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Challenges in outpatient psychiatry: When patients don’t pay
Editor’s note: This is the second in a series of articles by Dr. Miller about challenges in outpatient psychiatry.
Mr. A lived a life that seemed glamorous to me. There were lunches with professional athletes, swank social events, and designer everything from clothes to cars. It was a world that I was not familiar with, and while I knew my patient worried about money, it seemed he had it. When he started therapy with me, Mr. A came to every session with a check. At some point, I realized that I had missed a switch in his mood. Despite his therapeutic level of lithium, Mr. A had become manic, and the expression of this mania took the form of even more spending. What started as an exciting lifestyle suddenly became tens of thousands of dollars of debt. I felt guilty that I initially did not see this as pathology, and as a young psychiatrist, I sought consultation with an older and wiser mentor.
After discussing the case, the consulting psychiatrist said to me, “Make sure you get paid; these cases are difficult.” In fact, in the midst of the chaos, Mr. A had stopped bringing a check to the sessions. I sent monthly statements, and they went unpaid. He didn’t have the money for his living expenses and I let this go on without addressing it for much too long. Soon, Mr. A’s debt to me was just one more stress in his life and while I knew I would not pursue reimbursement through legal channels, I did encourage him to find a psychiatrist who was in his insurance network, something he did not want to do. I was too embarrassed to tell the consulting psychiatrist that Mr. A had already accrued well over a thousand dollars in unpaid professional fees. In my mind, I was offering pro bono care because the patient’s financial circumstances had changed, and because I felt guilty that I had not recognized this as mania sooner.
In a 2011 Shrink Rap blog post, Jesse Hellman, MD, a psychiatrist in private practice in Towson, Md., wrote about the meaning of payment in psychotherapy:
“Money is something loaded with meaning to most people. What does it mean that the patient forgets to pay? Does it mean ‘if you really cared about me you would not charge me’? Is it a reflection of anger for something that occurred in the last session? Is it a displacement of feelings from something else (‘my boss didn’t give me the raise I expected’)? Is it completely inadvertent (Freud famously said ‘Sometimes a cigar is only a cigar’)?”
There are so many possibilities, and the psychodynamic therapist wants to understand them. How the patient relates to the therapist is some part of how he relates to others. The patient hopefully starts to watch his own actions and attitudes and also tries to understand them. A nonjudgmental stance helps the patient do this.
The therapist himself needs to be comfortable dealing with the subject of money. Sometimes beginning physicians fluctuate between feeling they are too inexperienced to be paid and feeling that they deserve anything they ask. We physicians might even (unfortunately) take on the attitudes of the insurance companies themselves (“Identification with the Aggressor”).
The blog post was flooded with comments –120 in total, and more comments than any other single Shrink Rap post received for the blog’s 12-year run.
Steven Reidbord, MD, is a psychiatrist in private practice in San Francisco and also a blogger. Dr. Reidbord conversed with me through email about patients who don’t pay.
“In years past, I’ve had a few patients who met with me a few times, always ‘forgetting’ their payment and offering it ‘next time,’ until after three or four sessions, I refused to see them. I always wondered what such patients were thinking, as obviously this arrangement wouldn’t last long. Did they tell themselves they’d pay me at some point, in effect fooling themselves? Was it conscious theft of my services? A couple years ago, I started accepting charge cards, and perhaps as a result, this hasn’t happened. While it’s always useful to consider individual dynamics in explaining such behavior, it’s also important to consider normative psychology: Make it easier to pay, and more people will.”
While payment for out-of-network services is often clear cut – the patients pay and then requests reimbursement from their insurer – the logistics often are confusing for the patient. He or she may believe that she has excellent coverage, only to learn that the out-of-network deductible is very high, or that reimbursement is based on “usual and customary fees” that are much lower than his psychiatrist’s fees. Sometimes people take on the cost of psychiatric care and discover that it costs more than they assumed, or they have a change in their financial circumstances, as my patient did. Sometimes a parent is paying for treatment and decides he can no longer afford it.
“When someone’s financial circumstances change, they often let me know by proposing we meet less often, for example, every other week,” Dr. Reidbord wrote. “I ask to hear more and often offer to adjust my fee to allow weekly meetings to continue.”
Not all patients pay for psychiatric services, and that may make the discussion even harder. When psychiatrists participate with insurance, the patients are responsible for paying only their deductible and then a copay. The patients may unexpectedly be billed for the entire fee if their insurance terminates, or if it does not pay for a submitted claim. And patients who carry public insurance may be seen at sites where there is no out-of-pocket cost to the patient; salaried clinicians often never know if the insurance has paid. In both of these settings, finances are usually discussed with administrative personnel and not with clinical staff.
Anthony Massey, MD, is founder of Maryland’s Gladstone Psychiatry and Wellness. The group is a multidisciplinary organization, and the clinicians participate with employer-based commercial health insurances. The group accepts payment directly from the insurer, and the patient is responsible for payment of the deductible and a copay.
“We try to understand what someone owes before the first appointment. We do an eligibility check online, and we ask for payment at the time of the appointment,” Massey explained. “Sometimes the insurance changes and we don’t know, or sometimes a patient comes to the appointment without the copay. We try to work with people, but if someone builds up a balance over $500, we tell them they can’t be seen here until it’s paid down. We’ll give patients a 30-day prescription and the names of other psychiatrists who accept insurance, but we don’t keep seeing people who don’t pay for their treatment.”
In all medical settings, unpaid bills present a problem, and while most psychiatrists have a method to deal with these issues, there is no perfect answer for every doctor in every situation. There is this tension between wanting to be kind and understanding of the hardships that people have whether those hardships result from life circumstances or from their own choices and behaviors, and of our own need to make the living we feel we deserve and to pay our own bills.
“The only advice I’d give other psychiatrists is to catch it early,” Reidbord said. “ – and stick with it. If a patient doesn’t pay according to your clearly stated policy, explore it right away. Remember that pragmatic issues like poor budgeting or unexpected expenses are just as likely as intrapsychic conflict and ‘acting out.’ Both should be considered.”
I wish I could say that in the decades since I treated Mr. A that no patients have ever failed to pay their professional fees and that I have perfectly mastered my own issues with money as it pertains to professional fees. While the vast majority of patients do pay, there are still occasional circumstances in which someone’s financial circumstances change, or very rarely where someone ends his treatment without paying for the last few sessions.
Dr. Miller is the coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016) and has a private practice in Baltimore. Patient details were altered to preserve confidentiality.
Editor’s note: This is the second in a series of articles by Dr. Miller about challenges in outpatient psychiatry.
Mr. A lived a life that seemed glamorous to me. There were lunches with professional athletes, swank social events, and designer everything from clothes to cars. It was a world that I was not familiar with, and while I knew my patient worried about money, it seemed he had it. When he started therapy with me, Mr. A came to every session with a check. At some point, I realized that I had missed a switch in his mood. Despite his therapeutic level of lithium, Mr. A had become manic, and the expression of this mania took the form of even more spending. What started as an exciting lifestyle suddenly became tens of thousands of dollars of debt. I felt guilty that I initially did not see this as pathology, and as a young psychiatrist, I sought consultation with an older and wiser mentor.
After discussing the case, the consulting psychiatrist said to me, “Make sure you get paid; these cases are difficult.” In fact, in the midst of the chaos, Mr. A had stopped bringing a check to the sessions. I sent monthly statements, and they went unpaid. He didn’t have the money for his living expenses and I let this go on without addressing it for much too long. Soon, Mr. A’s debt to me was just one more stress in his life and while I knew I would not pursue reimbursement through legal channels, I did encourage him to find a psychiatrist who was in his insurance network, something he did not want to do. I was too embarrassed to tell the consulting psychiatrist that Mr. A had already accrued well over a thousand dollars in unpaid professional fees. In my mind, I was offering pro bono care because the patient’s financial circumstances had changed, and because I felt guilty that I had not recognized this as mania sooner.
In a 2011 Shrink Rap blog post, Jesse Hellman, MD, a psychiatrist in private practice in Towson, Md., wrote about the meaning of payment in psychotherapy:
“Money is something loaded with meaning to most people. What does it mean that the patient forgets to pay? Does it mean ‘if you really cared about me you would not charge me’? Is it a reflection of anger for something that occurred in the last session? Is it a displacement of feelings from something else (‘my boss didn’t give me the raise I expected’)? Is it completely inadvertent (Freud famously said ‘Sometimes a cigar is only a cigar’)?”
There are so many possibilities, and the psychodynamic therapist wants to understand them. How the patient relates to the therapist is some part of how he relates to others. The patient hopefully starts to watch his own actions and attitudes and also tries to understand them. A nonjudgmental stance helps the patient do this.
The therapist himself needs to be comfortable dealing with the subject of money. Sometimes beginning physicians fluctuate between feeling they are too inexperienced to be paid and feeling that they deserve anything they ask. We physicians might even (unfortunately) take on the attitudes of the insurance companies themselves (“Identification with the Aggressor”).
The blog post was flooded with comments –120 in total, and more comments than any other single Shrink Rap post received for the blog’s 12-year run.
Steven Reidbord, MD, is a psychiatrist in private practice in San Francisco and also a blogger. Dr. Reidbord conversed with me through email about patients who don’t pay.
“In years past, I’ve had a few patients who met with me a few times, always ‘forgetting’ their payment and offering it ‘next time,’ until after three or four sessions, I refused to see them. I always wondered what such patients were thinking, as obviously this arrangement wouldn’t last long. Did they tell themselves they’d pay me at some point, in effect fooling themselves? Was it conscious theft of my services? A couple years ago, I started accepting charge cards, and perhaps as a result, this hasn’t happened. While it’s always useful to consider individual dynamics in explaining such behavior, it’s also important to consider normative psychology: Make it easier to pay, and more people will.”
While payment for out-of-network services is often clear cut – the patients pay and then requests reimbursement from their insurer – the logistics often are confusing for the patient. He or she may believe that she has excellent coverage, only to learn that the out-of-network deductible is very high, or that reimbursement is based on “usual and customary fees” that are much lower than his psychiatrist’s fees. Sometimes people take on the cost of psychiatric care and discover that it costs more than they assumed, or they have a change in their financial circumstances, as my patient did. Sometimes a parent is paying for treatment and decides he can no longer afford it.
“When someone’s financial circumstances change, they often let me know by proposing we meet less often, for example, every other week,” Dr. Reidbord wrote. “I ask to hear more and often offer to adjust my fee to allow weekly meetings to continue.”
Not all patients pay for psychiatric services, and that may make the discussion even harder. When psychiatrists participate with insurance, the patients are responsible for paying only their deductible and then a copay. The patients may unexpectedly be billed for the entire fee if their insurance terminates, or if it does not pay for a submitted claim. And patients who carry public insurance may be seen at sites where there is no out-of-pocket cost to the patient; salaried clinicians often never know if the insurance has paid. In both of these settings, finances are usually discussed with administrative personnel and not with clinical staff.
Anthony Massey, MD, is founder of Maryland’s Gladstone Psychiatry and Wellness. The group is a multidisciplinary organization, and the clinicians participate with employer-based commercial health insurances. The group accepts payment directly from the insurer, and the patient is responsible for payment of the deductible and a copay.
“We try to understand what someone owes before the first appointment. We do an eligibility check online, and we ask for payment at the time of the appointment,” Massey explained. “Sometimes the insurance changes and we don’t know, or sometimes a patient comes to the appointment without the copay. We try to work with people, but if someone builds up a balance over $500, we tell them they can’t be seen here until it’s paid down. We’ll give patients a 30-day prescription and the names of other psychiatrists who accept insurance, but we don’t keep seeing people who don’t pay for their treatment.”
In all medical settings, unpaid bills present a problem, and while most psychiatrists have a method to deal with these issues, there is no perfect answer for every doctor in every situation. There is this tension between wanting to be kind and understanding of the hardships that people have whether those hardships result from life circumstances or from their own choices and behaviors, and of our own need to make the living we feel we deserve and to pay our own bills.
