“Better than a thousand days of diligent study is one day with a great teacher.”
—Japanese proverb

My chairman of medicine in medical school was a looming, intimidating, diagnostic genius—and one of the best teachers I have ever had. As a sub-intern it seemed I learned more in one month with him than in my prior six months of medical school.  After the rotation, I asked him how he became such an effective teacher. “Simple,” he said, “I invest significant time and effort.”

But time is limited and you have to be smart with how you invest it. Here are three pearls that are a wise investment—they will make you a better teacher.

Those who seem to teach effortlessly do so after substantial behind-the-scenes effort. Read on your patients before rounds. Identify key teaching points and useful literature. Get some questions ready to define knowledge gaps and create “Teaching Scripts.”

Teaching Scripts are preplanned summaries of specific topics that can be used on rounds or longer talks and are “triggered” by common scenarios (eg, hypoxia). Great teaching scripts use a “hook” to engage the learner (commonly a thought-provoking question or story), two to five teaching points, and purposeful questions, mnemonics, and visual representations.

You should aim to develop at least five teaching scripts on commonly encountered topics. Eventually, you should have twenty scripts you can easily reference.

Technology significantly enhances the efficiency and impact of your teaching. For example, on rounds use your cell phone to display and teach anatomy, radiographic images, and EKGs. Use an iPad as a mobile whiteboard. Use email to collate and disseminate teaching points or send links to valuable learning resources like procedural videos. At its best, you can develop new programs and recruit team members to create resources, like I did with an online series focused on teaching to teach using graphically-enhanced TED-style talks¹ and animated whiteboard videos.²

Do you easily remember the content from your medical school lectures?  Likely not. But you likely remember moments from your favorite comedian or TED talk. Unlike the many PowerPoint lectures you’ve sat through, I’ll bet you stay engaged in films and documentaries. Why the difference? In short—medical educators often don’t make content engaging, readily understood, or memorable. To be most effective in teaching, learn from experts in other fields. Think how storytelling, film, theater, and graphic design contribute to learning. Don’t be afraid to be different.

All of these disciplines recognize the power of storytelling to make their points more impactful and memorable. Leverage this by mixing lessons with stories to create teaching points that stick. Lessons of character and morals can be highlighted through stories of personal struggles, prior patients, or people you admire. Clinical tips can be reinforced through sharing a “clinical story”—concise retellings of high-yield patient cases with diagnosis or management tips.

These disciplines also recognize the importance of “setting the stage” to create an optimal experience. We too can learn from this by setting the stage for our learners. Build a learning environment that is positive, collaborative, and fun by being open, curious, and enthusiastic. Treat your team to coffee rounds or lunch and get to know each learner as you walk between patients. As Teddy Roosevelt said, “people don’t care how much you know, until they know how much you care.”

My chairman taught me that exceptional teaching is not a talent of the gifted, it is a skill of the diligent. If you invest in your teaching, you can make a tremendous impact in the lives of your learners. Are you ready to be empowered?

Acknowledgments

The author wishes to thank Rana Kabeer and Sally Salari for their assistance in storyboarding, graphic design, and video editing of the MENTOR Video Series.

Disclosures

Dr. Cronin has nothing to disclose.

 

“Better than a thousand days of diligent study is one day with a great teacher.”
—Japanese proverb

My chairman of medicine in medical school was a looming, intimidating, diagnostic genius—and one of the best teachers I have ever had. As a sub-intern it seemed I learned more in one month with him than in my prior six months of medical school.  After the rotation, I asked him how he became such an effective teacher. “Simple,” he said, “I invest significant time and effort.”

But time is limited and you have to be smart with how you invest it. Here are three pearls that are a wise investment—they will make you a better teacher.

Those who seem to teach effortlessly do so after substantial behind-the-scenes effort. Read on your patients before rounds. Identify key teaching points and useful literature. Get some questions ready to define knowledge gaps and create “Teaching Scripts.”

Teaching Scripts are preplanned summaries of specific topics that can be used on rounds or longer talks and are “triggered” by common scenarios (eg, hypoxia). Great teaching scripts use a “hook” to engage the learner (commonly a thought-provoking question or story), two to five teaching points, and purposeful questions, mnemonics, and visual representations.

You should aim to develop at least five teaching scripts on commonly encountered topics. Eventually, you should have twenty scripts you can easily reference.

Technology significantly enhances the efficiency and impact of your teaching. For example, on rounds use your cell phone to display and teach anatomy, radiographic images, and EKGs. Use an iPad as a mobile whiteboard. Use email to collate and disseminate teaching points or send links to valuable learning resources like procedural videos. At its best, you can develop new programs and recruit team members to create resources, like I did with an online series focused on teaching to teach using graphically-enhanced TED-style talks¹ and animated whiteboard videos.²

Do you easily remember the content from your medical school lectures?  Likely not. But you likely remember moments from your favorite comedian or TED talk. Unlike the many PowerPoint lectures you’ve sat through, I’ll bet you stay engaged in films and documentaries. Why the difference? In short—medical educators often don’t make content engaging, readily understood, or memorable. To be most effective in teaching, learn from experts in other fields. Think how storytelling, film, theater, and graphic design contribute to learning. Don’t be afraid to be different.

All of these disciplines recognize the power of storytelling to make their points more impactful and memorable. Leverage this by mixing lessons with stories to create teaching points that stick. Lessons of character and morals can be highlighted through stories of personal struggles, prior patients, or people you admire. Clinical tips can be reinforced through sharing a “clinical story”—concise retellings of high-yield patient cases with diagnosis or management tips.

These disciplines also recognize the importance of “setting the stage” to create an optimal experience. We too can learn from this by setting the stage for our learners. Build a learning environment that is positive, collaborative, and fun by being open, curious, and enthusiastic. Treat your team to coffee rounds or lunch and get to know each learner as you walk between patients. As Teddy Roosevelt said, “people don’t care how much you know, until they know how much you care.”

My chairman taught me that exceptional teaching is not a talent of the gifted, it is a skill of the diligent. If you invest in your teaching, you can make a tremendous impact in the lives of your learners. Are you ready to be empowered?

Acknowledgments

The author wishes to thank Rana Kabeer and Sally Salari for their assistance in storyboarding, graphic design, and video editing of the MENTOR Video Series.

Disclosures

Dr. Cronin has nothing to disclose.

 

“Better than a thousand days of diligent study is one day with a great teacher.”
—Japanese proverb

My chairman of medicine in medical school was a looming, intimidating, diagnostic genius—and one of the best teachers I have ever had. As a sub-intern it seemed I learned more in one month with him than in my prior six months of medical school.  After the rotation, I asked him how he became such an effective teacher. “Simple,” he said, “I invest significant time and effort.”

But time is limited and you have to be smart with how you invest it. Here are three pearls that are a wise investment—they will make you a better teacher.

Those who seem to teach effortlessly do so after substantial behind-the-scenes effort. Read on your patients before rounds. Identify key teaching points and useful literature. Get some questions ready to define knowledge gaps and create “Teaching Scripts.”

Teaching Scripts are preplanned summaries of specific topics that can be used on rounds or longer talks and are “triggered” by common scenarios (eg, hypoxia). Great teaching scripts use a “hook” to engage the learner (commonly a thought-provoking question or story), two to five teaching points, and purposeful questions, mnemonics, and visual representations.

You should aim to develop at least five teaching scripts on commonly encountered topics. Eventually, you should have twenty scripts you can easily reference.

Technology significantly enhances the efficiency and impact of your teaching. For example, on rounds use your cell phone to display and teach anatomy, radiographic images, and EKGs. Use an iPad as a mobile whiteboard. Use email to collate and disseminate teaching points or send links to valuable learning resources like procedural videos. At its best, you can develop new programs and recruit team members to create resources, like I did with an online series focused on teaching to teach using graphically-enhanced TED-style talks¹ and animated whiteboard videos.²

Do you easily remember the content from your medical school lectures?  Likely not. But you likely remember moments from your favorite comedian or TED talk. Unlike the many PowerPoint lectures you’ve sat through, I’ll bet you stay engaged in films and documentaries. Why the difference? In short—medical educators often don’t make content engaging, readily understood, or memorable. To be most effective in teaching, learn from experts in other fields. Think how storytelling, film, theater, and graphic design contribute to learning. Don’t be afraid to be different.

All of these disciplines recognize the power of storytelling to make their points more impactful and memorable. Leverage this by mixing lessons with stories to create teaching points that stick. Lessons of character and morals can be highlighted through stories of personal struggles, prior patients, or people you admire. Clinical tips can be reinforced through sharing a “clinical story”—concise retellings of high-yield patient cases with diagnosis or management tips.

These disciplines also recognize the importance of “setting the stage” to create an optimal experience. We too can learn from this by setting the stage for our learners. Build a learning environment that is positive, collaborative, and fun by being open, curious, and enthusiastic. Treat your team to coffee rounds or lunch and get to know each learner as you walk between patients. As Teddy Roosevelt said, “people don’t care how much you know, until they know how much you care.”

My chairman taught me that exceptional teaching is not a talent of the gifted, it is a skill of the diligent. If you invest in your teaching, you can make a tremendous impact in the lives of your learners. Are you ready to be empowered?

Acknowledgments

The author wishes to thank Rana Kabeer and Sally Salari for their assistance in storyboarding, graphic design, and video editing of the MENTOR Video Series.

Disclosures

Dr. Cronin has nothing to disclose.

 

Endoscopic submucosal dissection (ESD) is a viable treatment option for patients with submucosal (T1b) esophageal cancer who have a low risk of lymph node metastasis, according to an expert review.

Among patients with T1b esophageal cancer, ideal candidates for ESD have small (less than 2 cm), well-differentiated tumors that do not invade beyond the superficial submucosa (SM1) and lack lymphovascular invasion, reported lead author Mohamed O. Othman, MD, of Baylor College of Medicine in Houston, and colleagues. The literature review was recently commissioned by the American Gastroenterological Association (AGA), because of high clinical relevance.

“[ESD] has been gaining momentum as an alternative to surgery in treating early gastrointestinal neoplasms,” the investigators wrote in Clinical Gastroenterology and Hepatology.

Most patients who undergo surgical resection develop gastroesophageal reflux, the investigators noted, and many others develop serious complications or do not survive the procedure.

“Even a high-volume center such as Mayo Clinic reported a surgical mortality of 4% for T1a esophageal cancer,” the investigators wrote. “Moreover, 34% of patients developed postoperative complications such as anastomotic leaks, anastomotic strictures, cardiopulmonary complications, and feeding jejunostomy leaks. ... Therefore, a less-invasive alternative to esophagectomy would be extremely valuable in the management of early stage [esophageal cancer] if proven effective.”

The investigators reviewed studies evaluating safety and efficacy of surgical and endoscopic techniques, as well as available data for chemoradiation and radiofrequency ablation combinations, which could potentially optimize outcomes of endoscopic resection.

They concluded that most patients with esophageal cancer that does not extend beyond the mucosa (T1a) can be cured with endoscopic resection, based on 5-year survival rates from several Japanese trials. For patients with T1b disease, however, ESD is best suited for those with a low risk of lymph node metastasis. Unfortunately, identifying these candidates can be challenging, according to the investigators.

“The risk of lymph node metastasis depends on the depth of invasion, histologic type, and molecular characterization of the tumor,” the investigators explained, noting that depth of invasion is the trickiest to discern. Although endoscopic ultrasound (EUS) is still recommended for submucosal imaging, the review showed that EUS may overstage cancer in Barrett’s esophagus. The investigators suggested that volume laser endoscopy with infrared light could be a more accurate alternative, but it is not yet a clinical reality.

The review also showed potential for combining ESD with other modalities. For example, a study by Hamada and colleagues involving 66 patients with submucosal (T1b) esophageal squamous cell carcinoma found that a combination of ESD with chemoradiation led to similar 3- and 5-year survival rates as radical esophagectomy. The investigators highlighted the importance of lymph node metastasis in this study, as none of the 30 patients lacking lymph node involvement had metastatic recurrence, compared with 6 of the 36 patients who exhibited lymph node metastasis. According to the investigators, promising data are also anticipated for this combination among those with adenocarcinoma. And for patients with intestinal metaplasia and/or dysplasia, adding radiofrequency ablation after ESD appears to be an effective option; one recent study by Sharmila Subramaniam, BMBS, and colleagues found that this strategy led to clearance rates of 85% and 96% for metaplasia and dysplasia, respectively.

“Additional treatment should be determined by factors such as tumor grade, status of lymphovascular invasion, and depth of tumor, which have a direct influence on metastatic potential,” the investigators wrote.

The investigators suggested that, in the future, better diagnostics will be needed to characterize T1b disease, as this could streamline patient selection. “Future research should focus on novel biological and immunohistochemistry markers that can aid in the prediction of tumor behavior and [lymph node metastasis] in T1b esophageal cancer,” they concluded.

The study was commissioned by the American Gastroenterological Association. The investigators disclosed additional relationships with Boston Scientific, Olympus, Lumendi, and others.

SOURCE: Othman MO et al. CGH. 2019 Jun 4. doi: 10.1016/j.cgh.2019.05.045.

Endoscopic submucosal dissection (ESD) is a viable treatment option for patients with submucosal (T1b) esophageal cancer who have a low risk of lymph node metastasis, according to an expert review.

Among patients with T1b esophageal cancer, ideal candidates for ESD have small (less than 2 cm), well-differentiated tumors that do not invade beyond the superficial submucosa (SM1) and lack lymphovascular invasion, reported lead author Mohamed O. Othman, MD, of Baylor College of Medicine in Houston, and colleagues. The literature review was recently commissioned by the American Gastroenterological Association (AGA), because of high clinical relevance.

“[ESD] has been gaining momentum as an alternative to surgery in treating early gastrointestinal neoplasms,” the investigators wrote in Clinical Gastroenterology and Hepatology.

Most patients who undergo surgical resection develop gastroesophageal reflux, the investigators noted, and many others develop serious complications or do not survive the procedure.

“Even a high-volume center such as Mayo Clinic reported a surgical mortality of 4% for T1a esophageal cancer,” the investigators wrote. “Moreover, 34% of patients developed postoperative complications such as anastomotic leaks, anastomotic strictures, cardiopulmonary complications, and feeding jejunostomy leaks. ... Therefore, a less-invasive alternative to esophagectomy would be extremely valuable in the management of early stage [esophageal cancer] if proven effective.”

The investigators reviewed studies evaluating safety and efficacy of surgical and endoscopic techniques, as well as available data for chemoradiation and radiofrequency ablation combinations, which could potentially optimize outcomes of endoscopic resection.

They concluded that most patients with esophageal cancer that does not extend beyond the mucosa (T1a) can be cured with endoscopic resection, based on 5-year survival rates from several Japanese trials. For patients with T1b disease, however, ESD is best suited for those with a low risk of lymph node metastasis. Unfortunately, identifying these candidates can be challenging, according to the investigators.

“The risk of lymph node metastasis depends on the depth of invasion, histologic type, and molecular characterization of the tumor,” the investigators explained, noting that depth of invasion is the trickiest to discern. Although endoscopic ultrasound (EUS) is still recommended for submucosal imaging, the review showed that EUS may overstage cancer in Barrett’s esophagus. The investigators suggested that volume laser endoscopy with infrared light could be a more accurate alternative, but it is not yet a clinical reality.

The review also showed potential for combining ESD with other modalities. For example, a study by Hamada and colleagues involving 66 patients with submucosal (T1b) esophageal squamous cell carcinoma found that a combination of ESD with chemoradiation led to similar 3- and 5-year survival rates as radical esophagectomy. The investigators highlighted the importance of lymph node metastasis in this study, as none of the 30 patients lacking lymph node involvement had metastatic recurrence, compared with 6 of the 36 patients who exhibited lymph node metastasis. According to the investigators, promising data are also anticipated for this combination among those with adenocarcinoma. And for patients with intestinal metaplasia and/or dysplasia, adding radiofrequency ablation after ESD appears to be an effective option; one recent study by Sharmila Subramaniam, BMBS, and colleagues found that this strategy led to clearance rates of 85% and 96% for metaplasia and dysplasia, respectively.

“Additional treatment should be determined by factors such as tumor grade, status of lymphovascular invasion, and depth of tumor, which have a direct influence on metastatic potential,” the investigators wrote.

The investigators suggested that, in the future, better diagnostics will be needed to characterize T1b disease, as this could streamline patient selection. “Future research should focus on novel biological and immunohistochemistry markers that can aid in the prediction of tumor behavior and [lymph node metastasis] in T1b esophageal cancer,” they concluded.

The study was commissioned by the American Gastroenterological Association. The investigators disclosed additional relationships with Boston Scientific, Olympus, Lumendi, and others.

SOURCE: Othman MO et al. CGH. 2019 Jun 4. doi: 10.1016/j.cgh.2019.05.045.

Endoscopic submucosal dissection (ESD) is a viable treatment option for patients with submucosal (T1b) esophageal cancer who have a low risk of lymph node metastasis, according to an expert review.

Among patients with T1b esophageal cancer, ideal candidates for ESD have small (less than 2 cm), well-differentiated tumors that do not invade beyond the superficial submucosa (SM1) and lack lymphovascular invasion, reported lead author Mohamed O. Othman, MD, of Baylor College of Medicine in Houston, and colleagues. The literature review was recently commissioned by the American Gastroenterological Association (AGA), because of high clinical relevance.

“[ESD] has been gaining momentum as an alternative to surgery in treating early gastrointestinal neoplasms,” the investigators wrote in Clinical Gastroenterology and Hepatology.

Most patients who undergo surgical resection develop gastroesophageal reflux, the investigators noted, and many others develop serious complications or do not survive the procedure.

