Int he fourth of his five lecture series, Dr. Cady reviews precision pharmacology, the need for accurate diagnosis (and treatment !) of ADHD, and how to avoid killing your patient with a drug=drug interaction. The origins of TransCranial Magnetic Stimulation are also reviewed, and its current research, as well as a patient history, is presented.
Generalized Anxiety Disorder (GAD) is a long-lasting disorder in which patients experience excessive, uncontrollable worry about everyday life events. Some key causes may include genetics and certain personality traits. Symptoms include persistent worrying, restlessness, fatigue, muscle tension and sleep problems. Treatments include cognitive behavioral therapy and antidepressant medications to help manage excessive worries and learn skills to promote relaxation. GAD affects around 3% of the US population and is more common in women than men.
This document provides information about anxiety disorders that school counselors should know. It discusses how anxiety disorders are different from normal anxiety in that they are excessive, unreasonable, and impairing. It outlines common physical, psychological, and behavioral symptoms of anxiety disorders. The document emphasizes that anxiety disorders are highly prevalent but often underdiagnosed and undertreated conditions that typically begin in childhood/adolescence. Left untreated, they can negatively impact functioning and lead to other issues.
This document discusses generalized anxiety disorder (GAD). GAD is a common anxiety disorder characterized by excessive, uncontrollable worry about daily life events for at least six months. People with GAD may experience physical symptoms like restlessness, fatigue, difficulty sleeping, and increased heart rate. The document explores GAD from psychodynamic, humanistic, cognitive, and biological perspectives and their associated therapies, such as psychodynamic therapy focusing on childhood experiences, cognitive therapy challenging irrational thoughts, and biological therapy using medication.
This document provides an overview of migraines including common signs and symptoms, facts about prevalence, and tips for tracking migraines. It also shares a personal reflection from Claire, a long-time migraine sufferer, on how tracking her migraines helped identify triggers and managing stress has been most effective for reducing migraines. The document concludes with a trigger-free fish chowder recipe from a migraine cookbook.
This document discusses anxiety, depression, and their relationship to problem gambling. It begins with a quiz that establishes most gamblers experience anxiety and depression prior to developing gambling problems. It then cites a study that found 74.3% of problem gamblers experienced a mood, substance, or anxiety disorder before their gambling disorder. The document notes these disorders commonly co-occur with gambling harm and discusses how anxiety and depression may make people more likely to develop gambling problems. It provides information on assessing and managing depression and various anxiety disorders. Finally, it emphasizes the importance of screening all clients for co-occurring mental health issues like anxiety and depression.
Generalized Anxiety Disorder (GAD), Anxiety, Anxiety Disorders, Risk Factors , Signs and Symptoms of GAD, DSM V Diagnostic Criteria for Generalized Anxiety Disorder, ICD 10 CriteriaF41.1 Generalized anxiety disorder, Prevalence and Age of Onset, Treatment, Self-help Strategies For GAD
DISCLAIMER: THIS IS A PROJECT FOR A HIGH SCHOOL AP PSYCHOLOGY COURSE. THIS IS A FICTIONALIZED ACCOUNT OF HAVING A PHSCHOLOGICAL AILMENT. FOR QUESTIONS ABOUT THIS BLOG PROJECT OR ITS CONTENT PLEASE EMAIL THE TEACHER, LAURA ASTORIAN: LAURA.ASTORIAN@COBBK12.ORG
Zoned, Stoned And Blown Pain Psych R X And C D Cady At OliverLouis Cady, MD
Ā
Review by Louis B. Cady, MD (Cady Wellness Institute) of the interdigitation between psychiatric disorders, chemical dependency and issues in treatment and recovery. This presentation reviews the enormous intertwinement between untreated ADHD and the development and maintenance of substance use and chemical dependency, examining both biological and psychodynamic influences. It concludes with tips from the recovery community and recommendations on how treatment teams can collaborate with each other.
Generalized Anxiety Disorder (GAD) is a long-lasting disorder in which patients experience excessive, uncontrollable worry about everyday life events. Some key causes may include genetics and certain personality traits. Symptoms include persistent worrying, restlessness, fatigue, muscle tension and sleep problems. Treatments include cognitive behavioral therapy and antidepressant medications to help manage excessive worries and learn skills to promote relaxation. GAD affects around 3% of the US population and is more common in women than men.
This document provides information about anxiety disorders that school counselors should know. It discusses how anxiety disorders are different from normal anxiety in that they are excessive, unreasonable, and impairing. It outlines common physical, psychological, and behavioral symptoms of anxiety disorders. The document emphasizes that anxiety disorders are highly prevalent but often underdiagnosed and undertreated conditions that typically begin in childhood/adolescence. Left untreated, they can negatively impact functioning and lead to other issues.
This document discusses generalized anxiety disorder (GAD). GAD is a common anxiety disorder characterized by excessive, uncontrollable worry about daily life events for at least six months. People with GAD may experience physical symptoms like restlessness, fatigue, difficulty sleeping, and increased heart rate. The document explores GAD from psychodynamic, humanistic, cognitive, and biological perspectives and their associated therapies, such as psychodynamic therapy focusing on childhood experiences, cognitive therapy challenging irrational thoughts, and biological therapy using medication.
This document provides an overview of migraines including common signs and symptoms, facts about prevalence, and tips for tracking migraines. It also shares a personal reflection from Claire, a long-time migraine sufferer, on how tracking her migraines helped identify triggers and managing stress has been most effective for reducing migraines. The document concludes with a trigger-free fish chowder recipe from a migraine cookbook.
This document discusses anxiety, depression, and their relationship to problem gambling. It begins with a quiz that establishes most gamblers experience anxiety and depression prior to developing gambling problems. It then cites a study that found 74.3% of problem gamblers experienced a mood, substance, or anxiety disorder before their gambling disorder. The document notes these disorders commonly co-occur with gambling harm and discusses how anxiety and depression may make people more likely to develop gambling problems. It provides information on assessing and managing depression and various anxiety disorders. Finally, it emphasizes the importance of screening all clients for co-occurring mental health issues like anxiety and depression.
Generalized Anxiety Disorder (GAD), Anxiety, Anxiety Disorders, Risk Factors , Signs and Symptoms of GAD, DSM V Diagnostic Criteria for Generalized Anxiety Disorder, ICD 10 CriteriaF41.1 Generalized anxiety disorder, Prevalence and Age of Onset, Treatment, Self-help Strategies For GAD
DISCLAIMER: THIS IS A PROJECT FOR A HIGH SCHOOL AP PSYCHOLOGY COURSE. THIS IS A FICTIONALIZED ACCOUNT OF HAVING A PHSCHOLOGICAL AILMENT. FOR QUESTIONS ABOUT THIS BLOG PROJECT OR ITS CONTENT PLEASE EMAIL THE TEACHER, LAURA ASTORIAN: LAURA.ASTORIAN@COBBK12.ORG
Zoned, Stoned And Blown Pain Psych R X And C D Cady At OliverLouis Cady, MD
Ā
Review by Louis B. Cady, MD (Cady Wellness Institute) of the interdigitation between psychiatric disorders, chemical dependency and issues in treatment and recovery. This presentation reviews the enormous intertwinement between untreated ADHD and the development and maintenance of substance use and chemical dependency, examining both biological and psychodynamic influences. It concludes with tips from the recovery community and recommendations on how treatment teams can collaborate with each other.
This document discusses differentiating between attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder in children. It poses four key questions about whether they are separate illnesses, overlapping syndromes, coexistent symptoms, or if ADHD is a warning sign of bipolar disorder. It then provides background on the history and diagnostic criteria of ADHD, as well as statistics on its prevalence. It also discusses the challenges of diagnosing pediatric bipolar disorder and lists common developmental manifestations of manic symptoms in children. The document notes that ADHD and bipolar disorder are highly comorbid conditions and explores some ways to differentiate between the two.
Caregiver stress can manifest physically, emotionally, and psychologically and put caregivers at risk for poor health outcomes and early mortality. Screening tools like the Zarit Burden Interview can help physicians identify caregivers experiencing high levels of stress. Interventions may include reducing caregiving demands through respite services, counseling, or institutionalizing the care recipient in extreme cases. It is important to evaluate the health status and needs of both the caregiver and care recipient as a unit.
The document discusses anxiety in children and adolescents. It describes the differences between depressed mood versus a depressive episode, and lists the diagnostic criteria for a major depressive episode. It also discusses irritable mood and the various conditions it could indicate. The document provides information on generalized anxiety disorder, including prevalence, genetics, neurotransmitters involved, and treatment options. It covers specific phobias and social phobia, including diagnostic criteria, prevalence, etiology, and treatment.
The document summarizes research on generalized anxiety disorder. It discusses the symptoms of excessive worrying across multiple areas and how it differs from other anxiety disorders. Generalized anxiety is caused by both biological and psychological factors like genetics and life stressors. It is typically treated through medications like antidepressants and psychotherapy like cognitive behavioral therapy, which helps patients replace negative thoughts with positive ones.
Sally, a 49-year-old woman, has experienced increasing anxiety, sleep difficulties, and panic attacks over the past 6 months. She was prescribed Xanax by her doctor but stopped taking it due to rebound anxiety. Her sleep, nutrition, pain levels, libido, and cognitive patterns were assessed using the PACER method. She reports stress, worry, and difficulty concentrating associated with family, health, and financial concerns. Recommendations included improving sleep hygiene, managing stress and anxiety, and following up with her primary care doctor.
Separation anxiety disorder involves excessive anxiety regarding separation from home or attachment figures. It is characterized by distress when anticipating or experiencing separation, persistent worry about harm befalling attachment figures, and reluctance or refusal to go places alone. It is diagnosed when fears or avoidance last at least 4 weeks in children or typically 6 months in adults and cause impairment. Treatment involves cognitive behavioral therapy and may include medication, parenting techniques, or family therapy. Prognosis is generally good with treatment, though co-occurring conditions or actual threats of separation decrease likelihood of positive outcomes.
This document provides an overview of social anxiety disorder. It begins by defining social anxiety and noting that it will focus on using the term "social anxiety" in this presentation. It then outlines that it will present information separately on social anxiety in adults and children. The main points covered include: what social anxiety looks like, characteristics of specific vs. generalized social anxiety, how social anxiety manifests differently in children, brain characteristics associated with social anxiety, how it is differentiated from other disorders, and examples of differential diagnoses.
This document presents a case study of a 7 year old male, OT, who is exhibiting unpredictable, impulsive, aggressive, and threatening behavior towards family members. His mother reports he has had behavioral issues since age 3 that have continued without improvement. He has a history of suicidal threats and attempts. A psychiatric evaluation finds OT to have poor impulse control, judgment, attention, and concentration. He is started on multiple medications without significant response. The document discusses opinions on diagnosing and treating pediatric bipolar disorder, particularly around issues of rapid cycling and mixed episodes in children.
This class offers developmental learning for educators working with children who have been exposed to overwhelming life events. This can occur in up to 25% of children in certain contexts. Traumatic experiences change neurobiological, social and educational development. Addressing the impact of trauma on learning can impact the long-term possibilities in a child's life
This case study documents the psychotherapeutic treatment of a 25-year-old woman referred to a psychiatrist due to severe headaches and blackouts. During therapy, it was discovered she had multiple personality disorder, alternating between personalities of Eve White and Eve Black. Objective psychological tests found differences between the personalities, and family members corroborated behavioral changes. The therapy aimed to help the personalities integrate, with some success though others questioned this account. The case study provides evidence for multiple personality disorder but is limited by potential researcher bias and lack of independent verification.
A 2015 presentation by Victoria Costello, science journalist, author and mental health advocate, demonstrating how lay advocates can access and incorporate scientific evidence into their family and community advocacy for mental health for all. References Victoria Costello's memoir, A Lethal Inheritance, A Mother Uncovers the Science Behind Three Generations of Mental Illness, published by Prometheus in 2012. Presented on May 29, 2015 at the annual meeting of Parent Professional Advocacy League in MA. Website: http://www.mentalhealthmomblog.com
This document discusses depression, anxiety, and epilepsy in children and adolescents. It finds that depression and anxiety are very common psychiatric issues for those with epilepsy. Rates of depression are over 20% for those with epilepsy, compared to 3.7-6.7% in the general population. Anxiety affects up to 40% of youth with epilepsy. The document examines risk factors, screening tools, and treatments like cognitive behavioral therapy and antidepressant medications to address the high prevalence of these important mental health issues in pediatric epilepsy.
This document analyzes the biological, cognitive, and sociocultural etiologies of social anxiety disorder and depression. For social anxiety disorder, biological factors include an oversensitive amygdala and genetic predispositions, while cognitive factors involve negative core beliefs developed from social experiences. Sociocultural influences include parenting styles and societal emphasis on competition. For depression, biological theories point to genetic and neurotransmitter imbalances, while cognitive theories cite irrational thinking patterns. Sociocultural risk factors include life stressors and varying conceptions of depression across cultures. Both disorders vary in prevalence by gender and culture.
This document provides information on Unipolar Mood Disorder and defines Unipolar Disorder as a mental disorder characterized by pervasive and persistent low mood accompanied by low self-esteem and loss of interest in enjoyable activities. It discusses the manifestations of Unipolar Disorder which can affect daily life for weeks or longer by interfering with social, family, work, academic, and health aspects of life. The document also lists and describes several types of Depressive Disorders including Major Depressive Disorder, Persistent Depressive Disorder, and Premenstrual Dysphoric Disorder. It provides details on the diagnostic criteria, clinical manifestations, causes, assessment tools, prognosis, prevalence, and treatment options for these disorders.
