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A Clinically Useful Self-Report Measure of the DSM-5 MDD Anxious Distress Specifier

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.

Why Become a Psychiatrist? The Id Speaks.

“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.

References

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

Cost-Effectiveness and Patient Choice of PTSD Therapy

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.

Time to Move on Physical Activity as Usual Care for Mental Illness

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.

References

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

Reintegrating Psychiatry and Neurology Is Long Overdue: Part 2

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.

Do We Frown Because We Are Depressed or Are We Depressed Because We Frown?

Smiling makes us feel better! In a TED talk, researcher Ron Gutman discussed the facts that people with bigger smiles tended to live longer lives, have happier marriages, and appear more competent to others.1 In addition, smiling can reduce stress levels by decreasing cortisol, and improve mood by increasing endorphins.1 Gutman’s talk received criticism as it was unclear whether the link between smiling and success was correlative or causative.2

According to evolutionary theorist Charles Darwin and philosopher/psychologist William James, the relationship is causative—we are happy because we smile, we are sorry because we cry, and we are angry because we clench our teeth, not the other way around.3,4 In other words, changes in facial expression create and enhance emotion and are not merely a consequence of that emotion.

If facial expression can influence emotional experience, then what would happen if depressed patients were no longer able to frown?

Three recent studies5–7 (with sample sizes of 30 to 85) set out to answer this question. Male and female participants with major depressive disorder were injected with botulinum toxin A (BTA) into the forehead region, causing a reduced ability to frown (ie, paralysis of the corrugator and procerus muscles, which control expressions of fear, anxiety, and anguish). In all 3 double-blind, placebo-controlled trials, BTA was associated with a statistically significant reduction in depressive symptoms compared with placebo. More interestingly, in our 24-week trial,7 the antidepressant effects of BTA continued even after the cosmetic effects had worn off.

If botulinum toxin in the frown muscles improves symptoms of depression, why?

Some may argue that looking aesthetically better leads to feeling better, but our study7 excluded those with concern about their frown lines. Others argue that the more pleasant and less depressed we look, the more inviting we are to others, leading to improved social interactions and, subsequently, improved mood. These arguments, however, do not explain why mood continues to improve even when the BTA is no longer cosmetically active.

A final argument is that BTA in the forehead alters peripheral feedback to the brain. A recent study8 showed that people who were given BTA in the frown muscles had reduced activity in the left amygdala on functional magnetic resonance imaging (fMRI) when mimicking angry facial expressions. In theory, paralysis of the forehead muscles reduces sensory information from the trigeminal tract to the brainstem, which then alters activity between the brainstem and left amygdala. These findings are important as hyperactivity in the left amygdala has been linked to anxiety, depression, posttraumatic stress disorder, and heightened fear responses.9 In one study,10 20 depressed patients exhibited exaggerated left amygdala activity when shown pictures of emotional faces, especially fearful faces. After antidepressant treatment, left amygdala hyperactivity returned to normal.

Is botulinum toxin a viable treatment option for major depressive disorder?

Regardless of whether one subscribes to a more behavioral or biological mechanism of action, further trials are warranted to determine if BTA is indeed a viable therapeutic option for depression and if specific patient populations are more likely to respond (eg, a recent study11 showed that higher agitation scores are predictive of response). If larger trials can replicate the findings of the 3 small trials, BTA may become a novel treatment in the management of major depressive disorder.

Financial disclosure: Dr Magid received grant/research support from the Brain and Behavior Institute, Young Investigator Award, to fund this study. After completion and as a result of the study, Dr. Magid became a consultant for Allergan.

References

1. Gutman R. The hidden power of smiling. TED Talks. March 2011. http://www.ted.com/talks/ron_gutman_the_hidden_power_of_smiling.

2. Grohol J. Ron Gutman: smiling while confusing correlation with causation. http://psychcentral.com/blog/archives/2012/08/19/ron-gutman-smiling-while-confusing-correlation-with-causation/.

3. Darwin, C. The Expression of the Emotions in Man and Animals. London, England: John Murray; 1872.

4. James, William. The Principles of Psychology. New York, NY: Henry Holt & Co; 1890.

5. Wollmer MA, de Boer C, Kalak N, et al. Facing depression with botulinum toxin: a randomized controlled trial. J Psychiatr Res. 2012;46(5):574–581. PubMed

6. Finzi E, Rosenthal NE. Treatment of depression with onabotulinumtoxin A: a randomized, double-blind, placebo controlled trial [published online ahead of print December 16, 2013]. J Psychiatr Res. Abstract

