Journal of psychiatry and brain science最新文献

Introduction: The post-acute phase of anorexia nervosa (AN) following discharge from higher-level care is a high-risk period in which relapse rates are high and many individuals lack access to effective treatment. Even after acute nutritional stabilization, AN is characterized by decreased biobehavioral sensitivity towards general rewards and elevated sensitivity towards weight-loss cues. These reward patterns may continue to maintain eating disorder and comorbid affective symptoms. To address these gaps in the treatment literature for post-acute AN, we propose a randomized controlled trial comparing Positive Affect Treatment for AN (PAT-AN), a neuroscience-informed therapy adapted to target these reward imbalances in AN, to more standard psychoeducational and behavioral treatment (PBT) for eating disorders following acute care.

Method: Adult participants (N = 80) with broad AN, including atypical AN, discharged from intensive treatment (e.g., residential, partial hospitalization) for AN within the past 6 months will be randomly assigned to 24 weeks of remotely-delivered PAT-AN or PBT. We will compare the feasibility, acceptability, and efficacy of each treatment to augment post-acute outpatient care for AN. A multimodal neurocognitive and self-report battery will assess eating pathology, comorbid symptom, and putative reward mechanism changes over the course of treatment (i.e., baseline, mid-treatment, post-treatment, three-month follow-up) and on a week-to-week basis.

Discussion: This trial will, for the first time, directly target observed reward disturbances in the post-acute period of AN. Thus, this investigation has the potential to simultaneously evaluate a novel, efficacious treatment for AN and to further evaluate the role of reward dysfunction in AN maintenance.

Perinatal mood and anxiety disorders (PMAD), which include depression and/or anxiety in the year before and/or after delivery, are common complications of pregnancy, affecting up to one in four perinatal individuals, with costs of over $15 billion per year in the US. In this paper, we provide an overview of the disparities in utilization and delivery outcomes for individuals with perinatal mood and anxiety disorders in the US. In addition, we discuss the current US screening and treatment guidelines as well as the high societal costs of illness of PMAD for both perinatal individuals and children. Finally, we outline opportunities for quality improvement of PMAD care in the US, including leveraging increased engagement with healthcare system during prenatal care, working toward a more cohesive national strategy to address PMAD, leaning into evidence-based policymaking through collaboration with a panel of experts, and generating state-level profiles focused on PMAD.

It is important to consider reciprocal associations between maternal and offspring mental health problems during early childhood. Existing interventions often focus narrowly on either adult or child mental health, missing the opportunity for holistic care. We describe the rationale and development of a pilot randomized clinical trial that explores their integration, combining an evidence-based parenting intervention with depression treatment to improve both maternal and child outcomes. Our approach is part of a growing field of two-generation interventions that offer a promising approach to enhance mental health support for caregivers and their young children.

Background: Non-suicidal self-injury (NSSI) is a highly prevalent clinical concern in adolescents and is associated with impaired functioning and suicide risk. The BRIDGES (BRain Imaging Development of Girls' Emotion and Self) study was designed to collect longitudinal clinical and neurobiological data to advance our understanding of NSSI in adolescents. The purpose of this paper is to describe the clinical data collected as part of this study, including psychiatric diagnoses, depression symptoms, episodes of non-suicidal self-injury, suicidal thoughts and behaviors, childhood trauma, and personality domains.

Methods: The baseline sample included 164 adolescents aged 12-16 assigned female at birth (Mean age = 14.97, SD = 1.20) with NSSI histories ranging from none to severe. Participants and their parent/guardian were invited to provide data at three time points spaced approximately one year apart. Descriptive analyses were conducted to provide estimates of rates and trajectories of clinical data.

Results: Of the 164 study participants, 75.61% and 57.93% completed the second and third time points, respectively. Visual inspection of the data suggests an overall trend of decreasing severity of psychopathology over time, and adolescents with a history of NSSI appeared to have higher rates of psychopathology than those without.

Conclusions: This paper describes longitudinal clinical trajectories in adolescents with a range of NSSI histories and presents readers with an overview of the rich, publicly available dataset that we hope will inspire future research to advance the understanding of the neurodevelopmental trajectories associated with NSSI, depression, and suicide risk.

Background: Despite the effectiveness and growing availability of treatment for opioid use disorder (OUD) with buprenorphine, many people with OUD do not access treatment services. This article describes the rationale, methodological design, evolution, and progress of an ongoing clinical trial of treatment linkage strategies for people with untreated OUD.