“The only advice I’d give other psychiatrists is to catch it early,” Reidbord said. “ – and stick with it. If a patient doesn’t pay according to your clearly stated policy, explore it right away. Remember that pragmatic issues like poor budgeting or unexpected expenses are just as likely as intrapsychic conflict and ‘acting out.’ Both should be considered.”
I wish I could say that in the decades since I treated Mr. A that no patients have ever failed to pay their professional fees and that I have perfectly mastered my own issues with money as it pertains to professional fees. While the vast majority of patients do pay, there are still occasional circumstances in which someone’s financial circumstances change, or very rarely where someone ends his treatment without paying for the last few sessions.
Dr. Miller is the coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016) and has a private practice in Baltimore. Patient details were altered to preserve confidentiality.
Editor’s note: This is the second in a series of articles by Dr. Miller about challenges in outpatient psychiatry.
Mr. A lived a life that seemed glamorous to me. There were lunches with professional athletes, swank social events, and designer everything from clothes to cars. It was a world that I was not familiar with, and while I knew my patient worried about money, it seemed he had it. When he started therapy with me, Mr. A came to every session with a check. At some point, I realized that I had missed a switch in his mood. Despite his therapeutic level of lithium, Mr. A had become manic, and the expression of this mania took the form of even more spending. What started as an exciting lifestyle suddenly became tens of thousands of dollars of debt. I felt guilty that I initially did not see this as pathology, and as a young psychiatrist, I sought consultation with an older and wiser mentor.
After discussing the case, the consulting psychiatrist said to me, “Make sure you get paid; these cases are difficult.” In fact, in the midst of the chaos, Mr. A had stopped bringing a check to the sessions. I sent monthly statements, and they went unpaid. He didn’t have the money for his living expenses and I let this go on without addressing it for much too long. Soon, Mr. A’s debt to me was just one more stress in his life and while I knew I would not pursue reimbursement through legal channels, I did encourage him to find a psychiatrist who was in his insurance network, something he did not want to do. I was too embarrassed to tell the consulting psychiatrist that Mr. A had already accrued well over a thousand dollars in unpaid professional fees. In my mind, I was offering pro bono care because the patient’s financial circumstances had changed, and because I felt guilty that I had not recognized this as mania sooner.
In a 2011 Shrink Rap blog post, Jesse Hellman, MD, a psychiatrist in private practice in Towson, Md., wrote about the meaning of payment in psychotherapy:
“Money is something loaded with meaning to most people. What does it mean that the patient forgets to pay? Does it mean ‘if you really cared about me you would not charge me’? Is it a reflection of anger for something that occurred in the last session? Is it a displacement of feelings from something else (‘my boss didn’t give me the raise I expected’)? Is it completely inadvertent (Freud famously said ‘Sometimes a cigar is only a cigar’)?”
There are so many possibilities, and the psychodynamic therapist wants to understand them. How the patient relates to the therapist is some part of how he relates to others. The patient hopefully starts to watch his own actions and attitudes and also tries to understand them. A nonjudgmental stance helps the patient do this.
The therapist himself needs to be comfortable dealing with the subject of money. Sometimes beginning physicians fluctuate between feeling they are too inexperienced to be paid and feeling that they deserve anything they ask. We physicians might even (unfortunately) take on the attitudes of the insurance companies themselves (“Identification with the Aggressor”).
The blog post was flooded with comments –120 in total, and more comments than any other single Shrink Rap post received for the blog’s 12-year run.
Steven Reidbord, MD, is a psychiatrist in private practice in San Francisco and also a blogger. Dr. Reidbord conversed with me through email about patients who don’t pay.
“In years past, I’ve had a few patients who met with me a few times, always ‘forgetting’ their payment and offering it ‘next time,’ until after three or four sessions, I refused to see them. I always wondered what such patients were thinking, as obviously this arrangement wouldn’t last long. Did they tell themselves they’d pay me at some point, in effect fooling themselves? Was it conscious theft of my services? A couple years ago, I started accepting charge cards, and perhaps as a result, this hasn’t happened. While it’s always useful to consider individual dynamics in explaining such behavior, it’s also important to consider normative psychology: Make it easier to pay, and more people will.”
While payment for out-of-network services is often clear cut – the patients pay and then requests reimbursement from their insurer – the logistics often are confusing for the patient. He or she may believe that she has excellent coverage, only to learn that the out-of-network deductible is very high, or that reimbursement is based on “usual and customary fees” that are much lower than his psychiatrist’s fees. Sometimes people take on the cost of psychiatric care and discover that it costs more than they assumed, or they have a change in their financial circumstances, as my patient did. Sometimes a parent is paying for treatment and decides he can no longer afford it.
“When someone’s financial circumstances change, they often let me know by proposing we meet less often, for example, every other week,” Dr. Reidbord wrote. “I ask to hear more and often offer to adjust my fee to allow weekly meetings to continue.”
Not all patients pay for psychiatric services, and that may make the discussion even harder. When psychiatrists participate with insurance, the patients are responsible for paying only their deductible and then a copay. The patients may unexpectedly be billed for the entire fee if their insurance terminates, or if it does not pay for a submitted claim. And patients who carry public insurance may be seen at sites where there is no out-of-pocket cost to the patient; salaried clinicians often never know if the insurance has paid. In both of these settings, finances are usually discussed with administrative personnel and not with clinical staff.
Anthony Massey, MD, is founder of Maryland’s Gladstone Psychiatry and Wellness. The group is a multidisciplinary organization, and the clinicians participate with employer-based commercial health insurances. The group accepts payment directly from the insurer, and the patient is responsible for payment of the deductible and a copay.
“We try to understand what someone owes before the first appointment. We do an eligibility check online, and we ask for payment at the time of the appointment,” Massey explained. “Sometimes the insurance changes and we don’t know, or sometimes a patient comes to the appointment without the copay. We try to work with people, but if someone builds up a balance over $500, we tell them they can’t be seen here until it’s paid down. We’ll give patients a 30-day prescription and the names of other psychiatrists who accept insurance, but we don’t keep seeing people who don’t pay for their treatment.”
In all medical settings, unpaid bills present a problem, and while most psychiatrists have a method to deal with these issues, there is no perfect answer for every doctor in every situation. There is this tension between wanting to be kind and understanding of the hardships that people have whether those hardships result from life circumstances or from their own choices and behaviors, and of our own need to make the living we feel we deserve and to pay our own bills.
“The only advice I’d give other psychiatrists is to catch it early,” Reidbord said. “ – and stick with it. If a patient doesn’t pay according to your clearly stated policy, explore it right away. Remember that pragmatic issues like poor budgeting or unexpected expenses are just as likely as intrapsychic conflict and ‘acting out.’ Both should be considered.”
I wish I could say that in the decades since I treated Mr. A that no patients have ever failed to pay their professional fees and that I have perfectly mastered my own issues with money as it pertains to professional fees. While the vast majority of patients do pay, there are still occasional circumstances in which someone’s financial circumstances change, or very rarely where someone ends his treatment without paying for the last few sessions.
Dr. Miller is the coauthor with Annette Hanson, MD, of “Committed: The Battle Over Involuntary Psychiatric Care” (Baltimore: Johns Hopkins University Press, 2016) and has a private practice in Baltimore. Patient details were altered to preserve confidentiality.
fMRI might help differentiate MDD and bipolar disorder
The hippocampal functional connectivity (FC) found in patients with major depressive disorder is different from the FC found in patients with bipolar disorder, an analysis of functional MRI data shows.
“Ahmed Ameen Fateh and his associates wrote in Psychiatry Research: Neuroimaging.
Mr. Fateh and his associates recruited 29 participants with depression and 30 with bipolar disorder, from a mental health center of Chengdu, Sichuan, China. An additional 30 healthy controls were recruited through advertisements, reported Mr. Fateh, a doctoral student at the University of Electronic Science and Technology of China, Chengdu.
Using one-way analysis of variance, the investigators looked at possible differences in the participants’ hippocampal FC. The results showed that some regions exhibited significant differences in the hippocampal FC among the patients with major depression and bipolar disorder.
If their results could be replicated, the researchers wrote, “such differences may yield future trends towards improving the clinical differentiation between these two types of depression with significant therapeutic and prognostic implications.”
SOURCE: Fateh AA et al. Psychiatry Res Neuroimaging. 2019 Jan 12. doi: 10.1016/j.pscychresns.2019.01.004.
The hippocampal functional connectivity (FC) found in patients with major depressive disorder is different from the FC found in patients with bipolar disorder, an analysis of functional MRI data shows.
“Ahmed Ameen Fateh and his associates wrote in Psychiatry Research: Neuroimaging.
Mr. Fateh and his associates recruited 29 participants with depression and 30 with bipolar disorder, from a mental health center of Chengdu, Sichuan, China. An additional 30 healthy controls were recruited through advertisements, reported Mr. Fateh, a doctoral student at the University of Electronic Science and Technology of China, Chengdu.
Using one-way analysis of variance, the investigators looked at possible differences in the participants’ hippocampal FC. The results showed that some regions exhibited significant differences in the hippocampal FC among the patients with major depression and bipolar disorder.
If their results could be replicated, the researchers wrote, “such differences may yield future trends towards improving the clinical differentiation between these two types of depression with significant therapeutic and prognostic implications.”
SOURCE: Fateh AA et al. Psychiatry Res Neuroimaging. 2019 Jan 12. doi: 10.1016/j.pscychresns.2019.01.004.
The hippocampal functional connectivity (FC) found in patients with major depressive disorder is different from the FC found in patients with bipolar disorder, an analysis of functional MRI data shows.
“Ahmed Ameen Fateh and his associates wrote in Psychiatry Research: Neuroimaging.
Mr. Fateh and his associates recruited 29 participants with depression and 30 with bipolar disorder, from a mental health center of Chengdu, Sichuan, China. An additional 30 healthy controls were recruited through advertisements, reported Mr. Fateh, a doctoral student at the University of Electronic Science and Technology of China, Chengdu.
Using one-way analysis of variance, the investigators looked at possible differences in the participants’ hippocampal FC. The results showed that some regions exhibited significant differences in the hippocampal FC among the patients with major depression and bipolar disorder.
If their results could be replicated, the researchers wrote, “such differences may yield future trends towards improving the clinical differentiation between these two types of depression with significant therapeutic and prognostic implications.”
SOURCE: Fateh AA et al. Psychiatry Res Neuroimaging. 2019 Jan 12. doi: 10.1016/j.pscychresns.2019.01.004.
FROM PSYCHIATRY RESEARCH: NEUROIMAGING
Masterclass: Marlene Freeman on treating bipolar disorder in women
National Pregnancy Registry for Psychiatric Medications at Massachusetts General Hospital, where she also serves as associate director of Women’s Mental Health.
Amazon
Apple Podcasts
Google Podcasts
Spotify during pregnancy. Dr. Freeman, associate professor of psychiatry at Harvard Medical School, also shares preliminary data on the impact of exposure to atypical antipsychotics from the
National Pregnancy Registry for Psychiatric Medications at Massachusetts General Hospital, where she also serves as associate director of Women’s Mental Health.
Amazon
Apple Podcasts
Google Podcasts
Spotify during pregnancy. Dr. Freeman, associate professor of psychiatry at Harvard Medical School, also shares preliminary data on the impact of exposure to atypical antipsychotics from the
National Pregnancy Registry for Psychiatric Medications at Massachusetts General Hospital, where she also serves as associate director of Women’s Mental Health.
Amazon
Apple Podcasts
Google Podcasts
Spotify during pregnancy. Dr. Freeman, associate professor of psychiatry at Harvard Medical School, also shares preliminary data on the impact of exposure to atypical antipsychotics from the
Mood and behavior are different targets for irritability in children
BROOKLYN, N.Y. – As a target of therapy in children with a psychiatric disorder, irritability expressed as grumpy mood or anger should be uncoupled from irritability expressed as threatening behavior, according to an exploration of this common clinical issue at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
“Irritability is like fever,” reported Gabrielle A. Carlson, MD, professor of psychiatry and pediatrics, State University of New York at Stony Brook. “It is a nonspecific symptom that only tells you that something is wrong.”
