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Depression: a changing concept in the age of ketamine
What does it mean to define an amalgamation of symptoms as a “psychiatric disorder?” Are psychiatric disorders an extreme variation of normative human behavior? Is human behavior simply an output phenotype of some neurologic chemical processes that become disordered in mental illness? Can depression be localized in the brain and subsequently turned on or off? If depression were to be localized in the brain, would it be an excess of a neurotransmitter, the depletion of a receptor, a malfunctioning neuron, an overactive connectome, poorly processed genetic material, or something as yet undefined? Those questions always have been present in our minds and influenced our understanding of patients, but a recent development in psychiatry raises questions about one of the few things we were historically confident about.
A part of our foundational understanding of depression was that it is not sadness, per se. One can be sad for any amount of time. It is not uncommon to feel sad for any variety of reasons, such as watching an adorable 60-second commercial for dog food.1 Those fleeting moments of sadness can even be empowering; they remind us about the things we care about and would be sad to miss.
Sadness in oneself can demonstrate the experience of empathic sadness for others. On the contrary, depression appears to have little apparent purpose, and instead results in a maladaptive way of coping that is all-consuming and often very damaging. Depression is not a mood but a state of being, something that is not defined by how one feels but who one is or has become because of the disorder. So it comes as somewhat of a surprise when we heard that ketamine could alleviate depression in minutes.2,3 As described by a ketamine expert, symptoms are relieved in “no less than an hour.”4 The surprise is not so much that a treatment would work but that improvement could be defined in such a short time frame.
Psychiatry has debated the definition of depression for its entire existence. There are many ways to tackle the concept of depression. A lot of the debate has been about the causes of depression. One example of the continued evolution of our understanding of depression is our prior categorization of depression as “exogenous” or “endogenous.”5 Exogenous depression was described as happening in the context of social stressors and as best treated with therapy. Endogenous depression was a supposedly truer form of depression as a disorder and was more biologically based. Patients suffering from endogenous depression were thought to have chemical abnormalities in the brain that could be alleviated by tricyclic antidepressants and subsequently SSRIs. Like many prior debates about depression, this one appears to be little discussed nowadays. A review of the use of the term “endogenous depression” in books shows an onset in the 1930s, a peak in the 1980s, and a rapid decline since.6
More recently, psychiatrists have defined depression using the DSM-5 criteria. Depression is thought to be the presence of at least five out of nine symptoms listed in the manual for a period of 2 weeks that cause significant distress or impairment.7 The DSM attempts to address criticism by providing information on its limitations and best use, and encourages clinical interpretation of symptoms. The DSM does not portray itself as a gold standard but rather as a tool for treatment planning and effective communication between peers. Furthermore, the National Institute on Mental Health is promoting an alternative understanding of depression using its own Research Domain Criteria, which attempt to provide a more objective understanding of the disorder based on biological rather than subjective correlates.
The growing literature on ketamine partly hinges on the belief that depression is something that can be redefined and changed at any moment. Many trials ask patients whether their depression remains in remission in the subsequent hours, days, and weeks following administration of the drug. However, one wonders if that is even possible. If a patient’s depression is alleviated in an hour, was it really clinical depression? Is it truly in remission? Contrary to our previous understanding, is depression, in reality, a switch that can be turned off by an infusion of an N-methyl-D-aspartate (NMDA)–receptor antagonist? Without minimizing the suffering of patients seeking ketamine or the relief provided to patients who benefit from the treatment, we simply are pointing out that the definition of depression did not account for this reported phenomenon of relatively instantaneous relief. The seemingly miraculous effects of ketamine suggest a new paradigm where any intervention – whether chemical, social, or psychological – could turn off the devastating effects of depression in an instant.
After all, the most widely used scale of depression, the nine-item Patient Health Questionnaire (PHQ-9) asks patients, “Over the last 2 weeks, how often have you been bothered by any of the following problems?” The highest answer one can give is “Nearly every day.” Are we incorrect to think that if one were suicidal every minute of the past 2 weeks, one would still score, nearly every day, even if one’s symptoms were relieved for the past hour? Thus, a maximum score of 27 would remain a 27 no matter what happened in the past hour.
We do realize that we are being overly literal. Ketamine makes some people feel better quickly, and researchers try to capture that effect by asking patients about their symptoms within short intervals. Furthermore, one has to start somewhere. After the infusion is a reasonable time to ask patients how they feel. We are also cognizant that many ketamine researchers do more long-term follow-ups and/or have recommended longer-term studies. Nonetheless,
Expanding our definition of depression to encompass experiences with short time frames may have unintended consequences. As living circumstances rarely change in minutes, the emphasis on rapid recovery makes the patients more in control of their reported experiences and thus their diagnoses. One cannot assess a patient’s impairment or disability from minute to minute. One is left with emphasizing the patient’s subjective symptoms and deemphasizing their relationships, goals, and daily functioning. How could one measure eating habits, hygiene, or participation in hobbies every hour? Another consequence of this reduced time frame is the expansion of a diagnosis that no longer requires the presence of symptoms for 2 weeks. Considering the already vast number of people diagnosed with depression,9,10 this small change may further expand the number diagnosed with a mood disorder. Perhaps to many practitioners and patients these arguments seem obtuse and fastidious, but there is a core failure in modern psychiatry to clearly differentiate the human condition from mental illness. Said failure has vast implications for psychiatric epidemiology, the sociological understanding of psychic suffering and suicide, as well as the overprescribing of psychotropic medications.
Ketamine is an exciting prospect to many psychiatrists who feel like we have had little advancement and few novel treatments in a long time; advertised breakthroughs in the treatment of depression since fluoxetine have not been particularly impressive. Furthermore, the concerns about potential ketamine abuse are not theoretical but a very real problem in some parts of the world.11,12 The concerns about abuse are worsened considering recent evidence that suggests that ketamine’s effect may be driven by its opiate rather than NMDA effects.13 While some have discussed those concerns, we think that the field also needs to address the fact that the debate about ketamine is also changing our definition of depression.