Mental health disorders commonly co-occur with gambling harm. Around 96% of those meeting criteria for pathological gambling disorder also meet criteria for at least one other psychiatric disorder, with two-thirds meeting criteria for three or more disorders. The most common co-occurring disorders are substance use disorders (42%), mood disorders like depression (56%), and anxiety disorders (60%). Overall, around 74% of problem gamblers experienced the other disorder prior to developing problems with gambling. Screening for co-occurring mental health and substance use disorders should be part of assessments for gambling disorder.
Jen is an 18-year-old German male who has stopped attending high school due to obsessive-compulsive disorder. He experiences obsessions of contamination along with compulsions of excessive washing. His symptoms have worsened over time, interfering with activities and isolating him. While aware his thoughts are unreasonable, he feels unable to resist them. His symptoms meet criteria for OCD but no other disorders are present. Treatment options will be discussed.
This document provides information on helping elderly friends and family who may be depressed. It defines depression, lists common causes in the elderly like loneliness or illness, and signs to watch for like changes in mood or appetite. It recommends offering social support, encouraging activities, and seeing a doctor. Senior centers in the area are listed that can help connect seniors to programs, healthcare, and each other. A quiz called the Geriatric Depression Scale is included to help assess depression risk in the elderly.
Cognitive-behavioral therapy is the best approach for treating social anxiety disorder based on its past higher success rates compared to other approaches. CBT combines cognitive therapy to examine how negative thoughts contribute to anxiety with behavior therapy to examine how patients behave and react to anxiety-triggering situations. Studies have shown CBT to be superior to biological treatments like medication in the long run, with more successful outcomes than psychoanalysis, trait theory, and other approaches. While no approach is perfect, CBT provides patients with effective tools to overcome social anxiety by addressing both cognitions and behaviors.
This document discusses depression, including its definition, burden, causes, risk factors, diagnosis criteria, prevention, and treatment. It defines depression as a common and chronic mental disorder characterized by depressed mood and loss of pleasure. Risk factors include age, gender, family history, and genetics. Diagnosis is based on DSM-IV-TR criteria of symptoms present for two weeks. Treatment involves pharmacotherapy like SSRIs and SNRIs as well as non-pharmacological therapies. Prevention focuses on primary, secondary, and tertiary levels through health promotion, screening high-risk groups, and reducing relapse.
A divorced 39-year-old woman presented with physical symptoms but was found to have dysthymic disorder after being prescribed an SSRI. Dysthymic disorder is a chronic form of depression lasting at least two years characterized by less severe but persistent symptoms. It is important to treat as it can be as debilitating as major depression and increases the risk of developing additional disorders. Prognosis is often chronic without treatment but SSRIs and other therapies can provide relief of symptoms.
This document discusses differentiating between attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder in children. It poses four key questions about whether they are separate illnesses, overlapping syndromes, coexistent symptoms, or if ADHD is a warning sign of bipolar disorder. It then provides background on the history and diagnostic criteria of ADHD, as well as statistics on its prevalence. It also discusses the challenges of diagnosing pediatric bipolar disorder and lists common developmental manifestations of manic symptoms in children. The document notes that ADHD and bipolar disorder are highly comorbid conditions and explores some ways to differentiate between the two.
Caregiver stress can manifest physically, emotionally, and psychologically and put caregivers at risk for poor health outcomes and early mortality. Screening tools like the Zarit Burden Interview can help physicians identify caregivers experiencing high levels of stress. Interventions may include reducing caregiving demands through respite services, counseling, or institutionalizing the care recipient in extreme cases. It is important to evaluate the health status and needs of both the caregiver and care recipient as a unit.
The document discusses anxiety in children and adolescents. It describes the differences between depressed mood versus a depressive episode, and lists the diagnostic criteria for a major depressive episode. It also discusses irritable mood and the various conditions it could indicate. The document provides information on generalized anxiety disorder, including prevalence, genetics, neurotransmitters involved, and treatment options. It covers specific phobias and social phobia, including diagnostic criteria, prevalence, etiology, and treatment.
The document summarizes research on generalized anxiety disorder. It discusses the symptoms of excessive worrying across multiple areas and how it differs from other anxiety disorders. Generalized anxiety is caused by both biological and psychological factors like genetics and life stressors. It is typically treated through medications like antidepressants and psychotherapy like cognitive behavioral therapy, which helps patients replace negative thoughts with positive ones.
Sally, a 49-year-old woman, has experienced increasing anxiety, sleep difficulties, and panic attacks over the past 6 months. She was prescribed Xanax by her doctor but stopped taking it due to rebound anxiety. Her sleep, nutrition, pain levels, libido, and cognitive patterns were assessed using the PACER method. She reports stress, worry, and difficulty concentrating associated with family, health, and financial concerns. Recommendations included improving sleep hygiene, managing stress and anxiety, and following up with her primary care doctor.
Separation anxiety disorder involves excessive anxiety regarding separation from home or attachment figures. It is characterized by distress when anticipating or experiencing separation, persistent worry about harm befalling attachment figures, and reluctance or refusal to go places alone. It is diagnosed when fears or avoidance last at least 4 weeks in children or typically 6 months in adults and cause impairment. Treatment involves cognitive behavioral therapy and may include medication, parenting techniques, or family therapy. Prognosis is generally good with treatment, though co-occurring conditions or actual threats of separation decrease likelihood of positive outcomes.
This document provides an overview of social anxiety disorder. It begins by defining social anxiety and noting that it will focus on using the term "social anxiety" in this presentation. It then outlines that it will present information separately on social anxiety in adults and children. The main points covered include: what social anxiety looks like, characteristics of specific vs. generalized social anxiety, how social anxiety manifests differently in children, brain characteristics associated with social anxiety, how it is differentiated from other disorders, and examples of differential diagnoses.
This document presents a case study of a 7 year old male, OT, who is exhibiting unpredictable, impulsive, aggressive, and threatening behavior towards family members. His mother reports he has had behavioral issues since age 3 that have continued without improvement. He has a history of suicidal threats and attempts. A psychiatric evaluation finds OT to have poor impulse control, judgment, attention, and concentration. He is started on multiple medications without significant response. The document discusses opinions on diagnosing and treating pediatric bipolar disorder, particularly around issues of rapid cycling and mixed episodes in children.
This class offers developmental learning for educators working with children who have been exposed to overwhelming life events. This can occur in up to 25% of children in certain contexts. Traumatic experiences change neurobiological, social and educational development. Addressing the impact of trauma on learning can impact the long-term possibilities in a child's life
This case study documents the psychotherapeutic treatment of a 25-year-old woman referred to a psychiatrist due to severe headaches and blackouts. During therapy, it was discovered she had multiple personality disorder, alternating between personalities of Eve White and Eve Black. Objective psychological tests found differences between the personalities, and family members corroborated behavioral changes. The therapy aimed to help the personalities integrate, with some success though others questioned this account. The case study provides evidence for multiple personality disorder but is limited by potential researcher bias and lack of independent verification.
A 2015 presentation by Victoria Costello, science journalist, author and mental health advocate, demonstrating how lay advocates can access and incorporate scientific evidence into their family and community advocacy for mental health for all. References Victoria Costello's memoir, A Lethal Inheritance, A Mother Uncovers the Science Behind Three Generations of Mental Illness, published by Prometheus in 2012. Presented on May 29, 2015 at the annual meeting of Parent Professional Advocacy League in MA. Website: http://www.mentalhealthmomblog.com
This document discusses depression, anxiety, and epilepsy in children and adolescents. It finds that depression and anxiety are very common psychiatric issues for those with epilepsy. Rates of depression are over 20% for those with epilepsy, compared to 3.7-6.7% in the general population. Anxiety affects up to 40% of youth with epilepsy. The document examines risk factors, screening tools, and treatments like cognitive behavioral therapy and antidepressant medications to address the high prevalence of these important mental health issues in pediatric epilepsy.
This document analyzes the biological, cognitive, and sociocultural etiologies of social anxiety disorder and depression. For social anxiety disorder, biological factors include an oversensitive amygdala and genetic predispositions, while cognitive factors involve negative core beliefs developed from social experiences. Sociocultural influences include parenting styles and societal emphasis on competition. For depression, biological theories point to genetic and neurotransmitter imbalances, while cognitive theories cite irrational thinking patterns. Sociocultural risk factors include life stressors and varying conceptions of depression across cultures. Both disorders vary in prevalence by gender and culture.
This document provides information on Unipolar Mood Disorder and defines Unipolar Disorder as a mental disorder characterized by pervasive and persistent low mood accompanied by low self-esteem and loss of interest in enjoyable activities. It discusses the manifestations of Unipolar Disorder which can affect daily life for weeks or longer by interfering with social, family, work, academic, and health aspects of life. The document also lists and describes several types of Depressive Disorders including Major Depressive Disorder, Persistent Depressive Disorder, and Premenstrual Dysphoric Disorder. It provides details on the diagnostic criteria, clinical manifestations, causes, assessment tools, prognosis, prevalence, and treatment options for these disorders.
Mental health disorders commonly co-occur with gambling harm. Around 96% of those meeting criteria for pathological gambling disorder also meet criteria for at least one other psychiatric disorder, with two-thirds meeting criteria for three or more disorders. The most common co-occurring disorders are substance use disorders (42%), mood disorders like depression (56%), and anxiety disorders (60%). Overall, around 74% of problem gamblers experienced the other disorder prior to developing problems with gambling. Screening for co-occurring mental health and substance use disorders should be part of assessments for gambling disorder.
Jen is an 18-year-old German male who has stopped attending high school due to obsessive-compulsive disorder. He experiences obsessions of contamination along with compulsions of excessive washing. His symptoms have worsened over time, interfering with activities and isolating him. While aware his thoughts are unreasonable, he feels unable to resist them. His symptoms meet criteria for OCD but no other disorders are present. Treatment options will be discussed.
This document provides information on helping elderly friends and family who may be depressed. It defines depression, lists common causes in the elderly like loneliness or illness, and signs to watch for like changes in mood or appetite. It recommends offering social support, encouraging activities, and seeing a doctor. Senior centers in the area are listed that can help connect seniors to programs, healthcare, and each other. A quiz called the Geriatric Depression Scale is included to help assess depression risk in the elderly.
Cognitive-behavioral therapy is the best approach for treating social anxiety disorder based on its past higher success rates compared to other approaches. CBT combines cognitive therapy to examine how negative thoughts contribute to anxiety with behavior therapy to examine how patients behave and react to anxiety-triggering situations. Studies have shown CBT to be superior to biological treatments like medication in the long run, with more successful outcomes than psychoanalysis, trait theory, and other approaches. While no approach is perfect, CBT provides patients with effective tools to overcome social anxiety by addressing both cognitions and behaviors.
This document discusses depression, including its definition, burden, causes, risk factors, diagnosis criteria, prevention, and treatment. It defines depression as a common and chronic mental disorder characterized by depressed mood and loss of pleasure. Risk factors include age, gender, family history, and genetics. Diagnosis is based on DSM-IV-TR criteria of symptoms present for two weeks. Treatment involves pharmacotherapy like SSRIs and SNRIs as well as non-pharmacological therapies. Prevention focuses on primary, secondary, and tertiary levels through health promotion, screening high-risk groups, and reducing relapse.
A divorced 39-year-old woman presented with physical symptoms but was found to have dysthymic disorder after being prescribed an SSRI. Dysthymic disorder is a chronic form of depression lasting at least two years characterized by less severe but persistent symptoms. It is important to treat as it can be as debilitating as major depression and increases the risk of developing additional disorders. Prognosis is often chronic without treatment but SSRIs and other therapies can provide relief of symptoms.
Mood disorders are disturbances of emotions that affect many aspects of life. The three main types are depression, dysthymia, and bipolar disorder. Depression involves feeling sad for at least two weeks with symptoms like fatigue and guilt. Dysthymia is a chronic, milder form of depression lasting two years. Bipolar disorder causes alternating episodes of depression and mania, an elevated mood with increased energy. Treatment involves medication and psychotherapy, as finding an effective drug combination can take years due to side effects.
Amplified Adolescent Anxiety During A PandemicCyndy McDonald
Ā
In normal times teenagers experience a great amount of stress and anxiety. This stress and anxiety has been amplified during the pandemic. One of the greatest contributors has been the uncertainty around standardized testing options. If students can't go to school, how are they supposed to go take an exam?
The document summarizes research on depression among medical students. Some key findings:
- Depression rates are similar entering medical school but increase disproportionately over the course of study, peaking as students prepare for clinical work. Long hours, stress, and insecurity about examinations contribute.
- Over 50% of medical students seek help for depression or other mental health issues. Females are more likely to experience depression than males.
- Depression can be effectively treated with antidepressants and psychotherapy. Untreated, it can lead to disability, absenteeism, suicide and economic costs.
- A study of Gulf Medical University students found depression in 25% of students. Rates varied by gender, nationality,
Developmental psychopathology examines how development influences psychopathology and vice versa. Clinicians use statistical deviance, maladaptiveness, and personal distress to define abnormal behavior. Autism is characterized by impaired social skills, communication, and repetitive behaviors and has a biological basis. Attention deficit hyperactivity disorder involves inattention, impulsivity, and hyperactivity and may be linked to low neurotransmitter levels. Treating developmental disorders in children is challenging due to their cognitive levels and need for parental involvement. In Ethiopia, awareness of such disorders is low and traditional beliefs influence treatment.
Understanding DMDDTreating kids with protracted anger outbursts and irritabi...Stephen Grcevich, MD
Ā
Learning Objectives:
Examine why DMDD was established as a stand-alone diagnosis in DSM-5, review the diagnostic criteria for DMDD, along with the differential diagnosis from other common conditions and explore what we know about treating kids with DMDD
The document discusses the controversy around diagnosing pediatric bipolar disorder. It outlines key perspectives, diagnostic criteria, and a lack of conclusive research evidence. Symptoms used to diagnose bipolar disorder in children are subjective and overlap with other disorders. International views show more skepticism about the validity of the diagnosis in pre-pubescent children. Further research is still needed to definitively diagnose or rule out the existence of bipolar disorder in young children.
