Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder characterized by a persistent pattern of inattention, impulsivity, and/ or hyperactivity that causes functional impairment.1 ADHD begins in childhood, continues into adulthood, and has negative consequences in many facets of adult patients’ lives, including their careers, daily functioning, and interpersonal relationships.2 According to the National Institute of Health and Care Excellence’s recommendations, both pharmacotherapy and psychotherapy are advised for patients with ADHD.3 Although various pharmacotherapies are advised as first-line treatments for ADHD, they are frequently linked to unfavorable adverse effects, partial responses, chronic residual symptoms, high dropout rates, and issues with addiction.4 As a result, there is a need for evidence-based nonpharmacologic therapies. In a systematic review, Nimmo-Smith et al5 found that certain nonpharmacologic treatments can be effective in helping patients with ADHD manage their illness. In clinical and cognitive assessments of ADHD, a recent meta-analysis found that noninvasive brain stimulation had a small but significant effect.6 Some evidence suggests that in addition to noninvasive brain stimulation, other nonpharmacologic interventions, including psychoeducation (PE), mindfulness, cognitive-behavioral therapy (CBT), and chronotherapy, can be effective as an adjunct treatment to pharmacotherapy, and possibly as monotherapy. Part 1 of this 2-part article reviewed 6 randomized controlled trials (RCTs) of pharmacologic interventions for adult ADHD published within the last 5 years.7 Part 2 analyzes 6 RCTs of nonpharmacologic treatments for adult ADHD published within the last 5 years (Table,8-13 page 33).
{"title":"Adult ADHD: 6 studies of nonpharmacologic interventions","authors":"Melody Grace Santos","doi":"10.12788/cp.0398","DOIUrl":"https://doi.org/10.12788/cp.0398","url":null,"abstract":"Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder characterized by a persistent pattern of inattention, impulsivity, and/ or hyperactivity that causes functional impairment.1 ADHD begins in childhood, continues into adulthood, and has negative consequences in many facets of adult patients’ lives, including their careers, daily functioning, and interpersonal relationships.2 According to the National Institute of Health and Care Excellence’s recommendations, both pharmacotherapy and psychotherapy are advised for patients with ADHD.3 Although various pharmacotherapies are advised as first-line treatments for ADHD, they are frequently linked to unfavorable adverse effects, partial responses, chronic residual symptoms, high dropout rates, and issues with addiction.4 As a result, there is a need for evidence-based nonpharmacologic therapies. In a systematic review, Nimmo-Smith et al5 found that certain nonpharmacologic treatments can be effective in helping patients with ADHD manage their illness. In clinical and cognitive assessments of ADHD, a recent meta-analysis found that noninvasive brain stimulation had a small but significant effect.6 Some evidence suggests that in addition to noninvasive brain stimulation, other nonpharmacologic interventions, including psychoeducation (PE), mindfulness, cognitive-behavioral therapy (CBT), and chronotherapy, can be effective as an adjunct treatment to pharmacotherapy, and possibly as monotherapy. Part 1 of this 2-part article reviewed 6 randomized controlled trials (RCTs) of pharmacologic interventions for adult ADHD published within the last 5 years.7 Part 2 analyzes 6 RCTs of nonpharmacologic treatments for adult ADHD published within the last 5 years (Table,8-13 page 33).","PeriodicalId":10971,"journal":{"name":"Current psychiatry","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134935347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
When used to treat anxiety or depressive disorders, antidepressants can cause a variety of adverse effects, including emotional blunting. Emotional blunting has been described as emotional numbness, indifference, decreased responsiveness, or numbing. In a study of 669 patients who had been receiving antidepressants (selective serotonin reuptake inhibitors [SSRIs], serotonin-norepinephrine reuptake inhibitors [SNRIs], or other antidepressants), 46% said they had experienced emotional blunting.1 A 2019 study found that approximately one-third of patients with unipolar depression or bipolar depression stopped taking their antidepressant due to emotional blunting.2 Historically, there has been difficulty parsing out emotional blunting (a general decrease of all range of emotions) from anhedonia (a restriction of positive emotions). Additionally, some researchers have questioned if the blunting of emotions is part of depressive symptomatology. In a study of 38 adults, most felt able to differentiate emotional blunting due to antidepressants by considering the resolution of other depressive symptoms and timeline of onset.3 A significant limitation has been how clinicians measure or assess emotional blunting. The Oxford Depression Questionnaire (ODQ), previously known as the Oxford Questionnaire on the Emotional Side-effects of Antidepressants, was created based on a qualitative survey of patients who endorsed emotional blunting.4 A validated scale, the ODQ divides emotional blunting into 4 dimensions: • general reduction in emotions • reduction in positive emotions • emotional detachment from others • not caring.4 The sections of ODQ focus on exploring specific aspects of patients’ emotional experiences, comparing experiences in the past week to before the development of illness/ emotional blunting, and patients’ opinions about antidepressants. Example statements from the ODQ (Table,4 page 47) may help clinicians better understand and explore emotional blunting with their patients. There are 2 leading theories behind the mechanism of emotional blunting on antidepressants, both focused on serotonin. The first theory offers that SSRIs alter frontal lobe activity through serotonergic effects. The second theory is focused on the downward effects of serotonin on dopamine in reward pathways.5
