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Psychiatry Research Jun 2024On October 7, 2023, a war erupted in Israel following a mass terror attack including mass shootings, violent events, civilian abductions, and numerous fatalities,...
Mental Health Outcomes of Arab and Jewish Populations in Israel a Month after the Mass Trauma Events of October 7, 2023: A Cross-Sectional Survey of a Representative Sample.
On October 7, 2023, a war erupted in Israel following a mass terror attack including mass shootings, violent events, civilian abductions, and numerous fatalities, ranking as the third most deadliest terror attack. This cross-sectional, population-based study evaluated the impact on the mental health and utilization of mental health services in the Arab and Jewish populations. Conducted through a virtual platform, the study compared demographic factors, exposure to war-related events, anxiety, and post-traumatic stress symptoms among 517 participants in a representative sample of the adult population in Israel (79.1% Jewish, 20.9% Arab). Jews reported higher exposure to war-related events, but a majority expressed a lack of interest in mental help. In contrast, more Arabs desired mental help but faced barriers like stigma and scarce resources. Arabs showed a greater preference for group therapy and medical treatment. Trust in official bodies was consistently higher among Jews. Both populations exhibited similar levels (12-15.4%) of probable post-traumatic stress disorder (PTSD). This study equips clinicians, researchers and policymakers with real-time insights into improving mental health support for the culturally diverse needs of Jewish and Arab communities following exposure to mass trauma.
PubMed: 38945101
DOI: 10.1016/j.psychres.2024.116042 -
Biological Psychiatry. Cognitive... Jun 2024'Voice-hearing' (VH) is a transdiagnostic experience that is common in trauma-related disorders (trauma-D). However, the neural substrates underlying trauma-related VH...
BACKGROUND
'Voice-hearing' (VH) is a transdiagnostic experience that is common in trauma-related disorders (trauma-D). However, the neural substrates underlying trauma-related VH remain largely unexplored. While auditory perceptual dysfunction is among the abnormalities implicated in schizophrenia VH, whether VH in trauma-D also involves auditory perceptual alterations is unknown.
METHODS
We investigated auditory cortex (AC)-related functional connectivity (FC) in n=65 women with trauma-D related to childhood abuse with varying severities of VH. Using a novel, computationally-driven and individual-specific method of functionally parcellating the brain, we calculated the FC of two distinct AC subregions-Heschl's gyrus (HG, corresponding to primary AC) and lateral superior temporal gyrus (lSTG, in non-primary AC)- with both the cerebrum and cerebellum. We then measured the association between VH severity and FC using leave-one-out cross validation within the cerebrum, and voxel-wise multiple regression analyses in the cerebellum.
RESULTS
We found that VH severity positively correlated with left lSTG-frontoparietal network FC, while it negatively correlated with FC between left lSTG and both cerebral and cerebellar representations of the default mode network. VH severity was not predicted by FC of left HG or right AC subregions.
CONCLUSIONS
Our findings point to altered interactions between auditory perceptual processing and higher-level processes related to self-reference and executive functioning. This is the first study to show alterations in auditory cortical connectivity in trauma-related VH. While VH in trauma-D appears to be mediated by brain networks that are also implicated in schizophrenia VH, the results suggest a unique mechanism that could distinguish VH in trauma-D.
PubMed: 38944384
DOI: 10.1016/j.bpsc.2024.06.009 -
European Journal of Pharmacology Jun 2024Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) are prevalently co-occurring, important risk factors for a broad array of neuropsychiatric diseases....
Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) are prevalently co-occurring, important risk factors for a broad array of neuropsychiatric diseases. To date, how these two contrastive concomitant pairs increase the risk of neuropsychiatric states, notably exacerbating PTSD-related symptoms, remains unknown. Moreover, pharmacological interventions with agents that could reverse PTSD-AUD comorbidity, however, remained limited. Hence, we investigated the neuroprotective actions of naringin in mice comorbidly exposed to PTSD followed by repeated ethanol (EtOH)-induced AUD. Following a 7-day single-prolong-stress (SPS)-induced PTSD in mice, binge/heavy drinking, notably related to AUD was induced in the PTSD mice with every-other-day ethanol (2 g/kg, p.o.) administration, followed by daily treatments with naringin (25 and 50 mg/kg) or fluoxetine (10 mg/kg), from days 8-21. PTSD-AUD-related behavioral changes, alcohol preference, hypothalamic-pituitary-adrenal (HPA)-axis dysfunction-induced neurochemical alterations, oxidative/nitrergic stress, and inflammation were examined in the prefrontal-cortex, striatum, and hippocampus. PTSD-AUD mice showed aggravated anxiety, spatial-cognitive, social impairments and EtOH intake, which were abated by naringin, similar to fluoxetine. Our assays on the HPA-axis showed exacerbated increased corticosterone release and adrenal hypertrophy, accompanied by marked dopamine and serotonin increase, with depleted glutamic acid decarboxylase enzyme in the three brain regions, which naringin, however, reversed, respectively. PTSD-AUD mice also showed increased TNF-α, IL-6, malondialdehyde and nitrite levels, with decreased antioxidant elements in the prefrontal-cortex, striatum, and hippocampus compared to SPS-EtOH-mice; mainly exacerbating catalase and glutathione decrease in the hippocampus relative SPS-mice. These findings suggest that AUD exacerbates PTSD pathologies in different brain regions, notably comprising neurochemical dysregulations, oxidative/nitrergic and cytokine-mediated inflammation, with HPA dysfunction, which were, however, revocable by naringin.
PubMed: 38944175
DOI: 10.1016/j.ejphar.2024.176791 -
Psychoneuroendocrinology Jun 2024Brain-Derived Neurotrophic Factor (BDNF) is implicated in extinction learning, which is a primary mechanism of exposure therapy for posttraumatic stress disorder (PTSD)....
Brain-Derived Neurotrophic Factor (BDNF) is implicated in extinction learning, which is a primary mechanism of exposure therapy for posttraumatic stress disorder (PTSD). Brief aerobic exercise has been shown to promote BDNF release and augment extinction learning. On the premise that the Val allele of the BDNF Val66Met polymorphism facilitates greater release of BDNF, this study examined the extent to which the Val allele of the BDNF polymorphism predicted treatment response in PTSD patients who underwent exposure therapy combined with aerobic exercise or passive stretching. PTSD patients (N = 85) provided saliva samples in order to extract genomic DNA to identify Val/Val and Met carriers of the BDNF Val66Met genotype, and were assessed for PTSD severity prior to and following a 9-week course of exposure therapy combined with aerobic exercise or stretching. The sample comprised 52 Val/Val carriers and 33 Met carriers. Patients with the BDNF high-expression Val allele display greater reduction of PTSD symptoms at posttreatment than Met carriers. Hierarchical regression analysis indicated that greater PTSD reduction was specifically observed in Val/Val carriers who received exposure therapy in combination with the aerobic exercise. This finding accords with animal and human evidence that the BDNF Val allele promotes greater extinction learning, and that these individuals may benefit more from exercise-augmented extinction. Although preliminary, this result represents a possible avenue for augmented exposure therapy in patients with the BDNF Val allele.
PubMed: 38943720
DOI: 10.1016/j.psyneuen.2024.107106 -
American Journal of Industrial Medicine Jun 2024Posttraumatic stress disorder (PTSD) symptomatology and poorer pulmonary function are highly prevalent psychiatric and medical conditions. In the present study, we...
BACKGROUND
Posttraumatic stress disorder (PTSD) symptomatology and poorer pulmonary function are highly prevalent psychiatric and medical conditions. In the present study, we tested for the individual, additive, and modifying associations of PTSD symptomatology and pulmonary function with cognitive performance.
METHODS
In this cross-sectional study, a total of 1,401 World Trade Center (WTC) responders (mean age = 53, SD = 8 years, 92% males) participated in the study. Cogstate assessment measured cognitive performance. PTSD symptomatology was measured using the trauma-specific version of the posttraumatic stress disorder checklist (PCL-17) adapted for the WTC attacks. The 1-second forced expiratory volume and forced vital capacity (FEV1/FVC) ratio was used to measure pulmonary function. Linear regressions with cognitive performance as the outcome were conducted to assess individual, additive, and moderating associations of PTSD symptomatology and pulmonary function.
RESULTS
Higher PTSD symptomatology and poorer pulmonary function were negatively associated with cognitive performance. A 10% increase on the FEV1/FVC ratio moderated the association between PTSD symptomatology and cognition, whereby its association with cognition was stronger when PTSD symptomatology was higher (est. = 0.01, 95%CI = 0.004, 0.01, p < 0.001). When stratified by responder type, these associations persisted in trained (est. = 0.01, 95%CI = 0.01, 0.02, p < 0.001), but not in non-trained (est. = 0.004, 95% C.I. = -0.01, 0.02, p = 0.39) responders.