ADHD is a developmental disorder affecting 3-6% of children that impacts executive function in the brain. It causes problems with attention span, impulse control, and activity level. The main symptoms are inattention, hyperactivity, and impulsivity. While a real disorder, ADHD is often underestimated and management includes medication, therapy, classroom support, and nutrition.
This document summarizes a conference on new developments in pharmacological and therapeutic interventions for ADHD. Dr. Gabriel Kaplan and Dr. Bennett Silver presented on various topics. Dr. Kaplan discussed ADHD epidemiology and diagnosis, as well as non-stimulant treatments and new approaches. Dr. Silver presented on stimulant medications and non-medication approaches. The document provides an agenda and background on the speakers. It also reviews stimulant treatment options, side effects, and considerations for non-stimulant use.
General Anxiety Disorder and Panic Disorder.pptxChitra654025
Ā
Generalized Anxiety Disorder (GAD) is characterized by excessive, uncontrollable worry about everyday life events. Individuals with GAD experience intense worry for long periods and have difficulty controlling their worry through coping strategies. This interferes with daily tasks and causes physical symptoms like restlessness, fatigue, difficulty concentrating, and sleep problems. GAD is common, affecting about 3% of adults and 6% of children, and is often comorbid with depression and substance abuse disorders. Biological and genetic factors contribute to vulnerabilities for developing GAD.
A 42-year-old man is experiencing a recurrent major depressive episode. He had previously responded well to treatment with imipramine but did not tolerate the anticholinergic side effects. Given his history of responding well to antidepressants and preference to avoid side effects, an SSRI with fewer anticholinergic effects would be a suitable first-line treatment option for this episode. Close monitoring would also be important given his risk of recurrence.
Are you currently supporting someone with depression or even struggling with it yourself? Educating yourself on the topic can help you immensely with some great coping skills and even encourage the first step to getting professional help.
Zoned, Stoned And Blown - by Louis B. Cady, M.D. and Lisa Seif, LCSW, CADAC02...Louis Cady, MD
Ā
This presentation reviews the diagnosis, treatment, and sobriety maintenance of dual diagnosis disorders ( psychiatric disorders coupled with chemical dependency and/or alcoholism), using a synthetic blend of two talented clinicians' experiences, humor, and review of precision diagnosis, treatment formulations, and interventions.
Depression comes in several forms including major depression, dysthymic disorder, and bipolar disorder. It is a whole-body illness that affects mood, thoughts, and physical symptoms. Common causes include stressful life events, illness, loss, and substance abuse. Treatment involves medication, counseling, diet, exercise, and avoiding drugs/alcohol. Caregivers should understand the illness, support treatment, listen without judgment, and care for themselves. Depression affects about 1 in 10 Americans.
Depression is a mental condition characterized by feelings of severe despondency and dejection. It can cause a lack of energy and difficulty maintaining interest in activities. Common symptoms include feelings of hopelessness, guilt, worthlessness, difficulty concentrating and sleeping, changes in appetite, and thoughts of death or suicide. Depression is one of the most common mental illnesses, affecting about 20% of the population at some point in their lives. It is linked to changes in brain chemistry and activity, especially in the frontal and temporal lobes of the left side of the brain.
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Mood Disorders
...no longer Mood Disorders...
Major Depressive Disorder
!āÆ Depressed mood or loss of interest over a 2 week period
!āÆ 5 or more symptoms present (with at least 1 symptom being
depressed mood or loss of interest/pleasure)
!āÆ Depressed mood (in kids, can be irritability)
!āÆ Diminished interest or pleasure in all, or almost all, activities
!āÆ Significant weight loss or weight gain (not from dieting;
change of more than 5%)
!āÆ Insomnia or hypersomnia
!āÆ Psychomotor agitation or retardation
!āÆ Fatigue/loss of energy
!āÆ Feelings of worthlessness/excessive guilt
!āÆ Diminished ability to think or concentrate
!āÆ Suicidal ideation
!āÆ Criterion B: Symptoms cause clinically significant
distress or impairment in social/occupational
!āÆ Criterion C: Not attributable to physiological effects
of a substance or general medical condition
!āÆ Criterion D: Depressive episode not better
explained by schizoaffective disorder,
schizophrenia, schizophreniform disorder,
delusional disorder
!āÆ Criterion E: No history of manic or hypomanic
episode
Specifiers
!āÆ Severity: mild, moderate, severe
!āÆ With mixed features (experience at least 3 manic or
hypomanic symptoms during the course of a major
depressive episode)
!āÆ With anxious distress (experience of at least 2 anxiety
symptoms during course of depressive episode)
!āÆ Melancholic features, atypical features, mood-congruent
psychotic features, mood-incongruent psychotic
features, with catatonia, with seasonal pattern
Bye Bye Bereavement
Exclusion
!āÆ Removed exclusion that depression cannot be
diagnosed in context of bereavement within 2
months of loss
!āÆ Ensured that someone grieving was not diagnosed as
ill/depressed
!āÆ Why did DSM 5 get rid of it?
!āÆ Used Wakefieldās research against him
Wakefieldās Research on
Loss
!āÆ Why are/were other serious losses that can cause sadness
ignored? Why only exclusion for bereavement?
!āÆ Is bereavement different than other losses/stresses?
!āÆ Mined data from NIMH survey
!āÆ No differences between those whose symptoms were triggered
by bereavement vs. different losses (e.g., divorce, financial)
!āÆ Looked at how bereaved vs. nonbereaved differed on number of,
and duration of, symptoms (as well as which symptoms were
reported)
!āÆ Conclusion: other losses just as likely to leave a person
depressed
!āÆ No scientific reason to treat death of loved one differently
!āÆ Expand bereavement exclusion to āother life stressorsā to
distinguish disorder from suffering?
Wakefield vs. DSM 5
!āÆ Return to pre-DSM II idea that sadness in response
to loss is normal/human condition (reaction)
!āÆ Differentiates suffering from disorder
!āÆ DSM 5 taskforce: these findings show that
bereavement should not be a special exclusion
!āÆ All qualify as mentally ill
!āÆ Ohā¦I see what you did thereā¦
Persistent Depressive
Disorder
!āÆ The new dysthymia and chronic MDD
!āÆ This is ...
Similar to Scratching Your Head Psychiatry II: How to Practice INSIDE the Allopathic Box (20)
The Moral Imperative of Integrative Medicine 2024.pptxLouis Cady, MD
Ā
This presentation was presented to a nationwide seminar audience for the Psychiatry Redfined program on June 22, 2024. The following topics were covered:
- MTHFR polymoprhisms
- how to spot them
- how to treat them
- failed psychopharmacology
- schizophrnenia
- clozapine
- clozapine therapy for schizophrenia
In short, this entire presentation was about recognizing functional medicine abnormalities in things that we normally consdier as "biological" psychiatric conditiions.
SEND IN THE SHRINKS - 2009 Oliver CME seminarLouis Cady, MD
Ā
This one was fun.
I was invited by Dr. Randalll Oliver, MD, Founder of the Oliver Heachache and Pain Clinic in Evansville, to present to an audience of primary care practitioners about how to use pysychiatric mediations ("psychopharmacology") in clinical practice.
Along the way, I covered, ADHD and treatments, depression, anxiety, erectile dysfunction, hypoadrenia, and even touched on hypothyroidism. Although this presentation was in 2009, all of the drugs covered are stills in use, and, at times.... stupidly.
This presentation deconstructs the intricacies of selecting and antidepressant, particularly in the SSRI class.
What is the nature of QUALITY in medicine -for ASQ 11 14 2023.pptLouis Cady, MD
Ā
In this presentation, Dr. Cady deconstructs the tensions and stressors on both patients and health care providers in today's system.
This presentation reviews checklists foe liminating mistakes, the actual number of mistakes that are being made in medical practice, and what patients and their loved ones can do for self protection.
This isn't a "bash the doctor" presentation. It's a thoughtful, careful exploration of stresses and ramifications to the current US healthcare system.
This document provides information about a presentation given by Dr. Louis B. Cady on transcranial magnetic stimulation (TMS) as a treatment for depression. It begins with Dr. Cady's credentials and commercial disclosure stating he has received honoraria from several companies but that this presentation is not being underwritten by any company. The presentation then covers how TMS works, its safety and effectiveness compared to antidepressant medications and electroconvulsive therapy (ECT), and its inclusion in treatment guidelines for depression.
Hormones and Mental Health - Thyroid and Testosterone.pptxLouis Cady, MD
Ā
In this presentation for the Psychiatry Redefined program, Dr.
Cady breaks down and deconstructs the accepted, unthinking, "practice guideline based" notions of thyroid and tesotsterone, with there seemingly "normal" levels and dosing, versus what the actual peer reviewed medical literature says. In this presentation, do use of all forms of thyroid, and all forms of testosterone are reviewed. The idiocy of "T4 only treatment" is covered. The use of T4, T3, a combination of T4 and T3, and all of the porcine and compounded products is review.
In terms of testosterone, dr. Katie reviews the concept of "do you want to be optimal or do you want to be normal." He notes that it is "normal" for oil in cars to deteriorate and break down with age. It's also "normal" for men's and women's testosterone (as well as thyroid) to go down with age. The question is, "do we want to do anything about it?"
Logical ways of intervening in both the thyroid and female and male gonadal axes are covered. There is scrupulous attention paid to the thyroid hormone pathways, and the relevance of reverse T3 versus free T3. Similarly, in terms of women, the downstream effect of estradiol coming from testosterone is also reviewed.
The Moral Imperative of Integrative Medicine 2022.pptLouis Cady, MD
Ā
The document discusses the case of a 16-year-old teenager with a long history of treatment-resistant depression and anxiety. Previous medication trials with SSRIs, SNRIs, atypical antipsychotics, and lamotrigine had failed to provide sustained relief. Upon further evaluation, the doctor found potential contributing factors including an undiagnosed MTHFR gene mutation and hormonal imbalances. The doctor adjusted the teenager's supplements and medications, focusing on addressing the underlying functional issues. At follow-up several months later, the teenager reported significantly improved mood with only brief periods of low mood, though menstrual irregularities persisted.
Dr. Cady deconstructs some the medical literature about the use of nutrients - and the evidence of what happens in the presence of their insufficiency. Everything for decreased viral replication to decrease brain shrinkage is covered. The role of antioxidant and carotenoids, measured by the Pharmanex Biophotonic Scanner, is reviewed.
Please note - there is no representation that any nutrient or supplement can treat, prevent, mitigate, or cure any medical condition. It does seem, however, upon reflecting on the medical literature, that there seems to be a lot of evidence for therapeutic effect in the presence of good levels of nutrient, and harm to patients if they have insufficient levels.
Subtitle: The Moral Imperative of Integrative Medicine
This presentation, two hours in length, was delivered to the A4m MMI Audience in their Frontiers of Neurology - Module 3.
The following topics are reviewed:
- ADHD, Autism, Depression, Schizophrenia
- the impact of neuroinflammation on all of these.
- confounding factors and the ways to mitigate them: Omega6/Omega 3 imbalance in the Western diet, MTHFR polymorphism, the use of elemental lithium, the presence of intestinal dysbiosis and the role of gluten/dairy IgG Food allergies.
- pharmacogenomic testing
The Moral Imperative of Integrative Medicine - IMMH 2020Louis Cady, MD
Ā
IN this presentation, Dr. Cady reviews several of the handful of functional, integrative medicine techniques required for a holistic and comprehensive management of psychiatric issues. MTHFR, hormone balance, diagnosis and treating intestinal dysbiosis, need for trace elements, and hormones (including thyroid, testosterone and estradiol) are reviewed.
This brief webinar, a gift to the local Jewish community and Temple Adath B'Nai Israel here in Evansville, IN, reviews the tradition of mindfulness and the interdigitation of Buddhist practices with some Jewish traditions. Dr. Cady reviews the downstream effects of stress, how meditation and mindfulness are useful tools and techniques, and actually how to practice it. Multiple references without being complicated or overdone are provided.
Webinar 5: Designing Your Future: WHAT'S COMING NEXT?Louis Cady, MD
Ā
In this capstone webinar presentation, closing out Dr. Cady's series on dealing with COVID 19, he turns his attention to a nunmber of interesting thems:
- what's the REAL case fatality rate of COVID 19
- How is it likely that society will reopen?
- What's going to happen in education and medicine?
- What's going to happen when the robots and AI arrive?
- What's the future going to be out 500 years?
HOW TO SAVE MONEY ON YOUR HEALTHCARE: An Integrative Medicine ApproachLouis Cady, MD
Ā
In this webinar, the fourth in a series of five from Dr. Louis Cady and the Cady Wellness Institute, we focus on the actual dollars and cents of health care expenditures, and the societal and PERSONAL costs of poor health maintenance behavior. We examine the essentially passive US medical system, that would rather drug a symptom than fix the underlying problem.
Great attention is paid on not shaming the patient or the doctors as they exist in the current system. Both groups "do not know what they do not know." Confirmation bias is rampant.
This webinar points the way to living a more vital, energetic life, with a minimum of cost, grief, and misery.
The Do It To Yourself Treatment of Depression - Webinar #3Louis Cady, MD
Ā
This is the third in a series of five webinars. The first was on staying alive by boosting your immunity during COVID 19. The second was on not screwing yourself up inside your head. This third one encompasses a romp through the peer reviewed medical literature looking for supplements and nutrients that you could use to self treat depression at home, CAREFULLY. Numerous cautions and warnings are included.
The driving impetus to this program is that many people - due to social isolation and their mental health care, or medical practitioners' offices being closed down - have not been able to get help or succeed in optimizing their treatment for depression. There are multiple useful nutrients for both depression and anxiety in nature's abundant pharmacopeia, and this webinar touches on just a few of them.