{"title":"Emotional blunting in patients taking antidepressants","authors":"Gemma Espejo","doi":"10.12788/cp.0392","DOIUrl":"https://doi.org/10.12788/cp.0392","url":null,"abstract":"When used to treat anxiety or depressive disorders, antidepressants can cause a variety of adverse effects, including emotional blunting. Emotional blunting has been described as emotional numbness, indifference, decreased responsiveness, or numbing. In a study of 669 patients who had been receiving antidepressants (selective serotonin reuptake inhibitors [SSRIs], serotonin-norepinephrine reuptake inhibitors [SNRIs], or other antidepressants), 46% said they had experienced emotional blunting.1 A 2019 study found that approximately one-third of patients with unipolar depression or bipolar depression stopped taking their antidepressant due to emotional blunting.2 Historically, there has been difficulty parsing out emotional blunting (a general decrease of all range of emotions) from anhedonia (a restriction of positive emotions). Additionally, some researchers have questioned if the blunting of emotions is part of depressive symptomatology. In a study of 38 adults, most felt able to differentiate emotional blunting due to antidepressants by considering the resolution of other depressive symptoms and timeline of onset.3 A significant limitation has been how clinicians measure or assess emotional blunting. The Oxford Depression Questionnaire (ODQ), previously known as the Oxford Questionnaire on the Emotional Side-effects of Antidepressants, was created based on a qualitative survey of patients who endorsed emotional blunting.4 A validated scale, the ODQ divides emotional blunting into 4 dimensions: • general reduction in emotions • reduction in positive emotions • emotional detachment from others • not caring.4 The sections of ODQ focus on exploring specific aspects of patients’ emotional experiences, comparing experiences in the past week to before the development of illness/ emotional blunting, and patients’ opinions about antidepressants. Example statements from the ODQ (Table,4 page 47) may help clinicians better understand and explore emotional blunting with their patients. There are 2 leading theories behind the mechanism of emotional blunting on antidepressants, both focused on serotonin. The first theory offers that SSRIs alter frontal lobe activity through serotonergic effects. The second theory is focused on the downward effects of serotonin on dopamine in reward pathways.5","PeriodicalId":10971,"journal":{"name":"Current psychiatry","volume":"49 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134935357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common. One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.
{"title":"A street medicine view of tobacco use in patients with schizophrenia","authors":"John W Figg","doi":"10.12788/cp.0404","DOIUrl":"https://doi.org/10.12788/cp.0404","url":null,"abstract":"Throughout my psychiatric clerkship, I (JWF) participated in street medicine, the practice of providing care to patients (typically those who are homeless) at the location they currently reside, such as in a homeless encampment or community shelter. Our clinical team drove to locations that provided housing for patients diagnosed with schizophrenia, where we assisted with medications and blood draws. I remember pulling up the first day and seeing someone outside smoking a cigarette. I soon learned that many people living in such situations were smokers, and that among the substances they used, tobacco was the most common. One patient said the cigarettes helped him manage the “voices in his head” as well as some of the adverse effects from medication, such as parkinsonism and akathisia. I asked my attending physician about this and she explained that for some patients, using tobacco was a way to mitigate the positive symptoms of schizophrenia and make the adverse effects of their therapy, particularly extrapyramidal symptoms (EPS), more bearable. By the end of my 2-week rotation, I was sure of a trend: our patients with schizophrenia smoked incessantly. Near the end of my rotation, I asked a patient, “Why do you smoke”? The patient looked at me, puzzled, and replied: “I just do.” This exchange only piqued my curiosity, and I could not help but wonder: what is the relationship between tobacco use and schizophrenia? How is tobacco use related to the pathophysiology of schizophrenia? Does tobacco use among patients with schizophrenia ameliorate aspects of their psychosis? Street medicine offered me a window into a biomedically intriguing question, and I wanted to learn more.","PeriodicalId":10971,"journal":{"name":"Current psychiatry","volume":"64 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134935346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The pandemic has permanently changed us, and its biopsychosocial sequelae linger…","authors":"Henry A Nasrallah","doi":"10.12788/cp.0402","DOIUrl":"https://doi.org/10.12788/cp.0402","url":null,"abstract":"","PeriodicalId":10971,"journal":{"name":"Current psychiatry","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134935355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M r. S, age 77, is admitted to a longterm care facility due to progressive cognitive impairment and sexually inappropriate behavior. He has a history of sexual assault of medical staff. His medical history includes significant frontotemporal dementia (FTD) with behavioral disturbances, abnormal sexual behaviors, subclinical hypothyroidism, schizoid personality disorder, Parkinson disease, posttraumatic stress disorder, and hyperammonemia. Upon admission, Mr. S’s vital signs are within normal limits except for an elevated thyroid-stimulating hormone (4.54 mIU/L; reference range 0.40 to 4.50 mIU/L). Prior cognitive testing results and updated ammonia levels are unavailable. Mr. S’s current medications include acetaminophen 650 mg every 4 hours as needed for pain, calcium carbonate/vitamin D twice daily for bone health, carbidopa/levodopa 25/100 mg twice daily for Parkinson disease, melatonin 3 mg/d at bedtime for insomnia, quetiapine 25 mg twice daily for psychosis with disturbance of behavior and 12.5 mg every 4 hours as needed for agitation, and trazodone 50 mg/d at bedtime for insomnia. Before Mr. S was admitted, previous therapy with selective serotonin reuptake inhibitors (SSRIs) had been tapered and discontinued. Mr. S had also started antipsychotic therapy at another facility due to worsening behaviors.