CONCLUSIONS
In the presence of higher PTSD, better pulmonary functioning is associated with better cognitive performance. Early intervention efforts to mitigate preventable cognitive decline in high-risk populations should be studied, especially since intervention in one modality may have an impact on others.
PubMed: 38943489
DOI: 10.1002/ajim.23631 -
European Journal of Trauma and... Jun 2024Depressed skull fractures occur when a portion of the skull is displaced inward towards the brain, leading to complications such as intracranial hematoma, brain...
INTRODUCTION
Depressed skull fractures occur when a portion of the skull is displaced inward towards the brain, leading to complications such as intracranial hematoma, brain contusion, and intracranial infection. Managing these fractures necessitates a multidisciplinary approach, with postoperative management and rehabilitation playing crucial roles in optimizing patient outcomes. This study aimed to assess the predictive factors and outcomes of patients who underwent surgical treatment for depressed skull fractures.
METHOD
A comprehensive retrospective review was undertaken on the medical records of all patients who underwent surgery for depressed skull fractures at the University Comprehensive Specialized Hospital from January 1, 2021, to January 1, 2023 G.C. Patients with missile injuries were excluded from this study. The analysis incorporated a total of 163 patients.
RESULTS
A total of 163 patients (mean age 23.9; standard deviation 14.8; range 3-65) were studied, comprising 136 men (83.4%) and 27 women (16.6%). Among them, 153 (93.9%) were under 50 years old. Physical assault accounted for 102 (62.5%) of the injuries, with 62 (38%) involving a stone, 32 (19.6%) a stick, and 8 (5%) other objects (e.g., shovel, beer bottle). Using the Glasgow Coma Scale (GCS), minor head injuries were found in 123 individuals (75%). Fracture sites predominantly included frontal depressions (61 patients, 37.4%) and parietal depressions (53 patients, 32.5%). The associated injuries featured brain contusion (52 cases, 32%), epidural hematoma (26 cases, 16%), subdural hematoma (3 cases, 1.8%), and IVH/SAH (3 cases, 1.8%). Following surgery, full recovery occurred in 148 patients (91%), while sequelae-such as hemiparesis and aphasia-affected 15 patients (9%); unfortunately, three patients (1.8%) died due to critical head injuries prior to admission. Complications included meningitis (4 cases, 2.55%), brain abscesses (2 cases, 1.2%), surgical site infections (10 cases, 6.1%), hypocalcemia in one patient, post-traumatic stress disorder in two patients(1.6%), and osteomyelitis of the skull bone in two patients(1.2%). The multivariable logistic regression revealed that low GCS scores, compound fractures, hemiparesis, and the presence of an epidural hematoma were found to be substantially associated with a poorer outcome.
CONCLUSION
The overall outcome of patients with depressed skull fracture was favorable. Factors associated with worse outcomes include compound fracture, low Glasgow Coma Scale at admission, presence of weakness, and presence of epidural hematoma. Complications associated with depressed skull fractures observed in our patients include wound infection, meningitis, brain abscess, osteomyelitis, PTSD, and hypocalcemia.
PubMed: 38943025
DOI: 10.1007/s00068-024-02590-z -
Journal of Affective Disorders Jun 2024Post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) are psychiatric disorders that can present with overlapping symptoms and shared risk factors.... (Review)
Review
Similarities and differences between post-traumatic stress disorder and major depressive disorder: Evidence from task-evoked functional magnetic resonance imaging meta-analysis.
BACKGROUND
Post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) are psychiatric disorders that can present with overlapping symptoms and shared risk factors. However, the extent to which these disorders share common underlying neuropathological mechanisms remains unclear. To investigate the similarities and differences in task-evoked brain activation patterns between patients with PTSD and MDD.
METHODS
A coordinate-based meta-analysis was conducted across 35 PTSD studies (564 patients and 543 healthy controls) and 125 MDD studies (4049 patients and 4170 healthy controls) using anisotropic effect-size signed differential mapping software.
RESULTS
Both PTSD and MDD patients exhibited increased neural activation in the bilateral inferior frontal gyrus. However, PTSD patients showed increased neural activation in the right insula, left supplementary motor area extending to median cingulate gyrus and superior frontal gyrus (SFG), and left fusiform gyrus, and decreased neural activation in the right posterior cingulate gyrus, right middle temporal gyrus, right paracentral lobule, and right inferior parietal gyrus relative to MDD patients.
