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Premature mortality across most psychiatric disorders

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Premature mortality across most psychiatric disorders

The evidence is robust and disheartening: As if the personal suffering and societal stigma of mental illness are not bad enough, psychiatric patients also have a shorter life­span.1 In the past, most studies have focused on early mortality and loss of potential life-years in schizophrenia,2 but many subsequent reports indicate that premature death occurs in all major psychiatric disorders.

Here is a summary of the sobering facts:

  • Schizophrenia. In a study of 30,210 patients with schizophrenia, compared with >5 million individuals in the general population in Denmark (where they have an excellent registry), mortality was 16-fold higher among patients with schizophrenia if they had a single somatic illness.3 The illnesses were mostly respiratory, gastrointestinal, or cardiovascular).3 The loss of potential years of life was staggeringly high: 18.7 years for men, 16.3 years for women.4 A study conducted in 8 US states reported a loss of 2 to 3 decades of life across each of these states.5 The causes of death in patients with schizophrenia were mainly heart disease, cancer, stroke, and pulmonary diseases. A national database in Sweden found that unmedicated patients with schizophrenia had a significantly higher death rate than those receiving antipsychotics.6,7 Similar findings were reported by researchers in Finland.8 The Swedish study by Tiihonen et al6 also found that mortality was highest in patients receiving benzodiazepines along with antipsychotics, but there was no increased mortality among patients with schizophrenia receiving antidepressants.
  • Bipolar disorder. A shorter life expectancy has also been reported in bipolar disorder,9 with a loss of 13.6 years for men and 12.1 years for women. Early death was caused by physical illness (even when suicide deaths were excluded), especially cardio­vascular disease.10
  • Major depressive disorder (MDD). A reduction of life expectancy in persons with MDD (unipolar depression) has been reported, with a loss of 14 years in men and 10 years in women.11 Although suicide contributed to the shorter lifespan, death due to accidents was 500% higher among persons with unipolar depression; the largest causes of death were physical illnesses. Further, Zubenko et al12 reported alarming findings about excess mortality among first- and second-degree relatives of persons with early-onset depression (some of whom were bipolar). The relatives died an average of 8 years earlier than the local population, and 40% died before reaching age 65. Also, there was a 5-fold increase in infant mortality (in the first year of life) among the relatives. The most common causes of death in adult relatives were heart disease, cancer, and stroke. It is obvious that MDD has a significant negative impact on health and longevity in both patients and their relatives.
  • Attention-deficit/hyperactivity disorder (ADHD). A 220% increase in mortality was reported in persons with ADHD at all ages.13 Accidents were the most common cause of death. The mortality rate ratio (MRR) was 1.86 for ADHD before age 6, 1.58 for ADHD between age 6 to 17, and 4.25 for those age ≥18. The rate of early mortality was higher in girls and women (MRR = 2.85) than boys and men (MRR = 1.27).
  • Obsessive-compulsive disorder (OCD). A study from Denmark of 10,155 persons with OCD followed for 10 years reported a significantly higher risk of death from both natural (MRR = 1.68) and unnatural causes (MRR = 2.61), compared with the general population.14 Patients with OCD and comorbid depression, anxiety, or substance use had a further increase in mortality risk, but the mortality risk of individuals with OCD without psychiatric comorbidity was still 200% higher than that of the general population.
  • Anxiety disorders. One study found no increase in mortality among patients who have generalized anxiety, unless it was associated with depression.15 Another study reported that the presence of anxiety reduced the risk of cardiovascular mortality in persons with depression.16 The absence of increased mortality in anxiety disorders was also confirmed in a meta-analysis of 36 studies.17 However, a study of postmenopausal women with panic attacks found a 3-fold increase in coronary artery disease and stroke in that cohort,18 which confirmed the findings of an older study19 that demonstrated a 2-fold increase of mortality among 155 men with panic disorder after a 12-year follow-up. Also, a 25-year follow-up study found that suicide accounted for 20% of deaths in the anxiety group compared with 16.2% in the depression group,20 showing a significant risk of suicide in panic disorder, even exceeding that of depression.
  • Oppositional defiant disorder (ODD) and conduct disorder (CD). In a 12-year follow-up study of 9,495 individuals with “disruptive behavioral disorders,” which included ODD and CD, the mortality rate was >400% higher in these patients compared with 1.92 million individuals in the general population (9.66 vs 2.22 per 10,000 person­-years).21 Comorbid substance use disorder and ADHD further increased the mortality rate in this cohort.
  • Posttraumatic stress disorder (PTSD). Studies show that there is a significantly increased risk of early cardiovascular mortality in PTSD,22 and that the death rate may be associated with accelerated “DNA methylation age” that leads to a 13% increased risk for all-cause mortality.23
  • Borderline personality disorder (BPD). A recent longitudinal study (24 years of follow-up with evaluation every 2 years) reported a significantly higher mortality in patients with BPD compared with those with other personality disorders. The age range when the study started was 18 to 35. The rate of suicide death was Palatino LT Std>400% higher in BPD (5.9% vs 1.4%). Also, non-suicidal death was 250% higher in BPD (14% vs 5.5%). The causes of non-suicidal death included cardiovascular disease, substance-related complications, cancer, and accidents.24
  • Other personality disorders. Certain personality traits have been associated with shorter leukocyte telomeres, which signal early death. These traits include neuroticism, conscientiousness, harm avoidance, and reward dependence.25 Another study found shorter telomeres in persons with high neuroticism and low agreeableness26 regardless of age or sex. Short telomeres, which reflect accelerated cellular senescence and aging, have also been reported in several major psychiatric disorders (schizophrenia, bipolar disorder, MDD, and anxiety).27-29 The cumulative evidence is unassailable; psychiatric brain disorders are not only associated with premature death due to high suicide rates, but also with multiple medical diseases that lead to early mortality and a shorter lifespan. The shortened telomeres reflect high oxidative stress and inflammation, and both those toxic processes are known to be associated with major psychiatric disorders. Compounding the dismal facts about early mortality due to mental illness are the additional grave medical consequences of alcohol and substance use, which are highly comorbid with most psychiatric disorders, further exacerbating the premature death rates among psychiatric patients.

Continue to: There is an important take-home message...

 

 

There is an important take-home message in all of this: Our patients are at high risk for potentially fatal medical conditions that require early detection, and intensive ongoing treatment by a primary care clinician (not “provider”; I abhor the widespread use of that term for physicians or nurse practitioners) is an indispensable component of psychiatric care. Thus, collaborative care is vital to protect our psychiatric patients from early mortality and a shortened lifespan. Psychiatrists and psychiatric nurse practitioners must not only win the battle against mental illness, but also diligently avoid losing the war of life and death.

References

1. Walker ER, McGee RE, Druss BG. Mortality in mental disorders and global disease burden implications: a systematic review and meta-analysis. JAMA Psychiatry. 2015;72(4):334-341.
2. Laursen TM, Wahlbeck K, Hällgren J, et al. Life expectancy and death by diseases of the circulatory system in patients with bipolar disorder or schizophrenia in the Nordic countries. PLoS One. 2013;8(6):e67133. doi: 10.1371/journal.pone.0067133.
3. Kugathasan P, Stubbs B, Aagaard J, et al. Increased mortality from somatic multimorbidity in patients with schizophrenia: a Danish nationwide cohort study. Acta Psychiatr Scand. 2019. doi: 10.1111/acps.13076.
4. Laursen TM. Life expectancy among persons with schizophrenia or bipolar affective disorder. Schizophr Res. 2011;131(1-3):101-104.
5. Colton CW, Manderscheid RW. Congruencies in increased mortality rates, years of potential life lost, and causes of death among public mental health clients in eight states. Prev Chronic Dis. 2006;3(2):A42.
6. Tiihonen J, Mittendorfer-Rutz E, Torniainen M, et al. Mortality and cumulative exposure to anti­psychotics, antidepressants, and benzodiazepines in patients with schizophrenia: an observational follow-up study. Am J Psychiatry. 2016;173(6):600-606.
7. Torniainen M, Mittendorfer-Rutz E, Tanskanen A, et al. Antipsychotic treatment and mortality in schizophrenia. Schizophr Bull. 2015;41(3):656-663.
8. Tiihonen J, Lönnqvist J, Wahlbeck K, et al. 11-year follow-up of mortality in patients with schizophrenia: a population-based cohort study (FIN11 study). Lancet. 2009;374(9690):620-627.
9. Wilson R, Gaughran F, Whitburn T, et al. Place of death and other factors associated with unnatural mortality in patients with serious mental disorders: population-based retrospective cohort study. BJPsych Open. 2019;5(2):e23. doi: 10.1192/bjo.2019.5.
10. Ösby U, Westman J, Hällgren J, et al. Mortality trends in cardiovascular causes in schizophrenia, bipolar and unipolar mood disorder in Sweden 1987-2010. Eur J Public Health. 2016;26(5):867-871.
11. Laursen TM, Musliner KL, Benros ME, et al. Mortality and life expectancy in persons with severe unipolar depression. J Affect Disord. 2016;193:203-207.
12. Zubenko GS, Zubenko WN, Spiker DG, et al. Malignancy of recurrent, early-onset major depression: a family study. Am J Med Genet. 2001;105(8):690-699.
13. Dalsgaard S, Østergaard SD, Leckman JF, et al. Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: a nationwide cohort study. Lancet. 2015;385(9983):2190-2196.
14. Meier SM, Mattheisen M, Mors O, et al. Mortality among persons with obsessive-compulsive disorder in Denmark. JAMA Psychiatry. 2016;73(3):268-274.
15. Holwerda TJ, Schoevers RA, Dekker J, et al. The relationship between generalized anxiety disorder, depression and mortality in old age. Int J Geriatr Psychiatry. 2007;22(3):241-249.
16. Ivanovs R, Kivite A, Ziedonis D, et al. Association of depression and anxiety with the 10-year risk of cardiovascular mortality in a primary care population of Latvia using the SCORE system. Front Psychiatry. 2018;9:276.
17. Miloyan B, Bulley A, Bandeen-Roche K, et al. Anxiety disorders and all-cause mortality: systematic review and meta-analysis. Soc Psychiatry Psychiatr Epidemiol. 2016;51(11):1467-1475.
18. Smoller JW, Pollack MH, Wassertheil-Smoller S, et al. Panic attacks and risk of incident cardiovascular events among postmenopausal women in the Women’s Health Initiative Observational Study. Arch Gen Psychiatry. 2007;64(10):1153-1160.
19. Coryell W, Noyes R Jr, House JD. Mortality among outpatients with anxiety disorders. Am J Psychiatry. 1986;143(4):508-510.
20. Coryell W, Noyes R, Clancy J. Excess mortality in panic disorder. A comparison with primary unipolar depression. Arch Gen Psychiatry. 1982;39(6):701-703.
21. Scott JG, Giørtz Pedersen M, Erskine HE, et al. Mortality in individuals with disruptive behavior disorders diagnosed by specialist services - a nationwide cohort study. Psychiatry Res. 2017;251:255-260.
22. Burg MM, Soufer R. Post-traumatic stress disorder and cardiovascular disease. Curr Cardiol Rep. 2016;18(10):94.
23. Wolf EJ, Logue MW, Stoop TB, et al. Accelerated DNA methylation age: associations with PTSD and mortality. Psychosom Med. 2017. doi: 10.1097/PSY.0000000000000506.
24. Temes CM, Frankenburg FR, Fitzmaurice MC, et al. Deaths by suicide and other causes among patients with borderline personality disorder and personality-disordered comparison subjects over 24 years of prospective follow-up. J Clin Psychiatry. 2019;80(1). doi: 10.4088/JCP.18m12436.
25. Sadahiro R, Suzuki A, Enokido M, et al. Relationship between leukocyte telomere length and personality traits in healthy subjects. Eur Psychiatry. 2015;30(2):291-295.
26. Schoormans D, Verhoeven JE, Denollet J, et al. Leukocyte telomere length and personality: associations with the Big Five and Type D personality traits. Psychol Med. 2018;48(6):1008-1019.
27. Muneer A, Minhas FA. Telomere biology in mood disorders: an updated, comprehensive review of the literature. Clin Psychopharmacol Neurosci. 2019;17(3):343-363.
28. Vakonaki E, Tsiminikaki K, Plaitis S, et al. Common mental disorders and association with telomere length. Biomed Rep. 2018;8(2):111-116.
29. Malouff JM, Schutte NS. A meta-analysis of the relationship between anxiety and telomere length. Anxiety Stress Coping. 2017;30(3):264-272.

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The evidence is robust and disheartening: As if the personal suffering and societal stigma of mental illness are not bad enough, psychiatric patients also have a shorter life­span.1 In the past, most studies have focused on early mortality and loss of potential life-years in schizophrenia,2 but many subsequent reports indicate that premature death occurs in all major psychiatric disorders.

Here is a summary of the sobering facts:

  • Schizophrenia. In a study of 30,210 patients with schizophrenia, compared with >5 million individuals in the general population in Denmark (where they have an excellent registry), mortality was 16-fold higher among patients with schizophrenia if they had a single somatic illness.3 The illnesses were mostly respiratory, gastrointestinal, or cardiovascular).3 The loss of potential years of life was staggeringly high: 18.7 years for men, 16.3 years for women.4 A study conducted in 8 US states reported a loss of 2 to 3 decades of life across each of these states.5 The causes of death in patients with schizophrenia were mainly heart disease, cancer, stroke, and pulmonary diseases. A national database in Sweden found that unmedicated patients with schizophrenia had a significantly higher death rate than those receiving antipsychotics.6,7 Similar findings were reported by researchers in Finland.8 The Swedish study by Tiihonen et al6 also found that mortality was highest in patients receiving benzodiazepines along with antipsychotics, but there was no increased mortality among patients with schizophrenia receiving antidepressants.
  • Bipolar disorder. A shorter life expectancy has also been reported in bipolar disorder,9 with a loss of 13.6 years for men and 12.1 years for women. Early death was caused by physical illness (even when suicide deaths were excluded), especially cardio­vascular disease.10
  • Major depressive disorder (MDD). A reduction of life expectancy in persons with MDD (unipolar depression) has been reported, with a loss of 14 years in men and 10 years in women.11 Although suicide contributed to the shorter lifespan, death due to accidents was 500% higher among persons with unipolar depression; the largest causes of death were physical illnesses. Further, Zubenko et al12 reported alarming findings about excess mortality among first- and second-degree relatives of persons with early-onset depression (some of whom were bipolar). The relatives died an average of 8 years earlier than the local population, and 40% died before reaching age 65. Also, there was a 5-fold increase in infant mortality (in the first year of life) among the relatives. The most common causes of death in adult relatives were heart disease, cancer, and stroke. It is obvious that MDD has a significant negative impact on health and longevity in both patients and their relatives.
  • Attention-deficit/hyperactivity disorder (ADHD). A 220% increase in mortality was reported in persons with ADHD at all ages.13 Accidents were the most common cause of death. The mortality rate ratio (MRR) was 1.86 for ADHD before age 6, 1.58 for ADHD between age 6 to 17, and 4.25 for those age ≥18. The rate of early mortality was higher in girls and women (MRR = 2.85) than boys and men (MRR = 1.27).
  • Obsessive-compulsive disorder (OCD). A study from Denmark of 10,155 persons with OCD followed for 10 years reported a significantly higher risk of death from both natural (MRR = 1.68) and unnatural causes (MRR = 2.61), compared with the general population.14 Patients with OCD and comorbid depression, anxiety, or substance use had a further increase in mortality risk, but the mortality risk of individuals with OCD without psychiatric comorbidity was still 200% higher than that of the general population.
  • Anxiety disorders. One study found no increase in mortality among patients who have generalized anxiety, unless it was associated with depression.15 Another study reported that the presence of anxiety reduced the risk of cardiovascular mortality in persons with depression.16 The absence of increased mortality in anxiety disorders was also confirmed in a meta-analysis of 36 studies.17 However, a study of postmenopausal women with panic attacks found a 3-fold increase in coronary artery disease and stroke in that cohort,18 which confirmed the findings of an older study19 that demonstrated a 2-fold increase of mortality among 155 men with panic disorder after a 12-year follow-up. Also, a 25-year follow-up study found that suicide accounted for 20% of deaths in the anxiety group compared with 16.2% in the depression group,20 showing a significant risk of suicide in panic disorder, even exceeding that of depression.
  • Oppositional defiant disorder (ODD) and conduct disorder (CD). In a 12-year follow-up study of 9,495 individuals with “disruptive behavioral disorders,” which included ODD and CD, the mortality rate was >400% higher in these patients compared with 1.92 million individuals in the general population (9.66 vs 2.22 per 10,000 person­-years).21 Comorbid substance use disorder and ADHD further increased the mortality rate in this cohort.
  • Posttraumatic stress disorder (PTSD). Studies show that there is a significantly increased risk of early cardiovascular mortality in PTSD,22 and that the death rate may be associated with accelerated “DNA methylation age” that leads to a 13% increased risk for all-cause mortality.23
  • Borderline personality disorder (BPD). A recent longitudinal study (24 years of follow-up with evaluation every 2 years) reported a significantly higher mortality in patients with BPD compared with those with other personality disorders. The age range when the study started was 18 to 35. The rate of suicide death was Palatino LT Std>400% higher in BPD (5.9% vs 1.4%). Also, non-suicidal death was 250% higher in BPD (14% vs 5.5%). The causes of non-suicidal death included cardiovascular disease, substance-related complications, cancer, and accidents.24
  • Other personality disorders. Certain personality traits have been associated with shorter leukocyte telomeres, which signal early death. These traits include neuroticism, conscientiousness, harm avoidance, and reward dependence.25 Another study found shorter telomeres in persons with high neuroticism and low agreeableness26 regardless of age or sex. Short telomeres, which reflect accelerated cellular senescence and aging, have also been reported in several major psychiatric disorders (schizophrenia, bipolar disorder, MDD, and anxiety).27-29 The cumulative evidence is unassailable; psychiatric brain disorders are not only associated with premature death due to high suicide rates, but also with multiple medical diseases that lead to early mortality and a shorter lifespan. The shortened telomeres reflect high oxidative stress and inflammation, and both those toxic processes are known to be associated with major psychiatric disorders. Compounding the dismal facts about early mortality due to mental illness are the additional grave medical consequences of alcohol and substance use, which are highly comorbid with most psychiatric disorders, further exacerbating the premature death rates among psychiatric patients.

Continue to: There is an important take-home message...

 

 

There is an important take-home message in all of this: Our patients are at high risk for potentially fatal medical conditions that require early detection, and intensive ongoing treatment by a primary care clinician (not “provider”; I abhor the widespread use of that term for physicians or nurse practitioners) is an indispensable component of psychiatric care. Thus, collaborative care is vital to protect our psychiatric patients from early mortality and a shortened lifespan. Psychiatrists and psychiatric nurse practitioners must not only win the battle against mental illness, but also diligently avoid losing the war of life and death.

The evidence is robust and disheartening: As if the personal suffering and societal stigma of mental illness are not bad enough, psychiatric patients also have a shorter life­span.1 In the past, most studies have focused on early mortality and loss of potential life-years in schizophrenia,2 but many subsequent reports indicate that premature death occurs in all major psychiatric disorders.

