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

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

Diverse presentations

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

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

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

Pharmacotherapy is underutilized

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

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

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

Why hesitate to use pharmacotherapeutics?

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

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

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

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

Therapeutic options

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

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

Psychosocial interventions

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

The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.

In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.

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

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

Diverse presentations

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

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

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

Pharmacotherapy is underutilized

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

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

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

Why hesitate to use pharmacotherapeutics?

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

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

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

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

Therapeutic options

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

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

Psychosocial interventions

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

The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.

In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.

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

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

Diverse presentations

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

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

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

Pharmacotherapy is underutilized

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

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

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

Why hesitate to use pharmacotherapeutics?

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

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

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

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

Therapeutic options

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

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

Psychosocial interventions

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

The authors would like to thank Thomas M. Penders, MS, MD, Medical Director for Consultation-Liaison Psychiatry at Cape Cod Healthcare, Hyannis, Massachusetts, and Affiliate Professor at East Carolina University, Greenville, North Carolina, for all his guidance, support, and mentorship.

In July 2017, Dr. Stanciu will be entering PGY-5 Addiction Psychiatry Fellowship, Geisel School of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, and Dr. Gnanasegaram has accepted a Clinical Instructor position, Department of Psychiatric Medicine, Dartmouth-Hitchcock, New Hampshire.

Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).

As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.¹ In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.

How CES works

After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.¹ The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.^1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.³

There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.¹

Evidence of efficacy

There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.

• In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.⁴
• In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.⁵ Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.⁵
• In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.⁶

Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.⁵

Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.⁷ Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.

Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).

As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.¹ In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.

How CES works

After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.¹ The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.^1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.³

There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.¹

Evidence of efficacy

There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.

• In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.⁴
• In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.⁵ Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.⁵
• In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.⁶

Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.⁵

Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.⁷ Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.

Individuals with posttraumatic stress disorder (PTSD) often report cognitive and sleep disturbances, such as insomnia and poor concentration. Although many patients report improvement with traditional evidence-based treatments, such as pharmacotherapy and psychotherapy, it might be valuable to consider complementary or alternative therapies. Many patients seek treatments that they can self-administer as needed, at their convenience, particularly during symptom exacerbation. One treatment option is cranial electrotherapy stimulation (CES).

As a medical device, CES has been cleared—rather than approved, as is the case for medications—by the FDA to treat depression, insomnia, and anxiety.¹ In the United States, CES devices require a prescription from a licensed health care practitioner, but they are available without a prescription in other countries. Cost for devices range from $600 to $1,200 and $10 to $20 for electrodes and contact solution. However, insurance companies that provide coverage for durable medical equipment might cover some or all of this expense.

How CES works

After applying contact solution, depending on the device used, the user attaches electrodes to the earlobes, mastoid processes, or other parts of the head that deliver a pulsed current, usually from AA batteries for 20 to 60 minutes.¹ The current causes cortical deactivation and could affect emotional regulation by influencing neurotransmission in the thalamus, hypothalamus, and limbic system.^1,2 CES increases cerebrospinal fluid levels of beta-endorphin, adrenocorticotropic hormone, and serotonin, which play a role in depression and anxiety.³

There are no known contraindications for CES. Adverse effects are rare, temporary, and mild; skin irritation, vertigo, or headache are the most common.¹

Evidence of efficacy

There are no double-blind placebo-controlled trials evaluating the efficacy of CES for PTSD. However, there is a case series and a large survey of patients supporting its use.

• In a case series, 2 patients reported improved occupational functioning and reduced PTSD symptoms after using CES, 100 to 500 mA, 20 to 60 minutes a day, 3 to 5 days per week.⁴
• In an online survey of 145 veterans and active-duty military personnel, 60% of individuals used CES for PTSD, and 20% of those individuals were not receiving pharmacotherapy.⁵ Participants reported at least a 25% reduction in symptoms using CES for at least 20 minutes, once or twice daily, with a current of 100 to 600 mA.⁵
• In an expert opinion, patients noted improved sleep quality and reduced alcohol and drug withdrawal symptoms after 20-minute treatments, twice a day, with a current of 2 mA. Currents could be increased to 4 mA, if there was no improvement after 2 weeks.⁶

Some patients experiencing exacerbation of PTSD symptoms could benefit from using the device for 1 hour several times a day until symptoms subside.⁵

Optimal strength, frequency, and duration of treatment vary among patients, and further studies are needed to assess these parameters as well as efficacy because definitive studies are currently lacking. CES has not always shown efficacy, such as in some patients with depression.⁷ Despite the limited evidence base, it is reasonable to consider CES for patients with PTSD. This modality might be helpful for patients who have comorbid pain, anxiety, and insomnia, or for those who seek a complementary, convenient, safe, self-administered treatment.

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.

CASE › Stacey, a 12-year-old girl with mild persistent asthma, presents to her family physician (FP) with her mother for her annual well visit. Stacey reports no complaints, but has visited twice recently for acute exacerbations of her asthma, which had previously been well-controlled. When reviewing her social history, Stacey reports that she started her second year of middle school 3 months ago. When asked if she enjoys school, Stacey looks down and says, “School is fine.” Her mother quickly adds that Stacey has quit the school cheerleading team—much to the coach’s dismay—and is having difficulty in her math class, a class in which she normally excels. Stacey appears embarrassed that her mother has brought these things up. Her mother says that at the beginning of the year, 2 girls began picking on Stacey, calling her names and making fun of her on social media and in front of other students.

