In a recent article in The Primary Care Companion, my colleagues and I discussed the potentially toxic impact of rumors on the internal functioning of a psychiatric department. However, rumors also have the potential of heavily impacting people’s lives, which carries clinical significance for the practicing psychiatrist.
I have encountered clinical situations with patients who were seeking help for trauma resulting from rumors propagated via electronic media. One characteristic of this particular way of spreading rumors is the fact that, due to the anonymous nature of the Internet, these rumors tend to generate in victims a sense of severe helplessness and loss of control.
Ms A was a 40-year-old, married executive secretary, with a long career in the corporate world. She found herself in the midst of a family dispute with her 4 siblings over their father’s large estate. Over the period of a year, a relatively close-knit family became involved in contentious litigation over their father’s estate. At that point, a barrage of anonymous, calumnious statements about Ms A appeared on the Internet: a criminal history including prostitution, theft, drug possession, and tax evasion, as well as a teenage pregnancy and abortion. None of these allegations had any basis in truth, and thus Ms A confidently dismissed and ignored them. However, as they were posted on the Internet in association with her correct name and identity, they became part of the information readily retrievable to anyone typing her name into a search engine. What followed seemed surreal for Ms A. As she related in session, her world gradually became shattered over a period of 6 to 8 months. People at work started making innuendos. Then, her supervisor called her in to discuss the claims found on the Internet, apparently having been notified by coworkers. There were concerns about the corporate image. In spite of the fact that Ms A denied all of the allegations, a cloud of doubt about her past continued. This was unjustified given the fact that criminal activities and personal histories can be confirmed and denied through background checks. Friends, acquaintances, and coworkers seemed to slip into a state of ambiguity, despite having no proof for any of these allegations. This ambiguity created distance between Ms A and her entire support system. In time, Ms A became isolated. Her employer did not take any action. The entire matter was treated with silence, which may have contributed to the rumor effect.
When Ms A first visited my office, she presented with symptoms of PTSD, eg, intrusive thoughts about the rumors and the related consequences, nightmares, guardedness, and heightened suspicion. She developed depression and a chronic sense of anhedonia about everyday life activities, work, and previously enjoyed leisure activities. Treatment with psychotherapy included a restructuring of her trauma-related suspicious cognitions. In addition, supportive and dynamic techniques were utilized to create a new forum of reality, away from the cloud of rumors in which she was now operating. It was particularly helpful to tap into the resource of a supportive marriage. Therefore, occasional conjoint sessions were scheduled. In addition, Ms A showed a positive response to treatment with SSRIs, which decreased the rumination and obsessive thinking. Treatment has been maintained long-term. Today, a year later, Ms A has persistent guardedness about coworkers and friends, but her nightmares and depression have remitted. She has not maintained contact with any of her siblings, as it was suspected that the younger brother had initiated the rumors.
The above case illustrates the malignancy of rumors propagated over the Internet. The ambiguous nature of rumors makes them a pathogen that can produce particularly prolonged effects. Thus, the combination of the power of Internet information and the human tendency to believe legends and rumors, when misused, will shatter people’s lives. The Internet provides no sure privacy safeguards. Treatment for patients in these situations has to be focused on rebuilding their confidence, addressing their faulty cognition that everyone privy to the rumors will believe them, and encouraging them to move to a different stage in life. There is certainly evil and insecurity in the world. However, one of the long-term goals of treatment should be to penetrate the defenses of posttraumatic thinking and re-expand our patients’ vision to internalize the experience of good and beauty.
As a final note, we often underestimate the value of long-term maintenance treatment in enhancing functionality after severe trauma, as opposed to the limited treatment needed to achieve remission in the case of an episodic psychiatric disorder. Most clinical studies, especially in psychopharmacology, are short-term, lasting only until first remission, and often we have no information about outcome 5 or 10 years later. For some patients, recurrence is the rule; for others, the exception. Treating patients with trauma sometimes requires stepping aside from the norms set by the many treatment studies with limited timeframes.
Financial disclosure: Dr Novac had no relevant personal financial relationships to report.
Almost every day, I receive an e-mail from a desperate mother. She is writing because she suspects that her daughter has ADHD and is looking for help. In some instances, the girl is young, the symptoms are clear cut and agreed upon by parents and teachers, and mom is just looking for a referral. But, in too many cases, the girl has already been seen by a mental health professional and the diagnosis of ADHD has been missed or mom fears her daughter is misdiagnosed. The following e-mail was received recently and is unfortunately quite typical. (All identifiers have been removed or changed to maintain privacy.)
Dear Dr. Quinn,
My daughter is a sophomore (freshman, senior, etc) at XXXX High School (or College), where she is struggling. She was told by a school counselor (psychologist, psychiatrist) that she is most likely bipolar. She was recently prescribed medication for this diagnosis by a psychiatrist. However, we see her as ADHD: she can be moody and sensitive but has never been really depressed; she starts new projects with enthusiasm, but the follow-through is lacking. She can spend impulsively, and deadlines are always a challenge for her unless they relate to a high-interest activity. She is invariably good at what she does but is sensitive to perceived criticism. She is very bright but has a history of academic underachievement since middle school.
