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Family violence after COVID: Understanding coercive relationships
Despite the ability of some couples to pull together and manage through the COVID-19 pandemic, other couples and families failed to thrive. Increasing divorce rates have been noted nationwide with many disagreements being specifically about COVID.1
A review of over 1 million tweets, between April 12 and July 16, 2020, found an increase in calls to hotlines and increased reports of a variety of types of family violence. There were also more inquiries about social services for family violence, an increased presence from social movements, and more domestic violence-related news.2
The literature addressing family violence uses a variety of terms, so here are some definitions.
Domestic violence is defined as a pattern of behaviors used to gain or maintain power and control. Broadly speaking, domestic violence includes elder abuse, sibling abuse, child abuse, intimate partner abuse, parent abuse, and can also include people who don’t necessarily live together but who have an intimate relationship. Domestic violence centers use the Power and Control Wheel (see graphic) developed by the Domestic Abuse Intervention Project in Duluth, Minn., to describe how domestic violence occurs.
Intimate partner violence is more specific, referring to violence that happens between people in an ongoing or former intimate or romantic relationship, and is a subcategory of domestic violence.
Coercive control is the use of power for control and compliance. It is a dynamic and systematic process described in the top left corner of the Power and Control Wheel. Overt control occurs with the implication that “if you don’t follow the rules, I’ll kill you.” More subtle control is when obedience is forced through monopolizing resources, dictating preferred choices, microregulating a partner’s behavior, and deprivation of supports needed to exercise independent judgment.
All interpersonal relationships have elements of persuasion and influence; however, the goal of coercive relationships is to maintain power and control. It is a dynamic of the relationship. Coercive control emphasizes the systematic, organized, multifaceted, and patterned nature of this interpersonal dynamic and can be considered to originate in the patriarchal dynamic where men control women.
Most professionals who work in this interdisciplinary area now refer to domestic violence as coercive control. Victimizers target women whom they sense they can control to get their own needs met. They are disinclined to invest in relationships with women who stress their own points of view, who do not readily accept blame when there is a disagreement, and who offer nurturing only when it is reciprocated.
In my office, if I think there are elements of coercion in a relationship, I bring out the Power and Control Wheel and the patient and I go over it. Good education is our responsibility. However, we all have met women who decide to stay in unhealthy relationships.
Assessing people who stay in coercive relationships
Fear
The most important first step is to assess safety. Are they afraid of increased violence if they challenge their partner? Restraining orders or other legal deterrents may not offer solace, as many women are clear that their spouse will come after them, if not tomorrow, then next week, or even next month. They are sure that they will not be safe.
In these cases, I go over safety steps with them so that if they decide to go, they will be prepared. I bring out the “safety box,” which includes the following action steps:
- Memorize important phone numbers of people to call in an emergency.
- If your children are old enough, teach them important phone numbers, including when to dial 911.
- If you can, open your own bank account.
- Stay in touch with friends. Get to know your neighbors. Don’t cut yourself off from people, even if you feel like you want to be alone.
- Rehearse your escape plan until you know it by heart.
- Leave a set of car keys, extra money, a change of clothes and copies of important documents with a trusted friend or relative: your own and your children’s birth certificates, children’s school and medical records, bank books, welfare identification, passport/green card, immigration papers, social security card, lease agreements or mortgage payment books, insurance papers, important addresses, and telephone numbers.
- Keep information about domestic violence in a safe place, where your abuser won’t find it, but where you can get it when you need to review it.
Some women may acknowledge that the risk of physical violence is not the determining factor in their decision to stay and have difficulty explaining why they choose to stay. I suggest that we then consider the following frames that have their origin in the study of the impact of trauma.
Shame
From this lens, abusive events are humiliating experiences, now represented as shame experiences. Humiliation and shame hide hostile feelings that the patient is not able to acknowledge.
“In shame, the self is the failure and others may reject or be critical of this exposed, flawed self.”3 Women will therefore remain attached to an abuser to avoid the exposure of their defective self.
Action steps: Empathic engagement and acknowledgment of shame and humiliation are key. For someone to overcome shame, they must face their sense of their defective self and have strategies to manage these feelings. The development of such strategies is the next step.
Trauma repetition and trauma bonding
Women subjected to domestic violence often respond with incapacitating traumatic syndromes. The concept of “trauma repetition” is suggested as a cause of vulnerability to repeated abuse, and “trauma bonding” is the term for the intense and tenacious bond that can form between abusers and victims.4
Trauma bonding implies that a sense of safety and closeness and secure attachment can only be reached through highly abusive engagement; anything else is experienced as “superficial, cold, or irrelevant.”5 Trauma bonding may have its origins in emotional neglect, according to self reports of 116 women.6Action steps: The literature on trauma is growing and many patients will benefit from good curated sources. Having a good list of books and website on hand is important. Discussion and exploration of the impact of trauma will be needed, and can be provided by someone who is available on a consistent and frequent basis. This work may be time consuming and difficult.
Some asides
1. Some psychiatrists proffer the explanation that these women who stay must be masochistic. The misogynistic concept of masochism still haunts the halls of psychiatry. It is usually offered as a way to dismiss these women’s concerns.
2. One of the obstacles to recognizing chronic mistreatment in relationships is that most abusive men simply “do not seem like abusers.” They have many good qualities, including times of kindness, warmth, and humor, especially in the initial period of a relationship. An abuser’s friends may think the world of him. He may have a successful work life and have no problems with drugs or alcohol. He may simply not fit anyone’s image of a cruel or intimidating person. So, when a woman feels her relationship spinning out of control, it may not occur to her that her partner is an abuser. Even if she does consider her partner to be overly controlling, others may question her perception.
3. Neutrality in family courts is systemic sexism/misogyny. When it comes to domestic violence, family courts tend to split the difference. Stephanie Brandt, MD, notes that The assumption that it is violence alone that matters has formed the basis of much clinical and legal confusion.7 As an analyst, she has gone against the grain of a favored neutrality and become active in the courts, noting the secondary victimization that occurs when a woman enters the legal system.
In summary, psychiatrists must reclaim our expertise in systemic dynamics and point out the role of systemic misogyny. Justices and other court officials need to be educated. Ideally, justice should be based on the equality of men and women in a society free of systemic misogyny. Unfortunately our society has not yet reached this position. In the meanwhile, we must think systemically about interpersonal dynamics. This is our lane. This should not be controversial.
Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at [email protected]. Dr. Heru would like to thank Dr. Stephanie Brandt for discussing this topic with her and supporting this work.
References
1. Ellyatt H. Arguing with your partner over Covid? You’re not alone, with the pandemic straining many relationships. 2022 Jan 21. https://www.cnbc.com/2022/01/21/covid-has-put-pressures-and-strains-on-relationships.html
2. Xue J et al. J Med Internet Res. 2020 Nov 6;22(11):e24361. doi: 10.2196/24361.
3. Dorahy MJ. J Trauma Dissociation. 2017 May-Jun;18(3):383-96. doi: 10.1080/15299732.2017.1295422.
4. Dutton DG and Painter SL. Victimology. 1981 Jan;6(1):139-55.
5. Sachs A. J Trauma Dissociation. 2017 May-Jun;18(3):319-39. doi: 10.1080/15299732.2017.1295400.
6. Krüger C and Fletcher L. J Trauma Dissociation. 2017 May-Jun;18(3):356-72. doi: 10.1080/15299732.2017.1295420.
7. Brandt S and Rudden M. Int J Appl Psychoanal Studies. 2020 Sept;17(3):215-31. doi: 10.1002/aps.1671.
Despite the ability of some couples to pull together and manage through the COVID-19 pandemic, other couples and families failed to thrive. Increasing divorce rates have been noted nationwide with many disagreements being specifically about COVID.1
A review of over 1 million tweets, between April 12 and July 16, 2020, found an increase in calls to hotlines and increased reports of a variety of types of family violence. There were also more inquiries about social services for family violence, an increased presence from social movements, and more domestic violence-related news.2
The literature addressing family violence uses a variety of terms, so here are some definitions.
Domestic violence is defined as a pattern of behaviors used to gain or maintain power and control. Broadly speaking, domestic violence includes elder abuse, sibling abuse, child abuse, intimate partner abuse, parent abuse, and can also include people who don’t necessarily live together but who have an intimate relationship. Domestic violence centers use the Power and Control Wheel (see graphic) developed by the Domestic Abuse Intervention Project in Duluth, Minn., to describe how domestic violence occurs.
Intimate partner violence is more specific, referring to violence that happens between people in an ongoing or former intimate or romantic relationship, and is a subcategory of domestic violence.
Coercive control is the use of power for control and compliance. It is a dynamic and systematic process described in the top left corner of the Power and Control Wheel. Overt control occurs with the implication that “if you don’t follow the rules, I’ll kill you.” More subtle control is when obedience is forced through monopolizing resources, dictating preferred choices, microregulating a partner’s behavior, and deprivation of supports needed to exercise independent judgment.
All interpersonal relationships have elements of persuasion and influence; however, the goal of coercive relationships is to maintain power and control. It is a dynamic of the relationship. Coercive control emphasizes the systematic, organized, multifaceted, and patterned nature of this interpersonal dynamic and can be considered to originate in the patriarchal dynamic where men control women.
Most professionals who work in this interdisciplinary area now refer to domestic violence as coercive control. Victimizers target women whom they sense they can control to get their own needs met. They are disinclined to invest in relationships with women who stress their own points of view, who do not readily accept blame when there is a disagreement, and who offer nurturing only when it is reciprocated.
In my office, if I think there are elements of coercion in a relationship, I bring out the Power and Control Wheel and the patient and I go over it. Good education is our responsibility. However, we all have met women who decide to stay in unhealthy relationships.
Assessing people who stay in coercive relationships
Fear
The most important first step is to assess safety. Are they afraid of increased violence if they challenge their partner? Restraining orders or other legal deterrents may not offer solace, as many women are clear that their spouse will come after them, if not tomorrow, then next week, or even next month. They are sure that they will not be safe.
In these cases, I go over safety steps with them so that if they decide to go, they will be prepared. I bring out the “safety box,” which includes the following action steps:
- Memorize important phone numbers of people to call in an emergency.
- If your children are old enough, teach them important phone numbers, including when to dial 911.
- If you can, open your own bank account.
- Stay in touch with friends. Get to know your neighbors. Don’t cut yourself off from people, even if you feel like you want to be alone.
- Rehearse your escape plan until you know it by heart.
- Leave a set of car keys, extra money, a change of clothes and copies of important documents with a trusted friend or relative: your own and your children’s birth certificates, children’s school and medical records, bank books, welfare identification, passport/green card, immigration papers, social security card, lease agreements or mortgage payment books, insurance papers, important addresses, and telephone numbers.
- Keep information about domestic violence in a safe place, where your abuser won’t find it, but where you can get it when you need to review it.
Some women may acknowledge that the risk of physical violence is not the determining factor in their decision to stay and have difficulty explaining why they choose to stay. I suggest that we then consider the following frames that have their origin in the study of the impact of trauma.
Shame
From this lens, abusive events are humiliating experiences, now represented as shame experiences. Humiliation and shame hide hostile feelings that the patient is not able to acknowledge.
“In shame, the self is the failure and others may reject or be critical of this exposed, flawed self.”3 Women will therefore remain attached to an abuser to avoid the exposure of their defective self.
Action steps: Empathic engagement and acknowledgment of shame and humiliation are key. For someone to overcome shame, they must face their sense of their defective self and have strategies to manage these feelings. The development of such strategies is the next step.
Trauma repetition and trauma bonding
Women subjected to domestic violence often respond with incapacitating traumatic syndromes. The concept of “trauma repetition” is suggested as a cause of vulnerability to repeated abuse, and “trauma bonding” is the term for the intense and tenacious bond that can form between abusers and victims.4
Trauma bonding implies that a sense of safety and closeness and secure attachment can only be reached through highly abusive engagement; anything else is experienced as “superficial, cold, or irrelevant.”5 Trauma bonding may have its origins in emotional neglect, according to self reports of 116 women.6Action steps: The literature on trauma is growing and many patients will benefit from good curated sources. Having a good list of books and website on hand is important. Discussion and exploration of the impact of trauma will be needed, and can be provided by someone who is available on a consistent and frequent basis. This work may be time consuming and difficult.
Some asides
1. Some psychiatrists proffer the explanation that these women who stay must be masochistic. The misogynistic concept of masochism still haunts the halls of psychiatry. It is usually offered as a way to dismiss these women’s concerns.
2. One of the obstacles to recognizing chronic mistreatment in relationships is that most abusive men simply “do not seem like abusers.” They have many good qualities, including times of kindness, warmth, and humor, especially in the initial period of a relationship. An abuser’s friends may think the world of him. He may have a successful work life and have no problems with drugs or alcohol. He may simply not fit anyone’s image of a cruel or intimidating person. So, when a woman feels her relationship spinning out of control, it may not occur to her that her partner is an abuser. Even if she does consider her partner to be overly controlling, others may question her perception.
3. Neutrality in family courts is systemic sexism/misogyny. When it comes to domestic violence, family courts tend to split the difference. Stephanie Brandt, MD, notes that The assumption that it is violence alone that matters has formed the basis of much clinical and legal confusion.7 As an analyst, she has gone against the grain of a favored neutrality and become active in the courts, noting the secondary victimization that occurs when a woman enters the legal system.
In summary, psychiatrists must reclaim our expertise in systemic dynamics and point out the role of systemic misogyny. Justices and other court officials need to be educated. Ideally, justice should be based on the equality of men and women in a society free of systemic misogyny. Unfortunately our society has not yet reached this position. In the meanwhile, we must think systemically about interpersonal dynamics. This is our lane. This should not be controversial.
Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at [email protected]. Dr. Heru would like to thank Dr. Stephanie Brandt for discussing this topic with her and supporting this work.
References
1. Ellyatt H. Arguing with your partner over Covid? You’re not alone, with the pandemic straining many relationships. 2022 Jan 21. https://www.cnbc.com/2022/01/21/covid-has-put-pressures-and-strains-on-relationships.html
2. Xue J et al. J Med Internet Res. 2020 Nov 6;22(11):e24361. doi: 10.2196/24361.
3. Dorahy MJ. J Trauma Dissociation. 2017 May-Jun;18(3):383-96. doi: 10.1080/15299732.2017.1295422.
4. Dutton DG and Painter SL. Victimology. 1981 Jan;6(1):139-55.
5. Sachs A. J Trauma Dissociation. 2017 May-Jun;18(3):319-39. doi: 10.1080/15299732.2017.1295400.
6. Krüger C and Fletcher L. J Trauma Dissociation. 2017 May-Jun;18(3):356-72. doi: 10.1080/15299732.2017.1295420.
7. Brandt S and Rudden M. Int J Appl Psychoanal Studies. 2020 Sept;17(3):215-31. doi: 10.1002/aps.1671.
Despite the ability of some couples to pull together and manage through the COVID-19 pandemic, other couples and families failed to thrive. Increasing divorce rates have been noted nationwide with many disagreements being specifically about COVID.1
A review of over 1 million tweets, between April 12 and July 16, 2020, found an increase in calls to hotlines and increased reports of a variety of types of family violence. There were also more inquiries about social services for family violence, an increased presence from social movements, and more domestic violence-related news.2
The literature addressing family violence uses a variety of terms, so here are some definitions.
Domestic violence is defined as a pattern of behaviors used to gain or maintain power and control. Broadly speaking, domestic violence includes elder abuse, sibling abuse, child abuse, intimate partner abuse, parent abuse, and can also include people who don’t necessarily live together but who have an intimate relationship. Domestic violence centers use the Power and Control Wheel (see graphic) developed by the Domestic Abuse Intervention Project in Duluth, Minn., to describe how domestic violence occurs.
Intimate partner violence is more specific, referring to violence that happens between people in an ongoing or former intimate or romantic relationship, and is a subcategory of domestic violence.
Coercive control is the use of power for control and compliance. It is a dynamic and systematic process described in the top left corner of the Power and Control Wheel. Overt control occurs with the implication that “if you don’t follow the rules, I’ll kill you.” More subtle control is when obedience is forced through monopolizing resources, dictating preferred choices, microregulating a partner’s behavior, and deprivation of supports needed to exercise independent judgment.
All interpersonal relationships have elements of persuasion and influence; however, the goal of coercive relationships is to maintain power and control. It is a dynamic of the relationship. Coercive control emphasizes the systematic, organized, multifaceted, and patterned nature of this interpersonal dynamic and can be considered to originate in the patriarchal dynamic where men control women.
Most professionals who work in this interdisciplinary area now refer to domestic violence as coercive control. Victimizers target women whom they sense they can control to get their own needs met. They are disinclined to invest in relationships with women who stress their own points of view, who do not readily accept blame when there is a disagreement, and who offer nurturing only when it is reciprocated.
In my office, if I think there are elements of coercion in a relationship, I bring out the Power and Control Wheel and the patient and I go over it. Good education is our responsibility. However, we all have met women who decide to stay in unhealthy relationships.
Assessing people who stay in coercive relationships
Fear
The most important first step is to assess safety. Are they afraid of increased violence if they challenge their partner? Restraining orders or other legal deterrents may not offer solace, as many women are clear that their spouse will come after them, if not tomorrow, then next week, or even next month. They are sure that they will not be safe.
In these cases, I go over safety steps with them so that if they decide to go, they will be prepared. I bring out the “safety box,” which includes the following action steps:
- Memorize important phone numbers of people to call in an emergency.
- If your children are old enough, teach them important phone numbers, including when to dial 911.
- If you can, open your own bank account.
- Stay in touch with friends. Get to know your neighbors. Don’t cut yourself off from people, even if you feel like you want to be alone.
- Rehearse your escape plan until you know it by heart.
- Leave a set of car keys, extra money, a change of clothes and copies of important documents with a trusted friend or relative: your own and your children’s birth certificates, children’s school and medical records, bank books, welfare identification, passport/green card, immigration papers, social security card, lease agreements or mortgage payment books, insurance papers, important addresses, and telephone numbers.
- Keep information about domestic violence in a safe place, where your abuser won’t find it, but where you can get it when you need to review it.
Some women may acknowledge that the risk of physical violence is not the determining factor in their decision to stay and have difficulty explaining why they choose to stay. I suggest that we then consider the following frames that have their origin in the study of the impact of trauma.
Shame
From this lens, abusive events are humiliating experiences, now represented as shame experiences. Humiliation and shame hide hostile feelings that the patient is not able to acknowledge.
“In shame, the self is the failure and others may reject or be critical of this exposed, flawed self.”3 Women will therefore remain attached to an abuser to avoid the exposure of their defective self.
Action steps: Empathic engagement and acknowledgment of shame and humiliation are key. For someone to overcome shame, they must face their sense of their defective self and have strategies to manage these feelings. The development of such strategies is the next step.
Trauma repetition and trauma bonding
Women subjected to domestic violence often respond with incapacitating traumatic syndromes. The concept of “trauma repetition” is suggested as a cause of vulnerability to repeated abuse, and “trauma bonding” is the term for the intense and tenacious bond that can form between abusers and victims.4
Trauma bonding implies that a sense of safety and closeness and secure attachment can only be reached through highly abusive engagement; anything else is experienced as “superficial, cold, or irrelevant.”5 Trauma bonding may have its origins in emotional neglect, according to self reports of 116 women.6Action steps: The literature on trauma is growing and many patients will benefit from good curated sources. Having a good list of books and website on hand is important. Discussion and exploration of the impact of trauma will be needed, and can be provided by someone who is available on a consistent and frequent basis. This work may be time consuming and difficult.
Some asides
1. Some psychiatrists proffer the explanation that these women who stay must be masochistic. The misogynistic concept of masochism still haunts the halls of psychiatry. It is usually offered as a way to dismiss these women’s concerns.
2. One of the obstacles to recognizing chronic mistreatment in relationships is that most abusive men simply “do not seem like abusers.” They have many good qualities, including times of kindness, warmth, and humor, especially in the initial period of a relationship. An abuser’s friends may think the world of him. He may have a successful work life and have no problems with drugs or alcohol. He may simply not fit anyone’s image of a cruel or intimidating person. So, when a woman feels her relationship spinning out of control, it may not occur to her that her partner is an abuser. Even if she does consider her partner to be overly controlling, others may question her perception.
