Current Psychiatry

Differentiating the irritable, oppositional child with attention-deficit/hyperactivity disorder (ADHD) from the child with bipolar disorder (BD) often is difficult. To make matters more complicated, 50% to 70% of patients with BD have comorbid ADHD.^1,2 Accordingly, clinicians are often faced with the moody, irritable, dis­ruptive child whose parents want to know if he (she) is “bipolar” to try to deal with oppositional and mood behaviors.

In this article, we present an approach that will help you distinguish these 2 disorders from each other.

Precision medicineThere is a lack of evidence-based methods for diagnosing psychiat­ric disorders in children and adolescents. DSM-5 provides clinicians with diagnostic checklists that rely on the clinician’s judgment and training in evaluating a patient.³ In The innovator’s prescription: a dis­ruptive solution for health care, Christensen et al⁴ describe how medi­cine is moving from “intuitive medicine” to empirical medicine and toward “precision medicine.” Intuitive medicine depends on the clini­cian’s expertise, training, and exposure to different disorders, which is the traditional clinical model that predominates in child psychiatry. Empirical medicine relies on laboratory results, scans, scales, and other standardized tools.

Precision medicine occurs when a disorder can be precisely diag­nosed and its cause understood, and when it can be treated with effec­tive, evidence-based therapies. An example of this movement toward precision is Timothy syndrome (TS), a rare autosomal dominant disorder characterized by physical malformations, cardiac arrhyth­mias and structural heart defects, webbing of fingers and toes, and autism spectrum disorder. In the past, a child with TS would have been given a diagnosis of intellectual disability, or a specialist in developmental disorders might recognize the pattern of TS. It is now known that TS is caused by muta­tions in CACNA1C, the gene encoding the calcium channel Ca_v1.2α subunit, allowing precise diagnosis by genotyping.⁵

Although there are several tools that help clinicians assess symptoms of ADHD and BD, including rating scales such the Vanderbilt ADHD Diagnostic Rating Scale and Young Mania Rating Scale, none of these scales are diagnostic. Youngstrom et al^6,7 have developed an evidence-based strategy to diagnose pediatric BD. This method uses a nomogram that takes into account the base rate of BD in a clinical set­ting and family history of BD.

We will describe and contrast the epi­demiologic and clinical characteristics of pediatric BD from ADHD and use the Youngstrom nomogram to better define these patients. Although still far from pre­cision medicine, the type of approach rep­resents an ongoing effort in mental health care to increase diagnostic accuracy and improve treatment outcomes.

Pediatric bipolar disorder
Prevalence of pediatric BD is 1.8% (95% CI, 1.1% to 3.0%),⁸ which does not include sub-threshold cases of BD. ADHD and oppo­sitional defiant disorder (ODD) are 8 to 10 times more prevalent. For the purposes of the nomogram, the “base rate” is the rate at which a disorder occurs in different clinical settings. In general outpatient clinics, BD might occur 6% to 8% of the time, whereas in a county-run child psychiatry inpatient facility the rate is 11%.⁶ A reasonable rate in an outpatient pediatric setting is 6%.

Family history. In the Bipolar Offspring Study,9 the rate of BD in children of par­ents with BD was 13 times greater than that of controls, and the rate of anxiety and behavior disorders was approximately twice that of children of parents without BD (Table 1).⁹ This study evaluated 388 children of 233 parents with BD and 251 children of 143 demographically matched controls.

Elevated or expansive mood. The child might have a mood that is inappropriately giddy, silly, elated, or euphoric. Often this mood will be present without reason and last for several hours. It may be distin­guished from a transient cheerful mood by the intensity and duration of the episode. The child with BD may have little to no insight about the inappropriate nature of their elevated mood, when present. 

Irritable mood. The child might become markedly belligerent or irritated with intense outbursts of anger, 2 to 3 times a day for several hours. An adolescent might appear extremely oppositional, belliger­ent, or hostile with parents and others. 

Grandiosity or inflated self-esteem can be confused with brief childhood fanta­sies of increased capability. Typically, true grandiosity can manifest as assertion of great competency in all areas of life, which usually cannot be altered by contrary exter­nal evidence. Occasionally, this is bizarre and includes delusions of “super powers.” The child in a manic episode will not only assert that she can fly, but will jump off the garage roof to prove it. 

Decreased need for sleep. The child may only require 4 to 5 hours of sleep a night during a manic episode without feeling fatigued or showing evidence of tiredness. Consider substance use in this differential diagnosis, especially in adolescents.

Increased talkativeness. Lack of inhibi­tion to social norms may lead pediatric BD patients to blurt out answers during class or repeatedly be disciplined for talking to peers in class. Speech typically is rapid and pressured to the point where it might be continuous and seems to jump between loosely related subjects.

Flight of ideas or racing thoughts. The child or adolescent might report a subjec­tive feeling that his thoughts are moving so rapidly that his speech cannot keep up. Often this is differentiated from rapid speech by the degree of rapidity the patient expresses loosely related topics that might seem completely unrelated to the listener.

Distractibility, short attention span. During a manic episode, the child or ado­lescent might report that it is impossible to pay attention to class or other outside events because of rapidly changing focus of their thoughts. This symptom must be care­fully distinguished from the distractibility and inattention of ADHD, which typically is a more fixed and long-standing pattern rather than a brief episodic phenomenon in a manic or hypomanic episode.

Increase in goal-directed activity. During a mild manic episode, the child or adoles­cent may be capable of accomplishing a great deal of work. However, episodes that are more severe manifest as an individual starting numerous ambitious projects that she later is unable to complete.

Excessive risk-taking activities. The child or adolescent might become involved in forbidden, pleasurable activities that have a high risk of adverse consequences. This can manifest as hypersexual behavior, fre­quent fighting, increased recklessness, use of drugs and alcohol, shopping sprees, and reckless driving.

There are few studies comparing patients with comorbid BD and ADHD with patients with only ADHD. Geller et al¹¹ compared 60 children with BD and ADHD (mean age, 10) to age- and sex-matched patients with ADHD and no mood disorder. Compared with children who had ADHD, those with BD exhib­ited significantly greater elevated mood, grandiosity, flight and/or racing of ideas, decreased need for sleep, and hypersexual­ity (Figure 1,¹¹). Features common to both groups—and therefore not useful in differentiating the disorders—included irritability, hyperactivity, accelerated speech, and distractibility.
 

CASE REPORTIrritable and disruptiveBill, age 12, has been brought to see you by his mother because she is concerned about escalating behavior problems at home and school in the past several months. The school principal has called her about his obnoxious behavior with teachers and about other par­ents’ complaints that he has made unwanted sexual advances to girls who sit next to him in class.

Bill, who is in the 7th grade, is on the verge of being suspended for his inappropriate and disruptive behavior. His parents report that he is irritable around them and stays up all night, messaging his friends on the Internet from his iPad in his bedroom. They attribute his inappro­priate sexual behavior to puberty and possibly to the Web sites he views.

Bill’s mother is concerned about his:
   • increasing behavior problems during the last several months at home and school
   • intensifying irritability and depressive symptoms
   • staying up all night on the Internet, phoning friends, and doing projects
   • frequent unprovoked, outbursts of rage occurring with increasing frequency and intensity (almost daily)
   • moderate grandiosity, including telling the soccer coach and teachers how to do their jobs
   • inappropriate sexual behavior, including kissing and touching female classmates.

During your history, you learn that Bill has been a bright and artistic child, with good academic performance. His peer relation­ships have been satisfactory, but not excel­lent—he tends to be “bossy” with his peers. He is medically healthy and not taking any medications. As part of your history, you also talk with Bill and his family about exposure to trauma or significant stressors, which they deny. You learn that Bill’s father was diag­nosed with BD I at age 32.

Completing the nomogram developed by Youngstrom et al^6,7 using these variables (see this article at CurrentPsychiatry.com for Figure 2)^6,7 gives Bill a post-test probability of approximately 42%. The threshold for moving ahead with assessment and possible treat­ment, the “test-treatment threshold,” depends on your clinical setting.^12,13 Our clinical expe­rience is that, when the post-test probability exceeds 30%, further assessment for BD is warranted.

The next strategy is to look at Bill’s scores on externalizing behaviors using an instru­ment such as the Vanderbilt ADHD Diagnostic Parent Rating Scale. Few pediatric patients with BD will score low on externalizing behaviors.14 Bill scores in the clinically signifi­cant range for hyperactivity/impulsivity and positive on the screeners for ODD, conduct disorder (CD), and anxiety/depression.

You decide that Bill is at high risk of pedi­atric BD; he has a post-test probability of approximately 45%, and many externalizing behaviors on the Vanderbilt. You give Bill a diagnosis of BD I and ADHD and prescribe ris­peridone, 0.5 mg/d, which results in signifi­cant improvement in mood swings and other manic behaviors.

ADHD
Epidemiology. ADHD is one of the most common neurodevelopmental disorders in childhood, with prevalence estimates of 8% of U.S. children.^15,16 Overall, boys are more likely to be assigned a diagnosis of ADHD than girls.¹⁵ Although ADHD often is diagnosed in early childhood, research is working to clarify the lifetime preva­lence of ADHD into late adolescence and adulthood. Current estimates suggest that ADHD persists into adulthood in close to two-thirds of patients.¹⁷ However, the symptom presentation can change during adolescence and adulthood, with less overt hyperactivity and symptoms of impulsivity transitioning to risky behaviors involving trouble with the law, substance use, and sexual promiscuity.¹⁷

As in pediatric BD, comorbidity is com­mon in ADHD, with uncomplicated ADHD being the exception rather than the rule. Recent studies have suggested that approx­imately two-thirds of children who have a diagnosis of ADHD have ≥1 comorbid diag­noses.¹⁵ Common comorbidities are similar to those seen in BD, including ODD, CD, anxiety disorders, depression, and learning disability. Several tools and resources are available to help clinicians navigate these issues within their practices.

Family history. Genetics appear to play a large role in ADHD, with twin studies suggesting inheritance of approximately 76%.18 Environmental factors contribute, either in the development of ADHD or in the exacerbation of an underlying familial predisposition. Interestingly, in children with BD, family history often is significant for several family members who have both ADHD and BD. However, in children with ADHD only, family history often reflects an absence of family members with BD.19 Although not diagnostic, this pattern can be helpful when considering a diagnosis of BD vs ADHD.

Clinical picture. ADHD often is recog­nized in childhood; DSM-5 criteria spec­ify that symptoms be present before age 12 and persist for at least 6 months. This characterization of the timing of symp­toms helps exclude behavioral disruptions related to external factors such as trauma (eg, death of a caregiver) or abuse. It also is important to note that symptoms might be present earlier but not come to attention clinically until a later age, perhaps because of increasing demands placed on the child by school, peer groups, and extracurricu­lar activities. To make an ADHD diag­nosis, symptoms must be present in >1 setting and interfere with functioning or development.

Core symptoms of ADHD include inat­tention, hyperactivity, and impulsivity that are out of proportion to the child’s developmental level (Table 2).20 When considering diagnosis of ADHD, 6 of 9 symptoms for inattention and/or hyperactivity-impulsivity must be present at a clinically significant level.

Three different ADHD presentations are recognized: combined, inattentive, and hyperactive impulsive. Children with predominant impulsive and hyperactive behaviors generally come to clinical atten­tion at a younger age; inattentive symptoms often take longer to identify.

Children with ADHD have been noted to have lower tolerance for frustration, which might make anger outbursts and aggressive behavior more likely. Anger and aggression in ADHD often stem from impulsivity, rather than irritable mood seen with BD.18 Issues related to self-esteem, depression, substance use, and CD can contribute to symptoms of irrita­bility, anger, and aggression that can occur in children with ADHD. Although these symptoms can overlap with those seen in children with BD, other core symptoms of ADHD will not be present.

ODD is one of the most common comor­bidities among children with ADHD, and the combination of ODD and ADHD may be confused with BD. Children with ODD often are noted to exhibit a pattern of negative and defiant behavior that is out of proportion to what is seen in their peers and for their age and develop­mental level (Table 3).²⁰ When considering an ODD diagnosis, 4 out of 8 symptoms must be present at a clinically significant level.

The following case highlights the poten­tial similarities between ADHD/ODD and BD, with tips on how to distinguish them.

CASE REPORT

Angry and destructiveSam, age 7, has been given a diagnosis of ADHD, but his parents think that he isn’t improving with methylphenidate treatment. They are concerned that he has anger issues like his uncle, who has “bipolar disorder.”

Sam’s parents find that he gets frustrated easily and note that he has frequent short “meltdowns” and “mood swings.” During these episodes he yells, is aggressive towards others, and can be destructive. They are concerned because Sam will become angry quickly, then act as if nothing happened after the meltdown has blown over. Sam’s parents feel that he doesn’t listen to them and often argues when they make a request. His parents note that when they push harder, Sam digs in his heels, which can trigger his meltdowns.