I hope you enjoy it.
HOW TO COPE WITH THE PSYCHOLOGICAL IMPACT OF COVID 19 AND SOCIAL DISTANCINGis...Louis Cady, MD
Ā
In this presentation, Dr. Cady will review:
- What did Sparky learn about not being an emotional support animal?
- "Do it to yourself psychotherapy." Learn the following:
- What are the wrong - and the RIGHT ways of any sort of "behavioral therapy"?
- How to use a journal to think RATIONALLY and āget out of your head.ā
- How to get out of your HEAD and into your LIFE.
- We'll cover all 10 of David Burnsā cognitive distortions, customized and gift-wrapped for dealing with COVID 19.
- We will cover actionable examples of how to reprogram yourself.
We will review What are the 3 P's of Positive Psychology and Learned Optimism?
The Cady 5 "5Pāsā and āHow to shrink yourself."
Can we find the GOOD in COVID?
This presentation is meant to be provocative and to challenge you mentally, intellectually, and emotionally. Some of the great thinkers and exemplars of human performance and possibility are featured.
BOOSTING YOUR IMMUNITY During the COVID 19 PandemicLouis Cady, MD
Ā
In this presentation, presented as a live webinar on Monday, April 27th, Dr. Louis Cady of the Cady Wellness Institute reviewed practical, common-sense things that can be done to boost your immunity, with documentation from the peer-reviewed medical literature. Dr. Cady also reviews supplements and nutrients that are established in the peer-reviewed medical literature as having antiviral capabilities. These include Vitamins C,D, and E, Zinc, carotenoids and antioxidants, probiotics, the reishi mushroom, elderberry, cannabidiol (CBD - not marijuana or weed!).
Points presented are scrupulously documented from the medical literature. This presentation does not guarantee or represent that using ANY of these nutrients will "keep you from getting infected or dying" from COVID 19. They are presented for your thoughtful consideration.
The integrative treatment of schizophrenia brazil 2019Louis Cady, MD
Ā
This is the English language version of Dr. Cady's presentation given at UNIP (Campus Paraiso - Sao Paulo, SP Brazil) for the 2019 Congresso de Saude Mental (Conference on Mental Health). It was delivered April 20, 2019.
This presentation also includes extra slides in the appendix that were not presented, and, unfortunately, these slides of the appendix have not been translated in the Portuguse version of this presentation.
In this presentation (Portuguese presentation will also be posted next), Dr. Cady briefly reviews the history of schizophrenia, the failure of the dopamine D2 receptor blockage as a universal cure-all in schizophrenia, and various holistic interventions which can strongly and positively impact symptoms of schizophrenia. Included in Dr. Cady's survey were the role of essential fatty acids, nutrient deficiencies (particularly B vitamins), the danger of overgrowth of candida , pharmacogenomic testing, MTHFR polymorphisms, and more.
It was an honor and a privilege to deliver this presentation in
SĆ£o Paulo,.
For further information in Brazil on this topic, or to order a video/audio recording of the conference (in Portuguese),contact Luiz Dias of Laboratorio Great Plains in Brazil.
Natural Treatments for ADHD (TADH) in Sao Paulo, Brazil, for Laboratorio Grea...Louis Cady, MD
Ā
In this presentation, given at UNIP (Campus Paraiso - Sao Paulo, SP Brazo) for the 2019 Congresso de Saude Mental (Conference on Mental Health), Dr. Cady reviewed the prevalence, inheritability, and social ramifications of ADHD (TADH in Brazil). He specifically reviewed multiple holistic interventions, including limiting "electric screen time,"good quality diet with adequate amounts of essential fatty acids and critically important trace elements, and the use of pharmacogenomic testing as well as functional, integrative medicine testing, all to better characterize logical and reeasonmable points for holistic intervention.
This presentation was simultaneously translated into Portugue for the attendees, but unfortunately the slides were not available in translated form.
For further information in Brazil on this topic, or to order a video/audio recording of the conference (in Portuguese),contact Luiz Dias of Laboratorio Great Plains in Brazil.
The Children are very vulnerable to get affected with respiratory disease.
In our country, the respiratory Disease conditions are consider as major cause for mortality and Morbidity in Child.
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
āEnvironmental sanitation means the art and science of applying sanitary, biological and physical science principles and knowledge to improve and control the environment therein for the protection of the health and welfare of the publicā.The overall importance of sanitationĀ are to provide a healthy living environment for everyone, to protect the natural resources (such as surface water, groundwater, soil ), and to provide safety, security and dignity for people when they defecate or urinate .Sanitation refers to public health conditions such as drinking clean water, sewage treatment, etc. All the effective tools and actions that help in keeping the environment clean come under sanitation. Sanitation refers to public health conditions such as drinking clean water, sewage treatment. All the effective tools and actions that help in keeping the environment clean and promotes public health is the necessary in todays life.
Giloy in Ayurveda - Classical Categorization and SynonymsPlanet Ayurveda
Ā
Giloy, also known as Guduchi or Amrita in classical Ayurvedic texts, is a revered herb renowned for its myriad health benefits. It is categorized as a Rasayana, meaning it has rejuvenating properties that enhance vitality and longevity. Giloy is celebrated for its ability to boost the immune system, detoxify the body, and promote overall wellness. Its anti-inflammatory, antipyretic, and antioxidant properties make it a staple in managing conditions like fever, diabetes, and stress. The versatility and efficacy of Giloy in supporting health naturally highlight its importance in Ayurveda. At Planet Ayurveda, we provide a comprehensive range of health services and 100% herbal supplements that harness the power of natural ingredients like Giloy. Our products are globally available and affordable, ensuring that everyone can benefit from the ancient wisdom of Ayurveda. If you or your loved ones are dealing with health issues, contact Planet Ayurveda at 01725214040 to book an online video consultation with our professional doctors. Let us help you achieve optimal health and wellness naturally.
Dr. Tan's Balance Method.pdf (From Academy of Oriental Medicine at Austin)GeorgeKieling1
Ā
Home
Organization
Academy of Oriental Medicine at Austin
Academy of Oriental Medicine at Austin
Academy of Oriental Medicine at Austin
About AOMA: The Academy of Oriental Medicine at Austin offers a masters-level graduate program in acupuncture and Oriental medicine, preparing its students for careers as skilled, professional practitioners. AOMA is known for its internationally recognized faculty, award-winning student clinical internship program, and herbal medicine program. Since its founding in 1993, AOMA has grown rapidly in size and reputation, drawing students from around the nation and faculty from around the world. AOMA also conducts more than 20,000 patient visits annually in its student and professional clinics. AOMA collaborates with Western healthcare institutions including the Seton Family of Hospitals, and gives back to the community through partnerships with nonprofit organizations and by providing free and reduced price treatments to people who cannot afford them. The Academy of Oriental Medicine at Austin is located at 2700 West Anderson Lane. AOMA also serves patients and retail customers at its south Austin location, 4701 West Gate Blvd. For more information see www.aoma.edu or call 512-492-303434.
Congestive Heart failure is caused by low cardiac output and high sympathetic discharge. Diuretics reduce preload, ACE inhibitors lower afterload, beta blockers reduce sympathetic activity, and digitalis has inotropic effects. Newer medications target vasodilation and myosin activation to improve heart efficiency while lowering energy requirements. Combination therapy, following an assessment of cardiac function and volume status, is the most effective strategy to heart failure care.
Pharmacology of Drugs for Congestive Heart Failure
Ā
Scratching Your Head Psychiatry II: How to Practice INSIDE the Allopathic Box
1. SCRATCHING YOUR HEAD PSYCHIATRY II:
How to Think INSIDE the Allopathic Boxā¦
[and Practice Precisely, Effectively, and to
Maximum Benefit]
Louis B. Cady, MD ā CEO & Founder ā Cady Wellness
Institute Adjunct Assoc. Professor ā Indiana University School
of Medicine Department of Psychiatry
Child, Adolescent, Adult & Forensic Psychiatry ā Evansville,
Indiana
(c) 2012 Louis B. Cady, M.D. - all rights reserved
2. āSlumber not in the
tents of your fathers.
The world is advancing.
Advance with it.ā
- Giuseppe Mazzine
3. Relevance for your practice
ā¢ ALL PRESCRIBERS - donāt kill your patient
with a drug-drug interaction.
ā¢ ALL PARTICIPANTS - Know bad/stupid
psychopharmacology when you see it.
ā Be able to DO SOMETHING about it.
ā¢ Donāt diagnose someone as having ādrug
problemsā when they DONāT.
ā¢ Better āMOAā understanding
4. A quick look back in history
The Interpretation of Ugo Cerletti 1935
Prozac - 1987
Dreams ā 1885 - 1890
5. The Therapeutic Trifecta of Psychiatry:
Shrinking
Shocking
or Drugging
[Supposedly the only three things
you could do to a patientās
brainā¦]
6. Dangers with
Psychiatry/psychotropics
ā¢ Failure to diagnose
ā (E.g āhead caseā and then they die of a medical problem)
ā¢ Failure to adequately treat
ā¢ Failure to prescribe accurately (Rx-rx interaction)
ā¢ Giving people side effects
ā¢ Using the wrong drug
ā¢ Ignorance about best options because āI always did it that
way.ā
ā¢ Getting people addicted
ā¢ Practicing beyond your ability and expertise
ā¢ Violating black box warnings
7. *ACCURATE MEDICAL diagnosis a malpractice suit
Depression & Anxiety & āmood disorder due to a
in 1 Easy Lesson
general medical conditionā AND r/o bipolar disorder
DEPRESSION Gen. ANXIETY D.O.
SIG: E- CAPS! ā¢Somatic Sx (āenergyā,etc.)
ā¢ Sleep ā¢WORRY
ā¢ Sadness ā¢Irritability
ā¢ Interest loss ā¢Concentration
ā¢ Guilt ā¢Keyed up
ā¢ *Energy ā¢Insomnia (āsleepā)
ā¢ Concentration ā¢Restlessness
ā¢ Appetite BEWARE BEWARE ā ātoo muchā
ā¢ Psychomotor Sx energy
ā¢ Suicidal thinking SWICKIR is Quicker:
Worry + 3 = GAD (Baughman)
5of 9 with 1 of 2 x 2 weeks
9. Epidemiology of Depression
Prevalence of Major Depression
20
point prevalence (30 day)
15 lifetime prevalence
Percent 10
of Patients
5
0
Epidemiologic National Comorbidity
Catchment Area (ECA) Survey (NCS)
Regier et al., 1988; Blazer et al., 1994
10. PHQ-9 Symptom Checklist
More Nearly
1. Over the last 2 weeks, how often have you Not Several than half every
been bothered by the following problems? at all days the days day
0 1 2 3
a. Little interest or pleasure in doing things ļ£ ļ£ ļ£ ļ
b. Feeling down, depressed, or hopeless ļ£ ļ ļ£ ļ£
c. Trouble falling or staying asleep, or sleeping too much ļ£ ļ£ ļ ļ£
d. Feeling tired or having little energy ļ£ ļ£ ļ£ ļ
e. Poor appetite or overeating ļ£ ļ ļ£ ļ£
f. Feeling bad about yourself, or that you are a failureā¦ ļ£ ļ£ ļ ļ£
g. Trouble concentrating on things, such as readingā¦ ļ£ ļ£ ļ£ ļ
h. Moving or speaking so slowlyā¦ ļ ļ£ ļ£ ļ£
i. Thoughts that you would be better off deadā¦ ļ£ ļ ļ£ ļ£
Subtotals: 3 4 9
TOTAL: 16
Kroenke 2001.
11. DepressionāImpact on the
Healthcare System
ā¢ Compared with those without
depression, depressed individuals:
ā Utilize all types of healthcare services more
often
ā Incur 1Ā½ to 2 times greater healthcare costs
ā increased length of hospital stay
ā significant worsening of physical, social, and
role functioning
Simon 1995; Luber 2000; Verbosky 1993; Wells 1989.
12. Comorbidity of Depression and
Anxiety
Disability % Patients
Disabled 3+ Days
GAD + MDD 33.7%
MDD/no GAD 19.45%
GAD/no MDD 16.9%
no GAD/no MDD 3.1%
0 5 10 15 20 25 30 35 40 45
Percent of Patients With ā„1 Disability Day in Past Month
Wittchen, Depress Anxiety, 2002
14. Kids and Adults ā Differences in
HYPERACTIVE domain
AS A CHILD: AS AN ADULT:
ā¢ Squirming, fidgeting ā¢ Work inefficiencies
ā¢ Cannot stay seated ā¢ Canāt sit through meetings
ā¢ Cannot wait turn ā¢ Cannot wait in line
ā¢ Runs/climbs excessively ā¢ Drives too fast
ā¢ Cannot play quietly ā¢ Self-selects very active job
ā¢ On the go/driven by motor ā¢ Cannot tolerate frustration
ā¢ Talks excessively ā¢ Talks excessively
ā¢ Blurts out answers ā¢ Makes inappropriate
ā¢ Intrudes, interrupts others comments
ā¢ Interrupts others
Sources: DSM-IV (TR). APA 2000:85-93)
Weiss MD, Weiss JR. J Clin Psychiatry 2004;65(Suppl 3):27-37.
15. Horrigan J, et al. Presented at 47th Annual AACAP Meeting:
October 24-29, 2000. New York, NY.
