Neglecting the impact of social determinants of health has come at a big cost. Key points Social psychiatry strives to combat the social and environmental contributors to mental distress. Social determinants of health or SDoH are non-medical social factors that affect health outcomes. SDoH speak to the social fabric of our lives—the conditions to which we are born, raised, work, live, and age. The Social Determinants of Health Network promotes the education of professionals and the public about SDoH. In the mid-twentieth century, psychiatrists were, with much zeal, striving to combat the social and environmental contributors to mental distress by focusing on strengthening families, encouraging healthy lifestyles, and advocating relevant legal and health policy issues. Unfortunately, in subsequent decades, a lack of political will (admitting to the social antecedents of mental health issues would require elected officials to work to change laws) and withering public funding meant the social psychiatry approach became not only forgotten but also unpopular. The era of psychiatry I trained in, in the early 2000s, for the most part, had embraced (and continues to embrace) a biological approach. This means that today, a conversation with a psychiatrist about mental health symptoms will mostly be focused on neurobiology, genetics, misfiring brain structures, and neurotransmitters gone awry. And yes, well-trained psychiatric practitioners who approach their practice from a bio-psych-social approach will take into consideration social factors but too often this is cursory. Why? Twenty-first-century psychiatric practice is simply not enabled or encouraged to support an in-depth assessment of or response to the social determinants that are causing mental distress to our patients. Too often frontline clinicians feel their hands are tied. The consequences of abandoning social psychiatry I’ve witnessed how the abandonment of social psychiatry leads to highly unsatisfactory outcomes such as the over-pathologizing of mental distress in individuals with diagnoses such as depressive and anxiety disorders when, in fact, the real culprits are social factors. Also overmedicating with anti-depressant, anti-anxiety, and insomnia medications— all inadequate band aids that don’t address the root cause of the symptoms and come with side effects. The distinct trend in recent decades has been to ignore social psychiatry approaches that call out the mental health effects of broken systems and an unjust world. And this has come at a big cost with an over-reliance on individual responsibility and “fixing” brains or “altering” mindsets when changes to societal policies may have elevated the mental wellness of large swathes of the general population. Will the management of social determinants finally become a reality in health care? Imagine then, how delighted I was to come across this recent article about Past APA President Dilip Jeste, M.D., who wants to make the assessment and management of social determinants of health (SDoH) a reality in psychiatry and general medicine, not just an aspiration. He founded the Social Determinants of Health Network, a dedicated 501(c)(3) nonprofit foundation, to promote research and foster the education of healthcare professionals and the public about SDoH. What is the meaning of SDoH? SDoH are “non-medical social factors that affect health outcomes.” They are societal problems that affect both individuals and the larger population and have a well-established influence on mental health, risk for mental illnesses, and overall quality of life. SDoHs speak to the social fabric of our lives, the conditions in which we are born, raised, work, live, and age, and also the systemic and institutional forces that shape our everyday life circumstances. SDoH include: Exposure to childhood trauma including ACEs The presence or absence of supportive social connections Exposure to stigma and discrimination Your financial status (including issues related to access to education) Your employment Access to transportation Access to food and shelter To date, the problem has been less about the psychiatric profession resisting social determinants and more about practicality. What tools can practitioners use to formally assess and address the social determinants that affect our patients’ health in our clinics? What are the associated diagnostic terms? Are there expert consensus guidelines or algorithms that show us what actions we need to take when we identify SDoH that are affecting our patient’s health? How will health systems reimburse the time practitioners spend focusing on social determinants? I’m looking forward to embracing a new era that will provide solutions to these practicalities and normalize the management of social determinants as a routine part of health care because social psychiatry is long overdue for a comeback. Note: This article originally appeared on Psychology Today .

Key Takeaways GLP-1 receptor agonists effectively manage obesity, reducing appetite and achieving weight loss in patients with BMI ≥30 or ≥27 with comorbidities. The Confusion Assessment Method is optimal for diagnosing delirium, while the Geriatric Depression Scale is sensitive for detecting depression in older adults. Collaborative care models between family medicine and psychiatry enhance patient outcomes by addressing both physical and mental health needs. Reducing stigma and integrating behavioral health services in family medicine can improve access to psychiatric care. CONFERENCE SPOTLIGHT The Spotlight series highlights speakers at the Family Medicine Experience 2024 (FMX 2024), hosted by the American Academy of Family Physicians. Name Ecler Jaqua, MD, MBA, FAAFP, AGSF, FACLM, DipABOM, AAHIVS Title Associate Professor Institution Loma Linda University Hometown Pomona, CA Tell us about yourself. I am an associate professor of family medicine at Loma Linda University Health, specializing in family medicine and geriatrics. My work is driven by a passion for holistic and comprehensive care, ensuring the well-being of my patients across different stages of life. In addition to my clinical practice, I enjoy teaching and mentoring the next generation of physicians, and I have completed certifications in lifestyle medicine, obesity medicine, and HIV specialization. I am also actively involved in program leadership and quality improvement initiatives. Can you please discuss some key take home points from your presentation at the FMX 2024 conference? At the FMX conference, I presented on 2 key topics. First, I discussed the role of GLP-1 receptor agonists in managing obesity, emphasizing their ability to reduce appetite and achieve significant weight loss in patients with a body mass index greater than or equal to 30 or greater than or equal to 27 with comorbidities like type 2 diabetes. I also covered protocols for initiating treatment and managing adverse effects. In my second topic, I compared cognitive screening tools, highlighting the Confusion Assessment Method as the best tool for diagnosing delirium, while the Geriatric Depression Scale is highly sensitive for detecting depression in older adults . Do you have any suggestions for improving the integration between family medicine and psychiatry to enhance patient care? Improving integration between family medicine and psychiatry can be achieved by fostering collaborative care models where mental health professionals work closely with family physicians to address both physical and mental health needs. Regular interdisciplinary case reviews, shared care plans, and streamlined referral processes can enhance patient outcomes, ensuring timely and holistic treatment for conditions like depression, anxiety, and chronic illnesses with mental health components. Additionally, training family physicians in primary care psychiatry can help bridge the gap in access to mental health services . What do you believe to be some factors that prevent patients from seeking help at times from a psychiatrist? Any suggestions for improvement? Patients may avoid seeking help from a psychiatrist due to stigma surrounding mental health, fear of being judged, or a lack of understanding about psychiatric care. Limited access to services and financial concerns can also be barriers. To improve this, increasing mental health education, normalizing conversations about mental health in primary care settings, and integrating behavioral health services within family medicine can help reduce stigma and improve access to psychiatric care. How do you deal with patient compliance and managing adverse effects from various psychiatric medications? Managing patient compliance and adverse effects from psychiatric medications involves open communication, educating patients about potential adverse effects, and setting realistic expectations about treatment outcomes. I regularly assess patients for tolerance and adherence, adjusting medications as needed to minimize side effects while maintaining effectiveness. Collaborative decision-making, involving patients in their treatment plans, also helps improve compliance and addresses any concerns early on. What advice about patient care would you like to share with your medical colleagues in psychiatry? For my colleagues in psychiatry, I would emphasize the importance of maintaining a patient-centered approach by fostering trust and open dialogue. Collaborating with other health care providers, particularly in primary care, can provide a more comprehensive understanding of the patient’s overall well-being, improving outcomes. Any words of wisdom or favorite quotes? One of my favorite quotes is: "The good physician treats the disease; the great physician treats the patient who has the disease." – William Osler. Another quote I value is, "People don’t care how much you know until they know how much you care." – Theodore Roosevelt. This serves as a reminder that compassion and empathy are foundational in building strong patient relationships and delivering effective care. Note: This article originally appeared on Psychiatric Times .