References
1. https://www.youtube.com/watch?v=MpcUN6XvGmk.
2. J Clin Psychiatry. 2016 Jun;77(6):e719-25.
3. Emerg (Tehran). 2014 Winter;2(1):36-9.
4. “Is esketamine the game-changer for depression we want?” Rolling Stone. 2019 Mar 11.
5. Psychol Med. 1971;1(3):191-6.
6. https://books.google.com/ngrams.
7. Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). American Psychiatric Association, 2013.
8. Am J Psychiatry. 2014 Apr;171(4):395-7.
9. “Many people taking antidepressants discover they cannot quit.” New York Times. 2018 Apr 7.
10. “Antidepressants show greatest increase in number of prescription items dispensed.” National Health Service. 2015 Jul 5.
11. “The ketamine connection.” BBC News. 2015 Jul 10.
12. Front Psychiatry. 2018 Jul 17. doi: 10.33389/fpsyt.2018.00313.
13. Am J Psychiatry. 2018 Dec 1;175(2):1205-15.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. Among his writings is Coercion and the critical psychiatrist, chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Cham, Switzerland: Springer Nature Switzerland, 2019, pp. 155-77). Dr. Lehman is an associate professor of psychiatry at UCSD. He is codirector of all Acute and Intensive Psychiatric Treatment at the VA Medical Center in San Diego, where he practices clinical psychiatry. He also is the course director for the UCSD third-year medical student psychiatry clerkship.
*This article was updated 3/25/2019.
What does it mean to define an amalgamation of symptoms as a “psychiatric disorder?” Are psychiatric disorders an extreme variation of normative human behavior? Is human behavior simply an output phenotype of some neurologic chemical processes that become disordered in mental illness? Can depression be localized in the brain and subsequently turned on or off? If depression were to be localized in the brain, would it be an excess of a neurotransmitter, the depletion of a receptor, a malfunctioning neuron, an overactive connectome, poorly processed genetic material, or something as yet undefined? Those questions always have been present in our minds and influenced our understanding of patients, but a recent development in psychiatry raises questions about one of the few things we were historically confident about.
A part of our foundational understanding of depression was that it is not sadness, per se. One can be sad for any amount of time. It is not uncommon to feel sad for any variety of reasons, such as watching an adorable 60-second commercial for dog food.1 Those fleeting moments of sadness can even be empowering; they remind us about the things we care about and would be sad to miss.
Sadness in oneself can demonstrate the experience of empathic sadness for others. On the contrary, depression appears to have little apparent purpose, and instead results in a maladaptive way of coping that is all-consuming and often very damaging. Depression is not a mood but a state of being, something that is not defined by how one feels but who one is or has become because of the disorder. So it comes as somewhat of a surprise when we heard that ketamine could alleviate depression in minutes.2,3 As described by a ketamine expert, symptoms are relieved in “no less than an hour.”4 The surprise is not so much that a treatment would work but that improvement could be defined in such a short time frame.
Psychiatry has debated the definition of depression for its entire existence. There are many ways to tackle the concept of depression. A lot of the debate has been about the causes of depression. One example of the continued evolution of our understanding of depression is our prior categorization of depression as “exogenous” or “endogenous.”5 Exogenous depression was described as happening in the context of social stressors and as best treated with therapy. Endogenous depression was a supposedly truer form of depression as a disorder and was more biologically based. Patients suffering from endogenous depression were thought to have chemical abnormalities in the brain that could be alleviated by tricyclic antidepressants and subsequently SSRIs. Like many prior debates about depression, this one appears to be little discussed nowadays. A review of the use of the term “endogenous depression” in books shows an onset in the 1930s, a peak in the 1980s, and a rapid decline since.6
More recently, psychiatrists have defined depression using the DSM-5 criteria. Depression is thought to be the presence of at least five out of nine symptoms listed in the manual for a period of 2 weeks that cause significant distress or impairment.7 The DSM attempts to address criticism by providing information on its limitations and best use, and encourages clinical interpretation of symptoms. The DSM does not portray itself as a gold standard but rather as a tool for treatment planning and effective communication between peers. Furthermore, the National Institute on Mental Health is promoting an alternative understanding of depression using its own Research Domain Criteria, which attempt to provide a more objective understanding of the disorder based on biological rather than subjective correlates.
The growing literature on ketamine partly hinges on the belief that depression is something that can be redefined and changed at any moment. Many trials ask patients whether their depression remains in remission in the subsequent hours, days, and weeks following administration of the drug. However, one wonders if that is even possible. If a patient’s depression is alleviated in an hour, was it really clinical depression? Is it truly in remission? Contrary to our previous understanding, is depression, in reality, a switch that can be turned off by an infusion of an N-methyl-D-aspartate (NMDA)–receptor antagonist? Without minimizing the suffering of patients seeking ketamine or the relief provided to patients who benefit from the treatment, we simply are pointing out that the definition of depression did not account for this reported phenomenon of relatively instantaneous relief. The seemingly miraculous effects of ketamine suggest a new paradigm where any intervention – whether chemical, social, or psychological – could turn off the devastating effects of depression in an instant.
After all, the most widely used scale of depression, the nine-item Patient Health Questionnaire (PHQ-9) asks patients, “Over the last 2 weeks, how often have you been bothered by any of the following problems?” The highest answer one can give is “Nearly every day.” Are we incorrect to think that if one were suicidal every minute of the past 2 weeks, one would still score, nearly every day, even if one’s symptoms were relieved for the past hour? Thus, a maximum score of 27 would remain a 27 no matter what happened in the past hour.
