Current Psychiatry

We thank Dr. Helmuth and the principal investigators of CATIE for their interest in our article and the opportunity to further clarify a key learning point from CATIE.

Dr. Helmuth acknowledges our balanced review but suggests that cost and metabolic side effects should be considered along with lower EPS liability in selecting antipsychotic therapy. We agree. Avoiding EPS while obtaining a good antipsychotic effect is one key consideration in providing optimal antipsychotic therapy. Other adverse effects, patient preference, cost, and other factors are all important considerations in this complex process of individually optimizing antipsychotic treatment.

The CATIE investigators agree with our interpretation of the study’s principal findings. They take exception, however, to our suggestion that CATIE’s finding of no FGA-SGA difference in EPS and TD may be related to its relatively low assay sensitivity to detect such differences because the sample studied was at low risk for EPS and TD.

While accepting our description of the study sample as accurate, they disagree that it was at low risk for EPS and TD. Patients who have been ill for 16 years and received antipsychotic treatment for an average of 14 years without developing TD or severe EPS (as in CATIE) are by definition at low risk for EPS and TD.

We agree that patients without current TD and who are at risk for developing it comprise the best study population to investigate differential risk for TD; however, patients who have not developed it, despite 14 years of antipsychotic therapy, are at very low risk for developing it at all. First-episode patients without prior antipsychotic exposure would be an optimal study population, but such patients were excluded from CATIE.

Drs. Rosenheck and colleagues do not disagree with any of the other assertions in our article; they are, however, critical of “numerous factual errors in other published critiques of CATIE.” We cannot address such supposed inaccuracies, which are best taken up with authors of those commentaries.

To extract maximum value from this important initiative, we must better understand CATIE’s findings in the context of its study design and the results of other relevant studies. Neither mischaracterization nor overinterpretation of CATIE’s findings helps clinicians, patients, and policy-makers.

The essence of our article was that avoiding motor, cognitive, and affective EPS due to unmodulated dopamine blockade is the key to realizing the “atypical benefits” of a broader spectrum of efficacy and lower risk of TD during antipsychotic therapy. Neither Dr. Helmuth nor Drs. Rosenheck and colleagues appear to disagree with this assertion. Avoiding broadly defined EPS appears to be critical to improving cognition, dysphoria, and negative symptoms with SGAs and FGAs. The lower risk of TD observed with SGAs also appears to be related to the greater ease with which they can provide an equivalent antipsychotic effect without EPS.

Rajiv Tandon, MD
Adjunct professor of psychiatry
University of Florida, Tallahassee

Robert Constantine, PhD
Research associate professor
University of South Florida, Tampa

We thank Dr. Helmuth and the principal investigators of CATIE for their interest in our article and the opportunity to further clarify a key learning point from CATIE.

Dr. Helmuth acknowledges our balanced review but suggests that cost and metabolic side effects should be considered along with lower EPS liability in selecting antipsychotic therapy. We agree. Avoiding EPS while obtaining a good antipsychotic effect is one key consideration in providing optimal antipsychotic therapy. Other adverse effects, patient preference, cost, and other factors are all important considerations in this complex process of individually optimizing antipsychotic treatment.

The CATIE investigators agree with our interpretation of the study’s principal findings. They take exception, however, to our suggestion that CATIE’s finding of no FGA-SGA difference in EPS and TD may be related to its relatively low assay sensitivity to detect such differences because the sample studied was at low risk for EPS and TD.

While accepting our description of the study sample as accurate, they disagree that it was at low risk for EPS and TD. Patients who have been ill for 16 years and received antipsychotic treatment for an average of 14 years without developing TD or severe EPS (as in CATIE) are by definition at low risk for EPS and TD.

We agree that patients without current TD and who are at risk for developing it comprise the best study population to investigate differential risk for TD; however, patients who have not developed it, despite 14 years of antipsychotic therapy, are at very low risk for developing it at all. First-episode patients without prior antipsychotic exposure would be an optimal study population, but such patients were excluded from CATIE.

Drs. Rosenheck and colleagues do not disagree with any of the other assertions in our article; they are, however, critical of “numerous factual errors in other published critiques of CATIE.” We cannot address such supposed inaccuracies, which are best taken up with authors of those commentaries.

To extract maximum value from this important initiative, we must better understand CATIE’s findings in the context of its study design and the results of other relevant studies. Neither mischaracterization nor overinterpretation of CATIE’s findings helps clinicians, patients, and policy-makers.

The essence of our article was that avoiding motor, cognitive, and affective EPS due to unmodulated dopamine blockade is the key to realizing the “atypical benefits” of a broader spectrum of efficacy and lower risk of TD during antipsychotic therapy. Neither Dr. Helmuth nor Drs. Rosenheck and colleagues appear to disagree with this assertion. Avoiding broadly defined EPS appears to be critical to improving cognition, dysphoria, and negative symptoms with SGAs and FGAs. The lower risk of TD observed with SGAs also appears to be related to the greater ease with which they can provide an equivalent antipsychotic effect without EPS.

Rajiv Tandon, MD
Adjunct professor of psychiatry
University of Florida, Tallahassee

Robert Constantine, PhD
Research associate professor
University of South Florida, Tampa

We thank Dr. Helmuth and the principal investigators of CATIE for their interest in our article and the opportunity to further clarify a key learning point from CATIE.

Dr. Helmuth acknowledges our balanced review but suggests that cost and metabolic side effects should be considered along with lower EPS liability in selecting antipsychotic therapy. We agree. Avoiding EPS while obtaining a good antipsychotic effect is one key consideration in providing optimal antipsychotic therapy. Other adverse effects, patient preference, cost, and other factors are all important considerations in this complex process of individually optimizing antipsychotic treatment.

The CATIE investigators agree with our interpretation of the study’s principal findings. They take exception, however, to our suggestion that CATIE’s finding of no FGA-SGA difference in EPS and TD may be related to its relatively low assay sensitivity to detect such differences because the sample studied was at low risk for EPS and TD.

While accepting our description of the study sample as accurate, they disagree that it was at low risk for EPS and TD. Patients who have been ill for 16 years and received antipsychotic treatment for an average of 14 years without developing TD or severe EPS (as in CATIE) are by definition at low risk for EPS and TD.

We agree that patients without current TD and who are at risk for developing it comprise the best study population to investigate differential risk for TD; however, patients who have not developed it, despite 14 years of antipsychotic therapy, are at very low risk for developing it at all. First-episode patients without prior antipsychotic exposure would be an optimal study population, but such patients were excluded from CATIE.

Drs. Rosenheck and colleagues do not disagree with any of the other assertions in our article; they are, however, critical of “numerous factual errors in other published critiques of CATIE.” We cannot address such supposed inaccuracies, which are best taken up with authors of those commentaries.

To extract maximum value from this important initiative, we must better understand CATIE’s findings in the context of its study design and the results of other relevant studies. Neither mischaracterization nor overinterpretation of CATIE’s findings helps clinicians, patients, and policy-makers.

The essence of our article was that avoiding motor, cognitive, and affective EPS due to unmodulated dopamine blockade is the key to realizing the “atypical benefits” of a broader spectrum of efficacy and lower risk of TD during antipsychotic therapy. Neither Dr. Helmuth nor Drs. Rosenheck and colleagues appear to disagree with this assertion. Avoiding broadly defined EPS appears to be critical to improving cognition, dysphoria, and negative symptoms with SGAs and FGAs. The lower risk of TD observed with SGAs also appears to be related to the greater ease with which they can provide an equivalent antipsychotic effect without EPS.

Rajiv Tandon, MD
Adjunct professor of psychiatry
University of Florida, Tallahassee

Robert Constantine, PhD
Research associate professor
University of South Florida, Tampa

We agree with Drs. Tandon’s and Constantine’s explanation of the difference between the results of the CATIE trial¹ and previous studies—specifically that CATIE showed no differences between 4 SGAs and an intermediate potency FGA on EPS and tardive dyskinesia (TD). As the authors suggest, these results are best explained by the use of high-dose, high-potency haloperidol as the comparator in pre-CATIE studies, which magnified differences between FGAs and SGAs. A recent study has further suggested that in most of these trials the doses of haloperidol were above FDA-approved levels,² and few, if any, used prophylactic anticholinergics, further biasing the comparisons.

Drs. Tandon and Constantine further assert that the CATIE sample was at less risk of EPS or TD than previous samples because it excluded first-episode patients and those with TD and addressed a population that had used medications for 14 years without a history of adverse effects. CATIE—like any other ethical human investigation—excluded patients if they had well-documented, drug-related, adverse reactions to any of the proposed treatments.

Many, if not most, FDA registration trials (the source of most data on EPS with SGAs) excluded all patients with previous exposure to the new SGA drugs they tested but did not apply this criterion to patients exposed to older drugs. Thus the trials were more likely to include patients who would have responded poorly to FGAs than those who would have responded poorly to SGAs. Others have recognized that this reduces the validity of such FGA-SGA comparisons.³

Table

Study populations of SGA-FGA comparison trials

In the Table we present data comparing population characteristics from CATIE, from a meta-analysis that identified all 4 published controlled trials that have examined TD outcomes in FGA and SGAs,⁴ and from several other well-known comparable trials. The CATIE sample was similar to patients who participated in the other trials in average age, age of onset, and duration of illness.

Beasley et al⁵ similarly presented an analysis that excluded patients without TD at baseline, which we believe is the optimal population to use when evaluating medication-related risk for TD. CATIE is the only study that conducted a sound randomization comparing FGAs and SGAs in patients without current TD who are at risk for it, and—more than other studies—used an unbiased and thus more informative comparator.

Unfortunately there have been numerous factual errors in published critiques of CATIE. In one, CATIE was deemed disappointing⁶ because it had “a large percentage of discontinuations for all causes,” but the data presented for comparison were from a 28-week study⁷—less than half as long as the 72-week CATIE trial. CATIE, in fact, had better overall follow-up rates than the cited study at 28 weeks and also had better long-term follow-up rates than either the paper by Beasley et al⁵ or by Csernansky et al⁸—the most often cited “long-term” studies comparing FGAs and SGAs on TD.

Another commentary, like that of Drs. Tandon and Constantine, described CATIE patients as having more chronic illness that those in other trials, with “24 years since first treatment,”⁹ a misreading of the average age of first onset (which was 24) as if it was the average duration of illness (which was 16 years).

Many commentators have further asserted that because patients with TD at baseline “were not randomly assigned to conventional drugs” the comparison of either outcomes or TD risk was invalid.^6,9 As noted above, comparison of side effect risk is properly tested by trials involving patients without that risk at onset.

CATIE represented a major investment of public dollars to learn more about antipsychotic medications. Erroneous critiques needlessly mislead the professional community about what can be learned from this initiative.

The CATIE investigators
Robert Rosenheck, MD, New Haven, CT
T. Scott Stroup, MD, MPH, Chapel Hill, NC
Richard SE Keefe, PhD, Durham, NC
Joseph McEvoy, MD, Durham, NC
Marvin Swartz, MD, Durham, NC
Jeffrey Lieberman, MD, New York, NY

We agree with Drs. Tandon’s and Constantine’s explanation of the difference between the results of the CATIE trial¹ and previous studies—specifically that CATIE showed no differences between 4 SGAs and an intermediate potency FGA on EPS and tardive dyskinesia (TD). As the authors suggest, these results are best explained by the use of high-dose, high-potency haloperidol as the comparator in pre-CATIE studies, which magnified differences between FGAs and SGAs. A recent study has further suggested that in most of these trials the doses of haloperidol were above FDA-approved levels,² and few, if any, used prophylactic anticholinergics, further biasing the comparisons.

Drs. Tandon and Constantine further assert that the CATIE sample was at less risk of EPS or TD than previous samples because it excluded first-episode patients and those with TD and addressed a population that had used medications for 14 years without a history of adverse effects. CATIE—like any other ethical human investigation—excluded patients if they had well-documented, drug-related, adverse reactions to any of the proposed treatments.

Many, if not most, FDA registration trials (the source of most data on EPS with SGAs) excluded all patients with previous exposure to the new SGA drugs they tested but did not apply this criterion to patients exposed to older drugs. Thus the trials were more likely to include patients who would have responded poorly to FGAs than those who would have responded poorly to SGAs. Others have recognized that this reduces the validity of such FGA-SGA comparisons.³

Table

Study populations of SGA-FGA comparison trials

In the Table we present data comparing population characteristics from CATIE, from a meta-analysis that identified all 4 published controlled trials that have examined TD outcomes in FGA and SGAs,⁴ and from several other well-known comparable trials. The CATIE sample was similar to patients who participated in the other trials in average age, age of onset, and duration of illness.

Beasley et al⁵ similarly presented an analysis that excluded patients without TD at baseline, which we believe is the optimal population to use when evaluating medication-related risk for TD. CATIE is the only study that conducted a sound randomization comparing FGAs and SGAs in patients without current TD who are at risk for it, and—more than other studies—used an unbiased and thus more informative comparator.

Unfortunately there have been numerous factual errors in published critiques of CATIE. In one, CATIE was deemed disappointing⁶ because it had “a large percentage of discontinuations for all causes,” but the data presented for comparison were from a 28-week study⁷—less than half as long as the 72-week CATIE trial. CATIE, in fact, had better overall follow-up rates than the cited study at 28 weeks and also had better long-term follow-up rates than either the paper by Beasley et al⁵ or by Csernansky et al⁸—the most often cited “long-term” studies comparing FGAs and SGAs on TD.

Another commentary, like that of Drs. Tandon and Constantine, described CATIE patients as having more chronic illness that those in other trials, with “24 years since first treatment,”⁹ a misreading of the average age of first onset (which was 24) as if it was the average duration of illness (which was 16 years).

Many commentators have further asserted that because patients with TD at baseline “were not randomly assigned to conventional drugs” the comparison of either outcomes or TD risk was invalid.^6,9 As noted above, comparison of side effect risk is properly tested by trials involving patients without that risk at onset.

CATIE represented a major investment of public dollars to learn more about antipsychotic medications. Erroneous critiques needlessly mislead the professional community about what can be learned from this initiative.

