Personality Disorders

As forensic psychiatrists, one of our main roles is to apply the Dusky standard to assess competency. In this regard, multiple times a week, we see pretrial defendants who wait weeks, sometimes months, in jail, for their competency evaluations. Will they be permitted to attend court and continue with their legal proceedings, or will a judge remand them into an involuntary treatment unit to restore their competency? The number of defendants referred for competency evaluation is formally not measured, but estimates suggest it almost doubled from 1973¹ till 2000.²

The intent of ensuring the competency of the accused is fundamentally fair. While all would agree that only those who are convicted of committing crimes be found guilty, not every culture has paid attention to the question of whether those found guilty understand how and why that happened.

Defendant’s background

The defendant is a 40-something-year-old man who vacillates between homelessness and living with friends who partake in his penchant for alcohol. He has committed various crimes, including thefts, disorderly conduct, and possession of controlled substances. He went to prison once for selling narcotics but quickly retorts: “I don’t sell … . This [expletive] cop came and asked if I had any. She was hot. What did you want me to say? It was entrapment.”

Challenging behavior continues

During the course of the interview, he was able to demonstrate that he understands the meaning of making a threat, of committing a crime, and of the roles of the different courtroom personnel. However, the stress of court highlights his interpersonal problems. In this particular case, he recounts: “Court had not yet started; I was talking to my lawyer, and the judge interrupted me, so I answered: Wait your turn [expletive] … not my greatest idea.” When asked about his past referral for competency, he mentions it was in response to trying to fire a public defender because “she was Mexican. I don’t work with those.”

Given his behavior, it is unclear how else a judge or a lawyer could have acted. One could argue that it would be a mistake not to refer this defendant for a competency evaluation, considering his outbursts. On the other hand, he had been evaluated many times before, and the opinion of well-respected forensic psychiatrists was that he did not have a mental illness.

While we reflect on our experience with this defendant, we are unsure of the lessons to be learned. We ponder whether psychiatry does a disservice when not being clearer about what constitutes a serious mental illness. We wonder if we exacerbated the confusion by the removal of “Axis II” categories from the DSM, implying that severe personality disorders are no longer different from, say, schizophrenia and bipolar disorder. Rarely do we hear psychiatrists point out that unusual behaviors do not equal mental illness. We are often too pleased in advocating for more resources by saying that all crimes, all substance misuses, and all annoying behaviors are forms of mental illness when, in reality, the criminal4, the addictive5, and the less common6 are not always biologically based mental disorders or even the real problem, for that matter.

This defendant is difficult. He argues, he yells, he provokes, and he hurts others physically as well as emotionally. While many psychiatrists have decided to codify this pattern of behavior within the B cluster of personality traits, have we misled the public into thinking that patients with personality disorders require the same attention and care as patients with other forms of mental illness, like schizophrenia? Often, we see patients with schizophrenia, bipolar depression, or major depression, who even at their best, are too impaired to file their taxes, apply for an identity card, or understand the complexity of the legal system.

Psychiatry’s difficulty in verbalizing the difference between those disorders harms the public perception of mental disorders. As a result, we have a forensic system similar to the rest of the community health care system – with an abundance of individuals with severe mental illness not referred for treatment or evaluation, and several patients with personality disorders bogging down a system with very limited resources. It is our responsibility not only to educate the public on how to manage and contain the emotions that patients with personality disorders engender in us, but also to educate the public on how to recognize patients with profound mentally ill patients who are quietly suffering.

Dr. Badre is affiliated with the county of San Diego, the University of California at San Diego, and the University of San Diego. Dr. Rao is a San Diego–based board-certified psychiatrist with expertise in forensic psychiatry, correctional psychiatry, telepsychiatry, and inpatient psychiatry.
 

References

1. Competency to Stand Trial and Mental Illness: Final Report. Rockville, Md.: National Institute of Mental Health, 1973.

2. Youth on Trial: A Developmental Perspective on Juvenile Justice. Chicago: University of Chicago Press, 2000.

3. J Am Acad Psychiatry Law. 2007;35(4 Suppl):S3-72.

4. Clin Psychiatry News. 2017;45(8):5.

5. Law and Philosophy. 1999;18(6):589-610.

6. Am J Psychiatry. 1981 Feb;138(2):210-5.

As forensic psychiatrists, one of our main roles is to apply the Dusky standard to assess competency. In this regard, multiple times a week, we see pretrial defendants who wait weeks, sometimes months, in jail, for their competency evaluations. Will they be permitted to attend court and continue with their legal proceedings, or will a judge remand them into an involuntary treatment unit to restore their competency? The number of defendants referred for competency evaluation is formally not measured, but estimates suggest it almost doubled from 1973¹ till 2000.²

The intent of ensuring the competency of the accused is fundamentally fair. While all would agree that only those who are convicted of committing crimes be found guilty, not every culture has paid attention to the question of whether those found guilty understand how and why that happened.

Defendant’s background

The defendant is a 40-something-year-old man who vacillates between homelessness and living with friends who partake in his penchant for alcohol. He has committed various crimes, including thefts, disorderly conduct, and possession of controlled substances. He went to prison once for selling narcotics but quickly retorts: “I don’t sell … . This [expletive] cop came and asked if I had any. She was hot. What did you want me to say? It was entrapment.”

Challenging behavior continues

During the course of the interview, he was able to demonstrate that he understands the meaning of making a threat, of committing a crime, and of the roles of the different courtroom personnel. However, the stress of court highlights his interpersonal problems. In this particular case, he recounts: “Court had not yet started; I was talking to my lawyer, and the judge interrupted me, so I answered: Wait your turn [expletive] … not my greatest idea.” When asked about his past referral for competency, he mentions it was in response to trying to fire a public defender because “she was Mexican. I don’t work with those.”

Given his behavior, it is unclear how else a judge or a lawyer could have acted. One could argue that it would be a mistake not to refer this defendant for a competency evaluation, considering his outbursts. On the other hand, he had been evaluated many times before, and the opinion of well-respected forensic psychiatrists was that he did not have a mental illness.

While we reflect on our experience with this defendant, we are unsure of the lessons to be learned. We ponder whether psychiatry does a disservice when not being clearer about what constitutes a serious mental illness. We wonder if we exacerbated the confusion by the removal of “Axis II” categories from the DSM, implying that severe personality disorders are no longer different from, say, schizophrenia and bipolar disorder. Rarely do we hear psychiatrists point out that unusual behaviors do not equal mental illness. We are often too pleased in advocating for more resources by saying that all crimes, all substance misuses, and all annoying behaviors are forms of mental illness when, in reality, the criminal4, the addictive5, and the less common6 are not always biologically based mental disorders or even the real problem, for that matter.

This defendant is difficult. He argues, he yells, he provokes, and he hurts others physically as well as emotionally. While many psychiatrists have decided to codify this pattern of behavior within the B cluster of personality traits, have we misled the public into thinking that patients with personality disorders require the same attention and care as patients with other forms of mental illness, like schizophrenia? Often, we see patients with schizophrenia, bipolar depression, or major depression, who even at their best, are too impaired to file their taxes, apply for an identity card, or understand the complexity of the legal system.

Psychiatry’s difficulty in verbalizing the difference between those disorders harms the public perception of mental disorders. As a result, we have a forensic system similar to the rest of the community health care system – with an abundance of individuals with severe mental illness not referred for treatment or evaluation, and several patients with personality disorders bogging down a system with very limited resources. It is our responsibility not only to educate the public on how to manage and contain the emotions that patients with personality disorders engender in us, but also to educate the public on how to recognize patients with profound mentally ill patients who are quietly suffering.

Dr. Badre is affiliated with the county of San Diego, the University of California at San Diego, and the University of San Diego. Dr. Rao is a San Diego–based board-certified psychiatrist with expertise in forensic psychiatry, correctional psychiatry, telepsychiatry, and inpatient psychiatry.
 

References

1. Competency to Stand Trial and Mental Illness: Final Report. Rockville, Md.: National Institute of Mental Health, 1973.

2. Youth on Trial: A Developmental Perspective on Juvenile Justice. Chicago: University of Chicago Press, 2000.

3. J Am Acad Psychiatry Law. 2007;35(4 Suppl):S3-72.

4. Clin Psychiatry News. 2017;45(8):5.

5. Law and Philosophy. 1999;18(6):589-610.

6. Am J Psychiatry. 1981 Feb;138(2):210-5.

As forensic psychiatrists, one of our main roles is to apply the Dusky standard to assess competency. In this regard, multiple times a week, we see pretrial defendants who wait weeks, sometimes months, in jail, for their competency evaluations. Will they be permitted to attend court and continue with their legal proceedings, or will a judge remand them into an involuntary treatment unit to restore their competency? The number of defendants referred for competency evaluation is formally not measured, but estimates suggest it almost doubled from 1973¹ till 2000.²

The intent of ensuring the competency of the accused is fundamentally fair. While all would agree that only those who are convicted of committing crimes be found guilty, not every culture has paid attention to the question of whether those found guilty understand how and why that happened.

Defendant’s background

The defendant is a 40-something-year-old man who vacillates between homelessness and living with friends who partake in his penchant for alcohol. He has committed various crimes, including thefts, disorderly conduct, and possession of controlled substances. He went to prison once for selling narcotics but quickly retorts: “I don’t sell … . This [expletive] cop came and asked if I had any. She was hot. What did you want me to say? It was entrapment.”

Challenging behavior continues

During the course of the interview, he was able to demonstrate that he understands the meaning of making a threat, of committing a crime, and of the roles of the different courtroom personnel. However, the stress of court highlights his interpersonal problems. In this particular case, he recounts: “Court had not yet started; I was talking to my lawyer, and the judge interrupted me, so I answered: Wait your turn [expletive] … not my greatest idea.” When asked about his past referral for competency, he mentions it was in response to trying to fire a public defender because “she was Mexican. I don’t work with those.”

Given his behavior, it is unclear how else a judge or a lawyer could have acted. One could argue that it would be a mistake not to refer this defendant for a competency evaluation, considering his outbursts. On the other hand, he had been evaluated many times before, and the opinion of well-respected forensic psychiatrists was that he did not have a mental illness.

While we reflect on our experience with this defendant, we are unsure of the lessons to be learned. We ponder whether psychiatry does a disservice when not being clearer about what constitutes a serious mental illness. We wonder if we exacerbated the confusion by the removal of “Axis II” categories from the DSM, implying that severe personality disorders are no longer different from, say, schizophrenia and bipolar disorder. Rarely do we hear psychiatrists point out that unusual behaviors do not equal mental illness. We are often too pleased in advocating for more resources by saying that all crimes, all substance misuses, and all annoying behaviors are forms of mental illness when, in reality, the criminal4, the addictive5, and the less common6 are not always biologically based mental disorders or even the real problem, for that matter.

This defendant is difficult. He argues, he yells, he provokes, and he hurts others physically as well as emotionally. While many psychiatrists have decided to codify this pattern of behavior within the B cluster of personality traits, have we misled the public into thinking that patients with personality disorders require the same attention and care as patients with other forms of mental illness, like schizophrenia? Often, we see patients with schizophrenia, bipolar depression, or major depression, who even at their best, are too impaired to file their taxes, apply for an identity card, or understand the complexity of the legal system.

Psychiatry’s difficulty in verbalizing the difference between those disorders harms the public perception of mental disorders. As a result, we have a forensic system similar to the rest of the community health care system – with an abundance of individuals with severe mental illness not referred for treatment or evaluation, and several patients with personality disorders bogging down a system with very limited resources. It is our responsibility not only to educate the public on how to manage and contain the emotions that patients with personality disorders engender in us, but also to educate the public on how to recognize patients with profound mentally ill patients who are quietly suffering.

Dr. Badre is affiliated with the county of San Diego, the University of California at San Diego, and the University of San Diego. Dr. Rao is a San Diego–based board-certified psychiatrist with expertise in forensic psychiatry, correctional psychiatry, telepsychiatry, and inpatient psychiatry.
 

References

1. Competency to Stand Trial and Mental Illness: Final Report. Rockville, Md.: National Institute of Mental Health, 1973.

2. Youth on Trial: A Developmental Perspective on Juvenile Justice. Chicago: University of Chicago Press, 2000.

3. J Am Acad Psychiatry Law. 2007;35(4 Suppl):S3-72.

4. Clin Psychiatry News. 2017;45(8):5.

5. Law and Philosophy. 1999;18(6):589-610.

6. Am J Psychiatry. 1981 Feb;138(2):210-5.

Borderline personality disorder (BPD) is associated with impaired psychosocial functioning,^1-4 reduced health-related quality of life,⁵ high utilization of services,^6,7 and excess mortality.^8-10 Although BPD occurs in up to 40% of psychiatric inpatients¹¹ and 10% of outpatients,¹² it is underrecognized.^13-15 Often, patients with BPD do not receive an accurate diagnosis until ≥10 years after initially seeking treatment.¹⁶ The treatment and clinical implications of failing to recognize BPD include overprescribing medication and underutilizing empirically effective psychotherapies.¹⁴

This review summarizes studies of the underdiagnosis of BPD in routine clinical practice, describes which patients should be screened, and reviews alternative approaches to screening.

Underrecognition of BPD

The Rhode Island Methods to Improve Diagnostic Assessment and Services (MIDAS) project is an ongoing clinical research study involving the integration of research assessment methods into routine clinical practice.¹⁷ In an early report from the MIDAS project, BPD diagnoses derived from structured and unstructured clinical interviews were compared between 2 groups of psychiatric outpatients in the same practice.¹⁵ Individuals in the structured interview cohort were 35 times more often diagnosed with BPD than individuals evaluated with an unstructured clinical interview. Importantly, when the information from the structured interview was presented to the clinicians, BPD was more likely to be diagnosed clinically.

Other studies^13,16 also found that the rate of diagnosing BPD was higher when the diagnosis was based on a semi-structured diagnostic interview compared with an unstructured clinical interview, and that clinicians were reluctant to diagnose BPD during their routine intake diagnostic evaluation.

Clinicians, however, do not use semi-structured interviews in their practice, and they also do not tend to diagnose personality disorders (PDs) based on direct questioning, as they typically would when assessing a symptom-based disorder such as depression or anxiety. Rather, clinicians report that they rely on longitudinal observations to diagnose PDs.¹⁸ However, the results from the MIDAS project were inconsistent with clinicians’ reports. When clinicians were presented with the results of the semi-structured interview, they usually would diagnose BPD, even though it was the initial evaluation. If clinicians actually relied on longitudinal observations and considered information based on the direct question approach of research interviews to be irrelevant or invalid, then the results from the semi-structured interview should not have influenced the rate at which they diagnosed BPD. This suggests that the primary issue in diagnosing PDs is not the need for longi­tudinal observation but rather the need for more information, and that there is a role for screening questionnaires.

One potential criticism of studies demonstrating underrecognition of BPD in clinical practice is that patients typically were interviewed when they presented for treatment, when most were depressed or anxious. The possible pathologizing effects of psychiatric state on personality have been known for years.¹⁹ However, a large body of literature examining the treatment, prognostic, familial, and biological correlates of PDs supports the validity of diagnosing PDs in this manner. Moreover, from a clinical perspective, the sooner a clinician is aware of the presence of BPD, the more likely this information can be used for treatment planning.

Who should be screened for BPD?

BPD is underrecognized and underdiagnosed because patients with BPD often also have comorbid mood, anxiety, or substance use disorders.^20,21 The symptoms associated with these disorders are typically the chief concern of patients with undiagnosed BPD who present for treatment. Patients with BPD rarely present for an intake evaluation and state that they are struggling with abandonment fears, chronic feelings of emptiness, or an identity disturbance. If patients identified these problems as their chief concerns, BPD would be easier to recognize.

Although several studies have documented the frequency of BPD in patients with a specific psychiatric diagnosis such as major depressive disorder (MDD) or attention-deficit/hyperactivity disorder,^22-26 the MIDAS project examined the frequency of BPD in patients with various diagnoses and evaluated which disorders were associated with a significantly increased rate of BPD.²⁷ The highest rate of BPD was found in patients with bipolar disorder. Approximately 25% of patients with bipolar II disorder and one-third of those with bipolar I disorder were diagnosed with BPD; these rates were significantly higher than the rate of BPD in patients without these disorders (Table 1²⁷). The rate of BPD was second highest in patients with a principal diagnosis of posttraumatic stress disorder (PTSD) and MDD; however, the rate of BPD in these patients was not significantly elevated compared with patients who did not have these principal diagnoses. Three disorders were associated with a significantly lower rate of BPD: adjustment disorder, dysthymic disorder, and generalized anxiety disorder.

A brief review of screening statistics

Screening tests for most psychiatric disorders are based on multi-item scales in which a total score is computed from a sum of item scores, and a cutoff point is established to determine who does and does not screen positive on the test. However, sensitivity, specificity, and positive and negative predictive values are not invariant properties of a screening test with a continuous score distribution. Rather, the performance statistics of a scale can be altered by changing the threshold score to distinguish cases from non-cases. When the screening threshold is lowered, sensitivity increases and specificity decreases.

For screening, a broad net needs to be cast so that all (or almost all) cases are included. Therefore, the cutoff score should be set low to prioritize the sensitivity of the instrument. A screening scale also should have high negative predictive value so that the clinician can be confident that patients who screen negative on the test do not have the disorder.

Screening questionnaires for BPD

Several questionnaires have been developed to screen for PDs (Table 2^28-35). Some screen for each of the DSM PDs,^28,36-42 and some screen more broadly for the presence or absence of any PD.^29,43,44 The most commonly studied self-report scale for BPD is the McLean Screening Instrument for Borderline Personality Disorder (MSI-BPD),³⁰ a 10-item self-report scale derived from a subset of questions from the BPD module of a semi-structured diagnostic interview.

The initial validation study³⁰ found that the optimal cutoff score was 7, which resulted in a sensitivity of 81% and specificity of 89%. Three studies have evaluated the scale in adolescents and young adults,^45-47 and 3 studies examined the scale in adult outpatients.^48-50 Across all 6 studies, at the optimal cutoff scores determined in each study, the sensitivity of the MSI-BPD ranged from 68% to 94% (mean, 80%) and the specificity ranged from 66% to 80% (mean, 72%).

Problems with screening questionnaires. Although screening scales have been developed for many psychiatric disorders, they have not been widely used in mental health settings. In a previous commentary, I argued that the conceptual justification for using self-report screening scales for single disorders in psychiatric settings is questionable.⁵¹ Another problem with screening scales is their potential misuse as case-finding instruments. In the literature on bipolar disorder screening, several researchers misconstrued a positive screen to indicate caseness.⁵¹ Although this is not a problem with the screening measures or the selection of a cutoff score, caution must be taken to not confuse screening with diagnosis.⁵²

Screening for BPD as part of your diagnostic interview

An alternative approach to using self-administered questionnaires for screening is for clinicians to include questions in their evaluation as part of a psychiatric review of systems. When conducting a diagnostic interview, clinicians typically screen for disorders that are comorbid with the principal diagnosis by asking about the comorbid disorders’ necessary features or “gate criteria.” For example, in a patient with a principal diagnosis of MDD, the clinician would inquire about the presence of panic attacks, excessive worry, or substance use to screen for the presence of panic disorder, generalized anxiety disorder, or a substance use disorder. In contrast, for polythetically defined disorders such as BPD, there is no single gate criterion, because the disorder is diagnosed based on the presence of at least 5 of 9 criteria and no single one of these criteria is required to be present to establish the diagnosis.

As part of the MIDAS project, the psycho­metric properties of the BPD criteria were examined to determine if it was possible to identify 1 or 2 criteria that could serve as gate criteria to screen for the disorder. If the sensitivity of 1 criterion or a combination of 2 BPD criteria was sufficiently high (ie, >90%), then the assessment of this criterion (or these criteria) could be included in a psychiatric review of systems, thus potentially improving the detection of BPD. Researchers hypothesized that affective instability, considered first by Linehan⁵³ and later by other theorists⁵⁴ to be of central importance to the clinical manifestations of BPD, could function as a gate criterion. In the sample of 3,674 psychiatric outpatients who were evaluated with a semi-structured interview, the sensitivity of the affective instability criterion was 92.8%, and the negative predictive value of the criterion was 99%.

Borderline personality disorder (BPD) is associated with impaired psychosocial functioning,^1-4 reduced health-related quality of life,⁵ high utilization of services,^6,7 and excess mortality.^8-10 Although BPD occurs in up to 40% of psychiatric inpatients¹¹ and 10% of outpatients,¹² it is underrecognized.^13-15 Often, patients with BPD do not receive an accurate diagnosis until ≥10 years after initially seeking treatment.¹⁶ The treatment and clinical implications of failing to recognize BPD include overprescribing medication and underutilizing empirically effective psychotherapies.¹⁴

This review summarizes studies of the underdiagnosis of BPD in routine clinical practice, describes which patients should be screened, and reviews alternative approaches to screening.

Underrecognition of BPD

The Rhode Island Methods to Improve Diagnostic Assessment and Services (MIDAS) project is an ongoing clinical research study involving the integration of research assessment methods into routine clinical practice.¹⁷ In an early report from the MIDAS project, BPD diagnoses derived from structured and unstructured clinical interviews were compared between 2 groups of psychiatric outpatients in the same practice.¹⁵ Individuals in the structured interview cohort were 35 times more often diagnosed with BPD than individuals evaluated with an unstructured clinical interview. Importantly, when the information from the structured interview was presented to the clinicians, BPD was more likely to be diagnosed clinically.