I realize you can't diagnose her on the basis of this brief description, but I am concerned that she has been misdiagnosed. Her moods are always in response to life events: the scale and severity may seem atypical, but there is always a trigger. Can you refer me to someone who is informed and aware of the presenting symptoms and prevailing wisdom regarding treatment of ADHD (without hyperactivity)?
p.s. My daughter runs track, which may be a mitigating factor for her not demonstrating hyperactivity.
Does this girl have bipolar disorder, ADHD, or both? Unless you entertain the diagnosis of ADHD, you’re going to miss it. Let’s look at the odds for her having a diagnosis of ADHD versus bipolar disorder or both. First, ADHD is about twice as common as bipolar disorder in both children and adults.1,2 Bipolar disorder affects only a fraction of children and adolescents with ADHD; however, among those with bipolar disorder, the likelihood of having comorbid ADHD is high.1 Several research studies have demonstrated that the earlier the mood swings of bipolar disorder start, the more likely coexisting ADHD is; 40% to 90% of children and adolescents who are diagnosed with bipolar disorder also have ADHD symptoms.3-5 Among children with ADHD, however, only 23% have bipolar disorder.6
In adults, the pattern of comorbidity is the opposite. Studies7,8 estimate that 10% to 21% of adults with bipolar disorder also have ADHD diagnosed in adulthood, while 47% of adults with ADHD have bipolar disorder. Incidence of coexisting bipolar disorder varies by ADHD presentation in adults; one study9 found that 23% of those with combined type, 6% of those with inattentive type, and 38% of those with hyperactive type ADHD also had bipolar disorder.
Second, ADHD and bipolar disorder share several features, including mood fluctuations, increased energy levels, hypertalkativeness, impulsivity, “racing thoughts,” irritability, and sleep disturbances.1,10 In addition, they both have a chronic course with life-long impairment, as well as a strong genetic component. However, ADHD and bipolar disorder can be distinguished on the basis of several differences. These include age at onset, persistence of symptoms, and qualities of the mood fluctuations, including duration, stability, and whether they are in response to real stimuli in the environment.
Third, ADHD symptoms are present throughout the lifespan. For a diagnosis, symptoms must be present (although not necessarily impairing) by age 12 years.10 Conversely, bipolar disorder can be present in young children, but such an occurrence is rare. Thus, symptoms that begin prior to puberty are more often due to ADHD. In addition, symptoms of ADHD are always present while bipolar disorder is episodic, with normal moods occurring between episodes.
Women and girls with ADHD often have strong emotional reactions to the events in their lives. This clear triggering of mood shifts by real events distinguishes ADHD from bipolar mood shifts that come and go unrelated to life events.10 Rapid ADHD mood swings are usually the result of stimuli in the environment that can shift rapidly, sometimes within minutes. However, the mood swings of bipolar disorder often occur over days or weeks even in the most “rapid cyclers.” A rapid cycling bipolar disorder is defined as one in which an individual experiences at least 4 shifts of mood over a year. Many females with ADHD have that many mood shifts in a single day!
When ADHD and bipolar disorder occur together, both must be properly diagnosed and treated in order for these girls and women to improve. Great caution must be taken to make sure you don’t miss ADHD when making a diagnosis of bipolar disorder or misdiagnose ADHD as bipolar disorder in a discouraged (or depressed) female teen or young adult. Looking at what lies beneath often will give you the answer and keep my inbox clear!
Financial disclosure: Dr Quinn is a member of the speakers board for Shire.
1. Galanter CA, Liebenluft E. Frontiers between attention deficit hyperactivity disorder and bipolar disorder. Child Adolesc Psychiatr Clin N Am. 2008;17(2):325–346. PubMed
2. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62(6):593–602. PubMed
3. Sachs GS, Baldassano CF, Truman CJ, et al. Comorbidity of attention deficit hyperactivity disorder with early- and late-onset bipolar disorder. Am J Psychiatry. 2000;157(3):466–468. PubMed
4. Masi G, Perugi G, Toni C, et al. Attention-deficit hyperactivity disorder–bipolar comorbidity in children and adolescents. Bipolar Disord. 2006;8(4):373–381. PubMed
5. Joshi G, Wilens T. Comorbidity in pediatric bipolar disorder. Child Adolesc Psychiatr Clin N Am. 2009;18(2):291–319. PubMed
6. Beiderman J, Faraone SV, Mick E, et al. Attention-deficit hyperactivity disorder and juvenile mania: an overlooked comorbidity? J Am Acad Child Adolesc Psychiatry. 1996;35(8):997–1008. PubMed
7. Nierenberg AA, Miyahara S, Spencer T, et al. Clinical and diagnostic implications of lifetime attention-deficit/hyperactivity disorder comorbidity in adults with bipolar disorder: data from the first 1000 STEP-BD participants. Biol Psychiatry. 2005;57(11):1467–1473. PubMed
8. Wingo AP, Ghaemi SN. A systematic review of rates and diagnostic validity of comorbid adult attention-deficit/hyperactivity disorder and bipolar disorder. J Clin Psychiatry. 2007 Nov;68(11):1776-1784. Full Text
9. Wilens TE, Biederman J, Faraone SV, et al. Presenting ADHD symptoms, subtypes, and comorbid disorders in clinically referred adults with ADHD. J Clin Psychiatry. 2009;70(11):1557–1562. Full Text
10. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Washington, DC: American Psychiatric Association; 2013.