Here is a summary of the sobering facts:

  • Schizophrenia. In a study of 30,210 patients with schizophrenia, compared with >5 million individuals in the general population in Denmark (where they have an excellent registry), mortality was 16-fold higher among patients with schizophrenia if they had a single somatic illness.3 The illnesses were mostly respiratory, gastrointestinal, or cardiovascular).3 The loss of potential years of life was staggeringly high: 18.7 years for men, 16.3 years for women.4 A study conducted in 8 US states reported a loss of 2 to 3 decades of life across each of these states.5 The causes of death in patients with schizophrenia were mainly heart disease, cancer, stroke, and pulmonary diseases. A national database in Sweden found that unmedicated patients with schizophrenia had a significantly higher death rate than those receiving antipsychotics.6,7 Similar findings were reported by researchers in Finland.8 The Swedish study by Tiihonen et al6 also found that mortality was highest in patients receiving benzodiazepines along with antipsychotics, but there was no increased mortality among patients with schizophrenia receiving antidepressants.
  • Bipolar disorder. A shorter life expectancy has also been reported in bipolar disorder,9 with a loss of 13.6 years for men and 12.1 years for women. Early death was caused by physical illness (even when suicide deaths were excluded), especially cardio­vascular disease.10
  • Major depressive disorder (MDD). A reduction of life expectancy in persons with MDD (unipolar depression) has been reported, with a loss of 14 years in men and 10 years in women.11 Although suicide contributed to the shorter lifespan, death due to accidents was 500% higher among persons with unipolar depression; the largest causes of death were physical illnesses. Further, Zubenko et al12 reported alarming findings about excess mortality among first- and second-degree relatives of persons with early-onset depression (some of whom were bipolar). The relatives died an average of 8 years earlier than the local population, and 40% died before reaching age 65. Also, there was a 5-fold increase in infant mortality (in the first year of life) among the relatives. The most common causes of death in adult relatives were heart disease, cancer, and stroke. It is obvious that MDD has a significant negative impact on health and longevity in both patients and their relatives.
  • Attention-deficit/hyperactivity disorder (ADHD). A 220% increase in mortality was reported in persons with ADHD at all ages.13 Accidents were the most common cause of death. The mortality rate ratio (MRR) was 1.86 for ADHD before age 6, 1.58 for ADHD between age 6 to 17, and 4.25 for those age ≥18. The rate of early mortality was higher in girls and women (MRR = 2.85) than boys and men (MRR = 1.27).
  • Obsessive-compulsive disorder (OCD). A study from Denmark of 10,155 persons with OCD followed for 10 years reported a significantly higher risk of death from both natural (MRR = 1.68) and unnatural causes (MRR = 2.61), compared with the general population.14 Patients with OCD and comorbid depression, anxiety, or substance use had a further increase in mortality risk, but the mortality risk of individuals with OCD without psychiatric comorbidity was still 200% higher than that of the general population.
  • Anxiety disorders. One study found no increase in mortality among patients who have generalized anxiety, unless it was associated with depression.15 Another study reported that the presence of anxiety reduced the risk of cardiovascular mortality in persons with depression.16 The absence of increased mortality in anxiety disorders was also confirmed in a meta-analysis of 36 studies.17 However, a study of postmenopausal women with panic attacks found a 3-fold increase in coronary artery disease and stroke in that cohort,18 which confirmed the findings of an older study19 that demonstrated a 2-fold increase of mortality among 155 men with panic disorder after a 12-year follow-up. Also, a 25-year follow-up study found that suicide accounted for 20% of deaths in the anxiety group compared with 16.2% in the depression group,20 showing a significant risk of suicide in panic disorder, even exceeding that of depression.
  • Oppositional defiant disorder (ODD) and conduct disorder (CD). In a 12-year follow-up study of 9,495 individuals with “disruptive behavioral disorders,” which included ODD and CD, the mortality rate was >400% higher in these patients compared with 1.92 million individuals in the general population (9.66 vs 2.22 per 10,000 person­-years).21 Comorbid substance use disorder and ADHD further increased the mortality rate in this cohort.
  • Posttraumatic stress disorder (PTSD). Studies show that there is a significantly increased risk of early cardiovascular mortality in PTSD,22 and that the death rate may be associated with accelerated “DNA methylation age” that leads to a 13% increased risk for all-cause mortality.23
  • Borderline personality disorder (BPD). A recent longitudinal study (24 years of follow-up with evaluation every 2 years) reported a significantly higher mortality in patients with BPD compared with those with other personality disorders. The age range when the study started was 18 to 35. The rate of suicide death was Palatino LT Std>400% higher in BPD (5.9% vs 1.4%). Also, non-suicidal death was 250% higher in BPD (14% vs 5.5%). The causes of non-suicidal death included cardiovascular disease, substance-related complications, cancer, and accidents.24
  • Other personality disorders. Certain personality traits have been associated with shorter leukocyte telomeres, which signal early death. These traits include neuroticism, conscientiousness, harm avoidance, and reward dependence.25 Another study found shorter telomeres in persons with high neuroticism and low agreeableness26 regardless of age or sex. Short telomeres, which reflect accelerated cellular senescence and aging, have also been reported in several major psychiatric disorders (schizophrenia, bipolar disorder, MDD, and anxiety).27-29 The cumulative evidence is unassailable; psychiatric brain disorders are not only associated with premature death due to high suicide rates, but also with multiple medical diseases that lead to early mortality and a shorter lifespan. The shortened telomeres reflect high oxidative stress and inflammation, and both those toxic processes are known to be associated with major psychiatric disorders. Compounding the dismal facts about early mortality due to mental illness are the additional grave medical consequences of alcohol and substance use, which are highly comorbid with most psychiatric disorders, further exacerbating the premature death rates among psychiatric patients.

Continue to: There is an important take-home message...

 

 

There is an important take-home message in all of this: Our patients are at high risk for potentially fatal medical conditions that require early detection, and intensive ongoing treatment by a primary care clinician (not “provider”; I abhor the widespread use of that term for physicians or nurse practitioners) is an indispensable component of psychiatric care. Thus, collaborative care is vital to protect our psychiatric patients from early mortality and a shortened lifespan. Psychiatrists and psychiatric nurse practitioners must not only win the battle against mental illness, but also diligently avoid losing the war of life and death.

References

1. Walker ER, McGee RE, Druss BG. Mortality in mental disorders and global disease burden implications: a systematic review and meta-analysis. JAMA Psychiatry. 2015;72(4):334-341.
2. Laursen TM, Wahlbeck K, Hällgren J, et al. Life expectancy and death by diseases of the circulatory system in patients with bipolar disorder or schizophrenia in the Nordic countries. PLoS One. 2013;8(6):e67133. doi: 10.1371/journal.pone.0067133.
3. Kugathasan P, Stubbs B, Aagaard J, et al. Increased mortality from somatic multimorbidity in patients with schizophrenia: a Danish nationwide cohort study. Acta Psychiatr Scand. 2019. doi: 10.1111/acps.13076.
4. Laursen TM. Life expectancy among persons with schizophrenia or bipolar affective disorder. Schizophr Res. 2011;131(1-3):101-104.
5. Colton CW, Manderscheid RW. Congruencies in increased mortality rates, years of potential life lost, and causes of death among public mental health clients in eight states. Prev Chronic Dis. 2006;3(2):A42.
6. Tiihonen J, Mittendorfer-Rutz E, Torniainen M, et al. Mortality and cumulative exposure to anti­psychotics, antidepressants, and benzodiazepines in patients with schizophrenia: an observational follow-up study. Am J Psychiatry. 2016;173(6):600-606.
7. Torniainen M, Mittendorfer-Rutz E, Tanskanen A, et al. Antipsychotic treatment and mortality in schizophrenia. Schizophr Bull. 2015;41(3):656-663.
8. Tiihonen J, Lönnqvist J, Wahlbeck K, et al. 11-year follow-up of mortality in patients with schizophrenia: a population-based cohort study (FIN11 study). Lancet. 2009;374(9690):620-627.
9. Wilson R, Gaughran F, Whitburn T, et al. Place of death and other factors associated with unnatural mortality in patients with serious mental disorders: population-based retrospective cohort study. BJPsych Open. 2019;5(2):e23. doi: 10.1192/bjo.2019.5.
10. Ösby U, Westman J, Hällgren J, et al. Mortality trends in cardiovascular causes in schizophrenia, bipolar and unipolar mood disorder in Sweden 1987-2010. Eur J Public Health. 2016;26(5):867-871.
11. Laursen TM, Musliner KL, Benros ME, et al. Mortality and life expectancy in persons with severe unipolar depression. J Affect Disord. 2016;193:203-207.
12. Zubenko GS, Zubenko WN, Spiker DG, et al. Malignancy of recurrent, early-onset major depression: a family study. Am J Med Genet. 2001;105(8):690-699.
13. Dalsgaard S, Østergaard SD, Leckman JF, et al. Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: a nationwide cohort study. Lancet. 2015;385(9983):2190-2196.
14. Meier SM, Mattheisen M, Mors O, et al. Mortality among persons with obsessive-compulsive disorder in Denmark. JAMA Psychiatry. 2016;73(3):268-274.
15. Holwerda TJ, Schoevers RA, Dekker J, et al. The relationship between generalized anxiety disorder, depression and mortality in old age. Int J Geriatr Psychiatry. 2007;22(3):241-249.
16. Ivanovs R, Kivite A, Ziedonis D, et al. Association of depression and anxiety with the 10-year risk of cardiovascular mortality in a primary care population of Latvia using the SCORE system. Front Psychiatry. 2018;9:276.
17. Miloyan B, Bulley A, Bandeen-Roche K, et al. Anxiety disorders and all-cause mortality: systematic review and meta-analysis. Soc Psychiatry Psychiatr Epidemiol. 2016;51(11):1467-1475.
18. Smoller JW, Pollack MH, Wassertheil-Smoller S, et al. Panic attacks and risk of incident cardiovascular events among postmenopausal women in the Women’s Health Initiative Observational Study. Arch Gen Psychiatry. 2007;64(10):1153-1160.
19. Coryell W, Noyes R Jr, House JD. Mortality among outpatients with anxiety disorders. Am J Psychiatry. 1986;143(4):508-510.
20. Coryell W, Noyes R, Clancy J. Excess mortality in panic disorder. A comparison with primary unipolar depression. Arch Gen Psychiatry. 1982;39(6):701-703.
21. Scott JG, Giørtz Pedersen M, Erskine HE, et al. Mortality in individuals with disruptive behavior disorders diagnosed by specialist services - a nationwide cohort study. Psychiatry Res. 2017;251:255-260.
22. Burg MM, Soufer R. Post-traumatic stress disorder and cardiovascular disease. Curr Cardiol Rep. 2016;18(10):94.
23. Wolf EJ, Logue MW, Stoop TB, et al. Accelerated DNA methylation age: associations with PTSD and mortality. Psychosom Med. 2017. doi: 10.1097/PSY.0000000000000506.
24. Temes CM, Frankenburg FR, Fitzmaurice MC, et al. Deaths by suicide and other causes among patients with borderline personality disorder and personality-disordered comparison subjects over 24 years of prospective follow-up. J Clin Psychiatry. 2019;80(1). doi: 10.4088/JCP.18m12436.
25. Sadahiro R, Suzuki A, Enokido M, et al. Relationship between leukocyte telomere length and personality traits in healthy subjects. Eur Psychiatry. 2015;30(2):291-295.
26. Schoormans D, Verhoeven JE, Denollet J, et al. Leukocyte telomere length and personality: associations with the Big Five and Type D personality traits. Psychol Med. 2018;48(6):1008-1019.
27. Muneer A, Minhas FA. Telomere biology in mood disorders: an updated, comprehensive review of the literature. Clin Psychopharmacol Neurosci. 2019;17(3):343-363.
28. Vakonaki E, Tsiminikaki K, Plaitis S, et al. Common mental disorders and association with telomere length. Biomed Rep. 2018;8(2):111-116.
29. Malouff JM, Schutte NS. A meta-analysis of the relationship between anxiety and telomere length. Anxiety Stress Coping. 2017;30(3):264-272.

References

1. Walker ER, McGee RE, Druss BG. Mortality in mental disorders and global disease burden implications: a systematic review and meta-analysis. JAMA Psychiatry. 2015;72(4):334-341.
2. Laursen TM, Wahlbeck K, Hällgren J, et al. Life expectancy and death by diseases of the circulatory system in patients with bipolar disorder or schizophrenia in the Nordic countries. PLoS One. 2013;8(6):e67133. doi: 10.1371/journal.pone.0067133.
3. Kugathasan P, Stubbs B, Aagaard J, et al. Increased mortality from somatic multimorbidity in patients with schizophrenia: a Danish nationwide cohort study. Acta Psychiatr Scand. 2019. doi: 10.1111/acps.13076.
4. Laursen TM. Life expectancy among persons with schizophrenia or bipolar affective disorder. Schizophr Res. 2011;131(1-3):101-104.
5. Colton CW, Manderscheid RW. Congruencies in increased mortality rates, years of potential life lost, and causes of death among public mental health clients in eight states. Prev Chronic Dis. 2006;3(2):A42.
6. Tiihonen J, Mittendorfer-Rutz E, Torniainen M, et al. Mortality and cumulative exposure to anti­psychotics, antidepressants, and benzodiazepines in patients with schizophrenia: an observational follow-up study. Am J Psychiatry. 2016;173(6):600-606.
7. Torniainen M, Mittendorfer-Rutz E, Tanskanen A, et al. Antipsychotic treatment and mortality in schizophrenia. Schizophr Bull. 2015;41(3):656-663.
8. Tiihonen J, Lönnqvist J, Wahlbeck K, et al. 11-year follow-up of mortality in patients with schizophrenia: a population-based cohort study (FIN11 study). Lancet. 2009;374(9690):620-627.
9. Wilson R, Gaughran F, Whitburn T, et al. Place of death and other factors associated with unnatural mortality in patients with serious mental disorders: population-based retrospective cohort study. BJPsych Open. 2019;5(2):e23. doi: 10.1192/bjo.2019.5.
10. Ösby U, Westman J, Hällgren J, et al. Mortality trends in cardiovascular causes in schizophrenia, bipolar and unipolar mood disorder in Sweden 1987-2010. Eur J Public Health. 2016;26(5):867-871.
11. Laursen TM, Musliner KL, Benros ME, et al. Mortality and life expectancy in persons with severe unipolar depression. J Affect Disord. 2016;193:203-207.
12. Zubenko GS, Zubenko WN, Spiker DG, et al. Malignancy of recurrent, early-onset major depression: a family study. Am J Med Genet. 2001;105(8):690-699.
13. Dalsgaard S, Østergaard SD, Leckman JF, et al. Mortality in children, adolescents, and adults with attention deficit hyperactivity disorder: a nationwide cohort study. Lancet. 2015;385(9983):2190-2196.
14. Meier SM, Mattheisen M, Mors O, et al. Mortality among persons with obsessive-compulsive disorder in Denmark. JAMA Psychiatry. 2016;73(3):268-274.
15. Holwerda TJ, Schoevers RA, Dekker J, et al. The relationship between generalized anxiety disorder, depression and mortality in old age. Int J Geriatr Psychiatry. 2007;22(3):241-249.
16. Ivanovs R, Kivite A, Ziedonis D, et al. Association of depression and anxiety with the 10-year risk of cardiovascular mortality in a primary care population of Latvia using the SCORE system. Front Psychiatry. 2018;9:276.
17. Miloyan B, Bulley A, Bandeen-Roche K, et al. Anxiety disorders and all-cause mortality: systematic review and meta-analysis. Soc Psychiatry Psychiatr Epidemiol. 2016;51(11):1467-1475.
18. Smoller JW, Pollack MH, Wassertheil-Smoller S, et al. Panic attacks and risk of incident cardiovascular events among postmenopausal women in the Women’s Health Initiative Observational Study. Arch Gen Psychiatry. 2007;64(10):1153-1160.
19. Coryell W, Noyes R Jr, House JD. Mortality among outpatients with anxiety disorders. Am J Psychiatry. 1986;143(4):508-510.
20. Coryell W, Noyes R, Clancy J. Excess mortality in panic disorder. A comparison with primary unipolar depression. Arch Gen Psychiatry. 1982;39(6):701-703.
21. Scott JG, Giørtz Pedersen M, Erskine HE, et al. Mortality in individuals with disruptive behavior disorders diagnosed by specialist services - a nationwide cohort study. Psychiatry Res. 2017;251:255-260.
22. Burg MM, Soufer R. Post-traumatic stress disorder and cardiovascular disease. Curr Cardiol Rep. 2016;18(10):94.
23. Wolf EJ, Logue MW, Stoop TB, et al. Accelerated DNA methylation age: associations with PTSD and mortality. Psychosom Med. 2017. doi: 10.1097/PSY.0000000000000506.
24. Temes CM, Frankenburg FR, Fitzmaurice MC, et al. Deaths by suicide and other causes among patients with borderline personality disorder and personality-disordered comparison subjects over 24 years of prospective follow-up. J Clin Psychiatry. 2019;80(1). doi: 10.4088/JCP.18m12436.
25. Sadahiro R, Suzuki A, Enokido M, et al. Relationship between leukocyte telomere length and personality traits in healthy subjects. Eur Psychiatry. 2015;30(2):291-295.
26. Schoormans D, Verhoeven JE, Denollet J, et al. Leukocyte telomere length and personality: associations with the Big Five and Type D personality traits. Psychol Med. 2018;48(6):1008-1019.
27. Muneer A, Minhas FA. Telomere biology in mood disorders: an updated, comprehensive review of the literature. Clin Psychopharmacol Neurosci. 2019;17(3):343-363.
28. Vakonaki E, Tsiminikaki K, Plaitis S, et al. Common mental disorders and association with telomere length. Biomed Rep. 2018;8(2):111-116.
29. Malouff JM, Schutte NS. A meta-analysis of the relationship between anxiety and telomere length. Anxiety Stress Coping. 2017;30(3):264-272.

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Psychotherapy for psychiatric disorders: A review of 4 studies

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Psychotherapy for psychiatric disorders: A review of 4 studies

Psychotherapy is among the evidence-based treatment options for treating various psychiatric disorders. How we approach psychiatric disorders via psycho­therapy has been shaped by numerous theories of personality and psychopathology, including psychodynamic, behavioral, cognitive, systems, and existential-humanistic approaches. Whether used as primary treatment or in conjunction with medication, psychotherapy has played a pivotal role in shaping psychiatric disease management and treatment. Several evidence-based therapy modalities have been used throughout the years and continue to significantly improve and impact our patients’ lives. In the armamentarium of treatment modalities, therapy takes the leading role for several conditions. Here we review 4 studies from current psychotherapy literature; these studies are summarized in the Table.1-4

Psychotherapy for psychiatric disorders: 4 studies

1. Pompoli A, Furukawa TA, Efthimiou O, et al. Dismantling cognitive-behaviour therapy for panic disorder: a systematic review and component network meta-analysis. Psychol Med. 2018;48(12):1945-1953.

Panic disorder has a lifetime prevalence of 3.7% in the general population. Three treatment modalities recommended for patients with panic disorder are psychological therapy, pharmacologic therapy, and self-help. Among the psychological therapies, cognitive-behavioral therapy (CBT) is one of the most widely used.1

Cognitive-behavioral therapy for panic disorder has been proven to be an efficacious and impactful treatment. For panic disorder, CBT may consist of different combinations of several therapeutic components, such as relaxation, breathing retraining, cognitive restructuring, interoceptive exposure, and/or in vivo exposure. It is therefore important, both theoretically and clinically, to examine whether specific components of CBT or their combinations are superior to others for treating panic disorder.1

Pompoli et al1 conducted a component network meta-analysis (NMA) of 72 studies in order to determine which CBT components were the most efficacious in treating patients with panic disorder. Component NMA is an extension of standard NMA; it is used to disentangle the treatment effects of different components included in composite interventions.1

The aim of this study was to determine which specific component or combination of components was superior to others when treating panic disorder.1

Study design

  • Researchers reviewed 2,526 references from Medline, EMBASE, PsycINFO, and Cochrane Central and selected 72 studies that included 4,064 patients with panic disorder.1
  • The primary outcome was remission of panic disorder with or without agoraphobia in the short term (3 to 6 months). Remission was defined as achieving a score of ≤7 on the Panic Disorder Severity Scale (PDSS).1
  • Secondary outcomes included response (≥40% reduction in PDSS score from baseline) and dropout for any reason in the short term.1

Continue to: Outcomes

 

 

Outcomes

  • Using component NMA, researchers determined that interoceptive exposure and face-to-face setting (administration of therapeutic components in a face-to-face setting rather than through self-help means) led to better efficacy and acceptability. Muscle relaxation and virtual reality exposure corresponded to lower efficacy. Breathing retraining and in vivo exposure improved treatment acceptability, but had small effects on efficacy.1
  • Based on an analysis of remission rates, the most efficacious CBT incorporated cognitive restructuring and interoceptive exposure. The least efficacious CBT incorporated breathing retraining, muscle relaxation, in vivo exposure, and virtual reality exposure.1
  • Application of cognitive and behavioral therapeutic elements was superior to administration of behavioral elements alone. When administering CBT, face-to-face therapy led to better outcomes in response and remission rates. Dropout rates occurred at a lower frequency when CBT was administered face-to-face when compared with self-help groups. The placebo effect was associated with the highest dropout rate.1

Conclusion

  • Findings from this meta-analysis have high practical utility. Which CBT components are used can significantly alter CBT’s efficacy and acceptability in patients with panic disorder.1
  • The “most efficacious CBT” would include cognitive restructuring and interoceptive exposure delivered in a face-to-face setting. Breathing retraining, muscle relaxation, and virtual reality may have a minimal or even negative impact.1
  • Limitations of this meta-analysis include the high number of studies used for the data analysis, complex statistical analysis, inability to include unpublished studies, and limited relevant studies. A future implication of this study is the consideration of formal methodology based on the clinical application of efficacious CBT components when treating patients with panic disorder.1

2. Sloan DM, Marx BP, Lee DJ, et al. A brief exposure-based treatment vs cognitive processing therapy for posttraumatic stress disorder: a randomized noninferiority clinical trial. JAMA Psychiatry. 2018;75(3):233-239.