16. Persistence of ADHD Into Adulthood
ā¢ ADHD is a heterogeneous disorder associated with
considerable disability and comorbidity that, in many cases,
persists into adulthood1
ā Some studies have found persistence as high as 36.3% 2
ā¢ Mood, anxiety, and substance use disorders are
the most common comorbid disorders in adults with ADHD 3
ā¢ Current prevalence of ADHD persistent into
adulthood 4.4%4 (5% by new study ā Willcut ā Neurotherapeutics 2012
ā¢ Much of the treatment of adult ADHD can be based on
experience in treating children/adolescents5
1. Barkley et al. J Abnorm Psychol. 2002;111:279-289.
2. Kessler RC et al. Biol Psychiatry 2005 June;57(11):1442-51. [retrospective review of 3,197 14-44 yo
respondents in NCS-R]
3. Biederman et al. Am J Psychiatry. 1993;150:1792-1798. 4. Kessler et al. Am J Psychiatry. 2006;163(4):716-
23. 5. Dodson WW. J Clin Psychol. 2005;61:589-606.
17. Diagnostic Pearls - Cady
ā¢ Howās work?
ā How has your employment history been?
ā¢ Howās your mood? Your marriage (relationship)?
ā¢ How was school for you?
ā¢ Are people nervous driving with you?
ā¢ Are there periods of time when you have too much
energy for no particular reason?
ā¢ Do you ever have to have a beer at the end of the day to
relax?
ā [gently lead in to other substances, especially stimulants that
may have a CALMING effect]
ā āHave you ever taken any of your childās ADD Rx?ā [or other
stimulants, energy drinks, diet pills, or cocaine]
18. Pharmacology Failuresā¦
1. āBegin with the end in mind.ā (Covey)
2. Start LOW ā (rule of thumb ā Ā½ what the
drug rep and package insert says!)
3. Go up to the maximum tolerated dosage,
with finesse.
ā Tell them about āGoldilocksā
1. If it doesnāt work, add something
complimentary (that makes sense).
19. THE FACTS
ā¢ SSRIās treat depression AND/OR anxiety
ā¢ Patients may INITIALLY need something else for daytime
anxiety or sleep.
ā¢ BZDās of choice:
ā clonazepam 1 mg tablets ā Ā½ to 1 twice daily to three
times daily
ā Diazepam ā 5 mg =- Ā½ - 1 Ā½ twice daily to three times
daily
ā¢ (first pass and second pass effects)
ā¢ ANTIANXIETY RX (non BZD) ā Buspirone, per package
insert. Push to 20 mg THREE TIMES DAILY or to the
point of maximum tolerability for 4 ā 6 weeks AT THAT
DOSE.
ā Start with 5 mg. Can use WITH SSRIās
20. AVOID Alprazolam (Xanax Ā®)
ā¢ Addicting (and rapidly so)
ā¢ Can have seizures if rapidly withdrawn
(structurally similar to carbamazepine)
ā¢ MDās shot over it.
ā¢ NOT an āanti-anxietyā medication
ā¢ NOT a sleeper.
ā¢ Even if they need a BZD for anxiety, it
doesnāt have to be Xanax.
21. Sleepers ā my preferences
ā¢ Rozerem (brand) (a melatonin analog) ā 8 (up to 16* mg) at
bedtime. VASTLY under-rated. May need to take 2 weeks
before adequate effect. (* off-label dose)
ā Dual acting agent ā homeostatic and circadian effects. 70x
as potent as melatonin.
ā Melatonin SR may also be a good agent.
ā¢ Trazodone (50 ā 150mg Ā½ - 2 hrs before HS. (Note, off
label āunapproved.ā Warn on priapism).
ā¢ Lunesta (brand) ā 2 ā 3 mg. Try samples. Have
mouthwash on hand. (Probably most predictable agent)
ā¢ Ambien 12.5 mg CR (brand) ā legitimately lasts longer than
zolpidem. Probably not as effective as Lunesta.
ā¢ Zolpidem ā generic. People get hooked on it.
ā¢ Paradigm: SYMPTOMATIC treatment ā after depression is stabilized,
fade out the sleeper
28. āStrattera [coupled with
Prozac or Paxil] has been
great for our admissions. ā
-Dr. William Beute, MD
Pine Rest Campus Clinic
Grand Rapids, MI
April 21, 2004
[quoted with permission]
29. Cytochrome p-450 2D6 inhibition measured as %
increase in āDesipramine AUCā ā in vivo data
Critically important when
combining with other Rx
metabolized through 2D6
pathways
Preskhorn, Alderman, et al. Pharmacokinetics of desipramine coadministered
with sertraline or fluoxetine. J. Clin Psychopharmacol 1994;14:90-98;
Escitalopram package insert - note ā different source of data, but same method
31. The ānot so selectiveā SSRIās; how to
āDo yourself a favor.ā
drug SSRI? 2nd order effects Side effects possible
Escitalopram Yes NOTHING (excess serotonin side
(Lexapro) now effects only)
generic
Sertraline (Zoloft) Yes Dopamine (1/3 as Agitation, nervousness;
potent as improved [ ]
amphetamine)
Citalopram Yes AntiH1 Sedation (note- FDA
(Celexa) lowered max dose to
40mg)
Paroxetine (Paxil) Yes Ach Doped up, TCA effects,
NOT āNRIā neurocognitive problems,
withdrawal. Sexual,
Prostate sxs
Fluoxetine Yes 5HT2C Agitation, appetite
(Prozac) suppression
32. New Agents, New Mechanisms
(agent) (MOA) Differentiating points
Venlafaxine (āIRā and XR) SSRI, NRI Nausea, GI side effects, sxl
(Effexor) dysfunction
Duloxetine (Cymbalta) SSRI, NRI Same. Better tolerated. For pain
w/ dep.
Desvenlafaxine (Pristiq) ā SSRI, NRI Better tolerated
āson of Effexorā
Trazodone XR with 5HT2a/c Legitimate effect on
ContramidĀ® (OLEPTRO) BLOCKER, mild depression/anxiety without
SSRI doping up.
Vilazodone (Viibryd) SPA, SSRI ONLY SPARI. Weaker āSSRI.ā
Targets 5HT1A. Less sexual side
effects.
Bupropion (āXLā ā not āNDRIā Possibility of anxiety & āwound
āSRā) (Wellbutrin) up.ā Improved concentration.
Push to 450 mg. SZ warning..
33. An illustrative study on picking your
antidepressantā¦
Duloxetine (Cymbalta) Versus
Escitalopram (Lexapro) and Placebo:
An 8-month, Double-Blind Trial in
Patients With Major Depressive
Disorder
Pigott et al., Curr Med Res Opin, 2007
34. Retardatio
Comparison of Escitalopram and Duloxetine:
HAMD (MMRM)
8-Month Trial
17
Maier
Subscales
Sleep
*
Somatization
Anxiety/
Total Score
*p<0.05
Pigott et al., Curr Med Res Opin, 2007
35. Comparison of Escitalopram and Duloxetine: 8-
Month Trial
Significantly Different Adverse Events (p<0.05 Duloxetine vs Escitalopram)
Percent of Patients
Pigott et al., Curr Med Res Opin, 2007
36. Comparison of Escitalopram and
Duloxetine: 8-Month Trial
Conclusions: they both worked the same;
side effects were worse with duloxetine
ā¢ Remission rates for both escitalopram and duloxetine
continued to improve over time
ā¢ Significantly more escitalopram-treated patients
continued treatment compared to duloxetine-treated
patients
ā¢ Escitalopram showed significant improvement vs
duloxetine on the HAMD17 sleep subscale
ā¢ Compared to escitalopram, duloxetine significantly
increased pulse and systolic blood pressure
Pigott et al., Curr Med Res Opin, 2007
37. Two New Agents You Need to Know
ā¢ Extended release Trazodone
ā NOT āson of Trazodoneā
ā Possibility of legitimate antidepressant effect with anti-
anxiety effect WITHOUT doping patient up.
ā A āSARIā ā serotonin antagonist reuptake inhibitor
ā¢ Vilazodone ā the only SPARI available.
ā¢ How to appreciate:
ā 5HT1A is receptor for antidepressant effect of serotonin
ā 5HT2A and 5HT2 C: anxiety, sleep disruption, sexual
side effects.
ā ANYTHING which works preferentially on 5HT1A is
GOOD!
38. XR Trazodone steady state dosing study
ā¢ (Levels done after 7
days steady state)
ā¢ 300 mg XR Traz
AUC comparable to
100 mg IR Traz tid
ā¢ Cmax 42% lower
than IR Trazodone
ā Translation ā it
doesnāt dope the
patient up.
Kramer, WG et al. Once-daily Trazodone: Overview of Pharmacokinetic Properties.
Poster ā ACCP 38th Annual Meeting, San Antonio, TX 2005
39. XR Trazodone Food Effect Study
ā¢ PI says ātake at nightā
ā¢ CMax increase by 86%
(!!!) under fed conditions.
Peak is at 7 hours post
dose (with feeding).
ā¢ Note ā this may lead the
enlightened prescriber to
vary the time of dosing.
Kramer, WG et al. Once-daily Trazodone: Overview of Pharmacokinetic Properties.
Poster ā ACCP 38th Annual Meeting, San Antonio, TX 2005
40. Vilazodone ā a SPARI (per Stephen Stahl, MD, Ph.D.) ā
Serotonin Partial Agonist Reuptake Inhibitor
ā¢ Highly serotonergic. START LOW (5 mg).
ā¢ Because of 5HT1A agonism, LESS āSSRIā effect is
required.
41. ADHD Rx for frontline medicine
ā¢ Desiderata ā get control, and keep it consistent for
predictable period of time
ā¢ Rules of thumb: donāt be guided on SIZE. START LOW.
āKnow the Biederman maxā for MPH and amphetamine.
ā¢ Recommendations (for children and adult):
ā Focalin XR (Dexmethylphenidate XR) 5,10,15,20,30 and 40 mg
capsules)
ā¢ Rationale: MPH based. FAST. 8 ā 10 hours. Can dose twice daily (off-
label), a.m. >pm. (can also start with Ā½ capsule)
ā Vyvanse ā (lisdexamfetamine [sic]) ā 20,30,40,50,60,70 mg [= 7.5
ā 30 mg] amphetamine equivalents. Lasts 12 ā 14 hours. (Can
dissolve in water ā per PI!).
ā Kapvay/Intuniv ā FDA approved in kids.
ā¢ Kapvay easier to use, better tolerated.
ā¢ Intuniv more potent, but more side effects (sedation)
42. Practicing beyond your ability (and knowledge) ā
the second generation antipsychotics
ā¢ Definitions:
ā Mood stabilizer ā something that stabilizes mood
(Lithium, carbamazepine, VPA)
ā Antipsychotic ā something you give someone who is
PSYCHOTIC to get them UNPSYCHOTIC.
ā Antidepressant ā something for depression.
ā ā2nd generation antipsychotic (āSGAāsā) = S2/D2
blockers.ā
ā¢ Can āstabilize moodā as well as function as antipsychotics
ā¢ Now some FDA approved for either add-on use or single agents
for ābipolar depressionā (e.g., quietapine XR)
43. Know who youāre playing with
ā¢ SGAās and WEIGHT GAIN (Cady experience)
ā olanzapine/risperidone > quietapine>
aripiprazole/arsenapine> lurasidone/ziprasidone
ā¢ (Zyprexa/Risperdal>Seroquel> Abilify/Saphris> Latuda/Geodon)
ā¢ EXPENSIVE: $400 ā $600 /per month
ā¢ All will work for mania. NONE are pure āmood stabilizers.ā
Some make you fat.
ā¢ Some will work for depression but dope you up.
ā¢ Much less risky than 1st generation for tardive dyskinesia.
ā¢ Axiom: refine your psychopharmacology before going to
look for an SGA.
ā¢ If you have to use one (for bipolar or psychosis, Lurasidone
is probably most benign ā 40 ā 80 mg twice daily (or 160
mg HS)
44. Cady recommendation for SGAās in
primary care
ā¢ As little as possible.
ā¢ Do NOT use as primary mood stabilizers for bipolar disorder.
Use lithium (Type I) VPA (Type I/II) or Lamotrigine ā which is
a real option. Check levels and labs as needed
ā¢ Can use if single, or better yet, DOUBLE mood stabilizers
donāt work.
ā¢ Abilify (only ādopaminergicā SGA) probably best for
antidepressant augmentation at LOW DOSE.
ā 2 ā 4 or 5 mg is optimum dose for this. (Start with Ā½ of a 2
mg and go up)
ā Onset is FAST when it happens.
ā¢ Olanzapine is most dependable for rapid onset and control of
manic episode, or agitation, or EXTREME PANIC & anxiety
(off label).. Lurasidone may be best tolerated.
45. A quick look back in psychiatric tx:
The Interpretation of Ugo Cerletti 1935
Prozac - 1987
Dreams ā 1885 - 1890
46. The Therapeutic Trifecta of Psychiatry:
Shrinking
Shocking
or Drugging
[Supposedly] the only three
things you could do to a patientās
brainā¦]
47. STAR*D Study demonstrates that current
treatment has limited effectiveness
47
Trivedi (2006) Am J Psychiatry; Rush (2006) Am J Psychiatry; Fava (2006) Am J Psychiatry; McGrath (2006) Am J Psychiatry
48. Likelihood of discontinuing treatment increases
with each new medication attempt
Systemic Drug Side Effects
ļ± Weight Gain
ļ± Fatigue
ļ± Constipation ļ± Headache/
Migraine
ļ± Diarrhea
ļ± Abnormal
ļ± Nausea Ejaculation
ļ± Drowsiness ļ± Impotence
ļ± Insomnia ļ± Sweating
ļ± Decreased ļ± Tremor
Libido
ļ± Treatment
ļ± Nervous Discontinuati
Anxiety on Side
Effects
ļ± Increased
Appetite ļ± Weakness
ļ± Decreased ļ± Dry Mouth
Trivedi (2006) Am J Psychiatry; Rush (2006) Am J Psychiatry; Fava (2006) Am J Appetite
Psychiatry; McGrath (2006) Am J Psychiatry; Neuronetics, Inc. (data on file)
ļ± Dizziness
49. ECT ā origins
ā¢ Origin in 1700ās ā Middlesex Hospital
ā machine with weak electrical current used for range of illnesses.
