Current Psychiatry

In the United States, the average potency of Cannabis has increased significantly over the past few decades in response to consumer demand and policies in some states that have legalized marijuana for medicinal and recreational purposes.¹ Whereas the delta-9-tetrahydrocannabinol (THC) content of “street” marijuana was <1% in the 1970s and 4% in the 1990s, by 2012, analyses of Cannabis samples seized by law enforcement agencies documented a rise in average THC potency to >12%.^1-3

Although this increase in potency has been overstated in the media because studies did not control for the effects of changes in sampling methods on freshness, it is estimated that Cannabis potency increased 7-fold from 1970 to 2010.³ Also, Cannabis preparations such as hashish and hash oil extracts containing THC well above average—from 35% to 90% THC—are now more widely available. In states where marijuana has been legalized, high-potency Cannabis (HPC) in the form of “edibles” (eg, marijuana added to baked goods, candy, or drinks) and hash oil extracts (Table 1)^4-13 can be readily obtained from dispensaries or even at local farmers’ markets.

The potency of Cannabis, typically defined as the percentage of THC, its chief psychoactive component, varies depending on the genetic strain of the plant, cultivation techniques, and methods of processing and storage. For example, relative to “average marijuana,” hemp (Cannabis bred for industrial purposes) has very little THC, while sinsemilla (flowering buds from unpollinated female plants), hashish (Cannabis resin), and extracted hash oil contain increasing amounts of THC (Table 2).^1,2

Cannabis use disorder

Recent data indicate that the prevalence of Cannabis use disorders (eg, abuse and dependence) in the United States is approximately 3% among the general population and >30% among Cannabis users.¹⁶ The availability of increasingly potent forms of Cannabis has been cited as a possible explanation for this rise, despite no change in the prevalence of overall marijuana use between 1991 to 1992 and 2001 to 2002.¹⁷ However, while the prevalence of marijuana use disorders has continued to rise—nearly doubling from 2001 to 2002 to 2012 to 2013—this latest increase occurred with a significant increase in overall marijuana use, such that the actual rate of Cannabis use disorders among users seems to have plateaued, despite the continued rise in marijuana potency.¹⁶ This discrepancy could be explained if Cannabis users cut back past a specific threshold of increasing potency. However, 2 studies have called into question how effective such titration efforts might be in practice. In one study, Cannabis users who preferred more potent Cannabis inhaled lower volumes of smoke, but did not fully compensate for the increased potency, such that use of HPC still resulted in greater THC exposure.¹⁸ Another study found that HPC users rolled less marijuana into their joints but not enough to mitigate the impact of greater potency.¹⁹ Therefore, it appears that HPC users typically expose themselves to greater amounts of THC, which could place them at higher risk of addiction.

Although a causal association between increasing Cannabis potency and the rate of substance use disorders among users remains unclear based on epidemiologic studies from the United States, a recent study from the United Kingdom examined the impact of Cannabis potency on dependence.²⁰ This cross-sectional survey found that, although HPC was preferred by users and was rated as offering the “best high,” its use was associated with increasing severity of dependence, especially among young people. The limited available evidence supports a greater risk of Cannabis use disorders with increasing potency.

Psychosis

Based on longitudinal studies published over the past 30 years, it is clear that using Cannabis at a young age (age <15 to 18) increases the risk of developing a psychotic disorder.²¹ This association appears to be dose-dependent, with studies consistently demonstrating that psychosis risk increases with greater frequency of Cannabis use.²² The accumulated evidence to date is strong enough to view the psychotic potential of Cannabis as a significant public health concern.²¹

If risk of psychosis is proportional to the amount of Cannabis used as measured by frequency, it follows that this risk might be affected similarly by Cannabis potency. In another paper, I discussed the potential for greater risk of psychosis in the context of medical marijuana and synthetic cannabinoids.²³ My colleagues and I also have published case reports describing emerging psychosis among regular Cannabis users after escalating to higher potency medical marijuana²⁴ and a hyperconcentrated form of hash oil known as Cannabis “wax” or “dabs” that contains as much as 90% THC.⁴ Preliminary anecdotal evidence supports the plausibility of HPC being more psychotoxic than less potent forms.

Several studies from a research group in the United Kingdom, where sinsemilla has increasingly dominated the drug market, likewise have reported that the use of HPC is associated with a greater risk of psychosis. The first of these studies, published in 2009, found that adults hospitalized for first-episode psychosis were more likely to have used HPC than healthy controls.²⁵ Among Cannabis users, HPC use was associated with a 7-fold increased risk of psychosis, with daily HPC use associated with a 12-fold increased risk.

Based on a larger dataset, a second study reported that high-potency, but not low-potency, Cannabis increased the risk of first-episode psychosis with increasing frequency of use.²⁶ Daily users of HPC had a 5-fold higher risk of psychosis compared with those that had never used Cannabis. A third study reported that HPC use and daily Cannabis use were independently associated with an earlier onset of first-episode psychosis, with daily HPC users developing first-episode psychosis an average of 6 years earlier than non-Cannabis users.²⁷ Finally, a prospective study following patients with first-episode psychosis over 2 years found that the greatest risk of relapse—defined by hospital admission caused by exacerbation of psychotic symptoms—was found among self-reported daily users of HPC, while the lowest risk was among those who stopped using Cannabis after their initial psychotic episode.²⁸

The findings from these 4 studies suggest that the increased risk of psychosis with Cannabis is proportional to overall exposure, determined by both frequency of use and Cannabis potency.

Cognition

There is little doubt that using Cannabis can impair cognition acutely, “after all, this is the basic reason for its recreational use,” as one author wrote.²⁹ As with psychosis, the available evidence indicates that the degree of cognitive impairment is related to the frequency and duration of Cannabis use as well as age of onset of use.^30,31

Few studies have assessed cognitive functioning in relation to Cannabis potency with most only examining the effects of relatively low-potency Cannabis with inconsistent results. For example, 2 studies compared cognitive performance in individuals smoking Cannabis with 1.8% and 3.9% THC. One study found that using higher potency Cannabis resulted in prolonged time needed to complete certain cognitive tasks,³² whereas the other found greater impairment in performance on a decision-making task at both potencies compared with non-users but no differences between the 2 dosages.³³ Detecting significant differences may be difficult within the narrow range of low Cannabis potency studied where any findings have limited applicability in the context of today’s Cannabis with much higher THC content.

To date, only 1 study has assessed cognition at higher Cannabis potencies, comparing Cannabis with 4% THC to 13% THC.³⁴ Cognitive impairments increased with higher potency, especially in tasks that measured motor control and executive functioning. Therefore it appears that higher potency Cannabis use is associated with greater acute cognitive impairment.

The longer-term effects on cognition are less clear, with conflicting evidence about whether Cannabis use can result in residual cognitive impairment despite abstinence.^30,35 A recent review concluded that “the magnitude of neuropsychological impairment and the extent to which it persists after abstinence may depend on the frequency and the duration of Cannabis use, length of abstinence, and age at onset of use.”³¹ The effects of HPC on long-term cognitive deficits have not been studied.

Structural brain changes

A number of studies have determined an association between Cannabis use and brain changes involving structures governing memory and emotional processing, including reduced volume of the hippocampus,³⁶ temporal cortex, insula, and orbitofrontal cortex.³⁷ Although many of these changes appear to be dose-related, some morphologic changes have been reported among young recreational users without Cannabis dependence.³⁸ This has resulted in an understandable concern about the effects of Cannabis on the brains of young people with limited exposure; however, it is not yet clear to what extent detected brain changes are pathological and reflect functional deficits.

Recent research using newer neuroimaging modalities provides preliminary support of Cannabis use associated with white matter changes that, in turn, are correlated with cognitive impairment.³⁹ One study comparing low-potency Cannabis and HPC users with and without first-episode psychosis found a significant effect of Cannabis potency on disturbances in white matter microstructural organization in the corpus callosum.⁴⁰ These findings provide sufficient cause for concern that structural brain changes associated with cognitive impairment are more likely to occur with HPC use.

Recommendations for clinicians

Similar to any drug, the effects of THC and its psychiatric sequelae can be expected to increase with dosage. To date, much of the information about psychiatric risks has been based on studies of low- and moderate-potency Cannabis rather than the much higher potency Cannabis products, such as hyper-concentrated “wax dabs,” that are available today. Data from social media suggest that these products may be associated with novel patterns of use, such as with the intention of “passing out.”⁴¹ It is likely that clinicians will encounter greater psychiatric morbidity associated with HPC use.

Although clinicians may be accustomed to asking about the frequency and duration of Cannabis use, it is now prudent also to ask patients about Cannabis potency to better assess the potential risks of use. The potency of different marijuana products is openly advertised within some “medical marijuana” dispensaries, although the accuracy of information in products such as “edibles” has been called into question.⁵

Physicians are increasingly asked to provide recommendations on “medical marijuana” use. A recent paper outlined characteristics of appropriate candidates for “medical marijuana” including:

• having a debilitating condition that might benefit from Cannabis
• multiple failed trials of conventional pharmacotherapies including FDA-approved cannabinoids
• lack of substance use disorders, psychosis, or unstable mood or anxiety disorders
• residence in a state where “medical marijuana” is legal.⁴²

As part of the informed consent process, physicians providing recommendations for “medical marijuana” now must consider the effects of HPC when weighing potential risks against any benefits of Cannabis use. Those monitoring patients using Cannabis should be aware of the potential for greater psychiatric morbidity with HPC and should educate patients about that risk. Failure to adequately warn patients about such morbidity or to screen for risk factors such as psychosis could leave physicians vulnerable to malpractice litigation.

In the United States, the average potency of Cannabis has increased significantly over the past few decades in response to consumer demand and policies in some states that have legalized marijuana for medicinal and recreational purposes.¹ Whereas the delta-9-tetrahydrocannabinol (THC) content of “street” marijuana was <1% in the 1970s and 4% in the 1990s, by 2012, analyses of Cannabis samples seized by law enforcement agencies documented a rise in average THC potency to >12%.^1-3

Although this increase in potency has been overstated in the media because studies did not control for the effects of changes in sampling methods on freshness, it is estimated that Cannabis potency increased 7-fold from 1970 to 2010.³ Also, Cannabis preparations such as hashish and hash oil extracts containing THC well above average—from 35% to 90% THC—are now more widely available. In states where marijuana has been legalized, high-potency Cannabis (HPC) in the form of “edibles” (eg, marijuana added to baked goods, candy, or drinks) and hash oil extracts (Table 1)^4-13 can be readily obtained from dispensaries or even at local farmers’ markets.

The potency of Cannabis, typically defined as the percentage of THC, its chief psychoactive component, varies depending on the genetic strain of the plant, cultivation techniques, and methods of processing and storage. For example, relative to “average marijuana,” hemp (Cannabis bred for industrial purposes) has very little THC, while sinsemilla (flowering buds from unpollinated female plants), hashish (Cannabis resin), and extracted hash oil contain increasing amounts of THC (Table 2).^1,2

Cannabis use disorder

Recent data indicate that the prevalence of Cannabis use disorders (eg, abuse and dependence) in the United States is approximately 3% among the general population and >30% among Cannabis users.¹⁶ The availability of increasingly potent forms of Cannabis has been cited as a possible explanation for this rise, despite no change in the prevalence of overall marijuana use between 1991 to 1992 and 2001 to 2002.¹⁷ However, while the prevalence of marijuana use disorders has continued to rise—nearly doubling from 2001 to 2002 to 2012 to 2013—this latest increase occurred with a significant increase in overall marijuana use, such that the actual rate of Cannabis use disorders among users seems to have plateaued, despite the continued rise in marijuana potency.¹⁶ This discrepancy could be explained if Cannabis users cut back past a specific threshold of increasing potency. However, 2 studies have called into question how effective such titration efforts might be in practice. In one study, Cannabis users who preferred more potent Cannabis inhaled lower volumes of smoke, but did not fully compensate for the increased potency, such that use of HPC still resulted in greater THC exposure.¹⁸ Another study found that HPC users rolled less marijuana into their joints but not enough to mitigate the impact of greater potency.¹⁹ Therefore, it appears that HPC users typically expose themselves to greater amounts of THC, which could place them at higher risk of addiction.

Although a causal association between increasing Cannabis potency and the rate of substance use disorders among users remains unclear based on epidemiologic studies from the United States, a recent study from the United Kingdom examined the impact of Cannabis potency on dependence.²⁰ This cross-sectional survey found that, although HPC was preferred by users and was rated as offering the “best high,” its use was associated with increasing severity of dependence, especially among young people. The limited available evidence supports a greater risk of Cannabis use disorders with increasing potency.

Psychosis

Based on longitudinal studies published over the past 30 years, it is clear that using Cannabis at a young age (age <15 to 18) increases the risk of developing a psychotic disorder.²¹ This association appears to be dose-dependent, with studies consistently demonstrating that psychosis risk increases with greater frequency of Cannabis use.²² The accumulated evidence to date is strong enough to view the psychotic potential of Cannabis as a significant public health concern.²¹

If risk of psychosis is proportional to the amount of Cannabis used as measured by frequency, it follows that this risk might be affected similarly by Cannabis potency. In another paper, I discussed the potential for greater risk of psychosis in the context of medical marijuana and synthetic cannabinoids.²³ My colleagues and I also have published case reports describing emerging psychosis among regular Cannabis users after escalating to higher potency medical marijuana²⁴ and a hyperconcentrated form of hash oil known as Cannabis “wax” or “dabs” that contains as much as 90% THC.⁴ Preliminary anecdotal evidence supports the plausibility of HPC being more psychotoxic than less potent forms.

Several studies from a research group in the United Kingdom, where sinsemilla has increasingly dominated the drug market, likewise have reported that the use of HPC is associated with a greater risk of psychosis. The first of these studies, published in 2009, found that adults hospitalized for first-episode psychosis were more likely to have used HPC than healthy controls.²⁵ Among Cannabis users, HPC use was associated with a 7-fold increased risk of psychosis, with daily HPC use associated with a 12-fold increased risk.

Based on a larger dataset, a second study reported that high-potency, but not low-potency, Cannabis increased the risk of first-episode psychosis with increasing frequency of use.²⁶ Daily users of HPC had a 5-fold higher risk of psychosis compared with those that had never used Cannabis. A third study reported that HPC use and daily Cannabis use were independently associated with an earlier onset of first-episode psychosis, with daily HPC users developing first-episode psychosis an average of 6 years earlier than non-Cannabis users.²⁷ Finally, a prospective study following patients with first-episode psychosis over 2 years found that the greatest risk of relapse—defined by hospital admission caused by exacerbation of psychotic symptoms—was found among self-reported daily users of HPC, while the lowest risk was among those who stopped using Cannabis after their initial psychotic episode.²⁸

The findings from these 4 studies suggest that the increased risk of psychosis with Cannabis is proportional to overall exposure, determined by both frequency of use and Cannabis potency.

Cognition

There is little doubt that using Cannabis can impair cognition acutely, “after all, this is the basic reason for its recreational use,” as one author wrote.²⁹ As with psychosis, the available evidence indicates that the degree of cognitive impairment is related to the frequency and duration of Cannabis use as well as age of onset of use.^30,31

Few studies have assessed cognitive functioning in relation to Cannabis potency with most only examining the effects of relatively low-potency Cannabis with inconsistent results. For example, 2 studies compared cognitive performance in individuals smoking Cannabis with 1.8% and 3.9% THC. One study found that using higher potency Cannabis resulted in prolonged time needed to complete certain cognitive tasks,³² whereas the other found greater impairment in performance on a decision-making task at both potencies compared with non-users but no differences between the 2 dosages.³³ Detecting significant differences may be difficult within the narrow range of low Cannabis potency studied where any findings have limited applicability in the context of today’s Cannabis with much higher THC content.