Irritability might be nothing more than a negative mood, but it also can be the source of explosive aggression, leading to tantrums and destructive behaviors, according to Dr. Carlson. She placed them into two different categories when considering treatment. Irritability leading to annoyance, grumpiness, withdrawal, or persistent anger is characterized as the “internalizing” or “tonic” form of the symptom. As opposed to the aggressive subtype, the tonic form is more closely associated with depression or anxiety. Irritability leading to extreme verbal outbursts or physical violence is characterized as the “externalizing” or “phasic” form, Dr. Carlson said. This type of irritability, defined by behavior more than mood, might signal disruptive mood dysregulation disorder (DMDD). But it is important to recognize that DMDD can overlap with other conditions, such as attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, oppositional defiant disorder (ODD), and autism spectrum disorders.
In defining the impact of treatments on tonic versus phasic symptoms of irritability within the context of the underlying diagnoses, studies have not done a good job in separating relative effects on the two key forms of irritability, Dr. Carlson said.
“Irritability needs to be measured not only by how one feels but what one does,” said Dr. Carlson, explaining that the impact of therapy has not always been adequately described in therapy studies.
For the tonic form, irritability is likely to improve or resolve with control of the underlying psychiatric condition. Although this might also be true of the phasic form, this type of irritability often accompanies conditions that are less readily controlled even through the threat of self-harm, harm to others, or other destructive behaviors invites intervention specifically targeted at this symptom.
Unfortunately, the best approach to irritability is unclear for many underling pathologies.
“Clinicians should recognize that empirical evidence is still lacking as to aggression-targeted treatments with favorable benefit-risk profiles for children and adolescents with ADHD and severe aggression,” said Dr. Carlson, providing ADHD as one of several examples.
Psychological interventions, such as dialectical behavior therapy in children (DBT-C), have been associated with control of both tonic and phasic forms of irritability, but Dr. Carlson cautioned that few studies have adequately differentiated improvement in irritability as measured by behavior relative to mood. In addition, the baseline severity and the degree to which improvement meant adequate control have been unclear.
“Many psychological treatments are school based or group delivered, making it likely that patients are less impaired than explosive kids in psychiatry clinics and hospitals,” Dr. Carlson said.
Providing some practical tips for addressing the phasic form of irritability, She advised clinicians to “maximize the treatment of the base condition” but to add pharmacologic therapies to psychological interventions if symptoms persist.
“Our pendulum has swung from dishing out atypicals to eschewing them completely,” Dr. Carlson noted. Although she agreed these are no longer appropriate as first-line therapies, she suggested they might be employed judiciously if weight gain is monitored carefully.
“If they don’t work, stop them. If they do work, try to limit the duration of use,” Dr. Carlson said.
She reported having no relevant financial relationships to disclose.
BROOKLYN, N.Y. – As a target of therapy in children with a psychiatric disorder, irritability expressed as grumpy mood or anger should be uncoupled from irritability expressed as threatening behavior, according to an exploration of this common clinical issue at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
“Irritability is like fever,” reported Gabrielle A. Carlson, MD, professor of psychiatry and pediatrics, State University of New York at Stony Brook. “It is a nonspecific symptom that only tells you that something is wrong.”
Irritability might be nothing more than a negative mood, but it also can be the source of explosive aggression, leading to tantrums and destructive behaviors, according to Dr. Carlson. She placed them into two different categories when considering treatment. Irritability leading to annoyance, grumpiness, withdrawal, or persistent anger is characterized as the “internalizing” or “tonic” form of the symptom. As opposed to the aggressive subtype, the tonic form is more closely associated with depression or anxiety. Irritability leading to extreme verbal outbursts or physical violence is characterized as the “externalizing” or “phasic” form, Dr. Carlson said. This type of irritability, defined by behavior more than mood, might signal disruptive mood dysregulation disorder (DMDD). But it is important to recognize that DMDD can overlap with other conditions, such as attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, oppositional defiant disorder (ODD), and autism spectrum disorders.
In defining the impact of treatments on tonic versus phasic symptoms of irritability within the context of the underlying diagnoses, studies have not done a good job in separating relative effects on the two key forms of irritability, Dr. Carlson said.
“Irritability needs to be measured not only by how one feels but what one does,” said Dr. Carlson, explaining that the impact of therapy has not always been adequately described in therapy studies.
For the tonic form, irritability is likely to improve or resolve with control of the underlying psychiatric condition. Although this might also be true of the phasic form, this type of irritability often accompanies conditions that are less readily controlled even through the threat of self-harm, harm to others, or other destructive behaviors invites intervention specifically targeted at this symptom.
Unfortunately, the best approach to irritability is unclear for many underling pathologies.
“Clinicians should recognize that empirical evidence is still lacking as to aggression-targeted treatments with favorable benefit-risk profiles for children and adolescents with ADHD and severe aggression,” said Dr. Carlson, providing ADHD as one of several examples.
Psychological interventions, such as dialectical behavior therapy in children (DBT-C), have been associated with control of both tonic and phasic forms of irritability, but Dr. Carlson cautioned that few studies have adequately differentiated improvement in irritability as measured by behavior relative to mood. In addition, the baseline severity and the degree to which improvement meant adequate control have been unclear.
“Many psychological treatments are school based or group delivered, making it likely that patients are less impaired than explosive kids in psychiatry clinics and hospitals,” Dr. Carlson said.
Providing some practical tips for addressing the phasic form of irritability, She advised clinicians to “maximize the treatment of the base condition” but to add pharmacologic therapies to psychological interventions if symptoms persist.
“Our pendulum has swung from dishing out atypicals to eschewing them completely,” Dr. Carlson noted. Although she agreed these are no longer appropriate as first-line therapies, she suggested they might be employed judiciously if weight gain is monitored carefully.
“If they don’t work, stop them. If they do work, try to limit the duration of use,” Dr. Carlson said.
She reported having no relevant financial relationships to disclose.
BROOKLYN, N.Y. – As a target of therapy in children with a psychiatric disorder, irritability expressed as grumpy mood or anger should be uncoupled from irritability expressed as threatening behavior, according to an exploration of this common clinical issue at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
“Irritability is like fever,” reported Gabrielle A. Carlson, MD, professor of psychiatry and pediatrics, State University of New York at Stony Brook. “It is a nonspecific symptom that only tells you that something is wrong.”
Irritability might be nothing more than a negative mood, but it also can be the source of explosive aggression, leading to tantrums and destructive behaviors, according to Dr. Carlson. She placed them into two different categories when considering treatment. Irritability leading to annoyance, grumpiness, withdrawal, or persistent anger is characterized as the “internalizing” or “tonic” form of the symptom. As opposed to the aggressive subtype, the tonic form is more closely associated with depression or anxiety. Irritability leading to extreme verbal outbursts or physical violence is characterized as the “externalizing” or “phasic” form, Dr. Carlson said. This type of irritability, defined by behavior more than mood, might signal disruptive mood dysregulation disorder (DMDD). But it is important to recognize that DMDD can overlap with other conditions, such as attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, oppositional defiant disorder (ODD), and autism spectrum disorders.
In defining the impact of treatments on tonic versus phasic symptoms of irritability within the context of the underlying diagnoses, studies have not done a good job in separating relative effects on the two key forms of irritability, Dr. Carlson said.
“Irritability needs to be measured not only by how one feels but what one does,” said Dr. Carlson, explaining that the impact of therapy has not always been adequately described in therapy studies.
For the tonic form, irritability is likely to improve or resolve with control of the underlying psychiatric condition. Although this might also be true of the phasic form, this type of irritability often accompanies conditions that are less readily controlled even through the threat of self-harm, harm to others, or other destructive behaviors invites intervention specifically targeted at this symptom.
Unfortunately, the best approach to irritability is unclear for many underling pathologies.
“Clinicians should recognize that empirical evidence is still lacking as to aggression-targeted treatments with favorable benefit-risk profiles for children and adolescents with ADHD and severe aggression,” said Dr. Carlson, providing ADHD as one of several examples.
Psychological interventions, such as dialectical behavior therapy in children (DBT-C), have been associated with control of both tonic and phasic forms of irritability, but Dr. Carlson cautioned that few studies have adequately differentiated improvement in irritability as measured by behavior relative to mood. In addition, the baseline severity and the degree to which improvement meant adequate control have been unclear.
“Many psychological treatments are school based or group delivered, making it likely that patients are less impaired than explosive kids in psychiatry clinics and hospitals,” Dr. Carlson said.
Providing some practical tips for addressing the phasic form of irritability, She advised clinicians to “maximize the treatment of the base condition” but to add pharmacologic therapies to psychological interventions if symptoms persist.
“Our pendulum has swung from dishing out atypicals to eschewing them completely,” Dr. Carlson noted. Although she agreed these are no longer appropriate as first-line therapies, she suggested they might be employed judiciously if weight gain is monitored carefully.
“If they don’t work, stop them. If they do work, try to limit the duration of use,” Dr. Carlson said.
She reported having no relevant financial relationships to disclose.
REPORTING FROM The PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Tool might help assessment of prodromal symptoms in children
Brooklyn, N.Y. – A risk calculator for bipolar disorder that has reached late stages of development might merit a trial to test whether treating prodromal symptoms delays or prevents the disease from developing in young patients, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Clinicians often are confronted with children who have prodromal symptoms of bipolar disorder, but only about half of those children eventually convert to full disease expression. As a result, treatment is not routine practice, said Boris Birmaher, MD, Endowed Chair, Early Onset Bipolar Disease, at the University of Pittsburgh.
A risk calculator that more effectively identifies those at highest risk of converting might be a tool that could allow early intervention to be tested. Such a calculator has been in development for some years, and the most recent research suggests that it is nearing a degree of accuracy that is clinically meaningful (J Am Acad Child Adolesc Psychiatry. 2018;57:755-63).
Accuracy might improve further with the identification and incorporation of more predictive variables. High-risk features for conversion include a parent with bipolar disorder, particularly one with childhood onset, and specific clinical features, such as prominent episodes of mania.
“Once replicated, the risk calculator will be instrumental to predict personalized risk to develop bipolar disease,” Dr. Birmaher said. He compared it to risk calculators now in use in other fields of medicine, such as cancer and cardiovascular disease, which generate information used by patients and their physicians for treatment decisions.
In the most recent study with the risk calculator, which has been the topic of several previous publications, 140 children with a diagnosis of bipolar disorder not otherwise specified (BP-NOS) were assessed every 7 months for a median of 11.5 years. BP-NOS is the diagnosis of a prodromal syndrome that includes mood lability and other features of bipolar disorder but not at levels reaching DSM-5 diagnostic criteria. The primary outcome of the study was conversion from BP-NOS to bipolar I or II, which are DSM-5 categories.
At the end of follow-up, 53.6% of the population had converted to bipolar I or II, which is consistent with previous risk estimates in this population. In specific patients, the correlation between predicted and observed conversions was “excellent.” Furthermore, the risk calculator was reported to have provided “good” discrimination between converters and nonconverters.
The risk calculator already is accessible online (http://www.cabsresearch.pitt.edu/bpriskcalculator/). Dr. Birmaher invited clinicians to visit and “play around” with its features, but he also issued a warning. “Be careful because we need to further validate this, which we are doing now, to see if it’s truly accurate or not. If it is, it would be a very good tool for us,” he said.
There are many potential clinical applications of the risk calculator, but Dr. Birmaher emphasized its possible value in selecting at-risk patients for therapy studies. Although several therapy trials already have been conducted in high-risk children on the basis of clinical presentation alone, such as a double-blind trial in BP-NOS patients that associated aripiprazole with a reduction in mania (J Child Adolesc Psychopharmacol. 2017;27:864-74), Dr. Birmaher sees the risk calculator as potentially more precise in identifying candidates.