7. Magid M, Reichenberg JS, Poth PE, et al. Treatment of major depressive disorder using botulinum toxin A: a 24-week randomized, double-blind, placebo-controlled study. J Clin Psychiatry [published online ahead of print May 13, 2014]. Abstract

8. Hennenlotter A, Dresel C, Castrop F, et al. The link between facial feedback and neural activity within central circuitries of emotion—new insights from botulinum toxin-induced denervation of frown muscles. Cereb Cortex. 2009;19(3):537–542. PubMed

9. Shin LM, Liberzon I. The neurocircuitry of fear, stress, and anxiety disorders. Neuropsychopharmacology. 2010;35(1):169–191. PubMed

10. Sheline YI, Barch DM, Donnelly JM, et al. Increased amygdala response to masked emotional faces in depressed subjects resolves with antidepressant treatment: an fMRI study. Biol Psychiatry. 2001;50(9):651–658. PubMed

11. Wollmer MA, Kalak N, Jung S, et al. Agitation predicts response of depression to botulinum toxin treatment in a randomized controlled trial. Front Psychiatry. 2014;5:36. PubMed

Reintegrating Psychiatry and Neurology Is Long Overdue: Part 1

For over a century, neurology and psychiatry were united in one discipline and one department in medical schools, representing a brain specialty. Neuropsychiatry dealt with all aspects of that divinely complex organ, from sensory, motor, vascular, or neoplastic to cognition, speech, thought, emotions, and behavior. Upon graduating from a unified neuropsychiatric department, some physicians focused on the physical brain disorders such as stroke, epilepsy, Parkinson’s, or multiple sclerosis, while others focused on the mental brain disorders such as psychosis, depression, anxiety, or pathological behaviors. This is not different from contemporary ophthalmology departments, where graduates of training programs subspecialize in disorders of the cornea, the lens, the retina, neuro-opthalmology, or ocular infectious diseases.

So why did the unified brain specialty split during the 1950s? Although multifactorial, a prominent reason was the rise of the theoretical, nonempirical psychoanalytic model that permeated and dominated psychiatric departments in that era. That was in stark contrast with the empirical, nontheoretical neurologic training and practice. The “organic vs. functional” dichotomy was accentuated, and the jargon of psychiatry alienated neurologists, who adhered to traditional medical terminology. This led to the “secession” of neurology that created separate journals and associations and a separate board exam. For the past 60 years, psychiatry and neurology retreated into their respective silos in all medical schools and rarely interacted clinically, an amazing paradox given that they dealt with the same organ! However, the alienation became so entrenched that cynics regarded psychiatry as brainless and neurology as mindless!

Fortunately, the neuroscience revolution came to the rescue and has elucidated the multiple links between brain and mind. The past 3 to 4 decades witnessed unprecedented advances in elucidating brain-behavior linkages and the neuroanatomic, neurochemical, neurophysiologic, and neurologic correlates of mental functions. Thanks to breakthroughs in structural and functional neuroimaging and accelerating advances in molecular neurogenetics, the medical foundations of psychiatry have become well established. The neuropsychiatrists of a century ago always assumed that the mind is a product of cortical activity, but they lacked the technological tools to demonstrate it.

Thus, from a conceptual perspective, the splitting of neurology and psychiatry is no longer justified. However, reunification, while urgently desirable, will be slow because practitioners on both sides, trained and inculcated with the model of brain-mind dualism, may be reluctant to merge, and many might remain entrenched in their “separateness.” Nevertheless, the shift to a modern, scientifically valid paradigm of integrating psychiatry and neurology has begun and will ultimately be widely adopted. A motivated cadre of neuropsychiatrists and behavioral neurologists must serve as leaders and catalysts to overcome the inertia of decades of alienation.

In my next blog entry, I’ll discuss the numerous practical advantages of reuniting neurology and psychiatry into a single discipline.

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.

Science, Rhetoric, and the End of Psychosis

Recently, I have been told that incivility in the debate about early intervention in psychosis alienates the undecided. Exaggerated claims of cures and prevention on one side and caustic criticisms on the other side combine to reinforce the folk-wisdom of avoiding the company of fanatics, or at least of not discussing religion, politics, or psychosis at dinner parties.

The less partisan position appears to be a mildly skeptical suspension of judgment. Seductive hope that schizophrenia is a preventable neurodegenerative process is balanced against inconclusive evidence, leading to the thought, “I am open to the possibilities, but I am not yet convinced.”

As a critic of early intervention analysis, I have often heard, “Yes, evidence is lacking, but if rhetoric attracts greater funding, even for a small subset of patients, where’s the harm in pretending?”