For many years, bullying was trivialized. Some viewed it as a universal childhood experience; others considered it a rite of passage.^1,2 It was not examined as a public health issue until the 1970s. In fact, no legislation addressing bullying or “peer abuse” existed in the United States until the mass shooting at Columbine High School in Littleton, Colo, in 1999. Within 3 years of the Columbine tragedy, the number of state laws that mentioned bullying went from zero to 15; within 10 years of Columbine, 41 states had laws addressing bullying,¹ and by 2015, every state, the District of Columbia, and some territories had a bullying law in place.³

Ask patients, "Are you being bullied?" and then follow that with, "How often are you bullied?" and, "Does it happen at school? Online?" These details can help guide interventions.As research and advocacy regarding bullying has grown, its impact on the health of children, adolescents, and even adults has become more apparent. In a 2001 study of school-associated violent deaths in the United States between 1994 and 1999, the Centers for Disease Control and Prevention (CDC) found that among students, homicide perpetrators were more than twice as likely as homicide victims to have been bullied by peers.⁴ Given that homicide is the third leading cause of death in people ages 15 to 24,⁵ past exposure to bullying may be a significant contributing factor to mortality in this age group.⁴

In addition to a correlation with homicidal behavior, those involved in bullying—whether as the bully or victim—are at risk for a wide range of symptoms, conditions, and problems including poor psychosocial adjustment, depression, anxiety, suicide (the second leading cause of death in the 10-14 and 15-24 age groups⁵), academic decline, psychosomatic manifestations, fighting, alcohol use, smoking, and difficulty with the management of chronic diseases.^6-10 Not only does being a victim of bullying have a direct impact on a child’s current mental and physical well-being, but it can have lasting psychological and behavioral effects that can follow children well into adulthood.⁷ The significant impact of bullying on individuals and society as a whole mandates a multifaceted approach that begins in your exam room. What follows is practical advice on screening, counseling, and working with schools and the community at large to curb the bullying epidemic.

IMAGE: © ALICIA BUELOW

Clarifying the problem: The CDC’s definition

Recognizing that varying definitions of bullying were being used in research studies that looked at violent or aggressive behaviors in youth, the CDC published a consensus statement in 2014 that proposed the following definition for bullying:¹¹ any unwanted aggressive behavior by another youth or group of youths who are not siblings or current dating partners that involves an observed or perceived power imbalance and is repeated multiple times or is highly likely to be repeated. This expanded on an earlier definition by Olweus^12,13 that also identified a longitudinal nature and power imbalance as key features.

Types of bullying. Direct bullying entails blatant attacks on a targeted young person, while indirect bullying involves communication with others about the targeted individual (eg, spreading harmful rumors). Bullying may be physical, verbal, or relational (eg, excluding someone from their usual social circle, denying friendship, the silent treatment, writing mean letters, eye rolling, etc.) and may involve damage to property. Boys tend toward more direct bullying behaviors, while girls more often engage in indirect bullying, which may be more challenging for both adults and other students to recognize.^12,13 With increased use of technology and social media by adolescents, cyberbullying has become increasingly more prevalent, with its effects on adolescent health and academics being every bit as profound as those of traditional bullying.¹⁴

About 1 in 4/5 students suffer. The prevalence of bullying ranges by country and culture. The vast majority of early bullying research was conducted in Norway, which found that approximately 15% of students in elementary and secondary schools were involved in bullying in some capacity.¹² In a study involving over 200,000 adolescents from 40 European countries, 26% of adolescents reported being involved in bullying, ranging from 8.6% to 45.2% for boys and 4.8% to 35.8% for girls.¹⁵ Variations in prevalence may be due to cultural differences in the acts of bullying or differences in interpretation of the term “bullying.”^1,15

Among students, homicide perpetrators are more than twice as likely as homicide victims to have been bullied by their peers.In the United States, a 2001 survey of more than 15,000 students in public and private schools (grades 6-10) asked the students about their involvement in bullying: 13% said they'd been a bully, 10.6% a victim, and 6.3% said they'd been both.⁶ There was no significant difference in the frequency of self-reported bullying among urban, suburban, or rural settings.

Despite efforts to educate the public about bullying and work with schools to intervene and prevent bullying, incidence remains largely unchanged. In 2013, the National Crime Victimization Survey reported that approximately 22% of adolescents ages 12 through 18 were victims of bullying.¹⁶ Similarly, the CDC's 2015 Youth Risk Behavior Surveillance System reported that 20.2% of high school students experienced bullying on school property.¹⁷

Screening: Best practices

The FP’s role begins with screening children at risk for bullying (TABLE 1^18-22) or those whose complaints suggest that they may be victims of bullying.

Start screening when children enter elementary school

Given that providers’ time is limited for every patient visit, it is important to address bullying at times that are most likely to yield impactful results. The American Academy of Pediatrics recommends that the topic of bullying be introduced at the 6-year-old well-child visit (a typical age for entry to elementary school).⁷ Views in the literature are inconsistent regarding when and how to address bullying at other time points. One approach is to pre-screen those with risk factors associated with bullying (TABLE 1^18-22), and to focus screening on those with warning signs of bullying, which include mood disorders, psychosomatic or behavioral symptoms, substance abuse, self-harm behaviors, suicidal ideation or a suicide attempt, a decline in academic performance, and reports of school truancy. Parental concerns, such as when a child suddenly needs more money for lunch, is having aggressive outbursts, or is exhibiting unexplained physical injuries, should also be regarded as cues to screen.⁹

Screen patients in high-risk groups

A number of groups of children are at high risk for bullying and warrant targeted screening efforts.

