Key Takeaways Antipsychotics are frequently prescribed off-label for children, despite limited long-term efficacy data and potential adverse effects, including metabolic and neurological issues. Comprehensive assessment and nonpharmacological approaches should precede antipsychotic use, with careful monitoring and consideration of tapering when possible. Short-term antipsychotic use can stabilize symptoms, but long-term use requires regular evaluation of benefits versus risks, with a focus on minimizing dosage. Medication substitution with less toxic alternatives should be considered, especially when adverse effects are present or when tapering is unsuccessful. “Bridget,” a 15-year-old girl, is referred by her foster care case manager for continued aggression. She has diagnoses of attention-deficit/hyperactivity disorder (ADHD), conduct disorder, and posttraumatic stress disorder (PTSD) related to sexual abuse she experienced in a stepfamily setting from 9 to 12 years of age. Her mother is receiving inpatient behavioral health care in an extended stay program. Bridget’s father is not available, and her 2 younger siblings are in different foster care settings. Bridget is currently prescribed risperidone 3 mg daily, methylphenidate extended-release 54 mg daily, and clonidine immediate-release 0.2 mg nightly. Approximately 1% of children aged 7 to 12 years and 1.5% of individuals aged 13 to 18 years are prescribed antipsychotic medications, according to findings from a study. These medications are sometimes US Food and Drug Administration (FDA) approved for conditions such as schizophrenia, bipolar disorder, and irritability associated with autism.2 However, approximately 65% of antipsychotic medications for children and adolescents are prescribed for off-label uses, including managing aggression, agitation, disruptive behaviors, and irritability as well as adjunct treatment for ADHD.3 Although there are limited data on the long-term effectiveness of these medications, research has shown that they can lead to a reduction in neuronal tissue and various neurological and metabolic adverse effects.4 Additionally, high doses of antipsychotics have been linked to increased mortality rates in this age group. This article expands on our previous work and discusses the appropriate duration for antipsychotic use and strategies for safely tapering or discontinuing them. First Things First: Is There a Need? Although frank psychosis and bipolar mania remain clear indications for use or consideration of dopamine receptor 2 (D2)–blocking antipsychotic medications, in these circumstances and in all other cases, a comprehensive assessment is warranted to clarify the diagnoses and options for addressing the symptoms. For example, the differential diagnosis for an agitated teenager with seemingly mixed mania may include malignant catatonia, for which antipsychotic medication is generally contraindicated, as it is likely to exacerbate the condition. This is particularly more common in patients with autism. Another more common concern is aggression associated with ADHD; Blader found that well-crafted trials of stimulant medications (eg, first trying methylphenidate and then trying dextroamphetamine) were effective for managing aggression in approximately 60% to 80% of young patients. Given the potential severity of metabolic and neurologic adverse effects of antipsychotic medications, we wrote treatment algorithms to begin with nonpharmacological approaches and treatment of co-occurring conditions before approaching the use of antipsychotics. We also made recommendations for monitoring patients during their use and, once patients are stable, looking at whether, when, and how these medications might be discontinued. How Well Do Antipsychotics Work? Antipsychotics can be beneficial for short-term stabilization, such as preventing psychiatric hospitalization, helping a student remain in a less restrictive school environment, and reducing aggression or self-harming behaviors. However, the evidence does not strongly support their use in treating severe ADHD or oppositional defiant disorder.13 Even in cases where there is FDA approval, such as for managing irritability in autism, it is important to assess whether the patient meets the criteria for antipsychotic treatment (eg, aggression, self-injury, severe mood instability) and whether other approaches might be effective. This could include addressing sensory or communication challenges or considering medications with a safer adverse effect profile. For How Long Should They Be Used? The use of antipsychotic medications in children has primarily been studied and approved by the FDA for short-term treatment, generally up to 6 months.14 There is limited research on the long-term benefits and adverse effects of antipsychotic use in children.15 Concerns commonly associated with antipsychotic medications include the following: Metabolic effects (such as weight gain, diabetes, and hyperlipidemia) Somnolence Prolonged corrected QT interval Elevated prolactin levels Extrapyramidal symptoms Neuroleptic malignant syndrome How long should you use these medications? It will not always be possible to reduce D2-blocking antipsychotic medications, because some patients have symptoms related to psychosis or affective conditions that do not respond to other approaches and where the benefits of continuing the medication outweigh the risks, perhaps keeping the patient safe and/or functioning. We recommend that you use them with an intent to reduce and discontinue their use whenever and however possible, such as when an episode of mania has passed, when you can build a more robust therapy or community plan to support the patient, or when you can substitute less toxic medications, such as antiepileptic drugs for mood stability or stimulant medications for aggression in ADHD, as noted previously. Given these considerations, how do we minimize the use of D2-blocking antipsychotic medications? Start With Discontinuation in Mind When initiating antipsychotic medication, it is crucial to consider the end goal from the start. As part of the informed consent process, discuss the intended duration of treatment with patients and their families. Important topics to cover include the following: The severity of symptoms The natural progression of the condition The child’s age The response to other psychosocial treatments Since there is no set duration for antipsychotic use in nonpsychotic conditions, it is important to monitor the frequency and severity of specific symptoms. Collaborate with patients and families to determine the desired level and duration of improvement that would justify tapering or discontinuing the medication. As a possible guideline, when we use selective serotonin reuptake inhibitors (SSRIs) for depression, we like to see at least 6 to 12 months of remission before we consider tapering and to look at any seasonal or stress-related aspects such as fall/winter effects, school-related stress, or even loss of school structure. Still, the treatment period should be as brief as possible for most clinical situations in children and adolescents. When to Reduce Antipsychotics? At each appointment, discuss the ongoing treatment plan with the patient and their family, focusing on the following: How much improvement has occurred since the initial symptoms? Are there concerning adverse effects (eg, weight gain, elevated cholesterol level, drowsiness, involuntary movements)? How well is the patient adhering to the medication regimen and required monitoring? Are the patient and family open to the idea of tapering the medication? Tapering may not be feasible for patients with primary psychotic disorders or severe mood instability or those with previous failed tapering attempts. If there are ongoing symptoms, take another look at the differential diagnosis and possible treatment options. You do not want to continue ineffective treatment with potentially severe adverse effects. In any case, if you are continuing the medication, you should document the reasons for doing so and consistently monitor for metabolic and movement-related adverse effects. Refer to the American Academy of Child and Adolescent Psychiatry’s Practice Parameter for the Use of Atypical Antipsychotic Medication in Children and Adolescents for monitoring guidelines.17 When you take over care for patients already taking antipsychotic medications, reassess the decision to continue them during your evaluation. For patients on long-term antipsychotic treatment, revisit this discussion every 6 months to evaluate whether continuing the medication remains the best option, considering its effectiveness and potential adverse effects. Begin these conversations by asking patients and families what they perceive as the benefits and drawbacks of the medication. How Slow Should You Go? Tapering does not necessarily mean discontinuing the medication entirely. Even minor dose reductions can help alleviate adverse effects such as elevated cholesterol level or weight gain and lower the risk of neurological adverse effects, such as tardive dyskinesia.18 Once you and your patient agree to taper, consider the following strategies: This is ideal for straightforward cases without co-occurring conditions or a complicated medication history. Ensure at least 3 to 6 months of stability and choose a time without new stressors. Arrange for additional support (eg, therapeutic interventions, school-based services). Reduce the dose by no more than approximately 25% of the original dose every 3 to 6 months or 5% to 10% every 2 months.19 Although there are no clear data to guide the rate of the dosage reduction in children and teenagers, adult research supports very gradual reduction over many months to 2 or 3 years to reduce relapse rates of psychosis in patients who have been on long-term antipsychotic treatment. Consider gradual weekly reductions toward the new dose (eg, recommending the patient take the current dose daily and then substituting the new lower target dose for 1 of 7 days the first week, 2 of 7 days the second week, etc, until every day is at the new lower dose). Schedule regular follow-ups to monitor for any worsening of target symptoms. Bridget is now receiving therapy for her PTSD, and you have stabilized her aggression by shifting her from methylphenidate to dextroamphetamine. However, she is gradually gaining weight, and you decide to reduce her risperidone to 2.5 mg daily using a gradual weekly reduction over 6 weeks. Is Switching Medication an Option? In many situations, you can effectively substitute the antipsychotic or reduce it substantially by using other less potentially toxic medications, such as in the following suggestions: For ADHD with aggression, consider using different kinds of stimulants or even nonstimulant ADHD medications. If there is cooccurring anxiety or irritability, consider trying SSRIs. For behavioral dysregulation or aggression associated with underlying anxiety or autism, explore options such as α agonists or β-blockers. After 6 months, you have reduced Bridget’s risperidone to 0.5 mg daily. Her aggression is well managed, she is making friends, and she is doing better academically, although her appetite and weight have not stabilized. You attempt to discontinue the risperidone altogether, but Bridget becomes far more agitated. Intraclass Medication Substitution When a patient needs to stay on an antipsychotic due to severe symptoms (such as psychosis, self-injury, or mania), consider switching to a more weight-neutral option such as ziprasidone or lurasidone (keeping in mind that insurance coverage might make these medications challenging to start). This approach is also worth considering if a previous antipsychotic trial was unsuccessful or if the patient presents with psychotic symptoms or mania. Offer this alternative if a patient experiences adverse effects that lead to discontinuation of a medication such as risperidone or aripiprazole. Bridget has stability on ziprasidone 20 mg along with the dextroamphetamine and clonidine. Screening and follow-up ECG results are normal, and her weight gain has stabilized. Bridget’s mother is in a step-down psychiatric placement facility, and the family is beginning therapy aimed at possible reunification. Concluding Thoughts Antipsychotics can be lifesaving, but they should only be used when necessary and when accompanied by continuous discussions about the length of treatment and strategies to minimize dosage and adverse effects. Note: This article originally appeared on Psychiatric Times .