“Even a high-volume center such as Mayo Clinic reported a surgical mortality of 4% for T1a esophageal cancer,” the investigators wrote. “Moreover, 34% of patients developed postoperative complications such as anastomotic leaks, anastomotic strictures, cardiopulmonary complications, and feeding jejunostomy leaks. ... Therefore, a less-invasive alternative to esophagectomy would be extremely valuable in the management of early stage [esophageal cancer] if proven effective.”

The investigators reviewed studies evaluating safety and efficacy of surgical and endoscopic techniques, as well as available data for chemoradiation and radiofrequency ablation combinations, which could potentially optimize outcomes of endoscopic resection.

They concluded that most patients with esophageal cancer that does not extend beyond the mucosa (T1a) can be cured with endoscopic resection, based on 5-year survival rates from several Japanese trials. For patients with T1b disease, however, ESD is best suited for those with a low risk of lymph node metastasis. Unfortunately, identifying these candidates can be challenging, according to the investigators.

“The risk of lymph node metastasis depends on the depth of invasion, histologic type, and molecular characterization of the tumor,” the investigators explained, noting that depth of invasion is the trickiest to discern. Although endoscopic ultrasound (EUS) is still recommended for submucosal imaging, the review showed that EUS may overstage cancer in Barrett’s esophagus. The investigators suggested that volume laser endoscopy with infrared light could be a more accurate alternative, but it is not yet a clinical reality.

The review also showed potential for combining ESD with other modalities. For example, a study by Hamada and colleagues involving 66 patients with submucosal (T1b) esophageal squamous cell carcinoma found that a combination of ESD with chemoradiation led to similar 3- and 5-year survival rates as radical esophagectomy. The investigators highlighted the importance of lymph node metastasis in this study, as none of the 30 patients lacking lymph node involvement had metastatic recurrence, compared with 6 of the 36 patients who exhibited lymph node metastasis. According to the investigators, promising data are also anticipated for this combination among those with adenocarcinoma. And for patients with intestinal metaplasia and/or dysplasia, adding radiofrequency ablation after ESD appears to be an effective option; one recent study by Sharmila Subramaniam, BMBS, and colleagues found that this strategy led to clearance rates of 85% and 96% for metaplasia and dysplasia, respectively.

“Additional treatment should be determined by factors such as tumor grade, status of lymphovascular invasion, and depth of tumor, which have a direct influence on metastatic potential,” the investigators wrote.

The investigators suggested that, in the future, better diagnostics will be needed to characterize T1b disease, as this could streamline patient selection. “Future research should focus on novel biological and immunohistochemistry markers that can aid in the prediction of tumor behavior and [lymph node metastasis] in T1b esophageal cancer,” they concluded.

The study was commissioned by the American Gastroenterological Association. The investigators disclosed additional relationships with Boston Scientific, Olympus, Lumendi, and others.

SOURCE: Othman MO et al. CGH. 2019 Jun 4. doi: 10.1016/j.cgh.2019.05.045.

Studies have found that 1 in 2 psychiatrists,^1-4 and 1 in 5 psychologists, clinical social workers, and other mental health professionals,⁵ will lose a patient to suicide in the course of their career. This statistic suggests that losing a patient to suicide constitutes a clear occupational hazard.^6,7 Despite this, most mental health professionals continue to view suicide loss as an aberration. Consequently, there is often a lack of preparedness for such an event when it does occur.

This 2-part article summarizes what is currently known about the unique personal and professional issues experienced by clinician-survivors (clinicians who have lost patients and/or loved ones to suicide). In Part 1, I cover:

• the impact of losing a patient to suicide
• confidentiality-related constraints on the ability to discuss and process the loss
• legal and ethical issues
• colleagues’ reactions and stigma
• the effects of a suicide loss on one’s clinical work.

Part 2 will discuss the opportunities for personal growth that can result from experiencing a suicide loss, guidelines for optimal postventions, and steps clinicians can take to help support colleagues who have lost a patient to suicide. 

A neglected topic

For psychiatrists and other mental health professionals, the loss of a patient to suicide is certainly not uncommon.^1-5 Despite this, coping with a patient’s suicide is a “neglected topic”⁸ in residency and general mental health training.

There are many published articles on clinicians experiencing suicide loss (for a comprehensive bibliography, see McIntosh⁹), and several authors^10-19 have developed suggestions, guidelines, and detailed postvention protocols to help clinicians navigate the often-complicated sequelae to such a loss. However, these resources have generally not been integrated into clinical training, and tend to be poorly disseminated. In a national survey of chief residents, Melton and Coverdale²⁰ found that only 25% of residency training programs covered topics related to postvention, and 72% of chief residents felt this topic needed more attention. Thus, despite the existence of guidelines for optimal postvention and support, clinicians are often left to cope with the consequences of this difficult loss on their own, and under less-than-optimal conditions.

A patient’s suicide typically affects clinicians on multiple levels, both personally and professionally. In this article, I highlight the range of normative responses, as well as the factors that may facilitate or inhibit subsequent healing and growth, with the hope that this knowledge may be utilized to help current and future generations of clinician-survivors obtain optimal support, and that institutions who treat potentially suicidal individuals will develop optimal postvention responses following a suicide loss. Many aspects of what this article discusses also apply to clinicians who have experienced a suicide loss in their personal or family life, as this also tends to “spill over” into one’s professional roles and identity.

Grief and other emotional effects

In many ways, clinicians’ responses after a patient’s suicide are similar to those of other survivors after the loss of a loved one to suicide.²¹ Chemtob et al² found that approximately one-half of psychiatrists who lost a patient to suicide had scores on the Impact of an Event Scale that were comparable to those of a clinical population seeking treatment after the death of a parent.

Continue to: Jordan and McIntosh have detailed...

Jordan and McIntosh²² have detailed several elements and themes that differentiate suicide loss and its associated reactions from other types of loss and grief. In general, suicide loss is considered traumatic, and is often accompanied by intense confusion and existential questioning, reflecting a negative impact on one’s core beliefs and assumptive world. The subsequent need to address the myriad of “why” questions left in its wake are often tinted with what Jordan and Baugher²³ term the “tyranny of hindsight,” and take the form of implicit guilt for “sins of omission or commission” in relation to the lost individual.

Responses to suicide loss typically include initial shock, denial and numbness, intense sadness, anxiety, anger, and intense distress. Consistent with the traumatic nature of the loss, survivors are also likely to experience posttraumatic stress disorder symptoms such as intrusive thoughts, avoidance, and dissociation. Survivors also commonly experience significant guilt and shame, and this is likely to be socially reinforced by the general stigma associated with suicide as well as the actual blaming and avoidance responses of others.^24-27

Clinicians’ unique reactions

For clinicians, there are additional components that may further complicate or exacerbate these reactions and extend their duration. First and foremost, such a loss affects clinicians on both personal and professional levels, a phenomenon that Plakun and Tillman¹³ have termed a “twin bereavement.” Thus, in addition to the personal grief and trauma reactions entailed in losing a patient to suicide, this loss is likely to impact clinicians’ professional identities, their relationships with colleagues, and their clinical work.

Clinicians’ professional identities are often predicated on generally shared assumptions and beliefs that, as trained professionals, they should have the power, aptitude, and competence to heal, or at least improve, the lives of patients, to reduce their distress, and to provide safety. In addition, such assumptions about clinicians’ responsibility and ability to prevent suicide are often reinforced in the clinical literature.^28,29

These assumptions are often challenged, if not shattered, when patients take their own lives. A clinician’s sense of professional responsibility, the guilt and self-blame that may accompany this, self-doubts about one’s skills and clinical competence, the fear of (and actual) blame of colleagues and family members, and the real or imagined threat of litigation may all greatly exacerbate a clinician’s distress.¹¹

Continue to: Hendin et al found...

Hendin et al³⁰ found that mental health therapists have described losing a patient as “the most profoundly disturbing event of their professional careers,” noting that one-third of these clinicians experienced severe distress that lasted at least 1 year beyond the initial loss. In a 2004 study, Ruskin et al⁴ similarly found that one-quarter of psychiatrists and psychiatric trainees noted that losing a patient had a “profound and enduring effect on them.” In her article on surviving a patient’s suicide, Rycroft³¹ describes a “professional void” following the loss of her patient, in which “the world had changed, nothing was predictable any more, and it was no longer safe to assume anything.” Additionally, many clinicians experience an “acute sense of aloneness and isolation” subsequent to the loss.³²

Many clinicians have noted that they considered leaving the field after such a loss,^33,34 and it is hypothesized that many may have done so.^35-37 Others have noted that, at least temporarily, they stopped treating patients who were potentially suicidal.^29,35

Box 1

After losing a patient to suicide, a clinician may experience grief that proceeds through specific stages (Box 1^33,38-41). Box 2^{2-4,6,16,24,29,30,33,34,40,42-45}  describes a wide range of factors that affect each clinician’s unique response to losing a patient to suicide.

Box 2

Continue to: Implications of confidentiality restrictions

Confidentiality issues, as well as advice from attorneys to limit the disclosure of information about a patient, are likely to preclude a clinician’s ability to talk freely about the patient, the therapeutic relationship, and his/her reactions to the loss, all of which are known to facilitate movement through the grief process.⁴⁶

The development of trust and the sharing of pain are just 2 factors that can make the clinical encounter an intense emotional experience for both parties. Recent trends in the psychodynamic literature acknowledge the profundity and depth of the personal impact that patients have on the clinician, an impact that is neither pathological nor an indication of poor boundaries in the therapy dyad, but instead a recognition of how all aspects of the clinician’s person, whether consciously or not, are used within the context of a therapeutic relationship. Yet when clinicians lose a patient, confidentiality restrictions often leave them wondering if and where any aspects of their experiences can be shared. Legal counsel may advise a clinician against speaking to consultants or supervisors or even surviving family members for fear that these non-privileged communications are subject to discovery should any legal proceedings ensue. Furthermore, the usual grief rituals that facilitate the healing of loss and the processing of grief (eg, gathering with others who knew the deceased, sharing feelings and memories, attending memorials) are usually denied to the clinician, and are often compounded by the reactions of one’s professional colleagues, who tend not to view the therapist’s grief as “legitimate.” Thus, clinician-survivors, despite having experienced a profound and traumatic loss, have very few places where this may be processed or even validated. As one clinician in a clinician-survivors support group stated, “I felt like I was grieving in a vacuum, that I wasn’t allowed to talk about how much my patient meant to me or how I’m feeling about it.” The isolation of grieving alone is likely to be compounded by the general lack of resources for supporting clinicians after such a loss. In contrast to the general suicide “survivor” network of support groups for family members who have experienced a suicide loss, there is an almost complete lack of supportive resources for clinicians following such a loss, and most clinicians are not aware of the resources that are available, such as the Clinician Survivor Task Force of the American Association of Suicidology (Box 3¹²).

Box 3

Continue to: Doka has described...

Doka⁴⁷ has described “disenfranchised grief” in which the bereaved person does not receive the type and quality of support accorded to other bereaved persons, and thus is likely to internalize the view that his/her grief is not legitimate, and to believe that sharing related distress is a shame-ridden liability. This clearly relates to the sense of profound isolation and distress often described by clinician-survivors.

Other legal/ethical issues

The clinician-survivor’s concern about litigation, or an actual lawsuit, is likely to produce intense anxiety. This common fear is both understandable and credible. According to Bongar,⁴⁸ the most common malpractice lawsuits filed against clinicians are those that involve a patient’s suicide. Peterson et al⁴⁹ found that 34% of surviving family members considered bringing a lawsuit against the clinician, and of these, 57% consulted a lawyer.

In addition, an institution’s concern about protecting itself from liability may compromise its ability to support the clinician or trainee who sustained the loss. As noted above, the potential prohibitions around discussing the case can compromise the grief process. Additionally, the fear of (or actual) legal reprisals against supervisors and the larger institution may engender angry and blaming responses toward the treating clinician. In a personal communication (April 2008), Quinnett described an incident in which a supervising psychologist stomped into the grieving therapist’s office unannounced and shouted, “Now look what you’ve done! You’re going to get me sued!”

Other studies^29,50,51 note that clinician-survivors fear losing their job, and that their colleagues and supervisors will be reluctant to assign new patients to them. Spiegleman and Werth¹⁷ also note that trainees grapple with additional concerns over negative evaluations, suspension or termination from clinical sites or training programs, and a potential interruption of obtaining a degree. Such supervisory and institutional reactions are likely to intensify a clinician’s sense of shame and distress, and are antithetical to postvention responses that promote optimal personal and professional growth. Such negative reactions are also likely to contribute to a clinician or trainee’s subsequent reluctance to work with suicidal individuals, or their decision to discontinue their clinical work altogether. Lastly, other ethical issues, such as contact with the patient’s family following the suicide, attending the funeral, etc., are likely to be a source of additional anxiety and distress, particularly if the clinician needs to address these issues in isolation.

Professional relationships/colleagues’ reactions

Many clinician-survivors have described reactions from colleagues and supervisors that are hurtful and unsupportive. According to Jobes and Maltsberger,⁵² “the suicide death of a patient in active treatment is commonly taken as prima facie evidence that the therapist, somehow or another, has mismanaged the case,” and thus the clinician often faces unwarranted blame and censure from colleagues and supervisors. Hendin et al³⁰ noted that many trainees found reactions by their institutions to be insensitive and unsupportive, one noting that the department’s review of the case “felt more like a tribunal or inquest.” In a personal communication (April 2008), Quinnett noted that many clinicians he interviewed following a suicide loss reported a pattern of isolation and interpersonal discomfort with their colleagues, who implicitly or explicitly expressed concerns about their competence. He described how a respected colleague received “no understanding, no support, only abuse” from her supervisors. Such responses, while perhaps surprising from mental health professionals, probably reflect the long-standing cultural attitude of social condemnation of suicide, and of those who are associated with it.

Continue to: Negative reactions from professional colleagues...

Negative reactions from professional colleagues are most likely to occur immediately after the suicide loss and/or during the course of a subsequent investigation or psychological autopsy. Castelli-Dransart et al⁵³ found that the lack of institutional support after a clinician experiences a suicide loss contributed to significantly higher stress responses for impacted clinicians, and may lead to a well-founded ambivalence about disclosure to colleagues, and consequent resistance to seeking out optimal supervision/consultation or even personal therapy that could help the clinician gain clarity on the effects of these issues. Many mental health professionals have described how, after the distressing experience of losing a patient to suicide, they moved through this process in relative isolation and loneliness, feeling abandoned by their colleagues and by their own hopes and expectations for support.

Stigmatization. In clinical settings, when a patient in treatment completes suicide, the treating clinician becomes an easy scapegoat for family members and colleagues. To the extent that mental health professionals are not immune from the effects and imposition of stigma, this might also affect their previously mentioned tendency to project judgment, overtly or covertly, onto the treating clinician.

Stigma around suicide is well documented.²⁵ In The Surgeon General’s Call to Action to Prevent Suicide,⁵⁴ former Surgeon General David Satcher specifically described stigma around suicide as one of the biggest barriers to prevention. Studies have shown that individuals bereaved by suicide are also stigmatized, and that those who were in caregiving roles (parents, clinicians) are believed to be more psychologically disturbed, less likable, more blameworthy, and less worthy of receiving support than other bereaved individuals.^25,55-63 These judgments often mirror survivors’ self-punitive assessments, which then become exacerbated by and intertwined with both externally imposed and internalized stigma. Hence, it is not uncommon for suicide survivors to question their own right to grieve, to report low expectations of social support, and to feel compelled to deny or hide the mode of death. Feigelman et al²⁶ found that stigmatization after a suicide loss was specifically associated with ongoing grief difficulties, depression, and suicidal thinking.

In my long-term work with clinician-survivors, I’ve come to believe that in addition to stigma around suicide, there may also be stigma projected by colleagues in relation to a clinician’s perceived emotional vulnerability. A traumatized clinician potentially challenges the notion of the implicit dichotomy/power imbalance between professionals and the patients we treat: “Us”—the professional, competent, healthy, and benevolent clinicians who have the care to offer, and “Them”—our patients, being needy, pathological, looking to us for care. This “us/them” distinction may serve to bolster a clinician’s professional esteem and identity. But when one of “us” becomes one of “them”—when a professional colleague is perceived as being emotionally vulnerable—this can be threatening to the predicates of this distinction, leading to the need to put the affected clinician firmly into the “them” camp. Thus, unwarranted condemnations of the clinician-survivor’s handling of the case, and/or the pathologizing of their normative grief reactions after the suicide loss, can seem justified.

Stigma associated both with suicide and with professional vulnerability is likely to be internalized and to have a profound effect on the clinician’s decisions about disclosure, asking for support, and ultimately on one’s ability to integrate the loss. When this occurs, it is likely to lead to even more isolation, shame, and self-blame. It is not surprising that many clinicians consider leaving the profession after this type of experience.

Continue to: Effects on clinical work

A suicide loss is also likely to affect a clinician’s therapeutic work. Many authors^12,52,64-67 have found that this commonly leads therapists to question their abilities as clinicians, and to experience a sharp loss of confidence in their work with patients. The shattered beliefs and assumptions around the efficacy of the therapeutic process, a sense of guilt or self-blame, and any perceived or actual negative judgment from colleagues can dramatically compromise a clinician’s sense of competence. Hendin et al³⁰ noted that even the most experienced therapists expressed difficulty in trusting their own clinical judgment, or accurately assessing risk after a suicide loss.

In addition, the common grief and trauma-related responses to a suicide loss (including shock, numbness, sadness, anxiety, and generalized distress) are likely to result in at least some temporary disruption of a clinician’s optimal functioning. If trauma-related symptoms are more pronounced, the effect and longevity of such impairment may be exacerbated, and are likely to “impair clinical response and therapeutic judgment.”¹⁵ In addition, because such symptoms and states may be triggered by exposure to other potentially suicidal patients, they are more likely to impact clinical functioning when the clinician works with suicidal individuals. Thus, the normative responses to a suicide loss are likely to impact a clinician’s work, just as they are likely to impact the personal and occupational functioning of any survivor of suicide loss.