The CATIE investigators
Robert Rosenheck, MD, New Haven, CT
T. Scott Stroup, MD, MPH, Chapel Hill, NC
Richard SE Keefe, PhD, Durham, NC
Joseph McEvoy, MD, Durham, NC
Marvin Swartz, MD, Durham, NC
Jeffrey Lieberman, MD, New York, NY

We agree with Drs. Tandon’s and Constantine’s explanation of the difference between the results of the CATIE trial¹ and previous studies—specifically that CATIE showed no differences between 4 SGAs and an intermediate potency FGA on EPS and tardive dyskinesia (TD). As the authors suggest, these results are best explained by the use of high-dose, high-potency haloperidol as the comparator in pre-CATIE studies, which magnified differences between FGAs and SGAs. A recent study has further suggested that in most of these trials the doses of haloperidol were above FDA-approved levels,² and few, if any, used prophylactic anticholinergics, further biasing the comparisons.

Drs. Tandon and Constantine further assert that the CATIE sample was at less risk of EPS or TD than previous samples because it excluded first-episode patients and those with TD and addressed a population that had used medications for 14 years without a history of adverse effects. CATIE—like any other ethical human investigation—excluded patients if they had well-documented, drug-related, adverse reactions to any of the proposed treatments.

Many, if not most, FDA registration trials (the source of most data on EPS with SGAs) excluded all patients with previous exposure to the new SGA drugs they tested but did not apply this criterion to patients exposed to older drugs. Thus the trials were more likely to include patients who would have responded poorly to FGAs than those who would have responded poorly to SGAs. Others have recognized that this reduces the validity of such FGA-SGA comparisons.³

Table

Study populations of SGA-FGA comparison trials

In the Table we present data comparing population characteristics from CATIE, from a meta-analysis that identified all 4 published controlled trials that have examined TD outcomes in FGA and SGAs,⁴ and from several other well-known comparable trials. The CATIE sample was similar to patients who participated in the other trials in average age, age of onset, and duration of illness.

Beasley et al⁵ similarly presented an analysis that excluded patients without TD at baseline, which we believe is the optimal population to use when evaluating medication-related risk for TD. CATIE is the only study that conducted a sound randomization comparing FGAs and SGAs in patients without current TD who are at risk for it, and—more than other studies—used an unbiased and thus more informative comparator.

Unfortunately there have been numerous factual errors in published critiques of CATIE. In one, CATIE was deemed disappointing⁶ because it had “a large percentage of discontinuations for all causes,” but the data presented for comparison were from a 28-week study⁷—less than half as long as the 72-week CATIE trial. CATIE, in fact, had better overall follow-up rates than the cited study at 28 weeks and also had better long-term follow-up rates than either the paper by Beasley et al⁵ or by Csernansky et al⁸—the most often cited “long-term” studies comparing FGAs and SGAs on TD.

Another commentary, like that of Drs. Tandon and Constantine, described CATIE patients as having more chronic illness that those in other trials, with “24 years since first treatment,”⁹ a misreading of the average age of first onset (which was 24) as if it was the average duration of illness (which was 16 years).

Many commentators have further asserted that because patients with TD at baseline “were not randomly assigned to conventional drugs” the comparison of either outcomes or TD risk was invalid.^6,9 As noted above, comparison of side effect risk is properly tested by trials involving patients without that risk at onset.

CATIE represented a major investment of public dollars to learn more about antipsychotic medications. Erroneous critiques needlessly mislead the professional community about what can be learned from this initiative.

The CATIE investigators
Robert Rosenheck, MD, New Haven, CT
T. Scott Stroup, MD, MPH, Chapel Hill, NC
Richard SE Keefe, PhD, Durham, NC
Joseph McEvoy, MD, Durham, NC
Marvin Swartz, MD, Durham, NC
Jeffrey Lieberman, MD, New York, NY

Although the article “Avoiding EPS is key to realizing ‘atypical’ benefits,” by Drs. Rajiv Tandon and Robert J. Constantine (Current Psychiatry, November 2006), is more balanced than some reviews of the CATIE findings, it emphasized avoiding extrapyramidal symptoms (EPS) while ignoring two other features that are important when choosing an antipsychotic.

The first is the propensity for causing weight gain, hyperglycemia, and hyperlipidemia. The CATIE phase 1 investigation showed that second-generation antipsychotics (SGA)—especially olanzapine—are much more likely to cause these health-threatening complications compared with the first-generation antipsychotic (FGA) perphenazine.

The second consideration is cost. I am aware of economic arguments in favor of SGAs, especially if they prevent hospitalizations. However, in light of CATIE and the British CUtLASS 1 studies, it is unconscionable to not consider the huge difference in cost between SGAs and FGAs. Recent reports indicate that SGAs continue to outpace almost all other medications in price increases. This adds to society’s health-cost burden and creates a cruel inequity for those without prescription coverage.

It is an oversimplification of our clinical duty to refer to avoiding EPS as the “key” to antipsychotic treatment. We can only wish it were that simple.

Dennis Helmuth, MD, PhD
Clinical associate professor of psychiatry
Northeastern Ohio Universities College of Medicine,
Wooster, OH

Although the article “Avoiding EPS is key to realizing ‘atypical’ benefits,” by Drs. Rajiv Tandon and Robert J. Constantine (Current Psychiatry, November 2006), is more balanced than some reviews of the CATIE findings, it emphasized avoiding extrapyramidal symptoms (EPS) while ignoring two other features that are important when choosing an antipsychotic.

The first is the propensity for causing weight gain, hyperglycemia, and hyperlipidemia. The CATIE phase 1 investigation showed that second-generation antipsychotics (SGA)—especially olanzapine—are much more likely to cause these health-threatening complications compared with the first-generation antipsychotic (FGA) perphenazine.

The second consideration is cost. I am aware of economic arguments in favor of SGAs, especially if they prevent hospitalizations. However, in light of CATIE and the British CUtLASS 1 studies, it is unconscionable to not consider the huge difference in cost between SGAs and FGAs. Recent reports indicate that SGAs continue to outpace almost all other medications in price increases. This adds to society’s health-cost burden and creates a cruel inequity for those without prescription coverage.

It is an oversimplification of our clinical duty to refer to avoiding EPS as the “key” to antipsychotic treatment. We can only wish it were that simple.

Dennis Helmuth, MD, PhD
Clinical associate professor of psychiatry
Northeastern Ohio Universities College of Medicine,
Wooster, OH

Although the article “Avoiding EPS is key to realizing ‘atypical’ benefits,” by Drs. Rajiv Tandon and Robert J. Constantine (Current Psychiatry, November 2006), is more balanced than some reviews of the CATIE findings, it emphasized avoiding extrapyramidal symptoms (EPS) while ignoring two other features that are important when choosing an antipsychotic.

The first is the propensity for causing weight gain, hyperglycemia, and hyperlipidemia. The CATIE phase 1 investigation showed that second-generation antipsychotics (SGA)—especially olanzapine—are much more likely to cause these health-threatening complications compared with the first-generation antipsychotic (FGA) perphenazine.

The second consideration is cost. I am aware of economic arguments in favor of SGAs, especially if they prevent hospitalizations. However, in light of CATIE and the British CUtLASS 1 studies, it is unconscionable to not consider the huge difference in cost between SGAs and FGAs. Recent reports indicate that SGAs continue to outpace almost all other medications in price increases. This adds to society’s health-cost burden and creates a cruel inequity for those without prescription coverage.

It is an oversimplification of our clinical duty to refer to avoiding EPS as the “key” to antipsychotic treatment. We can only wish it were that simple.

Dennis Helmuth, MD, PhD
Clinical associate professor of psychiatry
Northeastern Ohio Universities College of Medicine,
Wooster, OH

Thank you for the interview, “Protect yourself against patient assault,” and the accompanying reprint of Dr. John Battaglia’s article “Is this patient dangerous?” (Current Psychiatry, November 2006). Both give sound clinical guidelines for psychiatrist safety without being insensitive or “blaming the victim” in the case of Dr. Wayne Fenton’s tragic death allegedly at the hands of a patient. Although implicit, however, the need to develop and maintain appropriate boundaries needs to be more explicit and discussed.

From what we know, Dr. Fenton saw the patient in his office on a weekend with no one else present other than the patient’s father, who waited outside. One eulogy said that Dr. Fenton helped install a carpet in a different patient’s residence after the patient was released from the hospital. Both examples surely are instances of going “the extra mile” to help troubled patients, and Dr. Fenton was known as a master clinician who received some of the most difficult cases.

On the other hand, customary boundaries regarding how and where to see patients were not taken. Perhaps Dr. Fenton thought the rewards of breaking these boundaries outweighed the risks. Nevertheless, development and maintenance of boundaries should be undertaken as one way to ensure safety. When making exceptions, extra precaution should be taken.

H. Steven Moffic, MD
Professor of psychiatry and behavioral medicine
Medical College of Wisconsin
Milwaukee

Dr. Battaglia responds

I wholeheartedly agree with Dr. Moffic’s points about the need to take extra precautions when going outside customary boundaries. However, our discipline treads in muddy waters on the issue of what is appropriate when working outside such boundaries.

The extremes of sexual or financial exploitation are clear, but otherwise the entire spectrum of interaction between patient and clinician can be appropriate under certain circumstances. For example, in my work with the Madison (WI) Program of Assertive Community Treatment, I often see patients in their homes, help them with grocery shopping, or assist them with other daily tasks. Although these behaviors do not fit an office model, they are not uncommon in community work and do not necessarily break boundaries.

John Battaglia, MD
Program of Assertive Community Treatment
Associate clinical professor of psychiatry
University of Wisconsin-Madison Medical School

Thank you for the interview, “Protect yourself against patient assault,” and the accompanying reprint of Dr. John Battaglia’s article “Is this patient dangerous?” (Current Psychiatry, November 2006). Both give sound clinical guidelines for psychiatrist safety without being insensitive or “blaming the victim” in the case of Dr. Wayne Fenton’s tragic death allegedly at the hands of a patient. Although implicit, however, the need to develop and maintain appropriate boundaries needs to be more explicit and discussed.

From what we know, Dr. Fenton saw the patient in his office on a weekend with no one else present other than the patient’s father, who waited outside. One eulogy said that Dr. Fenton helped install a carpet in a different patient’s residence after the patient was released from the hospital. Both examples surely are instances of going “the extra mile” to help troubled patients, and Dr. Fenton was known as a master clinician who received some of the most difficult cases.

On the other hand, customary boundaries regarding how and where to see patients were not taken. Perhaps Dr. Fenton thought the rewards of breaking these boundaries outweighed the risks. Nevertheless, development and maintenance of boundaries should be undertaken as one way to ensure safety. When making exceptions, extra precaution should be taken.

H. Steven Moffic, MD
Professor of psychiatry and behavioral medicine
Medical College of Wisconsin
Milwaukee

Dr. Battaglia responds

I wholeheartedly agree with Dr. Moffic’s points about the need to take extra precautions when going outside customary boundaries. However, our discipline treads in muddy waters on the issue of what is appropriate when working outside such boundaries.

The extremes of sexual or financial exploitation are clear, but otherwise the entire spectrum of interaction between patient and clinician can be appropriate under certain circumstances. For example, in my work with the Madison (WI) Program of Assertive Community Treatment, I often see patients in their homes, help them with grocery shopping, or assist them with other daily tasks. Although these behaviors do not fit an office model, they are not uncommon in community work and do not necessarily break boundaries.

John Battaglia, MD
Program of Assertive Community Treatment
Associate clinical professor of psychiatry
University of Wisconsin-Madison Medical School

Thank you for the interview, “Protect yourself against patient assault,” and the accompanying reprint of Dr. John Battaglia’s article “Is this patient dangerous?” (Current Psychiatry, November 2006). Both give sound clinical guidelines for psychiatrist safety without being insensitive or “blaming the victim” in the case of Dr. Wayne Fenton’s tragic death allegedly at the hands of a patient. Although implicit, however, the need to develop and maintain appropriate boundaries needs to be more explicit and discussed.

From what we know, Dr. Fenton saw the patient in his office on a weekend with no one else present other than the patient’s father, who waited outside. One eulogy said that Dr. Fenton helped install a carpet in a different patient’s residence after the patient was released from the hospital. Both examples surely are instances of going “the extra mile” to help troubled patients, and Dr. Fenton was known as a master clinician who received some of the most difficult cases.

On the other hand, customary boundaries regarding how and where to see patients were not taken. Perhaps Dr. Fenton thought the rewards of breaking these boundaries outweighed the risks. Nevertheless, development and maintenance of boundaries should be undertaken as one way to ensure safety. When making exceptions, extra precaution should be taken.

H. Steven Moffic, MD
Professor of psychiatry and behavioral medicine
Medical College of Wisconsin
Milwaukee

Dr. Battaglia responds

I wholeheartedly agree with Dr. Moffic’s points about the need to take extra precautions when going outside customary boundaries. However, our discipline treads in muddy waters on the issue of what is appropriate when working outside such boundaries.

The extremes of sexual or financial exploitation are clear, but otherwise the entire spectrum of interaction between patient and clinician can be appropriate under certain circumstances. For example, in my work with the Madison (WI) Program of Assertive Community Treatment, I often see patients in their homes, help them with grocery shopping, or assist them with other daily tasks. Although these behaviors do not fit an office model, they are not uncommon in community work and do not necessarily break boundaries.

John Battaglia, MD
Program of Assertive Community Treatment
Associate clinical professor of psychiatry
University of Wisconsin-Madison Medical School

The life span of the seriously mentally ill is even shorter than we had thought. Earlier studies showed a loss of 20% of the average life span or 15 to 16 years.¹ Recent figures are alarmingly higher, however, and vary from state to state.

Virginia has the "best" mortality rate among the seriously mentally ill with a loss of "only" 13.5 years of potential life, according to the Center for Mental Health Services (CMHS) and the Centers for Disease Control and Prevention (CDC).² Perhaps persons who suffer from schizophrenia should move to Virgina because the loss of potential life years in other states is much worse:   
   • Arizona: 31.8 years   
   • Texas: 29.3 years   
   • Missouri: 27.9 years   
   • Utah: 26.9 years   
   • Oklahoma: 26.3 years.

