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The placebo effect in psychiatric practice
“It is a mystery how a ubiquitous treatment used since antiquity was unknown, unnamed, and unidentified until recently. It is even more remarkable because this is the only treatment common to all societies and cultures.”1
The treatment discussed above is not a specific pill, surgery, plant, or herb. Rather, the authors are referring to placebo. Indeed, the history of medical treatment is largely a chronicle of placebos. When subjected to scientific scrutiny, the overwhelming majority of treatments have turned out to be devoid of intrinsic therapeutic value; they derived their benefits from the placebo effect. Despite these benefits, the term “placebo” comes with unfortunate baggage. Latin for “I shall please,” it is the first word of the Christian vespers for the dead. In the 12th century these vespers were commonly referred to as placebos. By the 1300s, the term had become secular and pejorative, suggesting a flatterer or sycophant. When the word entered medical terminology in the late 18th century, the negative connotation stuck. A placebo was defined as a medicine given to please patients rather than to benefit them. In the modern era, the lack of pharmacologic activity became part of the definition as well.
The word placebo brings with it connotations of deception, fakery, and ineffectiveness. But one of the things about placebos that contribute mightily to the health care community’s aversion toward them is, in fact, their effectiveness. They bring relief across a wide range of medical conditions.2 In doing so, placebos impugn the value of our most cherished remedies, hamper the development of new therapeutics, and threaten our livelihoods as health professionals.3
Placebos often are conceptualized as any treatment that lacks intrinsic therapeutic value, such as sugar pills. But looking at what placebo treatment actually entails, both in placebo-controlled treatment trials and in clinical settings, suggests a more comprehensive definition. Placebos encompass all the elements common to any treatment or healing situation. These include a recognized healer, evaluation, diagnosis, prognosis, plausible treatment, and most importantly, the expectation that one will recover. Along these lines, the placebo response can be thought of as the response to the common elements of the treatment or healing situation.3
Research regarding the placebo effect has mushroomed in the past 2 decades. Over this time, we have learned a good deal about both the mechanisms underlying the placebo effect and how the placebo effect can be applied to enhance the benefit of conventional treatment. Brain imaging technology has revealed that when placebo treatment alleviates pain, Parkinson’s disease, and depression, brain changes occur that are similar to those observed with active pharmacologic treatment.4,5 Recent studies also show that deliberate, open (nondeceptive) use of placebo can improve the symptoms of several conditions, including depression, pain, and irritable bowel syndrome.6 Furthermore, intermittent substitution of placebo pills for pharmacologically active treatment in a conditioning paradigm can be as effective as the “real” treatment.7 Also, research over the past decade has verified that certain common features of the treatment situation, particularly the quality of the doctor–patient encounter, contribute to the placebo response and have a demonstrable impact on the outcome of treatment.8 Clearly, the placebo effect has gone from being simply a nuisance that interferes with the evaluation of new treatments to a variable worthy of study and application in its own right. Although, for the most part, clinical practice has not kept up with these advances.
Placebos seem to have their greatest impact on the subjective symptoms of disease—pain, distress, and discouragement. It should come as no surprise, then, that placebos are particularly effective in certain psychiatric conditions. In some forms of anxiety and depressive disorders, for example, distress is the illness, and placebos reliably bring relief. Patients with panic disorder, mild to moderate depression, or generalized anxiety disorder get almost as much relief with placebo as they do with conventional treatment (about one-half improve with placebo).9-11 But <20% of those with obsessive-compulsive disorder improve with placebo, and placebo response rates are also low in patients with schizophrenia or dementia. Mania, attention-deficit/hyperactivity disorder (ADHD), and severe depression fall somewhere in the middle.3
Harnessing the placebo response
There may be a few circumstances in psychiatric practice when it makes sense to intentionally prescribe a placebo as treatment, and we discuss those below. But far more frequently, what we know about the elements that contribute to the placebo effect can be applied to enhance the benefits of any treatment. Patients might be best served if deliberate mobilization of the placebo effect was a standard adjunct to conventional clinical care.
Various components of the treatment situation, collectively referred to as placebo, are a powerful antidote for illness, and some of these healing components exert their influence without special activity on the clinician’s part:
- Simply seeking psychiatric care can bring relief by providing some sense of control over distressing symptoms. The standard trappings of the office or clinic and customary office procedures—from the presentation of one’s insurance card to taking a history—offer reassurance and evoke the expectation that improvement or recovery is around the corner.
- The comfort provided by the psychiatrist’s presence is enhanced when patients feel that they are in the hands of a recognized healer. Psychiatrists inspire confidence when they look like a psychiatrist, or more precisely, like the patient’s idea of what a psychiatrist should look like. In our culture, that means a white coat or business attire.
A thorough evaluation is one of the common treatment elements that does the most to reduce distress and inspire confidence. The quality of an evaluation bears a strong relationship to patients’ satisfaction with the medical encounter, and can influence the amount of disability they suffer.3,12-15
Although guidelines for conducting effective psychiatric interviews have been around for almost 100 years, psychiatrists vary considerably in the extent to which they elicit complete and accurate information, build rapport, give patients the sense that they are listened to, and provide a thorough assessment. The degree to which patients feel that the clinician is responsive to their concerns depends as much on the style of the interview as on the amount of time devoted to it. Nonverbal behavior can carry the message that the clinician is paying full attention. Something as simple as not answering the phone during an interview (this seems obvious, but a surprising and troubling number of mental health professionals take phone calls during interviews and treatment sessions) conveys an important message about the importance that the clinician places on the patient’s problems.3
The idea that the treatment situation itself provides reassurance and reduces distress, and in doing so, powers a good bit of the placebo effect, is enshrined in such concepts as the importance of good bedside manner. Many feel that the doctor’s thoughtful attention, positive regard, and optimism—so valued by patients—are justified on humanitarian grounds alone; actual evidence that this caring behavior contributes to healing isn’t required. To many, the healing properties of the treatment situation are self-evident. But as the costs of health care snowball and the demands for efficiency and cost-effectiveness rise, the time that psychiatrists can devote to patients has dwindled. Third-party payors demand evidence, beyond intuition and common sense, that diagnostic procedures and treatments have some usefulness, and rightly so.
Is there any evidence that the common components of the treatment situation provide benefit?3 More specifically, does the quality of the doctor–patient relationship and the patient’s feelings about a therapeutic encounter promote healing? Several studies suggest that the doctor–patient relationship has a demonstrable impact on symptom relief.16 In 1 study, oncologists were randomly assigned to receive a Communication Skills Training (CST) program or not. CST included a 1.5-day face-to-face workshop and 6 hours of monthly videoconferencing that focused on improving communication skills with patients.17 Lessons included building rapport, engaging in appropriate eye contact, and normalizing difficult experiences. One week after initially consulting with their physician, patients who saw an oncologist in the CST group experienced less anxiety and depression than those who saw an oncologist who did not receive CST. The benefit of CST for patient anxiety mostly persisted at a 3-month follow-up.
A recent meta-analysis pooled the results of 47 studies to examine the relationship between how much trust patients have for their doctors and health outcomes. There was a small to medium association: More trust was associated with greater improvement.18 It is possible that a good doctor–patient relationship enhances expectancies. However, it is also likely that a positive therapeutic relationship is inherently soothing and reduces distress or dysfunction independent of expectation. Regardless of the precise mechanism, these studies warrant attention. We all understand that it is important on ethical grounds to treat patients with respect and kindness. Research shows that this type of behavior also promotes recovery.
Patient expectations. The idea that expectation of improvement has a major impact on treatment outcome is firmly grounded in research on the placebo effect. Studies have shown that what people expect to experience as an outcome of treatment has a substantial impact on what they actually experience. In a classic study, a doctor told some patients with symptoms of minor illness that they would feel better soon and another group with the same symptoms that he didn’t know what ailed them.19 Two weeks later, 64% of patients in the “positive expectation” group were improved, compared with only 39% of patients in the “negative” group. In another study, adults were exposed to an allergen that caused a skin reaction.20 Hand lotion (ie, a therapeutically inert substance) was then spread on the skin. Patients were led to believe that the cream would either alleviate or exacerbate the itching. The experimentally-induced wheal-and-flare was measured in both groups a few minutes after the allergen and cream were applied. The wheal-and-flare were worse for participants in the group that expected exacerbation.
Not uncommonly, expectation can have more impact on clinical outcome than a drug’s pharmacologic activity. In a double-blind placebo-controlled study, patients with depression were treated with St. John’s wort, sertraline, or placebo.21 They improved to the same extent with all 3 treatments. But when patients were asked to guess the treatment to which they had been assigned, those who thought they had received placebo showed little improvement, irrespective of which intervention they actually received, and those who guessed they had been given St. John’s wort or sertraline showed uniformly large improvement, irrespective of which intervention they actually received (including placebo). The researchers concluded that “Patient beliefs regarding treatment may have a stronger association with clinical outcome than the actual medication received.”
Psychiatrists who wish to use all the therapeutic tools at their disposal must attend to and manage patient expectations. One part of channeling a patient’s expectation is to thoroughly assess the patient’s beliefs regarding the efficacy of various treatments. If a patient’s uncle said that a certain drug is a miracle cure for anxiety, and the patient believes it to be true, then that expectation must be taken into consideration. Many patients prefer alternative treatments to conventional therapies. As long as there is no reason to think an alternative treatment will cause harm, a compromise might be reasonable. For example, if a patient with schizophrenia wants to treat her symptoms with herbal tea, the psychiatrist could say, “In addition to the tea, I recommend that you also take clozapine. The combination is likely to improve your symptoms.”3 More than anything else, the words a psychiatrist uses when recommending treatment shape the patient’s expectations. “You should be feeling a lot less anxious soon after you start taking this” has a different effect than “Try this. It may help.”
Prescribing ‘open-label’ placebo
There may be some limited circumstances where an actual placebo (eg, a sugar pill) might be suitable as a treatment. These include when placebo and conventional treatment provide similar results and a patient is reluctant to take conventional medicine, or when there is no effective conventional treatment. The deceptive prescription of placebo (providing placebo and calling it a drug) has a long history and was considered ethical—and recommended by medical authorities—until the latter half of the 20th century. This practice was deemed unethical in the 1980s, because it was dishonest and violated patient autonomy. Because it was widely believed that placebos given openly would be ineffective, the end of placebo treatment seemed at hand. An intriguing body of evidence, however, suggests that placebos can be effective even when patients know they are taking a placebo. Patients given an “open-label” placebo are told something along the lines of “the pill being prescribed contains no medicine, but some people improve with it, perhaps because the pill stimulates the body’s self-healing.” Open-label placebo has been evaluated for depression,22 low back pain,23 irritable bowel syndrome,24 neurosis,25 allergic rhinitis,26 and anxiety.27 Most of these studies are small, and some were uncontrolled. Yet they consistently have shown that symptoms improve with a nondeceptive placebo, and improve to a greater extent than with no treatment.
The most recent trial is a promising example of the potential of open-label placebos. In this study, 96 patients with chronic low back pain were randomly assigned to 3 weeks of treatment as usual (TAU) or 3 weeks of TAU plus open-label placebo.23 Patients who received open-label placebo were educated about the placebo effect and shown a film clip describing promising results of a prior open-label placebo study. They were then given placebo pills to be take once daily, and clearly told the pills contained no active medication. After 3 weeks, patients in the TAU plus placebo group reported less pain and less disability than patients who received TAU without a placebo. Some patients even requested a placebo prescription at the end of the study.
The placebo response provides a rational basis for prescribing innocuous alternative therapies with no intrinsic therapeutic value. Patients who prefer and believe in the effectiveness of alternative remedies—herbal compounds, massage, magnets, homeopathic solutions, etc.—can be recommended these treatments to mobilize a placebo response.
Using a conditioning model. Prescribing a placebo to obtain a conditioned drug response has enormous but untapped clinical potential. Both animal and human research indicates that a wide range of drug responses, from immune suppression to motor stimulation, can be conditioned (a neutral stimulus, such as a pill or injection, associated with drug administration can in itself evoke the drug effect). In many conditioning or dose-extending models, a particular response to real medication (such as pain relief after analgesics) first becomes conditioned due to repeated exposure to the drug given in a particular vehicle. Then, the treatment shifts to some doses comprising of real medicine and some doses comprising of placebo. Because the drug response has been conditioned, it is thought that the response to an identically appearing placebo will mirror the drug response. The active drug often is only replaced by placebo for certain doses under a schedule of partial reinforcement, given the ubiquity of extinction (the conditioned response lessens when the conditioned stimulus is presented alone on repeated trials).
In 1 version of a conditioning study, children with ADHD were randomized to 1 of 3 groups.28 One group (full dose) took the standard dose of medication for 2 months, a second group (reduced dose) took a standard dose during 1 month followed by a half dose during the second month, and children in the third group (reduced dose with placebo) took the standard dose plus a visually distinctive placebo during the first month, followed by a half dose plus the visually distinctive placebo during the second month. Not surprisingly, ADHD symptoms were worse among children in the reduced-dose group. However, there was no difference between those in the reduced-dose with placebo group and those in the full-dose group. It appears as though the symptom reduction associated with a 100% dose was an unconditioned response that could be mimicked with the addition of a placebo pill.
In another study, patients with psoriasis were randomly assigned to receive a full dose of active medication (0.1% triamcinolone cream) twice a day, or a full dose of active medication for 25% to 50% of the doses, with a placebo (moisturizing cream) given for the other 50% to 75% of the doses.29 Relapse rates were not statistically different between groups.
1. Shapiro AK, Shapiro E. The powerful placebo: from ancient priest to modern physician. Baltimore, MD: Johns Hopkins University Press; 1997.
2. Beecher HK. The powerful placebo. J Am Med Assoc. 1955;159(17):1602-1606.
3. Brown WA. The placebo effect in clinical practice. New York, NY: Oxford University Press; 2013.
4. Mayberg HS, Silva JA, Brannan SK, et al. The functional neuroanatomy of the placebo effect. Am J Psychiatry. 2002;159(5):728-737.
5. de la Fuente-Fernández R, Ruth TJ, Sossi V, et al. Expectation and dopamine release: mechanism of the placebo effect in Parkinson’s disease. Science. 2001;293(5532):1164-1166.
6. Charlesworth JEG, Petkovic G, Kelley JM, et al. Effects of placebos without deception compared with no treatment: a systematic review and meta‐analysis. J Evid Based Med. 2017;10(2):97-107.
7. Colloca L, Enck P, DeGrazia D. Relieving pain using dose-extending placebos: a scoping review. Pain. 2016;157(8):1590-1598.
8. Kaptchuk TJ, Kelley JM, Conboy LA, et al. Components of placebo effect: randomised controlled trial in patients with irritable bowel syndrome. BMJ. 2008;336(7651):999-1003.
9. Khan A, Kolts RL, Rapaport MH, et al. Magnitude of placebo response and drug-placebo differences across psychiatric disorders. Psychol Med. 2005;35(5):743-749.
10. Walsh BT, Seidman SN, Sysko R, Gould M. Placebo response in studies of major depression: variable, substantial, and growing. JAMA. 2002;287(14):1840-1847.
11. Kirsch I, Deacon BJ, Huedo-Medina TB, et al. Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration. PLoS Med. 2008;5(2):e45.
12. Kaptchuk TJ. Acupuncture: theory, efficacy, and practice. Ann Intern Med. 2002;136(5):374-383.
13. Kelley JM, Kraft-Todd G, Schapira L, et al. The influence of the patient-clinician relationship on healthcare outcomes: a systematic review and meta-analysis of randomized controlled trials. PLoS One. 2014;9(4):e94207.
14. Olsson B, Olsson B, Tibblin G. Effect of patients’ expectations on recovery from acute tonsillitis. Fam Pract. 1989;6(3):188-192.
15. Sox HC, Margulies I, Sox CH. Psychologically mediated effects of diagnostic tests. Ann Intern Med. 1981;95(6):680-685.
16. Stewart MA. Effective physician-patient communication and health outcomes: a review. CMAJ. 1995;152(9):1423-1433.
17. Girgis A, Cockburn J, Butow P, et al. Improving patient emotional functioning and psychological morbidity: evaluation of a consultation skills training program for oncologists. Patient Educ Couns. 2009;77(3):456-462.
18. Birkhäuer J, Gaab J, Kossowsky J, et al. Trust in the health care professional and health outcome: a meta-analysis. PLoS One. 2017;12(2):e0170988.
19. Thomas KB. General practice consultations: is there any point in being positive? Br Med J (Clin Res Ed). 1987;294(6581):1200-1202.
20. Howe LC, Goyer JP, Crum AJ. Harnessing the placebo effect: exploring the influence of physician characteristics on placebo response [published online May 9, 2017]. Health Psychol. doi: 10.1037/hea0000499.
21. Chen JA, Papakostas GI, Youn SJ, et al. Association between patient beliefs regarding assigned treatment and clinical response: reanalysis of data from the Hypericum Depression Trial Study Group. J Clin Psychiatry. 2011;72(12):1669-1676.
22. Kelley JM, Kaptchuk TJ, Cusin C, et al. Open-label placebo for major depressive disorder: a pilot randomized controlled trial. Psychother Psychosom. 2012;81(5):312-314.
23. Carvalho C, Caetano JM, Cunha L, et al. Open-label placebo treatment in chronic low back pain: a randomized controlled trial. Pain. 2016;157(12):2766-2772.
24. Kaptchuk TJ, Friedlander E, Kelley JM, et al. Placebos without deception: a randomized controlled trial in irritable bowel syndrome. PLoS One. 2010;5(12):e15591.
25. Park LC, Covi L. Nonblind placebo trial: an exploration of neurotic patients’ responses to placebo when its inert content is disclosed. Arch Gen Psychiatry. 1965;12(4):336-345.
26. Schaefer M, Harke R, Denke C. Open-label placebos improve symptoms in allergic rhinitis: a randomized controlled trial. Psychother Psychosom. 2016;85(6):373-374.
27. Aulas JJ, Rosner I. Efficacy of a non blind placebo prescription [in French]. Encephale. 2003;29(1):68-71.
28. Sandler AD, Glesne CE, Bodfish JW. Conditioned placebo dose reduction: a new treatment in attention deficit hyperactivity disorder? J Dev Behav Pediatr. 2010;31(5):369-375.
29. Ader R, Mercurio MG, Walton J, et al. Conditioned pharmacotherapeutic effects: a preliminary study. Psychosom Med. 2010;72(2):192-197.
30. Weiss RD, O’Malley SS, Hosking JD, et al; COMBINE Study Research Group. Do patients with alcohol dependence respond to placebo? Results from the COMBINE Study. J Stud Alcohol Drugs. 2008;69(6):878-884.
31. Mattick RP, Breen C, Kimber J, et al. Buprenorphine maintenance versus placebo or methadone maintenance for opioid dependence. Cochrane Database Syst Rev. 2014;(2):CD002207.
“It is a mystery how a ubiquitous treatment used since antiquity was unknown, unnamed, and unidentified until recently. It is even more remarkable because this is the only treatment common to all societies and cultures.”1
The treatment discussed above is not a specific pill, surgery, plant, or herb. Rather, the authors are referring to placebo. Indeed, the history of medical treatment is largely a chronicle of placebos. When subjected to scientific scrutiny, the overwhelming majority of treatments have turned out to be devoid of intrinsic therapeutic value; they derived their benefits from the placebo effect. Despite these benefits, the term “placebo” comes with unfortunate baggage. Latin for “I shall please,” it is the first word of the Christian vespers for the dead. In the 12th century these vespers were commonly referred to as placebos. By the 1300s, the term had become secular and pejorative, suggesting a flatterer or sycophant. When the word entered medical terminology in the late 18th century, the negative connotation stuck. A placebo was defined as a medicine given to please patients rather than to benefit them. In the modern era, the lack of pharmacologic activity became part of the definition as well.