Despite clearly disobeying his parents, Sam often says that things aren’t his fault and blames his parents or siblings instead. Sam seems to disagree with people often. His mother reports “if I say the water looks blue, he’ll say it’s green.” Often, Sam seems to argue or pester others to get a rise out of them. This is causing problems for Sam with his siblings and peers, and significant stress for his parents. Family history suggests that Sam’s uncle may have ADHD with CD or a substance use disorder, rather than true BD. Other than Sam’s uncle, there is no family his­tory for BD.

Sam’s parents say that extended release methylphenidate, 20 mg/d, has helped with hyperactivity, but they are concerned that other symptoms have not improved. Aside from the symptoms listed above, Sam is described as a happy child. There is no his­tory of trauma, and no symptoms of anxiety are noted. Sam sometimes gets “down” when things don’t go his way, but this lasts only for a few hours. Sam has a history of delayed sleep onset, which responded well to melato­nin. No other symptoms that suggest mania are described.

You complete the pediatric bipolar nomo­gram (Figure 3)^6,7 and Sam’s parents com­plete a Vanderbilt ADHD Diagnostic Parent Rating Scale. At first, Sam seems to have sev­eral factors that might indicate BD: aggres­sive behavior, mood swings, sleep problems, and, possibly, a family history of BD.

However, a careful history provides several clues that Sam has a comorbid diagnosis of ODD. Sam is exhibiting the classic pattern of negativist behavior seen in children with ODD. In contrast to the episodic pattern of BD, these symptoms are prevalent and per­sistent, and manifest as an overall pattern of functioning. Impulsivity seen in children with ADHD can complicate the picture, but again appears as a consistent pattern rather than bouts of irritability. Sam’s core symptoms of ADHD (hyperactivity) improved with methyl­phenidate, but the underlying symptoms of ODD persisted.

Sleep problems are common in chil­dren who have ADHD and BD, but Sam’s delayed sleep onset responded to melato­nin, whereas the insomnia seen in BD often is refractory to lower-intensity interven­tions, such as melatonin. Taking a careful family history led you to believe that BD in the family is unlikely. Although this type of detail may not always be available, it can be helpful to ask about mental health symptoms that seem to “run in the family.”

Bottom Line

Distinguishing the child who has bipolar disorder from one who has attention-deficit/hyperactivity disorder can be challenging. A careful history helps ensure that you are on the path toward understanding the diagnostic possibilities. Tools such as the Vanderbilt Rating Scale can further clarify possible diagnoses, and the nomogram approach can provide even more predictive information when considering a diagnosis of bipolar disorder.

Related Resources
• Children and Adults with Attention Deficit/Hyperactivity Disorder (CHADD). www.chadd.org.
• American Academy of Child and Adolescent Psychiatry. Facts for Families. www.aacap.org/cs/root/facts_for_families/ facts_for_families.
• Froehlich TE, Delgado SV, Anixt JS. Expanding medica­tion options for pediatric ADHD. Current Psychiatry. 2013;(12)12:20-29.
• Passarotti AM, Pavuluri MN. Brain functional domains in­form therapeutic interventions in attention-deficit/hyper­activity disorder and pediatric bipolar disorder. Expert Rev Neurother. 2011;11(6):897-914.

Drug Brand Names
Methylphenidate • Ritalin,  Methylin, Metadate CD, Metadate ER, Methylin ER, Ritalin LA, Ritalin SR, Concerta, Quillivant XR, Daytrana

Risperidone • Risperdal

Differentiating the irritable, oppositional child with attention-deficit/hyperactivity disorder (ADHD) from the child with bipolar disorder (BD) often is difficult. To make matters more complicated, 50% to 70% of patients with BD have comorbid ADHD.^1,2 Accordingly, clinicians are often faced with the moody, irritable, dis­ruptive child whose parents want to know if he (she) is “bipolar” to try to deal with oppositional and mood behaviors.

In this article, we present an approach that will help you distinguish these 2 disorders from each other.

Precision medicineThere is a lack of evidence-based methods for diagnosing psychiat­ric disorders in children and adolescents. DSM-5 provides clinicians with diagnostic checklists that rely on the clinician’s judgment and training in evaluating a patient.³ In The innovator’s prescription: a dis­ruptive solution for health care, Christensen et al⁴ describe how medi­cine is moving from “intuitive medicine” to empirical medicine and toward “precision medicine.” Intuitive medicine depends on the clini­cian’s expertise, training, and exposure to different disorders, which is the traditional clinical model that predominates in child psychiatry. Empirical medicine relies on laboratory results, scans, scales, and other standardized tools.

Precision medicine occurs when a disorder can be precisely diag­nosed and its cause understood, and when it can be treated with effec­tive, evidence-based therapies. An example of this movement toward precision is Timothy syndrome (TS), a rare autosomal dominant disorder characterized by physical malformations, cardiac arrhyth­mias and structural heart defects, webbing of fingers and toes, and autism spectrum disorder. In the past, a child with TS would have been given a diagnosis of intellectual disability, or a specialist in developmental disorders might recognize the pattern of TS. It is now known that TS is caused by muta­tions in CACNA1C, the gene encoding the calcium channel Ca_v1.2α subunit, allowing precise diagnosis by genotyping.⁵

Although there are several tools that help clinicians assess symptoms of ADHD and BD, including rating scales such the Vanderbilt ADHD Diagnostic Rating Scale and Young Mania Rating Scale, none of these scales are diagnostic. Youngstrom et al^6,7 have developed an evidence-based strategy to diagnose pediatric BD. This method uses a nomogram that takes into account the base rate of BD in a clinical set­ting and family history of BD.

We will describe and contrast the epi­demiologic and clinical characteristics of pediatric BD from ADHD and use the Youngstrom nomogram to better define these patients. Although still far from pre­cision medicine, the type of approach rep­resents an ongoing effort in mental health care to increase diagnostic accuracy and improve treatment outcomes.

Pediatric bipolar disorder
Prevalence of pediatric BD is 1.8% (95% CI, 1.1% to 3.0%),⁸ which does not include sub-threshold cases of BD. ADHD and oppo­sitional defiant disorder (ODD) are 8 to 10 times more prevalent. For the purposes of the nomogram, the “base rate” is the rate at which a disorder occurs in different clinical settings. In general outpatient clinics, BD might occur 6% to 8% of the time, whereas in a county-run child psychiatry inpatient facility the rate is 11%.⁶ A reasonable rate in an outpatient pediatric setting is 6%.

Family history. In the Bipolar Offspring Study,9 the rate of BD in children of par­ents with BD was 13 times greater than that of controls, and the rate of anxiety and behavior disorders was approximately twice that of children of parents without BD (Table 1).⁹ This study evaluated 388 children of 233 parents with BD and 251 children of 143 demographically matched controls.

Elevated or expansive mood. The child might have a mood that is inappropriately giddy, silly, elated, or euphoric. Often this mood will be present without reason and last for several hours. It may be distin­guished from a transient cheerful mood by the intensity and duration of the episode. The child with BD may have little to no insight about the inappropriate nature of their elevated mood, when present. 

Irritable mood. The child might become markedly belligerent or irritated with intense outbursts of anger, 2 to 3 times a day for several hours. An adolescent might appear extremely oppositional, belliger­ent, or hostile with parents and others. 

Grandiosity or inflated self-esteem can be confused with brief childhood fanta­sies of increased capability. Typically, true grandiosity can manifest as assertion of great competency in all areas of life, which usually cannot be altered by contrary exter­nal evidence. Occasionally, this is bizarre and includes delusions of “super powers.” The child in a manic episode will not only assert that she can fly, but will jump off the garage roof to prove it. 

Decreased need for sleep. The child may only require 4 to 5 hours of sleep a night during a manic episode without feeling fatigued or showing evidence of tiredness. Consider substance use in this differential diagnosis, especially in adolescents.

Increased talkativeness. Lack of inhibi­tion to social norms may lead pediatric BD patients to blurt out answers during class or repeatedly be disciplined for talking to peers in class. Speech typically is rapid and pressured to the point where it might be continuous and seems to jump between loosely related subjects.

Flight of ideas or racing thoughts. The child or adolescent might report a subjec­tive feeling that his thoughts are moving so rapidly that his speech cannot keep up. Often this is differentiated from rapid speech by the degree of rapidity the patient expresses loosely related topics that might seem completely unrelated to the listener.

Distractibility, short attention span. During a manic episode, the child or ado­lescent might report that it is impossible to pay attention to class or other outside events because of rapidly changing focus of their thoughts. This symptom must be care­fully distinguished from the distractibility and inattention of ADHD, which typically is a more fixed and long-standing pattern rather than a brief episodic phenomenon in a manic or hypomanic episode.

Increase in goal-directed activity. During a mild manic episode, the child or adoles­cent may be capable of accomplishing a great deal of work. However, episodes that are more severe manifest as an individual starting numerous ambitious projects that she later is unable to complete.

Excessive risk-taking activities. The child or adolescent might become involved in forbidden, pleasurable activities that have a high risk of adverse consequences. This can manifest as hypersexual behavior, fre­quent fighting, increased recklessness, use of drugs and alcohol, shopping sprees, and reckless driving.

There are few studies comparing patients with comorbid BD and ADHD with patients with only ADHD. Geller et al¹¹ compared 60 children with BD and ADHD (mean age, 10) to age- and sex-matched patients with ADHD and no mood disorder. Compared with children who had ADHD, those with BD exhib­ited significantly greater elevated mood, grandiosity, flight and/or racing of ideas, decreased need for sleep, and hypersexual­ity (Figure 1,¹¹). Features common to both groups—and therefore not useful in differentiating the disorders—included irritability, hyperactivity, accelerated speech, and distractibility.
 

CASE REPORTIrritable and disruptiveBill, age 12, has been brought to see you by his mother because she is concerned about escalating behavior problems at home and school in the past several months. The school principal has called her about his obnoxious behavior with teachers and about other par­ents’ complaints that he has made unwanted sexual advances to girls who sit next to him in class.

Bill, who is in the 7th grade, is on the verge of being suspended for his inappropriate and disruptive behavior. His parents report that he is irritable around them and stays up all night, messaging his friends on the Internet from his iPad in his bedroom. They attribute his inappro­priate sexual behavior to puberty and possibly to the Web sites he views.

Bill’s mother is concerned about his:
   • increasing behavior problems during the last several months at home and school
   • intensifying irritability and depressive symptoms
   • staying up all night on the Internet, phoning friends, and doing projects
   • frequent unprovoked, outbursts of rage occurring with increasing frequency and intensity (almost daily)
   • moderate grandiosity, including telling the soccer coach and teachers how to do their jobs
   • inappropriate sexual behavior, including kissing and touching female classmates.

During your history, you learn that Bill has been a bright and artistic child, with good academic performance. His peer relation­ships have been satisfactory, but not excel­lent—he tends to be “bossy” with his peers. He is medically healthy and not taking any medications. As part of your history, you also talk with Bill and his family about exposure to trauma or significant stressors, which they deny. You learn that Bill’s father was diag­nosed with BD I at age 32.

Completing the nomogram developed by Youngstrom et al^6,7 using these variables (see this article at CurrentPsychiatry.com for Figure 2)^6,7 gives Bill a post-test probability of approximately 42%. The threshold for moving ahead with assessment and possible treat­ment, the “test-treatment threshold,” depends on your clinical setting.^12,13 Our clinical expe­rience is that, when the post-test probability exceeds 30%, further assessment for BD is warranted.

The next strategy is to look at Bill’s scores on externalizing behaviors using an instru­ment such as the Vanderbilt ADHD Diagnostic Parent Rating Scale. Few pediatric patients with BD will score low on externalizing behaviors.14 Bill scores in the clinically signifi­cant range for hyperactivity/impulsivity and positive on the screeners for ODD, conduct disorder (CD), and anxiety/depression.

You decide that Bill is at high risk of pedi­atric BD; he has a post-test probability of approximately 45%, and many externalizing behaviors on the Vanderbilt. You give Bill a diagnosis of BD I and ADHD and prescribe ris­peridone, 0.5 mg/d, which results in signifi­cant improvement in mood swings and other manic behaviors.

ADHD
Epidemiology. ADHD is one of the most common neurodevelopmental disorders in childhood, with prevalence estimates of 8% of U.S. children.^15,16 Overall, boys are more likely to be assigned a diagnosis of ADHD than girls.¹⁵ Although ADHD often is diagnosed in early childhood, research is working to clarify the lifetime preva­lence of ADHD into late adolescence and adulthood. Current estimates suggest that ADHD persists into adulthood in close to two-thirds of patients.¹⁷ However, the symptom presentation can change during adolescence and adulthood, with less overt hyperactivity and symptoms of impulsivity transitioning to risky behaviors involving trouble with the law, substance use, and sexual promiscuity.¹⁷

As in pediatric BD, comorbidity is com­mon in ADHD, with uncomplicated ADHD being the exception rather than the rule. Recent studies have suggested that approx­imately two-thirds of children who have a diagnosis of ADHD have ≥1 comorbid diag­noses.¹⁵ Common comorbidities are similar to those seen in BD, including ODD, CD, anxiety disorders, depression, and learning disability. Several tools and resources are available to help clinicians navigate these issues within their practices.