A recent Ohio study of mortality and medical illness found an average loss of 32 years of life among persons with schizophrenia.³

Why is the life span of mentally ill persons so short? Apart from their high rates of death from unnatural causes (suicide, homicide, and accidents), the most frequent killer is cardiovascular disease. High mortality rates are well-documented in schizophrenia from various ailments but especially heart disease.⁴ Bipolar disorder and major depression are also associated with high death rates from cardiovascular disease.⁵

The sad truth is that a “dual neglect” contributes to premature mortality of the seriously mentally ill: the system fails to provide ongoing basic primary healthcare, and patients neglect to seek or adhere to medical care.

Persons with serious mental illness often have risk factors associated with preventable causes of heart disease and stroke, including smoking, obesity, sedentary life styles, and poor nutrition. In addition, the metabolic syndrome—obesity, hypertension, hyperglycemia, and dyslipidemia—is highly associated with schizophrenia,⁶ bipolar disorder,⁷ and unipolar depression.⁸

Cardiovascular risk associated with metabolic syndrome requires ongoing medical follow-up, which many mentally ill patients do not receive. The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) found shockingly low treatment rates for diabetes, hypertension, and hyperglycemia among outpatients with schizophrenia around the country.⁹

Let us mobilize to correct this shameful health disparity, one patient at a time. The message to mental health professionals is clear:
   • In addition to controlling symptoms of psychosis, mania, depression, or anxiety, routinely screen patients for weight gain, hypertension, high fasting serum glucose, and elevated lipid levels.
   • Refer overweight and obese patients to primary care providers, dietitians, and exercise counselors to reduce their cardiovascular risks.

Psychiatrists and nurse practitioners must address both mental and medical health needs when formulating assessments, treatment plans, and patient education. For practical recommendations on managing medical comorbidities, see “7-point checkup for stable schizophrenia outpatients,” by Britton Ashley Arey, MD, and Stephen R. Marder, MD. The public mental health system also could help the seriously mentally ill by integrating primary healthcare with mental healthcare in community settings across the nation. There are no excuses to do anything less.

The life span of the seriously mentally ill is even shorter than we had thought. Earlier studies showed a loss of 20% of the average life span or 15 to 16 years.¹ Recent figures are alarmingly higher, however, and vary from state to state.

Virginia has the "best" mortality rate among the seriously mentally ill with a loss of "only" 13.5 years of potential life, according to the Center for Mental Health Services (CMHS) and the Centers for Disease Control and Prevention (CDC).² Perhaps persons who suffer from schizophrenia should move to Virgina because the loss of potential life years in other states is much worse:   
   • Arizona: 31.8 years   
   • Texas: 29.3 years   
   • Missouri: 27.9 years   
   • Utah: 26.9 years   
   • Oklahoma: 26.3 years.

A recent Ohio study of mortality and medical illness found an average loss of 32 years of life among persons with schizophrenia.³

Why is the life span of mentally ill persons so short? Apart from their high rates of death from unnatural causes (suicide, homicide, and accidents), the most frequent killer is cardiovascular disease. High mortality rates are well-documented in schizophrenia from various ailments but especially heart disease.⁴ Bipolar disorder and major depression are also associated with high death rates from cardiovascular disease.⁵

The sad truth is that a “dual neglect” contributes to premature mortality of the seriously mentally ill: the system fails to provide ongoing basic primary healthcare, and patients neglect to seek or adhere to medical care.

Persons with serious mental illness often have risk factors associated with preventable causes of heart disease and stroke, including smoking, obesity, sedentary life styles, and poor nutrition. In addition, the metabolic syndrome—obesity, hypertension, hyperglycemia, and dyslipidemia—is highly associated with schizophrenia,⁶ bipolar disorder,⁷ and unipolar depression.⁸

Cardiovascular risk associated with metabolic syndrome requires ongoing medical follow-up, which many mentally ill patients do not receive. The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) found shockingly low treatment rates for diabetes, hypertension, and hyperglycemia among outpatients with schizophrenia around the country.⁹

Let us mobilize to correct this shameful health disparity, one patient at a time. The message to mental health professionals is clear:
   • In addition to controlling symptoms of psychosis, mania, depression, or anxiety, routinely screen patients for weight gain, hypertension, high fasting serum glucose, and elevated lipid levels.
   • Refer overweight and obese patients to primary care providers, dietitians, and exercise counselors to reduce their cardiovascular risks.

Psychiatrists and nurse practitioners must address both mental and medical health needs when formulating assessments, treatment plans, and patient education. For practical recommendations on managing medical comorbidities, see “7-point checkup for stable schizophrenia outpatients,” by Britton Ashley Arey, MD, and Stephen R. Marder, MD. The public mental health system also could help the seriously mentally ill by integrating primary healthcare with mental healthcare in community settings across the nation. There are no excuses to do anything less.

The life span of the seriously mentally ill is even shorter than we had thought. Earlier studies showed a loss of 20% of the average life span or 15 to 16 years.¹ Recent figures are alarmingly higher, however, and vary from state to state.

Virginia has the "best" mortality rate among the seriously mentally ill with a loss of "only" 13.5 years of potential life, according to the Center for Mental Health Services (CMHS) and the Centers for Disease Control and Prevention (CDC).² Perhaps persons who suffer from schizophrenia should move to Virgina because the loss of potential life years in other states is much worse:   
   • Arizona: 31.8 years   
   • Texas: 29.3 years   
   • Missouri: 27.9 years   
   • Utah: 26.9 years   
   • Oklahoma: 26.3 years.

A recent Ohio study of mortality and medical illness found an average loss of 32 years of life among persons with schizophrenia.³

Why is the life span of mentally ill persons so short? Apart from their high rates of death from unnatural causes (suicide, homicide, and accidents), the most frequent killer is cardiovascular disease. High mortality rates are well-documented in schizophrenia from various ailments but especially heart disease.⁴ Bipolar disorder and major depression are also associated with high death rates from cardiovascular disease.⁵

The sad truth is that a “dual neglect” contributes to premature mortality of the seriously mentally ill: the system fails to provide ongoing basic primary healthcare, and patients neglect to seek or adhere to medical care.

Persons with serious mental illness often have risk factors associated with preventable causes of heart disease and stroke, including smoking, obesity, sedentary life styles, and poor nutrition. In addition, the metabolic syndrome—obesity, hypertension, hyperglycemia, and dyslipidemia—is highly associated with schizophrenia,⁶ bipolar disorder,⁷ and unipolar depression.⁸

Cardiovascular risk associated with metabolic syndrome requires ongoing medical follow-up, which many mentally ill patients do not receive. The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) found shockingly low treatment rates for diabetes, hypertension, and hyperglycemia among outpatients with schizophrenia around the country.⁹

Let us mobilize to correct this shameful health disparity, one patient at a time. The message to mental health professionals is clear:
   • In addition to controlling symptoms of psychosis, mania, depression, or anxiety, routinely screen patients for weight gain, hypertension, high fasting serum glucose, and elevated lipid levels.
   • Refer overweight and obese patients to primary care providers, dietitians, and exercise counselors to reduce their cardiovascular risks.

Psychiatrists and nurse practitioners must address both mental and medical health needs when formulating assessments, treatment plans, and patient education. For practical recommendations on managing medical comorbidities, see “7-point checkup for stable schizophrenia outpatients,” by Britton Ashley Arey, MD, and Stephen R. Marder, MD. The public mental health system also could help the seriously mentally ill by integrating primary healthcare with mental healthcare in community settings across the nation. There are no excuses to do anything less.

History: shop talk

Ms. B, age 46, presents to the ER at her brother’s insistence. For about 6 months, she says, she has been “hearing voices”—including that of her boss—talking to each other about work.

Ms. B has no personal or family psychiatric history but notes that her sister died 6 months ago, and her father died the following month. At work, she is having trouble getting along with her boss. She adds that she has been skipping church lately because she believes her church is under investigation and the inquiry might be targeting her.

Ms. B has been a company manager for 20 years. She is divorced, has no children, and lives alone. She says she does not smoke or use illicit drugs and seldom drinks alcohol. She denies suicidal or homicidal thoughts, depressed mood, or visual hallucinations. She says she is sleeping only 3 to 4 hours nightly and feels fatigued in the afternoon. She denies loss of concentration or functioning.

Mental status. Ms. B is well groomed, maintains good eye contact, and is superficially cooperative but increasingly guarded with further questioning. She describes her mood as “OK,” but her affect is blunted. Thought process is logical but circumstantial at times, and her thoughts consist of auditory hallucinations, paranoid thinking, persecutory delusions, and ideas of reference. She has poor insight into her symptoms and does not want to be admitted.

Physical examination and laboratory tests are unremarkable. Negative ethanol and urine drug screens rule out substance abuse, and preliminary noncontrast head CT shows no acute changes.

The author’s observations

In women, schizophrenia typically emerges between ages 17 and 37;¹ onset after age 45 is unusual.² Ms. B’s age, family history, and lack of a formal thought disorder or negative symptoms make late-onset schizophrenia unlikely, though it cannot be ruled out.

Ms. B denies mood symptoms, but significant stressors—such as the recent deaths of her sister and father and difficulties at work—could precipitate a mood disorder. Of the possible diagnoses, major depressive disorder is most likely at this time.^1,3 Because Ms. B’s symptoms do not clearly match any diagnosis, we speak with her brother and sister-in-law to seek collateral information.

Collateral history: beware of spies

Ms. B’s brother says his sister began behaving strangely about 8 months ago and has worsened lately. He says she suspects that her boss hired spies to watch her house, car, and her parent’s house. After work, she often parks in paid garages rather than at home to avoid being “followed.” When visiting, he says, she leaves her keys outside because she fears they contain a tracking device. Family members say Ms. B sometimes drops by at night—as late as 5 AM—complaining that she cannot sleep because she is being “watched.”

Ms. B’s family hired a private investigator 3 or 4 months ago to examine her house and car. Although no tracking devices were found, her brother says, Ms. B remains convinced she is being followed. He says she often speaks in “code” and whispers to herself.

According to her brother, Ms. B often hears voices while trying to sleep, saying such things as “Why won’t she turn over?” She reportedly wears a towel while showering because the “spies” are watching. During a conference she attended last week, she told her brother that a group of government investigators followed her there and arrested her boss.

Ms. B’s sister-in-law says the patient’s functioning has declined sharply, and that she has been helping Ms. B complete routine work. Neither she nor Ms. B’s brother have noticed a change in the patient’s energy, productivity, or speech production or speed, thus ruling out bipolar disorder. Ms. B’s brother confirms that there is no family history of mental illness.

The author’s observations

Collateral information about Ms. B points to psychosis rather than a mood disorder with psychotic features, but she lacks the formal thought disorder and negative symptoms common in primary psychotic disorders.

Because Ms. B’s presentation is atypical, we order brain MRI to check for a general medical condition (Figure 1). If brain MRI suggests a medical problem, we will follow with EEG, lumbar puncture, or other tests.

Figure 1 Clinical steps to rule out medical causes of late-onset psychosis

treatment, testing: what mri suggests

We admit Ms. B to the locked inpatient psychiatric unit—where she remains paranoid and guarded—and prescribe risperidone, 1 mg/d, to address her paranoia. She refuses medication at first because she feels she does not need psychiatric care, but we give her lorazepam, 0.5 mg/d for her anxiety, along with psychoeducation and family support. After 3 days, we stop lorazepam and Ms. B agrees to take risperidone.

Within 4 days of starting risperidone, Ms. B’s auditory hallucinations and paranoia have lessened and her insight is improved. We recommend increasing the dosage to 2 mg/d because we feel that 1 mg/d will not sufficiently control her symptoms. She remains paranoid but is reluctant to increase the dosage for fear of adverse effects, though she has reported none so far.

Brain MRI taken the night Ms. B was admitted shows:

• multiple focal, well-defined hyperintense periventricular lesions on fluid-attenuated inversion recovery (FLAIR)- and T2-weighted images (Figure 2). Some lesions are flame-shaped.
• a 1.5-cm lesion adjacent to the right frontal horn showing a hyperintense signal on T2-weighted images and a hypointense signal on T1-weighted images without contrast enhancement. White-matter edema surrounds this lesion.
• no gadolinium-enhancing lesions.

Two radiologists confirm possible demyelination, suggesting multiple sclerosis (MS). Final report of initial brain CT shows lowdensity, periventricular white matter changes consistent with the MRI findings.

Results of subsequent laboratory tests are normal. Erythrocyte sedimentation rate is slightly elevated at 35 mm/hr, suggesting a possible autoimmune disorder. ECG shows sinus bradycardia, and chest x-ray and MR angiogram are unremarkable, as are EEG and visual evoked potential results.

Lumbar puncture and CSF studies show increased immunoglobulin G to albumin ratio. CSF fluid is clear, blood counts and protein are normal, Gram’s stain and culture are negative, and cytologic findings show a marked increase in mature lymphocytes. These results suggest inflammation, but follow-up neurologic exam is unremarkable.

Figure 2 FLAIR-weighted image after Ms. B’s brain MRI

Right 1.5-cm lesion adjacent to right frontal horn and multiple left hyperintense lesions on fluid-attenuated inversion recovery (FLAIR)-weighted image.

The authors’ observations

Determining disease dissemination in time and space is key to diagnosing MS. Clinical presentation or MRI can determine both criteria (Table 1). Ms. B’s lesions and CSF results suggest that MS has disseminated throughout her body, but neurologic examination shows no objective clinical evidence of lesions.

Neuropsychological testing might help evaluate Ms. B’s cognition and executive functioning, but these deficits do not specifically suggest MS. The cortex, particularly the prefrontal cortex, is believed to coordinate organization, planning, and socially appropriate behavior. MS typically involves white matter rather than the cortex, but researchers have suggested that MS-related demyelination might disrupt the axonal circuits that connect the cortex to other brain areas.¹⁸

Increased lesion load has been correlated with decreased cognitive function. Neuropsychological testing could indirectly point to a lesion load increase by recording decreased cognitive function, but this decline cannot be attributed to MS without an MRI.

Ms. B’s psychotic symptoms could be clinical evidence of MS, but we cannot solidify the diagnosis until we establish dissemination in time. To do that, we need a second MRI 3 months after the first one. Concurrent late-onset paraphrenia and MS is possible but rare.

