Becoming an inner ally: the compassionate minds approach to self-compassion - an online programme.

A rapidly growing body of evidence indicates the enormous psychological burden of working in health care on nurses and other health professionals that is resulting in high levels of psychological problems. These will have profound effects on individuals and long-term ramifications for healthcare systems. Effective interventions that can counter the adverse psychological effects of caring during the COVID-19 pandemic and beyond are urgently required. With this in mind, the authors have created an online self-compassion programme to advance the health and wellbeing of the nursing workforce through developing proactive evidence-based preventive teaching and learning strategies to promote compassion satisfaction and prevent compassion fatigue by improving self-compassion. The online programme is underpinned by compassionate minds theories and research.

On what motivates us: a detailed review of intrinsic v. extrinsic motivation.

Motivational processes underlie behaviors that enrich the human experience, and impairments in motivation are commonly observed in psychiatric illness. While motivated behavior is often examined with respect to extrinsic reinforcers, not all actions are driven by reactions to external stimuli; some are driven by 'intrinsic' motivation. Intrinsically motivated behaviors are computationally similar to extrinsically motivated behaviors, in that they strive to maximize reward value and minimize punishment. However, our understanding of the neurocognitive mechanisms that underlie intrinsically motivated behavior remains limited. Dysfunction in intrinsic motivation represents an important trans-diagnostic facet of psychiatric symptomology, but due to a lack of clear consensus, the contribution of intrinsic motivation to psychopathology remains poorly understood. This review aims to provide an overview of the conceptualization, measurement, and neurobiology of intrinsic motivation, providing a framework for understanding its potential contributions to psychopathology and its treatment. Distinctions between intrinsic and extrinsic motivation are discussed, including divergence in the types of associated rewards or outcomes that drive behavioral action and choice. A useful framework for understanding intrinsic motivation, and thus separating it from extrinsic motivation, is developed and suggestions for optimization of paradigms to measure intrinsic motivation are proposed.

HIV at 40: reflections on and development of interdisciplinary working in HIV care.

This article reflects on 40 years of HIV and the growing need to work collaboratively to improve outcomes for people living with HIV. It reflects on the history of interdisciplinary working in HIV care in the UK and discusses the development of links between the professions of nursing and clinical psychology. Both professions had contributed to the development of the Standards for Psychological Support for Adults Living with HIV. One of the authors, who was chair of the National HIV Nurses Association, initiated an audit of the use of the standards within UK HIV clinics and invited local British Psychological Society members to participate in the development of the audit process. The audit results identified gaps in the provision of care that led to further close working relationships. In an era of highly effective antiretrovirals that address the medical aspects of HIV care, the focus of care has shifted to the management of psychosocial factors that contribute to poor outcomes in of HIV. Interdisciplinary work and cooperation is the most effective way to address those complex issues.

Stress-related reduction of hippocampal subfield volumes in major depressive disorder: A 7-Tesla study.

Background: Major depressive disorder (MDD) is a prevalent health problem with complex pathophysiology that is not clearly understood. Prior work has implicated the hippocampus in MDD, but how hippocampal subfields influence or are affected by MDD requires further characterization with high-resolution data. This will help ascertain the accuracy and reproducibility of previous subfield findings in depression as well as correlate subfield volumes with MDD symptom scores. The objective of this study was to assess volumetric differences in hippocampal subfields between MDD patients globally and healthy controls (HC) as well as between a subset of treatment-resistant depression (TRD) patients and HC using automatic segmentation of hippocampal subfields (ASHS) software and ultra-high field MRI. Methods: Thirty-five MDD patients and 28 HC underwent imaging using 7-Tesla MRI. ASHS software was applied to the imaging data to perform automated hippocampal segmentation and provide volumetrics for analysis. An exploratory analysis was also performed on associations between symptom scores for diagnostic testing and hippocampal subfield volumes. Results: Compared to HC, MDD and TRD patients showed reduced right-hemisphere CA2/3 subfield volume (p = 0.01, η 2 = 0.31 and p = 0.3, η 2 = 0.44, respectively). Additionally, negative associations were found between subfield volumes and life-stressor checklist scores, including left CA1 (p = 0.041, f 2 = 0.419), left CA4/DG (p = 0.010, f 2 = 0.584), right subiculum total (p = 0.038, f 2 = 0.354), left hippocampus total (p = 0.015, f 2 = 0.134), and right hippocampus total (p = 0.034, f 2 = 0.110). Caution should be exercised in interpreting these results due to the small sample size and low power. Conclusion: Determining biomarkers for MDD and TRD pathophysiology through segmentation on high-resolution MRI data and understanding the effects of stress on these regions can enable better assessment of biological response to treatment selection and may elucidate the underlying mechanisms of depression.