In clinician-survivor discussions and support groups I’ve led, participants have identified many common areas of clinical impact. Perhaps one of the most common early responses reported by clinician-survivors who continued to work with potentially suicidal individuals was to become hypervigilant in relation to any perceived suicide risk, to interpret such risk in such a way as to warrant more conservative interventions than are necessary, and to consequently minimize the patient’s own capacities for self-care.⁶⁸ Conversely, others reported a tendency to minimize or deny suicidal potential by, for example, avoiding asking patients directly about suicidal ideation, even when they later realized that such questioning was indicated.⁶⁹

Suicide loss may also lead to more subtle clinical reactions that have been observed not only with suicidal patients, but also in relation to patients who struggle with loss or grief. These include avoidant or even dissociative reactions in relation to their patient’s pain, which in turn can impact the clinician’s ability to “be fully present” or empathic in clinical encounters.^50,69 Still, other clinicians noted that they tended to project residual feelings of anger onto their current suicidal patients, or envied patients who seemed to have mastered their grief. Consistent with Maltsberger’s description of “atonement reactions,”⁴⁰ some clinicians found themselves doing more than should be expected for their patients, even losing their sense of professional boundaries in the process. Anderson⁷⁰ noted that in pushing herself beyond what she knew were her optimal clinical boundaries, she was “punishing herself” for failing to prevent her patient’s suicide because, as she realized, “doing ‘penance’ was better than feeling helpless and powerless.” And Schultz¹⁶ described how therapists may have subsequent difficulty in trusting other patients, especially if patients who completed suicide did not disclose or denied their suicidal intent.

Working toward a supportive solution

In summary, unless clinicians who lose a patient to suicide have more supportive experiences, the combination of confidentiality-related restrictions, confusion about legal/ethical repercussions, unsupportive reactions from colleagues, and unexpected impairments in clinical work are likely to lead to intensified distress, isolation, the perceived need to “hide” the impact in professional settings, and consideration of leaving the profession. However, as I will describe in Part 2 (Current Psychiatry. November 2019), losing a patient to suicide can paradoxically present opportunities for clinicians to experience profound and personal transformation, and postvention protocols can help them navigate the often-complicated sequelae to a patient’s suicide. There is also much we can do to help support a clinician colleague who has lost a patient to suicide.

Bottom Line

For mental health clinicians, losing a patient to suicide is a clear occupational hazard. After a suicide loss, clinicians often experience unique personal and professional challenges, including the impact of the loss on clinical work and professional identity, legal/ethical issues, and confidentiality-related constraints on the ability to discuss and process the loss.

Related Resources

• American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
• Gutin N. Helping survivors in the aftermath of suicide loss. Current Psychiatry. 2018;17(8):27-33.

Studies have found that 1 in 2 psychiatrists,^1-4 and 1 in 5 psychologists, clinical social workers, and other mental health professionals,⁵ will lose a patient to suicide in the course of their career. This statistic suggests that losing a patient to suicide constitutes a clear occupational hazard.^6,7 Despite this, most mental health professionals continue to view suicide loss as an aberration. Consequently, there is often a lack of preparedness for such an event when it does occur.

This 2-part article summarizes what is currently known about the unique personal and professional issues experienced by clinician-survivors (clinicians who have lost patients and/or loved ones to suicide). In Part 1, I cover:

• the impact of losing a patient to suicide
• confidentiality-related constraints on the ability to discuss and process the loss
• legal and ethical issues
• colleagues’ reactions and stigma
• the effects of a suicide loss on one’s clinical work.

Part 2 will discuss the opportunities for personal growth that can result from experiencing a suicide loss, guidelines for optimal postventions, and steps clinicians can take to help support colleagues who have lost a patient to suicide. 

A neglected topic

For psychiatrists and other mental health professionals, the loss of a patient to suicide is certainly not uncommon.^1-5 Despite this, coping with a patient’s suicide is a “neglected topic”⁸ in residency and general mental health training.

There are many published articles on clinicians experiencing suicide loss (for a comprehensive bibliography, see McIntosh⁹), and several authors^10-19 have developed suggestions, guidelines, and detailed postvention protocols to help clinicians navigate the often-complicated sequelae to such a loss. However, these resources have generally not been integrated into clinical training, and tend to be poorly disseminated. In a national survey of chief residents, Melton and Coverdale²⁰ found that only 25% of residency training programs covered topics related to postvention, and 72% of chief residents felt this topic needed more attention. Thus, despite the existence of guidelines for optimal postvention and support, clinicians are often left to cope with the consequences of this difficult loss on their own, and under less-than-optimal conditions.

A patient’s suicide typically affects clinicians on multiple levels, both personally and professionally. In this article, I highlight the range of normative responses, as well as the factors that may facilitate or inhibit subsequent healing and growth, with the hope that this knowledge may be utilized to help current and future generations of clinician-survivors obtain optimal support, and that institutions who treat potentially suicidal individuals will develop optimal postvention responses following a suicide loss. Many aspects of what this article discusses also apply to clinicians who have experienced a suicide loss in their personal or family life, as this also tends to “spill over” into one’s professional roles and identity.

Grief and other emotional effects

In many ways, clinicians’ responses after a patient’s suicide are similar to those of other survivors after the loss of a loved one to suicide.²¹ Chemtob et al² found that approximately one-half of psychiatrists who lost a patient to suicide had scores on the Impact of an Event Scale that were comparable to those of a clinical population seeking treatment after the death of a parent.

Continue to: Jordan and McIntosh have detailed...

Jordan and McIntosh²² have detailed several elements and themes that differentiate suicide loss and its associated reactions from other types of loss and grief. In general, suicide loss is considered traumatic, and is often accompanied by intense confusion and existential questioning, reflecting a negative impact on one’s core beliefs and assumptive world. The subsequent need to address the myriad of “why” questions left in its wake are often tinted with what Jordan and Baugher²³ term the “tyranny of hindsight,” and take the form of implicit guilt for “sins of omission or commission” in relation to the lost individual.

Responses to suicide loss typically include initial shock, denial and numbness, intense sadness, anxiety, anger, and intense distress. Consistent with the traumatic nature of the loss, survivors are also likely to experience posttraumatic stress disorder symptoms such as intrusive thoughts, avoidance, and dissociation. Survivors also commonly experience significant guilt and shame, and this is likely to be socially reinforced by the general stigma associated with suicide as well as the actual blaming and avoidance responses of others.^24-27

Clinicians’ unique reactions

For clinicians, there are additional components that may further complicate or exacerbate these reactions and extend their duration. First and foremost, such a loss affects clinicians on both personal and professional levels, a phenomenon that Plakun and Tillman¹³ have termed a “twin bereavement.” Thus, in addition to the personal grief and trauma reactions entailed in losing a patient to suicide, this loss is likely to impact clinicians’ professional identities, their relationships with colleagues, and their clinical work.

Clinicians’ professional identities are often predicated on generally shared assumptions and beliefs that, as trained professionals, they should have the power, aptitude, and competence to heal, or at least improve, the lives of patients, to reduce their distress, and to provide safety. In addition, such assumptions about clinicians’ responsibility and ability to prevent suicide are often reinforced in the clinical literature.^28,29

These assumptions are often challenged, if not shattered, when patients take their own lives. A clinician’s sense of professional responsibility, the guilt and self-blame that may accompany this, self-doubts about one’s skills and clinical competence, the fear of (and actual) blame of colleagues and family members, and the real or imagined threat of litigation may all greatly exacerbate a clinician’s distress.¹¹

Continue to: Hendin et al found...

Hendin et al³⁰ found that mental health therapists have described losing a patient as “the most profoundly disturbing event of their professional careers,” noting that one-third of these clinicians experienced severe distress that lasted at least 1 year beyond the initial loss. In a 2004 study, Ruskin et al⁴ similarly found that one-quarter of psychiatrists and psychiatric trainees noted that losing a patient had a “profound and enduring effect on them.” In her article on surviving a patient’s suicide, Rycroft³¹ describes a “professional void” following the loss of her patient, in which “the world had changed, nothing was predictable any more, and it was no longer safe to assume anything.” Additionally, many clinicians experience an “acute sense of aloneness and isolation” subsequent to the loss.³²

Many clinicians have noted that they considered leaving the field after such a loss,^33,34 and it is hypothesized that many may have done so.^35-37 Others have noted that, at least temporarily, they stopped treating patients who were potentially suicidal.^29,35

Box 1

After losing a patient to suicide, a clinician may experience grief that proceeds through specific stages (Box 1^33,38-41). Box 2^{2-4,6,16,24,29,30,33,34,40,42-45}  describes a wide range of factors that affect each clinician’s unique response to losing a patient to suicide.

Box 2

Continue to: Implications of confidentiality restrictions

Confidentiality issues, as well as advice from attorneys to limit the disclosure of information about a patient, are likely to preclude a clinician’s ability to talk freely about the patient, the therapeutic relationship, and his/her reactions to the loss, all of which are known to facilitate movement through the grief process.⁴⁶

The development of trust and the sharing of pain are just 2 factors that can make the clinical encounter an intense emotional experience for both parties. Recent trends in the psychodynamic literature acknowledge the profundity and depth of the personal impact that patients have on the clinician, an impact that is neither pathological nor an indication of poor boundaries in the therapy dyad, but instead a recognition of how all aspects of the clinician’s person, whether consciously or not, are used within the context of a therapeutic relationship. Yet when clinicians lose a patient, confidentiality restrictions often leave them wondering if and where any aspects of their experiences can be shared. Legal counsel may advise a clinician against speaking to consultants or supervisors or even surviving family members for fear that these non-privileged communications are subject to discovery should any legal proceedings ensue. Furthermore, the usual grief rituals that facilitate the healing of loss and the processing of grief (eg, gathering with others who knew the deceased, sharing feelings and memories, attending memorials) are usually denied to the clinician, and are often compounded by the reactions of one’s professional colleagues, who tend not to view the therapist’s grief as “legitimate.” Thus, clinician-survivors, despite having experienced a profound and traumatic loss, have very few places where this may be processed or even validated. As one clinician in a clinician-survivors support group stated, “I felt like I was grieving in a vacuum, that I wasn’t allowed to talk about how much my patient meant to me or how I’m feeling about it.” The isolation of grieving alone is likely to be compounded by the general lack of resources for supporting clinicians after such a loss. In contrast to the general suicide “survivor” network of support groups for family members who have experienced a suicide loss, there is an almost complete lack of supportive resources for clinicians following such a loss, and most clinicians are not aware of the resources that are available, such as the Clinician Survivor Task Force of the American Association of Suicidology (Box 3¹²).

Box 3

Continue to: Doka has described...

Doka⁴⁷ has described “disenfranchised grief” in which the bereaved person does not receive the type and quality of support accorded to other bereaved persons, and thus is likely to internalize the view that his/her grief is not legitimate, and to believe that sharing related distress is a shame-ridden liability. This clearly relates to the sense of profound isolation and distress often described by clinician-survivors.

Other legal/ethical issues

The clinician-survivor’s concern about litigation, or an actual lawsuit, is likely to produce intense anxiety. This common fear is both understandable and credible. According to Bongar,⁴⁸ the most common malpractice lawsuits filed against clinicians are those that involve a patient’s suicide. Peterson et al⁴⁹ found that 34% of surviving family members considered bringing a lawsuit against the clinician, and of these, 57% consulted a lawyer.

In addition, an institution’s concern about protecting itself from liability may compromise its ability to support the clinician or trainee who sustained the loss. As noted above, the potential prohibitions around discussing the case can compromise the grief process. Additionally, the fear of (or actual) legal reprisals against supervisors and the larger institution may engender angry and blaming responses toward the treating clinician. In a personal communication (April 2008), Quinnett described an incident in which a supervising psychologist stomped into the grieving therapist’s office unannounced and shouted, “Now look what you’ve done! You’re going to get me sued!”

Other studies^29,50,51 note that clinician-survivors fear losing their job, and that their colleagues and supervisors will be reluctant to assign new patients to them. Spiegleman and Werth¹⁷ also note that trainees grapple with additional concerns over negative evaluations, suspension or termination from clinical sites or training programs, and a potential interruption of obtaining a degree. Such supervisory and institutional reactions are likely to intensify a clinician’s sense of shame and distress, and are antithetical to postvention responses that promote optimal personal and professional growth. Such negative reactions are also likely to contribute to a clinician or trainee’s subsequent reluctance to work with suicidal individuals, or their decision to discontinue their clinical work altogether. Lastly, other ethical issues, such as contact with the patient’s family following the suicide, attending the funeral, etc., are likely to be a source of additional anxiety and distress, particularly if the clinician needs to address these issues in isolation.

Professional relationships/colleagues’ reactions

Many clinician-survivors have described reactions from colleagues and supervisors that are hurtful and unsupportive. According to Jobes and Maltsberger,⁵² “the suicide death of a patient in active treatment is commonly taken as prima facie evidence that the therapist, somehow or another, has mismanaged the case,” and thus the clinician often faces unwarranted blame and censure from colleagues and supervisors. Hendin et al³⁰ noted that many trainees found reactions by their institutions to be insensitive and unsupportive, one noting that the department’s review of the case “felt more like a tribunal or inquest.” In a personal communication (April 2008), Quinnett noted that many clinicians he interviewed following a suicide loss reported a pattern of isolation and interpersonal discomfort with their colleagues, who implicitly or explicitly expressed concerns about their competence. He described how a respected colleague received “no understanding, no support, only abuse” from her supervisors. Such responses, while perhaps surprising from mental health professionals, probably reflect the long-standing cultural attitude of social condemnation of suicide, and of those who are associated with it.

Continue to: Negative reactions from professional colleagues...

Negative reactions from professional colleagues are most likely to occur immediately after the suicide loss and/or during the course of a subsequent investigation or psychological autopsy. Castelli-Dransart et al⁵³ found that the lack of institutional support after a clinician experiences a suicide loss contributed to significantly higher stress responses for impacted clinicians, and may lead to a well-founded ambivalence about disclosure to colleagues, and consequent resistance to seeking out optimal supervision/consultation or even personal therapy that could help the clinician gain clarity on the effects of these issues. Many mental health professionals have described how, after the distressing experience of losing a patient to suicide, they moved through this process in relative isolation and loneliness, feeling abandoned by their colleagues and by their own hopes and expectations for support.

Stigmatization. In clinical settings, when a patient in treatment completes suicide, the treating clinician becomes an easy scapegoat for family members and colleagues. To the extent that mental health professionals are not immune from the effects and imposition of stigma, this might also affect their previously mentioned tendency to project judgment, overtly or covertly, onto the treating clinician.

Stigma around suicide is well documented.²⁵ In The Surgeon General’s Call to Action to Prevent Suicide,⁵⁴ former Surgeon General David Satcher specifically described stigma around suicide as one of the biggest barriers to prevention. Studies have shown that individuals bereaved by suicide are also stigmatized, and that those who were in caregiving roles (parents, clinicians) are believed to be more psychologically disturbed, less likable, more blameworthy, and less worthy of receiving support than other bereaved individuals.^25,55-63 These judgments often mirror survivors’ self-punitive assessments, which then become exacerbated by and intertwined with both externally imposed and internalized stigma. Hence, it is not uncommon for suicide survivors to question their own right to grieve, to report low expectations of social support, and to feel compelled to deny or hide the mode of death. Feigelman et al²⁶ found that stigmatization after a suicide loss was specifically associated with ongoing grief difficulties, depression, and suicidal thinking.

In my long-term work with clinician-survivors, I’ve come to believe that in addition to stigma around suicide, there may also be stigma projected by colleagues in relation to a clinician’s perceived emotional vulnerability. A traumatized clinician potentially challenges the notion of the implicit dichotomy/power imbalance between professionals and the patients we treat: “Us”—the professional, competent, healthy, and benevolent clinicians who have the care to offer, and “Them”—our patients, being needy, pathological, looking to us for care. This “us/them” distinction may serve to bolster a clinician’s professional esteem and identity. But when one of “us” becomes one of “them”—when a professional colleague is perceived as being emotionally vulnerable—this can be threatening to the predicates of this distinction, leading to the need to put the affected clinician firmly into the “them” camp. Thus, unwarranted condemnations of the clinician-survivor’s handling of the case, and/or the pathologizing of their normative grief reactions after the suicide loss, can seem justified.

Stigma associated both with suicide and with professional vulnerability is likely to be internalized and to have a profound effect on the clinician’s decisions about disclosure, asking for support, and ultimately on one’s ability to integrate the loss. When this occurs, it is likely to lead to even more isolation, shame, and self-blame. It is not surprising that many clinicians consider leaving the profession after this type of experience.

Continue to: Effects on clinical work

A suicide loss is also likely to affect a clinician’s therapeutic work. Many authors^12,52,64-67 have found that this commonly leads therapists to question their abilities as clinicians, and to experience a sharp loss of confidence in their work with patients. The shattered beliefs and assumptions around the efficacy of the therapeutic process, a sense of guilt or self-blame, and any perceived or actual negative judgment from colleagues can dramatically compromise a clinician’s sense of competence. Hendin et al³⁰ noted that even the most experienced therapists expressed difficulty in trusting their own clinical judgment, or accurately assessing risk after a suicide loss.

In addition, the common grief and trauma-related responses to a suicide loss (including shock, numbness, sadness, anxiety, and generalized distress) are likely to result in at least some temporary disruption of a clinician’s optimal functioning. If trauma-related symptoms are more pronounced, the effect and longevity of such impairment may be exacerbated, and are likely to “impair clinical response and therapeutic judgment.”¹⁵ In addition, because such symptoms and states may be triggered by exposure to other potentially suicidal patients, they are more likely to impact clinical functioning when the clinician works with suicidal individuals. Thus, the normative responses to a suicide loss are likely to impact a clinician’s work, just as they are likely to impact the personal and occupational functioning of any survivor of suicide loss.