• Children with special health needs. Research has shown that children with special health needs are at increased risk for being bullied.¹⁸ In fact, the presence of a chronic disease may increase the risk for bullying, and bullying often negatively impacts chronic disease management. As a result, it’s important to have a high index of suspicion with patients who have a chronic disease and who are not responding as expected to medical management or who experience deterioration after being previously well-controlled.¹⁸
• Children who are under- or overweight. Similarly, bullying based on a child's weight is a phenomenon that has been recognized to have a significant impact on children’s emotional health.¹⁹
• Youth who identify as lesbian, gay, bisexual, transgender, or queer/questioning (LGBTQ+) are more likely than non-LGBTQ+ peers to attempt suicide when exposed to a hostile social environment, such as that created by bullying.²⁰

Screening need not be complicated

One screening approach is simply to ask patients, “Are you being bullied?” followed by such questions as, “How often are you bullied?” or “How long have you been bullied?” Asking about the setting of the bullying (Does it happen at school? Traveling to/from school? Online?) and other details may help guide interventions and the provision of resources.⁹ Another approach is to provide patients with some type of written survey (see TABLE 2²³ for an example) to encourage responses that patients might be reluctant to disclose verbally.^23,24 (See “Barriers to screening.")

Provider and parental interventions

Interventions often entail counseling the patient and the family about bullying and its effects, empowering victims and their caregivers, and screening for bullying comorbidities and correlates.² Refer patients to behavioral health specialists when there is evidence of pervasive effects on mood, behavior, or social development, but keep in mind that counseling can begin in your own exam room.

Effective discussion starters. Affirming the problem and its unacceptability, talking about the different types of bullying and where bullying may occur, and asking about patient perceptions of bullying can be effective discussion starters. FPs should help patients identify bullying, open lines of communication between children and their parents and between parents and other caregivers, and demonstrate respect and kindness in their approach to discussing the topic. Encourage children to speak with trusted adults when exposed to bullying. Talk to them about standing up to bullies (saying “stop” confidently or walking away from difficult situations) and staying safe by staying near adults or groups of peers when bullies are present (TABLE 3²⁵).

Empowering caregivers. Encourage parents to spend time each day talking with their child about the child’s time away from home (TABLE 3²⁵). Counsel parents/caregivers to expand their role. Knowing a child’s friends, encouraging the child academically, and increasing communication are all associated with lower risks of bullying.²⁶ Similarly, parental oversight of Internet and social media use is associated with decreased participation in cyberbullying.²⁷

In addition, the Positive Parenting telephone-based parenting education curriculum has been shown to decrease bullying, physical fighting, physical injuries, and victimization of children.²⁸ The research-based, family strengthening program emphasizes 3 core elements of authoritative parenting: nurturance, discipline, and respect or granting of psychologic autonomy. The program entails 15- to 30-minute weekly phone conversations between parents and educators, as well as videos and a manual.

Are community programs in place—or are they needed?

Many schools have robust, state-mandated programs in place to identify bullying and provide support for students who are victims of bullying. (See “NJ’s harassment and bullying protocol: A case in point.”) Explaining this to victims and their families may help them come forward and seek assistance. FPs who want to advocate for their patients should start with local schools to support such programs and link students at risk with school counselors.

If programs are lacking in your community, there is much you can do to educate yourself about successful programs and advise local community organizations and schools about them. Among the most successful and well-studied interventions for thwarting the bullying epidemic have been school-based community ones. The most studied of these is the Olweus Bullying Prevention Program (OBPP), which is based on 4 principles:^1,29

1. Adults both at home and at school should take a positive and encouraging interest in students.
2. Unacceptable behavior should have strict and well-known limits.
3. Sanctions should be applied consistently and should be non-hostile in nature.
4. Adults both at home and in the educational environment should act as authorities.

In short, the program focuses on greater awareness and involvement on the part of adults, and employing measures at the school level (eg, surveys, better supervision during break and lunch times), the class level (eg, rules against bullying, regular class meetings with students), and the individual level (eg, serious talks with bullies, victims, parents of involved students).

Research has shown that the OBPP reduces bullying behaviors by as much as 50%, reduces vandalism and truancy, and reduces the number of new victims.¹² Limits to the more widespread implementation of the OBPP have consisted mainly of the inability to appropriately train adults, including teachers and other school personnel in educational settings. Despite these limitations, the OBPP has been praised and endorsed by numerous groups, including the US Department of Justice.³⁰

Encourage children who are bullied to stay safe by standing near adults or groups of peers when bullies are present.Other non-curricular, school-based programs exist, such as the School-Wide Positive Behavioral Interventions and Supports (SWPBIS). This program is a school-wide prevention strategy aimed at: 1) reducing behavior problems that lead to office discipline referrals and suspensions, and 2) changing perceptions of school safety. (For more information, see https://www.crimesolutions.gov/ProgramDetails.aspx?ID=385 and https://www.pbis.org/school/swpbis-for-beginners.)³¹

The research-based Second Step: Student Success Through Prevention (SS-SSTP) Middle School Program (http://www.cfchildren.org/second-step/middle-school)³² focuses on the often difficult middle school years. The program helps schools teach and model essential communication, coping, and decision-making skills to help adolescents navigate around common pitfalls such as peer pressure, substance abuse, and bullying (both in-person and online). The program aims to reduce aggression and provide support for a more inclusive environment that helps students stay in school, make good choices, and experience social and academic success.

The Positive Action Program (https://www.positiveaction.net/research/primer),³³ which is predicated on the notion that we feel good about ourselves when we do positive things, features scripted lessons and kits of materials (eg, posters, games, worksheets, puzzles) appropriate for each grade level.

