Personality Disorders

In Drs. Ali M. Hashmi and Dennis Vowell’s article “The manipulative self-harmer” (Cases That Test Your Skills, Current Psychiatry, June 2010, p. 44-48), the authors regard the patient’s outcome (“Recently she was placed in a more restrictive setting because her hostile and self-destructive behavior escalated”) as characteristic of borderline personality disorder (BPD) (“Ms. L is no different from most axis II Cluster B disordered patients.”). In my view, this is the greatest risk of calling a patient borderline—it tends to justify poor outcomes by thinking that it is just characteristic of the illness. Instead, shouldn’t we worry that our treatment may be suboptimal? Maybe we are missing something?

For example, Ms. L may have some degree of bipolarity (see the Harvard Bipolarity Index as a characterization of that concept, incorporating but going beyond the DSM-IV-TR) that could account for their observation, “Her mood and behavior continue to oscillate; she is relatively calm and satisfied 1 week, angry and assaultive the next.” Instead of concluding, “this stormy course is expected…” the authors should be wondering whether they might be contributing to it by restarting venlafaxine despite simultaneous carbamazepine initiation. Granted, the possibilities of bipolarity and antidepressant-induced rapid cycling are complex considerations, because we lack solid footing for differentiating BPD and bipolar disorder and for determining causality when a patient experiences rapid mood changes while taking an antidepressant. These are controversial issues, but why present the case as though it’s illustrative of accepted principles? I find it perfectly illustrative of how badly we’re floundering as a field.

Jim Phelps, MD
PsychEducation.org
Corvallis, OR

The authors respond

Dr. Phelps’ contention is that our observation that Ms. L’s “hostile and self-destructive behavior” makes her “no different from most axis II Cluster B disordered patients” somehow understates the extent of her illness, perhaps leading to poorer outcomes. Negative countertransference toward such patients is the norm and handling it empathically is an integral part of the treatment relationship. This is true even though the severity of Ms. L’s personality pathology, as evidenced by her placement in the “911 program,” may not be representative of all patients with BPD.

We agree that “the possibilities of…antidepressant-induced rapid cycling are complex considerations.” Even experts disagree on this. In fact, as we pointed out, Ms. L resisted medication tapers, at one point insisting that high doses of fluoxetine and venafaxine be used together for depression, a request we denied specifically for fear of worsening her mood lability. Fluoxetine was discontinued and venlafaxine restarted at a lower dose to treat her persistent depression as well as to help with her chronic back pain. Because by this time she was taking carbamazepine as well, we felt the risk was acceptable. Her positive long-term outcome has validated our approach.

We disagree that psychiatry is “floundering” as a field. In fact, exchanges like this are a core component of placing our specialty on a more solid, scientific basis to position it for future challenges.

Ali M. Hashmi, MD
Medical director
Mid-South Health Systems
Jonesboro, AR
Clinical instructor
Department of psychiatry
University of Arkansas for Medical Science
College of Medicine
Little Rock, AR

Dennis Vowell, PsyD
Clinical psychologist
Mid-South Health Systems
Paragould, AR

In Drs. Ali M. Hashmi and Dennis Vowell’s article “The manipulative self-harmer” (Cases That Test Your Skills, Current Psychiatry, June 2010, p. 44-48), the authors regard the patient’s outcome (“Recently she was placed in a more restrictive setting because her hostile and self-destructive behavior escalated”) as characteristic of borderline personality disorder (BPD) (“Ms. L is no different from most axis II Cluster B disordered patients.”). In my view, this is the greatest risk of calling a patient borderline—it tends to justify poor outcomes by thinking that it is just characteristic of the illness. Instead, shouldn’t we worry that our treatment may be suboptimal? Maybe we are missing something?

For example, Ms. L may have some degree of bipolarity (see the Harvard Bipolarity Index as a characterization of that concept, incorporating but going beyond the DSM-IV-TR) that could account for their observation, “Her mood and behavior continue to oscillate; she is relatively calm and satisfied 1 week, angry and assaultive the next.” Instead of concluding, “this stormy course is expected…” the authors should be wondering whether they might be contributing to it by restarting venlafaxine despite simultaneous carbamazepine initiation. Granted, the possibilities of bipolarity and antidepressant-induced rapid cycling are complex considerations, because we lack solid footing for differentiating BPD and bipolar disorder and for determining causality when a patient experiences rapid mood changes while taking an antidepressant. These are controversial issues, but why present the case as though it’s illustrative of accepted principles? I find it perfectly illustrative of how badly we’re floundering as a field.

Jim Phelps, MD
PsychEducation.org
Corvallis, OR

The authors respond

Dr. Phelps’ contention is that our observation that Ms. L’s “hostile and self-destructive behavior” makes her “no different from most axis II Cluster B disordered patients” somehow understates the extent of her illness, perhaps leading to poorer outcomes. Negative countertransference toward such patients is the norm and handling it empathically is an integral part of the treatment relationship. This is true even though the severity of Ms. L’s personality pathology, as evidenced by her placement in the “911 program,” may not be representative of all patients with BPD.

We agree that “the possibilities of…antidepressant-induced rapid cycling are complex considerations.” Even experts disagree on this. In fact, as we pointed out, Ms. L resisted medication tapers, at one point insisting that high doses of fluoxetine and venafaxine be used together for depression, a request we denied specifically for fear of worsening her mood lability. Fluoxetine was discontinued and venlafaxine restarted at a lower dose to treat her persistent depression as well as to help with her chronic back pain. Because by this time she was taking carbamazepine as well, we felt the risk was acceptable. Her positive long-term outcome has validated our approach.

We disagree that psychiatry is “floundering” as a field. In fact, exchanges like this are a core component of placing our specialty on a more solid, scientific basis to position it for future challenges.

Ali M. Hashmi, MD
Medical director
Mid-South Health Systems
Jonesboro, AR
Clinical instructor
Department of psychiatry
University of Arkansas for Medical Science
College of Medicine
Little Rock, AR

Dennis Vowell, PsyD
Clinical psychologist
Mid-South Health Systems
Paragould, AR

In Drs. Ali M. Hashmi and Dennis Vowell’s article “The manipulative self-harmer” (Cases That Test Your Skills, Current Psychiatry, June 2010, p. 44-48), the authors regard the patient’s outcome (“Recently she was placed in a more restrictive setting because her hostile and self-destructive behavior escalated”) as characteristic of borderline personality disorder (BPD) (“Ms. L is no different from most axis II Cluster B disordered patients.”). In my view, this is the greatest risk of calling a patient borderline—it tends to justify poor outcomes by thinking that it is just characteristic of the illness. Instead, shouldn’t we worry that our treatment may be suboptimal? Maybe we are missing something?

For example, Ms. L may have some degree of bipolarity (see the Harvard Bipolarity Index as a characterization of that concept, incorporating but going beyond the DSM-IV-TR) that could account for their observation, “Her mood and behavior continue to oscillate; she is relatively calm and satisfied 1 week, angry and assaultive the next.” Instead of concluding, “this stormy course is expected…” the authors should be wondering whether they might be contributing to it by restarting venlafaxine despite simultaneous carbamazepine initiation. Granted, the possibilities of bipolarity and antidepressant-induced rapid cycling are complex considerations, because we lack solid footing for differentiating BPD and bipolar disorder and for determining causality when a patient experiences rapid mood changes while taking an antidepressant. These are controversial issues, but why present the case as though it’s illustrative of accepted principles? I find it perfectly illustrative of how badly we’re floundering as a field.

Jim Phelps, MD
PsychEducation.org
Corvallis, OR

The authors respond

Dr. Phelps’ contention is that our observation that Ms. L’s “hostile and self-destructive behavior” makes her “no different from most axis II Cluster B disordered patients” somehow understates the extent of her illness, perhaps leading to poorer outcomes. Negative countertransference toward such patients is the norm and handling it empathically is an integral part of the treatment relationship. This is true even though the severity of Ms. L’s personality pathology, as evidenced by her placement in the “911 program,” may not be representative of all patients with BPD.

We agree that “the possibilities of…antidepressant-induced rapid cycling are complex considerations.” Even experts disagree on this. In fact, as we pointed out, Ms. L resisted medication tapers, at one point insisting that high doses of fluoxetine and venafaxine be used together for depression, a request we denied specifically for fear of worsening her mood lability. Fluoxetine was discontinued and venlafaxine restarted at a lower dose to treat her persistent depression as well as to help with her chronic back pain. Because by this time she was taking carbamazepine as well, we felt the risk was acceptable. Her positive long-term outcome has validated our approach.

We disagree that psychiatry is “floundering” as a field. In fact, exchanges like this are a core component of placing our specialty on a more solid, scientific basis to position it for future challenges.

Ali M. Hashmi, MD
Medical director
Mid-South Health Systems
Jonesboro, AR
Clinical instructor
Department of psychiatry
University of Arkansas for Medical Science
College of Medicine
Little Rock, AR

Dennis Vowell, PsyD
Clinical psychologist
Mid-South Health Systems
Paragould, AR

I appreciated “The woman who saw the light” (Current Psychiatry, July 2010, p. 44-48) in which Dr. R. Andrew Sewell et al describe a 30-year-old woman with schizoaffective disorder and a 7-year history of visual disturbances, including “flashing lights.” The authors’ differential diagnosis did not include the possibility of visual disturbance secondary to atypical anti-psychotic serotonergic antagonism. Photopsia and similar phenomena are not uncommon with 5HT antagonist antidepressants, such as nefazodone.¹ They also are well-known sequelae of lysergic acid diethylamide (LSD), a complex serotonin antagonist/agonist, and would be included under the DSM-IV-TR diagnosis hallucinogen persisting perceptual disorder (HPPD).² Risperidone, a 5HT2-blocking atypical, and selective serotonin reuptake inhibitors may worsen HPPD effects.^3,4 Visual disturbance with risperidone also has been reported in a patient with no LSD exposure.⁵ Dr. Sewell’s patient was treated sequentially with aripiprazole and olanzapine. Both have 5HT blocking properties.

I wonder if the patient has a history of hallucinogen or LSD exposure, or whether her visual symptoms might be related to the use of atypical anti-psychotics combined with sertraline. It would be interesting to see if her symptoms abated with use of a first-generation antipsychotic.

Charles Krasnow, MD
Adjunct clinical assistant professor of psychiatry
University of Michigan Medical School
Ann Arbor, MI

The authors respond

We agree with Dr. Krasnow that HPPD belongs within our differential diagnosis for photopsia and regret omitting it from our article. We consider this to be unlikely, however, because she had no prior LSD use, a history of well-formed visual hallucinations not characteristic of HPPD, and no other characteristic symptoms of HPPD (palinopsia, afterimages, illusory movement, etc.).

In addition, she tolerated olanzapine well, and there is anecdotal evidence and 1 case report to suggest that olanzapine exacerbates HPPD.¹

HPPD typically is considered a rare sequela of LSD use, although even more rarely it may be caused by other drugs. Common visual disturbances attributed to HPPD are recurrent geometric hallucinations, perception of peripheral movement, colored flashes, intensified colors, palinopsia, positive afterimages, haloes around objects, macropsia, and micropsia occurring spontaneously in individuals with no prior psychopathology. These disturbances can be intermittent or continuous, slowly reversible or irreversible, but are severe, intrusive, and cause functional debility. Sufferers retain insight that these phenomena are the consequence of LSD use and usually seek psychiatric help.

HPPD may be diagnosed by the presence of an identifiable trigger, prodromal symptoms, and presentation onset; by the characteristics of the perceptual disturbances, their frequency, duration, intensity, and course; and by the accompanying negative affect and preserved insight.²

This LSD-induced persistence of visual imagery after the image is removed from the visual field is thought to result from dysfunction of serotonergic cortical inhibitory interneurons with GABAergic outputs that normally suppress visual processors.³ Clonazepam often is helpful.²

R. Andrew Sewell, MD
VA Connecticut Healthcare/Yale University
School of Medicine
New Haven, CT

David Kozin
McLean Hospital/Harvard Medical School
Belmont, MA

Miles G. Cunningham, MD, PhD
McLean Hospital/Harvard Medical School
Belmont, MA

I appreciated “The woman who saw the light” (Current Psychiatry, July 2010, p. 44-48) in which Dr. R. Andrew Sewell et al describe a 30-year-old woman with schizoaffective disorder and a 7-year history of visual disturbances, including “flashing lights.” The authors’ differential diagnosis did not include the possibility of visual disturbance secondary to atypical anti-psychotic serotonergic antagonism. Photopsia and similar phenomena are not uncommon with 5HT antagonist antidepressants, such as nefazodone.¹ They also are well-known sequelae of lysergic acid diethylamide (LSD), a complex serotonin antagonist/agonist, and would be included under the DSM-IV-TR diagnosis hallucinogen persisting perceptual disorder (HPPD).² Risperidone, a 5HT2-blocking atypical, and selective serotonin reuptake inhibitors may worsen HPPD effects.^3,4 Visual disturbance with risperidone also has been reported in a patient with no LSD exposure.⁵ Dr. Sewell’s patient was treated sequentially with aripiprazole and olanzapine. Both have 5HT blocking properties.

I wonder if the patient has a history of hallucinogen or LSD exposure, or whether her visual symptoms might be related to the use of atypical anti-psychotics combined with sertraline. It would be interesting to see if her symptoms abated with use of a first-generation antipsychotic.

Charles Krasnow, MD
Adjunct clinical assistant professor of psychiatry
University of Michigan Medical School
Ann Arbor, MI

The authors respond

We agree with Dr. Krasnow that HPPD belongs within our differential diagnosis for photopsia and regret omitting it from our article. We consider this to be unlikely, however, because she had no prior LSD use, a history of well-formed visual hallucinations not characteristic of HPPD, and no other characteristic symptoms of HPPD (palinopsia, afterimages, illusory movement, etc.).

In addition, she tolerated olanzapine well, and there is anecdotal evidence and 1 case report to suggest that olanzapine exacerbates HPPD.¹

HPPD typically is considered a rare sequela of LSD use, although even more rarely it may be caused by other drugs. Common visual disturbances attributed to HPPD are recurrent geometric hallucinations, perception of peripheral movement, colored flashes, intensified colors, palinopsia, positive afterimages, haloes around objects, macropsia, and micropsia occurring spontaneously in individuals with no prior psychopathology. These disturbances can be intermittent or continuous, slowly reversible or irreversible, but are severe, intrusive, and cause functional debility. Sufferers retain insight that these phenomena are the consequence of LSD use and usually seek psychiatric help.

