Current Psychiatry

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

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

Dr. Warren responds

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

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

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

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

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

Dr. Warren responds

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

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

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

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

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

Dr. Warren responds

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Quality criteria for rating scales

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

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

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

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

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

Patient Health Questionnaire

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

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

Mood Disorder Questionnaire

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

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

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

Generalized Anxiety Disorder 7-item scale

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

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

CAGE questionnaire for detection of substance use

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

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

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

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

Columbia Suicide Severity Rating Scale (C-SSRS)

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

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

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

Using scales to augment care

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

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

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

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

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

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

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

Quality criteria for rating scales

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

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

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

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

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

Patient Health Questionnaire

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

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

Mood Disorder Questionnaire

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

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

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

Generalized Anxiety Disorder 7-item scale

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

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

CAGE questionnaire for detection of substance use

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

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

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

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

Columbia Suicide Severity Rating Scale (C-SSRS)

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

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

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

Using scales to augment care

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

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

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

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

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

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

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

Quality criteria for rating scales

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

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

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

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

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

Patient Health Questionnaire

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

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

Mood Disorder Questionnaire

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

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

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

Generalized Anxiety Disorder 7-item scale

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

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

CAGE questionnaire for detection of substance use

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

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

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

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

Columbia Suicide Severity Rating Scale (C-SSRS)

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

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

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

Using scales to augment care

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

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

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

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

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

What is your diagnosis at this point?

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

The authors’ observations

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

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

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

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

HISTORY High functioning

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

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

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

What would be your differential diagnosis at this time?

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

The authors’ observations

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

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

EVALUATION Questionable story

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

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

The authors’ observations

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

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

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

EVALUATION Cognitive deficits

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

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

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

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

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

Other causes of psychiatric symptoms in MS include:

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

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

How would you treat Ms. S?

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

Treating psychiatric symptoms in the context of MS

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

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

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

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

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

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

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

What is your diagnosis at this point?

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

The authors’ observations

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

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

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

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

HISTORY High functioning

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

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

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

What would be your differential diagnosis at this time?

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

The authors’ observations

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

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

EVALUATION Questionable story

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

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

The authors’ observations

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

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

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

EVALUATION Cognitive deficits

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

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

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

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

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

Other causes of psychiatric symptoms in MS include:

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

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

How would you treat Ms. S?

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

Treating psychiatric symptoms in the context of MS

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

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

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

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

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

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

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

What is your diagnosis at this point?

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

The authors’ observations

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

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

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

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

HISTORY High functioning

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

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

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

What would be your differential diagnosis at this time?

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

The authors’ observations

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

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

EVALUATION Questionable story

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

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

The authors’ observations

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

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

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

EVALUATION Cognitive deficits

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

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

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

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

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

Other causes of psychiatric symptoms in MS include:

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

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

How would you treat Ms. S?

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

Treating psychiatric symptoms in the context of MS

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

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

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

Many patients experience difficulty swallowing pills, for various reasons:

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

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

Crushing guidelines

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

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

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

Many patients experience difficulty swallowing pills, for various reasons:

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

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

Crushing guidelines

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

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

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

Many patients experience difficulty swallowing pills, for various reasons:

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

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

Crushing guidelines

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Revisiting delirious mania

After treating a young woman with delirious mania, we were compelled to comment on the case report “Confused and nearly naked after going on spending sprees” (Cases That Test Your Skills, Current Psychiatry. July 2014, p. 56-62).

A young woman with bipolar I disorder and mild intellectual disability was brought to our inpatient psychiatric unit after she disappeared from her home. Her family reported she was not compliant with her medications, and she recently showed deterioration marked by bizarre and violent behaviors for the previous month.

Although her presentation was consistent with earlier manic episodes, additional behaviors indicated an increase in severity. The patient was only oriented to name, was disrobing, had urinary and fecal incontinence, and showed purposeless hyperactivity such as continuously dancing in circles.

Because we thought she was experiencing a severe exacerbation of bipolar disorder, the patient was started on 4 different antipsychotic trials (typical and atypical) and 2 mood stabilizers, all of which did not produce adequate response. Even after augmentation with nightly long-acting benzodiazepines, the patient’s symptoms remained unchanged.

The patient received a diagnosis of delirious mania, with the underlying mechanism being severe catatonia. A literature search revealed electroconvulsive therapy (ECT) and benzodiazepines as first-line treatments, and discouraged use of typical antipsychotics because of an increased risk of neuroleptic malignant syndrome and malignant delirious mania.¹ Because ECT was not available at our facility, we initiated benzodiazepines, while continuing an atypical antipsychotic and mood stabilizer. The patient was discharged after her symptoms improved rapidly.