Brooklyn, N.Y. – A risk calculator for bipolar disorder that has reached late stages of development might merit a trial to test whether treating prodromal symptoms delays or prevents the disease from developing in young patients, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Clinicians often are confronted with children who have prodromal symptoms of bipolar disorder, but only about half of those children eventually convert to full disease expression. As a result, treatment is not routine practice, said Boris Birmaher, MD, Endowed Chair, Early Onset Bipolar Disease, at the University of Pittsburgh.
A risk calculator that more effectively identifies those at highest risk of converting might be a tool that could allow early intervention to be tested. Such a calculator has been in development for some years, and the most recent research suggests that it is nearing a degree of accuracy that is clinically meaningful (J Am Acad Child Adolesc Psychiatry. 2018;57:755-63).
Accuracy might improve further with the identification and incorporation of more predictive variables. High-risk features for conversion include a parent with bipolar disorder, particularly one with childhood onset, and specific clinical features, such as prominent episodes of mania.
“Once replicated, the risk calculator will be instrumental to predict personalized risk to develop bipolar disease,” Dr. Birmaher said. He compared it to risk calculators now in use in other fields of medicine, such as cancer and cardiovascular disease, which generate information used by patients and their physicians for treatment decisions.
In the most recent study with the risk calculator, which has been the topic of several previous publications, 140 children with a diagnosis of bipolar disorder not otherwise specified (BP-NOS) were assessed every 7 months for a median of 11.5 years. BP-NOS is the diagnosis of a prodromal syndrome that includes mood lability and other features of bipolar disorder but not at levels reaching DSM-5 diagnostic criteria. The primary outcome of the study was conversion from BP-NOS to bipolar I or II, which are DSM-5 categories.
At the end of follow-up, 53.6% of the population had converted to bipolar I or II, which is consistent with previous risk estimates in this population. In specific patients, the correlation between predicted and observed conversions was “excellent.” Furthermore, the risk calculator was reported to have provided “good” discrimination between converters and nonconverters.
The risk calculator already is accessible online (http://www.cabsresearch.pitt.edu/bpriskcalculator/). Dr. Birmaher invited clinicians to visit and “play around” with its features, but he also issued a warning. “Be careful because we need to further validate this, which we are doing now, to see if it’s truly accurate or not. If it is, it would be a very good tool for us,” he said.
There are many potential clinical applications of the risk calculator, but Dr. Birmaher emphasized its possible value in selecting at-risk patients for therapy studies. Although several therapy trials already have been conducted in high-risk children on the basis of clinical presentation alone, such as a double-blind trial in BP-NOS patients that associated aripiprazole with a reduction in mania (J Child Adolesc Psychopharmacol. 2017;27:864-74), Dr. Birmaher sees the risk calculator as potentially more precise in identifying candidates.
Brooklyn, N.Y. – A risk calculator for bipolar disorder that has reached late stages of development might merit a trial to test whether treating prodromal symptoms delays or prevents the disease from developing in young patients, an expert said at a pediatric psychopharmacology update held by the American Academy of Child and Adolescent Psychiatry.
Clinicians often are confronted with children who have prodromal symptoms of bipolar disorder, but only about half of those children eventually convert to full disease expression. As a result, treatment is not routine practice, said Boris Birmaher, MD, Endowed Chair, Early Onset Bipolar Disease, at the University of Pittsburgh.
A risk calculator that more effectively identifies those at highest risk of converting might be a tool that could allow early intervention to be tested. Such a calculator has been in development for some years, and the most recent research suggests that it is nearing a degree of accuracy that is clinically meaningful (J Am Acad Child Adolesc Psychiatry. 2018;57:755-63).
Accuracy might improve further with the identification and incorporation of more predictive variables. High-risk features for conversion include a parent with bipolar disorder, particularly one with childhood onset, and specific clinical features, such as prominent episodes of mania.
“Once replicated, the risk calculator will be instrumental to predict personalized risk to develop bipolar disease,” Dr. Birmaher said. He compared it to risk calculators now in use in other fields of medicine, such as cancer and cardiovascular disease, which generate information used by patients and their physicians for treatment decisions.
In the most recent study with the risk calculator, which has been the topic of several previous publications, 140 children with a diagnosis of bipolar disorder not otherwise specified (BP-NOS) were assessed every 7 months for a median of 11.5 years. BP-NOS is the diagnosis of a prodromal syndrome that includes mood lability and other features of bipolar disorder but not at levels reaching DSM-5 diagnostic criteria. The primary outcome of the study was conversion from BP-NOS to bipolar I or II, which are DSM-5 categories.
At the end of follow-up, 53.6% of the population had converted to bipolar I or II, which is consistent with previous risk estimates in this population. In specific patients, the correlation between predicted and observed conversions was “excellent.” Furthermore, the risk calculator was reported to have provided “good” discrimination between converters and nonconverters.
The risk calculator already is accessible online (http://www.cabsresearch.pitt.edu/bpriskcalculator/). Dr. Birmaher invited clinicians to visit and “play around” with its features, but he also issued a warning. “Be careful because we need to further validate this, which we are doing now, to see if it’s truly accurate or not. If it is, it would be a very good tool for us,” he said.
There are many potential clinical applications of the risk calculator, but Dr. Birmaher emphasized its possible value in selecting at-risk patients for therapy studies. Although several therapy trials already have been conducted in high-risk children on the basis of clinical presentation alone, such as a double-blind trial in BP-NOS patients that associated aripiprazole with a reduction in mania (J Child Adolesc Psychopharmacol. 2017;27:864-74), Dr. Birmaher sees the risk calculator as potentially more precise in identifying candidates.
REPORTING FROM the PSYCHOPHARMACOLOGY UPDATE INSTITUTE
Older-age bipolar disorder: A case series
Although the peak age of onset of bipolar disorder (BD) is between 20 and 40 years,1 some patients develop BD later in life. The International Society for Bipolar Disorders Task Force has classified the illness into 3 categories:
- early-onset bipolar disorder (EOBD), in which the first manic episode occurs before age 40
- late-onset bipolar disorder (LOBD), in which the initial manic/hypomanic episode occurs after age 50
- older-age bipolar disorder (OABD), in which the first manic/hypomanic episode occurs after age 60.2
OABD represents 25% of the population with BD.3 OABD differs from EOBD in its clinical presentation, biological factors, and psychiatric and somatic comorbidities.4 Studies suggest OABD warrants a more extensive workup to rule out organic causes because symptoms are often attributable to a variety of organic etiologies.
This article describes 3 cases of OABD, including treatments and outcomes. We discuss general treatment recommendations for patients with OABD as cited in the literature. Further research is needed to expand our ability to better care for this unique population.
CASE 1
Mr. D was a 66-year-old African American male with no psychiatric history. His medical history was significant for hypertension, poorly controlled diabetes mellitus, and chronic kidney disease. One year ago, he was diagnosed with cholangiocarcinoma, and underwent uncomplicated right trisegmentectomy, resection of extrahepatic biliary tree, and complete portal lymphadenectomy, with Roux-en-Y hepaticojejunostomy to 2 intrahepatic ducts. He presented to the emergency department (ED) with disorganized behavior for 3 weeks. During that time, Mr. D reported increased distractibility, irritability, hyper-religiosity, racing thoughts, decreased appetite, and decreased need for sleep. There was no pertinent family history.
On mental status examination, Mr. D was agitated, noncooperative, and guarded. His speech was loud and pressured. Mr. D was distractible, tangential, and goal-directed. His Young Mania Rating Scale (YMRS) score was 31, which is highly indicative of mania.5 Computed tomography (CT) scan of the head (Figure 1)
CASE 2
Mr. M was a 63-year-old African American male with no psychiatric history and a medical history significant for hypertension and hypercholesterolemia. He presented to the ED with behavioral changes for 2 weeks. During this time, he experienced decreased need for sleep, agitation, excessive spending, self-conversing, hypersexuality, and paranoia. His family history was significant for schizoaffective disorder, bipolar type.
A mental status examination revealed pressured speech, grandiose delusions, hyper-religiosity, flight of ideas, looseness of association, auditory hallucinations, and tangential thought processes. Mr. M’s initial YMRS score was 56. A CT scan of the head revealed no acute abnormality, but MRI of the brain (Figure 2) showed chronic microvascular ischemic change. Mr. M was diagnosed with bipolar I disorder and admitted. He was started on quetiapine extended release, which was titrated to 600 mg nightly. Divalproex sodium extended release was titrated to 1,500 mg nightly, with subsequent improvement. At discharge, his YMRS score was 15.
Continue to: CASE 3
CASE 3
Ms. F was a 69-year-old White female with no psychiatric history. Her medical history was significant for hypertension, osteoarthritis, and stage III-C ovarian adenocarcinoma with a debulking surgical procedure 5 years earlier. After that, she received adjuvant therapy with paclitaxel and carboplatin, which resulted in a 10-month disease-free interval. Subsequent progression led to cycles of doxorubicin liposomal and gemcitabine. She was in remission until 1 week earlier, when a CT scan of the abdomen/pelvis showed recurrence. She presented to the hospital after disrobing in the street due to hyper-religiosity and divine instruction. She endorsed elevated mood and increased energy despite sleeping only 2 hours daily. Her family psychiatric history was significant for her daughter’s suicide attempt.
A mental status examination revealed disorganized behavior and agitation. Her speech was loud and pressured. She described a “great” mood with congruent affect. Her thought process was circumstantial and illogical. She displayed flight of ideas, grandiose delusions, and paranoia. Ms. F’s initial YMRS score was 38. Vital signs were significant for an elevated blood pressure of 153/113 mm Hg. A CT scan of the head (Figure 3) showed age-related change with no acute findings. Ms. F was admitted with a diagnosis of bipolar I disorder and prescribed olanzapine, 2.5 mg nightly. Due to continued manic symptoms, olanzapine was discontinued, and Ms. F was started on quetiapine, 300 mg nightly, with subsequent improvement. At discharge, her YMRS score was 10.
Differences between EOBD and OABD
BD has always been considered a multi-system illness; however, comorbidity is much more common in OABD than in EOBD. Comorbid conditions are 3 to 4 times more common in patients with OABD.2 Common comorbidities include metabolic syndrome, allergic rhinitis, arthritis, asthma, and cardiovascular disease.
Compared with younger individuals, older patients with BD score lower on the YMRS in the areas of increased activity-energy, language-thought disorder, and sexual interest.6 Psychotic symptoms are less common or less severe in OABD. Although symptom severity is lower, the prevalence of rapid cycling illness is 20% higher in patients with OABD.6 OABD is less commonly associated with a family history.7 This may suggest a difference from the popular genetic component typically found in patients with EOBD.
Cognitive impairment is more commonly found in OABD. Patients with OABD suffer from neuropsychological deficits even during euthymic phases.8 While these deficits may also be found in patients with EOBD, compared with younger patients, older adults are more susceptible to accelerated decline in cognition. OABD can first present within the context of cardiovascular or neuropsychological impairment. It has also been linked to a greater prevalence of white matter hyperintensities compared with EOBD.9,10
Continue to: Treatment is not specific to OABD
Treatment is not specific to OABD
No established treatment guidelines specifically address OABD. It has been treated similarly to EOBD, with antipsychotics, mood stabilizers, antidepressants, and electroconvulsive therapy (ECT). Although lithium is effective, special precautions should be taken when prescribing it to older adults because these patients may be more sensitive to adverse events.11 Drug–drug interactions may also be more likely due to concomitant use of medications for common medical issues such as hypertension.