Other studies^13,16 also found that the rate of diagnosing BPD was higher when the diagnosis was based on a semi-structured diagnostic interview compared with an unstructured clinical interview, and that clinicians were reluctant to diagnose BPD during their routine intake diagnostic evaluation.

Clinicians, however, do not use semi-structured interviews in their practice, and they also do not tend to diagnose personality disorders (PDs) based on direct questioning, as they typically would when assessing a symptom-based disorder such as depression or anxiety. Rather, clinicians report that they rely on longitudinal observations to diagnose PDs.¹⁸ However, the results from the MIDAS project were inconsistent with clinicians’ reports. When clinicians were presented with the results of the semi-structured interview, they usually would diagnose BPD, even though it was the initial evaluation. If clinicians actually relied on longitudinal observations and considered information based on the direct question approach of research interviews to be irrelevant or invalid, then the results from the semi-structured interview should not have influenced the rate at which they diagnosed BPD. This suggests that the primary issue in diagnosing PDs is not the need for longi­tudinal observation but rather the need for more information, and that there is a role for screening questionnaires.

One potential criticism of studies demonstrating underrecognition of BPD in clinical practice is that patients typically were interviewed when they presented for treatment, when most were depressed or anxious. The possible pathologizing effects of psychiatric state on personality have been known for years.¹⁹ However, a large body of literature examining the treatment, prognostic, familial, and biological correlates of PDs supports the validity of diagnosing PDs in this manner. Moreover, from a clinical perspective, the sooner a clinician is aware of the presence of BPD, the more likely this information can be used for treatment planning.

Who should be screened for BPD?

BPD is underrecognized and underdiagnosed because patients with BPD often also have comorbid mood, anxiety, or substance use disorders.^20,21 The symptoms associated with these disorders are typically the chief concern of patients with undiagnosed BPD who present for treatment. Patients with BPD rarely present for an intake evaluation and state that they are struggling with abandonment fears, chronic feelings of emptiness, or an identity disturbance. If patients identified these problems as their chief concerns, BPD would be easier to recognize.

Although several studies have documented the frequency of BPD in patients with a specific psychiatric diagnosis such as major depressive disorder (MDD) or attention-deficit/hyperactivity disorder,^22-26 the MIDAS project examined the frequency of BPD in patients with various diagnoses and evaluated which disorders were associated with a significantly increased rate of BPD.²⁷ The highest rate of BPD was found in patients with bipolar disorder. Approximately 25% of patients with bipolar II disorder and one-third of those with bipolar I disorder were diagnosed with BPD; these rates were significantly higher than the rate of BPD in patients without these disorders (Table 1²⁷). The rate of BPD was second highest in patients with a principal diagnosis of posttraumatic stress disorder (PTSD) and MDD; however, the rate of BPD in these patients was not significantly elevated compared with patients who did not have these principal diagnoses. Three disorders were associated with a significantly lower rate of BPD: adjustment disorder, dysthymic disorder, and generalized anxiety disorder.

A brief review of screening statistics

Screening tests for most psychiatric disorders are based on multi-item scales in which a total score is computed from a sum of item scores, and a cutoff point is established to determine who does and does not screen positive on the test. However, sensitivity, specificity, and positive and negative predictive values are not invariant properties of a screening test with a continuous score distribution. Rather, the performance statistics of a scale can be altered by changing the threshold score to distinguish cases from non-cases. When the screening threshold is lowered, sensitivity increases and specificity decreases.

For screening, a broad net needs to be cast so that all (or almost all) cases are included. Therefore, the cutoff score should be set low to prioritize the sensitivity of the instrument. A screening scale also should have high negative predictive value so that the clinician can be confident that patients who screen negative on the test do not have the disorder.

Screening questionnaires for BPD

Several questionnaires have been developed to screen for PDs (Table 2^28-35). Some screen for each of the DSM PDs,^28,36-42 and some screen more broadly for the presence or absence of any PD.^29,43,44 The most commonly studied self-report scale for BPD is the McLean Screening Instrument for Borderline Personality Disorder (MSI-BPD),³⁰ a 10-item self-report scale derived from a subset of questions from the BPD module of a semi-structured diagnostic interview.

The initial validation study³⁰ found that the optimal cutoff score was 7, which resulted in a sensitivity of 81% and specificity of 89%. Three studies have evaluated the scale in adolescents and young adults,^45-47 and 3 studies examined the scale in adult outpatients.^48-50 Across all 6 studies, at the optimal cutoff scores determined in each study, the sensitivity of the MSI-BPD ranged from 68% to 94% (mean, 80%) and the specificity ranged from 66% to 80% (mean, 72%).

Problems with screening questionnaires. Although screening scales have been developed for many psychiatric disorders, they have not been widely used in mental health settings. In a previous commentary, I argued that the conceptual justification for using self-report screening scales for single disorders in psychiatric settings is questionable.⁵¹ Another problem with screening scales is their potential misuse as case-finding instruments. In the literature on bipolar disorder screening, several researchers misconstrued a positive screen to indicate caseness.⁵¹ Although this is not a problem with the screening measures or the selection of a cutoff score, caution must be taken to not confuse screening with diagnosis.⁵²

Screening for BPD as part of your diagnostic interview

An alternative approach to using self-administered questionnaires for screening is for clinicians to include questions in their evaluation as part of a psychiatric review of systems. When conducting a diagnostic interview, clinicians typically screen for disorders that are comorbid with the principal diagnosis by asking about the comorbid disorders’ necessary features or “gate criteria.” For example, in a patient with a principal diagnosis of MDD, the clinician would inquire about the presence of panic attacks, excessive worry, or substance use to screen for the presence of panic disorder, generalized anxiety disorder, or a substance use disorder. In contrast, for polythetically defined disorders such as BPD, there is no single gate criterion, because the disorder is diagnosed based on the presence of at least 5 of 9 criteria and no single one of these criteria is required to be present to establish the diagnosis.

As part of the MIDAS project, the psycho­metric properties of the BPD criteria were examined to determine if it was possible to identify 1 or 2 criteria that could serve as gate criteria to screen for the disorder. If the sensitivity of 1 criterion or a combination of 2 BPD criteria was sufficiently high (ie, >90%), then the assessment of this criterion (or these criteria) could be included in a psychiatric review of systems, thus potentially improving the detection of BPD. Researchers hypothesized that affective instability, considered first by Linehan⁵³ and later by other theorists⁵⁴ to be of central importance to the clinical manifestations of BPD, could function as a gate criterion. In the sample of 3,674 psychiatric outpatients who were evaluated with a semi-structured interview, the sensitivity of the affective instability criterion was 92.8%, and the negative predictive value of the criterion was 99%.

Borderline personality disorder (BPD) is associated with impaired psychosocial functioning,^1-4 reduced health-related quality of life,⁵ high utilization of services,^6,7 and excess mortality.^8-10 Although BPD occurs in up to 40% of psychiatric inpatients¹¹ and 10% of outpatients,¹² it is underrecognized.^13-15 Often, patients with BPD do not receive an accurate diagnosis until ≥10 years after initially seeking treatment.¹⁶ The treatment and clinical implications of failing to recognize BPD include overprescribing medication and underutilizing empirically effective psychotherapies.¹⁴

This review summarizes studies of the underdiagnosis of BPD in routine clinical practice, describes which patients should be screened, and reviews alternative approaches to screening.

Underrecognition of BPD

The Rhode Island Methods to Improve Diagnostic Assessment and Services (MIDAS) project is an ongoing clinical research study involving the integration of research assessment methods into routine clinical practice.¹⁷ In an early report from the MIDAS project, BPD diagnoses derived from structured and unstructured clinical interviews were compared between 2 groups of psychiatric outpatients in the same practice.¹⁵ Individuals in the structured interview cohort were 35 times more often diagnosed with BPD than individuals evaluated with an unstructured clinical interview. Importantly, when the information from the structured interview was presented to the clinicians, BPD was more likely to be diagnosed clinically.

Other studies^13,16 also found that the rate of diagnosing BPD was higher when the diagnosis was based on a semi-structured diagnostic interview compared with an unstructured clinical interview, and that clinicians were reluctant to diagnose BPD during their routine intake diagnostic evaluation.

Clinicians, however, do not use semi-structured interviews in their practice, and they also do not tend to diagnose personality disorders (PDs) based on direct questioning, as they typically would when assessing a symptom-based disorder such as depression or anxiety. Rather, clinicians report that they rely on longitudinal observations to diagnose PDs.¹⁸ However, the results from the MIDAS project were inconsistent with clinicians’ reports. When clinicians were presented with the results of the semi-structured interview, they usually would diagnose BPD, even though it was the initial evaluation. If clinicians actually relied on longitudinal observations and considered information based on the direct question approach of research interviews to be irrelevant or invalid, then the results from the semi-structured interview should not have influenced the rate at which they diagnosed BPD. This suggests that the primary issue in diagnosing PDs is not the need for longi­tudinal observation but rather the need for more information, and that there is a role for screening questionnaires.

One potential criticism of studies demonstrating underrecognition of BPD in clinical practice is that patients typically were interviewed when they presented for treatment, when most were depressed or anxious. The possible pathologizing effects of psychiatric state on personality have been known for years.¹⁹ However, a large body of literature examining the treatment, prognostic, familial, and biological correlates of PDs supports the validity of diagnosing PDs in this manner. Moreover, from a clinical perspective, the sooner a clinician is aware of the presence of BPD, the more likely this information can be used for treatment planning.

Who should be screened for BPD?

BPD is underrecognized and underdiagnosed because patients with BPD often also have comorbid mood, anxiety, or substance use disorders.^20,21 The symptoms associated with these disorders are typically the chief concern of patients with undiagnosed BPD who present for treatment. Patients with BPD rarely present for an intake evaluation and state that they are struggling with abandonment fears, chronic feelings of emptiness, or an identity disturbance. If patients identified these problems as their chief concerns, BPD would be easier to recognize.

Although several studies have documented the frequency of BPD in patients with a specific psychiatric diagnosis such as major depressive disorder (MDD) or attention-deficit/hyperactivity disorder,^22-26 the MIDAS project examined the frequency of BPD in patients with various diagnoses and evaluated which disorders were associated with a significantly increased rate of BPD.²⁷ The highest rate of BPD was found in patients with bipolar disorder. Approximately 25% of patients with bipolar II disorder and one-third of those with bipolar I disorder were diagnosed with BPD; these rates were significantly higher than the rate of BPD in patients without these disorders (Table 1²⁷). The rate of BPD was second highest in patients with a principal diagnosis of posttraumatic stress disorder (PTSD) and MDD; however, the rate of BPD in these patients was not significantly elevated compared with patients who did not have these principal diagnoses. Three disorders were associated with a significantly lower rate of BPD: adjustment disorder, dysthymic disorder, and generalized anxiety disorder.

A brief review of screening statistics

Screening tests for most psychiatric disorders are based on multi-item scales in which a total score is computed from a sum of item scores, and a cutoff point is established to determine who does and does not screen positive on the test. However, sensitivity, specificity, and positive and negative predictive values are not invariant properties of a screening test with a continuous score distribution. Rather, the performance statistics of a scale can be altered by changing the threshold score to distinguish cases from non-cases. When the screening threshold is lowered, sensitivity increases and specificity decreases.

For screening, a broad net needs to be cast so that all (or almost all) cases are included. Therefore, the cutoff score should be set low to prioritize the sensitivity of the instrument. A screening scale also should have high negative predictive value so that the clinician can be confident that patients who screen negative on the test do not have the disorder.

Screening questionnaires for BPD

Several questionnaires have been developed to screen for PDs (Table 2^28-35). Some screen for each of the DSM PDs,^28,36-42 and some screen more broadly for the presence or absence of any PD.^29,43,44 The most commonly studied self-report scale for BPD is the McLean Screening Instrument for Borderline Personality Disorder (MSI-BPD),³⁰ a 10-item self-report scale derived from a subset of questions from the BPD module of a semi-structured diagnostic interview.

The initial validation study³⁰ found that the optimal cutoff score was 7, which resulted in a sensitivity of 81% and specificity of 89%. Three studies have evaluated the scale in adolescents and young adults,^45-47 and 3 studies examined the scale in adult outpatients.^48-50 Across all 6 studies, at the optimal cutoff scores determined in each study, the sensitivity of the MSI-BPD ranged from 68% to 94% (mean, 80%) and the specificity ranged from 66% to 80% (mean, 72%).

Problems with screening questionnaires. Although screening scales have been developed for many psychiatric disorders, they have not been widely used in mental health settings. In a previous commentary, I argued that the conceptual justification for using self-report screening scales for single disorders in psychiatric settings is questionable.⁵¹ Another problem with screening scales is their potential misuse as case-finding instruments. In the literature on bipolar disorder screening, several researchers misconstrued a positive screen to indicate caseness.⁵¹ Although this is not a problem with the screening measures or the selection of a cutoff score, caution must be taken to not confuse screening with diagnosis.⁵²

Screening for BPD as part of your diagnostic interview

An alternative approach to using self-administered questionnaires for screening is for clinicians to include questions in their evaluation as part of a psychiatric review of systems. When conducting a diagnostic interview, clinicians typically screen for disorders that are comorbid with the principal diagnosis by asking about the comorbid disorders’ necessary features or “gate criteria.” For example, in a patient with a principal diagnosis of MDD, the clinician would inquire about the presence of panic attacks, excessive worry, or substance use to screen for the presence of panic disorder, generalized anxiety disorder, or a substance use disorder. In contrast, for polythetically defined disorders such as BPD, there is no single gate criterion, because the disorder is diagnosed based on the presence of at least 5 of 9 criteria and no single one of these criteria is required to be present to establish the diagnosis.

As part of the MIDAS project, the psycho­metric properties of the BPD criteria were examined to determine if it was possible to identify 1 or 2 criteria that could serve as gate criteria to screen for the disorder. If the sensitivity of 1 criterion or a combination of 2 BPD criteria was sufficiently high (ie, >90%), then the assessment of this criterion (or these criteria) could be included in a psychiatric review of systems, thus potentially improving the detection of BPD. Researchers hypothesized that affective instability, considered first by Linehan⁵³ and later by other theorists⁵⁴ to be of central importance to the clinical manifestations of BPD, could function as a gate criterion. In the sample of 3,674 psychiatric outpatients who were evaluated with a semi-structured interview, the sensitivity of the affective instability criterion was 92.8%, and the negative predictive value of the criterion was 99%.

CASE A lifelong habit

Ms. B, age 14, has diagnoses of attention-deficit/hyperactive disorder (ADHD) and oppositional defiant disorder, and is taking extended-release (ER) methylphenidate, 36 mg/d. Her mother brings her to the hospital with concerns that Ms. B has been stealing small objects, such as money, toys, and pencils from home, school, and her peers, even though she does not need them and her family can afford to buy them for her. Ms. B’s mother routinely searches her daughter when she leaves the house and when she returns and frequently finds things in Ms. B’s possession that do not belong to her.

The mother reports that Ms. B’s stealing has been a lifelong habit that worsened after Ms. B’s father died in a car accident last year.

Ms. B does not volunteer any information about her stealing. She is admitted to a partial hospitalization program for further evaluation and treatment.

[polldaddy:9837962]

EVALUATION Continued stealing

A week later, Ms. B remains reluctant to talk about her stealing habit. However, once a therapeutic alliance is established, she reveals that she experiences increased anxiety before stealing and feels pleasure during the theft. Her methylphenidate ER dosage is increased to 54 mg/d in an attempt to address poor impulse control and sub­sequent stealing behavior. Her ADHD symptoms are controlled, and she does not exhibit poor impulse control in any situation other than stealing.

However, Ms. B continues to have poor insight and impaired judgment about her behavior. During treatment, Ms. B steals markers from the psychiatrist’s office, which later are found in her bag. When the staff convinces Ms. B to return the markers to the psychiatrist, she denies knowing how they got there. Behavioral interventions, including covert sensitization, systemic desensitization, positive reinforcement, body and bag search, and reminders, occur consistently as part of treatment, but have little effect on her symptoms.

The author’s observations

Risk-taking and novelty-seeking behaviors are common in adolescent patients. Impulsivity, instant reward-seeking behavior, and poor judgment can lead to stealing in this population, but this behavior is not necessarily indicative of kleptomania.

Kleptomania is the recurrent failure to resist impulses to steal objects.² It differs from other forms of stealing in that the objects stolen by a patient with kleptomania are not needed for personal use or for their monetary value. Kleptomania usually begins in early adolescence, is found in about 0.5% of the general population, and is more common among females.³

• The psychoanalytical theory explains kleptomania as an immature defense against unconscious impulses, conflicts, and desires of destruction. By stealing, the individual protects the self from narcissistic injury and disintegration. The frantic search for objects helps to divert self-destructive aggressiveness and allows for the preservation of the self.⁴
• The biological model indicates that individuals with kleptomania have a significant deficit of white matter in inferior frontal regions and poor integrity of the tracts connecting the limbic system to the thalamus and to the prefrontal cortex.⁵ Reward system circuitry (ventral tegmental area–nucleus accumbens–orbital frontal cortex) is likely to be involved in impulse control disorders including kleptomania.⁶

Comorbidity. Kleptomania often is comorbid with substance use disorder (SUD), obsessive-compulsive disorder (OCD), and compulsive shopping, as well as depression, anxiety disorders, bulimia nervosa, and impulse control and conduct disorders.^3,6

Kleptomania shares many characteristics with SUD, including continued engagement in a behavior despite negative consequences and the temporary reduction in urges after the behavior’s completion, followed by a return of the urge to steal. There also is a bidirectional relationship between OCD and kleptomania. Individuals with both disorders frequently engage in excessive and unnecessary rituals even when it is ego-dystonic. First-degree relatives of kleptomania patients have high rates of SUD and OCD.³

Serotonin, dopamine, and opioid pathways play a role in both kleptomania and other behavioral addictions.⁶ Clinicians should be cautious in treating comorbid disorders with stimulants. These agents may help patients with high impulsivity, but lead to disinhibition and worsen impulse control in patients with low impulsivity.⁷

TREATMENT Naltrexone

The psychiatrist discusses pharmacologic options to treat kleptomania with Ms. B and her mother. After considering the risks, benefits, adverse effects, and alternative treatments (including the option of no pharma­cologic treatment), the mother consents and Ms. B assents to treatment with naltrexone, 25 mg/d. Before starting this medication, both the mother and Ms. B receive detailed psychoeducation describing naltrexone’s interactions with opioids. They are told that if Ms. B has a traumatic injury, they should inform the treatment team that she is taking naltrexone, which can acutely precipitate opiate withdrawal.

Before initiating pharmacotherapy, a comprehensive metabolic profile is obtained, and all values are within the normal range. After 1 week, naltrexone is increased to 50 mg/d. The medication is well tolerated, without any adverse effects.

[polldaddy:9837976]

The author’s observations

Behavioral interventions, such as covert sensitization and systemic desensitization, often are used to treat kleptomania.⁸ There are no FDA-approved medications for this condition. Opioid antagonists have been considered for the treatment of kleptomania.⁷

Mu-opioid receptors exist in highest concentrations in presynaptic neurons in the periaqueductal gray region and spinal cord and have high affinity for enkephalins and beta-endorphins. They also are involved in the reward and pleasure pathway. This neurocircuit is implicated in behavioral addiction.⁹

Naltrexone is an antagonist at μ-opioid receptors. It blocks the binding of endogenous and exogenous opioids at the receptors, particularly at the ventral tegmental area. By blocking the μ-receptor, naltrexone inhibits the processing of the reward and pleasure pathway involved in kleptomania. Naltrexone binds to these receptors, preventing the euphoric effects of behavioral addictions.¹⁰ This medication works best in conjunction with behavioral interventions.⁸

Naltrexone is a Schedule II drug. Use of naltrexone to treat kleptomania or other impulse control disorders is an off-label use of the medication. Naltrexone should not be prescribed to patients who are receiving opiates because it can cause acute opiate withdrawal.

Liver function tests should be monitored in all patients taking naltrexone. If liver function levels begin to rise, naltrexone should be discontinued. Naltrexone should be used with caution in patients with pre­existing liver disease.¹¹

OUTCOME Marked improvement

Ms. B’s K-SAS scores are evaluated 2 weeks after starting naltrexone. The results show a marked reduction in the urge to steal and in stealing behavior, and Ms. B’s mother reports no incidents of stealing in the previous week.

Ms. B is maintained on naltrexone, 50 mg/d, for 2 months. On repeated K-SAS scores, her mother rates Ms. B’s symptoms “very much improved” with “occasional” stealing. Ms. B is discharged from the intensive outpatient program.

CASE A lifelong habit

Ms. B, age 14, has diagnoses of attention-deficit/hyperactive disorder (ADHD) and oppositional defiant disorder, and is taking extended-release (ER) methylphenidate, 36 mg/d. Her mother brings her to the hospital with concerns that Ms. B has been stealing small objects, such as money, toys, and pencils from home, school, and her peers, even though she does not need them and her family can afford to buy them for her. Ms. B’s mother routinely searches her daughter when she leaves the house and when she returns and frequently finds things in Ms. B’s possession that do not belong to her.