HPPD may be diagnosed by the presence of an identifiable trigger, prodromal symptoms, and presentation onset; by the characteristics of the perceptual disturbances, their frequency, duration, intensity, and course; and by the accompanying negative affect and preserved insight.²

This LSD-induced persistence of visual imagery after the image is removed from the visual field is thought to result from dysfunction of serotonergic cortical inhibitory interneurons with GABAergic outputs that normally suppress visual processors.³ Clonazepam often is helpful.²

R. Andrew Sewell, MD
VA Connecticut Healthcare/Yale University
School of Medicine
New Haven, CT

David Kozin
McLean Hospital/Harvard Medical School
Belmont, MA

Miles G. Cunningham, MD, PhD
McLean Hospital/Harvard Medical School
Belmont, MA

I appreciated “The woman who saw the light” (Current Psychiatry, July 2010, p. 44-48) in which Dr. R. Andrew Sewell et al describe a 30-year-old woman with schizoaffective disorder and a 7-year history of visual disturbances, including “flashing lights.” The authors’ differential diagnosis did not include the possibility of visual disturbance secondary to atypical anti-psychotic serotonergic antagonism. Photopsia and similar phenomena are not uncommon with 5HT antagonist antidepressants, such as nefazodone.¹ They also are well-known sequelae of lysergic acid diethylamide (LSD), a complex serotonin antagonist/agonist, and would be included under the DSM-IV-TR diagnosis hallucinogen persisting perceptual disorder (HPPD).² Risperidone, a 5HT2-blocking atypical, and selective serotonin reuptake inhibitors may worsen HPPD effects.^3,4 Visual disturbance with risperidone also has been reported in a patient with no LSD exposure.⁵ Dr. Sewell’s patient was treated sequentially with aripiprazole and olanzapine. Both have 5HT blocking properties.

I wonder if the patient has a history of hallucinogen or LSD exposure, or whether her visual symptoms might be related to the use of atypical anti-psychotics combined with sertraline. It would be interesting to see if her symptoms abated with use of a first-generation antipsychotic.

Charles Krasnow, MD
Adjunct clinical assistant professor of psychiatry
University of Michigan Medical School
Ann Arbor, MI

The authors respond

We agree with Dr. Krasnow that HPPD belongs within our differential diagnosis for photopsia and regret omitting it from our article. We consider this to be unlikely, however, because she had no prior LSD use, a history of well-formed visual hallucinations not characteristic of HPPD, and no other characteristic symptoms of HPPD (palinopsia, afterimages, illusory movement, etc.).

In addition, she tolerated olanzapine well, and there is anecdotal evidence and 1 case report to suggest that olanzapine exacerbates HPPD.¹

HPPD typically is considered a rare sequela of LSD use, although even more rarely it may be caused by other drugs. Common visual disturbances attributed to HPPD are recurrent geometric hallucinations, perception of peripheral movement, colored flashes, intensified colors, palinopsia, positive afterimages, haloes around objects, macropsia, and micropsia occurring spontaneously in individuals with no prior psychopathology. These disturbances can be intermittent or continuous, slowly reversible or irreversible, but are severe, intrusive, and cause functional debility. Sufferers retain insight that these phenomena are the consequence of LSD use and usually seek psychiatric help.

HPPD may be diagnosed by the presence of an identifiable trigger, prodromal symptoms, and presentation onset; by the characteristics of the perceptual disturbances, their frequency, duration, intensity, and course; and by the accompanying negative affect and preserved insight.²

This LSD-induced persistence of visual imagery after the image is removed from the visual field is thought to result from dysfunction of serotonergic cortical inhibitory interneurons with GABAergic outputs that normally suppress visual processors.³ Clonazepam often is helpful.²

R. Andrew Sewell, MD
VA Connecticut Healthcare/Yale University
School of Medicine
New Haven, CT

David Kozin
McLean Hospital/Harvard Medical School
Belmont, MA

Miles G. Cunningham, MD, PhD
McLean Hospital/Harvard Medical School
Belmont, MA

CASE: Self-destructive behaviors

After being acquitted of 4 counts of second-degree forgery for writing checks from her mother’s bank account, Ms. L, age 52, is sent to the state hospital for a forensic examination to determine competency. Two years later she is granted conditional release from the hospital, transferred to our not-for-profit community mental health center, and enrolled in an intensive inpatient treatment program to monitor forensic patients. She is legally required to comply with treatment recommendations.

At admission, Ms. L is diagnosed with major depression, recurrent, and borderline personality disorder (BPD). She has no history of antisocial behavior or criminal acts other than forging checks and has never spent time in prison, which makes it unlikely she has co morbid antisocial personality disorder (Table 1).¹

Over the next 5 years Ms. L tests limits with the treatment team and acts out by engaging in self-harming behaviors. In 1 instance, she cuts her forearm deeply, stuffs the wound with mayonnaise and paper towels, and wraps her arm with a bandage. She wears a long-sleeved shirt to hide her wound, which is not discovered until a severe infection develops.

Ms. L has difficulty with coping skills and interpersonal relationships. She approaches others with ambivalence and mistrust and consistently expects them to demean or take advantage of her. Ms. L is manipulative, at times injuring herself after perceived wrongdoings by staff. For example, after her therapist reschedules a meeting because of an emergency, Ms. L pours scalding water on her foot.

Table 1

Cluster B personality disorders: Differential diagnosis

The authors’ observations

Ms. L consistently displays 3 common constructs of BPD:

• primitive defense mechanisms
• identity diffusion
• generally intact reality testing.²

Defense mechanisms are psychological attempts to deal with intrapsychic stress. Splitting—vacillating between extremes of idealization and devaluation—is a fundamental primitive defense mechanism that is the root of BPD.² Identity diffusion causes confusion about life goals and values and feelings of boredom and emptiness. This internal world leads a patient to have the same perception of the external world, which explains many symptoms of BPD, such as rapidly shifting moods, intense anger, lack of clear sense of self, fear of abandonment, and unstable and intense interpersonal relationships.²

Early in treatment, Ms. L had difficulty breaking a cycle of self-defeating behavior, such as destroying personal items, trying to hang herself, and gluing an ear plug in her ear. During an argument with a staff member, Ms. L punched a wall and fractured her left hand. BPD patients sometimes will “up the ante” when acting out. For example, one of our patients claimed to have planted a bomb in an elementary school and another swallowed inedible objects, including spoons, forks, and butter knives. In Ms. L’s case, we addressed her self-harm behavior by helping her:

• develop less destructive coping skills such as drawing or painting
• identify irrational thoughts that contribute to self harm.

HISTORY: Troubled past

Raised by her biologic parents, Ms. L met all developmental milestones. She denies a history of childhood abuse but reports experiencing “depression and memory loss” and relationship problems with her parents during adolescence. As a child she often missed school because she “did not want anyone to know what a disgusting person I was” and “I should have my head cut open and cut into little pieces for thinking such mean thoughts.” Ms. L dropped out of school in the twelfth grade but obtained her general educational development certificate.

Notes and letters Ms. L wrote while in treatment consistently refer to her negative self-image. Ms. L writes that she feels she does not deserve to “be a part of this world,” is “never good enough for anyone,” and “should be thrown away with the garbage.”

Ms. L vacillates between desiring a closer relationship with her parents, especially her mother, and wanting to “cut them out of my life for good.” She has minimal contact with her older sister. Ms. L is divorced and has 2 adult sons. She was involved sporadically in her sons’ lives when they were children, but now has no contact with them.

BPD and crime

Ms. L is enrolled in the “911 program,” which monitors individuals who have been found not guilty by reason of mental defect. Individuals with BPD often are convicted of serious and violent crimes, which may be because of BPD features such as interpersonal hostility and self-harm. Impulsivity, substance abuse, and parental neglect—all of which are associated with BPD—can increase risk of criminality.³ There is no evidence to suggest a direct link between BPD and criminality; however, over-representation of BPD in prison populations suggest that in severe cases it may increase criminogenic risk.^1,3

TREATMENT: Worsened depression

When Ms. L arrives at our facility, her medication regimen includes fluoxetine, 80 mg/d, risperidone, 2 mg/d, and buspirone, 20 mg/d. Risperidone and buspirone are discontinued because of perceived lack of efficacy. Venlafaxine XR is added and titrated to 300 mg/d, and Ms. L receives lorazepam, 1 and 2 mg as needed. However, lorazepam carries risks because impulsivity and impaired judgment—which are common in BPD—can lead to dependence and abuse. We feel that in a supervised setting the risks can be managed.

Recently, staff witnessed Ms. L experiencing an episode that appeared to be a grand mal seizure. After Ms. L is evaluated at the local emergency room, her EEG is normal, but a neurologic consult recommends discontinuing fluoxetine or venlafaxine XR because they may have contributed to the seizure. We taper and discontinue venlafaxine XR but Ms. L complains bitterly that she is getting increasingly depressed. On several occasions she attempts to pit team members against each other.

Ms. L falls, injures her back, and begins to abuse opiates. After her prescription runs out, she obtains more from an intellectually limited patient in her treatment program. Ms. L says she is getting more depressed, threatens suicide, and is placed in a more restrictive in-patient setting. We consider adding pregabalin to address her pain and help with anxiety and impulse control but the consulting neurologist prescribes carbamazepine, 400 mg/d, and her pain improves.^5,6

The authors’ observations

BPD treatment primarily is psychotherapeutic and emphasizes skill building (Table 2) with focused, symptom-targeted pharmacotherapy as indicated.⁴ Pharmacotherapy typically targets 3 domains:

• affective dysregulation
• impulsive-behavioral dyscontrol symptoms
• cognitive-perceptual symptoms.

Patients with prominent anxiety may benefit from benzodiazepines, although research on these agents for BPD is limited. Recent studies show efficacy with fluoxetine, olanzapine, or a combination of both,⁷ and divalproex.⁸ Preliminary data supports the use of topiramate, quetiapine, risperidone, ziprasidone, lamotrigine, and clonidine (Table 3).^9-14 A recent review and meta-analysis showed efficacy with topira-mate, lamotrigine, valproate, aripiprazole, and olanzapine.¹⁵

For Ms. L, we restart venlafaxine at a lower dose of 50 mg/d and titrate it to 150 mg/d, which is still lower than her previous dose of 300 mg/d. She has no recurrence of seizures and her depression improves.

Table 2

Features of psychotherapeutic modalities for BPD

Table 3

Pharmacotherapy for BPD: What the evidence says

OUTCOME: Some improvement

Ms. L has no dramatic suicidal gestures for 3 years. Although she continues to engage in self-injurious behaviors, the intensity and frequency are reduced and she does not inflict any serious injury for 18 months. Her mood and behavior continue to oscillate; she is relatively calm and satisfied 1 week, angry and assaultive the next. This stormy course is expected given her BPD diagnosis.

Initially, Ms. L resided in a locked residential unit and was minimally compliant with treatment recommendations and unit policies. As treatment progressed she moved to a different locked unit and eventually to an apartment. Recently, she was placed in a more restrictive setting because her hostile and self-destructive behavior escalated.

The authors’ observations

Ms. L is no different from most Axis II Cluster B disordered patients. During treatment she shows improvement by refraining from self-destructive behaviors for up to 18 months, but she then briefly reverts back to maladaptive behaviors. Ms. L resides in a very structured treatment setting. It is not clear if the gains she made in treatment would have been possible if she was living on her own in the community.

One year after finishing the court-mandated “911 program,” Ms. L lives in the community, draws and paints quite well, attends weekly individual and group therapy, and refrains from self-mutilation. She still experiences volatile moods, but can handle them without inflicting self injury.

Related resources

• Oldham JM. Guideline watch: practice guideline for the treatment of patients with borderline personality disorder. Arlington, VA: American Psychiatric Association; 2005. www.psychiatryonline.com/content.aspx?aID=148722.
• Koenigsberg HW, Kernberg OF, Stone MH, et al. Borderline patients: extending the limits of treatability. New York, NY: Basic Books; 2000.

Drug brand names

• Aripiprazole • Abilify
• Buspirone • Buspar
• Carbamazepine • Tegretol
• Clonidine • Catapres
• Divalproex • Depakote
• Fluoxetine • Prozac
• Fluoxetine-olanzapine • Symbyax
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Lorazepam • Ativan
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Pregabalin • Lyrica
• Risperidone • Risperdal
• Topiramate • Topamax
• Valproic acid • Depakene
• Venlafaxine XR • Effexor XR
• Ziprasidone • Geodon

Disclosures

Dr. Hashmi is on the speakers bureau for AstraZeneca, Eli Lilly and Company, and Janssen.

Dr. Vowell reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Self-destructive behaviors

After being acquitted of 4 counts of second-degree forgery for writing checks from her mother’s bank account, Ms. L, age 52, is sent to the state hospital for a forensic examination to determine competency. Two years later she is granted conditional release from the hospital, transferred to our not-for-profit community mental health center, and enrolled in an intensive inpatient treatment program to monitor forensic patients. She is legally required to comply with treatment recommendations.

At admission, Ms. L is diagnosed with major depression, recurrent, and borderline personality disorder (BPD). She has no history of antisocial behavior or criminal acts other than forging checks and has never spent time in prison, which makes it unlikely she has co morbid antisocial personality disorder (Table 1).¹

Over the next 5 years Ms. L tests limits with the treatment team and acts out by engaging in self-harming behaviors. In 1 instance, she cuts her forearm deeply, stuffs the wound with mayonnaise and paper towels, and wraps her arm with a bandage. She wears a long-sleeved shirt to hide her wound, which is not discovered until a severe infection develops.

Ms. L has difficulty with coping skills and interpersonal relationships. She approaches others with ambivalence and mistrust and consistently expects them to demean or take advantage of her. Ms. L is manipulative, at times injuring herself after perceived wrongdoings by staff. For example, after her therapist reschedules a meeting because of an emergency, Ms. L pours scalding water on her foot.

Table 1

Cluster B personality disorders: Differential diagnosis

The authors’ observations

Ms. L consistently displays 3 common constructs of BPD:

• primitive defense mechanisms
• identity diffusion
• generally intact reality testing.²

Defense mechanisms are psychological attempts to deal with intrapsychic stress. Splitting—vacillating between extremes of idealization and devaluation—is a fundamental primitive defense mechanism that is the root of BPD.² Identity diffusion causes confusion about life goals and values and feelings of boredom and emptiness. This internal world leads a patient to have the same perception of the external world, which explains many symptoms of BPD, such as rapidly shifting moods, intense anger, lack of clear sense of self, fear of abandonment, and unstable and intense interpersonal relationships.²

Early in treatment, Ms. L had difficulty breaking a cycle of self-defeating behavior, such as destroying personal items, trying to hang herself, and gluing an ear plug in her ear. During an argument with a staff member, Ms. L punched a wall and fractured her left hand. BPD patients sometimes will “up the ante” when acting out. For example, one of our patients claimed to have planted a bomb in an elementary school and another swallowed inedible objects, including spoons, forks, and butter knives. In Ms. L’s case, we addressed her self-harm behavior by helping her:

• develop less destructive coping skills such as drawing or painting
• identify irrational thoughts that contribute to self harm.

HISTORY: Troubled past

Raised by her biologic parents, Ms. L met all developmental milestones. She denies a history of childhood abuse but reports experiencing “depression and memory loss” and relationship problems with her parents during adolescence. As a child she often missed school because she “did not want anyone to know what a disgusting person I was” and “I should have my head cut open and cut into little pieces for thinking such mean thoughts.” Ms. L dropped out of school in the twelfth grade but obtained her general educational development certificate.

Notes and letters Ms. L wrote while in treatment consistently refer to her negative self-image. Ms. L writes that she feels she does not deserve to “be a part of this world,” is “never good enough for anyone,” and “should be thrown away with the garbage.”

Ms. L vacillates between desiring a closer relationship with her parents, especially her mother, and wanting to “cut them out of my life for good.” She has minimal contact with her older sister. Ms. L is divorced and has 2 adult sons. She was involved sporadically in her sons’ lives when they were children, but now has no contact with them.

