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TV watching linked to depression
While anxiety was at the top of my list of emotional states that generated office visits in my pediatric practice, depression always ran a close second. Not infrequently, patients would report symptoms that suggested they were harboring both morbidities.
Although some families appear to be prone to depression, I’m not aware that a definable genetic basis has been discovered. Like me, you may have wondered what factors determine whether an individual will become depressed or merely be unhappy when things aren’t going well. We all have known people who have weathered disappointment and life-altering calamities without even a hint of being depressed. On the other hand you probably have met numerous patients and acquaintances who have become significantly depressed as the result of simply worrying that some disaster might befall them.
Is this variable vulnerability to depression the result of some as yet undiscovered neurotransmitter? Or are there certain lifestyle features that make individuals more prone to depression? Or ... could it be both? In other words are there behaviors that can tweak a person’s telomeres in such a way that triggers a biochemical cascade that results in depression?
A recent paper in the American Journal of Psychiatry doesn’t drill down through the genetic and biochemical strata, but it does suggest that there are “modifiable” behaviors that may contribute to depression. The researchers based at Harvard Medical School in Boston accessed a database of more than 100,000 adults in the United Kingdom. With use of a two-stage method that included a strategy similar to that employed for identifying genetic risk factors for disease, the researchers scanned a large number of factors that they considered modifiable, searching for those that might be associated with the development of depression.
Not surprisingly, they discovered that those respondents who more frequently confided in others and more frequently visited with family and friends were less likely to become depressed. Of course, this protective effect of social connection can cut both ways during the pandemic. During this pandemic if those people you confide in are not currently in your “bubble,” you may have a problem. This may explain why, despite warnings of their dangers, bars continue to be so attractive. It’s probably not just the alcohol but it’s the bartenders and patrons who are willing to listen that patrons seek out. It would be helpful if more people felt comfortable sharing their feelings with members of their family bubble. But you and I know that many families don’t come even close to matching the Brady Bunch image of a functionality.
Somewhat surprisingly to the Harvard researchers was their finding that time watching television also was a significant risk factor for the development of depression. Their data did not allow them to determine whether this observation was linked to the sedentary nature of television watching or the content of the shows being viewed. I suspect that content is not the problem. But in addition to being a sedentary activity, television watching often is isolating. When television was first introduced to the mass market, families grouped around the household’s lone set, much as families did back when radios became popular. In their infancy radio listening and television viewing were social activities rich with discussion and shared emotions.
However, as televisions became less expensive and no longer required large pieces of furniture to house them, television viewing became a more solitary and individual activity. Televisions became obligatory furnishings of every bedroom, and parents and children could withdraw to their own spaces and be entertained free of any opportunity or obligation to interact with the rest of family.
This new research into the risk factors for depression suggests that again without any way of monitoring their usage. At least among children, television watching should be a modifiable behavior.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
While anxiety was at the top of my list of emotional states that generated office visits in my pediatric practice, depression always ran a close second. Not infrequently, patients would report symptoms that suggested they were harboring both morbidities.
Although some families appear to be prone to depression, I’m not aware that a definable genetic basis has been discovered. Like me, you may have wondered what factors determine whether an individual will become depressed or merely be unhappy when things aren’t going well. We all have known people who have weathered disappointment and life-altering calamities without even a hint of being depressed. On the other hand you probably have met numerous patients and acquaintances who have become significantly depressed as the result of simply worrying that some disaster might befall them.
Is this variable vulnerability to depression the result of some as yet undiscovered neurotransmitter? Or are there certain lifestyle features that make individuals more prone to depression? Or ... could it be both? In other words are there behaviors that can tweak a person’s telomeres in such a way that triggers a biochemical cascade that results in depression?
A recent paper in the American Journal of Psychiatry doesn’t drill down through the genetic and biochemical strata, but it does suggest that there are “modifiable” behaviors that may contribute to depression. The researchers based at Harvard Medical School in Boston accessed a database of more than 100,000 adults in the United Kingdom. With use of a two-stage method that included a strategy similar to that employed for identifying genetic risk factors for disease, the researchers scanned a large number of factors that they considered modifiable, searching for those that might be associated with the development of depression.
Not surprisingly, they discovered that those respondents who more frequently confided in others and more frequently visited with family and friends were less likely to become depressed. Of course, this protective effect of social connection can cut both ways during the pandemic. During this pandemic if those people you confide in are not currently in your “bubble,” you may have a problem. This may explain why, despite warnings of their dangers, bars continue to be so attractive. It’s probably not just the alcohol but it’s the bartenders and patrons who are willing to listen that patrons seek out. It would be helpful if more people felt comfortable sharing their feelings with members of their family bubble. But you and I know that many families don’t come even close to matching the Brady Bunch image of a functionality.
Somewhat surprisingly to the Harvard researchers was their finding that time watching television also was a significant risk factor for the development of depression. Their data did not allow them to determine whether this observation was linked to the sedentary nature of television watching or the content of the shows being viewed. I suspect that content is not the problem. But in addition to being a sedentary activity, television watching often is isolating. When television was first introduced to the mass market, families grouped around the household’s lone set, much as families did back when radios became popular. In their infancy radio listening and television viewing were social activities rich with discussion and shared emotions.
However, as televisions became less expensive and no longer required large pieces of furniture to house them, television viewing became a more solitary and individual activity. Televisions became obligatory furnishings of every bedroom, and parents and children could withdraw to their own spaces and be entertained free of any opportunity or obligation to interact with the rest of family.
This new research into the risk factors for depression suggests that again without any way of monitoring their usage. At least among children, television watching should be a modifiable behavior.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
While anxiety was at the top of my list of emotional states that generated office visits in my pediatric practice, depression always ran a close second. Not infrequently, patients would report symptoms that suggested they were harboring both morbidities.
Although some families appear to be prone to depression, I’m not aware that a definable genetic basis has been discovered. Like me, you may have wondered what factors determine whether an individual will become depressed or merely be unhappy when things aren’t going well. We all have known people who have weathered disappointment and life-altering calamities without even a hint of being depressed. On the other hand you probably have met numerous patients and acquaintances who have become significantly depressed as the result of simply worrying that some disaster might befall them.
Is this variable vulnerability to depression the result of some as yet undiscovered neurotransmitter? Or are there certain lifestyle features that make individuals more prone to depression? Or ... could it be both? In other words are there behaviors that can tweak a person’s telomeres in such a way that triggers a biochemical cascade that results in depression?
A recent paper in the American Journal of Psychiatry doesn’t drill down through the genetic and biochemical strata, but it does suggest that there are “modifiable” behaviors that may contribute to depression. The researchers based at Harvard Medical School in Boston accessed a database of more than 100,000 adults in the United Kingdom. With use of a two-stage method that included a strategy similar to that employed for identifying genetic risk factors for disease, the researchers scanned a large number of factors that they considered modifiable, searching for those that might be associated with the development of depression.
Not surprisingly, they discovered that those respondents who more frequently confided in others and more frequently visited with family and friends were less likely to become depressed. Of course, this protective effect of social connection can cut both ways during the pandemic. During this pandemic if those people you confide in are not currently in your “bubble,” you may have a problem. This may explain why, despite warnings of their dangers, bars continue to be so attractive. It’s probably not just the alcohol but it’s the bartenders and patrons who are willing to listen that patrons seek out. It would be helpful if more people felt comfortable sharing their feelings with members of their family bubble. But you and I know that many families don’t come even close to matching the Brady Bunch image of a functionality.
Somewhat surprisingly to the Harvard researchers was their finding that time watching television also was a significant risk factor for the development of depression. Their data did not allow them to determine whether this observation was linked to the sedentary nature of television watching or the content of the shows being viewed. I suspect that content is not the problem. But in addition to being a sedentary activity, television watching often is isolating. When television was first introduced to the mass market, families grouped around the household’s lone set, much as families did back when radios became popular. In their infancy radio listening and television viewing were social activities rich with discussion and shared emotions.
However, as televisions became less expensive and no longer required large pieces of furniture to house them, television viewing became a more solitary and individual activity. Televisions became obligatory furnishings of every bedroom, and parents and children could withdraw to their own spaces and be entertained free of any opportunity or obligation to interact with the rest of family.
This new research into the risk factors for depression suggests that again without any way of monitoring their usage. At least among children, television watching should be a modifiable behavior.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at pdnews@mdedge.com.
Golimumab approval extended to polyarticular-course JIA and juvenile PsA
after the Food and Drug Administration approved the tumor necrosis factor inhibitor for these indications on Sept. 30, according to an announcement from its manufacturer, Janssen.
Results from the open-label, single-arm, multicenter, phase 3, GO-VIVA clinical trial formed the basis for the agency’s approval of IV golimumab. GO-VIVA was conducted in 127 patients aged 2-17 years with JIA with arthritis in five or more joints (despite receiving treatment with methotrexate for at least 2 months) as part of a postmarketing requirement under the Pediatric Research Equity Act after the intravenous formulation of the biologic was approved for adults with rheumatoid arthritis in 2013. It demonstrated that pediatric patients had a level of pharmacokinetic exposure to golimumab that was similar to what was observed in two pivotal phase 3 trials in adults with moderately to severely active RA and active PsA, as well as efficacy that was generally consistent with responses seen in adult patients with RA, the manufacturer said.
Besides RA, intravenous golimumab was previously approved for adults with PsA and ankylosing spondylitis. As opposed to the IV dosing for adults with RA, PsA, and ankylosing spondylitis at 2 mg/kg infused over 30 minutes at weeks 0 and 4, and every 8 weeks thereafter, dosing for pediatric patients with pJIA and PsA is based on body surface area at 80 mg/m2, also given as an IV infusion over 30 minutes at weeks 0 and 4, and every 8 weeks thereafter.
The adverse reactions observed in GO-VIVA were consistent with the established safety profile of intravenous golimumab in adult patients with RA and PsA, according to Janssen.
The full prescribing information for intravenous golimumab can be found on the FDA website.
after the Food and Drug Administration approved the tumor necrosis factor inhibitor for these indications on Sept. 30, according to an announcement from its manufacturer, Janssen.
Results from the open-label, single-arm, multicenter, phase 3, GO-VIVA clinical trial formed the basis for the agency’s approval of IV golimumab. GO-VIVA was conducted in 127 patients aged 2-17 years with JIA with arthritis in five or more joints (despite receiving treatment with methotrexate for at least 2 months) as part of a postmarketing requirement under the Pediatric Research Equity Act after the intravenous formulation of the biologic was approved for adults with rheumatoid arthritis in 2013. It demonstrated that pediatric patients had a level of pharmacokinetic exposure to golimumab that was similar to what was observed in two pivotal phase 3 trials in adults with moderately to severely active RA and active PsA, as well as efficacy that was generally consistent with responses seen in adult patients with RA, the manufacturer said.
Besides RA, intravenous golimumab was previously approved for adults with PsA and ankylosing spondylitis. As opposed to the IV dosing for adults with RA, PsA, and ankylosing spondylitis at 2 mg/kg infused over 30 minutes at weeks 0 and 4, and every 8 weeks thereafter, dosing for pediatric patients with pJIA and PsA is based on body surface area at 80 mg/m2, also given as an IV infusion over 30 minutes at weeks 0 and 4, and every 8 weeks thereafter.
The adverse reactions observed in GO-VIVA were consistent with the established safety profile of intravenous golimumab in adult patients with RA and PsA, according to Janssen.
The full prescribing information for intravenous golimumab can be found on the FDA website.
after the Food and Drug Administration approved the tumor necrosis factor inhibitor for these indications on Sept. 30, according to an announcement from its manufacturer, Janssen.
Results from the open-label, single-arm, multicenter, phase 3, GO-VIVA clinical trial formed the basis for the agency’s approval of IV golimumab. GO-VIVA was conducted in 127 patients aged 2-17 years with JIA with arthritis in five or more joints (despite receiving treatment with methotrexate for at least 2 months) as part of a postmarketing requirement under the Pediatric Research Equity Act after the intravenous formulation of the biologic was approved for adults with rheumatoid arthritis in 2013. It demonstrated that pediatric patients had a level of pharmacokinetic exposure to golimumab that was similar to what was observed in two pivotal phase 3 trials in adults with moderately to severely active RA and active PsA, as well as efficacy that was generally consistent with responses seen in adult patients with RA, the manufacturer said.
Besides RA, intravenous golimumab was previously approved for adults with PsA and ankylosing spondylitis. As opposed to the IV dosing for adults with RA, PsA, and ankylosing spondylitis at 2 mg/kg infused over 30 minutes at weeks 0 and 4, and every 8 weeks thereafter, dosing for pediatric patients with pJIA and PsA is based on body surface area at 80 mg/m2, also given as an IV infusion over 30 minutes at weeks 0 and 4, and every 8 weeks thereafter.
The adverse reactions observed in GO-VIVA were consistent with the established safety profile of intravenous golimumab in adult patients with RA and PsA, according to Janssen.
The full prescribing information for intravenous golimumab can be found on the FDA website.
COVID-19’s psychological impact gets a name
During normal times, the U.K.-based charity No Panic offers itself as an easily accessible service to those with anxiety disorders and phobias. Visitors to the website who can receive immediate, remote support from trained volunteers. But this spring was anything but normal, as the reality of COVID-19’s worldwide spread became terrifyingly clear.
COVID-19 cases peaked in the United Kingdom in early April. Nationwide lockdown efforts contributed to a gradual but ultimately substantial decline in cases, yet, despite the favorable trend lines, No Panic has remained busier than ever.
Beyond the physical symptoms associated with COVID-19, the psychological outcomes are vast and, it seems, prolonged. Researchers have now formalized a definition of the long-term mental maladies associated with the pandemic, collectively deeming them “coronaphobia.”
The term is a catch-all phrase for the fear and the emotional and social strain experienced by the general public in response to COVID-19. Obsessive behaviors, distress, avoidance reaction, panic, anxiety, hoarding, paranoia, and depression are some of the responses associated with coronaphobia. On the surface, these appear to be normal, somewhat fitting reactions to this surreal and frightening moment in time. However, for those experiencing coronaphobia, they are distinctly maladaptive and harmful.
“We had a serious rise in the use of our services, notably the helpline and email enquiries,” explained Sarah Floyd, No Panic’s volunteer advisor and social media coordinator. “It has been up and down all along, but more of an up since lockdown is easing.”
The group’s experience offers yet more evidence that the anxieties and fears caused by this global pandemic don’t flatten alongside the curve but instead linger as chronic problems requiring ongoing care.
“Every week in my clinic, I’m seeing people who are experiencing more anxiety and hopelessness and having an emotional response that is perhaps out of proportion to what one would expect, which is directly related to what is going on in the world right now with coronavirus,” said Gregory Scott Brown, MD, founder and director of the Center for Green Psychiatry in West Lake Hills, Tex. “Simply put, I think what we are looking at is adjustment disorder. That is probably how the DSM would define it.”
Adjustment disorder is one of the most frequently diagnosed mental health conditions, although it is also relatively understudied. It is really a set of disorders that follow in the wake of a significant stressor, which can vary from serious illness or the death of a loved one to relocating or experiencing work problems. The resulting dysfunction and distress that the person experiences are considered out of proportion in duration or scale with what would normally be expected. Diagnosing an adjustment disorder is made difficult by the lack of a valid and reliable screening measure.
Recent literature suggests that coronaphobia may be likely to occur in those who feel vulnerable to disease, are predisposed to anxiety, or are intolerant of uncertainty. Preexisting mental health conditions can also be exacerbated by periods of quarantine, self-isolation, and lockdown, which can lead to panic attacks, chronophobia (fear of passing time), and suicidality.
Although imperfect comparisons, findings from earlier 21st century disease outbreaks, such as severe acute respiratory syndrome and the Ebola virus, signal that containment efforts themselves play a role in deteriorating mental health. A recent rapid review found that, in studies comparing persons who had previously undergone quarantines and those who had not, the former were significantly more likely to experience acute stress disorder, posttraumatic stress symptoms, and depression. Quarantine was found to result in long-term behavioral changes, such as avoiding crowds, among the general public and health care practitioners.
That tremendous psychological morbidity should accompany a global pandemic of this scale is not surprising, according to Amit Anand, MD, vice chair for research for the Center for Behavioral Health and director of the Mood and Emotional Disorders Across the Life Span program at the Cleveland Clinic.