3. Neutrality in family courts is systemic sexism/misogyny. When it comes to domestic violence, family courts tend to split the difference. Stephanie Brandt, MD, notes that The assumption that it is violence alone that matters has formed the basis of much clinical and legal confusion.7 As an analyst, she has gone against the grain of a favored neutrality and become active in the courts, noting the secondary victimization that occurs when a woman enters the legal system.
In summary, psychiatrists must reclaim our expertise in systemic dynamics and point out the role of systemic misogyny. Justices and other court officials need to be educated. Ideally, justice should be based on the equality of men and women in a society free of systemic misogyny. Unfortunately our society has not yet reached this position. In the meanwhile, we must think systemically about interpersonal dynamics. This is our lane. This should not be controversial.
Dr. Heru is professor of psychiatry at the University of Colorado at Denver, Aurora. She is editor of “Working With Families in Medical Settings: A Multidisciplinary Guide for Psychiatrists and Other Health Professionals” (New York: Routledge, 2013). She has no conflicts of interest to disclose. Contact Dr. Heru at [email protected]. Dr. Heru would like to thank Dr. Stephanie Brandt for discussing this topic with her and supporting this work.
References
1. Ellyatt H. Arguing with your partner over Covid? You’re not alone, with the pandemic straining many relationships. 2022 Jan 21. https://www.cnbc.com/2022/01/21/covid-has-put-pressures-and-strains-on-relationships.html
2. Xue J et al. J Med Internet Res. 2020 Nov 6;22(11):e24361. doi: 10.2196/24361.
3. Dorahy MJ. J Trauma Dissociation. 2017 May-Jun;18(3):383-96. doi: 10.1080/15299732.2017.1295422.
4. Dutton DG and Painter SL. Victimology. 1981 Jan;6(1):139-55.
5. Sachs A. J Trauma Dissociation. 2017 May-Jun;18(3):319-39. doi: 10.1080/15299732.2017.1295400.
6. Krüger C and Fletcher L. J Trauma Dissociation. 2017 May-Jun;18(3):356-72. doi: 10.1080/15299732.2017.1295420.
7. Brandt S and Rudden M. Int J Appl Psychoanal Studies. 2020 Sept;17(3):215-31. doi: 10.1002/aps.1671.
TikTok offers to ‘balance your hormones’ are pure hokum
With more than 306 million views, #hormonebalance and #hormonebalancing are among the latest hacks to take over the social media platform TikTok, on which users post short videos. Influencers offer advice such as eating raw carrots for “happy hormones,” eating protein followed by fat for breakfast to regulate blood glucose, or taking vitamin B2 supplements for thyroid health.
Have you ever wondered if you were asleep during the lecture on “hormone balancing” in medical school? No, you weren’t. It was never a class for good reason, and you didn’t fail to read any such breakthrough studies in The New England Journal of Medicine either.
There are over 50 different hormones produced by humans and animals, regulating sleep, growth, metabolism and reproduction, among many other biological processes, so there is certainly no one-size-fits-all solution to ensure these are all working in perfect harmony.
When someone mentions “hormone balancing,” my mind wanders to the last time I took my car to have my tires rotated and balanced. If only it were as simple to balance hormones in real life. The best we can hope for is to get a specific hormone within the ideal physiologic range for that person’s age.
The term “hormone” can mean many things to different people. When a woman comes in with a hormone question, for example, it is often related to estrogen, followed by thyroid hormones. A wealth of misinformation exists in popular literature regarding these hormones alone.
Estrogen can be replaced, but not everyone needs it replaced. It depends on variables including age, underlying medical conditions, the time of day a test was drawn, and concomitant medications. Having low levels of a given hormone does not necessarily call for replacement either.
Insulin is another example of a hormone that can never completely be replaced in people with diabetes in a way that exactly mimics the normal physiologic release.
There are many lesser-known hormones that are measurable and replaceable but are also more difficult to reset to original manufacturer specifications.
A Google search for “hormone balancing” often sends you to “naturopaths” or “integrative medicine” practitioners, who often propose similar solutions to the TikTok influencers. Users are told that their hormones are out of whack and that restoring this “balance” can be achieved by purchasing whatever “natural products” or concoction they are selling.
These TikTok videos and online “experts” are the home-brewed versions of the strip-mall hormone specialists. TikTok videos claiming to help “balance hormones” typically don’t name a specific hormone either, or the end organs that each would have an impact on. Rather, they lump all hormones into a monolithic entity, implying that there is a single solution for all health problems. And personal testimonials extolling the benefits of a TikTok intervention don’t constitute proof of efficacy no matter how many “likes” they get. These influencers assume that viewers can “sense” their hormones are out of tune and no lab tests can convince them otherwise.
In these inflationary times, the cost of seeking medical care from conventional channels is increasingly prohibitive. It’s easy to understand the appeal of getting free advice from TikTok or some other Internet site. At best, following the advice will not have much impact; at worst, it could be harmful.
Don’t try this at home
There are some things that should never be tried at home, and do-it-yourself hormone replacement or remediation both fall under this umbrella.
Generally, the body does a good job of balancing its own hormones. Most patients don’t need to be worried if they’re in good health. If they’re in doubt, they should seek advice from a doctor, ideally an endocrinologist, but an ob.gyn. or general practitioner are also good options.
One of the first questions to ask a patient is “Which hormone are you worried about?” or “What health issue is it specifically that is bothering you?” Narrowing the focus to a single thing, if possible, will lead to a more efficient evaluation.
Often, patients arrive with multiple concerns written on little pieces of paper. These ubiquitous pieces of paper are the red flag for the flood of questions to follow.
Ordering the appropriate tests for the conditions they are concerned about can help put their minds at ease. If there are any specific deficiencies, or excesses in any hormones, then appropriate solutions can be discussed.
TikTok hormone-balancing solutions are simply the 21st-century version of the snake oil sold on late-night cable TV in the 1990s.
Needless to say, you should gently encourage your patients to stay away from these non–FDA-approved products, without making them feel stupid. Off-label use of hormones when these are not indicated is also to be avoided, unless a medical practitioner feels it is warranted.
Dr. de la Rosa is an endocrinologist in Englewood, Fla. He disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
With more than 306 million views, #hormonebalance and #hormonebalancing are among the latest hacks to take over the social media platform TikTok, on which users post short videos. Influencers offer advice such as eating raw carrots for “happy hormones,” eating protein followed by fat for breakfast to regulate blood glucose, or taking vitamin B2 supplements for thyroid health.
Have you ever wondered if you were asleep during the lecture on “hormone balancing” in medical school? No, you weren’t. It was never a class for good reason, and you didn’t fail to read any such breakthrough studies in The New England Journal of Medicine either.
There are over 50 different hormones produced by humans and animals, regulating sleep, growth, metabolism and reproduction, among many other biological processes, so there is certainly no one-size-fits-all solution to ensure these are all working in perfect harmony.
When someone mentions “hormone balancing,” my mind wanders to the last time I took my car to have my tires rotated and balanced. If only it were as simple to balance hormones in real life. The best we can hope for is to get a specific hormone within the ideal physiologic range for that person’s age.
The term “hormone” can mean many things to different people. When a woman comes in with a hormone question, for example, it is often related to estrogen, followed by thyroid hormones. A wealth of misinformation exists in popular literature regarding these hormones alone.
Estrogen can be replaced, but not everyone needs it replaced. It depends on variables including age, underlying medical conditions, the time of day a test was drawn, and concomitant medications. Having low levels of a given hormone does not necessarily call for replacement either.
Insulin is another example of a hormone that can never completely be replaced in people with diabetes in a way that exactly mimics the normal physiologic release.
There are many lesser-known hormones that are measurable and replaceable but are also more difficult to reset to original manufacturer specifications.
A Google search for “hormone balancing” often sends you to “naturopaths” or “integrative medicine” practitioners, who often propose similar solutions to the TikTok influencers. Users are told that their hormones are out of whack and that restoring this “balance” can be achieved by purchasing whatever “natural products” or concoction they are selling.
These TikTok videos and online “experts” are the home-brewed versions of the strip-mall hormone specialists. TikTok videos claiming to help “balance hormones” typically don’t name a specific hormone either, or the end organs that each would have an impact on. Rather, they lump all hormones into a monolithic entity, implying that there is a single solution for all health problems. And personal testimonials extolling the benefits of a TikTok intervention don’t constitute proof of efficacy no matter how many “likes” they get. These influencers assume that viewers can “sense” their hormones are out of tune and no lab tests can convince them otherwise.
In these inflationary times, the cost of seeking medical care from conventional channels is increasingly prohibitive. It’s easy to understand the appeal of getting free advice from TikTok or some other Internet site. At best, following the advice will not have much impact; at worst, it could be harmful.
Don’t try this at home
There are some things that should never be tried at home, and do-it-yourself hormone replacement or remediation both fall under this umbrella.
Generally, the body does a good job of balancing its own hormones. Most patients don’t need to be worried if they’re in good health. If they’re in doubt, they should seek advice from a doctor, ideally an endocrinologist, but an ob.gyn. or general practitioner are also good options.
One of the first questions to ask a patient is “Which hormone are you worried about?” or “What health issue is it specifically that is bothering you?” Narrowing the focus to a single thing, if possible, will lead to a more efficient evaluation.
Often, patients arrive with multiple concerns written on little pieces of paper. These ubiquitous pieces of paper are the red flag for the flood of questions to follow.
Ordering the appropriate tests for the conditions they are concerned about can help put their minds at ease. If there are any specific deficiencies, or excesses in any hormones, then appropriate solutions can be discussed.
TikTok hormone-balancing solutions are simply the 21st-century version of the snake oil sold on late-night cable TV in the 1990s.
Needless to say, you should gently encourage your patients to stay away from these non–FDA-approved products, without making them feel stupid. Off-label use of hormones when these are not indicated is also to be avoided, unless a medical practitioner feels it is warranted.
Dr. de la Rosa is an endocrinologist in Englewood, Fla. He disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
With more than 306 million views, #hormonebalance and #hormonebalancing are among the latest hacks to take over the social media platform TikTok, on which users post short videos. Influencers offer advice such as eating raw carrots for “happy hormones,” eating protein followed by fat for breakfast to regulate blood glucose, or taking vitamin B2 supplements for thyroid health.
Have you ever wondered if you were asleep during the lecture on “hormone balancing” in medical school? No, you weren’t. It was never a class for good reason, and you didn’t fail to read any such breakthrough studies in The New England Journal of Medicine either.
There are over 50 different hormones produced by humans and animals, regulating sleep, growth, metabolism and reproduction, among many other biological processes, so there is certainly no one-size-fits-all solution to ensure these are all working in perfect harmony.
When someone mentions “hormone balancing,” my mind wanders to the last time I took my car to have my tires rotated and balanced. If only it were as simple to balance hormones in real life. The best we can hope for is to get a specific hormone within the ideal physiologic range for that person’s age.
The term “hormone” can mean many things to different people. When a woman comes in with a hormone question, for example, it is often related to estrogen, followed by thyroid hormones. A wealth of misinformation exists in popular literature regarding these hormones alone.
Estrogen can be replaced, but not everyone needs it replaced. It depends on variables including age, underlying medical conditions, the time of day a test was drawn, and concomitant medications. Having low levels of a given hormone does not necessarily call for replacement either.
Insulin is another example of a hormone that can never completely be replaced in people with diabetes in a way that exactly mimics the normal physiologic release.
There are many lesser-known hormones that are measurable and replaceable but are also more difficult to reset to original manufacturer specifications.
A Google search for “hormone balancing” often sends you to “naturopaths” or “integrative medicine” practitioners, who often propose similar solutions to the TikTok influencers. Users are told that their hormones are out of whack and that restoring this “balance” can be achieved by purchasing whatever “natural products” or concoction they are selling.
These TikTok videos and online “experts” are the home-brewed versions of the strip-mall hormone specialists. TikTok videos claiming to help “balance hormones” typically don’t name a specific hormone either, or the end organs that each would have an impact on. Rather, they lump all hormones into a monolithic entity, implying that there is a single solution for all health problems. And personal testimonials extolling the benefits of a TikTok intervention don’t constitute proof of efficacy no matter how many “likes” they get. These influencers assume that viewers can “sense” their hormones are out of tune and no lab tests can convince them otherwise.
In these inflationary times, the cost of seeking medical care from conventional channels is increasingly prohibitive. It’s easy to understand the appeal of getting free advice from TikTok or some other Internet site. At best, following the advice will not have much impact; at worst, it could be harmful.
Don’t try this at home
There are some things that should never be tried at home, and do-it-yourself hormone replacement or remediation both fall under this umbrella.
Generally, the body does a good job of balancing its own hormones. Most patients don’t need to be worried if they’re in good health. If they’re in doubt, they should seek advice from a doctor, ideally an endocrinologist, but an ob.gyn. or general practitioner are also good options.
One of the first questions to ask a patient is “Which hormone are you worried about?” or “What health issue is it specifically that is bothering you?” Narrowing the focus to a single thing, if possible, will lead to a more efficient evaluation.
Often, patients arrive with multiple concerns written on little pieces of paper. These ubiquitous pieces of paper are the red flag for the flood of questions to follow.
Ordering the appropriate tests for the conditions they are concerned about can help put their minds at ease. If there are any specific deficiencies, or excesses in any hormones, then appropriate solutions can be discussed.
TikTok hormone-balancing solutions are simply the 21st-century version of the snake oil sold on late-night cable TV in the 1990s.
Needless to say, you should gently encourage your patients to stay away from these non–FDA-approved products, without making them feel stupid. Off-label use of hormones when these are not indicated is also to be avoided, unless a medical practitioner feels it is warranted.
Dr. de la Rosa is an endocrinologist in Englewood, Fla. He disclosed no conflicts of interest.
A version of this article first appeared on Medscape.com.
One emergency is ending, and we’re ready for the next
I’ve always thought it was interesting that the first cases of COVID-19 were reported to the World Health Organization on December 31, 2019.1 How close we came to having COVID-20! On January 31, 2020, the US Department of Health and Human Services declared a national public health emergency due to COVID-19, and it’s been in effect ever since.
A national public health emergency allows the Department of Health and Human Services to access and designate funds to diagnose, treat, and prevent disease in response to the emergency. The declaration also facilitates the Centers for Disease Control and Prevention response to an infectious disease emergency. There are provisions for modifications to Medicare, Medicaid, and the Children’s Health Insurance Program so clinicians can continue seeing patients and be reimbursed for doing so, even in a situation in which the emergency disrupts usual reporting and documentation requirements. The declaration is essentially a shortcut through the typical bureaucracy that too often gums up the practice of medicine2; it allows for the rapid deployment of funds and personnel to a community affected by an emergency.
Unprecedented change. In the early days, plastic partitions were erected between patients in the hospital, and the scarce supply of N-95 masks was stored in paper bags and baked at low temperatures in ovens overnight.
My hospital enacted its incident command response procedures, just as we did the day our community experienced a mass shooting—except incident command stayed open for months. We had to adapt quickly. My office never closed to in-person visits; we decided that we took care of too many people who did not have other access to care to make closing practical. My practice partners and I spent a Friday afternoon in March 2020 writing policies. A policy for our residency practice. A policy for how to see patients who might have COVID. A policy for how to cover the residents and faculty when we inevitably got sick. A policy for how to do telehealth visits. By the following Monday, when the office reopened, we had already trained the staff on the new policies, and we were ready to implement them with our patients.
As COVID and our knowledge about it changed, we rewrote those policies dozens of times, and each time the staff retrained in a hurry. We all learned so much so quickly. So as the official public health emergency comes to an end, there are things that I think I will take from it, and things that I wish all of medicine could take from it too.
We adapted as a team. I will never forget the stress of the early days of the emergency, when the patient volume was overwhelming and the death rate was staggering. But shining through those dark times were wonderful moments of connection with the teams with which I worked. I think about the residents whose training shifted suddenly to full-time COVID, the nurses who learned new things every weekend for so many months, and everyone who went out on a limb to do the right thing.
We provided care without bureaucracy. I wish medicine could leave the bureaucracy behind along with the emergency. It was so much easier to practice medicine when we knew that the testing and treatment were covered, without “we’ll see” or “it depends on your insurance.” Telehealth is probably here to stay, thanks to widespread uptake by patients and clinicians alike during the pandemic. My wish is that we can make it as easy as possible to use going forward, instead of choosing to return to a more restricted and difficult path.3,4
Family physicians have much to be proud of. We can look back on the COVID-19 public health emergency as a time when we absorbed a huge amount of rapidly changing information and showed our adaptability to a frightening and uncertain environment. We are not returning to the office, as so many Americans are these days, because we never left the many settings where family physicians practice. We remained at work during the emergency and we took care of our patients.
When the next emergency is declared—whether it be national or local—we will once again be there for our patients.
1. CDC. CDC museum COVID-19 timeline. Updated March 15, 2023. Accessed March 28, 2023. www.cdc.gov/museum/timeline/covid19.html
2. US Department of Health and Human Services Administration for Strategic Preparedness & Response. A public health emer-gency declaration. Accessed March 28, 2023. https://aspr.hhs.gov/legal/PHE/Pages/Public-Health-Emergency-Declaration.aspx
3. US Department of Health and Human Services. Telehealth policy changes after the COVID-19 public health emergency. Updated February 16, 2023. Accessed March 28, 2023. https://telehealth.hhs.gov/providers/policy-changes-during-the-covid-19-public-health-emergency/policy-changes-after-the-covid-19-public-health-emergency
4. Cox C, Kates J, Cubanski J, et al. The end of the COVID-19 public health emergency: details on health coverage and access. Kaiser Family Foundation. Published February 3, 2023. Accessed March 28, 2023. www.kff.org/policy-watch/the-end-of-the-covid-19-public-health-emergency-details-on-health-coverage-and-access/
I’ve always thought it was interesting that the first cases of COVID-19 were reported to the World Health Organization on December 31, 2019.1 How close we came to having COVID-20! On January 31, 2020, the US Department of Health and Human Services declared a national public health emergency due to COVID-19, and it’s been in effect ever since.
A national public health emergency allows the Department of Health and Human Services to access and designate funds to diagnose, treat, and prevent disease in response to the emergency. The declaration also facilitates the Centers for Disease Control and Prevention response to an infectious disease emergency. There are provisions for modifications to Medicare, Medicaid, and the Children’s Health Insurance Program so clinicians can continue seeing patients and be reimbursed for doing so, even in a situation in which the emergency disrupts usual reporting and documentation requirements. The declaration is essentially a shortcut through the typical bureaucracy that too often gums up the practice of medicine2; it allows for the rapid deployment of funds and personnel to a community affected by an emergency.
Unprecedented change. In the early days, plastic partitions were erected between patients in the hospital, and the scarce supply of N-95 masks was stored in paper bags and baked at low temperatures in ovens overnight.
My hospital enacted its incident command response procedures, just as we did the day our community experienced a mass shooting—except incident command stayed open for months. We had to adapt quickly. My office never closed to in-person visits; we decided that we took care of too many people who did not have other access to care to make closing practical. My practice partners and I spent a Friday afternoon in March 2020 writing policies. A policy for our residency practice. A policy for how to see patients who might have COVID. A policy for how to cover the residents and faculty when we inevitably got sick. A policy for how to do telehealth visits. By the following Monday, when the office reopened, we had already trained the staff on the new policies, and we were ready to implement them with our patients.
As COVID and our knowledge about it changed, we rewrote those policies dozens of times, and each time the staff retrained in a hurry. We all learned so much so quickly. So as the official public health emergency comes to an end, there are things that I think I will take from it, and things that I wish all of medicine could take from it too.
We adapted as a team. I will never forget the stress of the early days of the emergency, when the patient volume was overwhelming and the death rate was staggering. But shining through those dark times were wonderful moments of connection with the teams with which I worked. I think about the residents whose training shifted suddenly to full-time COVID, the nurses who learned new things every weekend for so many months, and everyone who went out on a limb to do the right thing.