In clinician-survivor discussions and support groups I’ve led, participants have identified many common areas of clinical impact. Perhaps one of the most common early responses reported by clinician-survivors who continued to work with potentially suicidal individuals was to become hypervigilant in relation to any perceived suicide risk, to interpret such risk in such a way as to warrant more conservative interventions than are necessary, and to consequently minimize the patient’s own capacities for self-care.⁶⁸ Conversely, others reported a tendency to minimize or deny suicidal potential by, for example, avoiding asking patients directly about suicidal ideation, even when they later realized that such questioning was indicated.⁶⁹

Suicide loss may also lead to more subtle clinical reactions that have been observed not only with suicidal patients, but also in relation to patients who struggle with loss or grief. These include avoidant or even dissociative reactions in relation to their patient’s pain, which in turn can impact the clinician’s ability to “be fully present” or empathic in clinical encounters.^50,69 Still, other clinicians noted that they tended to project residual feelings of anger onto their current suicidal patients, or envied patients who seemed to have mastered their grief. Consistent with Maltsberger’s description of “atonement reactions,”⁴⁰ some clinicians found themselves doing more than should be expected for their patients, even losing their sense of professional boundaries in the process. Anderson⁷⁰ noted that in pushing herself beyond what she knew were her optimal clinical boundaries, she was “punishing herself” for failing to prevent her patient’s suicide because, as she realized, “doing ‘penance’ was better than feeling helpless and powerless.” And Schultz¹⁶ described how therapists may have subsequent difficulty in trusting other patients, especially if patients who completed suicide did not disclose or denied their suicidal intent.

Working toward a supportive solution

In summary, unless clinicians who lose a patient to suicide have more supportive experiences, the combination of confidentiality-related restrictions, confusion about legal/ethical repercussions, unsupportive reactions from colleagues, and unexpected impairments in clinical work are likely to lead to intensified distress, isolation, the perceived need to “hide” the impact in professional settings, and consideration of leaving the profession. However, as I will describe in Part 2 (Current Psychiatry. November 2019), losing a patient to suicide can paradoxically present opportunities for clinicians to experience profound and personal transformation, and postvention protocols can help them navigate the often-complicated sequelae to a patient’s suicide. There is also much we can do to help support a clinician colleague who has lost a patient to suicide.

Bottom Line

For mental health clinicians, losing a patient to suicide is a clear occupational hazard. After a suicide loss, clinicians often experience unique personal and professional challenges, including the impact of the loss on clinical work and professional identity, legal/ethical issues, and confidentiality-related constraints on the ability to discuss and process the loss.

Related Resources

• American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
• Gutin N. Helping survivors in the aftermath of suicide loss. Current Psychiatry. 2018;17(8):27-33.

Studies have found that 1 in 2 psychiatrists,^1-4 and 1 in 5 psychologists, clinical social workers, and other mental health professionals,⁵ will lose a patient to suicide in the course of their career. This statistic suggests that losing a patient to suicide constitutes a clear occupational hazard.^6,7 Despite this, most mental health professionals continue to view suicide loss as an aberration. Consequently, there is often a lack of preparedness for such an event when it does occur.

This 2-part article summarizes what is currently known about the unique personal and professional issues experienced by clinician-survivors (clinicians who have lost patients and/or loved ones to suicide). In Part 1, I cover:

• the impact of losing a patient to suicide
• confidentiality-related constraints on the ability to discuss and process the loss
• legal and ethical issues
• colleagues’ reactions and stigma
• the effects of a suicide loss on one’s clinical work.

Part 2 will discuss the opportunities for personal growth that can result from experiencing a suicide loss, guidelines for optimal postventions, and steps clinicians can take to help support colleagues who have lost a patient to suicide. 

A neglected topic

For psychiatrists and other mental health professionals, the loss of a patient to suicide is certainly not uncommon.^1-5 Despite this, coping with a patient’s suicide is a “neglected topic”⁸ in residency and general mental health training.

There are many published articles on clinicians experiencing suicide loss (for a comprehensive bibliography, see McIntosh⁹), and several authors^10-19 have developed suggestions, guidelines, and detailed postvention protocols to help clinicians navigate the often-complicated sequelae to such a loss. However, these resources have generally not been integrated into clinical training, and tend to be poorly disseminated. In a national survey of chief residents, Melton and Coverdale²⁰ found that only 25% of residency training programs covered topics related to postvention, and 72% of chief residents felt this topic needed more attention. Thus, despite the existence of guidelines for optimal postvention and support, clinicians are often left to cope with the consequences of this difficult loss on their own, and under less-than-optimal conditions.

A patient’s suicide typically affects clinicians on multiple levels, both personally and professionally. In this article, I highlight the range of normative responses, as well as the factors that may facilitate or inhibit subsequent healing and growth, with the hope that this knowledge may be utilized to help current and future generations of clinician-survivors obtain optimal support, and that institutions who treat potentially suicidal individuals will develop optimal postvention responses following a suicide loss. Many aspects of what this article discusses also apply to clinicians who have experienced a suicide loss in their personal or family life, as this also tends to “spill over” into one’s professional roles and identity.

Grief and other emotional effects

In many ways, clinicians’ responses after a patient’s suicide are similar to those of other survivors after the loss of a loved one to suicide.²¹ Chemtob et al² found that approximately one-half of psychiatrists who lost a patient to suicide had scores on the Impact of an Event Scale that were comparable to those of a clinical population seeking treatment after the death of a parent.

Continue to: Jordan and McIntosh have detailed...

Jordan and McIntosh²² have detailed several elements and themes that differentiate suicide loss and its associated reactions from other types of loss and grief. In general, suicide loss is considered traumatic, and is often accompanied by intense confusion and existential questioning, reflecting a negative impact on one’s core beliefs and assumptive world. The subsequent need to address the myriad of “why” questions left in its wake are often tinted with what Jordan and Baugher²³ term the “tyranny of hindsight,” and take the form of implicit guilt for “sins of omission or commission” in relation to the lost individual.

Responses to suicide loss typically include initial shock, denial and numbness, intense sadness, anxiety, anger, and intense distress. Consistent with the traumatic nature of the loss, survivors are also likely to experience posttraumatic stress disorder symptoms such as intrusive thoughts, avoidance, and dissociation. Survivors also commonly experience significant guilt and shame, and this is likely to be socially reinforced by the general stigma associated with suicide as well as the actual blaming and avoidance responses of others.^24-27

Clinicians’ unique reactions

For clinicians, there are additional components that may further complicate or exacerbate these reactions and extend their duration. First and foremost, such a loss affects clinicians on both personal and professional levels, a phenomenon that Plakun and Tillman¹³ have termed a “twin bereavement.” Thus, in addition to the personal grief and trauma reactions entailed in losing a patient to suicide, this loss is likely to impact clinicians’ professional identities, their relationships with colleagues, and their clinical work.

Clinicians’ professional identities are often predicated on generally shared assumptions and beliefs that, as trained professionals, they should have the power, aptitude, and competence to heal, or at least improve, the lives of patients, to reduce their distress, and to provide safety. In addition, such assumptions about clinicians’ responsibility and ability to prevent suicide are often reinforced in the clinical literature.^28,29

These assumptions are often challenged, if not shattered, when patients take their own lives. A clinician’s sense of professional responsibility, the guilt and self-blame that may accompany this, self-doubts about one’s skills and clinical competence, the fear of (and actual) blame of colleagues and family members, and the real or imagined threat of litigation may all greatly exacerbate a clinician’s distress.¹¹

Continue to: Hendin et al found...

Hendin et al³⁰ found that mental health therapists have described losing a patient as “the most profoundly disturbing event of their professional careers,” noting that one-third of these clinicians experienced severe distress that lasted at least 1 year beyond the initial loss. In a 2004 study, Ruskin et al⁴ similarly found that one-quarter of psychiatrists and psychiatric trainees noted that losing a patient had a “profound and enduring effect on them.” In her article on surviving a patient’s suicide, Rycroft³¹ describes a “professional void” following the loss of her patient, in which “the world had changed, nothing was predictable any more, and it was no longer safe to assume anything.” Additionally, many clinicians experience an “acute sense of aloneness and isolation” subsequent to the loss.³²

Many clinicians have noted that they considered leaving the field after such a loss,^33,34 and it is hypothesized that many may have done so.^35-37 Others have noted that, at least temporarily, they stopped treating patients who were potentially suicidal.^29,35

Box 1

After losing a patient to suicide, a clinician may experience grief that proceeds through specific stages (Box 1^33,38-41). Box 2^{2-4,6,16,24,29,30,33,34,40,42-45}  describes a wide range of factors that affect each clinician’s unique response to losing a patient to suicide.

Box 2

Continue to: Implications of confidentiality restrictions

Confidentiality issues, as well as advice from attorneys to limit the disclosure of information about a patient, are likely to preclude a clinician’s ability to talk freely about the patient, the therapeutic relationship, and his/her reactions to the loss, all of which are known to facilitate movement through the grief process.⁴⁶

The development of trust and the sharing of pain are just 2 factors that can make the clinical encounter an intense emotional experience for both parties. Recent trends in the psychodynamic literature acknowledge the profundity and depth of the personal impact that patients have on the clinician, an impact that is neither pathological nor an indication of poor boundaries in the therapy dyad, but instead a recognition of how all aspects of the clinician’s person, whether consciously or not, are used within the context of a therapeutic relationship. Yet when clinicians lose a patient, confidentiality restrictions often leave them wondering if and where any aspects of their experiences can be shared. Legal counsel may advise a clinician against speaking to consultants or supervisors or even surviving family members for fear that these non-privileged communications are subject to discovery should any legal proceedings ensue. Furthermore, the usual grief rituals that facilitate the healing of loss and the processing of grief (eg, gathering with others who knew the deceased, sharing feelings and memories, attending memorials) are usually denied to the clinician, and are often compounded by the reactions of one’s professional colleagues, who tend not to view the therapist’s grief as “legitimate.” Thus, clinician-survivors, despite having experienced a profound and traumatic loss, have very few places where this may be processed or even validated. As one clinician in a clinician-survivors support group stated, “I felt like I was grieving in a vacuum, that I wasn’t allowed to talk about how much my patient meant to me or how I’m feeling about it.” The isolation of grieving alone is likely to be compounded by the general lack of resources for supporting clinicians after such a loss. In contrast to the general suicide “survivor” network of support groups for family members who have experienced a suicide loss, there is an almost complete lack of supportive resources for clinicians following such a loss, and most clinicians are not aware of the resources that are available, such as the Clinician Survivor Task Force of the American Association of Suicidology (Box 3¹²).

Box 3

Continue to: Doka has described...

Doka⁴⁷ has described “disenfranchised grief” in which the bereaved person does not receive the type and quality of support accorded to other bereaved persons, and thus is likely to internalize the view that his/her grief is not legitimate, and to believe that sharing related distress is a shame-ridden liability. This clearly relates to the sense of profound isolation and distress often described by clinician-survivors.

Other legal/ethical issues

The clinician-survivor’s concern about litigation, or an actual lawsuit, is likely to produce intense anxiety. This common fear is both understandable and credible. According to Bongar,⁴⁸ the most common malpractice lawsuits filed against clinicians are those that involve a patient’s suicide. Peterson et al⁴⁹ found that 34% of surviving family members considered bringing a lawsuit against the clinician, and of these, 57% consulted a lawyer.

In addition, an institution’s concern about protecting itself from liability may compromise its ability to support the clinician or trainee who sustained the loss. As noted above, the potential prohibitions around discussing the case can compromise the grief process. Additionally, the fear of (or actual) legal reprisals against supervisors and the larger institution may engender angry and blaming responses toward the treating clinician. In a personal communication (April 2008), Quinnett described an incident in which a supervising psychologist stomped into the grieving therapist’s office unannounced and shouted, “Now look what you’ve done! You’re going to get me sued!”

Other studies^29,50,51 note that clinician-survivors fear losing their job, and that their colleagues and supervisors will be reluctant to assign new patients to them. Spiegleman and Werth¹⁷ also note that trainees grapple with additional concerns over negative evaluations, suspension or termination from clinical sites or training programs, and a potential interruption of obtaining a degree. Such supervisory and institutional reactions are likely to intensify a clinician’s sense of shame and distress, and are antithetical to postvention responses that promote optimal personal and professional growth. Such negative reactions are also likely to contribute to a clinician or trainee’s subsequent reluctance to work with suicidal individuals, or their decision to discontinue their clinical work altogether. Lastly, other ethical issues, such as contact with the patient’s family following the suicide, attending the funeral, etc., are likely to be a source of additional anxiety and distress, particularly if the clinician needs to address these issues in isolation.

Professional relationships/colleagues’ reactions

Many clinician-survivors have described reactions from colleagues and supervisors that are hurtful and unsupportive. According to Jobes and Maltsberger,⁵² “the suicide death of a patient in active treatment is commonly taken as prima facie evidence that the therapist, somehow or another, has mismanaged the case,” and thus the clinician often faces unwarranted blame and censure from colleagues and supervisors. Hendin et al³⁰ noted that many trainees found reactions by their institutions to be insensitive and unsupportive, one noting that the department’s review of the case “felt more like a tribunal or inquest.” In a personal communication (April 2008), Quinnett noted that many clinicians he interviewed following a suicide loss reported a pattern of isolation and interpersonal discomfort with their colleagues, who implicitly or explicitly expressed concerns about their competence. He described how a respected colleague received “no understanding, no support, only abuse” from her supervisors. Such responses, while perhaps surprising from mental health professionals, probably reflect the long-standing cultural attitude of social condemnation of suicide, and of those who are associated with it.

Continue to: Negative reactions from professional colleagues...

Negative reactions from professional colleagues are most likely to occur immediately after the suicide loss and/or during the course of a subsequent investigation or psychological autopsy. Castelli-Dransart et al⁵³ found that the lack of institutional support after a clinician experiences a suicide loss contributed to significantly higher stress responses for impacted clinicians, and may lead to a well-founded ambivalence about disclosure to colleagues, and consequent resistance to seeking out optimal supervision/consultation or even personal therapy that could help the clinician gain clarity on the effects of these issues. Many mental health professionals have described how, after the distressing experience of losing a patient to suicide, they moved through this process in relative isolation and loneliness, feeling abandoned by their colleagues and by their own hopes and expectations for support.

Stigmatization. In clinical settings, when a patient in treatment completes suicide, the treating clinician becomes an easy scapegoat for family members and colleagues. To the extent that mental health professionals are not immune from the effects and imposition of stigma, this might also affect their previously mentioned tendency to project judgment, overtly or covertly, onto the treating clinician.

Stigma around suicide is well documented.²⁵ In The Surgeon General’s Call to Action to Prevent Suicide,⁵⁴ former Surgeon General David Satcher specifically described stigma around suicide as one of the biggest barriers to prevention. Studies have shown that individuals bereaved by suicide are also stigmatized, and that those who were in caregiving roles (parents, clinicians) are believed to be more psychologically disturbed, less likable, more blameworthy, and less worthy of receiving support than other bereaved individuals.^25,55-63 These judgments often mirror survivors’ self-punitive assessments, which then become exacerbated by and intertwined with both externally imposed and internalized stigma. Hence, it is not uncommon for suicide survivors to question their own right to grieve, to report low expectations of social support, and to feel compelled to deny or hide the mode of death. Feigelman et al²⁶ found that stigmatization after a suicide loss was specifically associated with ongoing grief difficulties, depression, and suicidal thinking.

In my long-term work with clinician-survivors, I’ve come to believe that in addition to stigma around suicide, there may also be stigma projected by colleagues in relation to a clinician’s perceived emotional vulnerability. A traumatized clinician potentially challenges the notion of the implicit dichotomy/power imbalance between professionals and the patients we treat: “Us”—the professional, competent, healthy, and benevolent clinicians who have the care to offer, and “Them”—our patients, being needy, pathological, looking to us for care. This “us/them” distinction may serve to bolster a clinician’s professional esteem and identity. But when one of “us” becomes one of “them”—when a professional colleague is perceived as being emotionally vulnerable—this can be threatening to the predicates of this distinction, leading to the need to put the affected clinician firmly into the “them” camp. Thus, unwarranted condemnations of the clinician-survivor’s handling of the case, and/or the pathologizing of their normative grief reactions after the suicide loss, can seem justified.

Stigma associated both with suicide and with professional vulnerability is likely to be internalized and to have a profound effect on the clinician’s decisions about disclosure, asking for support, and ultimately on one’s ability to integrate the loss. When this occurs, it is likely to lead to even more isolation, shame, and self-blame. It is not surprising that many clinicians consider leaving the profession after this type of experience.

Continue to: Effects on clinical work

A suicide loss is also likely to affect a clinician’s therapeutic work. Many authors^12,52,64-67 have found that this commonly leads therapists to question their abilities as clinicians, and to experience a sharp loss of confidence in their work with patients. The shattered beliefs and assumptions around the efficacy of the therapeutic process, a sense of guilt or self-blame, and any perceived or actual negative judgment from colleagues can dramatically compromise a clinician’s sense of competence. Hendin et al³⁰ noted that even the most experienced therapists expressed difficulty in trusting their own clinical judgment, or accurately assessing risk after a suicide loss.

In addition, the common grief and trauma-related responses to a suicide loss (including shock, numbness, sadness, anxiety, and generalized distress) are likely to result in at least some temporary disruption of a clinician’s optimal functioning. If trauma-related symptoms are more pronounced, the effect and longevity of such impairment may be exacerbated, and are likely to “impair clinical response and therapeutic judgment.”¹⁵ In addition, because such symptoms and states may be triggered by exposure to other potentially suicidal patients, they are more likely to impact clinical functioning when the clinician works with suicidal individuals. Thus, the normative responses to a suicide loss are likely to impact a clinician’s work, just as they are likely to impact the personal and occupational functioning of any survivor of suicide loss.