“The technical definition of anxiety is an impending sense of doom, and I think all of us are living with that,” Dr. Anand said. “The basic question then becomes, what is normal and when does it become abnormal?”
He added that most classifications of psychiatric disorders are set during periods of relative stability, which the current moment is most certainly not.
“This is such an unusual situation, so I think it will depend on case-by-case basis, keeping the whole context in mind as whether the patient is thinking or behaving with an abnormal amount of anxiety,” Dr. Anand said.
Investigators are currently trying to give clinicians the tools to better make that determination. In the first scientific study of this clinical condition, Sherman Lee, MD, reported that five symptoms – dizziness, sleep disturbances, tonic immobility, appetite loss, and nausea/abdominal distress – were strong factors for distinguishing coronaphobia from otherwise normal concerns about COVID-19 that did not result in functional impairment. Dr. Lee and colleagues have since published further evidence that coronaphobia “is a unique predictor of psychological distress during the COVID-19 crisis.” They are working on validating a self-reported mental health screener for this condition.
Having the tools to identify patients struggling with coronaphobia may go some ways toward addressing another area of declining health. At the outset of the COVID-19 pandemic, there was a question as to whether doctors would be beset by a surge of the “worried well” – persons mistakenly believing themselves to be infected. Now months into the pandemic, the converse phenomenon – a fear of contracting COVID-19 that is driving patients away from practitioners – appears to be the more valid concern.
In early spring, the pandemic’s first surge was accompanied by reports of approximately 40% and 60% drops in visits to EDs and ambulatory centers, respectively. Stories of acute stroke patients avoiding treatment began to appear in the press. Major U.S. cities saw noteworthy declines in 911 calls, indicating a hesitancy to be taken to a hospital. That COVID-19 has been accompanied by mass unemployment and subsequent loss of insurance complicates the notion that fear alone is keeping people from treatment. In other countries, it has been explicitly linked. Investigators in Singapore noted that coronaphobia played a role in reducing willingness to attend in-person visits among adolescents with eating disorders. Similarly, case reports in Israel suggest that coronaphobia has contributed to delays in diagnoses of common pediatric diseases.
There is also a concern, colloquially termed “reentry anxiety,” that mental health problems caused by the pandemic, the accompanying lockdown, self-isolation, and quarantine practices will prove alarmingly durable. Even after this challenging moment in history draws to a close, many people may face substantial stress in returning to the normal activities of life – social, professional, familial – once taken for granted.
“We are in the beginning phase of that now,” said Dr. Anand. “ I think the longer it goes on for, the more difficult it will be.”
In the United States, that day may seem far away. Nonetheless, it is important to begin laying the therapeutic groundwork now, according to Dr. Brown.
“I am recommending unconventional therapies like meet-up groups, online forums,” he said. “Everything has shifted online, and so there are a lot of support groups that patients can participate to learn coping skills and really hear what other people are going through.”
Before reaching that stage, Dr. Brown recommends that clinicians first simply discuss such anxieties with their patients in order to normalize them.
“Realize that everyone essentially is going through some degree of this right now. The coronavirus pandemic is literally impacting every person on the face of the planet. Sometimes just pointing that out to people can really help,” he said.
A version of this article originally appeared on Medscape.com.
During normal times, the U.K.-based charity No Panic offers itself as an easily accessible service to those with anxiety disorders and phobias. Visitors to the website who can receive immediate, remote support from trained volunteers. But this spring was anything but normal, as the reality of COVID-19’s worldwide spread became terrifyingly clear.
COVID-19 cases peaked in the United Kingdom in early April. Nationwide lockdown efforts contributed to a gradual but ultimately substantial decline in cases, yet, despite the favorable trend lines, No Panic has remained busier than ever.
Beyond the physical symptoms associated with COVID-19, the psychological outcomes are vast and, it seems, prolonged. Researchers have now formalized a definition of the long-term mental maladies associated with the pandemic, collectively deeming them “coronaphobia.”
The term is a catch-all phrase for the fear and the emotional and social strain experienced by the general public in response to COVID-19. Obsessive behaviors, distress, avoidance reaction, panic, anxiety, hoarding, paranoia, and depression are some of the responses associated with coronaphobia. On the surface, these appear to be normal, somewhat fitting reactions to this surreal and frightening moment in time. However, for those experiencing coronaphobia, they are distinctly maladaptive and harmful.
“We had a serious rise in the use of our services, notably the helpline and email enquiries,” explained Sarah Floyd, No Panic’s volunteer advisor and social media coordinator. “It has been up and down all along, but more of an up since lockdown is easing.”
The group’s experience offers yet more evidence that the anxieties and fears caused by this global pandemic don’t flatten alongside the curve but instead linger as chronic problems requiring ongoing care.
“Every week in my clinic, I’m seeing people who are experiencing more anxiety and hopelessness and having an emotional response that is perhaps out of proportion to what one would expect, which is directly related to what is going on in the world right now with coronavirus,” said Gregory Scott Brown, MD, founder and director of the Center for Green Psychiatry in West Lake Hills, Tex. “Simply put, I think what we are looking at is adjustment disorder. That is probably how the DSM would define it.”
Adjustment disorder is one of the most frequently diagnosed mental health conditions, although it is also relatively understudied. It is really a set of disorders that follow in the wake of a significant stressor, which can vary from serious illness or the death of a loved one to relocating or experiencing work problems. The resulting dysfunction and distress that the person experiences are considered out of proportion in duration or scale with what would normally be expected. Diagnosing an adjustment disorder is made difficult by the lack of a valid and reliable screening measure.
Recent literature suggests that coronaphobia may be likely to occur in those who feel vulnerable to disease, are predisposed to anxiety, or are intolerant of uncertainty. Preexisting mental health conditions can also be exacerbated by periods of quarantine, self-isolation, and lockdown, which can lead to panic attacks, chronophobia (fear of passing time), and suicidality.
Although imperfect comparisons, findings from earlier 21st century disease outbreaks, such as severe acute respiratory syndrome and the Ebola virus, signal that containment efforts themselves play a role in deteriorating mental health. A recent rapid review found that, in studies comparing persons who had previously undergone quarantines and those who had not, the former were significantly more likely to experience acute stress disorder, posttraumatic stress symptoms, and depression. Quarantine was found to result in long-term behavioral changes, such as avoiding crowds, among the general public and health care practitioners.
That tremendous psychological morbidity should accompany a global pandemic of this scale is not surprising, according to Amit Anand, MD, vice chair for research for the Center for Behavioral Health and director of the Mood and Emotional Disorders Across the Life Span program at the Cleveland Clinic.
“The technical definition of anxiety is an impending sense of doom, and I think all of us are living with that,” Dr. Anand said. “The basic question then becomes, what is normal and when does it become abnormal?”
He added that most classifications of psychiatric disorders are set during periods of relative stability, which the current moment is most certainly not.
“This is such an unusual situation, so I think it will depend on case-by-case basis, keeping the whole context in mind as whether the patient is thinking or behaving with an abnormal amount of anxiety,” Dr. Anand said.
Investigators are currently trying to give clinicians the tools to better make that determination. In the first scientific study of this clinical condition, Sherman Lee, MD, reported that five symptoms – dizziness, sleep disturbances, tonic immobility, appetite loss, and nausea/abdominal distress – were strong factors for distinguishing coronaphobia from otherwise normal concerns about COVID-19 that did not result in functional impairment. Dr. Lee and colleagues have since published further evidence that coronaphobia “is a unique predictor of psychological distress during the COVID-19 crisis.” They are working on validating a self-reported mental health screener for this condition.
Having the tools to identify patients struggling with coronaphobia may go some ways toward addressing another area of declining health. At the outset of the COVID-19 pandemic, there was a question as to whether doctors would be beset by a surge of the “worried well” – persons mistakenly believing themselves to be infected. Now months into the pandemic, the converse phenomenon – a fear of contracting COVID-19 that is driving patients away from practitioners – appears to be the more valid concern.
In early spring, the pandemic’s first surge was accompanied by reports of approximately 40% and 60% drops in visits to EDs and ambulatory centers, respectively. Stories of acute stroke patients avoiding treatment began to appear in the press. Major U.S. cities saw noteworthy declines in 911 calls, indicating a hesitancy to be taken to a hospital. That COVID-19 has been accompanied by mass unemployment and subsequent loss of insurance complicates the notion that fear alone is keeping people from treatment. In other countries, it has been explicitly linked. Investigators in Singapore noted that coronaphobia played a role in reducing willingness to attend in-person visits among adolescents with eating disorders. Similarly, case reports in Israel suggest that coronaphobia has contributed to delays in diagnoses of common pediatric diseases.
There is also a concern, colloquially termed “reentry anxiety,” that mental health problems caused by the pandemic, the accompanying lockdown, self-isolation, and quarantine practices will prove alarmingly durable. Even after this challenging moment in history draws to a close, many people may face substantial stress in returning to the normal activities of life – social, professional, familial – once taken for granted.
“We are in the beginning phase of that now,” said Dr. Anand. “ I think the longer it goes on for, the more difficult it will be.”
In the United States, that day may seem far away. Nonetheless, it is important to begin laying the therapeutic groundwork now, according to Dr. Brown.
“I am recommending unconventional therapies like meet-up groups, online forums,” he said. “Everything has shifted online, and so there are a lot of support groups that patients can participate to learn coping skills and really hear what other people are going through.”
Before reaching that stage, Dr. Brown recommends that clinicians first simply discuss such anxieties with their patients in order to normalize them.
“Realize that everyone essentially is going through some degree of this right now. The coronavirus pandemic is literally impacting every person on the face of the planet. Sometimes just pointing that out to people can really help,” he said.
A version of this article originally appeared on Medscape.com.
During normal times, the U.K.-based charity No Panic offers itself as an easily accessible service to those with anxiety disorders and phobias. Visitors to the website who can receive immediate, remote support from trained volunteers. But this spring was anything but normal, as the reality of COVID-19’s worldwide spread became terrifyingly clear.
COVID-19 cases peaked in the United Kingdom in early April. Nationwide lockdown efforts contributed to a gradual but ultimately substantial decline in cases, yet, despite the favorable trend lines, No Panic has remained busier than ever.
Beyond the physical symptoms associated with COVID-19, the psychological outcomes are vast and, it seems, prolonged. Researchers have now formalized a definition of the long-term mental maladies associated with the pandemic, collectively deeming them “coronaphobia.”
The term is a catch-all phrase for the fear and the emotional and social strain experienced by the general public in response to COVID-19. Obsessive behaviors, distress, avoidance reaction, panic, anxiety, hoarding, paranoia, and depression are some of the responses associated with coronaphobia. On the surface, these appear to be normal, somewhat fitting reactions to this surreal and frightening moment in time. However, for those experiencing coronaphobia, they are distinctly maladaptive and harmful.
“We had a serious rise in the use of our services, notably the helpline and email enquiries,” explained Sarah Floyd, No Panic’s volunteer advisor and social media coordinator. “It has been up and down all along, but more of an up since lockdown is easing.”
The group’s experience offers yet more evidence that the anxieties and fears caused by this global pandemic don’t flatten alongside the curve but instead linger as chronic problems requiring ongoing care.
“Every week in my clinic, I’m seeing people who are experiencing more anxiety and hopelessness and having an emotional response that is perhaps out of proportion to what one would expect, which is directly related to what is going on in the world right now with coronavirus,” said Gregory Scott Brown, MD, founder and director of the Center for Green Psychiatry in West Lake Hills, Tex. “Simply put, I think what we are looking at is adjustment disorder. That is probably how the DSM would define it.”
Adjustment disorder is one of the most frequently diagnosed mental health conditions, although it is also relatively understudied. It is really a set of disorders that follow in the wake of a significant stressor, which can vary from serious illness or the death of a loved one to relocating or experiencing work problems. The resulting dysfunction and distress that the person experiences are considered out of proportion in duration or scale with what would normally be expected. Diagnosing an adjustment disorder is made difficult by the lack of a valid and reliable screening measure.
Recent literature suggests that coronaphobia may be likely to occur in those who feel vulnerable to disease, are predisposed to anxiety, or are intolerant of uncertainty. Preexisting mental health conditions can also be exacerbated by periods of quarantine, self-isolation, and lockdown, which can lead to panic attacks, chronophobia (fear of passing time), and suicidality.
Although imperfect comparisons, findings from earlier 21st century disease outbreaks, such as severe acute respiratory syndrome and the Ebola virus, signal that containment efforts themselves play a role in deteriorating mental health. A recent rapid review found that, in studies comparing persons who had previously undergone quarantines and those who had not, the former were significantly more likely to experience acute stress disorder, posttraumatic stress symptoms, and depression. Quarantine was found to result in long-term behavioral changes, such as avoiding crowds, among the general public and health care practitioners.
That tremendous psychological morbidity should accompany a global pandemic of this scale is not surprising, according to Amit Anand, MD, vice chair for research for the Center for Behavioral Health and director of the Mood and Emotional Disorders Across the Life Span program at the Cleveland Clinic.
“The technical definition of anxiety is an impending sense of doom, and I think all of us are living with that,” Dr. Anand said. “The basic question then becomes, what is normal and when does it become abnormal?”
He added that most classifications of psychiatric disorders are set during periods of relative stability, which the current moment is most certainly not.
“This is such an unusual situation, so I think it will depend on case-by-case basis, keeping the whole context in mind as whether the patient is thinking or behaving with an abnormal amount of anxiety,” Dr. Anand said.
Investigators are currently trying to give clinicians the tools to better make that determination. In the first scientific study of this clinical condition, Sherman Lee, MD, reported that five symptoms – dizziness, sleep disturbances, tonic immobility, appetite loss, and nausea/abdominal distress – were strong factors for distinguishing coronaphobia from otherwise normal concerns about COVID-19 that did not result in functional impairment. Dr. Lee and colleagues have since published further evidence that coronaphobia “is a unique predictor of psychological distress during the COVID-19 crisis.” They are working on validating a self-reported mental health screener for this condition.
Having the tools to identify patients struggling with coronaphobia may go some ways toward addressing another area of declining health. At the outset of the COVID-19 pandemic, there was a question as to whether doctors would be beset by a surge of the “worried well” – persons mistakenly believing themselves to be infected. Now months into the pandemic, the converse phenomenon – a fear of contracting COVID-19 that is driving patients away from practitioners – appears to be the more valid concern.
In early spring, the pandemic’s first surge was accompanied by reports of approximately 40% and 60% drops in visits to EDs and ambulatory centers, respectively. Stories of acute stroke patients avoiding treatment began to appear in the press. Major U.S. cities saw noteworthy declines in 911 calls, indicating a hesitancy to be taken to a hospital. That COVID-19 has been accompanied by mass unemployment and subsequent loss of insurance complicates the notion that fear alone is keeping people from treatment. In other countries, it has been explicitly linked. Investigators in Singapore noted that coronaphobia played a role in reducing willingness to attend in-person visits among adolescents with eating disorders. Similarly, case reports in Israel suggest that coronaphobia has contributed to delays in diagnoses of common pediatric diseases.
There is also a concern, colloquially termed “reentry anxiety,” that mental health problems caused by the pandemic, the accompanying lockdown, self-isolation, and quarantine practices will prove alarmingly durable. Even after this challenging moment in history draws to a close, many people may face substantial stress in returning to the normal activities of life – social, professional, familial – once taken for granted.
“We are in the beginning phase of that now,” said Dr. Anand. “ I think the longer it goes on for, the more difficult it will be.”
In the United States, that day may seem far away. Nonetheless, it is important to begin laying the therapeutic groundwork now, according to Dr. Brown.
“I am recommending unconventional therapies like meet-up groups, online forums,” he said. “Everything has shifted online, and so there are a lot of support groups that patients can participate to learn coping skills and really hear what other people are going through.”
Before reaching that stage, Dr. Brown recommends that clinicians first simply discuss such anxieties with their patients in order to normalize them.
“Realize that everyone essentially is going through some degree of this right now. The coronavirus pandemic is literally impacting every person on the face of the planet. Sometimes just pointing that out to people can really help,” he said.
A version of this article originally appeared on Medscape.com.