Although cycling acceleration was portrayed long ago, when Bleuler described a 50-hour cycle in a patient suffering from a mood disorder, the limited existing data do not allow clear conclusions regarding the clinical phenomenology, prevalence, and clinical correlates associated with rapid cycling.1
Additionally, misconceptions exist regarding overlap between this clinical variable and other clinical phenotypes. For example, patients with rapid cycling bipolar disorder are often misdiagnosed as suffering from a mixed episode. The only clinical situation, however, in which a manic or a hypomanic episode coexists in the same period of time as a full-blown major depressive one (as required by the modern classification systems) is within the nosological entity recognized as ultra-rapid cycling.2
Some fundamental questions about rapid cycling remain more or less unanswered. Is it a frequent clinical situation? How is it triggered? Is there a recognized relationship with environmental factors? Is there a specific biological substrate? Is it a real subtype with temporal stability or is it a course specifier?
To answer some of these questions, my colleagues and I performed a systematic review3 of the available data regarding rapid cycling, which was recently published in The Journal of Clinical Psychiatry.
We found some interesting answers. First of all, it seems that rapid cycling is a rather frequent clinical condition. Although the prevalence rates vary widely, we calculated that the mean weighted annual prevalence rate is 18.10%, while the lifetime prevalence rate is estimated to be 31.48%.3 Moreover, prevalence seems dissimilar among females and males, and a previous meta-analysis by Kupka and colleagues4 reported a close association between female gender and rapid cycling. Regarding age at onset, it seems that bipolar illness begins earlier among patients with rapid cycling (before 17 years) than among those without.
Does rapid cycling have a specific biological substrate? Do environmental triggers exist? A relationship between rapid cycling and hypothyroidism has been described (but not unanimously accepted) as a part of a more complex inter-correlation that also is associated with female gender and lithium treatment.5 Furthermore, the etiological relationship between the use of antidepressants and rapid cycling is less clear than once was thought, as it seems that only a fraction of patients will develop this course after the use of antidepressants.3 Beyond triggering factors, the findings from the field of genetics were not convincing. There is not an increased familial load for rapid cycling bipolar disorder.4 Furthermore, despite the existence of genetic studies, their limited number and the lack of replication is still a problem. Overall, the existing data are insufficient and cannot support the existence of a recognizable biological substrate. A hypothesis that deserves further exploration is that possibly temperament is the determining endophenotype, while rapid cycling serves as an intermediate phenotype.3
Finally, although rapid cycling seems like a worsening in the course of bipolar disorder, it does not happen in a predictable manner. Rapid cycling seems to represent a transitory phenomenon rather than a stable phase or feature of the disorder in the majority of cases.3
Financial disclosure: Dr Dimellis has received honoraria from Janssen-Cilag, Eli Lilly, Pfizer, Servier, and AstraZeneca and is a member of the speakers/advisory boards for Janssen-Cilag, Eli Lilly, Pfizer, Servier, AstraZeneca, and Sanofi.
1. Fountoulakis KN, Akiskal HS. Focus on bipolar illness. CNS Spectr. 2008;13(9):762. PubMed
2. Fountoulakis KN, Kontis D, Gonda X, et al. Treatment of mixed bipolar states. Int J Neuropsychopharmacol. 2012;15(7):1015–1026. PubMed
3. Carvalho AF, Dimellis D, Gonda X, et al. Rapid cycling in bipolar disorder: a systematic review. J Clin Psychiatry. 2014;75(6):e578–586. Abstract
4. Kupka RW, Luckenbaugh DA, Post RM, et al. Rapid and non-rapid cycling bipolar disorder: a meta-analysis of clinical studies. J Clin Psychiatry. 2003;64(12):1483–1494. Abstract
5. Bauer MS, Whybrow PC, Winokur A. Rapid cycling bipolar affective disorder: I. Association with grade I hypothyroidism. Arch Gen Psychiatry. 1990;47(5):427–432. PubMed
The phases of a woman’s life are demarcated by points of transition in her reproductive cycle. Global shifts in the hormonal milieu accomplish the transitions from child to woman, woman to mother, and mother to elder.