We provided care without bureaucracy. I wish medicine could leave the bureaucracy behind along with the emergency. It was so much easier to practice medicine when we knew that the testing and treatment were covered, without “we’ll see” or “it depends on your insurance.” Telehealth is probably here to stay, thanks to widespread uptake by patients and clinicians alike during the pandemic. My wish is that we can make it as easy as possible to use going forward, instead of choosing to return to a more restricted and difficult path.3,4
Family physicians have much to be proud of. We can look back on the COVID-19 public health emergency as a time when we absorbed a huge amount of rapidly changing information and showed our adaptability to a frightening and uncertain environment. We are not returning to the office, as so many Americans are these days, because we never left the many settings where family physicians practice. We remained at work during the emergency and we took care of our patients.
When the next emergency is declared—whether it be national or local—we will once again be there for our patients.
I’ve always thought it was interesting that the first cases of COVID-19 were reported to the World Health Organization on December 31, 2019.1 How close we came to having COVID-20! On January 31, 2020, the US Department of Health and Human Services declared a national public health emergency due to COVID-19, and it’s been in effect ever since.
A national public health emergency allows the Department of Health and Human Services to access and designate funds to diagnose, treat, and prevent disease in response to the emergency. The declaration also facilitates the Centers for Disease Control and Prevention response to an infectious disease emergency. There are provisions for modifications to Medicare, Medicaid, and the Children’s Health Insurance Program so clinicians can continue seeing patients and be reimbursed for doing so, even in a situation in which the emergency disrupts usual reporting and documentation requirements. The declaration is essentially a shortcut through the typical bureaucracy that too often gums up the practice of medicine2; it allows for the rapid deployment of funds and personnel to a community affected by an emergency.
Unprecedented change. In the early days, plastic partitions were erected between patients in the hospital, and the scarce supply of N-95 masks was stored in paper bags and baked at low temperatures in ovens overnight.
My hospital enacted its incident command response procedures, just as we did the day our community experienced a mass shooting—except incident command stayed open for months. We had to adapt quickly. My office never closed to in-person visits; we decided that we took care of too many people who did not have other access to care to make closing practical. My practice partners and I spent a Friday afternoon in March 2020 writing policies. A policy for our residency practice. A policy for how to see patients who might have COVID. A policy for how to cover the residents and faculty when we inevitably got sick. A policy for how to do telehealth visits. By the following Monday, when the office reopened, we had already trained the staff on the new policies, and we were ready to implement them with our patients.
As COVID and our knowledge about it changed, we rewrote those policies dozens of times, and each time the staff retrained in a hurry. We all learned so much so quickly. So as the official public health emergency comes to an end, there are things that I think I will take from it, and things that I wish all of medicine could take from it too.
We adapted as a team. I will never forget the stress of the early days of the emergency, when the patient volume was overwhelming and the death rate was staggering. But shining through those dark times were wonderful moments of connection with the teams with which I worked. I think about the residents whose training shifted suddenly to full-time COVID, the nurses who learned new things every weekend for so many months, and everyone who went out on a limb to do the right thing.
We provided care without bureaucracy. I wish medicine could leave the bureaucracy behind along with the emergency. It was so much easier to practice medicine when we knew that the testing and treatment were covered, without “we’ll see” or “it depends on your insurance.” Telehealth is probably here to stay, thanks to widespread uptake by patients and clinicians alike during the pandemic. My wish is that we can make it as easy as possible to use going forward, instead of choosing to return to a more restricted and difficult path.3,4
Family physicians have much to be proud of. We can look back on the COVID-19 public health emergency as a time when we absorbed a huge amount of rapidly changing information and showed our adaptability to a frightening and uncertain environment. We are not returning to the office, as so many Americans are these days, because we never left the many settings where family physicians practice. We remained at work during the emergency and we took care of our patients.
When the next emergency is declared—whether it be national or local—we will once again be there for our patients.
1. CDC. CDC museum COVID-19 timeline. Updated March 15, 2023. Accessed March 28, 2023. www.cdc.gov/museum/timeline/covid19.html
2. US Department of Health and Human Services Administration for Strategic Preparedness & Response. A public health emer-gency declaration. Accessed March 28, 2023. https://aspr.hhs.gov/legal/PHE/Pages/Public-Health-Emergency-Declaration.aspx
3. US Department of Health and Human Services. Telehealth policy changes after the COVID-19 public health emergency. Updated February 16, 2023. Accessed March 28, 2023. https://telehealth.hhs.gov/providers/policy-changes-during-the-covid-19-public-health-emergency/policy-changes-after-the-covid-19-public-health-emergency
4. Cox C, Kates J, Cubanski J, et al. The end of the COVID-19 public health emergency: details on health coverage and access. Kaiser Family Foundation. Published February 3, 2023. Accessed March 28, 2023. www.kff.org/policy-watch/the-end-of-the-covid-19-public-health-emergency-details-on-health-coverage-and-access/
1. CDC. CDC museum COVID-19 timeline. Updated March 15, 2023. Accessed March 28, 2023. www.cdc.gov/museum/timeline/covid19.html
2. US Department of Health and Human Services Administration for Strategic Preparedness & Response. A public health emer-gency declaration. Accessed March 28, 2023. https://aspr.hhs.gov/legal/PHE/Pages/Public-Health-Emergency-Declaration.aspx
3. US Department of Health and Human Services. Telehealth policy changes after the COVID-19 public health emergency. Updated February 16, 2023. Accessed March 28, 2023. https://telehealth.hhs.gov/providers/policy-changes-during-the-covid-19-public-health-emergency/policy-changes-after-the-covid-19-public-health-emergency
4. Cox C, Kates J, Cubanski J, et al. The end of the COVID-19 public health emergency: details on health coverage and access. Kaiser Family Foundation. Published February 3, 2023. Accessed March 28, 2023. www.kff.org/policy-watch/the-end-of-the-covid-19-public-health-emergency-details-on-health-coverage-and-access/
Picking up the premotor symptoms of Parkinson’s
This transcript has been edited for clarity.
Matthew F. Watto, MD: Welcome back to The Curbsiders. We had a great discussion on Parkinson’s Disease for Primary Care with Dr. Albert Hung. Paul, this was something that really made me nervous. I didn’t have a lot of comfort with it. But he taught us a lot of tips about how to recognize Parkinson’s.
I hadn’t been as aware of the premotor symptoms: constipation, hyposmia (loss of sense of smell), and rapid eye movement sleep behavior disorder. If patients have those early on and they aren’t explained by other things (especially the REM sleep behavior disorder), you should really key in because those patients are at risk of developing Parkinson’s years down the line. Those symptoms could present first, which just kind of blew my mind.
What tips do you have about how to recognize Parkinson’s? Do you want to talk about the physical exam?
Paul N. Williams, MD: You know I love the physical exam stuff, so I’m happy to talk about that.
You were deeply upset that cogwheel rigidity was not pathognomonic for Parkinson’s, but you made the point – and our guest agreed – that asymmetry tends to be the key here. And I really appreciated the point about reemergent tremor. This is this idea of a resting tremor. If someone has more parkinsonian features, you might see an intention tremor with essential tremor. If they reach out, it might seem steady at first, but if they hold long enough, then the tremor may kind of reemerge. I thought that was a neat distinction.
And this idea of cogwheel rigidity is a combination of some of the cardinal features of Parkinson’s – it’s a little bit of tremor and a little bit of rigidity too. There’s a baseline increase in tone, and then the tremor is superimposed on top of that. When you’re feeling cogwheeling, that’s actually what you’re feeling on examination. Parkinson’s, with all of its physical exam findings has always fascinated me.
Dr. Watto: He also told us about some red flags.
With classic idiopathic parkinsonism, there’s asymmetric involvement of the tremor. So red flags include a symmetric tremor, which might be something other than idiopathic parkinsonism. He also mentioned that one of the reasons you may want to get imaging (which is not always necessary if someone has a classic presentation), is if you see lower body–predominant symptoms of parkinsonism. These patients have rigidity or slowness of movement in their legs, but their upper bodies are not affected. They don’t have masked facies or the tremor in their hands. You might get an MRI in that case because that could be presentation of vascular dementia or vascular disease in the brain or even normal pressure hydrocephalus, which is a treatable condition. That would be one reason to get imaging.
What if the patient was exposed to a drug like a dopamine antagonist? They will get better in a couple of days, right?
Dr. Williams: This was a really fascinating point because we typically think if a patient’s symptoms are related to a drug exposure – in this case, drug-induced parkinsonism – we can just stop the medication and the symptoms will disappear in a couple of days as the drug leaves the system. But as it turns out, it might take much longer. A mistake that Dr Hung often sees is that the clinician stops the possibly offending agent, but when they don’t see an immediate relief of symptoms, they assume the drug wasn’t causing them. You really have to give the patient a fair shot off the medication to experience recovery because those symptoms can last weeks or even months after the drug is discontinued.
Dr. Watto: Dr Hung looks at the patient’s problem list and asks whether is there any reason this patient might have been exposed to one of these medications?
We’re not going to get too much into specific Parkinson’s treatment, but I was glad to hear that exercise actually improves mobility and may even have some neuroprotective effects. He mentioned ongoing trials looking at that. We always love an excuse to tell patients that they should be moving around more and being physically active.
Dr. Williams: That was one of the more shocking things I learned, that exercise might actually be good for you. That will deeply inform my practice. Many of the treatments that we use for Parkinson’s only address symptoms. They don’t address progression or fix anything, but exercise can help with that.
Dr. Watto: Paul, the last question I wanted to ask you is about our role in primary care. Patients with Parkinson’s have autonomic symptoms. They have neurocognitive symptoms. What is our role in that as primary care physicians?
Dr. Williams: Myriad symptoms can accompany Parkinson’s, and we have experience with most of them. We should all feel fairly comfortable dealing with constipation, which can be a very bothersome symptom. And we can use our full arsenal for symptoms such as depression, anxiety, and even apathy – the anhedonia, which apparently can be the predominant feature. We do have the tools to address these problems.
This might be a situation where we might reach for bupropion or a tricyclic antidepressant, which might not be your initial choice for a patient with a possibly annoying mood disorder. But for someone with Parkinson’s disease, this actually may be very helpful. We know how to manage a lot of the symptoms that come along with Parkinson’s that are not just the motor symptoms, and we should take ownership of those things.
Dr. Watto: You can hear the rest of this podcast here. This has been another episode of The Curbsiders bringing you a little knowledge food for your brain hole. Until next time, I’ve been Dr Matthew Frank Watto.
Dr. Williams: And I’m Dr Paul Nelson Williams.
Dr. Watto is a clinical assistant professor, department of medicine, at the University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, at Temple University, Philadelphia. Neither Dr. Watto nor Dr. Williams reported any relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Matthew F. Watto, MD: Welcome back to The Curbsiders. We had a great discussion on Parkinson’s Disease for Primary Care with Dr. Albert Hung. Paul, this was something that really made me nervous. I didn’t have a lot of comfort with it. But he taught us a lot of tips about how to recognize Parkinson’s.
I hadn’t been as aware of the premotor symptoms: constipation, hyposmia (loss of sense of smell), and rapid eye movement sleep behavior disorder. If patients have those early on and they aren’t explained by other things (especially the REM sleep behavior disorder), you should really key in because those patients are at risk of developing Parkinson’s years down the line. Those symptoms could present first, which just kind of blew my mind.
What tips do you have about how to recognize Parkinson’s? Do you want to talk about the physical exam?
Paul N. Williams, MD: You know I love the physical exam stuff, so I’m happy to talk about that.
You were deeply upset that cogwheel rigidity was not pathognomonic for Parkinson’s, but you made the point – and our guest agreed – that asymmetry tends to be the key here. And I really appreciated the point about reemergent tremor. This is this idea of a resting tremor. If someone has more parkinsonian features, you might see an intention tremor with essential tremor. If they reach out, it might seem steady at first, but if they hold long enough, then the tremor may kind of reemerge. I thought that was a neat distinction.
And this idea of cogwheel rigidity is a combination of some of the cardinal features of Parkinson’s – it’s a little bit of tremor and a little bit of rigidity too. There’s a baseline increase in tone, and then the tremor is superimposed on top of that. When you’re feeling cogwheeling, that’s actually what you’re feeling on examination. Parkinson’s, with all of its physical exam findings has always fascinated me.
Dr. Watto: He also told us about some red flags.
With classic idiopathic parkinsonism, there’s asymmetric involvement of the tremor. So red flags include a symmetric tremor, which might be something other than idiopathic parkinsonism. He also mentioned that one of the reasons you may want to get imaging (which is not always necessary if someone has a classic presentation), is if you see lower body–predominant symptoms of parkinsonism. These patients have rigidity or slowness of movement in their legs, but their upper bodies are not affected. They don’t have masked facies or the tremor in their hands. You might get an MRI in that case because that could be presentation of vascular dementia or vascular disease in the brain or even normal pressure hydrocephalus, which is a treatable condition. That would be one reason to get imaging.
What if the patient was exposed to a drug like a dopamine antagonist? They will get better in a couple of days, right?
Dr. Williams: This was a really fascinating point because we typically think if a patient’s symptoms are related to a drug exposure – in this case, drug-induced parkinsonism – we can just stop the medication and the symptoms will disappear in a couple of days as the drug leaves the system. But as it turns out, it might take much longer. A mistake that Dr Hung often sees is that the clinician stops the possibly offending agent, but when they don’t see an immediate relief of symptoms, they assume the drug wasn’t causing them. You really have to give the patient a fair shot off the medication to experience recovery because those symptoms can last weeks or even months after the drug is discontinued.
Dr. Watto: Dr Hung looks at the patient’s problem list and asks whether is there any reason this patient might have been exposed to one of these medications?
We’re not going to get too much into specific Parkinson’s treatment, but I was glad to hear that exercise actually improves mobility and may even have some neuroprotective effects. He mentioned ongoing trials looking at that. We always love an excuse to tell patients that they should be moving around more and being physically active.
Dr. Williams: That was one of the more shocking things I learned, that exercise might actually be good for you. That will deeply inform my practice. Many of the treatments that we use for Parkinson’s only address symptoms. They don’t address progression or fix anything, but exercise can help with that.
Dr. Watto: Paul, the last question I wanted to ask you is about our role in primary care. Patients with Parkinson’s have autonomic symptoms. They have neurocognitive symptoms. What is our role in that as primary care physicians?
Dr. Williams: Myriad symptoms can accompany Parkinson’s, and we have experience with most of them. We should all feel fairly comfortable dealing with constipation, which can be a very bothersome symptom. And we can use our full arsenal for symptoms such as depression, anxiety, and even apathy – the anhedonia, which apparently can be the predominant feature. We do have the tools to address these problems.
This might be a situation where we might reach for bupropion or a tricyclic antidepressant, which might not be your initial choice for a patient with a possibly annoying mood disorder. But for someone with Parkinson’s disease, this actually may be very helpful. We know how to manage a lot of the symptoms that come along with Parkinson’s that are not just the motor symptoms, and we should take ownership of those things.
Dr. Watto: You can hear the rest of this podcast here. This has been another episode of The Curbsiders bringing you a little knowledge food for your brain hole. Until next time, I’ve been Dr Matthew Frank Watto.
Dr. Williams: And I’m Dr Paul Nelson Williams.
Dr. Watto is a clinical assistant professor, department of medicine, at the University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, at Temple University, Philadelphia. Neither Dr. Watto nor Dr. Williams reported any relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Matthew F. Watto, MD: Welcome back to The Curbsiders. We had a great discussion on Parkinson’s Disease for Primary Care with Dr. Albert Hung. Paul, this was something that really made me nervous. I didn’t have a lot of comfort with it. But he taught us a lot of tips about how to recognize Parkinson’s.
I hadn’t been as aware of the premotor symptoms: constipation, hyposmia (loss of sense of smell), and rapid eye movement sleep behavior disorder. If patients have those early on and they aren’t explained by other things (especially the REM sleep behavior disorder), you should really key in because those patients are at risk of developing Parkinson’s years down the line. Those symptoms could present first, which just kind of blew my mind.
What tips do you have about how to recognize Parkinson’s? Do you want to talk about the physical exam?
Paul N. Williams, MD: You know I love the physical exam stuff, so I’m happy to talk about that.
You were deeply upset that cogwheel rigidity was not pathognomonic for Parkinson’s, but you made the point – and our guest agreed – that asymmetry tends to be the key here. And I really appreciated the point about reemergent tremor. This is this idea of a resting tremor. If someone has more parkinsonian features, you might see an intention tremor with essential tremor. If they reach out, it might seem steady at first, but if they hold long enough, then the tremor may kind of reemerge. I thought that was a neat distinction.
And this idea of cogwheel rigidity is a combination of some of the cardinal features of Parkinson’s – it’s a little bit of tremor and a little bit of rigidity too. There’s a baseline increase in tone, and then the tremor is superimposed on top of that. When you’re feeling cogwheeling, that’s actually what you’re feeling on examination. Parkinson’s, with all of its physical exam findings has always fascinated me.
Dr. Watto: He also told us about some red flags.
With classic idiopathic parkinsonism, there’s asymmetric involvement of the tremor. So red flags include a symmetric tremor, which might be something other than idiopathic parkinsonism. He also mentioned that one of the reasons you may want to get imaging (which is not always necessary if someone has a classic presentation), is if you see lower body–predominant symptoms of parkinsonism. These patients have rigidity or slowness of movement in their legs, but their upper bodies are not affected. They don’t have masked facies or the tremor in their hands. You might get an MRI in that case because that could be presentation of vascular dementia or vascular disease in the brain or even normal pressure hydrocephalus, which is a treatable condition. That would be one reason to get imaging.
What if the patient was exposed to a drug like a dopamine antagonist? They will get better in a couple of days, right?
Dr. Williams: This was a really fascinating point because we typically think if a patient’s symptoms are related to a drug exposure – in this case, drug-induced parkinsonism – we can just stop the medication and the symptoms will disappear in a couple of days as the drug leaves the system. But as it turns out, it might take much longer. A mistake that Dr Hung often sees is that the clinician stops the possibly offending agent, but when they don’t see an immediate relief of symptoms, they assume the drug wasn’t causing them. You really have to give the patient a fair shot off the medication to experience recovery because those symptoms can last weeks or even months after the drug is discontinued.
Dr. Watto: Dr Hung looks at the patient’s problem list and asks whether is there any reason this patient might have been exposed to one of these medications?
We’re not going to get too much into specific Parkinson’s treatment, but I was glad to hear that exercise actually improves mobility and may even have some neuroprotective effects. He mentioned ongoing trials looking at that. We always love an excuse to tell patients that they should be moving around more and being physically active.
Dr. Williams: That was one of the more shocking things I learned, that exercise might actually be good for you. That will deeply inform my practice. Many of the treatments that we use for Parkinson’s only address symptoms. They don’t address progression or fix anything, but exercise can help with that.
Dr. Watto: Paul, the last question I wanted to ask you is about our role in primary care. Patients with Parkinson’s have autonomic symptoms. They have neurocognitive symptoms. What is our role in that as primary care physicians?
Dr. Williams: Myriad symptoms can accompany Parkinson’s, and we have experience with most of them. We should all feel fairly comfortable dealing with constipation, which can be a very bothersome symptom. And we can use our full arsenal for symptoms such as depression, anxiety, and even apathy – the anhedonia, which apparently can be the predominant feature. We do have the tools to address these problems.
This might be a situation where we might reach for bupropion or a tricyclic antidepressant, which might not be your initial choice for a patient with a possibly annoying mood disorder. But for someone with Parkinson’s disease, this actually may be very helpful. We know how to manage a lot of the symptoms that come along with Parkinson’s that are not just the motor symptoms, and we should take ownership of those things.
Dr. Watto: You can hear the rest of this podcast here. This has been another episode of The Curbsiders bringing you a little knowledge food for your brain hole. Until next time, I’ve been Dr Matthew Frank Watto.
Dr. Williams: And I’m Dr Paul Nelson Williams.
Dr. Watto is a clinical assistant professor, department of medicine, at the University of Pennsylvania, Philadelphia. Dr. Williams is Associate Professor of Clinical Medicine, Department of General Internal Medicine, at Temple University, Philadelphia. Neither Dr. Watto nor Dr. Williams reported any relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Parkinson’s disease: What’s trauma got to do with it?