CASE › Stacey’s visit to her FP’s office has presented several clues that she may be a victim of bullying. Her mild persistent asthma appears to no longer be as well controlled as it was in the past. Direct questioning has revealed that 2 girls at school have been making fun of Stacey when she uses her inhaled corticosteroid in the morning before class, so she has stopped using it. These same students are on her cheerleading team, so she quit the team to avoid them. Her school-related anxiety is so great that she no longer pays attention in math class and is constantly worried that something is being posted about her online.

Stacy’s FP responds to this information with a multifaceted approach. In the exam room, he screens Stacy for depression. While she is negative and denies any suicidal ideation, Stacy is clearly having anxiety, so the FP refers Stacey to a counselor at a local mental health clinic. With Stacy’s permission, the FP discusses the issue with her mother and they decide together with Stacy that she should talk to a teacher at school about the ongoing bullying. Because this was not the first time that the FP has heard this from a child in the community, the FP plans to attend an upcoming school board meeting to advocate for an evidence-based bullying prevention program to help curb the ongoing problem facing his patients.

CORRESPONDENCE
Robert McClowry, MD, Department of Family and Community Medicine, Jefferson Family Medicine Associates, 833 Chestnut East, 3rd Floor, Suite 301, Philadelphia, PA, 19107-4414; [email protected].

CASE › Stacey, a 12-year-old girl with mild persistent asthma, presents to her family physician (FP) with her mother for her annual well visit. Stacey reports no complaints, but has visited twice recently for acute exacerbations of her asthma, which had previously been well-controlled. When reviewing her social history, Stacey reports that she started her second year of middle school 3 months ago. When asked if she enjoys school, Stacey looks down and says, “School is fine.” Her mother quickly adds that Stacey has quit the school cheerleading team—much to the coach’s dismay—and is having difficulty in her math class, a class in which she normally excels. Stacey appears embarrassed that her mother has brought these things up. Her mother says that at the beginning of the year, 2 girls began picking on Stacey, calling her names and making fun of her on social media and in front of other students.

For many years, bullying was trivialized. Some viewed it as a universal childhood experience; others considered it a rite of passage.^1,2 It was not examined as a public health issue until the 1970s. In fact, no legislation addressing bullying or “peer abuse” existed in the United States until the mass shooting at Columbine High School in Littleton, Colo, in 1999. Within 3 years of the Columbine tragedy, the number of state laws that mentioned bullying went from zero to 15; within 10 years of Columbine, 41 states had laws addressing bullying,¹ and by 2015, every state, the District of Columbia, and some territories had a bullying law in place.³

Ask patients, "Are you being bullied?" and then follow that with, "How often are you bullied?" and, "Does it happen at school? Online?" These details can help guide interventions.As research and advocacy regarding bullying has grown, its impact on the health of children, adolescents, and even adults has become more apparent. In a 2001 study of school-associated violent deaths in the United States between 1994 and 1999, the Centers for Disease Control and Prevention (CDC) found that among students, homicide perpetrators were more than twice as likely as homicide victims to have been bullied by peers.⁴ Given that homicide is the third leading cause of death in people ages 15 to 24,⁵ past exposure to bullying may be a significant contributing factor to mortality in this age group.⁴

In addition to a correlation with homicidal behavior, those involved in bullying—whether as the bully or victim—are at risk for a wide range of symptoms, conditions, and problems including poor psychosocial adjustment, depression, anxiety, suicide (the second leading cause of death in the 10-14 and 15-24 age groups⁵), academic decline, psychosomatic manifestations, fighting, alcohol use, smoking, and difficulty with the management of chronic diseases.^6-10 Not only does being a victim of bullying have a direct impact on a child’s current mental and physical well-being, but it can have lasting psychological and behavioral effects that can follow children well into adulthood.⁷ The significant impact of bullying on individuals and society as a whole mandates a multifaceted approach that begins in your exam room. What follows is practical advice on screening, counseling, and working with schools and the community at large to curb the bullying epidemic.

IMAGE: © ALICIA BUELOW

Clarifying the problem: The CDC’s definition

Recognizing that varying definitions of bullying were being used in research studies that looked at violent or aggressive behaviors in youth, the CDC published a consensus statement in 2014 that proposed the following definition for bullying:¹¹ any unwanted aggressive behavior by another youth or group of youths who are not siblings or current dating partners that involves an observed or perceived power imbalance and is repeated multiple times or is highly likely to be repeated. This expanded on an earlier definition by Olweus^12,13 that also identified a longitudinal nature and power imbalance as key features.

Types of bullying. Direct bullying entails blatant attacks on a targeted young person, while indirect bullying involves communication with others about the targeted individual (eg, spreading harmful rumors). Bullying may be physical, verbal, or relational (eg, excluding someone from their usual social circle, denying friendship, the silent treatment, writing mean letters, eye rolling, etc.) and may involve damage to property. Boys tend toward more direct bullying behaviors, while girls more often engage in indirect bullying, which may be more challenging for both adults and other students to recognize.^12,13 With increased use of technology and social media by adolescents, cyberbullying has become increasingly more prevalent, with its effects on adolescent health and academics being every bit as profound as those of traditional bullying.¹⁴

About 1 in 4/5 students suffer. The prevalence of bullying ranges by country and culture. The vast majority of early bullying research was conducted in Norway, which found that approximately 15% of students in elementary and secondary schools were involved in bullying in some capacity.¹² In a study involving over 200,000 adolescents from 40 European countries, 26% of adolescents reported being involved in bullying, ranging from 8.6% to 45.2% for boys and 4.8% to 35.8% for girls.¹⁵ Variations in prevalence may be due to cultural differences in the acts of bullying or differences in interpretation of the term “bullying.”^1,15

Among students, homicide perpetrators are more than twice as likely as homicide victims to have been bullied by their peers.In the United States, a 2001 survey of more than 15,000 students in public and private schools (grades 6-10) asked the students about their involvement in bullying: 13% said they'd been a bully, 10.6% a victim, and 6.3% said they'd been both.⁶ There was no significant difference in the frequency of self-reported bullying among urban, suburban, or rural settings.