Family history. Genetics appear to play a large role in ADHD, with twin studies suggesting inheritance of approximately 76%.18 Environmental factors contribute, either in the development of ADHD or in the exacerbation of an underlying familial predisposition. Interestingly, in children with BD, family history often is significant for several family members who have both ADHD and BD. However, in children with ADHD only, family history often reflects an absence of family members with BD.19 Although not diagnostic, this pattern can be helpful when considering a diagnosis of BD vs ADHD.

Clinical picture. ADHD often is recog­nized in childhood; DSM-5 criteria spec­ify that symptoms be present before age 12 and persist for at least 6 months. This characterization of the timing of symp­toms helps exclude behavioral disruptions related to external factors such as trauma (eg, death of a caregiver) or abuse. It also is important to note that symptoms might be present earlier but not come to attention clinically until a later age, perhaps because of increasing demands placed on the child by school, peer groups, and extracurricu­lar activities. To make an ADHD diag­nosis, symptoms must be present in >1 setting and interfere with functioning or development.

Core symptoms of ADHD include inat­tention, hyperactivity, and impulsivity that are out of proportion to the child’s developmental level (Table 2).20 When considering diagnosis of ADHD, 6 of 9 symptoms for inattention and/or hyperactivity-impulsivity must be present at a clinically significant level.

Three different ADHD presentations are recognized: combined, inattentive, and hyperactive impulsive. Children with predominant impulsive and hyperactive behaviors generally come to clinical atten­tion at a younger age; inattentive symptoms often take longer to identify.

Children with ADHD have been noted to have lower tolerance for frustration, which might make anger outbursts and aggressive behavior more likely. Anger and aggression in ADHD often stem from impulsivity, rather than irritable mood seen with BD.18 Issues related to self-esteem, depression, substance use, and CD can contribute to symptoms of irrita­bility, anger, and aggression that can occur in children with ADHD. Although these symptoms can overlap with those seen in children with BD, other core symptoms of ADHD will not be present.

ODD is one of the most common comor­bidities among children with ADHD, and the combination of ODD and ADHD may be confused with BD. Children with ODD often are noted to exhibit a pattern of negative and defiant behavior that is out of proportion to what is seen in their peers and for their age and develop­mental level (Table 3).²⁰ When considering an ODD diagnosis, 4 out of 8 symptoms must be present at a clinically significant level.

The following case highlights the poten­tial similarities between ADHD/ODD and BD, with tips on how to distinguish them.

CASE REPORT

Angry and destructiveSam, age 7, has been given a diagnosis of ADHD, but his parents think that he isn’t improving with methylphenidate treatment. They are concerned that he has anger issues like his uncle, who has “bipolar disorder.”

Sam’s parents find that he gets frustrated easily and note that he has frequent short “meltdowns” and “mood swings.” During these episodes he yells, is aggressive towards others, and can be destructive. They are concerned because Sam will become angry quickly, then act as if nothing happened after the meltdown has blown over. Sam’s parents feel that he doesn’t listen to them and often argues when they make a request. His parents note that when they push harder, Sam digs in his heels, which can trigger his meltdowns.

Despite clearly disobeying his parents, Sam often says that things aren’t his fault and blames his parents or siblings instead. Sam seems to disagree with people often. His mother reports “if I say the water looks blue, he’ll say it’s green.” Often, Sam seems to argue or pester others to get a rise out of them. This is causing problems for Sam with his siblings and peers, and significant stress for his parents. Family history suggests that Sam’s uncle may have ADHD with CD or a substance use disorder, rather than true BD. Other than Sam’s uncle, there is no family his­tory for BD.

Sam’s parents say that extended release methylphenidate, 20 mg/d, has helped with hyperactivity, but they are concerned that other symptoms have not improved. Aside from the symptoms listed above, Sam is described as a happy child. There is no his­tory of trauma, and no symptoms of anxiety are noted. Sam sometimes gets “down” when things don’t go his way, but this lasts only for a few hours. Sam has a history of delayed sleep onset, which responded well to melato­nin. No other symptoms that suggest mania are described.

You complete the pediatric bipolar nomo­gram (Figure 3)^6,7 and Sam’s parents com­plete a Vanderbilt ADHD Diagnostic Parent Rating Scale. At first, Sam seems to have sev­eral factors that might indicate BD: aggres­sive behavior, mood swings, sleep problems, and, possibly, a family history of BD.

However, a careful history provides several clues that Sam has a comorbid diagnosis of ODD. Sam is exhibiting the classic pattern of negativist behavior seen in children with ODD. In contrast to the episodic pattern of BD, these symptoms are prevalent and per­sistent, and manifest as an overall pattern of functioning. Impulsivity seen in children with ADHD can complicate the picture, but again appears as a consistent pattern rather than bouts of irritability. Sam’s core symptoms of ADHD (hyperactivity) improved with methyl­phenidate, but the underlying symptoms of ODD persisted.

Sleep problems are common in chil­dren who have ADHD and BD, but Sam’s delayed sleep onset responded to melato­nin, whereas the insomnia seen in BD often is refractory to lower-intensity interven­tions, such as melatonin. Taking a careful family history led you to believe that BD in the family is unlikely. Although this type of detail may not always be available, it can be helpful to ask about mental health symptoms that seem to “run in the family.”

Bottom Line

Distinguishing the child who has bipolar disorder from one who has attention-deficit/hyperactivity disorder can be challenging. A careful history helps ensure that you are on the path toward understanding the diagnostic possibilities. Tools such as the Vanderbilt Rating Scale can further clarify possible diagnoses, and the nomogram approach can provide even more predictive information when considering a diagnosis of bipolar disorder.

Related Resources
• Children and Adults with Attention Deficit/Hyperactivity Disorder (CHADD). www.chadd.org.
• American Academy of Child and Adolescent Psychiatry. Facts for Families. www.aacap.org/cs/root/facts_for_families/ facts_for_families.
• Froehlich TE, Delgado SV, Anixt JS. Expanding medica­tion options for pediatric ADHD. Current Psychiatry. 2013;(12)12:20-29.
• Passarotti AM, Pavuluri MN. Brain functional domains in­form therapeutic interventions in attention-deficit/hyper­activity disorder and pediatric bipolar disorder. Expert Rev Neurother. 2011;11(6):897-914.

Drug Brand Names
Methylphenidate • Ritalin,  Methylin, Metadate CD, Metadate ER, Methylin ER, Ritalin LA, Ritalin SR, Concerta, Quillivant XR, Daytrana

Risperidone • Risperdal

Differentiating the irritable, oppositional child with attention-deficit/hyperactivity disorder (ADHD) from the child with bipolar disorder (BD) often is difficult. To make matters more complicated, 50% to 70% of patients with BD have comorbid ADHD.^1,2 Accordingly, clinicians are often faced with the moody, irritable, dis­ruptive child whose parents want to know if he (she) is “bipolar” to try to deal with oppositional and mood behaviors.

In this article, we present an approach that will help you distinguish these 2 disorders from each other.

Precision medicineThere is a lack of evidence-based methods for diagnosing psychiat­ric disorders in children and adolescents. DSM-5 provides clinicians with diagnostic checklists that rely on the clinician’s judgment and training in evaluating a patient.³ In The innovator’s prescription: a dis­ruptive solution for health care, Christensen et al⁴ describe how medi­cine is moving from “intuitive medicine” to empirical medicine and toward “precision medicine.” Intuitive medicine depends on the clini­cian’s expertise, training, and exposure to different disorders, which is the traditional clinical model that predominates in child psychiatry. Empirical medicine relies on laboratory results, scans, scales, and other standardized tools.

Precision medicine occurs when a disorder can be precisely diag­nosed and its cause understood, and when it can be treated with effec­tive, evidence-based therapies. An example of this movement toward precision is Timothy syndrome (TS), a rare autosomal dominant disorder characterized by physical malformations, cardiac arrhyth­mias and structural heart defects, webbing of fingers and toes, and autism spectrum disorder. In the past, a child with TS would have been given a diagnosis of intellectual disability, or a specialist in developmental disorders might recognize the pattern of TS. It is now known that TS is caused by muta­tions in CACNA1C, the gene encoding the calcium channel Ca_v1.2α subunit, allowing precise diagnosis by genotyping.⁵

Although there are several tools that help clinicians assess symptoms of ADHD and BD, including rating scales such the Vanderbilt ADHD Diagnostic Rating Scale and Young Mania Rating Scale, none of these scales are diagnostic. Youngstrom et al^6,7 have developed an evidence-based strategy to diagnose pediatric BD. This method uses a nomogram that takes into account the base rate of BD in a clinical set­ting and family history of BD.

We will describe and contrast the epi­demiologic and clinical characteristics of pediatric BD from ADHD and use the Youngstrom nomogram to better define these patients. Although still far from pre­cision medicine, the type of approach rep­resents an ongoing effort in mental health care to increase diagnostic accuracy and improve treatment outcomes.

Pediatric bipolar disorder
Prevalence of pediatric BD is 1.8% (95% CI, 1.1% to 3.0%),⁸ which does not include sub-threshold cases of BD. ADHD and oppo­sitional defiant disorder (ODD) are 8 to 10 times more prevalent. For the purposes of the nomogram, the “base rate” is the rate at which a disorder occurs in different clinical settings. In general outpatient clinics, BD might occur 6% to 8% of the time, whereas in a county-run child psychiatry inpatient facility the rate is 11%.⁶ A reasonable rate in an outpatient pediatric setting is 6%.

Family history. In the Bipolar Offspring Study,9 the rate of BD in children of par­ents with BD was 13 times greater than that of controls, and the rate of anxiety and behavior disorders was approximately twice that of children of parents without BD (Table 1).⁹ This study evaluated 388 children of 233 parents with BD and 251 children of 143 demographically matched controls.

Elevated or expansive mood. The child might have a mood that is inappropriately giddy, silly, elated, or euphoric. Often this mood will be present without reason and last for several hours. It may be distin­guished from a transient cheerful mood by the intensity and duration of the episode. The child with BD may have little to no insight about the inappropriate nature of their elevated mood, when present. 

Irritable mood. The child might become markedly belligerent or irritated with intense outbursts of anger, 2 to 3 times a day for several hours. An adolescent might appear extremely oppositional, belliger­ent, or hostile with parents and others. 

Grandiosity or inflated self-esteem can be confused with brief childhood fanta­sies of increased capability. Typically, true grandiosity can manifest as assertion of great competency in all areas of life, which usually cannot be altered by contrary exter­nal evidence. Occasionally, this is bizarre and includes delusions of “super powers.” The child in a manic episode will not only assert that she can fly, but will jump off the garage roof to prove it. 

Decreased need for sleep. The child may only require 4 to 5 hours of sleep a night during a manic episode without feeling fatigued or showing evidence of tiredness. Consider substance use in this differential diagnosis, especially in adolescents.

Increased talkativeness. Lack of inhibi­tion to social norms may lead pediatric BD patients to blurt out answers during class or repeatedly be disciplined for talking to peers in class. Speech typically is rapid and pressured to the point where it might be continuous and seems to jump between loosely related subjects.

Flight of ideas or racing thoughts. The child or adolescent might report a subjec­tive feeling that his thoughts are moving so rapidly that his speech cannot keep up. Often this is differentiated from rapid speech by the degree of rapidity the patient expresses loosely related topics that might seem completely unrelated to the listener.

Distractibility, short attention span. During a manic episode, the child or ado­lescent might report that it is impossible to pay attention to class or other outside events because of rapidly changing focus of their thoughts. This symptom must be care­fully distinguished from the distractibility and inattention of ADHD, which typically is a more fixed and long-standing pattern rather than a brief episodic phenomenon in a manic or hypomanic episode.

Increase in goal-directed activity. During a mild manic episode, the child or adoles­cent may be capable of accomplishing a great deal of work. However, episodes that are more severe manifest as an individual starting numerous ambitious projects that she later is unable to complete.

Excessive risk-taking activities. The child or adolescent might become involved in forbidden, pleasurable activities that have a high risk of adverse consequences. This can manifest as hypersexual behavior, fre­quent fighting, increased recklessness, use of drugs and alcohol, shopping sprees, and reckless driving.