The major hormones of the female reproductive cycle include estrogens (estrone, estradiol and estriol), progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). The effects of these reproductive hormones on a woman’s mood are most prominent not at points of lowest or highest expression but rather at times of rapid change in serum concentration.1
The transition to menopause is accomplished over many years, beginning with gradual increases in the levels of FSH and LH while the woman maintains regular cycling. During perimenopause, menstrual cycles become intermittent, and, in the 6 months around the time of the final menstrual period, estrogen levels markedly decrease. A corresponding decline in FSH and LH quickly follows, ultimately resulting in stably low levels of all reproductive hormones in the postmenopausal period.2
An increase in risk for depressive symptoms occurs during the menopausal transition. Common symptoms of perimenopause like insomnia and vasomotor symptoms may be important contributors to low mood.3 The cessation of menstruation is not itself depressogenic, as depressive symptoms are reduced after the completion of menopause.4
Transdermal estradiol has been found effective for perimenopausal depression in randomized controlled trials.5 But, in accordance with the hypothesis that it is the rapid alteration in estrogen levels rather than low serum estrogen itself that predisposes perimenopausal women to depressive symptoms, treatment with estradiol alone appears less effective for depressed women who have completed menopause.6 However, estradiol treatment in postmenopausal women has been found to enhance7 or accelerate8 the effect of antidepressant treatment, resulting in improved global well-being and quality of life over and above that obtained with the antidepressant alone.9 Thus, combination of estrogen with an antidepressant can be an effective strategy that in some cases is greater than the sum of its parts.
Estrogen treatment has a positive effect on physiological symptoms associated with menopause.10 To some degree, the positive effect of estrogen on mood in perimenopausal women may be mediated by mitigation of physiological symptoms,3 but the extent of the interrelationship is not yet clear.
Potential adverse effects of estrogen replacement therapy in older women include increases in risk for the development of coronary heart disease, pulmonary embolism, and breast cancer.11 Combined treatment with estrogen and a progestin does not appear to mitigate these effects and may in fact increase breast cancer risk relative to use of estrogen alone.12
Thus, extended periods of hormone replacement therapy for postmenopausal women are not recommended and indeed are not indicated given the lack of effect of estrogen for depression after menopause. However, estrogen replacement therapy can be a reasonable short-term treatment for managing depressive as well as physiological symptoms associated with perimenopause. We suggest a treatment period of no longer than 6 months to cover the period of adjustment to the lower estrogen state while avoiding the multiple adverse effects associated with long-term use of hormone replacement therapy.
Financial disclosure: Dr Robakis has received grant/research support from NIMH. Dr Rasgon has received grant/research support and/or honoraria from and/or is a consultant for Magceutics, American Diabetes Association, Corcept, Shire, Sunovion, and Takeda.
1. Deecher D, Andree TH, Sloan D, et al. From menarche to menopause: exploring the underlying biology of depression in women experiencing hormonal changes. Psychoneuroendocrinology. 2008;33(1):3–17. PubMed
2. Rannevik G, Jeppsson S, Johnell O, et al. A longitudinal study of the perimenopausal transition: altered profiles of steroid and pituitary hormones, SHBG and bone mineral density. Maturitas. 1995;21(2):103–113. PubMed
3. Avis NE, Crawford S, Stellato R, et al. Longitudinal study of hormone levels and depression among women transitioning through menopause. Climacteric. 2001;4(3):243–249. PubMed
4. Freeman EW, Sammel MD, Liu L, et al. Hormones and menopausal status as predictors of depression in women in transition to menopause. Arch Gen Psychiatry, 2004;61(1):62–70. PubMed
5. Soares CN, Almeida OP, Joffe H, et al. Efficacy of estradiol for the treatment of depressive disorders in perimenopausal women: a double-blind, randomized, placebo-controlled trial. Arch Gen Psychiatry. 2001;58(6):529–534. PubMed
6. Morrison MF, Kallan MJ, Ten Have T, et al. Lack of efficacy of estradiol for depression in postmenopausal women: a randomized, controlled trial. Biol Psychiatry. 2004;55(4):406–412. PubMed
7. Schneider LS, Small GW, Hamilton SH, et al. Estrogen replacement and response to fluoxetine in a multicenter geriatric depression trial. Am J Geriatr Psychiatry. 1997;5(2):97–106. PubMed
8. Rasgon NL, Dunkin J, Fairbanks L, et al. Estrogen and response to sertraline in postmenopausal women with major depressive disorder: a pilot study. J Psychiatr Res. 2007;41(3–4):338–343. PubMed
9. Schneider LS, Small GW, Clary CM. Estrogen replacement therapy and antidepressant response to sertraline in older depressed women. Am J Geriatr Psychiatry. 2001;9(4):393–399. PubMed
10. Newton KM, Reed SD, LaCroix AZ, et al. Treatment of vasomotor symptoms of menopause with black cohosh, multibotanicals, soy, hormone therapy, or placebo: a randomized trial. Ann Internal Med. 2006;145(12):869–879. PubMed
11. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women's Health Initiative randomized controlled trial. JAMA. 2002;288(3):321–333. PubMed
12. Bakken K, Fournier A, Lund E, et al. Menopausal hormone therapy and breast cancer risk: impact of different treatments. The European Prospective Investigation into Cancer and Nutrition. Int J Cancer. 2011;128(1):144–156. PubMed
The recent death of Robin Williams has brought up questions about the links between addiction and depression, or dual diagnosis. The Epidemiologic Catchment Area study conducted by the National Institute of Mental Health reported that nearly a third of individuals with depression also have a comorbid substance disorder at some point.1 The daughter of former US Senator George McGovern, who was treated for depression, froze to death after having been drunk and passed out in the cold.2
With the DSM-5, we no longer make the distinction between substance abuse and substance dependency but place them together under the diagnosis of substance use disorder. It is interesting that alcohol and the various drugs of abuse all seem to cause activation of the brain’s reward circuits, especially the dopamine neurons located in the ventral tegmental area (VTA) with projections to the nucleus accumbens.3 Repeated activation leads to euphoria and an alteration in the reward mechanism, which is defined by the addict as “craving” when the drug is not present. This process is often referred to as sensitization. Eventually, with increased tolerance, the individual feels sick most of the time and will use the drug to feel “normal.” Given sufficient consequences for alcohol or drug use, the person with an addiction will seek help through rehab and/or a 12-Step program and may achieve a period of sobriety. Unfortunately, even one drink can again sensitize the neural circuits to want more and more. Last September, in an interview with Jon Stewart, Williams described the loss of 20 years of sobriety: “The moment I had the first sip…it was like…rahh…all of a sudden it was like, welcome back a**hole.”
