Caution about ‘miracle cures’

I thank Drs. Katherine Epstein and Helen Farrell for the balanced approach in their article “‘Miracle cures’ in psychiatry?” (Psychiatry 2.0, Current Psychiatry. September 2019, p. 13-16), which discussed the new psychiatric use of stimulants, dissociative agents, and hallucinogens. (Here I distinguish 3,4-methylenedioxymethamphetamine [MDMA], ketamine, and psilocybin by mechanisms.) The frustration psychiatrists have felt in attempting to get good results from their treatment efforts has long inspired bold new strategies. While Drs. Epstein and Farrell cited the long history of misguided enthusiasms in psychiatric therapeutics, they omitted more recent backfires: bilateral electroconvulsive therapy, cingulotomy, rapid neuroleptization, and the overselling of selective serotonin reuptake inhibitors. Chronic use and long-term adverse effects are usually underestimated at the beginning of new pharmacologies. Now, with an array of new psychoactive substances being introduced as therapies, we must learn from experience (the definition of mental health?) and use caution.

We need to pay serious attention to the small sample sizes and limited criteria for patient selection in trials of ketamine and MDMA, as well as to what sort of “psychotherapy” follows treatment with these agents. Many of us in psychiatric practice for the past 40 years have been humbled by patients’ idiosyncratic reactions to standard medications, let alone novel ones. Those of us who practiced psychiatry in the heyday of “party drugs” have seen many idiosyncratic reactions. Most early research with cannabinoids and lysergic acid diethylamide (and even Strassman’s trials with N,N-dimethyltryptamine [DMT]^1-5) highlighted the significance of response by drug-naïve patients vs drug-savvy individuals. Apart from Veterans Affairs trials for posttraumatic stress disorder, many trials of these drugs for treatment-resistant depression or end-of-life care have attracted non-naïve participants.^6-8 Private use of entheogens is quite different from medicalizing their use. This requires our best scrutiny. Our earnest interest in improving outcomes must not be influenced by the promise of a quick fix, let alone a miracle cure.

Sara Hartley, MD
Clinical Faculty
Interim Head of Admissions
UC Berkley/UCSF Joint Medical Program
Berkeley, California

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

References
1. Strassman RJ. Human psychopharmacology of N,N-dimethyltryptamine. Behav Brain Res. 1996;73(1-2):121-124.
2. Strassman RJ. DMT: the spirit molecule. A doctor’s revolutionary research into the biology of near-death and mystical experiences. Rochester, VT: Park Street Press; 2001.
3. Strassman RJ, Qualls CR. Dose-response study of N,N-dimethyltryptamine in humans. I. Neuroendocrine, autonomic, and cardiovascular effects. Arch Gen Psychiatry. 1994;51(2):85-97.
4. Strassman RJ, Qualls CR, Berg LM. Differential tolerance to biological and subjective effects of four closely spaced doses of N,N-dimethyltryptamine in humans. Biol Psychiatry. 1996;39(9):784-795.
5. Strassman RJ, Qualls CR, Uhlenhuth EH, et al. Dose-response study of N,N-dimethyltryptamine in humans. II. Subjective effects and preliminary results of a new rating scale. Arch Gen Psychiatry. 1994;51(2):98-108.
6. Albott CS, et al. Improvement in suicidal ideation after repeated ketamine infusions: Relationship to reductions in symptoms of posttraumatic stress disorder, depression, and pain. Presented at: The Anxiety and Depression Association of America Annual Conference; Mar. 28-31, 2019; Chicago.
7. Abdallah CG, Sanacora G, Duman RS, et al. Ketamine and rapid-acting antidepressants: a window into a new neurobiology for mood disorder therapeutics. Annu Rev Med. 2015;66:509-523.
8. Mithoefer MC, Mithoefer AT, Feduccia AA, et al. 3,4-Methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for post-traumatic stress disorder in military veterans, firefighters, and police officers: a randomised, double-blind, dose-response, phase 2 clinical trial. Lancet Psychiatry. 2018;5(6):486-497.

Continue to: Physician assistants and the psychiatrist shortage

Physician assistants and the psychiatrist shortage

J. Michael Smith’s article “Physician assistants in psychiatry: Helping to meet America’s mental health needs” (Commentary, Current Psychiatry. September 2019, p. 17-20,24) recommends the use of physician assistants (PAs) to alleviate the shortage of psychiatrists in the United States, but it fails to address the underlying issue. The use of both telepsychiatry as well as psychiatric PAs are inadequate attempts at solving the pressing matter of the psychiatrist shortage. Telepsychiatry was intended to provide care to underserved populations, but it has not succeeded. It is used more frequently in urban settings rather than in needier rural areas. Moreover, the use of PAs in psychiatry has also failed to solve the original problem. Psychiatrists are and should be the backbone of the practice of psychiatry, not PAs.

There needs to be a multifocal approach to incentivize medical students to choose psychiatry as a specialty. Several factors have discouraged medical students from going into psychiatry. The low reimbursement rates by insurance companies force psychiatrists to not accept insurances or to work for hospital or clinic organizations, where they become a part of the “medication management industry.” This scenario was created by the pharmaceutical industry and often leaves psychotherapy to other types of clinicians. In the not-too-distant future, advances in both neuroscience and artificial intelligence technologies will further reduce the role of medically trained psychiatrists, and might lead to them being replaced by other emerging professions (eg, psychiatric PAs) that are concentrated in urban settings where they are most profitable.

What can possibly be left for the future of the medically trained psychiatrist if a PA can diagnose and treat psychiatric patients? Why would we need more psychiatrists?

Marco T. Carpio, MD
Psychiatrist, private practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

The author responds

I appreciate Dr. Carpio’s comments, and I agree that the shortage of psychiatrists will not be addressed solely by the addition of other types of clinicians, such as PAs and nurse practitioners. However, the use of well-trained health care providers such as PAs will go a long way towards helping patients receive timely and appropriate access to care. Unfortunately, no single plan or method will be adequate to solve the shortage of psychiatrists in the United States, but that does not negate the need for utilizing all available options to improve access to quality mental health care. Physician assistants are well-trained to support this endeavor.

J. Michael Smith, DHSc, MPAS, PA-C, CAQ-Psychiatry
Post-Graduate PA Mental Health Residency Training Director
Physician Assistant, ACCESS Clinic, GMHC
Michael E. DeBakey VA Medical Center
Houston, Texas

Continue to: Additional anathemas in psychiatry

While reading Dr. Nasrallah’s “Anathemas of psychiatric practice” (From the Editor, Current Psychiatry. November 2019, p. 13-15), 2 additional anathemas immediately came to mind:

• Cash-only suboxone clinics. Suboxone was never intended to be used in “suboxone clinics”; it was meant to be part of an integrated treatment provided in an office-based practice. Nevertheless, this treatment has been used as such in this country. As part of this trend, an anathema has grown: cash-only suboxone clinics. Patients with severe substance use disorders can be found in every socioeconomic layer of our society, but many struggle with significant psychosocial adversity and outright poverty. Cash-only suboxone clinics put many patients in a bind. Patients spend their last dollars on a needed treatment or sell these medications to maintain their addiction, or even to purchase food.
• “Medical” marijuana. There is no credible evidence based upon methodologically sound research that cannabis has benefit for treating any mental illness. In fact, there is evidence to the contrary.¹ Yet, in many states, physicians—including psychiatrists—are supporting the approval of medical marijuana. I remember taking my Hippocratic Oath when I graduated from medical school, pledging to continue educating myself and my patients about evidenced-based medical science that benefits us all. I have not yet found credible evidence supporting medical marijuana.

Greed in general is a strong anathema in medicine.

Leo Bastiaens, MD
Clinical Associate Professor of Psychiatry
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Reference
1. Radhakrishnan R, Ranganathan M, D'Souza DC. Medical marijuana: what physicians need to know. J Clin Psychiatry. 2019;80(5):45-47.

Caution about ‘miracle cures’

I thank Drs. Katherine Epstein and Helen Farrell for the balanced approach in their article “‘Miracle cures’ in psychiatry?” (Psychiatry 2.0, Current Psychiatry. September 2019, p. 13-16), which discussed the new psychiatric use of stimulants, dissociative agents, and hallucinogens. (Here I distinguish 3,4-methylenedioxymethamphetamine [MDMA], ketamine, and psilocybin by mechanisms.) The frustration psychiatrists have felt in attempting to get good results from their treatment efforts has long inspired bold new strategies. While Drs. Epstein and Farrell cited the long history of misguided enthusiasms in psychiatric therapeutics, they omitted more recent backfires: bilateral electroconvulsive therapy, cingulotomy, rapid neuroleptization, and the overselling of selective serotonin reuptake inhibitors. Chronic use and long-term adverse effects are usually underestimated at the beginning of new pharmacologies. Now, with an array of new psychoactive substances being introduced as therapies, we must learn from experience (the definition of mental health?) and use caution.

We need to pay serious attention to the small sample sizes and limited criteria for patient selection in trials of ketamine and MDMA, as well as to what sort of “psychotherapy” follows treatment with these agents. Many of us in psychiatric practice for the past 40 years have been humbled by patients’ idiosyncratic reactions to standard medications, let alone novel ones. Those of us who practiced psychiatry in the heyday of “party drugs” have seen many idiosyncratic reactions. Most early research with cannabinoids and lysergic acid diethylamide (and even Strassman’s trials with N,N-dimethyltryptamine [DMT]^1-5) highlighted the significance of response by drug-naïve patients vs drug-savvy individuals. Apart from Veterans Affairs trials for posttraumatic stress disorder, many trials of these drugs for treatment-resistant depression or end-of-life care have attracted non-naïve participants.^6-8 Private use of entheogens is quite different from medicalizing their use. This requires our best scrutiny. Our earnest interest in improving outcomes must not be influenced by the promise of a quick fix, let alone a miracle cure.

Sara Hartley, MD
Clinical Faculty
Interim Head of Admissions
UC Berkley/UCSF Joint Medical Program
Berkeley, California

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

References
1. Strassman RJ. Human psychopharmacology of N,N-dimethyltryptamine. Behav Brain Res. 1996;73(1-2):121-124.
2. Strassman RJ. DMT: the spirit molecule. A doctor’s revolutionary research into the biology of near-death and mystical experiences. Rochester, VT: Park Street Press; 2001.
3. Strassman RJ, Qualls CR. Dose-response study of N,N-dimethyltryptamine in humans. I. Neuroendocrine, autonomic, and cardiovascular effects. Arch Gen Psychiatry. 1994;51(2):85-97.
4. Strassman RJ, Qualls CR, Berg LM. Differential tolerance to biological and subjective effects of four closely spaced doses of N,N-dimethyltryptamine in humans. Biol Psychiatry. 1996;39(9):784-795.
5. Strassman RJ, Qualls CR, Uhlenhuth EH, et al. Dose-response study of N,N-dimethyltryptamine in humans. II. Subjective effects and preliminary results of a new rating scale. Arch Gen Psychiatry. 1994;51(2):98-108.
6. Albott CS, et al. Improvement in suicidal ideation after repeated ketamine infusions: Relationship to reductions in symptoms of posttraumatic stress disorder, depression, and pain. Presented at: The Anxiety and Depression Association of America Annual Conference; Mar. 28-31, 2019; Chicago.
7. Abdallah CG, Sanacora G, Duman RS, et al. Ketamine and rapid-acting antidepressants: a window into a new neurobiology for mood disorder therapeutics. Annu Rev Med. 2015;66:509-523.
8. Mithoefer MC, Mithoefer AT, Feduccia AA, et al. 3,4-Methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for post-traumatic stress disorder in military veterans, firefighters, and police officers: a randomised, double-blind, dose-response, phase 2 clinical trial. Lancet Psychiatry. 2018;5(6):486-497.

Continue to: Physician assistants and the psychiatrist shortage

Physician assistants and the psychiatrist shortage

J. Michael Smith’s article “Physician assistants in psychiatry: Helping to meet America’s mental health needs” (Commentary, Current Psychiatry. September 2019, p. 17-20,24) recommends the use of physician assistants (PAs) to alleviate the shortage of psychiatrists in the United States, but it fails to address the underlying issue. The use of both telepsychiatry as well as psychiatric PAs are inadequate attempts at solving the pressing matter of the psychiatrist shortage. Telepsychiatry was intended to provide care to underserved populations, but it has not succeeded. It is used more frequently in urban settings rather than in needier rural areas. Moreover, the use of PAs in psychiatry has also failed to solve the original problem. Psychiatrists are and should be the backbone of the practice of psychiatry, not PAs.

There needs to be a multifocal approach to incentivize medical students to choose psychiatry as a specialty. Several factors have discouraged medical students from going into psychiatry. The low reimbursement rates by insurance companies force psychiatrists to not accept insurances or to work for hospital or clinic organizations, where they become a part of the “medication management industry.” This scenario was created by the pharmaceutical industry and often leaves psychotherapy to other types of clinicians. In the not-too-distant future, advances in both neuroscience and artificial intelligence technologies will further reduce the role of medically trained psychiatrists, and might lead to them being replaced by other emerging professions (eg, psychiatric PAs) that are concentrated in urban settings where they are most profitable.

What can possibly be left for the future of the medically trained psychiatrist if a PA can diagnose and treat psychiatric patients? Why would we need more psychiatrists?

Marco T. Carpio, MD
Psychiatrist, private practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

The author responds

I appreciate Dr. Carpio’s comments, and I agree that the shortage of psychiatrists will not be addressed solely by the addition of other types of clinicians, such as PAs and nurse practitioners. However, the use of well-trained health care providers such as PAs will go a long way towards helping patients receive timely and appropriate access to care. Unfortunately, no single plan or method will be adequate to solve the shortage of psychiatrists in the United States, but that does not negate the need for utilizing all available options to improve access to quality mental health care. Physician assistants are well-trained to support this endeavor.

J. Michael Smith, DHSc, MPAS, PA-C, CAQ-Psychiatry
Post-Graduate PA Mental Health Residency Training Director
Physician Assistant, ACCESS Clinic, GMHC
Michael E. DeBakey VA Medical Center
Houston, Texas

Continue to: Additional anathemas in psychiatry

While reading Dr. Nasrallah’s “Anathemas of psychiatric practice” (From the Editor, Current Psychiatry. November 2019, p. 13-15), 2 additional anathemas immediately came to mind:

• Cash-only suboxone clinics. Suboxone was never intended to be used in “suboxone clinics”; it was meant to be part of an integrated treatment provided in an office-based practice. Nevertheless, this treatment has been used as such in this country. As part of this trend, an anathema has grown: cash-only suboxone clinics. Patients with severe substance use disorders can be found in every socioeconomic layer of our society, but many struggle with significant psychosocial adversity and outright poverty. Cash-only suboxone clinics put many patients in a bind. Patients spend their last dollars on a needed treatment or sell these medications to maintain their addiction, or even to purchase food.
• “Medical” marijuana. There is no credible evidence based upon methodologically sound research that cannabis has benefit for treating any mental illness. In fact, there is evidence to the contrary.¹ Yet, in many states, physicians—including psychiatrists—are supporting the approval of medical marijuana. I remember taking my Hippocratic Oath when I graduated from medical school, pledging to continue educating myself and my patients about evidenced-based medical science that benefits us all. I have not yet found credible evidence supporting medical marijuana.

Greed in general is a strong anathema in medicine.

Leo Bastiaens, MD
Clinical Associate Professor of Psychiatry
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Reference
1. Radhakrishnan R, Ranganathan M, D'Souza DC. Medical marijuana: what physicians need to know. J Clin Psychiatry. 2019;80(5):45-47.

Caution about ‘miracle cures’

I thank Drs. Katherine Epstein and Helen Farrell for the balanced approach in their article “‘Miracle cures’ in psychiatry?” (Psychiatry 2.0, Current Psychiatry. September 2019, p. 13-16), which discussed the new psychiatric use of stimulants, dissociative agents, and hallucinogens. (Here I distinguish 3,4-methylenedioxymethamphetamine [MDMA], ketamine, and psilocybin by mechanisms.) The frustration psychiatrists have felt in attempting to get good results from their treatment efforts has long inspired bold new strategies. While Drs. Epstein and Farrell cited the long history of misguided enthusiasms in psychiatric therapeutics, they omitted more recent backfires: bilateral electroconvulsive therapy, cingulotomy, rapid neuroleptization, and the overselling of selective serotonin reuptake inhibitors. Chronic use and long-term adverse effects are usually underestimated at the beginning of new pharmacologies. Now, with an array of new psychoactive substances being introduced as therapies, we must learn from experience (the definition of mental health?) and use caution.

We need to pay serious attention to the small sample sizes and limited criteria for patient selection in trials of ketamine and MDMA, as well as to what sort of “psychotherapy” follows treatment with these agents. Many of us in psychiatric practice for the past 40 years have been humbled by patients’ idiosyncratic reactions to standard medications, let alone novel ones. Those of us who practiced psychiatry in the heyday of “party drugs” have seen many idiosyncratic reactions. Most early research with cannabinoids and lysergic acid diethylamide (and even Strassman’s trials with N,N-dimethyltryptamine [DMT]^1-5) highlighted the significance of response by drug-naïve patients vs drug-savvy individuals. Apart from Veterans Affairs trials for posttraumatic stress disorder, many trials of these drugs for treatment-resistant depression or end-of-life care have attracted non-naïve participants.^6-8 Private use of entheogens is quite different from medicalizing their use. This requires our best scrutiny. Our earnest interest in improving outcomes must not be influenced by the promise of a quick fix, let alone a miracle cure.