Despite efforts to educate the public about bullying and work with schools to intervene and prevent bullying, incidence remains largely unchanged. In 2013, the National Crime Victimization Survey reported that approximately 22% of adolescents ages 12 through 18 were victims of bullying.¹⁶ Similarly, the CDC's 2015 Youth Risk Behavior Surveillance System reported that 20.2% of high school students experienced bullying on school property.¹⁷

Screening: Best practices

The FP’s role begins with screening children at risk for bullying (TABLE 1^18-22) or those whose complaints suggest that they may be victims of bullying.

Start screening when children enter elementary school

Given that providers’ time is limited for every patient visit, it is important to address bullying at times that are most likely to yield impactful results. The American Academy of Pediatrics recommends that the topic of bullying be introduced at the 6-year-old well-child visit (a typical age for entry to elementary school).⁷ Views in the literature are inconsistent regarding when and how to address bullying at other time points. One approach is to pre-screen those with risk factors associated with bullying (TABLE 1^18-22), and to focus screening on those with warning signs of bullying, which include mood disorders, psychosomatic or behavioral symptoms, substance abuse, self-harm behaviors, suicidal ideation or a suicide attempt, a decline in academic performance, and reports of school truancy. Parental concerns, such as when a child suddenly needs more money for lunch, is having aggressive outbursts, or is exhibiting unexplained physical injuries, should also be regarded as cues to screen.⁹

Screen patients in high-risk groups

A number of groups of children are at high risk for bullying and warrant targeted screening efforts.

• Children with special health needs. Research has shown that children with special health needs are at increased risk for being bullied.¹⁸ In fact, the presence of a chronic disease may increase the risk for bullying, and bullying often negatively impacts chronic disease management. As a result, it’s important to have a high index of suspicion with patients who have a chronic disease and who are not responding as expected to medical management or who experience deterioration after being previously well-controlled.¹⁸
• Children who are under- or overweight. Similarly, bullying based on a child's weight is a phenomenon that has been recognized to have a significant impact on children’s emotional health.¹⁹
• Youth who identify as lesbian, gay, bisexual, transgender, or queer/questioning (LGBTQ+) are more likely than non-LGBTQ+ peers to attempt suicide when exposed to a hostile social environment, such as that created by bullying.²⁰

Screening need not be complicated

One screening approach is simply to ask patients, “Are you being bullied?” followed by such questions as, “How often are you bullied?” or “How long have you been bullied?” Asking about the setting of the bullying (Does it happen at school? Traveling to/from school? Online?) and other details may help guide interventions and the provision of resources.⁹ Another approach is to provide patients with some type of written survey (see TABLE 2²³ for an example) to encourage responses that patients might be reluctant to disclose verbally.^23,24 (See “Barriers to screening.")

Provider and parental interventions

Interventions often entail counseling the patient and the family about bullying and its effects, empowering victims and their caregivers, and screening for bullying comorbidities and correlates.² Refer patients to behavioral health specialists when there is evidence of pervasive effects on mood, behavior, or social development, but keep in mind that counseling can begin in your own exam room.

Effective discussion starters. Affirming the problem and its unacceptability, talking about the different types of bullying and where bullying may occur, and asking about patient perceptions of bullying can be effective discussion starters. FPs should help patients identify bullying, open lines of communication between children and their parents and between parents and other caregivers, and demonstrate respect and kindness in their approach to discussing the topic. Encourage children to speak with trusted adults when exposed to bullying. Talk to them about standing up to bullies (saying “stop” confidently or walking away from difficult situations) and staying safe by staying near adults or groups of peers when bullies are present (TABLE 3²⁵).

Empowering caregivers. Encourage parents to spend time each day talking with their child about the child’s time away from home (TABLE 3²⁵). Counsel parents/caregivers to expand their role. Knowing a child’s friends, encouraging the child academically, and increasing communication are all associated with lower risks of bullying.²⁶ Similarly, parental oversight of Internet and social media use is associated with decreased participation in cyberbullying.²⁷

In addition, the Positive Parenting telephone-based parenting education curriculum has been shown to decrease bullying, physical fighting, physical injuries, and victimization of children.²⁸ The research-based, family strengthening program emphasizes 3 core elements of authoritative parenting: nurturance, discipline, and respect or granting of psychologic autonomy. The program entails 15- to 30-minute weekly phone conversations between parents and educators, as well as videos and a manual.

Are community programs in place—or are they needed?

Many schools have robust, state-mandated programs in place to identify bullying and provide support for students who are victims of bullying. (See “NJ’s harassment and bullying protocol: A case in point.”) Explaining this to victims and their families may help them come forward and seek assistance. FPs who want to advocate for their patients should start with local schools to support such programs and link students at risk with school counselors.

If programs are lacking in your community, there is much you can do to educate yourself about successful programs and advise local community organizations and schools about them. Among the most successful and well-studied interventions for thwarting the bullying epidemic have been school-based community ones. The most studied of these is the Olweus Bullying Prevention Program (OBPP), which is based on 4 principles:^1,29

1. Adults both at home and at school should take a positive and encouraging interest in students.
2. Unacceptable behavior should have strict and well-known limits.
3. Sanctions should be applied consistently and should be non-hostile in nature.
4. Adults both at home and in the educational environment should act as authorities.