Table 1

Findings needed to determine MS diagnosis based on clinical presentation

Follow-up: where is she?

Ms. B is discharged after 10 days. She denies hallucinations, and staff notices decreased paranoia, brighter affect, and improved insight. We tell her to continue taking risperidone, 1 mg/d.

Three weeks later, Ms. B sees an outpatient psychiatrist. She is paranoid, guarded, and has not been taking risperidone.

Because Ms. B’s previous MRI results are suspect, we ask the hospital’s neurology service to examine her. Findings are unremarkable, but the neurologist recommends a followup brain MRI in 3 months or sooner if symptoms emerge. More than 2 years later, she has not completed a second MRI or contacted her psychiatrist or neurologist.

The authors’ observations

Ms. B’s case highlights the importance of:

• recognizing an atypical presentation of a primary psychotic disorder
• checking for a medical cause of psychosis (Table 2)
• knowing which psychiatric symptoms are common in MS.

Despite absence of neurologic symptoms, Ms. B’s psychosis could have been the initial presentation of MS, which is more prevalent among psychiatric inpatients than in the general population.^6,7 In a prospective study,⁸ 95% of patients with MS had neuropsychiatric symptoms, and 79% had depressive symptoms. Hallucinations and delusions were reported in 10% and 7% of MS patients, respectively. These findings suggest that mood disturbances are considerably more common than psychosis among patients with MS.

Diagnosis of MSrelated psychosis has been addressed only in case reports or small studies, most of which have not clearly defined psychosis or adequately described the symptoms or confounding factors such as medications. Findings on prevalence of psychosis as the initial presentation in MS are more limited and confounded by instances in which neurologic symptoms might have been overlooked.^9,11

Few studies have investigated whether lesion location correlates with specific neuropsychiatric symptoms. In one study,⁸ brain MRI taken within 9 months of presenting symptoms showed that MS was not significantly more severe among patients with psychosis compared with nonpsychotic MS patients. These data support psychosis as a possible early finding in MS.

At least two studies^12,13 suggest a correlation between temporal lobe lesions and psychosis, but both study samples were small (8 and 10 patients) and used a combination of diagnoses. One case report also supports this correlation.¹⁴

Table 2

Medical conditions that can cause psychotic symptoms

Treating ms-related psychosis

MS-related psychosis should abate with MS treatment, but no systematized studies have verified this or determined which antipsychotics would be suitable. Single case reports suggest successful treatment with risperidone,¹³ haloperidol,¹⁵ clozapine,¹⁶ or ziprasidone.¹⁷ Ms. B showed initial improvement with risperidone, but because she was lost to follow-up we cannot say if this medication would work long-term.

Related resources

• Feinstein A. The clinical neuropsychiatry of multiple sclerosis. New York: Cambridge University Press; 1999.
• National Multiple Sclerosis Society. www.nationalmssociety.org.

Drug brand name

• Clozapine • Clozaril
• Risperidone • Risperdal
• Haloperidol • Haldol
• Ziprasidone • Geodon
• Lorazepam • Ativan

Disclosures

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

Dr. Rafeyan is a speaker for AstraZeneca, BristolMyers Squibb Co., Eli Lilly and Co., GlaxoSmithKline, Pfizer, and Wyeth. He is also an advisor to Abbott Laboratories and Forest Pharmaceuticals.

History: shop talk

Ms. B, age 46, presents to the ER at her brother’s insistence. For about 6 months, she says, she has been “hearing voices”—including that of her boss—talking to each other about work.

Ms. B has no personal or family psychiatric history but notes that her sister died 6 months ago, and her father died the following month. At work, she is having trouble getting along with her boss. She adds that she has been skipping church lately because she believes her church is under investigation and the inquiry might be targeting her.

Ms. B has been a company manager for 20 years. She is divorced, has no children, and lives alone. She says she does not smoke or use illicit drugs and seldom drinks alcohol. She denies suicidal or homicidal thoughts, depressed mood, or visual hallucinations. She says she is sleeping only 3 to 4 hours nightly and feels fatigued in the afternoon. She denies loss of concentration or functioning.

Mental status. Ms. B is well groomed, maintains good eye contact, and is superficially cooperative but increasingly guarded with further questioning. She describes her mood as “OK,” but her affect is blunted. Thought process is logical but circumstantial at times, and her thoughts consist of auditory hallucinations, paranoid thinking, persecutory delusions, and ideas of reference. She has poor insight into her symptoms and does not want to be admitted.

Physical examination and laboratory tests are unremarkable. Negative ethanol and urine drug screens rule out substance abuse, and preliminary noncontrast head CT shows no acute changes.

The author’s observations

In women, schizophrenia typically emerges between ages 17 and 37;¹ onset after age 45 is unusual.² Ms. B’s age, family history, and lack of a formal thought disorder or negative symptoms make late-onset schizophrenia unlikely, though it cannot be ruled out.

Ms. B denies mood symptoms, but significant stressors—such as the recent deaths of her sister and father and difficulties at work—could precipitate a mood disorder. Of the possible diagnoses, major depressive disorder is most likely at this time.^1,3 Because Ms. B’s symptoms do not clearly match any diagnosis, we speak with her brother and sister-in-law to seek collateral information.

Collateral history: beware of spies

Ms. B’s brother says his sister began behaving strangely about 8 months ago and has worsened lately. He says she suspects that her boss hired spies to watch her house, car, and her parent’s house. After work, she often parks in paid garages rather than at home to avoid being “followed.” When visiting, he says, she leaves her keys outside because she fears they contain a tracking device. Family members say Ms. B sometimes drops by at night—as late as 5 AM—complaining that she cannot sleep because she is being “watched.”

Ms. B’s family hired a private investigator 3 or 4 months ago to examine her house and car. Although no tracking devices were found, her brother says, Ms. B remains convinced she is being followed. He says she often speaks in “code” and whispers to herself.

According to her brother, Ms. B often hears voices while trying to sleep, saying such things as “Why won’t she turn over?” She reportedly wears a towel while showering because the “spies” are watching. During a conference she attended last week, she told her brother that a group of government investigators followed her there and arrested her boss.

Ms. B’s sister-in-law says the patient’s functioning has declined sharply, and that she has been helping Ms. B complete routine work. Neither she nor Ms. B’s brother have noticed a change in the patient’s energy, productivity, or speech production or speed, thus ruling out bipolar disorder. Ms. B’s brother confirms that there is no family history of mental illness.

The author’s observations

Collateral information about Ms. B points to psychosis rather than a mood disorder with psychotic features, but she lacks the formal thought disorder and negative symptoms common in primary psychotic disorders.

Because Ms. B’s presentation is atypical, we order brain MRI to check for a general medical condition (Figure 1). If brain MRI suggests a medical problem, we will follow with EEG, lumbar puncture, or other tests.

Figure 1 Clinical steps to rule out medical causes of late-onset psychosis

treatment, testing: what mri suggests

We admit Ms. B to the locked inpatient psychiatric unit—where she remains paranoid and guarded—and prescribe risperidone, 1 mg/d, to address her paranoia. She refuses medication at first because she feels she does not need psychiatric care, but we give her lorazepam, 0.5 mg/d for her anxiety, along with psychoeducation and family support. After 3 days, we stop lorazepam and Ms. B agrees to take risperidone.

Within 4 days of starting risperidone, Ms. B’s auditory hallucinations and paranoia have lessened and her insight is improved. We recommend increasing the dosage to 2 mg/d because we feel that 1 mg/d will not sufficiently control her symptoms. She remains paranoid but is reluctant to increase the dosage for fear of adverse effects, though she has reported none so far.

Brain MRI taken the night Ms. B was admitted shows:

• multiple focal, well-defined hyperintense periventricular lesions on fluid-attenuated inversion recovery (FLAIR)- and T2-weighted images (Figure 2). Some lesions are flame-shaped.
• a 1.5-cm lesion adjacent to the right frontal horn showing a hyperintense signal on T2-weighted images and a hypointense signal on T1-weighted images without contrast enhancement. White-matter edema surrounds this lesion.
• no gadolinium-enhancing lesions.

Two radiologists confirm possible demyelination, suggesting multiple sclerosis (MS). Final report of initial brain CT shows lowdensity, periventricular white matter changes consistent with the MRI findings.

Results of subsequent laboratory tests are normal. Erythrocyte sedimentation rate is slightly elevated at 35 mm/hr, suggesting a possible autoimmune disorder. ECG shows sinus bradycardia, and chest x-ray and MR angiogram are unremarkable, as are EEG and visual evoked potential results.

Lumbar puncture and CSF studies show increased immunoglobulin G to albumin ratio. CSF fluid is clear, blood counts and protein are normal, Gram’s stain and culture are negative, and cytologic findings show a marked increase in mature lymphocytes. These results suggest inflammation, but follow-up neurologic exam is unremarkable.

Figure 2 FLAIR-weighted image after Ms. B’s brain MRI

Right 1.5-cm lesion adjacent to right frontal horn and multiple left hyperintense lesions on fluid-attenuated inversion recovery (FLAIR)-weighted image.

The authors’ observations

Determining disease dissemination in time and space is key to diagnosing MS. Clinical presentation or MRI can determine both criteria (Table 1). Ms. B’s lesions and CSF results suggest that MS has disseminated throughout her body, but neurologic examination shows no objective clinical evidence of lesions.

Neuropsychological testing might help evaluate Ms. B’s cognition and executive functioning, but these deficits do not specifically suggest MS. The cortex, particularly the prefrontal cortex, is believed to coordinate organization, planning, and socially appropriate behavior. MS typically involves white matter rather than the cortex, but researchers have suggested that MS-related demyelination might disrupt the axonal circuits that connect the cortex to other brain areas.¹⁸

Increased lesion load has been correlated with decreased cognitive function. Neuropsychological testing could indirectly point to a lesion load increase by recording decreased cognitive function, but this decline cannot be attributed to MS without an MRI.

Ms. B’s psychotic symptoms could be clinical evidence of MS, but we cannot solidify the diagnosis until we establish dissemination in time. To do that, we need a second MRI 3 months after the first one. Concurrent late-onset paraphrenia and MS is possible but rare.

Table 1

Findings needed to determine MS diagnosis based on clinical presentation

Follow-up: where is she?

Ms. B is discharged after 10 days. She denies hallucinations, and staff notices decreased paranoia, brighter affect, and improved insight. We tell her to continue taking risperidone, 1 mg/d.

Three weeks later, Ms. B sees an outpatient psychiatrist. She is paranoid, guarded, and has not been taking risperidone.

Because Ms. B’s previous MRI results are suspect, we ask the hospital’s neurology service to examine her. Findings are unremarkable, but the neurologist recommends a followup brain MRI in 3 months or sooner if symptoms emerge. More than 2 years later, she has not completed a second MRI or contacted her psychiatrist or neurologist.

The authors’ observations

Ms. B’s case highlights the importance of:

• recognizing an atypical presentation of a primary psychotic disorder
• checking for a medical cause of psychosis (Table 2)
• knowing which psychiatric symptoms are common in MS.

Despite absence of neurologic symptoms, Ms. B’s psychosis could have been the initial presentation of MS, which is more prevalent among psychiatric inpatients than in the general population.^6,7 In a prospective study,⁸ 95% of patients with MS had neuropsychiatric symptoms, and 79% had depressive symptoms. Hallucinations and delusions were reported in 10% and 7% of MS patients, respectively. These findings suggest that mood disturbances are considerably more common than psychosis among patients with MS.

Diagnosis of MSrelated psychosis has been addressed only in case reports or small studies, most of which have not clearly defined psychosis or adequately described the symptoms or confounding factors such as medications. Findings on prevalence of psychosis as the initial presentation in MS are more limited and confounded by instances in which neurologic symptoms might have been overlooked.^9,11

Few studies have investigated whether lesion location correlates with specific neuropsychiatric symptoms. In one study,⁸ brain MRI taken within 9 months of presenting symptoms showed that MS was not significantly more severe among patients with psychosis compared with nonpsychotic MS patients. These data support psychosis as a possible early finding in MS.

At least two studies^12,13 suggest a correlation between temporal lobe lesions and psychosis, but both study samples were small (8 and 10 patients) and used a combination of diagnoses. One case report also supports this correlation.¹⁴

Table 2

Medical conditions that can cause psychotic symptoms

Treating ms-related psychosis

MS-related psychosis should abate with MS treatment, but no systematized studies have verified this or determined which antipsychotics would be suitable. Single case reports suggest successful treatment with risperidone,¹³ haloperidol,¹⁵ clozapine,¹⁶ or ziprasidone.¹⁷ Ms. B showed initial improvement with risperidone, but because she was lost to follow-up we cannot say if this medication would work long-term.

Related resources

• Feinstein A. The clinical neuropsychiatry of multiple sclerosis. New York: Cambridge University Press; 1999.
• National Multiple Sclerosis Society. www.nationalmssociety.org.

Drug brand name

• Clozapine • Clozaril
• Risperidone • Risperdal
• Haloperidol • Haldol
• Ziprasidone • Geodon
• Lorazepam • Ativan

Disclosures

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

Dr. Rafeyan is a speaker for AstraZeneca, BristolMyers Squibb Co., Eli Lilly and Co., GlaxoSmithKline, Pfizer, and Wyeth. He is also an advisor to Abbott Laboratories and Forest Pharmaceuticals.

History: shop talk

Ms. B, age 46, presents to the ER at her brother’s insistence. For about 6 months, she says, she has been “hearing voices”—including that of her boss—talking to each other about work.

Ms. B has no personal or family psychiatric history but notes that her sister died 6 months ago, and her father died the following month. At work, she is having trouble getting along with her boss. She adds that she has been skipping church lately because she believes her church is under investigation and the inquiry might be targeting her.

Ms. B has been a company manager for 20 years. She is divorced, has no children, and lives alone. She says she does not smoke or use illicit drugs and seldom drinks alcohol. She denies suicidal or homicidal thoughts, depressed mood, or visual hallucinations. She says she is sleeping only 3 to 4 hours nightly and feels fatigued in the afternoon. She denies loss of concentration or functioning.