The boy whose arm wouldn’t work
CASE Drooling, unsteady, and not himself
B, age 10, who is left handed and has autism spectrum disorder, is brought to the emergency department (ED) with a 1-day history of drooling, unsteady gait, and left wrist in sustained flexion. His parents report that for the past week, B has had cold symptoms, including rhinorrhea, a low-grade fever (100.0°F), and cough. Earlier in the day, he was seen at his pediatrician’s office, where he was diagnosed with an acute respiratory infection and started on amoxicillin, 500 mg twice daily for 7 days.
At baseline, B is nonverbal. He requires some assistance with his activities of daily living. He usually is able to walk without assistance and dress himself, but he is not toilet trained. His parents report that in the past day, he has had significant difficulties with tasks involving his left hand. Normally, B is able to feed himself “finger foods” but has been unable to do so today. His parents say that he has been unsteady on his feet, and has been “falling forward” when he tries to walk.
Two years ago, B was started on risperidone, 0.5 mg nightly, for behavioral aggression and self-mutilation. Over the next 12 months, the dosage was steadily increased to 1 mg twice daily, with good response. He has been taking his current dosage, 1 mg twice daily, for the past 12 months without adjustment. His parents report there have been no other medication changes, other than starting amoxicillin earlier that day.
As part of his initial ED evaluation, B is found to be mildly dehydrated, with an elevated sedimentation rate on urinalysis. His complete blood count (CBC) with differential is within normal limits. A comprehensive metabolic panel shows a slight increase in his creatinine level, indicating dehydration. B is administered IV fluid replacement because he is having difficulty drinking due to excessive drooling.
The ED physician is concerned that B may be experiencing an acute dystonic reaction from risperidone, so the team holds this medication, and gives B a one-time dose of IV diphenhydramine, 25 mg, for presumptive acute dystonic reaction. After several minutes, there is no improvement in the sustained flexion of his left wrist.
[polldaddy:10615848]
The authors’ observations
B presented with new-onset neurologic findings after a recently diagnosed upper respiratory viral illness. His symptoms appeared to be confined to his left upper extremity, specifically demonstrating left arm extension at the elbow with flexion of the left wrist. He also had new-onset unsteady gait with a stooped forward posture and required assistance with walking. Interestingly, despite B’s history of antipsychotic use, administering an anticholinergic agent did not lessen the dystonic posturing at his wrist and elbow.
EVALUATION Laboratory results reveal new clues
While in the ED, B undergoes MRI of the brain and spinal cord to rule out any mass lesions that could be impinging upon the motor pathways. Both brain and spinal cord imaging appear to be essentially normal, without evidence of impingement of the spinal nerves or lesions involving the brainstem or cerebellum.
Continue to: Due to concerns...
Due to concerns of possible airway obstruction, a CT scan of the neck is obtained to rule out any acute pathology, such as epiglottitis compromising his airway. The scan shows some inflammation and edema in the soft tissues that is thought to be secondary to his acute viral illness. B is able to maintain his airway and oxygenation, so intubation is not necessary.
A CPK test is ordered because there are concerns of sustained muscle contraction of B’s left wrist and elbow. The CPK level is 884 U/L (reference range 26 to 192 U/L). The elevation in CPK is consistent with prior laboratory findings of dehydration and indicating skeletal muscle breakdown from sustained muscle contraction. All other laboratory results, including a comprehensive metabolic panel, urine drug screen, and thyroid screening panel, are within normal limits.
[polldaddy:10615850]
EVALUATION No variation in facial expression
B is admitted to the general pediatrics service. Maintenance IV fluids are started due to concerns of dehydration and possible rhabdomyolysis due to his elevated CPK level. Risperidone is held throughout the hospital course due to concerns for an acute dystonic reaction. B is monitored for several days without clinical improvement and eventually discharged home with a diagnosis of inflammatory mononeuropathy due to viral infection. The patient is told to discontinue risperidone as part of discharge instructions.
Five days later, B returns to the hospital because there was no improvement in his left extremity or walking. His left elbow remains extended with left wrist in flexion. Psychiatry is consulted for further diagnostic clarity and evaluation.
On physical examination, B’s left arm remains unchanged. Despite discontinuing risperidone, there is evidence of cogwheel rigidity of the left wrist joint. Reflexes in the upper and lower extremities are 2+ and symmetrical bilaterally, suggesting intact upper and lower motor pathways. Babinski sign is absent bilaterally, which is a normal finding in B’s age group. B continues to have difficulty with ambulating and appears to “fall forward” while trying to walk with assistance. His parents also say that B is not laughing, smiling, or showing any variation in facial expression.
Continue to: Additional family history...
Additional family history is gathered from B’s parents for possible hereditary movement disorders such as Wilson’s disease. They report that no family members have developed involuntary movements or other neurologic syndromes. Additional considerations on the differential diagnosis for B include juvenile ALS or mononeuropathy involving the C5 and C6 nerve roots. B’s parents deny any recent shoulder trauma, and radiographic studies did not demonstrate any involvement of the nerve roots.
TREATMENT A trial of bromocriptine
At this point, B’s neurologic workup is essentially normal, and he is given a provisional diagnosis of antipsychotic-induced tardive dystonia vs tardive parkinsonism. Risperidone continues to be held, and B is monitored for clinical improvement. B is administered a one-time dose of diphenhydramine, 25 mg, for dystonia with no improvement in symptoms. He is then started on bromocriptine, 1.25 mg twice daily with meals, for parkinsonian symptoms secondary to antipsychotic medication use. After 1 day of treatment, B shows less sustained flexion of his left wrist. He is able to relax his left arm, shows improvements in ambulation, and requires less assistance. B continues to be observed closely and continues to improve toward his baseline.
At Day 4, he is discharged. B is able to walk mostly without assistance and demonstrates improvement in left wrist flexion. He is scheduled to see a movement disorders specialist a week after discharge. The initial diagnosis given by the movement disorder specialist is tardive dystonia.
The authors’ observations
Tardive dyskinesia is a well-known iatrogenic effect of antipsychotic medications that are commonly used to manage conditions such as schizophrenia or behavioral agitation associated with autism spectrum disorder. Symptoms of tardive dyskinesia typically emerge after 1 to 2 years of continuous exposure to dopamine receptor blocking agents (DRBAs). Tardive dyskinesia symptoms include involuntary, repetitive, purposeless movements of the tongue, jaw, lips, face, trunk, and upper and lower extremities, with significant functional impairment.1
Tardive syndromes refer to a diverse array of hyperkinetic, hypokinetic, and sensory movement disorders resulting from at least 3 months of continuous DRBA therapy.2 Tardive dyskinesia is perhaps the most well-known of the tardive syndromes, but is not the only one to consider when assessing for antipsychotic-induced movement disorders. A key feature differentiating a tardive syndrome is the persistence of the movement disorder after the DRBA is discontinued. In this case, B had been receiving a stable dose of risperidone for >1 year. He developed dystonic posturing of his left wrist and elbow that was both unresponsive to anticholinergic medication and persisted after risperidone was discontinued. The term “tardive” emphasizes the delay in development of abnormal involuntary movement symptoms after initiating antipsychotic medications.3 Table 12 shows a comparison of tardive dystonia vs an acute dystonic reaction.
Continue to: Other tardive syndromes include...
Other tardive syndromes include:
- tardive tics
- tardive parkinsonism
- tardive pain
- tardive myoclonus
- tardive akathisia
- tardive tremors.
The incidence of tardive syndromes increases 5% annually for the first 5 years of treatment. At 10 years of treatment, the annual incidence is thought to be 49%, and at 25 years of treatment, 68%.4 The predominant theory of the pathophysiology of tardive syndromes is that the chronic use of DRBAs causes a gradual hypersensitization of dopamine receptors.4 The diagnosis of a tardive syndrome is based on history of exposure to a DRBA as well as clinical observation of symptoms.
Compared with classic tardive dyskinesia, tardive dystonia is more common among younger patients. The mean age of onset of tardive dystonia is 40, and it typically affects young males.5 Typical posturing observed in cases of tardive dystonia include extension of the arms and flexion at the wrists.6 In contrast to cases of primary dystonia, tardive dystonia is typically associated with stereotypies, akathisia, or other movement disorders. Anticholinergic agents, such as
The American Psychiatric Association has issued guidelines on screening for involuntary movement syndromes by using the Abnormal Involuntary Movement Scale (AIMS).7 The current recommendations include assessment every 6 months for patients receiving first-generation antipsychotics, and every 12 months for those receiving second-generation antipsychotics.7 Prescribers should also carefully assess for any pre-existing involuntary movements before prescribing a DRBA.7
[polldaddy:10615855]
The authors’ observations
In 2013, the American Academy of Neurology (AAN) published guidelines on the treatment of tardive dyskinesia. According to these guidelines, at that time, the treatments with the most evidence supporting their use were clonazepam, ginkgo biloba,
Continue to: In 2017, valbenazine and deutetrabenazine...
In 2017, valbenazine and deutetrabenazine became the first FDA-approved treatments for tardive dyskinesia in adults. Both medications block the vesicular monoamine transporter 2 (VMAT2) system, which results in decreased synaptic dopamine and dopamine receptor stimulation. Both VMAT2 inhibitor medications have a category level A supporting their use for treating tardive dyskinesia.8-10
Currently, there are no published treatment guidelines on pharmacologic management of tardive dystonia. In B’s case, bromocriptine, a dopamine agonist, was used to counter the dopamine-blocking effects of risperidone on the nigrostriatal pathway and improve parkinsonian features of B’s presentation, including bradykinesia, stooped forward posture, and masked facies. Bromocriptine was found to be effective in alleviating parkinsonian features; however, to date there is no evidence demonstrating its effectiveness in countering delayed dystonic effects of DRBAs.
OUTCOME Improvement of dystonia symptoms
One week after discharge, B is seen for a follow-up visit. He continues taking bromocriptine, 1.25 mg twice daily, with meals after discharge. On examination, he has some evidence of tardive dystonia, including flexion of left wrist and posturing while ambulating. B’s parkinsonian features, including stooped forward posture, masked facies, and cogwheel rigidity of the left wrist muscle, have resolved. B is now able to walk on his own without unsteadiness. Bromocriptine is discontinued after 1 month, and his symptoms of dystonia continue to improve.
Two months after hospitalization, B is started on quetiapine, 25 mg twice daily, for behavioral aggression. Quetiapine is chosen because it has a lower dopamine receptor affinity compared with risperidone, and theoretically, quetiapine is associated with a lower risk of developing tardive symptoms. During the next 6 months, B is monitored closely for recurrence of tardive symptoms. Quetiapine is slowly titrated to 25 mg in the morning, and 50 mg at bedtime. His behavioral agitation improves significantly and he does not have a recurrence of tardive symptoms.
Bottom Line
Tardive dystonia is a possible iatrogenic adverse effect for patients receiving long-term dopamine receptor blocking agent (DRBA) therapy. Tardive syndromes encompass delayed-onset movement disorders caused by long-term blockade of the dopamine receptor by antipsychotic agents. Tardive dystonia can be contrasted from acute dystonic reaction based on the time course of development as well as by the persistence of symptoms after DRBAs are withheld.
Continue to: Related Resources
Related Resources
- American Academy of Neurology. Summary of evidence-based guideline for clinicians: treatment of tardive syndromes. https://www.aan.com/Guidelines/Home/GetGuidelineContent/613. Published 2013.
- Dystonia Medical Research Foundation. https://dystonia-foundation.org/.
Drug Brand Names
Amantadine • Gocovri, Symmetrel
Amoxicillin • Amoxil
Baclofen • Kemstro, Liroesal
Benztropine • Cogentin
Bromocriptine • Parlodel
Clonazepam • Klonopin
Deutetrabenazine • Austedo
Galantamine • Razadyne
Quetiapine • Seroquel
Risperidone • Risperdal
Tetrabenazine • Xenazine
Trihexyphenidyl • Artane, Tremin
Valbenazine • Ingrezza
1. Margolese HC, Chouinard G, Kolivakis TT, et al. Tardive dyskinesia in the era of typical and atypical antipsychotics. Part 1: pathophysiology and mechanisms of induction. Can J Psychiatr. 2005;50(9):541-547.
2. Truong D, Frei K. Setting the record straight: the nosology of tardive syndromes. Parkinsonism Relat Disord. 2019;59:146-150.
3. Cornett EM, Novitch M, Kaye AD, et al. Medication-induced tardive dyskinesia: a review and update. Ochsner J. 2017;17(2):162-174.
4. Schooler NR, Kane JM. Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry. 1982;39(4):486-487.
5. Fahn S, Jankovic J, Hallett M. Principles and Practice of Movement Disorders. 2nd ed. Philadelphia, PA: Saunders; 2011:415-446.
6. Kang UJ, Burke RE, Fahn S. Natural history and treatment of tardive dystonia. Mov Disord. 1986;1(3):193-208.
7. Lehman AF, Lieberman JA, Dixon LB, et al. Practice guideline for the treatment of patients with schizophrenia, second edition. Am J Psychiatry. 2004;161(suppl 2):1-56.
8. Bhidayasiri R, Fahn S, Weiner WJ, et al, Evidence-based guideline: treatment of tardive syndromes: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;81(5):463-469.
9. Ingrezza [package insert]. San Diego, CA: Neurocrine Biosciences, Inc.; 2020.
10. Austedo [package insert]. North Wales, PA: Teva Pharmaceuticals; 2017.
CASE Drooling, unsteady, and not himself
B, age 10, who is left handed and has autism spectrum disorder, is brought to the emergency department (ED) with a 1-day history of drooling, unsteady gait, and left wrist in sustained flexion. His parents report that for the past week, B has had cold symptoms, including rhinorrhea, a low-grade fever (100.0°F), and cough. Earlier in the day, he was seen at his pediatrician’s office, where he was diagnosed with an acute respiratory infection and started on amoxicillin, 500 mg twice daily for 7 days.
At baseline, B is nonverbal. He requires some assistance with his activities of daily living. He usually is able to walk without assistance and dress himself, but he is not toilet trained. His parents report that in the past day, he has had significant difficulties with tasks involving his left hand. Normally, B is able to feed himself “finger foods” but has been unable to do so today. His parents say that he has been unsteady on his feet, and has been “falling forward” when he tries to walk.
Two years ago, B was started on risperidone, 0.5 mg nightly, for behavioral aggression and self-mutilation. Over the next 12 months, the dosage was steadily increased to 1 mg twice daily, with good response. He has been taking his current dosage, 1 mg twice daily, for the past 12 months without adjustment. His parents report there have been no other medication changes, other than starting amoxicillin earlier that day.
As part of his initial ED evaluation, B is found to be mildly dehydrated, with an elevated sedimentation rate on urinalysis. His complete blood count (CBC) with differential is within normal limits. A comprehensive metabolic panel shows a slight increase in his creatinine level, indicating dehydration. B is administered IV fluid replacement because he is having difficulty drinking due to excessive drooling.
The ED physician is concerned that B may be experiencing an acute dystonic reaction from risperidone, so the team holds this medication, and gives B a one-time dose of IV diphenhydramine, 25 mg, for presumptive acute dystonic reaction. After several minutes, there is no improvement in the sustained flexion of his left wrist.
[polldaddy:10615848]
The authors’ observations
B presented with new-onset neurologic findings after a recently diagnosed upper respiratory viral illness. His symptoms appeared to be confined to his left upper extremity, specifically demonstrating left arm extension at the elbow with flexion of the left wrist. He also had new-onset unsteady gait with a stooped forward posture and required assistance with walking. Interestingly, despite B’s history of antipsychotic use, administering an anticholinergic agent did not lessen the dystonic posturing at his wrist and elbow.
EVALUATION Laboratory results reveal new clues
While in the ED, B undergoes MRI of the brain and spinal cord to rule out any mass lesions that could be impinging upon the motor pathways. Both brain and spinal cord imaging appear to be essentially normal, without evidence of impingement of the spinal nerves or lesions involving the brainstem or cerebellum.
Continue to: Due to concerns...
Due to concerns of possible airway obstruction, a CT scan of the neck is obtained to rule out any acute pathology, such as epiglottitis compromising his airway. The scan shows some inflammation and edema in the soft tissues that is thought to be secondary to his acute viral illness. B is able to maintain his airway and oxygenation, so intubation is not necessary.
