elusive and appears to be multifactorial, rather than "purely" biological or psychosocial in origin. Thus, valid animal models of PSD would contribute to the study of the etiology (and treatment) of this disorder. METHODS: The present study depicts a rat model for PSD, using middle cerebral artery occlusion (MCAO). The two-way shuttle avoidance task, Porsolt forced-swim test, and sucrose preference test were employed to assess any depression-like behavior. Localized brain expressions of brain-derived neurotrophic factor (BDNF) protein levels were evaluated to examine the possible involvement of the brain neuronal plasticity in the observed behavioral syndrome. The raw data were subjected to unsupervised fuzzy clustering (UFC) algorithms to assess the sensitivity of bio-behavioral measures indicative of depressive symptoms post MCAO. RESULTS: About 56% of the rats developed significant depressive-like behavioral disruptions as a result of MCAO compared with 4% in the sham-operated control rats. A pattern of a depressive-like behavioral response was common to all affected MCAO animals, characterized by significantly more escape failures and reduced number of total avoidance shuttles, a significant elevation in immobility duration, and reduced sucrose preference. Significant downregulations of BDNF protein levels in the hippocampal sub-regions, frontal cortex, and hypothalamus were observed in all affected MCAO animals. CONCLUSION: The UFC analysis supports the behavioral analysis and thus, lends validity to our results.

Adjunctive treatment with brexpiprazole and escitalopram reduces behavioral stress responses and increase hypothalamic NPY immunoreactivity in a rat model of PTSD-like symptoms.

The study explored effects of brexpiprazole (partial D2/5-HT1A agonist, 5-HT2A and α1B/2C-adrenoceptor antagonist) in rats exposed to predator scent stress (PSS), a proposed model of PTSD-like phenotype. Brexpiprazole (3.0mg/kg, PO), escitalopram (5.0mg/kg, IP) and their combination were administered twice daily for 14 days, starting 14 days after exposure to PSS or sham-PSS, shortly after a situational stress reminder. One day after last treatment behavioral responsivity was assessed. Brexpiprazole+escitalopram-treated rats spent more time in open arms, entered open arms more often and exhibited a lower anxiety index in the elevated plus maze than vehicle-treated, PSS-exposed rats. Adjunct brexpiprazole+escitalopram treatment reduced startle amplitude, compared with vehicle-treated, PSS-exposed rats. Treatment with either drug alone did not attenuate anxiety-like behaviors following PSS exposure. Use of cut-off behavioral criteria confirmed that adjunct treatment shifted prevalence of PSS-exposed rats from extreme towards minimal behavioral responders. One day following behavioral tests, brains were prepared for immunohistochemical analysis of number of BDNF-positive cells and of NPY-positive cells/fibers. PSS exposure decreased BDNF levels in hippocampus, but this was not affected by drug treatments. PSS exposure decreased number of NPY positive cells/fibers in paraventricular and arcuate nuclei of hypothalamus. Adjunct treatment with brexpiprazole+escitalopram increased NPY in PSS- and sham-exposed rats. Treatment with brexpiprazole alone had no effects, while treatment with escitalopram alone increased NPY in the arcuate nucleus of PSS-exposed rats. In conclusion, treatment with brexpiprazole+escitalopram may be an effective intervention for the attenuation of PTSD-like stress responses, which in part may be mediated by activating NPY function.

Immediate Effects of Transcranial Direct Current Stimulation on Obsession-Induced Anxiety in Refractory Obsessive-Compulsive Disorder: A Pilot Study.