The mother reports that Ms. B’s stealing has been a lifelong habit that worsened after Ms. B’s father died in a car accident last year.

Ms. B does not volunteer any information about her stealing. She is admitted to a partial hospitalization program for further evaluation and treatment.

[polldaddy:9837962]

EVALUATION Continued stealing

A week later, Ms. B remains reluctant to talk about her stealing habit. However, once a therapeutic alliance is established, she reveals that she experiences increased anxiety before stealing and feels pleasure during the theft. Her methylphenidate ER dosage is increased to 54 mg/d in an attempt to address poor impulse control and sub­sequent stealing behavior. Her ADHD symptoms are controlled, and she does not exhibit poor impulse control in any situation other than stealing.

However, Ms. B continues to have poor insight and impaired judgment about her behavior. During treatment, Ms. B steals markers from the psychiatrist’s office, which later are found in her bag. When the staff convinces Ms. B to return the markers to the psychiatrist, she denies knowing how they got there. Behavioral interventions, including covert sensitization, systemic desensitization, positive reinforcement, body and bag search, and reminders, occur consistently as part of treatment, but have little effect on her symptoms.

The author’s observations

Risk-taking and novelty-seeking behaviors are common in adolescent patients. Impulsivity, instant reward-seeking behavior, and poor judgment can lead to stealing in this population, but this behavior is not necessarily indicative of kleptomania.

Kleptomania is the recurrent failure to resist impulses to steal objects.² It differs from other forms of stealing in that the objects stolen by a patient with kleptomania are not needed for personal use or for their monetary value. Kleptomania usually begins in early adolescence, is found in about 0.5% of the general population, and is more common among females.³

• The psychoanalytical theory explains kleptomania as an immature defense against unconscious impulses, conflicts, and desires of destruction. By stealing, the individual protects the self from narcissistic injury and disintegration. The frantic search for objects helps to divert self-destructive aggressiveness and allows for the preservation of the self.⁴
• The biological model indicates that individuals with kleptomania have a significant deficit of white matter in inferior frontal regions and poor integrity of the tracts connecting the limbic system to the thalamus and to the prefrontal cortex.⁵ Reward system circuitry (ventral tegmental area–nucleus accumbens–orbital frontal cortex) is likely to be involved in impulse control disorders including kleptomania.⁶

Comorbidity. Kleptomania often is comorbid with substance use disorder (SUD), obsessive-compulsive disorder (OCD), and compulsive shopping, as well as depression, anxiety disorders, bulimia nervosa, and impulse control and conduct disorders.^3,6

Kleptomania shares many characteristics with SUD, including continued engagement in a behavior despite negative consequences and the temporary reduction in urges after the behavior’s completion, followed by a return of the urge to steal. There also is a bidirectional relationship between OCD and kleptomania. Individuals with both disorders frequently engage in excessive and unnecessary rituals even when it is ego-dystonic. First-degree relatives of kleptomania patients have high rates of SUD and OCD.³

Serotonin, dopamine, and opioid pathways play a role in both kleptomania and other behavioral addictions.⁶ Clinicians should be cautious in treating comorbid disorders with stimulants. These agents may help patients with high impulsivity, but lead to disinhibition and worsen impulse control in patients with low impulsivity.⁷

TREATMENT Naltrexone

The psychiatrist discusses pharmacologic options to treat kleptomania with Ms. B and her mother. After considering the risks, benefits, adverse effects, and alternative treatments (including the option of no pharma­cologic treatment), the mother consents and Ms. B assents to treatment with naltrexone, 25 mg/d. Before starting this medication, both the mother and Ms. B receive detailed psychoeducation describing naltrexone’s interactions with opioids. They are told that if Ms. B has a traumatic injury, they should inform the treatment team that she is taking naltrexone, which can acutely precipitate opiate withdrawal.

Before initiating pharmacotherapy, a comprehensive metabolic profile is obtained, and all values are within the normal range. After 1 week, naltrexone is increased to 50 mg/d. The medication is well tolerated, without any adverse effects.

[polldaddy:9837976]

The author’s observations

Behavioral interventions, such as covert sensitization and systemic desensitization, often are used to treat kleptomania.⁸ There are no FDA-approved medications for this condition. Opioid antagonists have been considered for the treatment of kleptomania.⁷

Mu-opioid receptors exist in highest concentrations in presynaptic neurons in the periaqueductal gray region and spinal cord and have high affinity for enkephalins and beta-endorphins. They also are involved in the reward and pleasure pathway. This neurocircuit is implicated in behavioral addiction.⁹

Naltrexone is an antagonist at μ-opioid receptors. It blocks the binding of endogenous and exogenous opioids at the receptors, particularly at the ventral tegmental area. By blocking the μ-receptor, naltrexone inhibits the processing of the reward and pleasure pathway involved in kleptomania. Naltrexone binds to these receptors, preventing the euphoric effects of behavioral addictions.¹⁰ This medication works best in conjunction with behavioral interventions.⁸

Naltrexone is a Schedule II drug. Use of naltrexone to treat kleptomania or other impulse control disorders is an off-label use of the medication. Naltrexone should not be prescribed to patients who are receiving opiates because it can cause acute opiate withdrawal.

Liver function tests should be monitored in all patients taking naltrexone. If liver function levels begin to rise, naltrexone should be discontinued. Naltrexone should be used with caution in patients with pre­existing liver disease.¹¹

OUTCOME Marked improvement

Ms. B’s K-SAS scores are evaluated 2 weeks after starting naltrexone. The results show a marked reduction in the urge to steal and in stealing behavior, and Ms. B’s mother reports no incidents of stealing in the previous week.

Ms. B is maintained on naltrexone, 50 mg/d, for 2 months. On repeated K-SAS scores, her mother rates Ms. B’s symptoms “very much improved” with “occasional” stealing. Ms. B is discharged from the intensive outpatient program.

CASE A lifelong habit

Ms. B, age 14, has diagnoses of attention-deficit/hyperactive disorder (ADHD) and oppositional defiant disorder, and is taking extended-release (ER) methylphenidate, 36 mg/d. Her mother brings her to the hospital with concerns that Ms. B has been stealing small objects, such as money, toys, and pencils from home, school, and her peers, even though she does not need them and her family can afford to buy them for her. Ms. B’s mother routinely searches her daughter when she leaves the house and when she returns and frequently finds things in Ms. B’s possession that do not belong to her.

The mother reports that Ms. B’s stealing has been a lifelong habit that worsened after Ms. B’s father died in a car accident last year.

Ms. B does not volunteer any information about her stealing. She is admitted to a partial hospitalization program for further evaluation and treatment.

[polldaddy:9837962]

EVALUATION Continued stealing

A week later, Ms. B remains reluctant to talk about her stealing habit. However, once a therapeutic alliance is established, she reveals that she experiences increased anxiety before stealing and feels pleasure during the theft. Her methylphenidate ER dosage is increased to 54 mg/d in an attempt to address poor impulse control and sub­sequent stealing behavior. Her ADHD symptoms are controlled, and she does not exhibit poor impulse control in any situation other than stealing.

However, Ms. B continues to have poor insight and impaired judgment about her behavior. During treatment, Ms. B steals markers from the psychiatrist’s office, which later are found in her bag. When the staff convinces Ms. B to return the markers to the psychiatrist, she denies knowing how they got there. Behavioral interventions, including covert sensitization, systemic desensitization, positive reinforcement, body and bag search, and reminders, occur consistently as part of treatment, but have little effect on her symptoms.

The author’s observations

Risk-taking and novelty-seeking behaviors are common in adolescent patients. Impulsivity, instant reward-seeking behavior, and poor judgment can lead to stealing in this population, but this behavior is not necessarily indicative of kleptomania.

Kleptomania is the recurrent failure to resist impulses to steal objects.² It differs from other forms of stealing in that the objects stolen by a patient with kleptomania are not needed for personal use or for their monetary value. Kleptomania usually begins in early adolescence, is found in about 0.5% of the general population, and is more common among females.³

• The psychoanalytical theory explains kleptomania as an immature defense against unconscious impulses, conflicts, and desires of destruction. By stealing, the individual protects the self from narcissistic injury and disintegration. The frantic search for objects helps to divert self-destructive aggressiveness and allows for the preservation of the self.⁴
• The biological model indicates that individuals with kleptomania have a significant deficit of white matter in inferior frontal regions and poor integrity of the tracts connecting the limbic system to the thalamus and to the prefrontal cortex.⁵ Reward system circuitry (ventral tegmental area–nucleus accumbens–orbital frontal cortex) is likely to be involved in impulse control disorders including kleptomania.⁶

Comorbidity. Kleptomania often is comorbid with substance use disorder (SUD), obsessive-compulsive disorder (OCD), and compulsive shopping, as well as depression, anxiety disorders, bulimia nervosa, and impulse control and conduct disorders.^3,6

Kleptomania shares many characteristics with SUD, including continued engagement in a behavior despite negative consequences and the temporary reduction in urges after the behavior’s completion, followed by a return of the urge to steal. There also is a bidirectional relationship between OCD and kleptomania. Individuals with both disorders frequently engage in excessive and unnecessary rituals even when it is ego-dystonic. First-degree relatives of kleptomania patients have high rates of SUD and OCD.³

Serotonin, dopamine, and opioid pathways play a role in both kleptomania and other behavioral addictions.⁶ Clinicians should be cautious in treating comorbid disorders with stimulants. These agents may help patients with high impulsivity, but lead to disinhibition and worsen impulse control in patients with low impulsivity.⁷

TREATMENT Naltrexone

The psychiatrist discusses pharmacologic options to treat kleptomania with Ms. B and her mother. After considering the risks, benefits, adverse effects, and alternative treatments (including the option of no pharma­cologic treatment), the mother consents and Ms. B assents to treatment with naltrexone, 25 mg/d. Before starting this medication, both the mother and Ms. B receive detailed psychoeducation describing naltrexone’s interactions with opioids. They are told that if Ms. B has a traumatic injury, they should inform the treatment team that she is taking naltrexone, which can acutely precipitate opiate withdrawal.

Before initiating pharmacotherapy, a comprehensive metabolic profile is obtained, and all values are within the normal range. After 1 week, naltrexone is increased to 50 mg/d. The medication is well tolerated, without any adverse effects.

[polldaddy:9837976]

The author’s observations

Behavioral interventions, such as covert sensitization and systemic desensitization, often are used to treat kleptomania.⁸ There are no FDA-approved medications for this condition. Opioid antagonists have been considered for the treatment of kleptomania.⁷

Mu-opioid receptors exist in highest concentrations in presynaptic neurons in the periaqueductal gray region and spinal cord and have high affinity for enkephalins and beta-endorphins. They also are involved in the reward and pleasure pathway. This neurocircuit is implicated in behavioral addiction.⁹

Naltrexone is an antagonist at μ-opioid receptors. It blocks the binding of endogenous and exogenous opioids at the receptors, particularly at the ventral tegmental area. By blocking the μ-receptor, naltrexone inhibits the processing of the reward and pleasure pathway involved in kleptomania. Naltrexone binds to these receptors, preventing the euphoric effects of behavioral addictions.¹⁰ This medication works best in conjunction with behavioral interventions.⁸

Naltrexone is a Schedule II drug. Use of naltrexone to treat kleptomania or other impulse control disorders is an off-label use of the medication. Naltrexone should not be prescribed to patients who are receiving opiates because it can cause acute opiate withdrawal.

Liver function tests should be monitored in all patients taking naltrexone. If liver function levels begin to rise, naltrexone should be discontinued. Naltrexone should be used with caution in patients with pre­existing liver disease.¹¹

OUTCOME Marked improvement

Ms. B’s K-SAS scores are evaluated 2 weeks after starting naltrexone. The results show a marked reduction in the urge to steal and in stealing behavior, and Ms. B’s mother reports no incidents of stealing in the previous week.

Ms. B is maintained on naltrexone, 50 mg/d, for 2 months. On repeated K-SAS scores, her mother rates Ms. B’s symptoms “very much improved” with “occasional” stealing. Ms. B is discharged from the intensive outpatient program.

WASHINGTON – A view of borderline personality disorder as neurobiological in nature can help clinicians extend their patience and empathy to these notoriously difficult-to-treat patients, according to an expert.

“Unfortunately, there are those who ... are just too frustrated by” [patients with borderline personality disorder], said Carmen V. Pinto, MD, an Elizabethtown, Ky.–based psychiatrist who specializes in treating patients with the disorder.

The diagnosis occurs in up to 2% of the population and is twice as common in women. About three-quarters of borderline personality disorder patients will attempt suicide at least once, and up to 1 in 10 complete suicide, said Dr. Pinto, assistant clinical professor of psychiatry at the University of Louisville (Ky.).

“There is an art to dealing with patients who are impulsive, and sometimes dangerous and scary,” Dr. Pinto said at Summit in Neurology & Psychiatry, held by Global Academy for Medical Education.

He emphasized the effect of unstable interpersonal relationships combined with frontolimbic brain abnormalities on the lives of patients with borderline personality disorder. In some cases, borderline personality disorder patients experienced traumatic events such as sexual abuse that was personal and ongoing – and occurred while the personality was being formed.

“These are normal people who have been exposed to abnormal stress,” Dr. Pinto said. “So you have to be careful, and see them not as victims but as survivors still suffering.”

Citing several lines of study into the neurobiochemical mechanisms of action in the disorder, Dr. Pinto discussed the role of disruption to the brain’s cortical-limbic circuit that serves as the brain’s basic stress response. In this population, an overactive amygdala and hypofunctioning frontal cortex continually signal threats even when none exist – exciting the sympathetic nervous system – as well as the endocrine and immune systems.

“The circuit gets overwhelmed, either because there really is too much to deal with, or there was poor functioning to start with, so the brain is going off like a pinball machine,” Dr. Pinto said. “If [the patients perceive] even the slightest offense, their limbic system lights up, and they have trouble turning it off, which is why it can be so difficult to deal with these folks in therapy.”

He explained the borderline personality patient’s typical negative valence as the result of this hyper-threat detection, often rooted in experiences in which people who professed to care for them acted contrary to their words, as in cases of incest. “They learn they can’t trust what is said, so they rely on nonverbal cues,” Dr. Pinto said. “They aren’t listening to what is said to them.”

Dr. Pinto cited a study of how this patient population had trouble distinguishing neutral faces from faces expressing anger or boredom, resulting in their believing that most people they encounter are unhappy with them in some way, causing them to retreat or have stressful relationships with others.

“Therapeutic neutrality is not the best way to approach this person, because they read it as ‘you are mad at me’ or ‘you’re bored with me’ or ‘you don’t like me,’ ” Dr. Pinto said, noting that he likes to reassure patients that they are doing the best they can with what they have. However, he warned against how often, in these patients’ quest to feel loved and accepted, they might ask for hugs or other contact. Rather than panic, use the opportunity to help the patient practice having healthy boundaries by explaining that not hugging them is designed to protect them, Dr. Pinto said.

Among the DSM-5 criteria for diagnosing this disorder is that the patient has an “enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture.” Because there are no imaging or laboratory tests to confirm a deviant inner experience, the clinician must turn to the patient for assessment while quelling the impulse to assign meanings to action and insight.

“You really have to be quiet and listen. They are the expert with their inner experience, and you have to let them tell you what that is,” he said, noting that the distortion of how they view themselves in relation to others is painful and pervasive, crossing all areas of their lives.

Because relationships are so difficult for these patients to develop, Dr. Pinto urged keeping in mind that it is possible they have no other therapeutic relationship in their lives. “That is a scary responsibility, to think they have no one else to talk to but you,” he said. This underscores the need for clinicians to protect themselves, too. “If I don’t feel safe, I can’t do a good job for them – and I tell them that,” Dr. Pinto said.

Global Academy and this news organization are owned by the same company. Dr. Pinto had no relevant disclosures, although he said he is a paid speaker for Otsuka, Lundbeck, Janssen, and other pharmaceutical companies.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

WASHINGTON – A view of borderline personality disorder as neurobiological in nature can help clinicians extend their patience and empathy to these notoriously difficult-to-treat patients, according to an expert.

“Unfortunately, there are those who ... are just too frustrated by” [patients with borderline personality disorder], said Carmen V. Pinto, MD, an Elizabethtown, Ky.–based psychiatrist who specializes in treating patients with the disorder.

The diagnosis occurs in up to 2% of the population and is twice as common in women. About three-quarters of borderline personality disorder patients will attempt suicide at least once, and up to 1 in 10 complete suicide, said Dr. Pinto, assistant clinical professor of psychiatry at the University of Louisville (Ky.).

“There is an art to dealing with patients who are impulsive, and sometimes dangerous and scary,” Dr. Pinto said at Summit in Neurology & Psychiatry, held by Global Academy for Medical Education.

He emphasized the effect of unstable interpersonal relationships combined with frontolimbic brain abnormalities on the lives of patients with borderline personality disorder. In some cases, borderline personality disorder patients experienced traumatic events such as sexual abuse that was personal and ongoing – and occurred while the personality was being formed.

“These are normal people who have been exposed to abnormal stress,” Dr. Pinto said. “So you have to be careful, and see them not as victims but as survivors still suffering.”

Citing several lines of study into the neurobiochemical mechanisms of action in the disorder, Dr. Pinto discussed the role of disruption to the brain’s cortical-limbic circuit that serves as the brain’s basic stress response. In this population, an overactive amygdala and hypofunctioning frontal cortex continually signal threats even when none exist – exciting the sympathetic nervous system – as well as the endocrine and immune systems.

“The circuit gets overwhelmed, either because there really is too much to deal with, or there was poor functioning to start with, so the brain is going off like a pinball machine,” Dr. Pinto said. “If [the patients perceive] even the slightest offense, their limbic system lights up, and they have trouble turning it off, which is why it can be so difficult to deal with these folks in therapy.”

He explained the borderline personality patient’s typical negative valence as the result of this hyper-threat detection, often rooted in experiences in which people who professed to care for them acted contrary to their words, as in cases of incest. “They learn they can’t trust what is said, so they rely on nonverbal cues,” Dr. Pinto said. “They aren’t listening to what is said to them.”

Dr. Pinto cited a study of how this patient population had trouble distinguishing neutral faces from faces expressing anger or boredom, resulting in their believing that most people they encounter are unhappy with them in some way, causing them to retreat or have stressful relationships with others.

“Therapeutic neutrality is not the best way to approach this person, because they read it as ‘you are mad at me’ or ‘you’re bored with me’ or ‘you don’t like me,’ ” Dr. Pinto said, noting that he likes to reassure patients that they are doing the best they can with what they have. However, he warned against how often, in these patients’ quest to feel loved and accepted, they might ask for hugs or other contact. Rather than panic, use the opportunity to help the patient practice having healthy boundaries by explaining that not hugging them is designed to protect them, Dr. Pinto said.

Among the DSM-5 criteria for diagnosing this disorder is that the patient has an “enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture.” Because there are no imaging or laboratory tests to confirm a deviant inner experience, the clinician must turn to the patient for assessment while quelling the impulse to assign meanings to action and insight.

“You really have to be quiet and listen. They are the expert with their inner experience, and you have to let them tell you what that is,” he said, noting that the distortion of how they view themselves in relation to others is painful and pervasive, crossing all areas of their lives.

Because relationships are so difficult for these patients to develop, Dr. Pinto urged keeping in mind that it is possible they have no other therapeutic relationship in their lives. “That is a scary responsibility, to think they have no one else to talk to but you,” he said. This underscores the need for clinicians to protect themselves, too. “If I don’t feel safe, I can’t do a good job for them – and I tell them that,” Dr. Pinto said.

Global Academy and this news organization are owned by the same company. Dr. Pinto had no relevant disclosures, although he said he is a paid speaker for Otsuka, Lundbeck, Janssen, and other pharmaceutical companies.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

WASHINGTON – A view of borderline personality disorder as neurobiological in nature can help clinicians extend their patience and empathy to these notoriously difficult-to-treat patients, according to an expert.

“Unfortunately, there are those who ... are just too frustrated by” [patients with borderline personality disorder], said Carmen V. Pinto, MD, an Elizabethtown, Ky.–based psychiatrist who specializes in treating patients with the disorder.

The diagnosis occurs in up to 2% of the population and is twice as common in women. About three-quarters of borderline personality disorder patients will attempt suicide at least once, and up to 1 in 10 complete suicide, said Dr. Pinto, assistant clinical professor of psychiatry at the University of Louisville (Ky.).

“There is an art to dealing with patients who are impulsive, and sometimes dangerous and scary,” Dr. Pinto said at Summit in Neurology & Psychiatry, held by Global Academy for Medical Education.

He emphasized the effect of unstable interpersonal relationships combined with frontolimbic brain abnormalities on the lives of patients with borderline personality disorder. In some cases, borderline personality disorder patients experienced traumatic events such as sexual abuse that was personal and ongoing – and occurred while the personality was being formed.

“These are normal people who have been exposed to abnormal stress,” Dr. Pinto said. “So you have to be careful, and see them not as victims but as survivors still suffering.”

Citing several lines of study into the neurobiochemical mechanisms of action in the disorder, Dr. Pinto discussed the role of disruption to the brain’s cortical-limbic circuit that serves as the brain’s basic stress response. In this population, an overactive amygdala and hypofunctioning frontal cortex continually signal threats even when none exist – exciting the sympathetic nervous system – as well as the endocrine and immune systems.