In clinician-survivor discussions and support groups I’ve led, participants have identified many common areas of clinical impact. Perhaps one of the most common early responses reported by clinician-survivors who continued to work with potentially suicidal individuals was to become hypervigilant in relation to any perceived suicide risk, to interpret such risk in such a way as to warrant more conservative interventions than are necessary, and to consequently minimize the patient’s own capacities for self-care.⁶⁸ Conversely, others reported a tendency to minimize or deny suicidal potential by, for example, avoiding asking patients directly about suicidal ideation, even when they later realized that such questioning was indicated.⁶⁹

Suicide loss may also lead to more subtle clinical reactions that have been observed not only with suicidal patients, but also in relation to patients who struggle with loss or grief. These include avoidant or even dissociative reactions in relation to their patient’s pain, which in turn can impact the clinician’s ability to “be fully present” or empathic in clinical encounters.^50,69 Still, other clinicians noted that they tended to project residual feelings of anger onto their current suicidal patients, or envied patients who seemed to have mastered their grief. Consistent with Maltsberger’s description of “atonement reactions,”⁴⁰ some clinicians found themselves doing more than should be expected for their patients, even losing their sense of professional boundaries in the process. Anderson⁷⁰ noted that in pushing herself beyond what she knew were her optimal clinical boundaries, she was “punishing herself” for failing to prevent her patient’s suicide because, as she realized, “doing ‘penance’ was better than feeling helpless and powerless.” And Schultz¹⁶ described how therapists may have subsequent difficulty in trusting other patients, especially if patients who completed suicide did not disclose or denied their suicidal intent.

Working toward a supportive solution

In summary, unless clinicians who lose a patient to suicide have more supportive experiences, the combination of confidentiality-related restrictions, confusion about legal/ethical repercussions, unsupportive reactions from colleagues, and unexpected impairments in clinical work are likely to lead to intensified distress, isolation, the perceived need to “hide” the impact in professional settings, and consideration of leaving the profession. However, as I will describe in Part 2 (Current Psychiatry. November 2019), losing a patient to suicide can paradoxically present opportunities for clinicians to experience profound and personal transformation, and postvention protocols can help them navigate the often-complicated sequelae to a patient’s suicide. There is also much we can do to help support a clinician colleague who has lost a patient to suicide.

Bottom Line

For mental health clinicians, losing a patient to suicide is a clear occupational hazard. After a suicide loss, clinicians often experience unique personal and professional challenges, including the impact of the loss on clinical work and professional identity, legal/ethical issues, and confidentiality-related constraints on the ability to discuss and process the loss.

Related Resources

• American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
• Gutin N. Helping survivors in the aftermath of suicide loss. Current Psychiatry. 2018;17(8):27-33.

Ms. B, age 31, is brought to the emergency department (ED) via ambulance after emergency medical technicians used naloxone nasal spray to revive her following an overdose on heroin. She reports daily IV heroin use for the last 4 years as well as frequent use of other illicit substances, including marijuana and alprazolam, for which she does not have a prescription. She is unemployed, estranged from her family, and does not have stable housing. She refuses to be admitted to a drug rehabilitation facility for detoxification and asks to be immediately discharged.

How can you determine if Ms. B has the capacity to make decisions regarding her care?

Decisional capacity is defined as a patient’s ability to use information about an illness and the proposed treatment options to make a choice that is congruent with one’s own values and preferences.¹ Determining whether a patient has adequate capacity to make decisions regarding their care is an inherent aspect of all clinician-patient interactions.

Published reports have focused on the challenges clinicians face when assessing decisional capacity in patients with psychiatric and cognitive disorders. However, there is little evidence about assessing decisional capacity in patients with substance use disorders (SUDs), even though increasing numbers of patients with SUDs are presenting to EDs² and being admitted as inpatients in general hospitals.³ In this article, I discuss:

• the biologic basis for impaired decision-making in patients with SUDs
• common substance use–related conditions that may impact a patient’s decisional capacity
• the clinical challenges and legal considerations clinicians face when assessing decisional capacity in patients with SUDs
• how to assess decisional capacity in such patients.

Decisional capacity vs competence

“Capacity” and “competence” are not the same. Decisional capacity, which refers to the ability to make decisions, is a clinical construct that is determined by clinicians and is generally used in the acute clinical setting. Because cognition is the main determinant of capacity, conditions or treatments that affect cognition can impair an individual’s decision-making capacity.¹ Decisional capacity is not a global concept but a decision-specific one, subject to fluctuations depending on the time and the nature of the decision at hand. Therefore, requests for determination of decisional capacity in the clinical setting should be specific to an individual decision or set of decisions.

In contrast, competence is an enduring legal determination of incapacitation, typically made by a probate judge. It refers to the ability of an individual to perform actions needed to put decisions into effect. Decisional capacity as assessed by a clinician often serves as the basis for petitions submitted for the purpose of competency adjudication by the judicial system.

A biologic basis for impaired decision-making?

Jeste and Saks⁴ suggested that addiction itself is characterized by impaired decision-making because individuals keep using a substance despite experiencing recurrent physical, psychologic, or social problems caused or worsened by the substance. Several studies suggest there may be a biologic basis for impaired decision-making in these patients, even in the absence of severe psychiatric or cognitive disorders.

Continue to: Bechara and Damasio found...

Bechara and Damasio⁵ found that the decision-making impairment seen in some patients with SUDs was similar to that observed in patients who have lesions of the ventromedial prefrontal cortex. In both groups of patients, the impaired decision-making was characterized by a preference to opt for high immediate reward despite even higher future losses.

These deficits were also observed by Grant et al.⁶ In this study, patients with SUDs displayed markedly impaired performance on the Gambling Task, which examines decisions that result in long-term losses that exceed short-term gains. However, patients with SUDs performed similarly to controls on the Wisconsin Card Sorting Test, which evaluates the ability to form abstract concepts and to shift from established response sets.

MacDonald et al⁷ used a laboratory experiment and 2 field studies to test the hypothesis that alcohol affects attitudes and intentions toward drinking and driving. Their findings support the concept that alcohol intoxication decreases cognitive capacity such that people are more likely to attend to only the most salient cues.⁷

Whether the impairment documented in such studies is a contributing factor in addiction or is a result of addiction remains uncertain. While individuals with SUDs may have some level of impairment in decision-making in general, particularly in regard to their substance use, their decisional capacity on specific clinical decisions should be assessed carefully. In a study of 300 consecutive psychiatric consultations for decisional capacity at an urban hospital, Boettger et al⁸ found that 41% were related to SUDs. Of these, 37% were found to have impaired decisional capacity.

Impaired decision-making in patients with SUDs may specifically pertain to choices related to their addiction, including⁹:

• consent for addiction treatment
• consistency in maintaining a choice of recovery
• changing values regarding treatment over time
• capacity to participate in addiction research involving the use of addictive substances.

Continue to: It is important to recognize...

It is important to recognize that this impairment may not necessarily translate into altered decisional capacity regarding other health care decisions, such as consenting to surgery or other necessary medical interventions.⁹

Substance-related disorders that affect decisional capacity

Substance-related syndromes can affect mood, reality testing, and/or cognitive function, thereby directly impacting a patient’s decisional capacity. Substance-related syndromes can be divided into 2 categories: 1) disorders resulting from the direct effects of the substance, and 2) secondary disorders resulting from/or associated with substance use.

Disorders resulting from the direct effects of the substance

Temporary/reversible incapacitation

• Acute intoxication or intoxication delirium may be the most frequent type of temporary incapacitation. It can result from toxic levels of licit or illicit substances; alcohol is likely the most frequent offending agent. Although some individuals who are intoxicated may appear to be alert, oriented, and able to engage in lengthy conversations, the majority do not possess adequate decisional capacity.¹⁰
• Withdrawal delirium, associated with longstanding alcohol, sedative-hypnotic, or barbiturate dependence, is typically prolonged, but usually resolves, either spontaneously or with treatment. Although most deliria resolve once the underlying etiology is corrected, vulnerable individuals may experience irreversible cognitive impairment and permanent decisional incapacitation.^11,12
• Severe substance-induced depressive disorders, especially if accompanied by frank psychotic symptoms or severe depressive distortions of reality, may result in decisional incapacity. Substance abuse treatment that incorporates multiple strategies, sometimes in conjunction with pharmacotherapy to manage depression, should lead to sufficient recovery and restoration of decisional capacity.
• Transient psychotic disorders such as those associated with the use of stimulants are often treatable. Patients may recover decisional capacity spontaneously or with treatment.

Permanent incapacitation

• Dementia is associated with substance use, particularly alcohol use.¹³ For a patient who develops dementia, no appreciable recovery can be expected, even with prolonged abstinence.
• Persistent amnestic disorders (eg, Korsakoff syndrome) resulting from undiagnosed or untreated severe thiamine deficiency (Wernicke’s encephalopathy). Although an isolated Korsakoff syndrome consists primarily of anterograde amnesia, these patients may experience additional cognitive impairment resulting from years of alcohol consumption or associated with other neurodegenerative processes, and therefore are sufficiently impaired and lack decisional capacity. Even in the absence of such concomitant cognitive deficits, a very severe anterograde amnestic disorder directly impacts a patient’s capacity to perform the necessary tasks required to give informed consent. The inability to consolidate information about new medical developments, treatments, and procedures, even when they are thoroughly explained by the medical team, can pose serious challenges. For example, a patient may protest to being taken to surgery because he/she does not recall signing a consent form the previous day.
• Enduring severe and treatment-refractory psychotic disorders associated with drug use, specifically stimulants, can result in permanent incapacitation similar to that seen in severe primary psychotic disorders (such as treatment-resistant schizophrenia).

Secondary disorders resulting from/or associated with substance use

• Hepatic encephalopathy may be seen in patients with advanced cirrhosis of the liver (due to hepatitis C resulting from IV drug use, and/or alcohol use). In late stages of cirrhosis, the confusional state patients experience may become severe and may no longer be reversible unless liver transplantation is available and successful. This would therefore constitute a basis for permanent decisional incapacitation.
• Human immunodeficiency virus encephalitis or dementia can result from IV drug use.

Continue to: Clinical challenges

In intensive care settings, where a patient with a SUD may be treated for acute life-threatening intoxication or severe withdrawal delirium, an assumption of decisional incapacitation often exists as a result of medical acuity and impaired mentation. In these situations, treatment usually proceeds with consent obtained from next-of-kin, a guardian, or an administrative (hospital) authority when other substitute decision makers are unavailable or unwilling. In such cases, psychiatric consultation can play a dual role in documenting the patient’s decisional capacity and also in contributing to the care of patients with SUDs.

It is critical to perform a cognitive evaluation and mental status examination in a medically compromised patient with an SUD. Unfortunately, serious cognitive disorders can often be concealed by a superficially jovial or verbally skilled patient, or by an uncooperative individual who refuses to engage in a thorough conversation with his/her clinicians. These scenarios present significant challenges and may result in missed opportunities for care or premature discharges. Negative countertransference by clinicians toward patients with SUDs may also promote poor outcomes. For difficult cases, legal and ethical consultations may help mitigate risk and guide management approaches (Box¹⁴).

Box

How to assess decisional capacity

A direct conclusion of incapacity in an individual cannot be determined solely on the knowledge of the patient having a SUD-related clinical condition. (The possible exception to this may be a patient with severe dementia.) Evidence suggests that clinicians must conduct a specific assessment to determine the severity of the psychiatric or cognitive impairment and whether it directly impacts a patient’s ability to:

• understand the decision at hand
• discuss its benefits and risks
• describe alternatives
• demonstrate an appreciation of the implications of treatment or lack thereof
• communicate a clear and consistent choice.

Continue to: While most clinicians...

While most clinicians rely on a psychi­atric interview (with or without a cognitive examination) to make these determinations, several instruments have been developed to aid these evaluations, such as the MacArthur Competence Assessment Tool for Treatment (Mac-CAT-T).¹⁵ In patients with potentially reversible incapacitating conditions, serial examinations over time, especially re-evaluation when a patient has achieved and maintained sobriety, may be necessary and helpful.

The Table offers a guide to assessing decisional capacity in a patient with an SUD.

Who should conduct the assessment?

Mental health professionals—usually psychiatrists or psychologists—are consulted when there is uncertainty about a patient’s decisional capacity, and when a more thorough mental status examination is warranted to formulate an informed opinion.¹⁶ Unfortunately, this typically occurs only if a patient refuses treatment or demands to be discharged before treatment has been completed, or there is a high level of risk to the patient or others after discharge.

In acute settings, when a patient consents to treatment, a psychiatric consultation regarding decisional capacity is rarely requested. While it is often tempting for medical or surgical teams to proceed with an intervention in a cooperative patient who willingly signs a consent form without a formal assessment of his/her decisional capacity, doing so raises challenging ethical and legal questions in the event of an adverse outcome. It is therefore prudent to strongly recommend that medical and surgical colleagues obtain a psychiatric consultation when an individual’s decisional capacity is uncertain, especially when a patient is known to have a psychiatric or neurocognitive disorder, or exhibits evidence of recent mental status changes. In cases of potentially reversible impairment (eg, delirium, psychosis, or acute anxiety), targeted interventions may help restore capacity and allow treatment to proceed.

No jurisdictions mandate that the determination of decisional capacity should be made exclusively by a mental health professional. Any treating health care professional (usually the attending physician) can make a determination of decisional capacity in scenarios where there is no overt evidence the patient has a mental or cognitive disorder and the patient is communicating clear and reasoned choices, or when a patient is profoundly impaired and no meaningful communication can take place.

Continue to: CASE CONTINUED

The emergency physician requests a psychi­atric consultation. You assess Ms. B’s decisional capacity using the Mac-CAT-T along with a standard psychiatric evaluation. Her score of 14 reflects that she is able to understand the risks associated with her opioid use, and although irritated by engaging in such a discussion, is capable of reasoning through the various medical and psychosocial aspects of her addiction, and shows moderate appreciation of the impact of her choices on her future and that of significant others. The psychiatric evaluation fails to elicit any substantial mood, anxiety, or psychotic disorders associated with/or resulting from her addiction, and her cognitive examination is within normal limits. She does not exhibit severe withdrawal and is not delirious on examination. Finally, she did not harbor thoughts of intentional harm to self or others and is not deemed imminently dangerous.

You document that in your opinion, despite Ms. B’s unfortunate choices and questionable judgment, she does have the capacity to make informed decisions regarding her care and could be released against medical advice if she so chooses, while providing her with information about available resources should she decide to seek rehabilitation in the future.

An increasingly common scenario

Decisional capacity assessment in patients with SUDs is an increasingly common reason for psychiatric consultations. Primary and secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. The same principles that guide the assessment of decisional capacity in patients with other psychiatric or cognitive disorders should be applied to compromised individuals with SUDs. In challenging cases, a skilled psychiatric evaluation that is supported by a thorough cognitive examination and, when required, complemented by a legal or ethical consultation, can help clinicians make safe and judicious decisions.

Bottom Line

Assessing the decisional capacity of a patient with a substance use disorder can be challenging. Primary or secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. A skilled psychiatric evaluation that includes a thorough cognitive examination and is complemented by legal or ethical consultation can help in making judicious decisions.

Related Resources

• Tan SY. Determining patients’ decisional capacity. Clinical Psychiatry News. https://www.mdedge.com/psychiatry/article/137939/practice-management/determining-patients-decisional-capacity. Published May 10, 2017.
• Sorrentino R. Performing capacity evaluations: What’s expected from your consult. Current Psychiatry. 2014;13(1):41-44.

Drug Brand Names

Alprazolam • Xanax
Naloxone nasal spray • Narcan

Ms. B, age 31, is brought to the emergency department (ED) via ambulance after emergency medical technicians used naloxone nasal spray to revive her following an overdose on heroin. She reports daily IV heroin use for the last 4 years as well as frequent use of other illicit substances, including marijuana and alprazolam, for which she does not have a prescription. She is unemployed, estranged from her family, and does not have stable housing. She refuses to be admitted to a drug rehabilitation facility for detoxification and asks to be immediately discharged.

How can you determine if Ms. B has the capacity to make decisions regarding her care?

Decisional capacity is defined as a patient’s ability to use information about an illness and the proposed treatment options to make a choice that is congruent with one’s own values and preferences.¹ Determining whether a patient has adequate capacity to make decisions regarding their care is an inherent aspect of all clinician-patient interactions.

Published reports have focused on the challenges clinicians face when assessing decisional capacity in patients with psychiatric and cognitive disorders. However, there is little evidence about assessing decisional capacity in patients with substance use disorders (SUDs), even though increasing numbers of patients with SUDs are presenting to EDs² and being admitted as inpatients in general hospitals.³ In this article, I discuss:

• the biologic basis for impaired decision-making in patients with SUDs
• common substance use–related conditions that may impact a patient’s decisional capacity
• the clinical challenges and legal considerations clinicians face when assessing decisional capacity in patients with SUDs
• how to assess decisional capacity in such patients.

Decisional capacity vs competence

“Capacity” and “competence” are not the same. Decisional capacity, which refers to the ability to make decisions, is a clinical construct that is determined by clinicians and is generally used in the acute clinical setting. Because cognition is the main determinant of capacity, conditions or treatments that affect cognition can impair an individual’s decision-making capacity.¹ Decisional capacity is not a global concept but a decision-specific one, subject to fluctuations depending on the time and the nature of the decision at hand. Therefore, requests for determination of decisional capacity in the clinical setting should be specific to an individual decision or set of decisions.

In contrast, competence is an enduring legal determination of incapacitation, typically made by a probate judge. It refers to the ability of an individual to perform actions needed to put decisions into effect. Decisional capacity as assessed by a clinician often serves as the basis for petitions submitted for the purpose of competency adjudication by the judicial system.

A biologic basis for impaired decision-making?