ā John Birch, English neurosurgeon, used it to shock the brains of
depressed patients
ā Benjamin Franklin, after shocked, recommended electric shock for
tx of mental illness
ā¢ Ugo Cerletti ā 1935 ā noted (incorrectly) that epilepsy and
schizophrenia didnāt occur in same patient
ā¢ Problems with ECT ā memory loss, anesthesia risk
ā¢ Cost of $6400 for eight treatments
ā¢ 80% improvement
ā¢ 33,000 hospitalized Americans ā ECT in 1980, last year for
NIMH figures
ā http://www.faqs.org/health/topics/19/Electroconvulsive-therapy.html
50. But even before Freudā¦
ā¢ Electromagneitc
induction ā 1831
(Michael Faraday &
Joseph Henry)
ā¢ 1st demonstrated by
Faraday August 29,
1831
51. Faradayās Law of Induction
TMS Induced neuronal
Magnetic current
field
52. From electricity to
magnetism
ā¢ Bartholow, R (1874)
ā Stimulation of human brain
(exposed cortex) of patient with
cranial defect.
ā¢ dāArsonval ā āPhosphenes
and vertigoā induced inside
powerful magnetic coil
ā¢ Silvanus P. Thomson, Ph.D.
ā new type of magnetic Thompson, SP. āA Physiological
Effect of an Alternating Magnetic
stimulation (1910) Field.ā Proceedings of the Royal
Society of London B82:396-399, 1910
53. First patent application for magnetic
therapy:
ā¢ 1902 Adrian Pollacsek
and Berthold Beer ā
Vienna, Austria for a
ātherapeutical apparatusā
ā¢ Electromagnetic coil,
placed over the skull was
noted to āpass vibrations
into the skullā and ātreat
depression and
neuroses.ā
54. A quick look back in psychiatric history - redux
Shrinking Zapping Shocking Drugging
Freud: The Silvanus P. Ugo Cerletti 1935 Prozac - 1987
Interpretation of Thompson,
Dreams ā 1885 - Ph.D. (1910)
1890
55. First modern TMS:
ā¢ Barker AT, et al. āNon-
invasive magnetic
stimulation of the human
motor cortex. The
Lancet 1:1106-1107,
1985.
ā¢ 1st device ā designed by
Barker ā Univ. of
Sheffield, England.
ā 100 microsecond, 2 T
pulse
56. Coil types and rationale
From Matt Edwardson, MD ā Research Fellow and Acting
Instructor, Dept. of Neurology, Univ. of WA 10/16/2011
57. An unusual side effect
of imaging (2004)ā¦
ā¢ CONCLUSIONS: āThese preliminary data suggest
that the EP-MRSI scan induces electric field that
are associated with reported mood improvement in
subjects with bipolar disorder.ā
58.
59. NeuroStar TMS Directly Depolarizes
Cortical Neurons
Neuron
Pulsed magnetic fields
from NeuroStar:
ā¢induce a local electric
current in the cortex
which depolarizes
Neurons are neurons
āelectrochemical ā¢eliciting action potentials
cellsā and respond to ā¢causing the release of
either electrical or
chemical stimulation chemical
neurotransmitters
60. NeuroStar Releases Neurotransmitters
in the Brain
These effects
Depolarization of neurons in
the DLPFC causes local are associated
neurotransmitter release
with
improvements in
Dorsolateral
prefrontal
depressive
cortex
symptoms
Anterior
cingulate
cortex
Kito (2008) J Neuropsychiatry Clin
Neurosci
Depolarization of pyramidal
neurons in the DLPFC also Activation of deeper brain
causes neurotransmitter release neurons then exerts secondary
in deeper brain neurons effects on remaining portions of
targeted mood circuits
61. ECT TMS
Anesthesia, LOC ECT vs. TMS No
Yes
Induction of seizure Yes No
Systemic effects Anesthetic drugs, none
increase HR
Treatment schedule 3X/ week (8 -15 tx) Daily, M-F, six weeks (30
tx)
Rapidity of onset 2 ā 3 treatments 2 ā 3 weeks
Mechanism of action SEIZURE. Massive NT Precise, LOCAL release
release; rise in sz of NTās. Reactivation of
threshold neural circuits.
Side effects Memory loss, confusion Essentially none (mild HA
1st week)
Psychosocial impact canāt work Drive to and from txās,
work improved
After-effects Mild (usually transient) None. Pro-cognitive
memory loss
Insurance coverage Almost always Rare. Improving
64. Does it work?
ā¢ Original registration trial
ā 307 major depressed patients
ā¢ 67% women
ā¢ 93% recurrent depressives
ā¢ 43% had been hospitalized already
ā 42 sites
ā Treatment per label
ā¢ Results: Ā½ patients responded; 1/3 of
patients remitted.
ā¢ 80% patients completed the treatment.
65. Who Was Studied?
ā¢ Primary diagnosis: DSM-IV Major Depressive
Disorder
ā Unipolar type, non-psychotic
ā Moderate to severe symptoms at baseline
ā Approximately one-third of patients had a co-morbid anxiety
disorder (OCD excluded)
ā¢ Antidepressant Treatment History:
ā Average number of antidepressant medication trials in current
episode = 4 (range: 1 to 23 attempts)
ā¢ Majority of treatment attempts were unable to achieve adequate
dose and duration of treatment due to intolerance
ā In the indicated patient population, all patients failed to
achieve satisfactory benefit from one antidepressant
medication at an adequate dose and duration in current
episode
65
Demitrack and Thase (2009) Psychopharm
Bulletin
66. OāReardon, JP, et al. (2007) Efficacy and Safety of Transcranial Magnetic Stimulation in
the Acute Treatment of Major Depression: A Multi-Site Randomized Controlled Trial.
Biol Psychiatry 62:1208-1216.
67. Optimization of TMS (āOPT-TMSā) Study
Mark S. George, MD; Sarah H. Lisanby, MD; David Avery, MD; William M. McDonald, MD; Valerie Durkalski, PhD;
Martina Pavlicova, Phd; Berry Anderson, Phd, RN; Ziad Nahas, MD; Peter Bulow, MD; Paul Zarkowski, MD;
Paul E. Holtzheimer III, MD; Theresa Schwartz, MS; Harold A. Sackeim, PHD
Major Findings:
ā¢ NIMH-funded, independent of industry ā¢ MADRS total score decreased:16.6%
ā¢ N=190 patients, 4 premier academic sites (Active) vs 6.9% (Sham) p=0.01
ā¢ Primary outcome measure: (Effect size: 0.51)
% Remission - Active 15% vs Sham 4% (P = ā¢ 30% of patients achieved remission
0.015); Odds Ratio of achieving remission: in open-label extension phase
4.2 (95%CI, 1.3-13.2) ā¢ Excellent safety and adherence
Conclusion: āDaily left prefrontal rTMS as monotherapy produced
statistically significant and clinically meaningful antidepressant therapeutic
effects greater than sham.ā
68. Recent TMS Literature Review
ā¢ Roughly 30 controlled clinical research studies to date
ā¢ Most recent meta-analysis (Slotema, et al, 2010):
ā Included analysis of 34 studies involving 1,383 patients
ā Estimated standardized effect size = 0.55 (P < 0.001)
Conclusion: āā¦rTMS deserves a place in the
standard toolbox of psychiatric treatment
methods, as it is effective for depressionā¦and
has a mild side effect profileā¦.ā
1.Slotema, CW, Blom, JD, Hoek, HW, Sommer, IEC. (2010) Should we expand the toolbox of psychiatric
treatment methods to include repetitive transcranial magnetic stimulation (rTMS)J Clin Psych 71(7):873-84.
2.Schutter, DJLG. (2009) Antidepressant Efficacy of High-Frequency Transcranial Magnetic Stimulation Over
the Left Dorsolateral Prefrontal Cortex in Double-Blind Sham-Controlled Designs: A Meta-Analysis. Psychol
Medicine, 39:65-75.
69. NeuroStar TMS Therapy: Safety
Overview
ā¢ No systemic side effects
ā¢ No adverse effect on cognition
ā¢ Most common adverse event associated with
treatment was scalp pain or discomfort
ā < 5% of patients discontinued due to adverse events
ā¢ No seizures with NeuroStar device during clinical
studies (over 10,000 treatments)
ā¢ Rare risk of seizure with NeuroStar TMS in post-market
use (0.003% per treatment, <0.1% per acute treatment
course) (>150,000 treatments in post-marketing experience to
date)
ā¢ Long term safety demonstrated in 6 months follow-up
Janicak, et al. J Clin Psychiatry, 2008; Janicak, et al. Brain Stimulation, 2010.
70. No Evidence of Emergent Suicidal Ideation
4.0
NeuroStar TMS Therapy (n=155)
HAMD Item 3 Suicidal Ideation
3.5
Sham TMS (n=146)
3.0
Shift Score (%)*
2.5
2.0
1.5
1.0
0.5
0.0
Baseline Week 2 Week 4 Week 6
* Shift Score indicates the percent of subjects who experienced a change in HAMD Item 3 score from 0 or 1 at baseline
to 3 or 4 at later point in time.
Janicak (2008) J Clinical Psychiatry.
71. Long Term Follow Up After Acute
Treatment
RCT or Open-Label Extension Study Long-Term Follow-Up Study
ACUTE TAPER LONG TERM OUTCOME
BENEFIT (3 Weeks) ASSESSMENT
(6 Weeks) (6 Months)
Transition from Antidepressant medication
TMS to monotherapy w/TMS rescue as
pharmacotherapy add-on if needed through 6 Months
Janicak, et al. Brain Stimulation, 2010.
72. Long Term Follow Up After Acute Treatment
ā¢ Safety confirmed during long term, open-label 6 month
follow up period
ā¢ During open-label follow up on antidepressant
medication monotherapy,
ā ~37% of patients required TMS reintroduction
ā ~85% of patients who received TMS reintroduction benefited
ā¢ Net incidence of illness relapse under these open-label
follow up conditions: 11%
ā Six-month relapse with antidepressant treatment alone in
STAR*D study was 35-50% (Level 2 and 3 range)
Janicak, et al. Brain Stimulation, 2010.
73. The story of Geraldineā¦
IDS-SR
CGI -S
Photos used with patientās permission
74. Learning points I hope we have
achievedā¦
ā¢ Precise diagnosis.
ā¢ Improved concepts of ADHD presentation in
children and adults.
ā¢ Avoid obvious drug-drug interactions.
ā¢ Avoid excess/inappropriate BZDās.
ā¢ Avoid over-use of SGAās.
ā¢ Understand TMS and where it fits into
current psychiatric treatments
75. Contact information:
Louis B. Cady, M.D.
www.cadywellness.com
www.indianaTMS-cadywellness.com
Office: 812-429-0772
E-mail: lcady@cadywellness.com
4727 Rosebud Lane ā Suite F
Interstate Office Park
Newburgh, IN 47630 (USA)
Editor's Notes
Giuseppe Mazzini (22 June 1805 ā 10 March 1872), nicknamed "Soul of Italy,"[1] was an Italian politician, journalist and activist for the unification of Italy. His efforts helped bring about the independent and unified Italy[2] in place of the several separate states, many dominated by foreign powers, that existed until the 19th century. He also helped define the modern European movement for popular democracy in a republican state. [ citation needed ] ā Source - Wikipedia
In the following section of my talk, I ād like to discuss TMS in more detail. I will review its mechanism of action, and then discuss some of the most recent randomized clinical trial evidence supporting its efficacy and safety. I will also discuss recent outcomes in real-world practice settings obtained from an ongoing large, prospective outcomes study.
As demonstrated by this chart, psychiatric disorders are prevalent. 1-3 These data are from the National Comorbidity Survey (NCS) and the DSM-IV-TR ā¢ . The NCS is a collaborative epidemiologic investigation based on household survey data of over 8000 respondents from 1990 to 1992. 4
Depression can strike anyone at any age, but on average it begins in the late 20s. Depressive illness is a highly prevalent disorder associated with substantial morbidity and mortality. According to the World Health Organization, major depression is the leading cause of disability in the U.S. and worldwide. The annual costs associated with depression (both direct and indirect) in the U.S. were estimated to be $43.7 billion in 1990. Epidemiologic studies suggest that in any 30-day period, 2 to 5 percent of the U.S. population meet criteria for major depression. The lifetime probability of experiencing a major depressive episode has been estimated to be as high as 17 percent. Nearly twice as many women (21%) as men (13%) are affected by a depressive disorder during their lifetimes. References 1. Murray CJL, Lopez AD, eds. Summary: The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Cambridge, MA: Published by the Harvard School of Public Health on behalf of the World Health Organization and the World Bank, Harvard University Press; 1996. 2. Regier DA, Boyd JH, Burke JD Jr, Rae DS, Myers JK, Kramer M, Robins LN, George LK, Karno M, Locke BZ. One-month prevalence of mental disorders in the United States: based on five Epidemiologic Catchment Area sites. Arch Gen Psychiatry. 1988; 45:977-986. 3. Blazer DG, Kessler RC, McGonagle KA, Swartz MS. The prevalence and distribution of major depression in a national community sample: the National Comorbidity Survey. Am J Psychiatry . 1994;151:979-986. 4. Regier DA, Narrow WE, Rae DS, Manderscheid RW, Locke BZ, Goodwin FK. The de facto US mental and addictive disorders service system. Epidemiologic catchment area prospective 1-year prevalence rates of disorders and services. Arch Gen Psychiatry. 1993;50(2):85-94. Kessler RC, McGonagle KA, Swartz M, Blazer DG, Nelson CB. Sex and depression in the National Comorbidity Survey I: lifetime prevalence, chronicity and recurrence. J Affect Disord. 1993;29:85-96. Greenberg PE, Stiglin LE, Finkelstein SN, Berndt ER. The economic burden of depression in 1990. J Clin Psychiatry . 1993;54:405-418.