To date, only 1 study has assessed cognition at higher Cannabis potencies, comparing Cannabis with 4% THC to 13% THC.³⁴ Cognitive impairments increased with higher potency, especially in tasks that measured motor control and executive functioning. Therefore it appears that higher potency Cannabis use is associated with greater acute cognitive impairment.

The longer-term effects on cognition are less clear, with conflicting evidence about whether Cannabis use can result in residual cognitive impairment despite abstinence.^30,35 A recent review concluded that “the magnitude of neuropsychological impairment and the extent to which it persists after abstinence may depend on the frequency and the duration of Cannabis use, length of abstinence, and age at onset of use.”³¹ The effects of HPC on long-term cognitive deficits have not been studied.

Structural brain changes

A number of studies have determined an association between Cannabis use and brain changes involving structures governing memory and emotional processing, including reduced volume of the hippocampus,³⁶ temporal cortex, insula, and orbitofrontal cortex.³⁷ Although many of these changes appear to be dose-related, some morphologic changes have been reported among young recreational users without Cannabis dependence.³⁸ This has resulted in an understandable concern about the effects of Cannabis on the brains of young people with limited exposure; however, it is not yet clear to what extent detected brain changes are pathological and reflect functional deficits.

Recent research using newer neuroimaging modalities provides preliminary support of Cannabis use associated with white matter changes that, in turn, are correlated with cognitive impairment.³⁹ One study comparing low-potency Cannabis and HPC users with and without first-episode psychosis found a significant effect of Cannabis potency on disturbances in white matter microstructural organization in the corpus callosum.⁴⁰ These findings provide sufficient cause for concern that structural brain changes associated with cognitive impairment are more likely to occur with HPC use.

Recommendations for clinicians

Similar to any drug, the effects of THC and its psychiatric sequelae can be expected to increase with dosage. To date, much of the information about psychiatric risks has been based on studies of low- and moderate-potency Cannabis rather than the much higher potency Cannabis products, such as hyper-concentrated “wax dabs,” that are available today. Data from social media suggest that these products may be associated with novel patterns of use, such as with the intention of “passing out.”⁴¹ It is likely that clinicians will encounter greater psychiatric morbidity associated with HPC use.

Although clinicians may be accustomed to asking about the frequency and duration of Cannabis use, it is now prudent also to ask patients about Cannabis potency to better assess the potential risks of use. The potency of different marijuana products is openly advertised within some “medical marijuana” dispensaries, although the accuracy of information in products such as “edibles” has been called into question.⁵

Physicians are increasingly asked to provide recommendations on “medical marijuana” use. A recent paper outlined characteristics of appropriate candidates for “medical marijuana” including:

• having a debilitating condition that might benefit from Cannabis
• multiple failed trials of conventional pharmacotherapies including FDA-approved cannabinoids
• lack of substance use disorders, psychosis, or unstable mood or anxiety disorders
• residence in a state where “medical marijuana” is legal.⁴²

As part of the informed consent process, physicians providing recommendations for “medical marijuana” now must consider the effects of HPC when weighing potential risks against any benefits of Cannabis use. Those monitoring patients using Cannabis should be aware of the potential for greater psychiatric morbidity with HPC and should educate patients about that risk. Failure to adequately warn patients about such morbidity or to screen for risk factors such as psychosis could leave physicians vulnerable to malpractice litigation.

In the United States, the average potency of Cannabis has increased significantly over the past few decades in response to consumer demand and policies in some states that have legalized marijuana for medicinal and recreational purposes.¹ Whereas the delta-9-tetrahydrocannabinol (THC) content of “street” marijuana was <1% in the 1970s and 4% in the 1990s, by 2012, analyses of Cannabis samples seized by law enforcement agencies documented a rise in average THC potency to >12%.^1-3

Although this increase in potency has been overstated in the media because studies did not control for the effects of changes in sampling methods on freshness, it is estimated that Cannabis potency increased 7-fold from 1970 to 2010.³ Also, Cannabis preparations such as hashish and hash oil extracts containing THC well above average—from 35% to 90% THC—are now more widely available. In states where marijuana has been legalized, high-potency Cannabis (HPC) in the form of “edibles” (eg, marijuana added to baked goods, candy, or drinks) and hash oil extracts (Table 1)^4-13 can be readily obtained from dispensaries or even at local farmers’ markets.

The potency of Cannabis, typically defined as the percentage of THC, its chief psychoactive component, varies depending on the genetic strain of the plant, cultivation techniques, and methods of processing and storage. For example, relative to “average marijuana,” hemp (Cannabis bred for industrial purposes) has very little THC, while sinsemilla (flowering buds from unpollinated female plants), hashish (Cannabis resin), and extracted hash oil contain increasing amounts of THC (Table 2).^1,2

Cannabis use disorder

Recent data indicate that the prevalence of Cannabis use disorders (eg, abuse and dependence) in the United States is approximately 3% among the general population and >30% among Cannabis users.¹⁶ The availability of increasingly potent forms of Cannabis has been cited as a possible explanation for this rise, despite no change in the prevalence of overall marijuana use between 1991 to 1992 and 2001 to 2002.¹⁷ However, while the prevalence of marijuana use disorders has continued to rise—nearly doubling from 2001 to 2002 to 2012 to 2013—this latest increase occurred with a significant increase in overall marijuana use, such that the actual rate of Cannabis use disorders among users seems to have plateaued, despite the continued rise in marijuana potency.¹⁶ This discrepancy could be explained if Cannabis users cut back past a specific threshold of increasing potency. However, 2 studies have called into question how effective such titration efforts might be in practice. In one study, Cannabis users who preferred more potent Cannabis inhaled lower volumes of smoke, but did not fully compensate for the increased potency, such that use of HPC still resulted in greater THC exposure.¹⁸ Another study found that HPC users rolled less marijuana into their joints but not enough to mitigate the impact of greater potency.¹⁹ Therefore, it appears that HPC users typically expose themselves to greater amounts of THC, which could place them at higher risk of addiction.

Although a causal association between increasing Cannabis potency and the rate of substance use disorders among users remains unclear based on epidemiologic studies from the United States, a recent study from the United Kingdom examined the impact of Cannabis potency on dependence.²⁰ This cross-sectional survey found that, although HPC was preferred by users and was rated as offering the “best high,” its use was associated with increasing severity of dependence, especially among young people. The limited available evidence supports a greater risk of Cannabis use disorders with increasing potency.

Psychosis

Based on longitudinal studies published over the past 30 years, it is clear that using Cannabis at a young age (age <15 to 18) increases the risk of developing a psychotic disorder.²¹ This association appears to be dose-dependent, with studies consistently demonstrating that psychosis risk increases with greater frequency of Cannabis use.²² The accumulated evidence to date is strong enough to view the psychotic potential of Cannabis as a significant public health concern.²¹

If risk of psychosis is proportional to the amount of Cannabis used as measured by frequency, it follows that this risk might be affected similarly by Cannabis potency. In another paper, I discussed the potential for greater risk of psychosis in the context of medical marijuana and synthetic cannabinoids.²³ My colleagues and I also have published case reports describing emerging psychosis among regular Cannabis users after escalating to higher potency medical marijuana²⁴ and a hyperconcentrated form of hash oil known as Cannabis “wax” or “dabs” that contains as much as 90% THC.⁴ Preliminary anecdotal evidence supports the plausibility of HPC being more psychotoxic than less potent forms.

Several studies from a research group in the United Kingdom, where sinsemilla has increasingly dominated the drug market, likewise have reported that the use of HPC is associated with a greater risk of psychosis. The first of these studies, published in 2009, found that adults hospitalized for first-episode psychosis were more likely to have used HPC than healthy controls.²⁵ Among Cannabis users, HPC use was associated with a 7-fold increased risk of psychosis, with daily HPC use associated with a 12-fold increased risk.

Based on a larger dataset, a second study reported that high-potency, but not low-potency, Cannabis increased the risk of first-episode psychosis with increasing frequency of use.²⁶ Daily users of HPC had a 5-fold higher risk of psychosis compared with those that had never used Cannabis. A third study reported that HPC use and daily Cannabis use were independently associated with an earlier onset of first-episode psychosis, with daily HPC users developing first-episode psychosis an average of 6 years earlier than non-Cannabis users.²⁷ Finally, a prospective study following patients with first-episode psychosis over 2 years found that the greatest risk of relapse—defined by hospital admission caused by exacerbation of psychotic symptoms—was found among self-reported daily users of HPC, while the lowest risk was among those who stopped using Cannabis after their initial psychotic episode.²⁸

The findings from these 4 studies suggest that the increased risk of psychosis with Cannabis is proportional to overall exposure, determined by both frequency of use and Cannabis potency.

Cognition

There is little doubt that using Cannabis can impair cognition acutely, “after all, this is the basic reason for its recreational use,” as one author wrote.²⁹ As with psychosis, the available evidence indicates that the degree of cognitive impairment is related to the frequency and duration of Cannabis use as well as age of onset of use.^30,31

Few studies have assessed cognitive functioning in relation to Cannabis potency with most only examining the effects of relatively low-potency Cannabis with inconsistent results. For example, 2 studies compared cognitive performance in individuals smoking Cannabis with 1.8% and 3.9% THC. One study found that using higher potency Cannabis resulted in prolonged time needed to complete certain cognitive tasks,³² whereas the other found greater impairment in performance on a decision-making task at both potencies compared with non-users but no differences between the 2 dosages.³³ Detecting significant differences may be difficult within the narrow range of low Cannabis potency studied where any findings have limited applicability in the context of today’s Cannabis with much higher THC content.

To date, only 1 study has assessed cognition at higher Cannabis potencies, comparing Cannabis with 4% THC to 13% THC.³⁴ Cognitive impairments increased with higher potency, especially in tasks that measured motor control and executive functioning. Therefore it appears that higher potency Cannabis use is associated with greater acute cognitive impairment.

The longer-term effects on cognition are less clear, with conflicting evidence about whether Cannabis use can result in residual cognitive impairment despite abstinence.^30,35 A recent review concluded that “the magnitude of neuropsychological impairment and the extent to which it persists after abstinence may depend on the frequency and the duration of Cannabis use, length of abstinence, and age at onset of use.”³¹ The effects of HPC on long-term cognitive deficits have not been studied.

Structural brain changes

A number of studies have determined an association between Cannabis use and brain changes involving structures governing memory and emotional processing, including reduced volume of the hippocampus,³⁶ temporal cortex, insula, and orbitofrontal cortex.³⁷ Although many of these changes appear to be dose-related, some morphologic changes have been reported among young recreational users without Cannabis dependence.³⁸ This has resulted in an understandable concern about the effects of Cannabis on the brains of young people with limited exposure; however, it is not yet clear to what extent detected brain changes are pathological and reflect functional deficits.

Recent research using newer neuroimaging modalities provides preliminary support of Cannabis use associated with white matter changes that, in turn, are correlated with cognitive impairment.³⁹ One study comparing low-potency Cannabis and HPC users with and without first-episode psychosis found a significant effect of Cannabis potency on disturbances in white matter microstructural organization in the corpus callosum.⁴⁰ These findings provide sufficient cause for concern that structural brain changes associated with cognitive impairment are more likely to occur with HPC use.

Recommendations for clinicians

Similar to any drug, the effects of THC and its psychiatric sequelae can be expected to increase with dosage. To date, much of the information about psychiatric risks has been based on studies of low- and moderate-potency Cannabis rather than the much higher potency Cannabis products, such as hyper-concentrated “wax dabs,” that are available today. Data from social media suggest that these products may be associated with novel patterns of use, such as with the intention of “passing out.”⁴¹ It is likely that clinicians will encounter greater psychiatric morbidity associated with HPC use.

Although clinicians may be accustomed to asking about the frequency and duration of Cannabis use, it is now prudent also to ask patients about Cannabis potency to better assess the potential risks of use. The potency of different marijuana products is openly advertised within some “medical marijuana” dispensaries, although the accuracy of information in products such as “edibles” has been called into question.⁵

Physicians are increasingly asked to provide recommendations on “medical marijuana” use. A recent paper outlined characteristics of appropriate candidates for “medical marijuana” including:

• having a debilitating condition that might benefit from Cannabis
• multiple failed trials of conventional pharmacotherapies including FDA-approved cannabinoids
• lack of substance use disorders, psychosis, or unstable mood or anxiety disorders
• residence in a state where “medical marijuana” is legal.⁴²

As part of the informed consent process, physicians providing recommendations for “medical marijuana” now must consider the effects of HPC when weighing potential risks against any benefits of Cannabis use. Those monitoring patients using Cannabis should be aware of the potential for greater psychiatric morbidity with HPC and should educate patients about that risk. Failure to adequately warn patients about such morbidity or to screen for risk factors such as psychosis could leave physicians vulnerable to malpractice litigation.

Congratulations to Ricks Warren, PhD, ABPP, Elke Smeets, PhD, and Kristen Neff, MD, the authors of “Self-criticism and self-compassion: Risk and resilience,” (Evidence-Based Reviews, Current Psychiatry, December 2016, p. 18-21,24-28,32). I believe the application of the innovative and scholarly message of self-compassion will not only be a boon to patients and the public but also to psychiatrists and mental health clinicians. Why? We, psychiatrists, seem to be experiencing a rising and epidemic rate of burnout, and self-compassion can help us to stop blaming ourselves for being unable to do our best when the system inhibits us. In turn, if we help our own well-being, we will be better able to help our patients.

H. Steven Moffic, MD
Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Warren responds

We couldn’t agree more with Dr. Moffic’s perspective that psychiatrists and other mental health clinicians likely would benefit from self-compassion during our clinical work in a complex, demanding, and rapidly changing mental health environment. Fortunately, attention to the importance of self-compassion for caregivers has been advocated, and recent studies of self-compassion in health care professionals have reported promising results. Because the neuroticism and self-criticism personality traits are most associated with depression and burnout in physicians, interventions that promote self-compassion are likely to lead to improved mental health in psychiatrists and other health care professionals. Recent research has found that self-compassion in health care providers is associated with less burnout and compassion fatigue, increased resilience, adaptive emotion regulation, and reduced sleep disturbance.¹

The time is now right for clinical trials of self-compassion interventions in psychiatrists and other caregivers. Neff and Germer’s mindful self-compassion intervention,² discussed in our article, could be easily adapted for psychiatrists and other mental health professionals. As Mills and Chapman,³ stated, “While being self-critical and perfectionistic may be common among doctors, being kind to oneself is not a luxury: it is a necessity. Self-care is, in a sense, a sine qua non for giving care for patients.”

Ricks Warren, PhD, ABPP
Clinical Associate Professor
Department of Psychiatry
University of Michigan Medical School
Ann Arbor, Michigan

Congratulations to Ricks Warren, PhD, ABPP, Elke Smeets, PhD, and Kristen Neff, MD, the authors of “Self-criticism and self-compassion: Risk and resilience,” (Evidence-Based Reviews, Current Psychiatry, December 2016, p. 18-21,24-28,32). I believe the application of the innovative and scholarly message of self-compassion will not only be a boon to patients and the public but also to psychiatrists and mental health clinicians. Why? We, psychiatrists, seem to be experiencing a rising and epidemic rate of burnout, and self-compassion can help us to stop blaming ourselves for being unable to do our best when the system inhibits us. In turn, if we help our own well-being, we will be better able to help our patients.

H. Steven Moffic, MD
Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Warren responds

We couldn’t agree more with Dr. Moffic’s perspective that psychiatrists and other mental health clinicians likely would benefit from self-compassion during our clinical work in a complex, demanding, and rapidly changing mental health environment. Fortunately, attention to the importance of self-compassion for caregivers has been advocated, and recent studies of self-compassion in health care professionals have reported promising results. Because the neuroticism and self-criticism personality traits are most associated with depression and burnout in physicians, interventions that promote self-compassion are likely to lead to improved mental health in psychiatrists and other health care professionals. Recent research has found that self-compassion in health care providers is associated with less burnout and compassion fatigue, increased resilience, adaptive emotion regulation, and reduced sleep disturbance.¹

The time is now right for clinical trials of self-compassion interventions in psychiatrists and other caregivers. Neff and Germer’s mindful self-compassion intervention,² discussed in our article, could be easily adapted for psychiatrists and other mental health professionals. As Mills and Chapman,³ stated, “While being self-critical and perfectionistic may be common among doctors, being kind to oneself is not a luxury: it is a necessity. Self-care is, in a sense, a sine qua non for giving care for patients.”