Psychotherapy is also a useful modality for treating posttraumatic stress disorder (PTSD). Sloan et al2 compared brief exposure-based treatment with cognitive processing therapy (CPT) for PTSD. 

Clinical practice guidelines for the management of PTSD and acute stress disorder recommend the use of individual, trauma-focused therapies that focus on exposure and cognitive restructuring, such as prolonged exposure, CPT, and written narrative exposure.5

Continue to: One type of written narrative...

 

 

One type of written narrative exposure treatment is written exposure therapy (WET), which consists of 5 sessions during which patients write about their trauma. The first session is comprised of psychoeducation about PTSD and a review of treatment reasoning, followed by 30 minutes of writing. The therapist provides feedback and instructions. Written exposure therapy requires less therapist training and less supervision than prolonged exposure or CPT. Prior studies have suggested that WET can significantly reduce PTSD symptoms in various trauma survivors.2

Although efficacious for PTSD, WET had not been compared with CPT, which is the most commonly used first-line treatment of PTSD. The aim of this study was to determine whether WET is noninferior to CPT.2

Study design

  • In this randomized noninferiority clinical trial conducted in Boston, Massachusetts from February 28, 2013 to November 6, 2016, 126 veterans and non-veteran adults were randomized to WET or CPT. Participants met DSM-5 criteria for PTSD and were taking stable doses of their medications for at least 4 weeks.2 
  • Participants assigned to CPT (n = 63) underwent 12 sessions, and participants assigned to WET (n = 63) received 5 sessions. Cognitive processing therapy was conducted over 60-minute weekly sessions. Written exposure therapy consisted of an initial session that was 60 minutes long and four 40-minute follow-up sessions.2
  • Interviews were conducted by 4 independent evaluators at baseline and 6, 12, 24, and 36 weeks. During the WET sessions, participants wrote about a traumatic event while focusing on details, thoughts, and feelings associated with the event.2
  • Cognitive processing therapy involved 12 trauma-focused therapy sessions during which participants learn how to become aware of and address problematic cognitions about the trauma as well as thoughts about themselves and others. Between sessions, participants were required to write 2 trauma accounts and complete other assignments.2

Outcomes

  • The primary outcome was change in total score on the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5). The CAPS-5 scores for participants in the WET group were noninferior to those for participants in the CPT group at all assessment points.2
  • Participants did not significantly differ in age, education, income, or PTSD severity. Participants in the 2 groups did not differ in treatment expectations or level of satisfaction with treatment. Individuals assigned to CPT were more likely to drop out of the study: 20 participants in the CPT group dropped out in the first 5 sessions, whereas only 4 dropped out of the WET group. The dropout rate in the CPT group was 39.7%. Improvements in PTSD symptoms in the WET group were noninferior to improvements in the CPT group.2
  • Written exposure therapy showed no difference compared with CPT in decreasing PTSD symptoms. Furthermore, this study demonstrated that PTSD symptoms can decrease with a smaller number of shorter therapeutic sessions.2

Conclusion

  • This study demonstrated noninferiority between an established, commonly used PTSD therapy (CPT) and a version of exposure therapy that is briefer, simpler, and requires less homework and less therapist training and expertise. This “lower-dose” approach may improve access for the expanding number of patients who require treatment for PTSD, especially in the Veterans Affairs system.2
  • In summary, WET is well tolerated and time-efficient. Although it requires fewer sessions, WET was noninferior to CPT.2

Continue to: Multisystemic therapy versus management as usual...

 

 

3. Fonagy P, Butler S, Cottrell D, et al. Multisystemic therapy versus management as usual in the treatment of adolescent antisocial behaviour (START): a pragmatic, randomised controlled, superiority trial. Lancet Psychiatry. 2018;5(2):119-133.

Multisystemic therapy (MST) is an intensive, family-based, home-based intervention for young people with serious antisocial behavior. It has been found effective for childhood conduct disorders in the United States. However, previous studies that supported its efficacy were conducted by the therapy’s developers and used noncomprehensive comparators, such as individual therapy. Fonagy et al3 assessed the effectiveness and cost-effectiveness of MST vs management as usual for treating adolescent antisocial behavior. This is the first study that was performed by independent investigators and used a comprehensive control.3

Study design

  • This 18-month, multisite, pragmatic, randomized controlled superiority trial was conducted in England.3
  • Participants were age 11 to 17, with moderate to severe antisocial behavior. They had at least 3 severity criteria indicating difficulties across several settings and at least one of the 5 inclusion criteria for antisocial behavior. Six hundred eighty-four families were randomly assigned to MST or management as usual, and 491 families completed the study.3
  • For the MST intervention, therapists worked with the adolescent’s caregiver 3 times a week for 3 to 5 months to improve parenting skills, enhance family relationships, increase support from social networks, develop skills and resources, address communication problems, increase school attendance and achievement, and reduce the adolescent’s association with delinquent peers.3
  • For the management as usual intervention, management was based on local services for young people and was designed to be in line with current community practice.3

Outcomes

  • The primary outcome was the proportion of participants in out-of-home placements at 18 months. The secondary outcomes were time to first criminal offense and the total number of offenses.3
  • In terms of the risk of out-of-home placement, MST had no effect: 13% of participants in the MST group had out-of-home placement at 18 months, compared with 11% in the management-as-usual group.3
  • Multisystemic therapy also did not significantly delay the time to first offense (hazard ratio, 1.06; 95% confidence interval, 0.84 to 1.33). Also, at 18-month follow-up, participants in the MST group had committed more offenses than those in the management-as-usual group, although the difference was not statistically significant.3
  • Parents in the MST group reported increased parental support and involvement and reduced problems at 6 months, but the adolescents’ reports of parenting behavior indicated no significant effect for MST vs management as usual at any time point.3

Conclusion

  • Multisystemic therapy was not superior to management as usual in reducing out-of-home placements. Although the parents believed that MST brought about a rapid and effective change, this was not reflected in objective indicators of antisocial behavior. These results are contrary to previous studies in the United States. The substantial improvements observed in both groups reflected the effectiveness of routinely offered interventions for this group of young people, at least when observed in clinical trials.3

Continue to: Mindfulness-based cognitive therapy...

 

 

4. Janssen L, Kan CC, Carpentier PJ, et al. Mindfulness-based cognitive therapy v. treatment as usual in adults with ADHD: a multicentre, single-blind, randomised controlled trial. Psychol Med. 2019;49(1):55-65.

There is empirical support for using psychotherapy to treat attention-deficit/hyperactivity disorder (ADHD). Although medication management plays a leading role in treating ADHD, Janssen et al4 conducted a multicenter, single-blind trial comparing mindfulness-based cognitive therapy (MBCT) vs treatment as usual (TAU) for ADHD.

The aim of this study was to determine the efficacy of MBCT plus TAU vs TAU only in decreasing symptoms of adults with ADHD.4

Study design

  • This multicenter, single-blind randomized controlled trial was conducted in the Netherlands. Participants (N = 120) met criteria for ADHD and were age ≥18. Patients were randomly assigned to MBCT plus TAU (n = 60) or TAU only (n = 60). Patients in the MBCT plus TAU group received weekly group therapy sessions, meditation exercises, psychoeducation, and group discussions. Patients in the TAU-only group received pharmacotherapy and psychoeducation.4 
  • Blinded clinicians used the Connors’ Adult ADHD Rating Scale to assess ADHD symptoms.4
  • Secondary outcomes were determined by self-reported questionnaires that patients completed online.4
  • All statistical analyses were performed on an intention-to-treat sample as well as the per protocol sample.4

Outcomes

  • The primary outcome was ADHD symptoms rated by clinicians. Secondary outcomes included self-reported ADHD symptoms, executive functioning, mindfulness skills, positive mental health, and general functioning. Outcomes were examined at baseline and then at post treatment and 3- and 6-month follow-up.4
  • Patients in the MBCT plus TAU group had a significant decrease in clinician-rated ADHD symptoms that was maintained at 6-month follow-up. More patients in the MBCT plus TAU group (27%) vs patients in the TAU group (4%) showed a ≥30% reduction in ADHD symptoms. Compared with patients in the TAU group, patients in the MBCT plus TAU group had significant improvements in ADHD symptoms, mindfulness skills, and positive mental health at post treatment and at 6-month follow-up. Compared with those receiving TAU only, patients treated with MBCT plus TAU reported no improvement in executive functioning at post treatment, but did improve at 6-month follow-up.4

Continue to: Conclusion

 

 

Conclusion

  • Compared with TAU only, MBCT plus TAU is more effective in reducing ADHD symptoms, with a lasting effect at 6-month follow-up. In terms of secondary outcomes, MBCT plus TAU proved to be effective in improving mindfulness, self-compassion, positive mental health, and executive functioning. The results of this trial demonstrate that psychosocial treatments can be effective in addition to TAU in patients with ADHD, and MBCT holds promise for adult ADHD.4

References

1. Pompoli A, Furukawa TA, Efthimiou O, et al. Dismantling cognitive-behaviour therapy for panic disorder: a systematic review and component network meta-analysis. Psychol Med. 2018;48(12):1945-1953.
2. Sloan DM, Marx BP, Lee DJ, et al. A brief exposure-based treatment vs cognitive processing therapy for posttraumatic stress disorder: a randomized noninferiority clinical trial. JAMA Psychiatry. 2018;75(3):233-239.
3. Fonagy P, Butler S, Cottrell D, et al. Multisystemic therapy versus management as usual in the treatment of adolescent antisocial behaviour (START): a pragmatic, randomised controlled, superiority trial. Lancet Psychiatry. 2018;5(2):119-133.
4. Janssen L, Kan CC, Carpentier PJ, et al. Mindfulness-based cognitive therapy v. treatment as usual in adults with ADHD: a multicentre, single-blind, randomised controlled trial. Psychol Med. 2019;49(1):55-65.
5. US Department of Veterans Affairs and Department of Defense. VA/DoD clinical practice guideline for the management of posttraumatic stress disorder and acute stress disorder . https://www.healthquality.va.gov/guidelines/MH/ptsd/VADoDPTSDCPGFinal082917.pdf. Published June 2017. Accessed September 8, 2019.

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Disclosures
The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Dr. Saeed is Professor and Chair, Department of Psychiatry and Behavioral Medicine, East Carolina University Brody School of Medicine, Greenville, North Carolina. Dr. Muthukanagaraj is Assistant Professor, Department of Internal Medicine and Psychiatry, East Carolina University Brody School of Medicine, Greenville, North Carolina. Dr. Pastis is Clinical Assistant Professor, Department of Psychiatry, East Carolina University Brody School of Medicine, Greenville, North Carolina.

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The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Dr. Saeed is Professor and Chair, Department of Psychiatry and Behavioral Medicine, East Carolina University Brody School of Medicine, Greenville, North Carolina. Dr. Muthukanagaraj is Assistant Professor, Department of Internal Medicine and Psychiatry, East Carolina University Brody School of Medicine, Greenville, North Carolina. Dr. Pastis is Clinical Assistant Professor, Department of Psychiatry, East Carolina University Brody School of Medicine, Greenville, North Carolina.

Disclosures
The authors report no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

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Psychotherapy is among the evidence-based treatment options for treating various psychiatric disorders. How we approach psychiatric disorders via psycho­therapy has been shaped by numerous theories of personality and psychopathology, including psychodynamic, behavioral, cognitive, systems, and existential-humanistic approaches. Whether used as primary treatment or in conjunction with medication, psychotherapy has played a pivotal role in shaping psychiatric disease management and treatment. Several evidence-based therapy modalities have been used throughout the years and continue to significantly improve and impact our patients’ lives. In the armamentarium of treatment modalities, therapy takes the leading role for several conditions. Here we review 4 studies from current psychotherapy literature; these studies are summarized in the Table.1-4

Psychotherapy for psychiatric disorders: 4 studies

1. Pompoli A, Furukawa TA, Efthimiou O, et al. Dismantling cognitive-behaviour therapy for panic disorder: a systematic review and component network meta-analysis. Psychol Med. 2018;48(12):1945-1953.

Panic disorder has a lifetime prevalence of 3.7% in the general population. Three treatment modalities recommended for patients with panic disorder are psychological therapy, pharmacologic therapy, and self-help. Among the psychological therapies, cognitive-behavioral therapy (CBT) is one of the most widely used.1

Cognitive-behavioral therapy for panic disorder has been proven to be an efficacious and impactful treatment. For panic disorder, CBT may consist of different combinations of several therapeutic components, such as relaxation, breathing retraining, cognitive restructuring, interoceptive exposure, and/or in vivo exposure. It is therefore important, both theoretically and clinically, to examine whether specific components of CBT or their combinations are superior to others for treating panic disorder.1

Pompoli et al1 conducted a component network meta-analysis (NMA) of 72 studies in order to determine which CBT components were the most efficacious in treating patients with panic disorder. Component NMA is an extension of standard NMA; it is used to disentangle the treatment effects of different components included in composite interventions.1

The aim of this study was to determine which specific component or combination of components was superior to others when treating panic disorder.1

Study design

  • Researchers reviewed 2,526 references from Medline, EMBASE, PsycINFO, and Cochrane Central and selected 72 studies that included 4,064 patients with panic disorder.1
  • The primary outcome was remission of panic disorder with or without agoraphobia in the short term (3 to 6 months). Remission was defined as achieving a score of ≤7 on the Panic Disorder Severity Scale (PDSS).1
  • Secondary outcomes included response (≥40% reduction in PDSS score from baseline) and dropout for any reason in the short term.1

Continue to: Outcomes

 

 

Outcomes

  • Using component NMA, researchers determined that interoceptive exposure and face-to-face setting (administration of therapeutic components in a face-to-face setting rather than through self-help means) led to better efficacy and acceptability. Muscle relaxation and virtual reality exposure corresponded to lower efficacy. Breathing retraining and in vivo exposure improved treatment acceptability, but had small effects on efficacy.1
  • Based on an analysis of remission rates, the most efficacious CBT incorporated cognitive restructuring and interoceptive exposure. The least efficacious CBT incorporated breathing retraining, muscle relaxation, in vivo exposure, and virtual reality exposure.1
  • Application of cognitive and behavioral therapeutic elements was superior to administration of behavioral elements alone. When administering CBT, face-to-face therapy led to better outcomes in response and remission rates. Dropout rates occurred at a lower frequency when CBT was administered face-to-face when compared with self-help groups. The placebo effect was associated with the highest dropout rate.1

Conclusion

  • Findings from this meta-analysis have high practical utility. Which CBT components are used can significantly alter CBT’s efficacy and acceptability in patients with panic disorder.1
  • The “most efficacious CBT” would include cognitive restructuring and interoceptive exposure delivered in a face-to-face setting. Breathing retraining, muscle relaxation, and virtual reality may have a minimal or even negative impact.1
  • Limitations of this meta-analysis include the high number of studies used for the data analysis, complex statistical analysis, inability to include unpublished studies, and limited relevant studies. A future implication of this study is the consideration of formal methodology based on the clinical application of efficacious CBT components when treating patients with panic disorder.1

2. Sloan DM, Marx BP, Lee DJ, et al. A brief exposure-based treatment vs cognitive processing therapy for posttraumatic stress disorder: a randomized noninferiority clinical trial. JAMA Psychiatry. 2018;75(3):233-239.

Psychotherapy is also a useful modality for treating posttraumatic stress disorder (PTSD). Sloan et al2 compared brief exposure-based treatment with cognitive processing therapy (CPT) for PTSD. 

Clinical practice guidelines for the management of PTSD and acute stress disorder recommend the use of individual, trauma-focused therapies that focus on exposure and cognitive restructuring, such as prolonged exposure, CPT, and written narrative exposure.5

Continue to: One type of written narrative...

 

 

One type of written narrative exposure treatment is written exposure therapy (WET), which consists of 5 sessions during which patients write about their trauma. The first session is comprised of psychoeducation about PTSD and a review of treatment reasoning, followed by 30 minutes of writing. The therapist provides feedback and instructions. Written exposure therapy requires less therapist training and less supervision than prolonged exposure or CPT. Prior studies have suggested that WET can significantly reduce PTSD symptoms in various trauma survivors.2

Although efficacious for PTSD, WET had not been compared with CPT, which is the most commonly used first-line treatment of PTSD. The aim of this study was to determine whether WET is noninferior to CPT.2

Study design

  • In this randomized noninferiority clinical trial conducted in Boston, Massachusetts from February 28, 2013 to November 6, 2016, 126 veterans and non-veteran adults were randomized to WET or CPT. Participants met DSM-5 criteria for PTSD and were taking stable doses of their medications for at least 4 weeks.2 
  • Participants assigned to CPT (n = 63) underwent 12 sessions, and participants assigned to WET (n = 63) received 5 sessions. Cognitive processing therapy was conducted over 60-minute weekly sessions. Written exposure therapy consisted of an initial session that was 60 minutes long and four 40-minute follow-up sessions.2
  • Interviews were conducted by 4 independent evaluators at baseline and 6, 12, 24, and 36 weeks. During the WET sessions, participants wrote about a traumatic event while focusing on details, thoughts, and feelings associated with the event.2
  • Cognitive processing therapy involved 12 trauma-focused therapy sessions during which participants learn how to become aware of and address problematic cognitions about the trauma as well as thoughts about themselves and others. Between sessions, participants were required to write 2 trauma accounts and complete other assignments.2

Outcomes

  • The primary outcome was change in total score on the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5). The CAPS-5 scores for participants in the WET group were noninferior to those for participants in the CPT group at all assessment points.2
  • Participants did not significantly differ in age, education, income, or PTSD severity. Participants in the 2 groups did not differ in treatment expectations or level of satisfaction with treatment. Individuals assigned to CPT were more likely to drop out of the study: 20 participants in the CPT group dropped out in the first 5 sessions, whereas only 4 dropped out of the WET group. The dropout rate in the CPT group was 39.7%. Improvements in PTSD symptoms in the WET group were noninferior to improvements in the CPT group.2
  • Written exposure therapy showed no difference compared with CPT in decreasing PTSD symptoms. Furthermore, this study demonstrated that PTSD symptoms can decrease with a smaller number of shorter therapeutic sessions.2

Conclusion

  • This study demonstrated noninferiority between an established, commonly used PTSD therapy (CPT) and a version of exposure therapy that is briefer, simpler, and requires less homework and less therapist training and expertise. This “lower-dose” approach may improve access for the expanding number of patients who require treatment for PTSD, especially in the Veterans Affairs system.2
  • In summary, WET is well tolerated and time-efficient. Although it requires fewer sessions, WET was noninferior to CPT.2

Continue to: Multisystemic therapy versus management as usual...

 

 

3. Fonagy P, Butler S, Cottrell D, et al. Multisystemic therapy versus management as usual in the treatment of adolescent antisocial behaviour (START): a pragmatic, randomised controlled, superiority trial. Lancet Psychiatry. 2018;5(2):119-133.

Multisystemic therapy (MST) is an intensive, family-based, home-based intervention for young people with serious antisocial behavior. It has been found effective for childhood conduct disorders in the United States. However, previous studies that supported its efficacy were conducted by the therapy’s developers and used noncomprehensive comparators, such as individual therapy. Fonagy et al3 assessed the effectiveness and cost-effectiveness of MST vs management as usual for treating adolescent antisocial behavior. This is the first study that was performed by independent investigators and used a comprehensive control.3

Study design

  • This 18-month, multisite, pragmatic, randomized controlled superiority trial was conducted in England.3
  • Participants were age 11 to 17, with moderate to severe antisocial behavior. They had at least 3 severity criteria indicating difficulties across several settings and at least one of the 5 inclusion criteria for antisocial behavior. Six hundred eighty-four families were randomly assigned to MST or management as usual, and 491 families completed the study.3
  • For the MST intervention, therapists worked with the adolescent’s caregiver 3 times a week for 3 to 5 months to improve parenting skills, enhance family relationships, increase support from social networks, develop skills and resources, address communication problems, increase school attendance and achievement, and reduce the adolescent’s association with delinquent peers.3
  • For the management as usual intervention, management was based on local services for young people and was designed to be in line with current community practice.3

Outcomes

  • The primary outcome was the proportion of participants in out-of-home placements at 18 months. The secondary outcomes were time to first criminal offense and the total number of offenses.3
  • In terms of the risk of out-of-home placement, MST had no effect: 13% of participants in the MST group had out-of-home placement at 18 months, compared with 11% in the management-as-usual group.3
  • Multisystemic therapy also did not significantly delay the time to first offense (hazard ratio, 1.06; 95% confidence interval, 0.84 to 1.33). Also, at 18-month follow-up, participants in the MST group had committed more offenses than those in the management-as-usual group, although the difference was not statistically significant.3
  • Parents in the MST group reported increased parental support and involvement and reduced problems at 6 months, but the adolescents’ reports of parenting behavior indicated no significant effect for MST vs management as usual at any time point.3

Conclusion

  • Multisystemic therapy was not superior to management as usual in reducing out-of-home placements. Although the parents believed that MST brought about a rapid and effective change, this was not reflected in objective indicators of antisocial behavior. These results are contrary to previous studies in the United States. The substantial improvements observed in both groups reflected the effectiveness of routinely offered interventions for this group of young people, at least when observed in clinical trials.3

Continue to: Mindfulness-based cognitive therapy...