We do realize that we are being overly literal. Ketamine makes some people feel better quickly, and researchers try to capture that effect by asking patients about their symptoms within short intervals. Furthermore, one has to start somewhere. After the infusion is a reasonable time to ask patients how they feel. We are also cognizant that many ketamine researchers do more long-term follow-ups and/or have recommended longer-term studies. Nonetheless,
Expanding our definition of depression to encompass experiences with short time frames may have unintended consequences. As living circumstances rarely change in minutes, the emphasis on rapid recovery makes the patients more in control of their reported experiences and thus their diagnoses. One cannot assess a patient’s impairment or disability from minute to minute. One is left with emphasizing the patient’s subjective symptoms and deemphasizing their relationships, goals, and daily functioning. How could one measure eating habits, hygiene, or participation in hobbies every hour? Another consequence of this reduced time frame is the expansion of a diagnosis that no longer requires the presence of symptoms for 2 weeks. Considering the already vast number of people diagnosed with depression,9,10 this small change may further expand the number diagnosed with a mood disorder. Perhaps to many practitioners and patients these arguments seem obtuse and fastidious, but there is a core failure in modern psychiatry to clearly differentiate the human condition from mental illness. Said failure has vast implications for psychiatric epidemiology, the sociological understanding of psychic suffering and suicide, as well as the overprescribing of psychotropic medications.
Ketamine is an exciting prospect to many psychiatrists who feel like we have had little advancement and few novel treatments in a long time; advertised breakthroughs in the treatment of depression since fluoxetine have not been particularly impressive. Furthermore, the concerns about potential ketamine abuse are not theoretical but a very real problem in some parts of the world.11,12 The concerns about abuse are worsened considering recent evidence that suggests that ketamine’s effect may be driven by its opiate rather than NMDA effects.13 While some have discussed those concerns, we think that the field also needs to address the fact that the debate about ketamine is also changing our definition of depression.
References
1. https://www.youtube.com/watch?v=MpcUN6XvGmk.
2. J Clin Psychiatry. 2016 Jun;77(6):e719-25.
3. Emerg (Tehran). 2014 Winter;2(1):36-9.
4. “Is esketamine the game-changer for depression we want?” Rolling Stone. 2019 Mar 11.
5. Psychol Med. 1971;1(3):191-6.
6. https://books.google.com/ngrams.
7. Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). American Psychiatric Association, 2013.
8. Am J Psychiatry. 2014 Apr;171(4):395-7.
9. “Many people taking antidepressants discover they cannot quit.” New York Times. 2018 Apr 7.
10. “Antidepressants show greatest increase in number of prescription items dispensed.” National Health Service. 2015 Jul 5.
11. “The ketamine connection.” BBC News. 2015 Jul 10.
12. Front Psychiatry. 2018 Jul 17. doi: 10.33389/fpsyt.2018.00313.
13. Am J Psychiatry. 2018 Dec 1;175(2):1205-15.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. Among his writings is Coercion and the critical psychiatrist, chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Cham, Switzerland: Springer Nature Switzerland, 2019, pp. 155-77). Dr. Lehman is an associate professor of psychiatry at UCSD. He is codirector of all Acute and Intensive Psychiatric Treatment at the VA Medical Center in San Diego, where he practices clinical psychiatry. He also is the course director for the UCSD third-year medical student psychiatry clerkship.
*This article was updated 3/25/2019.
What does it mean to define an amalgamation of symptoms as a “psychiatric disorder?” Are psychiatric disorders an extreme variation of normative human behavior? Is human behavior simply an output phenotype of some neurologic chemical processes that become disordered in mental illness? Can depression be localized in the brain and subsequently turned on or off? If depression were to be localized in the brain, would it be an excess of a neurotransmitter, the depletion of a receptor, a malfunctioning neuron, an overactive connectome, poorly processed genetic material, or something as yet undefined? Those questions always have been present in our minds and influenced our understanding of patients, but a recent development in psychiatry raises questions about one of the few things we were historically confident about.
A part of our foundational understanding of depression was that it is not sadness, per se. One can be sad for any amount of time. It is not uncommon to feel sad for any variety of reasons, such as watching an adorable 60-second commercial for dog food.1 Those fleeting moments of sadness can even be empowering; they remind us about the things we care about and would be sad to miss.
Sadness in oneself can demonstrate the experience of empathic sadness for others. On the contrary, depression appears to have little apparent purpose, and instead results in a maladaptive way of coping that is all-consuming and often very damaging. Depression is not a mood but a state of being, something that is not defined by how one feels but who one is or has become because of the disorder. So it comes as somewhat of a surprise when we heard that ketamine could alleviate depression in minutes.2,3 As described by a ketamine expert, symptoms are relieved in “no less than an hour.”4 The surprise is not so much that a treatment would work but that improvement could be defined in such a short time frame.
Psychiatry has debated the definition of depression for its entire existence. There are many ways to tackle the concept of depression. A lot of the debate has been about the causes of depression. One example of the continued evolution of our understanding of depression is our prior categorization of depression as “exogenous” or “endogenous.”5 Exogenous depression was described as happening in the context of social stressors and as best treated with therapy. Endogenous depression was a supposedly truer form of depression as a disorder and was more biologically based. Patients suffering from endogenous depression were thought to have chemical abnormalities in the brain that could be alleviated by tricyclic antidepressants and subsequently SSRIs. Like many prior debates about depression, this one appears to be little discussed nowadays. A review of the use of the term “endogenous depression” in books shows an onset in the 1930s, a peak in the 1980s, and a rapid decline since.6
More recently, psychiatrists have defined depression using the DSM-5 criteria. Depression is thought to be the presence of at least five out of nine symptoms listed in the manual for a period of 2 weeks that cause significant distress or impairment.7 The DSM attempts to address criticism by providing information on its limitations and best use, and encourages clinical interpretation of symptoms. The DSM does not portray itself as a gold standard but rather as a tool for treatment planning and effective communication between peers. Furthermore, the National Institute on Mental Health is promoting an alternative understanding of depression using its own Research Domain Criteria, which attempt to provide a more objective understanding of the disorder based on biological rather than subjective correlates.
The growing literature on ketamine partly hinges on the belief that depression is something that can be redefined and changed at any moment. Many trials ask patients whether their depression remains in remission in the subsequent hours, days, and weeks following administration of the drug. However, one wonders if that is even possible. If a patient’s depression is alleviated in an hour, was it really clinical depression? Is it truly in remission? Contrary to our previous understanding, is depression, in reality, a switch that can be turned off by an infusion of an N-methyl-D-aspartate (NMDA)–receptor antagonist? Without minimizing the suffering of patients seeking ketamine or the relief provided to patients who benefit from the treatment, we simply are pointing out that the definition of depression did not account for this reported phenomenon of relatively instantaneous relief. The seemingly miraculous effects of ketamine suggest a new paradigm where any intervention – whether chemical, social, or psychological – could turn off the devastating effects of depression in an instant.