“The circuit gets overwhelmed, either because there really is too much to deal with, or there was poor functioning to start with, so the brain is going off like a pinball machine,” Dr. Pinto said. “If [the patients perceive] even the slightest offense, their limbic system lights up, and they have trouble turning it off, which is why it can be so difficult to deal with these folks in therapy.”

He explained the borderline personality patient’s typical negative valence as the result of this hyper-threat detection, often rooted in experiences in which people who professed to care for them acted contrary to their words, as in cases of incest. “They learn they can’t trust what is said, so they rely on nonverbal cues,” Dr. Pinto said. “They aren’t listening to what is said to them.”

Dr. Pinto cited a study of how this patient population had trouble distinguishing neutral faces from faces expressing anger or boredom, resulting in their believing that most people they encounter are unhappy with them in some way, causing them to retreat or have stressful relationships with others.

“Therapeutic neutrality is not the best way to approach this person, because they read it as ‘you are mad at me’ or ‘you’re bored with me’ or ‘you don’t like me,’ ” Dr. Pinto said, noting that he likes to reassure patients that they are doing the best they can with what they have. However, he warned against how often, in these patients’ quest to feel loved and accepted, they might ask for hugs or other contact. Rather than panic, use the opportunity to help the patient practice having healthy boundaries by explaining that not hugging them is designed to protect them, Dr. Pinto said.

Among the DSM-5 criteria for diagnosing this disorder is that the patient has an “enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture.” Because there are no imaging or laboratory tests to confirm a deviant inner experience, the clinician must turn to the patient for assessment while quelling the impulse to assign meanings to action and insight.

“You really have to be quiet and listen. They are the expert with their inner experience, and you have to let them tell you what that is,” he said, noting that the distortion of how they view themselves in relation to others is painful and pervasive, crossing all areas of their lives.

Because relationships are so difficult for these patients to develop, Dr. Pinto urged keeping in mind that it is possible they have no other therapeutic relationship in their lives. “That is a scary responsibility, to think they have no one else to talk to but you,” he said. This underscores the need for clinicians to protect themselves, too. “If I don’t feel safe, I can’t do a good job for them – and I tell them that,” Dr. Pinto said.

Global Academy and this news organization are owned by the same company. Dr. Pinto had no relevant disclosures, although he said he is a paid speaker for Otsuka, Lundbeck, Janssen, and other pharmaceutical companies.

wmcknight@frontlinemedcom.com

On Twitter @whitneymcknight

Current Psychiatry and the American Academy of Clinical Psychiatrists welcomed more than 500 psychiatric practitioners from across the United States and abroad to this annual conference, which was headed by Meeting Co-chairs Richard Balon, MD, and Donald W. Black, MD, March 30 to April 1, 2017, at the Marriott Chicago Magnificent Mile in Chicago, Illinois. Attendees earned as many as 18 AMA PRA Category 1 Credits™. We welcome you to join us at Psychiatry Update Encore in Las Vegas, December 10 to 12, 2017 or next year in Chicago, March 22 to 24, 2018.

View summaries from the event on the following pages.

Make Way for Possibilities of an Adjunctive Treatment for Major Depressive Disorder

In an industry-sponsored symposium, Dr. Mattingly reported that in the STAR-D study, approximately one-half of patients with major depressive disorder (MDD) did not experience adequate response to an initial selective serotonin reuptake inhibitor and 3 of 4 of those non-responding patients did not achieve full response with a second antidepressant, which prompts consideration of an adjunctive agent. Brexpiprazole (Rexulti) is a partial agonist for serotonin, dopamine, and noradrenergic systems. In pivotal trials as an adjunctive treatment in MDD, brexpiprazole, 2 mg/d, resulted in a statistically significant decrease in Montgomery-Åsburg Depression Rating Scale scores compared with placebo. Most common adverse reactions observed in ≥5% of patients and at least twice the rate of placebo included akathisia and weight increase.

Essentials of Malingering Assessment

Malingering is intentional lying with an external incentive, such as avoiding work or obtaining drugs. Dr. Mossman gave 2 examples of malingered posttraumatic stress disorder and psychosis. Although lying cannot be detected by careful examination of facial expressions or gestures, a detailed evaluation can reveal malingering. An individual who is malingering psychosis may describe symptoms, such as “I talk to voices all the time,” but clinicians never observe such behavior. Signs of malingering include using “textbook” terms for symptoms; inconsistencies in their history or symptoms; sudden onset of delusions; exaggerating; and being unpleasant, dishonest, or demanding.

Beyond Efficacy and Effectiveness: Neurotoxicity vs Neuroprotection are the REAL Differences Between Typical and Atypical Antipsychotics

Dr. Nasrallah discussed the difference between typical vs atypical antipsychotics—the former is neurotoxic, the latter is neuroprotective. Because patients with schizophrenia experience a loss of brain volume and cerebral grey matter and increased lateral ventricle volume, consider atypical antipsychotics for their neuroprotective properties.

In several studies typical antipsychotics, such as haloperidol, have been found to be neurotoxic, causing apoptosis and decreased cell viability. Atypical antipsychotics may be beneficial for patients with schizophrenia because they:

• stimulate production of new brain cells and increase neurotropic factors
• reverse PCP-induced changes in gene expression and loss of dendritic spines in the frontal cortex
• are neuroprotective against ischemic stroke damage
• prevent oligodendrocyte damage caused by interferon gamma-stimulated microglia.

Medicolegal Hazards in the Information Age: Malpractice and More

Dr. Mossman began by answering the question, “What should I do if a patient ‘friended’ me on Facebook?” Such online relationships can blur boundaries or risk breaching confidentiality, therefore medical organizations recommend ignoring a friend request. Telemedicine via Skype is cost effective and enhances outreach to patients in rural areas or who cannot travel to the office, but online clinical encounters lack multidimensional aspects of the interpersonal encounter and might not be HIPAA compliant. E-mail carries some of the same concerns, such as confidentially of personal information, although the practice—when employed appropriately—is supported by some medical associations, including the American Psychiatric Association.

Treatment-Resistance and Suicidality in Schizophrenia: 2 Major Management Challenges

Patients can seem treatment-resistant because of inadequate antipsychotic dosing, smoking, substance-induced relapse, nonadherence, or a general medical condition. Dr. Nasrallah discussed how to recognize true treatment-resistant schizophrenia and rule of spurious treatment resistance. If your patient is truly treatment-resistant, what do you do when everything else fails?

Risk factors for suicide include male sex, depressed mood, substance use, and social isolation. Clozapine, the only drug FDA-approved for refractory schizophrenia and suicidality, is underutilized for such patients. Dr. Nasrallah also presented evidence for the use of adjunctive modalities, such as lamotrigine, steroids, omega-3 fatty acids, NSAIDs, antidepressants, glutamatergic agents, and rTMS, as well as psychotherapy.

Luncheon Symposium

Depression, Its impact, and the Importance of Recognition and Treatment

Major depressive disorder (MDD) is the most commonly diagnosed condition, second to cardiovascular disease. Dr. Draud recommended using a wellness screen such as the WHO-5 (World Health Organization, 5 item well-being index) in addition to a depression screening tool such as the PHQ-9. He emphasized that the goal of treatment should not be merely remission—but remission without residual symptoms. Cognitive impairment is the most common residual symptom. Patients with residual symptoms relapse earlier (5.5 times faster) and at a greater rate than patients without residual symptoms (76% vs 25%, respectively). Continue treatment and monitoring even after symptoms appear to subside. Recommended treatment is multi-modal and should include cognitive therapy and exercise.

New and Old Treatments for Opioid Abuse and Dependence

Each day more than 1,000 people are treated in emergency departments for improper use of prescription opioids. But is naloxone saving lives or is overdose reversal nothing more than CPR? Dr. Gold spoke about the need for psychiatric assessment after a patient has been revived. Historically, treatment has stopped at abstinence or overdose treatment, but patients need ongoing treatment. Family therapy, vocational assistance, and psychotherapy are essential.

Dr. Gold reviewed established and newer treatments, including naloxone and naltrexone. Methadone and buprenorphine-naloxone can be effective for adherent patients who abuse only one drug. Naltrexone gives patients time to get their lives on track. Probuphine has comparable efficacy with buprenorphine-naloxone and methadone.

Impact of a Personality Disorder in Management of Comorbid Disorder

Personality disorder (PD) indicates patterns of long-term functioning and are not limited to episodes of illness. Abnormal personality traits are common among the general population, but are not considered a personality disorder unless they are inflexible, maladaptive, persisting, and cause distress either for the patient or the family. There are few cases of “pure” PDs without a comorbid psychiatric disorder. Personality disorders are not as stable as once understood; they wax and wane in response to stressors or depressed mood or anxiety. When a PD is comorbid with another disorder, patients are less likely to respond to medication and to experience remission from the comorbid psychiatric disorder. 

Evaluation and Treatment of Patients Who Abuse Methamphetamine or Cocaine

There are no FDA-approved medications or advancement in treatment for cocaine overdose—primary treatment is still ice baths. When assessing cocaine use, consider the route of ingestion and duration of use, which influence severity. Stimulants, whether methamphetamine or cocaine, cause changes in dopamine that are difficult to reverse. Substitute stimulants, such as modafinil, or vaccines have been proposed for cocaine abuse, but the evidence is not robust. Methamphetamine produces a schizophrenia-like illness, but antipsychotics are not effective. Naltrexone and bupropion showed some efficacy but was not statistically significant. There are no effective treatments for overdose or relapse prevention other than traditional group and residential treatment approaches.

Risks in Using Cannabis
Kevin Hill, MD, MHS, McLean Hospital

Although only 9% of Cannabis users become dependent, Dr. Hill recommended talking to all patients who use Cannabis about the risks, such as problems with work, school, and relationships. When treating patients with Cannabis use disorder, explore reasons that the individual would want to stop using Cannabis, take a careful history, and most importantly, build a good therapeutic alliance.

The most robust data for medical Cannabis is for chronic pain, neuropathic pain, and spasticity associated with multiple sclerosis; however, there are more than 70 indications among the 28 states that allow its use. Dr. Hill suggests having a written policy, engage in conversation about why the patient wants medical Cannabis, be open to evaluating such a patient, and consider treating the patient’s symptoms with traditional modalities.

To diagnose premenstrual dysphoric disorder, Dr. Freeman recommends asking your patient to document and rate daily moods using a mobile app or calendar. In perimenopause, the risk of depression increases because estrogen has antidepressant effects. Although, there are no guidelines for treating depression in women in perimenopause, consider serotonergic antidepressants, supplements such as omega-3 fatty acids, isoflavones, and black cohosh, and sleep aids for patients with insomnia—a common feature of menopause.

ADHD, Bipolar Disorder, and Depression in Children

Attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BD) may share an underlying biological etiology, Dr. Strawn explained. Shared risk factors include in utero events, dietary factors, and genetics. Differentiating ADHD from BD depends on the developmental stage of the patient. Symptoms overlap, which could lead to overdiagnosis of ADHD in youths with BD.

Dr. Strawn discussed how children with depression might display mood lability and irritability, rather than verbalizing feelings because they do not use language effectively until age 7. Children may have somatic symptoms early and irritability might decrease into adolescence. Anxiety disorder in children emerges early—usually as a phobia—around age 12 to 14, with an increase in onset of depressive disorders. Dr. Strawn reviewed screening tools to diagnose and track anxiety symptoms, as well as the pros and cons of pharmacological treatments.

Psychotic symptoms could be common in older adults; therefore it is important to evaluate whether these symptoms cause emotional suffering or impairment in daily function. Dr. Grossberg recommended that when treating psychotic disorders in geriatric patients to first evaluate and treat underlying medical problems and identify offending medications or environmental or psychosocial triggers, then consider psychosocial or environmental interventions. Consider antipsychotics for patients who are experiencing severe emotional distress or those who pose a high safety risk. If antipsychotics are necessary, pick an agent based on side effects, “start low, go slow,” and discuss the risks and benefits with the family.

Role of Psychiatrists in Long-term Care Facilities

In his presentation on the role of psychiatrists in long-term care facilities, Dr. Grossberg described common disorders including the behavioral and psychiatric symptoms of dementia, as well as risk for depression. Overprescribing is common in long-term care facilities; therefore when considering a patient’s medication regimen, often less is more. Dr. Grossberg also discussed common undertreated or undercorrected physical health problems, including hearing or vision deficits, obstructive sleep apnea, and malnutrition.

Fatigue

Fatigue experienced by patients with chronic fatigue syndrome is unrelenting, is not the result of ongoing exertion, and is unrelieved by rest. When approaching a patient with extreme fatigue, start with a thorough evaluation in collaboration with a primary care physician, Dr. Thompson said. Establish a rapport with the patient, limit iatrogenic harm, and treat chronic fatigue as you would any chronic condition. Rintatolimod and valganciclovir have showed some evidence of benefit, and graded exercise therapy has shown success.

Current Psychiatry and the American Academy of Clinical Psychiatrists welcomed more than 500 psychiatric practitioners from across the United States and abroad to this annual conference, which was headed by Meeting Co-chairs Richard Balon, MD, and Donald W. Black, MD, March 30 to April 1, 2017, at the Marriott Chicago Magnificent Mile in Chicago, Illinois. Attendees earned as many as 18 AMA PRA Category 1 Credits™. We welcome you to join us at Psychiatry Update Encore in Las Vegas, December 10 to 12, 2017 or next year in Chicago, March 22 to 24, 2018.

View summaries from the event on the following pages.

Make Way for Possibilities of an Adjunctive Treatment for Major Depressive Disorder

In an industry-sponsored symposium, Dr. Mattingly reported that in the STAR-D study, approximately one-half of patients with major depressive disorder (MDD) did not experience adequate response to an initial selective serotonin reuptake inhibitor and 3 of 4 of those non-responding patients did not achieve full response with a second antidepressant, which prompts consideration of an adjunctive agent. Brexpiprazole (Rexulti) is a partial agonist for serotonin, dopamine, and noradrenergic systems. In pivotal trials as an adjunctive treatment in MDD, brexpiprazole, 2 mg/d, resulted in a statistically significant decrease in Montgomery-Åsburg Depression Rating Scale scores compared with placebo. Most common adverse reactions observed in ≥5% of patients and at least twice the rate of placebo included akathisia and weight increase.

Essentials of Malingering Assessment

Malingering is intentional lying with an external incentive, such as avoiding work or obtaining drugs. Dr. Mossman gave 2 examples of malingered posttraumatic stress disorder and psychosis. Although lying cannot be detected by careful examination of facial expressions or gestures, a detailed evaluation can reveal malingering. An individual who is malingering psychosis may describe symptoms, such as “I talk to voices all the time,” but clinicians never observe such behavior. Signs of malingering include using “textbook” terms for symptoms; inconsistencies in their history or symptoms; sudden onset of delusions; exaggerating; and being unpleasant, dishonest, or demanding.

Beyond Efficacy and Effectiveness: Neurotoxicity vs Neuroprotection are the REAL Differences Between Typical and Atypical Antipsychotics

Dr. Nasrallah discussed the difference between typical vs atypical antipsychotics—the former is neurotoxic, the latter is neuroprotective. Because patients with schizophrenia experience a loss of brain volume and cerebral grey matter and increased lateral ventricle volume, consider atypical antipsychotics for their neuroprotective properties.

In several studies typical antipsychotics, such as haloperidol, have been found to be neurotoxic, causing apoptosis and decreased cell viability. Atypical antipsychotics may be beneficial for patients with schizophrenia because they:

• stimulate production of new brain cells and increase neurotropic factors
• reverse PCP-induced changes in gene expression and loss of dendritic spines in the frontal cortex
• are neuroprotective against ischemic stroke damage
• prevent oligodendrocyte damage caused by interferon gamma-stimulated microglia.

Medicolegal Hazards in the Information Age: Malpractice and More

Dr. Mossman began by answering the question, “What should I do if a patient ‘friended’ me on Facebook?” Such online relationships can blur boundaries or risk breaching confidentiality, therefore medical organizations recommend ignoring a friend request. Telemedicine via Skype is cost effective and enhances outreach to patients in rural areas or who cannot travel to the office, but online clinical encounters lack multidimensional aspects of the interpersonal encounter and might not be HIPAA compliant. E-mail carries some of the same concerns, such as confidentially of personal information, although the practice—when employed appropriately—is supported by some medical associations, including the American Psychiatric Association.

Treatment-Resistance and Suicidality in Schizophrenia: 2 Major Management Challenges

Patients can seem treatment-resistant because of inadequate antipsychotic dosing, smoking, substance-induced relapse, nonadherence, or a general medical condition. Dr. Nasrallah discussed how to recognize true treatment-resistant schizophrenia and rule of spurious treatment resistance. If your patient is truly treatment-resistant, what do you do when everything else fails?

Risk factors for suicide include male sex, depressed mood, substance use, and social isolation. Clozapine, the only drug FDA-approved for refractory schizophrenia and suicidality, is underutilized for such patients. Dr. Nasrallah also presented evidence for the use of adjunctive modalities, such as lamotrigine, steroids, omega-3 fatty acids, NSAIDs, antidepressants, glutamatergic agents, and rTMS, as well as psychotherapy.

Luncheon Symposium

Depression, Its impact, and the Importance of Recognition and Treatment

Major depressive disorder (MDD) is the most commonly diagnosed condition, second to cardiovascular disease. Dr. Draud recommended using a wellness screen such as the WHO-5 (World Health Organization, 5 item well-being index) in addition to a depression screening tool such as the PHQ-9. He emphasized that the goal of treatment should not be merely remission—but remission without residual symptoms. Cognitive impairment is the most common residual symptom. Patients with residual symptoms relapse earlier (5.5 times faster) and at a greater rate than patients without residual symptoms (76% vs 25%, respectively). Continue treatment and monitoring even after symptoms appear to subside. Recommended treatment is multi-modal and should include cognitive therapy and exercise.

New and Old Treatments for Opioid Abuse and Dependence

Each day more than 1,000 people are treated in emergency departments for improper use of prescription opioids. But is naloxone saving lives or is overdose reversal nothing more than CPR? Dr. Gold spoke about the need for psychiatric assessment after a patient has been revived. Historically, treatment has stopped at abstinence or overdose treatment, but patients need ongoing treatment. Family therapy, vocational assistance, and psychotherapy are essential.

Dr. Gold reviewed established and newer treatments, including naloxone and naltrexone. Methadone and buprenorphine-naloxone can be effective for adherent patients who abuse only one drug. Naltrexone gives patients time to get their lives on track. Probuphine has comparable efficacy with buprenorphine-naloxone and methadone.

Impact of a Personality Disorder in Management of Comorbid Disorder

Personality disorder (PD) indicates patterns of long-term functioning and are not limited to episodes of illness. Abnormal personality traits are common among the general population, but are not considered a personality disorder unless they are inflexible, maladaptive, persisting, and cause distress either for the patient or the family. There are few cases of “pure” PDs without a comorbid psychiatric disorder. Personality disorders are not as stable as once understood; they wax and wane in response to stressors or depressed mood or anxiety. When a PD is comorbid with another disorder, patients are less likely to respond to medication and to experience remission from the comorbid psychiatric disorder. 

Evaluation and Treatment of Patients Who Abuse Methamphetamine or Cocaine

There are no FDA-approved medications or advancement in treatment for cocaine overdose—primary treatment is still ice baths. When assessing cocaine use, consider the route of ingestion and duration of use, which influence severity. Stimulants, whether methamphetamine or cocaine, cause changes in dopamine that are difficult to reverse. Substitute stimulants, such as modafinil, or vaccines have been proposed for cocaine abuse, but the evidence is not robust. Methamphetamine produces a schizophrenia-like illness, but antipsychotics are not effective. Naltrexone and bupropion showed some efficacy but was not statistically significant. There are no effective treatments for overdose or relapse prevention other than traditional group and residential treatment approaches.

Risks in Using Cannabis
Kevin Hill, MD, MHS, McLean Hospital

Although only 9% of Cannabis users become dependent, Dr. Hill recommended talking to all patients who use Cannabis about the risks, such as problems with work, school, and relationships. When treating patients with Cannabis use disorder, explore reasons that the individual would want to stop using Cannabis, take a careful history, and most importantly, build a good therapeutic alliance.

The most robust data for medical Cannabis is for chronic pain, neuropathic pain, and spasticity associated with multiple sclerosis; however, there are more than 70 indications among the 28 states that allow its use. Dr. Hill suggests having a written policy, engage in conversation about why the patient wants medical Cannabis, be open to evaluating such a patient, and consider treating the patient’s symptoms with traditional modalities.

To diagnose premenstrual dysphoric disorder, Dr. Freeman recommends asking your patient to document and rate daily moods using a mobile app or calendar. In perimenopause, the risk of depression increases because estrogen has antidepressant effects. Although, there are no guidelines for treating depression in women in perimenopause, consider serotonergic antidepressants, supplements such as omega-3 fatty acids, isoflavones, and black cohosh, and sleep aids for patients with insomnia—a common feature of menopause.