The word placebo brings with it connotations of deception, fakery, and ineffectiveness. But one of the things about placebos that contribute mightily to the health care community’s aversion toward them is, in fact, their effectiveness. They bring relief across a wide range of medical conditions.2 In doing so, placebos impugn the value of our most cherished remedies, hamper the development of new therapeutics, and threaten our livelihoods as health professionals.3
Placebos often are conceptualized as any treatment that lacks intrinsic therapeutic value, such as sugar pills. But looking at what placebo treatment actually entails, both in placebo-controlled treatment trials and in clinical settings, suggests a more comprehensive definition. Placebos encompass all the elements common to any treatment or healing situation. These include a recognized healer, evaluation, diagnosis, prognosis, plausible treatment, and most importantly, the expectation that one will recover. Along these lines, the placebo response can be thought of as the response to the common elements of the treatment or healing situation.3
Research regarding the placebo effect has mushroomed in the past 2 decades. Over this time, we have learned a good deal about both the mechanisms underlying the placebo effect and how the placebo effect can be applied to enhance the benefit of conventional treatment. Brain imaging technology has revealed that when placebo treatment alleviates pain, Parkinson’s disease, and depression, brain changes occur that are similar to those observed with active pharmacologic treatment.4,5 Recent studies also show that deliberate, open (nondeceptive) use of placebo can improve the symptoms of several conditions, including depression, pain, and irritable bowel syndrome.6 Furthermore, intermittent substitution of placebo pills for pharmacologically active treatment in a conditioning paradigm can be as effective as the “real” treatment.7 Also, research over the past decade has verified that certain common features of the treatment situation, particularly the quality of the doctor–patient encounter, contribute to the placebo response and have a demonstrable impact on the outcome of treatment.8 Clearly, the placebo effect has gone from being simply a nuisance that interferes with the evaluation of new treatments to a variable worthy of study and application in its own right. Although, for the most part, clinical practice has not kept up with these advances.
Placebos seem to have their greatest impact on the subjective symptoms of disease—pain, distress, and discouragement. It should come as no surprise, then, that placebos are particularly effective in certain psychiatric conditions. In some forms of anxiety and depressive disorders, for example, distress is the illness, and placebos reliably bring relief. Patients with panic disorder, mild to moderate depression, or generalized anxiety disorder get almost as much relief with placebo as they do with conventional treatment (about one-half improve with placebo).9-11 But <20% of those with obsessive-compulsive disorder improve with placebo, and placebo response rates are also low in patients with schizophrenia or dementia. Mania, attention-deficit/hyperactivity disorder (ADHD), and severe depression fall somewhere in the middle.3
Harnessing the placebo response
There may be a few circumstances in psychiatric practice when it makes sense to intentionally prescribe a placebo as treatment, and we discuss those below. But far more frequently, what we know about the elements that contribute to the placebo effect can be applied to enhance the benefits of any treatment. Patients might be best served if deliberate mobilization of the placebo effect was a standard adjunct to conventional clinical care.
Various components of the treatment situation, collectively referred to as placebo, are a powerful antidote for illness, and some of these healing components exert their influence without special activity on the clinician’s part:
- Simply seeking psychiatric care can bring relief by providing some sense of control over distressing symptoms. The standard trappings of the office or clinic and customary office procedures—from the presentation of one’s insurance card to taking a history—offer reassurance and evoke the expectation that improvement or recovery is around the corner.
- The comfort provided by the psychiatrist’s presence is enhanced when patients feel that they are in the hands of a recognized healer. Psychiatrists inspire confidence when they look like a psychiatrist, or more precisely, like the patient’s idea of what a psychiatrist should look like. In our culture, that means a white coat or business attire.
A thorough evaluation is one of the common treatment elements that does the most to reduce distress and inspire confidence. The quality of an evaluation bears a strong relationship to patients’ satisfaction with the medical encounter, and can influence the amount of disability they suffer.3,12-15
Although guidelines for conducting effective psychiatric interviews have been around for almost 100 years, psychiatrists vary considerably in the extent to which they elicit complete and accurate information, build rapport, give patients the sense that they are listened to, and provide a thorough assessment. The degree to which patients feel that the clinician is responsive to their concerns depends as much on the style of the interview as on the amount of time devoted to it. Nonverbal behavior can carry the message that the clinician is paying full attention. Something as simple as not answering the phone during an interview (this seems obvious, but a surprising and troubling number of mental health professionals take phone calls during interviews and treatment sessions) conveys an important message about the importance that the clinician places on the patient’s problems.3
The idea that the treatment situation itself provides reassurance and reduces distress, and in doing so, powers a good bit of the placebo effect, is enshrined in such concepts as the importance of good bedside manner. Many feel that the doctor’s thoughtful attention, positive regard, and optimism—so valued by patients—are justified on humanitarian grounds alone; actual evidence that this caring behavior contributes to healing isn’t required. To many, the healing properties of the treatment situation are self-evident. But as the costs of health care snowball and the demands for efficiency and cost-effectiveness rise, the time that psychiatrists can devote to patients has dwindled. Third-party payors demand evidence, beyond intuition and common sense, that diagnostic procedures and treatments have some usefulness, and rightly so.
Is there any evidence that the common components of the treatment situation provide benefit?3 More specifically, does the quality of the doctor–patient relationship and the patient’s feelings about a therapeutic encounter promote healing? Several studies suggest that the doctor–patient relationship has a demonstrable impact on symptom relief.16 In 1 study, oncologists were randomly assigned to receive a Communication Skills Training (CST) program or not. CST included a 1.5-day face-to-face workshop and 6 hours of monthly videoconferencing that focused on improving communication skills with patients.17 Lessons included building rapport, engaging in appropriate eye contact, and normalizing difficult experiences. One week after initially consulting with their physician, patients who saw an oncologist in the CST group experienced less anxiety and depression than those who saw an oncologist who did not receive CST. The benefit of CST for patient anxiety mostly persisted at a 3-month follow-up.
A recent meta-analysis pooled the results of 47 studies to examine the relationship between how much trust patients have for their doctors and health outcomes. There was a small to medium association: More trust was associated with greater improvement.18 It is possible that a good doctor–patient relationship enhances expectancies. However, it is also likely that a positive therapeutic relationship is inherently soothing and reduces distress or dysfunction independent of expectation. Regardless of the precise mechanism, these studies warrant attention. We all understand that it is important on ethical grounds to treat patients with respect and kindness. Research shows that this type of behavior also promotes recovery.
Patient expectations. The idea that expectation of improvement has a major impact on treatment outcome is firmly grounded in research on the placebo effect. Studies have shown that what people expect to experience as an outcome of treatment has a substantial impact on what they actually experience. In a classic study, a doctor told some patients with symptoms of minor illness that they would feel better soon and another group with the same symptoms that he didn’t know what ailed them.19 Two weeks later, 64% of patients in the “positive expectation” group were improved, compared with only 39% of patients in the “negative” group. In another study, adults were exposed to an allergen that caused a skin reaction.20 Hand lotion (ie, a therapeutically inert substance) was then spread on the skin. Patients were led to believe that the cream would either alleviate or exacerbate the itching. The experimentally-induced wheal-and-flare was measured in both groups a few minutes after the allergen and cream were applied. The wheal-and-flare were worse for participants in the group that expected exacerbation.
Not uncommonly, expectation can have more impact on clinical outcome than a drug’s pharmacologic activity. In a double-blind placebo-controlled study, patients with depression were treated with St. John’s wort, sertraline, or placebo.21 They improved to the same extent with all 3 treatments. But when patients were asked to guess the treatment to which they had been assigned, those who thought they had received placebo showed little improvement, irrespective of which intervention they actually received, and those who guessed they had been given St. John’s wort or sertraline showed uniformly large improvement, irrespective of which intervention they actually received (including placebo). The researchers concluded that “Patient beliefs regarding treatment may have a stronger association with clinical outcome than the actual medication received.”
Psychiatrists who wish to use all the therapeutic tools at their disposal must attend to and manage patient expectations. One part of channeling a patient’s expectation is to thoroughly assess the patient’s beliefs regarding the efficacy of various treatments. If a patient’s uncle said that a certain drug is a miracle cure for anxiety, and the patient believes it to be true, then that expectation must be taken into consideration. Many patients prefer alternative treatments to conventional therapies. As long as there is no reason to think an alternative treatment will cause harm, a compromise might be reasonable. For example, if a patient with schizophrenia wants to treat her symptoms with herbal tea, the psychiatrist could say, “In addition to the tea, I recommend that you also take clozapine. The combination is likely to improve your symptoms.”3 More than anything else, the words a psychiatrist uses when recommending treatment shape the patient’s expectations. “You should be feeling a lot less anxious soon after you start taking this” has a different effect than “Try this. It may help.”
Prescribing ‘open-label’ placebo
There may be some limited circumstances where an actual placebo (eg, a sugar pill) might be suitable as a treatment. These include when placebo and conventional treatment provide similar results and a patient is reluctant to take conventional medicine, or when there is no effective conventional treatment. The deceptive prescription of placebo (providing placebo and calling it a drug) has a long history and was considered ethical—and recommended by medical authorities—until the latter half of the 20th century. This practice was deemed unethical in the 1980s, because it was dishonest and violated patient autonomy. Because it was widely believed that placebos given openly would be ineffective, the end of placebo treatment seemed at hand. An intriguing body of evidence, however, suggests that placebos can be effective even when patients know they are taking a placebo. Patients given an “open-label” placebo are told something along the lines of “the pill being prescribed contains no medicine, but some people improve with it, perhaps because the pill stimulates the body’s self-healing.” Open-label placebo has been evaluated for depression,22 low back pain,23 irritable bowel syndrome,24 neurosis,25 allergic rhinitis,26 and anxiety.27 Most of these studies are small, and some were uncontrolled. Yet they consistently have shown that symptoms improve with a nondeceptive placebo, and improve to a greater extent than with no treatment.
The most recent trial is a promising example of the potential of open-label placebos. In this study, 96 patients with chronic low back pain were randomly assigned to 3 weeks of treatment as usual (TAU) or 3 weeks of TAU plus open-label placebo.23 Patients who received open-label placebo were educated about the placebo effect and shown a film clip describing promising results of a prior open-label placebo study. They were then given placebo pills to be take once daily, and clearly told the pills contained no active medication. After 3 weeks, patients in the TAU plus placebo group reported less pain and less disability than patients who received TAU without a placebo. Some patients even requested a placebo prescription at the end of the study.
The placebo response provides a rational basis for prescribing innocuous alternative therapies with no intrinsic therapeutic value. Patients who prefer and believe in the effectiveness of alternative remedies—herbal compounds, massage, magnets, homeopathic solutions, etc.—can be recommended these treatments to mobilize a placebo response.
Using a conditioning model. Prescribing a placebo to obtain a conditioned drug response has enormous but untapped clinical potential. Both animal and human research indicates that a wide range of drug responses, from immune suppression to motor stimulation, can be conditioned (a neutral stimulus, such as a pill or injection, associated with drug administration can in itself evoke the drug effect). In many conditioning or dose-extending models, a particular response to real medication (such as pain relief after analgesics) first becomes conditioned due to repeated exposure to the drug given in a particular vehicle. Then, the treatment shifts to some doses comprising of real medicine and some doses comprising of placebo. Because the drug response has been conditioned, it is thought that the response to an identically appearing placebo will mirror the drug response. The active drug often is only replaced by placebo for certain doses under a schedule of partial reinforcement, given the ubiquity of extinction (the conditioned response lessens when the conditioned stimulus is presented alone on repeated trials).
In 1 version of a conditioning study, children with ADHD were randomized to 1 of 3 groups.28 One group (full dose) took the standard dose of medication for 2 months, a second group (reduced dose) took a standard dose during 1 month followed by a half dose during the second month, and children in the third group (reduced dose with placebo) took the standard dose plus a visually distinctive placebo during the first month, followed by a half dose plus the visually distinctive placebo during the second month. Not surprisingly, ADHD symptoms were worse among children in the reduced-dose group. However, there was no difference between those in the reduced-dose with placebo group and those in the full-dose group. It appears as though the symptom reduction associated with a 100% dose was an unconditioned response that could be mimicked with the addition of a placebo pill.
In another study, patients with psoriasis were randomly assigned to receive a full dose of active medication (0.1% triamcinolone cream) twice a day, or a full dose of active medication for 25% to 50% of the doses, with a placebo (moisturizing cream) given for the other 50% to 75% of the doses.29 Relapse rates were not statistically different between groups.
“It is a mystery how a ubiquitous treatment used since antiquity was unknown, unnamed, and unidentified until recently. It is even more remarkable because this is the only treatment common to all societies and cultures.”1
The treatment discussed above is not a specific pill, surgery, plant, or herb. Rather, the authors are referring to placebo. Indeed, the history of medical treatment is largely a chronicle of placebos. When subjected to scientific scrutiny, the overwhelming majority of treatments have turned out to be devoid of intrinsic therapeutic value; they derived their benefits from the placebo effect. Despite these benefits, the term “placebo” comes with unfortunate baggage. Latin for “I shall please,” it is the first word of the Christian vespers for the dead. In the 12th century these vespers were commonly referred to as placebos. By the 1300s, the term had become secular and pejorative, suggesting a flatterer or sycophant. When the word entered medical terminology in the late 18th century, the negative connotation stuck. A placebo was defined as a medicine given to please patients rather than to benefit them. In the modern era, the lack of pharmacologic activity became part of the definition as well.
The word placebo brings with it connotations of deception, fakery, and ineffectiveness. But one of the things about placebos that contribute mightily to the health care community’s aversion toward them is, in fact, their effectiveness. They bring relief across a wide range of medical conditions.2 In doing so, placebos impugn the value of our most cherished remedies, hamper the development of new therapeutics, and threaten our livelihoods as health professionals.3
Placebos often are conceptualized as any treatment that lacks intrinsic therapeutic value, such as sugar pills. But looking at what placebo treatment actually entails, both in placebo-controlled treatment trials and in clinical settings, suggests a more comprehensive definition. Placebos encompass all the elements common to any treatment or healing situation. These include a recognized healer, evaluation, diagnosis, prognosis, plausible treatment, and most importantly, the expectation that one will recover. Along these lines, the placebo response can be thought of as the response to the common elements of the treatment or healing situation.3
Research regarding the placebo effect has mushroomed in the past 2 decades. Over this time, we have learned a good deal about both the mechanisms underlying the placebo effect and how the placebo effect can be applied to enhance the benefit of conventional treatment. Brain imaging technology has revealed that when placebo treatment alleviates pain, Parkinson’s disease, and depression, brain changes occur that are similar to those observed with active pharmacologic treatment.4,5 Recent studies also show that deliberate, open (nondeceptive) use of placebo can improve the symptoms of several conditions, including depression, pain, and irritable bowel syndrome.6 Furthermore, intermittent substitution of placebo pills for pharmacologically active treatment in a conditioning paradigm can be as effective as the “real” treatment.7 Also, research over the past decade has verified that certain common features of the treatment situation, particularly the quality of the doctor–patient encounter, contribute to the placebo response and have a demonstrable impact on the outcome of treatment.8 Clearly, the placebo effect has gone from being simply a nuisance that interferes with the evaluation of new treatments to a variable worthy of study and application in its own right. Although, for the most part, clinical practice has not kept up with these advances.
Placebos seem to have their greatest impact on the subjective symptoms of disease—pain, distress, and discouragement. It should come as no surprise, then, that placebos are particularly effective in certain psychiatric conditions. In some forms of anxiety and depressive disorders, for example, distress is the illness, and placebos reliably bring relief. Patients with panic disorder, mild to moderate depression, or generalized anxiety disorder get almost as much relief with placebo as they do with conventional treatment (about one-half improve with placebo).9-11 But <20% of those with obsessive-compulsive disorder improve with placebo, and placebo response rates are also low in patients with schizophrenia or dementia. Mania, attention-deficit/hyperactivity disorder (ADHD), and severe depression fall somewhere in the middle.3
Harnessing the placebo response
There may be a few circumstances in psychiatric practice when it makes sense to intentionally prescribe a placebo as treatment, and we discuss those below. But far more frequently, what we know about the elements that contribute to the placebo effect can be applied to enhance the benefits of any treatment. Patients might be best served if deliberate mobilization of the placebo effect was a standard adjunct to conventional clinical care.
Various components of the treatment situation, collectively referred to as placebo, are a powerful antidote for illness, and some of these healing components exert their influence without special activity on the clinician’s part:
- Simply seeking psychiatric care can bring relief by providing some sense of control over distressing symptoms. The standard trappings of the office or clinic and customary office procedures—from the presentation of one’s insurance card to taking a history—offer reassurance and evoke the expectation that improvement or recovery is around the corner.
- The comfort provided by the psychiatrist’s presence is enhanced when patients feel that they are in the hands of a recognized healer. Psychiatrists inspire confidence when they look like a psychiatrist, or more precisely, like the patient’s idea of what a psychiatrist should look like. In our culture, that means a white coat or business attire.
A thorough evaluation is one of the common treatment elements that does the most to reduce distress and inspire confidence. The quality of an evaluation bears a strong relationship to patients’ satisfaction with the medical encounter, and can influence the amount of disability they suffer.3,12-15
Although guidelines for conducting effective psychiatric interviews have been around for almost 100 years, psychiatrists vary considerably in the extent to which they elicit complete and accurate information, build rapport, give patients the sense that they are listened to, and provide a thorough assessment. The degree to which patients feel that the clinician is responsive to their concerns depends as much on the style of the interview as on the amount of time devoted to it. Nonverbal behavior can carry the message that the clinician is paying full attention. Something as simple as not answering the phone during an interview (this seems obvious, but a surprising and troubling number of mental health professionals take phone calls during interviews and treatment sessions) conveys an important message about the importance that the clinician places on the patient’s problems.3
The idea that the treatment situation itself provides reassurance and reduces distress, and in doing so, powers a good bit of the placebo effect, is enshrined in such concepts as the importance of good bedside manner. Many feel that the doctor’s thoughtful attention, positive regard, and optimism—so valued by patients—are justified on humanitarian grounds alone; actual evidence that this caring behavior contributes to healing isn’t required. To many, the healing properties of the treatment situation are self-evident. But as the costs of health care snowball and the demands for efficiency and cost-effectiveness rise, the time that psychiatrists can devote to patients has dwindled. Third-party payors demand evidence, beyond intuition and common sense, that diagnostic procedures and treatments have some usefulness, and rightly so.
Is there any evidence that the common components of the treatment situation provide benefit?3 More specifically, does the quality of the doctor–patient relationship and the patient’s feelings about a therapeutic encounter promote healing? Several studies suggest that the doctor–patient relationship has a demonstrable impact on symptom relief.16 In 1 study, oncologists were randomly assigned to receive a Communication Skills Training (CST) program or not. CST included a 1.5-day face-to-face workshop and 6 hours of monthly videoconferencing that focused on improving communication skills with patients.17 Lessons included building rapport, engaging in appropriate eye contact, and normalizing difficult experiences. One week after initially consulting with their physician, patients who saw an oncologist in the CST group experienced less anxiety and depression than those who saw an oncologist who did not receive CST. The benefit of CST for patient anxiety mostly persisted at a 3-month follow-up.
A recent meta-analysis pooled the results of 47 studies to examine the relationship between how much trust patients have for their doctors and health outcomes. There was a small to medium association: More trust was associated with greater improvement.18 It is possible that a good doctor–patient relationship enhances expectancies. However, it is also likely that a positive therapeutic relationship is inherently soothing and reduces distress or dysfunction independent of expectation. Regardless of the precise mechanism, these studies warrant attention. We all understand that it is important on ethical grounds to treat patients with respect and kindness. Research shows that this type of behavior also promotes recovery.
Patient expectations. The idea that expectation of improvement has a major impact on treatment outcome is firmly grounded in research on the placebo effect. Studies have shown that what people expect to experience as an outcome of treatment has a substantial impact on what they actually experience. In a classic study, a doctor told some patients with symptoms of minor illness that they would feel better soon and another group with the same symptoms that he didn’t know what ailed them.19 Two weeks later, 64% of patients in the “positive expectation” group were improved, compared with only 39% of patients in the “negative” group. In another study, adults were exposed to an allergen that caused a skin reaction.20 Hand lotion (ie, a therapeutically inert substance) was then spread on the skin. Patients were led to believe that the cream would either alleviate or exacerbate the itching. The experimentally-induced wheal-and-flare was measured in both groups a few minutes after the allergen and cream were applied. The wheal-and-flare were worse for participants in the group that expected exacerbation.