Ricks Warren, PhD, ABPP
Clinical Associate Professor
Department of Psychiatry
University of Michigan Medical School
Ann Arbor, Michigan

Congratulations to Ricks Warren, PhD, ABPP, Elke Smeets, PhD, and Kristen Neff, MD, the authors of “Self-criticism and self-compassion: Risk and resilience,” (Evidence-Based Reviews, Current Psychiatry, December 2016, p. 18-21,24-28,32). I believe the application of the innovative and scholarly message of self-compassion will not only be a boon to patients and the public but also to psychiatrists and mental health clinicians. Why? We, psychiatrists, seem to be experiencing a rising and epidemic rate of burnout, and self-compassion can help us to stop blaming ourselves for being unable to do our best when the system inhibits us. In turn, if we help our own well-being, we will be better able to help our patients.

H. Steven Moffic, MD
Retired Tenured Professor of Psychiatry
Medical College of Wisconsin
Milwaukee, Wisconsin

Dr. Warren responds

We couldn’t agree more with Dr. Moffic’s perspective that psychiatrists and other mental health clinicians likely would benefit from self-compassion during our clinical work in a complex, demanding, and rapidly changing mental health environment. Fortunately, attention to the importance of self-compassion for caregivers has been advocated, and recent studies of self-compassion in health care professionals have reported promising results. Because the neuroticism and self-criticism personality traits are most associated with depression and burnout in physicians, interventions that promote self-compassion are likely to lead to improved mental health in psychiatrists and other health care professionals. Recent research has found that self-compassion in health care providers is associated with less burnout and compassion fatigue, increased resilience, adaptive emotion regulation, and reduced sleep disturbance.¹

The time is now right for clinical trials of self-compassion interventions in psychiatrists and other caregivers. Neff and Germer’s mindful self-compassion intervention,² discussed in our article, could be easily adapted for psychiatrists and other mental health professionals. As Mills and Chapman,³ stated, “While being self-critical and perfectionistic may be common among doctors, being kind to oneself is not a luxury: it is a necessity. Self-care is, in a sense, a sine qua non for giving care for patients.”

Ricks Warren, PhD, ABPP
Clinical Associate Professor
Department of Psychiatry
University of Michigan Medical School
Ann Arbor, Michigan

Providing care in a correctional facility is inherent with danger, complexities, and risks. The mnemonic CORRECT strives to shed light on some of these factors and to provide a window of understanding on the needs and experiences of patients and staff in correctional facilities.

Challenges. The inherently coercive environment of a correctional facility affects all those confined within—staff and inmates. Staff members have varied background and experience (ie, custody, medical services, and mental health services). A large percentage of incarcerated individuals have been diagnosed with antisocial personality disorder, substance use disorder, psychosis, or medical illnesses. Many of these individuals have received little, if any, treatment, and are monitored most of the time by custody staff, who have limited training in mental health care.

Inmates also have considerable interaction with medical services. The goals of medical and psychiatric providers differ from that of corrections: to diagnose and treat vs to confine, deter, and punish.¹ Disagreements and friction may be inevitable and require ongoing diplomacy.

Opportunity. Many inmates have a history of homelessness and arrive with untreated medical conditions; hypertension, impaired liver function, tuberculosis, and hepatitis C are common. Correctional facilities often become primary care providers for the physically and mentally ill. Inmates might have never received any form of patient education, and could respond well to patience, education, and compassion. Challenges can become opportunities to help this neglected, underserved, and underprivileged population.

Reflection. The need to continually assess a patient and provide a treatment plan is not unique to corrections. However, the patient caseload, the day-to-day continuum, and the need to complete patient care within time restrictions, can become a mundane process that could invite a sense of conditioned familiarity and boredom over the years, despite the predictable unpredictability of a correctional setting. The need to periodically stop and reflect is crucial, which can be done independently or with ongoing staff education.

Risks. A heightened level of risk starts from the time the incarcerated individual enters the correctional facility to the moment he (she) is released. This involves many facets, including physical, psychological, and medical exposure. Individuals could arrive in a state of drug withdrawal, and often in a state of delirium, which can complicate the presentation.

Potential inmate–inmate conflicts are a constant risk. Trading and swapping medications for sedative purposes or to get “high” is common in most correctional facilities, which has prompted many institutions to remove select medications from their formulary. Some individuals might prey on the novice, weak, or elderly inmates if they are taking sought-after medications. The suicide rate is high in correctional facilities. Because of these increased risks, the psychiatrist needs to be mindful of prescribing practices.

Experience. Despite years of education in medical school, residency, and fellowships, there is no substitute for clinical experience for novice correctional psychiatrists. Becoming competent can take years, and requires face-to-face evaluations, immersion, presence, and movement within a facility, and on-call responsibilities. Telepsychiatry is no replacement for the experience of being “in the trenches.” Despite a position of apparent power and superiority, physicians are human. Learning from mistakes is crucial to evolve and improve patient rapport.

Confidentiality. Lack of confidentiality often is the norm. Custody staff might be present during evaluations because of the potentially dangerous environment. Because certain areas of the facility require further caution, such as single cells or solitary confinement (as a result of unpredictability, dangerousness, specific charges, behavioral problems, etc.), the psychiatrist might be required to perform assessments at the front of the cell, in the presence of adjacent cells and other inmates and often an entire group. This might be unavoidable and requires a higher level of sensitivity. The need for correctional employees to maintain a sense of confidentiality has been well demonstrated in media events regarding serious boundary violations or sexual contact. 

Treatment. Psychiatrists “confined” in corrections could feel isolated from the “outside” world and from their professional colleagues. Therefore, clinicians employed in corrections could develop a specific variety of burnout. Avoiding burnout requires a mindful discipline in self-care, efforts in healthy socialization, recreation, and outdoor activities. It’s crucial to maintain and update one’s knowledge base in order to provide treatment within the standard of care.

Providing care in a correctional facility is inherent with danger, complexities, and risks. The mnemonic CORRECT strives to shed light on some of these factors and to provide a window of understanding on the needs and experiences of patients and staff in correctional facilities.

Challenges. The inherently coercive environment of a correctional facility affects all those confined within—staff and inmates. Staff members have varied background and experience (ie, custody, medical services, and mental health services). A large percentage of incarcerated individuals have been diagnosed with antisocial personality disorder, substance use disorder, psychosis, or medical illnesses. Many of these individuals have received little, if any, treatment, and are monitored most of the time by custody staff, who have limited training in mental health care.

Inmates also have considerable interaction with medical services. The goals of medical and psychiatric providers differ from that of corrections: to diagnose and treat vs to confine, deter, and punish.¹ Disagreements and friction may be inevitable and require ongoing diplomacy.

Opportunity. Many inmates have a history of homelessness and arrive with untreated medical conditions; hypertension, impaired liver function, tuberculosis, and hepatitis C are common. Correctional facilities often become primary care providers for the physically and mentally ill. Inmates might have never received any form of patient education, and could respond well to patience, education, and compassion. Challenges can become opportunities to help this neglected, underserved, and underprivileged population.

Reflection. The need to continually assess a patient and provide a treatment plan is not unique to corrections. However, the patient caseload, the day-to-day continuum, and the need to complete patient care within time restrictions, can become a mundane process that could invite a sense of conditioned familiarity and boredom over the years, despite the predictable unpredictability of a correctional setting. The need to periodically stop and reflect is crucial, which can be done independently or with ongoing staff education.

Risks. A heightened level of risk starts from the time the incarcerated individual enters the correctional facility to the moment he (she) is released. This involves many facets, including physical, psychological, and medical exposure. Individuals could arrive in a state of drug withdrawal, and often in a state of delirium, which can complicate the presentation.

Potential inmate–inmate conflicts are a constant risk. Trading and swapping medications for sedative purposes or to get “high” is common in most correctional facilities, which has prompted many institutions to remove select medications from their formulary. Some individuals might prey on the novice, weak, or elderly inmates if they are taking sought-after medications. The suicide rate is high in correctional facilities. Because of these increased risks, the psychiatrist needs to be mindful of prescribing practices.

Experience. Despite years of education in medical school, residency, and fellowships, there is no substitute for clinical experience for novice correctional psychiatrists. Becoming competent can take years, and requires face-to-face evaluations, immersion, presence, and movement within a facility, and on-call responsibilities. Telepsychiatry is no replacement for the experience of being “in the trenches.” Despite a position of apparent power and superiority, physicians are human. Learning from mistakes is crucial to evolve and improve patient rapport.

Confidentiality. Lack of confidentiality often is the norm. Custody staff might be present during evaluations because of the potentially dangerous environment. Because certain areas of the facility require further caution, such as single cells or solitary confinement (as a result of unpredictability, dangerousness, specific charges, behavioral problems, etc.), the psychiatrist might be required to perform assessments at the front of the cell, in the presence of adjacent cells and other inmates and often an entire group. This might be unavoidable and requires a higher level of sensitivity. The need for correctional employees to maintain a sense of confidentiality has been well demonstrated in media events regarding serious boundary violations or sexual contact. 

Treatment. Psychiatrists “confined” in corrections could feel isolated from the “outside” world and from their professional colleagues. Therefore, clinicians employed in corrections could develop a specific variety of burnout. Avoiding burnout requires a mindful discipline in self-care, efforts in healthy socialization, recreation, and outdoor activities. It’s crucial to maintain and update one’s knowledge base in order to provide treatment within the standard of care.

Providing care in a correctional facility is inherent with danger, complexities, and risks. The mnemonic CORRECT strives to shed light on some of these factors and to provide a window of understanding on the needs and experiences of patients and staff in correctional facilities.

Challenges. The inherently coercive environment of a correctional facility affects all those confined within—staff and inmates. Staff members have varied background and experience (ie, custody, medical services, and mental health services). A large percentage of incarcerated individuals have been diagnosed with antisocial personality disorder, substance use disorder, psychosis, or medical illnesses. Many of these individuals have received little, if any, treatment, and are monitored most of the time by custody staff, who have limited training in mental health care.

Inmates also have considerable interaction with medical services. The goals of medical and psychiatric providers differ from that of corrections: to diagnose and treat vs to confine, deter, and punish.¹ Disagreements and friction may be inevitable and require ongoing diplomacy.

Opportunity. Many inmates have a history of homelessness and arrive with untreated medical conditions; hypertension, impaired liver function, tuberculosis, and hepatitis C are common. Correctional facilities often become primary care providers for the physically and mentally ill. Inmates might have never received any form of patient education, and could respond well to patience, education, and compassion. Challenges can become opportunities to help this neglected, underserved, and underprivileged population.

Reflection. The need to continually assess a patient and provide a treatment plan is not unique to corrections. However, the patient caseload, the day-to-day continuum, and the need to complete patient care within time restrictions, can become a mundane process that could invite a sense of conditioned familiarity and boredom over the years, despite the predictable unpredictability of a correctional setting. The need to periodically stop and reflect is crucial, which can be done independently or with ongoing staff education.

Risks. A heightened level of risk starts from the time the incarcerated individual enters the correctional facility to the moment he (she) is released. This involves many facets, including physical, psychological, and medical exposure. Individuals could arrive in a state of drug withdrawal, and often in a state of delirium, which can complicate the presentation.

Potential inmate–inmate conflicts are a constant risk. Trading and swapping medications for sedative purposes or to get “high” is common in most correctional facilities, which has prompted many institutions to remove select medications from their formulary. Some individuals might prey on the novice, weak, or elderly inmates if they are taking sought-after medications. The suicide rate is high in correctional facilities. Because of these increased risks, the psychiatrist needs to be mindful of prescribing practices.

Experience. Despite years of education in medical school, residency, and fellowships, there is no substitute for clinical experience for novice correctional psychiatrists. Becoming competent can take years, and requires face-to-face evaluations, immersion, presence, and movement within a facility, and on-call responsibilities. Telepsychiatry is no replacement for the experience of being “in the trenches.” Despite a position of apparent power and superiority, physicians are human. Learning from mistakes is crucial to evolve and improve patient rapport.

Confidentiality. Lack of confidentiality often is the norm. Custody staff might be present during evaluations because of the potentially dangerous environment. Because certain areas of the facility require further caution, such as single cells or solitary confinement (as a result of unpredictability, dangerousness, specific charges, behavioral problems, etc.), the psychiatrist might be required to perform assessments at the front of the cell, in the presence of adjacent cells and other inmates and often an entire group. This might be unavoidable and requires a higher level of sensitivity. The need for correctional employees to maintain a sense of confidentiality has been well demonstrated in media events regarding serious boundary violations or sexual contact. 

Treatment. Psychiatrists “confined” in corrections could feel isolated from the “outside” world and from their professional colleagues. Therefore, clinicians employed in corrections could develop a specific variety of burnout. Avoiding burnout requires a mindful discipline in self-care, efforts in healthy socialization, recreation, and outdoor activities. It’s crucial to maintain and update one’s knowledge base in order to provide treatment within the standard of care.

Ms. M, age 71, was diagnosed with Alzheimer’s disease several months ago and her clinical presentation and Mini-Mental Status Exam score of 22 indicates mild dementia. In addition to chronic medications for hypertension, Ms. M has been taking lorazepam, 1 mg, 3 times daily, for >15 years for unspecified anxiety.

Ms. M becomes more confused at home over the course of a few days, and her daughter brings her to her primary care physician for evaluation. Recognizing that benzodiazepines can contribute to delirium, the physician discontinues lorazepam. Three days later, Ms. M’s confusion worsens, and she develops nausea and a tremor. She is taken to the local emergency department where she is admitted for benzodiazepine withdrawal and diagnosed with a urinary tract infection.

Because dementia is a strong risk factor for developing delirium,¹ withdrawing or changing

Consider withdrawing or replacing medications that are strongly implicated in causing delirium with another medication for the same indication with a lower potential for

In general, there are no firm rules for how to taper and discontinue potentially deliriogenic medications, as both the need to taper and the best strategy for doing so depends on a number of factors and requires clinical judgement. When determining how quickly to withdraw a potentially offending medication in a patient with suspected delirium, clinicians should consider:

Dosage and duration of treatment. Consider tapering and discontinuing benzodiazepines in a patient who is taking more than the minimal scheduled dosages for ≥2 weeks, especially after 8 weeks of scheduled treatment. Consider tapering opioids in a patient taking more than the minimal scheduled dosage for more than a few days. When attempting to rule out delirium, taper opioids as quickly and as safely possible, with a recommended reduction of ≤20% per day to prevent withdrawal symptoms. In general, potentially deliriogenic medications can be discontinued without tapering if they are taken on a non-daily, as-needed basis.

The half-life of a medication determines both the onset and duration of withdrawal symptoms. Withdrawal occurs earlier when discontinuing medications with short

Ms. M, age 71, was diagnosed with Alzheimer’s disease several months ago and her clinical presentation and Mini-Mental Status Exam score of 22 indicates mild dementia. In addition to chronic medications for hypertension, Ms. M has been taking lorazepam, 1 mg, 3 times daily, for >15 years for unspecified anxiety.

Ms. M becomes more confused at home over the course of a few days, and her daughter brings her to her primary care physician for evaluation. Recognizing that benzodiazepines can contribute to delirium, the physician discontinues lorazepam. Three days later, Ms. M’s confusion worsens, and she develops nausea and a tremor. She is taken to the local emergency department where she is admitted for benzodiazepine withdrawal and diagnosed with a urinary tract infection.