 

 

4. Janssen L, Kan CC, Carpentier PJ, et al. Mindfulness-based cognitive therapy v. treatment as usual in adults with ADHD: a multicentre, single-blind, randomised controlled trial. Psychol Med. 2019;49(1):55-65.

There is empirical support for using psychotherapy to treat attention-deficit/hyperactivity disorder (ADHD). Although medication management plays a leading role in treating ADHD, Janssen et al4 conducted a multicenter, single-blind trial comparing mindfulness-based cognitive therapy (MBCT) vs treatment as usual (TAU) for ADHD.

The aim of this study was to determine the efficacy of MBCT plus TAU vs TAU only in decreasing symptoms of adults with ADHD.4

Study design

  • This multicenter, single-blind randomized controlled trial was conducted in the Netherlands. Participants (N = 120) met criteria for ADHD and were age ≥18. Patients were randomly assigned to MBCT plus TAU (n = 60) or TAU only (n = 60). Patients in the MBCT plus TAU group received weekly group therapy sessions, meditation exercises, psychoeducation, and group discussions. Patients in the TAU-only group received pharmacotherapy and psychoeducation.4 
  • Blinded clinicians used the Connors’ Adult ADHD Rating Scale to assess ADHD symptoms.4
  • Secondary outcomes were determined by self-reported questionnaires that patients completed online.4
  • All statistical analyses were performed on an intention-to-treat sample as well as the per protocol sample.4

Outcomes

  • The primary outcome was ADHD symptoms rated by clinicians. Secondary outcomes included self-reported ADHD symptoms, executive functioning, mindfulness skills, positive mental health, and general functioning. Outcomes were examined at baseline and then at post treatment and 3- and 6-month follow-up.4
  • Patients in the MBCT plus TAU group had a significant decrease in clinician-rated ADHD symptoms that was maintained at 6-month follow-up. More patients in the MBCT plus TAU group (27%) vs patients in the TAU group (4%) showed a ≥30% reduction in ADHD symptoms. Compared with patients in the TAU group, patients in the MBCT plus TAU group had significant improvements in ADHD symptoms, mindfulness skills, and positive mental health at post treatment and at 6-month follow-up. Compared with those receiving TAU only, patients treated with MBCT plus TAU reported no improvement in executive functioning at post treatment, but did improve at 6-month follow-up.4

Continue to: Conclusion

 

 

Conclusion

  • Compared with TAU only, MBCT plus TAU is more effective in reducing ADHD symptoms, with a lasting effect at 6-month follow-up. In terms of secondary outcomes, MBCT plus TAU proved to be effective in improving mindfulness, self-compassion, positive mental health, and executive functioning. The results of this trial demonstrate that psychosocial treatments can be effective in addition to TAU in patients with ADHD, and MBCT holds promise for adult ADHD.4

Psychotherapy is among the evidence-based treatment options for treating various psychiatric disorders. How we approach psychiatric disorders via psycho­therapy has been shaped by numerous theories of personality and psychopathology, including psychodynamic, behavioral, cognitive, systems, and existential-humanistic approaches. Whether used as primary treatment or in conjunction with medication, psychotherapy has played a pivotal role in shaping psychiatric disease management and treatment. Several evidence-based therapy modalities have been used throughout the years and continue to significantly improve and impact our patients’ lives. In the armamentarium of treatment modalities, therapy takes the leading role for several conditions. Here we review 4 studies from current psychotherapy literature; these studies are summarized in the Table.1-4

Psychotherapy for psychiatric disorders: 4 studies

1. Pompoli A, Furukawa TA, Efthimiou O, et al. Dismantling cognitive-behaviour therapy for panic disorder: a systematic review and component network meta-analysis. Psychol Med. 2018;48(12):1945-1953.

Panic disorder has a lifetime prevalence of 3.7% in the general population. Three treatment modalities recommended for patients with panic disorder are psychological therapy, pharmacologic therapy, and self-help. Among the psychological therapies, cognitive-behavioral therapy (CBT) is one of the most widely used.1

Cognitive-behavioral therapy for panic disorder has been proven to be an efficacious and impactful treatment. For panic disorder, CBT may consist of different combinations of several therapeutic components, such as relaxation, breathing retraining, cognitive restructuring, interoceptive exposure, and/or in vivo exposure. It is therefore important, both theoretically and clinically, to examine whether specific components of CBT or their combinations are superior to others for treating panic disorder.1

Pompoli et al1 conducted a component network meta-analysis (NMA) of 72 studies in order to determine which CBT components were the most efficacious in treating patients with panic disorder. Component NMA is an extension of standard NMA; it is used to disentangle the treatment effects of different components included in composite interventions.1

The aim of this study was to determine which specific component or combination of components was superior to others when treating panic disorder.1

Study design

  • Researchers reviewed 2,526 references from Medline, EMBASE, PsycINFO, and Cochrane Central and selected 72 studies that included 4,064 patients with panic disorder.1
  • The primary outcome was remission of panic disorder with or without agoraphobia in the short term (3 to 6 months). Remission was defined as achieving a score of ≤7 on the Panic Disorder Severity Scale (PDSS).1
  • Secondary outcomes included response (≥40% reduction in PDSS score from baseline) and dropout for any reason in the short term.1

Continue to: Outcomes

 

 

Outcomes

  • Using component NMA, researchers determined that interoceptive exposure and face-to-face setting (administration of therapeutic components in a face-to-face setting rather than through self-help means) led to better efficacy and acceptability. Muscle relaxation and virtual reality exposure corresponded to lower efficacy. Breathing retraining and in vivo exposure improved treatment acceptability, but had small effects on efficacy.1
  • Based on an analysis of remission rates, the most efficacious CBT incorporated cognitive restructuring and interoceptive exposure. The least efficacious CBT incorporated breathing retraining, muscle relaxation, in vivo exposure, and virtual reality exposure.1
  • Application of cognitive and behavioral therapeutic elements was superior to administration of behavioral elements alone. When administering CBT, face-to-face therapy led to better outcomes in response and remission rates. Dropout rates occurred at a lower frequency when CBT was administered face-to-face when compared with self-help groups. The placebo effect was associated with the highest dropout rate.1

Conclusion

  • Findings from this meta-analysis have high practical utility. Which CBT components are used can significantly alter CBT’s efficacy and acceptability in patients with panic disorder.1
  • The “most efficacious CBT” would include cognitive restructuring and interoceptive exposure delivered in a face-to-face setting. Breathing retraining, muscle relaxation, and virtual reality may have a minimal or even negative impact.1
  • Limitations of this meta-analysis include the high number of studies used for the data analysis, complex statistical analysis, inability to include unpublished studies, and limited relevant studies. A future implication of this study is the consideration of formal methodology based on the clinical application of efficacious CBT components when treating patients with panic disorder.1

2. Sloan DM, Marx BP, Lee DJ, et al. A brief exposure-based treatment vs cognitive processing therapy for posttraumatic stress disorder: a randomized noninferiority clinical trial. JAMA Psychiatry. 2018;75(3):233-239.

Psychotherapy is also a useful modality for treating posttraumatic stress disorder (PTSD). Sloan et al2 compared brief exposure-based treatment with cognitive processing therapy (CPT) for PTSD. 

Clinical practice guidelines for the management of PTSD and acute stress disorder recommend the use of individual, trauma-focused therapies that focus on exposure and cognitive restructuring, such as prolonged exposure, CPT, and written narrative exposure.5

Continue to: One type of written narrative...

 

 

One type of written narrative exposure treatment is written exposure therapy (WET), which consists of 5 sessions during which patients write about their trauma. The first session is comprised of psychoeducation about PTSD and a review of treatment reasoning, followed by 30 minutes of writing. The therapist provides feedback and instructions. Written exposure therapy requires less therapist training and less supervision than prolonged exposure or CPT. Prior studies have suggested that WET can significantly reduce PTSD symptoms in various trauma survivors.2

Although efficacious for PTSD, WET had not been compared with CPT, which is the most commonly used first-line treatment of PTSD. The aim of this study was to determine whether WET is noninferior to CPT.2

Study design

  • In this randomized noninferiority clinical trial conducted in Boston, Massachusetts from February 28, 2013 to November 6, 2016, 126 veterans and non-veteran adults were randomized to WET or CPT. Participants met DSM-5 criteria for PTSD and were taking stable doses of their medications for at least 4 weeks.2 
  • Participants assigned to CPT (n = 63) underwent 12 sessions, and participants assigned to WET (n = 63) received 5 sessions. Cognitive processing therapy was conducted over 60-minute weekly sessions. Written exposure therapy consisted of an initial session that was 60 minutes long and four 40-minute follow-up sessions.2
  • Interviews were conducted by 4 independent evaluators at baseline and 6, 12, 24, and 36 weeks. During the WET sessions, participants wrote about a traumatic event while focusing on details, thoughts, and feelings associated with the event.2
  • Cognitive processing therapy involved 12 trauma-focused therapy sessions during which participants learn how to become aware of and address problematic cognitions about the trauma as well as thoughts about themselves and others. Between sessions, participants were required to write 2 trauma accounts and complete other assignments.2

Outcomes

  • The primary outcome was change in total score on the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5). The CAPS-5 scores for participants in the WET group were noninferior to those for participants in the CPT group at all assessment points.2
  • Participants did not significantly differ in age, education, income, or PTSD severity. Participants in the 2 groups did not differ in treatment expectations or level of satisfaction with treatment. Individuals assigned to CPT were more likely to drop out of the study: 20 participants in the CPT group dropped out in the first 5 sessions, whereas only 4 dropped out of the WET group. The dropout rate in the CPT group was 39.7%. Improvements in PTSD symptoms in the WET group were noninferior to improvements in the CPT group.2
  • Written exposure therapy showed no difference compared with CPT in decreasing PTSD symptoms. Furthermore, this study demonstrated that PTSD symptoms can decrease with a smaller number of shorter therapeutic sessions.2

Conclusion

  • This study demonstrated noninferiority between an established, commonly used PTSD therapy (CPT) and a version of exposure therapy that is briefer, simpler, and requires less homework and less therapist training and expertise. This “lower-dose” approach may improve access for the expanding number of patients who require treatment for PTSD, especially in the Veterans Affairs system.2
  • In summary, WET is well tolerated and time-efficient. Although it requires fewer sessions, WET was noninferior to CPT.2

Continue to: Multisystemic therapy versus management as usual...

 

 

3. Fonagy P, Butler S, Cottrell D, et al. Multisystemic therapy versus management as usual in the treatment of adolescent antisocial behaviour (START): a pragmatic, randomised controlled, superiority trial. Lancet Psychiatry. 2018;5(2):119-133.

Multisystemic therapy (MST) is an intensive, family-based, home-based intervention for young people with serious antisocial behavior. It has been found effective for childhood conduct disorders in the United States. However, previous studies that supported its efficacy were conducted by the therapy’s developers and used noncomprehensive comparators, such as individual therapy. Fonagy et al3 assessed the effectiveness and cost-effectiveness of MST vs management as usual for treating adolescent antisocial behavior. This is the first study that was performed by independent investigators and used a comprehensive control.3

Study design

  • This 18-month, multisite, pragmatic, randomized controlled superiority trial was conducted in England.3
  • Participants were age 11 to 17, with moderate to severe antisocial behavior. They had at least 3 severity criteria indicating difficulties across several settings and at least one of the 5 inclusion criteria for antisocial behavior. Six hundred eighty-four families were randomly assigned to MST or management as usual, and 491 families completed the study.3
  • For the MST intervention, therapists worked with the adolescent’s caregiver 3 times a week for 3 to 5 months to improve parenting skills, enhance family relationships, increase support from social networks, develop skills and resources, address communication problems, increase school attendance and achievement, and reduce the adolescent’s association with delinquent peers.3
  • For the management as usual intervention, management was based on local services for young people and was designed to be in line with current community practice.3

Outcomes

  • The primary outcome was the proportion of participants in out-of-home placements at 18 months. The secondary outcomes were time to first criminal offense and the total number of offenses.3
  • In terms of the risk of out-of-home placement, MST had no effect: 13% of participants in the MST group had out-of-home placement at 18 months, compared with 11% in the management-as-usual group.3
  • Multisystemic therapy also did not significantly delay the time to first offense (hazard ratio, 1.06; 95% confidence interval, 0.84 to 1.33). Also, at 18-month follow-up, participants in the MST group had committed more offenses than those in the management-as-usual group, although the difference was not statistically significant.3
  • Parents in the MST group reported increased parental support and involvement and reduced problems at 6 months, but the adolescents’ reports of parenting behavior indicated no significant effect for MST vs management as usual at any time point.3

Conclusion

  • Multisystemic therapy was not superior to management as usual in reducing out-of-home placements. Although the parents believed that MST brought about a rapid and effective change, this was not reflected in objective indicators of antisocial behavior. These results are contrary to previous studies in the United States. The substantial improvements observed in both groups reflected the effectiveness of routinely offered interventions for this group of young people, at least when observed in clinical trials.3

Continue to: Mindfulness-based cognitive therapy...

 

 

4. Janssen L, Kan CC, Carpentier PJ, et al. Mindfulness-based cognitive therapy v. treatment as usual in adults with ADHD: a multicentre, single-blind, randomised controlled trial. Psychol Med. 2019;49(1):55-65.

There is empirical support for using psychotherapy to treat attention-deficit/hyperactivity disorder (ADHD). Although medication management plays a leading role in treating ADHD, Janssen et al4 conducted a multicenter, single-blind trial comparing mindfulness-based cognitive therapy (MBCT) vs treatment as usual (TAU) for ADHD.

The aim of this study was to determine the efficacy of MBCT plus TAU vs TAU only in decreasing symptoms of adults with ADHD.4

Study design

  • This multicenter, single-blind randomized controlled trial was conducted in the Netherlands. Participants (N = 120) met criteria for ADHD and were age ≥18. Patients were randomly assigned to MBCT plus TAU (n = 60) or TAU only (n = 60). Patients in the MBCT plus TAU group received weekly group therapy sessions, meditation exercises, psychoeducation, and group discussions. Patients in the TAU-only group received pharmacotherapy and psychoeducation.4 
  • Blinded clinicians used the Connors’ Adult ADHD Rating Scale to assess ADHD symptoms.4
  • Secondary outcomes were determined by self-reported questionnaires that patients completed online.4
  • All statistical analyses were performed on an intention-to-treat sample as well as the per protocol sample.4

Outcomes

  • The primary outcome was ADHD symptoms rated by clinicians. Secondary outcomes included self-reported ADHD symptoms, executive functioning, mindfulness skills, positive mental health, and general functioning. Outcomes were examined at baseline and then at post treatment and 3- and 6-month follow-up.4
  • Patients in the MBCT plus TAU group had a significant decrease in clinician-rated ADHD symptoms that was maintained at 6-month follow-up. More patients in the MBCT plus TAU group (27%) vs patients in the TAU group (4%) showed a ≥30% reduction in ADHD symptoms. Compared with patients in the TAU group, patients in the MBCT plus TAU group had significant improvements in ADHD symptoms, mindfulness skills, and positive mental health at post treatment and at 6-month follow-up. Compared with those receiving TAU only, patients treated with MBCT plus TAU reported no improvement in executive functioning at post treatment, but did improve at 6-month follow-up.4

Continue to: Conclusion

 

 

Conclusion

  • Compared with TAU only, MBCT plus TAU is more effective in reducing ADHD symptoms, with a lasting effect at 6-month follow-up. In terms of secondary outcomes, MBCT plus TAU proved to be effective in improving mindfulness, self-compassion, positive mental health, and executive functioning. The results of this trial demonstrate that psychosocial treatments can be effective in addition to TAU in patients with ADHD, and MBCT holds promise for adult ADHD.4

References

1. Pompoli A, Furukawa TA, Efthimiou O, et al. Dismantling cognitive-behaviour therapy for panic disorder: a systematic review and component network meta-analysis. Psychol Med. 2018;48(12):1945-1953.
2. Sloan DM, Marx BP, Lee DJ, et al. A brief exposure-based treatment vs cognitive processing therapy for posttraumatic stress disorder: a randomized noninferiority clinical trial. JAMA Psychiatry. 2018;75(3):233-239.
3. Fonagy P, Butler S, Cottrell D, et al. Multisystemic therapy versus management as usual in the treatment of adolescent antisocial behaviour (START): a pragmatic, randomised controlled, superiority trial. Lancet Psychiatry. 2018;5(2):119-133.
4. Janssen L, Kan CC, Carpentier PJ, et al. Mindfulness-based cognitive therapy v. treatment as usual in adults with ADHD: a multicentre, single-blind, randomised controlled trial. Psychol Med. 2019;49(1):55-65.
5. US Department of Veterans Affairs and Department of Defense. VA/DoD clinical practice guideline for the management of posttraumatic stress disorder and acute stress disorder . https://www.healthquality.va.gov/guidelines/MH/ptsd/VADoDPTSDCPGFinal082917.pdf. Published June 2017. Accessed September 8, 2019.

References

1. Pompoli A, Furukawa TA, Efthimiou O, et al. Dismantling cognitive-behaviour therapy for panic disorder: a systematic review and component network meta-analysis. Psychol Med. 2018;48(12):1945-1953.
2. Sloan DM, Marx BP, Lee DJ, et al. A brief exposure-based treatment vs cognitive processing therapy for posttraumatic stress disorder: a randomized noninferiority clinical trial. JAMA Psychiatry. 2018;75(3):233-239.
3. Fonagy P, Butler S, Cottrell D, et al. Multisystemic therapy versus management as usual in the treatment of adolescent antisocial behaviour (START): a pragmatic, randomised controlled, superiority trial. Lancet Psychiatry. 2018;5(2):119-133.
4. Janssen L, Kan CC, Carpentier PJ, et al. Mindfulness-based cognitive therapy v. treatment as usual in adults with ADHD: a multicentre, single-blind, randomised controlled trial. Psychol Med. 2019;49(1):55-65.
5. US Department of Veterans Affairs and Department of Defense. VA/DoD clinical practice guideline for the management of posttraumatic stress disorder and acute stress disorder . https://www.healthquality.va.gov/guidelines/MH/ptsd/VADoDPTSDCPGFinal082917.pdf. Published June 2017. Accessed September 8, 2019.

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Beyond ‘selfies’: An epidemic of acquired narcissism

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Beyond ‘selfies’: An epidemic of acquired narcissism

Narcissism has an evil reputation. But is it justified? A modicum of narcissism is actually healthy. It can bolster self-confidence, assertiveness, and success in business and in the sociobiology of mating. Perhaps that’s why narcissism as a trait has a survival value from an evolutionary perspective.

Taking an excessive number of “selfies” with a smartphone is probably the most common and relatively benign form of mild narcissism (and not in DSM-5, yet). Narcissistic personality disorder (NPD), with a prevalence of 1%, is on the extreme end of the narcissism continuum. It has become tainted with such an intensely negative halo that it has become a despised trait, an insult, and even a vile epithet, like a 4-letter word. But as psychiatrists and other mental health professionals, we clinically relate to patients with NPD as being afflicted with a serious neuropsychiatric disorder, not as despicable individuals. Many people outside the mental health profession abhor persons with NPD because of their gargantuan hubris, insufferable selfishness, self-aggrandizement, emotional abuse of others, and irremediable vanity. Narcissistic personality disorder deprives its sufferers of the prosocial capacity for empathy, which leads them to belittle others or treat competent individuals with disdain, never as equals. They also seem to be incapable of experiencing shame as they inflate their self-importance and megalomania at the expense of those they degrade. They cannot tolerate any success by others because it threatens to overshadow their own exaggerated achievements. They can be mercilessly harsh towards their underlings. They are incapable of fostering warm, long-term loving relationships, where bidirectional respect is essential. Their lives often are replete with brief, broken-up relationships because they emotionally, physically, or sexually abuse their intimate partners.