Jeste and Saks⁴ suggested that addiction itself is characterized by impaired decision-making because individuals keep using a substance despite experiencing recurrent physical, psychologic, or social problems caused or worsened by the substance. Several studies suggest there may be a biologic basis for impaired decision-making in these patients, even in the absence of severe psychiatric or cognitive disorders.

Continue to: Bechara and Damasio found...

Bechara and Damasio⁵ found that the decision-making impairment seen in some patients with SUDs was similar to that observed in patients who have lesions of the ventromedial prefrontal cortex. In both groups of patients, the impaired decision-making was characterized by a preference to opt for high immediate reward despite even higher future losses.

These deficits were also observed by Grant et al.⁶ In this study, patients with SUDs displayed markedly impaired performance on the Gambling Task, which examines decisions that result in long-term losses that exceed short-term gains. However, patients with SUDs performed similarly to controls on the Wisconsin Card Sorting Test, which evaluates the ability to form abstract concepts and to shift from established response sets.

MacDonald et al⁷ used a laboratory experiment and 2 field studies to test the hypothesis that alcohol affects attitudes and intentions toward drinking and driving. Their findings support the concept that alcohol intoxication decreases cognitive capacity such that people are more likely to attend to only the most salient cues.⁷

Whether the impairment documented in such studies is a contributing factor in addiction or is a result of addiction remains uncertain. While individuals with SUDs may have some level of impairment in decision-making in general, particularly in regard to their substance use, their decisional capacity on specific clinical decisions should be assessed carefully. In a study of 300 consecutive psychiatric consultations for decisional capacity at an urban hospital, Boettger et al⁸ found that 41% were related to SUDs. Of these, 37% were found to have impaired decisional capacity.

Impaired decision-making in patients with SUDs may specifically pertain to choices related to their addiction, including⁹:

• consent for addiction treatment
• consistency in maintaining a choice of recovery
• changing values regarding treatment over time
• capacity to participate in addiction research involving the use of addictive substances.

Continue to: It is important to recognize...

It is important to recognize that this impairment may not necessarily translate into altered decisional capacity regarding other health care decisions, such as consenting to surgery or other necessary medical interventions.⁹

Substance-related disorders that affect decisional capacity

Substance-related syndromes can affect mood, reality testing, and/or cognitive function, thereby directly impacting a patient’s decisional capacity. Substance-related syndromes can be divided into 2 categories: 1) disorders resulting from the direct effects of the substance, and 2) secondary disorders resulting from/or associated with substance use.

Disorders resulting from the direct effects of the substance

Temporary/reversible incapacitation

• Acute intoxication or intoxication delirium may be the most frequent type of temporary incapacitation. It can result from toxic levels of licit or illicit substances; alcohol is likely the most frequent offending agent. Although some individuals who are intoxicated may appear to be alert, oriented, and able to engage in lengthy conversations, the majority do not possess adequate decisional capacity.¹⁰
• Withdrawal delirium, associated with longstanding alcohol, sedative-hypnotic, or barbiturate dependence, is typically prolonged, but usually resolves, either spontaneously or with treatment. Although most deliria resolve once the underlying etiology is corrected, vulnerable individuals may experience irreversible cognitive impairment and permanent decisional incapacitation.^11,12
• Severe substance-induced depressive disorders, especially if accompanied by frank psychotic symptoms or severe depressive distortions of reality, may result in decisional incapacity. Substance abuse treatment that incorporates multiple strategies, sometimes in conjunction with pharmacotherapy to manage depression, should lead to sufficient recovery and restoration of decisional capacity.
• Transient psychotic disorders such as those associated with the use of stimulants are often treatable. Patients may recover decisional capacity spontaneously or with treatment.

Permanent incapacitation

• Dementia is associated with substance use, particularly alcohol use.¹³ For a patient who develops dementia, no appreciable recovery can be expected, even with prolonged abstinence.
• Persistent amnestic disorders (eg, Korsakoff syndrome) resulting from undiagnosed or untreated severe thiamine deficiency (Wernicke’s encephalopathy). Although an isolated Korsakoff syndrome consists primarily of anterograde amnesia, these patients may experience additional cognitive impairment resulting from years of alcohol consumption or associated with other neurodegenerative processes, and therefore are sufficiently impaired and lack decisional capacity. Even in the absence of such concomitant cognitive deficits, a very severe anterograde amnestic disorder directly impacts a patient’s capacity to perform the necessary tasks required to give informed consent. The inability to consolidate information about new medical developments, treatments, and procedures, even when they are thoroughly explained by the medical team, can pose serious challenges. For example, a patient may protest to being taken to surgery because he/she does not recall signing a consent form the previous day.
• Enduring severe and treatment-refractory psychotic disorders associated with drug use, specifically stimulants, can result in permanent incapacitation similar to that seen in severe primary psychotic disorders (such as treatment-resistant schizophrenia).

Secondary disorders resulting from/or associated with substance use

• Hepatic encephalopathy may be seen in patients with advanced cirrhosis of the liver (due to hepatitis C resulting from IV drug use, and/or alcohol use). In late stages of cirrhosis, the confusional state patients experience may become severe and may no longer be reversible unless liver transplantation is available and successful. This would therefore constitute a basis for permanent decisional incapacitation.
• Human immunodeficiency virus encephalitis or dementia can result from IV drug use.

Continue to: Clinical challenges

In intensive care settings, where a patient with a SUD may be treated for acute life-threatening intoxication or severe withdrawal delirium, an assumption of decisional incapacitation often exists as a result of medical acuity and impaired mentation. In these situations, treatment usually proceeds with consent obtained from next-of-kin, a guardian, or an administrative (hospital) authority when other substitute decision makers are unavailable or unwilling. In such cases, psychiatric consultation can play a dual role in documenting the patient’s decisional capacity and also in contributing to the care of patients with SUDs.

It is critical to perform a cognitive evaluation and mental status examination in a medically compromised patient with an SUD. Unfortunately, serious cognitive disorders can often be concealed by a superficially jovial or verbally skilled patient, or by an uncooperative individual who refuses to engage in a thorough conversation with his/her clinicians. These scenarios present significant challenges and may result in missed opportunities for care or premature discharges. Negative countertransference by clinicians toward patients with SUDs may also promote poor outcomes. For difficult cases, legal and ethical consultations may help mitigate risk and guide management approaches (Box¹⁴).

Box

How to assess decisional capacity

A direct conclusion of incapacity in an individual cannot be determined solely on the knowledge of the patient having a SUD-related clinical condition. (The possible exception to this may be a patient with severe dementia.) Evidence suggests that clinicians must conduct a specific assessment to determine the severity of the psychiatric or cognitive impairment and whether it directly impacts a patient’s ability to:

• understand the decision at hand
• discuss its benefits and risks
• describe alternatives
• demonstrate an appreciation of the implications of treatment or lack thereof
• communicate a clear and consistent choice.

Continue to: While most clinicians...

While most clinicians rely on a psychi­atric interview (with or without a cognitive examination) to make these determinations, several instruments have been developed to aid these evaluations, such as the MacArthur Competence Assessment Tool for Treatment (Mac-CAT-T).¹⁵ In patients with potentially reversible incapacitating conditions, serial examinations over time, especially re-evaluation when a patient has achieved and maintained sobriety, may be necessary and helpful.

The Table offers a guide to assessing decisional capacity in a patient with an SUD.

Who should conduct the assessment?

Mental health professionals—usually psychiatrists or psychologists—are consulted when there is uncertainty about a patient’s decisional capacity, and when a more thorough mental status examination is warranted to formulate an informed opinion.¹⁶ Unfortunately, this typically occurs only if a patient refuses treatment or demands to be discharged before treatment has been completed, or there is a high level of risk to the patient or others after discharge.

In acute settings, when a patient consents to treatment, a psychiatric consultation regarding decisional capacity is rarely requested. While it is often tempting for medical or surgical teams to proceed with an intervention in a cooperative patient who willingly signs a consent form without a formal assessment of his/her decisional capacity, doing so raises challenging ethical and legal questions in the event of an adverse outcome. It is therefore prudent to strongly recommend that medical and surgical colleagues obtain a psychiatric consultation when an individual’s decisional capacity is uncertain, especially when a patient is known to have a psychiatric or neurocognitive disorder, or exhibits evidence of recent mental status changes. In cases of potentially reversible impairment (eg, delirium, psychosis, or acute anxiety), targeted interventions may help restore capacity and allow treatment to proceed.

No jurisdictions mandate that the determination of decisional capacity should be made exclusively by a mental health professional. Any treating health care professional (usually the attending physician) can make a determination of decisional capacity in scenarios where there is no overt evidence the patient has a mental or cognitive disorder and the patient is communicating clear and reasoned choices, or when a patient is profoundly impaired and no meaningful communication can take place.

Continue to: CASE CONTINUED

The emergency physician requests a psychi­atric consultation. You assess Ms. B’s decisional capacity using the Mac-CAT-T along with a standard psychiatric evaluation. Her score of 14 reflects that she is able to understand the risks associated with her opioid use, and although irritated by engaging in such a discussion, is capable of reasoning through the various medical and psychosocial aspects of her addiction, and shows moderate appreciation of the impact of her choices on her future and that of significant others. The psychiatric evaluation fails to elicit any substantial mood, anxiety, or psychotic disorders associated with/or resulting from her addiction, and her cognitive examination is within normal limits. She does not exhibit severe withdrawal and is not delirious on examination. Finally, she did not harbor thoughts of intentional harm to self or others and is not deemed imminently dangerous.

You document that in your opinion, despite Ms. B’s unfortunate choices and questionable judgment, she does have the capacity to make informed decisions regarding her care and could be released against medical advice if she so chooses, while providing her with information about available resources should she decide to seek rehabilitation in the future.

An increasingly common scenario

Decisional capacity assessment in patients with SUDs is an increasingly common reason for psychiatric consultations. Primary and secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. The same principles that guide the assessment of decisional capacity in patients with other psychiatric or cognitive disorders should be applied to compromised individuals with SUDs. In challenging cases, a skilled psychiatric evaluation that is supported by a thorough cognitive examination and, when required, complemented by a legal or ethical consultation, can help clinicians make safe and judicious decisions.

Bottom Line

Assessing the decisional capacity of a patient with a substance use disorder can be challenging. Primary or secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. A skilled psychiatric evaluation that includes a thorough cognitive examination and is complemented by legal or ethical consultation can help in making judicious decisions.

Related Resources

• Tan SY. Determining patients’ decisional capacity. Clinical Psychiatry News. https://www.mdedge.com/psychiatry/article/137939/practice-management/determining-patients-decisional-capacity. Published May 10, 2017.
• Sorrentino R. Performing capacity evaluations: What’s expected from your consult. Current Psychiatry. 2014;13(1):41-44.

Drug Brand Names

Alprazolam • Xanax
Naloxone nasal spray • Narcan

Ms. B, age 31, is brought to the emergency department (ED) via ambulance after emergency medical technicians used naloxone nasal spray to revive her following an overdose on heroin. She reports daily IV heroin use for the last 4 years as well as frequent use of other illicit substances, including marijuana and alprazolam, for which she does not have a prescription. She is unemployed, estranged from her family, and does not have stable housing. She refuses to be admitted to a drug rehabilitation facility for detoxification and asks to be immediately discharged.

How can you determine if Ms. B has the capacity to make decisions regarding her care?

Decisional capacity is defined as a patient’s ability to use information about an illness and the proposed treatment options to make a choice that is congruent with one’s own values and preferences.¹ Determining whether a patient has adequate capacity to make decisions regarding their care is an inherent aspect of all clinician-patient interactions.

Published reports have focused on the challenges clinicians face when assessing decisional capacity in patients with psychiatric and cognitive disorders. However, there is little evidence about assessing decisional capacity in patients with substance use disorders (SUDs), even though increasing numbers of patients with SUDs are presenting to EDs² and being admitted as inpatients in general hospitals.³ In this article, I discuss:

• the biologic basis for impaired decision-making in patients with SUDs
• common substance use–related conditions that may impact a patient’s decisional capacity
• the clinical challenges and legal considerations clinicians face when assessing decisional capacity in patients with SUDs
• how to assess decisional capacity in such patients.

Decisional capacity vs competence

“Capacity” and “competence” are not the same. Decisional capacity, which refers to the ability to make decisions, is a clinical construct that is determined by clinicians and is generally used in the acute clinical setting. Because cognition is the main determinant of capacity, conditions or treatments that affect cognition can impair an individual’s decision-making capacity.¹ Decisional capacity is not a global concept but a decision-specific one, subject to fluctuations depending on the time and the nature of the decision at hand. Therefore, requests for determination of decisional capacity in the clinical setting should be specific to an individual decision or set of decisions.

In contrast, competence is an enduring legal determination of incapacitation, typically made by a probate judge. It refers to the ability of an individual to perform actions needed to put decisions into effect. Decisional capacity as assessed by a clinician often serves as the basis for petitions submitted for the purpose of competency adjudication by the judicial system.

A biologic basis for impaired decision-making?

Jeste and Saks⁴ suggested that addiction itself is characterized by impaired decision-making because individuals keep using a substance despite experiencing recurrent physical, psychologic, or social problems caused or worsened by the substance. Several studies suggest there may be a biologic basis for impaired decision-making in these patients, even in the absence of severe psychiatric or cognitive disorders.

Continue to: Bechara and Damasio found...

Bechara and Damasio⁵ found that the decision-making impairment seen in some patients with SUDs was similar to that observed in patients who have lesions of the ventromedial prefrontal cortex. In both groups of patients, the impaired decision-making was characterized by a preference to opt for high immediate reward despite even higher future losses.

These deficits were also observed by Grant et al.⁶ In this study, patients with SUDs displayed markedly impaired performance on the Gambling Task, which examines decisions that result in long-term losses that exceed short-term gains. However, patients with SUDs performed similarly to controls on the Wisconsin Card Sorting Test, which evaluates the ability to form abstract concepts and to shift from established response sets.

MacDonald et al⁷ used a laboratory experiment and 2 field studies to test the hypothesis that alcohol affects attitudes and intentions toward drinking and driving. Their findings support the concept that alcohol intoxication decreases cognitive capacity such that people are more likely to attend to only the most salient cues.⁷

Whether the impairment documented in such studies is a contributing factor in addiction or is a result of addiction remains uncertain. While individuals with SUDs may have some level of impairment in decision-making in general, particularly in regard to their substance use, their decisional capacity on specific clinical decisions should be assessed carefully. In a study of 300 consecutive psychiatric consultations for decisional capacity at an urban hospital, Boettger et al⁸ found that 41% were related to SUDs. Of these, 37% were found to have impaired decisional capacity.

Impaired decision-making in patients with SUDs may specifically pertain to choices related to their addiction, including⁹:

• consent for addiction treatment
• consistency in maintaining a choice of recovery
• changing values regarding treatment over time
• capacity to participate in addiction research involving the use of addictive substances.

Continue to: It is important to recognize...

It is important to recognize that this impairment may not necessarily translate into altered decisional capacity regarding other health care decisions, such as consenting to surgery or other necessary medical interventions.⁹

Substance-related disorders that affect decisional capacity

Substance-related syndromes can affect mood, reality testing, and/or cognitive function, thereby directly impacting a patient’s decisional capacity. Substance-related syndromes can be divided into 2 categories: 1) disorders resulting from the direct effects of the substance, and 2) secondary disorders resulting from/or associated with substance use.

Disorders resulting from the direct effects of the substance

Temporary/reversible incapacitation

• Acute intoxication or intoxication delirium may be the most frequent type of temporary incapacitation. It can result from toxic levels of licit or illicit substances; alcohol is likely the most frequent offending agent. Although some individuals who are intoxicated may appear to be alert, oriented, and able to engage in lengthy conversations, the majority do not possess adequate decisional capacity.¹⁰
• Withdrawal delirium, associated with longstanding alcohol, sedative-hypnotic, or barbiturate dependence, is typically prolonged, but usually resolves, either spontaneously or with treatment. Although most deliria resolve once the underlying etiology is corrected, vulnerable individuals may experience irreversible cognitive impairment and permanent decisional incapacitation.^11,12
• Severe substance-induced depressive disorders, especially if accompanied by frank psychotic symptoms or severe depressive distortions of reality, may result in decisional incapacity. Substance abuse treatment that incorporates multiple strategies, sometimes in conjunction with pharmacotherapy to manage depression, should lead to sufficient recovery and restoration of decisional capacity.
• Transient psychotic disorders such as those associated with the use of stimulants are often treatable. Patients may recover decisional capacity spontaneously or with treatment.

Permanent incapacitation

• Dementia is associated with substance use, particularly alcohol use.¹³ For a patient who develops dementia, no appreciable recovery can be expected, even with prolonged abstinence.
• Persistent amnestic disorders (eg, Korsakoff syndrome) resulting from undiagnosed or untreated severe thiamine deficiency (Wernicke’s encephalopathy). Although an isolated Korsakoff syndrome consists primarily of anterograde amnesia, these patients may experience additional cognitive impairment resulting from years of alcohol consumption or associated with other neurodegenerative processes, and therefore are sufficiently impaired and lack decisional capacity. Even in the absence of such concomitant cognitive deficits, a very severe anterograde amnestic disorder directly impacts a patient’s capacity to perform the necessary tasks required to give informed consent. The inability to consolidate information about new medical developments, treatments, and procedures, even when they are thoroughly explained by the medical team, can pose serious challenges. For example, a patient may protest to being taken to surgery because he/she does not recall signing a consent form the previous day.
• Enduring severe and treatment-refractory psychotic disorders associated with drug use, specifically stimulants, can result in permanent incapacitation similar to that seen in severe primary psychotic disorders (such as treatment-resistant schizophrenia).

Secondary disorders resulting from/or associated with substance use

• Hepatic encephalopathy may be seen in patients with advanced cirrhosis of the liver (due to hepatitis C resulting from IV drug use, and/or alcohol use). In late stages of cirrhosis, the confusional state patients experience may become severe and may no longer be reversible unless liver transplantation is available and successful. This would therefore constitute a basis for permanent decisional incapacitation.
• Human immunodeficiency virus encephalitis or dementia can result from IV drug use.