Depression is one of the most common forms of mental illness, affecting about 15% of the population.4 A number of different brain areas are affected, which create different symptoms. The frontal cortex may be involved with disturbances of cognition,5 the hippocampus with feelings of suicidality,6 and the VTA and nucleus accumbens may mediate anhedonia and decreased motivation.7 The fact is that addiction and depression seem to share common neural substrates.8
An additional factor in Robin Williams’ death is the news from Mrs Williams that her husband had early Parkinson’s disease. Each illness—depression and Parkinson’s—can worsen the other, with increases in problems with concentration as well as movement problems and anxiety.9 In Parkinson’s disease, the dopamine-producing brain cells die, which we know are linked to reward and pleasure. In the 1990 movie Awakenings, Robin Williams portrayed a physician at a hospital in the Bronx caring for patients suffering from catatonia caused by an encephalitis epidemic. After attending a lecture, Dr Sayer (Robin Williams) believes the Parkinson’s drug L-Dopa may help, and he gives it to patient Leonard Lowe (Robert DeNiro). Leonard “awakens,” falls in love, and desires freedom, but then he develops facial and body tics. The tics grow more prominent, Leonard starts to shuffle, spasms, and then cannot move. Leonard returns to catatonia.
In a 2010 interview with comedian Marc Maron, Williams spoke about contemplating suicide but said the big picture was far more positive than any of the troubles of the present. It is possible that, following the diagnosis of Parkinson’s, the big picture changed for Mr Williams. He may have made the decision to end his life now rather than face a living death of depression, dementia, and the catatonic-like rigidity of Parkinson’s disease.
Financial disclosure: Dr King had no relevant personal financial relationships to report.
1. Regier DA, Farmer ME, Rae DS, et al. Comorbidity of mental disorders with alcohol and other drug abuse: results from the Epidemiologic Catchment Area (ECA) Study. JAMA. 1990;264(19):2511–2518. PubMed
2. McGovern G. Terry: My Daughter’s Life-and-Death Struggle With Alcoholism. New York, NY: Plume; 1997.
3. Gardner EL. Addiction and brain reward and antireward pathways. Adv Psychosom Med. 2011;30:22–60. PubMed
4. Bromet E, Andrade LH, Hwang I, et al. Cross-national epidemiology of DSM-IV major depressive episode. BMC Med. 2011;9:90. PubMed
5. Clark L, Chamberlain SR, Sahakian BJ. Neurocognitive mechanisms in depression: implications for treatment. Annu Rev Neurosci. 2009;32:57–74. PubMed
6. Labonté B, Suderman M, Maussion G, et al. Genome-wide methylation changes in the brains of suicide completers. Am J Psychiatry. 2013;170(5):511–520. PubMed
7. Kroemer NB, Guevara A, Teodorescu IC, et al. Balancing reward and work: anticipatory brain activation in NAcc and VTA predict effort differentially [published online ahead of print August 6, 2014]. Neuroimage. PubMed
8. Peña CJ, Bagot RC, Labonté B, et al. Epigenetic signaling in psychiatric disorders [published online ahead of print April 5, 2014]. J Mol Biol. PubMed
9. Raskind MA. Diagnosis and treatment of depression comorbid with neurologic disorders. Am J Med. 2008;121(11 suppl 2):S28–S37. PubMed
During the past 20 years, the clinical significance of co-existing anxiety disorders and anxiety symptoms in patients with major depressive disorder (MDD) has been increasingly recognized. The prevalence is high, with the majority of depressed patients having either symptoms of anxiety or a comorbid anxiety disorder. Anxiety in patients with MDD predicts greater morbidity than in those without anxiety. Co-occurring anxiety has been associated with increased suicidality, greater impairment in functioning, worse health-related quality of life, poorer longitudinal course, greater number of depressive episodes, and poorer response to treatment in controlled efficacy studies and uncontrolled effectiveness studies. Clinicians indicated that anxiety was the symptom that most commonly influenced their choice of antidepressant for patients with MDD.
To acknowledge the clinical significance of anxious features in depressed patients, DSM-5 included criteria for an anxious distress specifier for MDD. With increased attention likely to be given to anxious depression because of the addition of this specifier, it is important that rating scales be developed that measure symptoms of both depression and anxiety. The development of new scales is particularly timely in the context of recent recommendations to measure outcome during routine clinical practice. Measurement-based care has been emphasized in official treatment guidelines for depression, as well as in DSM-5. Self-report questionnaires are a cost-effective option to implement measurement-based care because they require little time to administer and correlate highly with clinician ratings.