A Randomized Controlled Trial of Repeated Ketamine Administration for Chronic Posttraumatic Stress Disorder.

Objective: Posttraumatic stress disorder (PTSD) is a chronic and disabling disorder, for which available pharmacotherapies have limited efficacy. The authors' previous proof-of-concept randomized controlled trial of single-dose intravenous ketamine infusion in individuals with PTSD showed significant and rapid PTSD symptom reduction 24 hours postinfusion. The present study is the first randomized controlled trial to test the efficacy and safety of repeated intravenous ketamine infusions for the treatment of chronic PTSD. Methods: Individuals with chronic PTSD (N=30) were randomly assigned (1:1) to receive six infusions of ketamine (0.5 mg/kg) or midazolam (0.045 mg/kg) (psychoactive placebo control) over 2 consecutive weeks. Clinician-rated and self-report assessments were administered 24 hours after the first infusion and at weekly visits. The primary outcome measure was change in PTSD symptom severity, as assessed with the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5), from baseline to 2 weeks (after completion of all infusions). Secondary outcome measures included the Impact of Event Scale-Revised, the Montgomery-Åsberg Depression Rating Scale (MADRS), and side effect measures. Results: The ketamine group showed a significantly greater improvement in CAPS-5 and MADRS total scores than the midazolam group from baseline to week 2. At week 2, the mean CAPS-5 total score was 11.88 points (SE=3.96) lower in the ketamine group than in the midazolam group (d=1.13, 95% CI=0.36, 1.91). Sixty-seven percent of participants in the ketamine group were treatment responders, compared with 20% in the midazolam group. Among ketamine responders, the median time to loss of response was 27.5 days following the 2-week course of infusions. Ketamine infusions were well tolerated overall, without serious adverse events. Conclusions: This randomized controlled trial provides the first evidence of efficacy of repeated ketamine infusions in reducing symptom severity in individuals with chronic PTSD. Further studies are warranted to understand ketamine's full potential as a treatment for chronic PTSD.Reprinted from Am J Psychiatry 2021; 178:193-202, with permission from American Psychiatric Association Publishing. Copyright © 2021.

Altered hippocampus and amygdala subregion connectome hierarchy in major depressive disorder.

The hippocampus and amygdala limbic structures are critical to the etiology of major depressive disorder (MDD). However, there are no high-resolution characterizations of the role of their subregions in the whole brain network (connectome). Connectomic examination of these subregions can uncover disorder-related patterns that are otherwise missed when treated as single structures. 38 MDD patients and 40 healthy controls (HC) underwent anatomical and diffusion imaging using 7-Tesla MRI. Whole-brain segmentation was performed along with hippocampus and amygdala subregion segmentation, each representing a node in the connectome. Graph theory analysis was applied to examine the importance of the limbic subregions within the brain network using centrality features measured by node strength (sum of weights of the node's connections), Betweenness (number of shortest paths that traverse the node), and clustering coefficient (how connected the node's neighbors are to one another and forming a cluster). Compared to HC, MDD patients showed decreased node strength of the right hippocampus cornu ammonis (CA) 3/4, indicating decreased connectivity to the rest of the brain, and decreased clustering coefficient of the right dentate gyrus, implying it is less embedded in a cluster. Additionally, within the MDD group, the greater the embedding of the right amygdala central nucleus (CeA) in a cluster, the greater the severity of depressive symptoms. The altered role of these limbic subregions in the whole-brain connectome is related to diagnosis and depression severity, contributing to our understanding of the limbic system involvement in MDD and may elucidate the underlying mechanisms of depression.

Perivascular spaces as a marker of psychological trauma in depression: A 7-Tesla MRI study.