TOPLINE: US diagnosis rates of autism spectrum disorder (ASD) increased by 175% from 2011 to 2022, a new study shows. Prevalence was highest in children aged 5-8 years, but the greatest relative increases were reported in young adults, women, and children in multiple racial and ethnic groups. METHODOLOGY: In this cross-sectional study, researchers examined annual diagnosis rates of ASD from 2011 to 2022 using more than 1.2 million electronic health records across 12 US health systems from the Mental Health Research Network. Participants were included if they were enrolled in a participating health system for at least 10 months of the year. Diagnoses of ASD were identified using International Classification of Diseases (Ninth and 10th Revision) codes. Sociodemographic characteristics of the participants were included, and data were stratified by participants' age, sex, race, and ethnicity. TAKEAWAY: A total of 77,683 participants had ASD. The overall diagnosis rate of ASD increased by 175% from 2011 to 2022. The rate was highest among 5- to 8-year-olds (30.3 per 1000 individuals), with the greatest relative increase in diagnosis rates observed among 26- to 34-year-olds (452%). Diagnosis rates were higher in women than in men, both for children (305% increase vs 185% increase) and adults (315% increase vs 215% increase). Relative increases in prevalence were highest among Black, Asian, American Indian or Alaska Native, and Hispanic children compared with White children. IN PRACTICE: "These findings forecast a substantial number of autistic people aging into adult care and can be used both to inform interventions for addressing disparities and to efficiently allocate resources to meet the support needs of autistic people across the lifespan," the authors wrote. LIMITATIONS: The study was limited by the high rates of missing or unknown data for race and ethnicity, which could have affected the accuracy of diagnosis rates. The findings may not be generalizable to individuals without insurance coverage or those seeking ASD-related services outside integrated health systems. DISCLOSURES: The study was funded by the National Institute of Mental Health . One author reported receiving grants from SAGE Therapeutics outside the submitted work. Note: This article originally appeared on Medscape .

The rising incidence of food allergies among children over the past decade appears to have been accompanied by a growing awareness among pediatric allergists that their patients may need mental health care to manage anxiety related to allergies, new research shows. From 2013 to 2023, referrals from pediatric allergists to mental health experts related to food allergies rose 11-fold at one children’s hospital system. Referrals in 2023 were 50% higher than in the period between 2018 and 2022, researchers reported at the 2024 annual scientific meeting of the American College of Allergy, Asthma and Immunology. “I hope this [study] increases awareness for pediatricians and allergists to discuss anxiety with families,” said David Stukus, MD, director of the Food Allergy Treatment Center at Nationwide Children’s Hospital in Columbus, Ohio, who helped conduct the research. “It is important to normalize this as much as possible as some people may see anxiety as a negative stigma.” Stukus and his colleagues said their study was not designed to draw conclusions about the incidence of pediatric anxiety linked to food allergies. “Our study was only designed to evaluate the number of referrals over time, and we observed a significant increase in referrals,” he said. “Our study was not designed to assess why or to evaluate if anxiety was increasing among all of our patients or the population of children with food allergy at large.” Clinicians and researchers now have a better understanding that anxiety is a component of having food allergies, “but I am not aware if anxiety itself has been increasing or we are simply more aware to assess for it and ask about it,” he said. The center was opened in 2021, and two psychologists were hired to help families and children dealing with anxiety in relation to allergies, Stukus said. His team conducted the study to characterize the use of the new psychology services. Stukus and his colleagues conducted a chart review of 250 referrals (141 male; median age, 9.5 years) to outpatient pediatric psychologists at Nationwide Children’s Hospital. The data included demographic information, medical history related to food allergies, and the number of psychology appointments. The findings revealed that 88% of patients were referred for psychological assessment owing to concerns related to food allergies, with 69% of the children exhibiting symptoms of anxiety related to their food restrictions. More than 50% had prior documented anaphylaxis. Of those referred, 60% followed through with at least one appointment, and on average, patients attended 5.5 follow-up appointments in the following year. Although awareness of the psychological impact of food allergies is growing, Stukus said not enough psychologists and therapists are available to help children. “And even those that are, they don’t necessarily have the background specific to food allergies and anxiety pertaining to those,” Stukus said. Zachary Rubin, MD, a pediatric allergist and immunologist at Oak Brook Allergists in Elmhurst, Illinois, said food allergies can play a large part in the mental health of patients. “When you have to constantly think about what you’re eating to make sure that it’s safe to consume and not have a severe allergic reaction, that can create a lot of problems psychologically,” Rubin said. “It is a chronic disease.” Kari Benson, PhD, a pediatric psychologist at Nationwide Children’s Hospital , said pediatricians usually refer patients to her when the anxiety begins to interfere with their day-to-day lives. “The kids have been avoiding eating lunch with their friends at school, maybe they only feel comfortable eating privately at their own table or at the allergen-free table, or maybe they won’t go to friends’ houses,” Benson said. “Or maybe they’re not necessarily avoiding anything but just that they spend a lot of their day worrying, and it’s really just having an impact on mood and stress.” Note: This article originally appeared on Medscape .