A CPK test is ordered because there are concerns of sustained muscle contraction of B’s left wrist and elbow. The CPK level is 884 U/L (reference range 26 to 192 U/L). The elevation in CPK is consistent with prior laboratory findings of dehydration and indicating skeletal muscle breakdown from sustained muscle contraction. All other laboratory results, including a comprehensive metabolic panel, urine drug screen, and thyroid screening panel, are within normal limits.
[polldaddy:10615850]
EVALUATION No variation in facial expression
B is admitted to the general pediatrics service. Maintenance IV fluids are started due to concerns of dehydration and possible rhabdomyolysis due to his elevated CPK level. Risperidone is held throughout the hospital course due to concerns for an acute dystonic reaction. B is monitored for several days without clinical improvement and eventually discharged home with a diagnosis of inflammatory mononeuropathy due to viral infection. The patient is told to discontinue risperidone as part of discharge instructions.
Five days later, B returns to the hospital because there was no improvement in his left extremity or walking. His left elbow remains extended with left wrist in flexion. Psychiatry is consulted for further diagnostic clarity and evaluation.
On physical examination, B’s left arm remains unchanged. Despite discontinuing risperidone, there is evidence of cogwheel rigidity of the left wrist joint. Reflexes in the upper and lower extremities are 2+ and symmetrical bilaterally, suggesting intact upper and lower motor pathways. Babinski sign is absent bilaterally, which is a normal finding in B’s age group. B continues to have difficulty with ambulating and appears to “fall forward” while trying to walk with assistance. His parents also say that B is not laughing, smiling, or showing any variation in facial expression.
Continue to: Additional family history...
Additional family history is gathered from B’s parents for possible hereditary movement disorders such as Wilson’s disease. They report that no family members have developed involuntary movements or other neurologic syndromes. Additional considerations on the differential diagnosis for B include juvenile ALS or mononeuropathy involving the C5 and C6 nerve roots. B’s parents deny any recent shoulder trauma, and radiographic studies did not demonstrate any involvement of the nerve roots.
TREATMENT A trial of bromocriptine
At this point, B’s neurologic workup is essentially normal, and he is given a provisional diagnosis of antipsychotic-induced tardive dystonia vs tardive parkinsonism. Risperidone continues to be held, and B is monitored for clinical improvement. B is administered a one-time dose of diphenhydramine, 25 mg, for dystonia with no improvement in symptoms. He is then started on bromocriptine, 1.25 mg twice daily with meals, for parkinsonian symptoms secondary to antipsychotic medication use. After 1 day of treatment, B shows less sustained flexion of his left wrist. He is able to relax his left arm, shows improvements in ambulation, and requires less assistance. B continues to be observed closely and continues to improve toward his baseline.
At Day 4, he is discharged. B is able to walk mostly without assistance and demonstrates improvement in left wrist flexion. He is scheduled to see a movement disorders specialist a week after discharge. The initial diagnosis given by the movement disorder specialist is tardive dystonia.
The authors’ observations
Tardive dyskinesia is a well-known iatrogenic effect of antipsychotic medications that are commonly used to manage conditions such as schizophrenia or behavioral agitation associated with autism spectrum disorder. Symptoms of tardive dyskinesia typically emerge after 1 to 2 years of continuous exposure to dopamine receptor blocking agents (DRBAs). Tardive dyskinesia symptoms include involuntary, repetitive, purposeless movements of the tongue, jaw, lips, face, trunk, and upper and lower extremities, with significant functional impairment.1
Tardive syndromes refer to a diverse array of hyperkinetic, hypokinetic, and sensory movement disorders resulting from at least 3 months of continuous DRBA therapy.2 Tardive dyskinesia is perhaps the most well-known of the tardive syndromes, but is not the only one to consider when assessing for antipsychotic-induced movement disorders. A key feature differentiating a tardive syndrome is the persistence of the movement disorder after the DRBA is discontinued. In this case, B had been receiving a stable dose of risperidone for >1 year. He developed dystonic posturing of his left wrist and elbow that was both unresponsive to anticholinergic medication and persisted after risperidone was discontinued. The term “tardive” emphasizes the delay in development of abnormal involuntary movement symptoms after initiating antipsychotic medications.3 Table 12 shows a comparison of tardive dystonia vs an acute dystonic reaction.
Continue to: Other tardive syndromes include...
Other tardive syndromes include:
- tardive tics
- tardive parkinsonism
- tardive pain
- tardive myoclonus
- tardive akathisia
- tardive tremors.
The incidence of tardive syndromes increases 5% annually for the first 5 years of treatment. At 10 years of treatment, the annual incidence is thought to be 49%, and at 25 years of treatment, 68%.4 The predominant theory of the pathophysiology of tardive syndromes is that the chronic use of DRBAs causes a gradual hypersensitization of dopamine receptors.4 The diagnosis of a tardive syndrome is based on history of exposure to a DRBA as well as clinical observation of symptoms.
Compared with classic tardive dyskinesia, tardive dystonia is more common among younger patients. The mean age of onset of tardive dystonia is 40, and it typically affects young males.5 Typical posturing observed in cases of tardive dystonia include extension of the arms and flexion at the wrists.6 In contrast to cases of primary dystonia, tardive dystonia is typically associated with stereotypies, akathisia, or other movement disorders. Anticholinergic agents, such as
The American Psychiatric Association has issued guidelines on screening for involuntary movement syndromes by using the Abnormal Involuntary Movement Scale (AIMS).7 The current recommendations include assessment every 6 months for patients receiving first-generation antipsychotics, and every 12 months for those receiving second-generation antipsychotics.7 Prescribers should also carefully assess for any pre-existing involuntary movements before prescribing a DRBA.7
[polldaddy:10615855]
The authors’ observations
In 2013, the American Academy of Neurology (AAN) published guidelines on the treatment of tardive dyskinesia. According to these guidelines, at that time, the treatments with the most evidence supporting their use were clonazepam, ginkgo biloba,
Continue to: In 2017, valbenazine and deutetrabenazine...
In 2017, valbenazine and deutetrabenazine became the first FDA-approved treatments for tardive dyskinesia in adults. Both medications block the vesicular monoamine transporter 2 (VMAT2) system, which results in decreased synaptic dopamine and dopamine receptor stimulation. Both VMAT2 inhibitor medications have a category level A supporting their use for treating tardive dyskinesia.8-10
Currently, there are no published treatment guidelines on pharmacologic management of tardive dystonia. In B’s case, bromocriptine, a dopamine agonist, was used to counter the dopamine-blocking effects of risperidone on the nigrostriatal pathway and improve parkinsonian features of B’s presentation, including bradykinesia, stooped forward posture, and masked facies. Bromocriptine was found to be effective in alleviating parkinsonian features; however, to date there is no evidence demonstrating its effectiveness in countering delayed dystonic effects of DRBAs.
OUTCOME Improvement of dystonia symptoms
One week after discharge, B is seen for a follow-up visit. He continues taking bromocriptine, 1.25 mg twice daily, with meals after discharge. On examination, he has some evidence of tardive dystonia, including flexion of left wrist and posturing while ambulating. B’s parkinsonian features, including stooped forward posture, masked facies, and cogwheel rigidity of the left wrist muscle, have resolved. B is now able to walk on his own without unsteadiness. Bromocriptine is discontinued after 1 month, and his symptoms of dystonia continue to improve.
Two months after hospitalization, B is started on quetiapine, 25 mg twice daily, for behavioral aggression. Quetiapine is chosen because it has a lower dopamine receptor affinity compared with risperidone, and theoretically, quetiapine is associated with a lower risk of developing tardive symptoms. During the next 6 months, B is monitored closely for recurrence of tardive symptoms. Quetiapine is slowly titrated to 25 mg in the morning, and 50 mg at bedtime. His behavioral agitation improves significantly and he does not have a recurrence of tardive symptoms.
Bottom Line
Tardive dystonia is a possible iatrogenic adverse effect for patients receiving long-term dopamine receptor blocking agent (DRBA) therapy. Tardive syndromes encompass delayed-onset movement disorders caused by long-term blockade of the dopamine receptor by antipsychotic agents. Tardive dystonia can be contrasted from acute dystonic reaction based on the time course of development as well as by the persistence of symptoms after DRBAs are withheld.
Continue to: Related Resources
Related Resources
- American Academy of Neurology. Summary of evidence-based guideline for clinicians: treatment of tardive syndromes. https://www.aan.com/Guidelines/Home/GetGuidelineContent/613. Published 2013.
- Dystonia Medical Research Foundation. https://dystonia-foundation.org/.
Drug Brand Names
Amantadine • Gocovri, Symmetrel
Amoxicillin • Amoxil
Baclofen • Kemstro, Liroesal
Benztropine • Cogentin
Bromocriptine • Parlodel
Clonazepam • Klonopin
Deutetrabenazine • Austedo
Galantamine • Razadyne
Quetiapine • Seroquel
Risperidone • Risperdal
Tetrabenazine • Xenazine
Trihexyphenidyl • Artane, Tremin
Valbenazine • Ingrezza
CASE Drooling, unsteady, and not himself
B, age 10, who is left handed and has autism spectrum disorder, is brought to the emergency department (ED) with a 1-day history of drooling, unsteady gait, and left wrist in sustained flexion. His parents report that for the past week, B has had cold symptoms, including rhinorrhea, a low-grade fever (100.0°F), and cough. Earlier in the day, he was seen at his pediatrician’s office, where he was diagnosed with an acute respiratory infection and started on amoxicillin, 500 mg twice daily for 7 days.
At baseline, B is nonverbal. He requires some assistance with his activities of daily living. He usually is able to walk without assistance and dress himself, but he is not toilet trained. His parents report that in the past day, he has had significant difficulties with tasks involving his left hand. Normally, B is able to feed himself “finger foods” but has been unable to do so today. His parents say that he has been unsteady on his feet, and has been “falling forward” when he tries to walk.
Two years ago, B was started on risperidone, 0.5 mg nightly, for behavioral aggression and self-mutilation. Over the next 12 months, the dosage was steadily increased to 1 mg twice daily, with good response. He has been taking his current dosage, 1 mg twice daily, for the past 12 months without adjustment. His parents report there have been no other medication changes, other than starting amoxicillin earlier that day.
As part of his initial ED evaluation, B is found to be mildly dehydrated, with an elevated sedimentation rate on urinalysis. His complete blood count (CBC) with differential is within normal limits. A comprehensive metabolic panel shows a slight increase in his creatinine level, indicating dehydration. B is administered IV fluid replacement because he is having difficulty drinking due to excessive drooling.
The ED physician is concerned that B may be experiencing an acute dystonic reaction from risperidone, so the team holds this medication, and gives B a one-time dose of IV diphenhydramine, 25 mg, for presumptive acute dystonic reaction. After several minutes, there is no improvement in the sustained flexion of his left wrist.
[polldaddy:10615848]
The authors’ observations
B presented with new-onset neurologic findings after a recently diagnosed upper respiratory viral illness. His symptoms appeared to be confined to his left upper extremity, specifically demonstrating left arm extension at the elbow with flexion of the left wrist. He also had new-onset unsteady gait with a stooped forward posture and required assistance with walking. Interestingly, despite B’s history of antipsychotic use, administering an anticholinergic agent did not lessen the dystonic posturing at his wrist and elbow.
EVALUATION Laboratory results reveal new clues
While in the ED, B undergoes MRI of the brain and spinal cord to rule out any mass lesions that could be impinging upon the motor pathways. Both brain and spinal cord imaging appear to be essentially normal, without evidence of impingement of the spinal nerves or lesions involving the brainstem or cerebellum.
Continue to: Due to concerns...
Due to concerns of possible airway obstruction, a CT scan of the neck is obtained to rule out any acute pathology, such as epiglottitis compromising his airway. The scan shows some inflammation and edema in the soft tissues that is thought to be secondary to his acute viral illness. B is able to maintain his airway and oxygenation, so intubation is not necessary.
A CPK test is ordered because there are concerns of sustained muscle contraction of B’s left wrist and elbow. The CPK level is 884 U/L (reference range 26 to 192 U/L). The elevation in CPK is consistent with prior laboratory findings of dehydration and indicating skeletal muscle breakdown from sustained muscle contraction. All other laboratory results, including a comprehensive metabolic panel, urine drug screen, and thyroid screening panel, are within normal limits.
[polldaddy:10615850]
EVALUATION No variation in facial expression
B is admitted to the general pediatrics service. Maintenance IV fluids are started due to concerns of dehydration and possible rhabdomyolysis due to his elevated CPK level. Risperidone is held throughout the hospital course due to concerns for an acute dystonic reaction. B is monitored for several days without clinical improvement and eventually discharged home with a diagnosis of inflammatory mononeuropathy due to viral infection. The patient is told to discontinue risperidone as part of discharge instructions.
Five days later, B returns to the hospital because there was no improvement in his left extremity or walking. His left elbow remains extended with left wrist in flexion. Psychiatry is consulted for further diagnostic clarity and evaluation.
On physical examination, B’s left arm remains unchanged. Despite discontinuing risperidone, there is evidence of cogwheel rigidity of the left wrist joint. Reflexes in the upper and lower extremities are 2+ and symmetrical bilaterally, suggesting intact upper and lower motor pathways. Babinski sign is absent bilaterally, which is a normal finding in B’s age group. B continues to have difficulty with ambulating and appears to “fall forward” while trying to walk with assistance. His parents also say that B is not laughing, smiling, or showing any variation in facial expression.
Continue to: Additional family history...
Additional family history is gathered from B’s parents for possible hereditary movement disorders such as Wilson’s disease. They report that no family members have developed involuntary movements or other neurologic syndromes. Additional considerations on the differential diagnosis for B include juvenile ALS or mononeuropathy involving the C5 and C6 nerve roots. B’s parents deny any recent shoulder trauma, and radiographic studies did not demonstrate any involvement of the nerve roots.
TREATMENT A trial of bromocriptine
At this point, B’s neurologic workup is essentially normal, and he is given a provisional diagnosis of antipsychotic-induced tardive dystonia vs tardive parkinsonism. Risperidone continues to be held, and B is monitored for clinical improvement. B is administered a one-time dose of diphenhydramine, 25 mg, for dystonia with no improvement in symptoms. He is then started on bromocriptine, 1.25 mg twice daily with meals, for parkinsonian symptoms secondary to antipsychotic medication use. After 1 day of treatment, B shows less sustained flexion of his left wrist. He is able to relax his left arm, shows improvements in ambulation, and requires less assistance. B continues to be observed closely and continues to improve toward his baseline.
At Day 4, he is discharged. B is able to walk mostly without assistance and demonstrates improvement in left wrist flexion. He is scheduled to see a movement disorders specialist a week after discharge. The initial diagnosis given by the movement disorder specialist is tardive dystonia.
The authors’ observations
Tardive dyskinesia is a well-known iatrogenic effect of antipsychotic medications that are commonly used to manage conditions such as schizophrenia or behavioral agitation associated with autism spectrum disorder. Symptoms of tardive dyskinesia typically emerge after 1 to 2 years of continuous exposure to dopamine receptor blocking agents (DRBAs). Tardive dyskinesia symptoms include involuntary, repetitive, purposeless movements of the tongue, jaw, lips, face, trunk, and upper and lower extremities, with significant functional impairment.1
Tardive syndromes refer to a diverse array of hyperkinetic, hypokinetic, and sensory movement disorders resulting from at least 3 months of continuous DRBA therapy.2 Tardive dyskinesia is perhaps the most well-known of the tardive syndromes, but is not the only one to consider when assessing for antipsychotic-induced movement disorders. A key feature differentiating a tardive syndrome is the persistence of the movement disorder after the DRBA is discontinued. In this case, B had been receiving a stable dose of risperidone for >1 year. He developed dystonic posturing of his left wrist and elbow that was both unresponsive to anticholinergic medication and persisted after risperidone was discontinued. The term “tardive” emphasizes the delay in development of abnormal involuntary movement symptoms after initiating antipsychotic medications.3 Table 12 shows a comparison of tardive dystonia vs an acute dystonic reaction.
Continue to: Other tardive syndromes include...
Other tardive syndromes include:
- tardive tics
- tardive parkinsonism
- tardive pain
- tardive myoclonus
- tardive akathisia
- tardive tremors.
