The current study investigated the relationship between trauma exposure and psychopathology in a sample of predominately African-American women of low socioeconomic status (SES). Women (N = 7430) were recruited from medical clinics at two large public hospitals in Atlanta, GA, from 2005 to 2017. Women were assessed for sociodemographics, life-course trauma burden, posttraumatic stress disorder (PTSD), and major depressive disorder (MDD) utilizing self-report and structured clinical interview assessments. The effects of trauma exposure on current and lifetime PTSD and MDD were examined. Ninety-one percent of women reported trauma exposure, 83% reported a monthly household income of less than $2000, and 41% reported a history of arrest. Regarding psychiatric diagnoses, 30.8% met the criteria for probable MDD, and 32.3% met the criteria for probable PTSD. History of childhood abuse and total lifetime trauma significantly increased PTSD and depressive symptoms with additional incremental trauma exposure. PTSD and depressive symptom scores (95% CI) increased from 5.5 (5.0–6.1) and 8.4 (7.9–9.0) in the no trauma group to 20.8 (20.1–21.5) and 20.4 (19.7–21.2), respectively, in those exposed to four or more types of trauma. These results show high rates of adult and childhood trauma exposure, PTSD, MDD, and an additive effect of lifetime trauma exposure on the development of PTSD and MDD in a sample of low SES African-American women. These findings bring light to the high psychiatric symptom burden in this population and call for increased availability of interventions to address symptoms as well as policies aimed at reducing trauma exposure across the lifespan.
The relationship of analgesic medication use with posttraumatic stress disorder (PTSD) diagnosis was investigated among a sample of 173 African Americans presenting for routine outpatient visits at an urban mental health center. Seventy-eight (43.5%) of the sample met DSM-IV PTSD criteria. Those with PTSD had significantly higher use of analgesic medication (both opiate and non-opiate), as compared with non-PTSD patients. PTSD symptoms, as measured by the Posttraumatic Symptom Scale, were significantly higher in subjects who were prescribed analgesics. The authors conclude that there may be a relationship between PTSD and use of pain medications warranting further examination of the endogenous opiate system in the pathophysiology of PTSD.
Background: Current observational literature on the mental health impact of the COVID-19 pandemic has focused on anxiety, depression, and sleep-disturbance among the public, healthcare workers, and COVID-19 patients. Case reports suggest catatonia and psychosis may be presenting symptoms of COVID-19 disease with a mechanism postulated to involve central nervous system changes in response to inflammation. There is a lack of robust evidence examining catatonia in this context. We sought to systematically review available case data and contextualize our findings. Case Presentations: We present three cases of patients with catatonia seen at a large metropolitan tertiary care hospital in which their catatonia was likely attributable to SARS-CoV-2 infection. Ms. A is a female in her 50s with no psychiatric history who presented with self-inflicted stab wounds following her COVID-19 diagnosis. Ms. B is a female in her 50s with a history of schizophrenia, but no history of catatonia, who presented with akinetic catatonia, SARS-CoV-2 infection, and Clostridium difficile infection, without respiratory manifestations of COVID-19. Ms. C is a female in her 20s with a history of bipolar disorder (type 1) without catatonic features who presented with akinetic catatonia without the physical symptoms of SARS-CoV-2 infection. Discussion: We present a brief review of six case reports detailing co-occurring catatonia and SARS-CoV-2 infection and one case report of catatonia attributed to the psychological stress of the COVID-19 pandemic in a patient without SARS-CoV-2 infection. We note one additional case of cooccurring catatonia and SARS-CoV-2 infection for which details are not available. COVID-19-associated catatonia may develop secondary to psychological and physical factors. Cases often report anxiety preceding catatonic symptoms. Developing evidence also suggests SARS-CoV-2 may act directly on the central nervous system or via a systemic inflammatory response. One of our cases featured significant anxiety preceding symptoms, and two had co-occurring elevated serum inflammatory markers. We suggest that clinicians should keep a high index of suspicion for both clinically significant anxiety disorders and catatonia.