Mental status. Ms. B is well groomed, maintains good eye contact, and is superficially cooperative but increasingly guarded with further questioning. She describes her mood as “OK,” but her affect is blunted. Thought process is logical but circumstantial at times, and her thoughts consist of auditory hallucinations, paranoid thinking, persecutory delusions, and ideas of reference. She has poor insight into her symptoms and does not want to be admitted.

Physical examination and laboratory tests are unremarkable. Negative ethanol and urine drug screens rule out substance abuse, and preliminary noncontrast head CT shows no acute changes.

The author’s observations

In women, schizophrenia typically emerges between ages 17 and 37;¹ onset after age 45 is unusual.² Ms. B’s age, family history, and lack of a formal thought disorder or negative symptoms make late-onset schizophrenia unlikely, though it cannot be ruled out.

Ms. B denies mood symptoms, but significant stressors—such as the recent deaths of her sister and father and difficulties at work—could precipitate a mood disorder. Of the possible diagnoses, major depressive disorder is most likely at this time.^1,3 Because Ms. B’s symptoms do not clearly match any diagnosis, we speak with her brother and sister-in-law to seek collateral information.

Collateral history: beware of spies

Ms. B’s brother says his sister began behaving strangely about 8 months ago and has worsened lately. He says she suspects that her boss hired spies to watch her house, car, and her parent’s house. After work, she often parks in paid garages rather than at home to avoid being “followed.” When visiting, he says, she leaves her keys outside because she fears they contain a tracking device. Family members say Ms. B sometimes drops by at night—as late as 5 AM—complaining that she cannot sleep because she is being “watched.”

Ms. B’s family hired a private investigator 3 or 4 months ago to examine her house and car. Although no tracking devices were found, her brother says, Ms. B remains convinced she is being followed. He says she often speaks in “code” and whispers to herself.

According to her brother, Ms. B often hears voices while trying to sleep, saying such things as “Why won’t she turn over?” She reportedly wears a towel while showering because the “spies” are watching. During a conference she attended last week, she told her brother that a group of government investigators followed her there and arrested her boss.

Ms. B’s sister-in-law says the patient’s functioning has declined sharply, and that she has been helping Ms. B complete routine work. Neither she nor Ms. B’s brother have noticed a change in the patient’s energy, productivity, or speech production or speed, thus ruling out bipolar disorder. Ms. B’s brother confirms that there is no family history of mental illness.

The author’s observations

Collateral information about Ms. B points to psychosis rather than a mood disorder with psychotic features, but she lacks the formal thought disorder and negative symptoms common in primary psychotic disorders.

Because Ms. B’s presentation is atypical, we order brain MRI to check for a general medical condition (Figure 1). If brain MRI suggests a medical problem, we will follow with EEG, lumbar puncture, or other tests.

Figure 1 Clinical steps to rule out medical causes of late-onset psychosis

treatment, testing: what mri suggests

We admit Ms. B to the locked inpatient psychiatric unit—where she remains paranoid and guarded—and prescribe risperidone, 1 mg/d, to address her paranoia. She refuses medication at first because she feels she does not need psychiatric care, but we give her lorazepam, 0.5 mg/d for her anxiety, along with psychoeducation and family support. After 3 days, we stop lorazepam and Ms. B agrees to take risperidone.

Within 4 days of starting risperidone, Ms. B’s auditory hallucinations and paranoia have lessened and her insight is improved. We recommend increasing the dosage to 2 mg/d because we feel that 1 mg/d will not sufficiently control her symptoms. She remains paranoid but is reluctant to increase the dosage for fear of adverse effects, though she has reported none so far.

Brain MRI taken the night Ms. B was admitted shows:

• multiple focal, well-defined hyperintense periventricular lesions on fluid-attenuated inversion recovery (FLAIR)- and T2-weighted images (Figure 2). Some lesions are flame-shaped.
• a 1.5-cm lesion adjacent to the right frontal horn showing a hyperintense signal on T2-weighted images and a hypointense signal on T1-weighted images without contrast enhancement. White-matter edema surrounds this lesion.
• no gadolinium-enhancing lesions.

Two radiologists confirm possible demyelination, suggesting multiple sclerosis (MS). Final report of initial brain CT shows lowdensity, periventricular white matter changes consistent with the MRI findings.

Results of subsequent laboratory tests are normal. Erythrocyte sedimentation rate is slightly elevated at 35 mm/hr, suggesting a possible autoimmune disorder. ECG shows sinus bradycardia, and chest x-ray and MR angiogram are unremarkable, as are EEG and visual evoked potential results.

Lumbar puncture and CSF studies show increased immunoglobulin G to albumin ratio. CSF fluid is clear, blood counts and protein are normal, Gram’s stain and culture are negative, and cytologic findings show a marked increase in mature lymphocytes. These results suggest inflammation, but follow-up neurologic exam is unremarkable.

Figure 2 FLAIR-weighted image after Ms. B’s brain MRI

Right 1.5-cm lesion adjacent to right frontal horn and multiple left hyperintense lesions on fluid-attenuated inversion recovery (FLAIR)-weighted image.

The authors’ observations

Determining disease dissemination in time and space is key to diagnosing MS. Clinical presentation or MRI can determine both criteria (Table 1). Ms. B’s lesions and CSF results suggest that MS has disseminated throughout her body, but neurologic examination shows no objective clinical evidence of lesions.

Neuropsychological testing might help evaluate Ms. B’s cognition and executive functioning, but these deficits do not specifically suggest MS. The cortex, particularly the prefrontal cortex, is believed to coordinate organization, planning, and socially appropriate behavior. MS typically involves white matter rather than the cortex, but researchers have suggested that MS-related demyelination might disrupt the axonal circuits that connect the cortex to other brain areas.¹⁸

Increased lesion load has been correlated with decreased cognitive function. Neuropsychological testing could indirectly point to a lesion load increase by recording decreased cognitive function, but this decline cannot be attributed to MS without an MRI.

Ms. B’s psychotic symptoms could be clinical evidence of MS, but we cannot solidify the diagnosis until we establish dissemination in time. To do that, we need a second MRI 3 months after the first one. Concurrent late-onset paraphrenia and MS is possible but rare.

Table 1

Findings needed to determine MS diagnosis based on clinical presentation

Follow-up: where is she?

Ms. B is discharged after 10 days. She denies hallucinations, and staff notices decreased paranoia, brighter affect, and improved insight. We tell her to continue taking risperidone, 1 mg/d.

Three weeks later, Ms. B sees an outpatient psychiatrist. She is paranoid, guarded, and has not been taking risperidone.

Because Ms. B’s previous MRI results are suspect, we ask the hospital’s neurology service to examine her. Findings are unremarkable, but the neurologist recommends a followup brain MRI in 3 months or sooner if symptoms emerge. More than 2 years later, she has not completed a second MRI or contacted her psychiatrist or neurologist.

The authors’ observations

Ms. B’s case highlights the importance of:

• recognizing an atypical presentation of a primary psychotic disorder
• checking for a medical cause of psychosis (Table 2)
• knowing which psychiatric symptoms are common in MS.

Despite absence of neurologic symptoms, Ms. B’s psychosis could have been the initial presentation of MS, which is more prevalent among psychiatric inpatients than in the general population.^6,7 In a prospective study,⁸ 95% of patients with MS had neuropsychiatric symptoms, and 79% had depressive symptoms. Hallucinations and delusions were reported in 10% and 7% of MS patients, respectively. These findings suggest that mood disturbances are considerably more common than psychosis among patients with MS.

Diagnosis of MSrelated psychosis has been addressed only in case reports or small studies, most of which have not clearly defined psychosis or adequately described the symptoms or confounding factors such as medications. Findings on prevalence of psychosis as the initial presentation in MS are more limited and confounded by instances in which neurologic symptoms might have been overlooked.^9,11

Few studies have investigated whether lesion location correlates with specific neuropsychiatric symptoms. In one study,⁸ brain MRI taken within 9 months of presenting symptoms showed that MS was not significantly more severe among patients with psychosis compared with nonpsychotic MS patients. These data support psychosis as a possible early finding in MS.

At least two studies^12,13 suggest a correlation between temporal lobe lesions and psychosis, but both study samples were small (8 and 10 patients) and used a combination of diagnoses. One case report also supports this correlation.¹⁴

Table 2

Medical conditions that can cause psychotic symptoms

Treating ms-related psychosis

MS-related psychosis should abate with MS treatment, but no systematized studies have verified this or determined which antipsychotics would be suitable. Single case reports suggest successful treatment with risperidone,¹³ haloperidol,¹⁵ clozapine,¹⁶ or ziprasidone.¹⁷ Ms. B showed initial improvement with risperidone, but because she was lost to follow-up we cannot say if this medication would work long-term.

Related resources

• Feinstein A. The clinical neuropsychiatry of multiple sclerosis. New York: Cambridge University Press; 1999.
• National Multiple Sclerosis Society. www.nationalmssociety.org.

Drug brand name

• Clozapine • Clozaril
• Risperidone • Risperdal
• Haloperidol • Haldol
• Ziprasidone • Geodon
• Lorazepam • Ativan

Disclosures

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

Dr. Rafeyan is a speaker for AstraZeneca, BristolMyers Squibb Co., Eli Lilly and Co., GlaxoSmithKline, Pfizer, and Wyeth. He is also an advisor to Abbott Laboratories and Forest Pharmaceuticals.

Whenever you feel you are doing more work than the patient and are more invested than he is, something has gone wrong in collaborative care.

With resistant or hostile patients, fight the urge to move quickly into clinical assessment and to prescribe what you think should be worked on and how. Instead, spend more time—especially when building the treatment alliance in the first 15 minutes (Box¹)—exploring their ideas on how, when, and where they feel they can achieve what is most important to them (Table 1²).

Resistant patients may have different agendas, but taking a pragmatic approach can merge their goals with yours.

Box

Table 1

How to merge the reluctant patient’s goals with clinical needs assessment

What does the patient want?

When a patient is difficult to engage, begin by listening for the most important concern that brought him to your office.

He may be depressed, anxious, or tired, but exploring why he decided to seek help now (“My wife said she would leave me if I didn’t get help”) reveals what is most important. The “treatment contract,” then, is helping this patient save his marriage.

Initial engagement

Collaborative treatment begins with a genuinely interested dialogue about what prompted the patient’s visit.

Therapist: “Thank you for choosing to work with me. How may I serve you? What is the most important thing you want me to help you with?”

Mr. L: “I didn’t choose you; they made me come.”

T: “I didn’t see anyone drag you in. What would happen if you had not come today?”

Mr. L: “I might lose my job. I came because my boss told me to.”

Focus on what the patient wants, not just what others have said he or she needs (treatment for substance abuse, angry outbursts, conflict at work). The patient may want to stay out of jail, keep his job or relationship, regain custody of his or her children, obtain housing, or get people to “leave me alone and quit locking me up against my will.” Although the patient’s problem may be obvious to us, he needs “discovery” work, not “recovery” work.

Why has the patient come now? What is his highest priority? Can we help him discover the link between his drinking or anger that affects his work performance?

Therapist: “So you want to get the boss off your back. You want people to leave you alone. You feel people treat you unfairly and want them to stop. But why did you come today and not last week or last month?”

Mr. L: “I came now because yesterday my boss said I could lose my job if I didn’t get some help.”

T: “So what you want most importantly is to keep your job, is that it?”

Mr. L: “Well yeah, but I don’t have a drinking problem or any problem with my temper. They’re just overreacting. It wasn’t as bad as they said.”

T: “OK, I am willing to work on helping you keep your job if that’s what is most important to you. Do you know what you are doing that makes them think you have a drinking or anger problem?

Mr. L: “All I did was come in late a couple of times and got into a little argument with a couple of people.”

T: “If we are going to help you keep your job, we could spend our time talking about how unfair your boss is and how she’s misjudging you. Or we could work to show her that she has you all wrong and that you are a productive worker who does not have a substance or anger problem.

“Let’s think together how we could gather the data that would prove you don’t have a substance problem. If all that data is squeaky clean, then I can write a very supportive letter to your boss and tell her all is well. If, however, we discover you do have a problem, I can still write a very supportive letter. But we’ll have to show her how you are taking care of any problems that interfere with your work performance.”

Reframe the presenting complaint

Few patients present fully ready to work on definitive behavioral health recovery. If patients at least attend sessions or talk with you, they must be motivated to do something. Otherwise, they would not show up.

Our task is help patients such as Mr. L get what they want, not what we think they should want. Eventually you will get to explore the patient’s substance use, impulse or parenting problems, mental health symptoms, or communication problems, but this discussion will be in the service of allying with his or her goals.

Rather than viewing patients as unmotivated or resistant, think of resistance as an interactional process. “If we are going to stop them from locking you up,” you might say, “let’s talk about what you are doing that makes you look like you are dangerous and out of control. And when you were not locked away, let’s think of how you kept ‘them’ off your back.”

Instead of interpreting resistance as pathology, view the behavior as an opportunity to understand and respond to the patient’s stage of readiness to change.

Stages of change

By being “difficult,” patients are often declaring that they are not invested in what you think the problem is or in working on that problem. Resistance thrives when we and the patient have not allied around a common goal and are at different stages of change. Think of the therapeutic alliance in the context of the widely-used and well-researched Transtheoretical Model’s stages of change:^3,4

Precontemplation. A person at this stage is not considering the possibility of change, although others are aware of a problem. He or she will seldom appear for treatment without coercion. The person could benefit from nonthreatening information to raise awareness of a possible “problem” and possibilities for change.

Contemplation. The person is ambivalent, undecided, vacillating about whether he has a “problem.” He wants to change, but this desire exists simultaneously with resistance to change. Motivational strategies can be useful, but aggressive or premature confrontation could provoke strong resistance and defensive behaviors. Many persons at this stage have indefinite plans to take action in the next 6 months or so.

Preparation takes the person from the contemplation stage to specific steps to solve the problem in the action stage. He or she develops increasing confidence in the decision to change and takes the first steps on the road to action. Most people at this stage plan to take action within 1 month and are making final adjustments before beginning to change.

Action. The person takes specific actions intended to bring about change. This busiest stage of change is characterized by overt modification of behavior and surroundings and requires the greatest time and energy. Support and encouragement are crucial to prevent drop-out and regression in readiness to change.