There are few studies comparing patients with comorbid BD and ADHD with patients with only ADHD. Geller et al¹¹ compared 60 children with BD and ADHD (mean age, 10) to age- and sex-matched patients with ADHD and no mood disorder. Compared with children who had ADHD, those with BD exhib­ited significantly greater elevated mood, grandiosity, flight and/or racing of ideas, decreased need for sleep, and hypersexual­ity (Figure 1,¹¹). Features common to both groups—and therefore not useful in differentiating the disorders—included irritability, hyperactivity, accelerated speech, and distractibility.
 

CASE REPORTIrritable and disruptiveBill, age 12, has been brought to see you by his mother because she is concerned about escalating behavior problems at home and school in the past several months. The school principal has called her about his obnoxious behavior with teachers and about other par­ents’ complaints that he has made unwanted sexual advances to girls who sit next to him in class.

Bill, who is in the 7th grade, is on the verge of being suspended for his inappropriate and disruptive behavior. His parents report that he is irritable around them and stays up all night, messaging his friends on the Internet from his iPad in his bedroom. They attribute his inappro­priate sexual behavior to puberty and possibly to the Web sites he views.

Bill’s mother is concerned about his:
   • increasing behavior problems during the last several months at home and school
   • intensifying irritability and depressive symptoms
   • staying up all night on the Internet, phoning friends, and doing projects
   • frequent unprovoked, outbursts of rage occurring with increasing frequency and intensity (almost daily)
   • moderate grandiosity, including telling the soccer coach and teachers how to do their jobs
   • inappropriate sexual behavior, including kissing and touching female classmates.

During your history, you learn that Bill has been a bright and artistic child, with good academic performance. His peer relation­ships have been satisfactory, but not excel­lent—he tends to be “bossy” with his peers. He is medically healthy and not taking any medications. As part of your history, you also talk with Bill and his family about exposure to trauma or significant stressors, which they deny. You learn that Bill’s father was diag­nosed with BD I at age 32.

Completing the nomogram developed by Youngstrom et al^6,7 using these variables (see this article at CurrentPsychiatry.com for Figure 2)^6,7 gives Bill a post-test probability of approximately 42%. The threshold for moving ahead with assessment and possible treat­ment, the “test-treatment threshold,” depends on your clinical setting.^12,13 Our clinical expe­rience is that, when the post-test probability exceeds 30%, further assessment for BD is warranted.

The next strategy is to look at Bill’s scores on externalizing behaviors using an instru­ment such as the Vanderbilt ADHD Diagnostic Parent Rating Scale. Few pediatric patients with BD will score low on externalizing behaviors.14 Bill scores in the clinically signifi­cant range for hyperactivity/impulsivity and positive on the screeners for ODD, conduct disorder (CD), and anxiety/depression.

You decide that Bill is at high risk of pedi­atric BD; he has a post-test probability of approximately 45%, and many externalizing behaviors on the Vanderbilt. You give Bill a diagnosis of BD I and ADHD and prescribe ris­peridone, 0.5 mg/d, which results in signifi­cant improvement in mood swings and other manic behaviors.

ADHD
Epidemiology. ADHD is one of the most common neurodevelopmental disorders in childhood, with prevalence estimates of 8% of U.S. children.^15,16 Overall, boys are more likely to be assigned a diagnosis of ADHD than girls.¹⁵ Although ADHD often is diagnosed in early childhood, research is working to clarify the lifetime preva­lence of ADHD into late adolescence and adulthood. Current estimates suggest that ADHD persists into adulthood in close to two-thirds of patients.¹⁷ However, the symptom presentation can change during adolescence and adulthood, with less overt hyperactivity and symptoms of impulsivity transitioning to risky behaviors involving trouble with the law, substance use, and sexual promiscuity.¹⁷

As in pediatric BD, comorbidity is com­mon in ADHD, with uncomplicated ADHD being the exception rather than the rule. Recent studies have suggested that approx­imately two-thirds of children who have a diagnosis of ADHD have ≥1 comorbid diag­noses.¹⁵ Common comorbidities are similar to those seen in BD, including ODD, CD, anxiety disorders, depression, and learning disability. Several tools and resources are available to help clinicians navigate these issues within their practices.

Family history. Genetics appear to play a large role in ADHD, with twin studies suggesting inheritance of approximately 76%.18 Environmental factors contribute, either in the development of ADHD or in the exacerbation of an underlying familial predisposition. Interestingly, in children with BD, family history often is significant for several family members who have both ADHD and BD. However, in children with ADHD only, family history often reflects an absence of family members with BD.19 Although not diagnostic, this pattern can be helpful when considering a diagnosis of BD vs ADHD.

Clinical picture. ADHD often is recog­nized in childhood; DSM-5 criteria spec­ify that symptoms be present before age 12 and persist for at least 6 months. This characterization of the timing of symp­toms helps exclude behavioral disruptions related to external factors such as trauma (eg, death of a caregiver) or abuse. It also is important to note that symptoms might be present earlier but not come to attention clinically until a later age, perhaps because of increasing demands placed on the child by school, peer groups, and extracurricu­lar activities. To make an ADHD diag­nosis, symptoms must be present in >1 setting and interfere with functioning or development.

Core symptoms of ADHD include inat­tention, hyperactivity, and impulsivity that are out of proportion to the child’s developmental level (Table 2).20 When considering diagnosis of ADHD, 6 of 9 symptoms for inattention and/or hyperactivity-impulsivity must be present at a clinically significant level.

Three different ADHD presentations are recognized: combined, inattentive, and hyperactive impulsive. Children with predominant impulsive and hyperactive behaviors generally come to clinical atten­tion at a younger age; inattentive symptoms often take longer to identify.

Children with ADHD have been noted to have lower tolerance for frustration, which might make anger outbursts and aggressive behavior more likely. Anger and aggression in ADHD often stem from impulsivity, rather than irritable mood seen with BD.18 Issues related to self-esteem, depression, substance use, and CD can contribute to symptoms of irrita­bility, anger, and aggression that can occur in children with ADHD. Although these symptoms can overlap with those seen in children with BD, other core symptoms of ADHD will not be present.

ODD is one of the most common comor­bidities among children with ADHD, and the combination of ODD and ADHD may be confused with BD. Children with ODD often are noted to exhibit a pattern of negative and defiant behavior that is out of proportion to what is seen in their peers and for their age and develop­mental level (Table 3).²⁰ When considering an ODD diagnosis, 4 out of 8 symptoms must be present at a clinically significant level.

The following case highlights the poten­tial similarities between ADHD/ODD and BD, with tips on how to distinguish them.

CASE REPORT

Angry and destructiveSam, age 7, has been given a diagnosis of ADHD, but his parents think that he isn’t improving with methylphenidate treatment. They are concerned that he has anger issues like his uncle, who has “bipolar disorder.”

Sam’s parents find that he gets frustrated easily and note that he has frequent short “meltdowns” and “mood swings.” During these episodes he yells, is aggressive towards others, and can be destructive. They are concerned because Sam will become angry quickly, then act as if nothing happened after the meltdown has blown over. Sam’s parents feel that he doesn’t listen to them and often argues when they make a request. His parents note that when they push harder, Sam digs in his heels, which can trigger his meltdowns.

Despite clearly disobeying his parents, Sam often says that things aren’t his fault and blames his parents or siblings instead. Sam seems to disagree with people often. His mother reports “if I say the water looks blue, he’ll say it’s green.” Often, Sam seems to argue or pester others to get a rise out of them. This is causing problems for Sam with his siblings and peers, and significant stress for his parents. Family history suggests that Sam’s uncle may have ADHD with CD or a substance use disorder, rather than true BD. Other than Sam’s uncle, there is no family his­tory for BD.

Sam’s parents say that extended release methylphenidate, 20 mg/d, has helped with hyperactivity, but they are concerned that other symptoms have not improved. Aside from the symptoms listed above, Sam is described as a happy child. There is no his­tory of trauma, and no symptoms of anxiety are noted. Sam sometimes gets “down” when things don’t go his way, but this lasts only for a few hours. Sam has a history of delayed sleep onset, which responded well to melato­nin. No other symptoms that suggest mania are described.

You complete the pediatric bipolar nomo­gram (Figure 3)^6,7 and Sam’s parents com­plete a Vanderbilt ADHD Diagnostic Parent Rating Scale. At first, Sam seems to have sev­eral factors that might indicate BD: aggres­sive behavior, mood swings, sleep problems, and, possibly, a family history of BD.

However, a careful history provides several clues that Sam has a comorbid diagnosis of ODD. Sam is exhibiting the classic pattern of negativist behavior seen in children with ODD. In contrast to the episodic pattern of BD, these symptoms are prevalent and per­sistent, and manifest as an overall pattern of functioning. Impulsivity seen in children with ADHD can complicate the picture, but again appears as a consistent pattern rather than bouts of irritability. Sam’s core symptoms of ADHD (hyperactivity) improved with methyl­phenidate, but the underlying symptoms of ODD persisted.

Sleep problems are common in chil­dren who have ADHD and BD, but Sam’s delayed sleep onset responded to melato­nin, whereas the insomnia seen in BD often is refractory to lower-intensity interven­tions, such as melatonin. Taking a careful family history led you to believe that BD in the family is unlikely. Although this type of detail may not always be available, it can be helpful to ask about mental health symptoms that seem to “run in the family.”

Bottom Line

Distinguishing the child who has bipolar disorder from one who has attention-deficit/hyperactivity disorder can be challenging. A careful history helps ensure that you are on the path toward understanding the diagnostic possibilities. Tools such as the Vanderbilt Rating Scale can further clarify possible diagnoses, and the nomogram approach can provide even more predictive information when considering a diagnosis of bipolar disorder.

Related Resources
• Children and Adults with Attention Deficit/Hyperactivity Disorder (CHADD). www.chadd.org.
• American Academy of Child and Adolescent Psychiatry. Facts for Families. www.aacap.org/cs/root/facts_for_families/ facts_for_families.
• Froehlich TE, Delgado SV, Anixt JS. Expanding medica­tion options for pediatric ADHD. Current Psychiatry. 2013;(12)12:20-29.
• Passarotti AM, Pavuluri MN. Brain functional domains in­form therapeutic interventions in attention-deficit/hyper­activity disorder and pediatric bipolar disorder. Expert Rev Neurother. 2011;11(6):897-914.

Drug Brand Names
Methylphenidate • Ritalin,  Methylin, Metadate CD, Metadate ER, Methylin ER, Ritalin LA, Ritalin SR, Concerta, Quillivant XR, Daytrana

Risperidone • Risperdal

Ataxia is a well-known complication of chronic alcohol abuse, which is attributed to degeneration of the cerebellar vermis. However, effective treatment approaches, as well as the timing and level of recovery, remain unclear. One cross-sectional study found that long-term abstainers from alcohol had less severe ataxia than short-term abstainers,¹ suggesting that improvement is possible with continued sobriety. However, a recent longitudinal study contradicts this finding, reporting no improvement in ataxia in patients abstinent for 10 weeks to 1 year.²

CASE REPORT
Unable to walk, heavy alcohol use

Mr. G, a 59-year-old white male with a history of daily, heavy alcohol use, presents to the emergency room reporting that he has “not been able to walk right” for 3 weeks. He is in a wheelchair because of ataxia and difficulty balancing. He denies headaches, visual changes, weakness, numbness, and difficulty speaking or swallowing.

Mr. G reports drinking one 40-oz bottle of malt liquor and 2 pints of vodka per day for more than 40 years. His alcohol abuse led to homelessness, unemployment, and divorce. Despite heavy drinking, he denies signs of withdrawal, including shaking, sweating, seizures, and delirium.

Mr. G has no other medical conditions. He denies a family history of neurologic disorders or substance abuse.

His pulse is 100 beats per minute, respirations of 16 breaths per minute, temperature of 37°C, and blood pressure of 143/89 mm Hg. Physical examination reveals a wide-based gait.

Mr. G is admitted to the inpatient psychiatric unit to monitor and treat his alcohol withdrawal and to undergo further workup of the gait disturbance.

A head CT scan shows non-specific changes; an EEG also is within normal limits. Complete blood count, basic metabolic panel, liver function test, HIV test, acute hepatitis panel, thyroid function test, erythrocyte sedimentation rate, and vitamin B₁₂ tests are within normal ranges.

A full neurologic exam reveals a wide-based gait, impaired heel-shin test, and dysmetria on finger-nose-finger test. Mr. G is given a diagnosis of ataxia due to alcoholic cerebellar degeneration. Thiamine repletion is suggested.

Treatment and outcome

Mr. G continues on thiamine, 100 mg, twice daily, and oxazepam, 15 mg, as needed, to manage withdrawal symptoms. He receives gait training 3 times per week.

Approximately 10 days after admission, Mr. G is able to ambulate with a walker. Three weeks after admission, his gait has improved and he walks with a cane. (See the video at CurrentPsychiatry.com for an illustration of this progressive recovery.)

After discharge, Mr. G is referred to an addiction psychiatrist and addiction psychotherapist for ongoing treatment of alcohol use disorder.