BPD and crime

Ms. L is enrolled in the “911 program,” which monitors individuals who have been found not guilty by reason of mental defect. Individuals with BPD often are convicted of serious and violent crimes, which may be because of BPD features such as interpersonal hostility and self-harm. Impulsivity, substance abuse, and parental neglect—all of which are associated with BPD—can increase risk of criminality.³ There is no evidence to suggest a direct link between BPD and criminality; however, over-representation of BPD in prison populations suggest that in severe cases it may increase criminogenic risk.^1,3

TREATMENT: Worsened depression

When Ms. L arrives at our facility, her medication regimen includes fluoxetine, 80 mg/d, risperidone, 2 mg/d, and buspirone, 20 mg/d. Risperidone and buspirone are discontinued because of perceived lack of efficacy. Venlafaxine XR is added and titrated to 300 mg/d, and Ms. L receives lorazepam, 1 and 2 mg as needed. However, lorazepam carries risks because impulsivity and impaired judgment—which are common in BPD—can lead to dependence and abuse. We feel that in a supervised setting the risks can be managed.

Recently, staff witnessed Ms. L experiencing an episode that appeared to be a grand mal seizure. After Ms. L is evaluated at the local emergency room, her EEG is normal, but a neurologic consult recommends discontinuing fluoxetine or venlafaxine XR because they may have contributed to the seizure. We taper and discontinue venlafaxine XR but Ms. L complains bitterly that she is getting increasingly depressed. On several occasions she attempts to pit team members against each other.

Ms. L falls, injures her back, and begins to abuse opiates. After her prescription runs out, she obtains more from an intellectually limited patient in her treatment program. Ms. L says she is getting more depressed, threatens suicide, and is placed in a more restrictive in-patient setting. We consider adding pregabalin to address her pain and help with anxiety and impulse control but the consulting neurologist prescribes carbamazepine, 400 mg/d, and her pain improves.^5,6

The authors’ observations

BPD treatment primarily is psychotherapeutic and emphasizes skill building (Table 2) with focused, symptom-targeted pharmacotherapy as indicated.⁴ Pharmacotherapy typically targets 3 domains:

• affective dysregulation
• impulsive-behavioral dyscontrol symptoms
• cognitive-perceptual symptoms.

Patients with prominent anxiety may benefit from benzodiazepines, although research on these agents for BPD is limited. Recent studies show efficacy with fluoxetine, olanzapine, or a combination of both,⁷ and divalproex.⁸ Preliminary data supports the use of topiramate, quetiapine, risperidone, ziprasidone, lamotrigine, and clonidine (Table 3).^9-14 A recent review and meta-analysis showed efficacy with topira-mate, lamotrigine, valproate, aripiprazole, and olanzapine.¹⁵

For Ms. L, we restart venlafaxine at a lower dose of 50 mg/d and titrate it to 150 mg/d, which is still lower than her previous dose of 300 mg/d. She has no recurrence of seizures and her depression improves.

Table 2

Features of psychotherapeutic modalities for BPD

Table 3

Pharmacotherapy for BPD: What the evidence says

OUTCOME: Some improvement

Ms. L has no dramatic suicidal gestures for 3 years. Although she continues to engage in self-injurious behaviors, the intensity and frequency are reduced and she does not inflict any serious injury for 18 months. Her mood and behavior continue to oscillate; she is relatively calm and satisfied 1 week, angry and assaultive the next. This stormy course is expected given her BPD diagnosis.

Initially, Ms. L resided in a locked residential unit and was minimally compliant with treatment recommendations and unit policies. As treatment progressed she moved to a different locked unit and eventually to an apartment. Recently, she was placed in a more restrictive setting because her hostile and self-destructive behavior escalated.

The authors’ observations

Ms. L is no different from most Axis II Cluster B disordered patients. During treatment she shows improvement by refraining from self-destructive behaviors for up to 18 months, but she then briefly reverts back to maladaptive behaviors. Ms. L resides in a very structured treatment setting. It is not clear if the gains she made in treatment would have been possible if she was living on her own in the community.

One year after finishing the court-mandated “911 program,” Ms. L lives in the community, draws and paints quite well, attends weekly individual and group therapy, and refrains from self-mutilation. She still experiences volatile moods, but can handle them without inflicting self injury.

Related resources

• Oldham JM. Guideline watch: practice guideline for the treatment of patients with borderline personality disorder. Arlington, VA: American Psychiatric Association; 2005. www.psychiatryonline.com/content.aspx?aID=148722.
• Koenigsberg HW, Kernberg OF, Stone MH, et al. Borderline patients: extending the limits of treatability. New York, NY: Basic Books; 2000.

Drug brand names

• Aripiprazole • Abilify
• Buspirone • Buspar
• Carbamazepine • Tegretol
• Clonidine • Catapres
• Divalproex • Depakote
• Fluoxetine • Prozac
• Fluoxetine-olanzapine • Symbyax
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Lorazepam • Ativan
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Pregabalin • Lyrica
• Risperidone • Risperdal
• Topiramate • Topamax
• Valproic acid • Depakene
• Venlafaxine XR • Effexor XR
• Ziprasidone • Geodon

Disclosures

Dr. Hashmi is on the speakers bureau for AstraZeneca, Eli Lilly and Company, and Janssen.

Dr. Vowell reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Self-destructive behaviors

After being acquitted of 4 counts of second-degree forgery for writing checks from her mother’s bank account, Ms. L, age 52, is sent to the state hospital for a forensic examination to determine competency. Two years later she is granted conditional release from the hospital, transferred to our not-for-profit community mental health center, and enrolled in an intensive inpatient treatment program to monitor forensic patients. She is legally required to comply with treatment recommendations.

At admission, Ms. L is diagnosed with major depression, recurrent, and borderline personality disorder (BPD). She has no history of antisocial behavior or criminal acts other than forging checks and has never spent time in prison, which makes it unlikely she has co morbid antisocial personality disorder (Table 1).¹

Over the next 5 years Ms. L tests limits with the treatment team and acts out by engaging in self-harming behaviors. In 1 instance, she cuts her forearm deeply, stuffs the wound with mayonnaise and paper towels, and wraps her arm with a bandage. She wears a long-sleeved shirt to hide her wound, which is not discovered until a severe infection develops.

Ms. L has difficulty with coping skills and interpersonal relationships. She approaches others with ambivalence and mistrust and consistently expects them to demean or take advantage of her. Ms. L is manipulative, at times injuring herself after perceived wrongdoings by staff. For example, after her therapist reschedules a meeting because of an emergency, Ms. L pours scalding water on her foot.

Table 1

Cluster B personality disorders: Differential diagnosis

The authors’ observations

Ms. L consistently displays 3 common constructs of BPD:

• primitive defense mechanisms
• identity diffusion
• generally intact reality testing.²

Defense mechanisms are psychological attempts to deal with intrapsychic stress. Splitting—vacillating between extremes of idealization and devaluation—is a fundamental primitive defense mechanism that is the root of BPD.² Identity diffusion causes confusion about life goals and values and feelings of boredom and emptiness. This internal world leads a patient to have the same perception of the external world, which explains many symptoms of BPD, such as rapidly shifting moods, intense anger, lack of clear sense of self, fear of abandonment, and unstable and intense interpersonal relationships.²

Early in treatment, Ms. L had difficulty breaking a cycle of self-defeating behavior, such as destroying personal items, trying to hang herself, and gluing an ear plug in her ear. During an argument with a staff member, Ms. L punched a wall and fractured her left hand. BPD patients sometimes will “up the ante” when acting out. For example, one of our patients claimed to have planted a bomb in an elementary school and another swallowed inedible objects, including spoons, forks, and butter knives. In Ms. L’s case, we addressed her self-harm behavior by helping her:

• develop less destructive coping skills such as drawing or painting
• identify irrational thoughts that contribute to self harm.

HISTORY: Troubled past

Raised by her biologic parents, Ms. L met all developmental milestones. She denies a history of childhood abuse but reports experiencing “depression and memory loss” and relationship problems with her parents during adolescence. As a child she often missed school because she “did not want anyone to know what a disgusting person I was” and “I should have my head cut open and cut into little pieces for thinking such mean thoughts.” Ms. L dropped out of school in the twelfth grade but obtained her general educational development certificate.

Notes and letters Ms. L wrote while in treatment consistently refer to her negative self-image. Ms. L writes that she feels she does not deserve to “be a part of this world,” is “never good enough for anyone,” and “should be thrown away with the garbage.”

Ms. L vacillates between desiring a closer relationship with her parents, especially her mother, and wanting to “cut them out of my life for good.” She has minimal contact with her older sister. Ms. L is divorced and has 2 adult sons. She was involved sporadically in her sons’ lives when they were children, but now has no contact with them.

BPD and crime

Ms. L is enrolled in the “911 program,” which monitors individuals who have been found not guilty by reason of mental defect. Individuals with BPD often are convicted of serious and violent crimes, which may be because of BPD features such as interpersonal hostility and self-harm. Impulsivity, substance abuse, and parental neglect—all of which are associated with BPD—can increase risk of criminality.³ There is no evidence to suggest a direct link between BPD and criminality; however, over-representation of BPD in prison populations suggest that in severe cases it may increase criminogenic risk.^1,3

TREATMENT: Worsened depression

When Ms. L arrives at our facility, her medication regimen includes fluoxetine, 80 mg/d, risperidone, 2 mg/d, and buspirone, 20 mg/d. Risperidone and buspirone are discontinued because of perceived lack of efficacy. Venlafaxine XR is added and titrated to 300 mg/d, and Ms. L receives lorazepam, 1 and 2 mg as needed. However, lorazepam carries risks because impulsivity and impaired judgment—which are common in BPD—can lead to dependence and abuse. We feel that in a supervised setting the risks can be managed.

Recently, staff witnessed Ms. L experiencing an episode that appeared to be a grand mal seizure. After Ms. L is evaluated at the local emergency room, her EEG is normal, but a neurologic consult recommends discontinuing fluoxetine or venlafaxine XR because they may have contributed to the seizure. We taper and discontinue venlafaxine XR but Ms. L complains bitterly that she is getting increasingly depressed. On several occasions she attempts to pit team members against each other.

Ms. L falls, injures her back, and begins to abuse opiates. After her prescription runs out, she obtains more from an intellectually limited patient in her treatment program. Ms. L says she is getting more depressed, threatens suicide, and is placed in a more restrictive in-patient setting. We consider adding pregabalin to address her pain and help with anxiety and impulse control but the consulting neurologist prescribes carbamazepine, 400 mg/d, and her pain improves.^5,6

The authors’ observations

BPD treatment primarily is psychotherapeutic and emphasizes skill building (Table 2) with focused, symptom-targeted pharmacotherapy as indicated.⁴ Pharmacotherapy typically targets 3 domains:

• affective dysregulation
• impulsive-behavioral dyscontrol symptoms
• cognitive-perceptual symptoms.

Patients with prominent anxiety may benefit from benzodiazepines, although research on these agents for BPD is limited. Recent studies show efficacy with fluoxetine, olanzapine, or a combination of both,⁷ and divalproex.⁸ Preliminary data supports the use of topiramate, quetiapine, risperidone, ziprasidone, lamotrigine, and clonidine (Table 3).^9-14 A recent review and meta-analysis showed efficacy with topira-mate, lamotrigine, valproate, aripiprazole, and olanzapine.¹⁵

For Ms. L, we restart venlafaxine at a lower dose of 50 mg/d and titrate it to 150 mg/d, which is still lower than her previous dose of 300 mg/d. She has no recurrence of seizures and her depression improves.

Table 2

Features of psychotherapeutic modalities for BPD

Table 3

Pharmacotherapy for BPD: What the evidence says

OUTCOME: Some improvement

Ms. L has no dramatic suicidal gestures for 3 years. Although she continues to engage in self-injurious behaviors, the intensity and frequency are reduced and she does not inflict any serious injury for 18 months. Her mood and behavior continue to oscillate; she is relatively calm and satisfied 1 week, angry and assaultive the next. This stormy course is expected given her BPD diagnosis.

Initially, Ms. L resided in a locked residential unit and was minimally compliant with treatment recommendations and unit policies. As treatment progressed she moved to a different locked unit and eventually to an apartment. Recently, she was placed in a more restrictive setting because her hostile and self-destructive behavior escalated.

The authors’ observations

Ms. L is no different from most Axis II Cluster B disordered patients. During treatment she shows improvement by refraining from self-destructive behaviors for up to 18 months, but she then briefly reverts back to maladaptive behaviors. Ms. L resides in a very structured treatment setting. It is not clear if the gains she made in treatment would have been possible if she was living on her own in the community.

One year after finishing the court-mandated “911 program,” Ms. L lives in the community, draws and paints quite well, attends weekly individual and group therapy, and refrains from self-mutilation. She still experiences volatile moods, but can handle them without inflicting self injury.

Related resources

• Oldham JM. Guideline watch: practice guideline for the treatment of patients with borderline personality disorder. Arlington, VA: American Psychiatric Association; 2005. www.psychiatryonline.com/content.aspx?aID=148722.
• Koenigsberg HW, Kernberg OF, Stone MH, et al. Borderline patients: extending the limits of treatability. New York, NY: Basic Books; 2000.

Drug brand names

• Aripiprazole • Abilify
• Buspirone • Buspar
• Carbamazepine • Tegretol
• Clonidine • Catapres
• Divalproex • Depakote
• Fluoxetine • Prozac
• Fluoxetine-olanzapine • Symbyax
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Lorazepam • Ativan
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Pregabalin • Lyrica
• Risperidone • Risperdal
• Topiramate • Topamax
• Valproic acid • Depakene
• Venlafaxine XR • Effexor XR
• Ziprasidone • Geodon

Disclosures

Dr. Hashmi is on the speakers bureau for AstraZeneca, Eli Lilly and Company, and Janssen.

Dr. Vowell reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Treating borderline personality disorder can seem like a no-win situation. If we try traditional cognitive-behavioral therapy (CBT) and emphasize change, patients feel unheard and invalidated; they may withdraw, quit, or even attack. But if we suggest ways to accept unhappy situations, they may feel we don’t understand their suffering.

A more effective approach is dialectical behavior therapy (DBT), first developed to treat highly suicidal persons with borderline personality disorder and used with other populations that have difficulty regulating their emotions.

This article describes how invalidating environments may damage emotional health and suggests how psychiatrists can use DBT’s methods when treating borderline personality disorder.

BIOLOGY PLUS ENVIRONMENT

For the patient, borderline personality disorder’s behavior clusters (Table 1):

• function to regulate emotions
• or result from emotion dysregulation.

DBT theory identifies emotion dysregulation as the primary deficit in borderline personality disorder. Biologically based emotional vulnerability is seen as interacting with an inability to modulate emotions because of a skills deficit.

Emotional vulnerability. Three characteristics—high sensitivity, high reactivity, and slow return to baseline emotional state—define high emotional vulnerability:

High sensitivity. The person reacts more quickly and to more things than do others in emotion-provoking situations. When walking, for example, they may pass someone who doesn’t say hello. Most people would shrug this off, but persons with high emotional sensitivity may quickly notice, assume there is a problem, feel they have done something wrong, then feel shame and anger.

High reactivity. Their emotional reactions are large, and the high arousal dysregulates cognitive processing.