Sara Hartley, MD
Clinical Faculty
Interim Head of Admissions
UC Berkley/UCSF Joint Medical Program
Berkeley, California

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

References
1. Strassman RJ. Human psychopharmacology of N,N-dimethyltryptamine. Behav Brain Res. 1996;73(1-2):121-124.
2. Strassman RJ. DMT: the spirit molecule. A doctor’s revolutionary research into the biology of near-death and mystical experiences. Rochester, VT: Park Street Press; 2001.
3. Strassman RJ, Qualls CR. Dose-response study of N,N-dimethyltryptamine in humans. I. Neuroendocrine, autonomic, and cardiovascular effects. Arch Gen Psychiatry. 1994;51(2):85-97.
4. Strassman RJ, Qualls CR, Berg LM. Differential tolerance to biological and subjective effects of four closely spaced doses of N,N-dimethyltryptamine in humans. Biol Psychiatry. 1996;39(9):784-795.
5. Strassman RJ, Qualls CR, Uhlenhuth EH, et al. Dose-response study of N,N-dimethyltryptamine in humans. II. Subjective effects and preliminary results of a new rating scale. Arch Gen Psychiatry. 1994;51(2):98-108.
6. Albott CS, et al. Improvement in suicidal ideation after repeated ketamine infusions: Relationship to reductions in symptoms of posttraumatic stress disorder, depression, and pain. Presented at: The Anxiety and Depression Association of America Annual Conference; Mar. 28-31, 2019; Chicago.
7. Abdallah CG, Sanacora G, Duman RS, et al. Ketamine and rapid-acting antidepressants: a window into a new neurobiology for mood disorder therapeutics. Annu Rev Med. 2015;66:509-523.
8. Mithoefer MC, Mithoefer AT, Feduccia AA, et al. 3,4-Methylenedioxymethamphetamine (MDMA)-assisted psychotherapy for post-traumatic stress disorder in military veterans, firefighters, and police officers: a randomised, double-blind, dose-response, phase 2 clinical trial. Lancet Psychiatry. 2018;5(6):486-497.

Continue to: Physician assistants and the psychiatrist shortage

Physician assistants and the psychiatrist shortage

J. Michael Smith’s article “Physician assistants in psychiatry: Helping to meet America’s mental health needs” (Commentary, Current Psychiatry. September 2019, p. 17-20,24) recommends the use of physician assistants (PAs) to alleviate the shortage of psychiatrists in the United States, but it fails to address the underlying issue. The use of both telepsychiatry as well as psychiatric PAs are inadequate attempts at solving the pressing matter of the psychiatrist shortage. Telepsychiatry was intended to provide care to underserved populations, but it has not succeeded. It is used more frequently in urban settings rather than in needier rural areas. Moreover, the use of PAs in psychiatry has also failed to solve the original problem. Psychiatrists are and should be the backbone of the practice of psychiatry, not PAs.

There needs to be a multifocal approach to incentivize medical students to choose psychiatry as a specialty. Several factors have discouraged medical students from going into psychiatry. The low reimbursement rates by insurance companies force psychiatrists to not accept insurances or to work for hospital or clinic organizations, where they become a part of the “medication management industry.” This scenario was created by the pharmaceutical industry and often leaves psychotherapy to other types of clinicians. In the not-too-distant future, advances in both neuroscience and artificial intelligence technologies will further reduce the role of medically trained psychiatrists, and might lead to them being replaced by other emerging professions (eg, psychiatric PAs) that are concentrated in urban settings where they are most profitable.

What can possibly be left for the future of the medically trained psychiatrist if a PA can diagnose and treat psychiatric patients? Why would we need more psychiatrists?

Marco T. Carpio, MD
Psychiatrist, private practice
Lynbrook, New York

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

The author responds

I appreciate Dr. Carpio’s comments, and I agree that the shortage of psychiatrists will not be addressed solely by the addition of other types of clinicians, such as PAs and nurse practitioners. However, the use of well-trained health care providers such as PAs will go a long way towards helping patients receive timely and appropriate access to care. Unfortunately, no single plan or method will be adequate to solve the shortage of psychiatrists in the United States, but that does not negate the need for utilizing all available options to improve access to quality mental health care. Physician assistants are well-trained to support this endeavor.

J. Michael Smith, DHSc, MPAS, PA-C, CAQ-Psychiatry
Post-Graduate PA Mental Health Residency Training Director
Physician Assistant, ACCESS Clinic, GMHC
Michael E. DeBakey VA Medical Center
Houston, Texas

Continue to: Additional anathemas in psychiatry

While reading Dr. Nasrallah’s “Anathemas of psychiatric practice” (From the Editor, Current Psychiatry. November 2019, p. 13-15), 2 additional anathemas immediately came to mind:

• Cash-only suboxone clinics. Suboxone was never intended to be used in “suboxone clinics”; it was meant to be part of an integrated treatment provided in an office-based practice. Nevertheless, this treatment has been used as such in this country. As part of this trend, an anathema has grown: cash-only suboxone clinics. Patients with severe substance use disorders can be found in every socioeconomic layer of our society, but many struggle with significant psychosocial adversity and outright poverty. Cash-only suboxone clinics put many patients in a bind. Patients spend their last dollars on a needed treatment or sell these medications to maintain their addiction, or even to purchase food.
• “Medical” marijuana. There is no credible evidence based upon methodologically sound research that cannabis has benefit for treating any mental illness. In fact, there is evidence to the contrary.¹ Yet, in many states, physicians—including psychiatrists—are supporting the approval of medical marijuana. I remember taking my Hippocratic Oath when I graduated from medical school, pledging to continue educating myself and my patients about evidenced-based medical science that benefits us all. I have not yet found credible evidence supporting medical marijuana.

Greed in general is a strong anathema in medicine.

Leo Bastiaens, MD
Clinical Associate Professor of Psychiatry
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania

Disclosure: The author reports no financial relationships with any companies whose products are mentioned in this article, or with manufacturers of competing products.

Reference
1. Radhakrishnan R, Ranganathan M, D'Souza DC. Medical marijuana: what physicians need to know. J Clin Psychiatry. 2019;80(5):45-47.

As a psychiatrist, you could be called to court to testify as a fact witness in a hearing or trial. Your role as a fact witness would differ from that of an expert witness in that you would likely testify about the information that you have gathered through direct observation of patients or others. Fact witnesses are generally not asked to give expert opinions regarding forensic issues, and treating psychiatrists should not do so about their patients. As a fact witness, depending on the form of litigation, you might be in one of the following 4 roles¹:

• Observer. As the term implies, you have observed an event. For example, you are asked to testify about a fight that you witnessed between another clinician’s patient and a nurse while you were making your rounds on an inpatient unit.
• Non-defendant treater. You are the treating psychiatrist for a patient who is involved in litigation to recover damages for injuries sustained from a third party. For example, you are asked to testify about your patient’s premorbid functioning before a claimed injury that spurred the lawsuit.
• Plaintiff. You are suing someone else and may be claiming your own damages. For example, in your attempt to claim damages as a plaintiff, you use your clinical knowledge to testify about your own mental health symptoms and the adverse impact these have had on you.
• Defendant treater. You are being sued by one of your patients. For example, a patient brings a malpractice case against you for allegations of not meeting the standard of care. You testify about your direct observations of the patient, the diagnoses you provided, and your rationale for the implemented treatment plan.

Preparing yourself as a fact witness

For many psychiatrists, testifying can be an intimidating process. Although there are similarities between testifying in a courtroom and giving a deposition, there are also significant differences. For guidelines on providing depositions, see Knoll and Resnick’s “Deposition dos and don’ts: How to answer 8 tricky questions” (Current Psychiatry. March 2008, p. 25-28,36,39-40).² Although not an exhaustive list, we offer the following practical tips for testifying as a fact witness.

Don’t panic. Although your first reaction may be to panic upon receiving a subpoena or court order, you should “keep your cool” and remember that the observations you made or treatment provided have already taken place.¹ Your role as a fact witness is to inform the judge and jury about what you saw and did.¹

Continue to: Refresh your memory and practice

Refresh your memory and practice. Gather all required information (eg, medical records, your notes, etc.) and review it before testifying. This will help you to recall the facts more accurately when you are asked a question. Consider practicing your testimony with the attorney who requested you to get feedback on how you present yourself.¹ However, do not try to memorize what you are going to say because this could make your testimony sound rehearsed and unconvincing.

Plan ahead, and have a pretrial conference. Because court proceedings are unpredictable, you should clear your schedule to allow enough time to appear in court. Before your court appearance, meet with the attorney who requested you to discuss any new facts or issues as well as learn what the attorney aims to accomplish with your testimony.¹

Speak clearly in your own words, and avoid jargon. Courtroom officials are unlikely to understand psychiatric jargon. Therefore, you should explain psychiatric terms in language that laypeople would comprehend. Because the court stenographer will require you to use actual words for the court transcripts, you should answer clearly and verbally or respond with a definitive “yes” or “no” (and not by nodding or shaking your head).

Testimony is also not a time for guessing. If you don’t know the answer, you should say “I don’t know.”

As a psychiatrist, you could be called to court to testify as a fact witness in a hearing or trial. Your role as a fact witness would differ from that of an expert witness in that you would likely testify about the information that you have gathered through direct observation of patients or others. Fact witnesses are generally not asked to give expert opinions regarding forensic issues, and treating psychiatrists should not do so about their patients. As a fact witness, depending on the form of litigation, you might be in one of the following 4 roles¹:

• Observer. As the term implies, you have observed an event. For example, you are asked to testify about a fight that you witnessed between another clinician’s patient and a nurse while you were making your rounds on an inpatient unit.
• Non-defendant treater. You are the treating psychiatrist for a patient who is involved in litigation to recover damages for injuries sustained from a third party. For example, you are asked to testify about your patient’s premorbid functioning before a claimed injury that spurred the lawsuit.
• Plaintiff. You are suing someone else and may be claiming your own damages. For example, in your attempt to claim damages as a plaintiff, you use your clinical knowledge to testify about your own mental health symptoms and the adverse impact these have had on you.
• Defendant treater. You are being sued by one of your patients. For example, a patient brings a malpractice case against you for allegations of not meeting the standard of care. You testify about your direct observations of the patient, the diagnoses you provided, and your rationale for the implemented treatment plan.

Preparing yourself as a fact witness

For many psychiatrists, testifying can be an intimidating process. Although there are similarities between testifying in a courtroom and giving a deposition, there are also significant differences. For guidelines on providing depositions, see Knoll and Resnick’s “Deposition dos and don’ts: How to answer 8 tricky questions” (Current Psychiatry. March 2008, p. 25-28,36,39-40).² Although not an exhaustive list, we offer the following practical tips for testifying as a fact witness.

Don’t panic. Although your first reaction may be to panic upon receiving a subpoena or court order, you should “keep your cool” and remember that the observations you made or treatment provided have already taken place.¹ Your role as a fact witness is to inform the judge and jury about what you saw and did.¹

Continue to: Refresh your memory and practice

Refresh your memory and practice. Gather all required information (eg, medical records, your notes, etc.) and review it before testifying. This will help you to recall the facts more accurately when you are asked a question. Consider practicing your testimony with the attorney who requested you to get feedback on how you present yourself.¹ However, do not try to memorize what you are going to say because this could make your testimony sound rehearsed and unconvincing.

Plan ahead, and have a pretrial conference. Because court proceedings are unpredictable, you should clear your schedule to allow enough time to appear in court. Before your court appearance, meet with the attorney who requested you to discuss any new facts or issues as well as learn what the attorney aims to accomplish with your testimony.¹

Speak clearly in your own words, and avoid jargon. Courtroom officials are unlikely to understand psychiatric jargon. Therefore, you should explain psychiatric terms in language that laypeople would comprehend. Because the court stenographer will require you to use actual words for the court transcripts, you should answer clearly and verbally or respond with a definitive “yes” or “no” (and not by nodding or shaking your head).

Testimony is also not a time for guessing. If you don’t know the answer, you should say “I don’t know.”

As a psychiatrist, you could be called to court to testify as a fact witness in a hearing or trial. Your role as a fact witness would differ from that of an expert witness in that you would likely testify about the information that you have gathered through direct observation of patients or others. Fact witnesses are generally not asked to give expert opinions regarding forensic issues, and treating psychiatrists should not do so about their patients. As a fact witness, depending on the form of litigation, you might be in one of the following 4 roles¹:

• Observer. As the term implies, you have observed an event. For example, you are asked to testify about a fight that you witnessed between another clinician’s patient and a nurse while you were making your rounds on an inpatient unit.
• Non-defendant treater. You are the treating psychiatrist for a patient who is involved in litigation to recover damages for injuries sustained from a third party. For example, you are asked to testify about your patient’s premorbid functioning before a claimed injury that spurred the lawsuit.
• Plaintiff. You are suing someone else and may be claiming your own damages. For example, in your attempt to claim damages as a plaintiff, you use your clinical knowledge to testify about your own mental health symptoms and the adverse impact these have had on you.
• Defendant treater. You are being sued by one of your patients. For example, a patient brings a malpractice case against you for allegations of not meeting the standard of care. You testify about your direct observations of the patient, the diagnoses you provided, and your rationale for the implemented treatment plan.

Preparing yourself as a fact witness

For many psychiatrists, testifying can be an intimidating process. Although there are similarities between testifying in a courtroom and giving a deposition, there are also significant differences. For guidelines on providing depositions, see Knoll and Resnick’s “Deposition dos and don’ts: How to answer 8 tricky questions” (Current Psychiatry. March 2008, p. 25-28,36,39-40).² Although not an exhaustive list, we offer the following practical tips for testifying as a fact witness.

Don’t panic. Although your first reaction may be to panic upon receiving a subpoena or court order, you should “keep your cool” and remember that the observations you made or treatment provided have already taken place.¹ Your role as a fact witness is to inform the judge and jury about what you saw and did.¹

Continue to: Refresh your memory and practice

Refresh your memory and practice. Gather all required information (eg, medical records, your notes, etc.) and review it before testifying. This will help you to recall the facts more accurately when you are asked a question. Consider practicing your testimony with the attorney who requested you to get feedback on how you present yourself.¹ However, do not try to memorize what you are going to say because this could make your testimony sound rehearsed and unconvincing.

Plan ahead, and have a pretrial conference. Because court proceedings are unpredictable, you should clear your schedule to allow enough time to appear in court. Before your court appearance, meet with the attorney who requested you to discuss any new facts or issues as well as learn what the attorney aims to accomplish with your testimony.¹

Speak clearly in your own words, and avoid jargon. Courtroom officials are unlikely to understand psychiatric jargon. Therefore, you should explain psychiatric terms in language that laypeople would comprehend. Because the court stenographer will require you to use actual words for the court transcripts, you should answer clearly and verbally or respond with a definitive “yes” or “no” (and not by nodding or shaking your head).

Testimony is also not a time for guessing. If you don’t know the answer, you should say “I don’t know.”

Since publication of the first Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1952,¹ the diagnosis of manic and hypomanic symptoms has evolved significantly. This evolution has changed my approach to patients who exhibit these symptoms, which include increased goal-directed activity, decreased need for sleep, and racing thoughts. Here I outline these diagnostic changes in each edition of the DSM and discuss their therapeutic importance and the possibility of future changes.

DSM-I (1952) described manic symptoms as having psychotic features.¹ The term “manic episode” was not used, but manic symptoms were described as having a “tendency to remission and recurrence.”¹

DSM-II (1968) introduced the term “manic episode” as having psychotic features.² Manic episodes were characterized by symptoms of excessive elation, irritability, talkativeness, flight of ideas, and accelerated speech and motor activity.²

DSM-III (1980) explained that a manic episode could occur without psychotic features.³ The term “hypomanic episode” was introduced. It described manic features that do not meet criteria for a manic episode.³

DSM-IV (1994) reiterated the criteria for a manic episode.⁴ In addition, it established criteria for a hypomanic episode as lasting at least 4 days and requires ≥3 symptoms.⁴

DSM-5 (2013) describes hypomanic symptoms that do not meet criteria for a hypomanic episode (Table).⁵ These symptoms may require treatment with a mood stabilizer or antipsychotic medication.⁵

Suggested changes for the next DSM

Although DSM-5 does not discuss the duration of different manic or hypomanic symptoms in the same patient, these can vary widely.⁶ The same patient may have increased activity for 2 days, increased irritability for 2 weeks, and racing thoughts every day. Future versions of the DSM could include the varying durations of different manic or hypomanic symptoms in the same patient.

Continue to: Racing thoughts without...

Racing thoughts without increased energy or activity occur frequently and often go unnoticed.⁷ They can be mistaken for severe worrying or obsessive ideation. Depending on the severity of the patient’s racing thoughts, treatment might include a mood stabilizer or antipsychotic. All 5 DSM-5 diagnoses listed in the Table⁵ may include this symptom pattern, but do not specifically mention it. A diagnosis or specifier, such as “racing thoughts without increased energy or activity,” might help clinicians better recognize and treat this symptom pattern.

Since publication of the first Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1952,¹ the diagnosis of manic and hypomanic symptoms has evolved significantly. This evolution has changed my approach to patients who exhibit these symptoms, which include increased goal-directed activity, decreased need for sleep, and racing thoughts. Here I outline these diagnostic changes in each edition of the DSM and discuss their therapeutic importance and the possibility of future changes.

DSM-I (1952) described manic symptoms as having psychotic features.¹ The term “manic episode” was not used, but manic symptoms were described as having a “tendency to remission and recurrence.”¹

DSM-II (1968) introduced the term “manic episode” as having psychotic features.² Manic episodes were characterized by symptoms of excessive elation, irritability, talkativeness, flight of ideas, and accelerated speech and motor activity.²

DSM-III (1980) explained that a manic episode could occur without psychotic features.³ The term “hypomanic episode” was introduced. It described manic features that do not meet criteria for a manic episode.³

DSM-IV (1994) reiterated the criteria for a manic episode.⁴ In addition, it established criteria for a hypomanic episode as lasting at least 4 days and requires ≥3 symptoms.⁴

DSM-5 (2013) describes hypomanic symptoms that do not meet criteria for a hypomanic episode (Table).⁵ These symptoms may require treatment with a mood stabilizer or antipsychotic medication.⁵

Suggested changes for the next DSM

Although DSM-5 does not discuss the duration of different manic or hypomanic symptoms in the same patient, these can vary widely.⁶ The same patient may have increased activity for 2 days, increased irritability for 2 weeks, and racing thoughts every day. Future versions of the DSM could include the varying durations of different manic or hypomanic symptoms in the same patient.