A widely accepted assumption in the addiction field is that neuroanatomical changes observed in young people who use alcohol or other substances are largely the consequence of exposure to these substances. But a new study suggests neuroanatomical features in children, including greater whole brain and cortical volumes, are evident before exposure to any substances. Investigators, led by Alex P. Miller, PhD, assistant professor, Department of Psychiatry, Indiana University, Indianapolis, noted that the findings add to a growing body of work that suggests individual brain structure, along with environmental exposure and genetic risk, may influence risk for substance use disorder. The findings were published online on December 30, 2024, in JAMA Network Open . Neuroanatomy a Predisposing Risk Factor? Earlier research showed that substance use is associated with lower gray matter volume, thinner cortex, and less white matter integrity. While it has been widely thought that these changes were induced by the use of alcohol or illicit drugs, recent longitudinal and genetic studies suggest that the neuroanatomical changes may also be predisposing risk factors for substance use. To better understand the issue, investigators analyzed data on 9804 children (mean baseline age, 9.9 years; 53% men; 76% White) at 22 US sites enrolled in the Adolescent Brain Cognitive Development (ABCD) Study that’s examining brain and behavioral development from middle childhood to young adulthood. Researchers collected information on the use of alcohol, nicotine, cannabis, and other illicit substances from in-person interviews at baseline and years 1, 2, and 3, as well as interim phone interviews at 6, 18, and 30 months. MRI scans provided extensive brain structural data, including global and regional cortical volume, thickness, surface area, sulcal depth, and subcortical volume. Of the total, 3460 participants (35%) initiated substance use before age 15, with 90% reporting alcohol use initiation. There was considerable overlap between initiation of alcohol, nicotine, and cannabis. Researchers tested whether baseline neuroanatomical variability was associated with any substance use initiation before or up to 3 years following initial neuroimaging scans. Study covariates included baseline age, sex, pubertal status, familial relationship (eg, sibling or twin), and prenatal substance exposures. Researchers didn’t control for sociodemographic characteristics as these could influence associations. Significant Brain Differences Compared with no substance use initiation, any substance use initiation was associated with larger global neuroanatomical indices, including whole brain (β = 0.05; P = 2.80 × 10−8), total intracranial (β = 0.04; P = 3.49 × 10−6), cortical (β = 0.05; P = 4.31 × 10−8), and subcortical volumes (β = 0.05; P = 4.39 × 10−8), as well as greater total cortical surface area (β = 0.04; P = 6.05 × 10−7). The direction of associations between cortical thickness and substance use initiation was regionally specific; any substance use initiation was characterized by thinner cortex in all frontal regions (eg, rostral middle frontal gyrus, β = −0.03; P = 6.99 × 10−6), but thicker cortex in all other lobes. It was also associated with larger regional brain volumes, deeper regional sulci, and differences in regional cortical surface area. The authors noted total cortical thickness peaks at age 1.7 years and steadily declines throughout life. By contrast, subcortical volumes peak at 14.4 years of age and generally remain stable before steep later life declines. Secondary analyses compared initiation of the three most commonly used substances in early adolescence (alcohol, nicotine, and cannabis) with no substance use. Findings for alcohol largely mirrored those for any substance use. However, the study uncovered additional significant associations, including greater left lateral occipital volume and bilateral para-hippocampal gyri cortical thickness and less bilateral superior frontal gyri cortical thickness. Nicotine use was associated with lower right superior frontal gyrus volume and deeper left lateral orbitofrontal cortex sulci. And cannabis use was associated with thinner left precentral gyrus and lower right inferior parietal gyrus and right caudate volumes. The authors noted results for nicotine and cannabis may not have had adequate statistical power, and small effects suggest these findings aren’t clinically informative for individuals. However, they wrote, “They do inform and challenge current theoretical models of addiction.” Associations Precede Substance Use A post hoc analysis further challenges current models of addiction. When researchers looked only at the 1203 youth who initiated substance use after the baseline neuroimaging session, they found most associations preceded substance use. “That regional associations may precede substance use initiation, including less cortical thickness in the right rostral middle frontal gyrus, challenges predominant interpretations that these associations arise largely due to neurotoxic consequences of exposure and increases the plausibility that these features may, at least partially, reflect markers of predispositional risk,” wrote the authors. A study limitation was that unmeasured confounders and undetected systemic differences in missing data may have influenced associations. Sociodemographic, environmental, and genetic variables that were not included as covariates are likely associated with both neuroanatomical variability and substance use initiation and may moderate associations between them, said the authors. The ABCD Study provides “a robust and large database of longitudinal data” that goes beyond previous neuroimaging research “to understand the bidirectional relationship between brain structure and substance use,” Miller said in a press release. “The hope is that these types of studies, in conjunction with other data on environmental exposures and genetic risk, could help change how we think about the development of substance use disorders and inform more accurate models of addiction moving forward,” Miller said. Reevaluating Causal Assumptions In an accompanying editorial, Felix Pichardo, MA, and Sylia Wilson, PhD, from the Institute of Child Development, University of Minnesota Twin Cities, Minneapolis, suggested that it may be time to “reevaluate the causal assumptions that underlie brain disease models of addiction” and the mechanisms by which it develops, persists, and becomes harmful. Neurotoxic effects of substances are central to current brain disease models of addiction, wrote Pichardo and Wilson. “Substance exposure is thought to affect cortical and subcortical regions that support interrelated systems, resulting in desensitization of reward-related processing, increased stress that prompts cravings, negative emotions when cravings are unsated, and weakening of cognitive control abilities that leads to repeated returns to use.” The editorial writers praised the ABCD Study for its large sample size for providing a level of precision, statistical accuracy, and ability to identify both larger and smaller effects, which are critical for addiction research. Unlike most addiction research that relies on cross-sectional designs, the current study used longitudinal assessments, which is another of its strengths, they noted. “Longitudinal study designs like in the ABCD Study are fundamental for establishing temporal ordering across constructs, which is important because establishing temporal precedence is a key step in determining causal links and underlying mechanisms.” The inclusion of several genetically informative components, such as the family study design, nested twin subsamples, and DNA collection, “allows researchers to extend beyond temporal precedence toward increased causal inference and identification of mechanisms,” they added. Note: This article originally appeared on Medscape .

TOPLINE: About one third of US adults aged 50-80 years report feeling lonely and socially isolated, a new study of data from 2018-2024 shows. While the levels have returned to the pre-pandemic range, investigators say the findings suggest clinicians should screen for loneliness and isolation. METHODOLOGY: Researchers conducted a nationally representative survey of US adults aged 50-80 years through the University of Michigan National Poll on Healthy Aging at six timepoints between 2018 and 2024. Data collection involved online surveys conducted using the Ipsos KnowledgePanel from 2018 to 2021, transitioning to online and phone surveys conducted using the National Opinion Research Center AmeriSpeak panel from 2022 to 2024. Sample sizes ranged between 2051 and 2576 respondents, with completion rates ranging from 61% to 78% across the survey periods. TAKEAWAY: Loneliness rates among adults aged 50-80 years showed notable fluctuation, starting at 34% (95% CI, 31.7%-36.2%) in 2018, rising to 41% (95% CI, 39.1%-43.7%) in 2020, and returning to 33% (95% CI, 31.7%-35.1%) by 2024. Social isolation showed a similar pattern in the study group, starting at 27% (95% CI, 24.5%-28.8%) in 2018, peaking at 56% (95% CI, 53.4%-58.1%) in 2020, and declining to 29% (95% CI, 27.5%-30.9%) by 2024. Higher loneliness and social isolation rates were frequently reported among individuals who did not work, lived alone, had lower household incomes, and had self-reported fair and poor physical and mental health than those who reported excellent, very good, or good health. IN PRACTICE: The findings suggest that “much like routinely asking about diet and exercise, clinicians should consider screening older adults for loneliness and social isolation and connect them with appropriate resources,” the investigators wrote. SOURCE: The study was led by Preeti N. Malani, MD, MSJ, University of Michigan Medical School, Ann Arbor, Michigan. It was published online on December 9 in JAMA. LIMITATIONS: The study was limited by possible recall bias, reliance on self-reported data, lack of longitudinal results, and differences in survey timing, panels, and question framing across years. The findings may not have been applicable to excluded groups such as nursing home residents or individuals aged > 80 years, which limited their generalizability. DISCLOSURES: The study was supported by AARP and Michigan Medicine and the Department of Veterans Affairs, Veterans Health Administration, and Health Systems Research. One author reported receiving consulting fees and honoraria from various organizations. Details are provided in the original article. Note: This article originally appeared on Medscape .