Primary NPD has been shown in twin studies to be highly genetic, and more strongly heritable than 17 other personality dimensions.1 It is also resistant to any effective psychotherapeutic, pharmacologic, or somatic treatments. This is particularly relevant given the proclivity of individuals with NPD to experience a crushing disappointment, commonly known as “narcissistic injury,” following a real or imagined failure. This could lead to a painful depression or an outburst of “narcissistic rage” directed at anyone perceived as undermining them, and may even lead to violent behavior.2

Apart from heritable narcissism, there is also another form of narcissism that can develop in some individuals following life events. That hazardous condition, known as “acquired narcissism,” is most often associated with achieving the coveted status of an exalted celebrity. At risk for this acquired personality affliction are famous actors, singers, movie directors, TV anchors, or politicians (although some politicians are natural-born narcissists, driven to seek the powers of public office), and less frequently physicians (perhaps because the practice of medicine is not done in front of spectators) or scientists (because research, no matter how momentous, rarely procures the glamour or public adulation of the entertainment industry). The ardent fans of those “celebs” shower them with such intense attention and adulation that it malignantly transforms previously “normal” individuals into narcissists who start believing they are indeed “very special” and superior to the rest of us mortals (especially as their earning power balloons into the millions after growing up with humble social or economic roots).

Social media has become a catalyst for acquired narcissism, with millions of followers on Twitter, Facebook, or YouTube. Cable TV also caters to politicians, some of whom morph into narcissists, intoxicated with their newfound eminence and stature among their partisan followers, and become genuinely convinced that they have supreme power or influence over the masses. They get carried away with their own exaggerated self-importance as oracles of the “truth,” regardless of how extreme their views may be. Celebrity, politics, social media, and cable TV have converged into a combustible mix, a crucible for acquired narcissism.

An interesting feature of acquired narcissism is “collective narcissism,” in which celebrities coalesce to consolidate their imagined superhuman attributes that go beyond the technical skills of their professions such as acting, singing, sports, or politics. Thus, entertainers or star athletes believe they can enunciate radical statements about contemporary social, political, or environmental issues (at both ends of the debate) as though their artistic success renders them wise arbiters of the truth. What complicates matters is their delirious fans, who revere and mimic whatever their idols say (and their fashion or their tattoos), which further intensifies the grandiosity and megalomania of acquired narcissism. Celebrity triggers mindless idolatry, fueling the narcissism of individuals who are blessed (or cursed?) with runaway personal success. Neuroscientists should conduct research into how the brain is neurobiologically altered by fame, but there are many more urgent questions that demand their attention. It would be important to know if it is reversible or enduring, even as fame inevitably dims.

Continue to: The pursuit of wealth and fame...

 

 

The pursuit of wealth and fame is widely prevalent and can be healthy if it is not all-consuming. But if achieved beyond the aspirer’s wildest dreams, he/she may reach an inflection point conducive to a pathologic degree of acquired narcissism. That’s what the French refer to as “les risques du métier” (ie, occupational hazard). I recall reading about celebrities who became enraged when a policeman “dared” to stop their car for some driving violation, confronting the officer with “Do you know who I am?” That question may be a clinical biomarker of acquired narcissism.

Interestingly, several years ago, when the American Psychiatry Association last revised the DSM—sometimes referred to as the “bible” of psychiatric nosology—it came close to dropping NPD from its listed disorders, but then reverted and kept it as one of the 275 diagnostic categories included in DSM-5.3 Had the NPD diagnosis been discarded, one wonders if the mythical god of narcissism would have suffered a transcendental “narcissistic injury”…

References

1. Livesley WJ, Jang KL, Jackson DN, et al. Genetic and environmental contributions to dimensions of personality disorder. Am J Psychiatry. 1993;150(12):1826-1831
2. Malmquist CP. Homicide: a psychiatric perspective. Washington, DC: American Psychiatric Publishing, Inc.; 2006:181-182.
3. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.

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Narcissism has an evil reputation. But is it justified? A modicum of narcissism is actually healthy. It can bolster self-confidence, assertiveness, and success in business and in the sociobiology of mating. Perhaps that’s why narcissism as a trait has a survival value from an evolutionary perspective.

Taking an excessive number of “selfies” with a smartphone is probably the most common and relatively benign form of mild narcissism (and not in DSM-5, yet). Narcissistic personality disorder (NPD), with a prevalence of 1%, is on the extreme end of the narcissism continuum. It has become tainted with such an intensely negative halo that it has become a despised trait, an insult, and even a vile epithet, like a 4-letter word. But as psychiatrists and other mental health professionals, we clinically relate to patients with NPD as being afflicted with a serious neuropsychiatric disorder, not as despicable individuals. Many people outside the mental health profession abhor persons with NPD because of their gargantuan hubris, insufferable selfishness, self-aggrandizement, emotional abuse of others, and irremediable vanity. Narcissistic personality disorder deprives its sufferers of the prosocial capacity for empathy, which leads them to belittle others or treat competent individuals with disdain, never as equals. They also seem to be incapable of experiencing shame as they inflate their self-importance and megalomania at the expense of those they degrade. They cannot tolerate any success by others because it threatens to overshadow their own exaggerated achievements. They can be mercilessly harsh towards their underlings. They are incapable of fostering warm, long-term loving relationships, where bidirectional respect is essential. Their lives often are replete with brief, broken-up relationships because they emotionally, physically, or sexually abuse their intimate partners.

Primary NPD has been shown in twin studies to be highly genetic, and more strongly heritable than 17 other personality dimensions.1 It is also resistant to any effective psychotherapeutic, pharmacologic, or somatic treatments. This is particularly relevant given the proclivity of individuals with NPD to experience a crushing disappointment, commonly known as “narcissistic injury,” following a real or imagined failure. This could lead to a painful depression or an outburst of “narcissistic rage” directed at anyone perceived as undermining them, and may even lead to violent behavior.2

Apart from heritable narcissism, there is also another form of narcissism that can develop in some individuals following life events. That hazardous condition, known as “acquired narcissism,” is most often associated with achieving the coveted status of an exalted celebrity. At risk for this acquired personality affliction are famous actors, singers, movie directors, TV anchors, or politicians (although some politicians are natural-born narcissists, driven to seek the powers of public office), and less frequently physicians (perhaps because the practice of medicine is not done in front of spectators) or scientists (because research, no matter how momentous, rarely procures the glamour or public adulation of the entertainment industry). The ardent fans of those “celebs” shower them with such intense attention and adulation that it malignantly transforms previously “normal” individuals into narcissists who start believing they are indeed “very special” and superior to the rest of us mortals (especially as their earning power balloons into the millions after growing up with humble social or economic roots).

Social media has become a catalyst for acquired narcissism, with millions of followers on Twitter, Facebook, or YouTube. Cable TV also caters to politicians, some of whom morph into narcissists, intoxicated with their newfound eminence and stature among their partisan followers, and become genuinely convinced that they have supreme power or influence over the masses. They get carried away with their own exaggerated self-importance as oracles of the “truth,” regardless of how extreme their views may be. Celebrity, politics, social media, and cable TV have converged into a combustible mix, a crucible for acquired narcissism.

An interesting feature of acquired narcissism is “collective narcissism,” in which celebrities coalesce to consolidate their imagined superhuman attributes that go beyond the technical skills of their professions such as acting, singing, sports, or politics. Thus, entertainers or star athletes believe they can enunciate radical statements about contemporary social, political, or environmental issues (at both ends of the debate) as though their artistic success renders them wise arbiters of the truth. What complicates matters is their delirious fans, who revere and mimic whatever their idols say (and their fashion or their tattoos), which further intensifies the grandiosity and megalomania of acquired narcissism. Celebrity triggers mindless idolatry, fueling the narcissism of individuals who are blessed (or cursed?) with runaway personal success. Neuroscientists should conduct research into how the brain is neurobiologically altered by fame, but there are many more urgent questions that demand their attention. It would be important to know if it is reversible or enduring, even as fame inevitably dims.

Continue to: The pursuit of wealth and fame...

 

 

The pursuit of wealth and fame is widely prevalent and can be healthy if it is not all-consuming. But if achieved beyond the aspirer’s wildest dreams, he/she may reach an inflection point conducive to a pathologic degree of acquired narcissism. That’s what the French refer to as “les risques du métier” (ie, occupational hazard). I recall reading about celebrities who became enraged when a policeman “dared” to stop their car for some driving violation, confronting the officer with “Do you know who I am?” That question may be a clinical biomarker of acquired narcissism.

Interestingly, several years ago, when the American Psychiatry Association last revised the DSM—sometimes referred to as the “bible” of psychiatric nosology—it came close to dropping NPD from its listed disorders, but then reverted and kept it as one of the 275 diagnostic categories included in DSM-5.3 Had the NPD diagnosis been discarded, one wonders if the mythical god of narcissism would have suffered a transcendental “narcissistic injury”…

Narcissism has an evil reputation. But is it justified? A modicum of narcissism is actually healthy. It can bolster self-confidence, assertiveness, and success in business and in the sociobiology of mating. Perhaps that’s why narcissism as a trait has a survival value from an evolutionary perspective.

Taking an excessive number of “selfies” with a smartphone is probably the most common and relatively benign form of mild narcissism (and not in DSM-5, yet). Narcissistic personality disorder (NPD), with a prevalence of 1%, is on the extreme end of the narcissism continuum. It has become tainted with such an intensely negative halo that it has become a despised trait, an insult, and even a vile epithet, like a 4-letter word. But as psychiatrists and other mental health professionals, we clinically relate to patients with NPD as being afflicted with a serious neuropsychiatric disorder, not as despicable individuals. Many people outside the mental health profession abhor persons with NPD because of their gargantuan hubris, insufferable selfishness, self-aggrandizement, emotional abuse of others, and irremediable vanity. Narcissistic personality disorder deprives its sufferers of the prosocial capacity for empathy, which leads them to belittle others or treat competent individuals with disdain, never as equals. They also seem to be incapable of experiencing shame as they inflate their self-importance and megalomania at the expense of those they degrade. They cannot tolerate any success by others because it threatens to overshadow their own exaggerated achievements. They can be mercilessly harsh towards their underlings. They are incapable of fostering warm, long-term loving relationships, where bidirectional respect is essential. Their lives often are replete with brief, broken-up relationships because they emotionally, physically, or sexually abuse their intimate partners.

Primary NPD has been shown in twin studies to be highly genetic, and more strongly heritable than 17 other personality dimensions.1 It is also resistant to any effective psychotherapeutic, pharmacologic, or somatic treatments. This is particularly relevant given the proclivity of individuals with NPD to experience a crushing disappointment, commonly known as “narcissistic injury,” following a real or imagined failure. This could lead to a painful depression or an outburst of “narcissistic rage” directed at anyone perceived as undermining them, and may even lead to violent behavior.2

Apart from heritable narcissism, there is also another form of narcissism that can develop in some individuals following life events. That hazardous condition, known as “acquired narcissism,” is most often associated with achieving the coveted status of an exalted celebrity. At risk for this acquired personality affliction are famous actors, singers, movie directors, TV anchors, or politicians (although some politicians are natural-born narcissists, driven to seek the powers of public office), and less frequently physicians (perhaps because the practice of medicine is not done in front of spectators) or scientists (because research, no matter how momentous, rarely procures the glamour or public adulation of the entertainment industry). The ardent fans of those “celebs” shower them with such intense attention and adulation that it malignantly transforms previously “normal” individuals into narcissists who start believing they are indeed “very special” and superior to the rest of us mortals (especially as their earning power balloons into the millions after growing up with humble social or economic roots).

Social media has become a catalyst for acquired narcissism, with millions of followers on Twitter, Facebook, or YouTube. Cable TV also caters to politicians, some of whom morph into narcissists, intoxicated with their newfound eminence and stature among their partisan followers, and become genuinely convinced that they have supreme power or influence over the masses. They get carried away with their own exaggerated self-importance as oracles of the “truth,” regardless of how extreme their views may be. Celebrity, politics, social media, and cable TV have converged into a combustible mix, a crucible for acquired narcissism.

An interesting feature of acquired narcissism is “collective narcissism,” in which celebrities coalesce to consolidate their imagined superhuman attributes that go beyond the technical skills of their professions such as acting, singing, sports, or politics. Thus, entertainers or star athletes believe they can enunciate radical statements about contemporary social, political, or environmental issues (at both ends of the debate) as though their artistic success renders them wise arbiters of the truth. What complicates matters is their delirious fans, who revere and mimic whatever their idols say (and their fashion or their tattoos), which further intensifies the grandiosity and megalomania of acquired narcissism. Celebrity triggers mindless idolatry, fueling the narcissism of individuals who are blessed (or cursed?) with runaway personal success. Neuroscientists should conduct research into how the brain is neurobiologically altered by fame, but there are many more urgent questions that demand their attention. It would be important to know if it is reversible or enduring, even as fame inevitably dims.

Continue to: The pursuit of wealth and fame...

 

 

The pursuit of wealth and fame is widely prevalent and can be healthy if it is not all-consuming. But if achieved beyond the aspirer’s wildest dreams, he/she may reach an inflection point conducive to a pathologic degree of acquired narcissism. That’s what the French refer to as “les risques du métier” (ie, occupational hazard). I recall reading about celebrities who became enraged when a policeman “dared” to stop their car for some driving violation, confronting the officer with “Do you know who I am?” That question may be a clinical biomarker of acquired narcissism.

Interestingly, several years ago, when the American Psychiatry Association last revised the DSM—sometimes referred to as the “bible” of psychiatric nosology—it came close to dropping NPD from its listed disorders, but then reverted and kept it as one of the 275 diagnostic categories included in DSM-5.3 Had the NPD diagnosis been discarded, one wonders if the mythical god of narcissism would have suffered a transcendental “narcissistic injury”…

References

1. Livesley WJ, Jang KL, Jackson DN, et al. Genetic and environmental contributions to dimensions of personality disorder. Am J Psychiatry. 1993;150(12):1826-1831
2. Malmquist CP. Homicide: a psychiatric perspective. Washington, DC: American Psychiatric Publishing, Inc.; 2006:181-182.
3. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.

References

1. Livesley WJ, Jang KL, Jackson DN, et al. Genetic and environmental contributions to dimensions of personality disorder. Am J Psychiatry. 1993;150(12):1826-1831
2. Malmquist CP. Homicide: a psychiatric perspective. Washington, DC: American Psychiatric Publishing, Inc.; 2006:181-182.
3. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.

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Genetics, neurobiology of borderline personality disorder remain uncertain

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Thu, 06/27/2019 - 09:03

– Borderline personality disorder has a genetic and neurobiological component, but researchers remain unable to discern exactly why specific genetic markers are attributed to the disease, Emil F. Coccaro, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“The neurobiology at this point gives us clues that what’s going on with borderline personality disorder isn’t simply developmental or environmental. That’s all that it tells us,” said Dr. Coccaro, director of the Clinical Neuroscience & Psychopharmacology Research Unit at the University of Chicago.

Similarly, studies in twins that show heritability of borderline personal disorder at rates between 31% and 49% “only show there’s something in the DNA,” he added. Dr. Coccaro called the evidence for the neurobiology of borderline personality disorder “hazy.” “The neurobiology of [borderline personality disorder] points to widespread brain network dysfunction affecting emotional processing and social cognition,” said Dr. Coccaro, also chairman of the university’s department of psychiatry and behavioral neuroscience.

That is true of a lot of disorders, he said, so only the details explain why patients with borderline personality disorder look different from those who might have “similar types of circuitry abnormalities,” he said.

For example, genomewide association studies have found links between borderline personality disorder and the genes DPYD and PKP4, indicating problems with pyrimidine metabolism and myelin production. The study also found a strong association between borderline personality disorder, bipolar disorder, major depression, and schizophrenia (Transl Psychiatry. 2017 Jun. doi: 10.1038/tp.2017.115). DPYD has been associated with schizophrenia, but the relationship between DPYD and borderline personality disorder is unknown, Dr. Coccaro said.

“These [associations] are suggestive of what’s going on genetically, but it hardly makes a story that’s coherent enough to sink your teeth into,” he said.

 

 


The neuroscience behind borderline personality disorder, meanwhile, appears more promising, Dr. Coccaro noted. Studies of brain function have shown that negative emotions in patients with borderline personality disorder lead to increased amygdala reactivity. With regard to the neuroendocrinology of borderline personality disorder, trauma in those patients appears similar to what can be seen in patients with posttraumatic stress disorder (PTSD) with “increased central and decreased peripheral stress hormone response.” In fact, he said, 75% of people with borderline personality disorder experienced childhood physical, sexual, or emotional abuse (Curr Psychiatry Rep. 2005 Mar;7[1]:39).

Dr. Coccaro noted that, although the prevalence of borderline personality disorder is likely between 2% and 3%, the illness is encountered at a rate of 20% for patients in clinic and 40% for those in hospitals and emergency departments. Borderline personality disorder is more prevalent and more severe in women, but no gender differences are apparent in affective disturbance, impulsivity, or suicidality. Borderline personality disorder also is likely to be comorbid with at least two conditions: Men with borderline personality disorder tend to have narcissistic and antisocial personality disorders; women with borderline personality disorder have higher rates of major depression, anorexia and bulimia, and PTSD.

Borderline personality was traditionally associated with a “dismal prognosis,” but the lifetime course of the disorder appears to be more promising. In the Collaborative Longitudinal Personality Disorder Study (CLPS), 25% of 668 patients had achieved remission after 2 years, which was defined as having fewer than two symptoms for more than 2 months. After a decade, 85% of those patients had reached remission for at least 12 months (JAMA Psychiatry. 2011;68[8]:827-37). Another trial, the McLean Study of Adult Development, analyzed 290 patients who had a remission rate at 16 years of 78% that lasted for at least 8 years (J Pers Disord. 2005 Oct;19[5]:505-23).

However, Dr. Coccaro noted, patients with borderline personality disorder likely do not achieve true remission. Instead, he said, patients simply fail to meet all the criteria to be diagnosed with borderline personality disorder. “They still have some of the features, but they are less intense,” Dr. Coccaro said.

Dr. Coccaro reported serving as a consultant to Azevan, Avanir Pharma, and Brackett. He also reported receiving grants from the National Institute on Mental Illness and the National Institute on Alcoholic Abuse and Alcoholism, and receiving royalties from UpToDate.

The meeting was presented by Global Academy for Medical Education. Global Academy and this news organization are owned by the same parent company.
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– Borderline personality disorder has a genetic and neurobiological component, but researchers remain unable to discern exactly why specific genetic markers are attributed to the disease, Emil F. Coccaro, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“The neurobiology at this point gives us clues that what’s going on with borderline personality disorder isn’t simply developmental or environmental. That’s all that it tells us,” said Dr. Coccaro, director of the Clinical Neuroscience & Psychopharmacology Research Unit at the University of Chicago.

Similarly, studies in twins that show heritability of borderline personal disorder at rates between 31% and 49% “only show there’s something in the DNA,” he added. Dr. Coccaro called the evidence for the neurobiology of borderline personality disorder “hazy.” “The neurobiology of [borderline personality disorder] points to widespread brain network dysfunction affecting emotional processing and social cognition,” said Dr. Coccaro, also chairman of the university’s department of psychiatry and behavioral neuroscience.

That is true of a lot of disorders, he said, so only the details explain why patients with borderline personality disorder look different from those who might have “similar types of circuitry abnormalities,” he said.

For example, genomewide association studies have found links between borderline personality disorder and the genes DPYD and PKP4, indicating problems with pyrimidine metabolism and myelin production. The study also found a strong association between borderline personality disorder, bipolar disorder, major depression, and schizophrenia (Transl Psychiatry. 2017 Jun. doi: 10.1038/tp.2017.115). DPYD has been associated with schizophrenia, but the relationship between DPYD and borderline personality disorder is unknown, Dr. Coccaro said.

“These [associations] are suggestive of what’s going on genetically, but it hardly makes a story that’s coherent enough to sink your teeth into,” he said.

 

 


The neuroscience behind borderline personality disorder, meanwhile, appears more promising, Dr. Coccaro noted. Studies of brain function have shown that negative emotions in patients with borderline personality disorder lead to increased amygdala reactivity. With regard to the neuroendocrinology of borderline personality disorder, trauma in those patients appears similar to what can be seen in patients with posttraumatic stress disorder (PTSD) with “increased central and decreased peripheral stress hormone response.” In fact, he said, 75% of people with borderline personality disorder experienced childhood physical, sexual, or emotional abuse (Curr Psychiatry Rep. 2005 Mar;7[1]:39).