Continue to: Racing thoughts without...

Racing thoughts without increased energy or activity occur frequently and often go unnoticed.⁷ They can be mistaken for severe worrying or obsessive ideation. Depending on the severity of the patient’s racing thoughts, treatment might include a mood stabilizer or antipsychotic. All 5 DSM-5 diagnoses listed in the Table⁵ may include this symptom pattern, but do not specifically mention it. A diagnosis or specifier, such as “racing thoughts without increased energy or activity,” might help clinicians better recognize and treat this symptom pattern.

Since publication of the first Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1952,¹ the diagnosis of manic and hypomanic symptoms has evolved significantly. This evolution has changed my approach to patients who exhibit these symptoms, which include increased goal-directed activity, decreased need for sleep, and racing thoughts. Here I outline these diagnostic changes in each edition of the DSM and discuss their therapeutic importance and the possibility of future changes.

DSM-I (1952) described manic symptoms as having psychotic features.¹ The term “manic episode” was not used, but manic symptoms were described as having a “tendency to remission and recurrence.”¹

DSM-II (1968) introduced the term “manic episode” as having psychotic features.² Manic episodes were characterized by symptoms of excessive elation, irritability, talkativeness, flight of ideas, and accelerated speech and motor activity.²

DSM-III (1980) explained that a manic episode could occur without psychotic features.³ The term “hypomanic episode” was introduced. It described manic features that do not meet criteria for a manic episode.³

DSM-IV (1994) reiterated the criteria for a manic episode.⁴ In addition, it established criteria for a hypomanic episode as lasting at least 4 days and requires ≥3 symptoms.⁴

DSM-5 (2013) describes hypomanic symptoms that do not meet criteria for a hypomanic episode (Table).⁵ These symptoms may require treatment with a mood stabilizer or antipsychotic medication.⁵

Suggested changes for the next DSM

Although DSM-5 does not discuss the duration of different manic or hypomanic symptoms in the same patient, these can vary widely.⁶ The same patient may have increased activity for 2 days, increased irritability for 2 weeks, and racing thoughts every day. Future versions of the DSM could include the varying durations of different manic or hypomanic symptoms in the same patient.

Continue to: Racing thoughts without...

Racing thoughts without increased energy or activity occur frequently and often go unnoticed.⁷ They can be mistaken for severe worrying or obsessive ideation. Depending on the severity of the patient’s racing thoughts, treatment might include a mood stabilizer or antipsychotic. All 5 DSM-5 diagnoses listed in the Table⁵ may include this symptom pattern, but do not specifically mention it. A diagnosis or specifier, such as “racing thoughts without increased energy or activity,” might help clinicians better recognize and treat this symptom pattern.

I know that many have already started the planning process for next year’s business priorities and therefore I remain hopeful that time was taken to reflect on the success stories already achieved to provide the foundation for next year’s business goals.

What is key, is that one recognizes that the planning process must begin this year to kickstart next year’s work soon after the holidays are over. This planning process should lay out the framework from which to assign the work so it’s part of the business operations wherein goals can be established and ultimately achieved.

As we move into a new decade the evolution of medicine and specifically gastroenterology hasn’t stopped. The question is, have you set yourself (and your practice) up for success in 2020? In the ever-changing world of the gastroenterology practice you don’t want to be left behind this year. Here are the top things you need to know for a productive and successful new year!
 

1. Use the new Medicare Beneficiary Identifier (MBI). Starting January 1, 2020, if you want to get paid by Medicare you must use the MBI when billing Medicare regardless of the date of service. Claims submitted without MBIs will be rejected, with some exceptions. The MBI replaces the social security number–based Health Insurance Claim Numbers (HICNs) from Medicare cards and is now used for Medicare transactions like billing, eligibility status, and claim status.

2. Prepare for Evaluation and Management (E/M) changes. Did you know that E/M coding and guidelines are about to undergo the most significant changes since their implementation? The changes to guidelines and coding for new and established office/outpatient visits (CPT codes 99202-99205, 99211-99215) won’t officially take place until January 1, 2021, but they are so significant that the American Medical Association has already released a preview of the CPT 2021 changes. Don’t miss out on the preview – https://www.ama-assn.org/system/files/2019-06/cpt-office-prolonged-svs-code-changes.pdf. Sit down with your coders or contact your medical billing company and create a plan for training physicians and staff for the changes for a smooth transition on Jan. 1, 2021. With changes this big, you may find you need all of 2020 to prepare.

3. Review your quality reporting under the Merit-Based Incentive System (MIPS). There have been several changes to the weights of quality and cost performance categories under MIPS for the 2020 performance year. These will go into effect January 1st and will impact your 2022 Medicare payments.

4. Evaluate your clinician participation level if you’re reporting under MIPS as a group. During the 2020 performance year, the threshold for clinician participation is increasing. At least 50% of clinicians from the group must participate in or perform an activity for the same continuous 90-day period to earn credit for that improvement activity.

5. Don’t forget to report under MIPS for 2019. Those not in an Advanced Alternative Payment Model (APM), a Medicare Accountable Care Organization (ACO) or other MIPS alternative must report the required data under the program or face payment cuts in 2021. The submission window for your 2019 data opens on January 2, 2020 and closes on March 31st!

January 2020
January 1 - MIPS Performance Year 2019 Begins 
January 2 - Submission Window Opens for MIPS Performance Year 2019

March 2020
March 31 - Submission Window Closes for MIPS Performance Year 2019

July 2020
 • CMS publishes proposed reimbursement values for the E/M codes in the 2021 MPFS proposed rule
• CMS “Targeted Review” opens once CMS makes your MIPS payment adjustment available
• July 1 - MIPS Performance Feedback Available. CMS will provide you with performance feedback based on the data you submitted for Performance Year 2019. You can use this feedback to improve your care and optimize the payments you receive from CMS.

August 2020
August 31 - Targeted Review period closes (appeals process)
 

September 2020
AMA releases CPT 2021 book with new E/M coding guidelines and new coding for new patient office/outpatient visits (99202-99205)

October 2020
October 1, 2020 – Final day to start QPP activities to meet 90-day minimum.

November 2020
CMS finalizes reimbursement values for the E/M codes in the MPFS final rule

December 2020
December 31, 2020 - Quality Payment Program Exception Applications Window Closes
December 31, 2020 – MIPS Performance year 2020 ends

Stress to your team that proper planning is the norm and not the exception, and that seeking improvement in all facets of your medical practice is critical to achieving long-term success. Be sure to write your plans in the future tense and to include timelines in your final work product, as well as delegate accountability to accomplish those goals.

Use the planning process as an opportunity to build your team so that everyone is focused on the future and stress that their participation is important to achieve the success required to remain an independent medical group.
 

Mr. Turner is chief executive officer, Indianapolis Gastroenterology and Hepatology, Indianapolis. [email protected]

I know that many have already started the planning process for next year’s business priorities and therefore I remain hopeful that time was taken to reflect on the success stories already achieved to provide the foundation for next year’s business goals.

What is key, is that one recognizes that the planning process must begin this year to kickstart next year’s work soon after the holidays are over. This planning process should lay out the framework from which to assign the work so it’s part of the business operations wherein goals can be established and ultimately achieved.

As we move into a new decade the evolution of medicine and specifically gastroenterology hasn’t stopped. The question is, have you set yourself (and your practice) up for success in 2020? In the ever-changing world of the gastroenterology practice you don’t want to be left behind this year. Here are the top things you need to know for a productive and successful new year!
 

1. Use the new Medicare Beneficiary Identifier (MBI). Starting January 1, 2020, if you want to get paid by Medicare you must use the MBI when billing Medicare regardless of the date of service. Claims submitted without MBIs will be rejected, with some exceptions. The MBI replaces the social security number–based Health Insurance Claim Numbers (HICNs) from Medicare cards and is now used for Medicare transactions like billing, eligibility status, and claim status.

2. Prepare for Evaluation and Management (E/M) changes. Did you know that E/M coding and guidelines are about to undergo the most significant changes since their implementation? The changes to guidelines and coding for new and established office/outpatient visits (CPT codes 99202-99205, 99211-99215) won’t officially take place until January 1, 2021, but they are so significant that the American Medical Association has already released a preview of the CPT 2021 changes. Don’t miss out on the preview – https://www.ama-assn.org/system/files/2019-06/cpt-office-prolonged-svs-code-changes.pdf. Sit down with your coders or contact your medical billing company and create a plan for training physicians and staff for the changes for a smooth transition on Jan. 1, 2021. With changes this big, you may find you need all of 2020 to prepare.

3. Review your quality reporting under the Merit-Based Incentive System (MIPS). There have been several changes to the weights of quality and cost performance categories under MIPS for the 2020 performance year. These will go into effect January 1st and will impact your 2022 Medicare payments.

4. Evaluate your clinician participation level if you’re reporting under MIPS as a group. During the 2020 performance year, the threshold for clinician participation is increasing. At least 50% of clinicians from the group must participate in or perform an activity for the same continuous 90-day period to earn credit for that improvement activity.

5. Don’t forget to report under MIPS for 2019. Those not in an Advanced Alternative Payment Model (APM), a Medicare Accountable Care Organization (ACO) or other MIPS alternative must report the required data under the program or face payment cuts in 2021. The submission window for your 2019 data opens on January 2, 2020 and closes on March 31st!

January 2020
January 1 - MIPS Performance Year 2019 Begins 
January 2 - Submission Window Opens for MIPS Performance Year 2019

March 2020
March 31 - Submission Window Closes for MIPS Performance Year 2019

July 2020
 • CMS publishes proposed reimbursement values for the E/M codes in the 2021 MPFS proposed rule
• CMS “Targeted Review” opens once CMS makes your MIPS payment adjustment available
• July 1 - MIPS Performance Feedback Available. CMS will provide you with performance feedback based on the data you submitted for Performance Year 2019. You can use this feedback to improve your care and optimize the payments you receive from CMS.

August 2020
August 31 - Targeted Review period closes (appeals process)
 

September 2020
AMA releases CPT 2021 book with new E/M coding guidelines and new coding for new patient office/outpatient visits (99202-99205)

October 2020
October 1, 2020 – Final day to start QPP activities to meet 90-day minimum.

November 2020
CMS finalizes reimbursement values for the E/M codes in the MPFS final rule

December 2020
December 31, 2020 - Quality Payment Program Exception Applications Window Closes
December 31, 2020 – MIPS Performance year 2020 ends

Stress to your team that proper planning is the norm and not the exception, and that seeking improvement in all facets of your medical practice is critical to achieving long-term success. Be sure to write your plans in the future tense and to include timelines in your final work product, as well as delegate accountability to accomplish those goals.

Use the planning process as an opportunity to build your team so that everyone is focused on the future and stress that their participation is important to achieve the success required to remain an independent medical group.
 

Mr. Turner is chief executive officer, Indianapolis Gastroenterology and Hepatology, Indianapolis. [email protected]

I know that many have already started the planning process for next year’s business priorities and therefore I remain hopeful that time was taken to reflect on the success stories already achieved to provide the foundation for next year’s business goals.

What is key, is that one recognizes that the planning process must begin this year to kickstart next year’s work soon after the holidays are over. This planning process should lay out the framework from which to assign the work so it’s part of the business operations wherein goals can be established and ultimately achieved.

As we move into a new decade the evolution of medicine and specifically gastroenterology hasn’t stopped. The question is, have you set yourself (and your practice) up for success in 2020? In the ever-changing world of the gastroenterology practice you don’t want to be left behind this year. Here are the top things you need to know for a productive and successful new year!
 

1. Use the new Medicare Beneficiary Identifier (MBI). Starting January 1, 2020, if you want to get paid by Medicare you must use the MBI when billing Medicare regardless of the date of service. Claims submitted without MBIs will be rejected, with some exceptions. The MBI replaces the social security number–based Health Insurance Claim Numbers (HICNs) from Medicare cards and is now used for Medicare transactions like billing, eligibility status, and claim status.

2. Prepare for Evaluation and Management (E/M) changes. Did you know that E/M coding and guidelines are about to undergo the most significant changes since their implementation? The changes to guidelines and coding for new and established office/outpatient visits (CPT codes 99202-99205, 99211-99215) won’t officially take place until January 1, 2021, but they are so significant that the American Medical Association has already released a preview of the CPT 2021 changes. Don’t miss out on the preview – https://www.ama-assn.org/system/files/2019-06/cpt-office-prolonged-svs-code-changes.pdf. Sit down with your coders or contact your medical billing company and create a plan for training physicians and staff for the changes for a smooth transition on Jan. 1, 2021. With changes this big, you may find you need all of 2020 to prepare.

3. Review your quality reporting under the Merit-Based Incentive System (MIPS). There have been several changes to the weights of quality and cost performance categories under MIPS for the 2020 performance year. These will go into effect January 1st and will impact your 2022 Medicare payments.

4. Evaluate your clinician participation level if you’re reporting under MIPS as a group. During the 2020 performance year, the threshold for clinician participation is increasing. At least 50% of clinicians from the group must participate in or perform an activity for the same continuous 90-day period to earn credit for that improvement activity.

5. Don’t forget to report under MIPS for 2019. Those not in an Advanced Alternative Payment Model (APM), a Medicare Accountable Care Organization (ACO) or other MIPS alternative must report the required data under the program or face payment cuts in 2021. The submission window for your 2019 data opens on January 2, 2020 and closes on March 31st!

January 2020
January 1 - MIPS Performance Year 2019 Begins 
January 2 - Submission Window Opens for MIPS Performance Year 2019

March 2020
March 31 - Submission Window Closes for MIPS Performance Year 2019

July 2020
 • CMS publishes proposed reimbursement values for the E/M codes in the 2021 MPFS proposed rule
• CMS “Targeted Review” opens once CMS makes your MIPS payment adjustment available
• July 1 - MIPS Performance Feedback Available. CMS will provide you with performance feedback based on the data you submitted for Performance Year 2019. You can use this feedback to improve your care and optimize the payments you receive from CMS.

August 2020
August 31 - Targeted Review period closes (appeals process)
 

September 2020
AMA releases CPT 2021 book with new E/M coding guidelines and new coding for new patient office/outpatient visits (99202-99205)

October 2020
October 1, 2020 – Final day to start QPP activities to meet 90-day minimum.

November 2020
CMS finalizes reimbursement values for the E/M codes in the MPFS final rule

December 2020
December 31, 2020 - Quality Payment Program Exception Applications Window Closes
December 31, 2020 – MIPS Performance year 2020 ends

Stress to your team that proper planning is the norm and not the exception, and that seeking improvement in all facets of your medical practice is critical to achieving long-term success. Be sure to write your plans in the future tense and to include timelines in your final work product, as well as delegate accountability to accomplish those goals.

Use the planning process as an opportunity to build your team so that everyone is focused on the future and stress that their participation is important to achieve the success required to remain an independent medical group.
 

Mr. Turner is chief executive officer, Indianapolis Gastroenterology and Hepatology, Indianapolis. [email protected]

Opioid use disorder (OUD) and deaths by opioid overdose are a major public health concern, especially with the advent of synthetic opioids such as fentanyl.¹ Enrolling patients with OUD into substance abuse treatment programs can be a difficult hurdle to cross because patients do not want to experience withdrawal. The fear of withdrawal leads many individuals to refuse appropriate interventions. For these patients, consider the alpha-2 agonist lofexidine, which was FDA-approved in 2018 to help diminish the signs and symptoms of opioid withdrawal.^1-3 Use of lofexidine might encourage more patients with OUD to accept substance abuse treatment.^1,4,5

How to prescribe lofexidine

For decades, clinicians in Britain have prescribed lofexidine to attenuate opioid withdrawal.¹An analog of clonidine, lofexidine is reportedly less likely than clonidine to induce hypotension.^1,4 While this agent does not diminish drug toxicity, it can provide symptomatic relief for patients undergoing opioid withdrawal, and is efficacious as a supplement to and/or replacement for methadone, buprenorphine, clonidine, or other symptomatic pharmacotherapies.^1,4,5

Lofexidine is available in 0.18-mg tablets. For patients experiencing overt symptoms of opioid withdrawal, initially prescribe 3 0.18-mg tablets, 4 times a day.³ The recommended maximum dosage is 2.88 mg/d, and each dose generally should not exceed 0.72 mg/d. Lofexidine may be continued for up to 14 days, with dosing guided by symptoms. Initiate a taper once the patient no longer experiences withdrawal symptoms.³

Adverse effects. Lofexidine’s efficacy and safety were evaluated in 3 randomized, double-blind, placebo-controlled trials that included 935 participants dependent on short-acting opioids who were experiencing abrupt opioid withdrawal and received lofexidine, 2.16 or 2.88 mg/d, or placebo.³ The most common adverse effects of lofexidine were insomnia, orthostatic hypotension, bradycardia, hypotension, dizziness, somnolence, sedation, and dry mouth.³ In the 3 trials, these effects were reported by ≥10% of patients receiving lofexidine, and occurred more frequently compared with placebo (Table³).

Take precautions when prescribing lofexidine because it can cause QT prolongation and CNS depression, especially when co-administered with sedative agents.³ It also can result in rebound hypertension once discontinued. This may be minimized by gradually reducing the dosage.³

A pathway to OUD treatment

Lofexidine can help relieve symptoms of opioid withdrawal, such as stomach cramps, muscle spasms or twitching, feeling cold, muscular tension, and aches and pains.^1-5 This new option might help clinicians encourage more patients with OUD to fully engage in substance abuse treatment.