This transcript has been edited for clarity.
Kathrin LaFaver, MD: Hello. I’m happy to talk today to Dr. Indu Subramanian, clinical professor at University of California, Los Angeles, and director of the Parkinson’s Disease Research, Education and Clinical Center in Los Angeles. I am a neurologist in Saratoga Springs, New York, and we will be talking today about Indu’s new paper on childhood trauma and Parkinson’s disease. Welcome and thanks for taking the time.
Indu Subramanian, MD: Thank you so much for letting us highlight this important topic.
Dr. LaFaver: There are many papers published every month on Parkinson’s disease, but this topic stands out because it’s not a thing that has been commonly looked at. What gave you the idea to study this?
Neurology behind other specialties
Dr. Subramanian: Kathrin, you and I have been looking at things that can inform us about our patients – the person who’s standing in front of us when they come in and we’re giving them this diagnosis. I think that so much of what we’ve done [in the past] is a cookie cutter approach to giving everybody the standard treatment. [We’ve been assuming that] It doesn’t matter if they’re a man or woman. It doesn’t matter if they’re a veteran. It doesn’t matter if they may be from a minoritized population.
We’ve also been interested in approaches that are outside the box, right? We have this integrative medicine and lifestyle medicine background. I’ve been going to those meetings and really been struck by the mounting evidence on the importance of things like early adverse childhood events (ACEs), what zip code you live in, what your pollution index is, and how these things can affect people through their life and their health.
I think that it is high time neurologists pay attention to this. There’s been mounting evidence throughout many disease states, various types of cancers, and mental health. Cardiology is much more advanced, but we haven’t had much data in neurology. In fact, when we went to write this paper, there were just one or two papers that were looking at multiple sclerosis or general neurologic issues, but really nothing in Parkinson’s disease.
We know that Parkinson’s disease is not only a motor disease that affects mental health, but that it also affects nonmotor issues. Childhood adversity may affect how people progress or how quickly they may get a disease, and we were interested in how it may manifest in a disease like Parkinson’s disease.
That was the framework going to meetings. As we wrote this paper and were in various editing stages, there was a beautiful paper that came out by Nadine Burke Harris and team that really was a call to action for neurologists and caring about trauma.
Dr. LaFaver: I couldn’t agree more. It’s really an underrecognized issue. With my own background, being very interested in functional movement disorders, psychosomatic disorders, and so on, it becomes much more evident how common a trauma background is, not only for people we were traditionally asking about.
Why don’t you summarize your findings for us?
Adverse childhood events
Dr. Subramanian: This is a web-based survey, so obviously, these are patient self-reports of their disease. We have a large cohort of people that we’ve been following over 7 years. I’m looking at modifiable variables and what really impacts Parkinson’s disease. Some of our previous papers have looked at diet, exercise, and loneliness. This is the same cohort.
We ended up putting the ACEs questionnaire, which is 10 questions looking at whether you were exposed to certain things in your household below the age of 18. This is a relatively standard questionnaire that’s administered one time, and you get a score out of 10. This is something that has been pushed, at least in the state of California, as something that we should be checking more in all people coming in.
We introduced the survey, and we didn’t force everyone to take it. Unfortunately, there was 20% or so of our patients who chose not to answer these questions. One has to ask, who are those people that didn’t answer the questions? Are they the ones that may have had trauma and these questions were triggering? It was a gap. We didn’t add extra questions to explore why people didn’t answer those questions.
We have to also put this in context. We have a patient population that’s largely quite affluent, who are able to access web-based surveys through their computer, and largely Caucasian; there are not many minoritized populations in our cohort. We want to do better with that. We actually were able to gather a decent number of women. We represent women quite well in our survey. I think that’s because of this online approach and some of the things that we’re studying.
In our survey, we broke it down into people who had no ACEs, one to three ACEs, or four or more ACEs. This is a standard way to break down ACEs so that we’re able to categorize what to do with these patient populations.
What we saw – and it’s preliminary evidence – is that people who had higher ACE scores seemed to have more symptom severity when we controlled for things like years since diagnosis, age, and gender. They also seem to have a worse quality of life. There was some indication that there were more nonmotor issues in those populations, as you might expect, such as anxiety, depression, and things that presumably ACEs can affect separately.
There are some confounders, but I think we really want to use this as the first piece of evidence to hopefully pave the way for caring about trauma in Parkinson’s disease moving forward.
Dr. LaFaver: Thank you so much for that summary. You already mentioned the main methodology you used.
What is the next step for you? How do you see these findings informing our clinical care? Do you have suggestions for all of the neurologists listening in this regard?
PD not yet considered ACE-related
Dr. Subramanian: Dr. Burke Harris was the former surgeon general in California. She’s a woman of color and a brilliant speaker, and she had worked in inner cities, I think in San Francisco, with pediatric populations, seeing these effects of adversity in that time frame.
You see this population at risk, and then you’re following this cohort, which we knew from the Kaiser cohort determines earlier morbidity and mortality across a number of disease states. We’re seeing things like more heart attacks, more diabetes, and all kinds of things in these populations. This is not new news; we just have not been focusing on this.
In her paper, this call to action, they had talked about some ACE-related conditions that currently do not include Parkinson’s disease. There are three ACE-related neurologic conditions that people should be aware of. One is in the headache/pain universe. Another is in the stroke universe, and that’s understandable, given cardiovascular risk factors . Then the third is in this dementia risk category. I think Parkinson’s disease, as we know, can be associated with dementia. A large percentage of our patients get dementia, but we don’t have Parkinson’s disease called out in this framework.
What people are talking about is if you have no ACEs or are in this middle category of one to three ACEs and you don’t have an ACE-related diagnosis – which Parkinson’s disease is not currently – we just give some basic counseling about the importance of lifestyle. I think we would love to see that anyway. They’re talking about things like exercise, diet, sleep, social connection, getting out in nature, things like that, so just general counseling on the importance of that.
Then if you’re in this higher-risk category, and so with these ACE-related neurologic conditions, including dementia, headache, and stroke, if you had this middle range of one to three ACEs, they’re getting additional resources. Some of them may be referred for social work help or mental health support and things like that.
I’d really love to see that happening in Parkinson’s disease, because I think we have so many needs in our population. I’m always hoping to advocate for more mental health needs that are scarce and resources in the social support realm because I believe that social connection and social support is a huge buffer for this trauma.
ACEs are just one type of trauma. I take care of veterans in the Veterans [Affairs Department]. We have some information now coming out about posttraumatic stress disorder, predisposing to certain things in Parkinson’s disease, possibly head injury, and things like that. I think we have populations at risk that we can hopefully screen at intake, and I’m really pushing for that.
Maybe it’s not the neurologist that does this intake. It might be someone else on the team that can spend some time doing these questionnaires and understand if your patient has a high ACE score. Unless you ask, many patients don’t necessarily come forward to talk about this. I really am pushing for trying to screen and trying to advocate for more research in this area so that we can classify Parkinson’s disease as an ACE-related condition and thus give more resources from the mental health world, and also the social support world, to our patients.
Dr. LaFaver: Thank you. There are many important points, and I think it’s a very important thing to recognize that it may not be only trauma in childhood but also throughout life, as you said, and might really influence nonmotor symptoms of Parkinson’s disease in particular, including anxiety and pain, which are often difficult to treat.
I think there’s much more to do in research, advocacy, and education. We’re going to educate patients about this, and also educate other neurologists and providers. I think you mentioned that trauma-informed care is getting its spotlight in primary care and other specialties. I think we have catching up to do in neurology, and I think this is a really important work toward that goal.
Thank you so much for your work and for taking the time to share your thoughts. I hope to talk to you again soon.
Dr. Subramanian: Thank you so much, Kathrin.
Dr. LaFaver has disclosed no relevant financial relationships. Dr. Subramanian disclosed ties with Acorda Therapeutics.
A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Kathrin LaFaver, MD: Hello. I’m happy to talk today to Dr. Indu Subramanian, clinical professor at University of California, Los Angeles, and director of the Parkinson’s Disease Research, Education and Clinical Center in Los Angeles. I am a neurologist in Saratoga Springs, New York, and we will be talking today about Indu’s new paper on childhood trauma and Parkinson’s disease. Welcome and thanks for taking the time.
Indu Subramanian, MD: Thank you so much for letting us highlight this important topic.
Dr. LaFaver: There are many papers published every month on Parkinson’s disease, but this topic stands out because it’s not a thing that has been commonly looked at. What gave you the idea to study this?
Neurology behind other specialties
Dr. Subramanian: Kathrin, you and I have been looking at things that can inform us about our patients – the person who’s standing in front of us when they come in and we’re giving them this diagnosis. I think that so much of what we’ve done [in the past] is a cookie cutter approach to giving everybody the standard treatment. [We’ve been assuming that] It doesn’t matter if they’re a man or woman. It doesn’t matter if they’re a veteran. It doesn’t matter if they may be from a minoritized population.
We’ve also been interested in approaches that are outside the box, right? We have this integrative medicine and lifestyle medicine background. I’ve been going to those meetings and really been struck by the mounting evidence on the importance of things like early adverse childhood events (ACEs), what zip code you live in, what your pollution index is, and how these things can affect people through their life and their health.
I think that it is high time neurologists pay attention to this. There’s been mounting evidence throughout many disease states, various types of cancers, and mental health. Cardiology is much more advanced, but we haven’t had much data in neurology. In fact, when we went to write this paper, there were just one or two papers that were looking at multiple sclerosis or general neurologic issues, but really nothing in Parkinson’s disease.
We know that Parkinson’s disease is not only a motor disease that affects mental health, but that it also affects nonmotor issues. Childhood adversity may affect how people progress or how quickly they may get a disease, and we were interested in how it may manifest in a disease like Parkinson’s disease.
That was the framework going to meetings. As we wrote this paper and were in various editing stages, there was a beautiful paper that came out by Nadine Burke Harris and team that really was a call to action for neurologists and caring about trauma.
Dr. LaFaver: I couldn’t agree more. It’s really an underrecognized issue. With my own background, being very interested in functional movement disorders, psychosomatic disorders, and so on, it becomes much more evident how common a trauma background is, not only for people we were traditionally asking about.
Why don’t you summarize your findings for us?
Adverse childhood events
Dr. Subramanian: This is a web-based survey, so obviously, these are patient self-reports of their disease. We have a large cohort of people that we’ve been following over 7 years. I’m looking at modifiable variables and what really impacts Parkinson’s disease. Some of our previous papers have looked at diet, exercise, and loneliness. This is the same cohort.
We ended up putting the ACEs questionnaire, which is 10 questions looking at whether you were exposed to certain things in your household below the age of 18. This is a relatively standard questionnaire that’s administered one time, and you get a score out of 10. This is something that has been pushed, at least in the state of California, as something that we should be checking more in all people coming in.
We introduced the survey, and we didn’t force everyone to take it. Unfortunately, there was 20% or so of our patients who chose not to answer these questions. One has to ask, who are those people that didn’t answer the questions? Are they the ones that may have had trauma and these questions were triggering? It was a gap. We didn’t add extra questions to explore why people didn’t answer those questions.
We have to also put this in context. We have a patient population that’s largely quite affluent, who are able to access web-based surveys through their computer, and largely Caucasian; there are not many minoritized populations in our cohort. We want to do better with that. We actually were able to gather a decent number of women. We represent women quite well in our survey. I think that’s because of this online approach and some of the things that we’re studying.
In our survey, we broke it down into people who had no ACEs, one to three ACEs, or four or more ACEs. This is a standard way to break down ACEs so that we’re able to categorize what to do with these patient populations.
What we saw – and it’s preliminary evidence – is that people who had higher ACE scores seemed to have more symptom severity when we controlled for things like years since diagnosis, age, and gender. They also seem to have a worse quality of life. There was some indication that there were more nonmotor issues in those populations, as you might expect, such as anxiety, depression, and things that presumably ACEs can affect separately.
There are some confounders, but I think we really want to use this as the first piece of evidence to hopefully pave the way for caring about trauma in Parkinson’s disease moving forward.
Dr. LaFaver: Thank you so much for that summary. You already mentioned the main methodology you used.
What is the next step for you? How do you see these findings informing our clinical care? Do you have suggestions for all of the neurologists listening in this regard?
PD not yet considered ACE-related
Dr. Subramanian: Dr. Burke Harris was the former surgeon general in California. She’s a woman of color and a brilliant speaker, and she had worked in inner cities, I think in San Francisco, with pediatric populations, seeing these effects of adversity in that time frame.
You see this population at risk, and then you’re following this cohort, which we knew from the Kaiser cohort determines earlier morbidity and mortality across a number of disease states. We’re seeing things like more heart attacks, more diabetes, and all kinds of things in these populations. This is not new news; we just have not been focusing on this.
In her paper, this call to action, they had talked about some ACE-related conditions that currently do not include Parkinson’s disease. There are three ACE-related neurologic conditions that people should be aware of. One is in the headache/pain universe. Another is in the stroke universe, and that’s understandable, given cardiovascular risk factors . Then the third is in this dementia risk category. I think Parkinson’s disease, as we know, can be associated with dementia. A large percentage of our patients get dementia, but we don’t have Parkinson’s disease called out in this framework.
What people are talking about is if you have no ACEs or are in this middle category of one to three ACEs and you don’t have an ACE-related diagnosis – which Parkinson’s disease is not currently – we just give some basic counseling about the importance of lifestyle. I think we would love to see that anyway. They’re talking about things like exercise, diet, sleep, social connection, getting out in nature, things like that, so just general counseling on the importance of that.
Then if you’re in this higher-risk category, and so with these ACE-related neurologic conditions, including dementia, headache, and stroke, if you had this middle range of one to three ACEs, they’re getting additional resources. Some of them may be referred for social work help or mental health support and things like that.
I’d really love to see that happening in Parkinson’s disease, because I think we have so many needs in our population. I’m always hoping to advocate for more mental health needs that are scarce and resources in the social support realm because I believe that social connection and social support is a huge buffer for this trauma.
ACEs are just one type of trauma. I take care of veterans in the Veterans [Affairs Department]. We have some information now coming out about posttraumatic stress disorder, predisposing to certain things in Parkinson’s disease, possibly head injury, and things like that. I think we have populations at risk that we can hopefully screen at intake, and I’m really pushing for that.
Maybe it’s not the neurologist that does this intake. It might be someone else on the team that can spend some time doing these questionnaires and understand if your patient has a high ACE score. Unless you ask, many patients don’t necessarily come forward to talk about this. I really am pushing for trying to screen and trying to advocate for more research in this area so that we can classify Parkinson’s disease as an ACE-related condition and thus give more resources from the mental health world, and also the social support world, to our patients.
Dr. LaFaver: Thank you. There are many important points, and I think it’s a very important thing to recognize that it may not be only trauma in childhood but also throughout life, as you said, and might really influence nonmotor symptoms of Parkinson’s disease in particular, including anxiety and pain, which are often difficult to treat.
I think there’s much more to do in research, advocacy, and education. We’re going to educate patients about this, and also educate other neurologists and providers. I think you mentioned that trauma-informed care is getting its spotlight in primary care and other specialties. I think we have catching up to do in neurology, and I think this is a really important work toward that goal.
Thank you so much for your work and for taking the time to share your thoughts. I hope to talk to you again soon.
Dr. Subramanian: Thank you so much, Kathrin.
Dr. LaFaver has disclosed no relevant financial relationships. Dr. Subramanian disclosed ties with Acorda Therapeutics.
A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Kathrin LaFaver, MD: Hello. I’m happy to talk today to Dr. Indu Subramanian, clinical professor at University of California, Los Angeles, and director of the Parkinson’s Disease Research, Education and Clinical Center in Los Angeles. I am a neurologist in Saratoga Springs, New York, and we will be talking today about Indu’s new paper on childhood trauma and Parkinson’s disease. Welcome and thanks for taking the time.
Indu Subramanian, MD: Thank you so much for letting us highlight this important topic.
Dr. LaFaver: There are many papers published every month on Parkinson’s disease, but this topic stands out because it’s not a thing that has been commonly looked at. What gave you the idea to study this?
Neurology behind other specialties
Dr. Subramanian: Kathrin, you and I have been looking at things that can inform us about our patients – the person who’s standing in front of us when they come in and we’re giving them this diagnosis. I think that so much of what we’ve done [in the past] is a cookie cutter approach to giving everybody the standard treatment. [We’ve been assuming that] It doesn’t matter if they’re a man or woman. It doesn’t matter if they’re a veteran. It doesn’t matter if they may be from a minoritized population.
We’ve also been interested in approaches that are outside the box, right? We have this integrative medicine and lifestyle medicine background. I’ve been going to those meetings and really been struck by the mounting evidence on the importance of things like early adverse childhood events (ACEs), what zip code you live in, what your pollution index is, and how these things can affect people through their life and their health.
I think that it is high time neurologists pay attention to this. There’s been mounting evidence throughout many disease states, various types of cancers, and mental health. Cardiology is much more advanced, but we haven’t had much data in neurology. In fact, when we went to write this paper, there were just one or two papers that were looking at multiple sclerosis or general neurologic issues, but really nothing in Parkinson’s disease.
We know that Parkinson’s disease is not only a motor disease that affects mental health, but that it also affects nonmotor issues. Childhood adversity may affect how people progress or how quickly they may get a disease, and we were interested in how it may manifest in a disease like Parkinson’s disease.
That was the framework going to meetings. As we wrote this paper and were in various editing stages, there was a beautiful paper that came out by Nadine Burke Harris and team that really was a call to action for neurologists and caring about trauma.
Dr. LaFaver: I couldn’t agree more. It’s really an underrecognized issue. With my own background, being very interested in functional movement disorders, psychosomatic disorders, and so on, it becomes much more evident how common a trauma background is, not only for people we were traditionally asking about.
Why don’t you summarize your findings for us?
Adverse childhood events
Dr. Subramanian: This is a web-based survey, so obviously, these are patient self-reports of their disease. We have a large cohort of people that we’ve been following over 7 years. I’m looking at modifiable variables and what really impacts Parkinson’s disease. Some of our previous papers have looked at diet, exercise, and loneliness. This is the same cohort.
We ended up putting the ACEs questionnaire, which is 10 questions looking at whether you were exposed to certain things in your household below the age of 18. This is a relatively standard questionnaire that’s administered one time, and you get a score out of 10. This is something that has been pushed, at least in the state of California, as something that we should be checking more in all people coming in.
We introduced the survey, and we didn’t force everyone to take it. Unfortunately, there was 20% or so of our patients who chose not to answer these questions. One has to ask, who are those people that didn’t answer the questions? Are they the ones that may have had trauma and these questions were triggering? It was a gap. We didn’t add extra questions to explore why people didn’t answer those questions.
We have to also put this in context. We have a patient population that’s largely quite affluent, who are able to access web-based surveys through their computer, and largely Caucasian; there are not many minoritized populations in our cohort. We want to do better with that. We actually were able to gather a decent number of women. We represent women quite well in our survey. I think that’s because of this online approach and some of the things that we’re studying.
In our survey, we broke it down into people who had no ACEs, one to three ACEs, or four or more ACEs. This is a standard way to break down ACEs so that we’re able to categorize what to do with these patient populations.
What we saw – and it’s preliminary evidence – is that people who had higher ACE scores seemed to have more symptom severity when we controlled for things like years since diagnosis, age, and gender. They also seem to have a worse quality of life. There was some indication that there were more nonmotor issues in those populations, as you might expect, such as anxiety, depression, and things that presumably ACEs can affect separately.
There are some confounders, but I think we really want to use this as the first piece of evidence to hopefully pave the way for caring about trauma in Parkinson’s disease moving forward.
Dr. LaFaver: Thank you so much for that summary. You already mentioned the main methodology you used.
What is the next step for you? How do you see these findings informing our clinical care? Do you have suggestions for all of the neurologists listening in this regard?
PD not yet considered ACE-related
Dr. Subramanian: Dr. Burke Harris was the former surgeon general in California. She’s a woman of color and a brilliant speaker, and she had worked in inner cities, I think in San Francisco, with pediatric populations, seeing these effects of adversity in that time frame.