Reduced heart rate variability (HRV) in response to stress is a biomarker of emotion dysregulation (ED) and is related to posttraumatic stress disorder (PTSD), yet less is known about its role with dissociation in trauma-exposed adults. The goals of the current study were to examine unique patterns of associations between ED, dissociation, and PTSD with HRV at 15, 30, and 45 min (T1, T2, T3) following an acute psychosocial stressor task in a sample of 49 trauma-exposed, urban-dwelling Black women. Associations with baseline psychophysiology measures were also examined. ED and dissociation were assessed using self-report; PTSD was determined using a semi-structured interview. Heart rate (HR) and HRV, indexed with low frequency/high frequency (LF/HF) ratio and respiratory sinus arrhythmia (RSA), were measured with electrocardiogram recordings. ED and dissociation were positively correlated with LF/HF ratio at T3 (p < .05). There were no significant differences between individuals with PTSD versus those without PTSD in HR or HRV following acute stressor; PTSD diagnosis was related to higher HR at baseline. Latent growth modeling revealed that ED was associated with higher LF/HF ratio directly following acute stressor, while dissociation was associated with increase in LF/HF ratio over time. These findings demonstrate that ED is related to higher sympathetic reactivity for a prolonged period of time following stress exposure, while dissociation shows a delayed association with LF/HF ratio, suggesting a distinct impaired parasympathetic activation pattern exists for dissociation.
Context
Genetic inheritance and developmental life stress both contribute to major depressive disorder in adults. Child abuse and trauma alter the endogenous stress response, principally corticotropin-releasing hormone and its downstream effectors, suggesting that a gene × environment interaction at this locus may be important in depression.
Objective
To examine whether the effects of child abuse on adult depressive symptoms are moderated by genetic polymorphisms within the corticotropin-releasing hormone type 1 receptor (CRHR1) gene.
Design
Association study examining gene × environment interactions between genetic polymorphisms at the CRHR1 locus and measures of child abuse on adult depressive symptoms.
Setting
General medical clinics of a large, public, urban hospital and Emory University, Atlanta, Georgia.
Participants
The primary participant population was 97.4% African American, of low socioeconomic status, and with high rates of lifetime trauma (n=422). A supportive independent sample (n=199) was distinct both ethnically (87.7% Caucasian) and socioeconomically (less impoverished).
Main Outcome Measures
Beck Depression Inventory scores and history of major depressive disorder by the Structured Clinical Interview for DSM-IV Axis I Disorders.
Results
Fifteen single-nucleotide polymorphisms spanning 57 kilobases of the CRHR1 gene were examined. We found significant gene × environment interactions with multiple individual single-nucleotide polymorphisms (eg, rs110402, P=.008) as well as with a common haplotype spanning intron 1 (P <.001). Specific CRHR1 polymorphisms appeared to moderate the effect of child abuse on the risk for adult depressive symptoms. These protective effects were supported with similar findings in a second independent sample (n=199).
Conclusions
These data support the corticotropin-releasing hormone hypothesis of depression and suggest that a gene × environment interaction is important for the expression of depressive symptoms in adults with CRHR1 risk or protective alleles who have a history of child abuse.
Context
In addition to trauma exposure, other factors contribute to risk for development of posttraumatic stress disorder (PTSD) in adulthood. Both genetic and environmental factors are contributory, with child abuse providing significant risk liability.
Objective
To increase understanding of genetic and environmental risk factors as well as their interaction in the development of PTSD by gene × environment interactions of child abuse, level of non–child abuse trauma exposure, and genetic polymorphisms at the stress-related gene FKBP5.
Design, Setting, and Participants
A cross-sectional study examining genetic and psychological risk factors in 900 non psychiatric clinic patients (762 included for all genotype studies) with significant levels of childhood abuse as well as non–child abuse trauma using a verbally presented survey combined with single-nucleotide polymorphism (SNP) genotyping. Participants were primarily urban, low-income, black (>95%) men and women seeking care in the general medical care and obstetrics-gynecology clinics of an urban public hospital in Atlanta, Georgia, between 2005 and 2007.
Main Outcome Measures
Severity of adult PTSD symptomatology, measured with the modified PTSD Symptom Scale, non–child abuse (primarily adult) trauma exposure and child abuse measured using the traumatic events inventory and 8 SNPs spanning the FKBP5 locus.