We agree it is prudent to rule out any medical illnesses that could cause delirium. Interestingly, in our patient a head CT revealed small calcifications suggestive of cysticercosis, which have been seen on imaging since age 13. We suggest that this finding contributed to her disinhibition, prolonged her recovery, and could explain why she did not respond adequately to medications.

Diagnosing and treating delirious mania in our patient was challenging. As mentioned by Davis et al, there is no classification of delirious mania in DSM-5. In addition, there are no large-scale studies to educate psychiatrists about the prevalence and appropriate treatment of this disorder.

Our treatment approach differed from that of Davis et al in that we chose scheduled benzodiazepines rather than antipsychotics to target the patient’s catatonia. However, both patients improved, prompting us to further question the mechanism behind this presentation.

We encourage the addition of delirious mania to the next edition of DSM. Without classification and establishment of this diagnosis, psychiatrists are unlikely to consider this serious and potentially fatal syndrome. Delirious mania is mysterious and rare and its inner workings are not fully elucidated.

Sabina Bera, MD MSc

PGY-2 Psychiatry Resident

Mohammed Molla, MD, DFAPA

Interim Joint Chair and Program Director

University of California Los Angeles-Kern

Psychiatry Training Program
Bakersfield, California

Reference

1. Jacobowski NL, Heckers S, Bobo WV. Delirious mania: detection, diagnosis, and clinical management in the acute setting. J Psychiatr Pract. 2013;19(1):15-28.

Correcting an error

In his informative guest editorial "Forget the myths and help your psychiatric patients quit smoking" (From the Editor, Current Psychiatry. October 2016, p. 23-25), Dr. Anthenelli makes a common statistical error, which may mislead readers, namely, confusing “percentage” with “percentage points.” He reports a difference in the rates of serious neuropsychiatric adverse events between a non-psychiatric cohort (2%) and a psychiatric cohort (6%) as “4%” (p. 25), when the percentage (relative) difference is 300% (ie, 3-fold). The absolute difference in rates is 4 percentage points, which may be what he wanted to report.

David A. Gorelick, MD, PhD

Professor of Psychiatry
Maryland Psychiatric Research Center
University of Maryland
Baltimore, Maryland

Revisiting delirious mania

After treating a young woman with delirious mania, we were compelled to comment on the case report “Confused and nearly naked after going on spending sprees” (Cases That Test Your Skills, Current Psychiatry. July 2014, p. 56-62).

A young woman with bipolar I disorder and mild intellectual disability was brought to our inpatient psychiatric unit after she disappeared from her home. Her family reported she was not compliant with her medications, and she recently showed deterioration marked by bizarre and violent behaviors for the previous month.

Although her presentation was consistent with earlier manic episodes, additional behaviors indicated an increase in severity. The patient was only oriented to name, was disrobing, had urinary and fecal incontinence, and showed purposeless hyperactivity such as continuously dancing in circles.

Because we thought she was experiencing a severe exacerbation of bipolar disorder, the patient was started on 4 different antipsychotic trials (typical and atypical) and 2 mood stabilizers, all of which did not produce adequate response. Even after augmentation with nightly long-acting benzodiazepines, the patient’s symptoms remained unchanged.

The patient received a diagnosis of delirious mania, with the underlying mechanism being severe catatonia. A literature search revealed electroconvulsive therapy (ECT) and benzodiazepines as first-line treatments, and discouraged use of typical antipsychotics because of an increased risk of neuroleptic malignant syndrome and malignant delirious mania.¹ Because ECT was not available at our facility, we initiated benzodiazepines, while continuing an atypical antipsychotic and mood stabilizer. The patient was discharged after her symptoms improved rapidly.

We agree it is prudent to rule out any medical illnesses that could cause delirium. Interestingly, in our patient a head CT revealed small calcifications suggestive of cysticercosis, which have been seen on imaging since age 13. We suggest that this finding contributed to her disinhibition, prolonged her recovery, and could explain why she did not respond adequately to medications.

Diagnosing and treating delirious mania in our patient was challenging. As mentioned by Davis et al, there is no classification of delirious mania in DSM-5. In addition, there are no large-scale studies to educate psychiatrists about the prevalence and appropriate treatment of this disorder.

Our treatment approach differed from that of Davis et al in that we chose scheduled benzodiazepines rather than antipsychotics to target the patient’s catatonia. However, both patients improved, prompting us to further question the mechanism behind this presentation.

We encourage the addition of delirious mania to the next edition of DSM. Without classification and establishment of this diagnosis, psychiatrists are unlikely to consider this serious and potentially fatal syndrome. Delirious mania is mysterious and rare and its inner workings are not fully elucidated.