My answer generally involves grabbing a lapel and offering a passionate defense of the scientific method. Early intense intervention for psychosis has not led to miraculous cures, although outcomes are better while the support continues.1 Pretending that early intervention modifies the disease prevents the scientific accumulation of knowledge, where each step depends on the accuracy of previous steps. Funding driven by optimistic misrepresentations of early intervention means alternative treatments that may actually modify the disease attract less funding.

The problem is compounded by the distorting effects of politics. Early interventionists in Australia have attracted public funds to specialist units2 based on optimistic misinterpretations of data. Once large sums have been sunk into bricks and mortar based on poor quality evidence, it becomes less politically possible to change course even if alternatives that do change the course of schizophrenia are empirically justified.

It is easy for skeptics to convince themselves of the prevalence of bias in the early intervention literature. My recent article provides many examples,3 and two are particularly illuminating. Consider the 10-year follow-up of the early detection of psychosis experiment by Hegelstad and colleagues.4 How convincing is a study that changed its primary outcome at 1 year, from relapse to symptoms, when the initial primary outcome showed no difference, and then changed its primary outcome again at 10 years, from symptoms to a novel measure of recovery, when symptom measures favored the control group? Next, compare McGorry’s statement that the OPUS study demonstrates the “disease-modifying” effect of early intense intervention5 with the conclusion by OPUS authors that “no basic changes in illness were seen after 5 years from the start of the program.”1(p770)

These examples demonstrate the confirmatory bias that dominates early intervention research. Until this evidence is accurately interpreted, the early intervention crusade will serve only to obscure the true nature of psychotic illness and retard scientific progress toward a cure.

Financial disclosure: Dr Amos had no relevant personal financial relationships to report.

References

1.  Bertelsen M, Jeppesen P, Petersen L, et al. Five-year follow-up of a randomized multicenter trial of intensive early intervention vs standard treatment for patients with a first episode of psychotic illness: the OPUS trial. Arch Gen Psychiatry. 2008;65(7):762–771. PubMed

2.  Department of Health and Ageing. Major Expansion for headspace as EPPIC Moves Forward. May 23, 2013. Available at: http://www.agedcare.com.au/aged_care_news.php?title=major_expansion_for_andltemandgtheadspaceandlt_emandgt_as_eppic_moves_forward_463. Accessed March 24, 2014.

3.  Amos AJ. A review of spin and bias use in the early intervention in psychosis literature. Prim Care Companion CNS Disord. 2014;16(1):e1–7. Abstract

4.  Hegelstad WT, Larsen TK, Auestad B, et al. Long-term follow-up of the TIPS early detection in psychosis study: effects on 10-year outcome. Am J Psychiatry. 2012;169(4):374–380. PubMed.

5.  McGorry PD. Truth and reality in early intervention. Aust N Z JPsychiatry. 2012;46(4):313–316. PubMed

Experiences in Implementing Collaborative Care

Wagner’s Chronic Care Model of disease management applied to the treatment of mental disorders in primary care has come to be known as integrated health care or collaborative care. The model is a systematic approach that involves integration of patient oversight by mental health specialists, care managers, and primary care physicians to proactively treat mental health disorders. That systematic integration of various disciplines moves team practices beyond parallel relationships to an interdisciplinary practice model that includes collaborative communication, collective action, a process orientation, and working together for common goals that are centered on whole-person care.

Our recent qualitative case study of an integrated health care model of service delivery for the treatment of depression in a low-income, uninsured adult population explored how a collaborative care model of service delivery works. We examined a single, interdisciplinary team of providers to explore how the integrated health care model of collaborative care was an effective strategy for providing mental health treatment to a predominantly Hispanic patient population at one grant-funded primary care safety-net clinic.

There is little doubt that the mental health treatment community has historically played a role in obstructing communication between providers, in the interest of protecting patients and advocating for privacy as it related to mental health diagnoses. However, despite common protests among professionals about private health information and the sharing of mental health records, in our study, the care manager expressed surprise at never meeting a patient who was concerned about who might gain knowledge about his or her mental disorder. In fact, she summarized, “They felt like, ‘I’ve got this team of people around me that care about me, that are all communicating.’ It’s like being a well-loved child.”

Another historical obstacle to collaboration between providers has been the influence of the traditional medical model, in which the primary care doctor maintains control of patient care and struggles with sharing responsibility, except to hand off care to a psychiatrist. Skepticism that collaborative care will create more work for the primary care physician is a common reaction to the implementation of the collaborative care model. In our clinic, we took several steps to combat resistance. A respected, experienced physician was asked to champion the model to skeptical physicians, and then the clinical social worker who was acting as care manager shadowed physicians during patient visits to learn their styles. Finally, our early focus on identifying the most problematic patients of each physician, who were then successfully treated with the assistance of the care manager, also helped build trust and ease the medical team into understanding and using the model.