Key Takeaways Neuroplasticity is central to psychiatry, with brain health factors like nutrition and exercise being crucial for its optimization. BDNF is a key intermediary in neuroplasticity, with decreased levels associated with psychiatric disorders. Treatments like psychotherapy, ECT, and certain medications enhance BDNF, promoting neuroplasticity. Medication-assisted psychotherapies using psychoplastogens show promise but face regulatory challenges. A new treatment paradigm is needed in psychiatry to support enduring neuroplastic changes for optimal patient outcomes. As Psychiatric Times celebrates its 40th year, psychiatry’s tapestry is just beginning. The threads that currently exist seem to be weaving into a magnificent fabric that we have named neuroplasticity. Our challenge and opportunity is to optimize all of the threads we currently understand and remain open to the many additional threads that are currently unknown or just beginning to appear. Some of the most important threads that facilitate brain health, which provides a necessary foundation for neuroplasticity to occur, get lost in the Western medical model treatment process, where time is limited and interventions commonly focus on medications and procedures. We know now that the same factors that maximize cardiac health also maximize brain health: healthy blood pressure/cholesterol levels/blood glucose/body mass index, minimal substance use, quality sleep, good nutrition, physical activity, ability to manage stress, and supportive relationships. In addition to these, the brain thrives when it is learning new information, encountering novel experiences, and solving problems. Although certainly not a panacea, neuroplasticity provides hope that we have an inborn ally during our journey toward healing and maximum functioning. The Birth of Neuroplasticity In the 1970s, experimental research that involved severing the afferent neuron of a monkey’s limb just before where it enters the spinal cord to ascend to the brain led to the revolutionary field of neuroplasticity. This research extended into the early 1990s when it demonstrated that the monkey’s brain undergoes cortical remapping and connects to any adjacent active neurons when it ceases receiving input from the deafferented limb. Thus, the neuroplasticity property of the human brain was born. Learning Music as a Model During that early excitement, researchers looked for potential models that could quantify brain changes over time in an activity that required rigorous ongoing training. Researchers hypothesized that musicians provided an ideal model to study brain plasticity by using neuroimaging to monitor brain structure and function before and after a period of intensive training. Another research team reported on structural brain changes in early childhood following 15 months of musical training. Structural changes correlated with improvements in relevant motor and auditory musical skills.3 Similarly, a review of studies looking at changes in brain structure and function in musicians after their musical practice, magnetic resonance imaging demonstrated structural plasticity while neurophysiological activation patterns demonstrated functional plasticity. The authors concluded “experience can shape brain anatomy and brain physiology. BDNF: A Proxy for Neuroplasticity An established intermediary in the process of neuroplasticity is brain-derived neurotrophic factor (BDNF), which is present throughout the peripheral and central nervous systems, especially in the hippocampus and prefrontal cortex. BDNF has been shown to facilitate the maturation, differentiation, and longevity of neurons. One well-established pathway involves a presynaptic glutamate surge. Postsynaptically, this agonizes AMPA-glutamate receptors, which induces production of BDNF. BDNF agonizes tropomyosin-related kinase B receptors, which promote a cascade of molecular events, culminating in increased activity of the mammalian target of rapamycin (mTOR). mTOR serves as the orchestrator of the synthesis of scaffolding proteins and dendritic growth/synaptogenesis. Many psychiatric disorders are associated with decreased levels of BDNF compared with those found in healthy individuals. A growing literature has looked at serum and/or plasma BDNF levels as a proxy for neuroplasticity in patients pre- and post treatment. The strongest data supporting BDNF as a proxy for neuroplasticity comes from research in psychopharmacology, with a growing body of evidence supporting BDNF’s role in psychotherapy. Psychotherapy and Other Treatments Jeffrey Schwartz, MD, a pioneer in demonstrating the ability of cognitive behavior therapy to change brain chemistry without medications in patients with obsessive-compulsive disorder,6 demonstrated a significant bilateral decrease in caudate nucleus metabolic rates of glucose through positron emission tomography after 10 weeks of intensive exposure-response prevention and cognitive behavior therapy treatment, resulting in symptomatic improvement. Subsequent research has supported the hypothesis that psychotherapy can facilitate a rewiring of the brain through the production of increased BDNF. Other investigators have even hypothesized that good quality psychotherapy may facilitate interbrain plasticity between the therapist and patient during their sessions as a result of recurrent exposure to high interbrain synchrony that can lead to enduring neuroplastic changes in the patient that are then activated in relationships outside of therapy. Beyond psychotherapy, there are other treatments that impact neuroplasticity. Electroconvulsive therapy (ECT), one of psychiatry’s oldest treatments, has demonstrated increased BDNF levels in individuals with medication-resistant depression. For most patients, the significant increase in BDNF appeared 1 month after the completion of the ECT. Psychopharmacology One intriguing property of certain psychiatric medications is their effect of increasing BDNF, sometimes as soon as several hours after administration. We are early in understanding the effect on BDNF by specific antidepressants and antipsychotics, although it is well-documented that BDNF plays an important role in depression, bipolar disorder, and psychosis, especially in the hippocampus and the prefrontal cortex. Lithium is an example of such an agent. It has been shown to upregulate BDNF, and chronic treatment with lithium has demonstrated an associated increase in BDNF when administered in therapeutic as well as low doses in both the hippocampal and cortical regions of the brain. Neuroimaging studies have demonstrated an association between long-term lithium treatment and increased gray matter volume in the ventral prefrontal cortex and other brain regions related to cognition and emotional processing. It has also been proposed that chronic lithium treatment in patients with bipolar disorder may delay or decrease the risk of the onset of dementia. Medication-Assisted Psychotherapy Psychoplastogens are a molecularly diverse class of medications that initiate rapid neuronal plasticity via the rapid production of BDNF.16,17 These medications include 3,4-methylenedioxymethamphetamine (MDMA), ketamine, esketamine, psilocybin, and lysergic acid diethylamide (LSD). The downstream effect is increased activity of mTOR. With medication-assisted psychotherapies (MAPs), the psychoplastogens are administered to patients early in treatment and commonly in a small number of doses—usually between 1 and 3—in the presence of the psychotherapist(s) with whom they will work intensively (for up to as many as 15 sessions). Hypothetically, the psychoplastogen (eg, MDMA) increases patients’ access to difficult psychological material, it facilitates a meaningful experience with a strong emotional response (as with psilocybin/LSD), and/or it creates a window of neuroplasticity that can enhance improved functioning of a dysregulated circuit (as with ketamine/esketamine). With all 3 agents, an extended period of neuroplasticity may allow for significant and enduring changes in neuronal connectivity through the intensive psychotherapeutic process that is an integral part of the treatment. (Disappointingly, MAP received a setback in August 2024 when the FDA decided against approving MDMA-assisted psychotherapy and requested an additional phase 3 study.) Conclusion Thirty years ago, the medical profession and neuroscientists believed that the human brain was fully wired at birth. In retrospect this was naive, as we have the ability to learn new information, languages, musical instruments, and technical skills, and adapt to significant changes throughout our lives. Where but in the brain would the capacity for all of this learning, adaptation, and mastery occur? The catch is that it takes time, motivation, practice, and intention for us to orchestrate this neuroplasticity. In my opinion, the current structure of clinical psychiatric practice lacks these qualities, with a focus on the 15-minute medication check as the common standard time spent with a patient. If our treatment goal is to facilitate enduring neuroplastic changes in our patients’ brains, we must create a new treatment paradigm that supports that process. Then we can truly continue to weave our tapestry. Note: This article originally appeared on Psychiatric Times .