TOPLINE: About 5% of people older than 65 years in the United States are prescribed benzodiazepine after acute ischemic stroke (AIS) despite warnings of potential side effects in older adults, a new study shows. Although the findings indicate a slight decrease in benzodiazepine use for post-stroke anxiety (PSA) over the past decade, investigators say overdiagnosis remains a problem. METHODOLOGY: Researchers analyzed a sample of US Medicare claims from April 2013 to September 2021. A total of 126,050 beneficiaries (mean age, 78 years; 54% women; 82% White) discharged alive following an AIS were included. Patients previously prescribed benzodiazepine and those with self-discharge or discharge to skilled nursing facilities were excluded. Researchers assessed the demographics and comorbidities of patients, initial prescription lengths, cumulative incidence of first fills of benzodiazepine within 90 days post-discharge, and geographic and yearly trends. TAKEAWAY: Within 90 days of discharge, 5% of stroke survivors were initiated on benzodiazepine, with lorazepam (40%) and alprazolam (33%) prescribed most often. Most (76%) of first-time benzodiazepine prescriptions had a supply of > 7 days, with 55% covering 15-30 days. Women had higher initiation rates than men (6% vs 4%), and Hispanic adults had a higher cumulative incidence (6%) than adults of other ethnicities. Prescription rates were the highest in the Southeast (5%) and lowest in the Midwest (4%), with a slight countrywide decline (cumulative incidence difference, 1.6%) during the study period. IN PRACTICE: “Despite declining trends in benzodiazepine prescriptions, it is necessary to note that use remains alarming in the United States as it represents the third most used illicit or prescription drug in the country,” the authors wrote. Authors of an accompanying editorial noted that ideally, patients with stroke would be screened for PSA at discharge to allow for early diagnosis and appropriate treatment. “Unfortunately, access to mental health services after stroke can be limited, and not all hospitals or clinics will have these types of resources available,” the authors wrote. “These limitations require stroke physicians to often become the first line of treatment for PSA and sometimes are the only option available.” Note: This article originally appeared on Medscape .

Depression symptoms can be hard to manage, especially for people with treatment-resistant depression, a persistent and severe form of the disorder. Fortunately, new therapies are emerging for such hard-to-treat conditions. One of these is the medication ketamine, which numerous NIMH-funded studies have shown has fact-acting and lasting effects in people with mood disorders like depression. The discovery of ketamine has been a game changer for people with severe depression, who often need rapid relief from life-threatening symptoms. Whereas most antidepressants take weeks or months to work, ketamine works within hours to strongly reduce depression symptoms in people for whom other treatments have not worked. Despite ketamine’s effectiveness as an antidepressant, serious concerns limit its use, including problematic side effects and a high risk of misuse. To address these concerns, the National Institutes of Health (NIH) is invested in finding medications that capitalize on the therapeutic effects of ketamine while avoiding its negative ones. What did the researchers look at in the study? New research funded through the NIH Blueprint Neurotherapeutics Network for Small Molecules program examined a novel ketamine-related medication known as RR-HNK. RR-HNK is a metabolite , or byproduct, of ketamine left over as the body breaks it down. RR-HNK showed antidepressant effects in preclinical studies with animals , but it had not yet been tested in humans. The study involved a broad collaboration of researchers in the intramural programs at NIH’s National Institute of Mental Health , National Center for Advancing Translational Sciences, and National Institute on Aging; the Duke University and the University of Maryland School of Medicine; and other national and international institutions. What did the researchers do in the study? This study examined the safety, tolerability, pharmacokinetics (how the drug moves through the body), and pharmacodynamics (how the drug affects the body) of RR-HNK for the first time in humans. Participants were healthy adults between 18–65 years. A total of 74 people participated across three randomized trials: 55 received RR-HNK and 19 received an inactive placebo. Both the medication and placebo were given intravenously, with participants and researchers unaware of which group the participants were in. In Trial 1, participants received one of six dose levels of RR-HNK a single time. In Trial 2, participants received one of two dose levels of RR-HNK four times over 2 weeks. In Trial 3, participants received a single dose of RR-HNK, and their cerebrospinal fluid (a liquid surrounding the brain and spinal cord) was collected. The study's primary aim was to determine if the medication is safe by first testing it in healthy adults without a diagnosed mental health condition. Throughout the study, the researchers closely monitored for adverse events, such as negative side effects. The comprehensive safety profile included physical examinations; laboratory results; vital signs; electrocardiograms of heart activity; and ratings of mood, suicide risk, and dissociation and sedation symptoms. Additionally, participants were asked to tell study staff if they experienced any concerns or side effects at any point. The researchers also collected blood and urine samples from all participants before, during, and after receiving the medication. These samples and the cerebrospinal fluid collected in Trial 3 were used to check whether the medication entered the body and the brain. As a final exploratory step, the researchers used brain imaging to examine participants’ gamma oscillations (a type of brain wave) before and after the medication. This measure of the brain’s response to stimuli is one of the few available biomarkers of a medication’s effects on the brain. What did the study find? RR-HNK revealed itself to be exceptionally safe, causing no serious adverse events and only mild side effects that resolved quickly without care. Participants also reported no symptoms of sedation or dissociation. The positive safety profile was maintained at all doses tested and after multiple doses. Together, the results indicate that RR-HNK is safe and tolerable, with limited abuse or misuse potential. Cerebrospinal fluid confirmed that RR-HNK entered the brain and remained at detectable levels several hours after administration. Results further showed a dose-proportional response to the medication, meaning that at higher levels of RR-HNK, the amount of the substance in the body also increased at the same rate. A predictable relationship between the amount of RR-HNK given and the amount of RR-HNK in the bloodstream is important for the clinical efficacy of the medication, allowing doctors and researchers to accurately calibrate doses to a person’s specific level and type of symptoms. In the test of brain activity, some participants who received low to moderate doses of RR-HNK, but not those who received high doses or the placebo, showed an increase in the power of gamma oscillations. Preliminary evidence that RR-HNK produces a change in brain activity strengthens the case for its use as an antidepressant and provides a clinical biomarker for measuring whether it works in future research. However, there was large variability in the results and, given the small number of participants, the researchers caution against drawing firm conclusions from these findings. What do the results mean? This study offers critical insight into the safety, tolerability, and effects of RR-HNK in a diverse population of healthy adults. Findings from this early stage study demonstrate that the ketamine metabolite does not cause ketamine’s negative side effects and is safe for use in humans. The results also help set dosing parameters for its use in future research and treatment. These data, particularly a strong safety profile, support the progression into the next phase of research aimed at developing new therapies for people with hard-to-treat mental disorders. Despite the small size of each trial, which makes it difficult to interpret some of the results, the findings hold promise for the future of mental health treatment. This study is a critical early step in NIMH’s mission to improve the treatment of mental illnesses through research, setting the stage for clinical trials that test whether RR-HNK effectively treats depression and other disorders. Note: This article originally appeared on NIMH .