Not uncommonly, expectation can have more impact on clinical outcome than a drug’s pharmacologic activity. In a double-blind placebo-controlled study, patients with depression were treated with St. John’s wort, sertraline, or placebo.21 They improved to the same extent with all 3 treatments. But when patients were asked to guess the treatment to which they had been assigned, those who thought they had received placebo showed little improvement, irrespective of which intervention they actually received, and those who guessed they had been given St. John’s wort or sertraline showed uniformly large improvement, irrespective of which intervention they actually received (including placebo). The researchers concluded that “Patient beliefs regarding treatment may have a stronger association with clinical outcome than the actual medication received.”
Psychiatrists who wish to use all the therapeutic tools at their disposal must attend to and manage patient expectations. One part of channeling a patient’s expectation is to thoroughly assess the patient’s beliefs regarding the efficacy of various treatments. If a patient’s uncle said that a certain drug is a miracle cure for anxiety, and the patient believes it to be true, then that expectation must be taken into consideration. Many patients prefer alternative treatments to conventional therapies. As long as there is no reason to think an alternative treatment will cause harm, a compromise might be reasonable. For example, if a patient with schizophrenia wants to treat her symptoms with herbal tea, the psychiatrist could say, “In addition to the tea, I recommend that you also take clozapine. The combination is likely to improve your symptoms.”3 More than anything else, the words a psychiatrist uses when recommending treatment shape the patient’s expectations. “You should be feeling a lot less anxious soon after you start taking this” has a different effect than “Try this. It may help.”
Prescribing ‘open-label’ placebo
There may be some limited circumstances where an actual placebo (eg, a sugar pill) might be suitable as a treatment. These include when placebo and conventional treatment provide similar results and a patient is reluctant to take conventional medicine, or when there is no effective conventional treatment. The deceptive prescription of placebo (providing placebo and calling it a drug) has a long history and was considered ethical—and recommended by medical authorities—until the latter half of the 20th century. This practice was deemed unethical in the 1980s, because it was dishonest and violated patient autonomy. Because it was widely believed that placebos given openly would be ineffective, the end of placebo treatment seemed at hand. An intriguing body of evidence, however, suggests that placebos can be effective even when patients know they are taking a placebo. Patients given an “open-label” placebo are told something along the lines of “the pill being prescribed contains no medicine, but some people improve with it, perhaps because the pill stimulates the body’s self-healing.” Open-label placebo has been evaluated for depression,22 low back pain,23 irritable bowel syndrome,24 neurosis,25 allergic rhinitis,26 and anxiety.27 Most of these studies are small, and some were uncontrolled. Yet they consistently have shown that symptoms improve with a nondeceptive placebo, and improve to a greater extent than with no treatment.
The most recent trial is a promising example of the potential of open-label placebos. In this study, 96 patients with chronic low back pain were randomly assigned to 3 weeks of treatment as usual (TAU) or 3 weeks of TAU plus open-label placebo.23 Patients who received open-label placebo were educated about the placebo effect and shown a film clip describing promising results of a prior open-label placebo study. They were then given placebo pills to be take once daily, and clearly told the pills contained no active medication. After 3 weeks, patients in the TAU plus placebo group reported less pain and less disability than patients who received TAU without a placebo. Some patients even requested a placebo prescription at the end of the study.
The placebo response provides a rational basis for prescribing innocuous alternative therapies with no intrinsic therapeutic value. Patients who prefer and believe in the effectiveness of alternative remedies—herbal compounds, massage, magnets, homeopathic solutions, etc.—can be recommended these treatments to mobilize a placebo response.
Using a conditioning model. Prescribing a placebo to obtain a conditioned drug response has enormous but untapped clinical potential. Both animal and human research indicates that a wide range of drug responses, from immune suppression to motor stimulation, can be conditioned (a neutral stimulus, such as a pill or injection, associated with drug administration can in itself evoke the drug effect). In many conditioning or dose-extending models, a particular response to real medication (such as pain relief after analgesics) first becomes conditioned due to repeated exposure to the drug given in a particular vehicle. Then, the treatment shifts to some doses comprising of real medicine and some doses comprising of placebo. Because the drug response has been conditioned, it is thought that the response to an identically appearing placebo will mirror the drug response. The active drug often is only replaced by placebo for certain doses under a schedule of partial reinforcement, given the ubiquity of extinction (the conditioned response lessens when the conditioned stimulus is presented alone on repeated trials).
In 1 version of a conditioning study, children with ADHD were randomized to 1 of 3 groups.28 One group (full dose) took the standard dose of medication for 2 months, a second group (reduced dose) took a standard dose during 1 month followed by a half dose during the second month, and children in the third group (reduced dose with placebo) took the standard dose plus a visually distinctive placebo during the first month, followed by a half dose plus the visually distinctive placebo during the second month. Not surprisingly, ADHD symptoms were worse among children in the reduced-dose group. However, there was no difference between those in the reduced-dose with placebo group and those in the full-dose group. It appears as though the symptom reduction associated with a 100% dose was an unconditioned response that could be mimicked with the addition of a placebo pill.
In another study, patients with psoriasis were randomly assigned to receive a full dose of active medication (0.1% triamcinolone cream) twice a day, or a full dose of active medication for 25% to 50% of the doses, with a placebo (moisturizing cream) given for the other 50% to 75% of the doses.29 Relapse rates were not statistically different between groups.
1. Shapiro AK, Shapiro E. The powerful placebo: from ancient priest to modern physician. Baltimore, MD: Johns Hopkins University Press; 1997.
2. Beecher HK. The powerful placebo. J Am Med Assoc. 1955;159(17):1602-1606.
3. Brown WA. The placebo effect in clinical practice. New York, NY: Oxford University Press; 2013.
4. Mayberg HS, Silva JA, Brannan SK, et al. The functional neuroanatomy of the placebo effect. Am J Psychiatry. 2002;159(5):728-737.
5. de la Fuente-Fernández R, Ruth TJ, Sossi V, et al. Expectation and dopamine release: mechanism of the placebo effect in Parkinson’s disease. Science. 2001;293(5532):1164-1166.
6. Charlesworth JEG, Petkovic G, Kelley JM, et al. Effects of placebos without deception compared with no treatment: a systematic review and meta‐analysis. J Evid Based Med. 2017;10(2):97-107.
7. Colloca L, Enck P, DeGrazia D. Relieving pain using dose-extending placebos: a scoping review. Pain. 2016;157(8):1590-1598.
8. Kaptchuk TJ, Kelley JM, Conboy LA, et al. Components of placebo effect: randomised controlled trial in patients with irritable bowel syndrome. BMJ. 2008;336(7651):999-1003.
9. Khan A, Kolts RL, Rapaport MH, et al. Magnitude of placebo response and drug-placebo differences across psychiatric disorders. Psychol Med. 2005;35(5):743-749.
10. Walsh BT, Seidman SN, Sysko R, Gould M. Placebo response in studies of major depression: variable, substantial, and growing. JAMA. 2002;287(14):1840-1847.
11. Kirsch I, Deacon BJ, Huedo-Medina TB, et al. Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration. PLoS Med. 2008;5(2):e45.
12. Kaptchuk TJ. Acupuncture: theory, efficacy, and practice. Ann Intern Med. 2002;136(5):374-383.
13. Kelley JM, Kraft-Todd G, Schapira L, et al. The influence of the patient-clinician relationship on healthcare outcomes: a systematic review and meta-analysis of randomized controlled trials. PLoS One. 2014;9(4):e94207.
14. Olsson B, Olsson B, Tibblin G. Effect of patients’ expectations on recovery from acute tonsillitis. Fam Pract. 1989;6(3):188-192.
15. Sox HC, Margulies I, Sox CH. Psychologically mediated effects of diagnostic tests. Ann Intern Med. 1981;95(6):680-685.
16. Stewart MA. Effective physician-patient communication and health outcomes: a review. CMAJ. 1995;152(9):1423-1433.
17. Girgis A, Cockburn J, Butow P, et al. Improving patient emotional functioning and psychological morbidity: evaluation of a consultation skills training program for oncologists. Patient Educ Couns. 2009;77(3):456-462.
18. Birkhäuer J, Gaab J, Kossowsky J, et al. Trust in the health care professional and health outcome: a meta-analysis. PLoS One. 2017;12(2):e0170988.
19. Thomas KB. General practice consultations: is there any point in being positive? Br Med J (Clin Res Ed). 1987;294(6581):1200-1202.
20. Howe LC, Goyer JP, Crum AJ. Harnessing the placebo effect: exploring the influence of physician characteristics on placebo response [published online May 9, 2017]. Health Psychol. doi: 10.1037/hea0000499.
21. Chen JA, Papakostas GI, Youn SJ, et al. Association between patient beliefs regarding assigned treatment and clinical response: reanalysis of data from the Hypericum Depression Trial Study Group. J Clin Psychiatry. 2011;72(12):1669-1676.
22. Kelley JM, Kaptchuk TJ, Cusin C, et al. Open-label placebo for major depressive disorder: a pilot randomized controlled trial. Psychother Psychosom. 2012;81(5):312-314.
23. Carvalho C, Caetano JM, Cunha L, et al. Open-label placebo treatment in chronic low back pain: a randomized controlled trial. Pain. 2016;157(12):2766-2772.
24. Kaptchuk TJ, Friedlander E, Kelley JM, et al. Placebos without deception: a randomized controlled trial in irritable bowel syndrome. PLoS One. 2010;5(12):e15591.
25. Park LC, Covi L. Nonblind placebo trial: an exploration of neurotic patients’ responses to placebo when its inert content is disclosed. Arch Gen Psychiatry. 1965;12(4):336-345.
26. Schaefer M, Harke R, Denke C. Open-label placebos improve symptoms in allergic rhinitis: a randomized controlled trial. Psychother Psychosom. 2016;85(6):373-374.
27. Aulas JJ, Rosner I. Efficacy of a non blind placebo prescription [in French]. Encephale. 2003;29(1):68-71.
28. Sandler AD, Glesne CE, Bodfish JW. Conditioned placebo dose reduction: a new treatment in attention deficit hyperactivity disorder? J Dev Behav Pediatr. 2010;31(5):369-375.
29. Ader R, Mercurio MG, Walton J, et al. Conditioned pharmacotherapeutic effects: a preliminary study. Psychosom Med. 2010;72(2):192-197.
30. Weiss RD, O’Malley SS, Hosking JD, et al; COMBINE Study Research Group. Do patients with alcohol dependence respond to placebo? Results from the COMBINE Study. J Stud Alcohol Drugs. 2008;69(6):878-884.
31. Mattick RP, Breen C, Kimber J, et al. Buprenorphine maintenance versus placebo or methadone maintenance for opioid dependence. Cochrane Database Syst Rev. 2014;(2):CD002207.
1. Shapiro AK, Shapiro E. The powerful placebo: from ancient priest to modern physician. Baltimore, MD: Johns Hopkins University Press; 1997.
2. Beecher HK. The powerful placebo. J Am Med Assoc. 1955;159(17):1602-1606.
3. Brown WA. The placebo effect in clinical practice. New York, NY: Oxford University Press; 2013.
4. Mayberg HS, Silva JA, Brannan SK, et al. The functional neuroanatomy of the placebo effect. Am J Psychiatry. 2002;159(5):728-737.
5. de la Fuente-Fernández R, Ruth TJ, Sossi V, et al. Expectation and dopamine release: mechanism of the placebo effect in Parkinson’s disease. Science. 2001;293(5532):1164-1166.
6. Charlesworth JEG, Petkovic G, Kelley JM, et al. Effects of placebos without deception compared with no treatment: a systematic review and meta‐analysis. J Evid Based Med. 2017;10(2):97-107.
7. Colloca L, Enck P, DeGrazia D. Relieving pain using dose-extending placebos: a scoping review. Pain. 2016;157(8):1590-1598.
8. Kaptchuk TJ, Kelley JM, Conboy LA, et al. Components of placebo effect: randomised controlled trial in patients with irritable bowel syndrome. BMJ. 2008;336(7651):999-1003.
9. Khan A, Kolts RL, Rapaport MH, et al. Magnitude of placebo response and drug-placebo differences across psychiatric disorders. Psychol Med. 2005;35(5):743-749.
10. Walsh BT, Seidman SN, Sysko R, Gould M. Placebo response in studies of major depression: variable, substantial, and growing. JAMA. 2002;287(14):1840-1847.
11. Kirsch I, Deacon BJ, Huedo-Medina TB, et al. Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration. PLoS Med. 2008;5(2):e45.
12. Kaptchuk TJ. Acupuncture: theory, efficacy, and practice. Ann Intern Med. 2002;136(5):374-383.
13. Kelley JM, Kraft-Todd G, Schapira L, et al. The influence of the patient-clinician relationship on healthcare outcomes: a systematic review and meta-analysis of randomized controlled trials. PLoS One. 2014;9(4):e94207.
14. Olsson B, Olsson B, Tibblin G. Effect of patients’ expectations on recovery from acute tonsillitis. Fam Pract. 1989;6(3):188-192.
15. Sox HC, Margulies I, Sox CH. Psychologically mediated effects of diagnostic tests. Ann Intern Med. 1981;95(6):680-685.
16. Stewart MA. Effective physician-patient communication and health outcomes: a review. CMAJ. 1995;152(9):1423-1433.
17. Girgis A, Cockburn J, Butow P, et al. Improving patient emotional functioning and psychological morbidity: evaluation of a consultation skills training program for oncologists. Patient Educ Couns. 2009;77(3):456-462.
18. Birkhäuer J, Gaab J, Kossowsky J, et al. Trust in the health care professional and health outcome: a meta-analysis. PLoS One. 2017;12(2):e0170988.
19. Thomas KB. General practice consultations: is there any point in being positive? Br Med J (Clin Res Ed). 1987;294(6581):1200-1202.
20. Howe LC, Goyer JP, Crum AJ. Harnessing the placebo effect: exploring the influence of physician characteristics on placebo response [published online May 9, 2017]. Health Psychol. doi: 10.1037/hea0000499.
21. Chen JA, Papakostas GI, Youn SJ, et al. Association between patient beliefs regarding assigned treatment and clinical response: reanalysis of data from the Hypericum Depression Trial Study Group. J Clin Psychiatry. 2011;72(12):1669-1676.
22. Kelley JM, Kaptchuk TJ, Cusin C, et al. Open-label placebo for major depressive disorder: a pilot randomized controlled trial. Psychother Psychosom. 2012;81(5):312-314.
23. Carvalho C, Caetano JM, Cunha L, et al. Open-label placebo treatment in chronic low back pain: a randomized controlled trial. Pain. 2016;157(12):2766-2772.
24. Kaptchuk TJ, Friedlander E, Kelley JM, et al. Placebos without deception: a randomized controlled trial in irritable bowel syndrome. PLoS One. 2010;5(12):e15591.
25. Park LC, Covi L. Nonblind placebo trial: an exploration of neurotic patients’ responses to placebo when its inert content is disclosed. Arch Gen Psychiatry. 1965;12(4):336-345.
26. Schaefer M, Harke R, Denke C. Open-label placebos improve symptoms in allergic rhinitis: a randomized controlled trial. Psychother Psychosom. 2016;85(6):373-374.
27. Aulas JJ, Rosner I. Efficacy of a non blind placebo prescription [in French]. Encephale. 2003;29(1):68-71.
28. Sandler AD, Glesne CE, Bodfish JW. Conditioned placebo dose reduction: a new treatment in attention deficit hyperactivity disorder? J Dev Behav Pediatr. 2010;31(5):369-375.
29. Ader R, Mercurio MG, Walton J, et al. Conditioned pharmacotherapeutic effects: a preliminary study. Psychosom Med. 2010;72(2):192-197.
30. Weiss RD, O’Malley SS, Hosking JD, et al; COMBINE Study Research Group. Do patients with alcohol dependence respond to placebo? Results from the COMBINE Study. J Stud Alcohol Drugs. 2008;69(6):878-884.
31. Mattick RP, Breen C, Kimber J, et al. Buprenorphine maintenance versus placebo or methadone maintenance for opioid dependence. Cochrane Database Syst Rev. 2014;(2):CD002207.
The placebo effect in psychiatric practice
Are we on the verge of a cocaine epidemic?
Lithium-induced bradycardia: A rare but serious adverse effect
Mr. C, age 30, with schizoaffective disorder, bipolar type, Cannabis abuse, and nicotine dependence, has been enrolled in a Program of Assertive Community Treatment (PACT) for approximately 5 years. He presents to the PACT clinic for follow-up with his psychiatrist. Mr. C reports dizziness, lightheadedness, blurred vision, and nausea worsening over the last few days, and he appears drowsy and hypoactive. He does not report any chest pain, abdominal pain, swelling, cold extremities, shortness of breath, vomiting, diarrhea, or blood loss. Mr. C admits he has eaten only once daily for several weeks because of delusional ideation that he is responsible for others suffering from anorexia nervosa.
His medical history includes gastroesophageal reflux disease. Mr. C’s medication regimen for the past year included total daily oral doses of
Because of Mr. C’s complaints, appearance, and low HR, the psychiatrist calls emergency medical services (EMS). Although the paramedics recommend emergency transport to the hospital, Mr. C refuses. The psychiatrist instructs Mr. C to stop taking lithium because of suspected lithium-induced bradycardia and a concern that he may be more susceptible to lithium toxicity with prolonged anorexia nervosa. When nursing staff evaluate Mr. C the next day, his vitals are HR 60 bpm, respirations 20 breaths per minute, and blood pressure 124/81 mm Hg; his dizziness, blurred vision, lightheadedness, and nausea are resolved.
Bradycardia is defined as a HR <60 bpm; however, symptoms may not occur until the HR is <50 bpm. Symptoms include fatigue, dizziness, lightheadedness, chest pain, shortness of breath, and syncope. The incidence of bradycardia during lithium treatment is unknown; it is considered a rare but serious adverse effect. A literature review reveals several case reports of bradycardia with lithium treatment,2-4 including symptomatic bradycardia after a single dose of lithium.5 Other possible causes of bradycardia include anorexia nervosa, hypothermia, hypothyroidism, hypoxia, infection, stroke, acute myocardial infarction, sedative or opiate use, increased vagal tone with exercise conditioning, and other medications including fluphenazine.6
Mr. C’s symptoms may have been assumed to be secondary to several possible causes, including bradycardia, dehydration from poor oral intake, lithium toxicity, or an undiagnosed medical condition. The combination of nausea, dizziness, anorexia nervosa, blurred vision, and lightheadedness in a patient receiving lithium would certainly trigger a clinician’s concern for lithium toxicity, but he (she) may not be aware of the risk of bradycardia as an adverse effect of lithium. Because Mr. C refused hospital transportation by EMS, discontinuing lithium appears to have been the safest option. Laboratory studies from the day after Mr. C presented to the clinic appeared to lessen the probability that lithium toxicity, hypothyroidism,
Although psychiatrists may be vigilant about monitoring for signs and symptoms of toxicity with lithium use by utilizing regular laboratory studies, they may not be as vigilant with monitoring vital signs at every patient visit (Table). This case demonstrates the importance of regular vital sign measurements to be able to detect this rare but serious adverse effect.
1. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239-245.
2. White B, Larry J, Kantharia BK. Protracted presyncope and profound bradycardia due to lithium toxicity. Int J Cardiol. 2008;125(3):e48-e50.
3. Palatnik A, Kates R. Bradycardia and medications: identify the dangerous pace. Nurs Manage. 2003;34(6):56A-56F.
4. La Rocca R, Foschi A, Preston NM, et al. QT interval prolongation and bradycardia in lithium-induced nephrogenic diabetes insipidus. Int J Cardiol. 2012;162(1):e1-e2.
5. Sabharwal MS, Annapureddy N, Agarwal SK, et al. Severe bradycardia caused by a single dose of lithium. Intern Med. 2013;52(7):767-769.
6. Homoud MK. Sinus bradycardia. UpToDate. www.uptodate.com/contents/sinus-bradycardia. Updated June 7, 2017. Accessed August 28, 2017.
Mr. C, age 30, with schizoaffective disorder, bipolar type, Cannabis abuse, and nicotine dependence, has been enrolled in a Program of Assertive Community Treatment (PACT) for approximately 5 years. He presents to the PACT clinic for follow-up with his psychiatrist. Mr. C reports dizziness, lightheadedness, blurred vision, and nausea worsening over the last few days, and he appears drowsy and hypoactive. He does not report any chest pain, abdominal pain, swelling, cold extremities, shortness of breath, vomiting, diarrhea, or blood loss. Mr. C admits he has eaten only once daily for several weeks because of delusional ideation that he is responsible for others suffering from anorexia nervosa.