Slow return to baseline. Events stack up because emotional reactions are long-lasting for persons with high emotional vulnerability. They don’t have time to get over one thing before something else happens.

DBT postulates that, over time, borderline personality disorder results from the transaction of biological emotional vulnerability and an invalidating environment. This therapeutic model asserts that biology and the environment are flexible, and interventions may influence both.

Invalidating environment. DBT acknowledges that invalidation occurs in all environments, even nuturing ones. It becomes detrimental when a vulnerable person is exposed to pervasive invalidation that is not related to the validity of the person’s behavior or to the person’s expressed emotions or thoughts.

An invalidating environment has three characteristic patterns. One is indiscriminate rejection of communication of private experiences and self-generated behaviors.

Case examples. Mary, age 8, says she’s been teased and it hurt her feelings. Her mother tells her she is making too much of the incident. Mary questions herself and searches the social environment for cues about how to respond to similar situations in the future.

Robbie, age 4, completes a drawing and shows it to his father with delight. His father points out some “sloppy” coloring. If his father repeatedly finds fault with his work, Robbie is likely to not show him his work or stop drawing, and his expressions of delight are likely to decrease.

Invalidating environments may also punish emotional displays and intermittently reinforce emotional escalation. Someone may show disapproval for or ignore a person’s genuine sadness or fear but attend to angry outbursts that result when the person feels ignored.

The third invalidating pattern is to oversimplify the ease of problem-solving and meeting goals.

Case example. As a child, when Susan asked for help, her mother would say “just do it,” without considering the skills her daughter needed to accomplish tasks. When Susan became frustrated, her mother demanded that she “just stop cying,” even though no person could modulate his or her emotions that quickly. As an adult, Susan now sets unrealistic goals and expectations for herself and despairs when she is unable to solve problems in her life.

These three invalidating patterns cause persons to search the social environment for cues about how to respond to situations. They may question themselves, their identity, and the appropriateness of any emotional expression. As a result, they may oscillate between emotional inhibition and extreme emotional styles, set unrealistic goals and expectations for themselves, and eventually despair of being able to solve their problems.

Specific to borderline personality disorder is that the environment ignores genuine emotional expression, and the individual’s emotions escalate. This pattern is reinforced when the listener finally rewards emotionally extreme behavior with attention or desired changes.

As the pattern is repeated over time, extreme emotional reactions become the norm rather than the exception, and the emotional chaos can make the person wish to die. Acting on that desire when past expressions of desperation have been ignored or invalidated can provide attention or interventions that would never happen after simple emotional expressions.

Thus, an environment that does not recognize or validate genuine emotional expression can reinforce suicidality.

Table 1

Diagnostic criteria for borderline personality disorder

SOLVING NO-WIN THERAPY

Pitfalls with emphasizing change. Therapy that emphasizes solving problems and getting things to change typically triggers high arousal in persons with borderline personality disorder. Feeling out of control, they respond by trying to get in control, including attempts to control the therapist.

Similarly, they see attempts to get them to change their behavior as invalidating their experiences or, worse, who they are. Intense emotions aroused by the message they hear—that they are the source of their problems—impair learning and intensify their efforts to gain control. In a battle for control, collaboration and therapy cannot occur.

Case example. Ms. K wants you to understand how difficult her life is because of difficulties with her boss. You start talking about what Ms. K can do to change the situation, without acknowledging how difficult it is to deal with her boss.

Ms. K feels upset and says you don’t understand. For her, the interaction has led to emotion dysregulation and impaired cognitive processing.

Pitfalls with emphasizing acceptance. Most persons who come to therapy very distressed want something in their lives to change. If your primary message is acceptance instead of change, they may lose confidence in you.

Case example. Ms. K wants help dealing with her boss, who is making life quite difficult. As her therapist, you respond with warmth and acceptance but offer no suggestions as to how she might change the situation. Ms. K likes the way you listen to her but abandons therapy. after several sessions.

At first, patients with borderline personality disorder may like the warmth of client-centered acceptance approaches. Over time, however, they may feel their therapy sessions are out of control. They may think the therapist doesn’t understand the situation, doesn’t know how to help, or that situations that are troubling them cannot be changed.

Balanced therapy. DBT solves the change-or-acceptance dilemma by attempting to help patients with borderline personality disorder change themselves and their lives while offering strategies for accepting themselves and their situations.^1,2 DBT includes problem-solving and acceptance strategies (Table 2).

Table 2

Strategies used in dialectical behavioral therapy

DBT’S 4 THERAPY STAGES

DBT is a comprehensive treatment. The original outpatient model for borderline personality disorder (Table 3) has been adapted to different settings and applied to other populations.

Outpatients meet weekly in individual psychotherapy and a skills training group.³ Therapists also meet weekly in a consultation team viewed as “therapy for the therapist.”

Between sessions, therapists consult with patients by telephone to:

• decrease suicide crisis behaviors
• increase generalization of behavioral skills
• decrease patients’ feelings of conflict, alienation, or distance with the therapist.

Four stages. DBT follows four stages. For persons with borderline personality disorder, researchers have evaluated the efficacy of stage-1 therapy. Studies on stage-3 DBT have been conducted with nonborderline-personality individuals with eating disorders. The goals at each stage are:

Stage 1. Move from severe behavioral dyscontrol to behavioral control. Decrease suicidal and other life-threatening behaviors and those that interfere with therapy and quality of life. Increase mindfulness, tolerance for distress, interpersonal effectiveness, and emotion regulation.

Stage 2. Move from quiet desperation to emotional experiencing.

Stage 3. Address problems in living, and move toward ordinary happiness/unhappiness.

Stage 4. Move from incompleteness to capacity for joy and freedom.

Seven randomized controlled trials have shown that DBT can be useful in treating borderline personality disorder.^4-10 The initial trial by Linehan et al⁴ included 47 women ages 18 to 45 who met criteria for borderline personality disorder and had at least two parasuicide incidents in the previous 5 years, with one in the previous 8 weeks. Treatment lasted 1 year, and subjects agreed to stop other individual psychotherapy if assigned to DBT.

Subjects were then randomly assigned to either DBT or “treatment as usual” in the community. In the various DBT studies, treatment-as-usual has included community therapists, Department of Veterans Affairs outpatient treatment, client-centered therapy, and treatment by persons identified by their peers as experts in their communities.

Subjects were assessed every 4 months while in treatment and for 1 year thereafter. DBT was more effective than usual treatment in:

• reducing suicide attempts and self-injury
• decreasing premature dropout from therapy
• reducing emergency room admissions and length of psychiatric hospitalization
• reducing drug abuse, depression, hopelessness, and anger.

Table 3

Modes of therapy in outpatient dialectical behavioral therapy

RECOMMENDATIONS

Some psychiatrists may find “borderline patients” frustrating and unpleasant to treat. DBT therapists, however, make two assumptions that can help anyone working with individuals with borderline personality disorder. To avoid falling into the trap of polarization with these patients, assume that:

• they are doing the best they can
• their efforts are insufficient to meet their needs.

They therefore need to do better, and the therapist’s job is to help them do so. Also assume that if you try to help a patient with borderline personality disorder, you will need help, too. We require DBT therapists to participate in consultation teams.

Training. DBT is a comprehensive program that requires familiarity with the manuals mentioned in this article (see Related resources). Some teams have learned DBT through self-study and consultation with other teams.

If you plan to offer DBT to patients with borderline personality disorder, we recommend that you be:

• trained in behavior therapy and CBT
• familiar with research on emotions and processes involved in emotion regulation.

If you have not had CBT training, find a behavior therapist to join your team or get consultation from a behavior therapist.

An intensive training course in DBT—with 2 weeks of instruction and case consultation and several months of consultation with someone well-versed in DBT—is an efficient way to become familiar with the most critical principles of the treatment. If you cannot train toward adherent delivery of individual therapy, we recommend referring patients to someone trained in DBT.

Related resources

• Lieb K, Zanarini MC, Schmahl C, et al. Borderline personality disorder. Lancet 2004;364(9432):453-61.
• University of Washington, Behavioral Research and Therapy Clinics. www.brtc.psych.washington.edu/frameResearch.htm;
  www.brtc.psych.washington.edu/framePublications.htm
• Behavioral Tech, LLC. Consultation and training in dialectical behavioral therapy. www.behavioraltech.org.

Disclosures

Dr. DuBose is president and CEO/co-owner of DBT Center of Seattle, PLLC, and a speaker for Behavioral Tech, LLC.

Dr. Linehan is a shareholder in Behavioral Tech Research, Inc., which develops computerized training for DBT, a DBT trainer for Behavioral Tech, LLC, and the author of two books on DBT. She also receives research grants from the National Institute of Mental Health and National Institute on Drug Abuse.

Treating borderline personality disorder can seem like a no-win situation. If we try traditional cognitive-behavioral therapy (CBT) and emphasize change, patients feel unheard and invalidated; they may withdraw, quit, or even attack. But if we suggest ways to accept unhappy situations, they may feel we don’t understand their suffering.

A more effective approach is dialectical behavior therapy (DBT), first developed to treat highly suicidal persons with borderline personality disorder and used with other populations that have difficulty regulating their emotions.

This article describes how invalidating environments may damage emotional health and suggests how psychiatrists can use DBT’s methods when treating borderline personality disorder.

BIOLOGY PLUS ENVIRONMENT

For the patient, borderline personality disorder’s behavior clusters (Table 1):

• function to regulate emotions
• or result from emotion dysregulation.

DBT theory identifies emotion dysregulation as the primary deficit in borderline personality disorder. Biologically based emotional vulnerability is seen as interacting with an inability to modulate emotions because of a skills deficit.

Emotional vulnerability. Three characteristics—high sensitivity, high reactivity, and slow return to baseline emotional state—define high emotional vulnerability:

High sensitivity. The person reacts more quickly and to more things than do others in emotion-provoking situations. When walking, for example, they may pass someone who doesn’t say hello. Most people would shrug this off, but persons with high emotional sensitivity may quickly notice, assume there is a problem, feel they have done something wrong, then feel shame and anger.

High reactivity. Their emotional reactions are large, and the high arousal dysregulates cognitive processing.

Slow return to baseline. Events stack up because emotional reactions are long-lasting for persons with high emotional vulnerability. They don’t have time to get over one thing before something else happens.

DBT postulates that, over time, borderline personality disorder results from the transaction of biological emotional vulnerability and an invalidating environment. This therapeutic model asserts that biology and the environment are flexible, and interventions may influence both.

Invalidating environment. DBT acknowledges that invalidation occurs in all environments, even nuturing ones. It becomes detrimental when a vulnerable person is exposed to pervasive invalidation that is not related to the validity of the person’s behavior or to the person’s expressed emotions or thoughts.

An invalidating environment has three characteristic patterns. One is indiscriminate rejection of communication of private experiences and self-generated behaviors.

Case examples. Mary, age 8, says she’s been teased and it hurt her feelings. Her mother tells her she is making too much of the incident. Mary questions herself and searches the social environment for cues about how to respond to similar situations in the future.

Robbie, age 4, completes a drawing and shows it to his father with delight. His father points out some “sloppy” coloring. If his father repeatedly finds fault with his work, Robbie is likely to not show him his work or stop drawing, and his expressions of delight are likely to decrease.

Invalidating environments may also punish emotional displays and intermittently reinforce emotional escalation. Someone may show disapproval for or ignore a person’s genuine sadness or fear but attend to angry outbursts that result when the person feels ignored.

The third invalidating pattern is to oversimplify the ease of problem-solving and meeting goals.

Case example. As a child, when Susan asked for help, her mother would say “just do it,” without considering the skills her daughter needed to accomplish tasks. When Susan became frustrated, her mother demanded that she “just stop cying,” even though no person could modulate his or her emotions that quickly. As an adult, Susan now sets unrealistic goals and expectations for herself and despairs when she is unable to solve problems in her life.

These three invalidating patterns cause persons to search the social environment for cues about how to respond to situations. They may question themselves, their identity, and the appropriateness of any emotional expression. As a result, they may oscillate between emotional inhibition and extreme emotional styles, set unrealistic goals and expectations for themselves, and eventually despair of being able to solve their problems.

Specific to borderline personality disorder is that the environment ignores genuine emotional expression, and the individual’s emotions escalate. This pattern is reinforced when the listener finally rewards emotionally extreme behavior with attention or desired changes.

As the pattern is repeated over time, extreme emotional reactions become the norm rather than the exception, and the emotional chaos can make the person wish to die. Acting on that desire when past expressions of desperation have been ignored or invalidated can provide attention or interventions that would never happen after simple emotional expressions.

Thus, an environment that does not recognize or validate genuine emotional expression can reinforce suicidality.

Table 1

Diagnostic criteria for borderline personality disorder

SOLVING NO-WIN THERAPY

Pitfalls with emphasizing change. Therapy that emphasizes solving problems and getting things to change typically triggers high arousal in persons with borderline personality disorder. Feeling out of control, they respond by trying to get in control, including attempts to control the therapist.

Similarly, they see attempts to get them to change their behavior as invalidating their experiences or, worse, who they are. Intense emotions aroused by the message they hear—that they are the source of their problems—impair learning and intensify their efforts to gain control. In a battle for control, collaboration and therapy cannot occur.

Case example. Ms. K wants you to understand how difficult her life is because of difficulties with her boss. You start talking about what Ms. K can do to change the situation, without acknowledging how difficult it is to deal with her boss.

Ms. K feels upset and says you don’t understand. For her, the interaction has led to emotion dysregulation and impaired cognitive processing.

Pitfalls with emphasizing acceptance. Most persons who come to therapy very distressed want something in their lives to change. If your primary message is acceptance instead of change, they may lose confidence in you.

Case example. Ms. K wants help dealing with her boss, who is making life quite difficult. As her therapist, you respond with warmth and acceptance but offer no suggestions as to how she might change the situation. Ms. K likes the way you listen to her but abandons therapy. after several sessions.

At first, patients with borderline personality disorder may like the warmth of client-centered acceptance approaches. Over time, however, they may feel their therapy sessions are out of control. They may think the therapist doesn’t understand the situation, doesn’t know how to help, or that situations that are troubling them cannot be changed.

Balanced therapy. DBT solves the change-or-acceptance dilemma by attempting to help patients with borderline personality disorder change themselves and their lives while offering strategies for accepting themselves and their situations.^1,2 DBT includes problem-solving and acceptance strategies (Table 2).

Table 2

Strategies used in dialectical behavioral therapy

DBT’S 4 THERAPY STAGES

DBT is a comprehensive treatment. The original outpatient model for borderline personality disorder (Table 3) has been adapted to different settings and applied to other populations.

Outpatients meet weekly in individual psychotherapy and a skills training group.³ Therapists also meet weekly in a consultation team viewed as “therapy for the therapist.”

Between sessions, therapists consult with patients by telephone to:

• decrease suicide crisis behaviors
• increase generalization of behavioral skills
• decrease patients’ feelings of conflict, alienation, or distance with the therapist.

Four stages. DBT follows four stages. For persons with borderline personality disorder, researchers have evaluated the efficacy of stage-1 therapy. Studies on stage-3 DBT have been conducted with nonborderline-personality individuals with eating disorders. The goals at each stage are:

Stage 1. Move from severe behavioral dyscontrol to behavioral control. Decrease suicidal and other life-threatening behaviors and those that interfere with therapy and quality of life. Increase mindfulness, tolerance for distress, interpersonal effectiveness, and emotion regulation.