CONCLUSION
Our meta-analysis suggests that PTSD and MDD share some similar patterns of brain activation, but also have distinct neural signatures. These findings contribute to our understanding of the potential neuropathology underlying these disorders and may inform the development of more targeted and effective treatment and intervention strategies. Moreover, these results may provide useful neuroimaging targets for the differential diagnosis of MDD and PTSD.
PubMed: 38942203
DOI: 10.1016/j.jad.2024.06.095 -
Epilepsy & Behavior : E&B Jun 2024
PubMed: 38941951
DOI: 10.1016/j.yebeh.2024.109902 -
European Journal of Psychotraumatology 2024Clonidine is a centrally acting anti-adrenergic agent that may have applications in post-traumatic stress disorder (PTSD), particularly for sleep. In this systematic... (Review)
Review
Clonidine is a centrally acting anti-adrenergic agent that may have applications in post-traumatic stress disorder (PTSD), particularly for sleep. In this systematic review, we aimed to summarize the effect of clonidine on sleep quality and duration, nightmares, and PTSD symptom severity in adults with PTSD. PubMed (Medline), Embase, PsycINFO, CINAHL, and clinicaltrials.gov were searched up to April 2023. Studies on clonidine use in adult PTSD patients reporting data on the effect on sleep, nightmares, and PTSD symptoms were included. A narrative summary and a meta-analysis of the study findings are presented. Ten reports, accounting for = 569 patients with PTSD (145 on clonidine and 436 controls), were included in the final selection. There were four case reports, four observational studies, one non-blind clinical trial, and one crossover randomized controlled trial (RCT). Median clonidine dose was 0.15 mg/day (range: 0.1-0.5 mg/day). Median follow-up time was 31 days (range: 3 days to 19 months). The quality of the evidence was rated from very low to low. There was marked between-study heterogeneity and low power in the individual studies, but many reported improved sleep quality, nightmare reduction, and improvement of PTSD symptoms for patients treated with clonidine. Meta-analysis was only possible for two studies reporting the effect of clonidine on nightmares, and showed no difference from the comparator (i.e. prazosin or terazosin) (odds ratio: 1.16; 95% confidence interval: 0.66 to 2.05), potentially pointing towards non-inferiority between these medications. Future research, such as well-powered RCTs, is needed to identify the efficacy in the lower dose range and the most suitable treatment group, and to obtain good evidence on the effects of clonidine in the treatment of sleep disorders related to PTSD.
Topics: Clonidine; Humans; Stress Disorders, Post-Traumatic; Dreams; Sleep Quality; Adrenergic alpha-2 Receptor Agonists
PubMed: 38941125
DOI: 10.1080/20008066.2024.2366049 -
Psychopharmacology Jun 2024Since the precise mechanisms of posttraumatic stress disorder (PTSD) remain unknown, effective treatment interventions have not yet been established. Impaired extinction...
RATIONALE
Since the precise mechanisms of posttraumatic stress disorder (PTSD) remain unknown, effective treatment interventions have not yet been established. Impaired extinction of fear memory (EFM) is one of the core symptoms of PTSD and is associated with stress-induced epigenetic change in gene expression.
OBJECTIVES
In this study, we examined whether the involvement of histone H3 lysine 9 dimethylation (H3K9me2) in EFM is mediated through brain-derived neurotrophic factor (BDNF) expression in the hippocampus, and whether BIX01294, a selective G9a and GLP histone methyltransferase inhibitor, could be treatment for impaired EFM in an animal model of PTSD.
METHODS
The single prolonged stress (SPS) paradigm was used to model PTSD. We measured BDNF mRNA levels by RT-PCR, and H3K9me2 levels in the BDNF gene promoters by chromatin immunoprecipitation-qPCR. After undergoing contextual fear conditioning and hippocampal injection of BIX01294, male rats were subjected to extinction training and extinction testing and their freezing times and BDNF mRNA levels were measured.
RESULTS
Compared to sham rats, SPS rats showed decreased BDNF mRNA levels 2 h after extinction training, no significant changes in levels of global H3K9me2 prior to extinction training, and increased levels of H3K9me2 in BDNF gene promoter IV, but not in BDNF gene promoter I. Administration of BIX01294 ameliorated the decrease in BDNF mRNA levels 2 h after extinction training and subsequently alleviated impaired EFM in extinction tests in SPS rats.
CONCLUSION
We conclude that reduced hippocampal levels of BDNF mRNA due to increase in H3K9me2 levels may play a role in PTSD-associated EFM impairment, and BIX01294 could be a PTSD treatment option.
PubMed: 38940908
DOI: 10.1007/s00213-024-06640-7