In short, the program focuses on greater awareness and involvement on the part of adults, and employing measures at the school level (eg, surveys, better supervision during break and lunch times), the class level (eg, rules against bullying, regular class meetings with students), and the individual level (eg, serious talks with bullies, victims, parents of involved students).

Research has shown that the OBPP reduces bullying behaviors by as much as 50%, reduces vandalism and truancy, and reduces the number of new victims.¹² Limits to the more widespread implementation of the OBPP have consisted mainly of the inability to appropriately train adults, including teachers and other school personnel in educational settings. Despite these limitations, the OBPP has been praised and endorsed by numerous groups, including the US Department of Justice.³⁰

Encourage children who are bullied to stay safe by standing near adults or groups of peers when bullies are present.Other non-curricular, school-based programs exist, such as the School-Wide Positive Behavioral Interventions and Supports (SWPBIS). This program is a school-wide prevention strategy aimed at: 1) reducing behavior problems that lead to office discipline referrals and suspensions, and 2) changing perceptions of school safety. (For more information, see https://www.crimesolutions.gov/ProgramDetails.aspx?ID=385 and https://www.pbis.org/school/swpbis-for-beginners.)³¹

The research-based Second Step: Student Success Through Prevention (SS-SSTP) Middle School Program (http://www.cfchildren.org/second-step/middle-school)³² focuses on the often difficult middle school years. The program helps schools teach and model essential communication, coping, and decision-making skills to help adolescents navigate around common pitfalls such as peer pressure, substance abuse, and bullying (both in-person and online). The program aims to reduce aggression and provide support for a more inclusive environment that helps students stay in school, make good choices, and experience social and academic success.

The Positive Action Program (https://www.positiveaction.net/research/primer),³³ which is predicated on the notion that we feel good about ourselves when we do positive things, features scripted lessons and kits of materials (eg, posters, games, worksheets, puzzles) appropriate for each grade level.

CASE › Stacey’s visit to her FP’s office has presented several clues that she may be a victim of bullying. Her mild persistent asthma appears to no longer be as well controlled as it was in the past. Direct questioning has revealed that 2 girls at school have been making fun of Stacey when she uses her inhaled corticosteroid in the morning before class, so she has stopped using it. These same students are on her cheerleading team, so she quit the team to avoid them. Her school-related anxiety is so great that she no longer pays attention in math class and is constantly worried that something is being posted about her online.

Stacy’s FP responds to this information with a multifaceted approach. In the exam room, he screens Stacy for depression. While she is negative and denies any suicidal ideation, Stacy is clearly having anxiety, so the FP refers Stacey to a counselor at a local mental health clinic. With Stacy’s permission, the FP discusses the issue with her mother and they decide together with Stacy that she should talk to a teacher at school about the ongoing bullying. Because this was not the first time that the FP has heard this from a child in the community, the FP plans to attend an upcoming school board meeting to advocate for an evidence-based bullying prevention program to help curb the ongoing problem facing his patients.

CORRESPONDENCE
Robert McClowry, MD, Department of Family and Community Medicine, Jefferson Family Medicine Associates, 833 Chestnut East, 3rd Floor, Suite 301, Philadelphia, PA, 19107-4414; [email protected].

CASE › Stacey, a 12-year-old girl with mild persistent asthma, presents to her family physician (FP) with her mother for her annual well visit. Stacey reports no complaints, but has visited twice recently for acute exacerbations of her asthma, which had previously been well-controlled. When reviewing her social history, Stacey reports that she started her second year of middle school 3 months ago. When asked if she enjoys school, Stacey looks down and says, “School is fine.” Her mother quickly adds that Stacey has quit the school cheerleading team—much to the coach’s dismay—and is having difficulty in her math class, a class in which she normally excels. Stacey appears embarrassed that her mother has brought these things up. Her mother says that at the beginning of the year, 2 girls began picking on Stacey, calling her names and making fun of her on social media and in front of other students.

For many years, bullying was trivialized. Some viewed it as a universal childhood experience; others considered it a rite of passage.^1,2 It was not examined as a public health issue until the 1970s. In fact, no legislation addressing bullying or “peer abuse” existed in the United States until the mass shooting at Columbine High School in Littleton, Colo, in 1999. Within 3 years of the Columbine tragedy, the number of state laws that mentioned bullying went from zero to 15; within 10 years of Columbine, 41 states had laws addressing bullying,¹ and by 2015, every state, the District of Columbia, and some territories had a bullying law in place.³

Ask patients, "Are you being bullied?" and then follow that with, "How often are you bullied?" and, "Does it happen at school? Online?" These details can help guide interventions.As research and advocacy regarding bullying has grown, its impact on the health of children, adolescents, and even adults has become more apparent. In a 2001 study of school-associated violent deaths in the United States between 1994 and 1999, the Centers for Disease Control and Prevention (CDC) found that among students, homicide perpetrators were more than twice as likely as homicide victims to have been bullied by peers.⁴ Given that homicide is the third leading cause of death in people ages 15 to 24,⁵ past exposure to bullying may be a significant contributing factor to mortality in this age group.⁴

In addition to a correlation with homicidal behavior, those involved in bullying—whether as the bully or victim—are at risk for a wide range of symptoms, conditions, and problems including poor psychosocial adjustment, depression, anxiety, suicide (the second leading cause of death in the 10-14 and 15-24 age groups⁵), academic decline, psychosomatic manifestations, fighting, alcohol use, smoking, and difficulty with the management of chronic diseases.^6-10 Not only does being a victim of bullying have a direct impact on a child’s current mental and physical well-being, but it can have lasting psychological and behavioral effects that can follow children well into adulthood.⁷ The significant impact of bullying on individuals and society as a whole mandates a multifaceted approach that begins in your exam room. What follows is practical advice on screening, counseling, and working with schools and the community at large to curb the bullying epidemic.