His medical history includes gastroesophageal reflux disease. Mr. C’s medication regimen for the past year included total daily oral doses of
Because of Mr. C’s complaints, appearance, and low HR, the psychiatrist calls emergency medical services (EMS). Although the paramedics recommend emergency transport to the hospital, Mr. C refuses. The psychiatrist instructs Mr. C to stop taking lithium because of suspected lithium-induced bradycardia and a concern that he may be more susceptible to lithium toxicity with prolonged anorexia nervosa. When nursing staff evaluate Mr. C the next day, his vitals are HR 60 bpm, respirations 20 breaths per minute, and blood pressure 124/81 mm Hg; his dizziness, blurred vision, lightheadedness, and nausea are resolved.
Bradycardia is defined as a HR <60 bpm; however, symptoms may not occur until the HR is <50 bpm. Symptoms include fatigue, dizziness, lightheadedness, chest pain, shortness of breath, and syncope. The incidence of bradycardia during lithium treatment is unknown; it is considered a rare but serious adverse effect. A literature review reveals several case reports of bradycardia with lithium treatment,2-4 including symptomatic bradycardia after a single dose of lithium.5 Other possible causes of bradycardia include anorexia nervosa, hypothermia, hypothyroidism, hypoxia, infection, stroke, acute myocardial infarction, sedative or opiate use, increased vagal tone with exercise conditioning, and other medications including fluphenazine.6
Mr. C’s symptoms may have been assumed to be secondary to several possible causes, including bradycardia, dehydration from poor oral intake, lithium toxicity, or an undiagnosed medical condition. The combination of nausea, dizziness, anorexia nervosa, blurred vision, and lightheadedness in a patient receiving lithium would certainly trigger a clinician’s concern for lithium toxicity, but he (she) may not be aware of the risk of bradycardia as an adverse effect of lithium. Because Mr. C refused hospital transportation by EMS, discontinuing lithium appears to have been the safest option. Laboratory studies from the day after Mr. C presented to the clinic appeared to lessen the probability that lithium toxicity, hypothyroidism,
Although psychiatrists may be vigilant about monitoring for signs and symptoms of toxicity with lithium use by utilizing regular laboratory studies, they may not be as vigilant with monitoring vital signs at every patient visit (Table). This case demonstrates the importance of regular vital sign measurements to be able to detect this rare but serious adverse effect.
Mr. C, age 30, with schizoaffective disorder, bipolar type, Cannabis abuse, and nicotine dependence, has been enrolled in a Program of Assertive Community Treatment (PACT) for approximately 5 years. He presents to the PACT clinic for follow-up with his psychiatrist. Mr. C reports dizziness, lightheadedness, blurred vision, and nausea worsening over the last few days, and he appears drowsy and hypoactive. He does not report any chest pain, abdominal pain, swelling, cold extremities, shortness of breath, vomiting, diarrhea, or blood loss. Mr. C admits he has eaten only once daily for several weeks because of delusional ideation that he is responsible for others suffering from anorexia nervosa.
His medical history includes gastroesophageal reflux disease. Mr. C’s medication regimen for the past year included total daily oral doses of
Because of Mr. C’s complaints, appearance, and low HR, the psychiatrist calls emergency medical services (EMS). Although the paramedics recommend emergency transport to the hospital, Mr. C refuses. The psychiatrist instructs Mr. C to stop taking lithium because of suspected lithium-induced bradycardia and a concern that he may be more susceptible to lithium toxicity with prolonged anorexia nervosa. When nursing staff evaluate Mr. C the next day, his vitals are HR 60 bpm, respirations 20 breaths per minute, and blood pressure 124/81 mm Hg; his dizziness, blurred vision, lightheadedness, and nausea are resolved.
Bradycardia is defined as a HR <60 bpm; however, symptoms may not occur until the HR is <50 bpm. Symptoms include fatigue, dizziness, lightheadedness, chest pain, shortness of breath, and syncope. The incidence of bradycardia during lithium treatment is unknown; it is considered a rare but serious adverse effect. A literature review reveals several case reports of bradycardia with lithium treatment,2-4 including symptomatic bradycardia after a single dose of lithium.5 Other possible causes of bradycardia include anorexia nervosa, hypothermia, hypothyroidism, hypoxia, infection, stroke, acute myocardial infarction, sedative or opiate use, increased vagal tone with exercise conditioning, and other medications including fluphenazine.6
Mr. C’s symptoms may have been assumed to be secondary to several possible causes, including bradycardia, dehydration from poor oral intake, lithium toxicity, or an undiagnosed medical condition. The combination of nausea, dizziness, anorexia nervosa, blurred vision, and lightheadedness in a patient receiving lithium would certainly trigger a clinician’s concern for lithium toxicity, but he (she) may not be aware of the risk of bradycardia as an adverse effect of lithium. Because Mr. C refused hospital transportation by EMS, discontinuing lithium appears to have been the safest option. Laboratory studies from the day after Mr. C presented to the clinic appeared to lessen the probability that lithium toxicity, hypothyroidism,
Although psychiatrists may be vigilant about monitoring for signs and symptoms of toxicity with lithium use by utilizing regular laboratory studies, they may not be as vigilant with monitoring vital signs at every patient visit (Table). This case demonstrates the importance of regular vital sign measurements to be able to detect this rare but serious adverse effect.
1. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239-245.
2. White B, Larry J, Kantharia BK. Protracted presyncope and profound bradycardia due to lithium toxicity. Int J Cardiol. 2008;125(3):e48-e50.
3. Palatnik A, Kates R. Bradycardia and medications: identify the dangerous pace. Nurs Manage. 2003;34(6):56A-56F.
4. La Rocca R, Foschi A, Preston NM, et al. QT interval prolongation and bradycardia in lithium-induced nephrogenic diabetes insipidus. Int J Cardiol. 2012;162(1):e1-e2.
5. Sabharwal MS, Annapureddy N, Agarwal SK, et al. Severe bradycardia caused by a single dose of lithium. Intern Med. 2013;52(7):767-769.
6. Homoud MK. Sinus bradycardia. UpToDate. www.uptodate.com/contents/sinus-bradycardia. Updated June 7, 2017. Accessed August 28, 2017.
1. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239-245.
2. White B, Larry J, Kantharia BK. Protracted presyncope and profound bradycardia due to lithium toxicity. Int J Cardiol. 2008;125(3):e48-e50.
3. Palatnik A, Kates R. Bradycardia and medications: identify the dangerous pace. Nurs Manage. 2003;34(6):56A-56F.
4. La Rocca R, Foschi A, Preston NM, et al. QT interval prolongation and bradycardia in lithium-induced nephrogenic diabetes insipidus. Int J Cardiol. 2012;162(1):e1-e2.
5. Sabharwal MS, Annapureddy N, Agarwal SK, et al. Severe bradycardia caused by a single dose of lithium. Intern Med. 2013;52(7):767-769.
6. Homoud MK. Sinus bradycardia. UpToDate. www.uptodate.com/contents/sinus-bradycardia. Updated June 7, 2017. Accessed August 28, 2017.
‘Self-anesthetizing’ to cope with grief
CASE Grieving, delusional
Mr. M, age 51, is brought to the emergency department (ED) because of new-onset delusions and decreased self-care over the last 2 weeks following the sudden death of his wife. He has become expansive and grandiose, with pressured speech, increased energy, and markedly reduced sleep. Mr. M is preoccupied with the idea that he is “the first to survive a human reboot process” and says that his and his wife’s bodies and brains had been “split apart.” Mr. M has limited his food and fluid intake and lost 15 lb within the past 2 to 3 weeks.
Mr. M has no history of any affective, psychotic, or other major mental disorders or treatment. He reports that he has regularly used Cannabis over the last 10 years, and a few years ago, he started occasionally using nitrous oxide (N2O). He says that in the week following his wife’s death, he used N2O almost daily and in copious amounts. In an attempt to “self-anesthetize” himself after his wife’s funeral, he isolated himself in his bedroom and used escalating amounts of Cannabis and N2O, while continually working on a book about their life together.
At first, Mr. M shows little emotion and describes his situation as “interesting and fascinating.” He mentions that he thinks he might have been “psychotic” the week after his wife’s death, but he shows no sustained insight and immediately relapses into psychotic thinking. Over several hours in the ED, he is tearful and sad about his wife’s death. Mr. M recalls a similar experience of grief after his mother died when he was a teenager, but at that time he did not abuse substances or have psychotic symptoms. He is fully alert, fully oriented, and has no significant deficits of attention or memory.
[polldaddy:9859135]
The authors’ observations
Grief was a precipitating event, but by itself grief cannot explain psychosis. Psychotic depression is a possibility, but Mr. M’s psychotic features are incongruent with his mood. Mania would be a diagnosis of exclusion. Mr. M had no prior history of major affective illness. Mr. M was abusing Cannabis, which might independently contribute to psychosis1; however, he had been using it recreationally for 10 years without psychiatric problems. N2O, however, can cause symptoms consistent with Mr. M’s presentation.
[polldaddy:9859140]
EVALUATION Laboratory tests
Mr. M’s physical examination is notable only for an elevated blood pressure of 196/120 mm Hg. Neurologic examination is normal. Toxicology is positive for cannabinoids and negative for amphetamines, cocaine, opiates, and phencyclidine. Chemistries are normal except for a potassium of 3.4 mEq/L (reference range, 3.7 to 5.2 mEq/L) and a blood urine nitrogen of 25 mg/dL (reference range, 6 to 20 mg/dL), which are consistent with reduced food and fluid intake. Mr. M shows no signs of anemia. Hematocrit is 42% and mean corpuscular volume is 90 fL. Syphilis screen is negative; a head CT scan is unremarkable.
The authors’ observations
N2O, also known as “laughing gas,” is routinely used by dentists and pediatric anesthesiologists, and has other medical uses. Some studies have examined an adjunctive use of N2O for pain control in the ED and during colonoscopies.3,4
In the 2013 U.S. National Survey on Drug Use and Health, 16% of respondents reported lifetime illicit use of N2O.5,6 It is readily available in tanks used in medicine and industry and in small dispensers called “whippits” that can be legally purchased. Acute effects of N2O include euphoric mood, numbness, feeling of warmth, dizziness, and auditory hallucinations.7 The anesthetic effects of N2O are linked to endogenous release of opiates, and recent research links its anxiolytic activity to the facilitation of GABAergic inhibitory and N-methyl-
Beginning with a 1960 report of a series of patients with “megaloblastic madness,”17 there have been calls for increased awareness of the potential for vitamin B12 deficiency–induced psychiatric disorders, even in the absence of other hematologic or neurologic sequelae that would alert clinicians of the deficiency. In a case series of 141 patients with a broad array of neurologic and psychiatric symptoms associated with vitamin B12 deficiency, 40 (28%) patients had no anemia or macrocytosis.2
Vitamin B12-responsive psychosis has been reported as the sole manifestation of illness, without associated neurologic or hematologic symptoms, in only a few case reports. Vitamin B12 levels in these cases ranged from 75 to 236 pg/mL (reference range, 160 to 950 pg/mL).18-20 In all of these cases, the vitamin B12 deficiency was traced to dietary causes. The clinical evaluation of suspected vitamin B12 deficiency is outlined in the Figure.21 Mr. M had used Cannabis recreationally for a long time, and his Cannabis use acutely escalated with use of N2O. Long-term use of Cannabis alone is a risk factor for psychotic illness.22 Combined abuse of Cannabis and N2O has been reported to provoke psychotic illness. In a case report of a 22-year-old male who was treated for paranoid delusions, using Cannabis and 100 cartridges of N2O daily was associated with low vitamin B12 and elevated homocysteine and methylmalonic acid levels.23
Cannabis use may have played a role in Mr. M’s escalating N2O use. In a study comparing 9 active Cannabis users with 9 non-using controls, users rated the subjective effects of N2O as more intense than non-users.24 In our patient’s case, Cannabis may have played a role in both sustaining his escalating N2O abuse and potentiating its psychotomimetic effects.
It also is possible that Mr. M may have been “self-medicating” his grief with N2O. In a recent placebo-controlled crossover trial of 20 patients with treatment-resistant depression, Nagele et al25 found a significant rapid and week-long antidepressant effect of subanesthetic N2O use. A model involving NMDA receptor activation has been proposed.25,26 Zorumski et al26 further reviewed possible antidepressant mechanisms of N2O. They compared N2O with ketamine as an NMDA receptor antagonist, but also noted its distinct effects on glutaminergic and GABAergic neurotransmitter systems as well as other receptors and channels.26 However, illicit use of N2O poses toxicity dangers and has no current indication for psychiatric treatment.
TREATMENT Supplementation
Mr. M is diagnosed with substance-induced psychotic disorder. His symptoms were precipitated by an acute increase in N2O use, which has been shown to cause vitamin B12 deficiency, which we consider was likely a primary contributor to his presentation. Other potential contributing factors are premorbid hyperthymic temperament, a possible propensity to psychotic thinking under stress, the sudden death of his wife, acute grief, the potentiating role of Cannabis, dehydration, and general malnutrition. The death of a loved one is associated with an increased risk of developing substance use disorders.27
During a 15-day psychiatric hospitalization, Mr. M is given olanzapine, increased to 15 mg/d and oral vitamin B12, 1,000 mcg/d for 4 days, then IM cyanocobalamin for 7 days. Mr. M’s symptoms steadily improve, with normalization of sleep and near-total resolution of delusions. On hospital Day 14, his vitamin B12 levels are within normal limits (844 pg/mL). At discharge, Mr. M shows residual mild grandiosity, with limited insight into his illness and what caused it, but frank delusional ideation has clearly receded. He still shows some signs of grief. Mr. M is advised to stop using Cannabis and N2O and about the potential consequences of continued use.
The authors’ observations
For patients with vitamin B12 deficiency, guidelines from the National Health Service in the United Kingdom and the British Society for Haematology recommend treatment with IM hydroxocobalamin, 1,000 IU, 3 times weekly, for 2 weeks.21,28 For patients with neurologic symptoms, the British National Foundation recommends treatment with IM hydroxocobalamin, 1,000 IU, on alternative days until there is no further improvement.21
This case is a reminder for clinicians to screen for inhalant use, specifically N2O, which can precipitate vitamin B12 deficiency with psychiatric symptoms as the only presenting concern. Clinicians should consider measuring vitamin B12 levels in psychiatric patients at risk of deficiency of this nutrient, including older adults, vegetarians, and those with alimentary disorders.29,30 Dietary sources of vitamin B12 include meat, milk, egg, fish, and shellfish.31 The body can store a total of 2 to 5 mg of vitamin B12; thus, it takes 2 to 5 years to develop vitamin B12 deficiency from malabsorption and can take as long as 20 years to develop vitamin B12 deficiency from vegetarianism.32 However, by chemically inactivating vitamin B12, N2O causes a rapid functional deficiency, as was seen in our patient.
OUTCOME Improved insight
At a 1-week follow-up appointment with a psychiatrist, Mr. M has no evident psychotic symptoms. He reports that he has not used Cannabis or N2O, and he discontinues olanzapine following this visit. Two weeks later, Mr. M shows no psychotic or affective symptoms other than grief, which is appropriately expressed. His insight has improved. He commits to not using Cannabis, N2O, or any other illicit substances. Mr. M is referred back to his long-standing primary care provider with the understanding that if any psychiatric symptoms recur he will see a psychiatrist again.
1. Semple DM, McIntosh AM, Lawrie SM. Cannabis as a risk factor for psychosis: systematic review. J Psychopharmacol. 2005;19(2):187-194.
2. Lindenbaum J, Healton EB, Savage DG, et al. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med. 1988;318(26)1720-1728.
3. Herres J, Chudnofsky CR, Manur R, et al. The use of inhaled nitrous oxide for analgesia in adult ED patients: a pilot study. Am J Emerg Med. 2016;34(2):269-273.
4. Aboumarzouk OM, Agarwal T, Syed Nong Chek SA, et al. Nitrous oxide for colonoscopy. Cochrane Database Syst Rev. 2011;(8):CD008506.
5. National Institute on Drug Abuse. Drug facts: inhalants. http://www.drugabuse.gov/publications/drugfacts/inhalants. Updated February 2017. Accessed September 30, 2017.
6. SAMHSA, Center for Behavioral Health Statistics and Quality, National Survey on Drug Use and Health 2012 and 2013: Table 1.88C. https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs2013.pdf. Published September 4, 2017. Accessed September 30, 2017.
7. Brouette T, Anton R. Clinical review of inhalants. Am J Addict. 2001;10(1):79-94.
8. Emmanouil DE, Quock RM. Advances in understanding the actions of nitrous oxide. Anesth Prog. 2007;54(1):9-18.
9. Garakani A, Jaffe RJ, Savla D, et al. Neurologic, psychiatric, and other medical manifestations of nitrous oxide abuse: a systematic review of the case literature. Am J Addict. 2016;25(5):358-369.
10. Hathout L, El-Saden S. Nitrous oxide-induced B12 deficiency myelopathy: perspectives on the clinical biochemistry of vitamin B12. J Neurol Sci. 2011;301(1-2):1-8.
11. van Tonder SV, Ruck A, van der Westhuyzen J, et al. Dissociation of methionine synthetase (EC 2.1.1.13) activity and impairment of DNA synthesis in fruit bats (Rousettus aegyptiacus) with nitrous oxide-induced vitamin B12 deficiency. Br J Nutr. 1986;55(1):187-192.
12. Schrier SL, Mentzer WC, Tirnauer JS. Diagnosis and treatment of vitamin B12 and folate deficiency. UpToDate. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-vitamin-b12-and-folate-deficiency. Updated September 30, 2011. Accessed September 8, 2015.
13. Sethi NK, Mullin P, Torgovnick J, et al. Nitrous oxide “whippit” abuse presenting with cobalamin responsive psychosis. J Med Toxicol. 2006;2(2):71-74.
14. Cousaert C, Heylens G, Audenaert K. Laughing gas abuse is no joke. An overview of the implications for psychiatric practice. Clin Neurol Neurosurg. 2013;115(7):859-862.
15. Brodsky L, Zuniga J. Nitrous oxide: a psychotogenic agent. Compr Psychiatry. 1975;16(2):185-188.
16. Wong SL, Harrison R, Mattman A, et al. Nitrous oxide (N2O)-induced acute psychosis. Can J Neurol Sci. 2014;41(5):672-674.
17. Smith AD. Megaloblastic madness. Br Med J. 1960;2(5216):1840-1845.
18. Masalha R, Chudakov B, Muhamad M, et al. Cobalamin-responsive psychosis as the sole manifestation of vitamin B12 deficiency. Isr Med Associ J. 2001;3(9):701-703.
19. Kuo SC, Yeh SB, Yeh YW, et al. Schizophrenia-like psychotic episode precipitated by cobalamin deficiency. Gen Hosp Psychiatry. 2009;31(6):586-588.
20. Raveendranathan D, Shiva L, Venkatasubramanian G, et al. Vitamin B12 deficiency masquerading as clozapine-resistant psychotic symptoms in schizophrenia. J Neuropsychiatry Clin Neurosci. 2013;25(2):E34-E35.
21. Devalia V, Hamilton MS, Molloy AM; British Committee for Standards in Haematology. Guidelines for the diagnosis and treatment of cobalamin and folate disorders. Br J Haematol. 2014;166(4):496-513.
22. Moore THM, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319-328.
23. Garakani A, Welch AK, Jaffe RJ, et al. Psychosis and low cyanocobalamin in a patient abusing nitrous oxide and cannabis. Psychosomatics. 2014;55(6):715-719.
24. Yajnik S, Thapar P, Lichtor JL, et al. Effects of marijuana history on the subjective, psychomotor, and reinforcing effects of nitrous oxide in human. Drug Alcohol Depend. 1994;36(3):227-236.
25. Nagele P, Duma A, Kopec M, et al. Nitrous oxide for treatment-resistant major depression: a proof-of-concept trial. Biol Psychiatry. 2015;78(1):10-18.