Opioid use disorder (OUD) and deaths by opioid overdose are a major public health concern, especially with the advent of synthetic opioids such as fentanyl.¹ Enrolling patients with OUD into substance abuse treatment programs can be a difficult hurdle to cross because patients do not want to experience withdrawal. The fear of withdrawal leads many individuals to refuse appropriate interventions. For these patients, consider the alpha-2 agonist lofexidine, which was FDA-approved in 2018 to help diminish the signs and symptoms of opioid withdrawal.^1-3 Use of lofexidine might encourage more patients with OUD to accept substance abuse treatment.^1,4,5

How to prescribe lofexidine

For decades, clinicians in Britain have prescribed lofexidine to attenuate opioid withdrawal.¹An analog of clonidine, lofexidine is reportedly less likely than clonidine to induce hypotension.^1,4 While this agent does not diminish drug toxicity, it can provide symptomatic relief for patients undergoing opioid withdrawal, and is efficacious as a supplement to and/or replacement for methadone, buprenorphine, clonidine, or other symptomatic pharmacotherapies.^1,4,5

Lofexidine is available in 0.18-mg tablets. For patients experiencing overt symptoms of opioid withdrawal, initially prescribe 3 0.18-mg tablets, 4 times a day.³ The recommended maximum dosage is 2.88 mg/d, and each dose generally should not exceed 0.72 mg/d. Lofexidine may be continued for up to 14 days, with dosing guided by symptoms. Initiate a taper once the patient no longer experiences withdrawal symptoms.³

Adverse effects. Lofexidine’s efficacy and safety were evaluated in 3 randomized, double-blind, placebo-controlled trials that included 935 participants dependent on short-acting opioids who were experiencing abrupt opioid withdrawal and received lofexidine, 2.16 or 2.88 mg/d, or placebo.³ The most common adverse effects of lofexidine were insomnia, orthostatic hypotension, bradycardia, hypotension, dizziness, somnolence, sedation, and dry mouth.³ In the 3 trials, these effects were reported by ≥10% of patients receiving lofexidine, and occurred more frequently compared with placebo (Table³).

Take precautions when prescribing lofexidine because it can cause QT prolongation and CNS depression, especially when co-administered with sedative agents.³ It also can result in rebound hypertension once discontinued. This may be minimized by gradually reducing the dosage.³

A pathway to OUD treatment

Lofexidine can help relieve symptoms of opioid withdrawal, such as stomach cramps, muscle spasms or twitching, feeling cold, muscular tension, and aches and pains.^1-5 This new option might help clinicians encourage more patients with OUD to fully engage in substance abuse treatment.

Opioid use disorder (OUD) and deaths by opioid overdose are a major public health concern, especially with the advent of synthetic opioids such as fentanyl.¹ Enrolling patients with OUD into substance abuse treatment programs can be a difficult hurdle to cross because patients do not want to experience withdrawal. The fear of withdrawal leads many individuals to refuse appropriate interventions. For these patients, consider the alpha-2 agonist lofexidine, which was FDA-approved in 2018 to help diminish the signs and symptoms of opioid withdrawal.^1-3 Use of lofexidine might encourage more patients with OUD to accept substance abuse treatment.^1,4,5

How to prescribe lofexidine

For decades, clinicians in Britain have prescribed lofexidine to attenuate opioid withdrawal.¹An analog of clonidine, lofexidine is reportedly less likely than clonidine to induce hypotension.^1,4 While this agent does not diminish drug toxicity, it can provide symptomatic relief for patients undergoing opioid withdrawal, and is efficacious as a supplement to and/or replacement for methadone, buprenorphine, clonidine, or other symptomatic pharmacotherapies.^1,4,5

Lofexidine is available in 0.18-mg tablets. For patients experiencing overt symptoms of opioid withdrawal, initially prescribe 3 0.18-mg tablets, 4 times a day.³ The recommended maximum dosage is 2.88 mg/d, and each dose generally should not exceed 0.72 mg/d. Lofexidine may be continued for up to 14 days, with dosing guided by symptoms. Initiate a taper once the patient no longer experiences withdrawal symptoms.³

Adverse effects. Lofexidine’s efficacy and safety were evaluated in 3 randomized, double-blind, placebo-controlled trials that included 935 participants dependent on short-acting opioids who were experiencing abrupt opioid withdrawal and received lofexidine, 2.16 or 2.88 mg/d, or placebo.³ The most common adverse effects of lofexidine were insomnia, orthostatic hypotension, bradycardia, hypotension, dizziness, somnolence, sedation, and dry mouth.³ In the 3 trials, these effects were reported by ≥10% of patients receiving lofexidine, and occurred more frequently compared with placebo (Table³).

Take precautions when prescribing lofexidine because it can cause QT prolongation and CNS depression, especially when co-administered with sedative agents.³ It also can result in rebound hypertension once discontinued. This may be minimized by gradually reducing the dosage.³

A pathway to OUD treatment

Lofexidine can help relieve symptoms of opioid withdrawal, such as stomach cramps, muscle spasms or twitching, feeling cold, muscular tension, and aches and pains.^1-5 This new option might help clinicians encourage more patients with OUD to fully engage in substance abuse treatment.

A significant unmet need exists for users of acute medications for the treatment of migraine attacks. These medications can be ineffective or associated with undesirable side effects. However, a novel unique therapy, ubrogepant, has demonstrated efficacy for the acute treatment of migraine.

Click here to read this supplement. 

Patient Handout:

Click here to access and print a guide for your patients on understanding and treating migraine attacks. 

Supplementary Podcasts:

General Migraine Background

1. Treatment Patterns and Unmet Needs in the Acute Treatment of Migraine

2. Pharmacology and Pharmacokinetics of Ubrogepant: A Potent, Selective Calcitonin Gene-Related Peptide Receptor Antagonist for the Acute Treatment of Migraine

3. Clinical Efficacy and Safety of Ubrogepant for the Acute Treatment of Migraine

Podcast References

 ^{1. Burch R, Rizzoli P, Loder E. The prevalence and impact of migraine and severe headache in the United States: figures and trends from government health studies. Headache. 2018;58(4):496-505.}

^{2. GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1789-858.}

^{3. Evers S, Marziniak M. Clinical features, pathophysiology, and treatment of medication-overuse headache. Lancet Neurol. 2010;9(4):391-401.}

 ^{4. Ahmed F. Headache disorders: differentiating and managing the common subtypes. Br J Pain. 2012;6(3):124-32.}  

^{5. Minen M, Shome A, Halpern A, Tishler L, Brennan KC, Loder E, et al. A migraine management training program for primary care providers: An overview of a survey and pilot study findings, lessons learned, and considerations for further research. Headache. 2016;56(4):725-40.}

^{6. Becker WJ. Acute migraine treatment in adults. Headache. 2015;55(6):778-93.}

^{7. Marmura MJ, Silberstein SD, Schwedt TJ. The acute treatment of migraine in adults: the American Headache Society evidence assessment of migraine pharmacotherapies. Headache. 2015;55(1):3-20.}

^{8. Bigal ME, Lipton RB. Excessive acute migraine medication use and migraine progression. Neurology. 2008;71(22):1821-8.}

^{9. Messali AJ, Yang M, Gillard P, Tsai K, Tepper SJ, Bloudek LM, et al. Treatment persistence and switching in triptan users: a systematic literature review. Headache. 2014;54(7):1120-30.}

^{10. Katic BJ, Rajagopalan S, Ho TW, Chen YT, Hu XH. Triptan persistency among newly initiated users in a pharmacy claims database. Cephalalgia. 2011;31(4):488-500.}

^{11. Iyengar S, Ossipov MH, Johnson KW. The role of calcitonin gene-related peptide in peripheral and central pain mechanisms including migraine. Pain. 2017;158(4):543-59.}  

^{12. Ho TW, Edvinsson L, Goadsby PJ. CGRP and its receptors provide new insights into migraine pathophysiology. Nat Rev Neurol. 2010;6(10):573-82.}

A significant unmet need exists for users of acute medications for the treatment of migraine attacks. These medications can be ineffective or associated with undesirable side effects. However, a novel unique therapy, ubrogepant, has demonstrated efficacy for the acute treatment of migraine.

Click here to read this supplement. 

Patient Handout:

Click here to access and print a guide for your patients on understanding and treating migraine attacks. 

Supplementary Podcasts:

General Migraine Background

1. Treatment Patterns and Unmet Needs in the Acute Treatment of Migraine

2. Pharmacology and Pharmacokinetics of Ubrogepant: A Potent, Selective Calcitonin Gene-Related Peptide Receptor Antagonist for the Acute Treatment of Migraine

3. Clinical Efficacy and Safety of Ubrogepant for the Acute Treatment of Migraine

Podcast References

 ^{1. Burch R, Rizzoli P, Loder E. The prevalence and impact of migraine and severe headache in the United States: figures and trends from government health studies. Headache. 2018;58(4):496-505.}

^{2. GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1789-858.}

^{3. Evers S, Marziniak M. Clinical features, pathophysiology, and treatment of medication-overuse headache. Lancet Neurol. 2010;9(4):391-401.}

 ^{4. Ahmed F. Headache disorders: differentiating and managing the common subtypes. Br J Pain. 2012;6(3):124-32.}  

^{5. Minen M, Shome A, Halpern A, Tishler L, Brennan KC, Loder E, et al. A migraine management training program for primary care providers: An overview of a survey and pilot study findings, lessons learned, and considerations for further research. Headache. 2016;56(4):725-40.}

^{6. Becker WJ. Acute migraine treatment in adults. Headache. 2015;55(6):778-93.}

^{7. Marmura MJ, Silberstein SD, Schwedt TJ. The acute treatment of migraine in adults: the American Headache Society evidence assessment of migraine pharmacotherapies. Headache. 2015;55(1):3-20.}

^{8. Bigal ME, Lipton RB. Excessive acute migraine medication use and migraine progression. Neurology. 2008;71(22):1821-8.}

^{9. Messali AJ, Yang M, Gillard P, Tsai K, Tepper SJ, Bloudek LM, et al. Treatment persistence and switching in triptan users: a systematic literature review. Headache. 2014;54(7):1120-30.}

^{10. Katic BJ, Rajagopalan S, Ho TW, Chen YT, Hu XH. Triptan persistency among newly initiated users in a pharmacy claims database. Cephalalgia. 2011;31(4):488-500.}

^{11. Iyengar S, Ossipov MH, Johnson KW. The role of calcitonin gene-related peptide in peripheral and central pain mechanisms including migraine. Pain. 2017;158(4):543-59.}  

^{12. Ho TW, Edvinsson L, Goadsby PJ. CGRP and its receptors provide new insights into migraine pathophysiology. Nat Rev Neurol. 2010;6(10):573-82.}

A significant unmet need exists for users of acute medications for the treatment of migraine attacks. These medications can be ineffective or associated with undesirable side effects. However, a novel unique therapy, ubrogepant, has demonstrated efficacy for the acute treatment of migraine.

Click here to read this supplement. 

Patient Handout:

Click here to access and print a guide for your patients on understanding and treating migraine attacks. 

Supplementary Podcasts:

General Migraine Background

1. Treatment Patterns and Unmet Needs in the Acute Treatment of Migraine

2. Pharmacology and Pharmacokinetics of Ubrogepant: A Potent, Selective Calcitonin Gene-Related Peptide Receptor Antagonist for the Acute Treatment of Migraine

3. Clinical Efficacy and Safety of Ubrogepant for the Acute Treatment of Migraine

Podcast References

 ^{1. Burch R, Rizzoli P, Loder E. The prevalence and impact of migraine and severe headache in the United States: figures and trends from government health studies. Headache. 2018;58(4):496-505.}

^{2. GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1789-858.}

^{3. Evers S, Marziniak M. Clinical features, pathophysiology, and treatment of medication-overuse headache. Lancet Neurol. 2010;9(4):391-401.}

 ^{4. Ahmed F. Headache disorders: differentiating and managing the common subtypes. Br J Pain. 2012;6(3):124-32.}  

^{5. Minen M, Shome A, Halpern A, Tishler L, Brennan KC, Loder E, et al. A migraine management training program for primary care providers: An overview of a survey and pilot study findings, lessons learned, and considerations for further research. Headache. 2016;56(4):725-40.}

^{6. Becker WJ. Acute migraine treatment in adults. Headache. 2015;55(6):778-93.}

^{7. Marmura MJ, Silberstein SD, Schwedt TJ. The acute treatment of migraine in adults: the American Headache Society evidence assessment of migraine pharmacotherapies. Headache. 2015;55(1):3-20.}

^{8. Bigal ME, Lipton RB. Excessive acute migraine medication use and migraine progression. Neurology. 2008;71(22):1821-8.}

^{9. Messali AJ, Yang M, Gillard P, Tsai K, Tepper SJ, Bloudek LM, et al. Treatment persistence and switching in triptan users: a systematic literature review. Headache. 2014;54(7):1120-30.}

^{10. Katic BJ, Rajagopalan S, Ho TW, Chen YT, Hu XH. Triptan persistency among newly initiated users in a pharmacy claims database. Cephalalgia. 2011;31(4):488-500.}

^{11. Iyengar S, Ossipov MH, Johnson KW. The role of calcitonin gene-related peptide in peripheral and central pain mechanisms including migraine. Pain. 2017;158(4):543-59.}  

^{12. Ho TW, Edvinsson L, Goadsby PJ. CGRP and its receptors provide new insights into migraine pathophysiology. Nat Rev Neurol. 2010;6(10):573-82.}

CASE Bipolar-like symptoms

Mr. R, age 48, presents to the psychiatric emergency department (ED) for the third time in 4 days after a change in his behavior over the last 2.5 weeks. He exhibits heightened extroversion, pressured speech, and uncharacteristic irritability. Mr. R’s wife reports that her husband normally is reserved.

Mr. R’s wife first became concerned when she noticed he was not sleeping and spending his nights changing the locks on their home. Mr. R, who is a business executive, occupied his time by taking notes on ways to protect his identity from the senior partners at his company.

Three weeks before his first ED visit, Mr. R had been treated for a neck abscess with incision and drainage. He was sent home with a 10-day course of amoxicillin/clavulanate, 875/125 mg by mouth twice daily. There were no reports of steroid use during or after the procedure. Four days after starting the antibiotic, he stopped taking it because he and his wife felt it was contributing to his mood changes and bizarre behavior.

During his first visit to the ED, Mr. R received a 1-time dose of olanzapine, 5 mg by mouth, which helped temporarily reduce his anxiety; however, he returned the following day with the same anxiety symptoms and was discharged with a 30-day prescription for olanzapine, 5 mg/d, to manage symptoms until he could establish care with an outpatient psychiatrist. Two days later, he returned to the ED yet again convinced people were spying on him and that his coworkers were plotting to have him fired. He was not taking his phone to work due to fears that it would be hacked.

Mr. R’s only home medication is clomiphene citrate, 100 mg/d by mouth, which he’s received for the past 7 months to treat low testosterone. He has no personal or family history of psychiatric illness and no prior signs of mania or hypomania.

At the current ED visit, Mr. R’s testosterone level is checked and is within normal limits. His urine drug screen, head CT, and standard laboratory test results are unremarkable, except for mild transaminitis that does not warrant acute management.

The clinicians in the ED establish a diagnosis of mania, unspecified, and psychotic disorder, unspecified. They recommend that Mr. R be admitted for mood stabilization.

[polldaddy:10485725]

Continue to: The authors' observations

Our initial impression was that Mr. R was experiencing a manic episode from undiagnosed bipolar I disorder. The diagnosis was equivocal considering his age, lack of family history, and absence of prior psychiatric symptoms. In most cases, the mean age of onset for mania is late adolescence to early adulthood. It would be less common for a patient to experience a first manic episode at age 48, although mania may emerge at any age. Results from a large British study showed that the incidence of a first manic episode drops from 13.81% in men age 16 to 25 to 2.62% in men age 46 to 55.¹ However, some estimates suggest that the prevalence of late-onset mania is much higher than previously expected; medical comorbidities, such as dementia and delirium, may play a significant role in posing as manic-type symptoms in these patients.²

In Mr. R’s case, he remained fully alert and oriented without waxing and waning attentional deficits, which made delirium less likely. His affective symptoms included a reduced need for sleep, anxiety, irritability, rapid speech, and grandiosity lasting at least 2 weeks. He also exhibited psychotic symptoms in the form of paranoia. Altogether, he fit diagnostic criteria for bipolar I disorder well.

At the time of his manic episode, Mr. R was taking clomiphene. Clomiphene-induced mania and psychosis has been reported scarcely in the literature.³ In these cases, behavioral changes occurred within the first month of clomiphene initiation, which is dissimilar from Mr. R’s timeline.⁴ However, there appeared to be a temporal relationship between Mr. R’s use of amoxicillin/clavulanate and his manic episode.

This led us to consider whether medication-induced bipolar disorder would be a more appropriate diagnosis. There are documented associations between mania and antibiotics⁵; however, to our knowledge, mania secondary specifically to amoxicillin/clavulanate has not been reported extensively in the American literature. We found 1 case of suspected amoxicillin-induced psychosis,⁶ as well as a case report from the Netherlands of possible amoxicillin/clavulanate-induced mania.⁷

EVALUATION Ongoing paranoia

During his psychiatric hospitalization, Mr. R remains cooperative and polite, but exhibits ongoing paranoia, pressured speech, and poor reality testing. He remains convinced that “people are out to get me,” and routinely scans the room for safety during daily evaluations. He reports that he feels safe in the hospital, but does not feel safe to leave. Mr. R does not recall if in the past he had taken any products containing amoxicillin, but he is able to appreciate changes in his mood after being prescribed the antibiotic. He reports that starting the antibiotic made him feel confident in social interactions.

Continue to: During Mr. R's psychiatric hospitalization...

During Mr. R’s psychiatric hospitalization, olanzapine is titrated to 10 mg at bedtime. Clomiphene citrate is discontinued to limit any potential precipitants of mania, and amoxicillin/clavulanate is not restarted.