After all, the most widely used scale of depression, the nine-item Patient Health Questionnaire (PHQ-9) asks patients, “Over the last 2 weeks, how often have you been bothered by any of the following problems?” The highest answer one can give is “Nearly every day.” Are we incorrect to think that if one were suicidal every minute of the past 2 weeks, one would still score, nearly every day, even if one’s symptoms were relieved for the past hour? Thus, a maximum score of 27 would remain a 27 no matter what happened in the past hour.
We do realize that we are being overly literal. Ketamine makes some people feel better quickly, and researchers try to capture that effect by asking patients about their symptoms within short intervals. Furthermore, one has to start somewhere. After the infusion is a reasonable time to ask patients how they feel. We are also cognizant that many ketamine researchers do more long-term follow-ups and/or have recommended longer-term studies. Nonetheless,
Expanding our definition of depression to encompass experiences with short time frames may have unintended consequences. As living circumstances rarely change in minutes, the emphasis on rapid recovery makes the patients more in control of their reported experiences and thus their diagnoses. One cannot assess a patient’s impairment or disability from minute to minute. One is left with emphasizing the patient’s subjective symptoms and deemphasizing their relationships, goals, and daily functioning. How could one measure eating habits, hygiene, or participation in hobbies every hour? Another consequence of this reduced time frame is the expansion of a diagnosis that no longer requires the presence of symptoms for 2 weeks. Considering the already vast number of people diagnosed with depression,9,10 this small change may further expand the number diagnosed with a mood disorder. Perhaps to many practitioners and patients these arguments seem obtuse and fastidious, but there is a core failure in modern psychiatry to clearly differentiate the human condition from mental illness. Said failure has vast implications for psychiatric epidemiology, the sociological understanding of psychic suffering and suicide, as well as the overprescribing of psychotropic medications.
Ketamine is an exciting prospect to many psychiatrists who feel like we have had little advancement and few novel treatments in a long time; advertised breakthroughs in the treatment of depression since fluoxetine have not been particularly impressive. Furthermore, the concerns about potential ketamine abuse are not theoretical but a very real problem in some parts of the world.11,12 The concerns about abuse are worsened considering recent evidence that suggests that ketamine’s effect may be driven by its opiate rather than NMDA effects.13 While some have discussed those concerns, we think that the field also needs to address the fact that the debate about ketamine is also changing our definition of depression.
References
1. https://www.youtube.com/watch?v=MpcUN6XvGmk.
2. J Clin Psychiatry. 2016 Jun;77(6):e719-25.
3. Emerg (Tehran). 2014 Winter;2(1):36-9.
4. “Is esketamine the game-changer for depression we want?” Rolling Stone. 2019 Mar 11.
5. Psychol Med. 1971;1(3):191-6.
6. https://books.google.com/ngrams.
7. Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5). American Psychiatric Association, 2013.
8. Am J Psychiatry. 2014 Apr;171(4):395-7.
9. “Many people taking antidepressants discover they cannot quit.” New York Times. 2018 Apr 7.
10. “Antidepressants show greatest increase in number of prescription items dispensed.” National Health Service. 2015 Jul 5.
11. “The ketamine connection.” BBC News. 2015 Jul 10.
12. Front Psychiatry. 2018 Jul 17. doi: 10.33389/fpsyt.2018.00313.
13. Am J Psychiatry. 2018 Dec 1;175(2):1205-15.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. Among his writings is Coercion and the critical psychiatrist, chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Cham, Switzerland: Springer Nature Switzerland, 2019, pp. 155-77). Dr. Lehman is an associate professor of psychiatry at UCSD. He is codirector of all Acute and Intensive Psychiatric Treatment at the VA Medical Center in San Diego, where he practices clinical psychiatry. He also is the course director for the UCSD third-year medical student psychiatry clerkship.
*This article was updated 3/25/2019.
A prescription for ‘deprescribing’: A case report
In 2016, Swapnil Gupta, MD, and John Daniel Cahill, MD, PhD, challenged the field of psychiatry to reexamine our prescribing patterns. They warned against our use of polypharmacy when not attached to improvement in functioning for our patients.1 They were concerned about the lack of evidence for those treatment regimens and for our diagnostic criteria. In their inspiring article, they described how psychiatrists might proceed in the process of “deprescribing” – which they define as a process of pharmacologic regimen optimization through reducing or ending medications for which “benefits no longer outweigh risks.”1
In my practice, I routinely confront medication regimens that I have never encountered in the literature. The evidence for two psychotropics is limited but certainly available, in particular adjunct treatment of antidepressants2 and mood stabilizers.3 The evidence supporting the use of more than two psychotropics, however, is quite sparse. Yet, patients often enter my office on more than five psychotropics. I am also confronted with poorly defined diagnostic labels – which present more as means to justify polypharmacy than a thorough review of the patient’s current state.
Dr. Gupta and Dr. Cahill recommend a series of steps aimed at attempting the deprescription of psychotropics. Those steps include timeliness, knowledge of the patient’s current regimen, discussion about the risk of prescriptions, discussion about deprescribing, choosing the right medications to stop, a plan for describing, and monitoring. In the case presented below, I used some of those steps in an effort to provide the best care for the patient. Key details of the case have been changed, including the name, to protect the patient’s confidentiality.
Overview of the case
Rosalie Bertin is a 54-year-old female who has been treated for depression by a variety of primary care physicians for the better part of the last 30 years. She had tried an array of antidepressants, including sertraline, citalopram, duloxetine, and mirtazapine, over that time. Each seemed to provide some benefit when reviewing the notes, but there is no mention of why she was continued on those medications despite the absence of continuing symptoms. Occasionally, Rosalie would present to her clinician tearful and endorsing sadness, though the record did not comment on reports of energy, concentration, sleep, appetite, and interest.