OBJECTIVE: Studies have shown that transcranial direct current stimulation (tDCS) has immediate effects on brain activity. The aim of this study was to investigate the potential use of tDCS to regulate obsession-induced anxiety immediately after symptom provocation in patients with refractory obsessive-compulsive disorder (OCD). METHODS: Twelve patients with refractory OCD received cathode, anode, and sham transcranial direct current stimulation over the medial prefrontal cortex conjugant to pharmacological treatment in a crossover design. Before and after the DC stimulation, patients graded the intensity of their anxiety after a short exposure to a provoking stimulus using the visual analogue scale. Clinical questionnaires assessing symptoms severity were also applied before each stimulation mode. RESULTS: We found a statistically significant decrease in the severity of the obsession-induced anxiety (decreased visual analogue scale) as a result of cathode tDCS in comparison with the anode and sham stimulation. Reduction in obsession-induced anxiety was consistent, yet short lasting, and was independent of symptom severity. CONCLUSIONS: Cathode tDCS could be potentially used to regulate obsession-induced anxiety in refractory OCD patients. Further studies are warranted to confirm our results as well as to determine whether tDCS can achieve prolonged benefits in OCD and be of aid in behavioral treatments based on exposure.

Secondary Prevention of Chronic PTSD by Early and Short-Term Administration of Escitalopram: A Prospective Randomized, Placebo-Controlled, Double-Blind Trial.

OBJECTIVE: Prospective studies have not identified a viable pharmacologic strategy for secondary prevention of posttraumatic stress disorder (PTSD). The authors examined whether preventive intervention via early and short-term administration of a selective serotonin reuptake inhibitor (SSRI), within 1 month of exposure to a traumatic event (before diagnosis of PTSD could be made), may reduce the severity of PTSD symptoms according to DSM-IV at 13 months' follow-up. METHODS: Over 25,000 screening calls to patients referred to an emergency department for a traumatic event performed between June 2006 and December 2008 yielded 353 participants who were recruited within the month following a traumatic event . Participants were randomly assigned in a double-blind design to escitalopram (n = 176) or placebo (n = 177). The per-protocol analysis comprised 198 participants (escitalopram, n = 102; placebo, n = 96) who received treatment for 12 to 24 weeks and were available for follow-up at week 56. RESULTS: The primary outcome measure, the Clinician Administered PTSD Scale (CAPS), revealed no prevention effect. However, a secondary outcome, the Pittsburgh Sleep Quality Inventory (PSQI), showed better results for the SSRI group than for the placebo group. For a subset of participants who experienced intentional trauma (missile attacks, rape, or physical assault; n = 50), the prevention effect was found on both primary and secondary measures (CAPS, PSQI and measures of depression and global illness severity). CONCLUSIONS: Early and short-term administration of escitalopram was not shown to prevent PTSD, although it did improve sleep quality. In a subgroup of participants who experienced intentional trauma, however, this early-treatment approach may be effective as secondary prevention. This large study is the first to investigate the preventive effect of early administration of escitalopram on PTSD. It highlights the relevance of the type of trauma (intentional vs unintentional) to the outcome. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT00300313​​.

Blunted basal corticosterone pulsatility predicts post-exposure susceptibility to PTSD phenotype in rats.

The basal activity of the hypothalamic-pituitary-adrenal axis is highly dynamic and is characterized by both circadian and ultradian (pulsatile) patterns of hormone secretion. Pulsatility of glucocorticoids has been determined to be critical for optimal transcriptional, neuroendocrine, and behavioral responses. We used an animal model of post-traumatic stress disorder (PTSD) to assess whether stress-induced impairment of behavioral responses is correlated with aberrant secretion of corticosterone. Serial blood samples were collected manually via the jugular vein cannula during the light-(inactive)-phase in conscious male rats at 20-min intervals for a period of 5h before and 6.5h after exposure to predator scent stress. The outcome measures included behavior in an elevated plus-maze and acoustic startle response 7days after exposure. Individual animals were retrospectively classified as having "extreme", "partial", or "minimal" behavioral responses according to pre-set cut-off criteria for behavioral response patterns. Corticosterone secretion patterns were analyzed retrospectively. Under basal conditions, the amplitude of ultradian oscillations of corticosterone levels, rather than the mean corticosterone level or the frequency of corticosterone pulsatility, was significantly reduced in individuals who displayed PTSD-phenotype 8days later. In addition, extreme disruption of behavior on day 8 post-exposure was also characterized by a blunting of corticosterone response to the stressor. Animals with behavior that was only partially affected or unaffected displayed none of the above changes. Blunted basal corticosterone pulse amplitude is a pre-existing susceptibility or risk factor for PTSD, which originates from prior (life) experiences and may therefore predict post-exposure PTSD-phenotype in rats.