Mr. R gradually shows improvement in sleep quality and duration and becomes less irritable. His speech returns to a regular rate and rhythm. He eventually begins to question whether his fears were reality-based. After 4 days, Mr. R is ready to be discharged home and return to work.

[polldaddy:10485726]

The authors’ observations

The term “antibiomania” is used to describe manic episodes that coincide with antibiotic usage.⁸ Clarithromycin and ciprofloxacin are the agents most frequently implicated in antibiomania.⁹ While numerous reports exist in the literature, antibiomania is still considered a rare or unusual adverse event.

The link between infections and neuropsychiatric symptoms is well documented, which makes it challenging to tease apart the role of the acute infection from the use of antibiotics in precipitating psychiatric symptoms. However, in most reported cases of antibiomania, the onset of manic symptoms typically occurs within the first week of antibiotic initiation and resolves 1 to 3 days after medication discontinuation. The temporal relationship between antibiotic initiation and onset of neuropsychiatric symptoms has been best highlighted in cases where clarithromycin is used to treat a chronic Helicobacter pylori infection.¹⁰

While reports of antibiomania date back more than 6 decades, the exact mechanism by which antibiotics cause psychiatric symptoms is mostly unknown, although there are several hypotheses.⁵ Many hypotheses suggest some antibiotics play a role in reducing gamma-aminobutyric acid (GABA) neurotransmission. Quinolones, for example, have been found to cross the blood–brain barrier and can inhibit GABA from binding to the receptor sites. This can result in hyper-excitability in the CNS. Several quinolones have been implicated in antibiomania (Table 1⁵). Penicillins are also thought to interfere with GABA neurotransmission in a similar fashion; however, amoxicillin-clavulanate has poor CNS penetration in the absence of blood–brain barrier disruption,¹¹ which makes this theory a less plausible explanation for Mr. R’s case.

Continue to: Another possible mechanism...

Another possible mechanism of antibiotic-induced CNS excitability is through the glutamatergic system. Cycloserine, an antitubercular agent, is an N-methyl-D-aspartate receptor (NMDA) partial agonist and has reported neuropsychiatric adverse effects.¹² It has been proposed that quinolones may also have NMDA agonist activity.

The prostaglandin hypothesis suggests that a decrease in GABA may increase concentrations of steroid hormones in the rat CNS.¹³ Steroids have been implicated in the breakdown of prostaglandin E1 (PGE1).¹³ A disruption in steroid regulation may prevent PGE1 breakdown. Lithium’s antimanic properties are thought to be caused at least in part by limiting prostaglandin production.¹⁴ Thus, a shift in PGE1 may lead to mood dysregulation.

Bipolar disorder has been linked with mitochondrial function abnormalities.¹⁵ Antibiotics that target ribosomal RNA may disrupt normal mitochondrial function and increase risk for mania precipitation.¹⁵ However, amoxicillin exerts its antibiotic effects through binding to penicillin-binding proteins, which leads to inhibition of the cell wall biosynthesis.

Lastly, research into the microbiome has elucidated the gut-brain axis. In animal studies, the microbiome has been found to play a role in immunity, cognitive function, and behavior. Dysbiosis in the microbiome is currently being investigated for its role in schizophrenia and bipolar disorder.¹⁶ Both the microbiome and changes in mitochondrial function are thought to develop over time, so while these are plausible explanations, an onset within 4 days of antibiotic initiation is likely too short of an exposure time to produce these changes.

The most likely causes of Mr. R’s manic episode were clomiphene or amoxicillin-clavulanate, and the time course seems to indicate the antibiotic was the most likely culprit. Table 2 lists things to consider if you suspect your patient may be experiencing antibiomania.

Continue to: TREATMENT Stable on olanzapine

TREATMENT Stable on olanzapine

During his first visit to the outpatient clinic 4 weeks after being discharged, Mr. R reports that he has successfully returned to work, and his paranoia has completely resolved. He continues to take olanzapine, 10 mg nightly, and has restarted clomiphene, 100 mg/d.

During this outpatient follow-up visit, Mr. R attributes his manic episode to an adverse reaction to amoxicillin/clavulanate, and requests to be tapered off olanzapine. After he and his psychiatrist discuss the risk of relapse in untreated bipolar disorder, olanzapine is reduced to 7.5 mg at bedtime with a plan to taper to discontinuation.

At his second follow-up visit 1 month later, Mr. R has also stopped clomiphene and is taking a herbal supplement instead, which he reports is helpful for his fatigue. He says his mood is stable and denies experiencing any manic or depressive symptoms. Olanzapine is discontinued at this visit.

[polldaddy:10485727]

OUTCOME Lasting euthymic mood

Mr. R agrees to our recommendation of continuing to monitor him every 3 months for at least 1 year. We provide him and his wife with education about early warning signs of mood instability. Eight months after his manic episode, Mr. R no longer receives any psychotropic medications and shows no signs of mood instability. His mood remains euthymic and he is able to function well at work and in his personal life.

Bottom Line

‘Antibiomania’ describes manic episodes that coincide with antibiotic usage. This adverse effect is rare but should be considered in patients who present with unexplained first-episode mania, particularly those with an initial onset of mania after early adulthood.

Continue to: Related Resources

• Rakofsky JJ, Dunlop BW. Nothing to sneeze at: Upper respiratory infections and mood disorders. Current Psychiatry. 2019;18(7):29-34.
• Adiba A, Jackson JC, Torrence CL. Older-age bipolar disorder: A case series. Current Psychiatry. 2019;18(2):24-29

Drug Brand Names

Amoxicillin • Amoxil
Amoxicillin/clavulanate • Augmentin
Ampicillin • Omnipen-N, Polycillin-N
Ciprofloxacin • Cipro
Clarithromycin • Biaxin
Clomiphene • Clomid
Cycloserine • Seromycin
Dapsone • Dapsone
Erythromycin • Erythrocin, Pediamycin
Ethambutol • Myambutol
Ethionamide • Trecator-SC
Gentamicin • Garamycin
Isoniazid • Hyzyd, Nydrazid
Lithium • Eskalith, Lithobid
Metronidazole • Flagyl
Minocycline • Dynacin, Solodyn
Norfloxacin • Noroxin
Ofloxacin • Floxin
Olanzapine • Zyprexa
Penicillin G procaine • Duracillin A-S, Pfizerpen
Sulfamethoxazole/trimethoprim • Bactrim, Septra

CASE Bipolar-like symptoms

Mr. R, age 48, presents to the psychiatric emergency department (ED) for the third time in 4 days after a change in his behavior over the last 2.5 weeks. He exhibits heightened extroversion, pressured speech, and uncharacteristic irritability. Mr. R’s wife reports that her husband normally is reserved.

Mr. R’s wife first became concerned when she noticed he was not sleeping and spending his nights changing the locks on their home. Mr. R, who is a business executive, occupied his time by taking notes on ways to protect his identity from the senior partners at his company.

Three weeks before his first ED visit, Mr. R had been treated for a neck abscess with incision and drainage. He was sent home with a 10-day course of amoxicillin/clavulanate, 875/125 mg by mouth twice daily. There were no reports of steroid use during or after the procedure. Four days after starting the antibiotic, he stopped taking it because he and his wife felt it was contributing to his mood changes and bizarre behavior.

During his first visit to the ED, Mr. R received a 1-time dose of olanzapine, 5 mg by mouth, which helped temporarily reduce his anxiety; however, he returned the following day with the same anxiety symptoms and was discharged with a 30-day prescription for olanzapine, 5 mg/d, to manage symptoms until he could establish care with an outpatient psychiatrist. Two days later, he returned to the ED yet again convinced people were spying on him and that his coworkers were plotting to have him fired. He was not taking his phone to work due to fears that it would be hacked.

Mr. R’s only home medication is clomiphene citrate, 100 mg/d by mouth, which he’s received for the past 7 months to treat low testosterone. He has no personal or family history of psychiatric illness and no prior signs of mania or hypomania.

At the current ED visit, Mr. R’s testosterone level is checked and is within normal limits. His urine drug screen, head CT, and standard laboratory test results are unremarkable, except for mild transaminitis that does not warrant acute management.

The clinicians in the ED establish a diagnosis of mania, unspecified, and psychotic disorder, unspecified. They recommend that Mr. R be admitted for mood stabilization.

[polldaddy:10485725]

Continue to: The authors' observations

Our initial impression was that Mr. R was experiencing a manic episode from undiagnosed bipolar I disorder. The diagnosis was equivocal considering his age, lack of family history, and absence of prior psychiatric symptoms. In most cases, the mean age of onset for mania is late adolescence to early adulthood. It would be less common for a patient to experience a first manic episode at age 48, although mania may emerge at any age. Results from a large British study showed that the incidence of a first manic episode drops from 13.81% in men age 16 to 25 to 2.62% in men age 46 to 55.¹ However, some estimates suggest that the prevalence of late-onset mania is much higher than previously expected; medical comorbidities, such as dementia and delirium, may play a significant role in posing as manic-type symptoms in these patients.²

In Mr. R’s case, he remained fully alert and oriented without waxing and waning attentional deficits, which made delirium less likely. His affective symptoms included a reduced need for sleep, anxiety, irritability, rapid speech, and grandiosity lasting at least 2 weeks. He also exhibited psychotic symptoms in the form of paranoia. Altogether, he fit diagnostic criteria for bipolar I disorder well.

At the time of his manic episode, Mr. R was taking clomiphene. Clomiphene-induced mania and psychosis has been reported scarcely in the literature.³ In these cases, behavioral changes occurred within the first month of clomiphene initiation, which is dissimilar from Mr. R’s timeline.⁴ However, there appeared to be a temporal relationship between Mr. R’s use of amoxicillin/clavulanate and his manic episode.

This led us to consider whether medication-induced bipolar disorder would be a more appropriate diagnosis. There are documented associations between mania and antibiotics⁵; however, to our knowledge, mania secondary specifically to amoxicillin/clavulanate has not been reported extensively in the American literature. We found 1 case of suspected amoxicillin-induced psychosis,⁶ as well as a case report from the Netherlands of possible amoxicillin/clavulanate-induced mania.⁷

EVALUATION Ongoing paranoia

During his psychiatric hospitalization, Mr. R remains cooperative and polite, but exhibits ongoing paranoia, pressured speech, and poor reality testing. He remains convinced that “people are out to get me,” and routinely scans the room for safety during daily evaluations. He reports that he feels safe in the hospital, but does not feel safe to leave. Mr. R does not recall if in the past he had taken any products containing amoxicillin, but he is able to appreciate changes in his mood after being prescribed the antibiotic. He reports that starting the antibiotic made him feel confident in social interactions.

Continue to: During Mr. R's psychiatric hospitalization...

During Mr. R’s psychiatric hospitalization, olanzapine is titrated to 10 mg at bedtime. Clomiphene citrate is discontinued to limit any potential precipitants of mania, and amoxicillin/clavulanate is not restarted.

Mr. R gradually shows improvement in sleep quality and duration and becomes less irritable. His speech returns to a regular rate and rhythm. He eventually begins to question whether his fears were reality-based. After 4 days, Mr. R is ready to be discharged home and return to work.

[polldaddy:10485726]

The authors’ observations

The term “antibiomania” is used to describe manic episodes that coincide with antibiotic usage.⁸ Clarithromycin and ciprofloxacin are the agents most frequently implicated in antibiomania.⁹ While numerous reports exist in the literature, antibiomania is still considered a rare or unusual adverse event.

The link between infections and neuropsychiatric symptoms is well documented, which makes it challenging to tease apart the role of the acute infection from the use of antibiotics in precipitating psychiatric symptoms. However, in most reported cases of antibiomania, the onset of manic symptoms typically occurs within the first week of antibiotic initiation and resolves 1 to 3 days after medication discontinuation. The temporal relationship between antibiotic initiation and onset of neuropsychiatric symptoms has been best highlighted in cases where clarithromycin is used to treat a chronic Helicobacter pylori infection.¹⁰

While reports of antibiomania date back more than 6 decades, the exact mechanism by which antibiotics cause psychiatric symptoms is mostly unknown, although there are several hypotheses.⁵ Many hypotheses suggest some antibiotics play a role in reducing gamma-aminobutyric acid (GABA) neurotransmission. Quinolones, for example, have been found to cross the blood–brain barrier and can inhibit GABA from binding to the receptor sites. This can result in hyper-excitability in the CNS. Several quinolones have been implicated in antibiomania (Table 1⁵). Penicillins are also thought to interfere with GABA neurotransmission in a similar fashion; however, amoxicillin-clavulanate has poor CNS penetration in the absence of blood–brain barrier disruption,¹¹ which makes this theory a less plausible explanation for Mr. R’s case.

Continue to: Another possible mechanism...

Another possible mechanism of antibiotic-induced CNS excitability is through the glutamatergic system. Cycloserine, an antitubercular agent, is an N-methyl-D-aspartate receptor (NMDA) partial agonist and has reported neuropsychiatric adverse effects.¹² It has been proposed that quinolones may also have NMDA agonist activity.

The prostaglandin hypothesis suggests that a decrease in GABA may increase concentrations of steroid hormones in the rat CNS.¹³ Steroids have been implicated in the breakdown of prostaglandin E1 (PGE1).¹³ A disruption in steroid regulation may prevent PGE1 breakdown. Lithium’s antimanic properties are thought to be caused at least in part by limiting prostaglandin production.¹⁴ Thus, a shift in PGE1 may lead to mood dysregulation.

Bipolar disorder has been linked with mitochondrial function abnormalities.¹⁵ Antibiotics that target ribosomal RNA may disrupt normal mitochondrial function and increase risk for mania precipitation.¹⁵ However, amoxicillin exerts its antibiotic effects through binding to penicillin-binding proteins, which leads to inhibition of the cell wall biosynthesis.

Lastly, research into the microbiome has elucidated the gut-brain axis. In animal studies, the microbiome has been found to play a role in immunity, cognitive function, and behavior. Dysbiosis in the microbiome is currently being investigated for its role in schizophrenia and bipolar disorder.¹⁶ Both the microbiome and changes in mitochondrial function are thought to develop over time, so while these are plausible explanations, an onset within 4 days of antibiotic initiation is likely too short of an exposure time to produce these changes.

The most likely causes of Mr. R’s manic episode were clomiphene or amoxicillin-clavulanate, and the time course seems to indicate the antibiotic was the most likely culprit. Table 2 lists things to consider if you suspect your patient may be experiencing antibiomania.

Continue to: TREATMENT Stable on olanzapine

TREATMENT Stable on olanzapine

During his first visit to the outpatient clinic 4 weeks after being discharged, Mr. R reports that he has successfully returned to work, and his paranoia has completely resolved. He continues to take olanzapine, 10 mg nightly, and has restarted clomiphene, 100 mg/d.

During this outpatient follow-up visit, Mr. R attributes his manic episode to an adverse reaction to amoxicillin/clavulanate, and requests to be tapered off olanzapine. After he and his psychiatrist discuss the risk of relapse in untreated bipolar disorder, olanzapine is reduced to 7.5 mg at bedtime with a plan to taper to discontinuation.

At his second follow-up visit 1 month later, Mr. R has also stopped clomiphene and is taking a herbal supplement instead, which he reports is helpful for his fatigue. He says his mood is stable and denies experiencing any manic or depressive symptoms. Olanzapine is discontinued at this visit.

[polldaddy:10485727]

OUTCOME Lasting euthymic mood

Mr. R agrees to our recommendation of continuing to monitor him every 3 months for at least 1 year. We provide him and his wife with education about early warning signs of mood instability. Eight months after his manic episode, Mr. R no longer receives any psychotropic medications and shows no signs of mood instability. His mood remains euthymic and he is able to function well at work and in his personal life.

Bottom Line

‘Antibiomania’ describes manic episodes that coincide with antibiotic usage. This adverse effect is rare but should be considered in patients who present with unexplained first-episode mania, particularly those with an initial onset of mania after early adulthood.

Continue to: Related Resources

• Rakofsky JJ, Dunlop BW. Nothing to sneeze at: Upper respiratory infections and mood disorders. Current Psychiatry. 2019;18(7):29-34.
• Adiba A, Jackson JC, Torrence CL. Older-age bipolar disorder: A case series. Current Psychiatry. 2019;18(2):24-29

Drug Brand Names

Amoxicillin • Amoxil
Amoxicillin/clavulanate • Augmentin
Ampicillin • Omnipen-N, Polycillin-N
Ciprofloxacin • Cipro
Clarithromycin • Biaxin
Clomiphene • Clomid
Cycloserine • Seromycin
Dapsone • Dapsone
Erythromycin • Erythrocin, Pediamycin
Ethambutol • Myambutol
Ethionamide • Trecator-SC
Gentamicin • Garamycin
Isoniazid • Hyzyd, Nydrazid
Lithium • Eskalith, Lithobid
Metronidazole • Flagyl
Minocycline • Dynacin, Solodyn
Norfloxacin • Noroxin
Ofloxacin • Floxin
Olanzapine • Zyprexa
Penicillin G procaine • Duracillin A-S, Pfizerpen
Sulfamethoxazole/trimethoprim • Bactrim, Septra

CASE Bipolar-like symptoms

Mr. R, age 48, presents to the psychiatric emergency department (ED) for the third time in 4 days after a change in his behavior over the last 2.5 weeks. He exhibits heightened extroversion, pressured speech, and uncharacteristic irritability. Mr. R’s wife reports that her husband normally is reserved.

Mr. R’s wife first became concerned when she noticed he was not sleeping and spending his nights changing the locks on their home. Mr. R, who is a business executive, occupied his time by taking notes on ways to protect his identity from the senior partners at his company.

Three weeks before his first ED visit, Mr. R had been treated for a neck abscess with incision and drainage. He was sent home with a 10-day course of amoxicillin/clavulanate, 875/125 mg by mouth twice daily. There were no reports of steroid use during or after the procedure. Four days after starting the antibiotic, he stopped taking it because he and his wife felt it was contributing to his mood changes and bizarre behavior.