Dr. Coccaro noted that, although the prevalence of borderline personality disorder is likely between 2% and 3%, the illness is encountered at a rate of 20% for patients in clinic and 40% for those in hospitals and emergency departments. Borderline personality disorder is more prevalent and more severe in women, but no gender differences are apparent in affective disturbance, impulsivity, or suicidality. Borderline personality disorder also is likely to be comorbid with at least two conditions: Men with borderline personality disorder tend to have narcissistic and antisocial personality disorders; women with borderline personality disorder have higher rates of major depression, anorexia and bulimia, and PTSD.

Borderline personality was traditionally associated with a “dismal prognosis,” but the lifetime course of the disorder appears to be more promising. In the Collaborative Longitudinal Personality Disorder Study (CLPS), 25% of 668 patients had achieved remission after 2 years, which was defined as having fewer than two symptoms for more than 2 months. After a decade, 85% of those patients had reached remission for at least 12 months (JAMA Psychiatry. 2011;68[8]:827-37). Another trial, the McLean Study of Adult Development, analyzed 290 patients who had a remission rate at 16 years of 78% that lasted for at least 8 years (J Pers Disord. 2005 Oct;19[5]:505-23).

However, Dr. Coccaro noted, patients with borderline personality disorder likely do not achieve true remission. Instead, he said, patients simply fail to meet all the criteria to be diagnosed with borderline personality disorder. “They still have some of the features, but they are less intense,” Dr. Coccaro said.

Dr. Coccaro reported serving as a consultant to Azevan, Avanir Pharma, and Brackett. He also reported receiving grants from the National Institute on Mental Illness and the National Institute on Alcoholic Abuse and Alcoholism, and receiving royalties from UpToDate.

The meeting was presented by Global Academy for Medical Education. Global Academy and this news organization are owned by the same parent company.

– Borderline personality disorder has a genetic and neurobiological component, but researchers remain unable to discern exactly why specific genetic markers are attributed to the disease, Emil F. Coccaro, MD, said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

“The neurobiology at this point gives us clues that what’s going on with borderline personality disorder isn’t simply developmental or environmental. That’s all that it tells us,” said Dr. Coccaro, director of the Clinical Neuroscience & Psychopharmacology Research Unit at the University of Chicago.

Similarly, studies in twins that show heritability of borderline personal disorder at rates between 31% and 49% “only show there’s something in the DNA,” he added. Dr. Coccaro called the evidence for the neurobiology of borderline personality disorder “hazy.” “The neurobiology of [borderline personality disorder] points to widespread brain network dysfunction affecting emotional processing and social cognition,” said Dr. Coccaro, also chairman of the university’s department of psychiatry and behavioral neuroscience.

That is true of a lot of disorders, he said, so only the details explain why patients with borderline personality disorder look different from those who might have “similar types of circuitry abnormalities,” he said.

For example, genomewide association studies have found links between borderline personality disorder and the genes DPYD and PKP4, indicating problems with pyrimidine metabolism and myelin production. The study also found a strong association between borderline personality disorder, bipolar disorder, major depression, and schizophrenia (Transl Psychiatry. 2017 Jun. doi: 10.1038/tp.2017.115). DPYD has been associated with schizophrenia, but the relationship between DPYD and borderline personality disorder is unknown, Dr. Coccaro said.

“These [associations] are suggestive of what’s going on genetically, but it hardly makes a story that’s coherent enough to sink your teeth into,” he said.

 

 


The neuroscience behind borderline personality disorder, meanwhile, appears more promising, Dr. Coccaro noted. Studies of brain function have shown that negative emotions in patients with borderline personality disorder lead to increased amygdala reactivity. With regard to the neuroendocrinology of borderline personality disorder, trauma in those patients appears similar to what can be seen in patients with posttraumatic stress disorder (PTSD) with “increased central and decreased peripheral stress hormone response.” In fact, he said, 75% of people with borderline personality disorder experienced childhood physical, sexual, or emotional abuse (Curr Psychiatry Rep. 2005 Mar;7[1]:39).

Dr. Coccaro noted that, although the prevalence of borderline personality disorder is likely between 2% and 3%, the illness is encountered at a rate of 20% for patients in clinic and 40% for those in hospitals and emergency departments. Borderline personality disorder is more prevalent and more severe in women, but no gender differences are apparent in affective disturbance, impulsivity, or suicidality. Borderline personality disorder also is likely to be comorbid with at least two conditions: Men with borderline personality disorder tend to have narcissistic and antisocial personality disorders; women with borderline personality disorder have higher rates of major depression, anorexia and bulimia, and PTSD.

Borderline personality was traditionally associated with a “dismal prognosis,” but the lifetime course of the disorder appears to be more promising. In the Collaborative Longitudinal Personality Disorder Study (CLPS), 25% of 668 patients had achieved remission after 2 years, which was defined as having fewer than two symptoms for more than 2 months. After a decade, 85% of those patients had reached remission for at least 12 months (JAMA Psychiatry. 2011;68[8]:827-37). Another trial, the McLean Study of Adult Development, analyzed 290 patients who had a remission rate at 16 years of 78% that lasted for at least 8 years (J Pers Disord. 2005 Oct;19[5]:505-23).

However, Dr. Coccaro noted, patients with borderline personality disorder likely do not achieve true remission. Instead, he said, patients simply fail to meet all the criteria to be diagnosed with borderline personality disorder. “They still have some of the features, but they are less intense,” Dr. Coccaro said.

Dr. Coccaro reported serving as a consultant to Azevan, Avanir Pharma, and Brackett. He also reported receiving grants from the National Institute on Mental Illness and the National Institute on Alcoholic Abuse and Alcoholism, and receiving royalties from UpToDate.

The meeting was presented by Global Academy for Medical Education. Global Academy and this news organization are owned by the same parent company.
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For borderline personality disorder, less may be more

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Tue, 05/28/2019 - 10:36

– Borderline personality disorder is often treated with long-running psychotherapy, but this could be a disservice to patients. Instead, stepped-care models may offer more benefit in a shorter period of time, conserving resources and potentially expanding the reach of therapeutic interventions.

“There is this legacy of psychoanalysis, this idea that if you’ve had a condition for 20 years, it’s going to take 20 years of therapy to get rid of it – which is not true,” Joel Paris, MD, said in an interview. Dr. Paris moderated a session on stepped-care interventions for borderline personality disorder at the annual meeting of the American Psychiatric Association.

He also pointed out that psychoanalysis can prove self-sustaining: “There’s something to talk about, so it can go on and if there’s money to pay for the service, why stop?”

But psychoanalysis can have diminishing returns, and that in turn can strain resources. “Some people won’t get better or won’t go beyond a certain point. You help them to a certain extent, and then you have to be able to say, ‘That’s enough; stop there. If you get in to bad trouble, you can always come back,’ ” said Dr. Paris, professor of psychiatry at McGill University, Montreal.

That realization has led Dr. McGill to introduce a stepped-care model, which has provided a 12-week program for 15 years. Dr. Paris presented a retrospective look at the program, including 479 patients who received individual and group therapy. The dropout rate was high at 30%, but only 12% of patients returned asking for more therapy. A total of 145 patients deemed to be more chronic or who did not respond to the short-term program had the option of completing additional individual or group therapy over a period of 6-24 months.

Eighty-eight percent of patients don’t come back, and we’re happy with that. There are also dropouts; maybe a quarter will not complete the program,” Dr. Paris said. “But that means 75% do, and most of them get better. There’s also good evidence that short therapy can help many people with substance abuse.”

Lois W. Choi-Kain, MD, assistant professor psychiatry at Harvard Medical School, Boston, presented evidence from several studies showing that shorter- and long-term courses of dialectical behavior therapy led to similar improvements, but that brief courses were associated with more rapid improvement. The short course consisted of weekly 1-hour individual sessions, while the longer course involved weekly 2-hour group sessions. The individual approach was associated with an 89% faster improvement in symptoms in the first 3 months (P less than .0001).

These kinds of findings underscore the need for shorter courses of therapy, at least for most patients, in order to conserve resources and broaden the availability of therapy, particularly in less affluent settings. “We saw in today’s symposium that most improvement takes place at the beginning of therapy, and you should quit while you’re ahead,” Dr. Paris said. “You should not try to do impossible things and make everybody into paradigms of mental health.”

Dr. Paris reported no relevant financial disclosures.

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– Borderline personality disorder is often treated with long-running psychotherapy, but this could be a disservice to patients. Instead, stepped-care models may offer more benefit in a shorter period of time, conserving resources and potentially expanding the reach of therapeutic interventions.

“There is this legacy of psychoanalysis, this idea that if you’ve had a condition for 20 years, it’s going to take 20 years of therapy to get rid of it – which is not true,” Joel Paris, MD, said in an interview. Dr. Paris moderated a session on stepped-care interventions for borderline personality disorder at the annual meeting of the American Psychiatric Association.

He also pointed out that psychoanalysis can prove self-sustaining: “There’s something to talk about, so it can go on and if there’s money to pay for the service, why stop?”

But psychoanalysis can have diminishing returns, and that in turn can strain resources. “Some people won’t get better or won’t go beyond a certain point. You help them to a certain extent, and then you have to be able to say, ‘That’s enough; stop there. If you get in to bad trouble, you can always come back,’ ” said Dr. Paris, professor of psychiatry at McGill University, Montreal.

That realization has led Dr. McGill to introduce a stepped-care model, which has provided a 12-week program for 15 years. Dr. Paris presented a retrospective look at the program, including 479 patients who received individual and group therapy. The dropout rate was high at 30%, but only 12% of patients returned asking for more therapy. A total of 145 patients deemed to be more chronic or who did not respond to the short-term program had the option of completing additional individual or group therapy over a period of 6-24 months.

Eighty-eight percent of patients don’t come back, and we’re happy with that. There are also dropouts; maybe a quarter will not complete the program,” Dr. Paris said. “But that means 75% do, and most of them get better. There’s also good evidence that short therapy can help many people with substance abuse.”

Lois W. Choi-Kain, MD, assistant professor psychiatry at Harvard Medical School, Boston, presented evidence from several studies showing that shorter- and long-term courses of dialectical behavior therapy led to similar improvements, but that brief courses were associated with more rapid improvement. The short course consisted of weekly 1-hour individual sessions, while the longer course involved weekly 2-hour group sessions. The individual approach was associated with an 89% faster improvement in symptoms in the first 3 months (P less than .0001).

These kinds of findings underscore the need for shorter courses of therapy, at least for most patients, in order to conserve resources and broaden the availability of therapy, particularly in less affluent settings. “We saw in today’s symposium that most improvement takes place at the beginning of therapy, and you should quit while you’re ahead,” Dr. Paris said. “You should not try to do impossible things and make everybody into paradigms of mental health.”

Dr. Paris reported no relevant financial disclosures.

– Borderline personality disorder is often treated with long-running psychotherapy, but this could be a disservice to patients. Instead, stepped-care models may offer more benefit in a shorter period of time, conserving resources and potentially expanding the reach of therapeutic interventions.

“There is this legacy of psychoanalysis, this idea that if you’ve had a condition for 20 years, it’s going to take 20 years of therapy to get rid of it – which is not true,” Joel Paris, MD, said in an interview. Dr. Paris moderated a session on stepped-care interventions for borderline personality disorder at the annual meeting of the American Psychiatric Association.

He also pointed out that psychoanalysis can prove self-sustaining: “There’s something to talk about, so it can go on and if there’s money to pay for the service, why stop?”

But psychoanalysis can have diminishing returns, and that in turn can strain resources. “Some people won’t get better or won’t go beyond a certain point. You help them to a certain extent, and then you have to be able to say, ‘That’s enough; stop there. If you get in to bad trouble, you can always come back,’ ” said Dr. Paris, professor of psychiatry at McGill University, Montreal.

That realization has led Dr. McGill to introduce a stepped-care model, which has provided a 12-week program for 15 years. Dr. Paris presented a retrospective look at the program, including 479 patients who received individual and group therapy. The dropout rate was high at 30%, but only 12% of patients returned asking for more therapy. A total of 145 patients deemed to be more chronic or who did not respond to the short-term program had the option of completing additional individual or group therapy over a period of 6-24 months.

Eighty-eight percent of patients don’t come back, and we’re happy with that. There are also dropouts; maybe a quarter will not complete the program,” Dr. Paris said. “But that means 75% do, and most of them get better. There’s also good evidence that short therapy can help many people with substance abuse.”

Lois W. Choi-Kain, MD, assistant professor psychiatry at Harvard Medical School, Boston, presented evidence from several studies showing that shorter- and long-term courses of dialectical behavior therapy led to similar improvements, but that brief courses were associated with more rapid improvement. The short course consisted of weekly 1-hour individual sessions, while the longer course involved weekly 2-hour group sessions. The individual approach was associated with an 89% faster improvement in symptoms in the first 3 months (P less than .0001).

These kinds of findings underscore the need for shorter courses of therapy, at least for most patients, in order to conserve resources and broaden the availability of therapy, particularly in less affluent settings. “We saw in today’s symposium that most improvement takes place at the beginning of therapy, and you should quit while you’re ahead,” Dr. Paris said. “You should not try to do impossible things and make everybody into paradigms of mental health.”

Dr. Paris reported no relevant financial disclosures.

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Alopecia areata linked to mental health disorders

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Tue, 04/02/2019 - 11:46

 

Alopecia areata is associated with greater frequency of mental health disorders, according to a new analysis of U.S. hospitalizations.

Specifically, the analysis found, alopecia areata patients are at risk for any mental health disorder, anxiety disorders, attention-deficit/hyperactivity disorder, dementia, mood disorders, personality disorders, and suicide or intentionally self-inflicted injury. The report was published in the Journal of the American Academy of Dermatology.

The researchers worked with 87,053,155 adult and child records from the 2002-2012 National Inpatient Sample, which represents 20% of U.S. hospitalizations. They identified inpatients with alopecia areata based on the ICD-9-CM code and compared them to all patients without the condition.

Overall, 5,605 patients had alopecia areata, which was the secondary diagnosis more than 99% of the time. Compared with inpatients without alopecia areata, those with the disorder were more likely to be younger (42.2 vs. 47.9 years; P less than .0001), female (61.7% vs. 58.6%; P = .0297), and uninsured (8.1% vs. 5.5%; P less than .0001). In addition, inpatients with alopecia areata had a greater frequency of mental health disorders (32.8% vs. 20.0%; P less than .0001) and were more likely to have a primary mental health diagnosis (5.5% vs. 2.2%; P less than .0001), reported Vivek Singam of Northwestern University, Chicago, and his associates.

Among 15 mental health or classes of disorders examined, alopecia areata patients were at greater risk in 13 of them. The only exceptions were delirium/dementia/amnestic/cognitive disorders and disorders diagnosed in infancy, childhood, or adolescence.

Alopecia areata patients with a mental health disorder had a mean hospital stay of 6.0 days (95% confidence interval, 5.4.-6.6) and hospitalization cost of $11,907 (95% CI, $10,312-$13,503).

Previous studies had shown similar relationships. However, previous studies showed lower risk of alopecia areata and schizophrenia and no increased risk of ADHD, compared with the current study’s findings. The authors could offer no explanation for those differences.

The strengths of the current analysis include its use of a large-scale, nationally representative cohort and its large sample size, as well its inclusion of a broad range of mental health disorders. Because of its cross-sectional design, the study could not establish the temporal relationship between alopecia areata and mental health disorders.

It is unclear whether psychosocial stress might cause or exacerbate alopecia areata, or whether alopecia areata can lead to or worsen mental health disorders.

The researchers called for additional studies to understand this relationship and potential mechanisms.

The Agency for Healthcare Research and Quality and the Dermatology Foundation funded the study. The researchers declared having no conflicts of interest.

SOURCE: Singam V et al. J Am Acad Dermatol. 2018 Aug 6. doi: 10.1016/j.jaad.2018.07.044.

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Alopecia areata is associated with greater frequency of mental health disorders, according to a new analysis of U.S. hospitalizations.

Specifically, the analysis found, alopecia areata patients are at risk for any mental health disorder, anxiety disorders, attention-deficit/hyperactivity disorder, dementia, mood disorders, personality disorders, and suicide or intentionally self-inflicted injury. The report was published in the Journal of the American Academy of Dermatology.

The researchers worked with 87,053,155 adult and child records from the 2002-2012 National Inpatient Sample, which represents 20% of U.S. hospitalizations. They identified inpatients with alopecia areata based on the ICD-9-CM code and compared them to all patients without the condition.

Overall, 5,605 patients had alopecia areata, which was the secondary diagnosis more than 99% of the time. Compared with inpatients without alopecia areata, those with the disorder were more likely to be younger (42.2 vs. 47.9 years; P less than .0001), female (61.7% vs. 58.6%; P = .0297), and uninsured (8.1% vs. 5.5%; P less than .0001). In addition, inpatients with alopecia areata had a greater frequency of mental health disorders (32.8% vs. 20.0%; P less than .0001) and were more likely to have a primary mental health diagnosis (5.5% vs. 2.2%; P less than .0001), reported Vivek Singam of Northwestern University, Chicago, and his associates.

Among 15 mental health or classes of disorders examined, alopecia areata patients were at greater risk in 13 of them. The only exceptions were delirium/dementia/amnestic/cognitive disorders and disorders diagnosed in infancy, childhood, or adolescence.

Alopecia areata patients with a mental health disorder had a mean hospital stay of 6.0 days (95% confidence interval, 5.4.-6.6) and hospitalization cost of $11,907 (95% CI, $10,312-$13,503).

Previous studies had shown similar relationships. However, previous studies showed lower risk of alopecia areata and schizophrenia and no increased risk of ADHD, compared with the current study’s findings. The authors could offer no explanation for those differences.

The strengths of the current analysis include its use of a large-scale, nationally representative cohort and its large sample size, as well its inclusion of a broad range of mental health disorders. Because of its cross-sectional design, the study could not establish the temporal relationship between alopecia areata and mental health disorders.

It is unclear whether psychosocial stress might cause or exacerbate alopecia areata, or whether alopecia areata can lead to or worsen mental health disorders.

The researchers called for additional studies to understand this relationship and potential mechanisms.

The Agency for Healthcare Research and Quality and the Dermatology Foundation funded the study. The researchers declared having no conflicts of interest.

SOURCE: Singam V et al. J Am Acad Dermatol. 2018 Aug 6. doi: 10.1016/j.jaad.2018.07.044.

 

Alopecia areata is associated with greater frequency of mental health disorders, according to a new analysis of U.S. hospitalizations.

Specifically, the analysis found, alopecia areata patients are at risk for any mental health disorder, anxiety disorders, attention-deficit/hyperactivity disorder, dementia, mood disorders, personality disorders, and suicide or intentionally self-inflicted injury. The report was published in the Journal of the American Academy of Dermatology.

The researchers worked with 87,053,155 adult and child records from the 2002-2012 National Inpatient Sample, which represents 20% of U.S. hospitalizations. They identified inpatients with alopecia areata based on the ICD-9-CM code and compared them to all patients without the condition.

Overall, 5,605 patients had alopecia areata, which was the secondary diagnosis more than 99% of the time. Compared with inpatients without alopecia areata, those with the disorder were more likely to be younger (42.2 vs. 47.9 years; P less than .0001), female (61.7% vs. 58.6%; P = .0297), and uninsured (8.1% vs. 5.5%; P less than .0001). In addition, inpatients with alopecia areata had a greater frequency of mental health disorders (32.8% vs. 20.0%; P less than .0001) and were more likely to have a primary mental health diagnosis (5.5% vs. 2.2%; P less than .0001), reported Vivek Singam of Northwestern University, Chicago, and his associates.

Among 15 mental health or classes of disorders examined, alopecia areata patients were at greater risk in 13 of them. The only exceptions were delirium/dementia/amnestic/cognitive disorders and disorders diagnosed in infancy, childhood, or adolescence.

Alopecia areata patients with a mental health disorder had a mean hospital stay of 6.0 days (95% confidence interval, 5.4.-6.6) and hospitalization cost of $11,907 (95% CI, $10,312-$13,503).

Previous studies had shown similar relationships. However, previous studies showed lower risk of alopecia areata and schizophrenia and no increased risk of ADHD, compared with the current study’s findings. The authors could offer no explanation for those differences.

The strengths of the current analysis include its use of a large-scale, nationally representative cohort and its large sample size, as well its inclusion of a broad range of mental health disorders. Because of its cross-sectional design, the study could not establish the temporal relationship between alopecia areata and mental health disorders.

It is unclear whether psychosocial stress might cause or exacerbate alopecia areata, or whether alopecia areata can lead to or worsen mental health disorders.

The researchers called for additional studies to understand this relationship and potential mechanisms.