List of Famous Psychoanalysts - origin of therapy List of Famous Psychoanalysts - origin of therapy What is Psychoanalysis? Psychoanalysis , method of treating mental disorders, shaped by psychoanalytic theory, which emphasizes unconscious mental processes and is sometimes described as “depth psychology.” The psychoanalytic movement originated in the clinical observations and formulations of Austrian psychiatrist Sigmund Freud, who coined the term psychoanalysis . During the 1890s, Freud worked with Austrian physician and physiologist Josef Breuer in studies of neurotic patients under hypnosis. Freud and Breuer observed that, when the sources of patients’ ideas and impulses were brought into consciousness during the hypnotic state, the patients showed improvement. Observing that most patients talked freely without being under hypnosis, Freud evolved the technique of free association of ideas. The patient was encouraged to say anything that came to mind, without regard to its assumed relevancy or propriety. Noting that patients sometimes had difficulty in making free associations, Freud concluded that certain painful experiences were repressed, or held back from conscious awareness. Freud noted that in the majority of the patients seen during his early practice, the events most frequently repressed were concerned with disturbing sexual experiences. Thus he hypothesized that anxiety was a consequence of the repressed energy (libido) attached to sexuality; the repressed energy found expression in various symptoms that served as psychological defense mechanisms. Freud and his followers later extended the concept of anxiety to include feelings of fear, guilt, and shame consequent to fantasies of aggression and hostility and to fear of loneliness caused by separation from a person on whom the sufferer is dependent. Freud’s free-association technique provided him with a tool for studying the meanings of dreams, slips of the tongue, forgetfulness, and other mistakes and errors in everyday life. From these investigations he was led to a new conception of the structure of personality: the id, ego, and superego. The id is the unconscious reservoir of drives and impulses derived from the genetic background and concerned with the preservation and propagation of life. The ego, according to Freud, operates in conscious and precociousness levels of awareness. It is the portion of the personality concerned with the tasks of reality: perception, cognition, and executive actions. In the superego lie the individual’s environmentally derived ideals and values and the mores of family and society; the superego serves as a censor on the ego functions. In the Freudian framework, conflicts among the three structures of the personality are repressed and lead to the arousal of anxiety. The person is protected from experiencing anxiety directly by the development of defense mechanisms, which are learned through family and cultural influences. These mechanisms become pathological when they inhibit pursuit of the satisfactions of living in a society. The existence of these patterns of adaptation or mechanisms of defense are quantitatively but not qualitatively different in the psychotic and neurotic states. Freud held that the patient’s emotional attachment to the analyst represented a transference of the patient’s relationship to parents or important parental figures. Freud held that those strong feelings, unconsciously projected to the analyst, influenced the patient’s capacity to make free associations. By objectively treating these responses and the resistances they evoked and by bringing the patient to analyze the origin of those feelings, Freud concluded that the analysis of the transference and the patient’s resistance to its analysis were the keystones of psychoanalytic therapy. Early schisms over such issues as the basic role that Freud ascribed to biological instinctual processes caused onetime associates Carl Jung, Otto Rank, and Alfred Adler to establish their own psychological theories. Other influential theorists, including some who introduced significant departures from Freudian theory or technique, included Melanie Klein, Karen Horney, Ronald Fairbairn, Harry Stack Sullivan, Donald Winnicott, Erich Fromm, Erik Erikson, and Heinz Kohut. At one time psychiatrists held a monopoly on psychoanalytic practice, but later nonmedical therapists also were admitted to psychoanalytic training institutes. Later developments included work on the technique and theory of psychoanalysis of children, pioneered by Klein and Anna Freud, Sigmund Freud’s daughter. The Freudian tripartite division of the mind into id, ego, and superego became progressively more elaborate, problems of anxiety received increasing attention, and explorations of female sexuality were undertaken. Psychoanalysis also found many extraclinical applications in other areas of social thought, particularly anthropology and sociology, and in literature and the arts. Source: Brittanica (2023)

Key Takeaways Complex PTSD is not formally recognized in DSM-5-TR, affecting clinical understanding and treatment development. Historical events, like the Vietnam War and women's rights movements, influenced PTSD's diagnostic evolution. Only two medications are FDA-approved for PTSD, highlighting the need for more treatment options. Clinicians should prioritize trauma screening and education to improve patient care and treatment outcomes. "This was a tragic exclusion,” wrote Bessel van der Kolk, MD, one of the world’s experts in posttraumatic stress disorder (PTSD), following the publication of DSM-IV in 1994 when it failed to include a new diagnosis of complex PTSD . Yet here we are, 30 years and 3 DSMs later, with no formal or professional recognition of complex PTSD as a very different disorder than what DSM-5-TR describes for PTSD. In fact, DSM-5-TR provides only 2 specifiers to further differentiate PTSD: PTSD with dissociative symptoms (depersonalization vs derealization) and PTSD with delayed expression (ie, “the full diagnostic criteria are not met until at least 6 months after the event”). This misstep has had a cascading impact on the lack of clinical understanding of the complexities and differences in symptoms that can result from the experience of different types of trauma. Additionally, it has created a cloud of confusion regarding the PTSD diagnosis , which in turn results in the lack of tools and treatments that should be utilized in subpopulations of individuals with varying trauma histories. Finally, the vagueness of the DSM’s characterization of trauma has likely prolonged the considerable unmet need of additional pharmacological treatments. It is possible that if the US Food and Drug Administration Advisory Board had a more comprehensive understanding of the effects of different types of trauma and the wide range of treatments that should be available, it would have reached a different conclusion when it recommended against approval of midomafetamine (MDMA)–assisted psychotherapy this past June. Notably, the 2 phase 3 studies submitted to the FDA primarily included individuals who likely would have met the diagnostic criteria for complex