During his first visit to the ED, Mr. R received a 1-time dose of olanzapine, 5 mg by mouth, which helped temporarily reduce his anxiety; however, he returned the following day with the same anxiety symptoms and was discharged with a 30-day prescription for olanzapine, 5 mg/d, to manage symptoms until he could establish care with an outpatient psychiatrist. Two days later, he returned to the ED yet again convinced people were spying on him and that his coworkers were plotting to have him fired. He was not taking his phone to work due to fears that it would be hacked.

Mr. R’s only home medication is clomiphene citrate, 100 mg/d by mouth, which he’s received for the past 7 months to treat low testosterone. He has no personal or family history of psychiatric illness and no prior signs of mania or hypomania.

At the current ED visit, Mr. R’s testosterone level is checked and is within normal limits. His urine drug screen, head CT, and standard laboratory test results are unremarkable, except for mild transaminitis that does not warrant acute management.

The clinicians in the ED establish a diagnosis of mania, unspecified, and psychotic disorder, unspecified. They recommend that Mr. R be admitted for mood stabilization.

[polldaddy:10485725]

Continue to: The authors' observations

Our initial impression was that Mr. R was experiencing a manic episode from undiagnosed bipolar I disorder. The diagnosis was equivocal considering his age, lack of family history, and absence of prior psychiatric symptoms. In most cases, the mean age of onset for mania is late adolescence to early adulthood. It would be less common for a patient to experience a first manic episode at age 48, although mania may emerge at any age. Results from a large British study showed that the incidence of a first manic episode drops from 13.81% in men age 16 to 25 to 2.62% in men age 46 to 55.¹ However, some estimates suggest that the prevalence of late-onset mania is much higher than previously expected; medical comorbidities, such as dementia and delirium, may play a significant role in posing as manic-type symptoms in these patients.²

In Mr. R’s case, he remained fully alert and oriented without waxing and waning attentional deficits, which made delirium less likely. His affective symptoms included a reduced need for sleep, anxiety, irritability, rapid speech, and grandiosity lasting at least 2 weeks. He also exhibited psychotic symptoms in the form of paranoia. Altogether, he fit diagnostic criteria for bipolar I disorder well.

At the time of his manic episode, Mr. R was taking clomiphene. Clomiphene-induced mania and psychosis has been reported scarcely in the literature.³ In these cases, behavioral changes occurred within the first month of clomiphene initiation, which is dissimilar from Mr. R’s timeline.⁴ However, there appeared to be a temporal relationship between Mr. R’s use of amoxicillin/clavulanate and his manic episode.

This led us to consider whether medication-induced bipolar disorder would be a more appropriate diagnosis. There are documented associations between mania and antibiotics⁵; however, to our knowledge, mania secondary specifically to amoxicillin/clavulanate has not been reported extensively in the American literature. We found 1 case of suspected amoxicillin-induced psychosis,⁶ as well as a case report from the Netherlands of possible amoxicillin/clavulanate-induced mania.⁷

EVALUATION Ongoing paranoia

During his psychiatric hospitalization, Mr. R remains cooperative and polite, but exhibits ongoing paranoia, pressured speech, and poor reality testing. He remains convinced that “people are out to get me,” and routinely scans the room for safety during daily evaluations. He reports that he feels safe in the hospital, but does not feel safe to leave. Mr. R does not recall if in the past he had taken any products containing amoxicillin, but he is able to appreciate changes in his mood after being prescribed the antibiotic. He reports that starting the antibiotic made him feel confident in social interactions.

Continue to: During Mr. R's psychiatric hospitalization...

During Mr. R’s psychiatric hospitalization, olanzapine is titrated to 10 mg at bedtime. Clomiphene citrate is discontinued to limit any potential precipitants of mania, and amoxicillin/clavulanate is not restarted.

Mr. R gradually shows improvement in sleep quality and duration and becomes less irritable. His speech returns to a regular rate and rhythm. He eventually begins to question whether his fears were reality-based. After 4 days, Mr. R is ready to be discharged home and return to work.

[polldaddy:10485726]

The authors’ observations

The term “antibiomania” is used to describe manic episodes that coincide with antibiotic usage.⁸ Clarithromycin and ciprofloxacin are the agents most frequently implicated in antibiomania.⁹ While numerous reports exist in the literature, antibiomania is still considered a rare or unusual adverse event.

The link between infections and neuropsychiatric symptoms is well documented, which makes it challenging to tease apart the role of the acute infection from the use of antibiotics in precipitating psychiatric symptoms. However, in most reported cases of antibiomania, the onset of manic symptoms typically occurs within the first week of antibiotic initiation and resolves 1 to 3 days after medication discontinuation. The temporal relationship between antibiotic initiation and onset of neuropsychiatric symptoms has been best highlighted in cases where clarithromycin is used to treat a chronic Helicobacter pylori infection.¹⁰

While reports of antibiomania date back more than 6 decades, the exact mechanism by which antibiotics cause psychiatric symptoms is mostly unknown, although there are several hypotheses.⁵ Many hypotheses suggest some antibiotics play a role in reducing gamma-aminobutyric acid (GABA) neurotransmission. Quinolones, for example, have been found to cross the blood–brain barrier and can inhibit GABA from binding to the receptor sites. This can result in hyper-excitability in the CNS. Several quinolones have been implicated in antibiomania (Table 1⁵). Penicillins are also thought to interfere with GABA neurotransmission in a similar fashion; however, amoxicillin-clavulanate has poor CNS penetration in the absence of blood–brain barrier disruption,¹¹ which makes this theory a less plausible explanation for Mr. R’s case.

Continue to: Another possible mechanism...

Another possible mechanism of antibiotic-induced CNS excitability is through the glutamatergic system. Cycloserine, an antitubercular agent, is an N-methyl-D-aspartate receptor (NMDA) partial agonist and has reported neuropsychiatric adverse effects.¹² It has been proposed that quinolones may also have NMDA agonist activity.

The prostaglandin hypothesis suggests that a decrease in GABA may increase concentrations of steroid hormones in the rat CNS.¹³ Steroids have been implicated in the breakdown of prostaglandin E1 (PGE1).¹³ A disruption in steroid regulation may prevent PGE1 breakdown. Lithium’s antimanic properties are thought to be caused at least in part by limiting prostaglandin production.¹⁴ Thus, a shift in PGE1 may lead to mood dysregulation.

Bipolar disorder has been linked with mitochondrial function abnormalities.¹⁵ Antibiotics that target ribosomal RNA may disrupt normal mitochondrial function and increase risk for mania precipitation.¹⁵ However, amoxicillin exerts its antibiotic effects through binding to penicillin-binding proteins, which leads to inhibition of the cell wall biosynthesis.

Lastly, research into the microbiome has elucidated the gut-brain axis. In animal studies, the microbiome has been found to play a role in immunity, cognitive function, and behavior. Dysbiosis in the microbiome is currently being investigated for its role in schizophrenia and bipolar disorder.¹⁶ Both the microbiome and changes in mitochondrial function are thought to develop over time, so while these are plausible explanations, an onset within 4 days of antibiotic initiation is likely too short of an exposure time to produce these changes.

The most likely causes of Mr. R’s manic episode were clomiphene or amoxicillin-clavulanate, and the time course seems to indicate the antibiotic was the most likely culprit. Table 2 lists things to consider if you suspect your patient may be experiencing antibiomania.

Continue to: TREATMENT Stable on olanzapine

TREATMENT Stable on olanzapine

During his first visit to the outpatient clinic 4 weeks after being discharged, Mr. R reports that he has successfully returned to work, and his paranoia has completely resolved. He continues to take olanzapine, 10 mg nightly, and has restarted clomiphene, 100 mg/d.

During this outpatient follow-up visit, Mr. R attributes his manic episode to an adverse reaction to amoxicillin/clavulanate, and requests to be tapered off olanzapine. After he and his psychiatrist discuss the risk of relapse in untreated bipolar disorder, olanzapine is reduced to 7.5 mg at bedtime with a plan to taper to discontinuation.

At his second follow-up visit 1 month later, Mr. R has also stopped clomiphene and is taking a herbal supplement instead, which he reports is helpful for his fatigue. He says his mood is stable and denies experiencing any manic or depressive symptoms. Olanzapine is discontinued at this visit.

[polldaddy:10485727]

OUTCOME Lasting euthymic mood

Mr. R agrees to our recommendation of continuing to monitor him every 3 months for at least 1 year. We provide him and his wife with education about early warning signs of mood instability. Eight months after his manic episode, Mr. R no longer receives any psychotropic medications and shows no signs of mood instability. His mood remains euthymic and he is able to function well at work and in his personal life.

Bottom Line

‘Antibiomania’ describes manic episodes that coincide with antibiotic usage. This adverse effect is rare but should be considered in patients who present with unexplained first-episode mania, particularly those with an initial onset of mania after early adulthood.

Continue to: Related Resources

• Rakofsky JJ, Dunlop BW. Nothing to sneeze at: Upper respiratory infections and mood disorders. Current Psychiatry. 2019;18(7):29-34.
• Adiba A, Jackson JC, Torrence CL. Older-age bipolar disorder: A case series. Current Psychiatry. 2019;18(2):24-29

Drug Brand Names

Amoxicillin • Amoxil
Amoxicillin/clavulanate • Augmentin
Ampicillin • Omnipen-N, Polycillin-N
Ciprofloxacin • Cipro
Clarithromycin • Biaxin
Clomiphene • Clomid
Cycloserine • Seromycin
Dapsone • Dapsone
Erythromycin • Erythrocin, Pediamycin
Ethambutol • Myambutol
Ethionamide • Trecator-SC
Gentamicin • Garamycin
Isoniazid • Hyzyd, Nydrazid
Lithium • Eskalith, Lithobid
Metronidazole • Flagyl
Minocycline • Dynacin, Solodyn
Norfloxacin • Noroxin
Ofloxacin • Floxin
Olanzapine • Zyprexa
Penicillin G procaine • Duracillin A-S, Pfizerpen
Sulfamethoxazole/trimethoprim • Bactrim, Septra

Every community practice gastroenterologist knows that private equity is making an aggressive push into our specialty. This is a tectonic shift in GI practice and the implications for private practice, academic training programs, and our GI societies are substantial. Gastro Health (Florida), Atlanta Gastro (Georgia), and GI Alliance (Texas) all closed deals with private equity in 2018 and there are reported to be 16-20 deals completed or in process currently. The three “first movers” formed practice management companies that now have acquired numerous large and small practices around the country. We have one practice with more than 200 physicians and we will see single groups of 500-1000 in the near future.

Imagine what a digestive health multi-state practice of 500 physicians (gastroenterologists, pathologists, surgeons), 200 advance practice providers (APPs) plus other ancillary professionals (psychology, nutrition) could accomplish. Gross revenues could top $1 billion. All back-office operations would be consolidated and managed professionally. Each provider would work top of license so much routine care would be shifted away from MDs. Negotiating power with payers, vendors, hospital systems, and referring providers would be immense (care would be taken to avoid the appearance of a monopoly, but Department of Justice scrutiny has already been evident). Referral sources (CVS, Optum, health systems, and a few remaining independent practices) would be secured by contract or favored reimbursement rates. Academic health systems will find competition challenging save for high tertiary and quaternary care, but even these complex procedures often will have been consolidated (and contained within risk-bundles) to a half dozen health systems by direct-to-employer contracting. Current society offerings such as meetings, journals, and clinical guidelines will become obsolete because of practice-distributed virtual education, open publishing, and internal outcomes measurement. The vast provider network will be on a single data platform so it can generate true outcomes based on a payer’s patient base (not guideline-restricted process measures), and these outcomes will be used for negotiating restricted networks.

I hope these trends will be a clarion call for our societies and training programs to awaken to a new world order and adapt their efforts to meet demands from our patients and the critical (and changing) needs of current and future digestive health professionals.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

Every community practice gastroenterologist knows that private equity is making an aggressive push into our specialty. This is a tectonic shift in GI practice and the implications for private practice, academic training programs, and our GI societies are substantial. Gastro Health (Florida), Atlanta Gastro (Georgia), and GI Alliance (Texas) all closed deals with private equity in 2018 and there are reported to be 16-20 deals completed or in process currently. The three “first movers” formed practice management companies that now have acquired numerous large and small practices around the country. We have one practice with more than 200 physicians and we will see single groups of 500-1000 in the near future.

Imagine what a digestive health multi-state practice of 500 physicians (gastroenterologists, pathologists, surgeons), 200 advance practice providers (APPs) plus other ancillary professionals (psychology, nutrition) could accomplish. Gross revenues could top $1 billion. All back-office operations would be consolidated and managed professionally. Each provider would work top of license so much routine care would be shifted away from MDs. Negotiating power with payers, vendors, hospital systems, and referring providers would be immense (care would be taken to avoid the appearance of a monopoly, but Department of Justice scrutiny has already been evident). Referral sources (CVS, Optum, health systems, and a few remaining independent practices) would be secured by contract or favored reimbursement rates. Academic health systems will find competition challenging save for high tertiary and quaternary care, but even these complex procedures often will have been consolidated (and contained within risk-bundles) to a half dozen health systems by direct-to-employer contracting. Current society offerings such as meetings, journals, and clinical guidelines will become obsolete because of practice-distributed virtual education, open publishing, and internal outcomes measurement. The vast provider network will be on a single data platform so it can generate true outcomes based on a payer’s patient base (not guideline-restricted process measures), and these outcomes will be used for negotiating restricted networks.

I hope these trends will be a clarion call for our societies and training programs to awaken to a new world order and adapt their efforts to meet demands from our patients and the critical (and changing) needs of current and future digestive health professionals.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

Every community practice gastroenterologist knows that private equity is making an aggressive push into our specialty. This is a tectonic shift in GI practice and the implications for private practice, academic training programs, and our GI societies are substantial. Gastro Health (Florida), Atlanta Gastro (Georgia), and GI Alliance (Texas) all closed deals with private equity in 2018 and there are reported to be 16-20 deals completed or in process currently. The three “first movers” formed practice management companies that now have acquired numerous large and small practices around the country. We have one practice with more than 200 physicians and we will see single groups of 500-1000 in the near future.

Imagine what a digestive health multi-state practice of 500 physicians (gastroenterologists, pathologists, surgeons), 200 advance practice providers (APPs) plus other ancillary professionals (psychology, nutrition) could accomplish. Gross revenues could top $1 billion. All back-office operations would be consolidated and managed professionally. Each provider would work top of license so much routine care would be shifted away from MDs. Negotiating power with payers, vendors, hospital systems, and referring providers would be immense (care would be taken to avoid the appearance of a monopoly, but Department of Justice scrutiny has already been evident). Referral sources (CVS, Optum, health systems, and a few remaining independent practices) would be secured by contract or favored reimbursement rates. Academic health systems will find competition challenging save for high tertiary and quaternary care, but even these complex procedures often will have been consolidated (and contained within risk-bundles) to a half dozen health systems by direct-to-employer contracting. Current society offerings such as meetings, journals, and clinical guidelines will become obsolete because of practice-distributed virtual education, open publishing, and internal outcomes measurement. The vast provider network will be on a single data platform so it can generate true outcomes based on a payer’s patient base (not guideline-restricted process measures), and these outcomes will be used for negotiating restricted networks.

I hope these trends will be a clarion call for our societies and training programs to awaken to a new world order and adapt their efforts to meet demands from our patients and the critical (and changing) needs of current and future digestive health professionals.
 

John I. Allen, MD, MBA, AGAF
Editor in Chief

Mrs. C, age 75, is transferred to our inpatient medical/surgical hospital from a psychiatric hospital after presenting with shortness of breath and altered mental status.

Eight days earlier, Mrs. C had been admitted to the psychiatric hospital for bipolar mania with psychotic features. While there, Mrs. C received quetiapine, 400 mg nightly, and an initial valproic acid (VPA) dosage of 500 mg 2 times daily. While receiving VPA 500 mg 2 times daily, her VPA total level was 62 µg/mL, which is on the lower end of the therapeutic range (50 to 125 µg/mL). This prompted the team at the psychiatric hospital to increase her VPA dosage to 500 mg 3 times daily the day before she was transferred to our hospital.

At our hospital, she is found to be in hypoxic respiratory failure secondary to pneumonia. Upon admission, her laboratory data show evidence of infection and anemia and she also has an albumin level of 3.0 g/dL (normal range: 3.5 to 5.5 g/dL). All other laboratory values, including liver enzymes, are unremarkable. She is started on IV levofloxacin. Her previous medications—quetiapine and VPA—are continued at their same dosages and frequencies from her inpatient psychiatric stay.

From hospital Day 3 to Day 6, Mrs. C experiences gradual improvement in her respiratory and mental status. However, on hospital Day 7, she has extreme somnolence and altered mental status without respiratory involvement. Our team suspects VPA toxicity and/or VPA-induced hyperammonemic encephalopathy (VHE).

VPA-induced hyperammonemia

Hyperammonemia can occur in individuals receiving VPA and is most often asymptomatic. However, elevations in ammonia may lead to VHE, which is a rare but serious adverse effect. VHE has been reported early in treatment, in acute VPA overdose, and in chronic VPA use despite normal doses and levels.¹ It also can occur in the absence of clinical and laboratory evidence of hepatotoxicity. VHE is associated with significant morbidity and CNS damage. Symptoms of VHE include vomiting, lethargy, and confusion. If left untreated, VHE can lead to coma and death.