INTRODUCTION: Emerging evidence in depression suggests that blood-brain barrier (BBB) breakdown and elevated inflammatory cytokines in states of persistent stress or trauma may contribute to the development of symptoms. Signal-to-noise ratio afforded by ultra-high field MRI may aid in the detection of maladaptations of the glymphatic system related to BBB integrity that may not be visualized at lower field strengths. METHODS: We investigated the link between glymphatic neuroanatomy via perivascular spaces (PVS) and trauma experience in patients with major depressive disorder (MDD) and in healthy controls using 7-Tesla MRI and a semi-automated segmentation algorithm. RESULTS: After controlling for age and gender, the number of traumatic events was correlated with total PVS volume in MDD patients (r = 0.50, p = .028) and the overall population (r = 0.34, p = .024). The number of traumatic events eliciting horror was positively correlated with total PVS volume in MDD patients (r = 0.50, p = .030) and the overall population (r = 0.32, p = .023). Age correlated positively with PVS count, PVS total volume, and PVS density in all participants (r > 0.35, p < .01). CONCLUSIONS: These results suggest a relationship between glymphatic dysfunction related to BBB integrity and psychological trauma, and that glymphatic impairment may play a role in trauma-related symptomatology.

Computer Vision-Based Assessment of Motor Functioning in Schizophrenia: Use of Smartphones for Remote Measurement of Schizophrenia Symptomatology.

INTRODUCTION: Motor abnormalities have been shown to be a distinct component of schizophrenia symptomatology. However, objective and scalable methods for assessment of motor functioning in schizophrenia are lacking. Advancements in machine learning-based digital tools have allowed for automated and remote "digital phenotyping" of disease symptomatology. Here, we assess the performance of a computer vision-based assessment of motor functioning as a characteristic of schizophrenia using video data collected remotely through smartphones. METHODS: Eighteen patients with schizophrenia and 9 healthy controls were asked to remotely participate in smartphone-based assessments daily for 14 days. Video recorded from the smartphone front-facing camera during these assessments was used to quantify the Euclidean distance of head movement between frames through a pretrained computer vision model. The ability of head movement measurements to distinguish between patients and healthy controls as well as their relationship to schizophrenia symptom severity as measured through traditional clinical scores was assessed. RESULTS: The rate of head movement in participants with schizophrenia (1.48 mm/frame) and those without differed significantly (2.50 mm/frame; p = 0.01), and a logistic regression demonstrated that head movement was a significant predictor of schizophrenia diagnosis (p = 0.02). Linear regression between head movement and clinical scores of schizophrenia showed that head movement has a negative relationship with schizophrenia symptom severity (p = 0.04), primarily with negative symptoms of schizophrenia. CONCLUSIONS: Remote, smartphone-based assessments were able to capture meaningful visual behavior for computer vision-based objective measurement of head movement. The measurements of head movement acquired were able to accurately classify schizophrenia diagnosis and quantify symptom severity in patients with schizophrenia.

Neuroimaging correlates and predictors of response to repeated-dose intravenous ketamine in PTSD: preliminary evidence.

Promising initial data indicate that the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine may be beneficial in post-traumatic stress disorder (PTSD). Here, we explore the neural correlates of ketamine-related changes in PTSD symptoms, using a rich battery of functional imaging data (two emotion-processing tasks and one task-free scan), collected from a subset of participants of a randomized clinical trial of repeated-dose intravenous ketamine vs midazolam (total N = 21). In a pre-registered analysis, we tested whether changes in an a priori set of imaging measures from a target neural circuit were predictive of improvement in PTSD symptoms, using leave-one-out cross-validated elastic-net regression models (regions of interest in the target circuit consisted of the dorsal and rostral anterior cingulate cortex, ventromedial prefrontal cortex, anterior hippocampus, anterior insula, and amygdala). Improvements in PTSD severity were associated with increased functional connectivity between the ventromedial prefrontal cortex (vmPFC) and amygdala during emotional face-viewing (change score retained in model with minimum predictive error in left-out subjects, standardized regression coefficient [ß] = 2.90). This effect was stronger in participants who received ketamine compared to midazolam (interaction ß = 0.86), and persisted following inclusion of concomitant change in depressive symptoms in the analysis model (ß = 0.69). Improvement following ketamine was also predicted by decreased dorsal anterior cingulate activity during emotional conflict regulation, and increased task-free connectivity between the vmPFC and anterior insula (ßs = -2.82, 0.60). Exploratory follow-up analysis via dynamic causal modelling revealed that whilst improvement in PTSD symptoms following either drug was associated with decreased excitatory modulation of amygdala→vmPFC connectivity during emotional face-viewing, increased top-down inhibition of the amygdala by the vmPFC was only observed in participants who improved under ketamine. Individuals with low prefrontal inhibition of amygdala responses to faces at baseline also showed greater improvements following ketamine treatment. These preliminary findings suggest that, specifically under ketamine, improvements in PTSD symptoms are accompanied by normalization of hypofrontal control over amygdala responses to social signals of threat.