Making the diagnosis

In a patient complaining of balance difficulties, consider ataxia secondary to cerebellar degeneration.

• Take a complete history. Ask about the onset and progression of ataxia.
• Obtain a family history. Some types of ataxia are genetic.
• Perform a neurologic examination, which may reveal signs of cerebellar deficits, particularly characteristic wide-based gait. These patients will have difficulty when walking in tandem. Other impairments on the neurologic exam that may raise suspicion for a cerebellar disorder include: impaired heel-shin test, impaired finger-nose-finger test (dysmetria), impaired rapid alternating movements (dysdiadochokinesia), nystagmus, impaired smooth pursuits, intention tremor, or speech abnormalities.
• Perform head imaging, such as a CT scan or MRI. In patients with ataxia secondary to alcohol abuse, imaging might reveal degeneration of the cerebellar vermis.
• Perform laboratory tests, such as inflammatory markers, vitamin levels, and thyroid function testing to detect possible toxic-metabolic or inflammatory causes.

Alcohol-induced ataxia can be diagnosed in patients with a history of heavy drinking if the workup does not reveal another possible cause for the gait disturbance. Other less common deficits associated with alcohol-induced cerebellar injury include:

• dysarthria
• abnormal rate and force of movement
• limb ataxia.³

Recommendations

• Be able to recognize the characteristic gait of patients with alcohol-induced ataxia.
• Provide thiamine supplementation.
• Refer patients to physical therapy.
• Educate your patients that their gait will not improve and may worsen if they continue to drink.
• Refer patients for ongoing treatment for alcohol use disorder, including medication management and psychotherapy.

Our experience suggests that patients with alcohol use disorder with cerebellar ataxia could have a good prognosis for ambulation. Improvement could occur over several weeks; it is unclear whether further gains can be expected with months or years of abstinence.

Ataxia is a well-known complication of chronic alcohol abuse, which is attributed to degeneration of the cerebellar vermis. However, effective treatment approaches, as well as the timing and level of recovery, remain unclear. One cross-sectional study found that long-term abstainers from alcohol had less severe ataxia than short-term abstainers,¹ suggesting that improvement is possible with continued sobriety. However, a recent longitudinal study contradicts this finding, reporting no improvement in ataxia in patients abstinent for 10 weeks to 1 year.²

CASE REPORT
Unable to walk, heavy alcohol use

Mr. G, a 59-year-old white male with a history of daily, heavy alcohol use, presents to the emergency room reporting that he has “not been able to walk right” for 3 weeks. He is in a wheelchair because of ataxia and difficulty balancing. He denies headaches, visual changes, weakness, numbness, and difficulty speaking or swallowing.

Mr. G reports drinking one 40-oz bottle of malt liquor and 2 pints of vodka per day for more than 40 years. His alcohol abuse led to homelessness, unemployment, and divorce. Despite heavy drinking, he denies signs of withdrawal, including shaking, sweating, seizures, and delirium.

Mr. G has no other medical conditions. He denies a family history of neurologic disorders or substance abuse.

His pulse is 100 beats per minute, respirations of 16 breaths per minute, temperature of 37°C, and blood pressure of 143/89 mm Hg. Physical examination reveals a wide-based gait.

Mr. G is admitted to the inpatient psychiatric unit to monitor and treat his alcohol withdrawal and to undergo further workup of the gait disturbance.

A head CT scan shows non-specific changes; an EEG also is within normal limits. Complete blood count, basic metabolic panel, liver function test, HIV test, acute hepatitis panel, thyroid function test, erythrocyte sedimentation rate, and vitamin B₁₂ tests are within normal ranges.

A full neurologic exam reveals a wide-based gait, impaired heel-shin test, and dysmetria on finger-nose-finger test. Mr. G is given a diagnosis of ataxia due to alcoholic cerebellar degeneration. Thiamine repletion is suggested.

Treatment and outcome

Mr. G continues on thiamine, 100 mg, twice daily, and oxazepam, 15 mg, as needed, to manage withdrawal symptoms. He receives gait training 3 times per week.

Approximately 10 days after admission, Mr. G is able to ambulate with a walker. Three weeks after admission, his gait has improved and he walks with a cane. (See the video at CurrentPsychiatry.com for an illustration of this progressive recovery.)

After discharge, Mr. G is referred to an addiction psychiatrist and addiction psychotherapist for ongoing treatment of alcohol use disorder.

Making the diagnosis

In a patient complaining of balance difficulties, consider ataxia secondary to cerebellar degeneration.

• Take a complete history. Ask about the onset and progression of ataxia.
• Obtain a family history. Some types of ataxia are genetic.
• Perform a neurologic examination, which may reveal signs of cerebellar deficits, particularly characteristic wide-based gait. These patients will have difficulty when walking in tandem. Other impairments on the neurologic exam that may raise suspicion for a cerebellar disorder include: impaired heel-shin test, impaired finger-nose-finger test (dysmetria), impaired rapid alternating movements (dysdiadochokinesia), nystagmus, impaired smooth pursuits, intention tremor, or speech abnormalities.
• Perform head imaging, such as a CT scan or MRI. In patients with ataxia secondary to alcohol abuse, imaging might reveal degeneration of the cerebellar vermis.
• Perform laboratory tests, such as inflammatory markers, vitamin levels, and thyroid function testing to detect possible toxic-metabolic or inflammatory causes.

Alcohol-induced ataxia can be diagnosed in patients with a history of heavy drinking if the workup does not reveal another possible cause for the gait disturbance. Other less common deficits associated with alcohol-induced cerebellar injury include:

• dysarthria
• abnormal rate and force of movement
• limb ataxia.³

Recommendations

• Be able to recognize the characteristic gait of patients with alcohol-induced ataxia.
• Provide thiamine supplementation.
• Refer patients to physical therapy.
• Educate your patients that their gait will not improve and may worsen if they continue to drink.
• Refer patients for ongoing treatment for alcohol use disorder, including medication management and psychotherapy.

Our experience suggests that patients with alcohol use disorder with cerebellar ataxia could have a good prognosis for ambulation. Improvement could occur over several weeks; it is unclear whether further gains can be expected with months or years of abstinence.

Ataxia is a well-known complication of chronic alcohol abuse, which is attributed to degeneration of the cerebellar vermis. However, effective treatment approaches, as well as the timing and level of recovery, remain unclear. One cross-sectional study found that long-term abstainers from alcohol had less severe ataxia than short-term abstainers,¹ suggesting that improvement is possible with continued sobriety. However, a recent longitudinal study contradicts this finding, reporting no improvement in ataxia in patients abstinent for 10 weeks to 1 year.²

CASE REPORT
Unable to walk, heavy alcohol use

Mr. G, a 59-year-old white male with a history of daily, heavy alcohol use, presents to the emergency room reporting that he has “not been able to walk right” for 3 weeks. He is in a wheelchair because of ataxia and difficulty balancing. He denies headaches, visual changes, weakness, numbness, and difficulty speaking or swallowing.

Mr. G reports drinking one 40-oz bottle of malt liquor and 2 pints of vodka per day for more than 40 years. His alcohol abuse led to homelessness, unemployment, and divorce. Despite heavy drinking, he denies signs of withdrawal, including shaking, sweating, seizures, and delirium.

Mr. G has no other medical conditions. He denies a family history of neurologic disorders or substance abuse.

His pulse is 100 beats per minute, respirations of 16 breaths per minute, temperature of 37°C, and blood pressure of 143/89 mm Hg. Physical examination reveals a wide-based gait.

Mr. G is admitted to the inpatient psychiatric unit to monitor and treat his alcohol withdrawal and to undergo further workup of the gait disturbance.

A head CT scan shows non-specific changes; an EEG also is within normal limits. Complete blood count, basic metabolic panel, liver function test, HIV test, acute hepatitis panel, thyroid function test, erythrocyte sedimentation rate, and vitamin B₁₂ tests are within normal ranges.

A full neurologic exam reveals a wide-based gait, impaired heel-shin test, and dysmetria on finger-nose-finger test. Mr. G is given a diagnosis of ataxia due to alcoholic cerebellar degeneration. Thiamine repletion is suggested.

Treatment and outcome

Mr. G continues on thiamine, 100 mg, twice daily, and oxazepam, 15 mg, as needed, to manage withdrawal symptoms. He receives gait training 3 times per week.

Approximately 10 days after admission, Mr. G is able to ambulate with a walker. Three weeks after admission, his gait has improved and he walks with a cane. (See the video at CurrentPsychiatry.com for an illustration of this progressive recovery.)

After discharge, Mr. G is referred to an addiction psychiatrist and addiction psychotherapist for ongoing treatment of alcohol use disorder.

Making the diagnosis

In a patient complaining of balance difficulties, consider ataxia secondary to cerebellar degeneration.

• Take a complete history. Ask about the onset and progression of ataxia.
• Obtain a family history. Some types of ataxia are genetic.
• Perform a neurologic examination, which may reveal signs of cerebellar deficits, particularly characteristic wide-based gait. These patients will have difficulty when walking in tandem. Other impairments on the neurologic exam that may raise suspicion for a cerebellar disorder include: impaired heel-shin test, impaired finger-nose-finger test (dysmetria), impaired rapid alternating movements (dysdiadochokinesia), nystagmus, impaired smooth pursuits, intention tremor, or speech abnormalities.
• Perform head imaging, such as a CT scan or MRI. In patients with ataxia secondary to alcohol abuse, imaging might reveal degeneration of the cerebellar vermis.
• Perform laboratory tests, such as inflammatory markers, vitamin levels, and thyroid function testing to detect possible toxic-metabolic or inflammatory causes.

Alcohol-induced ataxia can be diagnosed in patients with a history of heavy drinking if the workup does not reveal another possible cause for the gait disturbance. Other less common deficits associated with alcohol-induced cerebellar injury include:

• dysarthria
• abnormal rate and force of movement
• limb ataxia.³

Recommendations

• Be able to recognize the characteristic gait of patients with alcohol-induced ataxia.
• Provide thiamine supplementation.
• Refer patients to physical therapy.
• Educate your patients that their gait will not improve and may worsen if they continue to drink.
• Refer patients for ongoing treatment for alcohol use disorder, including medication management and psychotherapy.

Our experience suggests that patients with alcohol use disorder with cerebellar ataxia could have a good prognosis for ambulation. Improvement could occur over several weeks; it is unclear whether further gains can be expected with months or years of abstinence.

Difficulty with time management and organization is one of the most common complaints of patients with attention-deficit/hyperactivity disorder (ADHD). Being unproductive and inefficient also is anxiety-producing and depressing, leaving patients with additional comorbidity.

Although medication can help improve a person’s focus, if the patient is focusing on a set of poorly designed systems, he (she) will see little improvement. A comprehensive approach to improving day-to-day task management, similar to the one I describe here and use with my patients, is therefore as important as medication.

Needed: An ‘organizing principle’

Imagine that supermarkets displayed food in the order it arrives from the food distributors and producers. You’d walk in to the store and see a display of food that lacks hierarchy—1 random item placed next to another. The experience would be jarring, and shopping would be a much slower chore. Furthermore, what if you had to go to 5 stores to cover all your needs?

Yet, that is how most “to-do” lists are executed: A thought comes in, a thought goes down on paper. Or on a sticky note. Or in an app. Or in a calendar. Or all of the above! Often, there is neither an organizing principle (other than perhaps chronological order) or a central repository. No wonder it’s hard to feel present and clear-minded. Add to this disorganization the volume of information coming in from the environment—e-mails, voice mails, texts, notifications, dings, beeps, buzzes, and maybe even snail mail—and the feeling of being overwhelmed grows.

Unconscious motives for maintaining poor systems also might play a role. People with a “need to please” personality type or who are more passive-aggressive in their communication are more likely to overcommit, and then forget or be late completing their tasks, rather than saying “No” from the outset or delegating the work. 

Survival basics for time management

Assuming there is simply a skills deficit, you can teach basic time and project management skills to patients with ADHD (and to any patient with suboptimal executive functioning). Here are basic principles to adopt:

• If you can forget it, you will, so all tasks should go onto the to-do list.
• You should keep only 1 list. Adding on “stickies” is not allowed.
• Your list is like an extra lobe of your brain: It should be present at all times, whether you keep it in “the Cloud,” on your desktop, or on paper.
• Review your list and clean it up at least daily. This takes time, but it also saves time—in spades—when you can call upon the right task, at the right time, with energy and drive.
• The first action you should take in the daily review is to weed out or delegate tasks.
• Next, categorize remaining tasks. (Note: The free smartphone app Evernote allows you to do this with “tags.”) Categorizing allows you to process sets of tasks in buckets that can be tackled as a bundle and, therefore, more efficiently. For example, having all of your errands, items to research, and telephone calls that need to be returned in separate buckets allows for speedier processing—as opposed to veering back and forth between line items.
• Then, move remaining high-priority items to the top of the list. However, remember that, if everything is urgent, nothing is. Items that are low-hanging fruit that you can cross off the list in a matter of minutes can be prioritized even if they are not as urgent. By doing that, your list becomes more manageable and your brain can dive deeper into more complex tasks.
• Block out calendar time for each of your buckets with this formula: (1) Estimate how much time you’ll need to complete the tasks in each bucket, then add 50% for each bucket. (2) Add in commuting, set-up, or wind-down time, if you need it, to the grand total for all buckets, and then add 50% more than you’ve estimated

Set the brain free!