Mechanism of VHE. The exact mechanism of VHE is unknown.^1-3 Ammonia is a toxic base produced by deamination of amino acids. The liver eliminates ammonia via the urea cycle.² Valproic acid metabolites, propionate and 4-en-VPA, can directly inhibit N-acetyl glutamate, which can disrupt the urea cycle, leading to elevated ammonia levels.³ Long-term or high-dose VPA can lead to carnitine deficiency, primarily by inhibiting its biosynthesis and depleting stores.⁴ Carnitine deficiency leads to disturbances in mitochondrial function, causing inhibition of the urea cycle and increasing ammonia. CNS toxicity due to hyperammonemia is thought to be due to activation of glutamate receptors.³

Risk factors. Co-administration of other antiepileptic drugs (AEDs) with VPA is a risk factor for VHE.^1,5 This happens because enzyme-inducing AEDs such as phenytoin, phenobarbital, and carba­mazepine can increase toxic metabolites of VPA, which can lead to hyperammonemia. Topiramate can also inhibit the urea cycle, leading to increased ammonia levels. Additionally, co-administration of VPA with quetiapine, paliperidone, risperidone, or aripiprazole has been reported to increase the risk of VHE.^1,5 Intellectual disability, carnitine deficiency, low albumin, and abnormal liver function have also been reported to increase the risk of VHE.^1,5

Continue to: Diagnosis and management

Diagnosis and management. If a patient receiving VPA is experiencing nausea, fatigue, or somnolence, it is important to check the patient’s ammonia level (normal range: 11 to 32 µmol/L) and VPA total levels (therapeutic range: 50 to 125 µg/mL). Consider checking a VPA free level, especially in geriatric patients or patients who have low albumin; the therapeutic range of VPA free is  6 to 22 µg/mL.³ If the ammonia level is elevated, discontinue VPA immediately (Table).^1-3 Clinicians may also elect to prescribe lactulose until ammonia levels return to normal range. Adding levocarnitine may also help, although evidence is limited to small case series or retrospective studies.³ Currently, there is no known advantage in combining lactulose and levocarnitine to address VHE. Severe cases of VHE (ammonia levels >400 µmol/L) may require hemodialysis.¹

Prevention. Strategies to prevent VHE include avoiding polypharmacy, especially concurrent use of enzyme-inducing AEDs and possibly second-generation antipsychotics. Additionally, VPA should not be used in individuals with urea cycle disorders. It is unknown if levocarnitine supplementation is preventive, but this approach has been suggested.³

CASE CONTINUED

Mrs. C has several possible risk factors for VHE, including co-administration of quetiapine and VPA, and a low albumin level. A further laboratory workup for Mrs. C reveals a VPA free level of 19 µg/mL (21.1% free), a VPA total level of 90 µg/mL, and an ammonia level of 79 µmol/L, confirming our suspicions regarding VHE. We determine that Mrs. C’s altered mental status is likely due her elevated ammonia levels, because the infection had been improving in the days leading up to the sudden, extreme somnolence.

VPA is immediately stopped and Mrs. C receives 1 dose of lactulose. The following day, Mrs. C’s mental status improves, and her ammonia levels return to normal. On hospital Day 9, she is transferred back to the psychiatric facility for management of manic and psychotic symptoms.

Related Resources

• Brown LM, Cupples N, Moore TA. Levocarnitine for valproate-induced hyperammonemia in the psychiatric setting: a case series and literature review. Ment Health Clin. 2018;8(3):148-154.
• Aires CCP, van Cruchten A, Ijlat L, et al. New insights on the mechanisms of valproate-induced hyperammonemia: inhibition of hepatic N-acetylglutamate synthase activity by valproyl-CoA. J Hepatol. 2011;55(2):426-434.

Drug Brand Names

Aripiprazole • Abilify
Carbamazepine • Tegretol
Lactulose • Enulose
Levocarnitine • Carnitine, Carnitor
Levofloxacin • Levaquin IV
Paliperidone • Invega
Phenobarbital • Luminal
Phenytoin • Dilantin
Quetiapine • Seroquel
Risperidone • Risperdal
Topiramate • Topamax
Valproic acid • Depakene

Mrs. C, age 75, is transferred to our inpatient medical/surgical hospital from a psychiatric hospital after presenting with shortness of breath and altered mental status.

Eight days earlier, Mrs. C had been admitted to the psychiatric hospital for bipolar mania with psychotic features. While there, Mrs. C received quetiapine, 400 mg nightly, and an initial valproic acid (VPA) dosage of 500 mg 2 times daily. While receiving VPA 500 mg 2 times daily, her VPA total level was 62 µg/mL, which is on the lower end of the therapeutic range (50 to 125 µg/mL). This prompted the team at the psychiatric hospital to increase her VPA dosage to 500 mg 3 times daily the day before she was transferred to our hospital.

At our hospital, she is found to be in hypoxic respiratory failure secondary to pneumonia. Upon admission, her laboratory data show evidence of infection and anemia and she also has an albumin level of 3.0 g/dL (normal range: 3.5 to 5.5 g/dL). All other laboratory values, including liver enzymes, are unremarkable. She is started on IV levofloxacin. Her previous medications—quetiapine and VPA—are continued at their same dosages and frequencies from her inpatient psychiatric stay.

From hospital Day 3 to Day 6, Mrs. C experiences gradual improvement in her respiratory and mental status. However, on hospital Day 7, she has extreme somnolence and altered mental status without respiratory involvement. Our team suspects VPA toxicity and/or VPA-induced hyperammonemic encephalopathy (VHE).

VPA-induced hyperammonemia

Hyperammonemia can occur in individuals receiving VPA and is most often asymptomatic. However, elevations in ammonia may lead to VHE, which is a rare but serious adverse effect. VHE has been reported early in treatment, in acute VPA overdose, and in chronic VPA use despite normal doses and levels.¹ It also can occur in the absence of clinical and laboratory evidence of hepatotoxicity. VHE is associated with significant morbidity and CNS damage. Symptoms of VHE include vomiting, lethargy, and confusion. If left untreated, VHE can lead to coma and death.

Mechanism of VHE. The exact mechanism of VHE is unknown.^1-3 Ammonia is a toxic base produced by deamination of amino acids. The liver eliminates ammonia via the urea cycle.² Valproic acid metabolites, propionate and 4-en-VPA, can directly inhibit N-acetyl glutamate, which can disrupt the urea cycle, leading to elevated ammonia levels.³ Long-term or high-dose VPA can lead to carnitine deficiency, primarily by inhibiting its biosynthesis and depleting stores.⁴ Carnitine deficiency leads to disturbances in mitochondrial function, causing inhibition of the urea cycle and increasing ammonia. CNS toxicity due to hyperammonemia is thought to be due to activation of glutamate receptors.³

Risk factors. Co-administration of other antiepileptic drugs (AEDs) with VPA is a risk factor for VHE.^1,5 This happens because enzyme-inducing AEDs such as phenytoin, phenobarbital, and carba­mazepine can increase toxic metabolites of VPA, which can lead to hyperammonemia. Topiramate can also inhibit the urea cycle, leading to increased ammonia levels. Additionally, co-administration of VPA with quetiapine, paliperidone, risperidone, or aripiprazole has been reported to increase the risk of VHE.^1,5 Intellectual disability, carnitine deficiency, low albumin, and abnormal liver function have also been reported to increase the risk of VHE.^1,5

Continue to: Diagnosis and management

Diagnosis and management. If a patient receiving VPA is experiencing nausea, fatigue, or somnolence, it is important to check the patient’s ammonia level (normal range: 11 to 32 µmol/L) and VPA total levels (therapeutic range: 50 to 125 µg/mL). Consider checking a VPA free level, especially in geriatric patients or patients who have low albumin; the therapeutic range of VPA free is  6 to 22 µg/mL.³ If the ammonia level is elevated, discontinue VPA immediately (Table).^1-3 Clinicians may also elect to prescribe lactulose until ammonia levels return to normal range. Adding levocarnitine may also help, although evidence is limited to small case series or retrospective studies.³ Currently, there is no known advantage in combining lactulose and levocarnitine to address VHE. Severe cases of VHE (ammonia levels >400 µmol/L) may require hemodialysis.¹

Prevention. Strategies to prevent VHE include avoiding polypharmacy, especially concurrent use of enzyme-inducing AEDs and possibly second-generation antipsychotics. Additionally, VPA should not be used in individuals with urea cycle disorders. It is unknown if levocarnitine supplementation is preventive, but this approach has been suggested.³

CASE CONTINUED

Mrs. C has several possible risk factors for VHE, including co-administration of quetiapine and VPA, and a low albumin level. A further laboratory workup for Mrs. C reveals a VPA free level of 19 µg/mL (21.1% free), a VPA total level of 90 µg/mL, and an ammonia level of 79 µmol/L, confirming our suspicions regarding VHE. We determine that Mrs. C’s altered mental status is likely due her elevated ammonia levels, because the infection had been improving in the days leading up to the sudden, extreme somnolence.

VPA is immediately stopped and Mrs. C receives 1 dose of lactulose. The following day, Mrs. C’s mental status improves, and her ammonia levels return to normal. On hospital Day 9, she is transferred back to the psychiatric facility for management of manic and psychotic symptoms.

Related Resources

• Brown LM, Cupples N, Moore TA. Levocarnitine for valproate-induced hyperammonemia in the psychiatric setting: a case series and literature review. Ment Health Clin. 2018;8(3):148-154.
• Aires CCP, van Cruchten A, Ijlat L, et al. New insights on the mechanisms of valproate-induced hyperammonemia: inhibition of hepatic N-acetylglutamate synthase activity by valproyl-CoA. J Hepatol. 2011;55(2):426-434.

Drug Brand Names

Aripiprazole • Abilify
Carbamazepine • Tegretol
Lactulose • Enulose
Levocarnitine • Carnitine, Carnitor
Levofloxacin • Levaquin IV
Paliperidone • Invega
Phenobarbital • Luminal
Phenytoin • Dilantin
Quetiapine • Seroquel
Risperidone • Risperdal
Topiramate • Topamax
Valproic acid • Depakene

Mrs. C, age 75, is transferred to our inpatient medical/surgical hospital from a psychiatric hospital after presenting with shortness of breath and altered mental status.

Eight days earlier, Mrs. C had been admitted to the psychiatric hospital for bipolar mania with psychotic features. While there, Mrs. C received quetiapine, 400 mg nightly, and an initial valproic acid (VPA) dosage of 500 mg 2 times daily. While receiving VPA 500 mg 2 times daily, her VPA total level was 62 µg/mL, which is on the lower end of the therapeutic range (50 to 125 µg/mL). This prompted the team at the psychiatric hospital to increase her VPA dosage to 500 mg 3 times daily the day before she was transferred to our hospital.

At our hospital, she is found to be in hypoxic respiratory failure secondary to pneumonia. Upon admission, her laboratory data show evidence of infection and anemia and she also has an albumin level of 3.0 g/dL (normal range: 3.5 to 5.5 g/dL). All other laboratory values, including liver enzymes, are unremarkable. She is started on IV levofloxacin. Her previous medications—quetiapine and VPA—are continued at their same dosages and frequencies from her inpatient psychiatric stay.

From hospital Day 3 to Day 6, Mrs. C experiences gradual improvement in her respiratory and mental status. However, on hospital Day 7, she has extreme somnolence and altered mental status without respiratory involvement. Our team suspects VPA toxicity and/or VPA-induced hyperammonemic encephalopathy (VHE).

VPA-induced hyperammonemia

Hyperammonemia can occur in individuals receiving VPA and is most often asymptomatic. However, elevations in ammonia may lead to VHE, which is a rare but serious adverse effect. VHE has been reported early in treatment, in acute VPA overdose, and in chronic VPA use despite normal doses and levels.¹ It also can occur in the absence of clinical and laboratory evidence of hepatotoxicity. VHE is associated with significant morbidity and CNS damage. Symptoms of VHE include vomiting, lethargy, and confusion. If left untreated, VHE can lead to coma and death.

Mechanism of VHE. The exact mechanism of VHE is unknown.^1-3 Ammonia is a toxic base produced by deamination of amino acids. The liver eliminates ammonia via the urea cycle.² Valproic acid metabolites, propionate and 4-en-VPA, can directly inhibit N-acetyl glutamate, which can disrupt the urea cycle, leading to elevated ammonia levels.³ Long-term or high-dose VPA can lead to carnitine deficiency, primarily by inhibiting its biosynthesis and depleting stores.⁴ Carnitine deficiency leads to disturbances in mitochondrial function, causing inhibition of the urea cycle and increasing ammonia. CNS toxicity due to hyperammonemia is thought to be due to activation of glutamate receptors.³

Risk factors. Co-administration of other antiepileptic drugs (AEDs) with VPA is a risk factor for VHE.^1,5 This happens because enzyme-inducing AEDs such as phenytoin, phenobarbital, and carba­mazepine can increase toxic metabolites of VPA, which can lead to hyperammonemia. Topiramate can also inhibit the urea cycle, leading to increased ammonia levels. Additionally, co-administration of VPA with quetiapine, paliperidone, risperidone, or aripiprazole has been reported to increase the risk of VHE.^1,5 Intellectual disability, carnitine deficiency, low albumin, and abnormal liver function have also been reported to increase the risk of VHE.^1,5

Continue to: Diagnosis and management

Diagnosis and management. If a patient receiving VPA is experiencing nausea, fatigue, or somnolence, it is important to check the patient’s ammonia level (normal range: 11 to 32 µmol/L) and VPA total levels (therapeutic range: 50 to 125 µg/mL). Consider checking a VPA free level, especially in geriatric patients or patients who have low albumin; the therapeutic range of VPA free is  6 to 22 µg/mL.³ If the ammonia level is elevated, discontinue VPA immediately (Table).^1-3 Clinicians may also elect to prescribe lactulose until ammonia levels return to normal range. Adding levocarnitine may also help, although evidence is limited to small case series or retrospective studies.³ Currently, there is no known advantage in combining lactulose and levocarnitine to address VHE. Severe cases of VHE (ammonia levels >400 µmol/L) may require hemodialysis.¹

Prevention. Strategies to prevent VHE include avoiding polypharmacy, especially concurrent use of enzyme-inducing AEDs and possibly second-generation antipsychotics. Additionally, VPA should not be used in individuals with urea cycle disorders. It is unknown if levocarnitine supplementation is preventive, but this approach has been suggested.³

CASE CONTINUED

Mrs. C has several possible risk factors for VHE, including co-administration of quetiapine and VPA, and a low albumin level. A further laboratory workup for Mrs. C reveals a VPA free level of 19 µg/mL (21.1% free), a VPA total level of 90 µg/mL, and an ammonia level of 79 µmol/L, confirming our suspicions regarding VHE. We determine that Mrs. C’s altered mental status is likely due her elevated ammonia levels, because the infection had been improving in the days leading up to the sudden, extreme somnolence.

VPA is immediately stopped and Mrs. C receives 1 dose of lactulose. The following day, Mrs. C’s mental status improves, and her ammonia levels return to normal. On hospital Day 9, she is transferred back to the psychiatric facility for management of manic and psychotic symptoms.

Related Resources

• Brown LM, Cupples N, Moore TA. Levocarnitine for valproate-induced hyperammonemia in the psychiatric setting: a case series and literature review. Ment Health Clin. 2018;8(3):148-154.
• Aires CCP, van Cruchten A, Ijlat L, et al. New insights on the mechanisms of valproate-induced hyperammonemia: inhibition of hepatic N-acetylglutamate synthase activity by valproyl-CoA. J Hepatol. 2011;55(2):426-434.

Drug Brand Names

Aripiprazole • Abilify
Carbamazepine • Tegretol
Lactulose • Enulose
Levocarnitine • Carnitine, Carnitor
Levofloxacin • Levaquin IV
Paliperidone • Invega
Phenobarbital • Luminal
Phenytoin • Dilantin
Quetiapine • Seroquel
Risperidone • Risperdal
Topiramate • Topamax
Valproic acid • Depakene

The American Psychiatric Association (APA) is the largest psychiatric organization in the world, with >38,500 members across 100 countries. At 175 years of age, it is also the oldest medical association in the United States, 3 years older than the venerable American Medical Association, and 48 years older than its mental health sister, the American Psychological Association.

I am truly honored to be nominated as the next APA President-Elect (Note: Dr. Nasrallah has withdrawn his candidacy for APA President-Elect. For a statement of explanation, click here), which prompted me to delve into the history of this great association that unifies us, empowers us, and gives us a loud voice to advocate for our patients, for our noble medical profession, and for advancing the mental health of society at large.

Our APA was established by 13 superintendents of the “Insane Asylums and Hospitals” in 1844. Its first name was a mouthful—the Association of Medical Superintendents of American Institutions of the Insane, a term now regarded as pejorative and unscientific. Thankfully, the name was changed almost 50 years later (in 1893) to the American Medico-Psychological Association, which was refined 28 years later in 1921 to the American Psychiatric Association, a name that has lasted for the past 99 years. If I am fortunate enough to be elected by my peers this month as President-Elect, and assume the APA Presidency in May 2021, a full century after the name of APA was adopted in 1921 (the era of Kraepelin, Bleuler, and Freud), I will propose and ask the APA members to approve inserting “physicians” in the APA name so it will become the American Psychiatric Physicians Association, or APPA. This will clearly reflect our medical training and identity, and underscore the remarkable progress achieved by the inspiring and diligent work of countless psychiatric physicians over the past century.

By the way, per a Google search, the term “physician” came about in the 13th century, when the Anglo-Normans used the French term “physique” or remedy, to coin the English word “physic” or medicine. Science historian Howard Markel discussed how “physic” became “physician.” As for the term “psychiatrist,” it was coined in 1808 by the German physician Johann Christian Reil, and it essentially means “medical treatment of the soul.”

The APA has an amazing structure that is very democratic, enabling members to elect their leaders as well as their representatives on the Assembly. It has a Board of Trustees (Table 1) comprised of 22 members, 7 of whom comprise the Executive Committee, plus 3 attendees. Eight standing committees (Table 2) report to the Board. There are also 13 councils (Table 3), 11 caucuses (Table 4), and 7 minority and underrepresented caucuses (Table 5). The APA has a national network of 76 District Branches (DBs), each usually representing one state, except for large states that have several DBs (California has 5, and New York has 13). The District of Columbia, Puerto Rico, Western Canada, and Quebec/Eastern Canada each have DBs as well. The DBs have their own bylaws, governance structures, and annual dues, and within them, they may have local “societies” in large cities. Finally, each DB elects representatives to the Assembly, which is comprised of 7 Areas, each of which contains several states.