Stage 2. Move from quiet desperation to emotional experiencing.

Stage 3. Address problems in living, and move toward ordinary happiness/unhappiness.

Stage 4. Move from incompleteness to capacity for joy and freedom.

Seven randomized controlled trials have shown that DBT can be useful in treating borderline personality disorder.^4-10 The initial trial by Linehan et al⁴ included 47 women ages 18 to 45 who met criteria for borderline personality disorder and had at least two parasuicide incidents in the previous 5 years, with one in the previous 8 weeks. Treatment lasted 1 year, and subjects agreed to stop other individual psychotherapy if assigned to DBT.

Subjects were then randomly assigned to either DBT or “treatment as usual” in the community. In the various DBT studies, treatment-as-usual has included community therapists, Department of Veterans Affairs outpatient treatment, client-centered therapy, and treatment by persons identified by their peers as experts in their communities.

Subjects were assessed every 4 months while in treatment and for 1 year thereafter. DBT was more effective than usual treatment in:

• reducing suicide attempts and self-injury
• decreasing premature dropout from therapy
• reducing emergency room admissions and length of psychiatric hospitalization
• reducing drug abuse, depression, hopelessness, and anger.

Table 3

Modes of therapy in outpatient dialectical behavioral therapy

RECOMMENDATIONS

Some psychiatrists may find “borderline patients” frustrating and unpleasant to treat. DBT therapists, however, make two assumptions that can help anyone working with individuals with borderline personality disorder. To avoid falling into the trap of polarization with these patients, assume that:

• they are doing the best they can
• their efforts are insufficient to meet their needs.

They therefore need to do better, and the therapist’s job is to help them do so. Also assume that if you try to help a patient with borderline personality disorder, you will need help, too. We require DBT therapists to participate in consultation teams.

Training. DBT is a comprehensive program that requires familiarity with the manuals mentioned in this article (see Related resources). Some teams have learned DBT through self-study and consultation with other teams.

If you plan to offer DBT to patients with borderline personality disorder, we recommend that you be:

• trained in behavior therapy and CBT
• familiar with research on emotions and processes involved in emotion regulation.

If you have not had CBT training, find a behavior therapist to join your team or get consultation from a behavior therapist.

An intensive training course in DBT—with 2 weeks of instruction and case consultation and several months of consultation with someone well-versed in DBT—is an efficient way to become familiar with the most critical principles of the treatment. If you cannot train toward adherent delivery of individual therapy, we recommend referring patients to someone trained in DBT.

Related resources

• Lieb K, Zanarini MC, Schmahl C, et al. Borderline personality disorder. Lancet 2004;364(9432):453-61.
• University of Washington, Behavioral Research and Therapy Clinics. www.brtc.psych.washington.edu/frameResearch.htm;
  www.brtc.psych.washington.edu/framePublications.htm
• Behavioral Tech, LLC. Consultation and training in dialectical behavioral therapy. www.behavioraltech.org.

Disclosures

Dr. DuBose is president and CEO/co-owner of DBT Center of Seattle, PLLC, and a speaker for Behavioral Tech, LLC.

Dr. Linehan is a shareholder in Behavioral Tech Research, Inc., which develops computerized training for DBT, a DBT trainer for Behavioral Tech, LLC, and the author of two books on DBT. She also receives research grants from the National Institute of Mental Health and National Institute on Drug Abuse.

Treating borderline personality disorder can seem like a no-win situation. If we try traditional cognitive-behavioral therapy (CBT) and emphasize change, patients feel unheard and invalidated; they may withdraw, quit, or even attack. But if we suggest ways to accept unhappy situations, they may feel we don’t understand their suffering.

A more effective approach is dialectical behavior therapy (DBT), first developed to treat highly suicidal persons with borderline personality disorder and used with other populations that have difficulty regulating their emotions.

This article describes how invalidating environments may damage emotional health and suggests how psychiatrists can use DBT’s methods when treating borderline personality disorder.

BIOLOGY PLUS ENVIRONMENT

For the patient, borderline personality disorder’s behavior clusters (Table 1):

• function to regulate emotions
• or result from emotion dysregulation.

DBT theory identifies emotion dysregulation as the primary deficit in borderline personality disorder. Biologically based emotional vulnerability is seen as interacting with an inability to modulate emotions because of a skills deficit.

Emotional vulnerability. Three characteristics—high sensitivity, high reactivity, and slow return to baseline emotional state—define high emotional vulnerability:

High sensitivity. The person reacts more quickly and to more things than do others in emotion-provoking situations. When walking, for example, they may pass someone who doesn’t say hello. Most people would shrug this off, but persons with high emotional sensitivity may quickly notice, assume there is a problem, feel they have done something wrong, then feel shame and anger.

High reactivity. Their emotional reactions are large, and the high arousal dysregulates cognitive processing.

Slow return to baseline. Events stack up because emotional reactions are long-lasting for persons with high emotional vulnerability. They don’t have time to get over one thing before something else happens.

DBT postulates that, over time, borderline personality disorder results from the transaction of biological emotional vulnerability and an invalidating environment. This therapeutic model asserts that biology and the environment are flexible, and interventions may influence both.

Invalidating environment. DBT acknowledges that invalidation occurs in all environments, even nuturing ones. It becomes detrimental when a vulnerable person is exposed to pervasive invalidation that is not related to the validity of the person’s behavior or to the person’s expressed emotions or thoughts.

An invalidating environment has three characteristic patterns. One is indiscriminate rejection of communication of private experiences and self-generated behaviors.

Case examples. Mary, age 8, says she’s been teased and it hurt her feelings. Her mother tells her she is making too much of the incident. Mary questions herself and searches the social environment for cues about how to respond to similar situations in the future.

Robbie, age 4, completes a drawing and shows it to his father with delight. His father points out some “sloppy” coloring. If his father repeatedly finds fault with his work, Robbie is likely to not show him his work or stop drawing, and his expressions of delight are likely to decrease.

Invalidating environments may also punish emotional displays and intermittently reinforce emotional escalation. Someone may show disapproval for or ignore a person’s genuine sadness or fear but attend to angry outbursts that result when the person feels ignored.

The third invalidating pattern is to oversimplify the ease of problem-solving and meeting goals.

Case example. As a child, when Susan asked for help, her mother would say “just do it,” without considering the skills her daughter needed to accomplish tasks. When Susan became frustrated, her mother demanded that she “just stop cying,” even though no person could modulate his or her emotions that quickly. As an adult, Susan now sets unrealistic goals and expectations for herself and despairs when she is unable to solve problems in her life.

These three invalidating patterns cause persons to search the social environment for cues about how to respond to situations. They may question themselves, their identity, and the appropriateness of any emotional expression. As a result, they may oscillate between emotional inhibition and extreme emotional styles, set unrealistic goals and expectations for themselves, and eventually despair of being able to solve their problems.

Specific to borderline personality disorder is that the environment ignores genuine emotional expression, and the individual’s emotions escalate. This pattern is reinforced when the listener finally rewards emotionally extreme behavior with attention or desired changes.

As the pattern is repeated over time, extreme emotional reactions become the norm rather than the exception, and the emotional chaos can make the person wish to die. Acting on that desire when past expressions of desperation have been ignored or invalidated can provide attention or interventions that would never happen after simple emotional expressions.

Thus, an environment that does not recognize or validate genuine emotional expression can reinforce suicidality.

Table 1

Diagnostic criteria for borderline personality disorder

SOLVING NO-WIN THERAPY

Pitfalls with emphasizing change. Therapy that emphasizes solving problems and getting things to change typically triggers high arousal in persons with borderline personality disorder. Feeling out of control, they respond by trying to get in control, including attempts to control the therapist.

Similarly, they see attempts to get them to change their behavior as invalidating their experiences or, worse, who they are. Intense emotions aroused by the message they hear—that they are the source of their problems—impair learning and intensify their efforts to gain control. In a battle for control, collaboration and therapy cannot occur.

Case example. Ms. K wants you to understand how difficult her life is because of difficulties with her boss. You start talking about what Ms. K can do to change the situation, without acknowledging how difficult it is to deal with her boss.

Ms. K feels upset and says you don’t understand. For her, the interaction has led to emotion dysregulation and impaired cognitive processing.

Pitfalls with emphasizing acceptance. Most persons who come to therapy very distressed want something in their lives to change. If your primary message is acceptance instead of change, they may lose confidence in you.

Case example. Ms. K wants help dealing with her boss, who is making life quite difficult. As her therapist, you respond with warmth and acceptance but offer no suggestions as to how she might change the situation. Ms. K likes the way you listen to her but abandons therapy. after several sessions.

At first, patients with borderline personality disorder may like the warmth of client-centered acceptance approaches. Over time, however, they may feel their therapy sessions are out of control. They may think the therapist doesn’t understand the situation, doesn’t know how to help, or that situations that are troubling them cannot be changed.

Balanced therapy. DBT solves the change-or-acceptance dilemma by attempting to help patients with borderline personality disorder change themselves and their lives while offering strategies for accepting themselves and their situations.^1,2 DBT includes problem-solving and acceptance strategies (Table 2).

Table 2

Strategies used in dialectical behavioral therapy

DBT’S 4 THERAPY STAGES

DBT is a comprehensive treatment. The original outpatient model for borderline personality disorder (Table 3) has been adapted to different settings and applied to other populations.

Outpatients meet weekly in individual psychotherapy and a skills training group.³ Therapists also meet weekly in a consultation team viewed as “therapy for the therapist.”

Between sessions, therapists consult with patients by telephone to:

• decrease suicide crisis behaviors
• increase generalization of behavioral skills
• decrease patients’ feelings of conflict, alienation, or distance with the therapist.

Four stages. DBT follows four stages. For persons with borderline personality disorder, researchers have evaluated the efficacy of stage-1 therapy. Studies on stage-3 DBT have been conducted with nonborderline-personality individuals with eating disorders. The goals at each stage are:

Stage 1. Move from severe behavioral dyscontrol to behavioral control. Decrease suicidal and other life-threatening behaviors and those that interfere with therapy and quality of life. Increase mindfulness, tolerance for distress, interpersonal effectiveness, and emotion regulation.

Stage 2. Move from quiet desperation to emotional experiencing.

Stage 3. Address problems in living, and move toward ordinary happiness/unhappiness.

Stage 4. Move from incompleteness to capacity for joy and freedom.

Seven randomized controlled trials have shown that DBT can be useful in treating borderline personality disorder.^4-10 The initial trial by Linehan et al⁴ included 47 women ages 18 to 45 who met criteria for borderline personality disorder and had at least two parasuicide incidents in the previous 5 years, with one in the previous 8 weeks. Treatment lasted 1 year, and subjects agreed to stop other individual psychotherapy if assigned to DBT.

Subjects were then randomly assigned to either DBT or “treatment as usual” in the community. In the various DBT studies, treatment-as-usual has included community therapists, Department of Veterans Affairs outpatient treatment, client-centered therapy, and treatment by persons identified by their peers as experts in their communities.

Subjects were assessed every 4 months while in treatment and for 1 year thereafter. DBT was more effective than usual treatment in:

• reducing suicide attempts and self-injury
• decreasing premature dropout from therapy
• reducing emergency room admissions and length of psychiatric hospitalization
• reducing drug abuse, depression, hopelessness, and anger.

Table 3

Modes of therapy in outpatient dialectical behavioral therapy

RECOMMENDATIONS

Some psychiatrists may find “borderline patients” frustrating and unpleasant to treat. DBT therapists, however, make two assumptions that can help anyone working with individuals with borderline personality disorder. To avoid falling into the trap of polarization with these patients, assume that:

• they are doing the best they can
• their efforts are insufficient to meet their needs.

They therefore need to do better, and the therapist’s job is to help them do so. Also assume that if you try to help a patient with borderline personality disorder, you will need help, too. We require DBT therapists to participate in consultation teams.

Training. DBT is a comprehensive program that requires familiarity with the manuals mentioned in this article (see Related resources). Some teams have learned DBT through self-study and consultation with other teams.

If you plan to offer DBT to patients with borderline personality disorder, we recommend that you be:

• trained in behavior therapy and CBT
• familiar with research on emotions and processes involved in emotion regulation.

If you have not had CBT training, find a behavior therapist to join your team or get consultation from a behavior therapist.

An intensive training course in DBT—with 2 weeks of instruction and case consultation and several months of consultation with someone well-versed in DBT—is an efficient way to become familiar with the most critical principles of the treatment. If you cannot train toward adherent delivery of individual therapy, we recommend referring patients to someone trained in DBT.

Related resources

• Lieb K, Zanarini MC, Schmahl C, et al. Borderline personality disorder. Lancet 2004;364(9432):453-61.
• University of Washington, Behavioral Research and Therapy Clinics. www.brtc.psych.washington.edu/frameResearch.htm;
  www.brtc.psych.washington.edu/framePublications.htm
• Behavioral Tech, LLC. Consultation and training in dialectical behavioral therapy. www.behavioraltech.org.

Disclosures

Dr. DuBose is president and CEO/co-owner of DBT Center of Seattle, PLLC, and a speaker for Behavioral Tech, LLC.

Dr. Linehan is a shareholder in Behavioral Tech Research, Inc., which develops computerized training for DBT, a DBT trainer for Behavioral Tech, LLC, and the author of two books on DBT. She also receives research grants from the National Institute of Mental Health and National Institute on Drug Abuse.

I am rebutting “How to reduce aggression in patients with conduct disorder” (Current Psychiatry, April 2004).

A 15-year-old ended his first two visits with me under police custody and was committed both times. After the first commitment, his grandmother filed a petition alleging unruly/delinquent behavior, and a judge ordered the boy to take his prescribed mood stabilizers. That was necessary because the hospital psychiatrist had determined that the boy was not mentally ill and that his grandmother needed parenting classes. The youth’s original diagnosis—conduct disorder and oppositional-defiant disorder (ODD)—contradicted my diagnosis: bipolar disorder, mixed.

During the second hospitalization, a psychiatrist diagnosed the youth as having attentiondeficit/hyperactivity disorder (ADHD). The doctor prescribed methylphenidate and oxcarbazepine, but the patient’s guardian did not consent to the medications.

Facing a sentence at the county juvenile detention center, the youth started taking olanzapine, 10 mg at bedtime, and lamotrigine, 25 mg bid titrated to 50 mg bid, as I had prescribed. His grandmother says that he no longer exhibits defiant behavior. At his third visit, he shook my hand and said, “Thank you for finding the right medications for me.”

I have seen hundreds of similar cases over 10 years. To paraphrase a colleague, diagnosing somebody with conduct disorder or ODD is like diagnosing a patient with a runny nose after a thorough emergency room examination.

I applaud the American Association of Community Psychiatry’s efforts to urge the American Psychiatric Association (APA) to abolish the conduct disorder diagnosis. I also support the many researchers who are requesting elimination of conduct disorder and ODD. These are not real and specific diagnoses but are alleged syndromes that express several conditions.

Manuel Mota-Castillo MD
Orlando, FL

Dr. Malone responds

It is hard to assess Dr. Mota-Castillo’s case based on the information he provided. Still, one would not refute any psychiatric syndrome by citing a single case.