PTSD; all participants in one of the studies met the criteria for severe PTSD, and 73% of participants in the second. Exploring the Evolution of PTSD in Psychiatry In 1896, Sigmund Freud, MD, published “The Aetiology of Hysteria,”4 in which he hypothesized that hysteria was caused by the sexual abuse of children before the onset of puberty based on his analysis of 18 adult patients with hysteria who reported a history of childhood sexual abuse and incest; this became known as the seduction theory. When Freud presented this paper at Vienna’s Society for Psychiatry and Neurology, he received a cold reception from the audience. His colleague who presided over the presentation characterized the paper as “a scientific fairy tale.” Due to continued criticism from his medical and psychiatric colleagues, he publicly retracted the seduction theory by 1905. During World Wars I and II, millions were exposed to horrific warfare. Soldiers were particularly impacted and reported loss of memory and ability to feel. It was reported that during World War I, 40% of British battle casualties were due to “mental breakdowns.” Shell shock was the term used to describe what had caused the severe emotional distress of soldiers. Trauma expert Judith Herman, MD, wrote, “It was recognized for the first time that any man could break down under fire and that psychiatric casualties could be predicted in direct proportion to the severity of combat exposure.”5 Herman further wrote about how “the lasting effects of war trauma were once again forgotten,” shortly after World War II. During the 1960s and 1970s, the Vietnam War facilitated an upheaval throughout the US after Americans witnessed via television the horrific nature of war and gained a growing awareness of the impact of these violent experiences on individuals. Veterans who were traumatized—often decorated war heroes—would not let us forget. Vietnam veterans organized groups to support one another. In 1970, psychiatrists met with a veteran-formed group called Vietnam Veterans Against the War and saw firsthand the effects of combat trauma exposure. Coinciding with the activism of the Vietnam veterans, the country also saw a new wave of the women’s rights movement. In 1970, the 50th anniversary of suffrage, people participated in the Women’s Strike for Equality, the largest women’s rights demonstration since suffrage. This demonstration raised national awareness on many issues related to women’s rights, health, safety, and equality. In 1973, the National Organization for Women (NOW) started the NOW Task Force on Rape, advocating for legal reform at the state level. The convergence of this activism likely had a significant impact on updating and revising 1968’s DSM-II. In 1980, DSM-III was introduced with the new diagnostic entity “posttraumatic stress disorder.” Significantly, PTSD was clustered under the category of “anxiety disorders” from 1980 until the publication of DSM-5 in 2013. It was then separated into a new category titled “trauma- and stress- or related disorders,” where it remains today. The Diagnosis of ‘PTSD’ Is Too Nonspecific With the DSM-III acknowledging the primary role of trauma in psychological distress, the symptoms of PTSD, and as a common etiological primary factor contributing to other psychiatric and medical comorbidities, trauma-related research exploded. Experts in trauma-related disorders, including van der Kolk and Herman, quickly recognized the limitations of a single and generally defined diagnosis for individuals’ experiences and the life-altering impact of those experiences, either immediately after the trauma occurred or decades later. In the early 1990s, van der Kolk was put in charge of a field trial by Robert Spitzer, MD, as revisions to DSM-III were being considered to produce DSM-IV. The field trial used a rating scale incorporating the many trauma symptoms found in the medical literature; the scale was administered during the interviews with 525 adult patient participants across the US. The goal was to investigate whether subpopulations with differing traumatic exposures demonstrated clinically different symptoms. The study populations included adult patients who had been physically or sexually abused in childhood by their caregivers, adult patients who were victims of recent domestic violence, and adult patients who had recently experienced a natural disaster. Significantly, the adults who had been abused in childhood by their caregivers demonstrated very different symptoms in adulthood than the other groups. A previous study by van der Kolk et al demonstrated that a history of sexual or physical abuse in childhood was a strong risk factor for recurrent self-cutting and suicide attempts later in life.8 The authors hypothesized that early-life severe trauma instills a feeling of lack of safety with others, leaving a lacuna in the structure of the self in contrast to the other subpopulations that had a template for feeling safe from long ago that could be accessed again through healthy adult relationships or therapy. Upon completion of this field trial, van der Kolk’s DSM-IV PTSD work group voted 19 to 2 to create a new diagnosis for patients with significant symptoms resulting from severe interpersonal trauma. They recommended the addition of the diagnosis “disorders of extreme stress, not otherwise specified,” also known as “complex PTSD,” to the DSM-IV.9-12 To their surprise and disappointment, their recommendation was ignored; no one in the PTSD work group was consulted. Conclusion The good news is that much progress has been made in developing evidence-based nonpharmacological treatments (Table 2). Although only 2 medications are approved by the FDA for treating PTSD (the selective serotonin reuptake inhibitors sertraline [Zoloft], approved in 1999, and paroxetine [Paxil], approved in 2000), 2 agents with very different mechanisms of action are in the review process. Garnering recent press is MDMA, which is meant to be used as part of structured medication-assisted psychotherapy; the FDA requested an additional phase 3 study. Brexpiprazole (Rexulti; FDA vote on approval is expected on February 8, 2025) is meant to be used as an augmentation agent for patients already on sertraline who only partially respond to treatment. As clinicians, we can and should educate ourselves further about the important and complex field of trauma and its treatment. Screening for past trauma in new and established patients is essential. It may take months, years, or even decades before our patients with a significant history of trauma, especially early-life trauma, develop enough trust to share their story with us. Yet past trauma is likely a contributing factor in many patients who present with anxiety, depression, substance use disorders, and many somatic complaints or diagnoses. The aforementioned book by van der Kolk1 comprehensively reviews what we have learned since 1980, and I highly recommend it as a good starting point. Often, our patients don’t know what to say or how to start to talk about their trauma. They are quietly waiting for us to begin the conversation. Note: This article originally appeared on Psychiatric Times .