ADHD, Bipolar Disorder, and Depression in Children

Attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BD) may share an underlying biological etiology, Dr. Strawn explained. Shared risk factors include in utero events, dietary factors, and genetics. Differentiating ADHD from BD depends on the developmental stage of the patient. Symptoms overlap, which could lead to overdiagnosis of ADHD in youths with BD.

Dr. Strawn discussed how children with depression might display mood lability and irritability, rather than verbalizing feelings because they do not use language effectively until age 7. Children may have somatic symptoms early and irritability might decrease into adolescence. Anxiety disorder in children emerges early—usually as a phobia—around age 12 to 14, with an increase in onset of depressive disorders. Dr. Strawn reviewed screening tools to diagnose and track anxiety symptoms, as well as the pros and cons of pharmacological treatments.

Psychotic symptoms could be common in older adults; therefore it is important to evaluate whether these symptoms cause emotional suffering or impairment in daily function. Dr. Grossberg recommended that when treating psychotic disorders in geriatric patients to first evaluate and treat underlying medical problems and identify offending medications or environmental or psychosocial triggers, then consider psychosocial or environmental interventions. Consider antipsychotics for patients who are experiencing severe emotional distress or those who pose a high safety risk. If antipsychotics are necessary, pick an agent based on side effects, “start low, go slow,” and discuss the risks and benefits with the family.

Role of Psychiatrists in Long-term Care Facilities

In his presentation on the role of psychiatrists in long-term care facilities, Dr. Grossberg described common disorders including the behavioral and psychiatric symptoms of dementia, as well as risk for depression. Overprescribing is common in long-term care facilities; therefore when considering a patient’s medication regimen, often less is more. Dr. Grossberg also discussed common undertreated or undercorrected physical health problems, including hearing or vision deficits, obstructive sleep apnea, and malnutrition.

Fatigue

Fatigue experienced by patients with chronic fatigue syndrome is unrelenting, is not the result of ongoing exertion, and is unrelieved by rest. When approaching a patient with extreme fatigue, start with a thorough evaluation in collaboration with a primary care physician, Dr. Thompson said. Establish a rapport with the patient, limit iatrogenic harm, and treat chronic fatigue as you would any chronic condition. Rintatolimod and valganciclovir have showed some evidence of benefit, and graded exercise therapy has shown success.

Current Psychiatry and the American Academy of Clinical Psychiatrists welcomed more than 500 psychiatric practitioners from across the United States and abroad to this annual conference, which was headed by Meeting Co-chairs Richard Balon, MD, and Donald W. Black, MD, March 30 to April 1, 2017, at the Marriott Chicago Magnificent Mile in Chicago, Illinois. Attendees earned as many as 18 AMA PRA Category 1 Credits™. We welcome you to join us at Psychiatry Update Encore in Las Vegas, December 10 to 12, 2017 or next year in Chicago, March 22 to 24, 2018.

View summaries from the event on the following pages.

Make Way for Possibilities of an Adjunctive Treatment for Major Depressive Disorder

In an industry-sponsored symposium, Dr. Mattingly reported that in the STAR-D study, approximately one-half of patients with major depressive disorder (MDD) did not experience adequate response to an initial selective serotonin reuptake inhibitor and 3 of 4 of those non-responding patients did not achieve full response with a second antidepressant, which prompts consideration of an adjunctive agent. Brexpiprazole (Rexulti) is a partial agonist for serotonin, dopamine, and noradrenergic systems. In pivotal trials as an adjunctive treatment in MDD, brexpiprazole, 2 mg/d, resulted in a statistically significant decrease in Montgomery-Åsburg Depression Rating Scale scores compared with placebo. Most common adverse reactions observed in ≥5% of patients and at least twice the rate of placebo included akathisia and weight increase.

Essentials of Malingering Assessment

Malingering is intentional lying with an external incentive, such as avoiding work or obtaining drugs. Dr. Mossman gave 2 examples of malingered posttraumatic stress disorder and psychosis. Although lying cannot be detected by careful examination of facial expressions or gestures, a detailed evaluation can reveal malingering. An individual who is malingering psychosis may describe symptoms, such as “I talk to voices all the time,” but clinicians never observe such behavior. Signs of malingering include using “textbook” terms for symptoms; inconsistencies in their history or symptoms; sudden onset of delusions; exaggerating; and being unpleasant, dishonest, or demanding.

Beyond Efficacy and Effectiveness: Neurotoxicity vs Neuroprotection are the REAL Differences Between Typical and Atypical Antipsychotics

Dr. Nasrallah discussed the difference between typical vs atypical antipsychotics—the former is neurotoxic, the latter is neuroprotective. Because patients with schizophrenia experience a loss of brain volume and cerebral grey matter and increased lateral ventricle volume, consider atypical antipsychotics for their neuroprotective properties.

In several studies typical antipsychotics, such as haloperidol, have been found to be neurotoxic, causing apoptosis and decreased cell viability. Atypical antipsychotics may be beneficial for patients with schizophrenia because they:

• stimulate production of new brain cells and increase neurotropic factors
• reverse PCP-induced changes in gene expression and loss of dendritic spines in the frontal cortex
• are neuroprotective against ischemic stroke damage
• prevent oligodendrocyte damage caused by interferon gamma-stimulated microglia.

Medicolegal Hazards in the Information Age: Malpractice and More

Dr. Mossman began by answering the question, “What should I do if a patient ‘friended’ me on Facebook?” Such online relationships can blur boundaries or risk breaching confidentiality, therefore medical organizations recommend ignoring a friend request. Telemedicine via Skype is cost effective and enhances outreach to patients in rural areas or who cannot travel to the office, but online clinical encounters lack multidimensional aspects of the interpersonal encounter and might not be HIPAA compliant. E-mail carries some of the same concerns, such as confidentially of personal information, although the practice—when employed appropriately—is supported by some medical associations, including the American Psychiatric Association.

Treatment-Resistance and Suicidality in Schizophrenia: 2 Major Management Challenges

Patients can seem treatment-resistant because of inadequate antipsychotic dosing, smoking, substance-induced relapse, nonadherence, or a general medical condition. Dr. Nasrallah discussed how to recognize true treatment-resistant schizophrenia and rule of spurious treatment resistance. If your patient is truly treatment-resistant, what do you do when everything else fails?

Risk factors for suicide include male sex, depressed mood, substance use, and social isolation. Clozapine, the only drug FDA-approved for refractory schizophrenia and suicidality, is underutilized for such patients. Dr. Nasrallah also presented evidence for the use of adjunctive modalities, such as lamotrigine, steroids, omega-3 fatty acids, NSAIDs, antidepressants, glutamatergic agents, and rTMS, as well as psychotherapy.

Luncheon Symposium

Depression, Its impact, and the Importance of Recognition and Treatment

Major depressive disorder (MDD) is the most commonly diagnosed condition, second to cardiovascular disease. Dr. Draud recommended using a wellness screen such as the WHO-5 (World Health Organization, 5 item well-being index) in addition to a depression screening tool such as the PHQ-9. He emphasized that the goal of treatment should not be merely remission—but remission without residual symptoms. Cognitive impairment is the most common residual symptom. Patients with residual symptoms relapse earlier (5.5 times faster) and at a greater rate than patients without residual symptoms (76% vs 25%, respectively). Continue treatment and monitoring even after symptoms appear to subside. Recommended treatment is multi-modal and should include cognitive therapy and exercise.

New and Old Treatments for Opioid Abuse and Dependence

Each day more than 1,000 people are treated in emergency departments for improper use of prescription opioids. But is naloxone saving lives or is overdose reversal nothing more than CPR? Dr. Gold spoke about the need for psychiatric assessment after a patient has been revived. Historically, treatment has stopped at abstinence or overdose treatment, but patients need ongoing treatment. Family therapy, vocational assistance, and psychotherapy are essential.

Dr. Gold reviewed established and newer treatments, including naloxone and naltrexone. Methadone and buprenorphine-naloxone can be effective for adherent patients who abuse only one drug. Naltrexone gives patients time to get their lives on track. Probuphine has comparable efficacy with buprenorphine-naloxone and methadone.

Impact of a Personality Disorder in Management of Comorbid Disorder

Personality disorder (PD) indicates patterns of long-term functioning and are not limited to episodes of illness. Abnormal personality traits are common among the general population, but are not considered a personality disorder unless they are inflexible, maladaptive, persisting, and cause distress either for the patient or the family. There are few cases of “pure” PDs without a comorbid psychiatric disorder. Personality disorders are not as stable as once understood; they wax and wane in response to stressors or depressed mood or anxiety. When a PD is comorbid with another disorder, patients are less likely to respond to medication and to experience remission from the comorbid psychiatric disorder. 

Evaluation and Treatment of Patients Who Abuse Methamphetamine or Cocaine

There are no FDA-approved medications or advancement in treatment for cocaine overdose—primary treatment is still ice baths. When assessing cocaine use, consider the route of ingestion and duration of use, which influence severity. Stimulants, whether methamphetamine or cocaine, cause changes in dopamine that are difficult to reverse. Substitute stimulants, such as modafinil, or vaccines have been proposed for cocaine abuse, but the evidence is not robust. Methamphetamine produces a schizophrenia-like illness, but antipsychotics are not effective. Naltrexone and bupropion showed some efficacy but was not statistically significant. There are no effective treatments for overdose or relapse prevention other than traditional group and residential treatment approaches.

Risks in Using Cannabis
Kevin Hill, MD, MHS, McLean Hospital

Although only 9% of Cannabis users become dependent, Dr. Hill recommended talking to all patients who use Cannabis about the risks, such as problems with work, school, and relationships. When treating patients with Cannabis use disorder, explore reasons that the individual would want to stop using Cannabis, take a careful history, and most importantly, build a good therapeutic alliance.

The most robust data for medical Cannabis is for chronic pain, neuropathic pain, and spasticity associated with multiple sclerosis; however, there are more than 70 indications among the 28 states that allow its use. Dr. Hill suggests having a written policy, engage in conversation about why the patient wants medical Cannabis, be open to evaluating such a patient, and consider treating the patient’s symptoms with traditional modalities.

To diagnose premenstrual dysphoric disorder, Dr. Freeman recommends asking your patient to document and rate daily moods using a mobile app or calendar. In perimenopause, the risk of depression increases because estrogen has antidepressant effects. Although, there are no guidelines for treating depression in women in perimenopause, consider serotonergic antidepressants, supplements such as omega-3 fatty acids, isoflavones, and black cohosh, and sleep aids for patients with insomnia—a common feature of menopause.

ADHD, Bipolar Disorder, and Depression in Children

Attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BD) may share an underlying biological etiology, Dr. Strawn explained. Shared risk factors include in utero events, dietary factors, and genetics. Differentiating ADHD from BD depends on the developmental stage of the patient. Symptoms overlap, which could lead to overdiagnosis of ADHD in youths with BD.

Dr. Strawn discussed how children with depression might display mood lability and irritability, rather than verbalizing feelings because they do not use language effectively until age 7. Children may have somatic symptoms early and irritability might decrease into adolescence. Anxiety disorder in children emerges early—usually as a phobia—around age 12 to 14, with an increase in onset of depressive disorders. Dr. Strawn reviewed screening tools to diagnose and track anxiety symptoms, as well as the pros and cons of pharmacological treatments.

Psychotic symptoms could be common in older adults; therefore it is important to evaluate whether these symptoms cause emotional suffering or impairment in daily function. Dr. Grossberg recommended that when treating psychotic disorders in geriatric patients to first evaluate and treat underlying medical problems and identify offending medications or environmental or psychosocial triggers, then consider psychosocial or environmental interventions. Consider antipsychotics for patients who are experiencing severe emotional distress or those who pose a high safety risk. If antipsychotics are necessary, pick an agent based on side effects, “start low, go slow,” and discuss the risks and benefits with the family.

Role of Psychiatrists in Long-term Care Facilities

In his presentation on the role of psychiatrists in long-term care facilities, Dr. Grossberg described common disorders including the behavioral and psychiatric symptoms of dementia, as well as risk for depression. Overprescribing is common in long-term care facilities; therefore when considering a patient’s medication regimen, often less is more. Dr. Grossberg also discussed common undertreated or undercorrected physical health problems, including hearing or vision deficits, obstructive sleep apnea, and malnutrition.

Fatigue

Fatigue experienced by patients with chronic fatigue syndrome is unrelenting, is not the result of ongoing exertion, and is unrelieved by rest. When approaching a patient with extreme fatigue, start with a thorough evaluation in collaboration with a primary care physician, Dr. Thompson said. Establish a rapport with the patient, limit iatrogenic harm, and treat chronic fatigue as you would any chronic condition. Rintatolimod and valganciclovir have showed some evidence of benefit, and graded exercise therapy has shown success.

Psychotic symptoms in patients with borderline personality disorder (BPD) are common, distressing to patients, and challenging to treat. Issues of comorbidities and misdiagnoses in BPD patients further complicate matters and could lead to iatrogenic harm. The dissociation that patients with BPD experience could be confused with psychosis and exacerbate treatment and diagnostic confusion. Furthermore, BPD patients with unstable identity and who are sensitive to rejection could present in a bizarre, disorganized, or agitated manner when under stress.

Although pitfalls occur when managing psychotic symptoms in patients with BPD, there are trends and clues to help clinicians navigate diagnostic and treatment challenges. This article will review the literature, propose how to distinguish psychotic symptoms in BPD from those in primary psychotic disorders such as schizophrenia, and explore reasonable treatment options.

The scope of the problem

The DSM-5 criteria for BPD states that “during periods of extreme stress, transient paranoid ideation or dissociative symptoms may occur.”¹ The term “borderline” originated from the idea that symptoms bordered on the intersection of neurosis and psychosis.² However, psychotic symptoms in BPD are more varied and frequent than what DSM-5 criteria suggests.

The prevalence of psychotic symptoms in patients with BPD has been estimated between 20% to 50%.³ There also is evidence of frequent auditory and visual hallucinations in patients with BPD, and a recent study using structured psychiatric interviews demonstrated that most BPD patients report at least 1 symptom of psychosis.⁴ Considering that psychiatric comorbidities are the rule rather than the exception in BPD, the presence of psychotic symptoms further complicates the diagnostic picture. Recognizing the symptoms of BPD is essential for understanding the course of the symptoms and predicting response to treatment.⁵

Treatment of BPD is strikingly different than that of a primary psychotic disorder. There is some evidence that low-dosage antipsychotics could ease mood instability and perceptual disturbances in patients with BPD.⁶ Antipsychotic dosages used to treat hallucinations and delusions in a primary psychotic disorder are unlikely to be as effective for a patient with BPD, and are associated with significant adverse effects. Furthermore, these adverse effects—such as weight gain, hyperlipidemia, and diabetes—could become new sources of distress. Clinicians also might miss an opportunity to engage a BPD patient in psychotherapy if the focus is on the anticipated effect of a medication. The mainstay treatment of BPD is an evidence-based psychotherapy, such as dialectical behavioral therapy, transference-focused psychotherapy, mentalization-based therapy, or good psychiatric management.⁷

CASE Hallucinations during times of stress

Ms. K, a 20-year-old single college student, presents to the psychiatric emergency room with worsening mood swings, anxiety, and hallucinations. Her mood swings are brief and intense, lasting minutes to hours. Anxiety often is triggered by feelings of emptiness and fear of abandonment. She describes herself as a “social chameleon” and notes that she changes how she behaves depending on who she spends time with.

She often hears the voice of her ex-boyfriend instructing her to kill herself and saying that she is a “terrible person.” Their relationship was intense, with many break-ups and reunions. She also reports feeling disconnected from herself at times as though she is being controlled by an outside entity. To relieve her emotional suffering, she cuts herself superficially. Although she has no family history of psychiatric illness, she fears that she may have schizophrenia.

Ms. K’s outpatient psychiatrist prescribes antipsychotics at escalating dosages over a few months (she now takes olanzapine, 40 mg/d, aripiprazole, 30 mg/d, clonazepam, 3 mg/d, and escitalopram, 30 mg/d), but the hallucinations remain. These symptoms worsen during stressful situations, and she notices that they almost are constant as she studies for final exams, prompting her psychiatrist to discuss a clozapine trial. Ms. K is not in psychotherapy, and recognizes that she does not deal with stress well. Despite her symptoms, she is organized in her thought process, has excellent grooming and hygiene, has many social connections, and performs well in school.

How does one approach a patient such as Ms. K?

A chief concern of hallucinations, particularly in a young adult at an age when psychotic disorders such as schizophrenia often emerge, can contribute to a diagnostic quandary. What evidence can guide the clinician? There are some key features to consider:

• Her “mood swings” are notable in their intensity and brevity, making a primary mood disorder with psychotic features less likely.
• Hallucinations are present in the absence of a prodromal period of functional decline or negative symptoms, making a primary psychotic disorder less likely.
• She does not have a family history of psychiatric illness, particularly a primary psychotic disorder.
• She maintains social connections, although her relationships are intense and tumultuous.
• Psychotic symptoms have not changed with higher dosages of antipsychotics.
• Complaints of feeling “disconnected from herself” and “empty” are common symptoms of BPD and necessitate further exploration.
• Psychotic symptoms are largely transient and stress-related, with an overwhelmingly negative tone.
• Techniques that individuals with schizophrenia use, such as distraction or trying to tune out voices, are not being employed. Instead, Ms. K attends to the voices and is anxiously focused on them.
• The relationship of her symptoms to interpersonal stress is key.

When evaluating a patient such as Ms. K, it is important to explore both the nature and timing of the psychotic symptoms and any other related psychiatric symptoms. This helps to determine a less ambiguous diagnosis and clearer treatment plan. Understanding the patient’s perspective about the psychotic symptoms also is useful to gauge the patient’s level of distress and her impression of what the symptoms mean.

Diagnostic considerations

BPD is characterized by a chaotic emotional climate with impulsivity and instability of self-image, affect, and relationships. Most BPD symptoms, including psychosis, often are exacerbated by the perception of abandonment or rejection and other interpersonal stressors.¹ Both BPD and schizophrenia are estimated to affect at least 1% of the general population.^8,9 Patients with BPD frequently meet criteria for comorbid mental illnesses, including major depressive disorder, substance use disorder, posttraumatic stress disorder, anxiety, and eating disorders.¹⁰ Because psychotic symptoms can present in some of these disorders, the context and time course of these symptoms are crucial to consider.

Misdiagnosis is common with BPD, and patients can receive the wrong treatment for years before BPD is considered, likely because of the stigma surrounding the diagnosis.⁵ One also must keep in mind that, although rare, a patient can have both BPD and a primary psychotic disorder.¹¹ Although a patient with schizophrenia could be prone to social isolation because of delusions or paranoia, BPD patients are more apt to experience intense interpersonal relationships driven by the need to avoid abandonment. Manipulation, anger, and neediness in relationships with both peers and health care providers are common—stark contrasts to typical negative symptoms, blunted affect, and a lack of social drive characteristic of schizophrenia.¹²

Distinguishing between psychosis in BPD and a psychotic disorder

Studies have sought to explore the quality of psychotic symptoms in BPD vs primary psychotic disorders, which can be challenging to differentiate (Table 1). Some have found that transient symptoms, such as non-delusional paranoia, are more prevalent in BPD, and “true” psychotic symptoms that are long-lasting and bizarre are indicative of schizophrenia.^13,14 Also, there is evidence that the lower levels of interpersonal functioning often found in BPD are predictive of psychotic symptoms in that disorder but not in schizophrenia.¹⁵

Auditory hallucinations in patients with BPD predominantly are negative and critical in tone.⁴ However, there is no consistent evidence that the quality of auditory hallucinations in BPD vs schizophrenia is different in any meaningful way.¹⁶ Because of the frequency of dissociative symptoms in BPD, it is likely that clinicians could misinterpret these symptoms to indicate disorganized behavior associated with a primary psychotic disorder. In one study, 50% of individuals with BPD experienced auditory hallucinations.¹¹ Differentiating between “internal” or “external” voices did not help to clarify the diagnosis, and paranoid delusions occurred in less than one-third of patients with BPD, but in approximately two-third of those with a diagnosis of schizophrenia.

The McLean Study of Adult Develop­ment, a longitudinal study of BPD patients, found that the prevalence of psychotic symptoms diminished over time. It is unclear whether this was due to the spontaneus remission rate of BPD symptoms in general or because of effective treatment.¹³

Psychotic symptoms in BPD seem to react to stress and increase in intensity when patients are in crisis.¹⁷ Nonetheless, because of the prevalence of psychosis in BPD patients and the distress it causes, clinicians should be cautioned against using terms that imply that the symptoms are not “true” or “real.”³

Treatment recommendations

When considering pharmacologic management of psychotic symptoms in BPD, aim to limit antipsychotic medications to low dosages because of adverse effects and the limited evidence that escalating dosages—and especially using >1 antipsychotic concurrently—are more effective.¹⁸ Educate patients that in BPD medications are, at best, considered adjunctive treatments. Blaming psychotic symptoms on a purely biological process in BPD, not only is harmful because medications are unlikely to significantly or consistently help, but also because they can undermine patient autonomy and reinforce the need for an outside entity (ie, medication) to fix their problems.