Because dementia is a strong risk factor for developing delirium,¹ withdrawing or changing

Consider withdrawing or replacing medications that are strongly implicated in causing delirium with another medication for the same indication with a lower potential for

In general, there are no firm rules for how to taper and discontinue potentially deliriogenic medications, as both the need to taper and the best strategy for doing so depends on a number of factors and requires clinical judgement. When determining how quickly to withdraw a potentially offending medication in a patient with suspected delirium, clinicians should consider:

Dosage and duration of treatment. Consider tapering and discontinuing benzodiazepines in a patient who is taking more than the minimal scheduled dosages for ≥2 weeks, especially after 8 weeks of scheduled treatment. Consider tapering opioids in a patient taking more than the minimal scheduled dosage for more than a few days. When attempting to rule out delirium, taper opioids as quickly and as safely possible, with a recommended reduction of ≤20% per day to prevent withdrawal symptoms. In general, potentially deliriogenic medications can be discontinued without tapering if they are taken on a non-daily, as-needed basis.

The half-life of a medication determines both the onset and duration of withdrawal symptoms. Withdrawal occurs earlier when discontinuing medications with short

Ms. M, age 71, was diagnosed with Alzheimer’s disease several months ago and her clinical presentation and Mini-Mental Status Exam score of 22 indicates mild dementia. In addition to chronic medications for hypertension, Ms. M has been taking lorazepam, 1 mg, 3 times daily, for >15 years for unspecified anxiety.

Ms. M becomes more confused at home over the course of a few days, and her daughter brings her to her primary care physician for evaluation. Recognizing that benzodiazepines can contribute to delirium, the physician discontinues lorazepam. Three days later, Ms. M’s confusion worsens, and she develops nausea and a tremor. She is taken to the local emergency department where she is admitted for benzodiazepine withdrawal and diagnosed with a urinary tract infection.

Because dementia is a strong risk factor for developing delirium,¹ withdrawing or changing

Consider withdrawing or replacing medications that are strongly implicated in causing delirium with another medication for the same indication with a lower potential for

In general, there are no firm rules for how to taper and discontinue potentially deliriogenic medications, as both the need to taper and the best strategy for doing so depends on a number of factors and requires clinical judgement. When determining how quickly to withdraw a potentially offending medication in a patient with suspected delirium, clinicians should consider:

Dosage and duration of treatment. Consider tapering and discontinuing benzodiazepines in a patient who is taking more than the minimal scheduled dosages for ≥2 weeks, especially after 8 weeks of scheduled treatment. Consider tapering opioids in a patient taking more than the minimal scheduled dosage for more than a few days. When attempting to rule out delirium, taper opioids as quickly and as safely possible, with a recommended reduction of ≤20% per day to prevent withdrawal symptoms. In general, potentially deliriogenic medications can be discontinued without tapering if they are taken on a non-daily, as-needed basis.

The half-life of a medication determines both the onset and duration of withdrawal symptoms. Withdrawal occurs earlier when discontinuing medications with short

In the current health care environment, there is an increasing demand for objective assessment of disease states.¹ This is particularly apparent in psychiatry, where documentation of outcomes lags that of other areas of medicine.

In 2012, the additional health care costs incurred by persons with mental health diagnoses were estimated to be $293 billion among commercially insured, Medicaid, and Medicare beneficiaries in the United States—a figure that is 273% higher than the cost for those without psychiatric diagnoses.² Psychiatric and medical illnesses can be so tightly linked that accurate diagnosis and treatment of psychiatric disorders becomes essential to control medical illnesses. It is not surprising that there is increased scrutiny to the ways in which psychiatric care can be objectively assessed and monitored, and payers such as Centers for Medicare and Medicaid Services (CMS) increasingly require objective documentation of disease state improvement for payment.³

Support for objective assessment of disease derives from the collaborative care model. This model is designed to better integrate psychiatric and primary care by (among other practices) establishing the Patient-Centered Medical Home and emphasizing screening and monitoring patient-reported outcomes over time to assess treatment response.⁴ This approach, which is endorsed by the American Psychiatric Association, is associated with significant improvements in outcomes compared with usual care.⁵ It tracks a patient’s progress using validated clinical rating scales and other screening tools (eg, Patient Health Questionnaire [PHQ-9] for depression), an approach that is analogous to how patients with type 2 diabetes mellitus are monitored by hemoglobin A_1c laboratory tests.⁶ An increasingly extensive body of research supports the impact of this approach on treatment. A 2012 Cochrane Review associated collaborative care with significant improvements in depression and anxiety outcomes compared with usual treatment.⁷

Despite these findings, a recent Kennedy Forum brief asserts that behavioral health is characterized by a “lack of systematic measurement to determine whether patients are responding to treatment.”⁸ That same brief points to the many easy-to-administer and validated rating scales and other screening tools that can reliably measure the frequency and severity of psychiatric symptoms over time, and likens the lack of their use as “equivalent to treating high blood pressure without using a blood pressure cuff to measure if a patient’s blood pressure is improving.”⁸ It is estimated that only 18% of psychiatrists and 11% of psychologists administer them routinely.^9,10 This lack of use denies clinicians important information that can help detect deterioration or lack of improvement in their patients.
 

Psychiatry is replete with rating scales and screening tools, and the number of competing scales can make choosing a measure difficult.¹ Nonetheless, not all scales are appropriate for clinical use; many are designed for research, for instance, and are lengthy and difficult to administer.

This article reviews a number of rating scales that are brief, useful, and easy to administer. A framework for the screening tools addressed in this article is available on the federally funded Center for Integrated Health Systems Web site (www.integration.samhsa.gov). This site promotes the use of tools designed to assist in screening and monitoring for depression, anxiety, bipolar disorder, substance use, and suicidality.¹¹

Quality criteria for rating scales

The quality of a rating scale is determined by the following attributes¹²:

• Objectivity. The ability of a scale to obtain the same results, regardless of who administers, analyzes, or interprets it.
• Reliability. The ability of a scale to convey consistent and reproducible information across time, patients, and raters.
• Validity. The degree to which the scale measures what it is supposed to measure (eg, depressive symptoms). Sensitivity and specificity are measures of validity and provide additional information about the rating scale; namely, whether the scale can detect the presence of a disease (sensitivity) and whether it detects only that disease or condition and not another (specificity).
• Establishment of norms. Whether a scale provides reference values for different clinical groups.
• Practicability. The resources required to administer the assessment instrument in terms of time, staff, and material.

In addition to meeting these quality criteria, selection of a scale can be based on whether it is self-rated or observer-rated. Advantages to self-rated scales, such as the PHQ-9, Mood Disorder Questionnaire (MDQ), and Generalized Anxiety Disorder 7-item (GAD-7) scale, are their practicability—they are easy to administer and don’t require clinician or staff time—and their use in evaluating and raising awareness of subjective states.

However, reliability may be a concern, as some patients either may lack insight or exaggerate or mask symptoms when completing such scales.¹³ Both observer and self-rated scales can be used together to minimize bias, identify symptoms that might have been missed/not addressed in the clinical interview, and drive clinical decision-making. Both also can help patients communicate with their providers and make them feel more involved in clinical decision-making.⁸

The following scales have met many of the quality criteria described here and are endorsed by the government payer system. They can easily be incorporated into clinical practice and will provide useful clinical information that can assist in diagnosis and monitoring patient outcomes.

Patient Health Questionnaire

PHQ-9 is a 9-item self-report questionnaire that can help to detect the presence of depression and supplement a thorough psychiatric and mental health interview. It scores the 9 DSM-IV criteria for depression on a scale of 0 (not at all) to 3 (nearly every day). It is a public resource that is easy to find online, available without cost in several languages, and takes just a few minutes to complete.¹⁴

PHQ-9 has shown excellent test–retest reliability in screening for depression, and normative data on the instrument’s use are available in various clinical populations.¹⁵ Research has shown that as PHQ-9 depression scores increase, functional status decrease, while depressive symptoms, sick days, and health care utilization increase.¹⁵ In one study, a PHQ-9 score of ≥10 had 88% sensitivity and specificity for detecting depression, with scores of 5, 10, 15, and 20 indicating mild, moderate, moderately severe, and severe depression, respectively.¹⁶ In addition to its use as a screening tool, PHQ-9 is a responsive and reliable measure of depression treatment outcomes.¹⁷

Mood Disorder Questionnaire

MDQ is another brief, self-report questionnaire that is available online. It is designed to identify and monitor patients who are likely to meet diagnostic criteria for bipolar disorder.^18,19

The first question on the MDQ asks if the patient has experienced any of 13 common mood and behavior symptoms. The second question asks if these symptoms have ever occurred at the same time, and the third asks the degree to which the patient finds the symptoms to be problematic. The remaining 2 questions provide additional, clinical information, because they address family history of manic–depressive illness or bipolar disorder and whether a diagnosis of either disorder has been made.

The MDQ has shown validity in assessing bipolar disorder symptoms in a general population,²⁰ although recent research suggests that imprecise recall bias may limit its reliability in detecting hypomanic episodes earlier in life.²¹ Nonetheless, its specificity of >97% means that it will effectively screen out just about all true negatives.¹⁸

Generalized Anxiety Disorder 7-item scale

GAD-7 scale is a brief, self-administered questionnaire for screening and measuring severity of GAD.²² It asks patients to rate 7 items that represent problems with general anxiety and scores each item on a scale of 0 (not at all) to 3 (nearly every day). Similar to the other measures, it is easily accessible online.

Research evidence supports the reliability and validity of GAD-7 as a measure of anxiety in the general population. Sensitivity and specificity are 89% and 82%, respectively. Normative data for age and sex specific subgroups support its use across age groups and in both males and females.²³ The GAD-7 performs well for detecting and monitoring not only GAD but also panic disorder, social anxiety disorder, and posttraumatic stress disorder.²⁴

CAGE questionnaire for detection of substance use

The CAGE questionnaire is a widely-used screening tool that was originally developed to detect alcohol abuse, but has been adapted to assess other substance abuse.^25,26 The omission of substance abuse from diagnostic consideration can have a major effect on quality of care, because substance abuse can be the underlying cause of other diseases. Therefore, routine administration of this instrument in clinical practice can lead to better understanding and monitoring of patient health.²⁷

Similar to other instruments, CAGE is free and available online.²⁷ It contains 4 simple questions, with 1 point is assigned to each positive answer.

Have you ever:
1. Felt the need to cut down on your drinking or drug use?
2. Have people annoyed you by criticizing your drinking or drug use?
3. Have you felt bad or guilty about your drinking or drug use?
4. Have you ever had a drink or used drugs first thing in the morning to steady your nerves or to get rid of a hangover (eye-opener)?

The simple mnemonic CAGE makes the questions easy to remember and to administer in a clinical setting. CAGE has demonstrated validity, with one study determining that CAGE scores ≥2 had a specificity and sensitivity of 76% and 93%, respectively, for identifying excessive drinking, and a specificity and sensitivity of 77% and 91%, respectively, for identifying alcohol abuse.²⁸

Columbia Suicide Severity Rating Scale (C-SSRS)

C-SSRS was developed by researchers at Columbia University to assess the severity of and track changes over time in suicidal ideation and behavior. C-SSRS is 2 pages and takes only a few minutes to administer; however, it also may be completed as a self-report measure. The questions are phrased for use in an interview format, and clinicians are encouraged to receive training prior to its administration, although specific training in mental health is not required.

The “Lifetime/Recent” version allows practitioners to gather lifetime history of suicidality as well as any recent suicidal ideation and/or behavior, whereas the “Since Last Visit” version of the scale assesses suicidality in patients who have completed at least 1 Lifetime/Recent C-SSRS assessment. A truncated, 6-item “Screener” version is typically used in emergency situations. A risk assessment can be added to either the Full or Screener version to summarize the answers from C-SSRS and document risk and protective factors.²⁹

Several studies have found C-SSRS to be reliable and valid for identifying suicide risk in children and adults.^30,31USA Today reported that an individual exhibiting even a single behavior identified by the scale is 8 to 10 times more likely to complete suicide.³² In addition, the C-SSRS has helped reduce the suicide rate 65% in one of the largest providers of community-based behavioral health care in the United States.³²

Using scales to augment care

Each of the scales described in this article can easily be incorporated into clinical practice and offers psychiatrists important clinical information that may have been missed or not addressed in the initial clinical interview. This information can be used to follow progression of symptoms and effectiveness of treatment. Although rating scales should never be used alone to establish a diagnosis or clinical treatment plan, they can and should be used to augment information from the clinician’s assessment and follow-up interviews.⁵
 

In the current health care environment, there is an increasing demand for objective assessment of disease states.¹ This is particularly apparent in psychiatry, where documentation of outcomes lags that of other areas of medicine.

In 2012, the additional health care costs incurred by persons with mental health diagnoses were estimated to be $293 billion among commercially insured, Medicaid, and Medicare beneficiaries in the United States—a figure that is 273% higher than the cost for those without psychiatric diagnoses.² Psychiatric and medical illnesses can be so tightly linked that accurate diagnosis and treatment of psychiatric disorders becomes essential to control medical illnesses. It is not surprising that there is increased scrutiny to the ways in which psychiatric care can be objectively assessed and monitored, and payers such as Centers for Medicare and Medicaid Services (CMS) increasingly require objective documentation of disease state improvement for payment.³

Support for objective assessment of disease derives from the collaborative care model. This model is designed to better integrate psychiatric and primary care by (among other practices) establishing the Patient-Centered Medical Home and emphasizing screening and monitoring patient-reported outcomes over time to assess treatment response.⁴ This approach, which is endorsed by the American Psychiatric Association, is associated with significant improvements in outcomes compared with usual care.⁵ It tracks a patient’s progress using validated clinical rating scales and other screening tools (eg, Patient Health Questionnaire [PHQ-9] for depression), an approach that is analogous to how patients with type 2 diabetes mellitus are monitored by hemoglobin A_1c laboratory tests.⁶ An increasingly extensive body of research supports the impact of this approach on treatment. A 2012 Cochrane Review associated collaborative care with significant improvements in depression and anxiety outcomes compared with usual treatment.⁷

Despite these findings, a recent Kennedy Forum brief asserts that behavioral health is characterized by a “lack of systematic measurement to determine whether patients are responding to treatment.”⁸ That same brief points to the many easy-to-administer and validated rating scales and other screening tools that can reliably measure the frequency and severity of psychiatric symptoms over time, and likens the lack of their use as “equivalent to treating high blood pressure without using a blood pressure cuff to measure if a patient’s blood pressure is improving.”⁸ It is estimated that only 18% of psychiatrists and 11% of psychologists administer them routinely.^9,10 This lack of use denies clinicians important information that can help detect deterioration or lack of improvement in their patients.
 

Psychiatry is replete with rating scales and screening tools, and the number of competing scales can make choosing a measure difficult.¹ Nonetheless, not all scales are appropriate for clinical use; many are designed for research, for instance, and are lengthy and difficult to administer.

This article reviews a number of rating scales that are brief, useful, and easy to administer. A framework for the screening tools addressed in this article is available on the federally funded Center for Integrated Health Systems Web site (www.integration.samhsa.gov). This site promotes the use of tools designed to assist in screening and monitoring for depression, anxiety, bipolar disorder, substance use, and suicidality.¹¹

Quality criteria for rating scales

The quality of a rating scale is determined by the following attributes¹²:

• Objectivity. The ability of a scale to obtain the same results, regardless of who administers, analyzes, or interprets it.
• Reliability. The ability of a scale to convey consistent and reproducible information across time, patients, and raters.
• Validity. The degree to which the scale measures what it is supposed to measure (eg, depressive symptoms). Sensitivity and specificity are measures of validity and provide additional information about the rating scale; namely, whether the scale can detect the presence of a disease (sensitivity) and whether it detects only that disease or condition and not another (specificity).
• Establishment of norms. Whether a scale provides reference values for different clinical groups.
• Practicability. The resources required to administer the assessment instrument in terms of time, staff, and material.