The incidence of tardive syndromes increases 5% annually for the first 5 years of treatment. At 10 years of treatment, the annual incidence is thought to be 49%, and at 25 years of treatment, 68%.4 The predominant theory of the pathophysiology of tardive syndromes is that the chronic use of DRBAs causes a gradual hypersensitization of dopamine receptors.4 The diagnosis of a tardive syndrome is based on history of exposure to a DRBA as well as clinical observation of symptoms.
Compared with classic tardive dyskinesia, tardive dystonia is more common among younger patients. The mean age of onset of tardive dystonia is 40, and it typically affects young males.5 Typical posturing observed in cases of tardive dystonia include extension of the arms and flexion at the wrists.6 In contrast to cases of primary dystonia, tardive dystonia is typically associated with stereotypies, akathisia, or other movement disorders. Anticholinergic agents, such as
The American Psychiatric Association has issued guidelines on screening for involuntary movement syndromes by using the Abnormal Involuntary Movement Scale (AIMS).7 The current recommendations include assessment every 6 months for patients receiving first-generation antipsychotics, and every 12 months for those receiving second-generation antipsychotics.7 Prescribers should also carefully assess for any pre-existing involuntary movements before prescribing a DRBA.7
[polldaddy:10615855]
The authors’ observations
In 2013, the American Academy of Neurology (AAN) published guidelines on the treatment of tardive dyskinesia. According to these guidelines, at that time, the treatments with the most evidence supporting their use were clonazepam, ginkgo biloba,
Continue to: In 2017, valbenazine and deutetrabenazine...
In 2017, valbenazine and deutetrabenazine became the first FDA-approved treatments for tardive dyskinesia in adults. Both medications block the vesicular monoamine transporter 2 (VMAT2) system, which results in decreased synaptic dopamine and dopamine receptor stimulation. Both VMAT2 inhibitor medications have a category level A supporting their use for treating tardive dyskinesia.8-10
Currently, there are no published treatment guidelines on pharmacologic management of tardive dystonia. In B’s case, bromocriptine, a dopamine agonist, was used to counter the dopamine-blocking effects of risperidone on the nigrostriatal pathway and improve parkinsonian features of B’s presentation, including bradykinesia, stooped forward posture, and masked facies. Bromocriptine was found to be effective in alleviating parkinsonian features; however, to date there is no evidence demonstrating its effectiveness in countering delayed dystonic effects of DRBAs.
OUTCOME Improvement of dystonia symptoms
One week after discharge, B is seen for a follow-up visit. He continues taking bromocriptine, 1.25 mg twice daily, with meals after discharge. On examination, he has some evidence of tardive dystonia, including flexion of left wrist and posturing while ambulating. B’s parkinsonian features, including stooped forward posture, masked facies, and cogwheel rigidity of the left wrist muscle, have resolved. B is now able to walk on his own without unsteadiness. Bromocriptine is discontinued after 1 month, and his symptoms of dystonia continue to improve.
Two months after hospitalization, B is started on quetiapine, 25 mg twice daily, for behavioral aggression. Quetiapine is chosen because it has a lower dopamine receptor affinity compared with risperidone, and theoretically, quetiapine is associated with a lower risk of developing tardive symptoms. During the next 6 months, B is monitored closely for recurrence of tardive symptoms. Quetiapine is slowly titrated to 25 mg in the morning, and 50 mg at bedtime. His behavioral agitation improves significantly and he does not have a recurrence of tardive symptoms.
Bottom Line
Tardive dystonia is a possible iatrogenic adverse effect for patients receiving long-term dopamine receptor blocking agent (DRBA) therapy. Tardive syndromes encompass delayed-onset movement disorders caused by long-term blockade of the dopamine receptor by antipsychotic agents. Tardive dystonia can be contrasted from acute dystonic reaction based on the time course of development as well as by the persistence of symptoms after DRBAs are withheld.
Continue to: Related Resources
Related Resources
- American Academy of Neurology. Summary of evidence-based guideline for clinicians: treatment of tardive syndromes. https://www.aan.com/Guidelines/Home/GetGuidelineContent/613. Published 2013.
- Dystonia Medical Research Foundation. https://dystonia-foundation.org/.
Drug Brand Names
Amantadine • Gocovri, Symmetrel
Amoxicillin • Amoxil
Baclofen • Kemstro, Liroesal
Benztropine • Cogentin
Bromocriptine • Parlodel
Clonazepam • Klonopin
Deutetrabenazine • Austedo
Galantamine • Razadyne
Quetiapine • Seroquel
Risperidone • Risperdal
Tetrabenazine • Xenazine
Trihexyphenidyl • Artane, Tremin
Valbenazine • Ingrezza
1. Margolese HC, Chouinard G, Kolivakis TT, et al. Tardive dyskinesia in the era of typical and atypical antipsychotics. Part 1: pathophysiology and mechanisms of induction. Can J Psychiatr. 2005;50(9):541-547.
2. Truong D, Frei K. Setting the record straight: the nosology of tardive syndromes. Parkinsonism Relat Disord. 2019;59:146-150.
3. Cornett EM, Novitch M, Kaye AD, et al. Medication-induced tardive dyskinesia: a review and update. Ochsner J. 2017;17(2):162-174.
4. Schooler NR, Kane JM. Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry. 1982;39(4):486-487.
5. Fahn S, Jankovic J, Hallett M. Principles and Practice of Movement Disorders. 2nd ed. Philadelphia, PA: Saunders; 2011:415-446.
6. Kang UJ, Burke RE, Fahn S. Natural history and treatment of tardive dystonia. Mov Disord. 1986;1(3):193-208.
7. Lehman AF, Lieberman JA, Dixon LB, et al. Practice guideline for the treatment of patients with schizophrenia, second edition. Am J Psychiatry. 2004;161(suppl 2):1-56.
8. Bhidayasiri R, Fahn S, Weiner WJ, et al, Evidence-based guideline: treatment of tardive syndromes: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;81(5):463-469.
9. Ingrezza [package insert]. San Diego, CA: Neurocrine Biosciences, Inc.; 2020.
10. Austedo [package insert]. North Wales, PA: Teva Pharmaceuticals; 2017.
1. Margolese HC, Chouinard G, Kolivakis TT, et al. Tardive dyskinesia in the era of typical and atypical antipsychotics. Part 1: pathophysiology and mechanisms of induction. Can J Psychiatr. 2005;50(9):541-547.
2. Truong D, Frei K. Setting the record straight: the nosology of tardive syndromes. Parkinsonism Relat Disord. 2019;59:146-150.
3. Cornett EM, Novitch M, Kaye AD, et al. Medication-induced tardive dyskinesia: a review and update. Ochsner J. 2017;17(2):162-174.
4. Schooler NR, Kane JM. Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry. 1982;39(4):486-487.
5. Fahn S, Jankovic J, Hallett M. Principles and Practice of Movement Disorders. 2nd ed. Philadelphia, PA: Saunders; 2011:415-446.
6. Kang UJ, Burke RE, Fahn S. Natural history and treatment of tardive dystonia. Mov Disord. 1986;1(3):193-208.
7. Lehman AF, Lieberman JA, Dixon LB, et al. Practice guideline for the treatment of patients with schizophrenia, second edition. Am J Psychiatry. 2004;161(suppl 2):1-56.
8. Bhidayasiri R, Fahn S, Weiner WJ, et al, Evidence-based guideline: treatment of tardive syndromes: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;81(5):463-469.
9. Ingrezza [package insert]. San Diego, CA: Neurocrine Biosciences, Inc.; 2020.
10. Austedo [package insert]. North Wales, PA: Teva Pharmaceuticals; 2017.
Cancer disparities: One of the most pressing public health issues
“The burden of cancer is not shouldered equally by all segments of the U.S. population,” the AACR adds. “The adverse differences in cancer burden that exist among certain population groups are one of the most pressing public health challenges that we face in the United States.”
AACR president Antoni Ribas, MD, PhD, gave some examples of these disparities at a September 16 Congressional briefing that focused on the inaugural AACR Cancer Disparities Progress Report 2020.
He noted that:
- Black men have more than double the rate of death from prostate cancer compared with men of other racial and ethnic groups.
- Hispanic children are 24% more likely to develop leukemia than non-Hispanic children.
- Non-Hispanic Black children and adolescents with cancer are more than 50% more likely to die from the cancer than non-Hispanic white children and adolescents with cancer.
- Women of low socioeconomic status with early stage ovarian cancer are 50% less likely to receive recommended care than are women of high socioeconomic status.
- In addition to racial and ethnic minority groups, other populations that bear a disproportionate burden when it comes to cancer include individuals lacking adequate health insurance coverage, immigrants, those with disabilities, residents in rural areas, and members of the lesbian, gay, bisexual, and transgender communities.
“It is absolutely unacceptable that advances in cancer care and treatment are not benefiting everyone equally,” Ribas commented.
Making progress against cancer
Progress being made against cancer was highlighted in another publication, the annual AACR Cancer Progress Report 2020.
U.S. cancer deaths declined by 29% between 1991 and 2017, translating to nearly 3 million cancer deaths avoided, the report notes. In addition, 5-year survival rates for all cancers combined increased from 49% in the mid-1970s to 70% for patients diagnosed from 2010-2016.
Between August 2019 and July 31 of this year, the U.S. Food and Drug Administration approved 20 new anticancer drugs for various cancer types and 15 new indications for previously approved cancer drugs, marking the highest number of approvals in one 12-month period since AACR started producing these reports 10 years ago.
A continuing reduction in the cigarette smoking rate among US adults, which is now below 14%, is contributing greatly to declines in lung cancer rates, which have largely driven the improvements in cancer survival, the AACR noted.
This report also notes that progress has been made toward reducing cancer disparities. Overall disparities in cancer death rates among racial and ethnic groups are less pronounced now than they have been in the past two decades. For example, the overall cancer death rate for African American patients was 33% higher than for White patients in 1990 but just 14% higher in 2016.
However, both reports agree that more must be done to reduce cancer disparities even further.
They highlight initiatives that are underway, including:
- The draft guidance issued by the FDA to promote diversification of clinical trial populations.
- The National Institutes of Health’s (NIH’s) Continuing Umbrella of Research Experiences (CURE) program supporting underrepresented students and scientists along their academic and research career pathway.
- The Centers for Disease Control and Prevention’s Racial and Ethnic Approaches to Community Health (REACH) program, a grant-making program focused on encouraging preventive behaviors in underserved communities.
- The NIH’s All of Us program, which is gathering information from the genomes of 1 million healthy individuals with a focus on recruitment from historically underrepresented populations.
Ribas also announced that AACR has established a task force to focus on racial inequalities in cancer research.
Eliminating disparities would save money, argued John D. Carpten, PhD, from the University of Southern California, Los Angeles, who chaired the steering committee that developed the AACR Cancer Disparities Progress Report.
Carpten noted research showing that eliminating disparities for racial and ethnic minorities between 2003 and 2006 would have reduced health care costs by more than $1 trillion in the United States. This underscores the potentially far-reaching impact of efforts to eliminate disparities, he said.
“Without a doubt, socioeconomics and inequities in access to quality care represent major factors influencing cancer health disparities, and these disparities will persist until we address these issues” he said.
Both progress reports culminate in a call to action, largely focused on the need for “unwavering, bipartisan support from Congress, in the form of robust and sustained annual increases in funding for the NIH, NCI [National Cancer Institute], and FDA,” which is vital for accelerating the pace of progress.
The challenge is now compounded by the ongoing COVID-19 pandemic: Both progress reports note that racial and ethnic minorities, including African Americans, are not only affected disproportionately by cancer, but also by COVID-19, further highlighting the “stark inequities in health care.”
Ribas further called for action from national leadership and the scientific community.
“During this unprecedented time in our nation’s history, there is also a need for our nation’s leaders to take on a much bigger role in confronting and combating the structural and systemic racism that contributes to health disparities,” he said. The “pervasive racism and social injustices” that have contributed to disparities in both COVID-19 and cancer underscore the need for “the scientific community to step up and partner with Congress to assess and address this issue within the research community.”
This article first appeared on Medscape.com.
“The burden of cancer is not shouldered equally by all segments of the U.S. population,” the AACR adds. “The adverse differences in cancer burden that exist among certain population groups are one of the most pressing public health challenges that we face in the United States.”
AACR president Antoni Ribas, MD, PhD, gave some examples of these disparities at a September 16 Congressional briefing that focused on the inaugural AACR Cancer Disparities Progress Report 2020.
He noted that:
- Black men have more than double the rate of death from prostate cancer compared with men of other racial and ethnic groups.
- Hispanic children are 24% more likely to develop leukemia than non-Hispanic children.
- Non-Hispanic Black children and adolescents with cancer are more than 50% more likely to die from the cancer than non-Hispanic white children and adolescents with cancer.
- Women of low socioeconomic status with early stage ovarian cancer are 50% less likely to receive recommended care than are women of high socioeconomic status.
- In addition to racial and ethnic minority groups, other populations that bear a disproportionate burden when it comes to cancer include individuals lacking adequate health insurance coverage, immigrants, those with disabilities, residents in rural areas, and members of the lesbian, gay, bisexual, and transgender communities.
“It is absolutely unacceptable that advances in cancer care and treatment are not benefiting everyone equally,” Ribas commented.
Making progress against cancer
Progress being made against cancer was highlighted in another publication, the annual AACR Cancer Progress Report 2020.
U.S. cancer deaths declined by 29% between 1991 and 2017, translating to nearly 3 million cancer deaths avoided, the report notes. In addition, 5-year survival rates for all cancers combined increased from 49% in the mid-1970s to 70% for patients diagnosed from 2010-2016.
Between August 2019 and July 31 of this year, the U.S. Food and Drug Administration approved 20 new anticancer drugs for various cancer types and 15 new indications for previously approved cancer drugs, marking the highest number of approvals in one 12-month period since AACR started producing these reports 10 years ago.
A continuing reduction in the cigarette smoking rate among US adults, which is now below 14%, is contributing greatly to declines in lung cancer rates, which have largely driven the improvements in cancer survival, the AACR noted.
This report also notes that progress has been made toward reducing cancer disparities. Overall disparities in cancer death rates among racial and ethnic groups are less pronounced now than they have been in the past two decades. For example, the overall cancer death rate for African American patients was 33% higher than for White patients in 1990 but just 14% higher in 2016.
However, both reports agree that more must be done to reduce cancer disparities even further.
They highlight initiatives that are underway, including:
- The draft guidance issued by the FDA to promote diversification of clinical trial populations.
- The National Institutes of Health’s (NIH’s) Continuing Umbrella of Research Experiences (CURE) program supporting underrepresented students and scientists along their academic and research career pathway.
- The Centers for Disease Control and Prevention’s Racial and Ethnic Approaches to Community Health (REACH) program, a grant-making program focused on encouraging preventive behaviors in underserved communities.
- The NIH’s All of Us program, which is gathering information from the genomes of 1 million healthy individuals with a focus on recruitment from historically underrepresented populations.
Ribas also announced that AACR has established a task force to focus on racial inequalities in cancer research.
Eliminating disparities would save money, argued John D. Carpten, PhD, from the University of Southern California, Los Angeles, who chaired the steering committee that developed the AACR Cancer Disparities Progress Report.
Carpten noted research showing that eliminating disparities for racial and ethnic minorities between 2003 and 2006 would have reduced health care costs by more than $1 trillion in the United States. This underscores the potentially far-reaching impact of efforts to eliminate disparities, he said.
“Without a doubt, socioeconomics and inequities in access to quality care represent major factors influencing cancer health disparities, and these disparities will persist until we address these issues” he said.
Both progress reports culminate in a call to action, largely focused on the need for “unwavering, bipartisan support from Congress, in the form of robust and sustained annual increases in funding for the NIH, NCI [National Cancer Institute], and FDA,” which is vital for accelerating the pace of progress.
The challenge is now compounded by the ongoing COVID-19 pandemic: Both progress reports note that racial and ethnic minorities, including African Americans, are not only affected disproportionately by cancer, but also by COVID-19, further highlighting the “stark inequities in health care.”
Ribas further called for action from national leadership and the scientific community.