This process will seem like a burden at the beginning, when the synapses underneath it still need to get stronger (much like how the body responds to exercise). However, as long as these principles are put into action daily, they will become a trusted, second-nature system that frees the brain from distraction and anxiety—and, ultimately, for being more creative and mindful.

Difficulty with time management and organization is one of the most common complaints of patients with attention-deficit/hyperactivity disorder (ADHD). Being unproductive and inefficient also is anxiety-producing and depressing, leaving patients with additional comorbidity.

Although medication can help improve a person’s focus, if the patient is focusing on a set of poorly designed systems, he (she) will see little improvement. A comprehensive approach to improving day-to-day task management, similar to the one I describe here and use with my patients, is therefore as important as medication.

Needed: An ‘organizing principle’

Imagine that supermarkets displayed food in the order it arrives from the food distributors and producers. You’d walk in to the store and see a display of food that lacks hierarchy—1 random item placed next to another. The experience would be jarring, and shopping would be a much slower chore. Furthermore, what if you had to go to 5 stores to cover all your needs?

Yet, that is how most “to-do” lists are executed: A thought comes in, a thought goes down on paper. Or on a sticky note. Or in an app. Or in a calendar. Or all of the above! Often, there is neither an organizing principle (other than perhaps chronological order) or a central repository. No wonder it’s hard to feel present and clear-minded. Add to this disorganization the volume of information coming in from the environment—e-mails, voice mails, texts, notifications, dings, beeps, buzzes, and maybe even snail mail—and the feeling of being overwhelmed grows.

Unconscious motives for maintaining poor systems also might play a role. People with a “need to please” personality type or who are more passive-aggressive in their communication are more likely to overcommit, and then forget or be late completing their tasks, rather than saying “No” from the outset or delegating the work. 

Survival basics for time management

Assuming there is simply a skills deficit, you can teach basic time and project management skills to patients with ADHD (and to any patient with suboptimal executive functioning). Here are basic principles to adopt:

• If you can forget it, you will, so all tasks should go onto the to-do list.
• You should keep only 1 list. Adding on “stickies” is not allowed.
• Your list is like an extra lobe of your brain: It should be present at all times, whether you keep it in “the Cloud,” on your desktop, or on paper.
• Review your list and clean it up at least daily. This takes time, but it also saves time—in spades—when you can call upon the right task, at the right time, with energy and drive.
• The first action you should take in the daily review is to weed out or delegate tasks.
• Next, categorize remaining tasks. (Note: The free smartphone app Evernote allows you to do this with “tags.”) Categorizing allows you to process sets of tasks in buckets that can be tackled as a bundle and, therefore, more efficiently. For example, having all of your errands, items to research, and telephone calls that need to be returned in separate buckets allows for speedier processing—as opposed to veering back and forth between line items.
• Then, move remaining high-priority items to the top of the list. However, remember that, if everything is urgent, nothing is. Items that are low-hanging fruit that you can cross off the list in a matter of minutes can be prioritized even if they are not as urgent. By doing that, your list becomes more manageable and your brain can dive deeper into more complex tasks.
• Block out calendar time for each of your buckets with this formula: (1) Estimate how much time you’ll need to complete the tasks in each bucket, then add 50% for each bucket. (2) Add in commuting, set-up, or wind-down time, if you need it, to the grand total for all buckets, and then add 50% more than you’ve estimated

Set the brain free!

This process will seem like a burden at the beginning, when the synapses underneath it still need to get stronger (much like how the body responds to exercise). However, as long as these principles are put into action daily, they will become a trusted, second-nature system that frees the brain from distraction and anxiety—and, ultimately, for being more creative and mindful.

Difficulty with time management and organization is one of the most common complaints of patients with attention-deficit/hyperactivity disorder (ADHD). Being unproductive and inefficient also is anxiety-producing and depressing, leaving patients with additional comorbidity.

Although medication can help improve a person’s focus, if the patient is focusing on a set of poorly designed systems, he (she) will see little improvement. A comprehensive approach to improving day-to-day task management, similar to the one I describe here and use with my patients, is therefore as important as medication.

Needed: An ‘organizing principle’

Imagine that supermarkets displayed food in the order it arrives from the food distributors and producers. You’d walk in to the store and see a display of food that lacks hierarchy—1 random item placed next to another. The experience would be jarring, and shopping would be a much slower chore. Furthermore, what if you had to go to 5 stores to cover all your needs?

Yet, that is how most “to-do” lists are executed: A thought comes in, a thought goes down on paper. Or on a sticky note. Or in an app. Or in a calendar. Or all of the above! Often, there is neither an organizing principle (other than perhaps chronological order) or a central repository. No wonder it’s hard to feel present and clear-minded. Add to this disorganization the volume of information coming in from the environment—e-mails, voice mails, texts, notifications, dings, beeps, buzzes, and maybe even snail mail—and the feeling of being overwhelmed grows.

Unconscious motives for maintaining poor systems also might play a role. People with a “need to please” personality type or who are more passive-aggressive in their communication are more likely to overcommit, and then forget or be late completing their tasks, rather than saying “No” from the outset or delegating the work. 

Survival basics for time management

Assuming there is simply a skills deficit, you can teach basic time and project management skills to patients with ADHD (and to any patient with suboptimal executive functioning). Here are basic principles to adopt:

• If you can forget it, you will, so all tasks should go onto the to-do list.
• You should keep only 1 list. Adding on “stickies” is not allowed.
• Your list is like an extra lobe of your brain: It should be present at all times, whether you keep it in “the Cloud,” on your desktop, or on paper.
• Review your list and clean it up at least daily. This takes time, but it also saves time—in spades—when you can call upon the right task, at the right time, with energy and drive.
• The first action you should take in the daily review is to weed out or delegate tasks.
• Next, categorize remaining tasks. (Note: The free smartphone app Evernote allows you to do this with “tags.”) Categorizing allows you to process sets of tasks in buckets that can be tackled as a bundle and, therefore, more efficiently. For example, having all of your errands, items to research, and telephone calls that need to be returned in separate buckets allows for speedier processing—as opposed to veering back and forth between line items.
• Then, move remaining high-priority items to the top of the list. However, remember that, if everything is urgent, nothing is. Items that are low-hanging fruit that you can cross off the list in a matter of minutes can be prioritized even if they are not as urgent. By doing that, your list becomes more manageable and your brain can dive deeper into more complex tasks.
• Block out calendar time for each of your buckets with this formula: (1) Estimate how much time you’ll need to complete the tasks in each bucket, then add 50% for each bucket. (2) Add in commuting, set-up, or wind-down time, if you need it, to the grand total for all buckets, and then add 50% more than you’ve estimated

Set the brain free!

This process will seem like a burden at the beginning, when the synapses underneath it still need to get stronger (much like how the body responds to exercise). However, as long as these principles are put into action daily, they will become a trusted, second-nature system that frees the brain from distraction and anxiety—and, ultimately, for being more creative and mindful.

The National Ambulatory Medical Care Survey^1,2 (NAMCS) indicates that less than 1 out of 4 (23%) psychiatrists provide smoking cessation counseling to their patients, and even fewer prescribe medications.

What gives? How is it that so many psychiatrists endorse having recently helped a patient quit smoking when the data from large-scale surveys^1,2 indicate they do not?

From the “glass is half-full” perspective, the discrepancy might indicate that psychiatrists finally have bought into the message put forth 20 years ago when the American Psychiatric Association first published its clinical practice guidelines for treating nicotine dependence.³ Because the figures I cited from NAMCS reflect data from 2006 to 2010, it is possible that in the last 5 years more psychiatrists have started to help their patients quit smoking. Such an hypothesis is further supported by the increasing number of research papers on smoking cessation in individuals with mental illness published over the past 8 years—a period that coincides with the release of the second edition of the Treating tobacco use and dependence clinical practice guideline from the U.S. Agency for Healthcare Research and Quality, which highlighted the need for more research in this population of smokers.⁴

Regardless of the reason, the fact that my informal surveys indicate a likely uptick in activity among psychiatrists to help their patients quit smoking is welcome news. With nearly 1 out of 2 cigarettes sold in the United States being smoked by individuals with psychiatric and substance use disorders,⁵ psychiatrists and other mental health professionals play a vital role in addressing this epidemic. That our patients smoke at rates 2- to 4-times that of the general population and die decades earlier than their non-smoking, non-mentally ill counterparts⁶ are compelling reasons urging us to end our complacency and help our patients quit smoking.

EAGLES trial results help debunk the latest myth about smoking cessation

In an article that I wrote for Current Psychiatry 11 years ago,⁷ I attempted to debunk 3 myths that might have influenced some psychiatrists’ approach and motivation to intervene in tobacco dependence. Since that article appeared, a fourth myth has been promulgated—that the non-nicotine smoking cessation medications, bupropion and varenicline, are unsafe to use in patients with stable psychiatric disorders and cause serious neuropsychiatric adverse events (AEs) including suicide. Indeed, that is one implication of the “black-box” warning both of these medications received in July 2009, which caution that, “the risks of Zyban^®/Chantix^® should be weighed against the benefits of [their] use.”^8,9 For an illness that causes 480,000 deaths each year in the United States,¹⁰ and nearly 6 million across the globe,¹¹ tobacco treatment specialists find themselves in a quandary when 2 of the only 3 approved medications available—nicotine replacement therapy being the third—carry such a stern warning.

In addition to applying the “black-box” warning, the FDA issued a post-marketing requirement to the manufacturers of bupropion and varenicline to conduct a large randomized controlled trial—Evaluating Adverse Events in a Global Smoking Cessation Study (EAGLES)—the top-line results of which were published in The Lancet this spring.¹²

The researchers found no significant increase in serious neuropsychiatric AEs—a composite measure assessing depression, anxiety, suicidality, and 13 other symptom clusters—attributable to varenicline or bupropion compared with placebo or the nicotine patch in smokers with or without psychiatric disorders. The study did detect a significant difference—approximately 4% (2% in non-psychiatric cohort vs 6% in psychiatric cohort)—in the rate of serious neuropsychiatric AEs regardless of treatment condition. In both cohorts, varenicline was more effective than bupropion, which had similar efficacy to the nicotine patch; all interventions were superior to placebo. Importantly, all 3 medications significantly improved quit rates in smokers with and without psychiatric disorders. Although the efficacy of medications in smokers with or without psychiatric disorders was similar in terms of odds ratios, overall, those with psychiatric disorders had 20% to 30% lower quit rates compared with non-psychiatrically ill smokers.

The EAGLES study results, when viewed in the context of findings from other clinical trials and large-scale observational studies, provide further evidence that smokers with stable mental illness can use bupropion and varenicline safely. It also demonstrates that moderate to severe neuropsychiatric AEs occur during a smoking cessation attempt regardless of the medication used, therefore, monitoring smokers—especially those with psychiatric disorders—is important, a role that psychiatrists are uniquely poised to play.

That all 3 smoking cessation medications are effective in patients with mood, anxiety, and psychotic disorders is good news for our patients. Combined with the EAGLES safety findings, there is no better time to intervene in tobacco dependence

The National Ambulatory Medical Care Survey^1,2 (NAMCS) indicates that less than 1 out of 4 (23%) psychiatrists provide smoking cessation counseling to their patients, and even fewer prescribe medications.

What gives? How is it that so many psychiatrists endorse having recently helped a patient quit smoking when the data from large-scale surveys^1,2 indicate they do not?

From the “glass is half-full” perspective, the discrepancy might indicate that psychiatrists finally have bought into the message put forth 20 years ago when the American Psychiatric Association first published its clinical practice guidelines for treating nicotine dependence.³ Because the figures I cited from NAMCS reflect data from 2006 to 2010, it is possible that in the last 5 years more psychiatrists have started to help their patients quit smoking. Such an hypothesis is further supported by the increasing number of research papers on smoking cessation in individuals with mental illness published over the past 8 years—a period that coincides with the release of the second edition of the Treating tobacco use and dependence clinical practice guideline from the U.S. Agency for Healthcare Research and Quality, which highlighted the need for more research in this population of smokers.⁴

Regardless of the reason, the fact that my informal surveys indicate a likely uptick in activity among psychiatrists to help their patients quit smoking is welcome news. With nearly 1 out of 2 cigarettes sold in the United States being smoked by individuals with psychiatric and substance use disorders,⁵ psychiatrists and other mental health professionals play a vital role in addressing this epidemic. That our patients smoke at rates 2- to 4-times that of the general population and die decades earlier than their non-smoking, non-mentally ill counterparts⁶ are compelling reasons urging us to end our complacency and help our patients quit smoking.