In a recent report from the Rhode Island Methods to Improve Diagnostic Assessment and Services (MIDAS) project, my colleagues and I described a modification of a self-administered depression scale, the Clinically Useful Depression Outcome Scale (CUDOS), to include a 5-item subscale assessing the DSM-5 anxious distress specifier of MDD (CUDOS-A).
In a study of nearly 800 outpatients diagnosed with MDD, the CUDOS-A was found to be a reliable and valid measure of anxiety symptoms. The scale was more highly correlated with other self-report measures of anxiety than with measures of depression, substance use problems, eating disorders, and anger. The convergent and discriminant validity of the CUDOS-A was further supported by the finding that the measure was more highly correlated with clinician severity ratings of anxiety than of depression and irritability. In addition, CUDOS-A scores were significantly higher in depressed outpatients with anxiety disorders than in depressed outpatients without anxiety disorders. Consistent with other research on the high prevalence of anxiety in depressed patients, the majority of patients with MDD in our study met the DSM-5 anxious distress specifier on the CUDOS-A. Compared to patients who did not meet the DSM-5 specifier, the patients who did reported more functional impairment and poorer quality of life.
The CUDOS-A is the fourth in a series of “Clinically Useful” scales that were developed in the MIDAS project for use in clinical practice, with the other scales created to measure depression (CUDOS), anxiety (Clinically Useful Anxiety Outcome Scale [CUXOS]), and social anxiety (Clinically Useful Social Anxiety Disorder Outcome Scale). Each of the scales in the Clinically Useful series is intended to be brief, easily scored, and available to clinicians for personal use without cost. Each scale has the same rating instructions, which facilitates comparisons of symptom severity across varied symptom domains. The CUDOS and CUXOS are available for administration on the Internet on a free website that assists clinicians in monitoring the course of treatment (www.outcometracker.org).
Financial disclosure: Dr Zimmerman had no relevant personal financial relationships to report.
“I am not sure how you do it. I would never do this.” (Jolly good, then. I guess my job is safe for now, and so is the world…from you!)
“What is the point of wasting time on something you cannot cure?” (Ah, yes, and you just won the Nobel Prize for curing [insert illness name here]. What’s that? You can only manage it and not cure it? Interesting.)
There. I have finally blurted out the impure thoughts that have often crossed my mind during conversations with colleagues over the years. Years of simmering in a cauldron of narcissistic injury finally culminating in an eruption of bile, which, I suspect, I may have been stewing in all this while.
It comes as no surprise that a career in psychiatry is not particularly coveted by medical students worldwide,1 even though their clerkship experience may have positively influenced their attitudes toward the field.2 Stigma toward mental illness in general and stigmatization of students interested in psychiatry might serve as deterrents. A perceived lack of effectiveness of treatment and concerns about working with people with mental health issues may also turn students away from a career in the field.
Which begs the question, what makes me want to do it? Well, my interest in psychiatry could have something to do with fellow physicians who contemplated giving up their careers as their depression took root, the accomplished professor who was no longer able to do what she did best, the brilliant lawyer reduced to a shadow of herself, who were able to return to productive lives with the appropriate treatment. It may have to do with the medical student contemplating self-harm, who ultimately made it into a competitive residency program after receiving help. Or perhaps the manic lady who ranted for 45 minutes, only to capitulate and take her mood stabilizer “because you are the only one who has ever listened to me for this long.” The overwhelmed caregiver, the wife desperate to get her husband back, the son who lost his father to suicide, the anxious parents wanting their child to just be able to sit still for a while, and the wounded warrior unable to find solace even in the relative safety of his home. Their despair turning to hope as their treatment bore fruit. Their transformation, priceless.
Do any of these people sound like someone you might know? These people could easily be (and perhaps are) our loved ones, colleagues, and neighbors. And that is why a career in psychiatry matters. That is why, no matter how bad my workday might be, at the end of it, there is at least one person whose life is better for what I may have done for them. This is why I do what I do. Because it is worth it!
PS: The author reports no financial conflicts, but (in the recent words of a colleague) a number of ongoing psychological conflicts may be apparent to readers!
Financial disclosure: Dr Joshi had no relevant personal financial relationships to report.
1. Lyons Z. Attitudes of medical students toward psychiatry and psychiatry as a career: a systematic review. Acad Psychiatry. 2013;37(3):150–157. PubMed
2. Lyons Z. Impact of the psychiatry clerkship on medical student attitudes towards psychiatry and to psychiatry as a career. Acad Psychiatry. 2014;38(1):35–42. PubMed
Participation in a treatment begins with choice of treatment. In evaluating efficacy or effectiveness, though, we often do not pay attention to this act of choosing, nor do we give much thought to whether choice in and of itself may lead to lower economic costs or improved patient outcomes. Nowhere is choice more important than for mental health treatments. Mental disorders often have causes both inside and outside the body. Individuals may have strong opinions about treatments that target biology, cognition, or behavior. Because of this, they may experience some relief of their distress when they receive the treatment that they prefer. They may also adhere to treatment better and be more willing to persist with therapy during setbacks.