In addition to meeting these quality criteria, selection of a scale can be based on whether it is self-rated or observer-rated. Advantages to self-rated scales, such as the PHQ-9, Mood Disorder Questionnaire (MDQ), and Generalized Anxiety Disorder 7-item (GAD-7) scale, are their practicability—they are easy to administer and don’t require clinician or staff time—and their use in evaluating and raising awareness of subjective states.

However, reliability may be a concern, as some patients either may lack insight or exaggerate or mask symptoms when completing such scales.¹³ Both observer and self-rated scales can be used together to minimize bias, identify symptoms that might have been missed/not addressed in the clinical interview, and drive clinical decision-making. Both also can help patients communicate with their providers and make them feel more involved in clinical decision-making.⁸

The following scales have met many of the quality criteria described here and are endorsed by the government payer system. They can easily be incorporated into clinical practice and will provide useful clinical information that can assist in diagnosis and monitoring patient outcomes.

Patient Health Questionnaire

PHQ-9 is a 9-item self-report questionnaire that can help to detect the presence of depression and supplement a thorough psychiatric and mental health interview. It scores the 9 DSM-IV criteria for depression on a scale of 0 (not at all) to 3 (nearly every day). It is a public resource that is easy to find online, available without cost in several languages, and takes just a few minutes to complete.¹⁴

PHQ-9 has shown excellent test–retest reliability in screening for depression, and normative data on the instrument’s use are available in various clinical populations.¹⁵ Research has shown that as PHQ-9 depression scores increase, functional status decrease, while depressive symptoms, sick days, and health care utilization increase.¹⁵ In one study, a PHQ-9 score of ≥10 had 88% sensitivity and specificity for detecting depression, with scores of 5, 10, 15, and 20 indicating mild, moderate, moderately severe, and severe depression, respectively.¹⁶ In addition to its use as a screening tool, PHQ-9 is a responsive and reliable measure of depression treatment outcomes.¹⁷

Mood Disorder Questionnaire

MDQ is another brief, self-report questionnaire that is available online. It is designed to identify and monitor patients who are likely to meet diagnostic criteria for bipolar disorder.^18,19

The first question on the MDQ asks if the patient has experienced any of 13 common mood and behavior symptoms. The second question asks if these symptoms have ever occurred at the same time, and the third asks the degree to which the patient finds the symptoms to be problematic. The remaining 2 questions provide additional, clinical information, because they address family history of manic–depressive illness or bipolar disorder and whether a diagnosis of either disorder has been made.

The MDQ has shown validity in assessing bipolar disorder symptoms in a general population,²⁰ although recent research suggests that imprecise recall bias may limit its reliability in detecting hypomanic episodes earlier in life.²¹ Nonetheless, its specificity of >97% means that it will effectively screen out just about all true negatives.¹⁸

Generalized Anxiety Disorder 7-item scale

GAD-7 scale is a brief, self-administered questionnaire for screening and measuring severity of GAD.²² It asks patients to rate 7 items that represent problems with general anxiety and scores each item on a scale of 0 (not at all) to 3 (nearly every day). Similar to the other measures, it is easily accessible online.

Research evidence supports the reliability and validity of GAD-7 as a measure of anxiety in the general population. Sensitivity and specificity are 89% and 82%, respectively. Normative data for age and sex specific subgroups support its use across age groups and in both males and females.²³ The GAD-7 performs well for detecting and monitoring not only GAD but also panic disorder, social anxiety disorder, and posttraumatic stress disorder.²⁴

CAGE questionnaire for detection of substance use

The CAGE questionnaire is a widely-used screening tool that was originally developed to detect alcohol abuse, but has been adapted to assess other substance abuse.^25,26 The omission of substance abuse from diagnostic consideration can have a major effect on quality of care, because substance abuse can be the underlying cause of other diseases. Therefore, routine administration of this instrument in clinical practice can lead to better understanding and monitoring of patient health.²⁷

Similar to other instruments, CAGE is free and available online.²⁷ It contains 4 simple questions, with 1 point is assigned to each positive answer.

Have you ever:
1. Felt the need to cut down on your drinking or drug use?
2. Have people annoyed you by criticizing your drinking or drug use?
3. Have you felt bad or guilty about your drinking or drug use?
4. Have you ever had a drink or used drugs first thing in the morning to steady your nerves or to get rid of a hangover (eye-opener)?

The simple mnemonic CAGE makes the questions easy to remember and to administer in a clinical setting. CAGE has demonstrated validity, with one study determining that CAGE scores ≥2 had a specificity and sensitivity of 76% and 93%, respectively, for identifying excessive drinking, and a specificity and sensitivity of 77% and 91%, respectively, for identifying alcohol abuse.²⁸

Columbia Suicide Severity Rating Scale (C-SSRS)

C-SSRS was developed by researchers at Columbia University to assess the severity of and track changes over time in suicidal ideation and behavior. C-SSRS is 2 pages and takes only a few minutes to administer; however, it also may be completed as a self-report measure. The questions are phrased for use in an interview format, and clinicians are encouraged to receive training prior to its administration, although specific training in mental health is not required.

The “Lifetime/Recent” version allows practitioners to gather lifetime history of suicidality as well as any recent suicidal ideation and/or behavior, whereas the “Since Last Visit” version of the scale assesses suicidality in patients who have completed at least 1 Lifetime/Recent C-SSRS assessment. A truncated, 6-item “Screener” version is typically used in emergency situations. A risk assessment can be added to either the Full or Screener version to summarize the answers from C-SSRS and document risk and protective factors.²⁹

Several studies have found C-SSRS to be reliable and valid for identifying suicide risk in children and adults.^30,31USA Today reported that an individual exhibiting even a single behavior identified by the scale is 8 to 10 times more likely to complete suicide.³² In addition, the C-SSRS has helped reduce the suicide rate 65% in one of the largest providers of community-based behavioral health care in the United States.³²

Using scales to augment care

Each of the scales described in this article can easily be incorporated into clinical practice and offers psychiatrists important clinical information that may have been missed or not addressed in the initial clinical interview. This information can be used to follow progression of symptoms and effectiveness of treatment. Although rating scales should never be used alone to establish a diagnosis or clinical treatment plan, they can and should be used to augment information from the clinician’s assessment and follow-up interviews.⁵
 

In the current health care environment, there is an increasing demand for objective assessment of disease states.¹ This is particularly apparent in psychiatry, where documentation of outcomes lags that of other areas of medicine.

In 2012, the additional health care costs incurred by persons with mental health diagnoses were estimated to be $293 billion among commercially insured, Medicaid, and Medicare beneficiaries in the United States—a figure that is 273% higher than the cost for those without psychiatric diagnoses.² Psychiatric and medical illnesses can be so tightly linked that accurate diagnosis and treatment of psychiatric disorders becomes essential to control medical illnesses. It is not surprising that there is increased scrutiny to the ways in which psychiatric care can be objectively assessed and monitored, and payers such as Centers for Medicare and Medicaid Services (CMS) increasingly require objective documentation of disease state improvement for payment.³

Support for objective assessment of disease derives from the collaborative care model. This model is designed to better integrate psychiatric and primary care by (among other practices) establishing the Patient-Centered Medical Home and emphasizing screening and monitoring patient-reported outcomes over time to assess treatment response.⁴ This approach, which is endorsed by the American Psychiatric Association, is associated with significant improvements in outcomes compared with usual care.⁵ It tracks a patient’s progress using validated clinical rating scales and other screening tools (eg, Patient Health Questionnaire [PHQ-9] for depression), an approach that is analogous to how patients with type 2 diabetes mellitus are monitored by hemoglobin A_1c laboratory tests.⁶ An increasingly extensive body of research supports the impact of this approach on treatment. A 2012 Cochrane Review associated collaborative care with significant improvements in depression and anxiety outcomes compared with usual treatment.⁷

Despite these findings, a recent Kennedy Forum brief asserts that behavioral health is characterized by a “lack of systematic measurement to determine whether patients are responding to treatment.”⁸ That same brief points to the many easy-to-administer and validated rating scales and other screening tools that can reliably measure the frequency and severity of psychiatric symptoms over time, and likens the lack of their use as “equivalent to treating high blood pressure without using a blood pressure cuff to measure if a patient’s blood pressure is improving.”⁸ It is estimated that only 18% of psychiatrists and 11% of psychologists administer them routinely.^9,10 This lack of use denies clinicians important information that can help detect deterioration or lack of improvement in their patients.
 

Psychiatry is replete with rating scales and screening tools, and the number of competing scales can make choosing a measure difficult.¹ Nonetheless, not all scales are appropriate for clinical use; many are designed for research, for instance, and are lengthy and difficult to administer.

This article reviews a number of rating scales that are brief, useful, and easy to administer. A framework for the screening tools addressed in this article is available on the federally funded Center for Integrated Health Systems Web site (www.integration.samhsa.gov). This site promotes the use of tools designed to assist in screening and monitoring for depression, anxiety, bipolar disorder, substance use, and suicidality.¹¹

Quality criteria for rating scales

The quality of a rating scale is determined by the following attributes¹²:

• Objectivity. The ability of a scale to obtain the same results, regardless of who administers, analyzes, or interprets it.
• Reliability. The ability of a scale to convey consistent and reproducible information across time, patients, and raters.
• Validity. The degree to which the scale measures what it is supposed to measure (eg, depressive symptoms). Sensitivity and specificity are measures of validity and provide additional information about the rating scale; namely, whether the scale can detect the presence of a disease (sensitivity) and whether it detects only that disease or condition and not another (specificity).
• Establishment of norms. Whether a scale provides reference values for different clinical groups.
• Practicability. The resources required to administer the assessment instrument in terms of time, staff, and material.

In addition to meeting these quality criteria, selection of a scale can be based on whether it is self-rated or observer-rated. Advantages to self-rated scales, such as the PHQ-9, Mood Disorder Questionnaire (MDQ), and Generalized Anxiety Disorder 7-item (GAD-7) scale, are their practicability—they are easy to administer and don’t require clinician or staff time—and their use in evaluating and raising awareness of subjective states.

However, reliability may be a concern, as some patients either may lack insight or exaggerate or mask symptoms when completing such scales.¹³ Both observer and self-rated scales can be used together to minimize bias, identify symptoms that might have been missed/not addressed in the clinical interview, and drive clinical decision-making. Both also can help patients communicate with their providers and make them feel more involved in clinical decision-making.⁸

The following scales have met many of the quality criteria described here and are endorsed by the government payer system. They can easily be incorporated into clinical practice and will provide useful clinical information that can assist in diagnosis and monitoring patient outcomes.

Patient Health Questionnaire

PHQ-9 is a 9-item self-report questionnaire that can help to detect the presence of depression and supplement a thorough psychiatric and mental health interview. It scores the 9 DSM-IV criteria for depression on a scale of 0 (not at all) to 3 (nearly every day). It is a public resource that is easy to find online, available without cost in several languages, and takes just a few minutes to complete.¹⁴

PHQ-9 has shown excellent test–retest reliability in screening for depression, and normative data on the instrument’s use are available in various clinical populations.¹⁵ Research has shown that as PHQ-9 depression scores increase, functional status decrease, while depressive symptoms, sick days, and health care utilization increase.¹⁵ In one study, a PHQ-9 score of ≥10 had 88% sensitivity and specificity for detecting depression, with scores of 5, 10, 15, and 20 indicating mild, moderate, moderately severe, and severe depression, respectively.¹⁶ In addition to its use as a screening tool, PHQ-9 is a responsive and reliable measure of depression treatment outcomes.¹⁷

Mood Disorder Questionnaire

MDQ is another brief, self-report questionnaire that is available online. It is designed to identify and monitor patients who are likely to meet diagnostic criteria for bipolar disorder.^18,19

The first question on the MDQ asks if the patient has experienced any of 13 common mood and behavior symptoms. The second question asks if these symptoms have ever occurred at the same time, and the third asks the degree to which the patient finds the symptoms to be problematic. The remaining 2 questions provide additional, clinical information, because they address family history of manic–depressive illness or bipolar disorder and whether a diagnosis of either disorder has been made.

The MDQ has shown validity in assessing bipolar disorder symptoms in a general population,²⁰ although recent research suggests that imprecise recall bias may limit its reliability in detecting hypomanic episodes earlier in life.²¹ Nonetheless, its specificity of >97% means that it will effectively screen out just about all true negatives.¹⁸

Generalized Anxiety Disorder 7-item scale

GAD-7 scale is a brief, self-administered questionnaire for screening and measuring severity of GAD.²² It asks patients to rate 7 items that represent problems with general anxiety and scores each item on a scale of 0 (not at all) to 3 (nearly every day). Similar to the other measures, it is easily accessible online.

Research evidence supports the reliability and validity of GAD-7 as a measure of anxiety in the general population. Sensitivity and specificity are 89% and 82%, respectively. Normative data for age and sex specific subgroups support its use across age groups and in both males and females.²³ The GAD-7 performs well for detecting and monitoring not only GAD but also panic disorder, social anxiety disorder, and posttraumatic stress disorder.²⁴

CAGE questionnaire for detection of substance use

The CAGE questionnaire is a widely-used screening tool that was originally developed to detect alcohol abuse, but has been adapted to assess other substance abuse.^25,26 The omission of substance abuse from diagnostic consideration can have a major effect on quality of care, because substance abuse can be the underlying cause of other diseases. Therefore, routine administration of this instrument in clinical practice can lead to better understanding and monitoring of patient health.²⁷

Similar to other instruments, CAGE is free and available online.²⁷ It contains 4 simple questions, with 1 point is assigned to each positive answer.

Have you ever:
1. Felt the need to cut down on your drinking or drug use?
2. Have people annoyed you by criticizing your drinking or drug use?
3. Have you felt bad or guilty about your drinking or drug use?
4. Have you ever had a drink or used drugs first thing in the morning to steady your nerves or to get rid of a hangover (eye-opener)?

The simple mnemonic CAGE makes the questions easy to remember and to administer in a clinical setting. CAGE has demonstrated validity, with one study determining that CAGE scores ≥2 had a specificity and sensitivity of 76% and 93%, respectively, for identifying excessive drinking, and a specificity and sensitivity of 77% and 91%, respectively, for identifying alcohol abuse.²⁸

Columbia Suicide Severity Rating Scale (C-SSRS)

C-SSRS was developed by researchers at Columbia University to assess the severity of and track changes over time in suicidal ideation and behavior. C-SSRS is 2 pages and takes only a few minutes to administer; however, it also may be completed as a self-report measure. The questions are phrased for use in an interview format, and clinicians are encouraged to receive training prior to its administration, although specific training in mental health is not required.

The “Lifetime/Recent” version allows practitioners to gather lifetime history of suicidality as well as any recent suicidal ideation and/or behavior, whereas the “Since Last Visit” version of the scale assesses suicidality in patients who have completed at least 1 Lifetime/Recent C-SSRS assessment. A truncated, 6-item “Screener” version is typically used in emergency situations. A risk assessment can be added to either the Full or Screener version to summarize the answers from C-SSRS and document risk and protective factors.²⁹

Several studies have found C-SSRS to be reliable and valid for identifying suicide risk in children and adults.^30,31USA Today reported that an individual exhibiting even a single behavior identified by the scale is 8 to 10 times more likely to complete suicide.³² In addition, the C-SSRS has helped reduce the suicide rate 65% in one of the largest providers of community-based behavioral health care in the United States.³²

Using scales to augment care

Each of the scales described in this article can easily be incorporated into clinical practice and offers psychiatrists important clinical information that may have been missed or not addressed in the initial clinical interview. This information can be used to follow progression of symptoms and effectiveness of treatment. Although rating scales should never be used alone to establish a diagnosis or clinical treatment plan, they can and should be used to augment information from the clinician’s assessment and follow-up interviews.⁵
 

CASE Paranoia, ataxia
Ms. S, age 46, is admitted to the hospital for cellulitis and gait disturbance. She has been living in her car for the past week and presents to the local fire department to get help for housing. She is referred to this hospital where she was found to have cellulitis in her buttock secondary to urinary and fecal incontinence. She also was noted to have difficulty ambulating and a wide-based gait. Two weeks earlier, a hotel clerk found her on the floor, unable to get up. Ms. S was seen in a local emergency room (ER) and discharged after her glucose level was found to be normal.