Controlled Low-Pressure Blast-Wave Exposure Causes Distinct Behavioral and Morphological Responses Modelling Mild Traumatic Brain Injury, Post-Traumatic Stress Disorder, and Comorbid Mild Traumatic Brain Injury-Post-Traumatic Stress Disorder.

The intense focus in the clinical literature on the mental and neurocognitive sequelae of explosive blast-wave exposure, especially when comorbid with post-traumatic stress-related disorders (PTSD) is justified, and warrants the design of translationally valid animal studies to provide valid complementary basic data. We employed a controlled experimental blast-wave paradigm in which unanesthetized animals were exposed to visual, auditory, olfactory, and tactile effects of an explosive blast-wave produced by exploding a thin copper wire. By combining cognitive-behavioral paradigms and ex vivo brain MRI to assess mild traumatic brain injury (mTBI) phenotype with a validated behavioral model for PTSD, complemented by morphological assessments, this study sought to examine our ability to evaluate the biobehavioral effects of low-intensity blast overpressure on rats, in a translationally valid manner. There were no significant differences between blast- and sham-exposed rats on motor coordination and strength, or sensory function. Whereas most male rats exposed to the blast-wave displayed normal behavioral and cognitive responses, 23.6% of the rats displayed a significant retardation of spatial learning acquisition, fulfilling criteria for mTBI-like responses. In addition, 5.4% of the blast-exposed animals displayed an extreme response in the behavioral tasks used to define PTSD-like criteria, whereas 10.9% of the rats developed both long-lasting and progressively worsening behavioral and cognitive "symptoms," suggesting comorbid PTSD-mTBI-like behavioral and cognitive response patterns. Neither group displayed changes on MRI. Exposure to experimental blast-wave elicited distinct behavioral and morphological responses modelling mTBI-like, PTSD-like, and comorbid mTBI-PTSD-like responses. This experimental animal model can be a useful tool for elucidating neurobiological mechanisms underlying the effects of blast-wave-induced mTBI and PTSD and comorbid mTBI-PTSD.

Preventing sleep on the first resting phase following a traumatic event attenuates anxiety-related responses.

Sleep deprivation (SD) in the early aftermath of stress exposure at the onset of the inactive (resting)-phase, has been shown to ameliorate stress-related sequelae. We examined whether this effect is affected by the temporal proximity between SD and the stressful event or whether it was related to the prevention of sleep in the first resting phase following the exposure. Rats were exposed to stress at the onset of their active phase. Then, they were prevented from sleeping immediately thereafter [forced wakefulness (FW)], or during the first resting phase (SD). The behavior in the elevated plus-maze and acoustic startle response paradigms were assessed seven days post-exposure for retrospective classification into behavioral response groups. We found that resting phase SD (with or without FW) decreased PTSD-like phenotype, whereas immediate FW had no significant effect. The long-term anxiolytic effects of SD appear to stem from a diurnal cycle-dependent mechanism, such that preventing sleep during the first natural resting phase following the traumatic exposure is beneficial in preventing the traumatic sequelae.

Exercise Maintains Dendritic Complexity in an Animal Model of Posttraumatic Stress Disorder.