The Agency for Healthcare Research and Quality and the Dermatology Foundation funded the study. The researchers declared having no conflicts of interest.

SOURCE: Singam V et al. J Am Acad Dermatol. 2018 Aug 6. doi: 10.1016/j.jaad.2018.07.044.

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Key clinical point: Alopecia areata patients should be monitored closely for mental health disorders.

Major finding: Overall, 32.8% of hospitalized alopecia areata patients had a mental health disorder, compared with 20.0% of controls.

Study details: Retrospective analysis of 87,053,155 U.S. adults and children.

Disclosures: The Agency for Healthcare Research & Quality and the Dermatology Foundation funded the study. The researchers declared having no conflicts of interest.

Source: Singam V et al. J Am Acad Dermatol. 2018 Aug 6. doi: 10.1016/j.jaad.2018.07.044.

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Strategies for working with patients with personality disorders

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Patients with personality disorders can disrupt the treatment relationship, and may leave us feeling angry, ineffective, inadequate, and defeated. Although their behaviors may appear volitional and purposeful, they often are the result of a dysfunctional personality structure.1 These patients’ unbending patterns of viewing themselves, interacting with others, and navigating the world can be problematic in an inpatient or outpatient setting, causing distress for both the staff and patient. Because no 2 personalities are identical, there is no algorithm for managing patients with personality disorders. However, there are strategies that we can apply to provide effective clinical care.1,2

Discuss the responses the patient evokes. Patients with personality disorders can elicit strong responses from the treatment team. Each clinician can have a different response to the same patient, ranging from feeling the need to protect the patient to strongly disliking him or her. Because cohesion among staff is essential for effective patient care, we need to discuss these responses in an open forum with our team members so we can effectively manage our responses and provide the patient with consistent interactions. Limiting the delivery of inconsistent or conflicting messages will decrease staff splitting and increase team unity.

Reinforce appropriate behaviors. Patients with personality disorders usually have negative interpersonal interactions, such as acting out, misinterpreting neutral social cues, and seeking constant attention. However, when they are not engaging in detrimental behaviors, we should provide positive reinforcement for appropriate behaviors, such as remaining composed, that help maintain the treatment relationship. When a patient displays disruptive behaviors, take a neutral approach by stating, “You appear upset. I will come back later when you are feeling better.”1

Set limits. These patients are likely to have difficulty conforming to appropriate social boundaries. Our reflex reaction may be to set concrete rules that fit our preferences. This could lead to a power struggle between us and our patients, which is not helpful. Rather than a “one-size-fits-all” approach to rules, it may be prudent to tailor boundaries according to each patient’s unique personality. Also, allowing the patient to help set these limits could increase the chances that he or she will follow your treatment plan and reinforce the more positive aspects of his or her person­ality structure.

Offer empathy. Empathy can be conceptualized as a step further than sympathy; in addition to expressing concern and compassion, empathy involves recognizing and sharing the patient’s emotions. Seek to comprehend the reasons behind a patient’s negative reactions by identifying and understanding his or her feelings. Empathy also can help us avoid further resistance by considering what is appropriate to say to patients.

References

1. Riddle M, Meeks T, Alvarez C, et al. When personality is the problem: managing patients with difficult personalitie s on the acute care unit. J Hosp Med. 2016;11(12):873-878.
2. Strous RD, Ulman AM, Kotler M. The hateful patient revisited: relevance for 21st century medicine. Eur J Intern Med. 2006;17(6):387-393.

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Dr. Joshi is Associate Professor of Clinical Psychiatry and Associate Director, Forensic Psychiatry Fellowship, Department of Neuropsychiatry and Behavioral Science, University of South Carolina School of Medicine, Columbia, South Carolina.

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The author reports no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

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Dr. Joshi is Associate Professor of Clinical Psychiatry and Associate Director, Forensic Psychiatry Fellowship, Department of Neuropsychiatry and Behavioral Science, University of South Carolina School of Medicine, Columbia, South Carolina.

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Patients with personality disorders can disrupt the treatment relationship, and may leave us feeling angry, ineffective, inadequate, and defeated. Although their behaviors may appear volitional and purposeful, they often are the result of a dysfunctional personality structure.1 These patients’ unbending patterns of viewing themselves, interacting with others, and navigating the world can be problematic in an inpatient or outpatient setting, causing distress for both the staff and patient. Because no 2 personalities are identical, there is no algorithm for managing patients with personality disorders. However, there are strategies that we can apply to provide effective clinical care.1,2

Discuss the responses the patient evokes. Patients with personality disorders can elicit strong responses from the treatment team. Each clinician can have a different response to the same patient, ranging from feeling the need to protect the patient to strongly disliking him or her. Because cohesion among staff is essential for effective patient care, we need to discuss these responses in an open forum with our team members so we can effectively manage our responses and provide the patient with consistent interactions. Limiting the delivery of inconsistent or conflicting messages will decrease staff splitting and increase team unity.

Reinforce appropriate behaviors. Patients with personality disorders usually have negative interpersonal interactions, such as acting out, misinterpreting neutral social cues, and seeking constant attention. However, when they are not engaging in detrimental behaviors, we should provide positive reinforcement for appropriate behaviors, such as remaining composed, that help maintain the treatment relationship. When a patient displays disruptive behaviors, take a neutral approach by stating, “You appear upset. I will come back later when you are feeling better.”1

Set limits. These patients are likely to have difficulty conforming to appropriate social boundaries. Our reflex reaction may be to set concrete rules that fit our preferences. This could lead to a power struggle between us and our patients, which is not helpful. Rather than a “one-size-fits-all” approach to rules, it may be prudent to tailor boundaries according to each patient’s unique personality. Also, allowing the patient to help set these limits could increase the chances that he or she will follow your treatment plan and reinforce the more positive aspects of his or her person­ality structure.

Offer empathy. Empathy can be conceptualized as a step further than sympathy; in addition to expressing concern and compassion, empathy involves recognizing and sharing the patient’s emotions. Seek to comprehend the reasons behind a patient’s negative reactions by identifying and understanding his or her feelings. Empathy also can help us avoid further resistance by considering what is appropriate to say to patients.

Patients with personality disorders can disrupt the treatment relationship, and may leave us feeling angry, ineffective, inadequate, and defeated. Although their behaviors may appear volitional and purposeful, they often are the result of a dysfunctional personality structure.1 These patients’ unbending patterns of viewing themselves, interacting with others, and navigating the world can be problematic in an inpatient or outpatient setting, causing distress for both the staff and patient. Because no 2 personalities are identical, there is no algorithm for managing patients with personality disorders. However, there are strategies that we can apply to provide effective clinical care.1,2

Discuss the responses the patient evokes. Patients with personality disorders can elicit strong responses from the treatment team. Each clinician can have a different response to the same patient, ranging from feeling the need to protect the patient to strongly disliking him or her. Because cohesion among staff is essential for effective patient care, we need to discuss these responses in an open forum with our team members so we can effectively manage our responses and provide the patient with consistent interactions. Limiting the delivery of inconsistent or conflicting messages will decrease staff splitting and increase team unity.

Reinforce appropriate behaviors. Patients with personality disorders usually have negative interpersonal interactions, such as acting out, misinterpreting neutral social cues, and seeking constant attention. However, when they are not engaging in detrimental behaviors, we should provide positive reinforcement for appropriate behaviors, such as remaining composed, that help maintain the treatment relationship. When a patient displays disruptive behaviors, take a neutral approach by stating, “You appear upset. I will come back later when you are feeling better.”1

Set limits. These patients are likely to have difficulty conforming to appropriate social boundaries. Our reflex reaction may be to set concrete rules that fit our preferences. This could lead to a power struggle between us and our patients, which is not helpful. Rather than a “one-size-fits-all” approach to rules, it may be prudent to tailor boundaries according to each patient’s unique personality. Also, allowing the patient to help set these limits could increase the chances that he or she will follow your treatment plan and reinforce the more positive aspects of his or her person­ality structure.

Offer empathy. Empathy can be conceptualized as a step further than sympathy; in addition to expressing concern and compassion, empathy involves recognizing and sharing the patient’s emotions. Seek to comprehend the reasons behind a patient’s negative reactions by identifying and understanding his or her feelings. Empathy also can help us avoid further resistance by considering what is appropriate to say to patients.

References

1. Riddle M, Meeks T, Alvarez C, et al. When personality is the problem: managing patients with difficult personalitie s on the acute care unit. J Hosp Med. 2016;11(12):873-878.
2. Strous RD, Ulman AM, Kotler M. The hateful patient revisited: relevance for 21st century medicine. Eur J Intern Med. 2006;17(6):387-393.

References

1. Riddle M, Meeks T, Alvarez C, et al. When personality is the problem: managing patients with difficult personalitie s on the acute care unit. J Hosp Med. 2016;11(12):873-878.
2. Strous RD, Ulman AM, Kotler M. The hateful patient revisited: relevance for 21st century medicine. Eur J Intern Med. 2006;17(6):387-393.

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Goldwater Rule should be modified, debate audience at The College agrees

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TAMPA, FLA. – Most psychiatrists believe that the so-called “Goldwater Rule” should be amended if an informal poll conducted at the annual meeting of the American College of Psychiatrists reflects dominant opinion.

The poll was conducted at the end of a debate between Nada L. Stotland, MD, who argued for no change, and Steven S. Sharfstein, MD, who argued that the ethical standard may have made sense when created in 1973 “but is now outmoded.”

Ted Bosworth/Frontline Medical News
Dr. Nada L. Stotland (left) and Dr. Steven S. Sharfstein

The American Psychiatric Association introduced what is widely known as the Goldwater Rule into the APA code of ethics following an infamous survey of psychiatrists published in 1964. In that survey, the respondents overwhelmingly expressed the opinion that Barry Goldwater, the Arizona senator and 1964 candidate for president of the United States, was unfit to serve, an outcome that many considered an embarrassment for the APA.

As written, the ethical standard introduced by the APA proscribes psychiatrists from pronouncing a diagnosis of mental illness in public figures who they have not examined. The standard was later amended to disallow any professional opinion on mental health in public figures, not just a diagnosis.

This standard, always controversial, has been increasingly challenged as a result of concerns expressed frequently in public forums about the mental health of the current president. The moderator of the debate, John M. Oldman, MD, chair for personality disorders in the department of psychiatry and behavioral sciences at Baylor College of Medicine, Houston, commented that President Donald Trump “may be the death of the Goldwater rule.”

Even though not all agreed that a psychiatric diagnosis requires a face-to-face evaluation, the debate centered on the justification for banning psychiatrists from offering any opinion about the mental health of a public figure. Can an opinion be justified on the basis of First Amendment guarantees of free speech if the speaker identifies him or herself as a psychiatrist?

Dr. Sharfstein, who is president emeritus, Sheppard Pratt Health System, Baltimore, concluded that this prohibition is too far reaching. By his interpretation, psychiatrists who call a public figure “a jerk” are potentially violating the Goldwater Rule. Although he conceded that he is sensitive to the etiquette of demeaning public figures when speaking in the capacity of a psychiatrist, he said that banning the expression of opinions “is unenforceable.”

Dr. Stotland, professor of psychiatry at Rush Medical College, Chicago, disagreed. She argued that comments on mental health status expressed by a psychiatrist carry different weight than other citizens. Like boxers, whose fists are considered legal weapons in some states, a psychiatrist “should give up the right to express casual opinions” about psychopathology in a public figure, she said.

As professional opinions will almost certainly differ between psychiatrists, Dr. Stotland also suggested that an inevitable variety of opinions expressed by different psychiatrists about a public figure is not likely to contribute usefully to the general discourse. “Dissension in our public remarks undermines the credibility of our profession,” she said.

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TAMPA, FLA. – Most psychiatrists believe that the so-called “Goldwater Rule” should be amended if an informal poll conducted at the annual meeting of the American College of Psychiatrists reflects dominant opinion.

The poll was conducted at the end of a debate between Nada L. Stotland, MD, who argued for no change, and Steven S. Sharfstein, MD, who argued that the ethical standard may have made sense when created in 1973 “but is now outmoded.”

Ted Bosworth/Frontline Medical News
Dr. Nada L. Stotland (left) and Dr. Steven S. Sharfstein

The American Psychiatric Association introduced what is widely known as the Goldwater Rule into the APA code of ethics following an infamous survey of psychiatrists published in 1964. In that survey, the respondents overwhelmingly expressed the opinion that Barry Goldwater, the Arizona senator and 1964 candidate for president of the United States, was unfit to serve, an outcome that many considered an embarrassment for the APA.

As written, the ethical standard introduced by the APA proscribes psychiatrists from pronouncing a diagnosis of mental illness in public figures who they have not examined. The standard was later amended to disallow any professional opinion on mental health in public figures, not just a diagnosis.

This standard, always controversial, has been increasingly challenged as a result of concerns expressed frequently in public forums about the mental health of the current president. The moderator of the debate, John M. Oldman, MD, chair for personality disorders in the department of psychiatry and behavioral sciences at Baylor College of Medicine, Houston, commented that President Donald Trump “may be the death of the Goldwater rule.”

Even though not all agreed that a psychiatric diagnosis requires a face-to-face evaluation, the debate centered on the justification for banning psychiatrists from offering any opinion about the mental health of a public figure. Can an opinion be justified on the basis of First Amendment guarantees of free speech if the speaker identifies him or herself as a psychiatrist?

Dr. Sharfstein, who is president emeritus, Sheppard Pratt Health System, Baltimore, concluded that this prohibition is too far reaching. By his interpretation, psychiatrists who call a public figure “a jerk” are potentially violating the Goldwater Rule. Although he conceded that he is sensitive to the etiquette of demeaning public figures when speaking in the capacity of a psychiatrist, he said that banning the expression of opinions “is unenforceable.”

Dr. Stotland, professor of psychiatry at Rush Medical College, Chicago, disagreed. She argued that comments on mental health status expressed by a psychiatrist carry different weight than other citizens. Like boxers, whose fists are considered legal weapons in some states, a psychiatrist “should give up the right to express casual opinions” about psychopathology in a public figure, she said.

As professional opinions will almost certainly differ between psychiatrists, Dr. Stotland also suggested that an inevitable variety of opinions expressed by different psychiatrists about a public figure is not likely to contribute usefully to the general discourse. “Dissension in our public remarks undermines the credibility of our profession,” she said.

 

TAMPA, FLA. – Most psychiatrists believe that the so-called “Goldwater Rule” should be amended if an informal poll conducted at the annual meeting of the American College of Psychiatrists reflects dominant opinion.

The poll was conducted at the end of a debate between Nada L. Stotland, MD, who argued for no change, and Steven S. Sharfstein, MD, who argued that the ethical standard may have made sense when created in 1973 “but is now outmoded.”

Ted Bosworth/Frontline Medical News
Dr. Nada L. Stotland (left) and Dr. Steven S. Sharfstein

The American Psychiatric Association introduced what is widely known as the Goldwater Rule into the APA code of ethics following an infamous survey of psychiatrists published in 1964. In that survey, the respondents overwhelmingly expressed the opinion that Barry Goldwater, the Arizona senator and 1964 candidate for president of the United States, was unfit to serve, an outcome that many considered an embarrassment for the APA.

As written, the ethical standard introduced by the APA proscribes psychiatrists from pronouncing a diagnosis of mental illness in public figures who they have not examined. The standard was later amended to disallow any professional opinion on mental health in public figures, not just a diagnosis.

This standard, always controversial, has been increasingly challenged as a result of concerns expressed frequently in public forums about the mental health of the current president. The moderator of the debate, John M. Oldman, MD, chair for personality disorders in the department of psychiatry and behavioral sciences at Baylor College of Medicine, Houston, commented that President Donald Trump “may be the death of the Goldwater rule.”

Even though not all agreed that a psychiatric diagnosis requires a face-to-face evaluation, the debate centered on the justification for banning psychiatrists from offering any opinion about the mental health of a public figure. Can an opinion be justified on the basis of First Amendment guarantees of free speech if the speaker identifies him or herself as a psychiatrist?

Dr. Sharfstein, who is president emeritus, Sheppard Pratt Health System, Baltimore, concluded that this prohibition is too far reaching. By his interpretation, psychiatrists who call a public figure “a jerk” are potentially violating the Goldwater Rule. Although he conceded that he is sensitive to the etiquette of demeaning public figures when speaking in the capacity of a psychiatrist, he said that banning the expression of opinions “is unenforceable.”

Dr. Stotland, professor of psychiatry at Rush Medical College, Chicago, disagreed. She argued that comments on mental health status expressed by a psychiatrist carry different weight than other citizens. Like boxers, whose fists are considered legal weapons in some states, a psychiatrist “should give up the right to express casual opinions” about psychopathology in a public figure, she said.

As professional opinions will almost certainly differ between psychiatrists, Dr. Stotland also suggested that an inevitable variety of opinions expressed by different psychiatrists about a public figure is not likely to contribute usefully to the general discourse. “Dissension in our public remarks undermines the credibility of our profession,” she said.

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The stigma toward BPD

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In response to Dr. Mark Zimmerman’s article, “Improving the recognition of borderline personality disorder” (Current Psychiatry. October 2017, p. 13-19), I think the topic of improving the diagnosis of borderline personality disorder (BPD) requires us to examine our own biases and stigma toward this diagnosis. Let’s be honest: many psychiatrists don’t make the diagnosis because they don’t want to give their patient that diagnosis and they don’t want to treat a patient with that diagnosis. Evidence suggests that a great proportion of stigma aimed at BPD is initiated by mental health professionals.1,2

Why all the stigma? Because mental health professionals don’t have complete information. The assumption used to be that BPD was “intractable” with no treatment. Even if this were true, it still would not be a reason to fail to disclose a diagnosis, because in other fields of medicine, the concept of “therapeutic privilege” fell by the wayside long ago. However, we now know that in many individuals with BPD, symptoms improve over time, and there are several effective treatments.

In DSM-II, published in 1968, obsessive-compulsive disorder (OCD) was characterized as an “obsessive compulsive neurosis.” It was not reclassified as the current OCD diagnosis until DSM-III-R was published in 1987, after the FDA approved clomipramine. Why is this important? Because once people realized that there was a treatment, they started acknowledging OCD more often.

The first step in addressing the stigma toward BPD is that mental health professionals must recognize their own bias toward this diagnosis. We must be re-educated that this diagnosis carries hope, symptoms improve, and that there are effective treatments. This is how professionals will increase the recognition of BPD.

Michael Shapiro, MD, FAPA
Assistant Professor and Compliance Officer
Department of Psychiatry
University of Florida
Clinic Director
UF Child and Adolescent Psychiatry Clinic at Springhill Health Center
Gainesville, Florida

References

1. Unruh BT, Gunderson JG. “Good enough” psychiatric residency training in borderline personality disorder: challenges, choice points, and a model generalist curriculum. Harv Rev Psychiatry. 2016;24(5):367-377.
2. Sheehan L, Nieweglowski K, Corrigan P. The stigma of personality disorders. Curr Psychiatry Rep. 2016;18(1):11.

Continue to: The author responds

 

 

 

The author responds

I agree with Dr. Shapiro that stigma by mental health clinicians contributes to the underdiagnosis of BPD. Mental health professions often hold a negative view of patients with personality disorders, particularly those with BPD, and see these patients as being more difficult to treat.1-3 They are the patients that some clinicians are reluctant to treat.3,4 Clinicians perceive patients with personality disorders as less mentally ill, more manipulative, and more able to control their behavior than patients with other psychiatric disorders.3,5 Consistent with this, clinicians have less sympathetic attitudes and behave less empathically toward patients with BPD.5,6 The term “borderline” also is sometimes used pejoratively to describe patients.1

As I described in my article, there are several possible reasons BPD is under­diagnosed. Foremost is that mood disorders, anxiety disorders, and substance use disorders are common in patients with BPD, and the symptoms of these other disorders are typically patients’ chief concerns when they present for treatment. Patients with BPD do not usually report the features of BPD—such as abandonment fears, chronic feelings of emptiness, or an identity disturbance—as their chief concerns. If they did, BPD would likely be easier to recognize. On a related note, clinicians do not have the time, or do not take the time, to conduct a thorough enough evaluation to diagnose BPD when it occurs in a patient who presents for treatment of a mood disorder, anxiety disorder, or substance use disorder. Our clinical research group found that when psychiatrists are presented with the results of a semi-structured interview, BPD is much more frequently diagnosed.7 Such a finding would not be expected if stigma was the primary or sole reason for underdiagnosis.