Older adults at risk for dementia can be identified using mobile data obtained during a wayfinding task, a novel real-world study suggested. During a smartphone-assisted scavenger hunt on a university campus, researchers observed that older adults with subjective cognitive decline (SCD) paused more frequently, likely to reorient themselves, than those without SCD. This behavior served as an identifier of individuals with SCD. "Deficits in spatial navigation are one of the first signs of Alzheimer's disease," study investigator Nadine Diersch, PhD, guest researcher with the German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany, told Medscape Medical News. This study, said Diersch, provides "first evidence of how a digital footprint for early dementia-related cognitive decline might look like in real-world settings during a short (less than 30 minutes) and remotely performed wayfinding task." The study was published online on October 3 in PLOS Digital Health . Trouble With Orientation Seventy-two men and women in their mid-20s to mid-60s participated in the study; 23 of the 48 older adults had SCD but still scored normally on neuropsychological assessments. All study participants were instructed to independently find five buildings on the medical campus of the Otto-von-Guericke-University Magdeburg, Magdeburg, Germany, guided by a smartphone app developed by the study team. Their patterns of movement were tracked by GPS. All participants had similar knowledge of the campus, and all were experienced in using smartphones. They also practiced using the app beforehand. In most cases, participants reached the five destinations in less than half an hour. The younger participants performed better than the older ones; on average, the younger adults walked shorter distances and generally did not use the help function on the app as often as the older ones. In the older adults, the number of orientation stops was predictive of SCD status. The adults with SCD tended to hesitate more at intersections. A decline in executive functioning might explain this finding, Diersch said. "Intact executive functioning is an important component of efficient navigation, for example, when switching between different navigation strategies or planning a route. However, since this was the first study on that subject, more research is needed to determine the precise contribution of different cognitive processes on digital wayfinding data," said Diersch. With more study, "we think that such a smartphone-assisted wayfinding task, performed in the immediate surroundings, could be used as a low-threshold screening tool — for example, to stratify subjects with regard to the need of extended cognitive and clinical diagnostics in specialized care," she added. 'A Game Changer' Commenting on the research, Shaheen Lakhan, MD, PhD, neurologist and researcher based in Miami, Florida, who wasn't involved in the research, said the findings have the potential to "revolutionize" dementia care . "We've seen smartphones transform everything from banking to dating — now they're set to reshape brain health monitoring. This ingenious digital scavenger hunt detects cognitive decline in real-world scenarios, bypassing costly, complex tests. It's a game changer," said Lakhan. "Just as we track our steps and calories, we could soon track our cognitive health with a tap. This isn't just innovation; it's the future of dementia prevention and care unfolding on our smartphone screens. We're not just talking about convenience. We're talking about catching Alzheimer's before it catches us," he added. The next phase, Lakhan noted, would be to develop smartphone apps as digital therapeutics, not just to detect cognitive decline but to treat or even prevent it. "Imagine your phone not only flagging potential issues but also providing personalized brain training exercises to keep your mind sharp and resilient against dementia," Lakhan said. This work was funded by the Deutsche Forschungsgemeinschaft (German Research Foundation) within the Collaborative Research Center "Neural Resources of Cognition" and a DZNE Innovation-2-Application Award. Diersch is now a full-time employee of neotiv GmbH. Lakhan had no relevant disclosures. Note: This article originally appeared on Medscape .

Key Point: The context and timing of symptoms is critical for a timely and accurate bipolar diagnosis. CLINICIAN’S CORNER “Knowledge without context is confusion.” -Chuck D, Public Enemy Understanding the context and timing of symptoms is critical to making a timely and accurate bipolar diagnosis. Unfortunately, the context and timing of symptoms are often overlooked. The delay from onset of symptoms to bipolar diagnosis is 10 years on average. This underdiagnosis or delay of diagnosis of bipolar has often been made when the person's index presentation for psychiatric evaluation is during a depressive episode. Every person presenting with symptoms of depression must be, at a minimum, evaluated for previous symptoms of mania or hypomania (occurring in the absence of substance use) and familial history of bipolar illness. Understanding the broader context of the person's presentation and not accepting depressive symptoms at face value can reduce diagnostic errors and delays in appropriate medication management. Underdiagnosis and overdiagnosis of bipolar illness can both be attributed to inadvertently dismissing or attributing symptoms that occur during teen years and early 20s (the average age of onset for bipolar illness) as developmentally normal. It is important to determine that the presenting symptoms are a stark change from baseline.1 Late adolescence and early adulthood are times when impulsivity, irritability, risk-taking, poor sleep, and recreational substance use are pervasive. Data are trending towards a recent phenomenon of overdiagnosis of bipolar illness in certain settings.2-4 Anecdotally, some argue that the increase is not due to incorrect diagnosis or overdiagnosis, but an increase in appropriate screening. Others have balked at the increase and attributed the trend to undue patient influence via Google and wholesale misdiagnosis. Although not diagnostic, validated screening instruments can help frame the conversation of presenting symptoms and ensure that important context is not overlooked. Screenings are not diagnostic. In psychiatry, clinicians often fall into 2 categories: those who use validated screening instruments and those who do not. Research indicates that less than 20% of behavioral health practitioners utilize measurement-based care.5 The low utilization of rating scales is multi-factorial. It includes provider concerns for patient confidentiality, competing requirements of insurance and medical records, and a belief that clinical judgment is suitable.5 Using clinical