Key Takeaways Phantom limb syndrome is explained by cortical remapping, where the brain reassigns sensory inputs to adjacent areas post-amputation. Edward Taub's Constraint-Induced Movement Therapy (CIMT) promotes neuroplasticity, aiding recovery in stroke patients by constraining healthy limbs. Functional MRI studies confirm increased brain activity in areas associated with improved function, supporting the effectiveness of CIMT. Neuroplasticity enables the adult nervous system to reorganize post-lesion, enhancing rehabilitation outcomes and shifting paradigms in neurorehabilitation. After reading about cortical remapping of the monkey’s brain, neurologist V.S. Ramachandran, MD, PhD, surmised that a similar phenomenon may explain the baffling syndrome of phantom limb, which had befuddled medical researchers and clinicians alike since it was first described by Silas Weir Mitchell, MD, shortly after the Civil War. Ramachandran examined a 17-year-old adolescent who had his left arm amputated 3 weeks prior in a motor vehicle accident and reported that it felt as if this arm was still present. Having the patient keep his eyes tightly closed, Ramachandran brushed the patient’s left cheek with a cotton swab in various locations. Upon asking the patient where he felt the sensations, the patient noted it was on his left cheek, but also on his amputated hand, thumb, and index finger. Remarkably, the patient reported that when he felt an itch on his phantom palm, he felt relief by scratching his lower face. Ramachandran hypothesized that this patient’s brain had cortically remapped the postamputation silent somatosensory cortex on the postcentral gyrus associated with the left hand to the adjacent incoming neurons from the facial nerve. It is well established that the area of the postcentral gyrus that maps to the left hand borders the area that maps the left face. This was a concrete example of neuroplasticity in action. In the 1980s, Edward Taub, PhD, the chief scientist at the Institute for Behavioral Research in Silver Spring, Maryland, developed a hypothesis based on his research with monkeys: If the innervation of 1 arm was seriously damaged but the healthy arm was constrained so it could not be used to accomplish necessary tasks, the possibility existed for the patient to regain function in the damaged arm with structured physical therapy. During the 1990s this hypothesis was proven by research in post cerebral vascular accident (CVA) using a technique called Constraint-Induced Movement Therapy (CIMT). In a review article that detailed the clinical applications in humans that had thus far been established, the authors wrote, “Research from several laboratories has shown that the adult nervous system can reorganize after a lesion,” concretizing the paradigm shift toward human neuroplasticity. Also in 2002, researchers leveraged functional magnetic resonance imaging to confirm an increase in brain activity in the cortical area involved in the increased function. Using functional magnetic resonance imaging technology, patients who engage in this [CIMT] therapy have been shown to have increased activity in their contralateral premotor and secondary somatosensory cortex in association with improved function. A 2011 review on the management of CVAs summarized the research demonstrating the role of neuroplasticity in rehabilitation from strokes, and the effectiveness of CIMT. Note: This article originally appeared on Psychiatric Times .

Key Takeaways Cannabis-induced psychosis complicates criminal responsibility, with settled insanity as a potential defense if symptoms persist beyond intoxication. Legal standards for insanity and diminished capacity vary by jurisdiction, affecting the applicability of voluntary intoxication as a defense. Understanding the relationship between substance use and mental health is crucial for forensic evaluations, especially with increasing cannabis prevalence. Case Study “John,” a 25-year-old man with no prior criminal history, was arrested after breaking into a convenience store in the middle of the night and assaulting the clerk with a knife. Witnesses reported erratic and violent behavior, including shouting about being chased by invisible enemies. Upon arrest, John was incoherent, disoriented, responding to internal stimuli, and exhibiting signs of paranoia. He was charged with assault with a deadly weapon. While incarcerated for several months, John continued to exhibit signs of psychosis and was found incompetent to stand trial. His family revealed that John had heavily used high-potency cannabis for several years and had experienced increasing paranoia and auditory hallucinations over the past year. After more than 6 months of involuntary treatment with antipsychotic medication, John was ultimately deemed competent to stand trial. At trial, John’s defense team contended that he was not guilty by reason of insanity, asserting that his prolonged cannabis use had led to a state of settled insanity, which he was experiencing at the time of the crime. However, the prosecution countered by pointing to the fact that John’s psychosis resulted from voluntary intoxication, a condition often excluded from insanity defenses. Criminal Responsibility Findings from studies have shown an increased use of cannabis in the US resulting from its legalization for recreational purposes. However, findings from studies on the effects of recreational cannabis legalization on mental health issues have shown mixed results. Recent cases have highlighted the relationship between cannabis and criminal responsibility, particularly with regard to intoxication and its impact on a defendant’s mental state. Criminal responsibility refers to the extent to which a person can be held legally accountable for committing a crime. In such cases, defendants may raise various mental defenses to argue that their mental state at the time of the offense diminishes or negates their responsibility for the act. The insanity defense is one of the most well-known mental defenses. The exact standard for determining legal insanity has differed across time and jurisdictions, but it typically means that due to a mental illness or defect, an individual cannot recognize an act is wrong, fails to understand the nature or quality of the act, or is unable to control their behavior. Typically, a substance-induced disorder resulting from the voluntary consumption of an intoxicating substance, such as cannabis, does not constitute a mental disease or defect for the purposes of the insanity defense. However, in certain jurisdictions, the defense of settled insanity may offer an alternative route for defendants whose cannabis use leads to prolonged psychotic symptoms. If it can be shown that substance use triggered or worsened psychotic symptoms that continued beyond the acute effects of intoxication, the defendant may be eligible to use the defense of settled insanity. Settled Insanity The standard for settled insanity varies by jurisdiction and is not always clearly defined. Although the specific criteria may differ across regions, the challenge of separating the effects of mental illness from substance use remains consistent. Establishing a clear timeline for the onset of substance use and symptoms of mental illness can be difficult and at times even impossible. Evidence indicating that the defendant showed signs of mental illness close to the time of the offense but prior to substance use or that the symptoms present during the offense persisted beyond the effects of intoxication may support the determination of settled insanity. For instance, the persistence of psychotic symptoms far beyond what would be expected from cannabis intoxication alone, requiring significant clinical intervention, could support an opinion of symptoms that are more settled and not merely a result of acute intoxication. Once it is established that a lasting impairment may be at play, the forensic evaluator must assess whether the symptoms meet the statutory criteria for the insanity defense. Experts assessing defendants for a potential insanity defense in cases involving substance use may consider examining the factors outlined in the Table. Diminished Capacity All crimes, except strict liability offenses (where the prosecution is not required to prove that the defendant had intent or knowledge of committing the crime), require both an action (actus reus) and criminal intent (mens rea). If mens rea is absent, an individual cannot be found guilty of a crime that necessitates intent. Courts distinguish between general intent and specific intent crimes, with voluntary intoxication being relevant to the latter. Specific intent crimes require not only the intent to perform the criminal act but also the intention to achieve a specific result. If cannabis intoxication impaired the defendant’s ability to form this specific intent, it could serve as a partial defense. For example, a defendant charged with a specific intent crime, such as first-degree murder, may argue that due to cannabis-induced psychosis, they were unable to premeditate or intentionally carry out the killing. This in turn could result in a reduction of charges. A general intent crime requires that the defendant intended to commit the criminal act but not necessarily to achieve a particular result. For these crimes, it is enough that the individual acted with a wrongful purpose, even if they did not intend to cause a specific outcome. Voluntary intoxication is never accepted as a defense, not even a partial one, for general intent crimes. Mitigation Voluntary intoxication may be considered during the sentencing phase of a criminal proceeding. Some jurisdictions allow judges to consider the defendant’s intoxicated state when determining the severity of the sentence. In Texas, for example, voluntary intoxication may be cited as a mitigating factor in sentencing. A mitigating factor is a circumstance or piece of evidence that can reduce the severity of a defendant’s sentence or level of criminal responsibility, even if they are found guilty of a crime. Mitigating factors do not excuse the crime but help explain why it may have occurred, suggesting that a lesser punishment is more appropriate. Concluding Thoughts The laws regarding voluntary intoxication and mental health defenses differ significantly among jurisdictions, making it important for forensic psychiatrists to be well-versed in the legal standards of the area where a case is being tried. Whether or not voluntary intoxication can be used to argue diminished capacity or as a mitigating factor at sentencing varies widely. The recognition of settled insanity where long-term substance use results in lasting mental impairment even after intoxication has ended adds another layer of complexity. Understanding the complex relationship between substance use and mental health is critical to providing thorough and well-informed evaluations. Staying up to date on both the evolving science of substance-induced psychiatric conditions and jurisdiction-specific legal standards ensures that forensic assessments remain aligned with contemporary practices and legal standards. As cannabis and other substances become more prevalent in legal contexts, expertise in this area will only grow in importance. Note: This article originally appeared on Psychiatric Times .