In 2014, Rosalie’s husband passed away from lung cancer. His death was fairly quick, and initially, Rosalie did not mention any significant emotional complaints. However, when visiting her primary care physician 4 months later, she was noted to experience auditory hallucinations. “Sometimes I hear my husband when I am alone in my home,” she said. Rosalie was referred to a psychiatrist with a diagnosis of “psychosis not otherwise specified.”
When discussing her condition with the psychiatrist, Rosalie mentioned experiencing low mood, and having diminished interest in engaging in activities. “I miss Marc when I go places; I used to do everything with him.” She reported hearing him often but only when at her home. He would say things like, “I miss you,” or ask her about her day. She was diagnosed with “major depressive disorder with psychotic features.” Risperidone was added to the escitalopram, buspirone, and gabapentin that had been started by her primary care physician.
After several months of psychotropic management, the dose of risperidone was titrated to 8 mg per day. Her mood symptoms were unchanged, but she now was complaining of poor concentration and memory. The psychiatrist performed a Mini-Mental State Examination (MMSE). It was noted that taking the MMSE engendered significant anxiety for the patient. Rosalie received a score suggesting mild cognitive impairment. She was started on donepezil for the memory complaint, quetiapine for the continued voices, and recommended for disability.
Once on short-term disability, the patient relocated to live closer to her mother in San Diego and subsequently contacted me about continuing psychiatric care.
Initial visit
Rosalie is a petite white woman, raised in the Midwest, who married her high school sweetheart, and subsequently became an administrative assistant. Rosalie and Marc were unable to have children. Marc was an engineer, and a longtime smoker. She describes their lives as simple – “few friends, few vacations, few problems, few regrets.” She states she misses her husband and often cries when thinking about him.
When asked about psychiatric diagnoses, she answered: “I have psychosis. … My doctor said maybe schizophrenia, but he is not sure yet.” She described schizophrenia as hearing voices. Rosalie also mentioned having memory problems: “They cannot tell if it is Alzheimer’s disease until I die and they look at my brain, but the medication should delay the progression.”
She reported no significant effect from her prior antidepressant trials: “I am not sure if or how they helped.” Rosalie could not explain the role of the medication. “I take medications as prescribed by my doctor,” she said.
When discussing her antipsychotics, she mentioned: “Those are strong medications; it is hard for me to stay awake with them.” She declared having had no changes in the voices while on the risperidone but said they went away since also being on the quetiapine: “I wonder if the combination of the two really fixed my brain imbalance.”
Assessment
I admit that I have a critical bias against the overuse of psychotropics, and this might have painted how I interpreted Rosalie’s story. Nonetheless, I was honest with her and told her of my concerns. I informed her that her diagnosis was not consistent with my understanding of mood and thought disorders. Her initial reports of depression neither met the DSM criteria for depression nor felt consistent with my conceptualization of the illness. She had retained appropriate functioning and seemed to be responding with the sadness expected when facing difficult challenges like grief.
Her subsequent reports of auditory hallucinations were not associated with delusions or forms of disorganization that I would expect in someone with a thought disorder. Furthermore, the context of the onset gave me the impression that this was part of her process of grief. Her poor result in the dementia screen was most surprising and inconsistent with my evaluation. I told her that I suspected that she was not suffering from Alzheimer’s but from being overmedicated and from anxiety at the time of the testing.
She was excited and hesitant about my report. She was surprised by the length of our visit and interested in hearing more from me. Strangely, I wished she had challenged my different approach. I think that I was hoping she would question my conceptualization, the way I hoped she would have done with her prior clinicians. Nonetheless, she agreed to make a plan with me.
Treatment plan
We decided to review each of her medications and discuss their benefits and risks over a couple of visits. She was most eager to discontinue the donepezil, which had caused diarrhea. She was concerned when I informed her of the potential side effects of antipsychotics. “My doctor asked me if I had any side effects at each visit; I answered that I felt nothing wrong; I had not realized that side effects could appear later.”
She was adamant about staying on buspirone, as she felt it helped her the most with her anxiety at social events. She voiced concern about discontinuing the antipsychotics despite being unsettled by my review of their risks. She asked that we taper them slowly.
In regard to receiving psychosocial support throughout this period of deprescribing, Rosalie declined weekly psychotherapy. She reported having a good social network in San Diego that she wanted to rely on.
Outcome
I often worry about consequences of stopping a medication, especially when I was not present at the time of its initiation. I agonize that the patient might relapse from my need to carry out my agenda on deprescribing. I try to remind myself that the evidence supports my decision making. The risks of psychotropics often are slow to show up, making the benefit of deprescribing less tangible. However, this case was straightforward.
Rosalie quickly improved. Tapering the antipsychotics was astonishing to her: “I can think clearly again.” Within 6 months, she was on buspirone only – though willing to discuss its discontinuation. She had a lead for a job and was hoping to return to work soon. Rosalie continued to miss her husband but had not heard him in some time. She has not had symptoms of psychosis or depression. Her cognition and mood were intact on my clinical assessment.
Discussion
Sadly and shockingly, cases like that of Rosalie are common. In my practice, I routinely see patients on multiple psychotropics – often on more than one antipsychotic. Their diagnoses are vague and dubious, and include diagnoses such as “unspecified psychosis” and “cognitive impairments.” Clinicians occasionally worry about relapse and promote a narrative that treatment must be not only long term but lifelong.4 There is some evidence for this perspective in a research context, but the clinical world also is filled with patients like Rosalie.
Her reports of auditory hallucinations were better explained by her grief than by a psychotic process.5 Her memory complaints were better explained by anxiety at the time of her testing while suffering from the side effects from her numerous psychotropics.6 Her depressive complaints were better explained by appropriate sadness in response to stressors. Several months later with fewer diagnoses and far fewer psychotropics, she is functioning better.
Take-home points
- Polypharmacy can lead to psychiatric symptoms and functional impairment.
- Patients often are unaware of the complete risks of psychotropics.