Maintenance. Goals at this stage are to sustain the changes accomplished by previous action and to prevent relapse. Maintaining new behaviors requires different skills than were needed to initiate change. Gains are consolidated. “Maintenance” is not a static stage; it can last 6 months or up to a lifetime. The patient learns new coping and problem-solving strategies, replaces problem behaviors with a healthier life style, and works through emotional triggers of relapse.

Relapse/recycling can happen but is not inevitable. When setbacks occur, help the patient avoid becoming stuck, discouraged, or demoralized, and help him learn from relapse before committing to a new action cycle. Conduct a comprehensive, multidimensional assessment to explore all reasons for relapse.

Termination is the ultimate goal: to exit the cycle of change without fear of relapse. Certain problems may be terminated or merely kept in remission through maintenance strategies.

Match strategies with stages

Discovery planning. Engaging patients in collaborative care starts with honoring their stages of change and working with them and their families on different tasks for each stage of change.^4-6 A patient such as Mr. L, for example—who is at an early stage of change and thinks he has an “unfair boss problem” (not an alcohol problem) or a “nagging wife problem” (not an anger or domestic violence problem)—needs a discovery, drop-out prevention plan.

The cause of the patient’s work or relationship problem may be obvious to you, but a patient in early stages of change resists that information and, if pressed, gets frustrated and leaves treatment. A “discovery” treatment plan embraces the patient’s views and could be focused, for example, on gathering data that would prove to the employer that there is not an alcohol problem.

If random breath alcohol testing, feedback from family, and review of past job losses all prove negative for alcohol problems, the patient would have data to support his or her view that he does not have an alcohol problem. If, however, this exploration reveals an alcohol problem, the patient “discovers” he has more of a problem than he thought. For this plan, the challenge is to keep Mr. L engaged long enough to discover the connection between his alcohol problems and his employment or marital problems.

Recovery planning. On the other hand, a person at the action stage who wants to avoid becoming depressed again or wishes to live a life of sobriety collaborates on a recovery, relapse prevention plan. This patient is committed to developing the knowledge and skills to prevent relapse and open to whatever will promote health and well-being.

The Transtheoretical Model’s 9 processes of change^3,4 inform which interventions might be most effective at various stages of change (Table 2). For example, a patient might be proud of the fact that “I can hold my liquor and drink everyone under the table.” Consciousness-raising—such as by explaining that his high alcohol tolerance is a danger signal, not a beneficial ability—can enhance his change process. Even if he is not ready to commit to definitive change, at least exploring whether he has a problem may move him from precontemplation to a contemplation stage of change. Table 3 shows how other processes of change can help motivate patients in later stages of change.^4,5

Table 2

Transtheoretical model’s 9 processes of change: What happens at each step

Strategies and interventions to motivate patients at each stage of change

• Scott D. Miller, PhD. Institute for the Study of Therapeutic Change, Chicago, IL. (773) 404-5130; www.talkingcure.com.
  
• Miller WR, Rollnick S, Moyers TB. Motivational interviewing: professional training videotape series. Albuquerque, NM: University of New Mexico, 1998. Six videotapes (about $130 total); (505) 768-0279 or 0100.
  
• Miller WR, consensus panel chair. Treatment improvement protocol. Enhancing motivation for change in substance abuse treatment. Rockville, MD; Center for Substance Abuse Treatment, 1999. DHHS Publication 99-3354. Available from the National Clearinghouse for Alcohol/Drug Information, Rockville, MD; (800) 729-6686.
  

Dr. Mee-Lee is a board-certified psychiatrist and is certified by examination of the American Society of Addiction Medicine (ASAM). He is based in Davis, CA, and is involved in full-time training and consulting. For information, visit www.DMLMD.com.

Whenever you feel you are doing more work than the patient and are more invested than he is, something has gone wrong in collaborative care.

With resistant or hostile patients, fight the urge to move quickly into clinical assessment and to prescribe what you think should be worked on and how. Instead, spend more time—especially when building the treatment alliance in the first 15 minutes (Box¹)—exploring their ideas on how, when, and where they feel they can achieve what is most important to them (Table 1²).

Resistant patients may have different agendas, but taking a pragmatic approach can merge their goals with yours.

Box

Table 1

How to merge the reluctant patient’s goals with clinical needs assessment

What does the patient want?

When a patient is difficult to engage, begin by listening for the most important concern that brought him to your office.

He may be depressed, anxious, or tired, but exploring why he decided to seek help now (“My wife said she would leave me if I didn’t get help”) reveals what is most important. The “treatment contract,” then, is helping this patient save his marriage.

Initial engagement

Collaborative treatment begins with a genuinely interested dialogue about what prompted the patient’s visit.

Therapist: “Thank you for choosing to work with me. How may I serve you? What is the most important thing you want me to help you with?”

Mr. L: “I didn’t choose you; they made me come.”

T: “I didn’t see anyone drag you in. What would happen if you had not come today?”

Mr. L: “I might lose my job. I came because my boss told me to.”

Focus on what the patient wants, not just what others have said he or she needs (treatment for substance abuse, angry outbursts, conflict at work). The patient may want to stay out of jail, keep his job or relationship, regain custody of his or her children, obtain housing, or get people to “leave me alone and quit locking me up against my will.” Although the patient’s problem may be obvious to us, he needs “discovery” work, not “recovery” work.

Why has the patient come now? What is his highest priority? Can we help him discover the link between his drinking or anger that affects his work performance?

Therapist: “So you want to get the boss off your back. You want people to leave you alone. You feel people treat you unfairly and want them to stop. But why did you come today and not last week or last month?”

Mr. L: “I came now because yesterday my boss said I could lose my job if I didn’t get some help.”

T: “So what you want most importantly is to keep your job, is that it?”

Mr. L: “Well yeah, but I don’t have a drinking problem or any problem with my temper. They’re just overreacting. It wasn’t as bad as they said.”

T: “OK, I am willing to work on helping you keep your job if that’s what is most important to you. Do you know what you are doing that makes them think you have a drinking or anger problem?

Mr. L: “All I did was come in late a couple of times and got into a little argument with a couple of people.”

T: “If we are going to help you keep your job, we could spend our time talking about how unfair your boss is and how she’s misjudging you. Or we could work to show her that she has you all wrong and that you are a productive worker who does not have a substance or anger problem.

“Let’s think together how we could gather the data that would prove you don’t have a substance problem. If all that data is squeaky clean, then I can write a very supportive letter to your boss and tell her all is well. If, however, we discover you do have a problem, I can still write a very supportive letter. But we’ll have to show her how you are taking care of any problems that interfere with your work performance.”

Reframe the presenting complaint

Few patients present fully ready to work on definitive behavioral health recovery. If patients at least attend sessions or talk with you, they must be motivated to do something. Otherwise, they would not show up.

Our task is help patients such as Mr. L get what they want, not what we think they should want. Eventually you will get to explore the patient’s substance use, impulse or parenting problems, mental health symptoms, or communication problems, but this discussion will be in the service of allying with his or her goals.

Rather than viewing patients as unmotivated or resistant, think of resistance as an interactional process. “If we are going to stop them from locking you up,” you might say, “let’s talk about what you are doing that makes you look like you are dangerous and out of control. And when you were not locked away, let’s think of how you kept ‘them’ off your back.”

Instead of interpreting resistance as pathology, view the behavior as an opportunity to understand and respond to the patient’s stage of readiness to change.

Stages of change

By being “difficult,” patients are often declaring that they are not invested in what you think the problem is or in working on that problem. Resistance thrives when we and the patient have not allied around a common goal and are at different stages of change. Think of the therapeutic alliance in the context of the widely-used and well-researched Transtheoretical Model’s stages of change:^3,4

Precontemplation. A person at this stage is not considering the possibility of change, although others are aware of a problem. He or she will seldom appear for treatment without coercion. The person could benefit from nonthreatening information to raise awareness of a possible “problem” and possibilities for change.

Contemplation. The person is ambivalent, undecided, vacillating about whether he has a “problem.” He wants to change, but this desire exists simultaneously with resistance to change. Motivational strategies can be useful, but aggressive or premature confrontation could provoke strong resistance and defensive behaviors. Many persons at this stage have indefinite plans to take action in the next 6 months or so.

Preparation takes the person from the contemplation stage to specific steps to solve the problem in the action stage. He or she develops increasing confidence in the decision to change and takes the first steps on the road to action. Most people at this stage plan to take action within 1 month and are making final adjustments before beginning to change.

Action. The person takes specific actions intended to bring about change. This busiest stage of change is characterized by overt modification of behavior and surroundings and requires the greatest time and energy. Support and encouragement are crucial to prevent drop-out and regression in readiness to change.

Maintenance. Goals at this stage are to sustain the changes accomplished by previous action and to prevent relapse. Maintaining new behaviors requires different skills than were needed to initiate change. Gains are consolidated. “Maintenance” is not a static stage; it can last 6 months or up to a lifetime. The patient learns new coping and problem-solving strategies, replaces problem behaviors with a healthier life style, and works through emotional triggers of relapse.

Relapse/recycling can happen but is not inevitable. When setbacks occur, help the patient avoid becoming stuck, discouraged, or demoralized, and help him learn from relapse before committing to a new action cycle. Conduct a comprehensive, multidimensional assessment to explore all reasons for relapse.

Termination is the ultimate goal: to exit the cycle of change without fear of relapse. Certain problems may be terminated or merely kept in remission through maintenance strategies.

Match strategies with stages

Discovery planning. Engaging patients in collaborative care starts with honoring their stages of change and working with them and their families on different tasks for each stage of change.^4-6 A patient such as Mr. L, for example—who is at an early stage of change and thinks he has an “unfair boss problem” (not an alcohol problem) or a “nagging wife problem” (not an anger or domestic violence problem)—needs a discovery, drop-out prevention plan.

The cause of the patient’s work or relationship problem may be obvious to you, but a patient in early stages of change resists that information and, if pressed, gets frustrated and leaves treatment. A “discovery” treatment plan embraces the patient’s views and could be focused, for example, on gathering data that would prove to the employer that there is not an alcohol problem.

If random breath alcohol testing, feedback from family, and review of past job losses all prove negative for alcohol problems, the patient would have data to support his or her view that he does not have an alcohol problem. If, however, this exploration reveals an alcohol problem, the patient “discovers” he has more of a problem than he thought. For this plan, the challenge is to keep Mr. L engaged long enough to discover the connection between his alcohol problems and his employment or marital problems.

Recovery planning. On the other hand, a person at the action stage who wants to avoid becoming depressed again or wishes to live a life of sobriety collaborates on a recovery, relapse prevention plan. This patient is committed to developing the knowledge and skills to prevent relapse and open to whatever will promote health and well-being.

The Transtheoretical Model’s 9 processes of change^3,4 inform which interventions might be most effective at various stages of change (Table 2). For example, a patient might be proud of the fact that “I can hold my liquor and drink everyone under the table.” Consciousness-raising—such as by explaining that his high alcohol tolerance is a danger signal, not a beneficial ability—can enhance his change process. Even if he is not ready to commit to definitive change, at least exploring whether he has a problem may move him from precontemplation to a contemplation stage of change. Table 3 shows how other processes of change can help motivate patients in later stages of change.^4,5

Table 2

Transtheoretical model’s 9 processes of change: What happens at each step

Strategies and interventions to motivate patients at each stage of change

• Scott D. Miller, PhD. Institute for the Study of Therapeutic Change, Chicago, IL. (773) 404-5130; www.talkingcure.com.
  
• Miller WR, Rollnick S, Moyers TB. Motivational interviewing: professional training videotape series. Albuquerque, NM: University of New Mexico, 1998. Six videotapes (about $130 total); (505) 768-0279 or 0100.
  
• Miller WR, consensus panel chair. Treatment improvement protocol. Enhancing motivation for change in substance abuse treatment. Rockville, MD; Center for Substance Abuse Treatment, 1999. DHHS Publication 99-3354. Available from the National Clearinghouse for Alcohol/Drug Information, Rockville, MD; (800) 729-6686.
  

Dr. Mee-Lee is a board-certified psychiatrist and is certified by examination of the American Society of Addiction Medicine (ASAM). He is based in Davis, CA, and is involved in full-time training and consulting. For information, visit www.DMLMD.com.

Whenever you feel you are doing more work than the patient and are more invested than he is, something has gone wrong in collaborative care.

With resistant or hostile patients, fight the urge to move quickly into clinical assessment and to prescribe what you think should be worked on and how. Instead, spend more time—especially when building the treatment alliance in the first 15 minutes (Box¹)—exploring their ideas on how, when, and where they feel they can achieve what is most important to them (Table 1²).

Resistant patients may have different agendas, but taking a pragmatic approach can merge their goals with yours.

Box

Table 1

How to merge the reluctant patient’s goals with clinical needs assessment

What does the patient want?

When a patient is difficult to engage, begin by listening for the most important concern that brought him to your office.

He may be depressed, anxious, or tired, but exploring why he decided to seek help now (“My wife said she would leave me if I didn’t get help”) reveals what is most important. The “treatment contract,” then, is helping this patient save his marriage.

Initial engagement

Collaborative treatment begins with a genuinely interested dialogue about what prompted the patient’s visit.

Therapist: “Thank you for choosing to work with me. How may I serve you? What is the most important thing you want me to help you with?”

Mr. L: “I didn’t choose you; they made me come.”

T: “I didn’t see anyone drag you in. What would happen if you had not come today?”

Mr. L: “I might lose my job. I came because my boss told me to.”

Focus on what the patient wants, not just what others have said he or she needs (treatment for substance abuse, angry outbursts, conflict at work). The patient may want to stay out of jail, keep his job or relationship, regain custody of his or her children, obtain housing, or get people to “leave me alone and quit locking me up against my will.” Although the patient’s problem may be obvious to us, he needs “discovery” work, not “recovery” work.

Why has the patient come now? What is his highest priority? Can we help him discover the link between his drinking or anger that affects his work performance?

Therapist: “So you want to get the boss off your back. You want people to leave you alone. You feel people treat you unfairly and want them to stop. But why did you come today and not last week or last month?”

Mr. L: “I came now because yesterday my boss said I could lose my job if I didn’t get some help.”

T: “So what you want most importantly is to keep your job, is that it?”