A Randomized Controlled Trial of Repeated Ketamine Administration for Chronic Posttraumatic Stress Disorder.

OBJECTIVE: Posttraumatic stress disorder (PTSD) is a chronic and disabling disorder, for which available pharmacotherapies have limited efficacy. The authors' previous proof-of-concept randomized controlled trial of single-dose intravenous ketamine infusion in individuals with PTSD showed significant and rapid PTSD symptom reduction 24 hours postinfusion. The present study is the first randomized controlled trial to test the efficacy and safety of repeated intravenous ketamine infusions for the treatment of chronic PTSD. METHODS: Individuals with chronic PTSD (N=30) were randomly assigned (1:1) to receive six infusions of ketamine (0.5 mg/kg) or midazolam (0.045 mg/kg) (psychoactive placebo control) over 2 consecutive weeks. Clinician-rated and self-report assessments were administered 24 hours after the first infusion and at weekly visits. The primary outcome measure was change in PTSD symptom severity, as assessed with the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5), from baseline to 2 weeks (after completion of all infusions). Secondary outcome measures included the Impact of Event Scale-Revised, the Montgomery-Åsberg Depression Rating Scale (MADRS), and side effect measures. RESULTS: The ketamine group showed a significantly greater improvement in CAPS-5 and MADRS total scores than the midazolam group from baseline to week 2. At week 2, the mean CAPS-5 total score was 11.88 points (SE=3.96) lower in the ketamine group than in the midazolam group (d=1.13, 95% CI=0.36, 1.91). Sixty-seven percent of participants in the ketamine group were treatment responders, compared with 20% in the midazolam group. Among ketamine responders, the median time to loss of response was 27.5 days following the 2-week course of infusions. Ketamine infusions were well tolerated overall, without serious adverse events. CONCLUSIONS: This randomized controlled trial provides the first evidence of efficacy of repeated ketamine infusions in reducing symptom severity in individuals with chronic PTSD. Further studies are warranted to understand ketamine's full potential as a treatment for chronic PTSD.

The emergence of ketamine as a novel treatment for posttraumatic stress disorder.

A serious lack of effective pharmacotherapeutic interventions for posttraumatic stress disorder (PTSD) raises the urgent need for the development of novel treatments. Ketamine-a noncompetitive glutamate N-methyl-d-aspartate (NMDA) receptor antagonist in use for decades as an anesthetic and analgesic agent-has more recently been demonstrated to have rapid-onset antidepressant effects in patients with treatment-resistant depression (TRD). In the present review of ketamine as an emerging novel pharmacotherapeutic intervention for chronic PTSD, we discuss findings from the first proof-of-concept, randomized clinical trial (RCT) of single-dose intravenous ketamine in patients with chronic PTSD, as well as open-label studies and current practice. We introduce ongoing RCTs investigating the efficacy of repeated ketamine infusions in rapidly reducing symptoms and maintaining improvement in samples of individuals with PTSD stemming from civilian and military traumas. Additionally, we discuss mixed findings from published reports on ketamine administration in the acute aftermath of trauma. Studies in animal models of chronic stress have investigated molecular mechanisms underlying ketamine's effects, generating a shift in the conceptualization of PTSD as a disorder of impaired neural connectivity. We review animal studies examining the potential of ketamine to modify the expression of fear by altering memory reconsolidation or enhancing fear extinction, as well as others investigating ketamine administration prophylactically prior to stress exposure. We introduce the need for additional study in humans to evaluate whether ketamine might enhance the efficacy of psychotherapeutic interventions in individuals with chronic PTSD, harnessing a window of ketamine-induced neuroplasticity. While research on ketamine for PTSD is still in its early stages, it brings about the promise of novel and more effective treatments for this disabling condition.