“During this unprecedented time in our nation’s history, there is also a need for our nation’s leaders to take on a much bigger role in confronting and combating the structural and systemic racism that contributes to health disparities,” he said. The “pervasive racism and social injustices” that have contributed to disparities in both COVID-19 and cancer underscore the need for “the scientific community to step up and partner with Congress to assess and address this issue within the research community.”
This article first appeared on Medscape.com.
“The burden of cancer is not shouldered equally by all segments of the U.S. population,” the AACR adds. “The adverse differences in cancer burden that exist among certain population groups are one of the most pressing public health challenges that we face in the United States.”
AACR president Antoni Ribas, MD, PhD, gave some examples of these disparities at a September 16 Congressional briefing that focused on the inaugural AACR Cancer Disparities Progress Report 2020.
He noted that:
- Black men have more than double the rate of death from prostate cancer compared with men of other racial and ethnic groups.
- Hispanic children are 24% more likely to develop leukemia than non-Hispanic children.
- Non-Hispanic Black children and adolescents with cancer are more than 50% more likely to die from the cancer than non-Hispanic white children and adolescents with cancer.
- Women of low socioeconomic status with early stage ovarian cancer are 50% less likely to receive recommended care than are women of high socioeconomic status.
- In addition to racial and ethnic minority groups, other populations that bear a disproportionate burden when it comes to cancer include individuals lacking adequate health insurance coverage, immigrants, those with disabilities, residents in rural areas, and members of the lesbian, gay, bisexual, and transgender communities.
“It is absolutely unacceptable that advances in cancer care and treatment are not benefiting everyone equally,” Ribas commented.
Making progress against cancer
Progress being made against cancer was highlighted in another publication, the annual AACR Cancer Progress Report 2020.
U.S. cancer deaths declined by 29% between 1991 and 2017, translating to nearly 3 million cancer deaths avoided, the report notes. In addition, 5-year survival rates for all cancers combined increased from 49% in the mid-1970s to 70% for patients diagnosed from 2010-2016.
Between August 2019 and July 31 of this year, the U.S. Food and Drug Administration approved 20 new anticancer drugs for various cancer types and 15 new indications for previously approved cancer drugs, marking the highest number of approvals in one 12-month period since AACR started producing these reports 10 years ago.
A continuing reduction in the cigarette smoking rate among US adults, which is now below 14%, is contributing greatly to declines in lung cancer rates, which have largely driven the improvements in cancer survival, the AACR noted.
This report also notes that progress has been made toward reducing cancer disparities. Overall disparities in cancer death rates among racial and ethnic groups are less pronounced now than they have been in the past two decades. For example, the overall cancer death rate for African American patients was 33% higher than for White patients in 1990 but just 14% higher in 2016.
However, both reports agree that more must be done to reduce cancer disparities even further.
They highlight initiatives that are underway, including:
- The draft guidance issued by the FDA to promote diversification of clinical trial populations.
- The National Institutes of Health’s (NIH’s) Continuing Umbrella of Research Experiences (CURE) program supporting underrepresented students and scientists along their academic and research career pathway.
- The Centers for Disease Control and Prevention’s Racial and Ethnic Approaches to Community Health (REACH) program, a grant-making program focused on encouraging preventive behaviors in underserved communities.
- The NIH’s All of Us program, which is gathering information from the genomes of 1 million healthy individuals with a focus on recruitment from historically underrepresented populations.
Ribas also announced that AACR has established a task force to focus on racial inequalities in cancer research.
Eliminating disparities would save money, argued John D. Carpten, PhD, from the University of Southern California, Los Angeles, who chaired the steering committee that developed the AACR Cancer Disparities Progress Report.
Carpten noted research showing that eliminating disparities for racial and ethnic minorities between 2003 and 2006 would have reduced health care costs by more than $1 trillion in the United States. This underscores the potentially far-reaching impact of efforts to eliminate disparities, he said.
“Without a doubt, socioeconomics and inequities in access to quality care represent major factors influencing cancer health disparities, and these disparities will persist until we address these issues” he said.
Both progress reports culminate in a call to action, largely focused on the need for “unwavering, bipartisan support from Congress, in the form of robust and sustained annual increases in funding for the NIH, NCI [National Cancer Institute], and FDA,” which is vital for accelerating the pace of progress.
The challenge is now compounded by the ongoing COVID-19 pandemic: Both progress reports note that racial and ethnic minorities, including African Americans, are not only affected disproportionately by cancer, but also by COVID-19, further highlighting the “stark inequities in health care.”
Ribas further called for action from national leadership and the scientific community.
“During this unprecedented time in our nation’s history, there is also a need for our nation’s leaders to take on a much bigger role in confronting and combating the structural and systemic racism that contributes to health disparities,” he said. The “pervasive racism and social injustices” that have contributed to disparities in both COVID-19 and cancer underscore the need for “the scientific community to step up and partner with Congress to assess and address this issue within the research community.”
This article first appeared on Medscape.com.
FDA adds polyarticular-course JIA to approved indications for tofacitinib
The Food and Drug Administration has (pJIA).
The approval, announced Sept. 28 by tofacitinib’s manufacturer, Pfizer, marks the first JAK inhibitor to be approved for the condition in the United States and is the fourth indication to be approved for the drug after approvals in adult patients with moderate to severe rheumatoid arthritis following methotrexate failure, active psoriatic arthritis after disease-modifying antirheumatic drug failure, and moderate to severe ulcerative colitis after failure on a tumor necrosis factor inhibitor.
The agency based its approval on a phase 3, multinational, randomized, double-blind, controlled withdrawal study that had an 18-week, open-label, run-in phase involving 225 patients who twice daily took either a 5-mg tablet or, in patients under 40 kg, a weight-based lower dose in the form of a 1 mg/mL oral solution, according to the company press release. A total of 173 patients from this phase met JIA American College of Rheumatology 30 response criteria, defined as 30% or greater improvement in three of six JIA core set variables and worsening in no more than one of the core set variables; they were then randomized in part 2 of the study to continue the same dose of tofacitinib or receive placebo until 44 weeks. By the end of this period, 31% who received tofacitinib had a disease flare, compared with 55% on placebo (P = .0007). Disease flare was defined as a 30% or greater worsening in at least three of the six variables of the JIA core set, with no more than one of the remaining JIA core response variables improving by 30% or more after randomization.
The types of adverse drug reactions in patients with pJIA were consistent with those seen in adult rheumatoid arthritis patients, according to Pfizer. Serious adverse drug reactions have most commonly been serious infections that may lead to hospitalization or death, and most patients who developed these infections were taking concomitant immunosuppressants, such as methotrexate or corticosteroids. Common adverse drug reactions reported in 2% or more of patients during the first 3 months in controlled clinical trials in patients with rheumatoid arthritis taking tofacitinib at 5 mg twice daily were upper respiratory tract infection, nasopharyngitis, diarrhea, headache, and hypertension.
While the 5-mg tablet formulation is already available, Pfizer said it expects the oral solution to be available by the end of the first quarter in 2021.
Prescribing information can be found on the FDA website.
The Food and Drug Administration has (pJIA).
The approval, announced Sept. 28 by tofacitinib’s manufacturer, Pfizer, marks the first JAK inhibitor to be approved for the condition in the United States and is the fourth indication to be approved for the drug after approvals in adult patients with moderate to severe rheumatoid arthritis following methotrexate failure, active psoriatic arthritis after disease-modifying antirheumatic drug failure, and moderate to severe ulcerative colitis after failure on a tumor necrosis factor inhibitor.
The agency based its approval on a phase 3, multinational, randomized, double-blind, controlled withdrawal study that had an 18-week, open-label, run-in phase involving 225 patients who twice daily took either a 5-mg tablet or, in patients under 40 kg, a weight-based lower dose in the form of a 1 mg/mL oral solution, according to the company press release. A total of 173 patients from this phase met JIA American College of Rheumatology 30 response criteria, defined as 30% or greater improvement in three of six JIA core set variables and worsening in no more than one of the core set variables; they were then randomized in part 2 of the study to continue the same dose of tofacitinib or receive placebo until 44 weeks. By the end of this period, 31% who received tofacitinib had a disease flare, compared with 55% on placebo (P = .0007). Disease flare was defined as a 30% or greater worsening in at least three of the six variables of the JIA core set, with no more than one of the remaining JIA core response variables improving by 30% or more after randomization.
The types of adverse drug reactions in patients with pJIA were consistent with those seen in adult rheumatoid arthritis patients, according to Pfizer. Serious adverse drug reactions have most commonly been serious infections that may lead to hospitalization or death, and most patients who developed these infections were taking concomitant immunosuppressants, such as methotrexate or corticosteroids. Common adverse drug reactions reported in 2% or more of patients during the first 3 months in controlled clinical trials in patients with rheumatoid arthritis taking tofacitinib at 5 mg twice daily were upper respiratory tract infection, nasopharyngitis, diarrhea, headache, and hypertension.
While the 5-mg tablet formulation is already available, Pfizer said it expects the oral solution to be available by the end of the first quarter in 2021.
Prescribing information can be found on the FDA website.
The Food and Drug Administration has (pJIA).
The approval, announced Sept. 28 by tofacitinib’s manufacturer, Pfizer, marks the first JAK inhibitor to be approved for the condition in the United States and is the fourth indication to be approved for the drug after approvals in adult patients with moderate to severe rheumatoid arthritis following methotrexate failure, active psoriatic arthritis after disease-modifying antirheumatic drug failure, and moderate to severe ulcerative colitis after failure on a tumor necrosis factor inhibitor.
The agency based its approval on a phase 3, multinational, randomized, double-blind, controlled withdrawal study that had an 18-week, open-label, run-in phase involving 225 patients who twice daily took either a 5-mg tablet or, in patients under 40 kg, a weight-based lower dose in the form of a 1 mg/mL oral solution, according to the company press release. A total of 173 patients from this phase met JIA American College of Rheumatology 30 response criteria, defined as 30% or greater improvement in three of six JIA core set variables and worsening in no more than one of the core set variables; they were then randomized in part 2 of the study to continue the same dose of tofacitinib or receive placebo until 44 weeks. By the end of this period, 31% who received tofacitinib had a disease flare, compared with 55% on placebo (P = .0007). Disease flare was defined as a 30% or greater worsening in at least three of the six variables of the JIA core set, with no more than one of the remaining JIA core response variables improving by 30% or more after randomization.
The types of adverse drug reactions in patients with pJIA were consistent with those seen in adult rheumatoid arthritis patients, according to Pfizer. Serious adverse drug reactions have most commonly been serious infections that may lead to hospitalization or death, and most patients who developed these infections were taking concomitant immunosuppressants, such as methotrexate or corticosteroids. Common adverse drug reactions reported in 2% or more of patients during the first 3 months in controlled clinical trials in patients with rheumatoid arthritis taking tofacitinib at 5 mg twice daily were upper respiratory tract infection, nasopharyngitis, diarrhea, headache, and hypertension.
While the 5-mg tablet formulation is already available, Pfizer said it expects the oral solution to be available by the end of the first quarter in 2021.
Prescribing information can be found on the FDA website.
Children’s share of new COVID-19 cases is on the rise
The cumulative percentage of COVID-19 cases reported in children continues to climb, but “the history behind that cumulative number shows substantial change,” according to a new analysis of state health department data.
As of Sept. 10, the 549,432 cases in children represented 10.0% of all reported COVID-19 cases in the United States following a substantial rise over the course of the pandemic – the figure was 7.7% on July 16 and 3.2% on May 7, Blake Sisk, PhD, of the American Academy of Pediatrics and associates reported Sept. 29 in Pediatrics.
Unlike the cumulative number, the weekly proportion of cases in children fell early in the summer but then started climbing again in late July. Dr. Sisk and associates wrote.
Despite the increase, however, the proportion of pediatric COVID-19 cases is still well below children’s share of the overall population (22.6%). Also, “it is unclear how much of the increase in child cases is due to increased testing capacity, although CDC data from public and commercial laboratories show the share of all tests administered to children ages 0-17 has remained stable at 5%-7% since late April,” they said.
Data for the current report were drawn from 49 state health department websites (New York state does not report ages for COVID-19 cases), along with New York City, the District of Columbia, Puerto Rico, and Guam. Alabama changed its definition of a child case in August and was not included in the trend analysis (see graph), the investigators explained.
Those data show “substantial variation in case growth by region: in April, a preponderance of cases was in the Northeast. In June, cases surged in the South and West, followed by mid-July increases in the Midwest,” Dr. Sisk and associates said.
The increase among children in Midwest states is ongoing with the number of new cases reaching its highest level yet during the week ending Sept. 10, they reported.
SOURCE: Sisk B et al. Pediatrics. 2020 Sep 29. doi: 10.1542/peds.2020-027425.
The cumulative percentage of COVID-19 cases reported in children continues to climb, but “the history behind that cumulative number shows substantial change,” according to a new analysis of state health department data.
As of Sept. 10, the 549,432 cases in children represented 10.0% of all reported COVID-19 cases in the United States following a substantial rise over the course of the pandemic – the figure was 7.7% on July 16 and 3.2% on May 7, Blake Sisk, PhD, of the American Academy of Pediatrics and associates reported Sept. 29 in Pediatrics.
Unlike the cumulative number, the weekly proportion of cases in children fell early in the summer but then started climbing again in late July. Dr. Sisk and associates wrote.
Despite the increase, however, the proportion of pediatric COVID-19 cases is still well below children’s share of the overall population (22.6%). Also, “it is unclear how much of the increase in child cases is due to increased testing capacity, although CDC data from public and commercial laboratories show the share of all tests administered to children ages 0-17 has remained stable at 5%-7% since late April,” they said.
Data for the current report were drawn from 49 state health department websites (New York state does not report ages for COVID-19 cases), along with New York City, the District of Columbia, Puerto Rico, and Guam. Alabama changed its definition of a child case in August and was not included in the trend analysis (see graph), the investigators explained.
Those data show “substantial variation in case growth by region: in April, a preponderance of cases was in the Northeast. In June, cases surged in the South and West, followed by mid-July increases in the Midwest,” Dr. Sisk and associates said.
The increase among children in Midwest states is ongoing with the number of new cases reaching its highest level yet during the week ending Sept. 10, they reported.
SOURCE: Sisk B et al. Pediatrics. 2020 Sep 29. doi: 10.1542/peds.2020-027425.
The cumulative percentage of COVID-19 cases reported in children continues to climb, but “the history behind that cumulative number shows substantial change,” according to a new analysis of state health department data.
As of Sept. 10, the 549,432 cases in children represented 10.0% of all reported COVID-19 cases in the United States following a substantial rise over the course of the pandemic – the figure was 7.7% on July 16 and 3.2% on May 7, Blake Sisk, PhD, of the American Academy of Pediatrics and associates reported Sept. 29 in Pediatrics.
Unlike the cumulative number, the weekly proportion of cases in children fell early in the summer but then started climbing again in late July. Dr. Sisk and associates wrote.
Despite the increase, however, the proportion of pediatric COVID-19 cases is still well below children’s share of the overall population (22.6%). Also, “it is unclear how much of the increase in child cases is due to increased testing capacity, although CDC data from public and commercial laboratories show the share of all tests administered to children ages 0-17 has remained stable at 5%-7% since late April,” they said.
Data for the current report were drawn from 49 state health department websites (New York state does not report ages for COVID-19 cases), along with New York City, the District of Columbia, Puerto Rico, and Guam. Alabama changed its definition of a child case in August and was not included in the trend analysis (see graph), the investigators explained.
Those data show “substantial variation in case growth by region: in April, a preponderance of cases was in the Northeast. In June, cases surged in the South and West, followed by mid-July increases in the Midwest,” Dr. Sisk and associates said.
The increase among children in Midwest states is ongoing with the number of new cases reaching its highest level yet during the week ending Sept. 10, they reported.
SOURCE: Sisk B et al. Pediatrics. 2020 Sep 29. doi: 10.1542/peds.2020-027425.
FROM PEDIATRICS
Congenital Defect of the Toenail
The Diagnosis: Onychodystrophy Secondary to Polydactyly
Radiographs of the feet demonstrated an accessory distal phalanx of the left great toe with a similar smaller accessory distal phalanx on the right great toe (Figure). The patient was referred to orthopedic surgery, and surgical intervention was recommended for only the left great toe given recurrent skin inflammation and nail complications. An excision of the left great toe polydactyly was performed. The patient healed well without complications.