- Psychiatric symptoms are not always associated with a psychiatric disorder.
- Deprescribing can be performed safely and effectively.
- Deprescribing can be performed with the patient’s informed consent and agreement.
References
1. Psychiatr Serv. 2016 Aug 1;67(8):904-7.
2. Focus. 2016 Apr 13; doi: 10.1176/appi.focus.20150041.
3. Bipolar Disord. 2016 Dec;18(8):684-91.
4. Am J Psychiatry. 2017 Sep 1;174(9):840-9.
5. World Psychiatry. 2009 Jun;8(2):67-74.
6. Hosp Community Psychiatry. 1983 Sep;34(9):830-5.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Among his writings is chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Springer, 2019).
*This column was updated 1/11/2019.
In 2016, Swapnil Gupta, MD, and John Daniel Cahill, MD, PhD, challenged the field of psychiatry to reexamine our prescribing patterns. They warned against our use of polypharmacy when not attached to improvement in functioning for our patients.1 They were concerned about the lack of evidence for those treatment regimens and for our diagnostic criteria. In their inspiring article, they described how psychiatrists might proceed in the process of “deprescribing” – which they define as a process of pharmacologic regimen optimization through reducing or ending medications for which “benefits no longer outweigh risks.”1
In my practice, I routinely confront medication regimens that I have never encountered in the literature. The evidence for two psychotropics is limited but certainly available, in particular adjunct treatment of antidepressants2 and mood stabilizers.3 The evidence supporting the use of more than two psychotropics, however, is quite sparse. Yet, patients often enter my office on more than five psychotropics. I am also confronted with poorly defined diagnostic labels – which present more as means to justify polypharmacy than a thorough review of the patient’s current state.
Dr. Gupta and Dr. Cahill recommend a series of steps aimed at attempting the deprescription of psychotropics. Those steps include timeliness, knowledge of the patient’s current regimen, discussion about the risk of prescriptions, discussion about deprescribing, choosing the right medications to stop, a plan for describing, and monitoring. In the case presented below, I used some of those steps in an effort to provide the best care for the patient. Key details of the case have been changed, including the name, to protect the patient’s confidentiality.
Overview of the case
Rosalie Bertin is a 54-year-old female who has been treated for depression by a variety of primary care physicians for the better part of the last 30 years. She had tried an array of antidepressants, including sertraline, citalopram, duloxetine, and mirtazapine, over that time. Each seemed to provide some benefit when reviewing the notes, but there is no mention of why she was continued on those medications despite the absence of continuing symptoms. Occasionally, Rosalie would present to her clinician tearful and endorsing sadness, though the record did not comment on reports of energy, concentration, sleep, appetite, and interest.
In 2014, Rosalie’s husband passed away from lung cancer. His death was fairly quick, and initially, Rosalie did not mention any significant emotional complaints. However, when visiting her primary care physician 4 months later, she was noted to experience auditory hallucinations. “Sometimes I hear my husband when I am alone in my home,” she said. Rosalie was referred to a psychiatrist with a diagnosis of “psychosis not otherwise specified.”
When discussing her condition with the psychiatrist, Rosalie mentioned experiencing low mood, and having diminished interest in engaging in activities. “I miss Marc when I go places; I used to do everything with him.” She reported hearing him often but only when at her home. He would say things like, “I miss you,” or ask her about her day. She was diagnosed with “major depressive disorder with psychotic features.” Risperidone was added to the escitalopram, buspirone, and gabapentin that had been started by her primary care physician.
After several months of psychotropic management, the dose of risperidone was titrated to 8 mg per day. Her mood symptoms were unchanged, but she now was complaining of poor concentration and memory. The psychiatrist performed a Mini-Mental State Examination (MMSE). It was noted that taking the MMSE engendered significant anxiety for the patient. Rosalie received a score suggesting mild cognitive impairment. She was started on donepezil for the memory complaint, quetiapine for the continued voices, and recommended for disability.
Once on short-term disability, the patient relocated to live closer to her mother in San Diego and subsequently contacted me about continuing psychiatric care.
Initial visit
Rosalie is a petite white woman, raised in the Midwest, who married her high school sweetheart, and subsequently became an administrative assistant. Rosalie and Marc were unable to have children. Marc was an engineer, and a longtime smoker. She describes their lives as simple – “few friends, few vacations, few problems, few regrets.” She states she misses her husband and often cries when thinking about him.
When asked about psychiatric diagnoses, she answered: “I have psychosis. … My doctor said maybe schizophrenia, but he is not sure yet.” She described schizophrenia as hearing voices. Rosalie also mentioned having memory problems: “They cannot tell if it is Alzheimer’s disease until I die and they look at my brain, but the medication should delay the progression.”
She reported no significant effect from her prior antidepressant trials: “I am not sure if or how they helped.” Rosalie could not explain the role of the medication. “I take medications as prescribed by my doctor,” she said.
When discussing her antipsychotics, she mentioned: “Those are strong medications; it is hard for me to stay awake with them.” She declared having had no changes in the voices while on the risperidone but said they went away since also being on the quetiapine: “I wonder if the combination of the two really fixed my brain imbalance.”
Assessment
I admit that I have a critical bias against the overuse of psychotropics, and this might have painted how I interpreted Rosalie’s story. Nonetheless, I was honest with her and told her of my concerns. I informed her that her diagnosis was not consistent with my understanding of mood and thought disorders. Her initial reports of depression neither met the DSM criteria for depression nor felt consistent with my conceptualization of the illness. She had retained appropriate functioning and seemed to be responding with the sadness expected when facing difficult challenges like grief.
Her subsequent reports of auditory hallucinations were not associated with delusions or forms of disorganization that I would expect in someone with a thought disorder. Furthermore, the context of the onset gave me the impression that this was part of her process of grief. Her poor result in the dementia screen was most surprising and inconsistent with my evaluation. I told her that I suspected that she was not suffering from Alzheimer’s but from being overmedicated and from anxiety at the time of the testing.