Neural correlates of rumination in major depressive disorder: A brain network analysis.

Patients with major depressive disorder (MDD) exhibit higher levels of rumination, i.e., repetitive thinking patterns and exaggerated focus on negative states. Rumination is known to be associated with the cortical midline structures / default mode network (DMN) region activity, although the brain network topological organization underlying rumination remains unclear. Implementing a graph theoretical analysis based on ultra-high field 7-Tesla functional MRI data, we tested whether whole brain network connectivity hierarchies during resting state are associated with rumination in a dimensional manner across 20 patients with MDD and 20 healthy controls. Applying this data-driven approach we found a significant correlation between rumination tendency and connectivity strength degree of the right precuneus, a key node of the DMN. In order to interrogate this region further, we then applied the Dependency Network Analysis (DEPNA), a recently developed method used to quantify the connectivity influence of network nodes. This revealed that rumination was associated with lower connectivity influence of the left medial orbito-frontal cortex (MOFC) cortex on the right precuneus. Lastly, we used an information theory entropy measure that quantifies the cohesion of a network's correlation matrix. We show that subjects with higher rumination scores exhibit higher entropy levels within the DMN i.e. decreased overall connectivity within the DMN. These results emphasize the general DMN involvement during self-reflective processing related to maladaptive rumination in MDD. This work specifically highlights the impact of the MOFC on the precuneus, which might serve as a target for clinical neuromodulation treatment.

Comparison of self-report and clinician-rated schizotypal traits in schizotypal personality disorder and community controls.

Given the common use of self-report questionnaires to assess schizotypy in personality pathology and schizophrenia research, it is important to determine the concordance between self-report and clinician ratings. 250 individuals with schizotypal personality disorder (SPD) and 116 community controls (CTR) were assessed on schizotypal traits using a clinical interview, the Structured Interview for DSM-IV Personality disorders (SIDP), and a self-report questionnaire, the Schizotypal Personality Questionnaire (SPQ). Ordinal logistic regressions examined concordance between self-reported and clinician-rated scores in CTR and SPD separately. Analyses of variance examined how the SPQ performed on differentiating between CTR with low schizotypy, CTR with high schizotypy, and SPD. For both CTR and SPD, higher SPQ subscale scores were significantly associated with higher clinician ratings on the respective SIDP items for the Ideas of Reference, Magical Thinking, Unusual Perceptual Experience, Suspiciousness, and Social Anxiety items, but not the Odd Speech or Limited Affect items. Higher SPQ subscale scores for Odd Behavior and Lack of Close Friends were significantly associated with the clinician-rated SIDP item scores in CTR but not SPD. CTR with low schizotypy scored lower on all SPQ subscales than CTR with high schizotypy, who did not differ from SPD. Self-report ratings are concordant with clinician ratings for positive schizotypal traits, whereas certain disorganization and interpersonal traits are not, particularly for individuals with SPD. The SPQ can differentiate between high and low schizotypy controls, but not between high schizotypy controls and individuals with SPD. Assessment of schizotypal traits should include both self-report questionnaires and clinician ratings.

Vulvar Lesions in an 8-Year-Old Girl: Cutaneous Manifestations of Multisystem Langerhans Cell Histiocytosis.

BACKGROUND: Langerhans cell histiocytosis (LCH) is a rare localized or systemic disease characterized by proliferation of myeloid-derived dendritic cells. Vulvar lesions might be the herald symptom of LCH and might mimic other cutaneous lesions. Prognosis varies widely on the basis of the extent and spread of disease. CASE: An 8-year-old girl with a 4-month history of vulvar lesions resistant to topical steroids was referred by her pediatrician. Vulvar biopsy was diagnostic for LCH. Imaging studies revealed a left hip lesion consistent with LCH. The patient was subsequently treated for multisystem LCH with vinblastine and prednisone. SUMMARY AND CONCLUSION: Although rare, LCH might be diagnosed by gynecologic providers and should be included in the differential diagnosis of genital lesions. We recommend having a low threshold for performing biopsy of vulvar lesions.