Treatment with antipsychotics in older patients carries risks. Use of antipsychotics may result in higher rates of morbidity and mortality related to cardiovascular, metabolic, and infectious etiologies. Some literature recommends the use of antipsychotics for OABD; however, the potential benefits must outweigh the risks.6 Monotherapy followed by combination therapy has demonstrated effectiveness in OABD.11 Because symptoms of OABD are often less severe, it may be best to avoid maintenance antipsychotic therapy when possible. With a higher prevalence of depressed mood following manic episodes, use of antidepressant therapy is common in OABD.6 ECT should be considered for patients with treatment-refractory BD.11
Lessons from our case series
Our case series included 3 patients with OABD. These patients’ comorbid conditions included hypertension, hypercholesteremia, and diabetes mellitus. Two patients had a history of cancer, but there was no metastasis to the brain in either case. However, we considered the possibility of structural changes in the brain or cognitive impairment secondary to cancer or its treatment. A literature review confirmed that adult patients treated for noncentral nervous system cancer experienced cancer-related cognitive impairment (CRCI).12 New research suggests that CRCI could be related to altered neuronal integrity along with a disturbance of brain structure networks that process and integrate information.13
We used the YMRS to compare symptom severity and treatment response (Figure 4). Two patients were treated with atypical antipsychotics with a mood stabilizer, and the third patient was prescribed an antipsychotic only. We avoided lithium and carbamazepine as mood stabilizers due to their adverse effect profiles and potential for drug–drug interactions. Each patient responded well to treatment without adverse events.
Future studies are needed to clearly define the safest and most effective treatment guidelines in patients with OABD. We believe that OABD may require the development of a unique treatment algorithm due to the high likelihood of medical comorbidity and age-related variations in treatment response.
Continue to: Etiology of OABD may be different
Etiology of OABD may be different
OABD may be associated with manic presentations and vascular risk factors. MRI imaging that found more white matter hyperintensities and cerebrovascular lesions in patients with OABD compared with younger patients provides evidence of possible differing etiologies.14 Cassidy and Carroll15 found a higher incidence of smoking, hypertension, diabetes mellitus, coronary heart disease, and atrial fibrillation in patients in the older onset group. Bellivier et al16 proposed 3 subgroups of bipolar I disorder; the late-onset subgroup’s etiology was multifactorial. EOBD and OABD subgroups have similar gender ratios,17 first-episode descriptions, and alcohol use rates; however, OABD subgroups have more neurological comorbidity, lesser severe psychosis, and less genetic predisposition.
Although 25% of BD cases are late onset,3 there is still little consensus regarding subgroups and etiological causes. Therefore, additional research specifically focusing on vascular risks may provide much-needed information. Controlling and mitigating vascular risks in OABD may affect its development and course. Despite debated etiologies, the treatment of BD remains consistent, with anticonvulsants preferred over lithium in older individuals.
The Table summarizes clinical pearls about the features and treatment of OABD.
Bottom Line
Compared with younger patients with bipolar disorder (BD), those who develop BD later in life may be more likely to have rapid cycling, medical comorbidities, and cognitive impairment. Older patients with BD also may be more likely to experience adverse effects of the medications commonly used to treat BD, including antipsychotics, lithium, and carbamazepine.
Related Resources
- Carlino AR, Stinnett JL, Kim DR. New onset of bipolar disorder in late life. Psychosomatics. 2013;54(1):94-97.
- Sajatovic M, Kales HC, Mulsant BH. Prescribing antipsychotics in geriatric patients: Focus on schizophrenia and bipolar disorder. Current Psychiatry. 2017;16(10):20-26,28.
Drug Brand Names
Carbamazepine • Carbatrol, Tegretol
Carboplatin • Paraplatin
Divalproex sodium • Depakote
Doxorubicin liposome injection • Doxil
Gemcitabine injection • Gemzar
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Paclitaxel injection • Abraxane
Quetiapine • Seroquel
1. Prabhakar D, Balon R. Late-onset bipolar disorder: a case for careful appraisal. Psychiatry (Edgmont). 2010;7(1):34-37.
2. Sajatovic M, Strejilevich SA, Gildengers AG, et al. A report on older-age bipolar disorder from the International Society for Bipolar Disorders Task Force. Bipolar Disord. 2015;17(7):689-704.
3. Arciniegas DB. New-onset bipolar disorder in late life: a case of mistaken identity. Am J Psychiatry. 2006;163(2):198-203.
4. Chou P-H, Tseng W-J, Chen L-M, et al. Late onset bipolar disorder: a case report and review of the literature. Journal of Clinical Gerontology and Geriatrics. 2015;6(1):27-29.
5. Lukasiewicz M, Gerard S, Besnard A, et al; Emblem Study Group. Young Mania Rating Scale: how to interpret the numbers? Determination of a severity threshold and of the minimal clinically significant difference in the EMBLEM cohort. Int J Methods Psychiatr Res. 2013;22(1):46-58.
6. Oostervink F, Boomsma MM, Nolen WA; EMBLEM Advisory Board. Bipolar disorder in the elderly; different effects of age and of age of onset. J Affect Disord. 2009;116(3):176-183.
7. Depp CA, Jeste D V. Bipolar disorder in older adults: A critical review. Bipolar Disord. 2004;6(5):343-367.8.
8. Gildengers AG, Butters MA, et al. Cognitive functioning in late-life bipolar disorder. Am J Psychiatry. 2004. doi:10.1176/appi.ajp.161.4.736
9. Steffens DC, Krishnan KR. Structural neuroimaging and mood disorders: Recent findings, implications for classification, and future directions. Biological Psychiatry. 1998;43(10):705-712.
10. Tamashiro JH, Zung S, Zanetti MV, et al. Increased rates of white matter hyperintensities in late-onset bipolar disorder. Bipolar Disord. 2008;10(7):765-775.
11. Aziz R, Lorberg B, Tampi RR. Treatments for late-life bipolar disorder. Am J Geriatr Pharmacother. 2006;4(4):347-364.
12. Wefel JS, Kesler SR, Noll KR, et al. Clinical characteristics, pathophysiology, and management of noncentral nervous system cancer-related cognitive impairment in adults. CA Cancer J Clin. 2015;65(2):123-138.
13. Amidi A, Hosseini SMH, Leemans A, et al. Changes in brain structural networks and cognitive functions in testicular cancer patients receiving cisplatin-based chemotherapy. J Natl Cancer Inst. 2017;109(12). doi: 10.1093/jnci/djx085.
14. Torrence C, Jackson J. New onset mania in late life: case report and literature review. J Mississippi Acad Sci. 2016;61(1):159.
15. Cassidy F, Carroll BJ. Vascular risk factors in late onset mania. Psychol Med. 2002;32(2):359-362.
16. Bellivier F, Golmard JL, Rietschel M, et al. Age at onset in bipolar I affective disorder: further evidence for three subgroups. Am J Psychiatry. 2003;160(5):999-1001.
17. Almeida OP, Fenner S. Bipolar disorder: similarities and differences between patients with illness onset before and after 65 years of age. Int Psychogeriatr. 2002;14(3):311-322.
18. Schürhoff F, Bellivier F, Jouvent R, et al. Early and late onset bipolar disorders: two different forms of manic-depressive illness? J Affect Disord. 2000;58(3):215-21.
Although the peak age of onset of bipolar disorder (BD) is between 20 and 40 years,1 some patients develop BD later in life. The International Society for Bipolar Disorders Task Force has classified the illness into 3 categories:
- early-onset bipolar disorder (EOBD), in which the first manic episode occurs before age 40
- late-onset bipolar disorder (LOBD), in which the initial manic/hypomanic episode occurs after age 50
- older-age bipolar disorder (OABD), in which the first manic/hypomanic episode occurs after age 60.2
OABD represents 25% of the population with BD.3 OABD differs from EOBD in its clinical presentation, biological factors, and psychiatric and somatic comorbidities.4 Studies suggest OABD warrants a more extensive workup to rule out organic causes because symptoms are often attributable to a variety of organic etiologies.
This article describes 3 cases of OABD, including treatments and outcomes. We discuss general treatment recommendations for patients with OABD as cited in the literature. Further research is needed to expand our ability to better care for this unique population.
CASE 1
Mr. D was a 66-year-old African American male with no psychiatric history. His medical history was significant for hypertension, poorly controlled diabetes mellitus, and chronic kidney disease. One year ago, he was diagnosed with cholangiocarcinoma, and underwent uncomplicated right trisegmentectomy, resection of extrahepatic biliary tree, and complete portal lymphadenectomy, with Roux-en-Y hepaticojejunostomy to 2 intrahepatic ducts. He presented to the emergency department (ED) with disorganized behavior for 3 weeks. During that time, Mr. D reported increased distractibility, irritability, hyper-religiosity, racing thoughts, decreased appetite, and decreased need for sleep. There was no pertinent family history.
On mental status examination, Mr. D was agitated, noncooperative, and guarded. His speech was loud and pressured. Mr. D was distractible, tangential, and goal-directed. His Young Mania Rating Scale (YMRS) score was 31, which is highly indicative of mania.5 Computed tomography (CT) scan of the head (Figure 1)
CASE 2
Mr. M was a 63-year-old African American male with no psychiatric history and a medical history significant for hypertension and hypercholesterolemia. He presented to the ED with behavioral changes for 2 weeks. During this time, he experienced decreased need for sleep, agitation, excessive spending, self-conversing, hypersexuality, and paranoia. His family history was significant for schizoaffective disorder, bipolar type.
A mental status examination revealed pressured speech, grandiose delusions, hyper-religiosity, flight of ideas, looseness of association, auditory hallucinations, and tangential thought processes. Mr. M’s initial YMRS score was 56. A CT scan of the head revealed no acute abnormality, but MRI of the brain (Figure 2) showed chronic microvascular ischemic change. Mr. M was diagnosed with bipolar I disorder and admitted. He was started on quetiapine extended release, which was titrated to 600 mg nightly. Divalproex sodium extended release was titrated to 1,500 mg nightly, with subsequent improvement. At discharge, his YMRS score was 15.
Continue to: CASE 3
CASE 3
Ms. F was a 69-year-old White female with no psychiatric history. Her medical history was significant for hypertension, osteoarthritis, and stage III-C ovarian adenocarcinoma with a debulking surgical procedure 5 years earlier. After that, she received adjuvant therapy with paclitaxel and carboplatin, which resulted in a 10-month disease-free interval. Subsequent progression led to cycles of doxorubicin liposomal and gemcitabine. She was in remission until 1 week earlier, when a CT scan of the abdomen/pelvis showed recurrence. She presented to the hospital after disrobing in the street due to hyper-religiosity and divine instruction. She endorsed elevated mood and increased energy despite sleeping only 2 hours daily. Her family psychiatric history was significant for her daughter’s suicide attempt.
A mental status examination revealed disorganized behavior and agitation. Her speech was loud and pressured. She described a “great” mood with congruent affect. Her thought process was circumstantial and illogical. She displayed flight of ideas, grandiose delusions, and paranoia. Ms. F’s initial YMRS score was 38. Vital signs were significant for an elevated blood pressure of 153/113 mm Hg. A CT scan of the head (Figure 3) showed age-related change with no acute findings. Ms. F was admitted with a diagnosis of bipolar I disorder and prescribed olanzapine, 2.5 mg nightly. Due to continued manic symptoms, olanzapine was discontinued, and Ms. F was started on quetiapine, 300 mg nightly, with subsequent improvement. At discharge, her YMRS score was 10.
Differences between EOBD and OABD
BD has always been considered a multi-system illness; however, comorbidity is much more common in OABD than in EOBD. Comorbid conditions are 3 to 4 times more common in patients with OABD.2 Common comorbidities include metabolic syndrome, allergic rhinitis, arthritis, asthma, and cardiovascular disease.
Compared with younger individuals, older patients with BD score lower on the YMRS in the areas of increased activity-energy, language-thought disorder, and sexual interest.6 Psychotic symptoms are less common or less severe in OABD. Although symptom severity is lower, the prevalence of rapid cycling illness is 20% higher in patients with OABD.6 OABD is less commonly associated with a family history.7 This may suggest a difference from the popular genetic component typically found in patients with EOBD.