judgment alone, providers detected early deterioration in only 21.4% of patients.6 Clinical incorporation of measurement-based care may reduce deterioration by 4% to 8% and improve positive outcomes.7 Self-report patient assessments are a valuable tool, but these rating scales must be seen as the first step in a 2-stage process. If the screening is positive, a more definitive and extensive evaluation is warranted. A good screening instrument will detect almost all patients with the disorder (high sensitivity) and rule out the disorder for almost all patients who screen negative (high negative predictive value). While high specificity or high positive predictive value is less critical for screening, an effective screener helps clinicians identify almost all patients who need further evaluation for the disorder. To reduce false positive diagnoses, clinicians must uphold screening as a 2-stage process. In busy clinical practices, it is tempting to take a positive screener as diagnostic confirmation. One of the great challenges for patients and clinicians alike is the prevalence of cooccurring substance use for those living with bipolar illness. Current literature has a prevalence of cooccurring substance use ranging from 30% to 50%.1,8 If we can ascertain that the timing and context of symptoms were present before the substance use then the bipolar diagnosis is not complicated to make; however, the timing and context are often not so clearly defined. Further, other differentials and comorbidities such as borderline personality disorder and attention-deficit/hyperactivity disorder (ADHD) must also be ruled out. There are other contextual clues that can further inform our differential in the absence of clear history of manic or hypomanic features. A few scenarios that would prompt medication management consistent with the treatment for bipolar illness rather than unipolar depression (mood stabilizers and dopamine receptor blocking agents vs SSRI/SNRI), despite not meeting all DSM-5 diagnostic criteria: Patient has the genetic pedigree of multiple first and second-degree relatives with type 1 bipolar illness and reports the first onset of depression at age 8 in the absence of any lifetime trauma, bullying, or loss. Patient has a history of postpartum depression and an immediate response (within 48 hours) to an SSRI. That is not to say that these scenarios then rate a bipolar diagnosis; they do not. The patient must continue to be followed, and the longitudinal monitoring of symptoms noted. The context suggests that there is high suspicion for bipolar illness and the patient would likely benefit from a more nuanced approach to their medication management. Reducing false positives in the diagnosis of bipolar disorder requires careful consideration and implementation of key principles. Although bipolar disorder carries distinct diagnostic criteria, clinicians may misdiagnose a patient due to phenomenological overlap with other symptoms. For instance, patients misdiagnosed with bipolar disorder are more likely to carry features of borderline personality disorder. A comprehensive assessment, utilizing a semi-structured clinical interview remains the gold standard for the diagnosis of bipolar disorder. However, busy clinicians may have to balance thorough clinical assessments against practice settings with limited time and resources. Self-report rating scales can help clinicians identify patients who require a more thorough assessment. Another key principle in reducing the misdiagnosis of bipolar disorder is to reject the pressure to assign a bipolar diagnosis immediately. Mania/hypomania is rarely an index presentation in bipolar disorder. This means that most patients will present in psychiatric clinics with complaints of depression that are indistinguishable from unipolar depression. Longitudinal monitoring of patients’ symptoms can provide clarity of diagnosis. For example, if the patient’s cognitive complaints are persistent regardless of affective state, this may suggest a comorbid psychiatric diagnosis while cognitive dysfunction within the context of a mood episode may be suggestive of bipolar illness. Lastly, clinicians should take care to remember that medication response is not diagnostic. Often, clinicians may update a diagnosis based on a response to a new medication class. For example, a positive response to lithium augmentation in a refractory depression may tempt a new diagnosis of bipolar disorder in light of this positive response. Lithium and second-generation antipsychotics are effective augmenting agents in unipolar depression.10 Clinicians may also be tempted to convert to a bipolar diagnosis if a patient experiences irritability or agitation with an antidepressant trial. The use of antidepressants does not convey any diagnostic implications unless the patient experiences a manic switch.11 One of the more significant updates to bipolar diagnostic criteria between the DSM-IV to DSM-5 is the inclusion of antidepressant-induced mania as diagnostically sufficient provided that it is temporal and persists at a fully syndromal level.12 An antidepressant-induced manic episode is one of the few circumstances where a diagnostic change is informed by medication response. Just as bipolar disorder is both overdiagnosed and underdiagnosed, psychiatry has a similar relationship with diagnostic fidelity. In school, students are often taught a rigid adherence to diagnostic criteria, but early career clinicians frequently enter a clinical environment of ambiguity, symptom overlap, and diagnostic uncertainty. Early career clinicians must understand how diagnosis informs treatments, prognosis, and nearly every other aspect of care. Psychiatry remains a field of syndromes, meaning a group of signs and symptoms with known associated features that characterize a particular disorder. In the absence of biomarkers or other definitive testing, a careful and accurate diagnosis remains one of the most critical components of psychiatry. There has been increasing awareness and attention spent on the underdiagnosis of bipolar disorder. A delay in bipolar diagnosis may contribute to many adverse outcomes. However, our efforts to increase awareness of bipolar disorder must not overcorrect. Overdiagnosis of bipolar disorder poses significant challenges in mental health care , leading to inappropriate treatment and mismanagement of other underlying conditions. By understanding the limitations of screening instruments, recognizing the impact of comorbidities, and adhering to key principles in diagnostic assessment, clinicians can improve diagnostic accuracy. A careful and nuanced approach ensures that individuals receive appropriate and effective care, tailored to their specific needs. Note: This article originally appeared on Psychiatric Times .