She was excited and hesitant about my report. She was surprised by the length of our visit and interested in hearing more from me. Strangely, I wished she had challenged my different approach. I think that I was hoping she would question my conceptualization, the way I hoped she would have done with her prior clinicians. Nonetheless, she agreed to make a plan with me.
Treatment plan
We decided to review each of her medications and discuss their benefits and risks over a couple of visits. She was most eager to discontinue the donepezil, which had caused diarrhea. She was concerned when I informed her of the potential side effects of antipsychotics. “My doctor asked me if I had any side effects at each visit; I answered that I felt nothing wrong; I had not realized that side effects could appear later.”
She was adamant about staying on buspirone, as she felt it helped her the most with her anxiety at social events. She voiced concern about discontinuing the antipsychotics despite being unsettled by my review of their risks. She asked that we taper them slowly.
In regard to receiving psychosocial support throughout this period of deprescribing, Rosalie declined weekly psychotherapy. She reported having a good social network in San Diego that she wanted to rely on.
Outcome
I often worry about consequences of stopping a medication, especially when I was not present at the time of its initiation. I agonize that the patient might relapse from my need to carry out my agenda on deprescribing. I try to remind myself that the evidence supports my decision making. The risks of psychotropics often are slow to show up, making the benefit of deprescribing less tangible. However, this case was straightforward.
Rosalie quickly improved. Tapering the antipsychotics was astonishing to her: “I can think clearly again.” Within 6 months, she was on buspirone only – though willing to discuss its discontinuation. She had a lead for a job and was hoping to return to work soon. Rosalie continued to miss her husband but had not heard him in some time. She has not had symptoms of psychosis or depression. Her cognition and mood were intact on my clinical assessment.
Discussion
Sadly and shockingly, cases like that of Rosalie are common. In my practice, I routinely see patients on multiple psychotropics – often on more than one antipsychotic. Their diagnoses are vague and dubious, and include diagnoses such as “unspecified psychosis” and “cognitive impairments.” Clinicians occasionally worry about relapse and promote a narrative that treatment must be not only long term but lifelong.4 There is some evidence for this perspective in a research context, but the clinical world also is filled with patients like Rosalie.
Her reports of auditory hallucinations were better explained by her grief than by a psychotic process.5 Her memory complaints were better explained by anxiety at the time of her testing while suffering from the side effects from her numerous psychotropics.6 Her depressive complaints were better explained by appropriate sadness in response to stressors. Several months later with fewer diagnoses and far fewer psychotropics, she is functioning better.
Take-home points
- Polypharmacy can lead to psychiatric symptoms and functional impairment.
- Patients often are unaware of the complete risks of psychotropics.
- Psychiatric symptoms are not always associated with a psychiatric disorder.
- Deprescribing can be performed safely and effectively.
- Deprescribing can be performed with the patient’s informed consent and agreement.
References
1. Psychiatr Serv. 2016 Aug 1;67(8):904-7.
2. Focus. 2016 Apr 13; doi: 10.1176/appi.focus.20150041.
3. Bipolar Disord. 2016 Dec;18(8):684-91.
4. Am J Psychiatry. 2017 Sep 1;174(9):840-9.
5. World Psychiatry. 2009 Jun;8(2):67-74.
6. Hosp Community Psychiatry. 1983 Sep;34(9):830-5.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Among his writings is chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Springer, 2019).
*This column was updated 1/11/2019.
In 2016, Swapnil Gupta, MD, and John Daniel Cahill, MD, PhD, challenged the field of psychiatry to reexamine our prescribing patterns. They warned against our use of polypharmacy when not attached to improvement in functioning for our patients.1 They were concerned about the lack of evidence for those treatment regimens and for our diagnostic criteria. In their inspiring article, they described how psychiatrists might proceed in the process of “deprescribing” – which they define as a process of pharmacologic regimen optimization through reducing or ending medications for which “benefits no longer outweigh risks.”1
In my practice, I routinely confront medication regimens that I have never encountered in the literature. The evidence for two psychotropics is limited but certainly available, in particular adjunct treatment of antidepressants2 and mood stabilizers.3 The evidence supporting the use of more than two psychotropics, however, is quite sparse. Yet, patients often enter my office on more than five psychotropics. I am also confronted with poorly defined diagnostic labels – which present more as means to justify polypharmacy than a thorough review of the patient’s current state.
Dr. Gupta and Dr. Cahill recommend a series of steps aimed at attempting the deprescription of psychotropics. Those steps include timeliness, knowledge of the patient’s current regimen, discussion about the risk of prescriptions, discussion about deprescribing, choosing the right medications to stop, a plan for describing, and monitoring. In the case presented below, I used some of those steps in an effort to provide the best care for the patient. Key details of the case have been changed, including the name, to protect the patient’s confidentiality.
Overview of the case
Rosalie Bertin is a 54-year-old female who has been treated for depression by a variety of primary care physicians for the better part of the last 30 years. She had tried an array of antidepressants, including sertraline, citalopram, duloxetine, and mirtazapine, over that time. Each seemed to provide some benefit when reviewing the notes, but there is no mention of why she was continued on those medications despite the absence of continuing symptoms. Occasionally, Rosalie would present to her clinician tearful and endorsing sadness, though the record did not comment on reports of energy, concentration, sleep, appetite, and interest.
In 2014, Rosalie’s husband passed away from lung cancer. His death was fairly quick, and initially, Rosalie did not mention any significant emotional complaints. However, when visiting her primary care physician 4 months later, she was noted to experience auditory hallucinations. “Sometimes I hear my husband when I am alone in my home,” she said. Rosalie was referred to a psychiatrist with a diagnosis of “psychosis not otherwise specified.”
When discussing her condition with the psychiatrist, Rosalie mentioned experiencing low mood, and having diminished interest in engaging in activities. “I miss Marc when I go places; I used to do everything with him.” She reported hearing him often but only when at her home. He would say things like, “I miss you,” or ask her about her day. She was diagnosed with “major depressive disorder with psychotic features.” Risperidone was added to the escitalopram, buspirone, and gabapentin that had been started by her primary care physician.