Many clinically heterogeneous phenotypes exist for polydactyly and syndactyly, which both are common entities with incidences of 1 in 700 to 1000 births and 1 in 2000 to 3000 births, respectively.1 Both polydactyly and syndactyly can be an isolated variant in newborns or present with multiple concurrent malformations as part of a genetic syndrome, with more than 300 syndromic anomalies described. The genetic basis of these conditions is equally diverse, with homeobox genes, hedgehog pathways, fibroblast growth factors, and boneand cartilage-derived morphogenetic proteins implicated in their development.1
The differential diagnosis for our patient included congenital malalignment of the great toenails, nail-patella syndrome, onychodystrophy secondary to polydactyly, and congenital hypertrophy of the lateral nail fold. Given the strong family history, polydactyly was suspected.
Congenital malalignment of the great toenails results in lateral deviation of the nail plates.2 It is an underdiagnosed condition with different etiologies hypothesized, such as genetic factors with possible autosomal-dominant transmission and extrinsic factors.3 One proposed mechanism of pathogenesis is desynchronization during growth of the nail and distal phalanx of the hallux, leading to larger nail plates that grow laterally.4 Typical features associated with this disease are nail discoloration, nail plate thickening, and transversal grooves or ridges, none of which were seen in our patient.2
Children with nail-patella syndrome have dysplastic nails and associated bony abnormalities, such as absent patellae.5 This syndrome results from an autosomaldominant mutation in the LIM homeobox transcription factor 1-beta gene, LMX1B, which is responsible for dorsal-ventral patterning of the limb, as well as patterning of the nails, patellae and long bones, and even the kidney tubule.6 As such, patients with nail-patella syndrome have associated renal abnormalities. The findings in our patient were limited to the feet, making an underlying syndrome unlikely to be the cause.
First described in 1968 by Meadow,7 fetal hydantoin syndrome is a well-documented sequela in women taking phenytoin throughout pregnancy. Multiple malformations are possible, including cardiac defects, cleft lip/palate, digit and nail hypoplasia, abnormal facial features, mental disability, and growth abnormalities.8 The teratogenicity behind phenytoin results from reactive oxygen species that alter embryonic DNA, proteins, and lipids.9 The mother of this child was not on any seizure prophylaxis, eliminating it from the differential.
Congenital hypertrophy of the lateral nail fold is a defect of the soft tissue of the hallux leading to hypertrophy of the nail fold, commonly presenting with inflammation and pain10 possibly due to dyssynchronous growth between the soft tissue and nail plate.11 With this defect, a lip covering the nail plate is common, which was not seen in our patient.
As demonstrated in our patient, family history can help guide the diagnosis. Seven of 9 nonsyndromic forms of syndactyly are inherited in an autosomal-dominant fashion and range from mild presentations, as in our patient, to more severe deformations with underlying bone fusion and functional impairment.12 Polydactyly also often is expressed in an autosomal-dominant pattern, with up to 30% of patients having a positive family history. Polydactyly traditionally is classified by the location of the supernumerary digit as preaxial (radial), central, or postaxial (ulnar), and many further morphologic variations exist within these groups. Overall, preaxial polydactyly is relatively rare and represents 15% of polydactylies, with central and postaxial comprising the other 6% and 79%, respectively.13 Delineation of the underlying anatomy may reveal ray duplications (digit and corresponding metacarpal or metatarsal bone), metatarsal variants, and duplicated phalanges that may be hypoplastic or deformed. Patients may report difficulty finding comfortable footwear, cosmetic concerns, and nail-related complications. Although not always required, surgical intervention may provide definitive treatment but can leave residual deformities in the surrounding altered anatomy; thus, orthopedic or plastic surgery consultations are critical in appropriately counseling patients.
- Ahmed H, Akbari H, Emanmi A, et al. Genetic overview of syndactyly and polydactyly. Plast Reconstr Surg Glob Open. 2017;5:e1549.
- Catalfo P, Musumeci ML, Lacarrubba F, et al. Congenital malalignment of the great toenails: a review. Skin Appendage Disord. 2018;4:230-235.
- Kus S, Tahmaz E, Gurunluoglu R, et al. Congenital malalignment of the great toenails in dizygotic twins. Pediatr Dermatol. 2005;22:434-435.
- Chaniotakis I, Bonitsis N, Stergiopoulou C, et al. Dizygotic twins with congenital malalignment of the great toenails: reappraisal of the pathogenesis. J Am Acad Dermatol. 2007;57:711-715.
- Witzgall R. Nail-patella syndrome. Pflugers Arch. 2017;469:927-936.
- Dreyer SD, Zhou G, Baldini A, et al, Mutations in LMX1B cause abnormal skeletal patterning and renal dysplasia in nail patella syndrome. Nat Genet. 1998;19:47-50.
- Meadow SR. Anticonvulsant drugs and congenital abnormalities. Lancet. 1968;2:1296.
- Scheinfeld N. Phenytoin in cutaneous medicine: its uses, mechanisms and side effects. Dermatol Online J. 2003;9:6.
- Winn LM, Wells PG. Phenytoin-initiated DNA oxidation in murine embryo culture, and embryo protection by the antioxidative enzymes superoxide dismutase and catalase: evidence for reactive oxygen species-mediated DNA oxidation in the molecular mechanism of phenytoin teratogenicity. Mol Pharmacol. 1995;48:112-120.
- Piraccini BM, Parente GL, Varotti E, et al. Congenital hypertrophy of the lateral nail folds of the hallux: clinical features and follow-up of seven cases. Pediatr Dermatol. 2000;17:348-351.
- Martinet C, Pascal M, Civatte J, et al. Lateral nail-pad of the big toe in infants. apropos of 2 cases. Ann Dermatol Venereol. 1984;111:731-732.
- Malik S. Syndactyly: phenotypes, genetics and current classification. Eur J Hum Genet. 2012;20:817-824.
- Belthur MV, Linton JL, Barnes DA. The spectrum of preaxial polydactyly of the foot. J Pediatr Orthop. 2011;31:435-447.
The Diagnosis: Onychodystrophy Secondary to Polydactyly
Radiographs of the feet demonstrated an accessory distal phalanx of the left great toe with a similar smaller accessory distal phalanx on the right great toe (Figure). The patient was referred to orthopedic surgery, and surgical intervention was recommended for only the left great toe given recurrent skin inflammation and nail complications. An excision of the left great toe polydactyly was performed. The patient healed well without complications.
Many clinically heterogeneous phenotypes exist for polydactyly and syndactyly, which both are common entities with incidences of 1 in 700 to 1000 births and 1 in 2000 to 3000 births, respectively.1 Both polydactyly and syndactyly can be an isolated variant in newborns or present with multiple concurrent malformations as part of a genetic syndrome, with more than 300 syndromic anomalies described. The genetic basis of these conditions is equally diverse, with homeobox genes, hedgehog pathways, fibroblast growth factors, and boneand cartilage-derived morphogenetic proteins implicated in their development.1
The differential diagnosis for our patient included congenital malalignment of the great toenails, nail-patella syndrome, onychodystrophy secondary to polydactyly, and congenital hypertrophy of the lateral nail fold. Given the strong family history, polydactyly was suspected.
Congenital malalignment of the great toenails results in lateral deviation of the nail plates.2 It is an underdiagnosed condition with different etiologies hypothesized, such as genetic factors with possible autosomal-dominant transmission and extrinsic factors.3 One proposed mechanism of pathogenesis is desynchronization during growth of the nail and distal phalanx of the hallux, leading to larger nail plates that grow laterally.4 Typical features associated with this disease are nail discoloration, nail plate thickening, and transversal grooves or ridges, none of which were seen in our patient.2
Children with nail-patella syndrome have dysplastic nails and associated bony abnormalities, such as absent patellae.5 This syndrome results from an autosomaldominant mutation in the LIM homeobox transcription factor 1-beta gene, LMX1B, which is responsible for dorsal-ventral patterning of the limb, as well as patterning of the nails, patellae and long bones, and even the kidney tubule.6 As such, patients with nail-patella syndrome have associated renal abnormalities. The findings in our patient were limited to the feet, making an underlying syndrome unlikely to be the cause.
First described in 1968 by Meadow,7 fetal hydantoin syndrome is a well-documented sequela in women taking phenytoin throughout pregnancy. Multiple malformations are possible, including cardiac defects, cleft lip/palate, digit and nail hypoplasia, abnormal facial features, mental disability, and growth abnormalities.8 The teratogenicity behind phenytoin results from reactive oxygen species that alter embryonic DNA, proteins, and lipids.9 The mother of this child was not on any seizure prophylaxis, eliminating it from the differential.
Congenital hypertrophy of the lateral nail fold is a defect of the soft tissue of the hallux leading to hypertrophy of the nail fold, commonly presenting with inflammation and pain10 possibly due to dyssynchronous growth between the soft tissue and nail plate.11 With this defect, a lip covering the nail plate is common, which was not seen in our patient.
As demonstrated in our patient, family history can help guide the diagnosis. Seven of 9 nonsyndromic forms of syndactyly are inherited in an autosomal-dominant fashion and range from mild presentations, as in our patient, to more severe deformations with underlying bone fusion and functional impairment.12 Polydactyly also often is expressed in an autosomal-dominant pattern, with up to 30% of patients having a positive family history. Polydactyly traditionally is classified by the location of the supernumerary digit as preaxial (radial), central, or postaxial (ulnar), and many further morphologic variations exist within these groups. Overall, preaxial polydactyly is relatively rare and represents 15% of polydactylies, with central and postaxial comprising the other 6% and 79%, respectively.13 Delineation of the underlying anatomy may reveal ray duplications (digit and corresponding metacarpal or metatarsal bone), metatarsal variants, and duplicated phalanges that may be hypoplastic or deformed. Patients may report difficulty finding comfortable footwear, cosmetic concerns, and nail-related complications. Although not always required, surgical intervention may provide definitive treatment but can leave residual deformities in the surrounding altered anatomy; thus, orthopedic or plastic surgery consultations are critical in appropriately counseling patients.
The Diagnosis: Onychodystrophy Secondary to Polydactyly
Radiographs of the feet demonstrated an accessory distal phalanx of the left great toe with a similar smaller accessory distal phalanx on the right great toe (Figure). The patient was referred to orthopedic surgery, and surgical intervention was recommended for only the left great toe given recurrent skin inflammation and nail complications. An excision of the left great toe polydactyly was performed. The patient healed well without complications.
Many clinically heterogeneous phenotypes exist for polydactyly and syndactyly, which both are common entities with incidences of 1 in 700 to 1000 births and 1 in 2000 to 3000 births, respectively.1 Both polydactyly and syndactyly can be an isolated variant in newborns or present with multiple concurrent malformations as part of a genetic syndrome, with more than 300 syndromic anomalies described. The genetic basis of these conditions is equally diverse, with homeobox genes, hedgehog pathways, fibroblast growth factors, and boneand cartilage-derived morphogenetic proteins implicated in their development.1
The differential diagnosis for our patient included congenital malalignment of the great toenails, nail-patella syndrome, onychodystrophy secondary to polydactyly, and congenital hypertrophy of the lateral nail fold. Given the strong family history, polydactyly was suspected.
Congenital malalignment of the great toenails results in lateral deviation of the nail plates.2 It is an underdiagnosed condition with different etiologies hypothesized, such as genetic factors with possible autosomal-dominant transmission and extrinsic factors.3 One proposed mechanism of pathogenesis is desynchronization during growth of the nail and distal phalanx of the hallux, leading to larger nail plates that grow laterally.4 Typical features associated with this disease are nail discoloration, nail plate thickening, and transversal grooves or ridges, none of which were seen in our patient.2
Children with nail-patella syndrome have dysplastic nails and associated bony abnormalities, such as absent patellae.5 This syndrome results from an autosomaldominant mutation in the LIM homeobox transcription factor 1-beta gene, LMX1B, which is responsible for dorsal-ventral patterning of the limb, as well as patterning of the nails, patellae and long bones, and even the kidney tubule.6 As such, patients with nail-patella syndrome have associated renal abnormalities. The findings in our patient were limited to the feet, making an underlying syndrome unlikely to be the cause.
First described in 1968 by Meadow,7 fetal hydantoin syndrome is a well-documented sequela in women taking phenytoin throughout pregnancy. Multiple malformations are possible, including cardiac defects, cleft lip/palate, digit and nail hypoplasia, abnormal facial features, mental disability, and growth abnormalities.8 The teratogenicity behind phenytoin results from reactive oxygen species that alter embryonic DNA, proteins, and lipids.9 The mother of this child was not on any seizure prophylaxis, eliminating it from the differential.
Congenital hypertrophy of the lateral nail fold is a defect of the soft tissue of the hallux leading to hypertrophy of the nail fold, commonly presenting with inflammation and pain10 possibly due to dyssynchronous growth between the soft tissue and nail plate.11 With this defect, a lip covering the nail plate is common, which was not seen in our patient.
As demonstrated in our patient, family history can help guide the diagnosis. Seven of 9 nonsyndromic forms of syndactyly are inherited in an autosomal-dominant fashion and range from mild presentations, as in our patient, to more severe deformations with underlying bone fusion and functional impairment.12 Polydactyly also often is expressed in an autosomal-dominant pattern, with up to 30% of patients having a positive family history. Polydactyly traditionally is classified by the location of the supernumerary digit as preaxial (radial), central, or postaxial (ulnar), and many further morphologic variations exist within these groups. Overall, preaxial polydactyly is relatively rare and represents 15% of polydactylies, with central and postaxial comprising the other 6% and 79%, respectively.13 Delineation of the underlying anatomy may reveal ray duplications (digit and corresponding metacarpal or metatarsal bone), metatarsal variants, and duplicated phalanges that may be hypoplastic or deformed. Patients may report difficulty finding comfortable footwear, cosmetic concerns, and nail-related complications. Although not always required, surgical intervention may provide definitive treatment but can leave residual deformities in the surrounding altered anatomy; thus, orthopedic or plastic surgery consultations are critical in appropriately counseling patients.
- Ahmed H, Akbari H, Emanmi A, et al. Genetic overview of syndactyly and polydactyly. Plast Reconstr Surg Glob Open. 2017;5:e1549.
- Catalfo P, Musumeci ML, Lacarrubba F, et al. Congenital malalignment of the great toenails: a review. Skin Appendage Disord. 2018;4:230-235.
- Kus S, Tahmaz E, Gurunluoglu R, et al. Congenital malalignment of the great toenails in dizygotic twins. Pediatr Dermatol. 2005;22:434-435.
- Chaniotakis I, Bonitsis N, Stergiopoulou C, et al. Dizygotic twins with congenital malalignment of the great toenails: reappraisal of the pathogenesis. J Am Acad Dermatol. 2007;57:711-715.
- Witzgall R. Nail-patella syndrome. Pflugers Arch. 2017;469:927-936.
- Dreyer SD, Zhou G, Baldini A, et al, Mutations in LMX1B cause abnormal skeletal patterning and renal dysplasia in nail patella syndrome. Nat Genet. 1998;19:47-50.
- Meadow SR. Anticonvulsant drugs and congenital abnormalities. Lancet. 1968;2:1296.
- Scheinfeld N. Phenytoin in cutaneous medicine: its uses, mechanisms and side effects. Dermatol Online J. 2003;9:6.
- Winn LM, Wells PG. Phenytoin-initiated DNA oxidation in murine embryo culture, and embryo protection by the antioxidative enzymes superoxide dismutase and catalase: evidence for reactive oxygen species-mediated DNA oxidation in the molecular mechanism of phenytoin teratogenicity. Mol Pharmacol. 1995;48:112-120.
- Piraccini BM, Parente GL, Varotti E, et al. Congenital hypertrophy of the lateral nail folds of the hallux: clinical features and follow-up of seven cases. Pediatr Dermatol. 2000;17:348-351.
- Martinet C, Pascal M, Civatte J, et al. Lateral nail-pad of the big toe in infants. apropos of 2 cases. Ann Dermatol Venereol. 1984;111:731-732.
- Malik S. Syndactyly: phenotypes, genetics and current classification. Eur J Hum Genet. 2012;20:817-824.