Continue to: Clinical challenges

In intensive care settings, where a patient with a SUD may be treated for acute life-threatening intoxication or severe withdrawal delirium, an assumption of decisional incapacitation often exists as a result of medical acuity and impaired mentation. In these situations, treatment usually proceeds with consent obtained from next-of-kin, a guardian, or an administrative (hospital) authority when other substitute decision makers are unavailable or unwilling. In such cases, psychiatric consultation can play a dual role in documenting the patient’s decisional capacity and also in contributing to the care of patients with SUDs.

It is critical to perform a cognitive evaluation and mental status examination in a medically compromised patient with an SUD. Unfortunately, serious cognitive disorders can often be concealed by a superficially jovial or verbally skilled patient, or by an uncooperative individual who refuses to engage in a thorough conversation with his/her clinicians. These scenarios present significant challenges and may result in missed opportunities for care or premature discharges. Negative countertransference by clinicians toward patients with SUDs may also promote poor outcomes. For difficult cases, legal and ethical consultations may help mitigate risk and guide management approaches (Box¹⁴).

Box

How to assess decisional capacity

A direct conclusion of incapacity in an individual cannot be determined solely on the knowledge of the patient having a SUD-related clinical condition. (The possible exception to this may be a patient with severe dementia.) Evidence suggests that clinicians must conduct a specific assessment to determine the severity of the psychiatric or cognitive impairment and whether it directly impacts a patient’s ability to:

• understand the decision at hand
• discuss its benefits and risks
• describe alternatives
• demonstrate an appreciation of the implications of treatment or lack thereof
• communicate a clear and consistent choice.

Continue to: While most clinicians...

While most clinicians rely on a psychi­atric interview (with or without a cognitive examination) to make these determinations, several instruments have been developed to aid these evaluations, such as the MacArthur Competence Assessment Tool for Treatment (Mac-CAT-T).¹⁵ In patients with potentially reversible incapacitating conditions, serial examinations over time, especially re-evaluation when a patient has achieved and maintained sobriety, may be necessary and helpful.

The Table offers a guide to assessing decisional capacity in a patient with an SUD.

Who should conduct the assessment?

Mental health professionals—usually psychiatrists or psychologists—are consulted when there is uncertainty about a patient’s decisional capacity, and when a more thorough mental status examination is warranted to formulate an informed opinion.¹⁶ Unfortunately, this typically occurs only if a patient refuses treatment or demands to be discharged before treatment has been completed, or there is a high level of risk to the patient or others after discharge.

In acute settings, when a patient consents to treatment, a psychiatric consultation regarding decisional capacity is rarely requested. While it is often tempting for medical or surgical teams to proceed with an intervention in a cooperative patient who willingly signs a consent form without a formal assessment of his/her decisional capacity, doing so raises challenging ethical and legal questions in the event of an adverse outcome. It is therefore prudent to strongly recommend that medical and surgical colleagues obtain a psychiatric consultation when an individual’s decisional capacity is uncertain, especially when a patient is known to have a psychiatric or neurocognitive disorder, or exhibits evidence of recent mental status changes. In cases of potentially reversible impairment (eg, delirium, psychosis, or acute anxiety), targeted interventions may help restore capacity and allow treatment to proceed.

No jurisdictions mandate that the determination of decisional capacity should be made exclusively by a mental health professional. Any treating health care professional (usually the attending physician) can make a determination of decisional capacity in scenarios where there is no overt evidence the patient has a mental or cognitive disorder and the patient is communicating clear and reasoned choices, or when a patient is profoundly impaired and no meaningful communication can take place.

Continue to: CASE CONTINUED

The emergency physician requests a psychi­atric consultation. You assess Ms. B’s decisional capacity using the Mac-CAT-T along with a standard psychiatric evaluation. Her score of 14 reflects that she is able to understand the risks associated with her opioid use, and although irritated by engaging in such a discussion, is capable of reasoning through the various medical and psychosocial aspects of her addiction, and shows moderate appreciation of the impact of her choices on her future and that of significant others. The psychiatric evaluation fails to elicit any substantial mood, anxiety, or psychotic disorders associated with/or resulting from her addiction, and her cognitive examination is within normal limits. She does not exhibit severe withdrawal and is not delirious on examination. Finally, she did not harbor thoughts of intentional harm to self or others and is not deemed imminently dangerous.

You document that in your opinion, despite Ms. B’s unfortunate choices and questionable judgment, she does have the capacity to make informed decisions regarding her care and could be released against medical advice if she so chooses, while providing her with information about available resources should she decide to seek rehabilitation in the future.

An increasingly common scenario

Decisional capacity assessment in patients with SUDs is an increasingly common reason for psychiatric consultations. Primary and secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. The same principles that guide the assessment of decisional capacity in patients with other psychiatric or cognitive disorders should be applied to compromised individuals with SUDs. In challenging cases, a skilled psychiatric evaluation that is supported by a thorough cognitive examination and, when required, complemented by a legal or ethical consultation, can help clinicians make safe and judicious decisions.

Bottom Line

Assessing the decisional capacity of a patient with a substance use disorder can be challenging. Primary or secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. A skilled psychiatric evaluation that includes a thorough cognitive examination and is complemented by legal or ethical consultation can help in making judicious decisions.

Related Resources

• Tan SY. Determining patients’ decisional capacity. Clinical Psychiatry News. https://www.mdedge.com/psychiatry/article/137939/practice-management/determining-patients-decisional-capacity. Published May 10, 2017.
• Sorrentino R. Performing capacity evaluations: What’s expected from your consult. Current Psychiatry. 2014;13(1):41-44.

Drug Brand Names

Alprazolam • Xanax
Naloxone nasal spray • Narcan

A physician’s mental health is important for the delivery of quality health care to his/her patients. Early identification and treatment of physicians with mental illnesses is challenging because physicians may neglect their own mental health due to the associated stigma, time constraints, or uncertainty regarding where to seek help. Physicians often worry about whom to confide in and harbor a fear that others will doubt his/her competence after recovery.¹ Physicians have higher rates of suicide than the general population.² According to data from the National Violent Death Reporting System, a diagnosed mental illness or a job problem significantly contribute to suicide among physicians.³ Additionally, physicians also have high rates of substance use and affective disorders.^1,4

Here, we present the case of a physician we treated on an inpatient psychiatry unit who stirred profound emotions in us as trainees, and discuss how we managed this complicated scenario.

CASE REPORT

Dr. P, a 35-year-old male endocrinologist, was admitted to our inpatient psychiatry unit with a diagnosis of bipolar disorder, manic, severe, with psychotic features. Earlier that day, Dr. P had walked out of his private outpatient practice where he still had several appointments. After he had been missing for several hours, he was picked up by the police. Dr. P had 2 prior psychiatric admissions; the last one had occurred >10 years ago. A few weeks before this admission, he stopped taking lithium, while continuing escitalopram. He had not been keeping his appointments with his outpatient psychiatrist.

At admission, Dr. P had pressured speech, grandiose delusions, an expansive affect, and aggressive behavior. He was responding to internal stimuli with no insight into his illness. He was evasive when asked about hallucinations. Dr. P believed he was superior in intelligence and physical prowess to everyone in the emergency department (ED), and for that reason, the ED staff was persecuting him. His urine toxicology was negative.

On the inpatient unit, because Dr. P exhibited posturing, mutism, and negativism, catatonia associated with bipolar disorder was added to his diagnosis. For the first 2 days, his catatonia was managed with oral lorazepam, 2 mg twice daily. Dr. P was also observed giving medical advice to other patients on the unit, and was told to stop. Throughout his hospitalization, he dictated his own treatment and would frequently debate with his treatment team on the pharmacologic basis for treatment decisions, asserting his expertise as a physician and claiming to have a general clinical knowledge of the acute management of bipolar disorder.

Dr. P was eventually stabilized on oral lithium, 450 mg twice daily, and aripiprazole, 10 mg/d. He also received oral clonazepam, as needed for acute agitation, which was eventually tapered and discontinued. He gradually responded to treatment, and demonstrated improved insight. The treatment team met with Dr. P’s parents, who also were physicians, to discuss treatment goals, management considerations, and an aftercare plan. After spending 8 days in the hospital, Dr. P was discharged home to the care of his immediate family, and instructed to follow up with his outpatient psychiatrist. We do not know if he resumed clinical duties.

Managing an extremely knowledgeable patient

During his hospitalization, Dr. P frequently challenged our clinical knowledge; he would repeatedly remind us that he was a physician and that we were still trainees, which caused us to second-guess ourselves. Eventually, the attending physician on our team was able to impress upon Dr. P the clearly established roles of the treatment team and the patient. It was also important to maintain open communication channels with Dr. P and his family, and to address his anxiety by discussing the treatment plan in detail.⁵

Continue to: Although his queries on medication...

Although his queries on medication pharmacodynamics and pharmacokinetics were daunting, we empathized with him, recognizing that his knowledge invariably contributed to his anxiety. We engaged with Dr. P and his parents and elaborated on the rationale behind treatment decisions. This earned his trust and tremendously facilitated his recovery.

We were also cautious about using benzodiazepines to treat Dr. P’s catatonia because we were concerned that his knowledge could aid him in feigning symptoms to obtain these medications. Physicians have a high rate of prescription medication abuse, mainly opiates and benzodiazepines.² The abuse of prescription medications by physicians is related to several psychological and psychiatric factors, including anxiety, depression, stress at work, personality problems, loss of loved ones, and pain. While treating physician patients, treatment decisions that include the use of opiates and benzodiazepines should be carefully considered.⁴

A complicated scenario

Managing a physician patient can be a rewarding experience; however, there are several factors that can impact the experience, including:

• The treating physicians’ anxiety and countertransference/transference dynamics. We repeatedly imagined ourselves in Dr. P’s position and thought long and hard about how this scenario could happen to anyone in the medical profession; these thoughts induced significant anxiety in each of us. Further, interacting with Dr. P was reminiscent of our training under senior residents and attendings. Dr. P viewed us—his treatment team—as his trainees and challenged our clinical knowledge and actions.
• The physician-patient’s emotional responses, which may include anxiety, despair, denial, and an inability to accept role reversal.

Our medical culture needs a paradigm shift. We need a model designed to encourage early self-disclosure and treatment-seeking among physicians with mental illness. This will reduce the stigma towards mental illness in our profession.

A physician’s mental health is important for the delivery of quality health care to his/her patients. Early identification and treatment of physicians with mental illnesses is challenging because physicians may neglect their own mental health due to the associated stigma, time constraints, or uncertainty regarding where to seek help. Physicians often worry about whom to confide in and harbor a fear that others will doubt his/her competence after recovery.¹ Physicians have higher rates of suicide than the general population.² According to data from the National Violent Death Reporting System, a diagnosed mental illness or a job problem significantly contribute to suicide among physicians.³ Additionally, physicians also have high rates of substance use and affective disorders.^1,4

Here, we present the case of a physician we treated on an inpatient psychiatry unit who stirred profound emotions in us as trainees, and discuss how we managed this complicated scenario.

CASE REPORT

Dr. P, a 35-year-old male endocrinologist, was admitted to our inpatient psychiatry unit with a diagnosis of bipolar disorder, manic, severe, with psychotic features. Earlier that day, Dr. P had walked out of his private outpatient practice where he still had several appointments. After he had been missing for several hours, he was picked up by the police. Dr. P had 2 prior psychiatric admissions; the last one had occurred >10 years ago. A few weeks before this admission, he stopped taking lithium, while continuing escitalopram. He had not been keeping his appointments with his outpatient psychiatrist.

At admission, Dr. P had pressured speech, grandiose delusions, an expansive affect, and aggressive behavior. He was responding to internal stimuli with no insight into his illness. He was evasive when asked about hallucinations. Dr. P believed he was superior in intelligence and physical prowess to everyone in the emergency department (ED), and for that reason, the ED staff was persecuting him. His urine toxicology was negative.

On the inpatient unit, because Dr. P exhibited posturing, mutism, and negativism, catatonia associated with bipolar disorder was added to his diagnosis. For the first 2 days, his catatonia was managed with oral lorazepam, 2 mg twice daily. Dr. P was also observed giving medical advice to other patients on the unit, and was told to stop. Throughout his hospitalization, he dictated his own treatment and would frequently debate with his treatment team on the pharmacologic basis for treatment decisions, asserting his expertise as a physician and claiming to have a general clinical knowledge of the acute management of bipolar disorder.

Dr. P was eventually stabilized on oral lithium, 450 mg twice daily, and aripiprazole, 10 mg/d. He also received oral clonazepam, as needed for acute agitation, which was eventually tapered and discontinued. He gradually responded to treatment, and demonstrated improved insight. The treatment team met with Dr. P’s parents, who also were physicians, to discuss treatment goals, management considerations, and an aftercare plan. After spending 8 days in the hospital, Dr. P was discharged home to the care of his immediate family, and instructed to follow up with his outpatient psychiatrist. We do not know if he resumed clinical duties.

Managing an extremely knowledgeable patient

During his hospitalization, Dr. P frequently challenged our clinical knowledge; he would repeatedly remind us that he was a physician and that we were still trainees, which caused us to second-guess ourselves. Eventually, the attending physician on our team was able to impress upon Dr. P the clearly established roles of the treatment team and the patient. It was also important to maintain open communication channels with Dr. P and his family, and to address his anxiety by discussing the treatment plan in detail.⁵

Continue to: Although his queries on medication...

Although his queries on medication pharmacodynamics and pharmacokinetics were daunting, we empathized with him, recognizing that his knowledge invariably contributed to his anxiety. We engaged with Dr. P and his parents and elaborated on the rationale behind treatment decisions. This earned his trust and tremendously facilitated his recovery.

We were also cautious about using benzodiazepines to treat Dr. P’s catatonia because we were concerned that his knowledge could aid him in feigning symptoms to obtain these medications. Physicians have a high rate of prescription medication abuse, mainly opiates and benzodiazepines.² The abuse of prescription medications by physicians is related to several psychological and psychiatric factors, including anxiety, depression, stress at work, personality problems, loss of loved ones, and pain. While treating physician patients, treatment decisions that include the use of opiates and benzodiazepines should be carefully considered.⁴

A complicated scenario

Managing a physician patient can be a rewarding experience; however, there are several factors that can impact the experience, including:

• The treating physicians’ anxiety and countertransference/transference dynamics. We repeatedly imagined ourselves in Dr. P’s position and thought long and hard about how this scenario could happen to anyone in the medical profession; these thoughts induced significant anxiety in each of us. Further, interacting with Dr. P was reminiscent of our training under senior residents and attendings. Dr. P viewed us—his treatment team—as his trainees and challenged our clinical knowledge and actions.
• The physician-patient’s emotional responses, which may include anxiety, despair, denial, and an inability to accept role reversal.

Our medical culture needs a paradigm shift. We need a model designed to encourage early self-disclosure and treatment-seeking among physicians with mental illness. This will reduce the stigma towards mental illness in our profession.

A physician’s mental health is important for the delivery of quality health care to his/her patients. Early identification and treatment of physicians with mental illnesses is challenging because physicians may neglect their own mental health due to the associated stigma, time constraints, or uncertainty regarding where to seek help. Physicians often worry about whom to confide in and harbor a fear that others will doubt his/her competence after recovery.¹ Physicians have higher rates of suicide than the general population.² According to data from the National Violent Death Reporting System, a diagnosed mental illness or a job problem significantly contribute to suicide among physicians.³ Additionally, physicians also have high rates of substance use and affective disorders.^1,4

Here, we present the case of a physician we treated on an inpatient psychiatry unit who stirred profound emotions in us as trainees, and discuss how we managed this complicated scenario.

CASE REPORT

Dr. P, a 35-year-old male endocrinologist, was admitted to our inpatient psychiatry unit with a diagnosis of bipolar disorder, manic, severe, with psychotic features. Earlier that day, Dr. P had walked out of his private outpatient practice where he still had several appointments. After he had been missing for several hours, he was picked up by the police. Dr. P had 2 prior psychiatric admissions; the last one had occurred >10 years ago. A few weeks before this admission, he stopped taking lithium, while continuing escitalopram. He had not been keeping his appointments with his outpatient psychiatrist.

At admission, Dr. P had pressured speech, grandiose delusions, an expansive affect, and aggressive behavior. He was responding to internal stimuli with no insight into his illness. He was evasive when asked about hallucinations. Dr. P believed he was superior in intelligence and physical prowess to everyone in the emergency department (ED), and for that reason, the ED staff was persecuting him. His urine toxicology was negative.

On the inpatient unit, because Dr. P exhibited posturing, mutism, and negativism, catatonia associated with bipolar disorder was added to his diagnosis. For the first 2 days, his catatonia was managed with oral lorazepam, 2 mg twice daily. Dr. P was also observed giving medical advice to other patients on the unit, and was told to stop. Throughout his hospitalization, he dictated his own treatment and would frequently debate with his treatment team on the pharmacologic basis for treatment decisions, asserting his expertise as a physician and claiming to have a general clinical knowledge of the acute management of bipolar disorder.

Dr. P was eventually stabilized on oral lithium, 450 mg twice daily, and aripiprazole, 10 mg/d. He also received oral clonazepam, as needed for acute agitation, which was eventually tapered and discontinued. He gradually responded to treatment, and demonstrated improved insight. The treatment team met with Dr. P’s parents, who also were physicians, to discuss treatment goals, management considerations, and an aftercare plan. After spending 8 days in the hospital, Dr. P was discharged home to the care of his immediate family, and instructed to follow up with his outpatient psychiatrist. We do not know if he resumed clinical duties.