Mr. L: “Well yeah, but I don’t have a drinking problem or any problem with my temper. They’re just overreacting. It wasn’t as bad as they said.”

T: “OK, I am willing to work on helping you keep your job if that’s what is most important to you. Do you know what you are doing that makes them think you have a drinking or anger problem?

Mr. L: “All I did was come in late a couple of times and got into a little argument with a couple of people.”

T: “If we are going to help you keep your job, we could spend our time talking about how unfair your boss is and how she’s misjudging you. Or we could work to show her that she has you all wrong and that you are a productive worker who does not have a substance or anger problem.

“Let’s think together how we could gather the data that would prove you don’t have a substance problem. If all that data is squeaky clean, then I can write a very supportive letter to your boss and tell her all is well. If, however, we discover you do have a problem, I can still write a very supportive letter. But we’ll have to show her how you are taking care of any problems that interfere with your work performance.”

Reframe the presenting complaint

Few patients present fully ready to work on definitive behavioral health recovery. If patients at least attend sessions or talk with you, they must be motivated to do something. Otherwise, they would not show up.

Our task is help patients such as Mr. L get what they want, not what we think they should want. Eventually you will get to explore the patient’s substance use, impulse or parenting problems, mental health symptoms, or communication problems, but this discussion will be in the service of allying with his or her goals.

Rather than viewing patients as unmotivated or resistant, think of resistance as an interactional process. “If we are going to stop them from locking you up,” you might say, “let’s talk about what you are doing that makes you look like you are dangerous and out of control. And when you were not locked away, let’s think of how you kept ‘them’ off your back.”

Instead of interpreting resistance as pathology, view the behavior as an opportunity to understand and respond to the patient’s stage of readiness to change.

Stages of change

By being “difficult,” patients are often declaring that they are not invested in what you think the problem is or in working on that problem. Resistance thrives when we and the patient have not allied around a common goal and are at different stages of change. Think of the therapeutic alliance in the context of the widely-used and well-researched Transtheoretical Model’s stages of change:^3,4

Precontemplation. A person at this stage is not considering the possibility of change, although others are aware of a problem. He or she will seldom appear for treatment without coercion. The person could benefit from nonthreatening information to raise awareness of a possible “problem” and possibilities for change.

Contemplation. The person is ambivalent, undecided, vacillating about whether he has a “problem.” He wants to change, but this desire exists simultaneously with resistance to change. Motivational strategies can be useful, but aggressive or premature confrontation could provoke strong resistance and defensive behaviors. Many persons at this stage have indefinite plans to take action in the next 6 months or so.

Preparation takes the person from the contemplation stage to specific steps to solve the problem in the action stage. He or she develops increasing confidence in the decision to change and takes the first steps on the road to action. Most people at this stage plan to take action within 1 month and are making final adjustments before beginning to change.

Action. The person takes specific actions intended to bring about change. This busiest stage of change is characterized by overt modification of behavior and surroundings and requires the greatest time and energy. Support and encouragement are crucial to prevent drop-out and regression in readiness to change.

Maintenance. Goals at this stage are to sustain the changes accomplished by previous action and to prevent relapse. Maintaining new behaviors requires different skills than were needed to initiate change. Gains are consolidated. “Maintenance” is not a static stage; it can last 6 months or up to a lifetime. The patient learns new coping and problem-solving strategies, replaces problem behaviors with a healthier life style, and works through emotional triggers of relapse.

Relapse/recycling can happen but is not inevitable. When setbacks occur, help the patient avoid becoming stuck, discouraged, or demoralized, and help him learn from relapse before committing to a new action cycle. Conduct a comprehensive, multidimensional assessment to explore all reasons for relapse.

Termination is the ultimate goal: to exit the cycle of change without fear of relapse. Certain problems may be terminated or merely kept in remission through maintenance strategies.

Match strategies with stages

Discovery planning. Engaging patients in collaborative care starts with honoring their stages of change and working with them and their families on different tasks for each stage of change.^4-6 A patient such as Mr. L, for example—who is at an early stage of change and thinks he has an “unfair boss problem” (not an alcohol problem) or a “nagging wife problem” (not an anger or domestic violence problem)—needs a discovery, drop-out prevention plan.

The cause of the patient’s work or relationship problem may be obvious to you, but a patient in early stages of change resists that information and, if pressed, gets frustrated and leaves treatment. A “discovery” treatment plan embraces the patient’s views and could be focused, for example, on gathering data that would prove to the employer that there is not an alcohol problem.

If random breath alcohol testing, feedback from family, and review of past job losses all prove negative for alcohol problems, the patient would have data to support his or her view that he does not have an alcohol problem. If, however, this exploration reveals an alcohol problem, the patient “discovers” he has more of a problem than he thought. For this plan, the challenge is to keep Mr. L engaged long enough to discover the connection between his alcohol problems and his employment or marital problems.

Recovery planning. On the other hand, a person at the action stage who wants to avoid becoming depressed again or wishes to live a life of sobriety collaborates on a recovery, relapse prevention plan. This patient is committed to developing the knowledge and skills to prevent relapse and open to whatever will promote health and well-being.

The Transtheoretical Model’s 9 processes of change^3,4 inform which interventions might be most effective at various stages of change (Table 2). For example, a patient might be proud of the fact that “I can hold my liquor and drink everyone under the table.” Consciousness-raising—such as by explaining that his high alcohol tolerance is a danger signal, not a beneficial ability—can enhance his change process. Even if he is not ready to commit to definitive change, at least exploring whether he has a problem may move him from precontemplation to a contemplation stage of change. Table 3 shows how other processes of change can help motivate patients in later stages of change.^4,5

Table 2

Transtheoretical model’s 9 processes of change: What happens at each step

Strategies and interventions to motivate patients at each stage of change

• Scott D. Miller, PhD. Institute for the Study of Therapeutic Change, Chicago, IL. (773) 404-5130; www.talkingcure.com.
  
• Miller WR, Rollnick S, Moyers TB. Motivational interviewing: professional training videotape series. Albuquerque, NM: University of New Mexico, 1998. Six videotapes (about $130 total); (505) 768-0279 or 0100.
  
• Miller WR, consensus panel chair. Treatment improvement protocol. Enhancing motivation for change in substance abuse treatment. Rockville, MD; Center for Substance Abuse Treatment, 1999. DHHS Publication 99-3354. Available from the National Clearinghouse for Alcohol/Drug Information, Rockville, MD; (800) 729-6686.
  

Dr. Mee-Lee is a board-certified psychiatrist and is certified by examination of the American Society of Addiction Medicine (ASAM). He is based in Davis, CA, and is involved in full-time training and consulting. For information, visit www.DMLMD.com.

Some dependent patients are needy, clingy, and insecure—unable to make the smallest decisions without inordinate advice and reassurance—whereas others are less easy to recognize. Dependency can be expressed in many different ways: obvious or subtle, maladaptive or adaptive.

Dependent psychotherapy patients are compliant and eager to please but can have difficulty terminating treatment. This article offers recommendations for clinical work with dependent adults to help you:

• assess and diagnose dependent personality disorder (DPD)
  
• distinguish unhealthy from healthy dependency
  
• provide effective psychotherapy for DPD in inpatient and outpatient settings.
  

What is a dependent personality?

DPD is diagnosed when an individual exhibits long-standing, inflexible dependency that creates difficulties in social, sexual, and occupational functioning, according to DSM-IV-TR.¹ DPD’s essential feature is a pervasive and excessive need to be taken care of that leads to submissive and clinging behavior and fears of separation, beginning by early adulthood and present in a variety of contexts. To receive a DPD diagnosis, a patient must show 5 of 8 possible symptoms (Table 1).

Table 1

Symptoms of dependent personality disorder (DPD)*

Who has DPD? One of the more common Axis II disorders, DPD is not distributed equally across the population. No studies have assessed the impact of age on DPD risk, but variables that affect DPD prevalence include:

• gender (women are far more likely than men to receive a DPD diagnosis)
  
• practice setting (DPD is more prevalent in rehabilitation and psychiatric inpatient settings than in outpatient practices)
  
• race and ethnicity (dependency may be less prevalent in African-American than in Caucasian adults).^3,4
  

Interpersonal, intrapsychic dynamics

DPD is viewed as having 4 related components:^4,5

• Cognitive: A perception of oneself as powerless and ineffectual plus the belief that other people are comparatively confident and competent.
  
• Motivational: A strong desire to maintain close ties with protectors and caregivers.
  
• Emotional: Fear of abandonment or rejection; anxiety about evaluation by authority figures.
  
• Behavioral: A pattern of relationship-facilitating behavior designed to minimize the possibility of abandonment and rejection.
  

Interpersonal strategies. Dependent persons use interpersonal strategies to strengthen social ties and minimize the possibility of being rejected or abandoned (Table 2). Some strategies involve behavior that is active and assertive—even quite aggressive.⁸ Therefore, dependency does not necessarily equate with passivity.

Table 2

Self-presentation strategies
used by dependent persons to facilitate relationships

What causes DPD?

Three theoretical frameworks have been used to explain the development and dynamics of DPD. Each suggests intervention techniques for dealing with dependency-related problems.

Psychodynamic. Psychodynamic theorists conceptualize problematic dependency in terms of dependency conflicts (such as conflicts between a desire to be cared for and an urge to dominate and compete). Ego defenses used to manage the affect associated with these conflicts (such as denial or projection) help determine the manner in which underlying dependency needs are expressed.⁹

Cognitive. Cognitive theorists regard problematic dependency as stemming from self-defeating thought patterns,¹⁰ including:

• helplessness-inducing automatic thoughts (reflexive thoughts that reflect the person’s lack of self-confidence)
  
• negative self-statements (self-deprecating internal monologues in which dependent persons reaffirm their perceived lack of competence and skill).
  

Diagnosis and assessment

Three principles guide the diagnosis of DPD.

• Dependency, as noted, is not always characterized by passivity. Dependent patients may use active, dramatic self-presentation strategies—such as breakdown threats or parasuicide attempts—to protect themselves from being abandoned.^4,8
  
• Self-reports do not always give a true picture. Because dependency may be viewed as a sign of weakness and immaturity, many adults—especially men—are reluctant to acknowledge dependent thoughts and feelings.¹² Interviewing knowledgeable informants can be enlightening.
  
• Dependency’s severity varies over time and across situations. Depressive episodes are associated with temporary increases in self-reported dependency. Even modest mood changes can amplify dependency.^13,14
  

Questionnaires do not allow you to probe and follow-up, but paper-and-pencil tools are relatively inexpensive and efficient. They also avoid reliability problems that can occur with structured interviews. The 2 self-report instruments used most often to diagnose DPD are:

• Millon Clinical Multiaxial Inventory-III
  
• Personality Diagnostic Questionnaire-IV
  

Differential diagnosis

DPD must be distinguished from Axis I and II syndromes with often-overlapping symptoms and similar presentations. These include:

• mood disorders, panic disorder, agoraphobia, and dependency arising from one or more general medical conditions
  
• borderline personality disorder, histrionic personality disorder, and avoidant personality disorder.¹
  

Axis II comorbidity patterns likely reflect the generalized, nonspecific nature of personality pathology and the fact that patients may show personality disorder symptoms in one or more diagnostic categories.

DPD Treatment

Dependency is associated with patient cooperativeness and conscientiousness.^3,4,16,17 Compared with nondependent patients, those with dependent personalities:

• delay less time before seeking treatment for psychological or medical symptoms
  
• adhere more conscientiously to psychotherapeutic and psychotropic regimens
  
• miss fewer therapy sessions
  
• show higher rates of treatment completion in outpatient individual and group therapy.
  

Psychotherapy. Traditional psychotherapies—psychodynamic, cognitive, behavioral—modestly improve DPD symptoms.¹⁹ Most effective has been psychotherapy that combines various modalities.^2,4,20 Five interventions (Table 3) have been shown to:

• help the patient and therapist identify aspects of the patient’s environment that propagate dependent behavior
  
• provide the patient with coping skills needed to more effectively control dependency-related impulses.
  

Table 3

5 useful psychotherapeutic methods for dependent patients

Limitations and caveats

Clinical work with DPD patients traditionally has focused on diminishing problematic dependency. Recent research suggests, however, that expressing dependency strivings in a flexible, situation-appropriate manner can strengthen interpersonal ties and facilitate adaptation and healthy psychological functioning.^2,5 Thus, the most effective interventions emphasize replacing unhealthy, maladaptive dependency with flexible, adaptive dependency.

Beyond the strategies summarized in Table 3, several other considerations—such as setting limits—are important in managing DPD and in minimizing therapeutic obstacles and impasses.

Set firm limits on after-hours contact early in treatment. Unless you set firm limits at the outset of therapy, dependent patients tend to have a higher-than-average number of “pseudo-emergencies” and make frequent requests for between-sessions contact.

In inpatient settings, patients with DPD receive more consultations and psychotropic medications than do non-DPD patients with similar demographic and diagnostic profiles, and their treatment costs can become excessive.²¹

Shift responsibility. When you provide adequate structure early in treatment, the dependent patient will feel secure enough to open up and disclose troubling thoughts and feelings. Then, as therapy progresses, help the patient experience autonomy and competence within the therapeutic milieu by gradually requiring him or her to take on increasing responsibility for structuring treatment.¹⁰

Beware of countertransference. Many therapists infantilize dependent patients, and exploitation or abuse—financial or sexual—may follow. You must acknowledge and confront these problematic feelings when they occur, either in formal clinical supervision or in informal consultation with other mental health professionals.^4,21

Two countertransference reactions are particularly common (and problematic) in therapeutic work with dependent patients:

• the fantasy of insatiability (believing that no matter how much support and reassurance the patient receives, it will never be enough)
  
• the fantasy of permanence (believing the patient will become so comfortable in therapy’s protective cocoon that he or she will never leave treatment).
  

Because some studies suggest that dependent patients may be at increased risk for suicide, monitor them continuously for negative indicators.^8,9 Five danger signs (Table 4) suggest an increased risk of self-destructive behavior in dependent patients.