26. Zorumski CF, Nagele P, Mennerick S, et al. Treatment-resistant major depression: rationale for NMDA receptors as targets and nitrous oxide as therapy. Front Psychiatry. 2015;6:172.
27. Shear MK. Clinical practice. Complicated grief. N Engl J Med. 2015;372(2):153-160.
28. Knechtli CJC, Crowe JN. Guidelines for the investigation & management of vitamin B12 deficiency. Royal United Hospital Bath, National Health Service. http://www.ruh.nhs.uk/For_Clinicians/departments_ruh/Pathology/documents/haematology/B12_-_advice_on_investigation_management.pdf. Accessed June 14, 2016.
29. Jayaram N, Rao MG, Narashima A, et al. Vitamin B12 levels and psychiatric symptomatology: a case series. J Neuropsychiatry Clin Neurosci. 2013;25(2):150-152.
30. Marks PW, Zukerberg LR. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 30-2004. A 37-year-old woman with paresthesias of the arms and legs. N Engl J Med. 2004;351(13):1333-1341.
31. Watanabe F. Vitamin B12 sources and bioavailablility. Exp Biol Med (Maywood). 2007;232(10):1266-1274.
32. Green R, Kinsella LJ. Current concepts in the diagnosis of cobalamin deficiency. Neurology. 1995;45(8):1435-1440.
CASE Grieving, delusional
Mr. M, age 51, is brought to the emergency department (ED) because of new-onset delusions and decreased self-care over the last 2 weeks following the sudden death of his wife. He has become expansive and grandiose, with pressured speech, increased energy, and markedly reduced sleep. Mr. M is preoccupied with the idea that he is “the first to survive a human reboot process” and says that his and his wife’s bodies and brains had been “split apart.” Mr. M has limited his food and fluid intake and lost 15 lb within the past 2 to 3 weeks.
Mr. M has no history of any affective, psychotic, or other major mental disorders or treatment. He reports that he has regularly used Cannabis over the last 10 years, and a few years ago, he started occasionally using nitrous oxide (N2O). He says that in the week following his wife’s death, he used N2O almost daily and in copious amounts. In an attempt to “self-anesthetize” himself after his wife’s funeral, he isolated himself in his bedroom and used escalating amounts of Cannabis and N2O, while continually working on a book about their life together.
At first, Mr. M shows little emotion and describes his situation as “interesting and fascinating.” He mentions that he thinks he might have been “psychotic” the week after his wife’s death, but he shows no sustained insight and immediately relapses into psychotic thinking. Over several hours in the ED, he is tearful and sad about his wife’s death. Mr. M recalls a similar experience of grief after his mother died when he was a teenager, but at that time he did not abuse substances or have psychotic symptoms. He is fully alert, fully oriented, and has no significant deficits of attention or memory.
[polldaddy:9859135]
The authors’ observations
Grief was a precipitating event, but by itself grief cannot explain psychosis. Psychotic depression is a possibility, but Mr. M’s psychotic features are incongruent with his mood. Mania would be a diagnosis of exclusion. Mr. M had no prior history of major affective illness. Mr. M was abusing Cannabis, which might independently contribute to psychosis1; however, he had been using it recreationally for 10 years without psychiatric problems. N2O, however, can cause symptoms consistent with Mr. M’s presentation.
[polldaddy:9859140]
EVALUATION Laboratory tests
Mr. M’s physical examination is notable only for an elevated blood pressure of 196/120 mm Hg. Neurologic examination is normal. Toxicology is positive for cannabinoids and negative for amphetamines, cocaine, opiates, and phencyclidine. Chemistries are normal except for a potassium of 3.4 mEq/L (reference range, 3.7 to 5.2 mEq/L) and a blood urine nitrogen of 25 mg/dL (reference range, 6 to 20 mg/dL), which are consistent with reduced food and fluid intake. Mr. M shows no signs of anemia. Hematocrit is 42% and mean corpuscular volume is 90 fL. Syphilis screen is negative; a head CT scan is unremarkable.
The authors’ observations
N2O, also known as “laughing gas,” is routinely used by dentists and pediatric anesthesiologists, and has other medical uses. Some studies have examined an adjunctive use of N2O for pain control in the ED and during colonoscopies.3,4
In the 2013 U.S. National Survey on Drug Use and Health, 16% of respondents reported lifetime illicit use of N2O.5,6 It is readily available in tanks used in medicine and industry and in small dispensers called “whippits” that can be legally purchased. Acute effects of N2O include euphoric mood, numbness, feeling of warmth, dizziness, and auditory hallucinations.7 The anesthetic effects of N2O are linked to endogenous release of opiates, and recent research links its anxiolytic activity to the facilitation of GABAergic inhibitory and N-methyl-
Beginning with a 1960 report of a series of patients with “megaloblastic madness,”17 there have been calls for increased awareness of the potential for vitamin B12 deficiency–induced psychiatric disorders, even in the absence of other hematologic or neurologic sequelae that would alert clinicians of the deficiency. In a case series of 141 patients with a broad array of neurologic and psychiatric symptoms associated with vitamin B12 deficiency, 40 (28%) patients had no anemia or macrocytosis.2
Vitamin B12-responsive psychosis has been reported as the sole manifestation of illness, without associated neurologic or hematologic symptoms, in only a few case reports. Vitamin B12 levels in these cases ranged from 75 to 236 pg/mL (reference range, 160 to 950 pg/mL).18-20 In all of these cases, the vitamin B12 deficiency was traced to dietary causes. The clinical evaluation of suspected vitamin B12 deficiency is outlined in the Figure.21 Mr. M had used Cannabis recreationally for a long time, and his Cannabis use acutely escalated with use of N2O. Long-term use of Cannabis alone is a risk factor for psychotic illness.22 Combined abuse of Cannabis and N2O has been reported to provoke psychotic illness. In a case report of a 22-year-old male who was treated for paranoid delusions, using Cannabis and 100 cartridges of N2O daily was associated with low vitamin B12 and elevated homocysteine and methylmalonic acid levels.23
Cannabis use may have played a role in Mr. M’s escalating N2O use. In a study comparing 9 active Cannabis users with 9 non-using controls, users rated the subjective effects of N2O as more intense than non-users.24 In our patient’s case, Cannabis may have played a role in both sustaining his escalating N2O abuse and potentiating its psychotomimetic effects.
It also is possible that Mr. M may have been “self-medicating” his grief with N2O. In a recent placebo-controlled crossover trial of 20 patients with treatment-resistant depression, Nagele et al25 found a significant rapid and week-long antidepressant effect of subanesthetic N2O use. A model involving NMDA receptor activation has been proposed.25,26 Zorumski et al26 further reviewed possible antidepressant mechanisms of N2O. They compared N2O with ketamine as an NMDA receptor antagonist, but also noted its distinct effects on glutaminergic and GABAergic neurotransmitter systems as well as other receptors and channels.26 However, illicit use of N2O poses toxicity dangers and has no current indication for psychiatric treatment.
TREATMENT Supplementation
Mr. M is diagnosed with substance-induced psychotic disorder. His symptoms were precipitated by an acute increase in N2O use, which has been shown to cause vitamin B12 deficiency, which we consider was likely a primary contributor to his presentation. Other potential contributing factors are premorbid hyperthymic temperament, a possible propensity to psychotic thinking under stress, the sudden death of his wife, acute grief, the potentiating role of Cannabis, dehydration, and general malnutrition. The death of a loved one is associated with an increased risk of developing substance use disorders.27
During a 15-day psychiatric hospitalization, Mr. M is given olanzapine, increased to 15 mg/d and oral vitamin B12, 1,000 mcg/d for 4 days, then IM cyanocobalamin for 7 days. Mr. M’s symptoms steadily improve, with normalization of sleep and near-total resolution of delusions. On hospital Day 14, his vitamin B12 levels are within normal limits (844 pg/mL). At discharge, Mr. M shows residual mild grandiosity, with limited insight into his illness and what caused it, but frank delusional ideation has clearly receded. He still shows some signs of grief. Mr. M is advised to stop using Cannabis and N2O and about the potential consequences of continued use.
The authors’ observations
For patients with vitamin B12 deficiency, guidelines from the National Health Service in the United Kingdom and the British Society for Haematology recommend treatment with IM hydroxocobalamin, 1,000 IU, 3 times weekly, for 2 weeks.21,28 For patients with neurologic symptoms, the British National Foundation recommends treatment with IM hydroxocobalamin, 1,000 IU, on alternative days until there is no further improvement.21
This case is a reminder for clinicians to screen for inhalant use, specifically N2O, which can precipitate vitamin B12 deficiency with psychiatric symptoms as the only presenting concern. Clinicians should consider measuring vitamin B12 levels in psychiatric patients at risk of deficiency of this nutrient, including older adults, vegetarians, and those with alimentary disorders.29,30 Dietary sources of vitamin B12 include meat, milk, egg, fish, and shellfish.31 The body can store a total of 2 to 5 mg of vitamin B12; thus, it takes 2 to 5 years to develop vitamin B12 deficiency from malabsorption and can take as long as 20 years to develop vitamin B12 deficiency from vegetarianism.32 However, by chemically inactivating vitamin B12, N2O causes a rapid functional deficiency, as was seen in our patient.
OUTCOME Improved insight
At a 1-week follow-up appointment with a psychiatrist, Mr. M has no evident psychotic symptoms. He reports that he has not used Cannabis or N2O, and he discontinues olanzapine following this visit. Two weeks later, Mr. M shows no psychotic or affective symptoms other than grief, which is appropriately expressed. His insight has improved. He commits to not using Cannabis, N2O, or any other illicit substances. Mr. M is referred back to his long-standing primary care provider with the understanding that if any psychiatric symptoms recur he will see a psychiatrist again.
CASE Grieving, delusional
Mr. M, age 51, is brought to the emergency department (ED) because of new-onset delusions and decreased self-care over the last 2 weeks following the sudden death of his wife. He has become expansive and grandiose, with pressured speech, increased energy, and markedly reduced sleep. Mr. M is preoccupied with the idea that he is “the first to survive a human reboot process” and says that his and his wife’s bodies and brains had been “split apart.” Mr. M has limited his food and fluid intake and lost 15 lb within the past 2 to 3 weeks.
Mr. M has no history of any affective, psychotic, or other major mental disorders or treatment. He reports that he has regularly used Cannabis over the last 10 years, and a few years ago, he started occasionally using nitrous oxide (N2O). He says that in the week following his wife’s death, he used N2O almost daily and in copious amounts. In an attempt to “self-anesthetize” himself after his wife’s funeral, he isolated himself in his bedroom and used escalating amounts of Cannabis and N2O, while continually working on a book about their life together.
At first, Mr. M shows little emotion and describes his situation as “interesting and fascinating.” He mentions that he thinks he might have been “psychotic” the week after his wife’s death, but he shows no sustained insight and immediately relapses into psychotic thinking. Over several hours in the ED, he is tearful and sad about his wife’s death. Mr. M recalls a similar experience of grief after his mother died when he was a teenager, but at that time he did not abuse substances or have psychotic symptoms. He is fully alert, fully oriented, and has no significant deficits of attention or memory.
[polldaddy:9859135]
The authors’ observations
Grief was a precipitating event, but by itself grief cannot explain psychosis. Psychotic depression is a possibility, but Mr. M’s psychotic features are incongruent with his mood. Mania would be a diagnosis of exclusion. Mr. M had no prior history of major affective illness. Mr. M was abusing Cannabis, which might independently contribute to psychosis1; however, he had been using it recreationally for 10 years without psychiatric problems. N2O, however, can cause symptoms consistent with Mr. M’s presentation.
[polldaddy:9859140]
EVALUATION Laboratory tests
Mr. M’s physical examination is notable only for an elevated blood pressure of 196/120 mm Hg. Neurologic examination is normal. Toxicology is positive for cannabinoids and negative for amphetamines, cocaine, opiates, and phencyclidine. Chemistries are normal except for a potassium of 3.4 mEq/L (reference range, 3.7 to 5.2 mEq/L) and a blood urine nitrogen of 25 mg/dL (reference range, 6 to 20 mg/dL), which are consistent with reduced food and fluid intake. Mr. M shows no signs of anemia. Hematocrit is 42% and mean corpuscular volume is 90 fL. Syphilis screen is negative; a head CT scan is unremarkable.
The authors’ observations
N2O, also known as “laughing gas,” is routinely used by dentists and pediatric anesthesiologists, and has other medical uses. Some studies have examined an adjunctive use of N2O for pain control in the ED and during colonoscopies.3,4
In the 2013 U.S. National Survey on Drug Use and Health, 16% of respondents reported lifetime illicit use of N2O.5,6 It is readily available in tanks used in medicine and industry and in small dispensers called “whippits” that can be legally purchased. Acute effects of N2O include euphoric mood, numbness, feeling of warmth, dizziness, and auditory hallucinations.7 The anesthetic effects of N2O are linked to endogenous release of opiates, and recent research links its anxiolytic activity to the facilitation of GABAergic inhibitory and N-methyl-
Beginning with a 1960 report of a series of patients with “megaloblastic madness,”17 there have been calls for increased awareness of the potential for vitamin B12 deficiency–induced psychiatric disorders, even in the absence of other hematologic or neurologic sequelae that would alert clinicians of the deficiency. In a case series of 141 patients with a broad array of neurologic and psychiatric symptoms associated with vitamin B12 deficiency, 40 (28%) patients had no anemia or macrocytosis.2
Vitamin B12-responsive psychosis has been reported as the sole manifestation of illness, without associated neurologic or hematologic symptoms, in only a few case reports. Vitamin B12 levels in these cases ranged from 75 to 236 pg/mL (reference range, 160 to 950 pg/mL).18-20 In all of these cases, the vitamin B12 deficiency was traced to dietary causes. The clinical evaluation of suspected vitamin B12 deficiency is outlined in the Figure.21 Mr. M had used Cannabis recreationally for a long time, and his Cannabis use acutely escalated with use of N2O. Long-term use of Cannabis alone is a risk factor for psychotic illness.22 Combined abuse of Cannabis and N2O has been reported to provoke psychotic illness. In a case report of a 22-year-old male who was treated for paranoid delusions, using Cannabis and 100 cartridges of N2O daily was associated with low vitamin B12 and elevated homocysteine and methylmalonic acid levels.23
Cannabis use may have played a role in Mr. M’s escalating N2O use. In a study comparing 9 active Cannabis users with 9 non-using controls, users rated the subjective effects of N2O as more intense than non-users.24 In our patient’s case, Cannabis may have played a role in both sustaining his escalating N2O abuse and potentiating its psychotomimetic effects.
It also is possible that Mr. M may have been “self-medicating” his grief with N2O. In a recent placebo-controlled crossover trial of 20 patients with treatment-resistant depression, Nagele et al25 found a significant rapid and week-long antidepressant effect of subanesthetic N2O use. A model involving NMDA receptor activation has been proposed.25,26 Zorumski et al26 further reviewed possible antidepressant mechanisms of N2O. They compared N2O with ketamine as an NMDA receptor antagonist, but also noted its distinct effects on glutaminergic and GABAergic neurotransmitter systems as well as other receptors and channels.26 However, illicit use of N2O poses toxicity dangers and has no current indication for psychiatric treatment.
TREATMENT Supplementation
Mr. M is diagnosed with substance-induced psychotic disorder. His symptoms were precipitated by an acute increase in N2O use, which has been shown to cause vitamin B12 deficiency, which we consider was likely a primary contributor to his presentation. Other potential contributing factors are premorbid hyperthymic temperament, a possible propensity to psychotic thinking under stress, the sudden death of his wife, acute grief, the potentiating role of Cannabis, dehydration, and general malnutrition. The death of a loved one is associated with an increased risk of developing substance use disorders.27
During a 15-day psychiatric hospitalization, Mr. M is given olanzapine, increased to 15 mg/d and oral vitamin B12, 1,000 mcg/d for 4 days, then IM cyanocobalamin for 7 days. Mr. M’s symptoms steadily improve, with normalization of sleep and near-total resolution of delusions. On hospital Day 14, his vitamin B12 levels are within normal limits (844 pg/mL). At discharge, Mr. M shows residual mild grandiosity, with limited insight into his illness and what caused it, but frank delusional ideation has clearly receded. He still shows some signs of grief. Mr. M is advised to stop using Cannabis and N2O and about the potential consequences of continued use.
The authors’ observations
For patients with vitamin B12 deficiency, guidelines from the National Health Service in the United Kingdom and the British Society for Haematology recommend treatment with IM hydroxocobalamin, 1,000 IU, 3 times weekly, for 2 weeks.21,28 For patients with neurologic symptoms, the British National Foundation recommends treatment with IM hydroxocobalamin, 1,000 IU, on alternative days until there is no further improvement.21
This case is a reminder for clinicians to screen for inhalant use, specifically N2O, which can precipitate vitamin B12 deficiency with psychiatric symptoms as the only presenting concern. Clinicians should consider measuring vitamin B12 levels in psychiatric patients at risk of deficiency of this nutrient, including older adults, vegetarians, and those with alimentary disorders.29,30 Dietary sources of vitamin B12 include meat, milk, egg, fish, and shellfish.31 The body can store a total of 2 to 5 mg of vitamin B12; thus, it takes 2 to 5 years to develop vitamin B12 deficiency from malabsorption and can take as long as 20 years to develop vitamin B12 deficiency from vegetarianism.32 However, by chemically inactivating vitamin B12, N2O causes a rapid functional deficiency, as was seen in our patient.
OUTCOME Improved insight
At a 1-week follow-up appointment with a psychiatrist, Mr. M has no evident psychotic symptoms. He reports that he has not used Cannabis or N2O, and he discontinues olanzapine following this visit. Two weeks later, Mr. M shows no psychotic or affective symptoms other than grief, which is appropriately expressed. His insight has improved. He commits to not using Cannabis, N2O, or any other illicit substances. Mr. M is referred back to his long-standing primary care provider with the understanding that if any psychiatric symptoms recur he will see a psychiatrist again.
1. Semple DM, McIntosh AM, Lawrie SM. Cannabis as a risk factor for psychosis: systematic review. J Psychopharmacol. 2005;19(2):187-194.
2. Lindenbaum J, Healton EB, Savage DG, et al. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med. 1988;318(26)1720-1728.
3. Herres J, Chudnofsky CR, Manur R, et al. The use of inhaled nitrous oxide for analgesia in adult ED patients: a pilot study. Am J Emerg Med. 2016;34(2):269-273.
4. Aboumarzouk OM, Agarwal T, Syed Nong Chek SA, et al. Nitrous oxide for colonoscopy. Cochrane Database Syst Rev. 2011;(8):CD008506.
5. National Institute on Drug Abuse. Drug facts: inhalants. http://www.drugabuse.gov/publications/drugfacts/inhalants. Updated February 2017. Accessed September 30, 2017.
6. SAMHSA, Center for Behavioral Health Statistics and Quality, National Survey on Drug Use and Health 2012 and 2013: Table 1.88C. https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs2013.pdf. Published September 4, 2017. Accessed September 30, 2017.
7. Brouette T, Anton R. Clinical review of inhalants. Am J Addict. 2001;10(1):79-94.
8. Emmanouil DE, Quock RM. Advances in understanding the actions of nitrous oxide. Anesth Prog. 2007;54(1):9-18.
9. Garakani A, Jaffe RJ, Savla D, et al. Neurologic, psychiatric, and other medical manifestations of nitrous oxide abuse: a systematic review of the case literature. Am J Addict. 2016;25(5):358-369.
10. Hathout L, El-Saden S. Nitrous oxide-induced B12 deficiency myelopathy: perspectives on the clinical biochemistry of vitamin B12. J Neurol Sci. 2011;301(1-2):1-8.
11. van Tonder SV, Ruck A, van der Westhuyzen J, et al. Dissociation of methionine synthetase (EC 2.1.1.13) activity and impairment of DNA synthesis in fruit bats (Rousettus aegyptiacus) with nitrous oxide-induced vitamin B12 deficiency. Br J Nutr. 1986;55(1):187-192.
12. Schrier SL, Mentzer WC, Tirnauer JS. Diagnosis and treatment of vitamin B12 and folate deficiency. UpToDate. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-vitamin-b12-and-folate-deficiency. Updated September 30, 2011. Accessed September 8, 2015.