The number of US adults who will develop dementia each year is projected to increase from approximately 514,000 in 2020 to about 1 million in 2060, new research shows. In addition, the lifetime risk of developing dementia after age 55 is estimated at 42%. The research showed that the relative growth in dementia cases is particularly pronounced for Black adults. These new findings researchers say, “highlight the urgent need for policies that enhance healthy aging, with a focus on health equity.” “The aging of the population means that the increased burden of cognitive decline and dementia, particularly among the oldest age group, is going to be significant, and we need to be prepared for it,” study investigator Josef Coresh, MD, PhD, director of the Optimal Aging Institute at NYU Grossman School of Medicine, New York City, told Medscape Medical News. He added that dementia may be preventable through such strategies as controlling vascular risk factors, treating sleep disorders, detecting and correcting hearing loss, managing mood disorders, and improving access to social support. The findings were published online on January 13 in Nature Medicine . Diverse Cohort, More Rigorous Methodology Over the past century, the US population has aged substantially, resulting in a rise in late-life diseases. Once an uncommon condition, dementia now affects more than 6 million Americans. The lifetime risk for dementia is a critical public health measure that can be used to raise awareness, enhance patient engagement in prevention, and inform policymaking, the investigators noted. The often-cited Framingham Heart Study estimates that 11%-14% of men and 19%-23% of women will develop dementia during their lifetime. But, as Coresh noted, these estimates were based on a predominantly White, relatively affluent, and well educated cohort, as well as limited means of determining dementia cases. In contrast, this new study is based on a more diverse cohort and used more rigorous methodology, Coresh said. “It’s capturing the latest decade of risk, from age 85 to 95 years,” which is important because people are living longer, he added. The report analyzed data collected from 1987 to 2020 from 15,043 participants in the Atherosclerosis Risk in Communities (ARIC) study. Drawn from four US communities, these individuals were all dementia-free of dementia at age 55. One of the study sites was Jackson, Mississippi, where Black individuals comprise 82% of the population. Black individuals accounted for 26.9% of the total study population, 55.1% of participants were women, and 30.8% carried at least one copy of the apolipoprotein E (APOE) epsilon 4 allele (28.1% with one copy and 2.7% with two copies). Over the past three decades, study participants underwent clinical examinations, including cognitive testing, laboratory testing, and both in-person and telephone interviews. In addition to interviews, the ARIC study uses review of hospital records and death certificates to determine dementia, with cases adjudicated by a committee assisted by a computer algorithm. Over a median follow-up of 23 years, 3252 new cases of dementia were identified. At age 55, researchers estimated the lifetime risk for dementia (up to age 95) to be 42% (95% CI, 41-43). The cumulative incidence of dementia remained relatively low between 55 and 75 years of age (3.9%) but rose significantly beyond that. Over a median follow-up of 23 years, there were 3252 incident cases of dementia. The lifetime risk for dementia was higher in women (48%; 95% CI, 46-50) vs men (35%; 95% CI, 33-36) and in Black individuals (44%; 95% CI, 41-46) vs White individuals (41%; 95% CI, 40-43). Additionally, Black individuals experienced an earlier median age of dementia onset (79 years) compared with White individuals (82 years). “By age 75, the risk is 3% in our White participants and 7% in our Black participants, so the racial difference is expressed early, and it stays to age 85 and then sort of closes and becomes smaller by age 95,” said Coresh. Structural Racism The racial disparity in dementia risk may reflect the impact of structural racism and socioeconomic inequality, including limited access to quality education and nutrition, said Coresh. Additionally, it could be influenced by poorer access to healthcare and a higher prevalence of vascular risk factors, such as hypertension and diabetes, he added. “People who were born in the South a long time ago may not have had the same opportunities as people in other areas and of other races and ethnicities.” The substantially higher risk among women is thought to reflect women’s longer life expectancy. Adults with two copies of the APOE epsilon 4 allele had a higher lifetime risk for dementia (59%; 95% CI, 53-65) compared with those with one copy (48%; 95% CI, 45-50) and those with no copies (39%; 95% CI, 37-40). Dementia also occurred earlier in APOE epsilon 4 carriers (median age, 79 years in those with two copies, 81 years in those with one copy, and 82 years in those with no copies). Applying the lifetime risk estimates to US Census population projections, the researchers predict the annual number of incident dementia cases will increase from about 514,000 in 2020 to 1 million in 2060. The number of individuals who will develop dementia each year is expected to nearly double among White individuals and triple among their Black counterparts. These findings highlight the importance of addressing the growing number of Baby Boomers transitioning into the oldest age group, Coresh noted. As more individuals live into their 80s and beyond, the medical community must focus on managing early symptoms and implementing effective prevention strategies, he added. Such strategies should include managing risk factors, such as social isolation, disordered sleep, mood issues, poor cardiovascular health, and uncorrected hearing loss, he said. As it stands, research suggests only about 20% of US adults meet recommended lifestyle and cardiovascular health targets, and only 30% of older adults with hearing loss are using a hearing aid. Dementia before age 75 may be underestimated in the study because up until this age, dementia was ascertained retrospectively with phone interviews and review of hospital and death records. Other limitations of the study include the lack of external validation of the results, limited generalizability of the projections to the entire US population, and exclusion of racial groups other than White and Black from the analysis. A Crisis in the Making Commenting for Medscape Medical News, Maria C. Carrillo, PhD, chief science officer and medical affairs lead for the Alzheimer’s Association, said the new findings reinforce what the Alzheimer’s Association has long emphasized: that the risk and prevalence of Alzheimer’s disease and other dementias are expected to rise significantly in the coming years. “There’s an urgent need to address the crisis of Alzheimer’s disease and dementia in this country and globally,” she said. These new data confirm the high risk for dementia among minority groups as well as women who have often been underrepresented in research, said Carrillo. The good news, though, is that this is “an exciting and hopeful time” in the field, with Alzheimer’s treatments being approved that slow the progression of early disease and with more treatments in the pipeline. “There are also better ways available now to detect and diagnose Alzheimer’s, and we’re learning more every day about risk reduction for Alzheimer’s and all other dementias,” Carrillo said. Carrillo added the Alzheimer’s Association is leading the U.S. POINTER Study, a 2-year clinical trial evaluating whether lifestyle interventions targeting risk factors can protect cognitive function in older adults at increased risk for cognitive decline. Results of that study will be reported later this year at the Alzheimer’s Association International Conference. She also pointed to last summer’s Lancet Commission Report showing that 40% of global dementia is potentially avoidable with behavioral and lifestyle changes. “The main message is that there’s hope that we can, in fact, change the trajectory,” that by making such changes, “we won’t hit the numbers that this new paper talks about until 2060.” However, she noted there’s still more work to be done. For example, she said, there’s an urgent need for more research into how to detect dementia as early as possible. Carillo emphasized the importance of checking patients’ blood pressure and cholesterol, and conducting other tests to determine risk and discuss lifestyle changes that could result in dementia risk reduction. Note: This article originally appeared on Medscape .

Older adults with major depressive disorder (MDD) exhibit riskier driving behaviors than their nondepressed peers, including hard braking, cornering, and unpredictable driving patterns, new research showed. Data for the study came from commercial vehicle data trackers installed in participants’ vehicles. After about a year of follow-up, investigators found that MDD was associated with an increase in the amount and severity of risking driving, even after controlling for antidepressant use. Late-life depression often goes undiagnosed, and the new findings highlight the importance of routine depression screening and targeted interventions to ensure driving safety among older adults, the study team said. “By using longitudinal, real-world driving data rather than controlled settings or self-reports, the study provides robust evidence of how MDD influences driving behaviors in day-to-day contexts,” first author Ganesh M. Babulal, PhD, OTD, with the Department of Neurology, Washington University School of Medicine in St Louis, told Medscape Medical News. “By analyzing the influence of antidepressant use and overall medication load, the study disentangles the effects of MDD from those of driver-impairing medications, further clarifying the unique contributions of depression to driving behaviors,” Babulal noted. The study was published online on December 30 in JAMA Network Open . Road Risks As the number of older adults grows, safe driving practices in this age group become increasingly crucial. By 2050, one quarter of drivers in the United States will be older than 65 years. MDD affects about 8% of US adults and is linked to cognitive impairments that may compromise driving safety. Prior studies revealed a link between depression and increased car crash risk, regardless of age. And earlier research by Babulal and colleagues showed that older adults with depression were three times more likely to receive a marginal or failing score on a standardized road test. To further study the issue, Babulal and colleagues examined the impact of MDD on naturalistic driving behaviors among older adults using longitudinal data. Participants were recruited from the Driving Real-World In-Vehicle Evaluation System Project, where their daily driving behaviors were recorded using commercial vehicle data loggers installed in their personal vehicles. The cohort included 85 adults with MDD (mean age, 69 years; 71% women) and 310 adults without MDD (mean age, 70 years; 49% women). The majority of participants in both groups were non-Hispanic White individuals. Based on intercepts, adults with MDD had a propensity toward riskier driving habits with a higher frequency of speeding events and spending more time on the road than those without MDD, they found. Additionally, during a mean of 1.1 years of follow-up, compared with older adults without MDD, those with MDD exhibited significantly more hard braking (P < .001) and hard cornering events per trip (P = .04) over time. They also traveled farther from home and visited more unique destinations (P < .001 for both). Over time, older adults also displayed increased entropy in driving patterns (P < .001), indicated less predictable driving routes. “Driving unpredictability, as evidenced by increased random entropy, highlights the unique challenges posed by MDD in maintaining safe driving practices,” the researchers wrote. Adjusting for antidepressant use, which could impair driving, or total medication burden did not change the findings, suggesting MDD independently affects driving. “Most importantly, our findings demonstrate that MDD — a common and treatable illness in older adults — was associated with an increase in both the amount and magnitude of risky driving behaviors over time,” the researchers wrote. The researchers noted that the study did not account for changes in depression severity over time and other psychiatric conditions co-occurring with MDD were not adjusted for. Also, situational factors like weather or traffic conditions were not assessed. Clear Clinical Implications There is a “pressing need” for targeted interventions to manage and mitigate the driving risks associated with late-life depression, the researchers wrote. “The study emphasizes the need for interventions tailored to the mental health and driving behaviors of older adults. These could include cognitive retraining, driver rehabilitation programs, and routine depression screening to enhance road safety and preserve independence,” Babulal told Medscape Medical News. “Encouraging older adults with MDD to self-regulate their driving habits (e.g., avoiding night driving or high-traffic situations) and educating them about potential driving challenges related to their condition can enhance safety,” he added. Commenting on this study for Medscape Medical News , Ipsit Vahia, MD, McLean Hospital, Belmont, Massachusetts, and Harvard Medical School, Boston, said it “adds nuance to our understanding of how depression can impact driving among older adults.” “While the connection between depression and a higher incident of crashes is known, this study demonstrates an association with riskier driving behaviors such as speeding,” Vahia said. “It highlights the importance of clinicians proactively initiating discussion of driving and safety when working with older adults with depressive symptoms.” Note: This article originally appeared on Medscape .