TOPLINE: Older adults who experience falls are at a higher risk of developing dementia within a year. The study found that 10.6% of patients who fell were diagnosed with dementia compared with 6.1% with other injuries. METHODOLOGY: Researchers conducted a retrospective cohort study using US Medicare Fee-for-Service data from 2014 to 2015, including follow-up data for at least 1 year after the index encounter. A total of 2,453,655 older adults aged 66 years or older who experienced a traumatic injury were included, with 50.1% of injuries resulting from falls. The primary outcome was the diagnosis of dementia within 1 year after experiencing a fall, identified using International Classification of Diseases, Ninth Revision (ICD-9) and ICD-10 codes and analyzed using a Cox multivariable competing risk model. Covariates included patient demographics, Charlson Comorbidity Index, prior skilled nursing facility admission, injury severity, presence of head or neck trauma, surgery for hip fracture, and diagnosis of delirium during the index encounter. TAKEAWAY: Falls were associated with a 21% increased hazard of new dementia diagnosis compared with other injury mechanisms (hazard ratio [HR], 1.21; 95% CI, 1.20-1.21; P < .001). In older adults without a recent skilled nursing facility admission, falls were associated with a 27% increased hazard of new dementia diagnosis (HR, 1.27; 95% CI, 1.26-1.28; P < .001). The overall rate of incident dementia diagnosis was higher in patients with an inpatient admission than in those with an emergency department visit (12.2% vs 7.5%; P < .001). Delirium during the index encounter was associated with an increased risk for future dementia diagnosis (HR, 1.66; 95% CI, 1.64-1.69; P < .001). IN PRACTICE: "Implementing cognitive screening after injurious falls in older adults may aid in the timely diagnosis of dementia, which would allow patients and their families to plan for the future, implement supports to promote ongoing safety in the community, and gain access to treatments," the authors wrote. LIMITATIONS: This retrospective, observational study limited the ability to draw causal conclusions. The transition from ICD-9 to ICD-10 codes may have affected the accuracy of coding injury mechanisms. The sensitivity of identifying dementia diagnoses using Medicare claims is low, which may have potentially missed preexisting diagnoses. The low rate of delirium during the index encounter may have been due to inaccurate coding or failure of recognition. The data from 2014 to 2015 may not have reflected current trends, but the underlying association is unlikely to have changed. Note: This article originally appeared on Medscape .

COPENHAGEN, Denmark — A higher cumulative genetic burden for depression is associated with an increased risk for relapse and worsening disability in people with multiple sclerosis (MS), early results of a new study showed. Unlike the previous research, the current analysis used polygenic risk scores for depression, which summarize the estimated effect of genetic variants to determine the potential association with MS disease activity, so results are less likely to be explained by reverse causality. This study increases awareness of the link between depression and MS, study investigator Kaarina Kowalec, PhD, assistant professor, College of Pharmacy, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Manitoba, Canada, told Medscape Medical News. "We're starting to understand how depression affects relapses and disability progression in MS," she said. The findings were presented on September 20 at the 40th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) 2024. Common Comorbidity Depression is a common comorbidity in patients with MS and is associated with increased relapse and disability progression. Depression risk is partly polygenic in nature, involving numerous common genetic variants, said Kowalec. The case-control study included 3420 relapsing-onset MS cases of European ancestry from four existing cohorts in three countries. The Canadian cohort included those enrolled in a prospective longitudinal study of psychiatric comorbidity in chronic immune-mediated inflammatory disease (IMID), including MS; the Swedish cohort was an MS registry (SSReg) that encompasses 64 MS clinics (the cohort was split into two groups); and the US cohort was enrolled in a clinical trial of combined therapy with interferon and glatiramer acetate (CombiRx) in patients with MS. The median follow-up in these cohorts ranged from 3 to 5 years. Not surprisingly, most participants were women (from 71% in one of the Swedish cohorts to 83% in the Canadian cohort), and the age at MS onset ranged from 29 years in the Canadian cohort to 35 years in one of the Swedish cohorts. The median baseline Expanded Disability Status Scale (EDSS) score was higher in the Canadian cohort (3.5) than in the Swedish (1.5) and US (2.0) cohorts, "reflective of the Canadian cohort being slightly more progressed," said Kowalec. Inherited Variants To measure depression heritability, researchers generated a polygenic risk score in whole-genome imputed genotypes. The score reflects the number of inherited common genetic variants, weighted by effect sizes. Researchers investigated the association between depression polygenic risk scores (top 20% vs bottom 80%) with annualized relapse rate and worsening disability in MS measured by the rate of change in EDSS score. In the US cohort, they also explored the association between depression polygenic risk scores and time to relapse and confirmed EDSS worsening. Covariates included use of disease-modifying therapy, age, sex, and the first five genetic ancestry principal components. The latter was done to capture residual stratification by genetic ancestry, although Kowalec stressed analyses were done only in those of European ancestry. Investigators found a higher depression polygenic risk score was associated with relapse risk (incident rate ratio, 1.23; 95% CI, 1.01-1.49). "Essentially, for every one standard deviation increase in the depression polygenic score, we found a significant increased hazard of 23% for experiencing a relapse over the follow-up period," said Kowalec, who is also affiliated with the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. She noted the Canadian cohort did not have many relapses, while the US and Swedish cohorts "had an increased rate." Other analyses examined the risk of having a relapse or worsening disability. Every one SD increase in the depression polygenic risk score was significantly associated with a 2.2 greater risk of experiencing relapse (hazard ratio [HR], 2.20; 95% CI, 1.35-3.60) and a 51% increased risk for confirmed EDSS progression (HR, 1.51; 95% CI, 1.03-2.22). 'An Ideal Marker' Use of polygenetic risk scores reduces the possibility of reverse causation, noted Kowalec. "These markers are fixed at birth and don't change over your lifespan, so they're really an ideal marker." The results suggest polygenetic risk scores represent a potential biomarker for risk stratification in people with MS, said Kowalec. Although depression polygenic risk scores are not currently available in clinical practice, "I would hope this would change in the next 3-4 years," she said. Asked by a delegate if confounding by a third variable is possible, Kowalec said because genetic markers don't change over time, there is a hint that the direction is causal and that depression is driving the outcome. However, she added, further confirmation is needed. Kowalec noted that there were no data on antidepressant use but noted that about half of the Canadian and US cohorts — and likely the same number in the Swedish cohorts — self-reported depression. A limitation of the study was that it included only participants of European ancestry. Commenting on the research for Medscape Medical News, Lauren Gluck, MD, program director, Montefiore Multiple Sclerosis Center, Bronx, New York, described the study as "fascinating" but noted that it's unclear how to use this new information in clinical practice. "Clinicians frequently ask people with MS about mood symptoms and offer interventions like antidepressants and referrals to therapists. However, genetic testing is not routine, so we don't yet know who to target based on these data." Preexisting depression or more severe depression could be viewed as a "red flag" for risk for more disease activity in the future, she said. "This could encourage clinicians to use more highly effective therapy in these patients, similar to our strategies for people with MS with frequent attacks and more disease burden on MRIs." Note: This article originally appeared on Medscape .