You see this population at risk, and then you’re following this cohort, which we knew from the Kaiser cohort determines earlier morbidity and mortality across a number of disease states. We’re seeing things like more heart attacks, more diabetes, and all kinds of things in these populations. This is not new news; we just have not been focusing on this.
In her paper, this call to action, they had talked about some ACE-related conditions that currently do not include Parkinson’s disease. There are three ACE-related neurologic conditions that people should be aware of. One is in the headache/pain universe. Another is in the stroke universe, and that’s understandable, given cardiovascular risk factors . Then the third is in this dementia risk category. I think Parkinson’s disease, as we know, can be associated with dementia. A large percentage of our patients get dementia, but we don’t have Parkinson’s disease called out in this framework.
What people are talking about is if you have no ACEs or are in this middle category of one to three ACEs and you don’t have an ACE-related diagnosis – which Parkinson’s disease is not currently – we just give some basic counseling about the importance of lifestyle. I think we would love to see that anyway. They’re talking about things like exercise, diet, sleep, social connection, getting out in nature, things like that, so just general counseling on the importance of that.
Then if you’re in this higher-risk category, and so with these ACE-related neurologic conditions, including dementia, headache, and stroke, if you had this middle range of one to three ACEs, they’re getting additional resources. Some of them may be referred for social work help or mental health support and things like that.
I’d really love to see that happening in Parkinson’s disease, because I think we have so many needs in our population. I’m always hoping to advocate for more mental health needs that are scarce and resources in the social support realm because I believe that social connection and social support is a huge buffer for this trauma.
ACEs are just one type of trauma. I take care of veterans in the Veterans [Affairs Department]. We have some information now coming out about posttraumatic stress disorder, predisposing to certain things in Parkinson’s disease, possibly head injury, and things like that. I think we have populations at risk that we can hopefully screen at intake, and I’m really pushing for that.
Maybe it’s not the neurologist that does this intake. It might be someone else on the team that can spend some time doing these questionnaires and understand if your patient has a high ACE score. Unless you ask, many patients don’t necessarily come forward to talk about this. I really am pushing for trying to screen and trying to advocate for more research in this area so that we can classify Parkinson’s disease as an ACE-related condition and thus give more resources from the mental health world, and also the social support world, to our patients.
Dr. LaFaver: Thank you. There are many important points, and I think it’s a very important thing to recognize that it may not be only trauma in childhood but also throughout life, as you said, and might really influence nonmotor symptoms of Parkinson’s disease in particular, including anxiety and pain, which are often difficult to treat.
I think there’s much more to do in research, advocacy, and education. We’re going to educate patients about this, and also educate other neurologists and providers. I think you mentioned that trauma-informed care is getting its spotlight in primary care and other specialties. I think we have catching up to do in neurology, and I think this is a really important work toward that goal.
Thank you so much for your work and for taking the time to share your thoughts. I hope to talk to you again soon.
Dr. Subramanian: Thank you so much, Kathrin.
Dr. LaFaver has disclosed no relevant financial relationships. Dr. Subramanian disclosed ties with Acorda Therapeutics.
A version of this article originally appeared on Medscape.com.
Autism: Is it in the water?
This transcript has been edited for clarity.
Few diseases have stymied explanation like autism spectrum disorder (ASD). We know that the prevalence has been increasing dramatically, but we aren’t quite sure whether that is because of more screening and awareness or more fundamental changes. We know that much of the risk appears to be genetic, but there may be 1,000 genes involved in the syndrome. We know that certain environmental exposures, like pollution, might increase the risk – perhaps on a susceptible genetic background – but we’re not really sure which exposures are most harmful.
So, the search continues, across all domains of inquiry from cell culture to large epidemiologic analyses. And this week, a new player enters the field, and, as they say, it’s something in the water.
We’re talking about this paper, by Zeyan Liew and colleagues, appearing in JAMA Pediatrics.
Using the incredibly robust health data infrastructure in Denmark, the researchers were able to identify 8,842 children born between 2000 and 2013 with ASD and matched each one to five control kids of the same sex and age without autism.
They then mapped the location the mothers of these kids lived while they were pregnant – down to 5 meters resolution, actually – to groundwater lithium levels.
Once that was done, the analysis was straightforward. Would moms who were pregnant in areas with higher groundwater lithium levels be more likely to have kids with ASD?
The results show a rather steady and consistent association between higher lithium levels in groundwater and the prevalence of ASD in children.
We’re not talking huge numbers, but moms who lived in the areas of the highest quartile of lithium were about 46% more likely to have a child with ASD. That’s a relative risk, of course – this would be like an increase from 1 in 100 kids to 1.5 in 100 kids. But still, it’s intriguing.
But the case is far from closed here.
Groundwater concentration of lithium and the amount of lithium a pregnant mother ingests are not the same thing. It does turn out that virtually all drinking water in Denmark comes from groundwater sources – but not all lithium comes from drinking water. There are plenty of dietary sources of lithium as well. And, of course, there is medical lithium, but we’ll get to that in a second.
First, let’s talk about those lithium measurements. They were taken in 2013 – after all these kids were born. The authors acknowledge this limitation but show a high correlation between measured levels in 2013 and earlier measured levels from prior studies, suggesting that lithium levels in a given area are quite constant over time. That’s great – but if lithium levels are constant over time, this study does nothing to shed light on why autism diagnoses seem to be increasing.
Let’s put some numbers to the lithium concentrations the authors examined. The average was about 12 mcg/L.
As a reminder, a standard therapeutic dose of lithium used for bipolar disorder is like 600 mg. That means you’d need to drink more than 2,500 of those 5-gallon jugs that sit on your water cooler, per day, to approximate the dose you’d get from a lithium tablet. Of course, small doses can still cause toxicity – but I wanted to put this in perspective.
Also, we have some data on pregnant women who take medical lithium. An analysis of nine studies showed that first-trimester lithium use may be associated with congenital malformations – particularly some specific heart malformations – and some birth complications. But three of four separate studies looking at longer-term neurodevelopmental outcomes did not find any effect on development, attainment of milestones, or IQ. One study of 15 kids exposed to medical lithium in utero did note minor neurologic dysfunction in one child and a low verbal IQ in another – but that’s a very small study.
Of course, lithium levels vary around the world as well. The U.S. Geological Survey examined lithium content in groundwater in the United States, as you can see here.
Our numbers are pretty similar to Denmark’s – in the 0-60 range. But an area in the Argentine Andes has levels as high as 1,600 mcg/L. A study of 194 babies from that area found higher lithium exposure was associated with lower fetal size, but I haven’t seen follow-up on neurodevelopmental outcomes.
The point is that there is a lot of variability here. It would be really interesting to map groundwater lithium levels to autism rates around the world. As a teaser, I will point out that, if you look at worldwide autism rates, you may be able to convince yourself that they are higher in more arid climates, and arid climates tend to have more groundwater lithium. But I’m really reaching here. More work needs to be done.
And I hope it is done quickly. Lithium is in the midst of becoming a very important commodity thanks to the shift to electric vehicles. While we can hope that recycling will claim most of those batteries at the end of their life, some will escape reclamation and potentially put more lithium into the drinking water. I’d like to know how risky that is before it happens.
F. Perry Wilson, MD, MSCE, is an associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator. He has disclosed no relevant financial relationships. His science communication work can be found in the Huffington Post, on NPR, and here on Medscape. He tweets @fperrywilson and his new book, “How Medicine Works and When It Doesn’t”, is available now.
A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Few diseases have stymied explanation like autism spectrum disorder (ASD). We know that the prevalence has been increasing dramatically, but we aren’t quite sure whether that is because of more screening and awareness or more fundamental changes. We know that much of the risk appears to be genetic, but there may be 1,000 genes involved in the syndrome. We know that certain environmental exposures, like pollution, might increase the risk – perhaps on a susceptible genetic background – but we’re not really sure which exposures are most harmful.
So, the search continues, across all domains of inquiry from cell culture to large epidemiologic analyses. And this week, a new player enters the field, and, as they say, it’s something in the water.
We’re talking about this paper, by Zeyan Liew and colleagues, appearing in JAMA Pediatrics.
Using the incredibly robust health data infrastructure in Denmark, the researchers were able to identify 8,842 children born between 2000 and 2013 with ASD and matched each one to five control kids of the same sex and age without autism.
They then mapped the location the mothers of these kids lived while they were pregnant – down to 5 meters resolution, actually – to groundwater lithium levels.
Once that was done, the analysis was straightforward. Would moms who were pregnant in areas with higher groundwater lithium levels be more likely to have kids with ASD?
The results show a rather steady and consistent association between higher lithium levels in groundwater and the prevalence of ASD in children.
We’re not talking huge numbers, but moms who lived in the areas of the highest quartile of lithium were about 46% more likely to have a child with ASD. That’s a relative risk, of course – this would be like an increase from 1 in 100 kids to 1.5 in 100 kids. But still, it’s intriguing.
But the case is far from closed here.
Groundwater concentration of lithium and the amount of lithium a pregnant mother ingests are not the same thing. It does turn out that virtually all drinking water in Denmark comes from groundwater sources – but not all lithium comes from drinking water. There are plenty of dietary sources of lithium as well. And, of course, there is medical lithium, but we’ll get to that in a second.
First, let’s talk about those lithium measurements. They were taken in 2013 – after all these kids were born. The authors acknowledge this limitation but show a high correlation between measured levels in 2013 and earlier measured levels from prior studies, suggesting that lithium levels in a given area are quite constant over time. That’s great – but if lithium levels are constant over time, this study does nothing to shed light on why autism diagnoses seem to be increasing.
Let’s put some numbers to the lithium concentrations the authors examined. The average was about 12 mcg/L.
As a reminder, a standard therapeutic dose of lithium used for bipolar disorder is like 600 mg. That means you’d need to drink more than 2,500 of those 5-gallon jugs that sit on your water cooler, per day, to approximate the dose you’d get from a lithium tablet. Of course, small doses can still cause toxicity – but I wanted to put this in perspective.
Also, we have some data on pregnant women who take medical lithium. An analysis of nine studies showed that first-trimester lithium use may be associated with congenital malformations – particularly some specific heart malformations – and some birth complications. But three of four separate studies looking at longer-term neurodevelopmental outcomes did not find any effect on development, attainment of milestones, or IQ. One study of 15 kids exposed to medical lithium in utero did note minor neurologic dysfunction in one child and a low verbal IQ in another – but that’s a very small study.
Of course, lithium levels vary around the world as well. The U.S. Geological Survey examined lithium content in groundwater in the United States, as you can see here.
Our numbers are pretty similar to Denmark’s – in the 0-60 range. But an area in the Argentine Andes has levels as high as 1,600 mcg/L. A study of 194 babies from that area found higher lithium exposure was associated with lower fetal size, but I haven’t seen follow-up on neurodevelopmental outcomes.
The point is that there is a lot of variability here. It would be really interesting to map groundwater lithium levels to autism rates around the world. As a teaser, I will point out that, if you look at worldwide autism rates, you may be able to convince yourself that they are higher in more arid climates, and arid climates tend to have more groundwater lithium. But I’m really reaching here. More work needs to be done.
And I hope it is done quickly. Lithium is in the midst of becoming a very important commodity thanks to the shift to electric vehicles. While we can hope that recycling will claim most of those batteries at the end of their life, some will escape reclamation and potentially put more lithium into the drinking water. I’d like to know how risky that is before it happens.
F. Perry Wilson, MD, MSCE, is an associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator. He has disclosed no relevant financial relationships. His science communication work can be found in the Huffington Post, on NPR, and here on Medscape. He tweets @fperrywilson and his new book, “How Medicine Works and When It Doesn’t”, is available now.
A version of this article originally appeared on Medscape.com.
This transcript has been edited for clarity.
Few diseases have stymied explanation like autism spectrum disorder (ASD). We know that the prevalence has been increasing dramatically, but we aren’t quite sure whether that is because of more screening and awareness or more fundamental changes. We know that much of the risk appears to be genetic, but there may be 1,000 genes involved in the syndrome. We know that certain environmental exposures, like pollution, might increase the risk – perhaps on a susceptible genetic background – but we’re not really sure which exposures are most harmful.
So, the search continues, across all domains of inquiry from cell culture to large epidemiologic analyses. And this week, a new player enters the field, and, as they say, it’s something in the water.
We’re talking about this paper, by Zeyan Liew and colleagues, appearing in JAMA Pediatrics.
Using the incredibly robust health data infrastructure in Denmark, the researchers were able to identify 8,842 children born between 2000 and 2013 with ASD and matched each one to five control kids of the same sex and age without autism.
They then mapped the location the mothers of these kids lived while they were pregnant – down to 5 meters resolution, actually – to groundwater lithium levels.
Once that was done, the analysis was straightforward. Would moms who were pregnant in areas with higher groundwater lithium levels be more likely to have kids with ASD?
The results show a rather steady and consistent association between higher lithium levels in groundwater and the prevalence of ASD in children.
We’re not talking huge numbers, but moms who lived in the areas of the highest quartile of lithium were about 46% more likely to have a child with ASD. That’s a relative risk, of course – this would be like an increase from 1 in 100 kids to 1.5 in 100 kids. But still, it’s intriguing.
But the case is far from closed here.
Groundwater concentration of lithium and the amount of lithium a pregnant mother ingests are not the same thing. It does turn out that virtually all drinking water in Denmark comes from groundwater sources – but not all lithium comes from drinking water. There are plenty of dietary sources of lithium as well. And, of course, there is medical lithium, but we’ll get to that in a second.
First, let’s talk about those lithium measurements. They were taken in 2013 – after all these kids were born. The authors acknowledge this limitation but show a high correlation between measured levels in 2013 and earlier measured levels from prior studies, suggesting that lithium levels in a given area are quite constant over time. That’s great – but if lithium levels are constant over time, this study does nothing to shed light on why autism diagnoses seem to be increasing.
Let’s put some numbers to the lithium concentrations the authors examined. The average was about 12 mcg/L.
As a reminder, a standard therapeutic dose of lithium used for bipolar disorder is like 600 mg. That means you’d need to drink more than 2,500 of those 5-gallon jugs that sit on your water cooler, per day, to approximate the dose you’d get from a lithium tablet. Of course, small doses can still cause toxicity – but I wanted to put this in perspective.
Also, we have some data on pregnant women who take medical lithium. An analysis of nine studies showed that first-trimester lithium use may be associated with congenital malformations – particularly some specific heart malformations – and some birth complications. But three of four separate studies looking at longer-term neurodevelopmental outcomes did not find any effect on development, attainment of milestones, or IQ. One study of 15 kids exposed to medical lithium in utero did note minor neurologic dysfunction in one child and a low verbal IQ in another – but that’s a very small study.
Of course, lithium levels vary around the world as well. The U.S. Geological Survey examined lithium content in groundwater in the United States, as you can see here.
Our numbers are pretty similar to Denmark’s – in the 0-60 range. But an area in the Argentine Andes has levels as high as 1,600 mcg/L. A study of 194 babies from that area found higher lithium exposure was associated with lower fetal size, but I haven’t seen follow-up on neurodevelopmental outcomes.
The point is that there is a lot of variability here. It would be really interesting to map groundwater lithium levels to autism rates around the world. As a teaser, I will point out that, if you look at worldwide autism rates, you may be able to convince yourself that they are higher in more arid climates, and arid climates tend to have more groundwater lithium. But I’m really reaching here. More work needs to be done.
And I hope it is done quickly. Lithium is in the midst of becoming a very important commodity thanks to the shift to electric vehicles. While we can hope that recycling will claim most of those batteries at the end of their life, some will escape reclamation and potentially put more lithium into the drinking water. I’d like to know how risky that is before it happens.
F. Perry Wilson, MD, MSCE, is an associate professor of medicine and director of Yale’s Clinical and Translational Research Accelerator. He has disclosed no relevant financial relationships. His science communication work can be found in the Huffington Post, on NPR, and here on Medscape. He tweets @fperrywilson and his new book, “How Medicine Works and When It Doesn’t”, is available now.
A version of this article originally appeared on Medscape.com.
The sacrifice of orthodoxy: Maintaining collegiality in psychiatry
Psychiatrists practice in a wide array of ways. We approach our work and our patients with beliefs and preconceptions that develop over time. Our training has significant influence, though our own personalities and biases also affect our understanding.
Psychiatrists have philosophical lenses through which they see patients. We can reflect and see some standard archetypes. We are familiar with the reductionistic pharmacologist, the somatic treatment specialist, the psychodynamic ‘guru,’ and the medicolegally paralyzed practitioner. It is without judgment that we lay these out, for our very point is that we have these constituent parts within our own clinical identities. The intensity with which we subscribe to these clinical sensibilities could contribute to a biased orthodoxy.
Orthodoxy can be defined as an accepted theory that stems from an authoritative entity. This is a well-known phenomenon that continues to be visible. For example, one can quickly peruse psychodynamic literature to find one school of thought criticizing another. It is not without some confrontation and even interpersonal rifts that the lineage of psychoanalytic theory has evolved. This has always been of interest to us. A core facet of psychoanalysis is empathy, truly knowing the inner state of a different person. And yet, the very bastions of this clinical sensibility frequently resort to veiled attacks on those in their field who have opposing views. It then begs the question: If even enlightened institutions fail at a nonjudgmental approach toward their colleagues, what hope is there for the rest of us clinicians, mired in the thick of day-to-day clinical practice?
It is our contention that the odds are against us. Even the aforementioned critique of psychoanalytic orthodoxy is just another example of how we humans organize our experience. Even as we write an article in argument against unbridled critique, we find it difficult to do so without engaging in it. For to criticize another is to help shore up our own personal identities. This is especially the case when clinicians deal with issues that we feel strongly about. The human psyche has a need to organize its experience, as “our experience of ourselves is fundamental to how we operate in the world. Our subjective experience is the phenomenology of all that one might be aware of.”1
In this vein, we would like to cite attribution theory. This is a view of human behavior within social psychology. The Austrian psychologist Fritz Heider, PhD, investigated “the domain of social interactions, wondering how people perceive each other in interaction and especially how they make sense of each other’s behavior.”2 Attribution theory suggests that as humans organize our social interactions, we may make two basic assumptions. One is that our own behavior is highly affected by an environment that is beyond our control. The second is that when judging the behavior of others, we are more likely to attribute it to internal traits that they have. A classic example is automobile traffic. When we see someone driving erratically, we are more likely to blame them for being an inherently bad driver. However, if attention is called to our own driving, we are more likely to cite external factors such as rush hour, a bad driver around us, or a faulty vehicle.
We would like to reference one last model of human behavior. It has become customary within the field of neuroscience to view the brain as a predictive organ: “Theories of prediction in perception, action, and learning suggest that the brain serves to reduce the discrepancies between expectation and actual experience, i.e., by reducing the prediction error.”3 Perception itself has recently been described as a controlled hallucination, where the brain makes predictions of what it thinks it is about to see based on past experiences. Visual stimulus ultimately takes time to enter our eyes and be processed in the brain – “predictions would need to preactivate neural representations that would typically be driven by sensory input, before the actual arrival of that input.”4 It thus seems to be an inherent method of the brain to anticipate visual and even social events to help human beings sustain themselves.
Having spoken of a psychoanalytic conceptualization of self-organization, the theory of attribution, and research into social neuroscience, we turn our attention back to the central question that this article would like to address.
When we find ourselves busy in rote clinical practice, we believe the likelihood of intercollegiate mentalization is low; our ability to relate to our peers becomes strained. We ultimately do not practice in a vacuum. Psychiatrists, even those in a solo private practice, are ultimately part of a community of providers who, more or less, follow some emergent ‘standard of care.’ This can be a vague concept; but one that takes on a concrete form in the minds of certain clinicians and certainly in the setting of a medicolegal court. Yet, the psychiatrists that we know all have very stereotyped ways of practice. And at the heart of it, we all think that we are right.
We can use polypharmacy as an example. Imagine that you have a new patient intake, who tells you that they are transferring care from another psychiatrist. They inform you of their medication regimen. This patient presents on eight or more psychotropics. Many of us may have a visceral reaction at this point and, following the aforementioned attribution theory, we may ask ourselves what ‘quack’ of a doctor would do this. Yet some among us would think that a very competent psychopharmacologist was daring enough to use the full armamentarium of psychopharmacology to help this patient, who must be treatment refractory.