The gold standard in research, the randomized clinical trial, ignores these benefits of choice. In fact, by its nature, the traditional randomized clinical trial prohibits choice. An alternative to this approach is a doubly randomized preference trial. This type of trial randomizes participants to either their choice of treatment or further randomization to an assigned treatment. The benefit of this design is that it separates the effect of choice from the effect of treatment on outcome.
My colleagues and I evaluated cost-effectiveness in a prospective doubly randomized choice trial of 2 treatments for posttraumatic stress disorder (PTSD). Specifically, we studied the incremental cost of obtaining a unit health effect in quality-adjusted life-years. We chose to study the effect of choice, a psychological therapy (prolonged exposure), and a pharmacotherapy (sertraline). We administered each treatment for 10 weeks and tracked patients for 1 year. We collected information on direct and indirect medical costs as well as effectiveness. Results suggest that giving patients a choice between prolonged exposure therapy and sertraline is a cost-effective shared decision-making strategy. In the absence of choice, prolonged exposure is more cost-effective than sertraline.
The traditional restriction of choice in our research methods has affected the dialogue in evidence-based practice. Our concern has revolved around the question, “Which treatment has greater efficacy or effectiveness?” This question drives systematic reviews, meta-analyses, cost-effectiveness models, and, ultimately, guidelines of care. Yet, effective treatments are not discovered through rigid adherence to this narrow scientific question. They arise in the context of decisions made by patients about which treatment they choose to pursue. The notion of what constitutes an effective treatment may depend in part on patient preferences. Giving patients a choice of either sertraline or prolonged exposure therapy for chronic PTSD may yield a benefit of its own. In general, we need to further explore whether shared decision-making should play a greater role in mental health guidelines.
Financial disclosure: Dr Doctor is a consultant for Baxter Biosciences and Precision Health Economics and has received grant/research support from Baxter Biosciences.
Physical inactivity is estimated to cause 9% of premature mortality worldwide,1 but recognition of the benefits of being physically active is increasing. In addition to the cardiometabolic benefits of regular bodily movement, physical activity has repeatedly been shown to have antidepressant and anxiolytic qualities, both as monotherapy and as adjunctive therapy.2,3
For people experiencing mental conditions beyond depressive disorders and anxiety, little evidence on useful treatment strategies is available. However, support exists for the notion of addressing the limited participation in physical activity seen among people with serious mental illnesses like schizophrenia, because a sedentary lifestyle happens to be a key modifiable risk factor for the development of metabolic syndrome. A recent editorial4 in The British Journal of Psychiatry made an urgent call “for better clinical trial evidence to determine how best to increase levels of physical activity”(p239) in people with schizophrenia, while a subsequent letter5 made reference to mental health physiotherapists as professionals ready to lead the charge in delivering evidence-based interventions.
Our review6 of 39 studies with varying participant diagnoses, including major depressive disorder and schizophrenia, aimed to determine what effect physical activity has on symptoms of depression in people with a mental illness, while also determining the impact on symptoms of schizophrenia, anthropometry, aerobic capacity, and quality of life.
The key findings were unsurprising, revealing that indeed physical activity is effective in improving both the physical health and mental health of people experiencing mental illness. However, the effect sizes of methodologically stronger trials were smaller than those of studies of a poorer quality. We also found that the intervention protocols were often poorly described, failed to utilize clinicians with expertise in exercise prescription, and often failed to meet basic principles of exercise programming.
Critics of physical activity interventions in people with mental illness often cite studies with negative findings such as those of Chalder et al,7 in which a predominantly telephone-based intervention had little effect on mood in a sample of participants with depression. Such interventions are unlikely to be comparable to, for example, supervised exercise programs incorporating an individualized prescription and incorporating both resistance- and aerobic-based components provided by allied health clinicians (such as exercise physiologists and physiotherapists). Unfortunately, this criticism reflects the current conceptualization (and subsequent lack of funding) of the role of physical activity as a diversion strategy rather than as a clinically meaningful intervention requiring clinicians with unique expertise.
At what point do we decide that sufficient evidence exists for a cultural change within psychiatric care, whereby exercise physiologists or physical therapists (and indeed dietitians) are considered as standard members of the multidisciplinary mental health team? Such paradigm shifts are often limited by the bottom line. Rather than looking at the cost of delivering such interventions, we need to consider the cost of failing to do so.
Financial disclosure: Mr Rosenbaum had no relevant personal financial relationships to report.