Most psychiatric disorders are syndromes and affect heterogeneous groups. This is true for disorders that are more prevalent in adults—such as schizophrenia and mania—and for those that present in childhood and adolescence—such as conduct disorder, ODD, and ADHD. Heterogeneity within disorders is no doubt related to underlying individual differences in genetics and environment and contributes to differences in symptom expression and treatment response.

Dr. Mota-Castillo did not present symptoms listed under DSM-IV-TR, so it is unclear how the patient was diagnosed. Diagnoses:

• are one clinician’s impression or the consensus of several clinicians
• are based on one patient encounter or ongoing treatment
• occur with or without input from other sources, such as parents and school
• are made with or without validated structured interviews.

Conduct disorder and ODDare part of DSM diagnostic nomenclature,¹ and the APA and American Academy of Child and Adolescent Psychiatry recognize both disorders. Reducing aggression associated with either disorder has long been the most common reason for psychiatric consultation in children.²

Also, Dr. Mota-Castillo prescribed olanzapine and lamotrigine, apparently for simultaneous use. The main point of our case was to discourage polypharmacy—something most experts agree should be avoided³ —by carefully starting one drug before adding a second. When a child receives two drugs at once, we cannot know the effect of either.

In the 15-year-old’s case, as often happens, the prescribed treatment might not have changed the symptoms; some symptoms remit spontaneously.

Nor does drug response clarify diagnosis. For example, both bipolar disorder and aggression in conduct disorder (and in many other conditions) may respond to an antipsychotic.⁴ Lithium and other treatments for mania have been shown to reduce severe aggression in nonmanic children and adolescents with conduct disorder.^5,6

Richard P. Malone, MD
Associate professor
Eastern Pennsylvania Psychiatric Institute
Drexel University College of Medicine
Philadelphia, PA

References

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (4th ed-rev). Washington, DC: American Psychiatric Association, 2000.
2. Kazdin AE. Conduct disorders in childhood and adolescence, vol. 9: developmental clinical psychology and psychiatry series. Newbury Park, CA: Sage Publications, 1987.
3. Pappadopulos E, Macintyre JC II, Crismon ML, et al. Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY): Part II. J Am Acad Child Adolesc Psychiatry 2003;42(2):145–61.
4. Malone RP, Delaney MA. Psychopharmacologic interventions in children with aggression: neuroleptics, lithium, and anticonvulsants. In: Coccaro EF (ed). Aggression: assessment and treatment.New York: Marcel Dekker, 2003:331–49.
5. Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry 2000;57(7):649–54.
6. Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry 1995;34(4):445–53.

I am rebutting “How to reduce aggression in patients with conduct disorder” (Current Psychiatry, April 2004).

A 15-year-old ended his first two visits with me under police custody and was committed both times. After the first commitment, his grandmother filed a petition alleging unruly/delinquent behavior, and a judge ordered the boy to take his prescribed mood stabilizers. That was necessary because the hospital psychiatrist had determined that the boy was not mentally ill and that his grandmother needed parenting classes. The youth’s original diagnosis—conduct disorder and oppositional-defiant disorder (ODD)—contradicted my diagnosis: bipolar disorder, mixed.

During the second hospitalization, a psychiatrist diagnosed the youth as having attentiondeficit/hyperactivity disorder (ADHD). The doctor prescribed methylphenidate and oxcarbazepine, but the patient’s guardian did not consent to the medications.

Facing a sentence at the county juvenile detention center, the youth started taking olanzapine, 10 mg at bedtime, and lamotrigine, 25 mg bid titrated to 50 mg bid, as I had prescribed. His grandmother says that he no longer exhibits defiant behavior. At his third visit, he shook my hand and said, “Thank you for finding the right medications for me.”

I have seen hundreds of similar cases over 10 years. To paraphrase a colleague, diagnosing somebody with conduct disorder or ODD is like diagnosing a patient with a runny nose after a thorough emergency room examination.

I applaud the American Association of Community Psychiatry’s efforts to urge the American Psychiatric Association (APA) to abolish the conduct disorder diagnosis. I also support the many researchers who are requesting elimination of conduct disorder and ODD. These are not real and specific diagnoses but are alleged syndromes that express several conditions.

Manuel Mota-Castillo MD
Orlando, FL

Dr. Malone responds

It is hard to assess Dr. Mota-Castillo’s case based on the information he provided. Still, one would not refute any psychiatric syndrome by citing a single case.

Most psychiatric disorders are syndromes and affect heterogeneous groups. This is true for disorders that are more prevalent in adults—such as schizophrenia and mania—and for those that present in childhood and adolescence—such as conduct disorder, ODD, and ADHD. Heterogeneity within disorders is no doubt related to underlying individual differences in genetics and environment and contributes to differences in symptom expression and treatment response.

Dr. Mota-Castillo did not present symptoms listed under DSM-IV-TR, so it is unclear how the patient was diagnosed. Diagnoses:

• are one clinician’s impression or the consensus of several clinicians
• are based on one patient encounter or ongoing treatment
• occur with or without input from other sources, such as parents and school
• are made with or without validated structured interviews.

Conduct disorder and ODDare part of DSM diagnostic nomenclature,¹ and the APA and American Academy of Child and Adolescent Psychiatry recognize both disorders. Reducing aggression associated with either disorder has long been the most common reason for psychiatric consultation in children.²

Also, Dr. Mota-Castillo prescribed olanzapine and lamotrigine, apparently for simultaneous use. The main point of our case was to discourage polypharmacy—something most experts agree should be avoided³ —by carefully starting one drug before adding a second. When a child receives two drugs at once, we cannot know the effect of either.

In the 15-year-old’s case, as often happens, the prescribed treatment might not have changed the symptoms; some symptoms remit spontaneously.

Nor does drug response clarify diagnosis. For example, both bipolar disorder and aggression in conduct disorder (and in many other conditions) may respond to an antipsychotic.⁴ Lithium and other treatments for mania have been shown to reduce severe aggression in nonmanic children and adolescents with conduct disorder.^5,6

Richard P. Malone, MD
Associate professor
Eastern Pennsylvania Psychiatric Institute
Drexel University College of Medicine
Philadelphia, PA

References

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (4th ed-rev). Washington, DC: American Psychiatric Association, 2000.
2. Kazdin AE. Conduct disorders in childhood and adolescence, vol. 9: developmental clinical psychology and psychiatry series. Newbury Park, CA: Sage Publications, 1987.
3. Pappadopulos E, Macintyre JC II, Crismon ML, et al. Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY): Part II. J Am Acad Child Adolesc Psychiatry 2003;42(2):145–61.
4. Malone RP, Delaney MA. Psychopharmacologic interventions in children with aggression: neuroleptics, lithium, and anticonvulsants. In: Coccaro EF (ed). Aggression: assessment and treatment.New York: Marcel Dekker, 2003:331–49.
5. Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry 2000;57(7):649–54.
6. Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry 1995;34(4):445–53.

I am rebutting “How to reduce aggression in patients with conduct disorder” (Current Psychiatry, April 2004).

A 15-year-old ended his first two visits with me under police custody and was committed both times. After the first commitment, his grandmother filed a petition alleging unruly/delinquent behavior, and a judge ordered the boy to take his prescribed mood stabilizers. That was necessary because the hospital psychiatrist had determined that the boy was not mentally ill and that his grandmother needed parenting classes. The youth’s original diagnosis—conduct disorder and oppositional-defiant disorder (ODD)—contradicted my diagnosis: bipolar disorder, mixed.

During the second hospitalization, a psychiatrist diagnosed the youth as having attentiondeficit/hyperactivity disorder (ADHD). The doctor prescribed methylphenidate and oxcarbazepine, but the patient’s guardian did not consent to the medications.

Facing a sentence at the county juvenile detention center, the youth started taking olanzapine, 10 mg at bedtime, and lamotrigine, 25 mg bid titrated to 50 mg bid, as I had prescribed. His grandmother says that he no longer exhibits defiant behavior. At his third visit, he shook my hand and said, “Thank you for finding the right medications for me.”

I have seen hundreds of similar cases over 10 years. To paraphrase a colleague, diagnosing somebody with conduct disorder or ODD is like diagnosing a patient with a runny nose after a thorough emergency room examination.

I applaud the American Association of Community Psychiatry’s efforts to urge the American Psychiatric Association (APA) to abolish the conduct disorder diagnosis. I also support the many researchers who are requesting elimination of conduct disorder and ODD. These are not real and specific diagnoses but are alleged syndromes that express several conditions.

Manuel Mota-Castillo MD
Orlando, FL

Dr. Malone responds

It is hard to assess Dr. Mota-Castillo’s case based on the information he provided. Still, one would not refute any psychiatric syndrome by citing a single case.

Most psychiatric disorders are syndromes and affect heterogeneous groups. This is true for disorders that are more prevalent in adults—such as schizophrenia and mania—and for those that present in childhood and adolescence—such as conduct disorder, ODD, and ADHD. Heterogeneity within disorders is no doubt related to underlying individual differences in genetics and environment and contributes to differences in symptom expression and treatment response.

Dr. Mota-Castillo did not present symptoms listed under DSM-IV-TR, so it is unclear how the patient was diagnosed. Diagnoses:

• are one clinician’s impression or the consensus of several clinicians
• are based on one patient encounter or ongoing treatment
• occur with or without input from other sources, such as parents and school
• are made with or without validated structured interviews.

Conduct disorder and ODDare part of DSM diagnostic nomenclature,¹ and the APA and American Academy of Child and Adolescent Psychiatry recognize both disorders. Reducing aggression associated with either disorder has long been the most common reason for psychiatric consultation in children.²

Also, Dr. Mota-Castillo prescribed olanzapine and lamotrigine, apparently for simultaneous use. The main point of our case was to discourage polypharmacy—something most experts agree should be avoided³ —by carefully starting one drug before adding a second. When a child receives two drugs at once, we cannot know the effect of either.

In the 15-year-old’s case, as often happens, the prescribed treatment might not have changed the symptoms; some symptoms remit spontaneously.

Nor does drug response clarify diagnosis. For example, both bipolar disorder and aggression in conduct disorder (and in many other conditions) may respond to an antipsychotic.⁴ Lithium and other treatments for mania have been shown to reduce severe aggression in nonmanic children and adolescents with conduct disorder.^5,6

Richard P. Malone, MD
Associate professor
Eastern Pennsylvania Psychiatric Institute
Drexel University College of Medicine
Philadelphia, PA

References

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (4th ed-rev). Washington, DC: American Psychiatric Association, 2000.
2. Kazdin AE. Conduct disorders in childhood and adolescence, vol. 9: developmental clinical psychology and psychiatry series. Newbury Park, CA: Sage Publications, 1987.
3. Pappadopulos E, Macintyre JC II, Crismon ML, et al. Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY): Part II. J Am Acad Child Adolesc Psychiatry 2003;42(2):145–61.
4. Malone RP, Delaney MA. Psychopharmacologic interventions in children with aggression: neuroleptics, lithium, and anticonvulsants. In: Coccaro EF (ed). Aggression: assessment and treatment.New York: Marcel Dekker, 2003:331–49.
5. Malone RP, Delaney MA, Luebbert JF, et al. A double-blind placebo-controlled study of lithium in hospitalized aggressive children and adolescents with conduct disorder. Arch Gen Psychiatry 2000;57(7):649–54.
6. Campbell M, Adams PB, Small AM, et al. Lithium in hospitalized aggressive children with conduct disorder: a double-blind and placebo-controlled study. J Am Acad Child Adolesc Psychiatry 1995;34(4):445–53.

Mr. K, age 52, has Asperger’s disorder and attention-deficit/hyperactivity disorder. Recently he sent an e-mail to President Bush, Vice President Cheney, Homeland Security Secretary Tom Ridge, television news commentator Wolf Blitzer, and numerous government agencies. Mr. K’s psychiatrist also received a copy.

In his message, Mr. K expressed intense personal offense at his belief that U.S. Sen. John Kerry had called his “beloved president” a liar, and challenged the presidential candidate to a duel. If Kerry refused, Mr. K wrote, he would “take other effective measures” to avenge this “insult to me, my family, and all loyal Americans.”

Immediately after seeing the note, the psychiatrist called the Secret Service. Ninety minutes later, agents interviewed Mr. K, searched his apartment, and found weapons and travel documents that strongly suggested Mr. K planned to follow Kerry. The patient was taken into custody and admitted to a secure psychiatric facility.

Patients with Asperger’s disorder often become fixated on a person or incident. Such patients’ social judgment is severely impaired, and they tend to view the world in absolute terms with no gray areas. In a presidential election year, that fixation can manifest as a verbal or written threat against the president, vice president, or a presidential candidate.

As doctors, we have both a civic duty and sworn obligation under state standard-of-practice codes to immediately inform the Secret Service of such a threat. Call the Secret Service even if you are unsure whether the patient will carry it out.

How to reach the Secret Service

• Find the phone number for the local Secret Service headquarters in the phone book’s U.S. government listings—usually under “frequently called numbers.”
• Tell the operator you are a psychiatrist reporting an imminent threat to the president’s or a candidate’s life. An agent will come on the line immediately.

If there is no Secret Service office in your area, contact the regional long-distance operator and demand to be connected with the nearest Secret Service headquarters.

When reporting a threat, insist on speaking to a live agent immediately. If you cannot reach the Secret Service, call the FBI at once.

Do not contact the patient once you have called authorities. The Secret Service will direct the investigation independent of your point of view.

Mr. K, age 52, has Asperger’s disorder and attention-deficit/hyperactivity disorder. Recently he sent an e-mail to President Bush, Vice President Cheney, Homeland Security Secretary Tom Ridge, television news commentator Wolf Blitzer, and numerous government agencies. Mr. K’s psychiatrist also received a copy.

In his message, Mr. K expressed intense personal offense at his belief that U.S. Sen. John Kerry had called his “beloved president” a liar, and challenged the presidential candidate to a duel. If Kerry refused, Mr. K wrote, he would “take other effective measures” to avenge this “insult to me, my family, and all loyal Americans.”

Immediately after seeing the note, the psychiatrist called the Secret Service. Ninety minutes later, agents interviewed Mr. K, searched his apartment, and found weapons and travel documents that strongly suggested Mr. K planned to follow Kerry. The patient was taken into custody and admitted to a secure psychiatric facility.

Patients with Asperger’s disorder often become fixated on a person or incident. Such patients’ social judgment is severely impaired, and they tend to view the world in absolute terms with no gray areas. In a presidential election year, that fixation can manifest as a verbal or written threat against the president, vice president, or a presidential candidate.

As doctors, we have both a civic duty and sworn obligation under state standard-of-practice codes to immediately inform the Secret Service of such a threat. Call the Secret Service even if you are unsure whether the patient will carry it out.

How to reach the Secret Service

• Find the phone number for the local Secret Service headquarters in the phone book’s U.S. government listings—usually under “frequently called numbers.”
• Tell the operator you are a psychiatrist reporting an imminent threat to the president’s or a candidate’s life. An agent will come on the line immediately.

If there is no Secret Service office in your area, contact the regional long-distance operator and demand to be connected with the nearest Secret Service headquarters.

When reporting a threat, insist on speaking to a live agent immediately. If you cannot reach the Secret Service, call the FBI at once.

Do not contact the patient once you have called authorities. The Secret Service will direct the investigation independent of your point of view.