Cognitive impairment is more commonly found in OABD. Patients with OABD suffer from neuropsychological deficits even during euthymic phases.8 While these deficits may also be found in patients with EOBD, compared with younger patients, older adults are more susceptible to accelerated decline in cognition. OABD can first present within the context of cardiovascular or neuropsychological impairment. It has also been linked to a greater prevalence of white matter hyperintensities compared with EOBD.9,10
Continue to: Treatment is not specific to OABD
Treatment is not specific to OABD
No established treatment guidelines specifically address OABD. It has been treated similarly to EOBD, with antipsychotics, mood stabilizers, antidepressants, and electroconvulsive therapy (ECT). Although lithium is effective, special precautions should be taken when prescribing it to older adults because these patients may be more sensitive to adverse events.11 Drug–drug interactions may also be more likely due to concomitant use of medications for common medical issues such as hypertension.
Treatment with antipsychotics in older patients carries risks. Use of antipsychotics may result in higher rates of morbidity and mortality related to cardiovascular, metabolic, and infectious etiologies. Some literature recommends the use of antipsychotics for OABD; however, the potential benefits must outweigh the risks.6 Monotherapy followed by combination therapy has demonstrated effectiveness in OABD.11 Because symptoms of OABD are often less severe, it may be best to avoid maintenance antipsychotic therapy when possible. With a higher prevalence of depressed mood following manic episodes, use of antidepressant therapy is common in OABD.6 ECT should be considered for patients with treatment-refractory BD.11
Lessons from our case series
Our case series included 3 patients with OABD. These patients’ comorbid conditions included hypertension, hypercholesteremia, and diabetes mellitus. Two patients had a history of cancer, but there was no metastasis to the brain in either case. However, we considered the possibility of structural changes in the brain or cognitive impairment secondary to cancer or its treatment. A literature review confirmed that adult patients treated for noncentral nervous system cancer experienced cancer-related cognitive impairment (CRCI).12 New research suggests that CRCI could be related to altered neuronal integrity along with a disturbance of brain structure networks that process and integrate information.13
We used the YMRS to compare symptom severity and treatment response (Figure 4). Two patients were treated with atypical antipsychotics with a mood stabilizer, and the third patient was prescribed an antipsychotic only. We avoided lithium and carbamazepine as mood stabilizers due to their adverse effect profiles and potential for drug–drug interactions. Each patient responded well to treatment without adverse events.
Future studies are needed to clearly define the safest and most effective treatment guidelines in patients with OABD. We believe that OABD may require the development of a unique treatment algorithm due to the high likelihood of medical comorbidity and age-related variations in treatment response.
Continue to: Etiology of OABD may be different
Etiology of OABD may be different
OABD may be associated with manic presentations and vascular risk factors. MRI imaging that found more white matter hyperintensities and cerebrovascular lesions in patients with OABD compared with younger patients provides evidence of possible differing etiologies.14 Cassidy and Carroll15 found a higher incidence of smoking, hypertension, diabetes mellitus, coronary heart disease, and atrial fibrillation in patients in the older onset group. Bellivier et al16 proposed 3 subgroups of bipolar I disorder; the late-onset subgroup’s etiology was multifactorial. EOBD and OABD subgroups have similar gender ratios,17 first-episode descriptions, and alcohol use rates; however, OABD subgroups have more neurological comorbidity, lesser severe psychosis, and less genetic predisposition.
Although 25% of BD cases are late onset,3 there is still little consensus regarding subgroups and etiological causes. Therefore, additional research specifically focusing on vascular risks may provide much-needed information. Controlling and mitigating vascular risks in OABD may affect its development and course. Despite debated etiologies, the treatment of BD remains consistent, with anticonvulsants preferred over lithium in older individuals.
The Table summarizes clinical pearls about the features and treatment of OABD.
Bottom Line
Compared with younger patients with bipolar disorder (BD), those who develop BD later in life may be more likely to have rapid cycling, medical comorbidities, and cognitive impairment. Older patients with BD also may be more likely to experience adverse effects of the medications commonly used to treat BD, including antipsychotics, lithium, and carbamazepine.
Related Resources
- Carlino AR, Stinnett JL, Kim DR. New onset of bipolar disorder in late life. Psychosomatics. 2013;54(1):94-97.
- Sajatovic M, Kales HC, Mulsant BH. Prescribing antipsychotics in geriatric patients: Focus on schizophrenia and bipolar disorder. Current Psychiatry. 2017;16(10):20-26,28.
Drug Brand Names
Carbamazepine • Carbatrol, Tegretol
Carboplatin • Paraplatin
Divalproex sodium • Depakote
Doxorubicin liposome injection • Doxil
Gemcitabine injection • Gemzar
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Paclitaxel injection • Abraxane
Quetiapine • Seroquel
Although the peak age of onset of bipolar disorder (BD) is between 20 and 40 years,1 some patients develop BD later in life. The International Society for Bipolar Disorders Task Force has classified the illness into 3 categories:
- early-onset bipolar disorder (EOBD), in which the first manic episode occurs before age 40
- late-onset bipolar disorder (LOBD), in which the initial manic/hypomanic episode occurs after age 50
- older-age bipolar disorder (OABD), in which the first manic/hypomanic episode occurs after age 60.2
OABD represents 25% of the population with BD.3 OABD differs from EOBD in its clinical presentation, biological factors, and psychiatric and somatic comorbidities.4 Studies suggest OABD warrants a more extensive workup to rule out organic causes because symptoms are often attributable to a variety of organic etiologies.
This article describes 3 cases of OABD, including treatments and outcomes. We discuss general treatment recommendations for patients with OABD as cited in the literature. Further research is needed to expand our ability to better care for this unique population.
CASE 1
Mr. D was a 66-year-old African American male with no psychiatric history. His medical history was significant for hypertension, poorly controlled diabetes mellitus, and chronic kidney disease. One year ago, he was diagnosed with cholangiocarcinoma, and underwent uncomplicated right trisegmentectomy, resection of extrahepatic biliary tree, and complete portal lymphadenectomy, with Roux-en-Y hepaticojejunostomy to 2 intrahepatic ducts. He presented to the emergency department (ED) with disorganized behavior for 3 weeks. During that time, Mr. D reported increased distractibility, irritability, hyper-religiosity, racing thoughts, decreased appetite, and decreased need for sleep. There was no pertinent family history.
On mental status examination, Mr. D was agitated, noncooperative, and guarded. His speech was loud and pressured. Mr. D was distractible, tangential, and goal-directed. His Young Mania Rating Scale (YMRS) score was 31, which is highly indicative of mania.5 Computed tomography (CT) scan of the head (Figure 1)
CASE 2
Mr. M was a 63-year-old African American male with no psychiatric history and a medical history significant for hypertension and hypercholesterolemia. He presented to the ED with behavioral changes for 2 weeks. During this time, he experienced decreased need for sleep, agitation, excessive spending, self-conversing, hypersexuality, and paranoia. His family history was significant for schizoaffective disorder, bipolar type.
A mental status examination revealed pressured speech, grandiose delusions, hyper-religiosity, flight of ideas, looseness of association, auditory hallucinations, and tangential thought processes. Mr. M’s initial YMRS score was 56. A CT scan of the head revealed no acute abnormality, but MRI of the brain (Figure 2) showed chronic microvascular ischemic change. Mr. M was diagnosed with bipolar I disorder and admitted. He was started on quetiapine extended release, which was titrated to 600 mg nightly. Divalproex sodium extended release was titrated to 1,500 mg nightly, with subsequent improvement. At discharge, his YMRS score was 15.
Continue to: CASE 3
CASE 3
Ms. F was a 69-year-old White female with no psychiatric history. Her medical history was significant for hypertension, osteoarthritis, and stage III-C ovarian adenocarcinoma with a debulking surgical procedure 5 years earlier. After that, she received adjuvant therapy with paclitaxel and carboplatin, which resulted in a 10-month disease-free interval. Subsequent progression led to cycles of doxorubicin liposomal and gemcitabine. She was in remission until 1 week earlier, when a CT scan of the abdomen/pelvis showed recurrence. She presented to the hospital after disrobing in the street due to hyper-religiosity and divine instruction. She endorsed elevated mood and increased energy despite sleeping only 2 hours daily. Her family psychiatric history was significant for her daughter’s suicide attempt.
A mental status examination revealed disorganized behavior and agitation. Her speech was loud and pressured. She described a “great” mood with congruent affect. Her thought process was circumstantial and illogical. She displayed flight of ideas, grandiose delusions, and paranoia. Ms. F’s initial YMRS score was 38. Vital signs were significant for an elevated blood pressure of 153/113 mm Hg. A CT scan of the head (Figure 3) showed age-related change with no acute findings. Ms. F was admitted with a diagnosis of bipolar I disorder and prescribed olanzapine, 2.5 mg nightly. Due to continued manic symptoms, olanzapine was discontinued, and Ms. F was started on quetiapine, 300 mg nightly, with subsequent improvement. At discharge, her YMRS score was 10.
Differences between EOBD and OABD
BD has always been considered a multi-system illness; however, comorbidity is much more common in OABD than in EOBD. Comorbid conditions are 3 to 4 times more common in patients with OABD.2 Common comorbidities include metabolic syndrome, allergic rhinitis, arthritis, asthma, and cardiovascular disease.
Compared with younger individuals, older patients with BD score lower on the YMRS in the areas of increased activity-energy, language-thought disorder, and sexual interest.6 Psychotic symptoms are less common or less severe in OABD. Although symptom severity is lower, the prevalence of rapid cycling illness is 20% higher in patients with OABD.6 OABD is less commonly associated with a family history.7 This may suggest a difference from the popular genetic component typically found in patients with EOBD.
Cognitive impairment is more commonly found in OABD. Patients with OABD suffer from neuropsychological deficits even during euthymic phases.8 While these deficits may also be found in patients with EOBD, compared with younger patients, older adults are more susceptible to accelerated decline in cognition. OABD can first present within the context of cardiovascular or neuropsychological impairment. It has also been linked to a greater prevalence of white matter hyperintensities compared with EOBD.9,10
Continue to: Treatment is not specific to OABD
Treatment is not specific to OABD
No established treatment guidelines specifically address OABD. It has been treated similarly to EOBD, with antipsychotics, mood stabilizers, antidepressants, and electroconvulsive therapy (ECT). Although lithium is effective, special precautions should be taken when prescribing it to older adults because these patients may be more sensitive to adverse events.11 Drug–drug interactions may also be more likely due to concomitant use of medications for common medical issues such as hypertension.
Treatment with antipsychotics in older patients carries risks. Use of antipsychotics may result in higher rates of morbidity and mortality related to cardiovascular, metabolic, and infectious etiologies. Some literature recommends the use of antipsychotics for OABD; however, the potential benefits must outweigh the risks.6 Monotherapy followed by combination therapy has demonstrated effectiveness in OABD.11 Because symptoms of OABD are often less severe, it may be best to avoid maintenance antipsychotic therapy when possible. With a higher prevalence of depressed mood following manic episodes, use of antidepressant therapy is common in OABD.6 ECT should be considered for patients with treatment-refractory BD.11
Lessons from our case series
Our case series included 3 patients with OABD. These patients’ comorbid conditions included hypertension, hypercholesteremia, and diabetes mellitus. Two patients had a history of cancer, but there was no metastasis to the brain in either case. However, we considered the possibility of structural changes in the brain or cognitive impairment secondary to cancer or its treatment. A literature review confirmed that adult patients treated for noncentral nervous system cancer experienced cancer-related cognitive impairment (CRCI).12 New research suggests that CRCI could be related to altered neuronal integrity along with a disturbance of brain structure networks that process and integrate information.13
We used the YMRS to compare symptom severity and treatment response (Figure 4). Two patients were treated with atypical antipsychotics with a mood stabilizer, and the third patient was prescribed an antipsychotic only. We avoided lithium and carbamazepine as mood stabilizers due to their adverse effect profiles and potential for drug–drug interactions. Each patient responded well to treatment without adverse events.
Future studies are needed to clearly define the safest and most effective treatment guidelines in patients with OABD. We believe that OABD may require the development of a unique treatment algorithm due to the high likelihood of medical comorbidity and age-related variations in treatment response.