At admission, she has an intact sensorium and is described as disheveled, illogical, rambling, and paranoid. Her mental status exam shows she is alert and oriented to person and time, with guarded and childlike behavior. Her affect/mood is irritable and oddly related, and her thought processes are concrete and simple with some thought-blocking and paranoid content. She denies thoughts of harming herself or others, and her insight is limited and judgment is poor.

Neurology is consulted to evaluate her gait disturbance. Ms. S has decreased muscle bulk in both calves, with brisk knee reflexes bilaterally. CT imaging shows nonspecific scattered periventricular white matter hypodensities consistent with microvascular ischemic diagnosis, but a demyelinating process could not be ruled out. Ms. S reports that the gait disturbance began in childhood, and that her grandmother had the same gait disturbance. Neurology recommends an electromyogram and MRI.

During her stay in the hospital, she is unwilling to cooperate with exams, declines to answer questions regarding her past, and appears suspicious of her acute care treatment team. The psychiatric team is consulted for evaluation of her paranoia and “seeming disorganization,” and she is transferred to the psychiatric unit. She appears to be repulsed by the fact that she was in a psychiatric ward stating, “I don’t belong here” and “I’m scared of the other people here.” She denies any psychiatric history, previous hospitalizations, or substance use, and no documentation of inpatient or outpatient care was found in the county’s computerized record system. Although she is willing to take a small dose of tranquilizer (eg, lorazepam) she refuses to take antipsychotic medications saying, “My mother told me not to take [antipsychotics]. I’m not psychotic.”

What is your diagnosis at this point?

a) normal pressure hydrocephalus
b) Charcot-Marie-Tooth disease
c) schizophrenia spectrum disorder
d) multiple sclerosis (MS)
e) vascular dementia
f) cord lesion compression

The authors’ observations

The neurology team initially suspected Charcot-Marie-Tooth disease because her clinical presentation included pes cavus, distal lower extremity weakness, and lower extremity muscle atrophy with a self-reported family history of similar gait disturbance, all of which are consistent with Charcot-Marie-Tooth disease.

Subcortical syndrome—a feature of vascular dementia—is characterized by focal motor deficits, gait disturbance, history of unsteadiness with frequent falls, urinary symptoms, personality and mood changes, and cognitive dysfunction.^1-3 Subcortical syndrome is caused by chronic ischemia and lacunar infarctions that affect cerebral nuclei and white matter pathways.¹ On imaging, subcortical vascular dementia is characterized by leukoaraiosis, which are hypointense spherical-like lesions on CT and hyperintense lesions in periventricular areas on T2 MRI.⁴

Although normal pressure hydrocephalus could be suspected given her clinical presentation of the Hakim-Adams triad (ie,“wacky, wobbly, and wet”), her head CT did not show any changes consistent with this condition.

Her clinical presentation does not align with schizophrenia spectrum disorder because of her history of higher functioning, acute later onset, and the absence of hallucinations, fixed delusions, or markedly disorganized speech. Although she is paranoid of her surroundings, her delusions were ill-formed. A cord lesion compression cannot be ruled out, and MRI is required urgently.

HISTORY High functioning

When asked, Ms. S states that she was admitted to the hospital because “someone who looked like a fake police officer [a member of the fire department] told me it was nice here.” She indicates that she initially thought it would be a nice place to live temporarily but later regretted coming after realizing that she was in a psychiatry unit. Available documentation from her recent hospitalization indicated that she was living in a motel on her own. Ms. S says that she works as an actress and has had minor roles in famous movies. She says that she studied at a well-known performance arts school and that her parents are famous musicians; however, she refuses to identify her parents or give permission to contact them—or any other collateral informant—because she is embarrassed about her current situation stating, “They would never believe it.”

During this interview, Ms. S appears confused as well as disorganized—which was a challenge to clearly delineate—disheveled, and guarded with hypoverbal and hypophonic speech. Her thought process is circumstantial, and she seems to be confabulating. She denies visual or auditory hallucinations but appears paranoid and states that she thinks we are experimenting on her. Except for the neurological exam, the rest of her physical exam is within normal limits. Urine toxicology screen and labs are negative except for a positive antinuclear antibody homogenous pattern with a titer of 1:640; B₁₂ vitamin levels are not tested.

MRI is ordered, however, she does not consent to the scan saying, “It’s creepy, I don’t want people looking at my brain.” The team makes several attempts to encourage her for consent but she refuses. Because of the clinical urgency (ie, possible cord compression) and her refusal to provide a surrogate decision maker, the team felt the situation is urgent, confirmed by 2 physicians, which led them to perform the MRI on an emergent basis. The MRI reveals multiple periventricular, juxtacortical, infratentorial, and likely cervical spinal cord T2 hyperintense lesions (Figure).

What would be your differential diagnosis at this time?

a) acute disseminated encephalomyelitis (ADEM)
b) systemic lupus erythematous
c) multiple sclerosis
d) vascular dementia
e) vitamin B deficiency

The authors’ observations

Psychosis in the presence of white matter demyelination could be associated with autoimmune, vascular, or nutritional disturbances. Deficiencies in vitamins B6, 9, and 12 (pyridoxine, folate, cobalamin) have been shown to cause neuropsychiatric symptoms and white matter lesions.⁵ Low levels of vitamins B6, 9, and 12 are associated with elevated homocysteine, which can cause small vessel ischemia leading to white matter lesions similar to changes seen in vascular dementia.⁵ The exact pathophysiology of ADEM is unclear, however, it is thought that after an infection, antiviral antibodies cross react with autoantigens on myelin causing an autoimmune demyelinating disease. Another hypothesized mechanism is that circulating immune complexes and humoral factors increase vascular permeability and inflammation thereby opening the blood–brain barrier. Once it is open, cells such as lymphocytes, phagocytes, and microglia cause gliosis and demyelination. Case reports have described ADEM associated with psychotic features.⁶

Likewise, systemic lupus erythematous has been associated with psychosis and neuropsychiatric symptoms in 14% to 75% of patients. Of these patients, 40% will experience neuropsychiatric symptoms before onset of lupus symptoms.⁷ One study found the most common MRI finding in neuropsychiatric systemic lupus erythematous was leukoaraiosis, which appeared in 57.1% of patients.⁸ 
Ms. S’s MRI results strongly suggest a diagnosis of MS.

EVALUATION Questionable story

Ms. S appears delusional and grandiose when she meets with the psychiatry team. She states that before her hospitalization, she was an actress and could ambulate, rent a motel room, and drive a car without assistance. However, during the examination, she cannot walk without 2 staff members for support, and overall her self-reported history sounds questionable. There were several pieces of evidence that corroborate portions of her story: (1) a screen actors guild card was found among personal belongings; (2) she was transported to the ER from a local motel; (3) she had recently visited another hospital and, at that time, was deemed stable enough to be discharged.

On the Montreal Cognitive Assessment (MoCA) Ms. S scored 19/30, with deficits mainly in executive/visuospatial and delayed recall memory. An alternate form of the MoCA is administered 1 day later, and she scores 20/30 with similar deficits. After obtaining medication consent, she is given risperidone, up to 2 mg/d, and becomes more cooperative with the treatment team.

The authors’ observations

Approximately 40% to 65% of MS patients experience cognitive impairment.⁹ Cognitive dysfunction in a depressed patient with MS might appear as pseudo-dementia, but other possible diagnoses include:

• true dementia
• encephalitis or infection
• medication- or substance-induced.

White matter demyelination is associated with subcortical dementia, which is characterized by slowness of information processing, forgetfulness, apathy, depression, and impaired cognition. According to meta-analyses, the most prominent neuropsychological deficits in MS are found in the areas of verbal fluency, information processing speed, working memory, and long-term memory.¹⁰ Relapsing-remitting type MS patients generally have less cognitive impairment than those with the chronic progressive type of the disease.

EVALUATION Cognitive deficits

Because of her acute condition and resistance to the evaluation, a modified screening neuropsychological battery is used. During the evaluation Ms. S is guarded and demonstrates paucity of speech; her responses are odd at times or contain word-substitution errors. Hand stiffness, tremor, and imprecision are noted during writing and drawing. Results of testing indicate average-range premorbid intellectual ability, with impairments in memory and information processing speed and a mild weakness in phonemic verbal fluency. Ms. S endorses statements reflecting paranoia and hostility on a self-report measure of emotional and personality functioning, consistent with her behavioral presentation. However, her responses on other subscales, including depression and psychotic symptoms, are within normal limits. Her cognitive deficits would be unusual if she had a psychiatric illness alone and are likely associated with her positive neuroimaging findings that suggest a demyelinating process. Overall, the results of the evaluation support a MS diagnosis.

The authors’ observations
Psychosis is found at a higher rate among MS patients (2% to 3%) than the general population (0.5% to 1%).⁹ Although rare, psychosis often can cloud the diagnosis of MS. Psychiatric symptoms that can occur in MS include:

• hallucinations and delusions (>50%)
• irritability and agitation (20%)
• grandiosity (15%)
• confusion, blunted affect, flight of ideas, depression, reduced self-care, and pressured speech (10%).¹¹

A review of 10 studies found that depression was the most prevalent symptom in MS, and that schizophrenia occurred in up to 7% of MS patients.¹² There are currently 3 theories about the relationship between psychosis and MS:

• MS and psychosis are thought to share the same pathophysiological process.
• Psychotic symptoms arise from regional demyelination simultaneously with MS.
• Psychosis is caused by medical treatment of MS.⁹

Other causes of psychiatric symptoms in MS include:

• depression associated with brain atrophy and lesions
• depression and anxiety as a result of chronic illness
• depression resulting from inflammatory changes
• corticosteroid treatment causing depression, mania, or psychosis.¹²

The link between psychosis and MS is still poorly understood and further investigation is needed.

How would you treat Ms. S?

a) haloperidol
b) risperidone
c) corticosteroids
d) selective serotonin reuptake inhibitors

Treating psychiatric symptoms in the context of MS

The literature, mainly case reports, suggests several treatment modalities for psychosis with MS. Clozapine has been shown to be beneficial in several case reports, and risperidone⁹ and ziprasidone¹³ also have been effective. Other studies recommended low-dose chlorpromazine.⁹

For MS patients with cognitive impairment, one study showed that interferon beta-1b (IFN-1b) treatment resulted in significant improvement in concentration, attention, visual learning, and recall after 1 year compared with control patients.⁹ However, there are also case reports of IFN-1b and glucocorticoid-induced psychosis in patients, which resolved after discontinuing treatment.⁹

Psychotic symptoms have been shown to resolve after corticosteroid treatment of MS.¹⁴ In another case report, mania and delusions subsided 3 days after IV methylprednisolone, whereas risperidone had no effect on psychotic features. However, it was unclear whether risperidone was discontinued when methylprednisolone was administered, therefore the specific effect of methylprednisolone is difficult to discern.¹⁵ Finally, in a case of a patient who has chronic MS for 16 years and presented with acute onset paranoid psychosis, symptoms resolved with aripiprazole, 10 to 20 mg/d.¹⁶ Because of the limited utility of case reports, there is a need for further research in medical management of psychiatric symptoms in MS.

CASE Paranoia, ataxia
Ms. S, age 46, is admitted to the hospital for cellulitis and gait disturbance. She has been living in her car for the past week and presents to the local fire department to get help for housing. She is referred to this hospital where she was found to have cellulitis in her buttock secondary to urinary and fecal incontinence. She also was noted to have difficulty ambulating and a wide-based gait. Two weeks earlier, a hotel clerk found her on the floor, unable to get up. Ms. S was seen in a local emergency room (ER) and discharged after her glucose level was found to be normal.

At admission, she has an intact sensorium and is described as disheveled, illogical, rambling, and paranoid. Her mental status exam shows she is alert and oriented to person and time, with guarded and childlike behavior. Her affect/mood is irritable and oddly related, and her thought processes are concrete and simple with some thought-blocking and paranoid content. She denies thoughts of harming herself or others, and her insight is limited and judgment is poor.

Neurology is consulted to evaluate her gait disturbance. Ms. S has decreased muscle bulk in both calves, with brisk knee reflexes bilaterally. CT imaging shows nonspecific scattered periventricular white matter hypodensities consistent with microvascular ischemic diagnosis, but a demyelinating process could not be ruled out. Ms. S reports that the gait disturbance began in childhood, and that her grandmother had the same gait disturbance. Neurology recommends an electromyogram and MRI.

During her stay in the hospital, she is unwilling to cooperate with exams, declines to answer questions regarding her past, and appears suspicious of her acute care treatment team. The psychiatric team is consulted for evaluation of her paranoia and “seeming disorganization,” and she is transferred to the psychiatric unit. She appears to be repulsed by the fact that she was in a psychiatric ward stating, “I don’t belong here” and “I’m scared of the other people here.” She denies any psychiatric history, previous hospitalizations, or substance use, and no documentation of inpatient or outpatient care was found in the county’s computerized record system. Although she is willing to take a small dose of tranquilizer (eg, lorazepam) she refuses to take antipsychotic medications saying, “My mother told me not to take [antipsychotics]. I’m not psychotic.”

What is your diagnosis at this point?

a) normal pressure hydrocephalus
b) Charcot-Marie-Tooth disease
c) schizophrenia spectrum disorder
d) multiple sclerosis (MS)
e) vascular dementia
f) cord lesion compression

The authors’ observations

The neurology team initially suspected Charcot-Marie-Tooth disease because her clinical presentation included pes cavus, distal lower extremity weakness, and lower extremity muscle atrophy with a self-reported family history of similar gait disturbance, all of which are consistent with Charcot-Marie-Tooth disease.

Subcortical syndrome—a feature of vascular dementia—is characterized by focal motor deficits, gait disturbance, history of unsteadiness with frequent falls, urinary symptoms, personality and mood changes, and cognitive dysfunction.^1-3 Subcortical syndrome is caused by chronic ischemia and lacunar infarctions that affect cerebral nuclei and white matter pathways.¹ On imaging, subcortical vascular dementia is characterized by leukoaraiosis, which are hypointense spherical-like lesions on CT and hyperintense lesions in periventricular areas on T2 MRI.⁴

Although normal pressure hydrocephalus could be suspected given her clinical presentation of the Hakim-Adams triad (ie,“wacky, wobbly, and wet”), her head CT did not show any changes consistent with this condition.

Her clinical presentation does not align with schizophrenia spectrum disorder because of her history of higher functioning, acute later onset, and the absence of hallucinations, fixed delusions, or markedly disorganized speech. Although she is paranoid of her surroundings, her delusions were ill-formed. A cord lesion compression cannot be ruled out, and MRI is required urgently.

HISTORY High functioning

When asked, Ms. S states that she was admitted to the hospital because “someone who looked like a fake police officer [a member of the fire department] told me it was nice here.” She indicates that she initially thought it would be a nice place to live temporarily but later regretted coming after realizing that she was in a psychiatry unit. Available documentation from her recent hospitalization indicated that she was living in a motel on her own. Ms. S says that she works as an actress and has had minor roles in famous movies. She says that she studied at a well-known performance arts school and that her parents are famous musicians; however, she refuses to identify her parents or give permission to contact them—or any other collateral informant—because she is embarrassed about her current situation stating, “They would never believe it.”