The development of patient-centered collaborative care teams is a core tenet of health care reform, at a time when the culture of cross-education and training is quite limited. Collaboration requires team members from various disciplines to develop a common language, loosen hierarchical structures, pool bodies of knowledge and theories, and jointly develop new methods and analytical techniques within a philosophy of whole-person care. In this sense, the patient is also considered a vital part of the team. Without a doubt, collaborative care teams offer the best hope for achieving quality health care outcomes, particularly for vulnerable populations and patients with multiple comorbidities.

Financial disclosure: Dr Sanchez had no relevant personal financial relationships to report.

The Ideal Tool for Health Care: Clinician Perspective

In my previous blog post, I described the patient’s perspective on the ideal tool to guide mental health care in the patient-centered medical home (PCMH). Here, I consider the treatment team’s view, as well as existing building blocks for such a tool.

From the primary care team’s perspective, the tool should maximize transfer of information and communication with the patient and among the team. It should integrate into the PCMH’s medical record and efficiently summarize, including graphically, a patient’s functional status, symptoms, and disease concerns and priorities, highlighting both changes over time and comparisons with an appropriate reference population. The tool’s dashboard should provide summative information for a patient’s chronic disease and for PCMH population management and quality activities. It should push out alerts and reports both at the patient and panel level.

The tool would provide efficiency by using information to connect the patient to the right PCMH team professional. The tool will efficiently lead clinicians to diagnosis by highlighting problems in patient functioning and relationships, history, and symptoms requiring confirmation or further exploration. It can then help guide the patient and the professional in developing a shared understanding of the patient’s needs, strengths, and priorities and preferences upon which to develop a treatment plan.

During treatment selection, the tool might display expert guidance useful in individualizing therapy. Given the patient’s experiences, comorbidities (eg, pain, sleep dysfunction), or vulnerabilities (eg, early-life abuse), what treatments might be of particular value or high risk? What potential drug interactions should be considered? For example, a patient with prior reactions to regular doses of medications metabolized by CYP450 2D6 might be identified as a possible “slow metabolizer,” suggesting low initial doses of some antidepressants.

In follow-up care, both short- and long-term, changes identified in functioning and symptom experience can support treatment adjustments. The tool also can provide clinicians with patients’ communications regarding other changes, such as new or different priorities and goals.

A further critical role for such a tool is communication and coordination at the time of transitions, such as hospitalization, referral to specialty care (eg, for intensive treatment of PTSD), and return to the primary care team, or geographic moves requiring a change in treatment team. Such transitions often not only are major sources of stress for the patient, decreasing coping and making them vulnerable to worsening health status, but are times of high risk for the occurrence of medical errors, both of commission and omission.

We have the building blocks for such an instrument. Measurement tools are available, and the required computing power is a reality, as are mobile platforms. Most patients are “wired.” The PHQ-2/PHQ-9, Bipolar CIDI 3.0, and the PC-PTSD/PCL screener-and-questionnaire combos already provide models of two-step strategies. Other tools available include quality of life instruments (eg, Q-LES-Q), functioning measures (eg, Cognitive and Physical Functioning Questionnaire, Family and Work APGAR scales, Sheehan Disability Scale), and less-used history tools. Cognitive assessment tools are available online, as are tools for conditions such as ADHD and substance abuse and for focused populations such as menopausal women, the elderly and adolescents, and disabled individuals.

The building blocks are beginning to be aggregated into primitive systems like the tool I describe. Virtual patient advocates are already being used for patient education processes (eg, http://www.bu.edu/fammed/projectred/meetlouise.html). In a pilot study, patients reported preferring the virtual advocate to clinical staff. The M3 tool, available with an app interface, measures multiple psychiatric conditions, provides individual disorder scores and a summary score, and tracks treatment and treatment response and side effects over time. In some VA regions, mental health technicians at central hubs can pull from a range of mental health instruments and remotely interview patients and collect data for clinicians. A number of online resources measure patient cognitive ability and provide clinical data to physicians (eg, http://www.mybraintest.org/tag/cantab/ )

The value equation has been missing in the past to drive the development and then refinement (likely to take years) of such a tool. However, steps in this direction are underway by multiple groups, who are approaching the task with a variety of motivations, including financially based (on either the potential for profit or the fear of loss) and grant-supported intellectual challenge and drive to improve care. As these efforts converge over the coming years, they will transform how we provide care, to the benefit of patients, professionals, and society.

Financial disclosure: Dr Culpepper is a consultant for Forest, Lundbeck, Merck, Sunovion, and Takeda; has received travel support from Pamlab; and is a stock shareholder of M3 (My Mood Monitor).

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