Mr. K, age 52, has Asperger’s disorder and attention-deficit/hyperactivity disorder. Recently he sent an e-mail to President Bush, Vice President Cheney, Homeland Security Secretary Tom Ridge, television news commentator Wolf Blitzer, and numerous government agencies. Mr. K’s psychiatrist also received a copy.

In his message, Mr. K expressed intense personal offense at his belief that U.S. Sen. John Kerry had called his “beloved president” a liar, and challenged the presidential candidate to a duel. If Kerry refused, Mr. K wrote, he would “take other effective measures” to avenge this “insult to me, my family, and all loyal Americans.”

Immediately after seeing the note, the psychiatrist called the Secret Service. Ninety minutes later, agents interviewed Mr. K, searched his apartment, and found weapons and travel documents that strongly suggested Mr. K planned to follow Kerry. The patient was taken into custody and admitted to a secure psychiatric facility.

Patients with Asperger’s disorder often become fixated on a person or incident. Such patients’ social judgment is severely impaired, and they tend to view the world in absolute terms with no gray areas. In a presidential election year, that fixation can manifest as a verbal or written threat against the president, vice president, or a presidential candidate.

As doctors, we have both a civic duty and sworn obligation under state standard-of-practice codes to immediately inform the Secret Service of such a threat. Call the Secret Service even if you are unsure whether the patient will carry it out.

How to reach the Secret Service

• Find the phone number for the local Secret Service headquarters in the phone book’s U.S. government listings—usually under “frequently called numbers.”
• Tell the operator you are a psychiatrist reporting an imminent threat to the president’s or a candidate’s life. An agent will come on the line immediately.

If there is no Secret Service office in your area, contact the regional long-distance operator and demand to be connected with the nearest Secret Service headquarters.

When reporting a threat, insist on speaking to a live agent immediately. If you cannot reach the Secret Service, call the FBI at once.

Do not contact the patient once you have called authorities. The Secret Service will direct the investigation independent of your point of view.

Families and schools often pressure clinicians to “do something” when children or adolescents persistently bully, threaten, or injure others. This demand poses a treatment dilemma when psychosocial and educational interventions have failed to manage pediatric aggression.

Aggression is the main reason for drug therapy in youths with conduct disorder, but very little safety and efficacy data exist to help us choose medications. This places young patients at risk for polypharmacy, unmanaged symptoms, short-term side effects, and unknown long-term consequences of exposure to psychotropics.

Table 1

4 precautions when prescribing for pediatric aggression

This article reviews the limited data on using medications to reduce aggression in children and adolescents, focusing on double-blind, placebo-controlled trials in conduct disorder. Based on this evidence and our clinical experience, we offer a sample case and treatment recommendations.

Prescribing principles

Precautions. When prescribing drugs to treat aggressive youth, remember the American Academy of Child and Adolescent Psychiatry’s precautions (Table 1)¹ Recently published recommendations prepared by expert consensus are also valuable treatment guides.²

Linking treatment to diagnosis. Should we attempt to manage aggression as a manifestation of an underlying psychiatric disorder? Or should we treat it the same across all disorders? The latter approach is akin to the “fever model.”

Fever—regardless of cause—may be treated with a nonsteroidal anti-inflammatory drug. However, evidence from drug studies suggests that underlying psychiatric disorders should help determine the choice of aggression treatment. For example, a recent study in adults found that divalproex was effective for aggressive patients only within a specific diagnostic subgroup (in this case, cluster B personality disorders).³

Clinical experience also links aggression treatment with underlying diagnoses. For example, aggression secondary to agitated depression is treated with an antidepressant, whereas aggression secondary to command hallucinations in schizophrenia is treated with antipsychotics.

In treating aggression in conduct disorder (Table 2), first treat comorbid disorders—such as attention deficit/hyperactivity disorder (ADHD) or bipolar disorder—and address the child’s psychosocial and educational needs. Then if medication is appropriate, consider drugs with evidence of safety and efficacy, such as antipsychotics, lithium, and stimulants.

Antipsychotics

Three conventional antipsychotics—chlorpromazine, haloperidol, and thioridazine—are FDA-approved for controlling disruptive behaviors in children.⁴ No atypical antipsychotics are so indicated, but atypicals are preferred in children and adolescents because of lower risks for tardive dyskinesia, neuroleptic malignant syndrome, and extrapyramidal symptoms.²

Risperidone is the most-studied atypical antipsychotic for treating pediatric aggression, particularly in patients with low intellectual functioning or mental retardation. In a 6-week, double-blind, placebo-controlled trial, 118 children ages 5 to 12 with severely disruptive behavior and IQs of 36 to 84 were given low-dose risperidone (mean 1.16 mg/d). Risperidone reduced conduct problems significantly more than placebo, although aggression was not measured directly.⁵ Adverse events included somnolence, headache, vomiting, weight gain, and elevated serum prolactin. Similar results have been reported in other studies.⁶

Table 2

Diagnostic criteria for conduct disorder

Box 1

Risperidone also reduced aggression in children with normal intelligence in one small study.⁷ As a cautionary note, however, long-term risperidone treatment has been associated with withdrawal dyskinesias.⁸

Olanzapine, quetiapine, ziprasidone, and aripiprazole are less well-studied for treating pediatric aggression but are preferable to conventional agents when antipsychotics are considered.

Recommendation. Expert consensus opinion² recommends using atypicals when psychosocial treatments and first-line medications for primary conditions have failed. Start with low dosages, and titrate up slowly while monitoring symptoms and side effects. Because no studies have compared any atypical’s efficacy over others for aggressive behavior, base your choices on:

• discussions with the patient and family (Box 1)
• medical comorbidities
• how the patient responded to antipsychotics in the past
• side-effect profile
• long-term treatment planning.²

If the patient cannot tolerate the medication or does not respond after 4 to 6 weeks, try switching atypicals. To improve partial response, consider adding a mood stabilizer such as lithium or divalproex. If aggressive symptoms remit for 6 months or longer, attempt to taper or discontinue the antipsychotic.²

Lithium

In placebo-controlled trials, lithium reduced aggression in:

• male prisoners ages 16 to 24.⁹
• children ages 7 and 12 with conduct disorder¹⁰
• children and adolescents ages 10 to 17 with conduct disorder.¹¹

Among these studies, only ours¹¹ specifically measured aggression. We randomly assigned 40 children to receive 4 weeks of lithium, 900 to 2,100 mg/d (mean 1,425 ± 321 mg/d), or placebo. Serum lithium levels were 0.78 to 1.55 mEq/L (mean 1.07 ± 0.19 mEq/L). We used the Overt Aggression Scale (OAS)^12,13 (see Related resources) to track frequency and severity of verbal aggression, aggression against objects, aggression against others, and self-aggression.

Lithium reduced aggression more than did placebo, as measured by the clinician-rated Clinical Global Impressions (CGI) scale and staff-rated Global Clinical Judgments (Consensus) Scale (GCJCS). The CGI showed a 70% response rate with lithium and 20% with placebo. Similarly, the GCJCS scale showed 80% response with lithium and 30% with placebo.

The aggression reduction with lithium was statistically significant and clinically evident. Most subjects (37 of 40) experienced at least one adverse event, however, whether receiving lithium or placebo. Nausea, vomiting, and urinary frequency were significantly more common in the lithium-treated group than with placebo. Fewer adverse events were reported in a similar outpatient study,¹⁴ probably because of less-frequent monitoring.

Lithium did not reduce aggression in adolescent girls treated for 2 weeks¹⁵ or in an outpatient study of children with ADHD.¹⁶

Recommendation. Lithium has shown efficacy for reducing severe aggression in hospitalized children with conduct disorder but not in similar outpatients. Consider this drug to reduce severe aggression in children with conduct disorder, especially if they have failed other treatments.

Anticonvulsants

Anticonvulsants have been used to decrease aggression for more than 50 years, and epidemiologic data show their use is increasing markedly.¹⁷ Few controlled studies support this prescribing trend, however.¹⁸

Initial reports suggested that anticonvulsants reduce disruptive behaviors, but more-critically designed studies have not supported this finding. For example, phenytoin sodium (diphenylhydantoin) demonstrated efficacy in open trials, but controlled trials found this anticonvulsant no more effective than placebo. In fact, placebo may have reduced aggression more than the active drug. Likewise, earlier controlled trials of carbamazepine indicated efficacy, but more-carefully designed trials using specific measures of aggression did not.

Divalproex is the anticonvulsant most commonly used for aggression in children and adolescents. Only one small, placebo-controlled study has found it effective in reducing aggression in children.¹⁹

Twenty children ages 10 to 18 with conduct disorder or oppositional defiant disorder were randomized to divalproex, 750 to 1,500 mg/d, or placebo. Eighteen completed the first phase, and 15 crossed over to the other treatment. Concomitant drug treatment, including stimulants, was allowed. The authors reported that 12 of 15 subjects showed some response to divalproex.

A 7-week study compared divalproex in high dosages (up to 1,500 mg/d) versus low dosages (up to 250 mg/d). This study was not placebo-controlled, but aggression was reduced more in the high-dosage than in the low-dosage group.²⁰

Recommendation. If you use an anticonvulsant, first obtain informed consent from the patient and parent. Divalproex causes weight gain and has been associated with increased risk of polycystic ovary syndrome with masculinizing effects.²¹

Double-blind, placebo-controlled studies of divalproex and other anticonvulsants in treating aggression are needed, particularly as prescriptions for these agents are rising.

Stimulants

Some small controlled studies suggest that stimulants can reduce aggression in children with ADHD, but their effects on aggression in conduct disorder have not been well studied. Aggression was not measured directly in the National Institute of Mental Health Multimodal Treatment Study of Children with ADHD.²¹ Most other studies have been small and included children with ADHD but not necessarily conduct disorder.

Recommendation. Stimulants may help reduce aggression in children with ADHD, but studies gauging their effects in conduct disorder are needed.

Alpha agonists

Alpha agonists such as clonidine and guanfacine are increasingly being used to treat children with disruptive disorders, despite limited evidence. The small controlled studies that examined alpha agonists as monotherapy or add-ons in this population did not directly measure aggression.^22,23

Recommendation. Little data support alpha agonists for reducing aggression. They should probably be considered second-line treatment.

SSRIs

No double-blind, placebo-controlled studies have tested any selective serotonin reuptake inhibitor (SSRIs) for reducing aggression in conduct disorder. In a 6-week open study, citalopram (mean 27 mg/d) reduced impulsive aggression in 12 children with mixed diagnoses, as measured by the modified OAS,¹³ Child Behavior Checklist, and CGI.²⁴

Recommendation. Use caution when prescribing SSRIs to aggressive youth, as these drugs may contribute to aggression in some mood-disordered children. More evidence of SSRIs’ safety and efficacy in this population is needed.

Related resources

• Overt Aggression Scale. In: Coccaro EF, Harvey PD, Kupsaw-Lawrence E, et al. Development of neuropharmacologically-based behavioral assessments of impulsiveaggressive behavior. J Neuropsychiatry 1991;3(2):S44-S51.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Chlorpromazine • Thorazine
• Clonidine • Catapres
• Phenytoin sodium • Dilantin
• Divalproex • Depakote
• Guanfacine • Tenex
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Thioridazine • Mellaril
• Ziprasidone • Geodon

Disclosure

Dr. Malone receives research support from Pfizer Inc. and Eli Lilly and Co. and is a consultant to Janssen Pharmaceutica.

Dr. Delaney is a consultant to Shire Pharmaceuticals.

Dr. Sheikh reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Families and schools often pressure clinicians to “do something” when children or adolescents persistently bully, threaten, or injure others. This demand poses a treatment dilemma when psychosocial and educational interventions have failed to manage pediatric aggression.

Aggression is the main reason for drug therapy in youths with conduct disorder, but very little safety and efficacy data exist to help us choose medications. This places young patients at risk for polypharmacy, unmanaged symptoms, short-term side effects, and unknown long-term consequences of exposure to psychotropics.

Table 1

4 precautions when prescribing for pediatric aggression

This article reviews the limited data on using medications to reduce aggression in children and adolescents, focusing on double-blind, placebo-controlled trials in conduct disorder. Based on this evidence and our clinical experience, we offer a sample case and treatment recommendations.

Prescribing principles

Precautions. When prescribing drugs to treat aggressive youth, remember the American Academy of Child and Adolescent Psychiatry’s precautions (Table 1)¹ Recently published recommendations prepared by expert consensus are also valuable treatment guides.²

Linking treatment to diagnosis. Should we attempt to manage aggression as a manifestation of an underlying psychiatric disorder? Or should we treat it the same across all disorders? The latter approach is akin to the “fever model.”

Fever—regardless of cause—may be treated with a nonsteroidal anti-inflammatory drug. However, evidence from drug studies suggests that underlying psychiatric disorders should help determine the choice of aggression treatment. For example, a recent study in adults found that divalproex was effective for aggressive patients only within a specific diagnostic subgroup (in this case, cluster B personality disorders).³

Clinical experience also links aggression treatment with underlying diagnoses. For example, aggression secondary to agitated depression is treated with an antidepressant, whereas aggression secondary to command hallucinations in schizophrenia is treated with antipsychotics.

In treating aggression in conduct disorder (Table 2), first treat comorbid disorders—such as attention deficit/hyperactivity disorder (ADHD) or bipolar disorder—and address the child’s psychosocial and educational needs. Then if medication is appropriate, consider drugs with evidence of safety and efficacy, such as antipsychotics, lithium, and stimulants.

Antipsychotics

Three conventional antipsychotics—chlorpromazine, haloperidol, and thioridazine—are FDA-approved for controlling disruptive behaviors in children.⁴ No atypical antipsychotics are so indicated, but atypicals are preferred in children and adolescents because of lower risks for tardive dyskinesia, neuroleptic malignant syndrome, and extrapyramidal symptoms.²

Risperidone is the most-studied atypical antipsychotic for treating pediatric aggression, particularly in patients with low intellectual functioning or mental retardation. In a 6-week, double-blind, placebo-controlled trial, 118 children ages 5 to 12 with severely disruptive behavior and IQs of 36 to 84 were given low-dose risperidone (mean 1.16 mg/d). Risperidone reduced conduct problems significantly more than placebo, although aggression was not measured directly.⁵ Adverse events included somnolence, headache, vomiting, weight gain, and elevated serum prolactin. Similar results have been reported in other studies.⁶

Table 2

Diagnostic criteria for conduct disorder

Box 1

Risperidone also reduced aggression in children with normal intelligence in one small study.⁷ As a cautionary note, however, long-term risperidone treatment has been associated with withdrawal dyskinesias.⁸

Olanzapine, quetiapine, ziprasidone, and aripiprazole are less well-studied for treating pediatric aggression but are preferable to conventional agents when antipsychotics are considered.