13. Sethi NK, Mullin P, Torgovnick J, et al. Nitrous oxide “whippit” abuse presenting with cobalamin responsive psychosis. J Med Toxicol. 2006;2(2):71-74.
14. Cousaert C, Heylens G, Audenaert K. Laughing gas abuse is no joke. An overview of the implications for psychiatric practice. Clin Neurol Neurosurg. 2013;115(7):859-862.
15. Brodsky L, Zuniga J. Nitrous oxide: a psychotogenic agent. Compr Psychiatry. 1975;16(2):185-188.
16. Wong SL, Harrison R, Mattman A, et al. Nitrous oxide (N2O)-induced acute psychosis. Can J Neurol Sci. 2014;41(5):672-674.
17. Smith AD. Megaloblastic madness. Br Med J. 1960;2(5216):1840-1845.
18. Masalha R, Chudakov B, Muhamad M, et al. Cobalamin-responsive psychosis as the sole manifestation of vitamin B12 deficiency. Isr Med Associ J. 2001;3(9):701-703.
19. Kuo SC, Yeh SB, Yeh YW, et al. Schizophrenia-like psychotic episode precipitated by cobalamin deficiency. Gen Hosp Psychiatry. 2009;31(6):586-588.
20. Raveendranathan D, Shiva L, Venkatasubramanian G, et al. Vitamin B12 deficiency masquerading as clozapine-resistant psychotic symptoms in schizophrenia. J Neuropsychiatry Clin Neurosci. 2013;25(2):E34-E35.
21. Devalia V, Hamilton MS, Molloy AM; British Committee for Standards in Haematology. Guidelines for the diagnosis and treatment of cobalamin and folate disorders. Br J Haematol. 2014;166(4):496-513.
22. Moore THM, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319-328.
23. Garakani A, Welch AK, Jaffe RJ, et al. Psychosis and low cyanocobalamin in a patient abusing nitrous oxide and cannabis. Psychosomatics. 2014;55(6):715-719.
24. Yajnik S, Thapar P, Lichtor JL, et al. Effects of marijuana history on the subjective, psychomotor, and reinforcing effects of nitrous oxide in human. Drug Alcohol Depend. 1994;36(3):227-236.
25. Nagele P, Duma A, Kopec M, et al. Nitrous oxide for treatment-resistant major depression: a proof-of-concept trial. Biol Psychiatry. 2015;78(1):10-18.
26. Zorumski CF, Nagele P, Mennerick S, et al. Treatment-resistant major depression: rationale for NMDA receptors as targets and nitrous oxide as therapy. Front Psychiatry. 2015;6:172.
27. Shear MK. Clinical practice. Complicated grief. N Engl J Med. 2015;372(2):153-160.
28. Knechtli CJC, Crowe JN. Guidelines for the investigation & management of vitamin B12 deficiency. Royal United Hospital Bath, National Health Service. http://www.ruh.nhs.uk/For_Clinicians/departments_ruh/Pathology/documents/haematology/B12_-_advice_on_investigation_management.pdf. Accessed June 14, 2016.
29. Jayaram N, Rao MG, Narashima A, et al. Vitamin B12 levels and psychiatric symptomatology: a case series. J Neuropsychiatry Clin Neurosci. 2013;25(2):150-152.
30. Marks PW, Zukerberg LR. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 30-2004. A 37-year-old woman with paresthesias of the arms and legs. N Engl J Med. 2004;351(13):1333-1341.
31. Watanabe F. Vitamin B12 sources and bioavailablility. Exp Biol Med (Maywood). 2007;232(10):1266-1274.
32. Green R, Kinsella LJ. Current concepts in the diagnosis of cobalamin deficiency. Neurology. 1995;45(8):1435-1440.
1. Semple DM, McIntosh AM, Lawrie SM. Cannabis as a risk factor for psychosis: systematic review. J Psychopharmacol. 2005;19(2):187-194.
2. Lindenbaum J, Healton EB, Savage DG, et al. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med. 1988;318(26)1720-1728.
3. Herres J, Chudnofsky CR, Manur R, et al. The use of inhaled nitrous oxide for analgesia in adult ED patients: a pilot study. Am J Emerg Med. 2016;34(2):269-273.
4. Aboumarzouk OM, Agarwal T, Syed Nong Chek SA, et al. Nitrous oxide for colonoscopy. Cochrane Database Syst Rev. 2011;(8):CD008506.
5. National Institute on Drug Abuse. Drug facts: inhalants. http://www.drugabuse.gov/publications/drugfacts/inhalants. Updated February 2017. Accessed September 30, 2017.
6. SAMHSA, Center for Behavioral Health Statistics and Quality, National Survey on Drug Use and Health 2012 and 2013: Table 1.88C. https://www.samhsa.gov/data/sites/default/files/NSDUH-DetTabs2013.pdf. Published September 4, 2017. Accessed September 30, 2017.
7. Brouette T, Anton R. Clinical review of inhalants. Am J Addict. 2001;10(1):79-94.
8. Emmanouil DE, Quock RM. Advances in understanding the actions of nitrous oxide. Anesth Prog. 2007;54(1):9-18.
9. Garakani A, Jaffe RJ, Savla D, et al. Neurologic, psychiatric, and other medical manifestations of nitrous oxide abuse: a systematic review of the case literature. Am J Addict. 2016;25(5):358-369.
10. Hathout L, El-Saden S. Nitrous oxide-induced B12 deficiency myelopathy: perspectives on the clinical biochemistry of vitamin B12. J Neurol Sci. 2011;301(1-2):1-8.
11. van Tonder SV, Ruck A, van der Westhuyzen J, et al. Dissociation of methionine synthetase (EC 2.1.1.13) activity and impairment of DNA synthesis in fruit bats (Rousettus aegyptiacus) with nitrous oxide-induced vitamin B12 deficiency. Br J Nutr. 1986;55(1):187-192.
12. Schrier SL, Mentzer WC, Tirnauer JS. Diagnosis and treatment of vitamin B12 and folate deficiency. UpToDate. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-vitamin-b12-and-folate-deficiency. Updated September 30, 2011. Accessed September 8, 2015.
13. Sethi NK, Mullin P, Torgovnick J, et al. Nitrous oxide “whippit” abuse presenting with cobalamin responsive psychosis. J Med Toxicol. 2006;2(2):71-74.
14. Cousaert C, Heylens G, Audenaert K. Laughing gas abuse is no joke. An overview of the implications for psychiatric practice. Clin Neurol Neurosurg. 2013;115(7):859-862.
15. Brodsky L, Zuniga J. Nitrous oxide: a psychotogenic agent. Compr Psychiatry. 1975;16(2):185-188.
16. Wong SL, Harrison R, Mattman A, et al. Nitrous oxide (N2O)-induced acute psychosis. Can J Neurol Sci. 2014;41(5):672-674.
17. Smith AD. Megaloblastic madness. Br Med J. 1960;2(5216):1840-1845.
18. Masalha R, Chudakov B, Muhamad M, et al. Cobalamin-responsive psychosis as the sole manifestation of vitamin B12 deficiency. Isr Med Associ J. 2001;3(9):701-703.
19. Kuo SC, Yeh SB, Yeh YW, et al. Schizophrenia-like psychotic episode precipitated by cobalamin deficiency. Gen Hosp Psychiatry. 2009;31(6):586-588.
20. Raveendranathan D, Shiva L, Venkatasubramanian G, et al. Vitamin B12 deficiency masquerading as clozapine-resistant psychotic symptoms in schizophrenia. J Neuropsychiatry Clin Neurosci. 2013;25(2):E34-E35.
21. Devalia V, Hamilton MS, Molloy AM; British Committee for Standards in Haematology. Guidelines for the diagnosis and treatment of cobalamin and folate disorders. Br J Haematol. 2014;166(4):496-513.
22. Moore THM, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319-328.
23. Garakani A, Welch AK, Jaffe RJ, et al. Psychosis and low cyanocobalamin in a patient abusing nitrous oxide and cannabis. Psychosomatics. 2014;55(6):715-719.
24. Yajnik S, Thapar P, Lichtor JL, et al. Effects of marijuana history on the subjective, psychomotor, and reinforcing effects of nitrous oxide in human. Drug Alcohol Depend. 1994;36(3):227-236.
25. Nagele P, Duma A, Kopec M, et al. Nitrous oxide for treatment-resistant major depression: a proof-of-concept trial. Biol Psychiatry. 2015;78(1):10-18.
26. Zorumski CF, Nagele P, Mennerick S, et al. Treatment-resistant major depression: rationale for NMDA receptors as targets and nitrous oxide as therapy. Front Psychiatry. 2015;6:172.
27. Shear MK. Clinical practice. Complicated grief. N Engl J Med. 2015;372(2):153-160.
28. Knechtli CJC, Crowe JN. Guidelines for the investigation & management of vitamin B12 deficiency. Royal United Hospital Bath, National Health Service. http://www.ruh.nhs.uk/For_Clinicians/departments_ruh/Pathology/documents/haematology/B12_-_advice_on_investigation_management.pdf. Accessed June 14, 2016.
29. Jayaram N, Rao MG, Narashima A, et al. Vitamin B12 levels and psychiatric symptomatology: a case series. J Neuropsychiatry Clin Neurosci. 2013;25(2):150-152.
30. Marks PW, Zukerberg LR. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 30-2004. A 37-year-old woman with paresthesias of the arms and legs. N Engl J Med. 2004;351(13):1333-1341.
31. Watanabe F. Vitamin B12 sources and bioavailablility. Exp Biol Med (Maywood). 2007;232(10):1266-1274.
32. Green R, Kinsella LJ. Current concepts in the diagnosis of cobalamin deficiency. Neurology. 1995;45(8):1435-1440.
The art of psychopharmacology: Avoiding medication changes and slowing down
As physicians, we are cognizant of the importance of patient-centered care, active listening, empathy, and patience—the so-called “hidden curriculum of medicine.”1 However, our attempts to centralize these concepts may be overshadowed by the deeply rooted drive to treat and fix. At times, we are simply treating uncertainty, whether it be diagnostic uncertainty or the uncertainty arising from clinical responses and outcomes that are far from binary. Definitive actions, such as adding medications or altering dosages, may appear to both patients and physicians to be a step closer to a “cure.” However, watchful waiting, re-evaluation, and accepting uncertainty are the true skills of effective care.
Be savvy about psychopharmacology
Psychotropics can take weeks to months to reach their full potential, and have varying responses and adverse effects. Beware of changing regimens prematurely, and keep in mind basic, yet crucial, pharmacokinetic concepts (eg, 4 to 5 half-lives to reach steady state, variations in metabolism). Receptor binding and dosing heuristics are notably common in psychiatry. Although such concepts are important to grasp, there is no one-size-fits-all rule. The brain simply does not possess the heart’s machine-like, linear functioning. Therefore, targeting individual parts (ie, receptors) will not equate to fixing the whole organ systematically or predictably.
Is the patient truly treatment-resistant?
Even the best treatment regimen has no clinical benefit if the patient cannot afford the prescription or does not take the medication. If cost is an impediment, switch from brand name drugs to generic formulations or to older medications in the same class. Before declaring the patient “treatment-resistant” and making medication changes, assess for compliance. This may require assistance from collateral informants. Ask family members to count the number of pills remaining in the bottle, and call the pharmacy to find out the last refill dates. If the patient exhibits a partial response to what should be a therapeutic dose, consider obtaining drug plasma levels to rule out rapid metabolism before deeming the medication trial a failure.2
Medications as liabilities
Overreliance on medications can result in the medications becoming liabilities. The polypharmacy problem is not unique to psychiatry.3 However, psychiatric patients may be more likely to inadvertently use medications in a maladaptive manner and disrupt the fundamental goals of long-term care. Avoid making medication adjustments in response to a patient’s life stressors and normative situational reactions. Doing so is a disservice to patients, because we are robbing them of chances to develop necessary coping skills and defenses. This can be overtly damaging in certain patient populations, such as those with borderline personality disorder, who may use medication adjustments as a crutch during crises.4
Treat the patient, not yourself
We physicians mean well in prescribing evidence-based treatments; however, if the symptoms or adverse effects are not bothersome or cause functional impairment, we risk losing sight of the patient’s goals in treatment and imposing our own instead. Displacing the treatment focus can alienate the patient, harm the therapeutic alliance, and result in “pill fatigue.” For example, we may be tempted to treat antipsychotic-induced tardive dyskinesia, even if the patient is not concerned about abnormal movements. Although we see this adverse effect
Change does not happen overnight
Picking a treatment option out of a lineup of choices, à la UWorld questions, does not always translate into patients agreeing with the suggested treatment, let alone the idea of receiving treatment at all. Motivational interviewing is our chance to shine in such situations and the reason why we are physicians, rather than answer-picking bots. Patients cannot change if they are not ready. However, we should be ready to roll with resistance while looking for signs of readiness to change. We must accept that it may take a week, a month, a year, or even longer for patients to align with our plan of action. The only futile decision is deeming our efforts as futile while discounting the benefits of incremental care.
1. Hafferty FW, Gaufberg EH, O’Donnell JF. The role of the hidden curriculum in “on doctoring” courses. AMA J Ethics. 2015;17(2):130-139.
2. Horvitz-Lennon M, Mattke S, Predmore Z, et al. The role of antipsychotic plasma levels in the treatment of schizophrenia. Am J Psychiatry. 2017;174(5):421-426.
3. Kantor ED, Rehm CD, Haas JS, et al. Trends in prescription drug use among adults in the United States from 1999-2012. JAMA. 2015;314(17):1818-1831.
4. Gunderson JG. The emergence of a generalist model to meet public health needs for patients with borderline personality disorder. Am J Psychiatry. 2016;173(5):452-458.
5. Kikkert MJ, Schene AH, Koeter MW, et al. Medication adherence in schizophrenia: exploring patients’, carers’ and professionals’ views. Schizophr Bull. 2005;32(4):786-794.
As physicians, we are cognizant of the importance of patient-centered care, active listening, empathy, and patience—the so-called “hidden curriculum of medicine.”1 However, our attempts to centralize these concepts may be overshadowed by the deeply rooted drive to treat and fix. At times, we are simply treating uncertainty, whether it be diagnostic uncertainty or the uncertainty arising from clinical responses and outcomes that are far from binary. Definitive actions, such as adding medications or altering dosages, may appear to both patients and physicians to be a step closer to a “cure.” However, watchful waiting, re-evaluation, and accepting uncertainty are the true skills of effective care.
Be savvy about psychopharmacology
Psychotropics can take weeks to months to reach their full potential, and have varying responses and adverse effects. Beware of changing regimens prematurely, and keep in mind basic, yet crucial, pharmacokinetic concepts (eg, 4 to 5 half-lives to reach steady state, variations in metabolism). Receptor binding and dosing heuristics are notably common in psychiatry. Although such concepts are important to grasp, there is no one-size-fits-all rule. The brain simply does not possess the heart’s machine-like, linear functioning. Therefore, targeting individual parts (ie, receptors) will not equate to fixing the whole organ systematically or predictably.
Is the patient truly treatment-resistant?
Even the best treatment regimen has no clinical benefit if the patient cannot afford the prescription or does not take the medication. If cost is an impediment, switch from brand name drugs to generic formulations or to older medications in the same class. Before declaring the patient “treatment-resistant” and making medication changes, assess for compliance. This may require assistance from collateral informants. Ask family members to count the number of pills remaining in the bottle, and call the pharmacy to find out the last refill dates. If the patient exhibits a partial response to what should be a therapeutic dose, consider obtaining drug plasma levels to rule out rapid metabolism before deeming the medication trial a failure.2
Medications as liabilities
Overreliance on medications can result in the medications becoming liabilities. The polypharmacy problem is not unique to psychiatry.3 However, psychiatric patients may be more likely to inadvertently use medications in a maladaptive manner and disrupt the fundamental goals of long-term care. Avoid making medication adjustments in response to a patient’s life stressors and normative situational reactions. Doing so is a disservice to patients, because we are robbing them of chances to develop necessary coping skills and defenses. This can be overtly damaging in certain patient populations, such as those with borderline personality disorder, who may use medication adjustments as a crutch during crises.4
Treat the patient, not yourself
We physicians mean well in prescribing evidence-based treatments; however, if the symptoms or adverse effects are not bothersome or cause functional impairment, we risk losing sight of the patient’s goals in treatment and imposing our own instead. Displacing the treatment focus can alienate the patient, harm the therapeutic alliance, and result in “pill fatigue.” For example, we may be tempted to treat antipsychotic-induced tardive dyskinesia, even if the patient is not concerned about abnormal movements. Although we see this adverse effect
Change does not happen overnight
Picking a treatment option out of a lineup of choices, à la UWorld questions, does not always translate into patients agreeing with the suggested treatment, let alone the idea of receiving treatment at all. Motivational interviewing is our chance to shine in such situations and the reason why we are physicians, rather than answer-picking bots. Patients cannot change if they are not ready. However, we should be ready to roll with resistance while looking for signs of readiness to change. We must accept that it may take a week, a month, a year, or even longer for patients to align with our plan of action. The only futile decision is deeming our efforts as futile while discounting the benefits of incremental care.
As physicians, we are cognizant of the importance of patient-centered care, active listening, empathy, and patience—the so-called “hidden curriculum of medicine.”1 However, our attempts to centralize these concepts may be overshadowed by the deeply rooted drive to treat and fix. At times, we are simply treating uncertainty, whether it be diagnostic uncertainty or the uncertainty arising from clinical responses and outcomes that are far from binary. Definitive actions, such as adding medications or altering dosages, may appear to both patients and physicians to be a step closer to a “cure.” However, watchful waiting, re-evaluation, and accepting uncertainty are the true skills of effective care.
Be savvy about psychopharmacology
Psychotropics can take weeks to months to reach their full potential, and have varying responses and adverse effects. Beware of changing regimens prematurely, and keep in mind basic, yet crucial, pharmacokinetic concepts (eg, 4 to 5 half-lives to reach steady state, variations in metabolism). Receptor binding and dosing heuristics are notably common in psychiatry. Although such concepts are important to grasp, there is no one-size-fits-all rule. The brain simply does not possess the heart’s machine-like, linear functioning. Therefore, targeting individual parts (ie, receptors) will not equate to fixing the whole organ systematically or predictably.
Is the patient truly treatment-resistant?
Even the best treatment regimen has no clinical benefit if the patient cannot afford the prescription or does not take the medication. If cost is an impediment, switch from brand name drugs to generic formulations or to older medications in the same class. Before declaring the patient “treatment-resistant” and making medication changes, assess for compliance. This may require assistance from collateral informants. Ask family members to count the number of pills remaining in the bottle, and call the pharmacy to find out the last refill dates. If the patient exhibits a partial response to what should be a therapeutic dose, consider obtaining drug plasma levels to rule out rapid metabolism before deeming the medication trial a failure.2
Medications as liabilities
Overreliance on medications can result in the medications becoming liabilities. The polypharmacy problem is not unique to psychiatry.3 However, psychiatric patients may be more likely to inadvertently use medications in a maladaptive manner and disrupt the fundamental goals of long-term care. Avoid making medication adjustments in response to a patient’s life stressors and normative situational reactions. Doing so is a disservice to patients, because we are robbing them of chances to develop necessary coping skills and defenses. This can be overtly damaging in certain patient populations, such as those with borderline personality disorder, who may use medication adjustments as a crutch during crises.4
Treat the patient, not yourself
We physicians mean well in prescribing evidence-based treatments; however, if the symptoms or adverse effects are not bothersome or cause functional impairment, we risk losing sight of the patient’s goals in treatment and imposing our own instead. Displacing the treatment focus can alienate the patient, harm the therapeutic alliance, and result in “pill fatigue.” For example, we may be tempted to treat antipsychotic-induced tardive dyskinesia, even if the patient is not concerned about abnormal movements. Although we see this adverse effect
Change does not happen overnight
Picking a treatment option out of a lineup of choices, à la UWorld questions, does not always translate into patients agreeing with the suggested treatment, let alone the idea of receiving treatment at all. Motivational interviewing is our chance to shine in such situations and the reason why we are physicians, rather than answer-picking bots. Patients cannot change if they are not ready. However, we should be ready to roll with resistance while looking for signs of readiness to change. We must accept that it may take a week, a month, a year, or even longer for patients to align with our plan of action. The only futile decision is deeming our efforts as futile while discounting the benefits of incremental care.