1. Lee I-M, Shiroma EJ, Lobelo F, et al. Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy. Lancet. 2012;380(9838):219–229. PubMed
2. Cooney GM, Dwan K, Greig CA, et al. Exercise for depression. Cochrane Database Syst Rev. 2013;9:CD004366. PubMed
3. Jayakody K, Gunadasa S, Hosker C. Exercise for anxiety disorders: systematic review. Br J Sports Med. 2014;48(3):187–196. PubMed
4. McNamee L, Mead G, MacGillivray S, et al. Schizophrenia, poor physical health and physical activity: evidence-based interventions are required to reduce major health inequalities. Br J Psychiatry. 2013;203(3):239–241. PubMed
5. Stubbs B, Probst M, Soundy A, et al. Physiotherapists can help implement physical activity programmes in clinical practice. Br J Psychiatry. 2014;204(2):164. PubMed
6. Rosenbaum S, Tiedemann A, Sherrington C, et al. Physical activity interventions for people with mental illness: a systematic review and meta-analysis [published online ahead of print March 31, 2014]. J Clin Psychiatry. doi: 10.4088/JCP.13r08765. Abstract
7. Chalder M, Wiles NJ, Campbell J, et al. Facilitated physical activity as a treatment for depressed adults: randomised controlled trial. BMJ. 2012;344:e2758. PubMed
In my previous blog entry, I explained why the splitting of neurology and psychiatry is no longer conceptually justified. At the practical level, there are numerous advantages and very few drawbacks to reuniting neurology and psychiatry into a single discipline of clinical brain disorders. Using the academic tripartite mission, I’ll describe the expected benefits.
Research. All clinical knowledge has to be discovered before it is taught and applied to patient care, so the positive impact on research must be highlighted first. Neurology and psychiatry have separately conducted their own studies with barely any collaboration with each other. Thus, there has been a dearth of testable hypotheses that integrate both the hardware (brain) and software (mind). A tragically high number of investigative opportunities were lost by failing to collaborate. Every neuroscience discovery has implications for ordinary brain functions as well as higher brain functions. By reuniting and integrating the 2 specialties into 1 department, disruptive translational neuroscience discoveries are more likely to emerge, substantively changing the current models of conceptualizing, diagnosing, and treating brain disorders.
Teaching and Training. The training for future clinical neuroscience practitioners must integrate the current neurologic and psychiatric training methods in order to assess and manage every patient with any brain disorder in a 360° approach. Every graduate of an integrated department would concurrently conduct neurologic-psychiatric history and examination and amalgamate the findings into a 360° diagnostic and treatment plan. Trainees would become adept at (1) recognizing and localizing the primary and secondary brain “lesions” that produce the patients’ physical and mental symptoms and (2) consistently looking at the consequences of a neurologic lesion on sensory and motor functions and concomitantly on cognitive behavior, thought, emotions, mood, and behavior. Here is one example of how the current un-integrated training overlooks important findings: patients with first-episode psychosis are rarely given a full neurologic exam by a psychiatry resident. Yet, researchers have consistently found that a substantial proportion of drug-naïve patients with first-episode psychosis have hypokinesia, dyskinesias, and dystonias. Because they are not documented in clinical settings, those movement disorders are attributed to iatrogenic effects of antipsychotics following the initiation of pharmacotherapy. Such undetected findings have neurobiological, diagnostic, and treatment implications. Trainees of an integrated program will develop a multidimensional view of the brain and all of its neuropsychiatric dysfunctions and their effects on patients’ functional outcomes.
Clinical Care. The salutary effects of integrating neurology and psychiatry on patient care are a genuine no-brainer. Every patient with a brain disorder (including mental symptoms) deserves a comprehensive 360° evaluation and management. Clinical and functional outcomes will be optimized with a neuropsychiatric approach. Another important benefit to psychiatric patients under the integrated model is the reduction in the stigma of mental illness. When the mind is recognized as a neurologic component of the brain, the ignorant discrimination toward psychiatric disorders will gradually disappear.
In medical schools, another important benefit of combining neurology and psychiatry is the improved fiscal integrity of the unified department. Neurology is associated with many well-reimbursed procedures (eg, EEG, EMG, lumbar puncture, botulinum toxin injections), while psychiatry is not. Thus, a combined department is more likely to have a healthier bottom line than a psychiatry department. In addition, due to economy of scale (eg, 1 chair instead of 2, 1 set of committees, 1 set of clinic receptionists and staff), the overhead is lower, and the faculty have more time to see patients, teach, mentor, or write research grant applications.
In conclusion, there are conceptual, academic, and practical benefits of reintegrating the 2 currently separate neuroscience disciplines of neurology and psychiatry. Reintegration is what Saint Louis University School of Medicine boldly initiated 7 years ago. This model should be given serious consideration by medical school deans and adopted by all medical schools, leaving behind the archaic, old-fashioned model of sequestering brain and mind disorders in separate departmental silos. Our patients with brain disorders deserve better because every “neurologic” disorder is associated with psychiatric sequelae and every “psychiatric” disorder has neurologic underpinnings. The remarkable neuroscience revolution will thrive further with an integrated model of brain disorders.
Financial disclosure: Dr Nasrallah is a consultant for Boehringer-Ingelheim, Genentech, Gruenthal, Janssen, Lundbeck, Merck, Otsuka, Roche, and Sunovion; has received grant/research support from Roche, Forest, and Otsuka; has received honoraria from Boehringer-Ingelheim, Forum, Genentech, Gruenthal, Janssen, Lundbeck, Merck, Otsuka, Roche, and Sunovion; and is a member of the speakers/advisory boards for Janssen, Otsuka, Genentech, Forum, Merck, and Sunovion.