Dr. Shapiro highlights the clinical consequence of underrecognition and underdiagnosis: the underutilization of empirically supported psychotherapies for BPD. A corollary of underdiagnosing BPD is overdiagnosis of bipolar disorder and overprescription of medication.8

There are other consequences of bias and stigma toward BPD. Despite the high levels of psychosocial morbidity, reduced health-related quality of life, high utilization of services, and excess mortality associated with BPD, this disorder is not included in the Global Burden of Disease Study. Thus, the public health significance of BPD is less fully appreciated. Finally, there is evidence that the level of funding for research from the National Institutes of Health is not commensurate with the level of psychosocial morbidity, mortality, and health expenditures associated with the disorder.9 Thus, the stigma toward BPD exists in both clinical and research communities.

Mark Zimmerman, MD
Professor of Psychiatry and Human Behavior
Warren Alpert Medical School of Brown University
Rhode Island Hospital
Providence, Rhode Island

References

1. Cleary M, Siegfried N, Walter G. Experience, knowledge and attitudes of mental health staff regarding clients with a borderline personality disorder. Int J Ment Health Nurs. 2002;11(3):186-191.
2. Gallop R, Lancee WJ, Garfinkel P. How nursing staff respond to the label “borderline personality disorder.” Hosp Community Psychiatry. 1989;40(8):815-819.
3. Lewis G, Appleby L. Personality disorder: the patients psychiatrists dislike. Br J Psychiatry. 1988;153:44-49.
4. Black DW, Pfohl B, Blum N, et al. Attitudes toward borderline personality disorder: a survey of 706 mental health clinicians. CNS Spectr. 2011;16(3):67-74.
5. Markham D, Trower P. The effects of the psychiatric label ‘borderline personality disorder’ on nursing staff’s perceptions and causal attributions for challenging behaviours. Br J Clin Psychol. 2003;42(pt 3):243-256.
6. Fraser K, Gallop R. Nurses’ confirming/disconfirming responses to patients diagnosed with borderline personality disorder. Arch Psychiatr Nurs. 1993;7(6):336-341.
7. Zimmerman M, Mattia JI. Differences between clinical and research practices in diagnosing borderline personality disorder. Am J Psychiatry. 1999;156(10):1570-1574.
8. Zimmerman M, Ruggero CJ, Chelminski I, et al. Is bipolar disorder overdiagnosed? J Clin Psychiatry. 2008;69(6):935-940.
9. Zimmerman M, Gazarian D. Is research on borderline personality disorder underfunded by the National Institute of Health? Psychiatry Res. 2014;220(3):941-944.

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In response to Dr. Mark Zimmerman’s article, “Improving the recognition of borderline personality disorder” (Current Psychiatry. October 2017, p. 13-19), I think the topic of improving the diagnosis of borderline personality disorder (BPD) requires us to examine our own biases and stigma toward this diagnosis. Let’s be honest: many psychiatrists don’t make the diagnosis because they don’t want to give their patient that diagnosis and they don’t want to treat a patient with that diagnosis. Evidence suggests that a great proportion of stigma aimed at BPD is initiated by mental health professionals.1,2

Why all the stigma? Because mental health professionals don’t have complete information. The assumption used to be that BPD was “intractable” with no treatment. Even if this were true, it still would not be a reason to fail to disclose a diagnosis, because in other fields of medicine, the concept of “therapeutic privilege” fell by the wayside long ago. However, we now know that in many individuals with BPD, symptoms improve over time, and there are several effective treatments.

In DSM-II, published in 1968, obsessive-compulsive disorder (OCD) was characterized as an “obsessive compulsive neurosis.” It was not reclassified as the current OCD diagnosis until DSM-III-R was published in 1987, after the FDA approved clomipramine. Why is this important? Because once people realized that there was a treatment, they started acknowledging OCD more often.

The first step in addressing the stigma toward BPD is that mental health professionals must recognize their own bias toward this diagnosis. We must be re-educated that this diagnosis carries hope, symptoms improve, and that there are effective treatments. This is how professionals will increase the recognition of BPD.

Michael Shapiro, MD, FAPA
Assistant Professor and Compliance Officer
Department of Psychiatry
University of Florida
Clinic Director
UF Child and Adolescent Psychiatry Clinic at Springhill Health Center
Gainesville, Florida

References

1. Unruh BT, Gunderson JG. “Good enough” psychiatric residency training in borderline personality disorder: challenges, choice points, and a model generalist curriculum. Harv Rev Psychiatry. 2016;24(5):367-377.
2. Sheehan L, Nieweglowski K, Corrigan P. The stigma of personality disorders. Curr Psychiatry Rep. 2016;18(1):11.

Continue to: The author responds

 

 

 

The author responds

I agree with Dr. Shapiro that stigma by mental health clinicians contributes to the underdiagnosis of BPD. Mental health professions often hold a negative view of patients with personality disorders, particularly those with BPD, and see these patients as being more difficult to treat.1-3 They are the patients that some clinicians are reluctant to treat.3,4 Clinicians perceive patients with personality disorders as less mentally ill, more manipulative, and more able to control their behavior than patients with other psychiatric disorders.3,5 Consistent with this, clinicians have less sympathetic attitudes and behave less empathically toward patients with BPD.5,6 The term “borderline” also is sometimes used pejoratively to describe patients.1

As I described in my article, there are several possible reasons BPD is under­diagnosed. Foremost is that mood disorders, anxiety disorders, and substance use disorders are common in patients with BPD, and the symptoms of these other disorders are typically patients’ chief concerns when they present for treatment. Patients with BPD do not usually report the features of BPD—such as abandonment fears, chronic feelings of emptiness, or an identity disturbance—as their chief concerns. If they did, BPD would likely be easier to recognize. On a related note, clinicians do not have the time, or do not take the time, to conduct a thorough enough evaluation to diagnose BPD when it occurs in a patient who presents for treatment of a mood disorder, anxiety disorder, or substance use disorder. Our clinical research group found that when psychiatrists are presented with the results of a semi-structured interview, BPD is much more frequently diagnosed.7 Such a finding would not be expected if stigma was the primary or sole reason for underdiagnosis.

Dr. Shapiro highlights the clinical consequence of underrecognition and underdiagnosis: the underutilization of empirically supported psychotherapies for BPD. A corollary of underdiagnosing BPD is overdiagnosis of bipolar disorder and overprescription of medication.8

There are other consequences of bias and stigma toward BPD. Despite the high levels of psychosocial morbidity, reduced health-related quality of life, high utilization of services, and excess mortality associated with BPD, this disorder is not included in the Global Burden of Disease Study. Thus, the public health significance of BPD is less fully appreciated. Finally, there is evidence that the level of funding for research from the National Institutes of Health is not commensurate with the level of psychosocial morbidity, mortality, and health expenditures associated with the disorder.9 Thus, the stigma toward BPD exists in both clinical and research communities.

Mark Zimmerman, MD
Professor of Psychiatry and Human Behavior
Warren Alpert Medical School of Brown University
Rhode Island Hospital
Providence, Rhode Island

References

1. Cleary M, Siegfried N, Walter G. Experience, knowledge and attitudes of mental health staff regarding clients with a borderline personality disorder. Int J Ment Health Nurs. 2002;11(3):186-191.
2. Gallop R, Lancee WJ, Garfinkel P. How nursing staff respond to the label “borderline personality disorder.” Hosp Community Psychiatry. 1989;40(8):815-819.
3. Lewis G, Appleby L. Personality disorder: the patients psychiatrists dislike. Br J Psychiatry. 1988;153:44-49.
4. Black DW, Pfohl B, Blum N, et al. Attitudes toward borderline personality disorder: a survey of 706 mental health clinicians. CNS Spectr. 2011;16(3):67-74.
5. Markham D, Trower P. The effects of the psychiatric label ‘borderline personality disorder’ on nursing staff’s perceptions and causal attributions for challenging behaviours. Br J Clin Psychol. 2003;42(pt 3):243-256.
6. Fraser K, Gallop R. Nurses’ confirming/disconfirming responses to patients diagnosed with borderline personality disorder. Arch Psychiatr Nurs. 1993;7(6):336-341.
7. Zimmerman M, Mattia JI. Differences between clinical and research practices in diagnosing borderline personality disorder. Am J Psychiatry. 1999;156(10):1570-1574.
8. Zimmerman M, Ruggero CJ, Chelminski I, et al. Is bipolar disorder overdiagnosed? J Clin Psychiatry. 2008;69(6):935-940.
9. Zimmerman M, Gazarian D. Is research on borderline personality disorder underfunded by the National Institute of Health? Psychiatry Res. 2014;220(3):941-944.

 

In response to Dr. Mark Zimmerman’s article, “Improving the recognition of borderline personality disorder” (Current Psychiatry. October 2017, p. 13-19), I think the topic of improving the diagnosis of borderline personality disorder (BPD) requires us to examine our own biases and stigma toward this diagnosis. Let’s be honest: many psychiatrists don’t make the diagnosis because they don’t want to give their patient that diagnosis and they don’t want to treat a patient with that diagnosis. Evidence suggests that a great proportion of stigma aimed at BPD is initiated by mental health professionals.1,2

Why all the stigma? Because mental health professionals don’t have complete information. The assumption used to be that BPD was “intractable” with no treatment. Even if this were true, it still would not be a reason to fail to disclose a diagnosis, because in other fields of medicine, the concept of “therapeutic privilege” fell by the wayside long ago. However, we now know that in many individuals with BPD, symptoms improve over time, and there are several effective treatments.

In DSM-II, published in 1968, obsessive-compulsive disorder (OCD) was characterized as an “obsessive compulsive neurosis.” It was not reclassified as the current OCD diagnosis until DSM-III-R was published in 1987, after the FDA approved clomipramine. Why is this important? Because once people realized that there was a treatment, they started acknowledging OCD more often.

The first step in addressing the stigma toward BPD is that mental health professionals must recognize their own bias toward this diagnosis. We must be re-educated that this diagnosis carries hope, symptoms improve, and that there are effective treatments. This is how professionals will increase the recognition of BPD.

Michael Shapiro, MD, FAPA
Assistant Professor and Compliance Officer
Department of Psychiatry
University of Florida
Clinic Director
UF Child and Adolescent Psychiatry Clinic at Springhill Health Center
Gainesville, Florida

References

1. Unruh BT, Gunderson JG. “Good enough” psychiatric residency training in borderline personality disorder: challenges, choice points, and a model generalist curriculum. Harv Rev Psychiatry. 2016;24(5):367-377.
2. Sheehan L, Nieweglowski K, Corrigan P. The stigma of personality disorders. Curr Psychiatry Rep. 2016;18(1):11.

Continue to: The author responds

 

 

 

The author responds

I agree with Dr. Shapiro that stigma by mental health clinicians contributes to the underdiagnosis of BPD. Mental health professions often hold a negative view of patients with personality disorders, particularly those with BPD, and see these patients as being more difficult to treat.1-3 They are the patients that some clinicians are reluctant to treat.3,4 Clinicians perceive patients with personality disorders as less mentally ill, more manipulative, and more able to control their behavior than patients with other psychiatric disorders.3,5 Consistent with this, clinicians have less sympathetic attitudes and behave less empathically toward patients with BPD.5,6 The term “borderline” also is sometimes used pejoratively to describe patients.1

As I described in my article, there are several possible reasons BPD is under­diagnosed. Foremost is that mood disorders, anxiety disorders, and substance use disorders are common in patients with BPD, and the symptoms of these other disorders are typically patients’ chief concerns when they present for treatment. Patients with BPD do not usually report the features of BPD—such as abandonment fears, chronic feelings of emptiness, or an identity disturbance—as their chief concerns. If they did, BPD would likely be easier to recognize. On a related note, clinicians do not have the time, or do not take the time, to conduct a thorough enough evaluation to diagnose BPD when it occurs in a patient who presents for treatment of a mood disorder, anxiety disorder, or substance use disorder. Our clinical research group found that when psychiatrists are presented with the results of a semi-structured interview, BPD is much more frequently diagnosed.7 Such a finding would not be expected if stigma was the primary or sole reason for underdiagnosis.

Dr. Shapiro highlights the clinical consequence of underrecognition and underdiagnosis: the underutilization of empirically supported psychotherapies for BPD. A corollary of underdiagnosing BPD is overdiagnosis of bipolar disorder and overprescription of medication.8

There are other consequences of bias and stigma toward BPD. Despite the high levels of psychosocial morbidity, reduced health-related quality of life, high utilization of services, and excess mortality associated with BPD, this disorder is not included in the Global Burden of Disease Study. Thus, the public health significance of BPD is less fully appreciated. Finally, there is evidence that the level of funding for research from the National Institutes of Health is not commensurate with the level of psychosocial morbidity, mortality, and health expenditures associated with the disorder.9 Thus, the stigma toward BPD exists in both clinical and research communities.

Mark Zimmerman, MD
Professor of Psychiatry and Human Behavior
Warren Alpert Medical School of Brown University
Rhode Island Hospital
Providence, Rhode Island

References

1. Cleary M, Siegfried N, Walter G. Experience, knowledge and attitudes of mental health staff regarding clients with a borderline personality disorder. Int J Ment Health Nurs. 2002;11(3):186-191.
2. Gallop R, Lancee WJ, Garfinkel P. How nursing staff respond to the label “borderline personality disorder.” Hosp Community Psychiatry. 1989;40(8):815-819.
3. Lewis G, Appleby L. Personality disorder: the patients psychiatrists dislike. Br J Psychiatry. 1988;153:44-49.
4. Black DW, Pfohl B, Blum N, et al. Attitudes toward borderline personality disorder: a survey of 706 mental health clinicians. CNS Spectr. 2011;16(3):67-74.
5. Markham D, Trower P. The effects of the psychiatric label ‘borderline personality disorder’ on nursing staff’s perceptions and causal attributions for challenging behaviours. Br J Clin Psychol. 2003;42(pt 3):243-256.
6. Fraser K, Gallop R. Nurses’ confirming/disconfirming responses to patients diagnosed with borderline personality disorder. Arch Psychiatr Nurs. 1993;7(6):336-341.
7. Zimmerman M, Mattia JI. Differences between clinical and research practices in diagnosing borderline personality disorder. Am J Psychiatry. 1999;156(10):1570-1574.
8. Zimmerman M, Ruggero CJ, Chelminski I, et al. Is bipolar disorder overdiagnosed? J Clin Psychiatry. 2008;69(6):935-940.
9. Zimmerman M, Gazarian D. Is research on borderline personality disorder underfunded by the National Institute of Health? Psychiatry Res. 2014;220(3):941-944.

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Inhaled loxapine quells agitation in personality disorders

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– The inhaled powder formulation of loxapine appears to be a safe and effective treatment for acute agitation in patients with personality disorders, Diego R. Mendez Mareque, MD, reported at the annual congress of the European College of Neuropsychopharmacology.

Inhaled loxapine is approved for the treatment of acute agitation associated with schizophrenia or bipolar I disorder. Its use in patients with borderline personality and other personality disorders is off label. But this inhaled typical antipsychotic shows promise in filling an unmet need for a rapid-acting, minimally invasive treatment for acute agitation in patients with personality disorders, a very common scenario in psychiatric wards and emergency departments, and one that can quickly escalate to aggression and violence, noted Dr. Mendez Mareque of the Galician Health Service in Ferrol, Spain.

He presented a prospective, longitudinal, observational pilot study of 14 patients with personality disorders treated with a single 10-mg dose of inhaled loxapine while experiencing acute agitation in a psychiatric emergency department or psychiatric ward. Their mean baseline score on the Excited Component of the Positive and Negative Syndrome Scale (PANSS-EC) was 20.8 out of a possible 35 points. The scale assesses five domains: excitement, tension, uncooperativeness, hostility, and poor impulse control.

Within 10 minutes after administration of inhaled loxapine by a health care professional, 11 patients showed a significant drop on the PANSS-EC. They were calm, nonsedated, and ready for assessment. Within 20 minutes, their PANSS-EC scores were reduced by roughly half, compared with baseline.

Three patients were nonresponders. They received rescue treatment with oral or injectable antipsychotics and benzodiazepines.

None of the 14 patients had a history of airway disease, and none experienced bronchospasm, a known possible side effect of inhaled loxapine, the psychiatrist noted.

The results of this Spanish observational study confirm the benefits of inhaled loxapine for treating agitation in patients with borderline personality disorder previously described in a German case series (J Clin Psychopharmacol. 2015 Dec;35[6]:741-3).

Dr. Mendez Mareque reported having no financial conflicts of interest regarding his study.

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– The inhaled powder formulation of loxapine appears to be a safe and effective treatment for acute agitation in patients with personality disorders, Diego R. Mendez Mareque, MD, reported at the annual congress of the European College of Neuropsychopharmacology.

Inhaled loxapine is approved for the treatment of acute agitation associated with schizophrenia or bipolar I disorder. Its use in patients with borderline personality and other personality disorders is off label. But this inhaled typical antipsychotic shows promise in filling an unmet need for a rapid-acting, minimally invasive treatment for acute agitation in patients with personality disorders, a very common scenario in psychiatric wards and emergency departments, and one that can quickly escalate to aggression and violence, noted Dr. Mendez Mareque of the Galician Health Service in Ferrol, Spain.

He presented a prospective, longitudinal, observational pilot study of 14 patients with personality disorders treated with a single 10-mg dose of inhaled loxapine while experiencing acute agitation in a psychiatric emergency department or psychiatric ward. Their mean baseline score on the Excited Component of the Positive and Negative Syndrome Scale (PANSS-EC) was 20.8 out of a possible 35 points. The scale assesses five domains: excitement, tension, uncooperativeness, hostility, and poor impulse control.

Within 10 minutes after administration of inhaled loxapine by a health care professional, 11 patients showed a significant drop on the PANSS-EC. They were calm, nonsedated, and ready for assessment. Within 20 minutes, their PANSS-EC scores were reduced by roughly half, compared with baseline.

Three patients were nonresponders. They received rescue treatment with oral or injectable antipsychotics and benzodiazepines.

None of the 14 patients had a history of airway disease, and none experienced bronchospasm, a known possible side effect of inhaled loxapine, the psychiatrist noted.

The results of this Spanish observational study confirm the benefits of inhaled loxapine for treating agitation in patients with borderline personality disorder previously described in a German case series (J Clin Psychopharmacol. 2015 Dec;35[6]:741-3).

Dr. Mendez Mareque reported having no financial conflicts of interest regarding his study.

 

– The inhaled powder formulation of loxapine appears to be a safe and effective treatment for acute agitation in patients with personality disorders, Diego R. Mendez Mareque, MD, reported at the annual congress of the European College of Neuropsychopharmacology.

Inhaled loxapine is approved for the treatment of acute agitation associated with schizophrenia or bipolar I disorder. Its use in patients with borderline personality and other personality disorders is off label. But this inhaled typical antipsychotic shows promise in filling an unmet need for a rapid-acting, minimally invasive treatment for acute agitation in patients with personality disorders, a very common scenario in psychiatric wards and emergency departments, and one that can quickly escalate to aggression and violence, noted Dr. Mendez Mareque of the Galician Health Service in Ferrol, Spain.

He presented a prospective, longitudinal, observational pilot study of 14 patients with personality disorders treated with a single 10-mg dose of inhaled loxapine while experiencing acute agitation in a psychiatric emergency department or psychiatric ward. Their mean baseline score on the Excited Component of the Positive and Negative Syndrome Scale (PANSS-EC) was 20.8 out of a possible 35 points. The scale assesses five domains: excitement, tension, uncooperativeness, hostility, and poor impulse control.

Within 10 minutes after administration of inhaled loxapine by a health care professional, 11 patients showed a significant drop on the PANSS-EC. They were calm, nonsedated, and ready for assessment. Within 20 minutes, their PANSS-EC scores were reduced by roughly half, compared with baseline.

Three patients were nonresponders. They received rescue treatment with oral or injectable antipsychotics and benzodiazepines.

None of the 14 patients had a history of airway disease, and none experienced bronchospasm, a known possible side effect of inhaled loxapine, the psychiatrist noted.

The results of this Spanish observational study confirm the benefits of inhaled loxapine for treating agitation in patients with borderline personality disorder previously described in a German case series (J Clin Psychopharmacol. 2015 Dec;35[6]:741-3).

Dr. Mendez Mareque reported having no financial conflicts of interest regarding his study.

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Key clinical point: Inhaled loxapine appears to offer a novel safe and effective option for treatment of acute agitation in patients with personality disorders.

Major finding: Eleven of 14 acutely agitated patients with various personality disorders were calm, nonsedated, and ready for assessment within 10 minutes after a single dose of inhaled loxapine.

Data source: A prospective observational pilot study of inhaled loxapine in 14 acutely agitated patients with personality disorders.

Disclosures: The study presenter reported having no financial conflicts of interest.

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