INTRODUCTION: This study examined the effect of endurance exercise on dendritic arborization in the dentate gyrus subregion in rodents exposed to a predator scent stress (PSS). METHODS: Sprague-Dawley rats were randomly assigned to one of four treatment groups. In two of the groups, rats were unexposed to PSS but either remained sedentary (SED + UNEXP) or were exercised (EX + UNEXP). In the other two groups, rats were exposed to the PSS but either remained sedentary (SED + PSS) or were exercised (EX + PSS). After 6 wk of either exercise or sedentary lifestyle, rats were exposed to either the PSS or a sham protocol. During exercise, the animals ran on a treadmill at 15 m·min, 5 min·d gradually increasing to 20 min·d, 5 d·wk for 6 wk. Eight days after exposure to either PSS or sham protocol, changes in the cytoarchitecture (dendritic number, dendritic length, and dendrite spine density) of the dentate gyrus subregion of the hippocampus were assessed. RESULTS: No differences (P = 0.493) were noted in dendritic number between the groups. However, dendritic length and dendrite spine density for SED + PSS was significantly smaller (P < 0.001) than that observed in all other groups. In addition, neurons from animals in SED + PSS had significantly fewer (P < 0.001) dendritic intersections than all other groups. CONCLUSION: The results of this study indicate that 6 wk of endurance training can protect dendritic length and complexity, suggesting a degree of resiliency to stress. This provides further evidence for supporting the inclusion of an exercise regimen for reducing the risk of posttraumatic stress disorder.

Distinctive cardiac autonomic dysfunction following stress exposure in both sexes in an animal model of PTSD.

It is unclear whether the poor autonomic flexibility or dysregulation observed in patients with posttraumatic stress disorder (PTSD) represents a pre-trauma vulnerability factor or results from exposure to trauma. We used an animal model of PTSD to assess the association between the behavioral response to predator scent stress (PSS) and the cardiac autonomic modulation in male and female rats. The rats were surgically implanted with radiotelemetry devices to measure their electrocardiograms and locomotor activity (LMA). Following baseline telemetric monitoring, the animals were exposed to PSS or sham-PSS. Continuous telemetric monitoring (24h/day sampling) was performed over the course of 7days. The electrocardiographic recordings were analyzed using the time- and frequency-domain indexes of heart rate variability (HRV). The behavioral response patterns were assessed using the elevated plus maze and acoustic startle response paradigms for the retrospective classification of individuals according to the PTSD-related cut-off behavioral criteria. During resting conditions, the male rats had significantly higher heart rates (HR) and lower HRV parameters than the female rats during both the active and inactive phases of the daily cycle. Immediately after PSS exposure, both the female and male rats demonstrated a robust increase in HR and a marked drop in HRV parameters, with a shift of sympathovagal balance towards sympathetic predominance. In both sexes, autonomic system habituation and recovery were selectively inhibited in the rats whose behavior was extremely disrupted after exposure to PSS. However, in the female rats, exposure to the PSS produced fewer EBR rats, with a more rapid recovery curve than that of the male rats. PSS did not induce changes to the circadian rhythm of the LMA. According to our results, PTSD can be conceptualized as a disorder that is related to failure-of-recovery mechanisms that impede the restitution of physiological homeostasis.

Predator-scent stress, ethanol consumption and the opioid system in an animal model of PTSD.

Emerging literature points to stress exposure as a potential contributor to the development of alcohol abuse, but animal models have yielded inconsistent results. Converging experimental data indicate that the endogenous opioid system modulates alcohol consumption and stress regulation. The aim of the present study is to examine the interplay between stress exposure, behavioral stress responses, ethanol (EtOH) consumption and the endogenous opioid system in an animal model of posttraumatic stress disorder. Rats were exposed to stress and then tested in a two-bottle free choice (TBC) assay or in a conditioned place preference paradigm. In some experiments, the endogenous opioid system was pharmacologically manipulated prior to stress exposure. The behavioral outcomes of stress exposure were assessed in an elevated plus-maze, with the acoustic startle response, and by monitoring the freezing response to trauma reminder. Immunoreactivity of phosphorylated opioid receptors in hippocampal subregions was also measured. Stress significantly increased the consumption of EtOH in the TBC assay. The severity of the behavioral response to stress was associated with EtOH consumption, cue-triggered freezing response to a trauma reminder, and endogenous levels of phosphorylated opioid receptors in the hippocampus. Pharmacologically manipulating the endogenous opioid system prior to stress exposure attenuated trauma cue-triggered freezing responses and blocked predator scent stress-induced potentiation of EtOH consumption. These data demonstrate a stress-induced potentiation of EtOH self-administration and reveal a clear association between individual patterns of the behavioral response to stress and alcohol preference, while indicating a role for the endogenous opioid system in the neurobiological response to stress.