When speaking with such a patient, we would be quick to reflect on our own parsimonious use of medications. We would tell ourselves that we are responsible providers and would be quick to recommend discontinuation of medications. This would help us feel better about ourselves, and would of course assuage the ever-present medicolegal ‘big brother’ in our minds. It is through this very process that we affirm our self-identities. For if this patient’s previous physician was a bad psychiatrist, then we are a good psychiatrist. It is through this process that our clinical selves find confirmation.
We do not mean to reduce the complexities of human behavior to quick stereotypes. However, it is our belief that when confronted with clinical or philosophical disputes with our colleagues, the basic rules of human behavior will attempt to dissolve and override efforts at mentalization, collegiality, or interpersonal sensitivity. For to accept a clinical practice view that is different from ours would be akin to giving up the essence of our clinical identities. It could be compared to the fragmentation process of a vulnerable psyche when confronted with a reality that is at odds with preconceived notions and experiences.
While we may be able to appreciate the nuances and sensibilities of another provider, we believe it would be particularly difficult for most of us to actually attempt to practice in a fashion that is not congruent with our own organizers of experience. Whether or not our practice style is ‘perfect,’ it has worked for us. Social neuroscience and our understanding of the organization of the self would predict that we would hold onto our way of practice with all the mind’s defenses. Externalization, denial, and projection could all be called into action in this battle against existential fragmentation.
Do we seek to portray a clinical world where there is no hope for genuine modeling of clinical sensibilities to other psychiatrists? That is not our intention. Yet it seems that many of the theoretical frameworks that we subscribe to argue against this possibility. We would be hypocritical if we did not here state that our own theoretical frameworks are yet other examples of “organizers of experience.” Attribution theory, intersubjectivity, and social neuroscience are simply our ways of organizing the chaos of perceptions, ideas, and intricacies of human behavior.
If we accept that psychiatrists, like all human beings, are trapped in a subjective experience, then we can be more playful and flexible when interacting with our colleagues. We do not have to be as defensive of our practices and accusatory of others. If we practice daily according to some orthodoxy, then we color our experiences of the patient and of our colleagues’ ways of practice. We automatically start off on the wrong foot. And yet, to give up this orthodoxy would, by definition, be disorganizing and fragmenting to us. For as Nietzsche said, “truth is an illusion without which a certain species could not survive.”5
Dr. Khalafian practices full time as a general outpatient psychiatrist. He trained at the University of California, San Diego, for his psychiatric residency and currently works as a telepsychiatrist, serving an outpatient clinic population in northern California. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Khalafian have no conflicts of interest.
References
1. Buirski P and Haglund P. Making sense together: The intersubjective approach to psychotherapy. Northvale, NJ: Jason Aronson; 2001.
2. Malle BF. Attribution theories: How people make sense of behavior. In Chadee D (ed.), Theories in social psychology. pp. 72-95. Wiley-Blackwell; 2011.
3. Brown EC and Brune M. The role of prediction in social neuroscience. Front Hum Neurosci. 2012 May 24;6:147. doi: 10.3389/fnhum.2012.00147.
4. Blom T et al. Predictions drive neural representations of visual events ahead of incoming sensory information. Proc Natl Acad Sci USA. 2020 Mar 31;117(13):7510-7515. doi: 10.1073/pnas.1917777117.
5. Yalom I. The Gift of Therapy. Harper Perennial; 2002.
Psychiatrists practice in a wide array of ways. We approach our work and our patients with beliefs and preconceptions that develop over time. Our training has significant influence, though our own personalities and biases also affect our understanding.
Psychiatrists have philosophical lenses through which they see patients. We can reflect and see some standard archetypes. We are familiar with the reductionistic pharmacologist, the somatic treatment specialist, the psychodynamic ‘guru,’ and the medicolegally paralyzed practitioner. It is without judgment that we lay these out, for our very point is that we have these constituent parts within our own clinical identities. The intensity with which we subscribe to these clinical sensibilities could contribute to a biased orthodoxy.
Orthodoxy can be defined as an accepted theory that stems from an authoritative entity. This is a well-known phenomenon that continues to be visible. For example, one can quickly peruse psychodynamic literature to find one school of thought criticizing another. It is not without some confrontation and even interpersonal rifts that the lineage of psychoanalytic theory has evolved. This has always been of interest to us. A core facet of psychoanalysis is empathy, truly knowing the inner state of a different person. And yet, the very bastions of this clinical sensibility frequently resort to veiled attacks on those in their field who have opposing views. It then begs the question: If even enlightened institutions fail at a nonjudgmental approach toward their colleagues, what hope is there for the rest of us clinicians, mired in the thick of day-to-day clinical practice?
It is our contention that the odds are against us. Even the aforementioned critique of psychoanalytic orthodoxy is just another example of how we humans organize our experience. Even as we write an article in argument against unbridled critique, we find it difficult to do so without engaging in it. For to criticize another is to help shore up our own personal identities. This is especially the case when clinicians deal with issues that we feel strongly about. The human psyche has a need to organize its experience, as “our experience of ourselves is fundamental to how we operate in the world. Our subjective experience is the phenomenology of all that one might be aware of.”1
In this vein, we would like to cite attribution theory. This is a view of human behavior within social psychology. The Austrian psychologist Fritz Heider, PhD, investigated “the domain of social interactions, wondering how people perceive each other in interaction and especially how they make sense of each other’s behavior.”2 Attribution theory suggests that as humans organize our social interactions, we may make two basic assumptions. One is that our own behavior is highly affected by an environment that is beyond our control. The second is that when judging the behavior of others, we are more likely to attribute it to internal traits that they have. A classic example is automobile traffic. When we see someone driving erratically, we are more likely to blame them for being an inherently bad driver. However, if attention is called to our own driving, we are more likely to cite external factors such as rush hour, a bad driver around us, or a faulty vehicle.
We would like to reference one last model of human behavior. It has become customary within the field of neuroscience to view the brain as a predictive organ: “Theories of prediction in perception, action, and learning suggest that the brain serves to reduce the discrepancies between expectation and actual experience, i.e., by reducing the prediction error.”3 Perception itself has recently been described as a controlled hallucination, where the brain makes predictions of what it thinks it is about to see based on past experiences. Visual stimulus ultimately takes time to enter our eyes and be processed in the brain – “predictions would need to preactivate neural representations that would typically be driven by sensory input, before the actual arrival of that input.”4 It thus seems to be an inherent method of the brain to anticipate visual and even social events to help human beings sustain themselves.
Having spoken of a psychoanalytic conceptualization of self-organization, the theory of attribution, and research into social neuroscience, we turn our attention back to the central question that this article would like to address.
When we find ourselves busy in rote clinical practice, we believe the likelihood of intercollegiate mentalization is low; our ability to relate to our peers becomes strained. We ultimately do not practice in a vacuum. Psychiatrists, even those in a solo private practice, are ultimately part of a community of providers who, more or less, follow some emergent ‘standard of care.’ This can be a vague concept; but one that takes on a concrete form in the minds of certain clinicians and certainly in the setting of a medicolegal court. Yet, the psychiatrists that we know all have very stereotyped ways of practice. And at the heart of it, we all think that we are right.
We can use polypharmacy as an example. Imagine that you have a new patient intake, who tells you that they are transferring care from another psychiatrist. They inform you of their medication regimen. This patient presents on eight or more psychotropics. Many of us may have a visceral reaction at this point and, following the aforementioned attribution theory, we may ask ourselves what ‘quack’ of a doctor would do this. Yet some among us would think that a very competent psychopharmacologist was daring enough to use the full armamentarium of psychopharmacology to help this patient, who must be treatment refractory.
When speaking with such a patient, we would be quick to reflect on our own parsimonious use of medications. We would tell ourselves that we are responsible providers and would be quick to recommend discontinuation of medications. This would help us feel better about ourselves, and would of course assuage the ever-present medicolegal ‘big brother’ in our minds. It is through this very process that we affirm our self-identities. For if this patient’s previous physician was a bad psychiatrist, then we are a good psychiatrist. It is through this process that our clinical selves find confirmation.
We do not mean to reduce the complexities of human behavior to quick stereotypes. However, it is our belief that when confronted with clinical or philosophical disputes with our colleagues, the basic rules of human behavior will attempt to dissolve and override efforts at mentalization, collegiality, or interpersonal sensitivity. For to accept a clinical practice view that is different from ours would be akin to giving up the essence of our clinical identities. It could be compared to the fragmentation process of a vulnerable psyche when confronted with a reality that is at odds with preconceived notions and experiences.
While we may be able to appreciate the nuances and sensibilities of another provider, we believe it would be particularly difficult for most of us to actually attempt to practice in a fashion that is not congruent with our own organizers of experience. Whether or not our practice style is ‘perfect,’ it has worked for us. Social neuroscience and our understanding of the organization of the self would predict that we would hold onto our way of practice with all the mind’s defenses. Externalization, denial, and projection could all be called into action in this battle against existential fragmentation.
Do we seek to portray a clinical world where there is no hope for genuine modeling of clinical sensibilities to other psychiatrists? That is not our intention. Yet it seems that many of the theoretical frameworks that we subscribe to argue against this possibility. We would be hypocritical if we did not here state that our own theoretical frameworks are yet other examples of “organizers of experience.” Attribution theory, intersubjectivity, and social neuroscience are simply our ways of organizing the chaos of perceptions, ideas, and intricacies of human behavior.
If we accept that psychiatrists, like all human beings, are trapped in a subjective experience, then we can be more playful and flexible when interacting with our colleagues. We do not have to be as defensive of our practices and accusatory of others. If we practice daily according to some orthodoxy, then we color our experiences of the patient and of our colleagues’ ways of practice. We automatically start off on the wrong foot. And yet, to give up this orthodoxy would, by definition, be disorganizing and fragmenting to us. For as Nietzsche said, “truth is an illusion without which a certain species could not survive.”5
Dr. Khalafian practices full time as a general outpatient psychiatrist. He trained at the University of California, San Diego, for his psychiatric residency and currently works as a telepsychiatrist, serving an outpatient clinic population in northern California. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Khalafian have no conflicts of interest.
References
1. Buirski P and Haglund P. Making sense together: The intersubjective approach to psychotherapy. Northvale, NJ: Jason Aronson; 2001.
2. Malle BF. Attribution theories: How people make sense of behavior. In Chadee D (ed.), Theories in social psychology. pp. 72-95. Wiley-Blackwell; 2011.
3. Brown EC and Brune M. The role of prediction in social neuroscience. Front Hum Neurosci. 2012 May 24;6:147. doi: 10.3389/fnhum.2012.00147.
4. Blom T et al. Predictions drive neural representations of visual events ahead of incoming sensory information. Proc Natl Acad Sci USA. 2020 Mar 31;117(13):7510-7515. doi: 10.1073/pnas.1917777117.
5. Yalom I. The Gift of Therapy. Harper Perennial; 2002.
Psychiatrists practice in a wide array of ways. We approach our work and our patients with beliefs and preconceptions that develop over time. Our training has significant influence, though our own personalities and biases also affect our understanding.
Psychiatrists have philosophical lenses through which they see patients. We can reflect and see some standard archetypes. We are familiar with the reductionistic pharmacologist, the somatic treatment specialist, the psychodynamic ‘guru,’ and the medicolegally paralyzed practitioner. It is without judgment that we lay these out, for our very point is that we have these constituent parts within our own clinical identities. The intensity with which we subscribe to these clinical sensibilities could contribute to a biased orthodoxy.
Orthodoxy can be defined as an accepted theory that stems from an authoritative entity. This is a well-known phenomenon that continues to be visible. For example, one can quickly peruse psychodynamic literature to find one school of thought criticizing another. It is not without some confrontation and even interpersonal rifts that the lineage of psychoanalytic theory has evolved. This has always been of interest to us. A core facet of psychoanalysis is empathy, truly knowing the inner state of a different person. And yet, the very bastions of this clinical sensibility frequently resort to veiled attacks on those in their field who have opposing views. It then begs the question: If even enlightened institutions fail at a nonjudgmental approach toward their colleagues, what hope is there for the rest of us clinicians, mired in the thick of day-to-day clinical practice?
It is our contention that the odds are against us. Even the aforementioned critique of psychoanalytic orthodoxy is just another example of how we humans organize our experience. Even as we write an article in argument against unbridled critique, we find it difficult to do so without engaging in it. For to criticize another is to help shore up our own personal identities. This is especially the case when clinicians deal with issues that we feel strongly about. The human psyche has a need to organize its experience, as “our experience of ourselves is fundamental to how we operate in the world. Our subjective experience is the phenomenology of all that one might be aware of.”1
In this vein, we would like to cite attribution theory. This is a view of human behavior within social psychology. The Austrian psychologist Fritz Heider, PhD, investigated “the domain of social interactions, wondering how people perceive each other in interaction and especially how they make sense of each other’s behavior.”2 Attribution theory suggests that as humans organize our social interactions, we may make two basic assumptions. One is that our own behavior is highly affected by an environment that is beyond our control. The second is that when judging the behavior of others, we are more likely to attribute it to internal traits that they have. A classic example is automobile traffic. When we see someone driving erratically, we are more likely to blame them for being an inherently bad driver. However, if attention is called to our own driving, we are more likely to cite external factors such as rush hour, a bad driver around us, or a faulty vehicle.
We would like to reference one last model of human behavior. It has become customary within the field of neuroscience to view the brain as a predictive organ: “Theories of prediction in perception, action, and learning suggest that the brain serves to reduce the discrepancies between expectation and actual experience, i.e., by reducing the prediction error.”3 Perception itself has recently been described as a controlled hallucination, where the brain makes predictions of what it thinks it is about to see based on past experiences. Visual stimulus ultimately takes time to enter our eyes and be processed in the brain – “predictions would need to preactivate neural representations that would typically be driven by sensory input, before the actual arrival of that input.”4 It thus seems to be an inherent method of the brain to anticipate visual and even social events to help human beings sustain themselves.
Having spoken of a psychoanalytic conceptualization of self-organization, the theory of attribution, and research into social neuroscience, we turn our attention back to the central question that this article would like to address.
When we find ourselves busy in rote clinical practice, we believe the likelihood of intercollegiate mentalization is low; our ability to relate to our peers becomes strained. We ultimately do not practice in a vacuum. Psychiatrists, even those in a solo private practice, are ultimately part of a community of providers who, more or less, follow some emergent ‘standard of care.’ This can be a vague concept; but one that takes on a concrete form in the minds of certain clinicians and certainly in the setting of a medicolegal court. Yet, the psychiatrists that we know all have very stereotyped ways of practice. And at the heart of it, we all think that we are right.
We can use polypharmacy as an example. Imagine that you have a new patient intake, who tells you that they are transferring care from another psychiatrist. They inform you of their medication regimen. This patient presents on eight or more psychotropics. Many of us may have a visceral reaction at this point and, following the aforementioned attribution theory, we may ask ourselves what ‘quack’ of a doctor would do this. Yet some among us would think that a very competent psychopharmacologist was daring enough to use the full armamentarium of psychopharmacology to help this patient, who must be treatment refractory.
When speaking with such a patient, we would be quick to reflect on our own parsimonious use of medications. We would tell ourselves that we are responsible providers and would be quick to recommend discontinuation of medications. This would help us feel better about ourselves, and would of course assuage the ever-present medicolegal ‘big brother’ in our minds. It is through this very process that we affirm our self-identities. For if this patient’s previous physician was a bad psychiatrist, then we are a good psychiatrist. It is through this process that our clinical selves find confirmation.
We do not mean to reduce the complexities of human behavior to quick stereotypes. However, it is our belief that when confronted with clinical or philosophical disputes with our colleagues, the basic rules of human behavior will attempt to dissolve and override efforts at mentalization, collegiality, or interpersonal sensitivity. For to accept a clinical practice view that is different from ours would be akin to giving up the essence of our clinical identities. It could be compared to the fragmentation process of a vulnerable psyche when confronted with a reality that is at odds with preconceived notions and experiences.
While we may be able to appreciate the nuances and sensibilities of another provider, we believe it would be particularly difficult for most of us to actually attempt to practice in a fashion that is not congruent with our own organizers of experience. Whether or not our practice style is ‘perfect,’ it has worked for us. Social neuroscience and our understanding of the organization of the self would predict that we would hold onto our way of practice with all the mind’s defenses. Externalization, denial, and projection could all be called into action in this battle against existential fragmentation.
Do we seek to portray a clinical world where there is no hope for genuine modeling of clinical sensibilities to other psychiatrists? That is not our intention. Yet it seems that many of the theoretical frameworks that we subscribe to argue against this possibility. We would be hypocritical if we did not here state that our own theoretical frameworks are yet other examples of “organizers of experience.” Attribution theory, intersubjectivity, and social neuroscience are simply our ways of organizing the chaos of perceptions, ideas, and intricacies of human behavior.
If we accept that psychiatrists, like all human beings, are trapped in a subjective experience, then we can be more playful and flexible when interacting with our colleagues. We do not have to be as defensive of our practices and accusatory of others. If we practice daily according to some orthodoxy, then we color our experiences of the patient and of our colleagues’ ways of practice. We automatically start off on the wrong foot. And yet, to give up this orthodoxy would, by definition, be disorganizing and fragmenting to us. For as Nietzsche said, “truth is an illusion without which a certain species could not survive.”5
Dr. Khalafian practices full time as a general outpatient psychiatrist. He trained at the University of California, San Diego, for his psychiatric residency and currently works as a telepsychiatrist, serving an outpatient clinic population in northern California. Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com. Dr. Badre and Dr. Khalafian have no conflicts of interest.
References
1. Buirski P and Haglund P. Making sense together: The intersubjective approach to psychotherapy. Northvale, NJ: Jason Aronson; 2001.
2. Malle BF. Attribution theories: How people make sense of behavior. In Chadee D (ed.), Theories in social psychology. pp. 72-95. Wiley-Blackwell; 2011.
3. Brown EC and Brune M. The role of prediction in social neuroscience. Front Hum Neurosci. 2012 May 24;6:147. doi: 10.3389/fnhum.2012.00147.
4. Blom T et al. Predictions drive neural representations of visual events ahead of incoming sensory information. Proc Natl Acad Sci USA. 2020 Mar 31;117(13):7510-7515. doi: 10.1073/pnas.1917777117.
5. Yalom I. The Gift of Therapy. Harper Perennial; 2002.
TNT: You need it, but guidelines won’t give it to you
Hi, everyone. I’m Dr Kenny Lin. I am a family physician and associate director of the Lancaster (Pa.) General Hospital Family Medicine Residency, and I blog at Common Sense Family Doctor.
For most of my career, I have precepted residents in primary care clinics. Generally, 1st years are scheduled to see a patient every 45 minutes on average, then every 30 minutes after the first 6 months. By the 3rd year, residents are scheduled to see a patient every 15 minutes to approximate the frequency at which patients are routinely seen in practice. Adult health maintenance visits are typically allotted two slots, for a total of 30 minutes.
The gradually increased pace of seeing patients is a challenge for many residents. It requires them to not only perform more focused medical histories and physical examinations but also to address a select handful of issues in patients who may have a long list of health concerns or preventive care needs. Prioritizing tasks into those that are necessary to do today vs. those that can be deferred to a follow-up visit is an essential skill that is equal parts art and science. In a previous commentary, I wrote about a research group’s efforts to create visual decision aids to generate individualized estimates of life expectancy gains from various preventive services.
Of course, it’s uncommon to have the luxury of focusing exclusively on preventive care in older adults, most of whom have one or more chronic conditions. Obesity, diabetes, hypertension, hypothyroidism, chronic obstructive pulmonary disease, coronary artery disease, and chronic kidney disease each has its own set of management guidelines. According to a recent estimate, following all guideline recommendations for chronic diseases plus those for preventive and acute care would require a primary care physician with a nationally representative panel of adult patients to work an impossible 27-hour day. That’s another good reason for me to continue seeing children in practice!