IMAGE: © ALICIA BUELOW

Clarifying the problem: The CDC’s definition

Recognizing that varying definitions of bullying were being used in research studies that looked at violent or aggressive behaviors in youth, the CDC published a consensus statement in 2014 that proposed the following definition for bullying:¹¹ any unwanted aggressive behavior by another youth or group of youths who are not siblings or current dating partners that involves an observed or perceived power imbalance and is repeated multiple times or is highly likely to be repeated. This expanded on an earlier definition by Olweus^12,13 that also identified a longitudinal nature and power imbalance as key features.

Types of bullying. Direct bullying entails blatant attacks on a targeted young person, while indirect bullying involves communication with others about the targeted individual (eg, spreading harmful rumors). Bullying may be physical, verbal, or relational (eg, excluding someone from their usual social circle, denying friendship, the silent treatment, writing mean letters, eye rolling, etc.) and may involve damage to property. Boys tend toward more direct bullying behaviors, while girls more often engage in indirect bullying, which may be more challenging for both adults and other students to recognize.^12,13 With increased use of technology and social media by adolescents, cyberbullying has become increasingly more prevalent, with its effects on adolescent health and academics being every bit as profound as those of traditional bullying.¹⁴

About 1 in 4/5 students suffer. The prevalence of bullying ranges by country and culture. The vast majority of early bullying research was conducted in Norway, which found that approximately 15% of students in elementary and secondary schools were involved in bullying in some capacity.¹² In a study involving over 200,000 adolescents from 40 European countries, 26% of adolescents reported being involved in bullying, ranging from 8.6% to 45.2% for boys and 4.8% to 35.8% for girls.¹⁵ Variations in prevalence may be due to cultural differences in the acts of bullying or differences in interpretation of the term “bullying.”^1,15

Among students, homicide perpetrators are more than twice as likely as homicide victims to have been bullied by their peers.In the United States, a 2001 survey of more than 15,000 students in public and private schools (grades 6-10) asked the students about their involvement in bullying: 13% said they'd been a bully, 10.6% a victim, and 6.3% said they'd been both.⁶ There was no significant difference in the frequency of self-reported bullying among urban, suburban, or rural settings.

Despite efforts to educate the public about bullying and work with schools to intervene and prevent bullying, incidence remains largely unchanged. In 2013, the National Crime Victimization Survey reported that approximately 22% of adolescents ages 12 through 18 were victims of bullying.¹⁶ Similarly, the CDC's 2015 Youth Risk Behavior Surveillance System reported that 20.2% of high school students experienced bullying on school property.¹⁷

Screening: Best practices

The FP’s role begins with screening children at risk for bullying (TABLE 1^18-22) or those whose complaints suggest that they may be victims of bullying.

Start screening when children enter elementary school

Given that providers’ time is limited for every patient visit, it is important to address bullying at times that are most likely to yield impactful results. The American Academy of Pediatrics recommends that the topic of bullying be introduced at the 6-year-old well-child visit (a typical age for entry to elementary school).⁷ Views in the literature are inconsistent regarding when and how to address bullying at other time points. One approach is to pre-screen those with risk factors associated with bullying (TABLE 1^18-22), and to focus screening on those with warning signs of bullying, which include mood disorders, psychosomatic or behavioral symptoms, substance abuse, self-harm behaviors, suicidal ideation or a suicide attempt, a decline in academic performance, and reports of school truancy. Parental concerns, such as when a child suddenly needs more money for lunch, is having aggressive outbursts, or is exhibiting unexplained physical injuries, should also be regarded as cues to screen.⁹

Screen patients in high-risk groups

A number of groups of children are at high risk for bullying and warrant targeted screening efforts.

• Children with special health needs. Research has shown that children with special health needs are at increased risk for being bullied.¹⁸ In fact, the presence of a chronic disease may increase the risk for bullying, and bullying often negatively impacts chronic disease management. As a result, it’s important to have a high index of suspicion with patients who have a chronic disease and who are not responding as expected to medical management or who experience deterioration after being previously well-controlled.¹⁸
• Children who are under- or overweight. Similarly, bullying based on a child's weight is a phenomenon that has been recognized to have a significant impact on children’s emotional health.¹⁹
• Youth who identify as lesbian, gay, bisexual, transgender, or queer/questioning (LGBTQ+) are more likely than non-LGBTQ+ peers to attempt suicide when exposed to a hostile social environment, such as that created by bullying.²⁰

Screening need not be complicated

One screening approach is simply to ask patients, “Are you being bullied?” followed by such questions as, “How often are you bullied?” or “How long have you been bullied?” Asking about the setting of the bullying (Does it happen at school? Traveling to/from school? Online?) and other details may help guide interventions and the provision of resources.⁹ Another approach is to provide patients with some type of written survey (see TABLE 2²³ for an example) to encourage responses that patients might be reluctant to disclose verbally.^23,24 (See “Barriers to screening.")