{"title":"Abnormal sexual behaviors in frontotemporal dementia","authors":"Alivia D Price","doi":"10.12788/cp.0382","DOIUrl":"https://doi.org/10.12788/cp.0382","url":null,"abstract":"M r. S, age 77, is admitted to a longterm care facility due to progressive cognitive impairment and sexually inappropriate behavior. He has a history of sexual assault of medical staff. His medical history includes significant frontotemporal dementia (FTD) with behavioral disturbances, abnormal sexual behaviors, subclinical hypothyroidism, schizoid personality disorder, Parkinson disease, posttraumatic stress disorder, and hyperammonemia. Upon admission, Mr. S’s vital signs are within normal limits except for an elevated thyroid-stimulating hormone (4.54 mIU/L; reference range 0.40 to 4.50 mIU/L). Prior cognitive testing results and updated ammonia levels are unavailable. Mr. S’s current medications include acetaminophen 650 mg every 4 hours as needed for pain, calcium carbonate/vitamin D twice daily for bone health, carbidopa/levodopa 25/100 mg twice daily for Parkinson disease, melatonin 3 mg/d at bedtime for insomnia, quetiapine 25 mg twice daily for psychosis with disturbance of behavior and 12.5 mg every 4 hours as needed for agitation, and trazodone 50 mg/d at bedtime for insomnia. Before Mr. S was admitted, previous therapy with selective serotonin reuptake inhibitors (SSRIs) had been tapered and discontinued. Mr. S had also started antipsychotic therapy at another facility due to worsening behaviors.","PeriodicalId":10971,"journal":{"name":"Current psychiatry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49032396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.3 It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country. Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”4 The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim. Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression The governance of our country is fractured like a dysfunctional family and could be negatively impacting the mental health of the citizenry Henry A. Nasrallah, MD, DLFAPA Editor-in-Chief
{"title":"A toxic and fractured political system can breed angst and PTSD","authors":"Henry A. Nasrallah","doi":"10.12788/cp.0393","DOIUrl":"https://doi.org/10.12788/cp.0393","url":null,"abstract":"Perhaps one of the worst experiences for a child is to witness bitterly adversarial parents (their vital role models) who argue viciously, despise each other, and hurl insults (and even punches) at each other. Such a chronically and emotionally traumatic upbringing can haunt kids well into adulthood, disrupting their hypothalamic-pituitary-adrenal axis and triggering anxiety, depression, and even psychosis due to epigenetic changes that ultimately lead to abnormal brain development.3 It often feels that the governance of our country, or the national “political family,” is seriously fractured like a hopelessly dysfunctional family. Could that be negatively impacting the mental health of the citizenry? Having 2 antagonistic political parties expressing visceral hatred and undisguised contempt for each other 24/7 (thanks to the enabling era of cable TV, the internet, and social media) has transformed each party’s fanatic followers from fellow citizens to ideological combatants. In this poisonous societal zeitgeist of bidirectional acrimony and mutual detestation, the opposing parties and their “intellectual militias” label each other as “extremists” or “radicals.” They become completely blind to any redeeming social value in the ideas or principles of their political opponents. They spend enormous time and energy on undermining each other instead of attending to the myriad vital issues involved in the governance of a massive and complex country. Winston Churchill said, “Democracy is the worst form of government, except for all the others that have been tried.”4 The current toxic cloud of intense “hyperpartisanship” is emblematic of the dark Machiavellian side of democracy. But those who lament the current distorted version of democracy should contemplate living in a dictatorship or totalitarian regime, where a despot would execute any dissenter or invade and destroy an adjacent country at a whim. Churchill made that statement in 1947. The internet, social media, and smartphones were science fiction back then. Those technological advances have added fuel to the political process and significantly stoked the flames of hyperpartisanship. It’s now democracy on steroids, where freedom of expression The governance of our country is fractured like a dysfunctional family and could be negatively impacting the mental health of the citizenry Henry A. Nasrallah, MD, DLFAPA Editor-in-Chief","PeriodicalId":10971,"journal":{"name":"Current psychiatry","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43193231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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