EAGLES trial results help debunk the latest myth about smoking cessation

In an article that I wrote for Current Psychiatry 11 years ago,⁷ I attempted to debunk 3 myths that might have influenced some psychiatrists’ approach and motivation to intervene in tobacco dependence. Since that article appeared, a fourth myth has been promulgated—that the non-nicotine smoking cessation medications, bupropion and varenicline, are unsafe to use in patients with stable psychiatric disorders and cause serious neuropsychiatric adverse events (AEs) including suicide. Indeed, that is one implication of the “black-box” warning both of these medications received in July 2009, which caution that, “the risks of Zyban^®/Chantix^® should be weighed against the benefits of [their] use.”^8,9 For an illness that causes 480,000 deaths each year in the United States,¹⁰ and nearly 6 million across the globe,¹¹ tobacco treatment specialists find themselves in a quandary when 2 of the only 3 approved medications available—nicotine replacement therapy being the third—carry such a stern warning.

In addition to applying the “black-box” warning, the FDA issued a post-marketing requirement to the manufacturers of bupropion and varenicline to conduct a large randomized controlled trial—Evaluating Adverse Events in a Global Smoking Cessation Study (EAGLES)—the top-line results of which were published in The Lancet this spring.¹²

The researchers found no significant increase in serious neuropsychiatric AEs—a composite measure assessing depression, anxiety, suicidality, and 13 other symptom clusters—attributable to varenicline or bupropion compared with placebo or the nicotine patch in smokers with or without psychiatric disorders. The study did detect a significant difference—approximately 4% (2% in non-psychiatric cohort vs 6% in psychiatric cohort)—in the rate of serious neuropsychiatric AEs regardless of treatment condition. In both cohorts, varenicline was more effective than bupropion, which had similar efficacy to the nicotine patch; all interventions were superior to placebo. Importantly, all 3 medications significantly improved quit rates in smokers with and without psychiatric disorders. Although the efficacy of medications in smokers with or without psychiatric disorders was similar in terms of odds ratios, overall, those with psychiatric disorders had 20% to 30% lower quit rates compared with non-psychiatrically ill smokers.

The EAGLES study results, when viewed in the context of findings from other clinical trials and large-scale observational studies, provide further evidence that smokers with stable mental illness can use bupropion and varenicline safely. It also demonstrates that moderate to severe neuropsychiatric AEs occur during a smoking cessation attempt regardless of the medication used, therefore, monitoring smokers—especially those with psychiatric disorders—is important, a role that psychiatrists are uniquely poised to play.

That all 3 smoking cessation medications are effective in patients with mood, anxiety, and psychotic disorders is good news for our patients. Combined with the EAGLES safety findings, there is no better time to intervene in tobacco dependence

The National Ambulatory Medical Care Survey^1,2 (NAMCS) indicates that less than 1 out of 4 (23%) psychiatrists provide smoking cessation counseling to their patients, and even fewer prescribe medications.

What gives? How is it that so many psychiatrists endorse having recently helped a patient quit smoking when the data from large-scale surveys^1,2 indicate they do not?

From the “glass is half-full” perspective, the discrepancy might indicate that psychiatrists finally have bought into the message put forth 20 years ago when the American Psychiatric Association first published its clinical practice guidelines for treating nicotine dependence.³ Because the figures I cited from NAMCS reflect data from 2006 to 2010, it is possible that in the last 5 years more psychiatrists have started to help their patients quit smoking. Such an hypothesis is further supported by the increasing number of research papers on smoking cessation in individuals with mental illness published over the past 8 years—a period that coincides with the release of the second edition of the Treating tobacco use and dependence clinical practice guideline from the U.S. Agency for Healthcare Research and Quality, which highlighted the need for more research in this population of smokers.⁴

Regardless of the reason, the fact that my informal surveys indicate a likely uptick in activity among psychiatrists to help their patients quit smoking is welcome news. With nearly 1 out of 2 cigarettes sold in the United States being smoked by individuals with psychiatric and substance use disorders,⁵ psychiatrists and other mental health professionals play a vital role in addressing this epidemic. That our patients smoke at rates 2- to 4-times that of the general population and die decades earlier than their non-smoking, non-mentally ill counterparts⁶ are compelling reasons urging us to end our complacency and help our patients quit smoking.

EAGLES trial results help debunk the latest myth about smoking cessation

In an article that I wrote for Current Psychiatry 11 years ago,⁷ I attempted to debunk 3 myths that might have influenced some psychiatrists’ approach and motivation to intervene in tobacco dependence. Since that article appeared, a fourth myth has been promulgated—that the non-nicotine smoking cessation medications, bupropion and varenicline, are unsafe to use in patients with stable psychiatric disorders and cause serious neuropsychiatric adverse events (AEs) including suicide. Indeed, that is one implication of the “black-box” warning both of these medications received in July 2009, which caution that, “the risks of Zyban^®/Chantix^® should be weighed against the benefits of [their] use.”^8,9 For an illness that causes 480,000 deaths each year in the United States,¹⁰ and nearly 6 million across the globe,¹¹ tobacco treatment specialists find themselves in a quandary when 2 of the only 3 approved medications available—nicotine replacement therapy being the third—carry such a stern warning.

In addition to applying the “black-box” warning, the FDA issued a post-marketing requirement to the manufacturers of bupropion and varenicline to conduct a large randomized controlled trial—Evaluating Adverse Events in a Global Smoking Cessation Study (EAGLES)—the top-line results of which were published in The Lancet this spring.¹²

The researchers found no significant increase in serious neuropsychiatric AEs—a composite measure assessing depression, anxiety, suicidality, and 13 other symptom clusters—attributable to varenicline or bupropion compared with placebo or the nicotine patch in smokers with or without psychiatric disorders. The study did detect a significant difference—approximately 4% (2% in non-psychiatric cohort vs 6% in psychiatric cohort)—in the rate of serious neuropsychiatric AEs regardless of treatment condition. In both cohorts, varenicline was more effective than bupropion, which had similar efficacy to the nicotine patch; all interventions were superior to placebo. Importantly, all 3 medications significantly improved quit rates in smokers with and without psychiatric disorders. Although the efficacy of medications in smokers with or without psychiatric disorders was similar in terms of odds ratios, overall, those with psychiatric disorders had 20% to 30% lower quit rates compared with non-psychiatrically ill smokers.

The EAGLES study results, when viewed in the context of findings from other clinical trials and large-scale observational studies, provide further evidence that smokers with stable mental illness can use bupropion and varenicline safely. It also demonstrates that moderate to severe neuropsychiatric AEs occur during a smoking cessation attempt regardless of the medication used, therefore, monitoring smokers—especially those with psychiatric disorders—is important, a role that psychiatrists are uniquely poised to play.

That all 3 smoking cessation medications are effective in patients with mood, anxiety, and psychotic disorders is good news for our patients. Combined with the EAGLES safety findings, there is no better time to intervene in tobacco dependence

There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).

Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.

Diverse presentations

Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?

Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.

As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.¹ Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.² Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.

Pharmacotherapy is underutilized

Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is under­utilized: only 3% of patients have received an FDA-approved treatment.^2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.³ Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.

Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.^4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.

Neuroscience supports the brain disease model of addiction, with neuro­plasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.⁶

Why hesitate to use pharmacotherapeutics?

There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.^4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?

Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:

• lack of familiarity with available agents
• absence of guidelines for use
• disbelief that the condition is treatable.

Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.

Therapeutic options

Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.

There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.

Psychosocial interventions

Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psychosocial therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on
fellowship, accountability, monitoring, and anonymity; the forum can compete with
motivational interviewing for efficacy in increasing abstinence and preventing relapse.

There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).

Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.

Diverse presentations

Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?

Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.

As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.¹ Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.² Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.

Pharmacotherapy is underutilized

Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is under­utilized: only 3% of patients have received an FDA-approved treatment.^2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.³ Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.

Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.^4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.

Neuroscience supports the brain disease model of addiction, with neuro­plasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.⁶

Why hesitate to use pharmacotherapeutics?

There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.^4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?

Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:

• lack of familiarity with available agents
• absence of guidelines for use
• disbelief that the condition is treatable.

Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.

Therapeutic options

Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.

There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.

Psychosocial interventions

Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psychosocial therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on
fellowship, accountability, monitoring, and anonymity; the forum can compete with
motivational interviewing for efficacy in increasing abstinence and preventing relapse.

There is ample evidence in the medical literature, as well as clinical experience, that patients seeking help for chemical dependency benefit from pharmacotherapy. It is common, however, for physicians, patients, and family to balk at the idea. Even within the psychiatry community, where there should be better understanding of substance use disorders, many practitioners hesitate to employ medications, especially for alcohol use disorder (AUD).

Efficacy for such FDA-approved medications has been demonstrated in well-designed, randomized controlled trials, but many trainees, and even experienced professionals, have never seen these medications used effectively and appropriately. Medication-assisted treatment (MAT) is not an alternative to biopsychosocial approaches but is an augmentation that can (1) help stabilize the patient until he (she) can be educated in relapse prevention skills and (2) allow the brain to rewire and heal until he regains impulse control.

Diverse presentations

Do you remember that patient who often arrived for appointments intoxicated, promising that he plans to cut down? How about the man you saw in the emergency department with an elevated blood alcohol level, who was constantly endorsing suicidal thoughts that subsided when he reached clinical sobriety? What about the college student who often was treated for alcohol poisoning after binge drinking on weekends, but who never considered this behavior problematic? And, how about the elderly woman who was evaluated for anxiety, but had been drinking 4 beers nightly for the past 30 years?

Despite the diverse presentations, these patients all have a chronic disease and we fail them when we do not apply evidence-based medicine to their treatment.

As psychiatrists, we encounter many patients with AUD as a primary or comorbid diagnosis. This is a global problem associated with significant human and financial cost. With 80% of American adolescents having reported using alcohol in the past year, the problem will continue to grow.¹ Furthermore, a greater prevalence of AUD is noted in clinical populations undergoing psychiatric treatment.² Ongoing alcohol abuse complicates the course of medical and psychiatric conditions and incites significant societal exclusion.

Pharmacotherapy is underutilized

Despite an increase in the use of psychotropic medications for treating psychiatric illness, pharmacotherapy for AUD is under­utilized: only 3% of patients have received an FDA-approved treatment.^2,3 Nearly one-third of adults are affected by AUD during their lifetime, yet only 20% seek help.³ Management today remains limited to episodic, brief inpatient detoxification and psychosocial therapy.

Recovery rates are highest when addiction treatment that monitors abstinence is continuous; yet, for most part, alcohol addiction is treated in discrete episodes upon relapse. Although MAT is recommended by experts for “moderate” and “severe” substance use disorders, practitioners, in general, have demonstrated considerable resistance to using this modality as part of routine practice.^4,5 This is regrettable: Regardless of terminology used to describe their condition, these people suffer a potentially fatal disease characterized by high post-treatment recidivism.

Neuroscience supports the brain disease model of addiction, with neuro­plasticity changes being made during phases of drug use. Medications are shown to assist in preventing relapse while the brain is healing and normal emotional and decision-making capacities are being restored.⁶

Why hesitate to use pharmacotherapeutics?

There are diverse pharmacotherapeutic options that can be pursued for treating AUD with minimal disruption to home and work life. Alarmingly, many trainees have never prescribed or even considered such medications. Despite modest effect sizes in randomized controlled trials, efficacy has been demonstrated in reducing relapse rates and overall severity of drinking days.^4,5 So, from where does the ambivalence of patients and providers about using these treatments to achieve lasting recovery stem?

Starting MAT certainly requires both parties to be in agreement. A patient might decline medication because of a fear of dependence or because he overestimates his ability to achieve remission on his own. There also may be financial barriers in a current alcohol treatment system that is traditionally non-medically oriented. Prescribers also fail to offer medications because of:

• lack of familiarity with available agents
• absence of guidelines for use
• disbelief that the condition is treatable.

Given that treatment often is based on a 12-step approach, such as Alcoholics Anonymous (AA), providers might hesitate to prescribe medication for an illness that is thought to be managed through psychosocial interventions, such as group and motivational therapy.

Therapeutic options

Choice of medication depends on the prescriber’s comfort level, reputation of the medication, potential side-effect profile, medical contraindications, and affordability; the most important consideration, however, should be the overall goals and expectations of the patient.

There are 4 FDA-approved medications for AUD (Table); many others are off-label. It is advisable to start with an FDA-approved medication such as disulfiram for the motivated patient who has a collaborator and desires complete abstinence; naltrexone for a patient who wants to cut down on intake (a long-acting formulation can be used for poorly adherent patients); and acamprosate for a patient with at least some established sobriety who needs help with post-withdrawal sleep disturbances.