Continue to: Etiology of OABD may be different
Etiology of OABD may be different
OABD may be associated with manic presentations and vascular risk factors. MRI imaging that found more white matter hyperintensities and cerebrovascular lesions in patients with OABD compared with younger patients provides evidence of possible differing etiologies.14 Cassidy and Carroll15 found a higher incidence of smoking, hypertension, diabetes mellitus, coronary heart disease, and atrial fibrillation in patients in the older onset group. Bellivier et al16 proposed 3 subgroups of bipolar I disorder; the late-onset subgroup’s etiology was multifactorial. EOBD and OABD subgroups have similar gender ratios,17 first-episode descriptions, and alcohol use rates; however, OABD subgroups have more neurological comorbidity, lesser severe psychosis, and less genetic predisposition.
Although 25% of BD cases are late onset,3 there is still little consensus regarding subgroups and etiological causes. Therefore, additional research specifically focusing on vascular risks may provide much-needed information. Controlling and mitigating vascular risks in OABD may affect its development and course. Despite debated etiologies, the treatment of BD remains consistent, with anticonvulsants preferred over lithium in older individuals.
The Table summarizes clinical pearls about the features and treatment of OABD.
Bottom Line
Compared with younger patients with bipolar disorder (BD), those who develop BD later in life may be more likely to have rapid cycling, medical comorbidities, and cognitive impairment. Older patients with BD also may be more likely to experience adverse effects of the medications commonly used to treat BD, including antipsychotics, lithium, and carbamazepine.
Related Resources
- Carlino AR, Stinnett JL, Kim DR. New onset of bipolar disorder in late life. Psychosomatics. 2013;54(1):94-97.
- Sajatovic M, Kales HC, Mulsant BH. Prescribing antipsychotics in geriatric patients: Focus on schizophrenia and bipolar disorder. Current Psychiatry. 2017;16(10):20-26,28.
Drug Brand Names
Carbamazepine • Carbatrol, Tegretol
Carboplatin • Paraplatin
Divalproex sodium • Depakote
Doxorubicin liposome injection • Doxil
Gemcitabine injection • Gemzar
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Paclitaxel injection • Abraxane
Quetiapine • Seroquel
1. Prabhakar D, Balon R. Late-onset bipolar disorder: a case for careful appraisal. Psychiatry (Edgmont). 2010;7(1):34-37.
2. Sajatovic M, Strejilevich SA, Gildengers AG, et al. A report on older-age bipolar disorder from the International Society for Bipolar Disorders Task Force. Bipolar Disord. 2015;17(7):689-704.
3. Arciniegas DB. New-onset bipolar disorder in late life: a case of mistaken identity. Am J Psychiatry. 2006;163(2):198-203.
4. Chou P-H, Tseng W-J, Chen L-M, et al. Late onset bipolar disorder: a case report and review of the literature. Journal of Clinical Gerontology and Geriatrics. 2015;6(1):27-29.
5. Lukasiewicz M, Gerard S, Besnard A, et al; Emblem Study Group. Young Mania Rating Scale: how to interpret the numbers? Determination of a severity threshold and of the minimal clinically significant difference in the EMBLEM cohort. Int J Methods Psychiatr Res. 2013;22(1):46-58.
6. Oostervink F, Boomsma MM, Nolen WA; EMBLEM Advisory Board. Bipolar disorder in the elderly; different effects of age and of age of onset. J Affect Disord. 2009;116(3):176-183.
7. Depp CA, Jeste D V. Bipolar disorder in older adults: A critical review. Bipolar Disord. 2004;6(5):343-367.8.
8. Gildengers AG, Butters MA, et al. Cognitive functioning in late-life bipolar disorder. Am J Psychiatry. 2004. doi:10.1176/appi.ajp.161.4.736
9. Steffens DC, Krishnan KR. Structural neuroimaging and mood disorders: Recent findings, implications for classification, and future directions. Biological Psychiatry. 1998;43(10):705-712.
10. Tamashiro JH, Zung S, Zanetti MV, et al. Increased rates of white matter hyperintensities in late-onset bipolar disorder. Bipolar Disord. 2008;10(7):765-775.
11. Aziz R, Lorberg B, Tampi RR. Treatments for late-life bipolar disorder. Am J Geriatr Pharmacother. 2006;4(4):347-364.
12. Wefel JS, Kesler SR, Noll KR, et al. Clinical characteristics, pathophysiology, and management of noncentral nervous system cancer-related cognitive impairment in adults. CA Cancer J Clin. 2015;65(2):123-138.
13. Amidi A, Hosseini SMH, Leemans A, et al. Changes in brain structural networks and cognitive functions in testicular cancer patients receiving cisplatin-based chemotherapy. J Natl Cancer Inst. 2017;109(12). doi: 10.1093/jnci/djx085.
14. Torrence C, Jackson J. New onset mania in late life: case report and literature review. J Mississippi Acad Sci. 2016;61(1):159.
15. Cassidy F, Carroll BJ. Vascular risk factors in late onset mania. Psychol Med. 2002;32(2):359-362.
16. Bellivier F, Golmard JL, Rietschel M, et al. Age at onset in bipolar I affective disorder: further evidence for three subgroups. Am J Psychiatry. 2003;160(5):999-1001.
17. Almeida OP, Fenner S. Bipolar disorder: similarities and differences between patients with illness onset before and after 65 years of age. Int Psychogeriatr. 2002;14(3):311-322.
18. Schürhoff F, Bellivier F, Jouvent R, et al. Early and late onset bipolar disorders: two different forms of manic-depressive illness? J Affect Disord. 2000;58(3):215-21.
1. Prabhakar D, Balon R. Late-onset bipolar disorder: a case for careful appraisal. Psychiatry (Edgmont). 2010;7(1):34-37.
2. Sajatovic M, Strejilevich SA, Gildengers AG, et al. A report on older-age bipolar disorder from the International Society for Bipolar Disorders Task Force. Bipolar Disord. 2015;17(7):689-704.
3. Arciniegas DB. New-onset bipolar disorder in late life: a case of mistaken identity. Am J Psychiatry. 2006;163(2):198-203.
4. Chou P-H, Tseng W-J, Chen L-M, et al. Late onset bipolar disorder: a case report and review of the literature. Journal of Clinical Gerontology and Geriatrics. 2015;6(1):27-29.
5. Lukasiewicz M, Gerard S, Besnard A, et al; Emblem Study Group. Young Mania Rating Scale: how to interpret the numbers? Determination of a severity threshold and of the minimal clinically significant difference in the EMBLEM cohort. Int J Methods Psychiatr Res. 2013;22(1):46-58.
6. Oostervink F, Boomsma MM, Nolen WA; EMBLEM Advisory Board. Bipolar disorder in the elderly; different effects of age and of age of onset. J Affect Disord. 2009;116(3):176-183.
7. Depp CA, Jeste D V. Bipolar disorder in older adults: A critical review. Bipolar Disord. 2004;6(5):343-367.8.
8. Gildengers AG, Butters MA, et al. Cognitive functioning in late-life bipolar disorder. Am J Psychiatry. 2004. doi:10.1176/appi.ajp.161.4.736
9. Steffens DC, Krishnan KR. Structural neuroimaging and mood disorders: Recent findings, implications for classification, and future directions. Biological Psychiatry. 1998;43(10):705-712.
10. Tamashiro JH, Zung S, Zanetti MV, et al. Increased rates of white matter hyperintensities in late-onset bipolar disorder. Bipolar Disord. 2008;10(7):765-775.
11. Aziz R, Lorberg B, Tampi RR. Treatments for late-life bipolar disorder. Am J Geriatr Pharmacother. 2006;4(4):347-364.
12. Wefel JS, Kesler SR, Noll KR, et al. Clinical characteristics, pathophysiology, and management of noncentral nervous system cancer-related cognitive impairment in adults. CA Cancer J Clin. 2015;65(2):123-138.
13. Amidi A, Hosseini SMH, Leemans A, et al. Changes in brain structural networks and cognitive functions in testicular cancer patients receiving cisplatin-based chemotherapy. J Natl Cancer Inst. 2017;109(12). doi: 10.1093/jnci/djx085.
14. Torrence C, Jackson J. New onset mania in late life: case report and literature review. J Mississippi Acad Sci. 2016;61(1):159.
15. Cassidy F, Carroll BJ. Vascular risk factors in late onset mania. Psychol Med. 2002;32(2):359-362.
16. Bellivier F, Golmard JL, Rietschel M, et al. Age at onset in bipolar I affective disorder: further evidence for three subgroups. Am J Psychiatry. 2003;160(5):999-1001.
17. Almeida OP, Fenner S. Bipolar disorder: similarities and differences between patients with illness onset before and after 65 years of age. Int Psychogeriatr. 2002;14(3):311-322.
18. Schürhoff F, Bellivier F, Jouvent R, et al. Early and late onset bipolar disorders: two different forms of manic-depressive illness? J Affect Disord. 2000;58(3):215-21.
Bipolar patients’ ability to consent can be measured with MacCAT-CR
, according to Christina C. Klein and her associates.
A total of 50 patients who were enrolled in a clinical trial of approved, standard treatments for bipolar disease were included in the consent study. The MacCAT-CR was administered after patients had given consent to be included in the trial, but before the trial had started. Four patients lacked the ability to provide consent for the trial after receiving the MacCAT-CR. After these patients were reeducated and went through the consent process a second time, three were enrolled and one declined enrollment.
Patients with higher Schedule for Assessment of Positive Symptoms scores were more likely to have worse MacCAT-CR Understanding and Appreciation subscale scores; lower Hamilton Depression Rating Scale and higher Clinical Global Impression–Severity scores were associated with worse Reasoning and Understanding subscale scores.
Comorbid ADHD, sex, IQ scores, and age at onset of bipolar disorder were not correlated with any subscale scores. In addition, a history of substance use disorder was associated with higher Appreciation and Reasoning subscale scores.
“The current study provides important information for clinicians and researchers to consider when obtaining informed consent from an individual with bipolar disorder. The MacCAT-CR may serve to identify patients, specifically those with higher psychotic symptoms or global illness severity, as needing additional education regarding informed consent,” the investigators concluded.
Three study coauthors reported conflicts of interest with numerous pharmaceutical companies.
SOURCE: Klein CC et al. J Affect Disord. 2018 Aug 13. doi: 10.1016/j.jad.2018.08.049.
, according to Christina C. Klein and her associates.
A total of 50 patients who were enrolled in a clinical trial of approved, standard treatments for bipolar disease were included in the consent study. The MacCAT-CR was administered after patients had given consent to be included in the trial, but before the trial had started. Four patients lacked the ability to provide consent for the trial after receiving the MacCAT-CR. After these patients were reeducated and went through the consent process a second time, three were enrolled and one declined enrollment.
Patients with higher Schedule for Assessment of Positive Symptoms scores were more likely to have worse MacCAT-CR Understanding and Appreciation subscale scores; lower Hamilton Depression Rating Scale and higher Clinical Global Impression–Severity scores were associated with worse Reasoning and Understanding subscale scores.
Comorbid ADHD, sex, IQ scores, and age at onset of bipolar disorder were not correlated with any subscale scores. In addition, a history of substance use disorder was associated with higher Appreciation and Reasoning subscale scores.
“The current study provides important information for clinicians and researchers to consider when obtaining informed consent from an individual with bipolar disorder. The MacCAT-CR may serve to identify patients, specifically those with higher psychotic symptoms or global illness severity, as needing additional education regarding informed consent,” the investigators concluded.
Three study coauthors reported conflicts of interest with numerous pharmaceutical companies.
SOURCE: Klein CC et al. J Affect Disord. 2018 Aug 13. doi: 10.1016/j.jad.2018.08.049.
, according to Christina C. Klein and her associates.
A total of 50 patients who were enrolled in a clinical trial of approved, standard treatments for bipolar disease were included in the consent study. The MacCAT-CR was administered after patients had given consent to be included in the trial, but before the trial had started. Four patients lacked the ability to provide consent for the trial after receiving the MacCAT-CR. After these patients were reeducated and went through the consent process a second time, three were enrolled and one declined enrollment.