When treatment is ineffective and symptoms do not improve, a patient with BPD likely will experience mounting distress. This, in turn, could exacerbate impulsive, suicidal, and self-injurious behaviors. Emphasize psychotherapy, particularly for those whose psychotic symptoms are transient, stress-related, and present during acute crises (Table 2). With evidence-based psychotherapy, BPD patients can become active participants in treatment, coupling developing insight with concrete skills and teachable principles. This leads to increased interpersonal effectiveness and resilience during times of stress. Challenging the patient’s psychotic symptoms as false or “made up” rarely is helpful and usually harmful, leading to the possible severance of the therapeutic alliance.³

Bottom Line

Psychotic symptoms in patients with borderline personality disorder (BPD) could look similar to those in primary psychotic disorders. Factors suggesting BPD include a pattern of worsening psychotic symptoms during stress, long-term symptom instability, lack of delusions, presence of dissociation, and nonresponse to antipsychotics. Although low-dosage antipsychotics could provide some relief of psychotic symptoms in a patient with BPD, they often are not consistently effective and frequently lead to adverse effects. Emphasize evidence-based psychotherapies.

Psychotic symptoms in patients with borderline personality disorder (BPD) are common, distressing to patients, and challenging to treat. Issues of comorbidities and misdiagnoses in BPD patients further complicate matters and could lead to iatrogenic harm. The dissociation that patients with BPD experience could be confused with psychosis and exacerbate treatment and diagnostic confusion. Furthermore, BPD patients with unstable identity and who are sensitive to rejection could present in a bizarre, disorganized, or agitated manner when under stress.

Although pitfalls occur when managing psychotic symptoms in patients with BPD, there are trends and clues to help clinicians navigate diagnostic and treatment challenges. This article will review the literature, propose how to distinguish psychotic symptoms in BPD from those in primary psychotic disorders such as schizophrenia, and explore reasonable treatment options.

The scope of the problem

The DSM-5 criteria for BPD states that “during periods of extreme stress, transient paranoid ideation or dissociative symptoms may occur.”¹ The term “borderline” originated from the idea that symptoms bordered on the intersection of neurosis and psychosis.² However, psychotic symptoms in BPD are more varied and frequent than what DSM-5 criteria suggests.

The prevalence of psychotic symptoms in patients with BPD has been estimated between 20% to 50%.³ There also is evidence of frequent auditory and visual hallucinations in patients with BPD, and a recent study using structured psychiatric interviews demonstrated that most BPD patients report at least 1 symptom of psychosis.⁴ Considering that psychiatric comorbidities are the rule rather than the exception in BPD, the presence of psychotic symptoms further complicates the diagnostic picture. Recognizing the symptoms of BPD is essential for understanding the course of the symptoms and predicting response to treatment.⁵

Treatment of BPD is strikingly different than that of a primary psychotic disorder. There is some evidence that low-dosage antipsychotics could ease mood instability and perceptual disturbances in patients with BPD.⁶ Antipsychotic dosages used to treat hallucinations and delusions in a primary psychotic disorder are unlikely to be as effective for a patient with BPD, and are associated with significant adverse effects. Furthermore, these adverse effects—such as weight gain, hyperlipidemia, and diabetes—could become new sources of distress. Clinicians also might miss an opportunity to engage a BPD patient in psychotherapy if the focus is on the anticipated effect of a medication. The mainstay treatment of BPD is an evidence-based psychotherapy, such as dialectical behavioral therapy, transference-focused psychotherapy, mentalization-based therapy, or good psychiatric management.⁷

CASE Hallucinations during times of stress

Ms. K, a 20-year-old single college student, presents to the psychiatric emergency room with worsening mood swings, anxiety, and hallucinations. Her mood swings are brief and intense, lasting minutes to hours. Anxiety often is triggered by feelings of emptiness and fear of abandonment. She describes herself as a “social chameleon” and notes that she changes how she behaves depending on who she spends time with.

She often hears the voice of her ex-boyfriend instructing her to kill herself and saying that she is a “terrible person.” Their relationship was intense, with many break-ups and reunions. She also reports feeling disconnected from herself at times as though she is being controlled by an outside entity. To relieve her emotional suffering, she cuts herself superficially. Although she has no family history of psychiatric illness, she fears that she may have schizophrenia.

Ms. K’s outpatient psychiatrist prescribes antipsychotics at escalating dosages over a few months (she now takes olanzapine, 40 mg/d, aripiprazole, 30 mg/d, clonazepam, 3 mg/d, and escitalopram, 30 mg/d), but the hallucinations remain. These symptoms worsen during stressful situations, and she notices that they almost are constant as she studies for final exams, prompting her psychiatrist to discuss a clozapine trial. Ms. K is not in psychotherapy, and recognizes that she does not deal with stress well. Despite her symptoms, she is organized in her thought process, has excellent grooming and hygiene, has many social connections, and performs well in school.

How does one approach a patient such as Ms. K?

A chief concern of hallucinations, particularly in a young adult at an age when psychotic disorders such as schizophrenia often emerge, can contribute to a diagnostic quandary. What evidence can guide the clinician? There are some key features to consider:

• Her “mood swings” are notable in their intensity and brevity, making a primary mood disorder with psychotic features less likely.
• Hallucinations are present in the absence of a prodromal period of functional decline or negative symptoms, making a primary psychotic disorder less likely.
• She does not have a family history of psychiatric illness, particularly a primary psychotic disorder.
• She maintains social connections, although her relationships are intense and tumultuous.
• Psychotic symptoms have not changed with higher dosages of antipsychotics.
• Complaints of feeling “disconnected from herself” and “empty” are common symptoms of BPD and necessitate further exploration.
• Psychotic symptoms are largely transient and stress-related, with an overwhelmingly negative tone.
• Techniques that individuals with schizophrenia use, such as distraction or trying to tune out voices, are not being employed. Instead, Ms. K attends to the voices and is anxiously focused on them.
• The relationship of her symptoms to interpersonal stress is key.

When evaluating a patient such as Ms. K, it is important to explore both the nature and timing of the psychotic symptoms and any other related psychiatric symptoms. This helps to determine a less ambiguous diagnosis and clearer treatment plan. Understanding the patient’s perspective about the psychotic symptoms also is useful to gauge the patient’s level of distress and her impression of what the symptoms mean.

Diagnostic considerations

BPD is characterized by a chaotic emotional climate with impulsivity and instability of self-image, affect, and relationships. Most BPD symptoms, including psychosis, often are exacerbated by the perception of abandonment or rejection and other interpersonal stressors.¹ Both BPD and schizophrenia are estimated to affect at least 1% of the general population.^8,9 Patients with BPD frequently meet criteria for comorbid mental illnesses, including major depressive disorder, substance use disorder, posttraumatic stress disorder, anxiety, and eating disorders.¹⁰ Because psychotic symptoms can present in some of these disorders, the context and time course of these symptoms are crucial to consider.

Misdiagnosis is common with BPD, and patients can receive the wrong treatment for years before BPD is considered, likely because of the stigma surrounding the diagnosis.⁵ One also must keep in mind that, although rare, a patient can have both BPD and a primary psychotic disorder.¹¹ Although a patient with schizophrenia could be prone to social isolation because of delusions or paranoia, BPD patients are more apt to experience intense interpersonal relationships driven by the need to avoid abandonment. Manipulation, anger, and neediness in relationships with both peers and health care providers are common—stark contrasts to typical negative symptoms, blunted affect, and a lack of social drive characteristic of schizophrenia.¹²

Distinguishing between psychosis in BPD and a psychotic disorder

Studies have sought to explore the quality of psychotic symptoms in BPD vs primary psychotic disorders, which can be challenging to differentiate (Table 1). Some have found that transient symptoms, such as non-delusional paranoia, are more prevalent in BPD, and “true” psychotic symptoms that are long-lasting and bizarre are indicative of schizophrenia.^13,14 Also, there is evidence that the lower levels of interpersonal functioning often found in BPD are predictive of psychotic symptoms in that disorder but not in schizophrenia.¹⁵

Auditory hallucinations in patients with BPD predominantly are negative and critical in tone.⁴ However, there is no consistent evidence that the quality of auditory hallucinations in BPD vs schizophrenia is different in any meaningful way.¹⁶ Because of the frequency of dissociative symptoms in BPD, it is likely that clinicians could misinterpret these symptoms to indicate disorganized behavior associated with a primary psychotic disorder. In one study, 50% of individuals with BPD experienced auditory hallucinations.¹¹ Differentiating between “internal” or “external” voices did not help to clarify the diagnosis, and paranoid delusions occurred in less than one-third of patients with BPD, but in approximately two-third of those with a diagnosis of schizophrenia.

The McLean Study of Adult Develop­ment, a longitudinal study of BPD patients, found that the prevalence of psychotic symptoms diminished over time. It is unclear whether this was due to the spontaneus remission rate of BPD symptoms in general or because of effective treatment.¹³

Psychotic symptoms in BPD seem to react to stress and increase in intensity when patients are in crisis.¹⁷ Nonetheless, because of the prevalence of psychosis in BPD patients and the distress it causes, clinicians should be cautioned against using terms that imply that the symptoms are not “true” or “real.”³

Treatment recommendations

When considering pharmacologic management of psychotic symptoms in BPD, aim to limit antipsychotic medications to low dosages because of adverse effects and the limited evidence that escalating dosages—and especially using >1 antipsychotic concurrently—are more effective.¹⁸ Educate patients that in BPD medications are, at best, considered adjunctive treatments. Blaming psychotic symptoms on a purely biological process in BPD, not only is harmful because medications are unlikely to significantly or consistently help, but also because they can undermine patient autonomy and reinforce the need for an outside entity (ie, medication) to fix their problems.

When treatment is ineffective and symptoms do not improve, a patient with BPD likely will experience mounting distress. This, in turn, could exacerbate impulsive, suicidal, and self-injurious behaviors. Emphasize psychotherapy, particularly for those whose psychotic symptoms are transient, stress-related, and present during acute crises (Table 2). With evidence-based psychotherapy, BPD patients can become active participants in treatment, coupling developing insight with concrete skills and teachable principles. This leads to increased interpersonal effectiveness and resilience during times of stress. Challenging the patient’s psychotic symptoms as false or “made up” rarely is helpful and usually harmful, leading to the possible severance of the therapeutic alliance.³

Bottom Line

Psychotic symptoms in patients with borderline personality disorder (BPD) could look similar to those in primary psychotic disorders. Factors suggesting BPD include a pattern of worsening psychotic symptoms during stress, long-term symptom instability, lack of delusions, presence of dissociation, and nonresponse to antipsychotics. Although low-dosage antipsychotics could provide some relief of psychotic symptoms in a patient with BPD, they often are not consistently effective and frequently lead to adverse effects. Emphasize evidence-based psychotherapies.

Psychotic symptoms in patients with borderline personality disorder (BPD) are common, distressing to patients, and challenging to treat. Issues of comorbidities and misdiagnoses in BPD patients further complicate matters and could lead to iatrogenic harm. The dissociation that patients with BPD experience could be confused with psychosis and exacerbate treatment and diagnostic confusion. Furthermore, BPD patients with unstable identity and who are sensitive to rejection could present in a bizarre, disorganized, or agitated manner when under stress.

Although pitfalls occur when managing psychotic symptoms in patients with BPD, there are trends and clues to help clinicians navigate diagnostic and treatment challenges. This article will review the literature, propose how to distinguish psychotic symptoms in BPD from those in primary psychotic disorders such as schizophrenia, and explore reasonable treatment options.

The scope of the problem

The DSM-5 criteria for BPD states that “during periods of extreme stress, transient paranoid ideation or dissociative symptoms may occur.”¹ The term “borderline” originated from the idea that symptoms bordered on the intersection of neurosis and psychosis.² However, psychotic symptoms in BPD are more varied and frequent than what DSM-5 criteria suggests.

The prevalence of psychotic symptoms in patients with BPD has been estimated between 20% to 50%.³ There also is evidence of frequent auditory and visual hallucinations in patients with BPD, and a recent study using structured psychiatric interviews demonstrated that most BPD patients report at least 1 symptom of psychosis.⁴ Considering that psychiatric comorbidities are the rule rather than the exception in BPD, the presence of psychotic symptoms further complicates the diagnostic picture. Recognizing the symptoms of BPD is essential for understanding the course of the symptoms and predicting response to treatment.⁵

Treatment of BPD is strikingly different than that of a primary psychotic disorder. There is some evidence that low-dosage antipsychotics could ease mood instability and perceptual disturbances in patients with BPD.⁶ Antipsychotic dosages used to treat hallucinations and delusions in a primary psychotic disorder are unlikely to be as effective for a patient with BPD, and are associated with significant adverse effects. Furthermore, these adverse effects—such as weight gain, hyperlipidemia, and diabetes—could become new sources of distress. Clinicians also might miss an opportunity to engage a BPD patient in psychotherapy if the focus is on the anticipated effect of a medication. The mainstay treatment of BPD is an evidence-based psychotherapy, such as dialectical behavioral therapy, transference-focused psychotherapy, mentalization-based therapy, or good psychiatric management.⁷

CASE Hallucinations during times of stress

Ms. K, a 20-year-old single college student, presents to the psychiatric emergency room with worsening mood swings, anxiety, and hallucinations. Her mood swings are brief and intense, lasting minutes to hours. Anxiety often is triggered by feelings of emptiness and fear of abandonment. She describes herself as a “social chameleon” and notes that she changes how she behaves depending on who she spends time with.

She often hears the voice of her ex-boyfriend instructing her to kill herself and saying that she is a “terrible person.” Their relationship was intense, with many break-ups and reunions. She also reports feeling disconnected from herself at times as though she is being controlled by an outside entity. To relieve her emotional suffering, she cuts herself superficially. Although she has no family history of psychiatric illness, she fears that she may have schizophrenia.

Ms. K’s outpatient psychiatrist prescribes antipsychotics at escalating dosages over a few months (she now takes olanzapine, 40 mg/d, aripiprazole, 30 mg/d, clonazepam, 3 mg/d, and escitalopram, 30 mg/d), but the hallucinations remain. These symptoms worsen during stressful situations, and she notices that they almost are constant as she studies for final exams, prompting her psychiatrist to discuss a clozapine trial. Ms. K is not in psychotherapy, and recognizes that she does not deal with stress well. Despite her symptoms, she is organized in her thought process, has excellent grooming and hygiene, has many social connections, and performs well in school.

How does one approach a patient such as Ms. K?

A chief concern of hallucinations, particularly in a young adult at an age when psychotic disorders such as schizophrenia often emerge, can contribute to a diagnostic quandary. What evidence can guide the clinician? There are some key features to consider:

• Her “mood swings” are notable in their intensity and brevity, making a primary mood disorder with psychotic features less likely.
• Hallucinations are present in the absence of a prodromal period of functional decline or negative symptoms, making a primary psychotic disorder less likely.
• She does not have a family history of psychiatric illness, particularly a primary psychotic disorder.
• She maintains social connections, although her relationships are intense and tumultuous.
• Psychotic symptoms have not changed with higher dosages of antipsychotics.
• Complaints of feeling “disconnected from herself” and “empty” are common symptoms of BPD and necessitate further exploration.
• Psychotic symptoms are largely transient and stress-related, with an overwhelmingly negative tone.
• Techniques that individuals with schizophrenia use, such as distraction or trying to tune out voices, are not being employed. Instead, Ms. K attends to the voices and is anxiously focused on them.
• The relationship of her symptoms to interpersonal stress is key.

When evaluating a patient such as Ms. K, it is important to explore both the nature and timing of the psychotic symptoms and any other related psychiatric symptoms. This helps to determine a less ambiguous diagnosis and clearer treatment plan. Understanding the patient’s perspective about the psychotic symptoms also is useful to gauge the patient’s level of distress and her impression of what the symptoms mean.

Diagnostic considerations

BPD is characterized by a chaotic emotional climate with impulsivity and instability of self-image, affect, and relationships. Most BPD symptoms, including psychosis, often are exacerbated by the perception of abandonment or rejection and other interpersonal stressors.¹ Both BPD and schizophrenia are estimated to affect at least 1% of the general population.^8,9 Patients with BPD frequently meet criteria for comorbid mental illnesses, including major depressive disorder, substance use disorder, posttraumatic stress disorder, anxiety, and eating disorders.¹⁰ Because psychotic symptoms can present in some of these disorders, the context and time course of these symptoms are crucial to consider.

Misdiagnosis is common with BPD, and patients can receive the wrong treatment for years before BPD is considered, likely because of the stigma surrounding the diagnosis.⁵ One also must keep in mind that, although rare, a patient can have both BPD and a primary psychotic disorder.¹¹ Although a patient with schizophrenia could be prone to social isolation because of delusions or paranoia, BPD patients are more apt to experience intense interpersonal relationships driven by the need to avoid abandonment. Manipulation, anger, and neediness in relationships with both peers and health care providers are common—stark contrasts to typical negative symptoms, blunted affect, and a lack of social drive characteristic of schizophrenia.¹²

Distinguishing between psychosis in BPD and a psychotic disorder

Studies have sought to explore the quality of psychotic symptoms in BPD vs primary psychotic disorders, which can be challenging to differentiate (Table 1). Some have found that transient symptoms, such as non-delusional paranoia, are more prevalent in BPD, and “true” psychotic symptoms that are long-lasting and bizarre are indicative of schizophrenia.^13,14 Also, there is evidence that the lower levels of interpersonal functioning often found in BPD are predictive of psychotic symptoms in that disorder but not in schizophrenia.¹⁵

Auditory hallucinations in patients with BPD predominantly are negative and critical in tone.⁴ However, there is no consistent evidence that the quality of auditory hallucinations in BPD vs schizophrenia is different in any meaningful way.¹⁶ Because of the frequency of dissociative symptoms in BPD, it is likely that clinicians could misinterpret these symptoms to indicate disorganized behavior associated with a primary psychotic disorder. In one study, 50% of individuals with BPD experienced auditory hallucinations.¹¹ Differentiating between “internal” or “external” voices did not help to clarify the diagnosis, and paranoid delusions occurred in less than one-third of patients with BPD, but in approximately two-third of those with a diagnosis of schizophrenia.

The McLean Study of Adult Develop­ment, a longitudinal study of BPD patients, found that the prevalence of psychotic symptoms diminished over time. It is unclear whether this was due to the spontaneus remission rate of BPD symptoms in general or because of effective treatment.¹³

Psychotic symptoms in BPD seem to react to stress and increase in intensity when patients are in crisis.¹⁷ Nonetheless, because of the prevalence of psychosis in BPD patients and the distress it causes, clinicians should be cautioned against using terms that imply that the symptoms are not “true” or “real.”³

Treatment recommendations

When considering pharmacologic management of psychotic symptoms in BPD, aim to limit antipsychotic medications to low dosages because of adverse effects and the limited evidence that escalating dosages—and especially using >1 antipsychotic concurrently—are more effective.¹⁸ Educate patients that in BPD medications are, at best, considered adjunctive treatments. Blaming psychotic symptoms on a purely biological process in BPD, not only is harmful because medications are unlikely to significantly or consistently help, but also because they can undermine patient autonomy and reinforce the need for an outside entity (ie, medication) to fix their problems.

When treatment is ineffective and symptoms do not improve, a patient with BPD likely will experience mounting distress. This, in turn, could exacerbate impulsive, suicidal, and self-injurious behaviors. Emphasize psychotherapy, particularly for those whose psychotic symptoms are transient, stress-related, and present during acute crises (Table 2). With evidence-based psychotherapy, BPD patients can become active participants in treatment, coupling developing insight with concrete skills and teachable principles. This leads to increased interpersonal effectiveness and resilience during times of stress. Challenging the patient’s psychotic symptoms as false or “made up” rarely is helpful and usually harmful, leading to the possible severance of the therapeutic alliance.³

Bottom Line

Psychotic symptoms in patients with borderline personality disorder (BPD) could look similar to those in primary psychotic disorders. Factors suggesting BPD include a pattern of worsening psychotic symptoms during stress, long-term symptom instability, lack of delusions, presence of dissociation, and nonresponse to antipsychotics. Although low-dosage antipsychotics could provide some relief of psychotic symptoms in a patient with BPD, they often are not consistently effective and frequently lead to adverse effects. Emphasize evidence-based psychotherapies.

We all know these patients:

The young man who, when his name shows up on the ED board, everyone lets out a little groan, knowing his hospital stay will be long and tumultuous.

The middle-aged woman who seems to do want your care and attention and yet rebuffs your attempts to help her, meanwhile, making constant demands on nursing staff.

The older man who trusts no one and will not cooperate with any of his needed care, frustrating staff and physicians alike.

Caring for the patient is integral to the art of doctoring, and yet, there are some people for whom this is incredibly hard to do. They frustrate even the most seasoned professional and work their way under our skin. While their disruptive acts may feel volitional to those of us attempting to provide care, these individuals may suffer from a personality disorder.

Megan Riddle, MD, PhD, is based in the department of psychiatry and behavioral sciences at the University of Washington, Seattle.

NOTES

1. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Arlington, VA: American Psychiatric Association; 2013.

2. Riddle M, Meeks T, Alvarez C, Dubovsky A. When personality is the problem: Managing patients with difficult personalities on the acute care unit. J Hosp Med. 2016 Dec;11(12):873-878.

3. Bukh JD, Bock C, Kessing LV. Association between genetic polymorphisms in the serotonergic system and comorbid personality disorders among patients with first-episode depression. J Pers Disord. 2014 Jun;28(3):365-378.