[NONINVASIVE BRAIN STIMULATION IN NEUROPSYCHIATRIC DISORDERS].

INTRODUCTION: Noninvasive brain stimulation is a growing field of treatment for many neuropsychiatric problems. In this review, several of the more common brain stimulation devices are presented. Specifically, we will review Transcranial Magnetic Stimulation (TMS), Transcranial Direct Current Stimulation (tDCS), Alternating Current Stimulation (ACS), Infrared Stimulation, Electroencephalography Neurofeedback (EEG-NF) and functional Magnetic Resonance Imagining Neurofeedback (fMRI-NF). We will outline some of the properties of these devices including the mechanism, side effect profile, using sham for research and major future developments.

[CAN POST-TRAUMATIC STRESS DISORDER BE PREVENTED WITH GLUCOCORTICOIDS?]

INTRODUCTION: Glucocorticoids (GCs) play a major role in orchestrating the complex physiological and behavioral reactions essential for the maintenance of homeostasis. These compounds enable the organism to prepare for, respond to and cope with the acute demands of physical and emotional stressors. The appropriate GC release, commensurate with stressor severity, enables the body to properly contain stress responses so as to promote recovery by rapidly restoring homeostasis. Indeed, inadequate GC release following stress not only delays recovery by disrupting biological homeostasis in the short run but can also interfere with the processing or interpretation of stressful information that results in long-term disruptions in memory integration. While conventional wisdom holds that people who develop post-traumatic stress disorder (PTSD) following exposure to extreme trauma might have sustained elevations in GCs, several studies have reported that lower cortisol levels in the acute aftermath of trauma are predictors for subsequent PTSD symptoms. Therefore, it is possible that the administration of exogenous cortisol immediately after exposure to a trauma might alter the trajectory of trauma exposure by promoting recovery. Our group has initiated a series of studies examining the role of GCs in susceptibility to "PTSD-like behaviors" in a well-validated animal model for PTSD. The results of these studies highlight the importance of an initial bolus of endogenous corticosteroids in the normative response to stress as a key to a return to homeostasis. Aberrations in the normative response play an equally pivotal role in determining long-term cyto-architecture, and also localized brain biomolecular and overall neuro-hormonal disruptions underlying the PTSD-like behavioral responses in animals, and may be related to the emotional and behavioral symptoms of PTSD in patients. The data provides initial evidence that a single dose of hydrocortisone administered in the acute aftermath of trauma promotes recovery while promoting enhanced synaptic plasticity and connectivity in the secondary prevention of PTSD. We suggested that exogenous hydrocortisone, if given during the 'window of opportunity' - right after the exposure and before consolidation of the traumatic memory - may promote the restoration of homeostasis by constraining central nervous system activity.

[BEHAVIORAL, PHYSIOLOGICAL AND MORPHOLOGICAL CHARACTERISTICS ASSOCIATED WITH POST-TRAUMATIC RESPONSE TO CONTINUOUS EXPOSURE VERSUS ALTERNATE EXPOSURE IN AN ANIMAL MODEL OF POST-TRAUMATIC STRESS DISORDER].