Results
Level of child abuse and non–child abuse trauma each separately predicted level of adult PTSD symptomatology (mean [SD], PTSD Symptom Scale for no child abuse, 8.03 [10.48] vs ≥2 types of abuse, 20.93 [14.32]; and for no non–child abuse trauma, 3.58 [6.27] vs ≥4 types, 16.74 [12.90]; P<.001). Although FKBP5 SNPs did not directly predict PTSD symptom outcome or interact with level of non–child abuse trauma to predict PTSD symptom severity, 4 SNPs in the FKBP5 locus significantly interacted (rs9296158, rs3800373, rs1360780, and rs9470080; minimum P=.0004) with the severity of child abuse to predict level of adult PTSD symptoms after correcting for multiple testing. This gene × environment interaction remained significant when controlling for depression severity scores, age, sex, levels of non–child abuse trauma exposure, and genetic ancestry. This genetic interaction was also paralleled by FKBP5 genotype-dependent and PTSD-dependent effects on glucocorticoid receptor sensitivity, measured by the dexamethasone suppression test.
Conclusions
Four SNPs of the FKBP5 gene interacted with severity of child abuse as a predictor of adult PTSD symptoms. There were no main effects of the SNPs on PTSD symptoms and no significant genetic interactions with level of non–child abuse trauma as predictor of adult PTSD symptoms, suggesting a potential gene-childhood environment interaction for adult PTSD.
One in seven people in the USA, or 14.3% of the population, develops a substance use disorder at some point in their lifetime [1]. Of the over 20.1 million Americans with substance use disorder, fewer than 7% receive treatment [2]. Despite this high disease prevalence and low treatment rate, general psychiatry training programs are required to provide only 1 month of addiction psychiatry training [3]. As a result, general psychiatry residents may graduate from residency underprepared for treating patients with substance use disorder in the context of a dearth of subspecialty-boarded physicians in addiction psychiatry and addiction medicine.
Objective:
This study was undertaken to increase understanding of environmental risk factors for PTSD and MDD within an urban, impoverished, population.
Method:
This study examined the demographic characteristics, patterns of trauma exposure, prevalence of PTSD and MDD, and predictors of post-traumatic stress and depressive symptomatology using a verbally-presented survey and structured clinical interviews administered to low-income, primarily African-American (>93%), women and men seeking care in the primary care and obstetrics-gynecology clinics of an urban public hospital.
Results:
87.8% (N=1256) of the sample reported some form of significant trauma in their lifetime. Accidents were the most common form of trauma exposure followed by interpersonal violence and sexual assault. Childhood level of trauma and adult level of trauma separately, and in combination, predicted level of adult PTSD and depressive symptomatology. The lifetime prevalence of PTSD was 46.2% and the lifetime prevalence of MDD was 36.7%.
Conclusions:
These data document high levels of childhood and adult trauma exposure, principally interpersonal violence, in a large sample of an inner-city primary care population. Within this group of subjects, PTSD and depression are highly prevalent conditions.
Despite the value of family-centered care (FCC) in intensive care units (ICUs), this approach is rarely a reality in this context. This article aims to increase the likelihood that ICU-based care incorporates best practices for FCC. Consistent with this goal, this article begins by overviewing FCC and its merits and challenges in ICUs. It then offers a systemic framework for conceptualizing FCC in this challenging environment, as such a model can help guide the implementation of this invaluable approach. This systemic framework combined with previous guidelines for FCC in the ICU are used to inform the series of recommended best practices for FCC in the ICU that balance the needs and realities of patients, families, and the interprofessional healthcare team. These best practices reflect an integration of the existing literature and previously published guidelines as well as our experiences as healthcare providers, family members, and patients. We encourage healthcare leaders and interprofessional ICU healthcare teams to adopt these best practices and modify them for the specific healthcare needs of the patients they serve and their families.
The World Health Organization declared the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to be a pandemic on March 11, 2020.1 As of February 25, 2021, there have been approximately 112 million cases and 2.5 million confirmed deaths attributable to COVID-19 disease.2 The physical, biochemical, and imaging characteristics of SARS-CoV-2 infection are well described.3 , 4 Recent data implicate SARS-CoV-2 involvement in a wide range of central nervous system (CNS) manifestations of the disease.5 SARS-CoV-2 is postulated to enter the CNS via translocation from the cribriform plate to the orbitofrontal cortex6 or via hematologic spread.7 The potential mechanisms for the neurological and neuropsychiatric effects of the virus are many and include direct viral encephalitis, as well as less direct effect of the infection, including inflammation, hypoxia, hypercoagulability, postinfectious auto-immunity, or effects of immunomodulatory treatments