I am glad to have been a member of the APA for more than 4 decades, since my residency days. Although most psychiatrists in the United States and Canada belong to the APA, some do not, either because they never joined, or they dropped out because they think the dues are high (although dues are less than half of 1% of the average psychiatrist’s annual income, which is a great bargain). So, for my colleagues who do belong, and especially for those who do not, I provide 20 reasons why being an APA member offers so many advantages, professionally and personally, and has a tremendous benefit to us individually and collectively:

1. It makes eminent sense to unify as members of a medical profession to enable us to be strong and influential, to overcome our challenges, and to achieve our goals.

Continue to: #2

2. The APA’s main objectives are to advocate for our patients, for member psychiatrists, and for the growth and success of the discipline of psychiatric medicine.

3. Being an APA member helps fight the hurtful stigma and disparity of parity, which we must all strive for together every day for our psychiatric patients.

4. A strong APA will fight for us to eliminate practice hassles such as outrageous pre-authorizations, complicated maintenance of certification process, cumbersome and time-consuming electronic medical records, and medico-legal constraints.

5. Unity affords our Association moral authority and social gravitas so that we become more credible when we educate the public to dispel the many myths and misconceptions about mental illness.

6. The APA provides us with the necessary political power and influence because medical care can be significantly impacted by good or bad legislation.

Continue to: #7

7. Our economic welfare needs a strong APA to which we all belong.

8. The antipsychiatry movement is a malignant antiscientific ideology that must be countered by all of us through a robust APA to which we all must belong.

9. The APA provides an enormous array of services and resources to all of us, individually or as groups. Many members don’t know that because they never ask.

10. While it is good to have subspecialty societies within the APA, we are all psychiatric physicians who have the same medical and psychiatric training and share the same core values. By joining the APA as our Mother Organization, we avoid Balkanization of our profession, which weakens all of us if we are divided into smaller groups.

11. The APA helps cultivate and recruit more medical students to choose psychiatry as a career. This is vital for the health of our field.

Continue to: #12

12. Mentoring residents about the professional issues of our specialty and involving them in committees is one of the priorities of the APA, which extends into the post-residency phase (early career psychiatrists).

13. The APA provides a “Big Tent” of diverse groups of colleagues across a rich mosaic of racial and ethnic groups, genders, national origins, sexual orientations, and practice settings. Our patients are diverse, and so are we.

14. Education is a top priority for the APA, providing its members with a wide array of opportunities for ongoing and life-long learning. This includes the spectacular annual meeting with its cornucopia of educational offers and newsletters, as well as many initiatives throughout the year.

15. The APA journals, especially its flagship American Journal of Psychiatry (AJP), are among the most cited publications in the world. We get them for free, even though the cost of a personal subscription to the AJP alone for non-APA members is equivalent to the entire annual dues!

16. The APA has many top researchers among its members, spread across more than 150 medical schools. Those members generate new knowledge that continuously advances the field of psychiatry and provides new evidence-based tools for psychiatric practitioners.

Continue to: #17

17. The APA is our community, an ecosystem that sustains us as psychiatrists, and connects us in many gratifying ways that keep us rejuvenated and helps us avoid burnout that may occur in absence of a supportive network of supportive peers.

18. The APA provides us discounts on malpractice insurance and other products.

19. Opportunities for personal and professional growth are available within the APA. This includes leadership skills via participation in the DBs or at the national level via committees, councils, caucuses, and the Assembly.

20. Last but not least, the APA represents all of us in The House of Medicine. It has very productive partnerships and collaborations with many other medical organizations that support us and help us achieve our cherished mission. Besides adding “Physicians” to the APA name, working closely with other physicians across many specialties (especially primary care) will consolidate our medical identity and lead to better outcomes for our patients through collaborative care initiatives.

I thank all my colleagues who are APA members or Fellows, and urge all the readers of Current Psychiatry who never joined the APA or dropped out for any reason to come home to our Mother Organization. I hope you not only join, but become actively involved in the APA democratic governance structure, and contribute your considerable talents and skills to take the APA (which will hopefully become APPA in 2021) to its next level of preeminence. We will all be better for it.

PS. Please VOTE in this month’s APA election! It’s our sacred duty. 

The American Psychiatric Association (APA) is the largest psychiatric organization in the world, with >38,500 members across 100 countries. At 175 years of age, it is also the oldest medical association in the United States, 3 years older than the venerable American Medical Association, and 48 years older than its mental health sister, the American Psychological Association.

I am truly honored to be nominated as the next APA President-Elect (Note: Dr. Nasrallah has withdrawn his candidacy for APA President-Elect. For a statement of explanation, click here), which prompted me to delve into the history of this great association that unifies us, empowers us, and gives us a loud voice to advocate for our patients, for our noble medical profession, and for advancing the mental health of society at large.

Our APA was established by 13 superintendents of the “Insane Asylums and Hospitals” in 1844. Its first name was a mouthful—the Association of Medical Superintendents of American Institutions of the Insane, a term now regarded as pejorative and unscientific. Thankfully, the name was changed almost 50 years later (in 1893) to the American Medico-Psychological Association, which was refined 28 years later in 1921 to the American Psychiatric Association, a name that has lasted for the past 99 years. If I am fortunate enough to be elected by my peers this month as President-Elect, and assume the APA Presidency in May 2021, a full century after the name of APA was adopted in 1921 (the era of Kraepelin, Bleuler, and Freud), I will propose and ask the APA members to approve inserting “physicians” in the APA name so it will become the American Psychiatric Physicians Association, or APPA. This will clearly reflect our medical training and identity, and underscore the remarkable progress achieved by the inspiring and diligent work of countless psychiatric physicians over the past century.

By the way, per a Google search, the term “physician” came about in the 13th century, when the Anglo-Normans used the French term “physique” or remedy, to coin the English word “physic” or medicine. Science historian Howard Markel discussed how “physic” became “physician.” As for the term “psychiatrist,” it was coined in 1808 by the German physician Johann Christian Reil, and it essentially means “medical treatment of the soul.”

The APA has an amazing structure that is very democratic, enabling members to elect their leaders as well as their representatives on the Assembly. It has a Board of Trustees (Table 1) comprised of 22 members, 7 of whom comprise the Executive Committee, plus 3 attendees. Eight standing committees (Table 2) report to the Board. There are also 13 councils (Table 3), 11 caucuses (Table 4), and 7 minority and underrepresented caucuses (Table 5). The APA has a national network of 76 District Branches (DBs), each usually representing one state, except for large states that have several DBs (California has 5, and New York has 13). The District of Columbia, Puerto Rico, Western Canada, and Quebec/Eastern Canada each have DBs as well. The DBs have their own bylaws, governance structures, and annual dues, and within them, they may have local “societies” in large cities. Finally, each DB elects representatives to the Assembly, which is comprised of 7 Areas, each of which contains several states.

I am glad to have been a member of the APA for more than 4 decades, since my residency days. Although most psychiatrists in the United States and Canada belong to the APA, some do not, either because they never joined, or they dropped out because they think the dues are high (although dues are less than half of 1% of the average psychiatrist’s annual income, which is a great bargain). So, for my colleagues who do belong, and especially for those who do not, I provide 20 reasons why being an APA member offers so many advantages, professionally and personally, and has a tremendous benefit to us individually and collectively:

1. It makes eminent sense to unify as members of a medical profession to enable us to be strong and influential, to overcome our challenges, and to achieve our goals.

Continue to: #2

2. The APA’s main objectives are to advocate for our patients, for member psychiatrists, and for the growth and success of the discipline of psychiatric medicine.

3. Being an APA member helps fight the hurtful stigma and disparity of parity, which we must all strive for together every day for our psychiatric patients.

4. A strong APA will fight for us to eliminate practice hassles such as outrageous pre-authorizations, complicated maintenance of certification process, cumbersome and time-consuming electronic medical records, and medico-legal constraints.

5. Unity affords our Association moral authority and social gravitas so that we become more credible when we educate the public to dispel the many myths and misconceptions about mental illness.

6. The APA provides us with the necessary political power and influence because medical care can be significantly impacted by good or bad legislation.

Continue to: #7

7. Our economic welfare needs a strong APA to which we all belong.

8. The antipsychiatry movement is a malignant antiscientific ideology that must be countered by all of us through a robust APA to which we all must belong.

9. The APA provides an enormous array of services and resources to all of us, individually or as groups. Many members don’t know that because they never ask.

10. While it is good to have subspecialty societies within the APA, we are all psychiatric physicians who have the same medical and psychiatric training and share the same core values. By joining the APA as our Mother Organization, we avoid Balkanization of our profession, which weakens all of us if we are divided into smaller groups.

11. The APA helps cultivate and recruit more medical students to choose psychiatry as a career. This is vital for the health of our field.

Continue to: #12

12. Mentoring residents about the professional issues of our specialty and involving them in committees is one of the priorities of the APA, which extends into the post-residency phase (early career psychiatrists).

13. The APA provides a “Big Tent” of diverse groups of colleagues across a rich mosaic of racial and ethnic groups, genders, national origins, sexual orientations, and practice settings. Our patients are diverse, and so are we.

14. Education is a top priority for the APA, providing its members with a wide array of opportunities for ongoing and life-long learning. This includes the spectacular annual meeting with its cornucopia of educational offers and newsletters, as well as many initiatives throughout the year.

15. The APA journals, especially its flagship American Journal of Psychiatry (AJP), are among the most cited publications in the world. We get them for free, even though the cost of a personal subscription to the AJP alone for non-APA members is equivalent to the entire annual dues!

16. The APA has many top researchers among its members, spread across more than 150 medical schools. Those members generate new knowledge that continuously advances the field of psychiatry and provides new evidence-based tools for psychiatric practitioners.

Continue to: #17

17. The APA is our community, an ecosystem that sustains us as psychiatrists, and connects us in many gratifying ways that keep us rejuvenated and helps us avoid burnout that may occur in absence of a supportive network of supportive peers.

18. The APA provides us discounts on malpractice insurance and other products.

19. Opportunities for personal and professional growth are available within the APA. This includes leadership skills via participation in the DBs or at the national level via committees, councils, caucuses, and the Assembly.

20. Last but not least, the APA represents all of us in The House of Medicine. It has very productive partnerships and collaborations with many other medical organizations that support us and help us achieve our cherished mission. Besides adding “Physicians” to the APA name, working closely with other physicians across many specialties (especially primary care) will consolidate our medical identity and lead to better outcomes for our patients through collaborative care initiatives.

I thank all my colleagues who are APA members or Fellows, and urge all the readers of Current Psychiatry who never joined the APA or dropped out for any reason to come home to our Mother Organization. I hope you not only join, but become actively involved in the APA democratic governance structure, and contribute your considerable talents and skills to take the APA (which will hopefully become APPA in 2021) to its next level of preeminence. We will all be better for it.

PS. Please VOTE in this month’s APA election! It’s our sacred duty. 

The American Psychiatric Association (APA) is the largest psychiatric organization in the world, with >38,500 members across 100 countries. At 175 years of age, it is also the oldest medical association in the United States, 3 years older than the venerable American Medical Association, and 48 years older than its mental health sister, the American Psychological Association.

I am truly honored to be nominated as the next APA President-Elect (Note: Dr. Nasrallah has withdrawn his candidacy for APA President-Elect. For a statement of explanation, click here), which prompted me to delve into the history of this great association that unifies us, empowers us, and gives us a loud voice to advocate for our patients, for our noble medical profession, and for advancing the mental health of society at large.

Our APA was established by 13 superintendents of the “Insane Asylums and Hospitals” in 1844. Its first name was a mouthful—the Association of Medical Superintendents of American Institutions of the Insane, a term now regarded as pejorative and unscientific. Thankfully, the name was changed almost 50 years later (in 1893) to the American Medico-Psychological Association, which was refined 28 years later in 1921 to the American Psychiatric Association, a name that has lasted for the past 99 years. If I am fortunate enough to be elected by my peers this month as President-Elect, and assume the APA Presidency in May 2021, a full century after the name of APA was adopted in 1921 (the era of Kraepelin, Bleuler, and Freud), I will propose and ask the APA members to approve inserting “physicians” in the APA name so it will become the American Psychiatric Physicians Association, or APPA. This will clearly reflect our medical training and identity, and underscore the remarkable progress achieved by the inspiring and diligent work of countless psychiatric physicians over the past century.

By the way, per a Google search, the term “physician” came about in the 13th century, when the Anglo-Normans used the French term “physique” or remedy, to coin the English word “physic” or medicine. Science historian Howard Markel discussed how “physic” became “physician.” As for the term “psychiatrist,” it was coined in 1808 by the German physician Johann Christian Reil, and it essentially means “medical treatment of the soul.”

The APA has an amazing structure that is very democratic, enabling members to elect their leaders as well as their representatives on the Assembly. It has a Board of Trustees (Table 1) comprised of 22 members, 7 of whom comprise the Executive Committee, plus 3 attendees. Eight standing committees (Table 2) report to the Board. There are also 13 councils (Table 3), 11 caucuses (Table 4), and 7 minority and underrepresented caucuses (Table 5). The APA has a national network of 76 District Branches (DBs), each usually representing one state, except for large states that have several DBs (California has 5, and New York has 13). The District of Columbia, Puerto Rico, Western Canada, and Quebec/Eastern Canada each have DBs as well. The DBs have their own bylaws, governance structures, and annual dues, and within them, they may have local “societies” in large cities. Finally, each DB elects representatives to the Assembly, which is comprised of 7 Areas, each of which contains several states.

I am glad to have been a member of the APA for more than 4 decades, since my residency days. Although most psychiatrists in the United States and Canada belong to the APA, some do not, either because they never joined, or they dropped out because they think the dues are high (although dues are less than half of 1% of the average psychiatrist’s annual income, which is a great bargain). So, for my colleagues who do belong, and especially for those who do not, I provide 20 reasons why being an APA member offers so many advantages, professionally and personally, and has a tremendous benefit to us individually and collectively:

1. It makes eminent sense to unify as members of a medical profession to enable us to be strong and influential, to overcome our challenges, and to achieve our goals.

Continue to: #2

2. The APA’s main objectives are to advocate for our patients, for member psychiatrists, and for the growth and success of the discipline of psychiatric medicine.

3. Being an APA member helps fight the hurtful stigma and disparity of parity, which we must all strive for together every day for our psychiatric patients.

4. A strong APA will fight for us to eliminate practice hassles such as outrageous pre-authorizations, complicated maintenance of certification process, cumbersome and time-consuming electronic medical records, and medico-legal constraints.

5. Unity affords our Association moral authority and social gravitas so that we become more credible when we educate the public to dispel the many myths and misconceptions about mental illness.

6. The APA provides us with the necessary political power and influence because medical care can be significantly impacted by good or bad legislation.

Continue to: #7

7. Our economic welfare needs a strong APA to which we all belong.

8. The antipsychiatry movement is a malignant antiscientific ideology that must be countered by all of us through a robust APA to which we all must belong.

9. The APA provides an enormous array of services and resources to all of us, individually or as groups. Many members don’t know that because they never ask.

10. While it is good to have subspecialty societies within the APA, we are all psychiatric physicians who have the same medical and psychiatric training and share the same core values. By joining the APA as our Mother Organization, we avoid Balkanization of our profession, which weakens all of us if we are divided into smaller groups.

11. The APA helps cultivate and recruit more medical students to choose psychiatry as a career. This is vital for the health of our field.

Continue to: #12

12. Mentoring residents about the professional issues of our specialty and involving them in committees is one of the priorities of the APA, which extends into the post-residency phase (early career psychiatrists).

13. The APA provides a “Big Tent” of diverse groups of colleagues across a rich mosaic of racial and ethnic groups, genders, national origins, sexual orientations, and practice settings. Our patients are diverse, and so are we.

14. Education is a top priority for the APA, providing its members with a wide array of opportunities for ongoing and life-long learning. This includes the spectacular annual meeting with its cornucopia of educational offers and newsletters, as well as many initiatives throughout the year.

15. The APA journals, especially its flagship American Journal of Psychiatry (AJP), are among the most cited publications in the world. We get them for free, even though the cost of a personal subscription to the AJP alone for non-APA members is equivalent to the entire annual dues!

16. The APA has many top researchers among its members, spread across more than 150 medical schools. Those members generate new knowledge that continuously advances the field of psychiatry and provides new evidence-based tools for psychiatric practitioners.

Continue to: #17

17. The APA is our community, an ecosystem that sustains us as psychiatrists, and connects us in many gratifying ways that keep us rejuvenated and helps us avoid burnout that may occur in absence of a supportive network of supportive peers.

18. The APA provides us discounts on malpractice insurance and other products.

19. Opportunities for personal and professional growth are available within the APA. This includes leadership skills via participation in the DBs or at the national level via committees, councils, caucuses, and the Assembly.

20. Last but not least, the APA represents all of us in The House of Medicine. It has very productive partnerships and collaborations with many other medical organizations that support us and help us achieve our cherished mission. Besides adding “Physicians” to the APA name, working closely with other physicians across many specialties (especially primary care) will consolidate our medical identity and lead to better outcomes for our patients through collaborative care initiatives.

I thank all my colleagues who are APA members or Fellows, and urge all the readers of Current Psychiatry who never joined the APA or dropped out for any reason to come home to our Mother Organization. I hope you not only join, but become actively involved in the APA democratic governance structure, and contribute your considerable talents and skills to take the APA (which will hopefully become APPA in 2021) to its next level of preeminence. We will all be better for it.

PS. Please VOTE in this month’s APA election! It’s our sacred duty.