Methods: The study, titled Opioid Use Disorder Treatment Linkage at Strategic Touchpoints using Buprenorphine (OUTLAST-B), uses "strategic touchpoints", initially sexual health clinics and subsequently broadened to other service venues and participant social networks, for recruitment and screening. Adults with untreated OUD (target N = 360) are randomized to one of the three arms: Usual Care (UC, enhanced with overdose education and naloxone distribution), Patient Navigation (PN), or Patient Navigation with an immediate short-term bridge prescription for buprenorphine (PN + BUP). In the PN and PN + BUP arms, the Patient Navigator works with participants for 2 months to facilitate treatment entry and early retention, resolve barriers (e.g., ID cards, transportation), and provide motivational support.

Results: The primary outcome is OUD treatment entry within 30 days of enrollment. Participants are assessed at baseline and followed at 3- and 6-months post-enrollment on measures of healthcare utilization, substance use, and general functioning. Challenges and recruitment adaptations pursuant to the COVID-19 pandemic are discussed.

Conclusions: This study could provide insights on how to reach people with untreated OUD and link them to care through non-traditional routes.

Trial registration: The study is registered at ClinicalTrials.gov (NCT04991974).

High titers of anti-NMDAR1 IgG autoantibodies were found in the brains of patients with anti-NMDAR1 encephalitis that exhibits psychosis, impaired memory, and many other psychiatric symptoms in addition to neurological symptoms. Low titers of blood circulating anti-NMDAR1 IgG autoantibodies are sufficient to robustly impair spatial working memory in mice with intact blood-brain barriers (BBB). On the other hand, anti-NMDAR1 autoantibodies were reported to protect against neuronal excitotoxicity caused by excessive glutamate in neurological diseases. Activation of extrasynaptic NMDARs is responsible for neuronal excitotoxicity, whereas activation of synaptic NMDARs within the synaptic cleft is pro-survival and essential for NMDAR-mediated neurotransmission. Unlike small IgG, IgM antibodies are large and pentameric (diameter of ~30 nm). It is plausible that IgM anti-NMDAR1 autoantibodies may be restricted to bind extrasynaptic NMDARs and thereby specifically inhibit neuronal excitotoxicity, but physically too large to enter the synaptic cleft (width: 20-30 nm) to suppress synaptic NMDAR-mediated neurotransmission in modulation of cognitive function and neuronal pro-survival signaling. Hence, blood circulating anti-NMDAR1 IgM autoantibodies are both neuroprotective and pro-cognitive, whereas blood circulating anti-NMDAR1 IgG and IgA autoantibodies are detrimental to cognitive function. Investigation of anti-NMDAR1 IgM autoantibodies may open up a new avenue for the development of long-lasting preventive and therapeutic IgM anti-NMDAR1 autoantibodies that protect from neuronal excitotoxicity in many neurological diseases and psychiatric disorders.

The risk for developing schizophrenia is increased among first-degree relatives of those with psychotic disorders, but the risk is even higher in those meeting established criteria for clinical high risk (CHR), a clinical construct most often comprising of attenuated psychotic experiences. Conversion to psychosis among CHR youth has been reported to be about 15-35% over three years. Accurately identifying individuals whose psychotic symptoms will worsen would facilitate earlier intervention, but this has been difficult to do using behavior measures alone. Brain-based risk markers have the potential to improve the accuracy of predicting outcomes in CHR youth. This narrative review provides an overview of neuroimaging studies used to investigate psychosis risk, including studies involving structural, functional, and diffusion imaging, functional connectivity, positron emission tomography, arterial spin labeling, magnetic resonance spectroscopy, and multi-modality approaches. We present findings separately in those observed in the CHR state and those associated with psychosis progression or resilience. Finally, we discuss future research directions that could improve clinical care for those at high risk for developing psychotic disorders.

Astrocytes, despite some shared features as glial cells supporting neuronal function in gray and white matter, participate and adapt their morphology and neurochemistry in a plethora of distinct regulatory tasks in specific neural environments. In the white matter, a large proportion of the processes branching from the astrocytes' cell bodies establish contacts with oligodendrocytes and the myelin they form, while the tips of many astrocyte branches closely associate with nodes of Ranvier. Stability of myelin has been shown to greatly depend on astrocyte-to-oligodendrocyte communication, while the integrity of action potentials that regenerate at nodes of Ranvier has been shown to depend on extracellular matrix components heavily contributed by astrocytes. Several lines of evidence are starting to show that in human subjects with affective disorders and in animal models of chronic stress there are significant changes in myelin components, white matter astrocytes and nodes of Ranvier that have direct relevance to connectivity alterations in those disorders. Some of these changes involve the expression of connexins supporting astrocyte-to-oligodendrocyte gap junctions, extracellular matrix components produced by astrocytes around nodes of Ranvier, specific types of astrocyte glutamate transporters, and neurotrophic factors secreted by astrocytes that are involved in the development and plasticity of myelin. Future studies should further examine the mechanisms responsible for those changes in white matter astrocytes, their putative contribution to pathological connectivity in affective disorders, and the possibility of leveraging that knowledge to design new therapies for psychiatric disorders.