In a commentary in The BMJ, Dr Minna Johansson and colleagues argued that guideline panels should explicitly consider the estimated clinician time needed to improve the desired outcome for one person in the targeted population, a metric that they call “time needed to treat” (TNT). For example, to implement a National Institute for Health and Care Excellence (NICE) guideline for U.K. general practitioners (GPs) about providing advice to physically inactive adults would require 3 hours for one more person to increase their self-reported physical activity. For a patient panel of 2000 adults, the absolute TNT would be 167 hours per GP, representing 15% of yearly total face time with all patients, which seems clearly excessive.
In fact, the U.S. Preventive Services Task Force does occasionally consider the “opportunity costs” of recommending preventive services. When they first reviewed screening for chronic obstructive pulmonary disease (COPD) in 2008, the USPSTF reasoned that the minimal benefit of screening hundreds of patients to prevent a single COPD exacerbation was at least offset by the time and resources it would take to perform spirometry on every adult with a smoking history, a conclusion that it reaffirmed last year. In contrast to NICE, the USPSTF recommends selectively counseling adults without cardiovascular risk factors to promote a healthy diet and physical activity rather than counseling every single person.
Other US guideline groups would do well to adopt the advice of Johansson and colleagues to consider TNT. Last year, the Women’s Preventive Services Initiative (WPSI) recommended counseling every woman aged 40-60 years with normal or overweight body mass index “to maintain weight or limit weight gain to prevent obesity.” Though preventing obesity is a laudable goal, I’d prefer to counsel those who are obese and suffering from obesity-related conditions and spend my 15 or 30 minutes with others doing something more valuable, like listening to the patient. As Dr. Johansson and colleagues wrote in their commentary, “Healthcare policies also need to account for the time clinicians should spend listening in silence, noticing carefully, and cocreating sensible plans of care with patients.”
Having served on several guideline panels in the past, I believe that thoughtfully developed evidence-based guidelines can help family physicians care for patients. But guidelines will never make up all of medicine, particularly primary care, where following too many well-intended recommendations can sometimes get in the way of being a good doctor.
A version of this article first appeared on Medscape.com.
Hi, everyone. I’m Dr Kenny Lin. I am a family physician and associate director of the Lancaster (Pa.) General Hospital Family Medicine Residency, and I blog at Common Sense Family Doctor.
For most of my career, I have precepted residents in primary care clinics. Generally, 1st years are scheduled to see a patient every 45 minutes on average, then every 30 minutes after the first 6 months. By the 3rd year, residents are scheduled to see a patient every 15 minutes to approximate the frequency at which patients are routinely seen in practice. Adult health maintenance visits are typically allotted two slots, for a total of 30 minutes.
The gradually increased pace of seeing patients is a challenge for many residents. It requires them to not only perform more focused medical histories and physical examinations but also to address a select handful of issues in patients who may have a long list of health concerns or preventive care needs. Prioritizing tasks into those that are necessary to do today vs. those that can be deferred to a follow-up visit is an essential skill that is equal parts art and science. In a previous commentary, I wrote about a research group’s efforts to create visual decision aids to generate individualized estimates of life expectancy gains from various preventive services.
Of course, it’s uncommon to have the luxury of focusing exclusively on preventive care in older adults, most of whom have one or more chronic conditions. Obesity, diabetes, hypertension, hypothyroidism, chronic obstructive pulmonary disease, coronary artery disease, and chronic kidney disease each has its own set of management guidelines. According to a recent estimate, following all guideline recommendations for chronic diseases plus those for preventive and acute care would require a primary care physician with a nationally representative panel of adult patients to work an impossible 27-hour day. That’s another good reason for me to continue seeing children in practice!
In a commentary in The BMJ, Dr Minna Johansson and colleagues argued that guideline panels should explicitly consider the estimated clinician time needed to improve the desired outcome for one person in the targeted population, a metric that they call “time needed to treat” (TNT). For example, to implement a National Institute for Health and Care Excellence (NICE) guideline for U.K. general practitioners (GPs) about providing advice to physically inactive adults would require 3 hours for one more person to increase their self-reported physical activity. For a patient panel of 2000 adults, the absolute TNT would be 167 hours per GP, representing 15% of yearly total face time with all patients, which seems clearly excessive.
In fact, the U.S. Preventive Services Task Force does occasionally consider the “opportunity costs” of recommending preventive services. When they first reviewed screening for chronic obstructive pulmonary disease (COPD) in 2008, the USPSTF reasoned that the minimal benefit of screening hundreds of patients to prevent a single COPD exacerbation was at least offset by the time and resources it would take to perform spirometry on every adult with a smoking history, a conclusion that it reaffirmed last year. In contrast to NICE, the USPSTF recommends selectively counseling adults without cardiovascular risk factors to promote a healthy diet and physical activity rather than counseling every single person.
Other US guideline groups would do well to adopt the advice of Johansson and colleagues to consider TNT. Last year, the Women’s Preventive Services Initiative (WPSI) recommended counseling every woman aged 40-60 years with normal or overweight body mass index “to maintain weight or limit weight gain to prevent obesity.” Though preventing obesity is a laudable goal, I’d prefer to counsel those who are obese and suffering from obesity-related conditions and spend my 15 or 30 minutes with others doing something more valuable, like listening to the patient. As Dr. Johansson and colleagues wrote in their commentary, “Healthcare policies also need to account for the time clinicians should spend listening in silence, noticing carefully, and cocreating sensible plans of care with patients.”
Having served on several guideline panels in the past, I believe that thoughtfully developed evidence-based guidelines can help family physicians care for patients. But guidelines will never make up all of medicine, particularly primary care, where following too many well-intended recommendations can sometimes get in the way of being a good doctor.
A version of this article first appeared on Medscape.com.
Hi, everyone. I’m Dr Kenny Lin. I am a family physician and associate director of the Lancaster (Pa.) General Hospital Family Medicine Residency, and I blog at Common Sense Family Doctor.
For most of my career, I have precepted residents in primary care clinics. Generally, 1st years are scheduled to see a patient every 45 minutes on average, then every 30 minutes after the first 6 months. By the 3rd year, residents are scheduled to see a patient every 15 minutes to approximate the frequency at which patients are routinely seen in practice. Adult health maintenance visits are typically allotted two slots, for a total of 30 minutes.
The gradually increased pace of seeing patients is a challenge for many residents. It requires them to not only perform more focused medical histories and physical examinations but also to address a select handful of issues in patients who may have a long list of health concerns or preventive care needs. Prioritizing tasks into those that are necessary to do today vs. those that can be deferred to a follow-up visit is an essential skill that is equal parts art and science. In a previous commentary, I wrote about a research group’s efforts to create visual decision aids to generate individualized estimates of life expectancy gains from various preventive services.
Of course, it’s uncommon to have the luxury of focusing exclusively on preventive care in older adults, most of whom have one or more chronic conditions. Obesity, diabetes, hypertension, hypothyroidism, chronic obstructive pulmonary disease, coronary artery disease, and chronic kidney disease each has its own set of management guidelines. According to a recent estimate, following all guideline recommendations for chronic diseases plus those for preventive and acute care would require a primary care physician with a nationally representative panel of adult patients to work an impossible 27-hour day. That’s another good reason for me to continue seeing children in practice!
In a commentary in The BMJ, Dr Minna Johansson and colleagues argued that guideline panels should explicitly consider the estimated clinician time needed to improve the desired outcome for one person in the targeted population, a metric that they call “time needed to treat” (TNT). For example, to implement a National Institute for Health and Care Excellence (NICE) guideline for U.K. general practitioners (GPs) about providing advice to physically inactive adults would require 3 hours for one more person to increase their self-reported physical activity. For a patient panel of 2000 adults, the absolute TNT would be 167 hours per GP, representing 15% of yearly total face time with all patients, which seems clearly excessive.
In fact, the U.S. Preventive Services Task Force does occasionally consider the “opportunity costs” of recommending preventive services. When they first reviewed screening for chronic obstructive pulmonary disease (COPD) in 2008, the USPSTF reasoned that the minimal benefit of screening hundreds of patients to prevent a single COPD exacerbation was at least offset by the time and resources it would take to perform spirometry on every adult with a smoking history, a conclusion that it reaffirmed last year. In contrast to NICE, the USPSTF recommends selectively counseling adults without cardiovascular risk factors to promote a healthy diet and physical activity rather than counseling every single person.
Other US guideline groups would do well to adopt the advice of Johansson and colleagues to consider TNT. Last year, the Women’s Preventive Services Initiative (WPSI) recommended counseling every woman aged 40-60 years with normal or overweight body mass index “to maintain weight or limit weight gain to prevent obesity.” Though preventing obesity is a laudable goal, I’d prefer to counsel those who are obese and suffering from obesity-related conditions and spend my 15 or 30 minutes with others doing something more valuable, like listening to the patient. As Dr. Johansson and colleagues wrote in their commentary, “Healthcare policies also need to account for the time clinicians should spend listening in silence, noticing carefully, and cocreating sensible plans of care with patients.”
Having served on several guideline panels in the past, I believe that thoughtfully developed evidence-based guidelines can help family physicians care for patients. But guidelines will never make up all of medicine, particularly primary care, where following too many well-intended recommendations can sometimes get in the way of being a good doctor.
A version of this article first appeared on Medscape.com.
Mpox (Monkeypox) Clinical Pearls
The 2022 mpox (monkeypox) virus outbreak represents the latest example of how infectious diseases with previously limited reach can spread in a globalized society. More than 86,000 cases have been reported worldwide, with more than 30,000 cases in the United States as of March 15, 2023.1 Herein, we summarize the key features of mpox infection for the dermatologist.
Mpox Transmission
The mpox virus is a double-stranded DNA virus of the Orthopoxvirus genus and Poxviridae family.2,3 There are 2 types of the mpox virus: clade I (formerly the Congo Basin clade) and clade II (formerly the West African clade). Clade I causes more severe disease (10% mortality rate), while clade II is associated with lower mortality (1%–3%) and has been split into subclades of IIa (exhibits zoonotic transmission) and IIb (exhibits human-to-human spread).3,4 The current outbreak is caused by clade IIb, and patients typically have no travel history to classic endemic regions.5,6
In endemic countries, mpox transmission is zoonotic from small forest animals. In nonendemic countries, sporadic cases rarely have been reported, including a cluster in the United States in 2003 related to pet prairie dogs. In stark contrast, human-to-human transmission is occurring in the current epidemic mainly via intimate skin-to-skin contact and possibly via sexual fluids, meeting the criteria for a sexually transmitted infection. However, nonsexual transmission does still occur, though it is less common.7 Many of the reported cases so far are in young to middle-aged men who have sex with men (MSM).2,8 However, it is crucial to understand that mpox is not exclusive to the MSM population; the virus has been transmitted to heterosexual males, females, children, and even household pets of infected individuals.2,9,10 Labeling mpox as exclusive to the MSM community is both inaccurate and inappropriately stigmatizing.
Cutaneous Presentation and Diagnosis of Mpox
Mpox has an incubation time of approximately 9 days (range, 7–21 days), after which affected persons develop macular lesions that evolve over 2 to 4 weeks into papules, vesicles, and deep-seated pustules before crusting over and resolving with possible residual scarring.2,3,5,9,11,12 Palmoplantar involvement is a key feature.11 Although in some cases there will be multiple lesions with centrifugal progression, the lesions also may be few in number, with some patients presenting with a single lesion in the anogenital region or on the face, hand, or foot (Figure).6,9 Systemic symptoms such as prodromal fever, lymphadenopathy, and headache are common but not universal.9,13 Potential complications include penile edema, proctitis, bacterial superinfection, tonsillitis, conjunctivitis, encephalitis, and pneumonia.5,9,13
A high index of suspicion is needed to diagnose mpox infection. The differential diagnosis includes smallpox; varicella-zoster virus (primary or reactivation); secondary syphilis; measles; herpes simplex virus; molluscum contagiosum; hand, foot, and mouth disease; and disseminated gonococcal infection.2,3 For lesions confined to the genital area, sexually transmitted infections (eg, chancroid, lymphogranuloma venereum) as well as non–sexually related acute genital ulcers (Lipschütz ulcers) should be considered.2
Certain clinical features may help in distinguishing mpox from other diseases. Mpox exhibits synchronous progression and centrifugal distribution when multiple lesions are present; in contrast, the lesions of primary varicella (chickenpox) appear in multiple different stages, and those of localized herpes zoster (shingles) exhibit a dermatomal distribution. When these features are present, mpox causes a greater degree of lymphadenopathy and systemic symptoms than primary varicella.3Clinical diagnosis of mpox is more than 90% sensitive but only 9% to 26% specific.3 To confirm the diagnosis, a viral swab vigorously obtained from active skin lesions should be sent in viral transport media for mpox DNA-specific polymerase chain reaction testing, which is available from major laboratories.2,3 Other supportive tests include serum studies for anti–mpox virus immunoglobulins and immunohistochemical staining for viral antigens on skin biopsy specimens.2 When evaluating suspected and confirmed mpox cases, dermatologists should wear a gown, gloves, a fitted N95 mask, and eye protection to prevent infection.5
Treating Mpox
Symptomatic mpox infection can last for up to 2 to 5 weeks.3 The patient is no longer infectious once the lesions have crusted over.3,11 The majority of cases require supportive care only.2,3,5,14 However, mpox remains a potentially fatal disease, with 38 deaths to date in the current outbreak.1 High-risk populations include children younger than 8 years, pregnant women, and individuals who are immunocompromised.15 Tecovirimat, an antiviral medication approved by the US Food and Drug Administration (FDA) for smallpox, is available via the expanded access Investigational New Drug (EA-IND) protocol to treat severe mpox cases but is not widely available in the United States.6,16-18 Brincidofovir, a prodrug of the antiviral cidofovir, possesses single-patient emergency use Investigational New Drug (e-IND) status for treatment of mpox but also is not widely available in the United States.17 Intravenous vaccinia immune globulin is under consideration for high-risk individuals, but little is known regarding its efficacy against mpox.5,16,17
Two smallpox vaccines—JYNNEOS (Bavarian Nordic) and ACAM2000 (Emergent Bio Solutions)—are available for both preexposure and postexposure prophylaxis against mpox virus.19 At this time, only JYNNEOS is FDA approved for the prevention of mpox; ACAM2000 can be used against mpox under the FDA’s EA-IND protocol, which involves additional requirements, including informed consent from the patient.20 ACAM2000 is a live, replication-competent vaccine that carries a warning of increased risk for side effects in patients with cardiac disease, pregnancy, immunocompromise, and a history or presence of eczema and other skin conditions.3,21,22 JYNNEOS is a live but replication-deficient virus and therefore does not carry these warnings.3,21,22
Final Thoughts
Mpox is no longer an obscure illness occurring in limited geographic areas. Dermatologists must remain highly vigilant when evaluating any patient for new-onset vesicular or pustular eruptions to combat this ongoing public health threat. This issue of Cutis® also features a thorough mpox update on the clinical presentation, vaccine guidance, and management.23
- Centers for Disease Control and Prevention. Mpox: 2022 Outbreak Cases and Data. Updated March 15, 2023. Accessed March 121, 2023. https://www.cdc.gov/poxvirus/monkeypox/response/2022/
- Srivastava G. Human monkeypox disease [published online August 10, 2022]. Clin Dermatol. doi:10.1016/j.clindermatol.2022.08.009
- Bryer J, Freeman EE, Rosenbach M. Monkeypox emerges on a global scale: a historical review and dermatologic primer [published online July 8, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.07.007
- Americo JL, Earl PL, Moss B. Virulence differences of mpox (monkeypox) virus clades I, IIa, and IIb.1 in a small animal model. Proc Natl Acad Sci U S A. 2023;120:E2220415120. doi:10.1073 /pnas.2220415120
- Guarner J, Del Rio C, Malani PN. Monkeypox in 2022—what clinicians need to know. JAMA. 2022;328:139-140. doi:10.1001/jama.2022.10802
- Looi MK. Monkeypox: what we know about the 2022 outbreak so far [published online August 23, 2022]. BMJ. doi:10.1136/bmj.o2058
- Allan-Blitz LT, Gandhi M, Adamson P, et al. A position statement on mpox as a sexually transmitted disease [published online December 22, 2022]. Clin Infect Dis. doi:10.1093/cid/ciac960
- Cabanillas B, Murdaca G, Guemari A, et al. A compilation answering 50 questions on monkeypox virus and the current monkeypox outbreak. Allergy. 2023;78:639-662. doi:10.1111/all.15633
- Tarín-Vicente EJ, Alemany A, Agud-Dios M, et al. Clinical presentation and virological assessment of confirmed human monkeypox virus cases in Spain: a prospective observational cohort study [published online August 8, 2022]. Lancet. doi:10.1016/S0140-6736(22)01436-2
- Seang S, Burrel S, Todesco E, et al. Evidence of human-to-dog transmission of monkeypox virus. Lancet. 2022;400:658-659. doi:10.1016 /s0140-6736(22)01487-8
- Ramdass P, Mullick S, Farber HF. Viral skin diseases. Prim Care. 2015;42:517-67. doi:10.1016/j.pop.2015.08.006
- Centers for Disease Control and Prevention. Mpox: Clinical Recognition. Updated August 23, 2022. Accessed March 21, 2023. https://www.cdc .gov/poxvirus/monkeypox/clinicians/clinical-recognition.html
- Mpox Cases by Age and Gender, Race/Ethnicity, and Symptoms. Centers for Disease Control and Prevention. Updated March 15, 2023. Accessed March 21, 2023. https://www.cdc.gov/poxvirus/monkeypox /response/2022/demographics.html
- Kawsar A, Hussain K, Roberts N. The return of monkeypox: key pointers for dermatologists [published online July 29, 2022]. Clin Exp Dermatol. doi:10.1111/ced.15357
- Khanna U, Bishnoi A, Vinay K. Current outbreak of monkeypox— essentials for the dermatologist [published online June 23, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.06.1170
- Fox T, Gould S, Princy N, et al. Therapeutics for treating mpox in humans. Cochrane Database Syst Rev. 2023;3:CD015769. doi:10.1002/14651858 .CD015769
- Centers for Disease Control and Prevention. Treatment information for healthcare professionals. Updated March 3, 2023. Accessed March 24, 2023. https://www.cdc.gov/poxvirus/mpox/clinicians /treatment.html#anchor_1666886364947
- Centers for Disease Control and Prevention. Guidance for tecovirimat use. Updated February 23, 2023. Accessed March 24, 2023. https://www .cdc.gov/poxvirus/mpox/clinicians/Tecovirimat.html
- Interim Clinical Considerations for Use of JYNNEOS and ACAM2000 Vaccines During the 2022 U.S. Monkeypox Outbreak. Centers for Disease Control and Prevention. Updated October 19, 2022. Accessed March 21, 2023. https://www.cdc.gov/poxvirus/monkeypox/health-departments/vaccine-considerations.html
- Key Facts About Vaccines to Prevent Monkeypox Disease. US Food and Drug Administration. Updated August 18, 2022. Accessed March 21, 2023. https://www.fda.gov/vaccines-blood-biologics/vaccines/key-facts-aboutvaccines-prevent-monkeypox-disease
- Smallpox: Vaccines. Centers for Disease Control and Prevention. Updated August 8, 2022. Accessed March 21, 2023. https://www.cdc.gov/smallpox/clinicians/vaccines.html
- ACAM2000. Package insert. Emergent Product Development Gaithersburg Inc; 2019.
- Cices A, Prasad S, Akselrad M, et al. Mpox update: clinical presentation, vaccination guidance, and management. Cutis. 2023;111:197-202. doi:10.12788/cutis.0745
The 2022 mpox (monkeypox) virus outbreak represents the latest example of how infectious diseases with previously limited reach can spread in a globalized society. More than 86,000 cases have been reported worldwide, with more than 30,000 cases in the United States as of March 15, 2023.1 Herein, we summarize the key features of mpox infection for the dermatologist.