4. Perez-Rodriguez MM, Weinstein S, New AS, et al. Tryptophan-hydroxylase 2 haplotype association with borderline personality disorder and aggression in a sample of patients with personality disorders and healthy controls. J Psychiatr Res. 2010 Nov; 44(15):1075-1081.

5. Checknita D, Maussion G, Labonte B, et al. Monoamine oxidase: A gene promoter methylation and transcriptional downregulation in an offender population with antisocial personality disorder. Br J Psychiatry. 2015 Mar;206(3):216-222.

6. Boen E, Westlye LT, Elvsashagen T, et al. Regional cortical thinning may be a biological marker for borderline personality disorder. Acta Psychiatr Scand. 2014 Sep;130(3):193-204.

7. Thoma P, Friedmann C, Suchan B. Empathy and social problem solving in alcohol dependence, mood disorders and selected personality disorders. Neurosci Biobehav Rev. 2013 Mar;37(3):448-470.

8. Liu H, Liao J, Jiang W, Wang W. Changes in low-frequency fluctuations in patients with antisocial personality disorder revealed by resting-state functional MRI. PLoS One. 2014 Mar 5;9(3):e89790.

9. Yang Y, Raine A. Prefrontal structural and functional brain imaging findings in antisocial, violent, and psychopathic individuals: A meta-analysis. Psychiatry Res. 2009 Nov 30;174(2):81-88.

10. Fok ML, Hayes RD, Chang CK, Stewart R, Callard FJ, Moran P. Life expectancy at birth and all-cause mortality among people with personality disorder. J Psychosom Res. 2012 Aug;73(2):104-107.

11. Tyrer P, Reed GM, Crawford MJ. Classification, assessment, prevalence, and effect of personality disorder. Lancet. 2015 Feb 21;385:717-726.

12. Groves JE. Taking care of the hateful patient. N Engl J Med. 1978 Apr 20; 298:883-887.

13. Groves JE. Management of the borderline patient on a medical or surgical ward: The psychiatric consultant’s role. Int J Psychiatry Med. 1975;6(3):337-348.

14. Bodner E, Cohen-Fridel S, Mashiah M, et al. The attitudes of psychiatric hospital staff toward hospitalization and treatment of patients with borderline personality disorder. BMC psychiatry. 2015 Jan 22;15:2.

15. Colli A, Tanzilli A, Dimaggio G, Lingiardi V. Patient personality and therapist response: An empirical investigation. Am J Psychiatry. 2014 Jan;171(1):102-108.

16. Ingenhoven T, Lafay P, Rinne T, Passchier J, Duivenvoorden H. Effectiveness of pharmacotherapy for severe personality disorders: Meta-analyses of randomized controlled trials. J Clin Psychiatry. 2010 Jan;71(1):14-25.

We all know these patients:

The young man who, when his name shows up on the ED board, everyone lets out a little groan, knowing his hospital stay will be long and tumultuous.

The middle-aged woman who seems to do want your care and attention and yet rebuffs your attempts to help her, meanwhile, making constant demands on nursing staff.

The older man who trusts no one and will not cooperate with any of his needed care, frustrating staff and physicians alike.

Caring for the patient is integral to the art of doctoring, and yet, there are some people for whom this is incredibly hard to do. They frustrate even the most seasoned professional and work their way under our skin. While their disruptive acts may feel volitional to those of us attempting to provide care, these individuals may suffer from a personality disorder.

Megan Riddle, MD, PhD, is based in the department of psychiatry and behavioral sciences at the University of Washington, Seattle.

NOTES

1. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Arlington, VA: American Psychiatric Association; 2013.

2. Riddle M, Meeks T, Alvarez C, Dubovsky A. When personality is the problem: Managing patients with difficult personalities on the acute care unit. J Hosp Med. 2016 Dec;11(12):873-878.

3. Bukh JD, Bock C, Kessing LV. Association between genetic polymorphisms in the serotonergic system and comorbid personality disorders among patients with first-episode depression. J Pers Disord. 2014 Jun;28(3):365-378.

4. Perez-Rodriguez MM, Weinstein S, New AS, et al. Tryptophan-hydroxylase 2 haplotype association with borderline personality disorder and aggression in a sample of patients with personality disorders and healthy controls. J Psychiatr Res. 2010 Nov; 44(15):1075-1081.

5. Checknita D, Maussion G, Labonte B, et al. Monoamine oxidase: A gene promoter methylation and transcriptional downregulation in an offender population with antisocial personality disorder. Br J Psychiatry. 2015 Mar;206(3):216-222.

6. Boen E, Westlye LT, Elvsashagen T, et al. Regional cortical thinning may be a biological marker for borderline personality disorder. Acta Psychiatr Scand. 2014 Sep;130(3):193-204.

7. Thoma P, Friedmann C, Suchan B. Empathy and social problem solving in alcohol dependence, mood disorders and selected personality disorders. Neurosci Biobehav Rev. 2013 Mar;37(3):448-470.

8. Liu H, Liao J, Jiang W, Wang W. Changes in low-frequency fluctuations in patients with antisocial personality disorder revealed by resting-state functional MRI. PLoS One. 2014 Mar 5;9(3):e89790.

9. Yang Y, Raine A. Prefrontal structural and functional brain imaging findings in antisocial, violent, and psychopathic individuals: A meta-analysis. Psychiatry Res. 2009 Nov 30;174(2):81-88.

10. Fok ML, Hayes RD, Chang CK, Stewart R, Callard FJ, Moran P. Life expectancy at birth and all-cause mortality among people with personality disorder. J Psychosom Res. 2012 Aug;73(2):104-107.

11. Tyrer P, Reed GM, Crawford MJ. Classification, assessment, prevalence, and effect of personality disorder. Lancet. 2015 Feb 21;385:717-726.

12. Groves JE. Taking care of the hateful patient. N Engl J Med. 1978 Apr 20; 298:883-887.

13. Groves JE. Management of the borderline patient on a medical or surgical ward: The psychiatric consultant’s role. Int J Psychiatry Med. 1975;6(3):337-348.

14. Bodner E, Cohen-Fridel S, Mashiah M, et al. The attitudes of psychiatric hospital staff toward hospitalization and treatment of patients with borderline personality disorder. BMC psychiatry. 2015 Jan 22;15:2.

15. Colli A, Tanzilli A, Dimaggio G, Lingiardi V. Patient personality and therapist response: An empirical investigation. Am J Psychiatry. 2014 Jan;171(1):102-108.

16. Ingenhoven T, Lafay P, Rinne T, Passchier J, Duivenvoorden H. Effectiveness of pharmacotherapy for severe personality disorders: Meta-analyses of randomized controlled trials. J Clin Psychiatry. 2010 Jan;71(1):14-25.

We all know these patients:

The young man who, when his name shows up on the ED board, everyone lets out a little groan, knowing his hospital stay will be long and tumultuous.

The middle-aged woman who seems to do want your care and attention and yet rebuffs your attempts to help her, meanwhile, making constant demands on nursing staff.

The older man who trusts no one and will not cooperate with any of his needed care, frustrating staff and physicians alike.

Caring for the patient is integral to the art of doctoring, and yet, there are some people for whom this is incredibly hard to do. They frustrate even the most seasoned professional and work their way under our skin. While their disruptive acts may feel volitional to those of us attempting to provide care, these individuals may suffer from a personality disorder.

Megan Riddle, MD, PhD, is based in the department of psychiatry and behavioral sciences at the University of Washington, Seattle.

NOTES

1. Diagnostic and Statistical Manual of Mental Disorders, 5th Edition. Arlington, VA: American Psychiatric Association; 2013.

2. Riddle M, Meeks T, Alvarez C, Dubovsky A. When personality is the problem: Managing patients with difficult personalities on the acute care unit. J Hosp Med. 2016 Dec;11(12):873-878.

3. Bukh JD, Bock C, Kessing LV. Association between genetic polymorphisms in the serotonergic system and comorbid personality disorders among patients with first-episode depression. J Pers Disord. 2014 Jun;28(3):365-378.

4. Perez-Rodriguez MM, Weinstein S, New AS, et al. Tryptophan-hydroxylase 2 haplotype association with borderline personality disorder and aggression in a sample of patients with personality disorders and healthy controls. J Psychiatr Res. 2010 Nov; 44(15):1075-1081.

5. Checknita D, Maussion G, Labonte B, et al. Monoamine oxidase: A gene promoter methylation and transcriptional downregulation in an offender population with antisocial personality disorder. Br J Psychiatry. 2015 Mar;206(3):216-222.

6. Boen E, Westlye LT, Elvsashagen T, et al. Regional cortical thinning may be a biological marker for borderline personality disorder. Acta Psychiatr Scand. 2014 Sep;130(3):193-204.

7. Thoma P, Friedmann C, Suchan B. Empathy and social problem solving in alcohol dependence, mood disorders and selected personality disorders. Neurosci Biobehav Rev. 2013 Mar;37(3):448-470.

8. Liu H, Liao J, Jiang W, Wang W. Changes in low-frequency fluctuations in patients with antisocial personality disorder revealed by resting-state functional MRI. PLoS One. 2014 Mar 5;9(3):e89790.

9. Yang Y, Raine A. Prefrontal structural and functional brain imaging findings in antisocial, violent, and psychopathic individuals: A meta-analysis. Psychiatry Res. 2009 Nov 30;174(2):81-88.

10. Fok ML, Hayes RD, Chang CK, Stewart R, Callard FJ, Moran P. Life expectancy at birth and all-cause mortality among people with personality disorder. J Psychosom Res. 2012 Aug;73(2):104-107.

11. Tyrer P, Reed GM, Crawford MJ. Classification, assessment, prevalence, and effect of personality disorder. Lancet. 2015 Feb 21;385:717-726.

12. Groves JE. Taking care of the hateful patient. N Engl J Med. 1978 Apr 20; 298:883-887.

13. Groves JE. Management of the borderline patient on a medical or surgical ward: The psychiatric consultant’s role. Int J Psychiatry Med. 1975;6(3):337-348.

14. Bodner E, Cohen-Fridel S, Mashiah M, et al. The attitudes of psychiatric hospital staff toward hospitalization and treatment of patients with borderline personality disorder. BMC psychiatry. 2015 Jan 22;15:2.

15. Colli A, Tanzilli A, Dimaggio G, Lingiardi V. Patient personality and therapist response: An empirical investigation. Am J Psychiatry. 2014 Jan;171(1):102-108.

16. Ingenhoven T, Lafay P, Rinne T, Passchier J, Duivenvoorden H. Effectiveness of pharmacotherapy for severe personality disorders: Meta-analyses of randomized controlled trials. J Clin Psychiatry. 2010 Jan;71(1):14-25.

Even among healthy individuals, feelings of paranoia are not unusual. In modern psychiatry, we consider paranoia to be a pattern of unfounded thinking, centered on the fearful experience of perceived victimization or threat of intentional harm. This means that a patient with paranoia is, by nature, difficult to engage in treatment. A patient might perceive the clinician as attempting to mislead or manipulate him. A therapeutic alliance could require patience on the part of the clinician, creativity,¹ and abandoning attempts at rational “therapeutic” persuasion. The severity of symptoms determines the approach.

In this article, we review the nature of paranoia and the continuum of syndromes to which it is a central feature, as well as treatment approaches.

Categorization and etiology

Until recently, clinicians considered “paranoid” to be a subtype of schizophrenia (Box^2-7); in DSM-5 the limited diagnostic stability and reliability of the categorization rendered the distinction obsolete.⁸ There are several levels of severity of paranoia; this thought process can present in simple variations of normal fears and concerns or in severe forms, with highly organized delusional systems.

The etiology of paranoia is not clear. Over the years, it has been attributed to defense mechanisms of the ego, habitual fears from repetitive exposure, or irregular activity of the amygdala. It is possible that various types of paranoia could have different causes. Functional MRIs indicate that the amygdala is involved in anxiety and threat perception in both primates and humans.⁹

Rational fear vs paranoia

Under the right circumstances, anyone could sense that he (she) is being threatened. Such feelings are normal in occupied countries and nations at war, and are not pathologic in such contexts. Anxiety about potential danger and harassment under truly oppressive circumstances might be biologically ingrained and have value for survival. It is important to employ cultural sensitivity when distinguishing pathological and nonpathological paranoia because some immigrant populations might have increased prevalence rates but without a true mental illness.¹⁰

Perhaps the key to separating realistic fear from paranoia is the recognition of whether the environment is truly safe or hostile; sometimes this is not initially evident to the clinician. The first author (J.A.W.) experienced this when discovering that a patient who was thought to be paranoid was indeed being stalked by another patient.

Rapid social change makes sweeping explanations about the range of threats experienced by any one person of limited value. Persons living with serious and persistent mental illness experience stigma—harassment, abuse, disgrace—and, similar to victims of repeated sexual abuse and other violence, are not necessarily unreasonable in their inner experience of omnipresent threat. In addition, advances in surveillance technology, as well as the media proliferation of depictions of vulnerability and threat, can plant generalized doubt of historically trusted individuals and systems. Under conditions of severe social discrimination or life under a totalitarian regime, constant fear for safety and worry about the intentions of others is reasonable. We must remember that during the Cold War many people in Eastern Europe had legitimate concerns that their phones were tapped. There are still many places in the world where the fear of government or of one’s neighbors exists.

• paranoid personality disorder
• delusional disorder
• paranoia in schizophrenia (Table).

Paranoid personality disorder

The nature of any personality disorder is a long-standing psychological and behavioral pattern that differs significantly from the expectations of one’s culture. Such beliefs and behaviors typically are pervasive across most aspects of the individual’s interactions, and these enduring patterns of personality usually are evident by adolescence or young adulthood. Paranoid personality disorder is marked by pervasive distrust of others. Typical features include:

• suspicion about other people’s motives
• sensitivity to criticism
• keeping grudges against alleged offenders.⁸

The patient must have 4 of the following symptoms to confirm the diagnosis:

• suspicion of others and their motives
• reluctance to confide in others, due to lack of trust
• recurrent doubts about the fidelity of a significant other
• preoccupation with doubt regarding trusting others
• seeing threatening meanings behind benign remarks or events
• perception of attacks upon one’s character or reputation
• bears persistent grudges.⁸

Individuals with paranoid personality disorder tend to lead maladaptive lifestyles and might present as irritable, unpleasant, and emotionally guarded. Paranoid personality disorder is not a form of delusion, but is a pattern of habitual distrust of others.

The disorder generally is expressed verbally, and is seldom accompanied by hallucinations or unpredictable behavior. Distrust of others might result in social isolation and litigious behavior.⁸ Alternately, a patient with this disorder might not present for treatment until later in life after the loss of significant supporting factors, such as the death of parents or loss of steady employment. Examination of these older individuals is likely to reveal long-standing suspiciousness and distrust that previously was hidden by family members. For example, a 68-year-old woman might present saying that she can’t trust her daughter, but her recently deceased spouse would not let her discuss the topic outside of the home.

The etiology of paranoid personality disorder is unknown. Family studies suggest a possible a genetic connection to paranoia in schizophrenia.¹² Others hypothesize that this dysfunction of personality might originate in early feelings of anxiety and low self-esteem, learned from a controlling, cruel, or sadistic parent; the patient then expects others to reject him (her) as the parent did.^13,14 Such individuals might develop deep-seated distrust of others as a defense mechanism. Under stress, such as during a medical illness, patients could develop brief psychoses. Antipsychotic treatment might be useful in some cases of paranoid personality disorder, but should be limited.

Delusional disorder

Delusional disorder is a unique form of psychosis. Patients with delusional disorder might appear rational—as long as they are in independent roles—and their general functioning could go unnoticed. This could change when the delusions predominate their thoughts, or their delusional behavior is unacceptable in a structured environment. Such individuals often suffer from a highly specific delusion fixed on 1 topic. These delusions generally are the only psychotic feature. The most common theme is that of persecution. For example, a person firmly believes he is being followed by foreign agents or by a religious organization, which is blatantly untrue. Another common theme is infidelity.

Paranoia in delusional disorder is about something that is not actually occurring, but could.³ In other words, the delusion is not necessarily bizarre. The patient may have no evidence or could invent “evidence,” yet remain completely resistant to any logical argument against his belief system. In many situations, individuals with delusional disorder function normally in society, until the delusion becomes severe enough to prompt clinical attention.


Paranoia in schizophrenia

In patients with schizophrenia with paranoia, the typical symptoms of disorganization and disturbed affect are less prominent. The condition develops in young adulthood, but could start at any age. Its course typically is chronic and requires psychiatric treatment; the patient may require hospital care.

Although patients with delusional disorder and those with schizophrenia both have delusions, the delusions of the latter typically are bizarre and unlikely to be possible. For example, the patient might believe that her body has been replaced with the inner workings of an alien being or a robot. The paranoid delusions of persons with delusional disorder are much more mundane and could be plausible. Karl Jaspers, a clinician and researcher in the early 20th century, separated delusional disorder from paranoid schizophrenia by noting that the former could be “understandable, even if untrue” while the latter was “not within the realm of understandability.”⁵

A patient with schizophrenia with paranoid delusions usually experiences auditory hallucinations, such as voices threatening persecution or harm. When predominant, patients could be aroused by these fears and can be dangerous to others.^2,4,5

Other presentations of paranoia

Paranoia can occur in affective disorders as well.¹³ Although the cause is only now being understood, clinicians have put forth theories for many years. A depressed person might suffer from excessive guilt and feel that he deserves to be persecuted, while a manic patient might think she is being persecuted for her greatness. In the past, response to electroconvulsive therapy was used to distinguish affective paranoia from other types.²

Paranoia in organic states

Substance use. Psychostimulants, which are known for their motor activity and arousal enhancing properties, as well as the potential for abuse and other negative consequences, could lead to acute paranoid states in susceptible individuals.^15-17 In addition, tetrahydrocannabinol, the active chemical in Cannabis, can cause acute psychotic symptoms, such as paranoia,^18,19 in a dose-dependent manner. A growing body of evidence suggests that a combination of Cannabis use with a genetic predisposition to psychosis may put some individuals at high risk of decompensation.¹⁹ Of growing concern is the evidence that synthetic cannabinoids, which are among the most commonly used new psychoactive substances, could be associated with psychosis, including paranoia.²⁰

Dementia. Persons with dementia often are paranoid. In geriatric patients with dementia, a delusion of thievery is common. When a person has misplaced objects and can’t remember where, the “default” cognition is that someone has taken them. This confabulation may progress to a persistent paranoia and can be draining on caregivers.

Treating paranoia

A patient with paranoia usually has poor insight and cannot be reasoned with. Such individuals are quick to incorporate others into their delusional theories and easily develop notions of conspiracy. In acute psychosis, when the patient presents with fixed beliefs that are not amenable to reality orientation, and poses a threat to his well-being or that of others, alleviating underlying fear and anxiety is the first priority. Swift pharma­cologic measures are required to decrease the patient’s underlying anxiety or anger, before you can try to earn his trust.

Psychopharmacologic interventions should be specific to the diagnosis. Anti­psychotic medications generally will help decrease most paranoia, but affective syndromes usually require lithium or divalproex for best results.^14,21

Develop a therapeutic relationship. The clinician must approach the patient in a practical and straightforward manner, and should not expect a quick therapeutic alliance. Transference and countertransference develop easily in the context of paranoia. Focus on behaviors that are problematic for the patient or the milieu, such as to ensure a safe environment. The patient needs to be aware of how he could come across to others. Clear feedback about behavior, such as “I cannot really listen to you when you’re yelling,” may be effective. It might be unwise to confront delusional paranoia in an agitated patient. Honesty and respect must continue in all communications to build trust. During assessment of a paranoid individual, evaluate the level of dangerousness. Ask your patient if he feels like acting on his beliefs or harming the people that are the targets of his paranoia.

As the patient begins to manage his anxiety and fear, you can develop a therapeutic alliance. The goals of treatment need be those of the patient—such as staying out of the hospital, or behaving in a manner that is required for employment. Over time, work toward growing the patient’s capacity for social interaction and productive activity. Insight might be elusive; however, some patients with paranoia can learn to take a detached view of their thoughts and emotions, and consider them impermanent events of the mind that make their lives difficult. Practice good judgment when aiming for recovery in a patient who does not have insight. For example, a patient can recognize that although there could be a microchip in his brain, he feels better when he takes medication.

In the case of paranoid personality disorder, treatment, as with most personality disorders, can be difficult. The patient might be unlikely to accept help and could distrust caregivers. Cognitive-behavioral therapy could be useful, if the patient can be engaged in the therapeutic process. Although it might be difficult to obtain enhanced insight, the patient could accept logical explanations for situations that provoke distrust. As long as anxiety and anger can be kept under control, the individual might learn the value of adopting the lessons of therapy. Pharmacological treatments are aimed at reducing the anxiety and anger experienced by the paranoid individual. Antipsychotics may be useful for short periods or during a crisis.^14,21

The clinician must remain calm and reassuring when approaching an individual with paranoia, and not react to the projection of paranoid feelings from the patient. Respect for the patient can be conveyed without agreeing with delusions or bizarre thinking. The clinician must keep agreements and appointments with the client to prevent the erosion of trust. Paranoid conditions might respond slowly to pharmacological treatment, therefore establishing a consistent therapeutic relationship is essential.