During this interview, Ms. S appears confused as well as disorganized—which was a challenge to clearly delineate—disheveled, and guarded with hypoverbal and hypophonic speech. Her thought process is circumstantial, and she seems to be confabulating. She denies visual or auditory hallucinations but appears paranoid and states that she thinks we are experimenting on her. Except for the neurological exam, the rest of her physical exam is within normal limits. Urine toxicology screen and labs are negative except for a positive antinuclear antibody homogenous pattern with a titer of 1:640; B₁₂ vitamin levels are not tested.

MRI is ordered, however, she does not consent to the scan saying, “It’s creepy, I don’t want people looking at my brain.” The team makes several attempts to encourage her for consent but she refuses. Because of the clinical urgency (ie, possible cord compression) and her refusal to provide a surrogate decision maker, the team felt the situation is urgent, confirmed by 2 physicians, which led them to perform the MRI on an emergent basis. The MRI reveals multiple periventricular, juxtacortical, infratentorial, and likely cervical spinal cord T2 hyperintense lesions (Figure).

What would be your differential diagnosis at this time?

a) acute disseminated encephalomyelitis (ADEM)
b) systemic lupus erythematous
c) multiple sclerosis
d) vascular dementia
e) vitamin B deficiency

The authors’ observations

Psychosis in the presence of white matter demyelination could be associated with autoimmune, vascular, or nutritional disturbances. Deficiencies in vitamins B6, 9, and 12 (pyridoxine, folate, cobalamin) have been shown to cause neuropsychiatric symptoms and white matter lesions.⁵ Low levels of vitamins B6, 9, and 12 are associated with elevated homocysteine, which can cause small vessel ischemia leading to white matter lesions similar to changes seen in vascular dementia.⁵ The exact pathophysiology of ADEM is unclear, however, it is thought that after an infection, antiviral antibodies cross react with autoantigens on myelin causing an autoimmune demyelinating disease. Another hypothesized mechanism is that circulating immune complexes and humoral factors increase vascular permeability and inflammation thereby opening the blood–brain barrier. Once it is open, cells such as lymphocytes, phagocytes, and microglia cause gliosis and demyelination. Case reports have described ADEM associated with psychotic features.⁶

Likewise, systemic lupus erythematous has been associated with psychosis and neuropsychiatric symptoms in 14% to 75% of patients. Of these patients, 40% will experience neuropsychiatric symptoms before onset of lupus symptoms.⁷ One study found the most common MRI finding in neuropsychiatric systemic lupus erythematous was leukoaraiosis, which appeared in 57.1% of patients.⁸ 
Ms. S’s MRI results strongly suggest a diagnosis of MS.

EVALUATION Questionable story

Ms. S appears delusional and grandiose when she meets with the psychiatry team. She states that before her hospitalization, she was an actress and could ambulate, rent a motel room, and drive a car without assistance. However, during the examination, she cannot walk without 2 staff members for support, and overall her self-reported history sounds questionable. There were several pieces of evidence that corroborate portions of her story: (1) a screen actors guild card was found among personal belongings; (2) she was transported to the ER from a local motel; (3) she had recently visited another hospital and, at that time, was deemed stable enough to be discharged.

On the Montreal Cognitive Assessment (MoCA) Ms. S scored 19/30, with deficits mainly in executive/visuospatial and delayed recall memory. An alternate form of the MoCA is administered 1 day later, and she scores 20/30 with similar deficits. After obtaining medication consent, she is given risperidone, up to 2 mg/d, and becomes more cooperative with the treatment team.

The authors’ observations

Approximately 40% to 65% of MS patients experience cognitive impairment.⁹ Cognitive dysfunction in a depressed patient with MS might appear as pseudo-dementia, but other possible diagnoses include:

• true dementia
• encephalitis or infection
• medication- or substance-induced.

White matter demyelination is associated with subcortical dementia, which is characterized by slowness of information processing, forgetfulness, apathy, depression, and impaired cognition. According to meta-analyses, the most prominent neuropsychological deficits in MS are found in the areas of verbal fluency, information processing speed, working memory, and long-term memory.¹⁰ Relapsing-remitting type MS patients generally have less cognitive impairment than those with the chronic progressive type of the disease.

EVALUATION Cognitive deficits

Because of her acute condition and resistance to the evaluation, a modified screening neuropsychological battery is used. During the evaluation Ms. S is guarded and demonstrates paucity of speech; her responses are odd at times or contain word-substitution errors. Hand stiffness, tremor, and imprecision are noted during writing and drawing. Results of testing indicate average-range premorbid intellectual ability, with impairments in memory and information processing speed and a mild weakness in phonemic verbal fluency. Ms. S endorses statements reflecting paranoia and hostility on a self-report measure of emotional and personality functioning, consistent with her behavioral presentation. However, her responses on other subscales, including depression and psychotic symptoms, are within normal limits. Her cognitive deficits would be unusual if she had a psychiatric illness alone and are likely associated with her positive neuroimaging findings that suggest a demyelinating process. Overall, the results of the evaluation support a MS diagnosis.

The authors’ observations
Psychosis is found at a higher rate among MS patients (2% to 3%) than the general population (0.5% to 1%).⁹ Although rare, psychosis often can cloud the diagnosis of MS. Psychiatric symptoms that can occur in MS include:

• hallucinations and delusions (>50%)
• irritability and agitation (20%)
• grandiosity (15%)
• confusion, blunted affect, flight of ideas, depression, reduced self-care, and pressured speech (10%).¹¹

A review of 10 studies found that depression was the most prevalent symptom in MS, and that schizophrenia occurred in up to 7% of MS patients.¹² There are currently 3 theories about the relationship between psychosis and MS:

• MS and psychosis are thought to share the same pathophysiological process.
• Psychotic symptoms arise from regional demyelination simultaneously with MS.
• Psychosis is caused by medical treatment of MS.⁹

Other causes of psychiatric symptoms in MS include:

• depression associated with brain atrophy and lesions
• depression and anxiety as a result of chronic illness
• depression resulting from inflammatory changes
• corticosteroid treatment causing depression, mania, or psychosis.¹²

The link between psychosis and MS is still poorly understood and further investigation is needed.

How would you treat Ms. S?

a) haloperidol
b) risperidone
c) corticosteroids
d) selective serotonin reuptake inhibitors

Treating psychiatric symptoms in the context of MS

The literature, mainly case reports, suggests several treatment modalities for psychosis with MS. Clozapine has been shown to be beneficial in several case reports, and risperidone⁹ and ziprasidone¹³ also have been effective. Other studies recommended low-dose chlorpromazine.⁹

For MS patients with cognitive impairment, one study showed that interferon beta-1b (IFN-1b) treatment resulted in significant improvement in concentration, attention, visual learning, and recall after 1 year compared with control patients.⁹ However, there are also case reports of IFN-1b and glucocorticoid-induced psychosis in patients, which resolved after discontinuing treatment.⁹

Psychotic symptoms have been shown to resolve after corticosteroid treatment of MS.¹⁴ In another case report, mania and delusions subsided 3 days after IV methylprednisolone, whereas risperidone had no effect on psychotic features. However, it was unclear whether risperidone was discontinued when methylprednisolone was administered, therefore the specific effect of methylprednisolone is difficult to discern.¹⁵ Finally, in a case of a patient who has chronic MS for 16 years and presented with acute onset paranoid psychosis, symptoms resolved with aripiprazole, 10 to 20 mg/d.¹⁶ Because of the limited utility of case reports, there is a need for further research in medical management of psychiatric symptoms in MS.

CASE Paranoia, ataxia
Ms. S, age 46, is admitted to the hospital for cellulitis and gait disturbance. She has been living in her car for the past week and presents to the local fire department to get help for housing. She is referred to this hospital where she was found to have cellulitis in her buttock secondary to urinary and fecal incontinence. She also was noted to have difficulty ambulating and a wide-based gait. Two weeks earlier, a hotel clerk found her on the floor, unable to get up. Ms. S was seen in a local emergency room (ER) and discharged after her glucose level was found to be normal.

At admission, she has an intact sensorium and is described as disheveled, illogical, rambling, and paranoid. Her mental status exam shows she is alert and oriented to person and time, with guarded and childlike behavior. Her affect/mood is irritable and oddly related, and her thought processes are concrete and simple with some thought-blocking and paranoid content. She denies thoughts of harming herself or others, and her insight is limited and judgment is poor.

Neurology is consulted to evaluate her gait disturbance. Ms. S has decreased muscle bulk in both calves, with brisk knee reflexes bilaterally. CT imaging shows nonspecific scattered periventricular white matter hypodensities consistent with microvascular ischemic diagnosis, but a demyelinating process could not be ruled out. Ms. S reports that the gait disturbance began in childhood, and that her grandmother had the same gait disturbance. Neurology recommends an electromyogram and MRI.

During her stay in the hospital, she is unwilling to cooperate with exams, declines to answer questions regarding her past, and appears suspicious of her acute care treatment team. The psychiatric team is consulted for evaluation of her paranoia and “seeming disorganization,” and she is transferred to the psychiatric unit. She appears to be repulsed by the fact that she was in a psychiatric ward stating, “I don’t belong here” and “I’m scared of the other people here.” She denies any psychiatric history, previous hospitalizations, or substance use, and no documentation of inpatient or outpatient care was found in the county’s computerized record system. Although she is willing to take a small dose of tranquilizer (eg, lorazepam) she refuses to take antipsychotic medications saying, “My mother told me not to take [antipsychotics]. I’m not psychotic.”

What is your diagnosis at this point?

a) normal pressure hydrocephalus
b) Charcot-Marie-Tooth disease
c) schizophrenia spectrum disorder
d) multiple sclerosis (MS)
e) vascular dementia
f) cord lesion compression

The authors’ observations

The neurology team initially suspected Charcot-Marie-Tooth disease because her clinical presentation included pes cavus, distal lower extremity weakness, and lower extremity muscle atrophy with a self-reported family history of similar gait disturbance, all of which are consistent with Charcot-Marie-Tooth disease.

Subcortical syndrome—a feature of vascular dementia—is characterized by focal motor deficits, gait disturbance, history of unsteadiness with frequent falls, urinary symptoms, personality and mood changes, and cognitive dysfunction.^1-3 Subcortical syndrome is caused by chronic ischemia and lacunar infarctions that affect cerebral nuclei and white matter pathways.¹ On imaging, subcortical vascular dementia is characterized by leukoaraiosis, which are hypointense spherical-like lesions on CT and hyperintense lesions in periventricular areas on T2 MRI.⁴

Although normal pressure hydrocephalus could be suspected given her clinical presentation of the Hakim-Adams triad (ie,“wacky, wobbly, and wet”), her head CT did not show any changes consistent with this condition.

Her clinical presentation does not align with schizophrenia spectrum disorder because of her history of higher functioning, acute later onset, and the absence of hallucinations, fixed delusions, or markedly disorganized speech. Although she is paranoid of her surroundings, her delusions were ill-formed. A cord lesion compression cannot be ruled out, and MRI is required urgently.

HISTORY High functioning

When asked, Ms. S states that she was admitted to the hospital because “someone who looked like a fake police officer [a member of the fire department] told me it was nice here.” She indicates that she initially thought it would be a nice place to live temporarily but later regretted coming after realizing that she was in a psychiatry unit. Available documentation from her recent hospitalization indicated that she was living in a motel on her own. Ms. S says that she works as an actress and has had minor roles in famous movies. She says that she studied at a well-known performance arts school and that her parents are famous musicians; however, she refuses to identify her parents or give permission to contact them—or any other collateral informant—because she is embarrassed about her current situation stating, “They would never believe it.”

During this interview, Ms. S appears confused as well as disorganized—which was a challenge to clearly delineate—disheveled, and guarded with hypoverbal and hypophonic speech. Her thought process is circumstantial, and she seems to be confabulating. She denies visual or auditory hallucinations but appears paranoid and states that she thinks we are experimenting on her. Except for the neurological exam, the rest of her physical exam is within normal limits. Urine toxicology screen and labs are negative except for a positive antinuclear antibody homogenous pattern with a titer of 1:640; B₁₂ vitamin levels are not tested.

MRI is ordered, however, she does not consent to the scan saying, “It’s creepy, I don’t want people looking at my brain.” The team makes several attempts to encourage her for consent but she refuses. Because of the clinical urgency (ie, possible cord compression) and her refusal to provide a surrogate decision maker, the team felt the situation is urgent, confirmed by 2 physicians, which led them to perform the MRI on an emergent basis. The MRI reveals multiple periventricular, juxtacortical, infratentorial, and likely cervical spinal cord T2 hyperintense lesions (Figure).

What would be your differential diagnosis at this time?

a) acute disseminated encephalomyelitis (ADEM)
b) systemic lupus erythematous
c) multiple sclerosis
d) vascular dementia
e) vitamin B deficiency

The authors’ observations

Psychosis in the presence of white matter demyelination could be associated with autoimmune, vascular, or nutritional disturbances. Deficiencies in vitamins B6, 9, and 12 (pyridoxine, folate, cobalamin) have been shown to cause neuropsychiatric symptoms and white matter lesions.⁵ Low levels of vitamins B6, 9, and 12 are associated with elevated homocysteine, which can cause small vessel ischemia leading to white matter lesions similar to changes seen in vascular dementia.⁵ The exact pathophysiology of ADEM is unclear, however, it is thought that after an infection, antiviral antibodies cross react with autoantigens on myelin causing an autoimmune demyelinating disease. Another hypothesized mechanism is that circulating immune complexes and humoral factors increase vascular permeability and inflammation thereby opening the blood–brain barrier. Once it is open, cells such as lymphocytes, phagocytes, and microglia cause gliosis and demyelination. Case reports have described ADEM associated with psychotic features.⁶

Likewise, systemic lupus erythematous has been associated with psychosis and neuropsychiatric symptoms in 14% to 75% of patients. Of these patients, 40% will experience neuropsychiatric symptoms before onset of lupus symptoms.⁷ One study found the most common MRI finding in neuropsychiatric systemic lupus erythematous was leukoaraiosis, which appeared in 57.1% of patients.⁸ 
Ms. S’s MRI results strongly suggest a diagnosis of MS.

EVALUATION Questionable story

Ms. S appears delusional and grandiose when she meets with the psychiatry team. She states that before her hospitalization, she was an actress and could ambulate, rent a motel room, and drive a car without assistance. However, during the examination, she cannot walk without 2 staff members for support, and overall her self-reported history sounds questionable. There were several pieces of evidence that corroborate portions of her story: (1) a screen actors guild card was found among personal belongings; (2) she was transported to the ER from a local motel; (3) she had recently visited another hospital and, at that time, was deemed stable enough to be discharged.

On the Montreal Cognitive Assessment (MoCA) Ms. S scored 19/30, with deficits mainly in executive/visuospatial and delayed recall memory. An alternate form of the MoCA is administered 1 day later, and she scores 20/30 with similar deficits. After obtaining medication consent, she is given risperidone, up to 2 mg/d, and becomes more cooperative with the treatment team.

The authors’ observations

Approximately 40% to 65% of MS patients experience cognitive impairment.⁹ Cognitive dysfunction in a depressed patient with MS might appear as pseudo-dementia, but other possible diagnoses include:

• true dementia
• encephalitis or infection
• medication- or substance-induced.

White matter demyelination is associated with subcortical dementia, which is characterized by slowness of information processing, forgetfulness, apathy, depression, and impaired cognition. According to meta-analyses, the most prominent neuropsychological deficits in MS are found in the areas of verbal fluency, information processing speed, working memory, and long-term memory.¹⁰ Relapsing-remitting type MS patients generally have less cognitive impairment than those with the chronic progressive type of the disease.

EVALUATION Cognitive deficits

Because of her acute condition and resistance to the evaluation, a modified screening neuropsychological battery is used. During the evaluation Ms. S is guarded and demonstrates paucity of speech; her responses are odd at times or contain word-substitution errors. Hand stiffness, tremor, and imprecision are noted during writing and drawing. Results of testing indicate average-range premorbid intellectual ability, with impairments in memory and information processing speed and a mild weakness in phonemic verbal fluency. Ms. S endorses statements reflecting paranoia and hostility on a self-report measure of emotional and personality functioning, consistent with her behavioral presentation. However, her responses on other subscales, including depression and psychotic symptoms, are within normal limits. Her cognitive deficits would be unusual if she had a psychiatric illness alone and are likely associated with her positive neuroimaging findings that suggest a demyelinating process. Overall, the results of the evaluation support a MS diagnosis.