Mpox Transmission
The mpox virus is a double-stranded DNA virus of the Orthopoxvirus genus and Poxviridae family.2,3 There are 2 types of the mpox virus: clade I (formerly the Congo Basin clade) and clade II (formerly the West African clade). Clade I causes more severe disease (10% mortality rate), while clade II is associated with lower mortality (1%–3%) and has been split into subclades of IIa (exhibits zoonotic transmission) and IIb (exhibits human-to-human spread).3,4 The current outbreak is caused by clade IIb, and patients typically have no travel history to classic endemic regions.5,6
In endemic countries, mpox transmission is zoonotic from small forest animals. In nonendemic countries, sporadic cases rarely have been reported, including a cluster in the United States in 2003 related to pet prairie dogs. In stark contrast, human-to-human transmission is occurring in the current epidemic mainly via intimate skin-to-skin contact and possibly via sexual fluids, meeting the criteria for a sexually transmitted infection. However, nonsexual transmission does still occur, though it is less common.7 Many of the reported cases so far are in young to middle-aged men who have sex with men (MSM).2,8 However, it is crucial to understand that mpox is not exclusive to the MSM population; the virus has been transmitted to heterosexual males, females, children, and even household pets of infected individuals.2,9,10 Labeling mpox as exclusive to the MSM community is both inaccurate and inappropriately stigmatizing.
Cutaneous Presentation and Diagnosis of Mpox
Mpox has an incubation time of approximately 9 days (range, 7–21 days), after which affected persons develop macular lesions that evolve over 2 to 4 weeks into papules, vesicles, and deep-seated pustules before crusting over and resolving with possible residual scarring.2,3,5,9,11,12 Palmoplantar involvement is a key feature.11 Although in some cases there will be multiple lesions with centrifugal progression, the lesions also may be few in number, with some patients presenting with a single lesion in the anogenital region or on the face, hand, or foot (Figure).6,9 Systemic symptoms such as prodromal fever, lymphadenopathy, and headache are common but not universal.9,13 Potential complications include penile edema, proctitis, bacterial superinfection, tonsillitis, conjunctivitis, encephalitis, and pneumonia.5,9,13
A high index of suspicion is needed to diagnose mpox infection. The differential diagnosis includes smallpox; varicella-zoster virus (primary or reactivation); secondary syphilis; measles; herpes simplex virus; molluscum contagiosum; hand, foot, and mouth disease; and disseminated gonococcal infection.2,3 For lesions confined to the genital area, sexually transmitted infections (eg, chancroid, lymphogranuloma venereum) as well as non–sexually related acute genital ulcers (Lipschütz ulcers) should be considered.2
Certain clinical features may help in distinguishing mpox from other diseases. Mpox exhibits synchronous progression and centrifugal distribution when multiple lesions are present; in contrast, the lesions of primary varicella (chickenpox) appear in multiple different stages, and those of localized herpes zoster (shingles) exhibit a dermatomal distribution. When these features are present, mpox causes a greater degree of lymphadenopathy and systemic symptoms than primary varicella.3Clinical diagnosis of mpox is more than 90% sensitive but only 9% to 26% specific.3 To confirm the diagnosis, a viral swab vigorously obtained from active skin lesions should be sent in viral transport media for mpox DNA-specific polymerase chain reaction testing, which is available from major laboratories.2,3 Other supportive tests include serum studies for anti–mpox virus immunoglobulins and immunohistochemical staining for viral antigens on skin biopsy specimens.2 When evaluating suspected and confirmed mpox cases, dermatologists should wear a gown, gloves, a fitted N95 mask, and eye protection to prevent infection.5
Treating Mpox
Symptomatic mpox infection can last for up to 2 to 5 weeks.3 The patient is no longer infectious once the lesions have crusted over.3,11 The majority of cases require supportive care only.2,3,5,14 However, mpox remains a potentially fatal disease, with 38 deaths to date in the current outbreak.1 High-risk populations include children younger than 8 years, pregnant women, and individuals who are immunocompromised.15 Tecovirimat, an antiviral medication approved by the US Food and Drug Administration (FDA) for smallpox, is available via the expanded access Investigational New Drug (EA-IND) protocol to treat severe mpox cases but is not widely available in the United States.6,16-18 Brincidofovir, a prodrug of the antiviral cidofovir, possesses single-patient emergency use Investigational New Drug (e-IND) status for treatment of mpox but also is not widely available in the United States.17 Intravenous vaccinia immune globulin is under consideration for high-risk individuals, but little is known regarding its efficacy against mpox.5,16,17
Two smallpox vaccines—JYNNEOS (Bavarian Nordic) and ACAM2000 (Emergent Bio Solutions)—are available for both preexposure and postexposure prophylaxis against mpox virus.19 At this time, only JYNNEOS is FDA approved for the prevention of mpox; ACAM2000 can be used against mpox under the FDA’s EA-IND protocol, which involves additional requirements, including informed consent from the patient.20 ACAM2000 is a live, replication-competent vaccine that carries a warning of increased risk for side effects in patients with cardiac disease, pregnancy, immunocompromise, and a history or presence of eczema and other skin conditions.3,21,22 JYNNEOS is a live but replication-deficient virus and therefore does not carry these warnings.3,21,22
Final Thoughts
Mpox is no longer an obscure illness occurring in limited geographic areas. Dermatologists must remain highly vigilant when evaluating any patient for new-onset vesicular or pustular eruptions to combat this ongoing public health threat. This issue of Cutis® also features a thorough mpox update on the clinical presentation, vaccine guidance, and management.23
The 2022 mpox (monkeypox) virus outbreak represents the latest example of how infectious diseases with previously limited reach can spread in a globalized society. More than 86,000 cases have been reported worldwide, with more than 30,000 cases in the United States as of March 15, 2023.1 Herein, we summarize the key features of mpox infection for the dermatologist.
Mpox Transmission
The mpox virus is a double-stranded DNA virus of the Orthopoxvirus genus and Poxviridae family.2,3 There are 2 types of the mpox virus: clade I (formerly the Congo Basin clade) and clade II (formerly the West African clade). Clade I causes more severe disease (10% mortality rate), while clade II is associated with lower mortality (1%–3%) and has been split into subclades of IIa (exhibits zoonotic transmission) and IIb (exhibits human-to-human spread).3,4 The current outbreak is caused by clade IIb, and patients typically have no travel history to classic endemic regions.5,6
In endemic countries, mpox transmission is zoonotic from small forest animals. In nonendemic countries, sporadic cases rarely have been reported, including a cluster in the United States in 2003 related to pet prairie dogs. In stark contrast, human-to-human transmission is occurring in the current epidemic mainly via intimate skin-to-skin contact and possibly via sexual fluids, meeting the criteria for a sexually transmitted infection. However, nonsexual transmission does still occur, though it is less common.7 Many of the reported cases so far are in young to middle-aged men who have sex with men (MSM).2,8 However, it is crucial to understand that mpox is not exclusive to the MSM population; the virus has been transmitted to heterosexual males, females, children, and even household pets of infected individuals.2,9,10 Labeling mpox as exclusive to the MSM community is both inaccurate and inappropriately stigmatizing.
Cutaneous Presentation and Diagnosis of Mpox
Mpox has an incubation time of approximately 9 days (range, 7–21 days), after which affected persons develop macular lesions that evolve over 2 to 4 weeks into papules, vesicles, and deep-seated pustules before crusting over and resolving with possible residual scarring.2,3,5,9,11,12 Palmoplantar involvement is a key feature.11 Although in some cases there will be multiple lesions with centrifugal progression, the lesions also may be few in number, with some patients presenting with a single lesion in the anogenital region or on the face, hand, or foot (Figure).6,9 Systemic symptoms such as prodromal fever, lymphadenopathy, and headache are common but not universal.9,13 Potential complications include penile edema, proctitis, bacterial superinfection, tonsillitis, conjunctivitis, encephalitis, and pneumonia.5,9,13
A high index of suspicion is needed to diagnose mpox infection. The differential diagnosis includes smallpox; varicella-zoster virus (primary or reactivation); secondary syphilis; measles; herpes simplex virus; molluscum contagiosum; hand, foot, and mouth disease; and disseminated gonococcal infection.2,3 For lesions confined to the genital area, sexually transmitted infections (eg, chancroid, lymphogranuloma venereum) as well as non–sexually related acute genital ulcers (Lipschütz ulcers) should be considered.2
Certain clinical features may help in distinguishing mpox from other diseases. Mpox exhibits synchronous progression and centrifugal distribution when multiple lesions are present; in contrast, the lesions of primary varicella (chickenpox) appear in multiple different stages, and those of localized herpes zoster (shingles) exhibit a dermatomal distribution. When these features are present, mpox causes a greater degree of lymphadenopathy and systemic symptoms than primary varicella.3Clinical diagnosis of mpox is more than 90% sensitive but only 9% to 26% specific.3 To confirm the diagnosis, a viral swab vigorously obtained from active skin lesions should be sent in viral transport media for mpox DNA-specific polymerase chain reaction testing, which is available from major laboratories.2,3 Other supportive tests include serum studies for anti–mpox virus immunoglobulins and immunohistochemical staining for viral antigens on skin biopsy specimens.2 When evaluating suspected and confirmed mpox cases, dermatologists should wear a gown, gloves, a fitted N95 mask, and eye protection to prevent infection.5
Treating Mpox
Symptomatic mpox infection can last for up to 2 to 5 weeks.3 The patient is no longer infectious once the lesions have crusted over.3,11 The majority of cases require supportive care only.2,3,5,14 However, mpox remains a potentially fatal disease, with 38 deaths to date in the current outbreak.1 High-risk populations include children younger than 8 years, pregnant women, and individuals who are immunocompromised.15 Tecovirimat, an antiviral medication approved by the US Food and Drug Administration (FDA) for smallpox, is available via the expanded access Investigational New Drug (EA-IND) protocol to treat severe mpox cases but is not widely available in the United States.6,16-18 Brincidofovir, a prodrug of the antiviral cidofovir, possesses single-patient emergency use Investigational New Drug (e-IND) status for treatment of mpox but also is not widely available in the United States.17 Intravenous vaccinia immune globulin is under consideration for high-risk individuals, but little is known regarding its efficacy against mpox.5,16,17
Two smallpox vaccines—JYNNEOS (Bavarian Nordic) and ACAM2000 (Emergent Bio Solutions)—are available for both preexposure and postexposure prophylaxis against mpox virus.19 At this time, only JYNNEOS is FDA approved for the prevention of mpox; ACAM2000 can be used against mpox under the FDA’s EA-IND protocol, which involves additional requirements, including informed consent from the patient.20 ACAM2000 is a live, replication-competent vaccine that carries a warning of increased risk for side effects in patients with cardiac disease, pregnancy, immunocompromise, and a history or presence of eczema and other skin conditions.3,21,22 JYNNEOS is a live but replication-deficient virus and therefore does not carry these warnings.3,21,22
Final Thoughts
Mpox is no longer an obscure illness occurring in limited geographic areas. Dermatologists must remain highly vigilant when evaluating any patient for new-onset vesicular or pustular eruptions to combat this ongoing public health threat. This issue of Cutis® also features a thorough mpox update on the clinical presentation, vaccine guidance, and management.23
- Centers for Disease Control and Prevention. Mpox: 2022 Outbreak Cases and Data. Updated March 15, 2023. Accessed March 121, 2023. https://www.cdc.gov/poxvirus/monkeypox/response/2022/
- Srivastava G. Human monkeypox disease [published online August 10, 2022]. Clin Dermatol. doi:10.1016/j.clindermatol.2022.08.009
- Bryer J, Freeman EE, Rosenbach M. Monkeypox emerges on a global scale: a historical review and dermatologic primer [published online July 8, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.07.007
- Americo JL, Earl PL, Moss B. Virulence differences of mpox (monkeypox) virus clades I, IIa, and IIb.1 in a small animal model. Proc Natl Acad Sci U S A. 2023;120:E2220415120. doi:10.1073 /pnas.2220415120
- Guarner J, Del Rio C, Malani PN. Monkeypox in 2022—what clinicians need to know. JAMA. 2022;328:139-140. doi:10.1001/jama.2022.10802
- Looi MK. Monkeypox: what we know about the 2022 outbreak so far [published online August 23, 2022]. BMJ. doi:10.1136/bmj.o2058
- Allan-Blitz LT, Gandhi M, Adamson P, et al. A position statement on mpox as a sexually transmitted disease [published online December 22, 2022]. Clin Infect Dis. doi:10.1093/cid/ciac960
- Cabanillas B, Murdaca G, Guemari A, et al. A compilation answering 50 questions on monkeypox virus and the current monkeypox outbreak. Allergy. 2023;78:639-662. doi:10.1111/all.15633
- Tarín-Vicente EJ, Alemany A, Agud-Dios M, et al. Clinical presentation and virological assessment of confirmed human monkeypox virus cases in Spain: a prospective observational cohort study [published online August 8, 2022]. Lancet. doi:10.1016/S0140-6736(22)01436-2
- Seang S, Burrel S, Todesco E, et al. Evidence of human-to-dog transmission of monkeypox virus. Lancet. 2022;400:658-659. doi:10.1016 /s0140-6736(22)01487-8
- Ramdass P, Mullick S, Farber HF. Viral skin diseases. Prim Care. 2015;42:517-67. doi:10.1016/j.pop.2015.08.006
- Centers for Disease Control and Prevention. Mpox: Clinical Recognition. Updated August 23, 2022. Accessed March 21, 2023. https://www.cdc .gov/poxvirus/monkeypox/clinicians/clinical-recognition.html
- Mpox Cases by Age and Gender, Race/Ethnicity, and Symptoms. Centers for Disease Control and Prevention. Updated March 15, 2023. Accessed March 21, 2023. https://www.cdc.gov/poxvirus/monkeypox /response/2022/demographics.html
- Kawsar A, Hussain K, Roberts N. The return of monkeypox: key pointers for dermatologists [published online July 29, 2022]. Clin Exp Dermatol. doi:10.1111/ced.15357
- Khanna U, Bishnoi A, Vinay K. Current outbreak of monkeypox— essentials for the dermatologist [published online June 23, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.06.1170
- Fox T, Gould S, Princy N, et al. Therapeutics for treating mpox in humans. Cochrane Database Syst Rev. 2023;3:CD015769. doi:10.1002/14651858 .CD015769
- Centers for Disease Control and Prevention. Treatment information for healthcare professionals. Updated March 3, 2023. Accessed March 24, 2023. https://www.cdc.gov/poxvirus/mpox/clinicians /treatment.html#anchor_1666886364947
- Centers for Disease Control and Prevention. Guidance for tecovirimat use. Updated February 23, 2023. Accessed March 24, 2023. https://www .cdc.gov/poxvirus/mpox/clinicians/Tecovirimat.html
- Interim Clinical Considerations for Use of JYNNEOS and ACAM2000 Vaccines During the 2022 U.S. Monkeypox Outbreak. Centers for Disease Control and Prevention. Updated October 19, 2022. Accessed March 21, 2023. https://www.cdc.gov/poxvirus/monkeypox/health-departments/vaccine-considerations.html
- Key Facts About Vaccines to Prevent Monkeypox Disease. US Food and Drug Administration. Updated August 18, 2022. Accessed March 21, 2023. https://www.fda.gov/vaccines-blood-biologics/vaccines/key-facts-aboutvaccines-prevent-monkeypox-disease
- Smallpox: Vaccines. Centers for Disease Control and Prevention. Updated August 8, 2022. Accessed March 21, 2023. https://www.cdc.gov/smallpox/clinicians/vaccines.html
- ACAM2000. Package insert. Emergent Product Development Gaithersburg Inc; 2019.
- Cices A, Prasad S, Akselrad M, et al. Mpox update: clinical presentation, vaccination guidance, and management. Cutis. 2023;111:197-202. doi:10.12788/cutis.0745
- Centers for Disease Control and Prevention. Mpox: 2022 Outbreak Cases and Data. Updated March 15, 2023. Accessed March 121, 2023. https://www.cdc.gov/poxvirus/monkeypox/response/2022/
- Srivastava G. Human monkeypox disease [published online August 10, 2022]. Clin Dermatol. doi:10.1016/j.clindermatol.2022.08.009
- Bryer J, Freeman EE, Rosenbach M. Monkeypox emerges on a global scale: a historical review and dermatologic primer [published online July 8, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.07.007
- Americo JL, Earl PL, Moss B. Virulence differences of mpox (monkeypox) virus clades I, IIa, and IIb.1 in a small animal model. Proc Natl Acad Sci U S A. 2023;120:E2220415120. doi:10.1073 /pnas.2220415120
- Guarner J, Del Rio C, Malani PN. Monkeypox in 2022—what clinicians need to know. JAMA. 2022;328:139-140. doi:10.1001/jama.2022.10802
- Looi MK. Monkeypox: what we know about the 2022 outbreak so far [published online August 23, 2022]. BMJ. doi:10.1136/bmj.o2058
- Allan-Blitz LT, Gandhi M, Adamson P, et al. A position statement on mpox as a sexually transmitted disease [published online December 22, 2022]. Clin Infect Dis. doi:10.1093/cid/ciac960
- Cabanillas B, Murdaca G, Guemari A, et al. A compilation answering 50 questions on monkeypox virus and the current monkeypox outbreak. Allergy. 2023;78:639-662. doi:10.1111/all.15633
- Tarín-Vicente EJ, Alemany A, Agud-Dios M, et al. Clinical presentation and virological assessment of confirmed human monkeypox virus cases in Spain: a prospective observational cohort study [published online August 8, 2022]. Lancet. doi:10.1016/S0140-6736(22)01436-2
- Seang S, Burrel S, Todesco E, et al. Evidence of human-to-dog transmission of monkeypox virus. Lancet. 2022;400:658-659. doi:10.1016 /s0140-6736(22)01487-8
- Ramdass P, Mullick S, Farber HF. Viral skin diseases. Prim Care. 2015;42:517-67. doi:10.1016/j.pop.2015.08.006
- Centers for Disease Control and Prevention. Mpox: Clinical Recognition. Updated August 23, 2022. Accessed March 21, 2023. https://www.cdc .gov/poxvirus/monkeypox/clinicians/clinical-recognition.html
- Mpox Cases by Age and Gender, Race/Ethnicity, and Symptoms. Centers for Disease Control and Prevention. Updated March 15, 2023. Accessed March 21, 2023. https://www.cdc.gov/poxvirus/monkeypox /response/2022/demographics.html
- Kawsar A, Hussain K, Roberts N. The return of monkeypox: key pointers for dermatologists [published online July 29, 2022]. Clin Exp Dermatol. doi:10.1111/ced.15357
- Khanna U, Bishnoi A, Vinay K. Current outbreak of monkeypox— essentials for the dermatologist [published online June 23, 2022]. J Am Acad Dermatol. doi:10.1016/j.jaad.2022.06.1170
- Fox T, Gould S, Princy N, et al. Therapeutics for treating mpox in humans. Cochrane Database Syst Rev. 2023;3:CD015769. doi:10.1002/14651858 .CD015769
- Centers for Disease Control and Prevention. Treatment information for healthcare professionals. Updated March 3, 2023. Accessed March 24, 2023. https://www.cdc.gov/poxvirus/mpox/clinicians /treatment.html#anchor_1666886364947
- Centers for Disease Control and Prevention. Guidance for tecovirimat use. Updated February 23, 2023. Accessed March 24, 2023. https://www .cdc.gov/poxvirus/mpox/clinicians/Tecovirimat.html
- Interim Clinical Considerations for Use of JYNNEOS and ACAM2000 Vaccines During the 2022 U.S. Monkeypox Outbreak. Centers for Disease Control and Prevention. Updated October 19, 2022. Accessed March 21, 2023. https://www.cdc.gov/poxvirus/monkeypox/health-departments/vaccine-considerations.html
- Key Facts About Vaccines to Prevent Monkeypox Disease. US Food and Drug Administration. Updated August 18, 2022. Accessed March 21, 2023. https://www.fda.gov/vaccines-blood-biologics/vaccines/key-facts-aboutvaccines-prevent-monkeypox-disease
- Smallpox: Vaccines. Centers for Disease Control and Prevention. Updated August 8, 2022. Accessed March 21, 2023. https://www.cdc.gov/smallpox/clinicians/vaccines.html
- ACAM2000. Package insert. Emergent Product Development Gaithersburg Inc; 2019.
- Cices A, Prasad S, Akselrad M, et al. Mpox update: clinical presentation, vaccination guidance, and management. Cutis. 2023;111:197-202. doi:10.12788/cutis.0745