AIMS: The aim of this study was to approximate these conditions in an animal model of post-traumatic stress disorder (PTSD). More specifically, the neurobiological basis of these conditions, focusing on stress-related behavioral changes, HPA-axis and morphological were evaluated. The intention was to employ this well-validated, reproducible and reliable model for PTSD, to elicit data which will provide some guidance in the planning of a prospective study involving military personal. BACKGROUND: Combat personnel are exposed to significant stress and hardship, both physical and emotional, during their service and especially during active combat. Military forces are increasingly involved in conflicts involving nonmilitary or paramilitary adversaries in which they are exposed not to battles but to sporadic events, in what has come to be labeled "low intensity conflict". "Low intensity conflict" refers to a level of hostilities or use of military power that falls short of a full scale conventional or general war. These are characterized by brief periods of extreme stress and tangible danger interspersed by prolonged periods of siege. Whereas the potentially traumatizing effect of battle conditions is well documented, the risks of the sporadic highly stressful nature of "low intensity conflict" have not been studied. Furthermore, in recent years, soldiers commonly receive "relaxation periods" before re-engaging in battle. This new policy may possibly contradict the traditional treatment principles, focusing on "proximity" and "continuity" to the battlefield and its effects have not been studied. METHODS: Continuous and sporadic stresses, representing battlefield conditions, were induced in a validated rat animalmodel for PTSD and behavioral changes, hormonal levels and brain morphology were evaluated. RESULTS: Behavioral response, hormonal levels and brain morphological changes suggest that PTSD-like reactions were significantly higher in rats exposed to continuous stress compared to those exposed to intermittent stress and the control group. CONCLUSIONS: The results support the assumption that "refreshing" during warfare may reduce the incidence of PTSD. Since this study is based on an animal model, its conclusions should also be validated in human observation studies.

[SUPPRESSION OF A NON-TRAUMA-RELATED THREATENING THOUGHT AS AN AVOIDANCE STRATEGY IN POST-TRAUMATIC STRESS DISORDER PATIENTS].

AIMS: Our goal was to examine how suppression of nontrauma- related thoughts differs between PTSD patients and patients with non-PTSD anxiety disorder compared to a group of matched controls. BACKGROUND: Intrusive recollections of aspects of the traumatic event and its sequelae are at the core of the post-traumatic stress disorder (PTSD). People who have suffered a traumatic event may implement some form of avoidance coping strategies in order to deal with the unwanted memories that accompany them. Thought suppression refers to the conscious effort that is made in order NOT to think about a particular thought and is used to regulate affect. The effects of thought suppression on trauma survivors indicates that suppression of trauma related thoughts produces a rebound effect, increasing frequency of negative autobiographical memory recall and may result in the maintenance of PTSD symptoms. RESULTS: The results show that PTSD patients differed in their performance of purposeful suppression of non-traumarelated thoughts, and spent significantly longer time thinking about the target thought during suppression as compared to the control groups. The duration to disengage attention from any thought content was significantly longer in PTSD patients as compared to the anxiety group and controls. CONCLUSIONS: We suggest that PTSD patients demonstrated a mental control deficient in self-regulatory mechanisms involved in coping with threat. DISCUSSION: While PTSD patients used external objects in the room, the control groups used mental contents as distractors. When given suppression instructions, such as distraction thought, all groups demonstrated shorter duration to disengage attention, but the PTSD patients exhibited the significant advantage.

Evaluating low-resolution tomography neurofeedback by single dissociation of mental grotation task from stop signal task performance.

Electroencephalography source localization neurofeedback, i.e Standardized low-resolution tomography (sLORETA) neurofeedback are non-invasive method for altering region specific brain activity. This is an improvement over traditional neurofeedback which were based on recordings from a single scalp-electrode. We proposed three criteria clusters as a methodological framework to evaluate electroencephalography source localization neurofeedback and present relevant data. Our objective was to evaluate standardized low resolution EEG tomography neurofeedback by examining how training one neuroanatomical area effects the mental rotation task (which is related to the activity of bilateral Parietal regions) and the stop-signal test (which is related to frontal structures). Twelve healthy participants were enrolled in a single session sLORETA neurofeedback protocol. The participants completed both the mental rotation task and the stop-signal test before and after one sLORETA neurofeedback session. During sLORETA neurofeedback sessions participants watched one sitcom episode while the picture quality co-varied with activity in the superior parietal lobule. Participants were rewarded for increasing activity in this region only. Results showed a significant reaction time decrease and an increase in accuracy after sLORETA neurofeedback on the mental rotation task but not after stop signal task. Together with behavioral changes a significant activity increase was found at the left parietal brain after sLORETA neurofeedback compared with baseline. We concluded that activity increase in the parietal region had a specific effect on the mental rotation task. Tasks unrelated to parietal brain activity were unaffected. Therefore, sLORETA neurofeedback could be used as a research, or clinical tool for cognitive disorders.