The authors’ observations
Psychosis is found at a higher rate among MS patients (2% to 3%) than the general population (0.5% to 1%).⁹ Although rare, psychosis often can cloud the diagnosis of MS. Psychiatric symptoms that can occur in MS include:

• hallucinations and delusions (>50%)
• irritability and agitation (20%)
• grandiosity (15%)
• confusion, blunted affect, flight of ideas, depression, reduced self-care, and pressured speech (10%).¹¹

A review of 10 studies found that depression was the most prevalent symptom in MS, and that schizophrenia occurred in up to 7% of MS patients.¹² There are currently 3 theories about the relationship between psychosis and MS:

• MS and psychosis are thought to share the same pathophysiological process.
• Psychotic symptoms arise from regional demyelination simultaneously with MS.
• Psychosis is caused by medical treatment of MS.⁹

Other causes of psychiatric symptoms in MS include:

• depression associated with brain atrophy and lesions
• depression and anxiety as a result of chronic illness
• depression resulting from inflammatory changes
• corticosteroid treatment causing depression, mania, or psychosis.¹²

The link between psychosis and MS is still poorly understood and further investigation is needed.

How would you treat Ms. S?

a) haloperidol
b) risperidone
c) corticosteroids
d) selective serotonin reuptake inhibitors

Treating psychiatric symptoms in the context of MS

The literature, mainly case reports, suggests several treatment modalities for psychosis with MS. Clozapine has been shown to be beneficial in several case reports, and risperidone⁹ and ziprasidone¹³ also have been effective. Other studies recommended low-dose chlorpromazine.⁹

For MS patients with cognitive impairment, one study showed that interferon beta-1b (IFN-1b) treatment resulted in significant improvement in concentration, attention, visual learning, and recall after 1 year compared with control patients.⁹ However, there are also case reports of IFN-1b and glucocorticoid-induced psychosis in patients, which resolved after discontinuing treatment.⁹

Psychotic symptoms have been shown to resolve after corticosteroid treatment of MS.¹⁴ In another case report, mania and delusions subsided 3 days after IV methylprednisolone, whereas risperidone had no effect on psychotic features. However, it was unclear whether risperidone was discontinued when methylprednisolone was administered, therefore the specific effect of methylprednisolone is difficult to discern.¹⁵ Finally, in a case of a patient who has chronic MS for 16 years and presented with acute onset paranoid psychosis, symptoms resolved with aripiprazole, 10 to 20 mg/d.¹⁶ Because of the limited utility of case reports, there is a need for further research in medical management of psychiatric symptoms in MS.

Many patients experience difficulty swallowing pills, for various reasons:

• discomfort (particularly pediatric and geriatric patients)
• postsurgical need for an alternate route of enteral intake (nasogastric tube, gastrostomy, jejunostomy)
• dysphagia due to a neurologic disorder (multiple sclerosis, impaired gag reflex, dementing processes)
• odynophagia (pain upon swallowing) due to gastroesophageal reflux or a structural abnormality
• a structural abnormality of the head or neck that impairs swallowing.¹

If these difficulties are not addressed, they can interfere with medication adherence. In those instances, using an alternative dosage form or manipulating an available formulation might be required.

Crushing guidelines

There are limited data on crushed-form products and their impact on efficacy. Therefore, when patients have difficulty taking pills, switching to liquid solution or orally disintegrating forms is recommended. However, most psychotropics are available only as tablets or capsules. Patients can crush their pills immediately before administration for easier intake. The following are some general guidelines for doing so:²

• Scored tablets typically can be crushed.
• Crushing sublingual and buccal tablets can alter their effectiveness.
• Crushing sustained-release medications can eliminate the sustained-release action.³
• Enteric-coated medications should not be crushed, because this can alter drug absorption.
• Capsules generally can be opened to administer powdered contents, unless the capsule has time-release properties or an enteric coating.

The accompanying Table, organized by drug class, indicates whether a drug can be crushed to a powdered form, which usually is mixed with food or liquid for easier intake. The Table also lists liquid and orally disintegrating forms available, and other routes, including injectable immediate and long-acting formulations. Helping patients find a medication formulation that suits their needs strengthens adherence and the therapeutic relationship.

Many patients experience difficulty swallowing pills, for various reasons:

• discomfort (particularly pediatric and geriatric patients)
• postsurgical need for an alternate route of enteral intake (nasogastric tube, gastrostomy, jejunostomy)
• dysphagia due to a neurologic disorder (multiple sclerosis, impaired gag reflex, dementing processes)
• odynophagia (pain upon swallowing) due to gastroesophageal reflux or a structural abnormality
• a structural abnormality of the head or neck that impairs swallowing.¹

If these difficulties are not addressed, they can interfere with medication adherence. In those instances, using an alternative dosage form or manipulating an available formulation might be required.

Crushing guidelines

There are limited data on crushed-form products and their impact on efficacy. Therefore, when patients have difficulty taking pills, switching to liquid solution or orally disintegrating forms is recommended. However, most psychotropics are available only as tablets or capsules. Patients can crush their pills immediately before administration for easier intake. The following are some general guidelines for doing so:²

• Scored tablets typically can be crushed.
• Crushing sublingual and buccal tablets can alter their effectiveness.
• Crushing sustained-release medications can eliminate the sustained-release action.³
• Enteric-coated medications should not be crushed, because this can alter drug absorption.
• Capsules generally can be opened to administer powdered contents, unless the capsule has time-release properties or an enteric coating.

The accompanying Table, organized by drug class, indicates whether a drug can be crushed to a powdered form, which usually is mixed with food or liquid for easier intake. The Table also lists liquid and orally disintegrating forms available, and other routes, including injectable immediate and long-acting formulations. Helping patients find a medication formulation that suits their needs strengthens adherence and the therapeutic relationship.

Many patients experience difficulty swallowing pills, for various reasons:

• discomfort (particularly pediatric and geriatric patients)
• postsurgical need for an alternate route of enteral intake (nasogastric tube, gastrostomy, jejunostomy)
• dysphagia due to a neurologic disorder (multiple sclerosis, impaired gag reflex, dementing processes)
• odynophagia (pain upon swallowing) due to gastroesophageal reflux or a structural abnormality
• a structural abnormality of the head or neck that impairs swallowing.¹

If these difficulties are not addressed, they can interfere with medication adherence. In those instances, using an alternative dosage form or manipulating an available formulation might be required.

Crushing guidelines

There are limited data on crushed-form products and their impact on efficacy. Therefore, when patients have difficulty taking pills, switching to liquid solution or orally disintegrating forms is recommended. However, most psychotropics are available only as tablets or capsules. Patients can crush their pills immediately before administration for easier intake. The following are some general guidelines for doing so:²

• Scored tablets typically can be crushed.
• Crushing sublingual and buccal tablets can alter their effectiveness.
• Crushing sustained-release medications can eliminate the sustained-release action.³
• Enteric-coated medications should not be crushed, because this can alter drug absorption.
• Capsules generally can be opened to administer powdered contents, unless the capsule has time-release properties or an enteric coating.

The accompanying Table, organized by drug class, indicates whether a drug can be crushed to a powdered form, which usually is mixed with food or liquid for easier intake. The Table also lists liquid and orally disintegrating forms available, and other routes, including injectable immediate and long-acting formulations. Helping patients find a medication formulation that suits their needs strengthens adherence and the therapeutic relationship.

Burnout among psychiatric clinicians can lead to reduced job satisfaction, poorer quality of patient care, and depression.¹ Signs of burnout include a feeling of cynicism (eg, negative attitudes toward patients), overwhelming exhaustion (eg, feeling depleted), and a sense of ineffectiveness (eg, reduced productivity).¹ Workplace variables and other factors that could perpetuate burnout among psychiatrists include, but are not limited to:

• too much work
• chronic staff shortages
• working with difficult patients
• inability to meet self-imposed demands
• a lack of meaningful relationships with colleagues and supervisors.^1,2

The mnemonic REIGNITE provides strategies to reduce the risk of burnout.^1,3

Recognize your limits. Although saying “no” may be difficult for mental health clinicians, saying “yes” too often can be detrimental. Techniques for setting limits without alienating colleagues include:

• declining tasks (“I appreciate you thinking of me to do that, but I can’t complete it right now”)
• delaying an answer (“Let me ponder what you are asking”)
• delegating tasks (“I could really use your help”)
• avoid taking on too much (“I thought that I could do that extra task, but I realize that taking on the additional assignment isn’t going to work out”).

Expand your portfolio. Developing a diverse work portfolio (eg, teaching part-time) could diminish stagnation. Adding regenerative activities (eg, outdoor activities) could be restorative.

Itemize your priorities. Ask yourself what is important to you. Is it work? If so, can work be modified so it continues to be rewarding without resulting in burnout? If it isn’t work, then what is? Money? Family? Evaluating what is important and pursuing those priorities could increase overall life satisfaction.

Go after your passions. What do you like to do aside from work? Do you paint or play a musical instrument? Pursuing hobbies and interests can revitalize your spirit.

Now. We as a profession are notorious for saying to ourselves, “I will get to it (being happy) someday.” We delay happiness until we catch up with work, save enough money, and so on. This approach is unrealistic. It is better to live in the present because there are a finite number of days to seize the day. Focus your energy in the moment.

Interact. Isolating oneself will lead to burnout. If you are in solo practice, connect with other providers or get involved in community activities. If you work with other providers, interact with them in a meaningful manner (eg, don’t complain but rather air your concerns, accept honest feedback, be open to suggestions, and seek assistance; it is acceptable to admit that you can’t do everything).

Take time off and take care of yourself. Although that seems intuitive, psychiatrists, as a group, don’t do a good job of it. Waiting until you are burned out to take a vacation is counterproductive because you will be too drained to enjoy it. Taking care of your physical and mental health is equally important.

Enjoyment in and at work. We make a difference in our patients’ lives throughthe emotional connections we develop with them. By viewing what we do as fulfilling a higher calling, we can learn to enjoy what we do rather than feeling burdened by it. Advocating for better recognition—whether financial, institutional, or social—can create opportunities for personal satisfaction.

Burnout among psychiatric clinicians can lead to reduced job satisfaction, poorer quality of patient care, and depression.¹ Signs of burnout include a feeling of cynicism (eg, negative attitudes toward patients), overwhelming exhaustion (eg, feeling depleted), and a sense of ineffectiveness (eg, reduced productivity).¹ Workplace variables and other factors that could perpetuate burnout among psychiatrists include, but are not limited to:

• too much work
• chronic staff shortages
• working with difficult patients
• inability to meet self-imposed demands
• a lack of meaningful relationships with colleagues and supervisors.^1,2

The mnemonic REIGNITE provides strategies to reduce the risk of burnout.^1,3

Recognize your limits. Although saying “no” may be difficult for mental health clinicians, saying “yes” too often can be detrimental. Techniques for setting limits without alienating colleagues include:

• declining tasks (“I appreciate you thinking of me to do that, but I can’t complete it right now”)
• delaying an answer (“Let me ponder what you are asking”)
• delegating tasks (“I could really use your help”)
• avoid taking on too much (“I thought that I could do that extra task, but I realize that taking on the additional assignment isn’t going to work out”).

Expand your portfolio. Developing a diverse work portfolio (eg, teaching part-time) could diminish stagnation. Adding regenerative activities (eg, outdoor activities) could be restorative.

Itemize your priorities. Ask yourself what is important to you. Is it work? If so, can work be modified so it continues to be rewarding without resulting in burnout? If it isn’t work, then what is? Money? Family? Evaluating what is important and pursuing those priorities could increase overall life satisfaction.

Go after your passions. What do you like to do aside from work? Do you paint or play a musical instrument? Pursuing hobbies and interests can revitalize your spirit.

Now. We as a profession are notorious for saying to ourselves, “I will get to it (being happy) someday.” We delay happiness until we catch up with work, save enough money, and so on. This approach is unrealistic. It is better to live in the present because there are a finite number of days to seize the day. Focus your energy in the moment.

Interact. Isolating oneself will lead to burnout. If you are in solo practice, connect with other providers or get involved in community activities. If you work with other providers, interact with them in a meaningful manner (eg, don’t complain but rather air your concerns, accept honest feedback, be open to suggestions, and seek assistance; it is acceptable to admit that you can’t do everything).

Take time off and take care of yourself. Although that seems intuitive, psychiatrists, as a group, don’t do a good job of it. Waiting until you are burned out to take a vacation is counterproductive because you will be too drained to enjoy it. Taking care of your physical and mental health is equally important.

Enjoyment in and at work. We make a difference in our patients’ lives throughthe emotional connections we develop with them. By viewing what we do as fulfilling a higher calling, we can learn to enjoy what we do rather than feeling burdened by it. Advocating for better recognition—whether financial, institutional, or social—can create opportunities for personal satisfaction.

Burnout among psychiatric clinicians can lead to reduced job satisfaction, poorer quality of patient care, and depression.¹ Signs of burnout include a feeling of cynicism (eg, negative attitudes toward patients), overwhelming exhaustion (eg, feeling depleted), and a sense of ineffectiveness (eg, reduced productivity).¹ Workplace variables and other factors that could perpetuate burnout among psychiatrists include, but are not limited to:

• too much work
• chronic staff shortages
• working with difficult patients
• inability to meet self-imposed demands
• a lack of meaningful relationships with colleagues and supervisors.^1,2

The mnemonic REIGNITE provides strategies to reduce the risk of burnout.^1,3

Recognize your limits. Although saying “no” may be difficult for mental health clinicians, saying “yes” too often can be detrimental. Techniques for setting limits without alienating colleagues include:

• declining tasks (“I appreciate you thinking of me to do that, but I can’t complete it right now”)
• delaying an answer (“Let me ponder what you are asking”)
• delegating tasks (“I could really use your help”)
• avoid taking on too much (“I thought that I could do that extra task, but I realize that taking on the additional assignment isn’t going to work out”).

Expand your portfolio. Developing a diverse work portfolio (eg, teaching part-time) could diminish stagnation. Adding regenerative activities (eg, outdoor activities) could be restorative.

Itemize your priorities. Ask yourself what is important to you. Is it work? If so, can work be modified so it continues to be rewarding without resulting in burnout? If it isn’t work, then what is? Money? Family? Evaluating what is important and pursuing those priorities could increase overall life satisfaction.

Go after your passions. What do you like to do aside from work? Do you paint or play a musical instrument? Pursuing hobbies and interests can revitalize your spirit.

Now. We as a profession are notorious for saying to ourselves, “I will get to it (being happy) someday.” We delay happiness until we catch up with work, save enough money, and so on. This approach is unrealistic. It is better to live in the present because there are a finite number of days to seize the day. Focus your energy in the moment.

Interact. Isolating oneself will lead to burnout. If you are in solo practice, connect with other providers or get involved in community activities. If you work with other providers, interact with them in a meaningful manner (eg, don’t complain but rather air your concerns, accept honest feedback, be open to suggestions, and seek assistance; it is acceptable to admit that you can’t do everything).

Take time off and take care of yourself. Although that seems intuitive, psychiatrists, as a group, don’t do a good job of it. Waiting until you are burned out to take a vacation is counterproductive because you will be too drained to enjoy it. Taking care of your physical and mental health is equally important.

Enjoyment in and at work. We make a difference in our patients’ lives throughthe emotional connections we develop with them. By viewing what we do as fulfilling a higher calling, we can learn to enjoy what we do rather than feeling burdened by it. Advocating for better recognition—whether financial, institutional, or social—can create opportunities for personal satisfaction.