- Belthur MV, Linton JL, Barnes DA. The spectrum of preaxial polydactyly of the foot. J Pediatr Orthop. 2011;31:435-447.
- Ahmed H, Akbari H, Emanmi A, et al. Genetic overview of syndactyly and polydactyly. Plast Reconstr Surg Glob Open. 2017;5:e1549.
- Catalfo P, Musumeci ML, Lacarrubba F, et al. Congenital malalignment of the great toenails: a review. Skin Appendage Disord. 2018;4:230-235.
- Kus S, Tahmaz E, Gurunluoglu R, et al. Congenital malalignment of the great toenails in dizygotic twins. Pediatr Dermatol. 2005;22:434-435.
- Chaniotakis I, Bonitsis N, Stergiopoulou C, et al. Dizygotic twins with congenital malalignment of the great toenails: reappraisal of the pathogenesis. J Am Acad Dermatol. 2007;57:711-715.
- Witzgall R. Nail-patella syndrome. Pflugers Arch. 2017;469:927-936.
- Dreyer SD, Zhou G, Baldini A, et al, Mutations in LMX1B cause abnormal skeletal patterning and renal dysplasia in nail patella syndrome. Nat Genet. 1998;19:47-50.
- Meadow SR. Anticonvulsant drugs and congenital abnormalities. Lancet. 1968;2:1296.
- Scheinfeld N. Phenytoin in cutaneous medicine: its uses, mechanisms and side effects. Dermatol Online J. 2003;9:6.
- Winn LM, Wells PG. Phenytoin-initiated DNA oxidation in murine embryo culture, and embryo protection by the antioxidative enzymes superoxide dismutase and catalase: evidence for reactive oxygen species-mediated DNA oxidation in the molecular mechanism of phenytoin teratogenicity. Mol Pharmacol. 1995;48:112-120.
- Piraccini BM, Parente GL, Varotti E, et al. Congenital hypertrophy of the lateral nail folds of the hallux: clinical features and follow-up of seven cases. Pediatr Dermatol. 2000;17:348-351.
- Martinet C, Pascal M, Civatte J, et al. Lateral nail-pad of the big toe in infants. apropos of 2 cases. Ann Dermatol Venereol. 1984;111:731-732.
- Malik S. Syndactyly: phenotypes, genetics and current classification. Eur J Hum Genet. 2012;20:817-824.
- Belthur MV, Linton JL, Barnes DA. The spectrum of preaxial polydactyly of the foot. J Pediatr Orthop. 2011;31:435-447.
An 18-month-old girl presented for evaluation of nail dystrophy. The patient’s parents stated that the left great toenail had been dystrophic since birth, leading to skin irritation and “snagging” of the toenail on socks and footwear. Additional history revealed that the patient also had webbed toes, and there was a paternal family history of polydactyly and syndactyly. Physical examination revealed webbing of the second and third toes to the distal interphalangeal joints on both feet, marked nail plate dystrophy on the left big toe, and an irregularly shaped nail plate on the right big toe. The patient had no similar findings on the hands.
My opus was myopic
I had been in practice only 6 or 7 years when I got the itch to do some writing. I had been exchanging letters with my father since I left for college. He was a professional writer but I had never done more than was required to get through school. What motivated me to sit down at the keyboard of his old hand-me-down portable typewriter was my frustration with grandmothers, as nearly every day I found myself struggling to counter some grandmother’s well-intentioned but somewhat off-the-mark childrearing advice.
Occasionally this would be during a face-to-face encounter with a grandmother who had tagged along to the well-baby visit. More often, I was trying to arm a mother or father with the “facts” (at least as I understood them) that they could carry home and use to defend my position as the child care expert for the family.
These were not knock-down-drag-out disagreements but I always felt badly that I might be tarnishing a grandmother’s reputation. Grandfathers seemed to have learned it was best to keep silent on childrearing. I knew from my own family that most grandmothers had years of experience raising children that, if properly delivered, could make childrearing a more positive experience for new parents. My father, whose mother was widowed when he was an infant, was raised by his grandmother. However, too often I found that grandmotherly advice came packaged with just enough old wives’ tales and factually incorrect medical information to be dangerous.
The title of my opus would be “The Good Grandmother Handbook” and it would be an effort to update grandmothers with the latest information on childrearing from a recently trained and cocky board-certified pediatrician with only 6 years’ practice under his belt. The book would reassure grandmothers that, although some of the things they had done as parents are now frowned upon, most of what they did has stood the test of time and probably is worth sharing.
The final chapter of the book would be about grandparent etiquette. How to deal with the fact that there is another set of grandparents who have opinions and would like to have time with their grandchildren. When and how to give advice: Basically, only if asked or you feel your grandchild’s life is at stake. And, finally, how to deal with the disappointment of not being asked for advice and not being involved.
Not surprisingly that sophomoric and condescending effort never got further than the first draft. It reflected my early experiences in a minimally diverse and relatively affluent community. As my world view broadened, I realized that for many families it’s not a question of how to deal with a grandmother’s unsolicited advice. There are numerous grandparents who have been forced to become safe havens in which a family in distress can ride out the turbulent economic times and societal upheaval.
A Pediatrics article estimates that 2% of children in this country are being raised by their grandparents. And, it turns out that grandparents are doing a surprisingly good job. The researchers concluded that: “Despite caring for children with greater developmental problems and poorer temperament grandparent caregivers seem to cope with parenting about as well as parents.”
As pediatricians we must continue to reach out to grandmothers and grandfathers who are caring for some of our most challenged patients. They need our medical advice but even more they need our compassion and emotional support. Over the last 5 decades I’ve come to learn that, although there are some grandmothers who can be meddlesome dispensers of old wives’ tales, many are the backbone of families in need.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
I had been in practice only 6 or 7 years when I got the itch to do some writing. I had been exchanging letters with my father since I left for college. He was a professional writer but I had never done more than was required to get through school. What motivated me to sit down at the keyboard of his old hand-me-down portable typewriter was my frustration with grandmothers, as nearly every day I found myself struggling to counter some grandmother’s well-intentioned but somewhat off-the-mark childrearing advice.
Occasionally this would be during a face-to-face encounter with a grandmother who had tagged along to the well-baby visit. More often, I was trying to arm a mother or father with the “facts” (at least as I understood them) that they could carry home and use to defend my position as the child care expert for the family.
These were not knock-down-drag-out disagreements but I always felt badly that I might be tarnishing a grandmother’s reputation. Grandfathers seemed to have learned it was best to keep silent on childrearing. I knew from my own family that most grandmothers had years of experience raising children that, if properly delivered, could make childrearing a more positive experience for new parents. My father, whose mother was widowed when he was an infant, was raised by his grandmother. However, too often I found that grandmotherly advice came packaged with just enough old wives’ tales and factually incorrect medical information to be dangerous.
The title of my opus would be “The Good Grandmother Handbook” and it would be an effort to update grandmothers with the latest information on childrearing from a recently trained and cocky board-certified pediatrician with only 6 years’ practice under his belt. The book would reassure grandmothers that, although some of the things they had done as parents are now frowned upon, most of what they did has stood the test of time and probably is worth sharing.
The final chapter of the book would be about grandparent etiquette. How to deal with the fact that there is another set of grandparents who have opinions and would like to have time with their grandchildren. When and how to give advice: Basically, only if asked or you feel your grandchild’s life is at stake. And, finally, how to deal with the disappointment of not being asked for advice and not being involved.
Not surprisingly that sophomoric and condescending effort never got further than the first draft. It reflected my early experiences in a minimally diverse and relatively affluent community. As my world view broadened, I realized that for many families it’s not a question of how to deal with a grandmother’s unsolicited advice. There are numerous grandparents who have been forced to become safe havens in which a family in distress can ride out the turbulent economic times and societal upheaval.
A Pediatrics article estimates that 2% of children in this country are being raised by their grandparents. And, it turns out that grandparents are doing a surprisingly good job. The researchers concluded that: “Despite caring for children with greater developmental problems and poorer temperament grandparent caregivers seem to cope with parenting about as well as parents.”
As pediatricians we must continue to reach out to grandmothers and grandfathers who are caring for some of our most challenged patients. They need our medical advice but even more they need our compassion and emotional support. Over the last 5 decades I’ve come to learn that, although there are some grandmothers who can be meddlesome dispensers of old wives’ tales, many are the backbone of families in need.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
I had been in practice only 6 or 7 years when I got the itch to do some writing. I had been exchanging letters with my father since I left for college. He was a professional writer but I had never done more than was required to get through school. What motivated me to sit down at the keyboard of his old hand-me-down portable typewriter was my frustration with grandmothers, as nearly every day I found myself struggling to counter some grandmother’s well-intentioned but somewhat off-the-mark childrearing advice.
Occasionally this would be during a face-to-face encounter with a grandmother who had tagged along to the well-baby visit. More often, I was trying to arm a mother or father with the “facts” (at least as I understood them) that they could carry home and use to defend my position as the child care expert for the family.
These were not knock-down-drag-out disagreements but I always felt badly that I might be tarnishing a grandmother’s reputation. Grandfathers seemed to have learned it was best to keep silent on childrearing. I knew from my own family that most grandmothers had years of experience raising children that, if properly delivered, could make childrearing a more positive experience for new parents. My father, whose mother was widowed when he was an infant, was raised by his grandmother. However, too often I found that grandmotherly advice came packaged with just enough old wives’ tales and factually incorrect medical information to be dangerous.
The title of my opus would be “The Good Grandmother Handbook” and it would be an effort to update grandmothers with the latest information on childrearing from a recently trained and cocky board-certified pediatrician with only 6 years’ practice under his belt. The book would reassure grandmothers that, although some of the things they had done as parents are now frowned upon, most of what they did has stood the test of time and probably is worth sharing.
The final chapter of the book would be about grandparent etiquette. How to deal with the fact that there is another set of grandparents who have opinions and would like to have time with their grandchildren. When and how to give advice: Basically, only if asked or you feel your grandchild’s life is at stake. And, finally, how to deal with the disappointment of not being asked for advice and not being involved.
Not surprisingly that sophomoric and condescending effort never got further than the first draft. It reflected my early experiences in a minimally diverse and relatively affluent community. As my world view broadened, I realized that for many families it’s not a question of how to deal with a grandmother’s unsolicited advice. There are numerous grandparents who have been forced to become safe havens in which a family in distress can ride out the turbulent economic times and societal upheaval.
A Pediatrics article estimates that 2% of children in this country are being raised by their grandparents. And, it turns out that grandparents are doing a surprisingly good job. The researchers concluded that: “Despite caring for children with greater developmental problems and poorer temperament grandparent caregivers seem to cope with parenting about as well as parents.”
As pediatricians we must continue to reach out to grandmothers and grandfathers who are caring for some of our most challenged patients. They need our medical advice but even more they need our compassion and emotional support. Over the last 5 decades I’ve come to learn that, although there are some grandmothers who can be meddlesome dispensers of old wives’ tales, many are the backbone of families in need.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
High schoolers send mixed signals on contraceptive use
according to data from the Youth Risk Behavior Survey (YRBS).
Nonuse of birth control in this population dropped to 11.9% in 2019, but the overall trend is one of no significant change since 2003. Meanwhile, the use of birth control pills has taken a different path, with prevalence rising significantly from 16.0% in 2007 to 23.0% in 2019, the Centers for Disease Control and Prevention reported.
The prevalence of condom use among sexually active students was 54.3% in 2019, up from 53.8% in 2017 – the survey is conducted every 2 years – but down from a high of 63.0% in 2003, the YRBS data show.
Condoms were the most prevalent method of contraception, but the finding that “only approximately half of sexually active students reported any condom use at last sexual intercourse … is concerning given the high risk for STDs among this population,” Leigh E. Szucs, PhD, and associates said in the Morbidity and Mortality Weekly Report.
In 2019, White (55.8%) and Hispanic (56.2%) students were more likely than Blacks (48.2%) to have used a condom during their last sexual intercourse, but use of birth control pills was much higher among Whites (29.1%) than Hispanics (15.4%) or Blacks (12.9%).The Black respondents were much more likely (23.0%) to use no contraceptive method, compared with Whites (8.4%) or Hispanics (13.3%), they said.
“Meeting the unintended pregnancy and STD/HIV prevention needs of black and Hispanic youths is vital,” wrote Dr. Szucs of the CDC’s National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention and associates. “Understanding and addressing structural barriers that might contribute to the observed differences are important next steps.”
The high school students taking the YRBS were considered sexually active if they had intercourse with at least one person in the previous 3 months. Overall, 3,226 (27.4%) of respondents in 2019 reported being sexually active: 52.2% were female and 47.8% were male, the CDC said.
SOURCE: Szucs LE et al. MMWR. 2019 Aug 21;69(SS-01)11-8.
according to data from the Youth Risk Behavior Survey (YRBS).
Nonuse of birth control in this population dropped to 11.9% in 2019, but the overall trend is one of no significant change since 2003. Meanwhile, the use of birth control pills has taken a different path, with prevalence rising significantly from 16.0% in 2007 to 23.0% in 2019, the Centers for Disease Control and Prevention reported.
The prevalence of condom use among sexually active students was 54.3% in 2019, up from 53.8% in 2017 – the survey is conducted every 2 years – but down from a high of 63.0% in 2003, the YRBS data show.
Condoms were the most prevalent method of contraception, but the finding that “only approximately half of sexually active students reported any condom use at last sexual intercourse … is concerning given the high risk for STDs among this population,” Leigh E. Szucs, PhD, and associates said in the Morbidity and Mortality Weekly Report.
In 2019, White (55.8%) and Hispanic (56.2%) students were more likely than Blacks (48.2%) to have used a condom during their last sexual intercourse, but use of birth control pills was much higher among Whites (29.1%) than Hispanics (15.4%) or Blacks (12.9%).The Black respondents were much more likely (23.0%) to use no contraceptive method, compared with Whites (8.4%) or Hispanics (13.3%), they said.
“Meeting the unintended pregnancy and STD/HIV prevention needs of black and Hispanic youths is vital,” wrote Dr. Szucs of the CDC’s National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention and associates. “Understanding and addressing structural barriers that might contribute to the observed differences are important next steps.”
The high school students taking the YRBS were considered sexually active if they had intercourse with at least one person in the previous 3 months. Overall, 3,226 (27.4%) of respondents in 2019 reported being sexually active: 52.2% were female and 47.8% were male, the CDC said.
SOURCE: Szucs LE et al. MMWR. 2019 Aug 21;69(SS-01)11-8.
according to data from the Youth Risk Behavior Survey (YRBS).
Nonuse of birth control in this population dropped to 11.9% in 2019, but the overall trend is one of no significant change since 2003. Meanwhile, the use of birth control pills has taken a different path, with prevalence rising significantly from 16.0% in 2007 to 23.0% in 2019, the Centers for Disease Control and Prevention reported.
The prevalence of condom use among sexually active students was 54.3% in 2019, up from 53.8% in 2017 – the survey is conducted every 2 years – but down from a high of 63.0% in 2003, the YRBS data show.
Condoms were the most prevalent method of contraception, but the finding that “only approximately half of sexually active students reported any condom use at last sexual intercourse … is concerning given the high risk for STDs among this population,” Leigh E. Szucs, PhD, and associates said in the Morbidity and Mortality Weekly Report.
In 2019, White (55.8%) and Hispanic (56.2%) students were more likely than Blacks (48.2%) to have used a condom during their last sexual intercourse, but use of birth control pills was much higher among Whites (29.1%) than Hispanics (15.4%) or Blacks (12.9%).The Black respondents were much more likely (23.0%) to use no contraceptive method, compared with Whites (8.4%) or Hispanics (13.3%), they said.
“Meeting the unintended pregnancy and STD/HIV prevention needs of black and Hispanic youths is vital,” wrote Dr. Szucs of the CDC’s National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention and associates. “Understanding and addressing structural barriers that might contribute to the observed differences are important next steps.”
The high school students taking the YRBS were considered sexually active if they had intercourse with at least one person in the previous 3 months. Overall, 3,226 (27.4%) of respondents in 2019 reported being sexually active: 52.2% were female and 47.8% were male, the CDC said.
SOURCE: Szucs LE et al. MMWR. 2019 Aug 21;69(SS-01)11-8.