Andrew N. Wilner, MD: Welcome to Medscape. I’m your host, Dr Andrew Wilner. Today, I have the privilege of speaking with Dr Jessi Gold. Dr Gold is an associate professor of psychiatry at the University of Tennessee Health Science Center and the author of How Do You Feel? Today, we’re going to talk about her book and her role as chief wellness officer at the University of Tennessee. Welcome, Dr Gold. Jessica A. Gold, MD, MS: Thank you so much for having me. Wilner: Dr Gold, let’s start with your book. Why did you write it? Tiptoeing Into Self Disclosure Gold: It’s not like there was an “aha” moment precisely, but I’ve been being a clinician who takes care of healthcare workers as a psychiatrist since the pandemic, if not before, and for the most part, I’ve been hearing the same stories over and over again. They always end with “I’ve never told anyone that before,” “No one else feels this way,” or “I feel alone in this.” For me, many of the stories have the same themes and we shouldn’t feel alone in it. To be able to tell stories of my patients and tell my own story in a way that might make this information accessible and might make people feel seen was the ultimate goal there. Wilner: I read your book and I found it very interesting. Also, it was quite intimate. There was a large amount of self-reveal. How did you feel about that? Gold: I’ve tiptoed into self-disclosure for a while, and I’ve been on social media for a while, talking about my own therapy. I wrote a piece a bit ago about my own meds and noticed that the response wasn’t that I combusted or that people thought I was a horrible person or judged me for it. As I’ve tiptoed into it, I’ve felt more comfortable and recognized the need for it. I also realized in being an expert in an article on burnout that, when they asked me how I was feeling and I said the real answer and then the article changed to me being the lead story, clearly we weren’t talking about this enough. Being a person, again, who’s like the clinician of healthcare workers, I wanted to model that and also thought if I could start the conversation, maybe other people would feel more comfortable being vulnerable. I took the leap to do that. Wilner: In your book, you talk about how COVID-19 affected you. Also, I believe you had four patients and their stories with the different mental health issues that they struggle with. COVID-19 is a little bit behind us, so has anything changed, do you think, in the mental health world? Gold: I think in many ways people want to believe that COVID-19 came down from the clouds, made us sad, went back to the clouds, and we’re fine again. It just never was going to be that way. As healthcare workers, we had high rates of burnout and mental health conditions long before COVID-19. It just gave us new stressors. COVID-19 also really exposed many of the issues in healthcare, including access and who gets access to things, people dying, ventilators, and protective equipment. All of these things were maybe new stressors or cracks in existing stressors, so it only compounded our bad baseline mental health. In my experience, just because it’s been better and those stressors are different doesn’t mean we’re okay now. I think there’s a desire to pretend that we’re okay now, but for me, it’s important that this conversation is still happening and that we’re not only talking about people who are caregivers or who work in frontline work in the height of a pandemic, but we also recognize that their jobs are always hard, that their jobs are going to be impacted by those years of their life, and that it should be a conversation we continue to have. Reducing Stigma Wilner: I’m going to read a line from your book: “People who ask for help are the subject of gossip and are judged.” What you’re talking about there is stigma. Particularly for physicians, it’s very difficult for them to ask for help. As a wellness officer, what’s going on there? Gold: There are some data about that. Basically, medical students, when they’re going into medical school, are asked if getting mental health help is a weakness. A very small percentage of them say yes to that. Then they say, well, what about all this other noise in the culture? What about your supervisors? What about your colleagues? What about residency applications? What about patients? Over 50% of them — closer to 60% in many of those cases — are saying my patients would judge me, my colleagues would judge me, my supervisors would judge me, and my next level of applications, residency programs, would judge me. It ends on this question that’s like, well then if you get help, would you talk about it? It’s a tiny number. Basically, just because we come in with our own beliefs — and maybe they aren’t even stigmatizing — maybe we actually think mental health is health, once we get into this culture of healthcare to what we’re seeing around us, to what we’re seeing modeled, that changes. Maybe we still get help but we’re not talking about it, or maybe we don’t get help, which is obviously the worst outcome. We have high rates of suicide in our profession, and the people who show up at my door tend to be quite sick by the time that they show up. It’s a little skewed because I am a psychiatrist and not a therapist, but in so many ways, it’s like, oh, it’s not interfering with my work yet. Many of my patients also say, “I haven’t hurt anyone yet,” which has never been my favorite response because I don’t think we should measure our own well-being by whether we made an error or whether we’re in a position where patients are going to notice. I think we should care about ourselves. People come pretty late. I think that is a product of stigma. It’s what we see. I think the stigma comes from what you see modeled. Nobody else is talking about it. I think it comes from even those little jokes that they make about psychiatry or mental health patients. If you see somebody who is in the emergency department for a mental health thing and the people around you make dark-humor jokes about it, then you say, well, I have that same thing. Like, I’m not going to disclose it. We also have a culture of showing up no matter what and using that as a badge of honor. If we wouldn’t show up if we were actively hemorrhaging, why wouldn’t we skip for mental health? It just doesn’t meet the criteria for not showing up. All of those things combined lead to us thinking I just have to deal with it myself, or My job is to serve other people, not to serve myself. Therefore, I just have to ignore what’s going on with me. Wilner: I know I would feel differently telling my residents, “Hey, I have to leave early today. I have a dentist appointment at 4 PM” vs “I have to leave early today. I have to see my therapist.” Gold: Do you think you feel at all better than when you started your medical career, or do you think that it has been the same for you the whole time? Wilner: I think I would be more open today, but I think that probably is related to the gray hair and wrinkles I’ve accumulated. Gold: I think when you have more power and flexibility, you care less about what all these other noises are. But I also think that as a culture, we’ve evolved to being more comfortable with mental health in general. I think people have become more comfortable talking about it out loud, but in our profession, much less than others. I feel like it’s also hard with therapy because you’re probably going every week or every other week. There are only a few things you would need to do that for, so even if you didn’t say, “I’m leaving at 4 PMbecause I have therapy,” if you left at 4 PM every week for an appointment, it’s either physical therapy or mental therapy. You don’t have many options, and residents, medical students, trainees, and other health professions don’t have the ability to take that much time off, but if they did and they had to ask for it, it would be much harder. What Does a Wellness Officer Do? Wilner: I don’t remember wellness officers when I was in medical school. Is that a new thing? Gold: It’s a newer thing. It’s developed under the concept that having somebody overseeing all of this stuff and valuing it at a higher level is important to making sure things actually get done. Places like Stanford are among the first that had chief wellness officers in the hospital system. Many hospitals have grown to have them. I’m in a different role in that I’m the University of Tennessee system, which includes the undergraduate schools, so it’s a bit different from the people who are just in health. The point is to have somebody whose goals, values, and things that they’re thinking about are always about the well-being of the people that are in the institution — students, faculty, and staff. That’s not always what the bottom line is for everybody else in administrative positions. It makes sure some stuff gets done and that you’re in the right rooms to make it happen. Wilner: Give me an example of one of those things that qualify as stuff. Gold: Much of what the chief wellness officers who work in hospitals are working on includes, how do we think about the role of the electronic medical record? How do we think about staffing? How do we think about control in your workplace, and what does that look like? Is our well-being matching up to what our productivity measures are? Are we actually measuring the right thing? You see much of the system focus from the chief wellness officers that are in the healthcare system. I have a little bit of a different bent just because I’m not exclusively in the healthcare system, so much of what I’m looking at is why we focus so much on the intervention side and are there enough things that we could be looking at, and what kind of options would we have for prevention on our campuses? It’s always going to be stopping the bleeding that’s going to take your attention, right? If there’s a crisis, you have to address the crisis, but we don’t all need to get to the crisis. When you have a little bit of breathing room and time to step back and actually look at what’s going on, how do we make sure that we have preventive options and that we have things for folks to try to do along the way that aren’t just like, oh, they got to crisis again. That’s what I’m looking at. What does that look like? Is that a peer support program? Is that a coaching program? Is that just making sure that they know of all the resources and where to access them when they need them? Is it regular screening tools for themselves that they can monitor? There are many things that people have implemented, but across the spectrum and across our whole state, we’re looking at what makes sense and what programs are working or not. Advice for Improving Wellness Wilner: We’re just about out of time. I have one more question. Apart from seeing you, do you have any advice for physicians and other healthcare workers trying to improve their own wellness? Gold: We’re people that do this job, not robots that do this job, so pretending that our job doesn’t affect us doesn’t help. It should. It’s a hard job. We listen to hard stuff; we see hard stuff. Pretending that somehow, you can see all that stuff and hear all that and be fine, doesn’t make sense. Instead, you should think about how you can deal with that and approach it that way. I’m not saying that the healthcare system is great because there are so many problems in the system, but if you’d like to stay in it for as long as you have, or you’d like to stay in it at least for a while, you do have to figure out what it looks like for you to do that. For me, it’s been things like checking in on myself and my feelings, making sure I take my vacation days, working on self-compassion and that mean voice in my head when I do things wrong or when I think I did things wrong, looking at how email takes over your life, and making really strict boundaries around certain things like talks or all those extra asks that come up in academics. There are ways that we can manage it, and this isn’t to say this is somehow a resiliency problem, because our resilience is higher than any other field. It is to say that we can do something, and I think that’s more important than doing nothing. Wilner: Dr Gold, thanks for joining me for this Medscape interview. Gold: Thanks for having me. Note: This article originally appeared on Medscape .