Provider and parental interventions

Interventions often entail counseling the patient and the family about bullying and its effects, empowering victims and their caregivers, and screening for bullying comorbidities and correlates.² Refer patients to behavioral health specialists when there is evidence of pervasive effects on mood, behavior, or social development, but keep in mind that counseling can begin in your own exam room.

Effective discussion starters. Affirming the problem and its unacceptability, talking about the different types of bullying and where bullying may occur, and asking about patient perceptions of bullying can be effective discussion starters. FPs should help patients identify bullying, open lines of communication between children and their parents and between parents and other caregivers, and demonstrate respect and kindness in their approach to discussing the topic. Encourage children to speak with trusted adults when exposed to bullying. Talk to them about standing up to bullies (saying “stop” confidently or walking away from difficult situations) and staying safe by staying near adults or groups of peers when bullies are present (TABLE 3²⁵).

Empowering caregivers. Encourage parents to spend time each day talking with their child about the child’s time away from home (TABLE 3²⁵). Counsel parents/caregivers to expand their role. Knowing a child’s friends, encouraging the child academically, and increasing communication are all associated with lower risks of bullying.²⁶ Similarly, parental oversight of Internet and social media use is associated with decreased participation in cyberbullying.²⁷

In addition, the Positive Parenting telephone-based parenting education curriculum has been shown to decrease bullying, physical fighting, physical injuries, and victimization of children.²⁸ The research-based, family strengthening program emphasizes 3 core elements of authoritative parenting: nurturance, discipline, and respect or granting of psychologic autonomy. The program entails 15- to 30-minute weekly phone conversations between parents and educators, as well as videos and a manual.

Are community programs in place—or are they needed?

Many schools have robust, state-mandated programs in place to identify bullying and provide support for students who are victims of bullying. (See “NJ’s harassment and bullying protocol: A case in point.”) Explaining this to victims and their families may help them come forward and seek assistance. FPs who want to advocate for their patients should start with local schools to support such programs and link students at risk with school counselors.

If programs are lacking in your community, there is much you can do to educate yourself about successful programs and advise local community organizations and schools about them. Among the most successful and well-studied interventions for thwarting the bullying epidemic have been school-based community ones. The most studied of these is the Olweus Bullying Prevention Program (OBPP), which is based on 4 principles:^1,29

1. Adults both at home and at school should take a positive and encouraging interest in students.
2. Unacceptable behavior should have strict and well-known limits.
3. Sanctions should be applied consistently and should be non-hostile in nature.
4. Adults both at home and in the educational environment should act as authorities.

In short, the program focuses on greater awareness and involvement on the part of adults, and employing measures at the school level (eg, surveys, better supervision during break and lunch times), the class level (eg, rules against bullying, regular class meetings with students), and the individual level (eg, serious talks with bullies, victims, parents of involved students).

Research has shown that the OBPP reduces bullying behaviors by as much as 50%, reduces vandalism and truancy, and reduces the number of new victims.¹² Limits to the more widespread implementation of the OBPP have consisted mainly of the inability to appropriately train adults, including teachers and other school personnel in educational settings. Despite these limitations, the OBPP has been praised and endorsed by numerous groups, including the US Department of Justice.³⁰

Encourage children who are bullied to stay safe by standing near adults or groups of peers when bullies are present.Other non-curricular, school-based programs exist, such as the School-Wide Positive Behavioral Interventions and Supports (SWPBIS). This program is a school-wide prevention strategy aimed at: 1) reducing behavior problems that lead to office discipline referrals and suspensions, and 2) changing perceptions of school safety. (For more information, see https://www.crimesolutions.gov/ProgramDetails.aspx?ID=385 and https://www.pbis.org/school/swpbis-for-beginners.)³¹

The research-based Second Step: Student Success Through Prevention (SS-SSTP) Middle School Program (http://www.cfchildren.org/second-step/middle-school)³² focuses on the often difficult middle school years. The program helps schools teach and model essential communication, coping, and decision-making skills to help adolescents navigate around common pitfalls such as peer pressure, substance abuse, and bullying (both in-person and online). The program aims to reduce aggression and provide support for a more inclusive environment that helps students stay in school, make good choices, and experience social and academic success.

The Positive Action Program (https://www.positiveaction.net/research/primer),³³ which is predicated on the notion that we feel good about ourselves when we do positive things, features scripted lessons and kits of materials (eg, posters, games, worksheets, puzzles) appropriate for each grade level.

CASE › Stacey’s visit to her FP’s office has presented several clues that she may be a victim of bullying. Her mild persistent asthma appears to no longer be as well controlled as it was in the past. Direct questioning has revealed that 2 girls at school have been making fun of Stacey when she uses her inhaled corticosteroid in the morning before class, so she has stopped using it. These same students are on her cheerleading team, so she quit the team to avoid them. Her school-related anxiety is so great that she no longer pays attention in math class and is constantly worried that something is being posted about her online.

Stacy’s FP responds to this information with a multifaceted approach. In the exam room, he screens Stacy for depression. While she is negative and denies any suicidal ideation, Stacy is clearly having anxiety, so the FP refers Stacey to a counselor at a local mental health clinic. With Stacy’s permission, the FP discusses the issue with her mother and they decide together with Stacy that she should talk to a teacher at school about the ongoing bullying. Because this was not the first time that the FP has heard this from a child in the community, the FP plans to attend an upcoming school board meeting to advocate for an evidence-based bullying prevention program to help curb the ongoing problem facing his patients.

CORRESPONDENCE
Robert McClowry, MD, Department of Family and Community Medicine, Jefferson Family Medicine Associates, 833 Chestnut East, 3rd Floor, Suite 301, Philadelphia, PA, 19107-4414; [email protected].