Even among healthy individuals, feelings of paranoia are not unusual. In modern psychiatry, we consider paranoia to be a pattern of unfounded thinking, centered on the fearful experience of perceived victimization or threat of intentional harm. This means that a patient with paranoia is, by nature, difficult to engage in treatment. A patient might perceive the clinician as attempting to mislead or manipulate him. A therapeutic alliance could require patience on the part of the clinician, creativity,¹ and abandoning attempts at rational “therapeutic” persuasion. The severity of symptoms determines the approach.

In this article, we review the nature of paranoia and the continuum of syndromes to which it is a central feature, as well as treatment approaches.

Categorization and etiology

Until recently, clinicians considered “paranoid” to be a subtype of schizophrenia (Box^2-7); in DSM-5 the limited diagnostic stability and reliability of the categorization rendered the distinction obsolete.⁸ There are several levels of severity of paranoia; this thought process can present in simple variations of normal fears and concerns or in severe forms, with highly organized delusional systems.

The etiology of paranoia is not clear. Over the years, it has been attributed to defense mechanisms of the ego, habitual fears from repetitive exposure, or irregular activity of the amygdala. It is possible that various types of paranoia could have different causes. Functional MRIs indicate that the amygdala is involved in anxiety and threat perception in both primates and humans.⁹

Rational fear vs paranoia

Under the right circumstances, anyone could sense that he (she) is being threatened. Such feelings are normal in occupied countries and nations at war, and are not pathologic in such contexts. Anxiety about potential danger and harassment under truly oppressive circumstances might be biologically ingrained and have value for survival. It is important to employ cultural sensitivity when distinguishing pathological and nonpathological paranoia because some immigrant populations might have increased prevalence rates but without a true mental illness.¹⁰

Perhaps the key to separating realistic fear from paranoia is the recognition of whether the environment is truly safe or hostile; sometimes this is not initially evident to the clinician. The first author (J.A.W.) experienced this when discovering that a patient who was thought to be paranoid was indeed being stalked by another patient.

Rapid social change makes sweeping explanations about the range of threats experienced by any one person of limited value. Persons living with serious and persistent mental illness experience stigma—harassment, abuse, disgrace—and, similar to victims of repeated sexual abuse and other violence, are not necessarily unreasonable in their inner experience of omnipresent threat. In addition, advances in surveillance technology, as well as the media proliferation of depictions of vulnerability and threat, can plant generalized doubt of historically trusted individuals and systems. Under conditions of severe social discrimination or life under a totalitarian regime, constant fear for safety and worry about the intentions of others is reasonable. We must remember that during the Cold War many people in Eastern Europe had legitimate concerns that their phones were tapped. There are still many places in the world where the fear of government or of one’s neighbors exists.

• paranoid personality disorder
• delusional disorder
• paranoia in schizophrenia (Table).

Paranoid personality disorder

The nature of any personality disorder is a long-standing psychological and behavioral pattern that differs significantly from the expectations of one’s culture. Such beliefs and behaviors typically are pervasive across most aspects of the individual’s interactions, and these enduring patterns of personality usually are evident by adolescence or young adulthood. Paranoid personality disorder is marked by pervasive distrust of others. Typical features include:

• suspicion about other people’s motives
• sensitivity to criticism
• keeping grudges against alleged offenders.⁸

The patient must have 4 of the following symptoms to confirm the diagnosis:

• suspicion of others and their motives
• reluctance to confide in others, due to lack of trust
• recurrent doubts about the fidelity of a significant other
• preoccupation with doubt regarding trusting others
• seeing threatening meanings behind benign remarks or events
• perception of attacks upon one’s character or reputation
• bears persistent grudges.⁸

Individuals with paranoid personality disorder tend to lead maladaptive lifestyles and might present as irritable, unpleasant, and emotionally guarded. Paranoid personality disorder is not a form of delusion, but is a pattern of habitual distrust of others.

The disorder generally is expressed verbally, and is seldom accompanied by hallucinations or unpredictable behavior. Distrust of others might result in social isolation and litigious behavior.⁸ Alternately, a patient with this disorder might not present for treatment until later in life after the loss of significant supporting factors, such as the death of parents or loss of steady employment. Examination of these older individuals is likely to reveal long-standing suspiciousness and distrust that previously was hidden by family members. For example, a 68-year-old woman might present saying that she can’t trust her daughter, but her recently deceased spouse would not let her discuss the topic outside of the home.

The etiology of paranoid personality disorder is unknown. Family studies suggest a possible a genetic connection to paranoia in schizophrenia.¹² Others hypothesize that this dysfunction of personality might originate in early feelings of anxiety and low self-esteem, learned from a controlling, cruel, or sadistic parent; the patient then expects others to reject him (her) as the parent did.^13,14 Such individuals might develop deep-seated distrust of others as a defense mechanism. Under stress, such as during a medical illness, patients could develop brief psychoses. Antipsychotic treatment might be useful in some cases of paranoid personality disorder, but should be limited.

Delusional disorder

Delusional disorder is a unique form of psychosis. Patients with delusional disorder might appear rational—as long as they are in independent roles—and their general functioning could go unnoticed. This could change when the delusions predominate their thoughts, or their delusional behavior is unacceptable in a structured environment. Such individuals often suffer from a highly specific delusion fixed on 1 topic. These delusions generally are the only psychotic feature. The most common theme is that of persecution. For example, a person firmly believes he is being followed by foreign agents or by a religious organization, which is blatantly untrue. Another common theme is infidelity.

Paranoia in delusional disorder is about something that is not actually occurring, but could.³ In other words, the delusion is not necessarily bizarre. The patient may have no evidence or could invent “evidence,” yet remain completely resistant to any logical argument against his belief system. In many situations, individuals with delusional disorder function normally in society, until the delusion becomes severe enough to prompt clinical attention.


Paranoia in schizophrenia

In patients with schizophrenia with paranoia, the typical symptoms of disorganization and disturbed affect are less prominent. The condition develops in young adulthood, but could start at any age. Its course typically is chronic and requires psychiatric treatment; the patient may require hospital care.

Although patients with delusional disorder and those with schizophrenia both have delusions, the delusions of the latter typically are bizarre and unlikely to be possible. For example, the patient might believe that her body has been replaced with the inner workings of an alien being or a robot. The paranoid delusions of persons with delusional disorder are much more mundane and could be plausible. Karl Jaspers, a clinician and researcher in the early 20th century, separated delusional disorder from paranoid schizophrenia by noting that the former could be “understandable, even if untrue” while the latter was “not within the realm of understandability.”⁵

A patient with schizophrenia with paranoid delusions usually experiences auditory hallucinations, such as voices threatening persecution or harm. When predominant, patients could be aroused by these fears and can be dangerous to others.^2,4,5

Other presentations of paranoia

Paranoia can occur in affective disorders as well.¹³ Although the cause is only now being understood, clinicians have put forth theories for many years. A depressed person might suffer from excessive guilt and feel that he deserves to be persecuted, while a manic patient might think she is being persecuted for her greatness. In the past, response to electroconvulsive therapy was used to distinguish affective paranoia from other types.²

Paranoia in organic states

Substance use. Psychostimulants, which are known for their motor activity and arousal enhancing properties, as well as the potential for abuse and other negative consequences, could lead to acute paranoid states in susceptible individuals.^15-17 In addition, tetrahydrocannabinol, the active chemical in Cannabis, can cause acute psychotic symptoms, such as paranoia,^18,19 in a dose-dependent manner. A growing body of evidence suggests that a combination of Cannabis use with a genetic predisposition to psychosis may put some individuals at high risk of decompensation.¹⁹ Of growing concern is the evidence that synthetic cannabinoids, which are among the most commonly used new psychoactive substances, could be associated with psychosis, including paranoia.²⁰

Dementia. Persons with dementia often are paranoid. In geriatric patients with dementia, a delusion of thievery is common. When a person has misplaced objects and can’t remember where, the “default” cognition is that someone has taken them. This confabulation may progress to a persistent paranoia and can be draining on caregivers.

Treating paranoia

A patient with paranoia usually has poor insight and cannot be reasoned with. Such individuals are quick to incorporate others into their delusional theories and easily develop notions of conspiracy. In acute psychosis, when the patient presents with fixed beliefs that are not amenable to reality orientation, and poses a threat to his well-being or that of others, alleviating underlying fear and anxiety is the first priority. Swift pharma­cologic measures are required to decrease the patient’s underlying anxiety or anger, before you can try to earn his trust.

Psychopharmacologic interventions should be specific to the diagnosis. Anti­psychotic medications generally will help decrease most paranoia, but affective syndromes usually require lithium or divalproex for best results.^14,21

Develop a therapeutic relationship. The clinician must approach the patient in a practical and straightforward manner, and should not expect a quick therapeutic alliance. Transference and countertransference develop easily in the context of paranoia. Focus on behaviors that are problematic for the patient or the milieu, such as to ensure a safe environment. The patient needs to be aware of how he could come across to others. Clear feedback about behavior, such as “I cannot really listen to you when you’re yelling,” may be effective. It might be unwise to confront delusional paranoia in an agitated patient. Honesty and respect must continue in all communications to build trust. During assessment of a paranoid individual, evaluate the level of dangerousness. Ask your patient if he feels like acting on his beliefs or harming the people that are the targets of his paranoia.

As the patient begins to manage his anxiety and fear, you can develop a therapeutic alliance. The goals of treatment need be those of the patient—such as staying out of the hospital, or behaving in a manner that is required for employment. Over time, work toward growing the patient’s capacity for social interaction and productive activity. Insight might be elusive; however, some patients with paranoia can learn to take a detached view of their thoughts and emotions, and consider them impermanent events of the mind that make their lives difficult. Practice good judgment when aiming for recovery in a patient who does not have insight. For example, a patient can recognize that although there could be a microchip in his brain, he feels better when he takes medication.

In the case of paranoid personality disorder, treatment, as with most personality disorders, can be difficult. The patient might be unlikely to accept help and could distrust caregivers. Cognitive-behavioral therapy could be useful, if the patient can be engaged in the therapeutic process. Although it might be difficult to obtain enhanced insight, the patient could accept logical explanations for situations that provoke distrust. As long as anxiety and anger can be kept under control, the individual might learn the value of adopting the lessons of therapy. Pharmacological treatments are aimed at reducing the anxiety and anger experienced by the paranoid individual. Antipsychotics may be useful for short periods or during a crisis.^14,21

The clinician must remain calm and reassuring when approaching an individual with paranoia, and not react to the projection of paranoid feelings from the patient. Respect for the patient can be conveyed without agreeing with delusions or bizarre thinking. The clinician must keep agreements and appointments with the client to prevent the erosion of trust. Paranoid conditions might respond slowly to pharmacological treatment, therefore establishing a consistent therapeutic relationship is essential.

Even among healthy individuals, feelings of paranoia are not unusual. In modern psychiatry, we consider paranoia to be a pattern of unfounded thinking, centered on the fearful experience of perceived victimization or threat of intentional harm. This means that a patient with paranoia is, by nature, difficult to engage in treatment. A patient might perceive the clinician as attempting to mislead or manipulate him. A therapeutic alliance could require patience on the part of the clinician, creativity,¹ and abandoning attempts at rational “therapeutic” persuasion. The severity of symptoms determines the approach.

In this article, we review the nature of paranoia and the continuum of syndromes to which it is a central feature, as well as treatment approaches.

Categorization and etiology

Until recently, clinicians considered “paranoid” to be a subtype of schizophrenia (Box^2-7); in DSM-5 the limited diagnostic stability and reliability of the categorization rendered the distinction obsolete.⁸ There are several levels of severity of paranoia; this thought process can present in simple variations of normal fears and concerns or in severe forms, with highly organized delusional systems.

The etiology of paranoia is not clear. Over the years, it has been attributed to defense mechanisms of the ego, habitual fears from repetitive exposure, or irregular activity of the amygdala. It is possible that various types of paranoia could have different causes. Functional MRIs indicate that the amygdala is involved in anxiety and threat perception in both primates and humans.⁹

Rational fear vs paranoia

Under the right circumstances, anyone could sense that he (she) is being threatened. Such feelings are normal in occupied countries and nations at war, and are not pathologic in such contexts. Anxiety about potential danger and harassment under truly oppressive circumstances might be biologically ingrained and have value for survival. It is important to employ cultural sensitivity when distinguishing pathological and nonpathological paranoia because some immigrant populations might have increased prevalence rates but without a true mental illness.¹⁰

Perhaps the key to separating realistic fear from paranoia is the recognition of whether the environment is truly safe or hostile; sometimes this is not initially evident to the clinician. The first author (J.A.W.) experienced this when discovering that a patient who was thought to be paranoid was indeed being stalked by another patient.

Rapid social change makes sweeping explanations about the range of threats experienced by any one person of limited value. Persons living with serious and persistent mental illness experience stigma—harassment, abuse, disgrace—and, similar to victims of repeated sexual abuse and other violence, are not necessarily unreasonable in their inner experience of omnipresent threat. In addition, advances in surveillance technology, as well as the media proliferation of depictions of vulnerability and threat, can plant generalized doubt of historically trusted individuals and systems. Under conditions of severe social discrimination or life under a totalitarian regime, constant fear for safety and worry about the intentions of others is reasonable. We must remember that during the Cold War many people in Eastern Europe had legitimate concerns that their phones were tapped. There are still many places in the world where the fear of government or of one’s neighbors exists.

• paranoid personality disorder
• delusional disorder
• paranoia in schizophrenia (Table).

Paranoid personality disorder

The nature of any personality disorder is a long-standing psychological and behavioral pattern that differs significantly from the expectations of one’s culture. Such beliefs and behaviors typically are pervasive across most aspects of the individual’s interactions, and these enduring patterns of personality usually are evident by adolescence or young adulthood. Paranoid personality disorder is marked by pervasive distrust of others. Typical features include:

• suspicion about other people’s motives
• sensitivity to criticism
• keeping grudges against alleged offenders.⁸

The patient must have 4 of the following symptoms to confirm the diagnosis:

• suspicion of others and their motives
• reluctance to confide in others, due to lack of trust
• recurrent doubts about the fidelity of a significant other
• preoccupation with doubt regarding trusting others
• seeing threatening meanings behind benign remarks or events
• perception of attacks upon one’s character or reputation
• bears persistent grudges.⁸

Individuals with paranoid personality disorder tend to lead maladaptive lifestyles and might present as irritable, unpleasant, and emotionally guarded. Paranoid personality disorder is not a form of delusion, but is a pattern of habitual distrust of others.

The disorder generally is expressed verbally, and is seldom accompanied by hallucinations or unpredictable behavior. Distrust of others might result in social isolation and litigious behavior.⁸ Alternately, a patient with this disorder might not present for treatment until later in life after the loss of significant supporting factors, such as the death of parents or loss of steady employment. Examination of these older individuals is likely to reveal long-standing suspiciousness and distrust that previously was hidden by family members. For example, a 68-year-old woman might present saying that she can’t trust her daughter, but her recently deceased spouse would not let her discuss the topic outside of the home.

The etiology of paranoid personality disorder is unknown. Family studies suggest a possible a genetic connection to paranoia in schizophrenia.¹² Others hypothesize that this dysfunction of personality might originate in early feelings of anxiety and low self-esteem, learned from a controlling, cruel, or sadistic parent; the patient then expects others to reject him (her) as the parent did.^13,14 Such individuals might develop deep-seated distrust of others as a defense mechanism. Under stress, such as during a medical illness, patients could develop brief psychoses. Antipsychotic treatment might be useful in some cases of paranoid personality disorder, but should be limited.

Delusional disorder

Delusional disorder is a unique form of psychosis. Patients with delusional disorder might appear rational—as long as they are in independent roles—and their general functioning could go unnoticed. This could change when the delusions predominate their thoughts, or their delusional behavior is unacceptable in a structured environment. Such individuals often suffer from a highly specific delusion fixed on 1 topic. These delusions generally are the only psychotic feature. The most common theme is that of persecution. For example, a person firmly believes he is being followed by foreign agents or by a religious organization, which is blatantly untrue. Another common theme is infidelity.

Paranoia in delusional disorder is about something that is not actually occurring, but could.³ In other words, the delusion is not necessarily bizarre. The patient may have no evidence or could invent “evidence,” yet remain completely resistant to any logical argument against his belief system. In many situations, individuals with delusional disorder function normally in society, until the delusion becomes severe enough to prompt clinical attention.


Paranoia in schizophrenia

In patients with schizophrenia with paranoia, the typical symptoms of disorganization and disturbed affect are less prominent. The condition develops in young adulthood, but could start at any age. Its course typically is chronic and requires psychiatric treatment; the patient may require hospital care.

Although patients with delusional disorder and those with schizophrenia both have delusions, the delusions of the latter typically are bizarre and unlikely to be possible. For example, the patient might believe that her body has been replaced with the inner workings of an alien being or a robot. The paranoid delusions of persons with delusional disorder are much more mundane and could be plausible. Karl Jaspers, a clinician and researcher in the early 20th century, separated delusional disorder from paranoid schizophrenia by noting that the former could be “understandable, even if untrue” while the latter was “not within the realm of understandability.”⁵

A patient with schizophrenia with paranoid delusions usually experiences auditory hallucinations, such as voices threatening persecution or harm. When predominant, patients could be aroused by these fears and can be dangerous to others.^2,4,5

Other presentations of paranoia

Paranoia can occur in affective disorders as well.¹³ Although the cause is only now being understood, clinicians have put forth theories for many years. A depressed person might suffer from excessive guilt and feel that he deserves to be persecuted, while a manic patient might think she is being persecuted for her greatness. In the past, response to electroconvulsive therapy was used to distinguish affective paranoia from other types.²

Paranoia in organic states

Substance use. Psychostimulants, which are known for their motor activity and arousal enhancing properties, as well as the potential for abuse and other negative consequences, could lead to acute paranoid states in susceptible individuals.^15-17 In addition, tetrahydrocannabinol, the active chemical in Cannabis, can cause acute psychotic symptoms, such as paranoia,^18,19 in a dose-dependent manner. A growing body of evidence suggests that a combination of Cannabis use with a genetic predisposition to psychosis may put some individuals at high risk of decompensation.¹⁹ Of growing concern is the evidence that synthetic cannabinoids, which are among the most commonly used new psychoactive substances, could be associated with psychosis, including paranoia.²⁰

Dementia. Persons with dementia often are paranoid. In geriatric patients with dementia, a delusion of thievery is common. When a person has misplaced objects and can’t remember where, the “default” cognition is that someone has taken them. This confabulation may progress to a persistent paranoia and can be draining on caregivers.

Treating paranoia

A patient with paranoia usually has poor insight and cannot be reasoned with. Such individuals are quick to incorporate others into their delusional theories and easily develop notions of conspiracy. In acute psychosis, when the patient presents with fixed beliefs that are not amenable to reality orientation, and poses a threat to his well-being or that of others, alleviating underlying fear and anxiety is the first priority. Swift pharma­cologic measures are required to decrease the patient’s underlying anxiety or anger, before you can try to earn his trust.

Psychopharmacologic interventions should be specific to the diagnosis. Anti­psychotic medications generally will help decrease most paranoia, but affective syndromes usually require lithium or divalproex for best results.^14,21

Develop a therapeutic relationship. The clinician must approach the patient in a practical and straightforward manner, and should not expect a quick therapeutic alliance. Transference and countertransference develop easily in the context of paranoia. Focus on behaviors that are problematic for the patient or the milieu, such as to ensure a safe environment. The patient needs to be aware of how he could come across to others. Clear feedback about behavior, such as “I cannot really listen to you when you’re yelling,” may be effective. It might be unwise to confront delusional paranoia in an agitated patient. Honesty and respect must continue in all communications to build trust. During assessment of a paranoid individual, evaluate the level of dangerousness. Ask your patient if he feels like acting on his beliefs or harming the people that are the targets of his paranoia.

As the patient begins to manage his anxiety and fear, you can develop a therapeutic alliance. The goals of treatment need be those of the patient—such as staying out of the hospital, or behaving in a manner that is required for employment. Over time, work toward growing the patient’s capacity for social interaction and productive activity. Insight might be elusive; however, some patients with paranoia can learn to take a detached view of their thoughts and emotions, and consider them impermanent events of the mind that make their lives difficult. Practice good judgment when aiming for recovery in a patient who does not have insight. For example, a patient can recognize that although there could be a microchip in his brain, he feels better when he takes medication.

In the case of paranoid personality disorder, treatment, as with most personality disorders, can be difficult. The patient might be unlikely to accept help and could distrust caregivers. Cognitive-behavioral therapy could be useful, if the patient can be engaged in the therapeutic process. Although it might be difficult to obtain enhanced insight, the patient could accept logical explanations for situations that provoke distrust. As long as anxiety and anger can be kept under control, the individual might learn the value of adopting the lessons of therapy. Pharmacological treatments are aimed at reducing the anxiety and anger experienced by the paranoid individual. Antipsychotics may be useful for short periods or during a crisis.^14,21

The clinician must remain calm and reassuring when approaching an individual with paranoia, and not react to the projection of paranoid feelings from the patient. Respect for the patient can be conveyed without agreeing with delusions or bizarre thinking. The clinician must keep agreements and appointments with the client to prevent the erosion of trust. Paranoid conditions might respond slowly to pharmacological treatment, therefore establishing a consistent therapeutic relationship is essential.