1. Hafferty FW, Gaufberg EH, O’Donnell JF. The role of the hidden curriculum in “on doctoring” courses. AMA J Ethics. 2015;17(2):130-139.
2. Horvitz-Lennon M, Mattke S, Predmore Z, et al. The role of antipsychotic plasma levels in the treatment of schizophrenia. Am J Psychiatry. 2017;174(5):421-426.
3. Kantor ED, Rehm CD, Haas JS, et al. Trends in prescription drug use among adults in the United States from 1999-2012. JAMA. 2015;314(17):1818-1831.
4. Gunderson JG. The emergence of a generalist model to meet public health needs for patients with borderline personality disorder. Am J Psychiatry. 2016;173(5):452-458.
5. Kikkert MJ, Schene AH, Koeter MW, et al. Medication adherence in schizophrenia: exploring patients’, carers’ and professionals’ views. Schizophr Bull. 2005;32(4):786-794.
1. Hafferty FW, Gaufberg EH, O’Donnell JF. The role of the hidden curriculum in “on doctoring” courses. AMA J Ethics. 2015;17(2):130-139.
2. Horvitz-Lennon M, Mattke S, Predmore Z, et al. The role of antipsychotic plasma levels in the treatment of schizophrenia. Am J Psychiatry. 2017;174(5):421-426.
3. Kantor ED, Rehm CD, Haas JS, et al. Trends in prescription drug use among adults in the United States from 1999-2012. JAMA. 2015;314(17):1818-1831.
4. Gunderson JG. The emergence of a generalist model to meet public health needs for patients with borderline personality disorder. Am J Psychiatry. 2016;173(5):452-458.
5. Kikkert MJ, Schene AH, Koeter MW, et al. Medication adherence in schizophrenia: exploring patients’, carers’ and professionals’ views. Schizophr Bull. 2005;32(4):786-794.
Providing psychotherapy? Keep these principles in mind
Although the biological aspects of psychiatry are crucial, psychotherapy is an integral part of psychiatry. Unfortunately, the emphasis on psychotherapy training in psychiatry residency programs has declined compared with a decade or more ago. In an era of dwindling psychotherapy training and resources, the quality and type of psychotherapy training has become more variable. In addition to helping maintain the therapeutic alliance, nuanced psychotherapy by a trained professional can be transformational by helping patients to:
- process complex life events and emotions
- feel understood
- overcome psychological barriers to recovery
- enhance self-esteem.
When providing psychotherapy for adult patients, consider these basic, but salient points that are often overlooked.
Refrain from making life decisions for patients, except in exceptional circumstances, such as in situations of abuse and other crises.1 Telling an adult patient what to do about life decisions that he finds challenging fits more under life coaching than psychotherapy. Through therapy, patients should be helped in processing the pros and cons of certain decisions and in navigating the decision-making process to arrive at a decision that makes the most sense to them. Also, it’s not uncommon for therapeutic relationships to rupture when therapists give advice such as suggesting that a patient divorce his spouse, date a certain individual, or have children.
There are many reasons why giving advice in psychotherapy is not recommended. Giving advice can be an impediment to the therapeutic process.2 What is good advice for one patient may not be good for another. Therapists who give advice often do so from their own lens and perspective. This perspective may not only be different from the patient’s priorities and life circumstances, but the therapist also may have inadequate information about the patient’s situation,1,2 which could lead to providing advice that could even harm the patient. In addition, providing advice might prevent a patient from gaining adequate agency or self-directedness while promoting an unhealthy dependence on the therapist and reinforcing the patient’s self-doubt or lack of confidence. In these cases, the patient may later resent the therapist for the advice.
Address the ‘here and now.’1 Pay attention to immediate issues or themes that emerge, and address them with the patient gently and thoughtfully, as appropriate. Ignoring these may create risks of missing vital, underlying material that could reveal more of the patient’s inner world, as these themes can sometimes reflect other themes of the patient’s life outside of treatment.
Acknowledging and empathizing, when appropriate, are key initial steps that help decrease resistance and facilitate the therapeutic process.
Explore the affect. Paying attention to the patient’s emotional state is critical.3 This holds true for all types of psychotherapy. For example, if a patient suddenly becomes tearful when telling his story or describing recent events, this is usually a sign that the subject matter affects or holds value to the patient in a significant or meaningful way and should be further explored.
‘Meet the patient where they are.’ This doesn’t mean you should yield to the patient or give in to his demands. It implies that you should assess the patient’s readiness for a particular intervention and devise interventions from that standpoint, exploring the patient’s ambivalence, noticing resistance, and continuing to acknowledge and empathize with where the patient is in life or treatment. When utilized judiciously, this technique can help the therapist align with the patient, and help the patient move forward through resistance and ambivalence.
Be nonjudgmental and empathetic. Patients place trust in their therapists when they disclose thoughts or emotions that are sensitive, meaningful, or close to the heart. A nonjudgmental response helps the patient accept his experiences and emotions. Being empathetic requires putting oneself in another’s shoes; it does not mean agreeing with the patient. Of course, if you learn that your patient abused a child or an older adult, you are required to report it to the appropriate state agency. In addition, follow the duty to warn and protect in case of any other safety issues, as appropriate.
Do not assume. Open-ended questions and exploration are key. For example, a patient told her resident therapist that her father recently passed away. The therapist expressed to the patient how hard this must be for her. However, the patient said she was relieved by her father’s death, because he had been abusive to her for years. Because of the therapist’s comment, the patient doubted her own reaction and felt guilty for not being more upset about her father’s death.
Avoid over-identifying with your patient. If you find yourself over-identifying with a patient because you have a common background or life events, seek supervision. Over-identification not only can pose barriers to objectively identifying patterns and trends in the patient’s behavior or presentation but also can increase the risk of crossing boundaries or even minimizing the patient’s experience. Exercise caution if you find yourself wanting to be liked by your patient; this is a common mistake among beginning therapists.4
Seek supervision. If you are feeling angry, frustrated, indifferent, or overly attached toward a patient, recognize this countertransference and seek consultation or supervision from an experienced colleague or supervisor. These emotions can be valuable tools that shed light not only on the patient’s life and the session itself, but also help you identify any other factors, such as your own feelings or experiences, that might be contributing to these reactions.
1. Yalom ID. The gift of therapy: an open letter to a new generation of therapists and their patients. New York, NY: HarperCollins Publishers; 2002:46-73,142-145.
2. Bender S, Messner E. Management of impasses. In: Bender S, Messner E. Becoming a therapist: what do I say, and why? New York, NY: The Guilford Press; 2003:235-258.
3.
4. Buckley P, Karasu TB, Charles E. Common mistakes in psychotherapy. Am J Psychiatry. 1979;136(12):1578-1580.
Although the biological aspects of psychiatry are crucial, psychotherapy is an integral part of psychiatry. Unfortunately, the emphasis on psychotherapy training in psychiatry residency programs has declined compared with a decade or more ago. In an era of dwindling psychotherapy training and resources, the quality and type of psychotherapy training has become more variable. In addition to helping maintain the therapeutic alliance, nuanced psychotherapy by a trained professional can be transformational by helping patients to:
- process complex life events and emotions
- feel understood
- overcome psychological barriers to recovery
- enhance self-esteem.
When providing psychotherapy for adult patients, consider these basic, but salient points that are often overlooked.
Refrain from making life decisions for patients, except in exceptional circumstances, such as in situations of abuse and other crises.1 Telling an adult patient what to do about life decisions that he finds challenging fits more under life coaching than psychotherapy. Through therapy, patients should be helped in processing the pros and cons of certain decisions and in navigating the decision-making process to arrive at a decision that makes the most sense to them. Also, it’s not uncommon for therapeutic relationships to rupture when therapists give advice such as suggesting that a patient divorce his spouse, date a certain individual, or have children.
There are many reasons why giving advice in psychotherapy is not recommended. Giving advice can be an impediment to the therapeutic process.2 What is good advice for one patient may not be good for another. Therapists who give advice often do so from their own lens and perspective. This perspective may not only be different from the patient’s priorities and life circumstances, but the therapist also may have inadequate information about the patient’s situation,1,2 which could lead to providing advice that could even harm the patient. In addition, providing advice might prevent a patient from gaining adequate agency or self-directedness while promoting an unhealthy dependence on the therapist and reinforcing the patient’s self-doubt or lack of confidence. In these cases, the patient may later resent the therapist for the advice.
Address the ‘here and now.’1 Pay attention to immediate issues or themes that emerge, and address them with the patient gently and thoughtfully, as appropriate. Ignoring these may create risks of missing vital, underlying material that could reveal more of the patient’s inner world, as these themes can sometimes reflect other themes of the patient’s life outside of treatment.
Acknowledging and empathizing, when appropriate, are key initial steps that help decrease resistance and facilitate the therapeutic process.
Explore the affect. Paying attention to the patient’s emotional state is critical.3 This holds true for all types of psychotherapy. For example, if a patient suddenly becomes tearful when telling his story or describing recent events, this is usually a sign that the subject matter affects or holds value to the patient in a significant or meaningful way and should be further explored.
‘Meet the patient where they are.’ This doesn’t mean you should yield to the patient or give in to his demands. It implies that you should assess the patient’s readiness for a particular intervention and devise interventions from that standpoint, exploring the patient’s ambivalence, noticing resistance, and continuing to acknowledge and empathize with where the patient is in life or treatment. When utilized judiciously, this technique can help the therapist align with the patient, and help the patient move forward through resistance and ambivalence.
Be nonjudgmental and empathetic. Patients place trust in their therapists when they disclose thoughts or emotions that are sensitive, meaningful, or close to the heart. A nonjudgmental response helps the patient accept his experiences and emotions. Being empathetic requires putting oneself in another’s shoes; it does not mean agreeing with the patient. Of course, if you learn that your patient abused a child or an older adult, you are required to report it to the appropriate state agency. In addition, follow the duty to warn and protect in case of any other safety issues, as appropriate.
Do not assume. Open-ended questions and exploration are key. For example, a patient told her resident therapist that her father recently passed away. The therapist expressed to the patient how hard this must be for her. However, the patient said she was relieved by her father’s death, because he had been abusive to her for years. Because of the therapist’s comment, the patient doubted her own reaction and felt guilty for not being more upset about her father’s death.
Avoid over-identifying with your patient. If you find yourself over-identifying with a patient because you have a common background or life events, seek supervision. Over-identification not only can pose barriers to objectively identifying patterns and trends in the patient’s behavior or presentation but also can increase the risk of crossing boundaries or even minimizing the patient’s experience. Exercise caution if you find yourself wanting to be liked by your patient; this is a common mistake among beginning therapists.4
Seek supervision. If you are feeling angry, frustrated, indifferent, or overly attached toward a patient, recognize this countertransference and seek consultation or supervision from an experienced colleague or supervisor. These emotions can be valuable tools that shed light not only on the patient’s life and the session itself, but also help you identify any other factors, such as your own feelings or experiences, that might be contributing to these reactions.
Although the biological aspects of psychiatry are crucial, psychotherapy is an integral part of psychiatry. Unfortunately, the emphasis on psychotherapy training in psychiatry residency programs has declined compared with a decade or more ago. In an era of dwindling psychotherapy training and resources, the quality and type of psychotherapy training has become more variable. In addition to helping maintain the therapeutic alliance, nuanced psychotherapy by a trained professional can be transformational by helping patients to:
- process complex life events and emotions
- feel understood
- overcome psychological barriers to recovery
- enhance self-esteem.
When providing psychotherapy for adult patients, consider these basic, but salient points that are often overlooked.
Refrain from making life decisions for patients, except in exceptional circumstances, such as in situations of abuse and other crises.1 Telling an adult patient what to do about life decisions that he finds challenging fits more under life coaching than psychotherapy. Through therapy, patients should be helped in processing the pros and cons of certain decisions and in navigating the decision-making process to arrive at a decision that makes the most sense to them. Also, it’s not uncommon for therapeutic relationships to rupture when therapists give advice such as suggesting that a patient divorce his spouse, date a certain individual, or have children.
There are many reasons why giving advice in psychotherapy is not recommended. Giving advice can be an impediment to the therapeutic process.2 What is good advice for one patient may not be good for another. Therapists who give advice often do so from their own lens and perspective. This perspective may not only be different from the patient’s priorities and life circumstances, but the therapist also may have inadequate information about the patient’s situation,1,2 which could lead to providing advice that could even harm the patient. In addition, providing advice might prevent a patient from gaining adequate agency or self-directedness while promoting an unhealthy dependence on the therapist and reinforcing the patient’s self-doubt or lack of confidence. In these cases, the patient may later resent the therapist for the advice.
Address the ‘here and now.’1 Pay attention to immediate issues or themes that emerge, and address them with the patient gently and thoughtfully, as appropriate. Ignoring these may create risks of missing vital, underlying material that could reveal more of the patient’s inner world, as these themes can sometimes reflect other themes of the patient’s life outside of treatment.
Acknowledging and empathizing, when appropriate, are key initial steps that help decrease resistance and facilitate the therapeutic process.
Explore the affect. Paying attention to the patient’s emotional state is critical.3 This holds true for all types of psychotherapy. For example, if a patient suddenly becomes tearful when telling his story or describing recent events, this is usually a sign that the subject matter affects or holds value to the patient in a significant or meaningful way and should be further explored.
‘Meet the patient where they are.’ This doesn’t mean you should yield to the patient or give in to his demands. It implies that you should assess the patient’s readiness for a particular intervention and devise interventions from that standpoint, exploring the patient’s ambivalence, noticing resistance, and continuing to acknowledge and empathize with where the patient is in life or treatment. When utilized judiciously, this technique can help the therapist align with the patient, and help the patient move forward through resistance and ambivalence.
Be nonjudgmental and empathetic. Patients place trust in their therapists when they disclose thoughts or emotions that are sensitive, meaningful, or close to the heart. A nonjudgmental response helps the patient accept his experiences and emotions. Being empathetic requires putting oneself in another’s shoes; it does not mean agreeing with the patient. Of course, if you learn that your patient abused a child or an older adult, you are required to report it to the appropriate state agency. In addition, follow the duty to warn and protect in case of any other safety issues, as appropriate.
Do not assume. Open-ended questions and exploration are key. For example, a patient told her resident therapist that her father recently passed away. The therapist expressed to the patient how hard this must be for her. However, the patient said she was relieved by her father’s death, because he had been abusive to her for years. Because of the therapist’s comment, the patient doubted her own reaction and felt guilty for not being more upset about her father’s death.
Avoid over-identifying with your patient. If you find yourself over-identifying with a patient because you have a common background or life events, seek supervision. Over-identification not only can pose barriers to objectively identifying patterns and trends in the patient’s behavior or presentation but also can increase the risk of crossing boundaries or even minimizing the patient’s experience. Exercise caution if you find yourself wanting to be liked by your patient; this is a common mistake among beginning therapists.4
Seek supervision. If you are feeling angry, frustrated, indifferent, or overly attached toward a patient, recognize this countertransference and seek consultation or supervision from an experienced colleague or supervisor. These emotions can be valuable tools that shed light not only on the patient’s life and the session itself, but also help you identify any other factors, such as your own feelings or experiences, that might be contributing to these reactions.
1. Yalom ID. The gift of therapy: an open letter to a new generation of therapists and their patients. New York, NY: HarperCollins Publishers; 2002:46-73,142-145.
2. Bender S, Messner E. Management of impasses. In: Bender S, Messner E. Becoming a therapist: what do I say, and why? New York, NY: The Guilford Press; 2003:235-258.
3.
4. Buckley P, Karasu TB, Charles E. Common mistakes in psychotherapy. Am J Psychiatry. 1979;136(12):1578-1580.
1. Yalom ID. The gift of therapy: an open letter to a new generation of therapists and their patients. New York, NY: HarperCollins Publishers; 2002:46-73,142-145.
2. Bender S, Messner E. Management of impasses. In: Bender S, Messner E. Becoming a therapist: what do I say, and why? New York, NY: The Guilford Press; 2003:235-258.
3.
4. Buckley P, Karasu TB, Charles E. Common mistakes in psychotherapy. Am J Psychiatry. 1979;136(12):1578-1580.
Use the ABCs when managing problem behaviors in autism
Despite a lack of evidence, polypharmacy often is used to treat autism spectrum disorder (ASD),1 while educational techniques are underutilized. Compared with the general population, children with ASD may be more prone to the adverse effects of the medications used to treat symptoms, such as antipsychotics and antidepressants.2 Therefore, when addressing problem behaviors, such as tantrums, aggressiveness, or self-injury, in a patient with ASD, before prescribing a medication, consider the ABCs of these behaviors.3
Antecedents. What happened before the behavior occurred? Where and when did the behavior occur? Was the individual unable to get a desired tangible item, such as a preferred food, toy, or another object? Was the individual told complete a task that he (she) did not want to do? Did the individual see someone else getting attention?
Behaviors. What behavior(s) occurred after each antecedent?
Consequences. What happened after the behavior occurred? Did the caregiver give the individual the item he wanted? Was the individual able to get out of doing work that he did not want to do or become the center of attention?
Having parents document the ABCs is useful not only for finding out why a behavior occurred, but also for objectively determining if and how a medication is affecting the frequency of a behavior. Charts that parents can use to document ABC data are available online (eg, http://www.positivelyautism.com/downloads/datasheet_abc.pdf). Once this data is collected, it can be used to implement appropriate interventions, which I describe as DEFG.
Differential reinforcement of other behaviors is a procedure that provides positive reinforcement for not engaging in a problem behavior or for staying on task. For example, use a token board to reward positive behaviors, with physical tokens or written marks. However, some patients require immediate reinforcement. I suggest that parents or caregivers carry small pieces of preferred food to give to the patient to reinforce positive behavior.
Exercise. A review of 18 studies reported that physical exercise, such as jogging, weight training, and bike riding, can help reduce problem behaviors in individuals with ASD.4 Among 64 participants with ASD, there was a decrease in aggression, stereotypy, off-task behavior, and elopement, and improvements in on-task and motor behavior such as playing catch.
Function. Refer to the ABCs to determine why a specific problem behavior is occurring. Each behavior can have 1 or multiple functions; therefore, develop a plan specific to the reason the patient engages in the behavior. For example, if the individual engages in a behavior to avoid a task, the parent or caregiver can give individual tokens that the individual can later exchange for a break, instead of engaging in the problem behavior to avoid the task. If a behavior appears to be done for attention, instruct the caregivers to provide frequent periods of attention when the individual engages in positive behaviors.
Go to the appropriate placement. By law, persons age ≤21 have the right to an education and to make meaningful progress. If a patient with ASD exhibits behaviors that interfere with learning, he is entitled to a placement that can provide intensive applied behavior analysis. If you feel that the child needs a different school, write an evaluation for the parent or guardian to submit to the school district and clearly outline the patient’s needs and requirements.
1. Spencer D, Marshall J, Post B, et al. Psychotropic medication use and polypharmacy in children with autism spectrum disorders. Pediatrics. 2013;132(5):833-840.
2. Azeem MW, Imran N, Khawaja IS. Autism spectrum disorder: an update. Psychiatr Ann. 2016;46(1):58-62.
3. Pratt C, Dubie M. Observing behavior using A-B-C data. Indiana Resource Center for Autism. https://www.iidc.indiana.edu/pages/observing-behavior-using-a-b-c-data. Accessed October 4, 2017.
4. Lang R, Kern Koegel LK, Ashbaugh K, et al. Physical exercise and individuals with autism spectrum disorders: a systematic review. Res Autism Spectr Dis. 2010;4(4):565-576.
Despite a lack of evidence, polypharmacy often is used to treat autism spectrum disorder (ASD),1 while educational techniques are underutilized. Compared with the general population, children with ASD may be more prone to the adverse effects of the medications used to treat symptoms, such as antipsychotics and antidepressants.2 Therefore, when addressing problem behaviors, such as tantrums, aggressiveness, or self-injury, in a patient with ASD, before prescribing a medication, consider the ABCs of these behaviors.3
Antecedents. What happened before the behavior occurred? Where and when did the behavior occur? Was the individual unable to get a desired tangible item, such as a preferred food, toy, or another object? Was the individual told complete a task that he (she) did not want to do? Did the individual see someone else getting attention?