The PHQ-9 symptom checklist asks the patients in a self-report format, ā Over the last 2 weeks, how often have you been bothered by the: following problems? Little interest or pleasure in doing things; feeling down, depressed or hopeless; trouble falling or staying asleep or sleeping too much; feeling tired or having little energy; poor appetite or overeating; feeling bad about yourself or that you are a failure; trouble concentrating on things; moving or speaking slowly; thoughts that you might be better off dead. ā These are all depression DSM-IV-TR items. Patients can score for themselves how often they have experienced these individual symptoms. 37
In addition to utilizing services related to their depression, patients also tend to be high utilizers of general medical care services. It has been shown that depressed patients utilize all types of healthcare services more often than nondepressed patients and incur overall healthcare costs 1 Ā½ to 2 times higher than the average nondepressed patient. 27,28 It has also been demonstrated that depressed individuals were hospitalized longer and had significant worsening of physical, social, and role functioning, compared with nondepressed individuals. 28-30
Both MDD and GAD are associated with considerable functional impairment and disability. Comorbid depression and GAD tends to result in greater levels of disability as measured by the proportion of patients who report 1 or more days of disability in a 30-day period. Patients experience diminished functioning both at work and socially, with many reporting moderate or severe social disability. Reference Wittchen HU. Generalized anxiety disorder: prevalence, burden, and cost to society. Depress Anxiety . 2002;16:162-171.
ADHD is a heterogeneous disorder associated with considerable disability and comorbidity that, in many cases, persists into adulthood. 1 Mood, anxiety, and substance use disorders are the most common comorbid disorders in adults with ADHD. 2 ADHD in adults is more prevalent than once thought. The National Comorbidity Survey found the estimated lifetime prevalence of ADHD in adults to be 8.1%. 3 According to DSM-IV criteria, adults diagnosed with ADHD must have had childhood onset and persistent and current symptoms, although allowance is made for partial remission. 4 Due to the great syndromatic continuity between childhood and adult ADHD, much of the medication management of adults with ADHD can be based on the experience gained from treating children and adolescents. 5 Barkley RA, Fischer M, Smallish L, Fletcher K. The persistence of attention-deficit/hyperactivity disorder into young adulthood as a function of reporting source and definition of disorder. J Abnormal Psychol. 2002;111:279-289. Biederman J, Faraone SV, Spencer T, et al. Patterns of psychiatric comorbidity, cognition, and psychosocial functioning in adults with attention deficit hyperactivity disorder. Am J Psychiatry . 1993;150:1792-1798. Kessler RC, Berglund P, Demler O, Jin R, Walters EE. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry . 2005;62:593-602. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders . 4th ed. ( DSM-IV ļ¤ ). Washington, DC: American Psychiatric Association; 1994:78-85. Dodson WW. Pharmacotherapy of adult ADHD. J Clin Psychol . 2005;61:589-606.
In a flexible dose study evaluating the safety and efficacy of escitalopram in the treatment of panic disorder (with or without agoraphobia), outpatients were randomized to receive placebo, citalopram or escitalopram. There were approximately 120 patients per treatment group. Following a 2-week single-blind lead-in period, patients received 10 weeks of double-blind treatment. Treatment was initiated at a low dose (10 mg/day for citalopram and 5 mg/day for escitalopram) and then titrated after one week to 20 mg/day for citalopram and 10 mg/day for escitalopram. After week 4, dose could be increased to 40 mg/day citalopram and 20 mg/day citalopram. The Panic and Anticipatory Anxiety Scale (PAAS) and the Panic and Agoraphobia (P&A) scale were used to quantify panic attacks, anticipatory anxiety, and phobic avoidance.
Duloxetine versus escitalopram and placebo: an 8-month, double-blind trial in patients with major depressive disorder. Curr Med Res Opin. 2007 Apr 27;
Overall effects of treatment of depression were assessed by the HAMD 17 total score using MMRM analysis. Treatment effects related to the somatic symptoms associated with depression were assessed by the anxiety/somatization subscale that consists of HAMD 17 items 10 (psychiatric anxiety), 11 (somatic anxiety), 12 (gastrointestinal-related symptoms), 13 (general somatic symptoms), 15 (hypochondriasis), and 17 (insight). The sleep subscale (HAMD 17 items 4, 5, and 6) was used to assess the treatment effects on insomnia (initial, middle, and terminal). The Maier subscale measures the core symptoms of depression and comprises HAMD 17 items 1 (depressed mood), 2 (feelings of guilt), 7 (work and activities), 8 (retardation), 9 (agitation), and 10 (psychic anxiety). The impact of treatment on energy and interest levels was evaluated by the retardation subscale: HAMD 17 items 1 (depressed mood), 7 (work and activities), 8 (retardation), and 14 (genital symptoms). After 8 months of treatment, duloxetine (60-120 mg/day) and escitalopram (10-20 mg/day) showed similar efficacy on HAMD 17 total and subscale scores, except the sleep subscale. On the HAMD 17 sleep subscale, escitalopram was significantly more efficacious than duloxetine (p<0.05). Rates of remission were not significantly different between escitalopram and duloxetine over the 8-month course of the study (50% vs 47%; respectively). Because so few patients on placebo (n=15) completed the entire 8-month study, the power to detect a difference between placebo and active treatments after 8 weeks was significantly decreased and very likely to be insufficient. Reference Pigott TA, Prakash A, Arnold LM, Aaronson ST, Mallinckrodt CH, Wohlreich MM. Duloxetine versus escitalopram and placebo: an 8-month, double-blind trial in patients with major depressive disorder. Curr Med Res Opin . 2007;23(6)1303-1318.
This slide shows the adverse events that were significantly different between escitalopram and duloxetine. Nausea, dry mouth, vomiting, yawning, and night sweats were reported at a significantly higher rate with duloxetine than with escitalopram, whereas only migraine was more frequently reported in the escitalopram group than in the duloxetine group. References: Pigott TA, Prakash A, Arnold LM, Aaronson ST, Mallinckrodt CH, Wohlreich MM. Duloxetine versus escitalopram and placebo: an 8-month, double-blind trial in patients with major depressive disorder. Curr Med Res Opin . 2007;23(6)1303-1318.
Throughout this 8-month extension study, escitalopram and duloxetine showed similar efficacy on all study measures except on the HAMD 17 sleep subscale. On the HAMD 17 sleep subscale, escitalopram was significantly more efficacious than duloxetine. Remission rates between escitalopram and duloxetine were not significantly different and both treatments lead to continued improvement over time. Significantly more escitalopram-treated patients continued treatment compared to duloxetine-treated patients, and duloxetine treatment led to an increase in both pulse and systolic blood pressure. References: Pigott TA, Prakash A, Arnold LM, Aaronson ST, Mallinckrodt CH, Wohlreich MM. Duloxetine versus escitalopram and placebo: an 8-month, double-blind trial in patients with major depressive disorder. Curr Med Res Opin . 2007;23(6)1303-1318.
In the following section of my talk, I ād like to discuss TMS in more detail. I will review its mechanism of action, and then discuss some of the most recent randomized clinical trial evidence supporting its efficacy and safety. I will also discuss recent outcomes in real-world practice settings obtained from an ongoing large, prospective outcomes study.
Let ās take a closer look at the evidence generated in the STAR*D Study. The design of this study involved four treatment Levels. These Levels were pre-specified by expert consensus, and were intended to reflect the general approach taken in clinical practice at the time STAR*D was constructed, which was about 10 years ago. Ā Patients treated in STAR*D were either first episode patients, or treatment-responsive patients. To get into the study, the patient could not have previously been treated with and failed to benefit from any of the options offered in either Level 1 or 2. Patients were recruited from both primary care and specialty psychiatric treatment settings in the United States. About 4,000 patients entered into this study. Ā The first Level results showed that in response to an adequate course of treatment with an SSRI (in this study, citalopram was the option used) only about 28% of patients were able to achieve remission as measured using the 17 Item Hamilton Depression Rating Scale. Ā At Level 2, the results are shown for those patients who were offered a switch to another antidepressant of the same or a different class (these options included sertraline, bupropion SR, or venlafaxine SR). You can already observe the drop in likelihood of remission, here at about 21% after failure of only one prior adequate antidepressant treatment. Ā At Level 3, the switch options offered were either mirtazapine or nortriptyline, and again the remission likelihood degrades further. Ā Finally, at Level 4, the switch option offered was the MAOI tranylcypromine. Here the likelihood of remission after failure of three prior adequate treatments was 6.9%. Ā References : Fava, M., A. J. Rush, et al. (2006). "A Comparison of Mirtazapine and Nortriptyline Following Two Consecutive Failed Medication Treatments for Depressed Outpatients: A Star*D Report." Am J Psychiatry 163 (7): 1161-1172. McGrath, P. J., J. W. Stewart, et al. (2006). "Tranylcypromine Versus Venlafaxine Plus Mirtazapine Following Three Failed Antidepressant Medication Trials for Depression: A STAR*D Report." Am J Psychiatry 163 (9): 1531-1541. Nierenberg, A. A., M. Fava, et al. (2006). "A Comparison of Lithium and T 3 Augmentation Following Two Failed Medication Treatments for Depression: A STAR*D Report." Am J Psychiatry 163 (9): 1519-1530. Rush, A. J. (2007). "STAR*D: What have we learned?" Am J Psychiatry 164 (2): 201-204. Rush, A. J., M. H. Trivedi, et al. (2006). "Acute and Longer-Term Outcomes in Depressed Outpatients Requiring One or Several Treatment Steps: A STAR*D Report." Am J Psychiatry 163 (11): 1905-1917. Trivedi, M. H., M. Fava, et al. (2006). "Medication Augmentation after the Failure of SSRIs for Depression." New England Journal of Medicine 354 (12): 1243-1252. Trivedi, M. H., A. J. Rush, et al. (2006). "Evaluation of Outcomes with Citalopram for Depression Using Measurement-Based Care in STAR*D Implications for Clinical Practice." Am J Psychiatry 163 (1): 28-40.
What about antidepressant tolerability and treatment adherence? A close look at the reported results of STAR*D reveals some important findings. Ā We have learned from the STAR*D Study, that the likelihood of a patient dropping out of treatment because of side effects rises dramatically, nearly tripling in the transition from Level 1 ( about 9% ) to Level 2 ( about 23% ). By the time a patient had failed to benefit from three prior treatment attempts, the likelihood of their discontinuing due to adverse events from the next offered antidepressant monotherapy (in this case the MAOI tranylcypromine), was quite notable: slightly greater than 41% . Ā There are many reasons why the intolerance to treatment rises with progressive levels of treatment resistance, and a full consideration of this is beyond the scope of this presentation. In general, this finding is both a reflection of how physically uncomfortable depression is as a disease, as well as the fact that each next treatment offering in this study brought the potential for an even greater degree of uncomfortable adverse events. Ā Shown on the right side of this diagram is a list of those adverse events reported in product labels for all contemporary antidepressant medications, including the augmentation agents such as the atypical antipsychotics. The list specifically shows those adverse events that in each product ās labeling were observed to occur at an incidence of at least 5% in the antidepressant-treated group, and occurred at a rate at least twice as high as the incidence of that event reported in the placebo group. Ā References : Fava, M., A. J. Rush, et al. (2006). "A Comparison of Mirtazapine and Nortriptyline Following Two Consecutive Failed Medication Treatments for Depressed Outpatients: A Star*D Report." Am J Psychiatry 163 (7): 1161-1172. McGrath, P. J., J. W. Stewart, et al. (2006). "Tranylcypromine Versus Venlafaxine Plus Mirtazapine Following Three Failed Antidepressant Medication Trials for Depression: A STAR*D Report." Am J Psychiatry 163 (9): 1531-1541. Nierenberg, A. A., M. Fava, et al. (2006). "A Comparison of Lithium and T 3 Augmentation Following Two Failed Medication Treatments for Depression: A STAR*D Report." Am J Psychiatry 163 (9): 1519-1530. Rush, A. J. (2007). "STAR*D: What have we learned?" Am J Psychiatry 164 (2): 201-204. Rush, A. J., M. H. Trivedi, et al. (2006). "Acute and Longer-Term Outcomes in Depressed Outpatients Requiring One or Several Treatment Steps: A STAR*D Report." Am J Psychiatry 163 (11): 1905-1917. Trivedi, M. H., M. Fava, et al. (2006). "Medication Augmentation after the Failure of SSRIs for Depression." New England Journal of Medicine 354 (12): 1243-1252. Trivedi, M. H., A. J. Rush, et al. (2006). "Evaluation of Outcomes with Citalopram for Depression Using Measurement-Based Care in STAR*D Implications for Clinical Practice." Am J Psychiatry 163 (1): 28-40. Product Labeling for currently marketed antidepressants (Neuronetics, Inc., data on file)
Capacitors of the day did not permit high intensity or rapid frequency use. The ā phosphenes ā were either generate from effects on the occipital cortex or directly on the retina of the eye. 1959 ā Kolin et al ā first to demonstrate magnetic field could stimulation a peripheral frog muscle preparation.
The underlying rationale for the use of TMS exploits the fact that neurons are electrochemical cells. This means that neuronal activity can be affected either chemically, via the use of drugs, or electrically, via interventions like TMS. Ā Unlike drug action, whose effects tend to be anatomically diffuse, the effects of TMS are anatomically focused, and by design are non-invasive and non-systemic in action. Under normal conditions of use, TMS therefore incurs far fewer adverse events, and is devoid of undesired systemic adverse events commonly observed with antidepressant medications. The TMS device is a powerful electromagnet, which is turned on and off in a rapid fashion, producing a pattern of āpulsedā magnetic fields. When pulsed magnetic fields are positioned close to an electrical conductor, like neurons, a local electrical current is produced in that conductor. This electric current is powerful enough right under the magnetic coil to elicit action potentials, which then travel down the neuron, ultimately causing the release of neurotransmitters at the synapse (Post 2001, p. 193A) . References : Post A, Keck ME. Transcranial magnetic stimulation as a therapeutic tool in psychiatry: what do we know about the neurobiological mechanisms? J Psychiatric Research. 2001;35: 193-215.