Patients with higher Schedule for Assessment of Positive Symptoms scores were more likely to have worse MacCAT-CR Understanding and Appreciation subscale scores; lower Hamilton Depression Rating Scale and higher Clinical Global Impression–Severity scores were associated with worse Reasoning and Understanding subscale scores.
Comorbid ADHD, sex, IQ scores, and age at onset of bipolar disorder were not correlated with any subscale scores. In addition, a history of substance use disorder was associated with higher Appreciation and Reasoning subscale scores.
“The current study provides important information for clinicians and researchers to consider when obtaining informed consent from an individual with bipolar disorder. The MacCAT-CR may serve to identify patients, specifically those with higher psychotic symptoms or global illness severity, as needing additional education regarding informed consent,” the investigators concluded.
Three study coauthors reported conflicts of interest with numerous pharmaceutical companies.
SOURCE: Klein CC et al. J Affect Disord. 2018 Aug 13. doi: 10.1016/j.jad.2018.08.049.
FROM THE JOURNAL OF AFFECTIVE DISORDERS
Early maladaptive schemas increase suicide risk, ideation in bipolar
The entitlement, social isolation, and defectiveness early maladaptive schemas (EMSs) were associated with increased suicide risk and ideation in patients with bipolar disorder, according to Vahid Khosravani of Shahid Beheshti University of Medical Sciences, Tehran, Iran, and his associates.
“These findings were in line with previous studies (J Nerv Ment Dis. 2016 Mar. 204[3]:236-9) showing higher scores of social isolation and entitlement in [bipolar disorder] patients with suicide attempts than those without such attempts,” Mr. Khosravani and his associates wrote in Psychiatry Research.
For the study, 100 inpatients with bipolar disorder completed the Young Schema Questionnaire–Short Form (YSQ-SF), the Bipolar Depression Rating Scale (BDRS), the Young Mania Rating Scale (YMRS), and the Beck Scale for Suicidal Ideation (BSSI). Of that group, 59% had attempted suicide and 59% had a BSSI score of 6 or higher, indicating high suicidal risk, reported Mr. Khosravani and his associates.
; they also had higher levels of depressive and hypomanic/manic symptoms. Current suicide ideation was associated with higher entitlement and defectiveness EMS scores, as well as with increased hypomanic/manic symptoms.
“The findings suggest that manic symptoms as well as specific EMSs including social isolation, entitlement, and defectiveness emerge as potentially implicated in suicidality in BD patients,” the investigators noted. “Therefore, providing social support in the economic, social, political, cultural, and educational spheres may be a factor in preventing suicide.”
Mr. Khosravani and his associates said their study received no funding from public, commercial, or nonprofit agencies. The investigators declared no conflicts of interest.
SOURCE: Khosravani V et al. Psychiatry Res. 2019 Jan. (271):351-9.
The entitlement, social isolation, and defectiveness early maladaptive schemas (EMSs) were associated with increased suicide risk and ideation in patients with bipolar disorder, according to Vahid Khosravani of Shahid Beheshti University of Medical Sciences, Tehran, Iran, and his associates.
“These findings were in line with previous studies (J Nerv Ment Dis. 2016 Mar. 204[3]:236-9) showing higher scores of social isolation and entitlement in [bipolar disorder] patients with suicide attempts than those without such attempts,” Mr. Khosravani and his associates wrote in Psychiatry Research.
For the study, 100 inpatients with bipolar disorder completed the Young Schema Questionnaire–Short Form (YSQ-SF), the Bipolar Depression Rating Scale (BDRS), the Young Mania Rating Scale (YMRS), and the Beck Scale for Suicidal Ideation (BSSI). Of that group, 59% had attempted suicide and 59% had a BSSI score of 6 or higher, indicating high suicidal risk, reported Mr. Khosravani and his associates.
; they also had higher levels of depressive and hypomanic/manic symptoms. Current suicide ideation was associated with higher entitlement and defectiveness EMS scores, as well as with increased hypomanic/manic symptoms.
“The findings suggest that manic symptoms as well as specific EMSs including social isolation, entitlement, and defectiveness emerge as potentially implicated in suicidality in BD patients,” the investigators noted. “Therefore, providing social support in the economic, social, political, cultural, and educational spheres may be a factor in preventing suicide.”
Mr. Khosravani and his associates said their study received no funding from public, commercial, or nonprofit agencies. The investigators declared no conflicts of interest.
SOURCE: Khosravani V et al. Psychiatry Res. 2019 Jan. (271):351-9.
The entitlement, social isolation, and defectiveness early maladaptive schemas (EMSs) were associated with increased suicide risk and ideation in patients with bipolar disorder, according to Vahid Khosravani of Shahid Beheshti University of Medical Sciences, Tehran, Iran, and his associates.
“These findings were in line with previous studies (J Nerv Ment Dis. 2016 Mar. 204[3]:236-9) showing higher scores of social isolation and entitlement in [bipolar disorder] patients with suicide attempts than those without such attempts,” Mr. Khosravani and his associates wrote in Psychiatry Research.
For the study, 100 inpatients with bipolar disorder completed the Young Schema Questionnaire–Short Form (YSQ-SF), the Bipolar Depression Rating Scale (BDRS), the Young Mania Rating Scale (YMRS), and the Beck Scale for Suicidal Ideation (BSSI). Of that group, 59% had attempted suicide and 59% had a BSSI score of 6 or higher, indicating high suicidal risk, reported Mr. Khosravani and his associates.
; they also had higher levels of depressive and hypomanic/manic symptoms. Current suicide ideation was associated with higher entitlement and defectiveness EMS scores, as well as with increased hypomanic/manic symptoms.
“The findings suggest that manic symptoms as well as specific EMSs including social isolation, entitlement, and defectiveness emerge as potentially implicated in suicidality in BD patients,” the investigators noted. “Therefore, providing social support in the economic, social, political, cultural, and educational spheres may be a factor in preventing suicide.”
Mr. Khosravani and his associates said their study received no funding from public, commercial, or nonprofit agencies. The investigators declared no conflicts of interest.
SOURCE: Khosravani V et al. Psychiatry Res. 2019 Jan. (271):351-9.
FROM PSYCHIATRY RESEARCH
ADHD more likely, causes worse outcomes in patients with BD
ADHD is significantly more common and is associated with worse outcomes in patients with bipolar disorder, according to Ross J. Baldessarini, MD, of McLean Hospital and Harvard Medical School, Boston, and his associates.
In a study of 703 patients diagnosed with bipolar disorder (BD) type I or II who were evaluated, treated, and followed at the Lucio Bini Mood Disorder Centers in Rome and Cagliari, Italy, 173 patients had co-occurring lifetime ADHD. Co-occurring conditions were more likely in men and in those with BD-I. The lifetime ADHD prevalence rate of 24.6% in patients with bipolar disorder is significantly higher than the incidence in the general population, the investigators wrote in the Journal of Affective Disorders.
Patients with co-occurring ADHD and BD were more likely to have performed worse in school, have higher Adult ADHD Self-Report Scale scores, be unemployed, have lower socioeconomic status, be married, have separated, have substance abuse, have attempted suicide, and have hypomania, compared with patients with only BD. However, they were less likely to have an anxiety disorder or a family history of mood disorders.
“The association of ADHD with a less successful and stable educational history, more unemployment, lack of or failed marriages, and greater risk of suicide attempts and substance abuse indicates unfavorable effects of having ADHD with BD. Such effects may arise by the impact of ADHD early during development,” the investigators concluded.
The study was partly supported by a research award from the Aretaeus Association of Rome and grants from the Bruce J. Anderson Foundation and the McLean Private Donors Research Fund. No conflicts of interest were reported.
SOURCE: Baldessarini RJ et al. J Affect Disord. 2018 Sep 17. doi: 10.1016/j.jad.2018.09.038.
ADHD is significantly more common and is associated with worse outcomes in patients with bipolar disorder, according to Ross J. Baldessarini, MD, of McLean Hospital and Harvard Medical School, Boston, and his associates.
In a study of 703 patients diagnosed with bipolar disorder (BD) type I or II who were evaluated, treated, and followed at the Lucio Bini Mood Disorder Centers in Rome and Cagliari, Italy, 173 patients had co-occurring lifetime ADHD. Co-occurring conditions were more likely in men and in those with BD-I. The lifetime ADHD prevalence rate of 24.6% in patients with bipolar disorder is significantly higher than the incidence in the general population, the investigators wrote in the Journal of Affective Disorders.
Patients with co-occurring ADHD and BD were more likely to have performed worse in school, have higher Adult ADHD Self-Report Scale scores, be unemployed, have lower socioeconomic status, be married, have separated, have substance abuse, have attempted suicide, and have hypomania, compared with patients with only BD. However, they were less likely to have an anxiety disorder or a family history of mood disorders.
“The association of ADHD with a less successful and stable educational history, more unemployment, lack of or failed marriages, and greater risk of suicide attempts and substance abuse indicates unfavorable effects of having ADHD with BD. Such effects may arise by the impact of ADHD early during development,” the investigators concluded.
The study was partly supported by a research award from the Aretaeus Association of Rome and grants from the Bruce J. Anderson Foundation and the McLean Private Donors Research Fund. No conflicts of interest were reported.
SOURCE: Baldessarini RJ et al. J Affect Disord. 2018 Sep 17. doi: 10.1016/j.jad.2018.09.038.
ADHD is significantly more common and is associated with worse outcomes in patients with bipolar disorder, according to Ross J. Baldessarini, MD, of McLean Hospital and Harvard Medical School, Boston, and his associates.
In a study of 703 patients diagnosed with bipolar disorder (BD) type I or II who were evaluated, treated, and followed at the Lucio Bini Mood Disorder Centers in Rome and Cagliari, Italy, 173 patients had co-occurring lifetime ADHD. Co-occurring conditions were more likely in men and in those with BD-I. The lifetime ADHD prevalence rate of 24.6% in patients with bipolar disorder is significantly higher than the incidence in the general population, the investigators wrote in the Journal of Affective Disorders.
Patients with co-occurring ADHD and BD were more likely to have performed worse in school, have higher Adult ADHD Self-Report Scale scores, be unemployed, have lower socioeconomic status, be married, have separated, have substance abuse, have attempted suicide, and have hypomania, compared with patients with only BD. However, they were less likely to have an anxiety disorder or a family history of mood disorders.
“The association of ADHD with a less successful and stable educational history, more unemployment, lack of or failed marriages, and greater risk of suicide attempts and substance abuse indicates unfavorable effects of having ADHD with BD. Such effects may arise by the impact of ADHD early during development,” the investigators concluded.
The study was partly supported by a research award from the Aretaeus Association of Rome and grants from the Bruce J. Anderson Foundation and the McLean Private Donors Research Fund. No conflicts of interest were reported.
SOURCE: Baldessarini RJ et al. J Affect Disord. 2018 Sep 17. doi: 10.1016/j.jad.2018.09.038.
FROM THE JOURNAL OF AFFECTIVE DISORDERS
Best of Psychopharmacology: Stimulants, ketamine, benzodiazapines
Amazon In this episode we go back to the summer for two master classes on ketamine and stimulants, respectively and we drop in on two conversations between Lorenzo Norris, MD on anxiety and comorbid ADHD as well as a conversation on benzodiazapines. The Psychcast will be back with new content in 2019.
Apple
Google
Spotify
Amazon In this episode we go back to the summer for two master classes on ketamine and stimulants, respectively and we drop in on two conversations between Lorenzo Norris, MD on anxiety and comorbid ADHD as well as a conversation on benzodiazapines. The Psychcast will be back with new content in 2019.
Apple
Google
Spotify
Amazon In this episode we go back to the summer for two master classes on ketamine and stimulants, respectively and we drop in on two conversations between Lorenzo Norris, MD on anxiety and comorbid ADHD as well as a conversation on benzodiazapines. The Psychcast will be back with new content in 2019.
Apple
Google
Spotify