After several months of psychotropic management, the dose of risperidone was titrated to 8 mg per day. Her mood symptoms were unchanged, but she now was complaining of poor concentration and memory. The psychiatrist performed a Mini-Mental State Examination (MMSE). It was noted that taking the MMSE engendered significant anxiety for the patient. Rosalie received a score suggesting mild cognitive impairment. She was started on donepezil for the memory complaint, quetiapine for the continued voices, and recommended for disability.
Once on short-term disability, the patient relocated to live closer to her mother in San Diego and subsequently contacted me about continuing psychiatric care.
Initial visit
Rosalie is a petite white woman, raised in the Midwest, who married her high school sweetheart, and subsequently became an administrative assistant. Rosalie and Marc were unable to have children. Marc was an engineer, and a longtime smoker. She describes their lives as simple – “few friends, few vacations, few problems, few regrets.” She states she misses her husband and often cries when thinking about him.
When asked about psychiatric diagnoses, she answered: “I have psychosis. … My doctor said maybe schizophrenia, but he is not sure yet.” She described schizophrenia as hearing voices. Rosalie also mentioned having memory problems: “They cannot tell if it is Alzheimer’s disease until I die and they look at my brain, but the medication should delay the progression.”
She reported no significant effect from her prior antidepressant trials: “I am not sure if or how they helped.” Rosalie could not explain the role of the medication. “I take medications as prescribed by my doctor,” she said.
When discussing her antipsychotics, she mentioned: “Those are strong medications; it is hard for me to stay awake with them.” She declared having had no changes in the voices while on the risperidone but said they went away since also being on the quetiapine: “I wonder if the combination of the two really fixed my brain imbalance.”
Assessment
I admit that I have a critical bias against the overuse of psychotropics, and this might have painted how I interpreted Rosalie’s story. Nonetheless, I was honest with her and told her of my concerns. I informed her that her diagnosis was not consistent with my understanding of mood and thought disorders. Her initial reports of depression neither met the DSM criteria for depression nor felt consistent with my conceptualization of the illness. She had retained appropriate functioning and seemed to be responding with the sadness expected when facing difficult challenges like grief.
Her subsequent reports of auditory hallucinations were not associated with delusions or forms of disorganization that I would expect in someone with a thought disorder. Furthermore, the context of the onset gave me the impression that this was part of her process of grief. Her poor result in the dementia screen was most surprising and inconsistent with my evaluation. I told her that I suspected that she was not suffering from Alzheimer’s but from being overmedicated and from anxiety at the time of the testing.
She was excited and hesitant about my report. She was surprised by the length of our visit and interested in hearing more from me. Strangely, I wished she had challenged my different approach. I think that I was hoping she would question my conceptualization, the way I hoped she would have done with her prior clinicians. Nonetheless, she agreed to make a plan with me.
Treatment plan
We decided to review each of her medications and discuss their benefits and risks over a couple of visits. She was most eager to discontinue the donepezil, which had caused diarrhea. She was concerned when I informed her of the potential side effects of antipsychotics. “My doctor asked me if I had any side effects at each visit; I answered that I felt nothing wrong; I had not realized that side effects could appear later.”
She was adamant about staying on buspirone, as she felt it helped her the most with her anxiety at social events. She voiced concern about discontinuing the antipsychotics despite being unsettled by my review of their risks. She asked that we taper them slowly.
In regard to receiving psychosocial support throughout this period of deprescribing, Rosalie declined weekly psychotherapy. She reported having a good social network in San Diego that she wanted to rely on.
Outcome
I often worry about consequences of stopping a medication, especially when I was not present at the time of its initiation. I agonize that the patient might relapse from my need to carry out my agenda on deprescribing. I try to remind myself that the evidence supports my decision making. The risks of psychotropics often are slow to show up, making the benefit of deprescribing less tangible. However, this case was straightforward.
Rosalie quickly improved. Tapering the antipsychotics was astonishing to her: “I can think clearly again.” Within 6 months, she was on buspirone only – though willing to discuss its discontinuation. She had a lead for a job and was hoping to return to work soon. Rosalie continued to miss her husband but had not heard him in some time. She has not had symptoms of psychosis or depression. Her cognition and mood were intact on my clinical assessment.
Discussion
Sadly and shockingly, cases like that of Rosalie are common. In my practice, I routinely see patients on multiple psychotropics – often on more than one antipsychotic. Their diagnoses are vague and dubious, and include diagnoses such as “unspecified psychosis” and “cognitive impairments.” Clinicians occasionally worry about relapse and promote a narrative that treatment must be not only long term but lifelong.4 There is some evidence for this perspective in a research context, but the clinical world also is filled with patients like Rosalie.
Her reports of auditory hallucinations were better explained by her grief than by a psychotic process.5 Her memory complaints were better explained by anxiety at the time of her testing while suffering from the side effects from her numerous psychotropics.6 Her depressive complaints were better explained by appropriate sadness in response to stressors. Several months later with fewer diagnoses and far fewer psychotropics, she is functioning better.
Take-home points
- Polypharmacy can lead to psychiatric symptoms and functional impairment.
- Patients often are unaware of the complete risks of psychotropics.
- Psychiatric symptoms are not always associated with a psychiatric disorder.
- Deprescribing can be performed safely and effectively.
- Deprescribing can be performed with the patient’s informed consent and agreement.
References
1. Psychiatr Serv. 2016 Aug 1;67(8):904-7.
2. Focus. 2016 Apr 13; doi: 10.1176/appi.focus.20150041.
3. Bipolar Disord. 2016 Dec;18(8):684-91.
4. Am J Psychiatry. 2017 Sep 1;174(9):840-9.
5. World Psychiatry. 2009 Jun;8(2):67-74.
6. Hosp Community Psychiatry. 1983 Sep;34(9):830-5.
Dr. Badre is a forensic psychiatrist in San Diego and an expert in correctional mental health. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Among his writings is chapter 7 in the new book “Critical Psychiatry: Controversies and Clinical Implications” (Springer, 2019).
*This column was updated 1/11/2019.