Recommendation. Expert consensus opinion² recommends using atypicals when psychosocial treatments and first-line medications for primary conditions have failed. Start with low dosages, and titrate up slowly while monitoring symptoms and side effects. Because no studies have compared any atypical’s efficacy over others for aggressive behavior, base your choices on:

• discussions with the patient and family (Box 1)
• medical comorbidities
• how the patient responded to antipsychotics in the past
• side-effect profile
• long-term treatment planning.²

If the patient cannot tolerate the medication or does not respond after 4 to 6 weeks, try switching atypicals. To improve partial response, consider adding a mood stabilizer such as lithium or divalproex. If aggressive symptoms remit for 6 months or longer, attempt to taper or discontinue the antipsychotic.²

Lithium

In placebo-controlled trials, lithium reduced aggression in:

• male prisoners ages 16 to 24.⁹
• children ages 7 and 12 with conduct disorder¹⁰
• children and adolescents ages 10 to 17 with conduct disorder.¹¹

Among these studies, only ours¹¹ specifically measured aggression. We randomly assigned 40 children to receive 4 weeks of lithium, 900 to 2,100 mg/d (mean 1,425 ± 321 mg/d), or placebo. Serum lithium levels were 0.78 to 1.55 mEq/L (mean 1.07 ± 0.19 mEq/L). We used the Overt Aggression Scale (OAS)^12,13 (see Related resources) to track frequency and severity of verbal aggression, aggression against objects, aggression against others, and self-aggression.

Lithium reduced aggression more than did placebo, as measured by the clinician-rated Clinical Global Impressions (CGI) scale and staff-rated Global Clinical Judgments (Consensus) Scale (GCJCS). The CGI showed a 70% response rate with lithium and 20% with placebo. Similarly, the GCJCS scale showed 80% response with lithium and 30% with placebo.

The aggression reduction with lithium was statistically significant and clinically evident. Most subjects (37 of 40) experienced at least one adverse event, however, whether receiving lithium or placebo. Nausea, vomiting, and urinary frequency were significantly more common in the lithium-treated group than with placebo. Fewer adverse events were reported in a similar outpatient study,¹⁴ probably because of less-frequent monitoring.

Lithium did not reduce aggression in adolescent girls treated for 2 weeks¹⁵ or in an outpatient study of children with ADHD.¹⁶

Recommendation. Lithium has shown efficacy for reducing severe aggression in hospitalized children with conduct disorder but not in similar outpatients. Consider this drug to reduce severe aggression in children with conduct disorder, especially if they have failed other treatments.

Anticonvulsants

Anticonvulsants have been used to decrease aggression for more than 50 years, and epidemiologic data show their use is increasing markedly.¹⁷ Few controlled studies support this prescribing trend, however.¹⁸

Initial reports suggested that anticonvulsants reduce disruptive behaviors, but more-critically designed studies have not supported this finding. For example, phenytoin sodium (diphenylhydantoin) demonstrated efficacy in open trials, but controlled trials found this anticonvulsant no more effective than placebo. In fact, placebo may have reduced aggression more than the active drug. Likewise, earlier controlled trials of carbamazepine indicated efficacy, but more-carefully designed trials using specific measures of aggression did not.

Divalproex is the anticonvulsant most commonly used for aggression in children and adolescents. Only one small, placebo-controlled study has found it effective in reducing aggression in children.¹⁹

Twenty children ages 10 to 18 with conduct disorder or oppositional defiant disorder were randomized to divalproex, 750 to 1,500 mg/d, or placebo. Eighteen completed the first phase, and 15 crossed over to the other treatment. Concomitant drug treatment, including stimulants, was allowed. The authors reported that 12 of 15 subjects showed some response to divalproex.

A 7-week study compared divalproex in high dosages (up to 1,500 mg/d) versus low dosages (up to 250 mg/d). This study was not placebo-controlled, but aggression was reduced more in the high-dosage than in the low-dosage group.²⁰

Recommendation. If you use an anticonvulsant, first obtain informed consent from the patient and parent. Divalproex causes weight gain and has been associated with increased risk of polycystic ovary syndrome with masculinizing effects.²¹

Double-blind, placebo-controlled studies of divalproex and other anticonvulsants in treating aggression are needed, particularly as prescriptions for these agents are rising.

Stimulants

Some small controlled studies suggest that stimulants can reduce aggression in children with ADHD, but their effects on aggression in conduct disorder have not been well studied. Aggression was not measured directly in the National Institute of Mental Health Multimodal Treatment Study of Children with ADHD.²¹ Most other studies have been small and included children with ADHD but not necessarily conduct disorder.

Recommendation. Stimulants may help reduce aggression in children with ADHD, but studies gauging their effects in conduct disorder are needed.

Alpha agonists

Alpha agonists such as clonidine and guanfacine are increasingly being used to treat children with disruptive disorders, despite limited evidence. The small controlled studies that examined alpha agonists as monotherapy or add-ons in this population did not directly measure aggression.^22,23

Recommendation. Little data support alpha agonists for reducing aggression. They should probably be considered second-line treatment.

SSRIs

No double-blind, placebo-controlled studies have tested any selective serotonin reuptake inhibitor (SSRIs) for reducing aggression in conduct disorder. In a 6-week open study, citalopram (mean 27 mg/d) reduced impulsive aggression in 12 children with mixed diagnoses, as measured by the modified OAS,¹³ Child Behavior Checklist, and CGI.²⁴

Recommendation. Use caution when prescribing SSRIs to aggressive youth, as these drugs may contribute to aggression in some mood-disordered children. More evidence of SSRIs’ safety and efficacy in this population is needed.

Related resources

• Overt Aggression Scale. In: Coccaro EF, Harvey PD, Kupsaw-Lawrence E, et al. Development of neuropharmacologically-based behavioral assessments of impulsiveaggressive behavior. J Neuropsychiatry 1991;3(2):S44-S51.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Chlorpromazine • Thorazine
• Clonidine • Catapres
• Phenytoin sodium • Dilantin
• Divalproex • Depakote
• Guanfacine • Tenex
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Thioridazine • Mellaril
• Ziprasidone • Geodon

Disclosure

Dr. Malone receives research support from Pfizer Inc. and Eli Lilly and Co. and is a consultant to Janssen Pharmaceutica.

Dr. Delaney is a consultant to Shire Pharmaceuticals.

Dr. Sheikh reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Families and schools often pressure clinicians to “do something” when children or adolescents persistently bully, threaten, or injure others. This demand poses a treatment dilemma when psychosocial and educational interventions have failed to manage pediatric aggression.

Aggression is the main reason for drug therapy in youths with conduct disorder, but very little safety and efficacy data exist to help us choose medications. This places young patients at risk for polypharmacy, unmanaged symptoms, short-term side effects, and unknown long-term consequences of exposure to psychotropics.

Table 1

4 precautions when prescribing for pediatric aggression

This article reviews the limited data on using medications to reduce aggression in children and adolescents, focusing on double-blind, placebo-controlled trials in conduct disorder. Based on this evidence and our clinical experience, we offer a sample case and treatment recommendations.

Prescribing principles

Precautions. When prescribing drugs to treat aggressive youth, remember the American Academy of Child and Adolescent Psychiatry’s precautions (Table 1)¹ Recently published recommendations prepared by expert consensus are also valuable treatment guides.²

Linking treatment to diagnosis. Should we attempt to manage aggression as a manifestation of an underlying psychiatric disorder? Or should we treat it the same across all disorders? The latter approach is akin to the “fever model.”

Fever—regardless of cause—may be treated with a nonsteroidal anti-inflammatory drug. However, evidence from drug studies suggests that underlying psychiatric disorders should help determine the choice of aggression treatment. For example, a recent study in adults found that divalproex was effective for aggressive patients only within a specific diagnostic subgroup (in this case, cluster B personality disorders).³

Clinical experience also links aggression treatment with underlying diagnoses. For example, aggression secondary to agitated depression is treated with an antidepressant, whereas aggression secondary to command hallucinations in schizophrenia is treated with antipsychotics.

In treating aggression in conduct disorder (Table 2), first treat comorbid disorders—such as attention deficit/hyperactivity disorder (ADHD) or bipolar disorder—and address the child’s psychosocial and educational needs. Then if medication is appropriate, consider drugs with evidence of safety and efficacy, such as antipsychotics, lithium, and stimulants.

Antipsychotics

Three conventional antipsychotics—chlorpromazine, haloperidol, and thioridazine—are FDA-approved for controlling disruptive behaviors in children.⁴ No atypical antipsychotics are so indicated, but atypicals are preferred in children and adolescents because of lower risks for tardive dyskinesia, neuroleptic malignant syndrome, and extrapyramidal symptoms.²

Risperidone is the most-studied atypical antipsychotic for treating pediatric aggression, particularly in patients with low intellectual functioning or mental retardation. In a 6-week, double-blind, placebo-controlled trial, 118 children ages 5 to 12 with severely disruptive behavior and IQs of 36 to 84 were given low-dose risperidone (mean 1.16 mg/d). Risperidone reduced conduct problems significantly more than placebo, although aggression was not measured directly.⁵ Adverse events included somnolence, headache, vomiting, weight gain, and elevated serum prolactin. Similar results have been reported in other studies.⁶

Table 2

Diagnostic criteria for conduct disorder

Box 1

Risperidone also reduced aggression in children with normal intelligence in one small study.⁷ As a cautionary note, however, long-term risperidone treatment has been associated with withdrawal dyskinesias.⁸

Olanzapine, quetiapine, ziprasidone, and aripiprazole are less well-studied for treating pediatric aggression but are preferable to conventional agents when antipsychotics are considered.

Recommendation. Expert consensus opinion² recommends using atypicals when psychosocial treatments and first-line medications for primary conditions have failed. Start with low dosages, and titrate up slowly while monitoring symptoms and side effects. Because no studies have compared any atypical’s efficacy over others for aggressive behavior, base your choices on:

• discussions with the patient and family (Box 1)
• medical comorbidities
• how the patient responded to antipsychotics in the past
• side-effect profile
• long-term treatment planning.²

If the patient cannot tolerate the medication or does not respond after 4 to 6 weeks, try switching atypicals. To improve partial response, consider adding a mood stabilizer such as lithium or divalproex. If aggressive symptoms remit for 6 months or longer, attempt to taper or discontinue the antipsychotic.²

Lithium

In placebo-controlled trials, lithium reduced aggression in:

• male prisoners ages 16 to 24.⁹
• children ages 7 and 12 with conduct disorder¹⁰
• children and adolescents ages 10 to 17 with conduct disorder.¹¹

Among these studies, only ours¹¹ specifically measured aggression. We randomly assigned 40 children to receive 4 weeks of lithium, 900 to 2,100 mg/d (mean 1,425 ± 321 mg/d), or placebo. Serum lithium levels were 0.78 to 1.55 mEq/L (mean 1.07 ± 0.19 mEq/L). We used the Overt Aggression Scale (OAS)^12,13 (see Related resources) to track frequency and severity of verbal aggression, aggression against objects, aggression against others, and self-aggression.

Lithium reduced aggression more than did placebo, as measured by the clinician-rated Clinical Global Impressions (CGI) scale and staff-rated Global Clinical Judgments (Consensus) Scale (GCJCS). The CGI showed a 70% response rate with lithium and 20% with placebo. Similarly, the GCJCS scale showed 80% response with lithium and 30% with placebo.

The aggression reduction with lithium was statistically significant and clinically evident. Most subjects (37 of 40) experienced at least one adverse event, however, whether receiving lithium or placebo. Nausea, vomiting, and urinary frequency were significantly more common in the lithium-treated group than with placebo. Fewer adverse events were reported in a similar outpatient study,¹⁴ probably because of less-frequent monitoring.

Lithium did not reduce aggression in adolescent girls treated for 2 weeks¹⁵ or in an outpatient study of children with ADHD.¹⁶

Recommendation. Lithium has shown efficacy for reducing severe aggression in hospitalized children with conduct disorder but not in similar outpatients. Consider this drug to reduce severe aggression in children with conduct disorder, especially if they have failed other treatments.

Anticonvulsants

Anticonvulsants have been used to decrease aggression for more than 50 years, and epidemiologic data show their use is increasing markedly.¹⁷ Few controlled studies support this prescribing trend, however.¹⁸

Initial reports suggested that anticonvulsants reduce disruptive behaviors, but more-critically designed studies have not supported this finding. For example, phenytoin sodium (diphenylhydantoin) demonstrated efficacy in open trials, but controlled trials found this anticonvulsant no more effective than placebo. In fact, placebo may have reduced aggression more than the active drug. Likewise, earlier controlled trials of carbamazepine indicated efficacy, but more-carefully designed trials using specific measures of aggression did not.

Divalproex is the anticonvulsant most commonly used for aggression in children and adolescents. Only one small, placebo-controlled study has found it effective in reducing aggression in children.¹⁹

Twenty children ages 10 to 18 with conduct disorder or oppositional defiant disorder were randomized to divalproex, 750 to 1,500 mg/d, or placebo. Eighteen completed the first phase, and 15 crossed over to the other treatment. Concomitant drug treatment, including stimulants, was allowed. The authors reported that 12 of 15 subjects showed some response to divalproex.

A 7-week study compared divalproex in high dosages (up to 1,500 mg/d) versus low dosages (up to 250 mg/d). This study was not placebo-controlled, but aggression was reduced more in the high-dosage than in the low-dosage group.²⁰

Recommendation. If you use an anticonvulsant, first obtain informed consent from the patient and parent. Divalproex causes weight gain and has been associated with increased risk of polycystic ovary syndrome with masculinizing effects.²¹

Double-blind, placebo-controlled studies of divalproex and other anticonvulsants in treating aggression are needed, particularly as prescriptions for these agents are rising.

Stimulants

Some small controlled studies suggest that stimulants can reduce aggression in children with ADHD, but their effects on aggression in conduct disorder have not been well studied. Aggression was not measured directly in the National Institute of Mental Health Multimodal Treatment Study of Children with ADHD.²¹ Most other studies have been small and included children with ADHD but not necessarily conduct disorder.

Recommendation. Stimulants may help reduce aggression in children with ADHD, but studies gauging their effects in conduct disorder are needed.

Alpha agonists

Alpha agonists such as clonidine and guanfacine are increasingly being used to treat children with disruptive disorders, despite limited evidence. The small controlled studies that examined alpha agonists as monotherapy or add-ons in this population did not directly measure aggression.^22,23

Recommendation. Little data support alpha agonists for reducing aggression. They should probably be considered second-line treatment.

SSRIs

No double-blind, placebo-controlled studies have tested any selective serotonin reuptake inhibitor (SSRIs) for reducing aggression in conduct disorder. In a 6-week open study, citalopram (mean 27 mg/d) reduced impulsive aggression in 12 children with mixed diagnoses, as measured by the modified OAS,¹³ Child Behavior Checklist, and CGI.²⁴

Recommendation. Use caution when prescribing SSRIs to aggressive youth, as these drugs may contribute to aggression in some mood-disordered children. More evidence of SSRIs’ safety and efficacy in this population is needed.

Related resources

• Overt Aggression Scale. In: Coccaro EF, Harvey PD, Kupsaw-Lawrence E, et al. Development of neuropharmacologically-based behavioral assessments of impulsiveaggressive behavior. J Neuropsychiatry 1991;3(2):S44-S51.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Chlorpromazine • Thorazine
• Clonidine • Catapres
• Phenytoin sodium • Dilantin
• Divalproex • Depakote
• Guanfacine • Tenex
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Thioridazine • Mellaril
• Ziprasidone • Geodon

Disclosure

Dr. Malone receives research support from Pfizer Inc. and Eli Lilly and Co. and is a consultant to Janssen Pharmaceutica.

Dr. Delaney is a consultant to Shire Pharmaceuticals.

Dr. Sheikh reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.