Sabina Bera, MD MSc

PGY-2 Psychiatry Resident

Mohammed Molla, MD, DFAPA

Interim Joint Chair and Program Director

University of California Los Angeles-Kern

Psychiatry Training Program
Bakersfield, California

Reference

1. Jacobowski NL, Heckers S, Bobo WV. Delirious mania: detection, diagnosis, and clinical management in the acute setting. J Psychiatr Pract. 2013;19(1):15-28.

Correcting an error

In his informative guest editorial "Forget the myths and help your psychiatric patients quit smoking" (From the Editor, Current Psychiatry. October 2016, p. 23-25), Dr. Anthenelli makes a common statistical error, which may mislead readers, namely, confusing “percentage” with “percentage points.” He reports a difference in the rates of serious neuropsychiatric adverse events between a non-psychiatric cohort (2%) and a psychiatric cohort (6%) as “4%” (p. 25), when the percentage (relative) difference is 300% (ie, 3-fold). The absolute difference in rates is 4 percentage points, which may be what he wanted to report.

David A. Gorelick, MD, PhD

Professor of Psychiatry
Maryland Psychiatric Research Center
University of Maryland
Baltimore, Maryland

Revisiting delirious mania

After treating a young woman with delirious mania, we were compelled to comment on the case report “Confused and nearly naked after going on spending sprees” (Cases That Test Your Skills, Current Psychiatry. July 2014, p. 56-62).

A young woman with bipolar I disorder and mild intellectual disability was brought to our inpatient psychiatric unit after she disappeared from her home. Her family reported she was not compliant with her medications, and she recently showed deterioration marked by bizarre and violent behaviors for the previous month.

Although her presentation was consistent with earlier manic episodes, additional behaviors indicated an increase in severity. The patient was only oriented to name, was disrobing, had urinary and fecal incontinence, and showed purposeless hyperactivity such as continuously dancing in circles.

Because we thought she was experiencing a severe exacerbation of bipolar disorder, the patient was started on 4 different antipsychotic trials (typical and atypical) and 2 mood stabilizers, all of which did not produce adequate response. Even after augmentation with nightly long-acting benzodiazepines, the patient’s symptoms remained unchanged.

The patient received a diagnosis of delirious mania, with the underlying mechanism being severe catatonia. A literature search revealed electroconvulsive therapy (ECT) and benzodiazepines as first-line treatments, and discouraged use of typical antipsychotics because of an increased risk of neuroleptic malignant syndrome and malignant delirious mania.¹ Because ECT was not available at our facility, we initiated benzodiazepines, while continuing an atypical antipsychotic and mood stabilizer. The patient was discharged after her symptoms improved rapidly.

We agree it is prudent to rule out any medical illnesses that could cause delirium. Interestingly, in our patient a head CT revealed small calcifications suggestive of cysticercosis, which have been seen on imaging since age 13. We suggest that this finding contributed to her disinhibition, prolonged her recovery, and could explain why she did not respond adequately to medications.

Diagnosing and treating delirious mania in our patient was challenging. As mentioned by Davis et al, there is no classification of delirious mania in DSM-5. In addition, there are no large-scale studies to educate psychiatrists about the prevalence and appropriate treatment of this disorder.

Our treatment approach differed from that of Davis et al in that we chose scheduled benzodiazepines rather than antipsychotics to target the patient’s catatonia. However, both patients improved, prompting us to further question the mechanism behind this presentation.

We encourage the addition of delirious mania to the next edition of DSM. Without classification and establishment of this diagnosis, psychiatrists are unlikely to consider this serious and potentially fatal syndrome. Delirious mania is mysterious and rare and its inner workings are not fully elucidated.

Sabina Bera, MD MSc

PGY-2 Psychiatry Resident

Mohammed Molla, MD, DFAPA

Interim Joint Chair and Program Director

University of California Los Angeles-Kern

Psychiatry Training Program
Bakersfield, California

Reference

1. Jacobowski NL, Heckers S, Bobo WV. Delirious mania: detection, diagnosis, and clinical management in the acute setting. J Psychiatr Pract. 2013;19(1):15-28.

Correcting an error

In his informative guest editorial "Forget the myths and help your psychiatric patients quit smoking" (From the Editor, Current Psychiatry. October 2016, p. 23-25), Dr. Anthenelli makes a common statistical error, which may mislead readers, namely, confusing “percentage” with “percentage points.” He reports a difference in the rates of serious neuropsychiatric adverse events between a non-psychiatric cohort (2%) and a psychiatric cohort (6%) as “4%” (p. 25), when the percentage (relative) difference is 300% (ie, 3-fold). The absolute difference in rates is 4 percentage points, which may be what he wanted to report.

David A. Gorelick, MD, PhD

Professor of Psychiatry
Maryland Psychiatric Research Center
University of Maryland
Baltimore, Maryland