TOPLINE: Listening to recordings of natural soundscapes may help reduce anxiety and stress, but adding in high-traffic noise can mask the potential benefit, new research shows. METHODOLOGY: Researchers enrolled 68 adults (ages 18-42 years) from the University of the West of England Psychology participant pool. Three 3-minute soundscape files were used: A natural soundscape with bird songs and two mixed soundscapes combining natural sounds with traffic noise recorded at speed limits of 20 mi/h or 40 mi/h. Each participant was exposed to three rounds of a stressor video for 1 minute and a soundscape playback of 3 minutes, then answered questions after each exposure. Subjective stress and pleasure scores (hedonic tone) were measured using the University of Wales Institute of Science and Technology Mood Adjective Checklist, and anxiety was measured using the State-Trait Anxiety Inventory scale. TAKEAWAY: Natural soundscapes were strongly associated with the lowest levels of anxiety and stress, whereas mixed soundscapes with 40 mi/h traffic noise were associated with the highest stress (P < .01) and anxiety (P < .001) levels. Higher pleasure scores occurred after exposure to natural soundscapes, but these scores decreased when the natural soundscapes were combined with 40 mi/h traffic noise. Traffic noise masked the positive impact of a natural soundscape on stress and anxiety in participants irrespective of age, sex, or a predisposed preference for natural environments. IN PRACTICE: "Our study shows that listening to natural soundscapes can reduce stress and anxiety, and that anthropogenic sounds such as traffic noise can mask potential positive impacts," the investigators said in a press release. “Reducing traffic speeds in cities is therefore an important step toward more people experiencing the positive effects of nature on their health and well-being,” they added. Note: This article originally appeared on Medscape .

NIMH-funded study used universal screening, risk assessment, and safety planning to reduce suicide attempts among adult primary care patients Suicide is a leading cause of death in the United States and a major public health concern. Previous research has shown that identifying and helping people at risk for suicide during regular care visits can help prevent it. Primary care clinics are particularly important in this regard, as research has shown that over 40% of people who died by suicide were seen in this setting in the month before their death. A recent study funded by the National Institute of Mental Health (NIMH) found that when primary care clinics added suicide care practices to routine visits, suicide attempts dropped by 25% in the 3 months after the visit. The findings highlight how impactful it can be for primary care clinics to take an active role in preventing suicide and help empower health systems to integrate those practices into clinical care. What did the researchers do in the study? Primary care clinicians screen for depression during most care visits, and depression screeners often include questions about suicide risk. Prior NIMH-supported research found that screening for suicidal thoughts and behaviors followed by brief safety planning can reduce the risk of suicide attempts . Researchers led by Julie Angerhofer Richards, Ph.D., M.P.H. , at the Kaiser Permanente Washington Health Research Institute aimed to see if integrating suicide care into routine adult primary care visits could prevent subsequent suicide attempts. This study analyzed secondary data from a larger integrated study of the National Zero Suicide Model . The comprehensive Zero Suicide approach is the first U.S. program linked to a substantial decrease in suicides among behavioral health patients. The research team previously examined this model in a separate NIMH-funded study at six health systems across the United States. Before the intervention, providers delivered care as usual, which did not include population-based suicide screening or follow-up. The 22 participating clinics were randomly assigned to start delivering suicide care on staggered dates (4 months apart) over a 2-year period. During the study, 333,593 patients were seen for over 1.5 million primary care visits. Suicide care consisted of: Depression screening: All patients completed a brief two-question depression screener, followed by a longer depression symptom scale for those who scored positive on either question. Depression symptom scale: The screener was followed by a longer depression symptom scale for patients who scored positive on either question. Suicide risk assessment: Patients with thoughts of self-harm or suicide completed a measure of suicidal thoughts and behaviors. Suicide safety planning: Patients who reported intent or plans for suicide in the last month were referred to designated care staff, including mental health social workers, for same-day suicide safety planning. Safety planning was a collaborative process between patients and providers that involved identifying warning signs, listing coping strategies and supports, and creating safe environments to manage a suicidal crisis. Three key strategies supported the intervention: Skilled facilitators led trainings at each clinic and met with staff on an ongoing basis to offer support and solve problems. Clinical decision support, including pre-visit reminders and visit prompts, came from the clinics’ electronic medical record system. Regular performance monitoring of medical records reported on clinician rates of screening and assessment. The researchers compared clinics delivering suicide care to clinics delivering usual care on: Providers’ rates of documenting suicide risk assessment and safety planning in the medical record within 2 weeks of an at-risk patient’s primary care visit Patients’ rates of suicide attempt or death by suicide in the 90 days after their primary care visit What did the results of the study show? Integrating suicide care into routine adult primary care visits led to significantly higher rates of suicide risk screening, assessment, and collaborative safety planning. The intervention in turn resulted in a 25% decrease in suicide attempts in the 90 days after a primary care visit compared to usual care clinics. Together, the results demonstrate that integrating suicide prevention practices into adult primary care leads to more people being screened for suicidal thoughts and behaviors and fewer suicide attempts once they leave the clinic. These findings support NIMH’s prioritization of suicide prevention in health care settings , with the ultimate goal of reducing the suicide rate in the United States. The study provides the critical next steps for providers and care teams in responding to suicidal concerns during clinical practice, helping save lives in the process. Note: This article originally appeared on NIMH .