Behaviors. What behavior(s) occurred after each antecedent?
Consequences. What happened after the behavior occurred? Did the caregiver give the individual the item he wanted? Was the individual able to get out of doing work that he did not want to do or become the center of attention?
Having parents document the ABCs is useful not only for finding out why a behavior occurred, but also for objectively determining if and how a medication is affecting the frequency of a behavior. Charts that parents can use to document ABC data are available online (eg, http://www.positivelyautism.com/downloads/datasheet_abc.pdf). Once this data is collected, it can be used to implement appropriate interventions, which I describe as DEFG.
Differential reinforcement of other behaviors is a procedure that provides positive reinforcement for not engaging in a problem behavior or for staying on task. For example, use a token board to reward positive behaviors, with physical tokens or written marks. However, some patients require immediate reinforcement. I suggest that parents or caregivers carry small pieces of preferred food to give to the patient to reinforce positive behavior.
Exercise. A review of 18 studies reported that physical exercise, such as jogging, weight training, and bike riding, can help reduce problem behaviors in individuals with ASD.4 Among 64 participants with ASD, there was a decrease in aggression, stereotypy, off-task behavior, and elopement, and improvements in on-task and motor behavior such as playing catch.
Function. Refer to the ABCs to determine why a specific problem behavior is occurring. Each behavior can have 1 or multiple functions; therefore, develop a plan specific to the reason the patient engages in the behavior. For example, if the individual engages in a behavior to avoid a task, the parent or caregiver can give individual tokens that the individual can later exchange for a break, instead of engaging in the problem behavior to avoid the task. If a behavior appears to be done for attention, instruct the caregivers to provide frequent periods of attention when the individual engages in positive behaviors.
Go to the appropriate placement. By law, persons age ≤21 have the right to an education and to make meaningful progress. If a patient with ASD exhibits behaviors that interfere with learning, he is entitled to a placement that can provide intensive applied behavior analysis. If you feel that the child needs a different school, write an evaluation for the parent or guardian to submit to the school district and clearly outline the patient’s needs and requirements.
Despite a lack of evidence, polypharmacy often is used to treat autism spectrum disorder (ASD),1 while educational techniques are underutilized. Compared with the general population, children with ASD may be more prone to the adverse effects of the medications used to treat symptoms, such as antipsychotics and antidepressants.2 Therefore, when addressing problem behaviors, such as tantrums, aggressiveness, or self-injury, in a patient with ASD, before prescribing a medication, consider the ABCs of these behaviors.3
Antecedents. What happened before the behavior occurred? Where and when did the behavior occur? Was the individual unable to get a desired tangible item, such as a preferred food, toy, or another object? Was the individual told complete a task that he (she) did not want to do? Did the individual see someone else getting attention?
Behaviors. What behavior(s) occurred after each antecedent?
Consequences. What happened after the behavior occurred? Did the caregiver give the individual the item he wanted? Was the individual able to get out of doing work that he did not want to do or become the center of attention?
Having parents document the ABCs is useful not only for finding out why a behavior occurred, but also for objectively determining if and how a medication is affecting the frequency of a behavior. Charts that parents can use to document ABC data are available online (eg, http://www.positivelyautism.com/downloads/datasheet_abc.pdf). Once this data is collected, it can be used to implement appropriate interventions, which I describe as DEFG.
Differential reinforcement of other behaviors is a procedure that provides positive reinforcement for not engaging in a problem behavior or for staying on task. For example, use a token board to reward positive behaviors, with physical tokens or written marks. However, some patients require immediate reinforcement. I suggest that parents or caregivers carry small pieces of preferred food to give to the patient to reinforce positive behavior.
Exercise. A review of 18 studies reported that physical exercise, such as jogging, weight training, and bike riding, can help reduce problem behaviors in individuals with ASD.4 Among 64 participants with ASD, there was a decrease in aggression, stereotypy, off-task behavior, and elopement, and improvements in on-task and motor behavior such as playing catch.
Function. Refer to the ABCs to determine why a specific problem behavior is occurring. Each behavior can have 1 or multiple functions; therefore, develop a plan specific to the reason the patient engages in the behavior. For example, if the individual engages in a behavior to avoid a task, the parent or caregiver can give individual tokens that the individual can later exchange for a break, instead of engaging in the problem behavior to avoid the task. If a behavior appears to be done for attention, instruct the caregivers to provide frequent periods of attention when the individual engages in positive behaviors.
Go to the appropriate placement. By law, persons age ≤21 have the right to an education and to make meaningful progress. If a patient with ASD exhibits behaviors that interfere with learning, he is entitled to a placement that can provide intensive applied behavior analysis. If you feel that the child needs a different school, write an evaluation for the parent or guardian to submit to the school district and clearly outline the patient’s needs and requirements.
1. Spencer D, Marshall J, Post B, et al. Psychotropic medication use and polypharmacy in children with autism spectrum disorders. Pediatrics. 2013;132(5):833-840.
2. Azeem MW, Imran N, Khawaja IS. Autism spectrum disorder: an update. Psychiatr Ann. 2016;46(1):58-62.
3. Pratt C, Dubie M. Observing behavior using A-B-C data. Indiana Resource Center for Autism. https://www.iidc.indiana.edu/pages/observing-behavior-using-a-b-c-data. Accessed October 4, 2017.
4. Lang R, Kern Koegel LK, Ashbaugh K, et al. Physical exercise and individuals with autism spectrum disorders: a systematic review. Res Autism Spectr Dis. 2010;4(4):565-576.
1. Spencer D, Marshall J, Post B, et al. Psychotropic medication use and polypharmacy in children with autism spectrum disorders. Pediatrics. 2013;132(5):833-840.
2. Azeem MW, Imran N, Khawaja IS. Autism spectrum disorder: an update. Psychiatr Ann. 2016;46(1):58-62.
3. Pratt C, Dubie M. Observing behavior using A-B-C data. Indiana Resource Center for Autism. https://www.iidc.indiana.edu/pages/observing-behavior-using-a-b-c-data. Accessed October 4, 2017.
4. Lang R, Kern Koegel LK, Ashbaugh K, et al. Physical exercise and individuals with autism spectrum disorders: a systematic review. Res Autism Spectr Dis. 2010;4(4):565-576.
Employment contracts: What to check before you sign
Most psychiatrists are required to sign an employment contract before taking a job, but few of us have received any training on reviewing such contracts. We often rely on coworkers and attorneys to navigate this process for us. However, the contract is crucial, because it outlines your employer’s clinical and administrative expectations for the position, and it gives you the opportunity to lay out what you want.1 Because an employment contract is legally binding, you should thoroughly read it and look for clauses that may not work in your best interest. Although not a complete list, the following items should be reviewed before signing a contract.1,2
Benefits. Make sure you are offered a reasonable salary, but balance the dollar amount with benefits such as:
- continuing medical education allowances
- educational loan forgiveness
- health/malpractice/disability insurance
- retirement benefits
- compensation for call schedule.
In some cases, there may be a delay before you are eligible to obtain certain benefits.
Work expectations. Many contracts state that the position is “full-time” or have other nonspecific parameters for work expectations. You should inquire about objective work parameters, such as duty hours, the average frequency of the current call schedule, timeframe for completing medical documentation, and penalties for not meeting clinical or administrative requirements, so you are not surprised by:
- working longer-than-planned shifts
- performing on-call duties
- working on days that you were not expecting
- having your credentialing status placed in jeopardy.
Some group practices allow for a half-day of no scheduled appointments with patients, so you can complete paperwork and return phone calls.
Noncompete clause. This restricts you from working within a certain geographic area or for a competing employer for a finite time period after the contract terminates or expires. A noncompete clause could restrict you from practicing within a large geographical area, especially if the job is located in a densely populated area. Some noncompete clauses do not include a temporal or geographic restriction, but can limit your ability to bring patients with you to a new practice or facility when the contract expires.
Malpractice insurance. Two types of malpractice insurance are occurrence and claims-made:
- Occurrence insurance protects you whenever an action is brought against you, even if the action is brought after the contract terminates or expires.
- Claims-made insurance provides coverage if the policy with the same insurer was in effect when the malpractice was committed and when the actual action was commenced.
Although claims-made insurance is less expensive, it can leave you without coverage should you leave your employer and no longer maintain the same insurance policy. Claims-made can be converted into occurrence through the purchase of a tail endorsement. If the employer does not offer you tail coverage, then it is your responsibility to pay for this insurance, which can be expensive.
Termination language. Every contract features a termination section that lists potential causes for terminating your employment. This list is usually not exhaustive, but it sets the framework for a realistic view of reasonable causes. Contracts also commonly contain provisions that permit termination “without cause” after notice of termination is provided. Although you could negotiate for more notice time, “without cause” clauses are unlikely to be removed from the contract.
1. Claussen K. Eight physician employment contract items you need to know about. The Doctor Weighs In. https://thedoctorweighsin.com/8-physician-employment-contract-items-you-need-to-know-about. Published March 8, 2017. Accessed October 11, 2017.
2. Blustein AE, Keller LB. Physician employment contracts: what you need to know before you sign. J Am Acad Dermatol. https://www.aad.org/members/publications/directions-in-residency/archiveyment-contracts-what-you-need-to-know-before-you-sign. Accessed October 11, 2017.
Most psychiatrists are required to sign an employment contract before taking a job, but few of us have received any training on reviewing such contracts. We often rely on coworkers and attorneys to navigate this process for us. However, the contract is crucial, because it outlines your employer’s clinical and administrative expectations for the position, and it gives you the opportunity to lay out what you want.1 Because an employment contract is legally binding, you should thoroughly read it and look for clauses that may not work in your best interest. Although not a complete list, the following items should be reviewed before signing a contract.1,2
Benefits. Make sure you are offered a reasonable salary, but balance the dollar amount with benefits such as:
- continuing medical education allowances
- educational loan forgiveness
- health/malpractice/disability insurance
- retirement benefits
- compensation for call schedule.
In some cases, there may be a delay before you are eligible to obtain certain benefits.
Work expectations. Many contracts state that the position is “full-time” or have other nonspecific parameters for work expectations. You should inquire about objective work parameters, such as duty hours, the average frequency of the current call schedule, timeframe for completing medical documentation, and penalties for not meeting clinical or administrative requirements, so you are not surprised by:
- working longer-than-planned shifts
- performing on-call duties
- working on days that you were not expecting
- having your credentialing status placed in jeopardy.
Some group practices allow for a half-day of no scheduled appointments with patients, so you can complete paperwork and return phone calls.
Noncompete clause. This restricts you from working within a certain geographic area or for a competing employer for a finite time period after the contract terminates or expires. A noncompete clause could restrict you from practicing within a large geographical area, especially if the job is located in a densely populated area. Some noncompete clauses do not include a temporal or geographic restriction, but can limit your ability to bring patients with you to a new practice or facility when the contract expires.
Malpractice insurance. Two types of malpractice insurance are occurrence and claims-made:
- Occurrence insurance protects you whenever an action is brought against you, even if the action is brought after the contract terminates or expires.
- Claims-made insurance provides coverage if the policy with the same insurer was in effect when the malpractice was committed and when the actual action was commenced.
Although claims-made insurance is less expensive, it can leave you without coverage should you leave your employer and no longer maintain the same insurance policy. Claims-made can be converted into occurrence through the purchase of a tail endorsement. If the employer does not offer you tail coverage, then it is your responsibility to pay for this insurance, which can be expensive.
Termination language. Every contract features a termination section that lists potential causes for terminating your employment. This list is usually not exhaustive, but it sets the framework for a realistic view of reasonable causes. Contracts also commonly contain provisions that permit termination “without cause” after notice of termination is provided. Although you could negotiate for more notice time, “without cause” clauses are unlikely to be removed from the contract.
Most psychiatrists are required to sign an employment contract before taking a job, but few of us have received any training on reviewing such contracts. We often rely on coworkers and attorneys to navigate this process for us. However, the contract is crucial, because it outlines your employer’s clinical and administrative expectations for the position, and it gives you the opportunity to lay out what you want.1 Because an employment contract is legally binding, you should thoroughly read it and look for clauses that may not work in your best interest. Although not a complete list, the following items should be reviewed before signing a contract.1,2
Benefits. Make sure you are offered a reasonable salary, but balance the dollar amount with benefits such as:
- continuing medical education allowances
- educational loan forgiveness
- health/malpractice/disability insurance
- retirement benefits
- compensation for call schedule.
In some cases, there may be a delay before you are eligible to obtain certain benefits.
Work expectations. Many contracts state that the position is “full-time” or have other nonspecific parameters for work expectations. You should inquire about objective work parameters, such as duty hours, the average frequency of the current call schedule, timeframe for completing medical documentation, and penalties for not meeting clinical or administrative requirements, so you are not surprised by:
- working longer-than-planned shifts
- performing on-call duties
- working on days that you were not expecting
- having your credentialing status placed in jeopardy.
Some group practices allow for a half-day of no scheduled appointments with patients, so you can complete paperwork and return phone calls.
Noncompete clause. This restricts you from working within a certain geographic area or for a competing employer for a finite time period after the contract terminates or expires. A noncompete clause could restrict you from practicing within a large geographical area, especially if the job is located in a densely populated area. Some noncompete clauses do not include a temporal or geographic restriction, but can limit your ability to bring patients with you to a new practice or facility when the contract expires.
Malpractice insurance. Two types of malpractice insurance are occurrence and claims-made:
- Occurrence insurance protects you whenever an action is brought against you, even if the action is brought after the contract terminates or expires.
- Claims-made insurance provides coverage if the policy with the same insurer was in effect when the malpractice was committed and when the actual action was commenced.
Although claims-made insurance is less expensive, it can leave you without coverage should you leave your employer and no longer maintain the same insurance policy. Claims-made can be converted into occurrence through the purchase of a tail endorsement. If the employer does not offer you tail coverage, then it is your responsibility to pay for this insurance, which can be expensive.
Termination language. Every contract features a termination section that lists potential causes for terminating your employment. This list is usually not exhaustive, but it sets the framework for a realistic view of reasonable causes. Contracts also commonly contain provisions that permit termination “without cause” after notice of termination is provided. Although you could negotiate for more notice time, “without cause” clauses are unlikely to be removed from the contract.
1. Claussen K. Eight physician employment contract items you need to know about. The Doctor Weighs In. https://thedoctorweighsin.com/8-physician-employment-contract-items-you-need-to-know-about. Published March 8, 2017. Accessed October 11, 2017.
2. Blustein AE, Keller LB. Physician employment contracts: what you need to know before you sign. J Am Acad Dermatol. https://www.aad.org/members/publications/directions-in-residency/archiveyment-contracts-what-you-need-to-know-before-you-sign. Accessed October 11, 2017.
1. Claussen K. Eight physician employment contract items you need to know about. The Doctor Weighs In. https://thedoctorweighsin.com/8-physician-employment-contract-items-you-need-to-know-about. Published March 8, 2017. Accessed October 11, 2017.
2. Blustein AE, Keller LB. Physician employment contracts: what you need to know before you sign. J Am Acad Dermatol. https://www.aad.org/members/publications/directions-in-residency/archiveyment-contracts-what-you-need-to-know-before-you-sign. Accessed October 11, 2017.
3 Approaches to PMS
Throughout my 40 years in private psychiatric practice, I have found some treatments for premenstrual syndrome (PMS) that were not mentioned in “Etiology of premenstrual dysphoric disorder: 5 interwoven pieces” (Evidence-Based Reviews, Current Psychiatry. September 2017, p. 20-28).
This started in 1972 when I was serving in the Army in Oklahoma. A 28-year-old woman with severe PMS had been treated by internal medicine, an OB/GYN, and endocrinology, all to no avail. Three days before her menses began, she would start driving north. When menses commenced, she would find herself in Nebraska and have to call her husband so he could wire her money to come back.
Through my evaluation, I found that she would gain 10 lb before her menses. I prescribed a diuretic and instructed her to start taking it when she began swelling and to stop taking it after her menses began. This alleviated all of her symptoms. If a woman gains more than 3 to 5 lb, her brain also will swell, along with everything else. Because the brain is encapsulated in the skull, the swelling puts pressure on the brain, which might have been the cause of these brief psychotic episodes.
If a woman who develops PMS does not experience significant weight gain, the first thing I try is vitamin B6, 100 mg/d, prior to menses. Vitamin B6 is a cofactor in the production of numerous neurotransmitters. I found that prescribing vitamin B6 would alleviate about 20% of PMS symptoms. If the patient has a personal or family history of affective disorder, I often try antidepressants prior to menses, which alleviate approximately another 20% of her symptoms. If none of the previous 3 factors are present, I often add a low dose of progesterone, which appears to help. If all else fails, I will try a low dose of lithium, 300 mg/d, before menses. This also seems to have some positive effect.
I have not written an article about these approaches to PMS, although I have discussed them with OB/GYNs, who never seem to follow these recommendations. Because I am not university-based, I have not been able to put thes
Throughout my 40 years in private psychiatric practice, I have found some treatments for premenstrual syndrome (PMS) that were not mentioned in “Etiology of premenstrual dysphoric disorder: 5 interwoven pieces” (Evidence-Based Reviews, Current Psychiatry. September 2017, p. 20-28).
This started in 1972 when I was serving in the Army in Oklahoma. A 28-year-old woman with severe PMS had been treated by internal medicine, an OB/GYN, and endocrinology, all to no avail. Three days before her menses began, she would start driving north. When menses commenced, she would find herself in Nebraska and have to call her husband so he could wire her money to come back.
Through my evaluation, I found that she would gain 10 lb before her menses. I prescribed a diuretic and instructed her to start taking it when she began swelling and to stop taking it after her menses began. This alleviated all of her symptoms. If a woman gains more than 3 to 5 lb, her brain also will swell, along with everything else. Because the brain is encapsulated in the skull, the swelling puts pressure on the brain, which might have been the cause of these brief psychotic episodes.
If a woman who develops PMS does not experience significant weight gain, the first thing I try is vitamin B6, 100 mg/d, prior to menses. Vitamin B6 is a cofactor in the production of numerous neurotransmitters. I found that prescribing vitamin B6 would alleviate about 20% of PMS symptoms. If the patient has a personal or family history of affective disorder, I often try antidepressants prior to menses, which alleviate approximately another 20% of her symptoms. If none of the previous 3 factors are present, I often add a low dose of progesterone, which appears to help. If all else fails, I will try a low dose of lithium, 300 mg/d, before menses. This also seems to have some positive effect.
I have not written an article about these approaches to PMS, although I have discussed them with OB/GYNs, who never seem to follow these recommendations. Because I am not university-based, I have not been able to put thes
Throughout my 40 years in private psychiatric practice, I have found some treatments for premenstrual syndrome (PMS) that were not mentioned in “Etiology of premenstrual dysphoric disorder: 5 interwoven pieces” (Evidence-Based Reviews, Current Psychiatry. September 2017, p. 20-28).
This started in 1972 when I was serving in the Army in Oklahoma. A 28-year-old woman with severe PMS had been treated by internal medicine, an OB/GYN, and endocrinology, all to no avail. Three days before her menses began, she would start driving north. When menses commenced, she would find herself in Nebraska and have to call her husband so he could wire her money to come back.
Through my evaluation, I found that she would gain 10 lb before her menses. I prescribed a diuretic and instructed her to start taking it when she began swelling and to stop taking it after her menses began. This alleviated all of her symptoms. If a woman gains more than 3 to 5 lb, her brain also will swell, along with everything else. Because the brain is encapsulated in the skull, the swelling puts pressure on the brain, which might have been the cause of these brief psychotic episodes.
If a woman who develops PMS does not experience significant weight gain, the first thing I try is vitamin B6, 100 mg/d, prior to menses. Vitamin B6 is a cofactor in the production of numerous neurotransmitters. I found that prescribing vitamin B6 would alleviate about 20% of PMS symptoms. If the patient has a personal or family history of affective disorder, I often try antidepressants prior to menses, which alleviate approximately another 20% of her symptoms. If none of the previous 3 factors are present, I often add a low dose of progesterone, which appears to help. If all else fails, I will try a low dose of lithium, 300 mg/d, before menses. This also seems to have some positive effect.
I have not written an article about these approaches to PMS, although I have discussed them with OB/GYNs, who never seem to follow these recommendations. Because I am not university-based, I have not been able to put thes