When the pulsed magnetic fields from the TMS coil are applied to the left dorsolateral prefrontal cortex, there are a series of events that are thought to underlie the therapeutic effects of TMS in the treatment of major depression: First, direct neuronal depolarization under the coil leads to local action potentials in neurons and the local release of neurotransmitters in the cortex. In addition to these local effects, neuronal depolarization of cortical pyramidal neurons is thought to occur (as represented by the blue neural pathway), reaching to deeper brain regions that lie outside the direct action of the pulsed magnetic fields. Activation of these deeper brain regions is then presumed to lead to secondary activation of brainstem neurotransmitter centers, which are then presumed to result in upward influences on the remaining brain regions involved in mood regulation (represented by the purple neural pathway). As a result, dopamine (Kanno 2004, pp. 75A, 76A, 77A) and serotonin (Juckel 1999, pp. 393A, 394A) activity are increased in areas of the brain whose low neurotransmitter activity have been linked to depression. The activity may be increased both in the short term by increasing release of neurotransmitters and in the long term by modulating expression of proteins involved in neurotransmitters signaling (Post 2001, p. 200A,B). Presumably, as a result of these changes, depression lifts (Slotema 2010, p. 876A). The net action of TMS is therefore targeted on the specific brain areas known to be involved in the regulation of mood, and is comprehensive in that its action has both direct effects on local neurons in the cerebral cortex, and then results in deeper actions on brain regions that are distant from the site of stimulation, but neurally connected to these cortical areas. These effects can be demonstrated in human neuroimaging studies of patients who have undergone treatment with TMS for their depression, as shown in the SPECT (single photon emission computed tomography) scan on the right (Kito, et al, 2008). In this image, the TMS coil has been positioned over the dorsolateral prefrontal cortex on the left side of the head. The area just underneath the coil is showing increased metabolic activity as a direct result of the magnetic stimulation. You can also see that the increase in metabolism reaches secondarily the deeper brain regions, in this case the regions of the cingulate cortex also show increased activation. References : Kanno M, Matsumoto M, et al. Effects of acute repetitive transcranial magnetic stimulation on dopamine release in rat dorsolateral striatum. J Neurological Sciences. 2004;217:73-81. Juckel G, Mendlin MA, et al. Electrical Stimulation of Rat Medial Prefrontal Cortex Enhances Forebrain Serotonin Output: Implications for Electroconvulsive Therapy and Transcranial Magnetic Stimulation in Depression. Neuropsychopharmacology. 1999;21(3):391-398. Slotema CW, Blom JD, et al. Should we expand the toolbox of psychiatric treatment methods to include repetitive transcranial magnetic stimulation (rTMS)? A meta-analysis of the efficacy of rTMS in psychiatric disorders. J Clin Psychiatry. 2010;71(7):873-884. Kito, S, Fujita, K, Koga, Y. Changes in Regional Cerebral Blood Flow After Repetitive Transcranial Magnetic Stimulation of the Left Dorsolateral Prefrontal Cortex in Treatment-Resistant Depression . J Neuropsychiatry Clin Neurosci. 2008; 20(1):74-80.
This slide describes some of the major demographic and clinical characteristics of the patients studied in the registration clinical trials that led to FDA clearance for the NeuroStar TMS Therapy system. Ā All patients had a diagnosis of unipolar, non-psychotic major depression, with moderate to severe symptoms at entry to the study. About a third of all patients had a concurrent secondary diagnosis of an anxiety disorder. Ā All patients received a rigorous characterization of their antidepressant medication treatment history in the current illness episode. Most patients had received numerous medication treatment attempts, with one of these treatment attempts being administered at an adequate daily dose and for at least four weeks without clinical benefit. The average number of overall treatment attempts (which includes all antidepressant medications administered in the current episode, regardless of whether they reached an adequate dose and duration) was 4, with a range across the study population from 1 to as many as 23 treatment attempts. Ā Consistent with the data that I reviewed earlier in this presentation, about 75% of the time, these antidepressant treatment attempts were unable to achieve this minimum level of exposure adequacy (usually because of treatment intolerance, or failure to adhere to the recommended treatment regimen). Ā References : Demitrack, MA , Thase, ME,. (2009) Clinical significance of transcranial magnetic stimulation (TMS) in the treatment of pharmacoresistant depression: synthesis of recent data. Psychopharm Bulletin 42(2) :5-38
Subsequent to the FDA clearance of the NeuroStar TMS system, the second-largest, randomized, sham-controlled clinical trial examining the safety and efficacy of TMS in major depression has now been reported. Ā This study has been referred to as the Optimization of TMS Study, or āOPT-TMSā by its investigators. It is a very important study for several reasons: Ā It was conducted independent of industry, and was funded and sponsored by the NIMH, It studied patients similar in inclusion and exclusion criteria to those studied in the Neuronetics trial, It used the same device as was used in the Neuronetics trial, the NeuroStar TMS Therapy System, It incorporated several additional innovations, including the use of an active sham condition to address questions of adequacy of the study blind in TMS trials, and The results were published in the Archives of General Psychiatry. Ā The main results of this study confirmed the observations of the earlier Neuronetics trial, and showed a statistically and clinically significant outcome on the primary efficacy measure of remission. Ā For those patients on sham treatment who did not improve, an open-label extension study was also offered. In that open-label extension, about 30% of patients were able to achieve remission after treatment with TMS. Ā This study also confirmed the safety and tolerability of TMS Therapy observed in prior studies, with a similar adverse event profile and with nearly 90% of patients fully adherent to the prescribed acute phase treatment course. Ā References : George, MS, Lisanby, SH, Avery, D, McDonald, WM, Durkalski, V, Pavlicova, M, Anderson, B, Nahas, Z, Bulow, P, Zarkowski, P, Holtzheimer, P, Schwartz, T, Sackeim, HA. (2010) Daily left prefrontal transcranial magnetic stimulation therapy for major depressive disorder: A sham-controlled randomized trial. Archives of General Psychiatry 67(5) :507-516
The published scientific evidence supporting the antidepressant effect of TMS is substantial, and now spans nearly twenty years of scientific research, involving more than 30 published studies, and over 2000 patients. Ā There are twelve published meta-analyses or qualitative reviews of this research. The most recent and comprehensive of these was reported by Slotema and colleagues last year. They analyzed the results of 34 studies involving 1,383 patients. They computed an effect size of 0.55 (P < 0.001), which represents a moderate to large clinical effect of TMS in the treatment of depression. Ā In their conclusion, they noted that āā¦rTMS deserves a place in the standard toolbox of psychiatric treatment methods, as it is effective for depressionā¦and has a mild side effect profileā¦ā. Ā References: Slotema, CW, Blom, JD, Hoek, HW, Sommer, IEC. (2010) Should we expand the toolbox of psychiatric treatment methods to include repetitive transcranial magnetic stimulation (rTMS)? A Meta-analysis of the efficacy of rTMS in psychiatric disorders. Journal of Clinical Psychiatry 71(7) :873-84. Schutter, DJLG. (2009) Antidepressant Efficacy of High-Frequency Transcranial Magnetic Stimulation Over the Left Dorsolateral Prefrontal Cortex in Double-Blind Sham-Controlled Designs: A Meta-Analysis. Psychol Medicine , 39 :65-75.
An overall summary of the main safety findings are shown on this slide: Ā As I discussed earlier in reviewing its mechanism of action, TMS showed no systemic side effects, There were no adverse effects on cognition as measured by formal cognitive testing using the Mini Mental Status Examination (a measure of global cognitive function), the Buschke Selective Reminding Test (a measure of short-term memory), and the Autobiographical Memory Interview Short Form (a measure of long-term memory), The most commonly reported device-related adverse event was scalp pain or discomfort in about a third of all patients, Only about 5% of patients discontinued due to adverse events, and for the majority of patients, the device-related adverse events subsided substantially after the first week of treatment Long term safety was confirmed in a six month period of follow up after benefit from acute treatment Ā Seizure is the major, medically significant potential safety risk of TMS. During clinical trials, no seizures were observed with the NeuroStar TMS system. In post-market use, the risk of seizure is rare. Since market introduction and based on current usage, an estimated risk of seizure is approximately 0.003% per treatmentĀ exposure, and <0.1% per acute treatment course. To date, over 150,000 treatments and more than 5,000 patients have been treated with the NeuroStar TMS Therapy system which confirms its safe use in the treatment of depression. Ā References : Janicak, PG, OāReardon, JP, Sampson, SM, Husain, MM, Lisanby, SH, Rado, JT, Demitrack, MA. (2008) Transcranial Magnetic Stimulation (TMS) in the Treatment of Major Depression: A Comprehensive Summary of Safety Experience from Acute and Extended Exposure and During Reintroduction Treatment. J Clin Psychiatry 69(2) :222-232. Janicak, PG, Nahas, Z, Lisanby, SH, Sovason, HB, Sampson, SM, McDonald, WM, Marangell, LB, Rosenquist, PB, McCall, WV, Kimball, J, OāReardon, J, Loo, C, Husain, MH, Krystal, A, Gilmer, W, Dowd, SM, Demitrack, MA, Schatzberg, AF: (2010) Long-Term Durability of Acute Response to Transcranial Magnetic Stimulation (TMS) in the Treatment of Pharmacoresistant Major Depression. Brain Stimulation 3 :187-199.
This slide shows another important safety observation. The risk of emergent suicidal ideation is a concern with any antidepressant treatment. Ā In the analysis shown on this slide, Item 3 of the Hamilton Depression Rating Scale (the Suicidal Ideation item), which ranges from 0 to 4, was used. The slide depicts the proportion of patients in either the active TMS or sham TMS treatment group in the randomized controlled trial who came in with no suicidal ideation (an Item 3 score of 0 or 1) at baseline, and who later experienced an abrupt emergence of suicidal ideation (a score of 3 or 4) at any later time point. Ā It can be seen that virtually all of these instances occurred only in the sham treatment condition. This indicates that TMS is not associated with provoking emergent suicidal ideation during acute treatment in the indicated patient population. Ā References : Neuronetics, Inc., data on file. Janicak, PG, OāReardon, JP, Sampson, SM, Husain, MM, Lisanby, SH, Rado, JT, Demitrack, MA. (2008) Transcranial Magnetic Stimulation (TMS) in the Treatment of Major Depression: A Comprehensive Summary of Safety Experience from Acute and Extended Exposure and During Reintroduction Treatment. J Clin Psychiatry 69(2) :222-232.
TMS employs the same type of pulsed magnetic field technology used in modern MR imaging equipment. While the safety of this medical technology in short and long term exposure is well established, Neuronetics also characterized the long-term safety outcomes of patients treated with TMS during six months of follow up after cessation of acute treatment. Ā The design of this open-label follow up study is shown in this diagram. Following completion of acute treatment with TMS alone, all patients were transitioned during a 3 week Taper Phase off of TMS and onto single antidepressant medication maintenance. Ā The choice of medication was based on clinician and patient preference, but could not include use of a medication to which the patient had previously been non-responsive. The most commonly used medications in this study in long-term follow up were duloxetine and bupropion. Ā During the 6 months of follow up, patients were not permitted to modify or add to the single medication regimen in any way. TMS treatment was permitted if the patient experienced symptom recurrence, as measured by the protocol rating scales. Ā References : Janicak, PG, Nahas, Z, Lisanby, SH, Sovason, HB, Sampson, SM, McDonald, WM, Marangell, LB, Rosenquist, PB, McCall, WV, Kimball, J, OāReardon, J, Loo, C, Husain, MH, Krystal, A, Gilmer, W, Dowd, SM, Demitrack, MA, Schatzberg, AF: (2010) Long-Term Durability of Acute Response to Transcranial Magnetic Stimulation (TMS) in the Treatment of Pharmacoresistant Major Depression. Brain Stimulation 3 :187-199.
The major results of this long-term, open-label safety follow up are shown here. Ā No new safety observations related to TMS were reported. Ā Approximately 37% of patients experienced symptom recurrence requiring reintroduction of TMS. For those patients, about 85% benefited from reintroduction of TMS given in addition to their ongoing antidepressant medication. Ā Over 6 months of follow up, the net incidence of illness relapse (ie, those patients who deteriorated without receiving TMS and exited the study, or those patients for whom TMS reintroduction was not effective) was about 11%. This compares favorably to the long-term relapse reported in open-label naturalistic follow up in the STAR*D study, where 6 month relapse rates in Level 2 or 3 patients ranged as high as 35-50% despite continued best efforts at treatment as usual. Ā References : Janicak, PG, Nahas, Z, Lisanby, SH, Sovason, HB, Sampson, SM, McDonald, WM, Marangell, LB, Rosenquist, PB, McCall, WV, Kimball, J, OāReardon, J, Loo, C, Husain, MH, Krystal, A, Gilmer, W, Dowd, SM, Demitrack, MA, Schatzberg, AF: (2010) Long-Term Durability of Acute Response to Transcranial Magnetic Stimulation (TMS) in the Treatment of Pharmacoresistant Major Depression. Brain Stimulation 3 :187-199. Rush, A. J., M. H. Trivedi, et al. (2006). "Acute and Longer-Term Outcomes in Depressed Outpatients Requiring One or Several Treatment Steps: A STAR*D Report." Am J Psychiatry 163 (11): 1905-1917.