Depression and anxiety are among the most common complications of stroke, affecting 1 in 3 and about 1 in 4 survivors, respectively. These disorders are associated with higher mortality rates, often obscuring the path to recovery. The American Heart Association (AHA)/American Stroke Association (ASA) last published its scientific statement on poststroke depression (PSD) in 2016. Although this statement doesn’t cover poststroke anxiety (PSA), the 2019 Canadian Stroke Best Practices update recommends screening for PSA and apathy, which often coexist in the absence of PSD. It advises management with pharmacotherapy, psychotherapy, or nonpharmacologic interventions such as exercise or music therapy, while noting there is limited evidence for the use of psychostimulants. New research on the most effective treatments for depression and the lack of information on anxiety after stroke have prompted some neurologists to ask: Is it time for new guidance? What’s the Prevalence, Who’s at Risk? Recent data from the South London Stroke Register Study, which followed 2295 patients with PSD for 18 years, revealed that 33% of those with stroke experienced PSD in the first 3 months following the event, 55% within a year, and 88% within 5 years. The study’s investigators noted that individuals with PSD were at substantial risk for persistent depression within a year and recommended PSD screening in all patients within the first 3-6 months following stroke. “The course of PSD is dynamic,” Nada El Husseini, MD, director of the Stroke Research Fellowship Program at Duke University Medical Center, Durham, North Carolina, and a co-author of the AHA/ASA 2016 statement on PSD, told Medscape Medical News. Some people experience depression soon after a stroke and recover within a year, whereas others develop PSD a year after stroke, she noted. Risk factors for PSD in the first 3 months following stroke include previous mental illness, a family history of mental illness, female gender, being younger than 70, and stroke severity. A recent analysis in the Journal of Affective Disorders examined three cohorts from STROKOG (The Stroke and Cognition Consortium), revealing a PSA prevalence of 35%. Investigators found risk factors for PSA included female gender, co-occurrence of PSD, and poststroke cognitive impairment. Most cases of PSA surface within the first year after stroke. Phobia and generalized anxiety disorder were the most common anxiety subtypes. In addition to screening, early and aggressive intervention for PSD is necessary, Bruce Ovbiagele, MD, vice chair of the committee that developed the statement, told Medscape Medical News. “With stroke, we speak about the three dreaded Ds: death, dementia, and disability. But there is a fourth, and that is depression, and it is not addressed to the degree it should be,” said Ovbiagele, professor of neurology, health policy, and global health at the University of California, San Francisco. PSD is underdiagnosed and undertreated, he added. The same appears to be true for PSA, the authors of a commentary published in October in Stroke wrote. “While awareness of PSA has increased in recent years, research into the identification and treatment of PSA continues to receive less attention than poststroke depressive disorders,” they added. “With similar prevalence rates between PSA and poststroke depression, an increased understanding of the diagnosis and treatment of PSA disorders is needed.” What Causes PSD and PSA? Although psychosocial factors can contribute to the development of depression or anxiety after a stroke, research suggests that neurologic damage caused by the stroke itself plays a significant role. A 2023 literature review examining the potential mechanisms underlying PSD showed stroke in regions such as the prefrontal cortex, limbic area, and basal ganglia can disrupt key pathways of mood-related neurotransmitters, potentially leading to depressive disorders. The review also cited numerous studies linking PSD to neuroinflammation. Some experts theorize that inflammation from stroke causes the release of pro-inflammatory cytokines, which can lead to decreased serotonin. Serotonin deficiency is believed to play a significant role in the development of depressive symptoms. Another 2023 study revealed that more than 80% of immune proteins associated with mood were elevated among individuals with PSD, suggesting a link between an overactive immune system and the disorder. These investigators also found that several pro-inflammatory cytokines, such as interleukin-6, were associated with PSD. Experts believe that such biomarkers can be used to guide treatment. Depression and anxiety after stroke often co-occur alongside cognitive impairment, physical disability, and neurologic damage, making the conditions more challenging to treat than depression or anxiety in the general population, Ovbiagele noted. Effective treatment may require a multidisciplinary approach, he added. For instance, if depressive symptoms appear at any point as a stroke patient transitions from the acute setting to rehabilitation to primary care, there must be clear communication between the patient’s treatment team about treatment strategies. Ongoing treatment may involve a psychiatric consult and psychotherapy, he said, and all clinicians should remain informed about the treatment plan. As reported previously by Medscape Medical News, there are a few theories about what distinguishes PSD from nonstroke depression. A 2023 meta-analysis showed greater severity and prevalence of emotional dysregulation and less anhedonia in people with PSD compared with their counterparts with depression and no stroke history. People with PSD were more likely to have cognitive impairment and difficulty controlling muscle contractions, which is not uncommon after stroke. Unlike major depression, PSD is linked to the ischemic event, a 2018 review suggests. In particular, the size and number of ischemic lesions, and whether the lesions disrupt the midbrain, limbic, and medial prefrontal cortical circuitry, are implicated in depression. “In particular, white matter lesions are associated with metabolic alterations in this circuitry and are correlated with major depression,” the article states. What Works for PSD? As the authors of the 2016 AHA/ASA statement noted, there are few large studies to help guide clinical management of PSD. However, some evidence suggests that escitalopram and sertraline may be effective treatment options. A 2022 meta-analysis of seven randomized controlled trials showed a standardized mean difference of -1.25 on Hamilton Depression Scale (HAM-D) scores (P < .001) among participants allocated to escitalopram vs placebo. A 2024 study added to those findings. The randomized controlled trial of 60 stroke patients showed that treatment with sertraline (100 mg) or escitalopram (20 mg) was associated with a statistically significant decrease in HAM-D scores (P < .05) after 8 weeks of treatment. Data on fluoxetine are mixed. As previously reported by Medscape Medical News , the 2021 AFFINITY trial showed that 20 mg of fluoxetine for 26 weeks did not prevent or alleviate PSD. However, a post hoc analysis of the EFFECTS trial published in 2022 showed that stroke patients reported lower depression scores after receiving 20 mg daily for 6 months. There has also been some debate over whether the use of selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) might be linked to an increased risk for bleeding in stroke patients. A study published about a decade ago showed that SSRI users experienced a higher risk for overall major bleeding that contributed to mortality rates. A subsequent study, also covered by Medscape Medical News, revealed that SSRI use in patients with intracerebral hemorrhage increased the risk for recurrence. However, other research showed no such increased risk. But new data appear to put this controversy to rest. In an analysis presented at the 2024 AHA annual meeting, researchers examined the health records of more than 650,000 stroke patients, comparing the bleeding risk among those taking SSRIs/SNRIs vs that in patients who took other antidepressants or none at all. Early use of SSRIs or SNRIs during the subacute recovery phase of acute ischemic stroke was not associated with increased bleeding risk in most patients, although a 29% higher risk for hemorrhagic stroke was observed in those who took antidepressants while also on dual antiplatelet therapy. Bleeding risk was also 15% higher with the use of other antidepressants compared with SSRIs or SNRIs. “Our findings should reassure clinicians that for most stroke survivors, it is safe to prescribe SSRI and/or SNRI antidepressants early after stroke to treat post-stroke depression and anxiety, which may help optimize their patients’ recovery,” lead investigator Kent Simmonds, DO, PhD, UT Southwestern Medical Center, Dallas, Texas, said in a press release. What Works for PSA? If research on PSD is lacking, data on the most effective treatments for PSA are even more scarce. In fact, authors of a 2021 narrative review published in Stroke found only three small trials on treatments for PSA. One study compared paroxetine or paroxetine plus psychotherapy vs standard care. Another examined buspirone hydrochloride vs standard care. The third study included data on a relaxation compact disc vs a waitlist control. Reviewers said the studies were sufficient to guide clinical practice, citing a high risk of methodological bias in all three. A fourth study, on the feasibility of a guided self-help cognitive-behavioral therapy (CBT) program delivered online and over the phone, was inconclusive. “Thus, large-scale, adequately powered, well-designed trials are needed to evaluate interventions to treat poststroke anxiety,” the authors wrote. In the absence of more defined recommendations, recent data suggest that more clinicians may be turning to benzodiazepines, often prescribing far more than the American Geriatrics Society advises. Use of these drugs in adults older than 65 years is associated with higher risk for cognitive impairment, delirium, falls, fractures, and motor vehicle accidents. In addition, some research shows that benzodiazepine use is associated with increased poststroke mortality at 90 days. Despite these warnings, investigators at Massachusetts General Hospital in Boston recently reported that nearly 5% of Medicare patients with acute ischemic stroke received a prescription for benzodiazepines within 90 days of discharge. Of these patients, 55% were prescribed benzodiazepines for durations ranging from 15 to 30 days. Guidance from the World Health Organization suggests that benzodiazepines should be prescribed for no more than 7 days. In an editorial accompanying this study, Justin J. MacKenzie, PhD, and Veronica Moreno-Gomez, MD, said the findings highlight “a concerning pattern of possible BZD [benzodiazepine] overprescription in vulnerable adults following ischemic stroke.” Some evidence suggests that various nonpharmacologic treatments are effective for PSA and PSD. A 2021 meta-analysis of 10 studies showed CBT was associated with improvement in PSD and PSA symptoms and that the benefits persisted up to 3 months after treatment. Other studies suggest potential benefits from exercise, acupuncture, and neuromodulation, although many of these trials were small or yielded inconsistent results. Time for New Guidance? Updated guidance for managing PSD and PSA would enable physicians to screen stroke patients more effectively for symptoms, Moreno-Gomez, who is an associate professor of neurology at the University of Utah in Salt Lake City, told Medscape Medical News. Any new guidance should identify the most effective and safest pharmacologic and nonpharmacologic treatments, she added. “While there is still room for improvement, the development of standardized guidelines for the short- and long-term management of anxiety will help minimize the misuse of benzodiazepines and their associated risks,” Moreno-Gomez said. The majority of studies published since the release of the statement are meta-analyses of randomized clinical trials (RCTs) with small numbers, of short duration, or with problematic diagnostic approaches, Ovbiagele said. As a result, the AHA/ASA currently has no plans to update its 2016 statement on PSD. “What we really need is a large, multidisciplinary RCT headed by neurologists, psychiatrists, and perhaps primary care physicians — all of whom play a role in the diagnosis and treatment of patients with PSD,” Ovbiagele said. The results of such large-scale research would provide a solid foundation for developing new guidance on the screening, treatment and management of PSD and PSA, he added. Amytis Towfighi, MD, chair of the AHA/ASA panel that developed the 2016 statement, told Medscape Medical News that although she could not comment on the need for updated guidance, she agreed there is a need for PSD and PSA screening. She also noted that repeated screening might be necessary because the timeline of PSD is unclear. Towfighi, chief of neurology at Los Angeles General Hospital and professor of neurology at the University of Southern California, agreed with Ovbiagele that more large-scale studies are needed to identify the most effective therapies. She highlighted the importance of including research on nonpharmacologic strategies such as music therapy, mindfulness, deep breathing, meditation, visualization, physical activity, motivational interviewing, acupuncture, and herbal remedies. Note: This article originally appeared on Medscape .