Managing an extremely knowledgeable patient

During his hospitalization, Dr. P frequently challenged our clinical knowledge; he would repeatedly remind us that he was a physician and that we were still trainees, which caused us to second-guess ourselves. Eventually, the attending physician on our team was able to impress upon Dr. P the clearly established roles of the treatment team and the patient. It was also important to maintain open communication channels with Dr. P and his family, and to address his anxiety by discussing the treatment plan in detail.⁵

Continue to: Although his queries on medication...

Although his queries on medication pharmacodynamics and pharmacokinetics were daunting, we empathized with him, recognizing that his knowledge invariably contributed to his anxiety. We engaged with Dr. P and his parents and elaborated on the rationale behind treatment decisions. This earned his trust and tremendously facilitated his recovery.

We were also cautious about using benzodiazepines to treat Dr. P’s catatonia because we were concerned that his knowledge could aid him in feigning symptoms to obtain these medications. Physicians have a high rate of prescription medication abuse, mainly opiates and benzodiazepines.² The abuse of prescription medications by physicians is related to several psychological and psychiatric factors, including anxiety, depression, stress at work, personality problems, loss of loved ones, and pain. While treating physician patients, treatment decisions that include the use of opiates and benzodiazepines should be carefully considered.⁴

A complicated scenario

Managing a physician patient can be a rewarding experience; however, there are several factors that can impact the experience, including:

• The treating physicians’ anxiety and countertransference/transference dynamics. We repeatedly imagined ourselves in Dr. P’s position and thought long and hard about how this scenario could happen to anyone in the medical profession; these thoughts induced significant anxiety in each of us. Further, interacting with Dr. P was reminiscent of our training under senior residents and attendings. Dr. P viewed us—his treatment team—as his trainees and challenged our clinical knowledge and actions.
• The physician-patient’s emotional responses, which may include anxiety, despair, denial, and an inability to accept role reversal.

Our medical culture needs a paradigm shift. We need a model designed to encourage early self-disclosure and treatment-seeking among physicians with mental illness. This will reduce the stigma towards mental illness in our profession.

Ms. G, a 36-year-old woman, presented to the emergency department (ED) requesting a neurologic evaluation. She told clinicians she had “NMDA receptor encephalitis.”

Ms. G reported successful self-treatment of “life-long” body pain that was precipitated by multiple external stimuli (food, social encounters, interpersonal conflict, etc.). Through her own research, she had learned that both ketamine and magnesium could alter nociception in rats through N-methyl-d-aspartic acid (NMDA) receptor antagonism, and so she decided to try treating her pain with Delsym, an over-the-counter cough syrup containing dextromethorphan polistirex (DXM), which at high doses acts as an NMDA receptor antagonist. She said she was taking Delsym, 120 mg/d, and magnesium oxide, 600 mg/d.

In the ED, Ms. G had a labile affect, pressured speech, and flight of ideas. She denied any history of psychiatric treatment, suicide attempts, or substance abuse. Ms. G’s family reported she had been unusually social, talkative, and impulsive. She was admitted to the inpatient psychiatric unit with a diagnosis of mania.

On psychiatric evaluation, Ms. G was grandiose, irritable, and perseverative about her aberrant symptoms. She felt she did not experience the world as other people did, but found relief from her chronic pain after taking Delsym. She was not taking other medications. Ms. G did not report a family history of bipolar disorder or psychosis. Her laboratory results, including a comprehensive metabolic panel, complete blood count, lipid panel, thyroid studies, urine drug screening, and urinalysis, were unremarkable. Her blood pressure was mildly elevated (141/82 mm Hg).

Ms. G’s eventual diagnosis was substance-induced mania (DXM). The DXM-containing cough syrup and magnesium were discontinued in the hospital. She was stabilized on lithium extended-release, 900 mg/d (blood level 0.8 mmol/L), and olanzapine, 10 mg/d at bedtime. However, after discharge, Ms. G resumed using Delsym, which resulted in 3 subsequent psychiatric hospitalizations for mania during the next year.

I first treated Ms. G as an outpatient after her second hospitalization. At that point, she was stable. Her mental status was calm and cooperative, and she had a linear thought process. At her baseline, in the absence of mania, she had a blunted affect. She understood that DXM caused her to have manic symptoms, but she continued to believe that Delsym and magnesium cured her physical suffering and social inhibition. I noticed Ms. G would use figurative language inappropriately. I later learned she had sensitivities to food textures and a specialized interest in electronics. Because of this, I suspected Ms. G was on the autism spectrum; she met several DSM-5 criteria for autism spectrum disorder (ASD), particularly deficits in social-emotional reciprocity, highly restricted interests, and hyperreactivity to sensory input.

Upon routine lab screening, Ms. G was found to have hypothyroidism, with a thyroid-stimulating hormone level of 6.67 mcIU/mL. This resolved after discontinuing lithium. Olanzapine caused adverse metabolic effects and also was discontinued. Ms. G remained euthymic without any mood-stabilizing medication, except during periods when she abused DXM, when she would again become manic. Eventually, her motivation to avoid hospitalization would promote her abstinence.

Continue to: Implications of NMDA receptor antagonism

Implications of NMDA receptor antagonism

The use of ketamine as an NMDA receptor antagonist for treating depression and other psychiatric illnesses has gained momentum. Esketamine, the S-enantiomer of racemic ketamine, is now available as an FDA-approved intranasal formulation for treatment-resistant depression. Ketamine stops afferent nociception to the brain and is used as an analgesic (at low concentrations) and anesthetic (at high concentrations).¹

Dextromethorphan is abused as a recreational drug because at high doses it works similarly to both ketamine and phencyclidine. Individuals who abuse DXM can develop psychosis, motor/cognitive impairment, agitation, fevers, hypertension, tachycardia, and death.² In patients with ASD, researchers have identified genetic variations of NMDA receptors that are linked to dysfunction of these receptors.³ In animal models, as well as in humans, researchers have found that suppression or excitation of the NMDA receptor can ameliorate ASD symptoms, including social withdrawal and repetitive behaviors.³

Many individuals with ASD suffer from sensory abnormalities, including a reduced sensitivity to pain or a crippling sensitivity to various stimuli. Patients with ASD may have difficulty describing these abnormalities, and as a result, they may be misdiagnosed. One case report described a 15-year-old girl diagnosed with social anxiety and chronic generalized pain when in social situations.⁴ Pediatric rheumatologists had diagnosed her with “amplified pain syndrome.” When she presented to a mental health clinic for a neurodevelopmental evaluation, she explained to clinicians how she simply “did not ‘get’ people; they are just empty shells” and subsequently was given a diagnosis of ASD.⁴

In psychiatric patients who have comorbid substance use disorders, it is vital for clinicians to not only detect the presence of substance misuse, but also to understand what drives the patient toward abuse. Ms. G’s case, with its combination of substance abuse and ASD, illustrates the importance of listening to our patients for more precise diagnostic formulations, which then shape our treatment recommendations.

Ms. G, a 36-year-old woman, presented to the emergency department (ED) requesting a neurologic evaluation. She told clinicians she had “NMDA receptor encephalitis.”

Ms. G reported successful self-treatment of “life-long” body pain that was precipitated by multiple external stimuli (food, social encounters, interpersonal conflict, etc.). Through her own research, she had learned that both ketamine and magnesium could alter nociception in rats through N-methyl-d-aspartic acid (NMDA) receptor antagonism, and so she decided to try treating her pain with Delsym, an over-the-counter cough syrup containing dextromethorphan polistirex (DXM), which at high doses acts as an NMDA receptor antagonist. She said she was taking Delsym, 120 mg/d, and magnesium oxide, 600 mg/d.

In the ED, Ms. G had a labile affect, pressured speech, and flight of ideas. She denied any history of psychiatric treatment, suicide attempts, or substance abuse. Ms. G’s family reported she had been unusually social, talkative, and impulsive. She was admitted to the inpatient psychiatric unit with a diagnosis of mania.

On psychiatric evaluation, Ms. G was grandiose, irritable, and perseverative about her aberrant symptoms. She felt she did not experience the world as other people did, but found relief from her chronic pain after taking Delsym. She was not taking other medications. Ms. G did not report a family history of bipolar disorder or psychosis. Her laboratory results, including a comprehensive metabolic panel, complete blood count, lipid panel, thyroid studies, urine drug screening, and urinalysis, were unremarkable. Her blood pressure was mildly elevated (141/82 mm Hg).

Ms. G’s eventual diagnosis was substance-induced mania (DXM). The DXM-containing cough syrup and magnesium were discontinued in the hospital. She was stabilized on lithium extended-release, 900 mg/d (blood level 0.8 mmol/L), and olanzapine, 10 mg/d at bedtime. However, after discharge, Ms. G resumed using Delsym, which resulted in 3 subsequent psychiatric hospitalizations for mania during the next year.

I first treated Ms. G as an outpatient after her second hospitalization. At that point, she was stable. Her mental status was calm and cooperative, and she had a linear thought process. At her baseline, in the absence of mania, she had a blunted affect. She understood that DXM caused her to have manic symptoms, but she continued to believe that Delsym and magnesium cured her physical suffering and social inhibition. I noticed Ms. G would use figurative language inappropriately. I later learned she had sensitivities to food textures and a specialized interest in electronics. Because of this, I suspected Ms. G was on the autism spectrum; she met several DSM-5 criteria for autism spectrum disorder (ASD), particularly deficits in social-emotional reciprocity, highly restricted interests, and hyperreactivity to sensory input.

Upon routine lab screening, Ms. G was found to have hypothyroidism, with a thyroid-stimulating hormone level of 6.67 mcIU/mL. This resolved after discontinuing lithium. Olanzapine caused adverse metabolic effects and also was discontinued. Ms. G remained euthymic without any mood-stabilizing medication, except during periods when she abused DXM, when she would again become manic. Eventually, her motivation to avoid hospitalization would promote her abstinence.

Continue to: Implications of NMDA receptor antagonism

Implications of NMDA receptor antagonism

The use of ketamine as an NMDA receptor antagonist for treating depression and other psychiatric illnesses has gained momentum. Esketamine, the S-enantiomer of racemic ketamine, is now available as an FDA-approved intranasal formulation for treatment-resistant depression. Ketamine stops afferent nociception to the brain and is used as an analgesic (at low concentrations) and anesthetic (at high concentrations).¹

Dextromethorphan is abused as a recreational drug because at high doses it works similarly to both ketamine and phencyclidine. Individuals who abuse DXM can develop psychosis, motor/cognitive impairment, agitation, fevers, hypertension, tachycardia, and death.² In patients with ASD, researchers have identified genetic variations of NMDA receptors that are linked to dysfunction of these receptors.³ In animal models, as well as in humans, researchers have found that suppression or excitation of the NMDA receptor can ameliorate ASD symptoms, including social withdrawal and repetitive behaviors.³

Many individuals with ASD suffer from sensory abnormalities, including a reduced sensitivity to pain or a crippling sensitivity to various stimuli. Patients with ASD may have difficulty describing these abnormalities, and as a result, they may be misdiagnosed. One case report described a 15-year-old girl diagnosed with social anxiety and chronic generalized pain when in social situations.⁴ Pediatric rheumatologists had diagnosed her with “amplified pain syndrome.” When she presented to a mental health clinic for a neurodevelopmental evaluation, she explained to clinicians how she simply “did not ‘get’ people; they are just empty shells” and subsequently was given a diagnosis of ASD.⁴

In psychiatric patients who have comorbid substance use disorders, it is vital for clinicians to not only detect the presence of substance misuse, but also to understand what drives the patient toward abuse. Ms. G’s case, with its combination of substance abuse and ASD, illustrates the importance of listening to our patients for more precise diagnostic formulations, which then shape our treatment recommendations.

Ms. G, a 36-year-old woman, presented to the emergency department (ED) requesting a neurologic evaluation. She told clinicians she had “NMDA receptor encephalitis.”

Ms. G reported successful self-treatment of “life-long” body pain that was precipitated by multiple external stimuli (food, social encounters, interpersonal conflict, etc.). Through her own research, she had learned that both ketamine and magnesium could alter nociception in rats through N-methyl-d-aspartic acid (NMDA) receptor antagonism, and so she decided to try treating her pain with Delsym, an over-the-counter cough syrup containing dextromethorphan polistirex (DXM), which at high doses acts as an NMDA receptor antagonist. She said she was taking Delsym, 120 mg/d, and magnesium oxide, 600 mg/d.

In the ED, Ms. G had a labile affect, pressured speech, and flight of ideas. She denied any history of psychiatric treatment, suicide attempts, or substance abuse. Ms. G’s family reported she had been unusually social, talkative, and impulsive. She was admitted to the inpatient psychiatric unit with a diagnosis of mania.

On psychiatric evaluation, Ms. G was grandiose, irritable, and perseverative about her aberrant symptoms. She felt she did not experience the world as other people did, but found relief from her chronic pain after taking Delsym. She was not taking other medications. Ms. G did not report a family history of bipolar disorder or psychosis. Her laboratory results, including a comprehensive metabolic panel, complete blood count, lipid panel, thyroid studies, urine drug screening, and urinalysis, were unremarkable. Her blood pressure was mildly elevated (141/82 mm Hg).

Ms. G’s eventual diagnosis was substance-induced mania (DXM). The DXM-containing cough syrup and magnesium were discontinued in the hospital. She was stabilized on lithium extended-release, 900 mg/d (blood level 0.8 mmol/L), and olanzapine, 10 mg/d at bedtime. However, after discharge, Ms. G resumed using Delsym, which resulted in 3 subsequent psychiatric hospitalizations for mania during the next year.

I first treated Ms. G as an outpatient after her second hospitalization. At that point, she was stable. Her mental status was calm and cooperative, and she had a linear thought process. At her baseline, in the absence of mania, she had a blunted affect. She understood that DXM caused her to have manic symptoms, but she continued to believe that Delsym and magnesium cured her physical suffering and social inhibition. I noticed Ms. G would use figurative language inappropriately. I later learned she had sensitivities to food textures and a specialized interest in electronics. Because of this, I suspected Ms. G was on the autism spectrum; she met several DSM-5 criteria for autism spectrum disorder (ASD), particularly deficits in social-emotional reciprocity, highly restricted interests, and hyperreactivity to sensory input.

Upon routine lab screening, Ms. G was found to have hypothyroidism, with a thyroid-stimulating hormone level of 6.67 mcIU/mL. This resolved after discontinuing lithium. Olanzapine caused adverse metabolic effects and also was discontinued. Ms. G remained euthymic without any mood-stabilizing medication, except during periods when she abused DXM, when she would again become manic. Eventually, her motivation to avoid hospitalization would promote her abstinence.

Continue to: Implications of NMDA receptor antagonism

Implications of NMDA receptor antagonism

The use of ketamine as an NMDA receptor antagonist for treating depression and other psychiatric illnesses has gained momentum. Esketamine, the S-enantiomer of racemic ketamine, is now available as an FDA-approved intranasal formulation for treatment-resistant depression. Ketamine stops afferent nociception to the brain and is used as an analgesic (at low concentrations) and anesthetic (at high concentrations).¹

Dextromethorphan is abused as a recreational drug because at high doses it works similarly to both ketamine and phencyclidine. Individuals who abuse DXM can develop psychosis, motor/cognitive impairment, agitation, fevers, hypertension, tachycardia, and death.² In patients with ASD, researchers have identified genetic variations of NMDA receptors that are linked to dysfunction of these receptors.³ In animal models, as well as in humans, researchers have found that suppression or excitation of the NMDA receptor can ameliorate ASD symptoms, including social withdrawal and repetitive behaviors.³

Many individuals with ASD suffer from sensory abnormalities, including a reduced sensitivity to pain or a crippling sensitivity to various stimuli. Patients with ASD may have difficulty describing these abnormalities, and as a result, they may be misdiagnosed. One case report described a 15-year-old girl diagnosed with social anxiety and chronic generalized pain when in social situations.⁴ Pediatric rheumatologists had diagnosed her with “amplified pain syndrome.” When she presented to a mental health clinic for a neurodevelopmental evaluation, she explained to clinicians how she simply “did not ‘get’ people; they are just empty shells” and subsequently was given a diagnosis of ASD.⁴

In psychiatric patients who have comorbid substance use disorders, it is vital for clinicians to not only detect the presence of substance misuse, but also to understand what drives the patient toward abuse. Ms. G’s case, with its combination of substance abuse and ASD, illustrates the importance of listening to our patients for more precise diagnostic formulations, which then shape our treatment recommendations.

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

Here is a summary of the sobering facts:

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

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

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

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

Here is a summary of the sobering facts:

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

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

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

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

Here is a summary of the sobering facts:

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

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

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

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

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

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

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

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

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

Study design

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

Continue to: Outcomes

Outcomes

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

Conclusion

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

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

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

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

Continue to: One type of written narrative...

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

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

Study design

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

Outcomes

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

Conclusion

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

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

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

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

Study design

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

Outcomes

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

Conclusion

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

Continue to: Mindfulness-based cognitive therapy...

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

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

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

Study design

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

Outcomes

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

Continue to: Conclusion

Conclusion

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

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

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

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

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

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

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

Study design

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

Continue to: Outcomes

Outcomes

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

Conclusion

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

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

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

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

Continue to: One type of written narrative...

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

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

Study design

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

Outcomes

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

Conclusion

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

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

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

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

Study design

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

Outcomes

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

Conclusion

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

Continue to: Mindfulness-based cognitive therapy...

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

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

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

Study design

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

Outcomes

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

Continue to: Conclusion

Conclusion

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

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

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

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

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

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

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

Study design

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

Continue to: Outcomes

Outcomes

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

Conclusion

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

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

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

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

Continue to: One type of written narrative...

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

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

Study design

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

Outcomes

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

Conclusion

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

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

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

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

Study design

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

Outcomes

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

Conclusion

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

Continue to: Mindfulness-based cognitive therapy...

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

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

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

Study design

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

Outcomes

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

Continue to: Conclusion

Conclusion

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