Psychosocial interventions

Medications are just 1 tool in recovery; patients should be engaged in a program of counseling. Encourage attendance at AA meetings. An up-and-coming concept is the use of smartphone applications to prevent relapse (or even induce remission); apps that provide an accurate blood alcohol tracking systems and integrated psychosocial therapies are in the pipeline. The novel Reddit online forum r/StopDrinking is a 24-hour peer-support community that relies on
fellowship, accountability, monitoring, and anonymity; the forum can compete with
motivational interviewing for efficacy in increasing abstinence and preventing relapse.

‘Enough!’ We need to take back our profession

Every day, I am grateful that I became a physician and a psychiatrist. Every minute that I spend with patients is an honor and a privilege. I have never forgotten that. But it is heartbreaking to see my precious profession being destroyed by bureaucrats.

An example: I am concerned about the effect that passage of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) will have on physicians. I read articles telling us how we should handle this new plan for reimbursement, but I also read that 86% of physicians are not in favor of MACRA. How did we get stuck with it?

Another example of why it has become virtually impossible to do our job: I spend a fair amount of time obtaining prior authorization for generic medications that are available at big-box stores for $10 or $15; often, these authorizations need approval by the medical director. I have been beaten down enough over the years to learn that I should no longer prescribe brand-name medications—only generic medications (which still require authorization!), even when my patient has been taking the medication for 10 or 15 years. The last time I sought authorization to prescribe a medication, the reviewer asked me why I had not tried 3 different generics over the past year. I had to remind her that I had an active prior authorization in place from the year before, and so why would I do what she was proposing?

Physicians are some of the most highly trained professionals. It takes 7 to 15 years to be able to be somewhat proficient at the job, then another 30 or 40 years of practice to become really good at it. But we’ve become technicians at the mercy of business executives: We go to our office and spend our time checking off boxes, trying to figure out proper coding and the proper diagnosis, so that we can get an appropriate amount of money for the service we’re providing. How has it come to this? Why can’t we take back our profession?

Another problem is that physicians are being paid for their performance and the outcomes they produce. But people are not refrigerators: We can do everything right and the patient still dies. I have a number of patients who have no insight into their psychiatric illness; no matter what I say, or do, or how much time I spend with them, they are nonadherent. How is this my fault?

Physicians are not given the opportunity to think for themselves, or to prescribe treatments that they see fit and document in ways that they were trained. Where is the American Medical Association, the Connecticut State Medical Society, the Hartford County Medical Association, and all the other associations that supposedly represent us? How have they allowed this to happen?

In the future, health care will be provided by physician assistants and nurse practitioners; physicians will provide background supervision, or perform surgery, but the patient will never meet them. I respect NPs and PAs, but they do not have the rigorous training that physicians have. But they’re less expensive—and isn’t that what it’s all about?

If we are not going to speak up, or if we are not going to elect officials to truly represent us and advocate for us, then we have nobody to blame but ourselves.

Carole Black Cohen, MD

Private psychiatric practice

Farmington, Connecticut

In Dr. Nasrallah’s August essay (From the Editor, Current Psychiatry. "Unresolved questions about the specialty lurk in the cortex of psychiatrists," p. 10,11,19,19A), he asks, as he often does, provocative, unanswered questions. There are probably many more questions to include in his list, but I’ll just add 1—the one that I think is the biggest problem in our field: Why is the burnout rate of physicians steadily climbing, to the extent that it exceeds the epidemic rate of 50%? Although you would think that we, as psychiatrists, should be expert at understanding and addressing this problem, our own burnout rate is >40%. Moreover, why haven’t we developed programs to prevent and reduce burnout, when other specialties, such as urology and emergency medicine, have done so?

H. Steven Moffic, MD

Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Nasrallah responds

Dr. Moffic is spot-on about the escalating rate of burnout among physicians, including psychiatrists. The reason I did not include burnout in the list of questions is because I intended to pose questions related to external forces that interfere with patient care. Burnout is a vicious internal typhoon of emotional turmoil that might be related to multiple idiosyncratic personal variables and only partially to frustrations in clinical practice.

Burnout is, one might say, a subcortical event (generated in the amygdala?)—not a cortical process like the “why” questions that beg for answers. Admittedly, however, the cumulative burden of practice frustrations—especially the inability to erase the personal, social, financial, and vocational stigmata that plague our patients’ lives—can, eventually, take a toll on our morale and quality of life.

Fortunately, we psychiatrists generally are a resilient breed. We can manage personal stress using techniques that we employ in our practices. That might be why burnout is lower in psychiatry than it is in other medical specialties.

Henry A. Nasrallah, MD

Professor and Chair
Department of Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri

‘Enough!’ We need to take back our profession

Every day, I am grateful that I became a physician and a psychiatrist. Every minute that I spend with patients is an honor and a privilege. I have never forgotten that. But it is heartbreaking to see my precious profession being destroyed by bureaucrats.

An example: I am concerned about the effect that passage of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) will have on physicians. I read articles telling us how we should handle this new plan for reimbursement, but I also read that 86% of physicians are not in favor of MACRA. How did we get stuck with it?

Another example of why it has become virtually impossible to do our job: I spend a fair amount of time obtaining prior authorization for generic medications that are available at big-box stores for $10 or $15; often, these authorizations need approval by the medical director. I have been beaten down enough over the years to learn that I should no longer prescribe brand-name medications—only generic medications (which still require authorization!), even when my patient has been taking the medication for 10 or 15 years. The last time I sought authorization to prescribe a medication, the reviewer asked me why I had not tried 3 different generics over the past year. I had to remind her that I had an active prior authorization in place from the year before, and so why would I do what she was proposing?

Physicians are some of the most highly trained professionals. It takes 7 to 15 years to be able to be somewhat proficient at the job, then another 30 or 40 years of practice to become really good at it. But we’ve become technicians at the mercy of business executives: We go to our office and spend our time checking off boxes, trying to figure out proper coding and the proper diagnosis, so that we can get an appropriate amount of money for the service we’re providing. How has it come to this? Why can’t we take back our profession?

Another problem is that physicians are being paid for their performance and the outcomes they produce. But people are not refrigerators: We can do everything right and the patient still dies. I have a number of patients who have no insight into their psychiatric illness; no matter what I say, or do, or how much time I spend with them, they are nonadherent. How is this my fault?

Physicians are not given the opportunity to think for themselves, or to prescribe treatments that they see fit and document in ways that they were trained. Where is the American Medical Association, the Connecticut State Medical Society, the Hartford County Medical Association, and all the other associations that supposedly represent us? How have they allowed this to happen?

In the future, health care will be provided by physician assistants and nurse practitioners; physicians will provide background supervision, or perform surgery, but the patient will never meet them. I respect NPs and PAs, but they do not have the rigorous training that physicians have. But they’re less expensive—and isn’t that what it’s all about?

If we are not going to speak up, or if we are not going to elect officials to truly represent us and advocate for us, then we have nobody to blame but ourselves.

Carole Black Cohen, MD

Private psychiatric practice

Farmington, Connecticut

In Dr. Nasrallah’s August essay (From the Editor, Current Psychiatry. "Unresolved questions about the specialty lurk in the cortex of psychiatrists," p. 10,11,19,19A), he asks, as he often does, provocative, unanswered questions. There are probably many more questions to include in his list, but I’ll just add 1—the one that I think is the biggest problem in our field: Why is the burnout rate of physicians steadily climbing, to the extent that it exceeds the epidemic rate of 50%? Although you would think that we, as psychiatrists, should be expert at understanding and addressing this problem, our own burnout rate is >40%. Moreover, why haven’t we developed programs to prevent and reduce burnout, when other specialties, such as urology and emergency medicine, have done so?

H. Steven Moffic, MD

Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Nasrallah responds

Dr. Moffic is spot-on about the escalating rate of burnout among physicians, including psychiatrists. The reason I did not include burnout in the list of questions is because I intended to pose questions related to external forces that interfere with patient care. Burnout is a vicious internal typhoon of emotional turmoil that might be related to multiple idiosyncratic personal variables and only partially to frustrations in clinical practice.

Burnout is, one might say, a subcortical event (generated in the amygdala?)—not a cortical process like the “why” questions that beg for answers. Admittedly, however, the cumulative burden of practice frustrations—especially the inability to erase the personal, social, financial, and vocational stigmata that plague our patients’ lives—can, eventually, take a toll on our morale and quality of life.

Fortunately, we psychiatrists generally are a resilient breed. We can manage personal stress using techniques that we employ in our practices. That might be why burnout is lower in psychiatry than it is in other medical specialties.

Henry A. Nasrallah, MD

Professor and Chair
Department of Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri

‘Enough!’ We need to take back our profession

Every day, I am grateful that I became a physician and a psychiatrist. Every minute that I spend with patients is an honor and a privilege. I have never forgotten that. But it is heartbreaking to see my precious profession being destroyed by bureaucrats.

An example: I am concerned about the effect that passage of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) will have on physicians. I read articles telling us how we should handle this new plan for reimbursement, but I also read that 86% of physicians are not in favor of MACRA. How did we get stuck with it?

Another example of why it has become virtually impossible to do our job: I spend a fair amount of time obtaining prior authorization for generic medications that are available at big-box stores for $10 or $15; often, these authorizations need approval by the medical director. I have been beaten down enough over the years to learn that I should no longer prescribe brand-name medications—only generic medications (which still require authorization!), even when my patient has been taking the medication for 10 or 15 years. The last time I sought authorization to prescribe a medication, the reviewer asked me why I had not tried 3 different generics over the past year. I had to remind her that I had an active prior authorization in place from the year before, and so why would I do what she was proposing?

Physicians are some of the most highly trained professionals. It takes 7 to 15 years to be able to be somewhat proficient at the job, then another 30 or 40 years of practice to become really good at it. But we’ve become technicians at the mercy of business executives: We go to our office and spend our time checking off boxes, trying to figure out proper coding and the proper diagnosis, so that we can get an appropriate amount of money for the service we’re providing. How has it come to this? Why can’t we take back our profession?

Another problem is that physicians are being paid for their performance and the outcomes they produce. But people are not refrigerators: We can do everything right and the patient still dies. I have a number of patients who have no insight into their psychiatric illness; no matter what I say, or do, or how much time I spend with them, they are nonadherent. How is this my fault?

Physicians are not given the opportunity to think for themselves, or to prescribe treatments that they see fit and document in ways that they were trained. Where is the American Medical Association, the Connecticut State Medical Society, the Hartford County Medical Association, and all the other associations that supposedly represent us? How have they allowed this to happen?

In the future, health care will be provided by physician assistants and nurse practitioners; physicians will provide background supervision, or perform surgery, but the patient will never meet them. I respect NPs and PAs, but they do not have the rigorous training that physicians have. But they’re less expensive—and isn’t that what it’s all about?

If we are not going to speak up, or if we are not going to elect officials to truly represent us and advocate for us, then we have nobody to blame but ourselves.

Carole Black Cohen, MD

Private psychiatric practice

Farmington, Connecticut

In Dr. Nasrallah’s August essay (From the Editor, Current Psychiatry. "Unresolved questions about the specialty lurk in the cortex of psychiatrists," p. 10,11,19,19A), he asks, as he often does, provocative, unanswered questions. There are probably many more questions to include in his list, but I’ll just add 1—the one that I think is the biggest problem in our field: Why is the burnout rate of physicians steadily climbing, to the extent that it exceeds the epidemic rate of 50%? Although you would think that we, as psychiatrists, should be expert at understanding and addressing this problem, our own burnout rate is >40%. Moreover, why haven’t we developed programs to prevent and reduce burnout, when other specialties, such as urology and emergency medicine, have done so?

H. Steven Moffic, MD

Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Nasrallah responds

Dr. Moffic is spot-on about the escalating rate of burnout among physicians, including psychiatrists. The reason I did not include burnout in the list of questions is because I intended to pose questions related to external forces that interfere with patient care. Burnout is a vicious internal typhoon of emotional turmoil that might be related to multiple idiosyncratic personal variables and only partially to frustrations in clinical practice.

Burnout is, one might say, a subcortical event (generated in the amygdala?)—not a cortical process like the “why” questions that beg for answers. Admittedly, however, the cumulative burden of practice frustrations—especially the inability to erase the personal, social, financial, and vocational stigmata that plague our patients’ lives—can, eventually, take a toll on our morale and quality of life.

Fortunately, we psychiatrists generally are a resilient breed. We can manage personal stress using techniques that we employ in our practices. That might be why burnout is lower in psychiatry than it is in other medical specialties.

Henry A. Nasrallah, MD

Professor and Chair
Department of Psychiatry
Saint Louis University School of Medicine
St. Louis, Missouri