Table 4

5 warning signs of self-destructive behavior in dependent patients

Because dependent persons often construct interpersonal milieus that foster and propagate their dependency, concurrent marital and/or family therapy may be warranted to disrupt entrenched dysfunctional patterns.^16,17 Examine the rewards dependent patients obtain for behaving helpless and vulnerable and ways in which their dependency may reward friends, family members, and coworkers.

Related resources

• Baltes MM. The many faces of dependency in old age. Cambridge, UK: Cambridge University Press; 1996.
  
• Bornstein RF. The dependent personality: developmental, social, and clinical perspectives. Psychol Bull 1992;112(1):3-23.
  
• Millon T. Disorders of personality: DSM-IV and beyond. New York: Wiley; 1996.
  

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

Some dependent patients are needy, clingy, and insecure—unable to make the smallest decisions without inordinate advice and reassurance—whereas others are less easy to recognize. Dependency can be expressed in many different ways: obvious or subtle, maladaptive or adaptive.

Dependent psychotherapy patients are compliant and eager to please but can have difficulty terminating treatment. This article offers recommendations for clinical work with dependent adults to help you:

• assess and diagnose dependent personality disorder (DPD)
  
• distinguish unhealthy from healthy dependency
  
• provide effective psychotherapy for DPD in inpatient and outpatient settings.
  

What is a dependent personality?

DPD is diagnosed when an individual exhibits long-standing, inflexible dependency that creates difficulties in social, sexual, and occupational functioning, according to DSM-IV-TR.¹ DPD’s essential feature is a pervasive and excessive need to be taken care of that leads to submissive and clinging behavior and fears of separation, beginning by early adulthood and present in a variety of contexts. To receive a DPD diagnosis, a patient must show 5 of 8 possible symptoms (Table 1).

Table 1

Symptoms of dependent personality disorder (DPD)*

Who has DPD? One of the more common Axis II disorders, DPD is not distributed equally across the population. No studies have assessed the impact of age on DPD risk, but variables that affect DPD prevalence include:

• gender (women are far more likely than men to receive a DPD diagnosis)
  
• practice setting (DPD is more prevalent in rehabilitation and psychiatric inpatient settings than in outpatient practices)
  
• race and ethnicity (dependency may be less prevalent in African-American than in Caucasian adults).^3,4
  

Interpersonal, intrapsychic dynamics

DPD is viewed as having 4 related components:^4,5

• Cognitive: A perception of oneself as powerless and ineffectual plus the belief that other people are comparatively confident and competent.
  
• Motivational: A strong desire to maintain close ties with protectors and caregivers.
  
• Emotional: Fear of abandonment or rejection; anxiety about evaluation by authority figures.
  
• Behavioral: A pattern of relationship-facilitating behavior designed to minimize the possibility of abandonment and rejection.
  

Interpersonal strategies. Dependent persons use interpersonal strategies to strengthen social ties and minimize the possibility of being rejected or abandoned (Table 2). Some strategies involve behavior that is active and assertive—even quite aggressive.⁸ Therefore, dependency does not necessarily equate with passivity.

Table 2

Self-presentation strategies
used by dependent persons to facilitate relationships

What causes DPD?

Three theoretical frameworks have been used to explain the development and dynamics of DPD. Each suggests intervention techniques for dealing with dependency-related problems.

Psychodynamic. Psychodynamic theorists conceptualize problematic dependency in terms of dependency conflicts (such as conflicts between a desire to be cared for and an urge to dominate and compete). Ego defenses used to manage the affect associated with these conflicts (such as denial or projection) help determine the manner in which underlying dependency needs are expressed.⁹

Cognitive. Cognitive theorists regard problematic dependency as stemming from self-defeating thought patterns,¹⁰ including:

• helplessness-inducing automatic thoughts (reflexive thoughts that reflect the person’s lack of self-confidence)
  
• negative self-statements (self-deprecating internal monologues in which dependent persons reaffirm their perceived lack of competence and skill).
  

Diagnosis and assessment

Three principles guide the diagnosis of DPD.

• Dependency, as noted, is not always characterized by passivity. Dependent patients may use active, dramatic self-presentation strategies—such as breakdown threats or parasuicide attempts—to protect themselves from being abandoned.^4,8
  
• Self-reports do not always give a true picture. Because dependency may be viewed as a sign of weakness and immaturity, many adults—especially men—are reluctant to acknowledge dependent thoughts and feelings.¹² Interviewing knowledgeable informants can be enlightening.
  
• Dependency’s severity varies over time and across situations. Depressive episodes are associated with temporary increases in self-reported dependency. Even modest mood changes can amplify dependency.^13,14
  

Questionnaires do not allow you to probe and follow-up, but paper-and-pencil tools are relatively inexpensive and efficient. They also avoid reliability problems that can occur with structured interviews. The 2 self-report instruments used most often to diagnose DPD are:

• Millon Clinical Multiaxial Inventory-III
  
• Personality Diagnostic Questionnaire-IV
  

Differential diagnosis

DPD must be distinguished from Axis I and II syndromes with often-overlapping symptoms and similar presentations. These include:

• mood disorders, panic disorder, agoraphobia, and dependency arising from one or more general medical conditions
  
• borderline personality disorder, histrionic personality disorder, and avoidant personality disorder.¹
  

Axis II comorbidity patterns likely reflect the generalized, nonspecific nature of personality pathology and the fact that patients may show personality disorder symptoms in one or more diagnostic categories.

DPD Treatment

Dependency is associated with patient cooperativeness and conscientiousness.^3,4,16,17 Compared with nondependent patients, those with dependent personalities:

• delay less time before seeking treatment for psychological or medical symptoms
  
• adhere more conscientiously to psychotherapeutic and psychotropic regimens
  
• miss fewer therapy sessions
  
• show higher rates of treatment completion in outpatient individual and group therapy.
  

Psychotherapy. Traditional psychotherapies—psychodynamic, cognitive, behavioral—modestly improve DPD symptoms.¹⁹ Most effective has been psychotherapy that combines various modalities.^2,4,20 Five interventions (Table 3) have been shown to:

• help the patient and therapist identify aspects of the patient’s environment that propagate dependent behavior
  
• provide the patient with coping skills needed to more effectively control dependency-related impulses.
  

Table 3

5 useful psychotherapeutic methods for dependent patients

Limitations and caveats

Clinical work with DPD patients traditionally has focused on diminishing problematic dependency. Recent research suggests, however, that expressing dependency strivings in a flexible, situation-appropriate manner can strengthen interpersonal ties and facilitate adaptation and healthy psychological functioning.^2,5 Thus, the most effective interventions emphasize replacing unhealthy, maladaptive dependency with flexible, adaptive dependency.

Beyond the strategies summarized in Table 3, several other considerations—such as setting limits—are important in managing DPD and in minimizing therapeutic obstacles and impasses.

Set firm limits on after-hours contact early in treatment. Unless you set firm limits at the outset of therapy, dependent patients tend to have a higher-than-average number of “pseudo-emergencies” and make frequent requests for between-sessions contact.

In inpatient settings, patients with DPD receive more consultations and psychotropic medications than do non-DPD patients with similar demographic and diagnostic profiles, and their treatment costs can become excessive.²¹

Shift responsibility. When you provide adequate structure early in treatment, the dependent patient will feel secure enough to open up and disclose troubling thoughts and feelings. Then, as therapy progresses, help the patient experience autonomy and competence within the therapeutic milieu by gradually requiring him or her to take on increasing responsibility for structuring treatment.¹⁰

Beware of countertransference. Many therapists infantilize dependent patients, and exploitation or abuse—financial or sexual—may follow. You must acknowledge and confront these problematic feelings when they occur, either in formal clinical supervision or in informal consultation with other mental health professionals.^4,21

Two countertransference reactions are particularly common (and problematic) in therapeutic work with dependent patients:

• the fantasy of insatiability (believing that no matter how much support and reassurance the patient receives, it will never be enough)
  
• the fantasy of permanence (believing the patient will become so comfortable in therapy’s protective cocoon that he or she will never leave treatment).
  

Because some studies suggest that dependent patients may be at increased risk for suicide, monitor them continuously for negative indicators.^8,9 Five danger signs (Table 4) suggest an increased risk of self-destructive behavior in dependent patients.

Table 4

5 warning signs of self-destructive behavior in dependent patients

Because dependent persons often construct interpersonal milieus that foster and propagate their dependency, concurrent marital and/or family therapy may be warranted to disrupt entrenched dysfunctional patterns.^16,17 Examine the rewards dependent patients obtain for behaving helpless and vulnerable and ways in which their dependency may reward friends, family members, and coworkers.

Related resources

• Baltes MM. The many faces of dependency in old age. Cambridge, UK: Cambridge University Press; 1996.
  
• Bornstein RF. The dependent personality: developmental, social, and clinical perspectives. Psychol Bull 1992;112(1):3-23.
  
• Millon T. Disorders of personality: DSM-IV and beyond. New York: Wiley; 1996.
  

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

Some dependent patients are needy, clingy, and insecure—unable to make the smallest decisions without inordinate advice and reassurance—whereas others are less easy to recognize. Dependency can be expressed in many different ways: obvious or subtle, maladaptive or adaptive.

Dependent psychotherapy patients are compliant and eager to please but can have difficulty terminating treatment. This article offers recommendations for clinical work with dependent adults to help you:

• assess and diagnose dependent personality disorder (DPD)
  
• distinguish unhealthy from healthy dependency
  
• provide effective psychotherapy for DPD in inpatient and outpatient settings.
  

What is a dependent personality?

DPD is diagnosed when an individual exhibits long-standing, inflexible dependency that creates difficulties in social, sexual, and occupational functioning, according to DSM-IV-TR.¹ DPD’s essential feature is a pervasive and excessive need to be taken care of that leads to submissive and clinging behavior and fears of separation, beginning by early adulthood and present in a variety of contexts. To receive a DPD diagnosis, a patient must show 5 of 8 possible symptoms (Table 1).

Table 1

Symptoms of dependent personality disorder (DPD)*

Who has DPD? One of the more common Axis II disorders, DPD is not distributed equally across the population. No studies have assessed the impact of age on DPD risk, but variables that affect DPD prevalence include:

• gender (women are far more likely than men to receive a DPD diagnosis)
  
• practice setting (DPD is more prevalent in rehabilitation and psychiatric inpatient settings than in outpatient practices)
  
• race and ethnicity (dependency may be less prevalent in African-American than in Caucasian adults).^3,4
  

Interpersonal, intrapsychic dynamics

DPD is viewed as having 4 related components:^4,5

• Cognitive: A perception of oneself as powerless and ineffectual plus the belief that other people are comparatively confident and competent.
  
• Motivational: A strong desire to maintain close ties with protectors and caregivers.
  
• Emotional: Fear of abandonment or rejection; anxiety about evaluation by authority figures.
  
• Behavioral: A pattern of relationship-facilitating behavior designed to minimize the possibility of abandonment and rejection.
  

Interpersonal strategies. Dependent persons use interpersonal strategies to strengthen social ties and minimize the possibility of being rejected or abandoned (Table 2). Some strategies involve behavior that is active and assertive—even quite aggressive.⁸ Therefore, dependency does not necessarily equate with passivity.

Table 2

Self-presentation strategies
used by dependent persons to facilitate relationships

What causes DPD?

Three theoretical frameworks have been used to explain the development and dynamics of DPD. Each suggests intervention techniques for dealing with dependency-related problems.

Psychodynamic. Psychodynamic theorists conceptualize problematic dependency in terms of dependency conflicts (such as conflicts between a desire to be cared for and an urge to dominate and compete). Ego defenses used to manage the affect associated with these conflicts (such as denial or projection) help determine the manner in which underlying dependency needs are expressed.⁹

Cognitive. Cognitive theorists regard problematic dependency as stemming from self-defeating thought patterns,¹⁰ including:

• helplessness-inducing automatic thoughts (reflexive thoughts that reflect the person’s lack of self-confidence)
  
• negative self-statements (self-deprecating internal monologues in which dependent persons reaffirm their perceived lack of competence and skill).
  

Diagnosis and assessment

Three principles guide the diagnosis of DPD.

• Dependency, as noted, is not always characterized by passivity. Dependent patients may use active, dramatic self-presentation strategies—such as breakdown threats or parasuicide attempts—to protect themselves from being abandoned.^4,8
  
• Self-reports do not always give a true picture. Because dependency may be viewed as a sign of weakness and immaturity, many adults—especially men—are reluctant to acknowledge dependent thoughts and feelings.¹² Interviewing knowledgeable informants can be enlightening.
  
• Dependency’s severity varies over time and across situations. Depressive episodes are associated with temporary increases in self-reported dependency. Even modest mood changes can amplify dependency.^13,14
  

Questionnaires do not allow you to probe and follow-up, but paper-and-pencil tools are relatively inexpensive and efficient. They also avoid reliability problems that can occur with structured interviews. The 2 self-report instruments used most often to diagnose DPD are:

• Millon Clinical Multiaxial Inventory-III
  
• Personality Diagnostic Questionnaire-IV
  

Differential diagnosis

DPD must be distinguished from Axis I and II syndromes with often-overlapping symptoms and similar presentations. These include:

• mood disorders, panic disorder, agoraphobia, and dependency arising from one or more general medical conditions
  
• borderline personality disorder, histrionic personality disorder, and avoidant personality disorder.¹
  

Axis II comorbidity patterns likely reflect the generalized, nonspecific nature of personality pathology and the fact that patients may show personality disorder symptoms in one or more diagnostic categories.

DPD Treatment

Dependency is associated with patient cooperativeness and conscientiousness.^3,4,16,17 Compared with nondependent patients, those with dependent personalities:

• delay less time before seeking treatment for psychological or medical symptoms
  
• adhere more conscientiously to psychotherapeutic and psychotropic regimens
  
• miss fewer therapy sessions
  
• show higher rates of treatment completion in outpatient individual and group therapy.
  

Psychotherapy. Traditional psychotherapies—psychodynamic, cognitive, behavioral—modestly improve DPD symptoms.¹⁹ Most effective has been psychotherapy that combines various modalities.^2,4,20 Five interventions (Table 3) have been shown to:

• help the patient and therapist identify aspects of the patient’s environment that propagate dependent behavior
  
• provide the patient with coping skills needed to more effectively control dependency-related impulses.
  

Table 3

5 useful psychotherapeutic methods for dependent patients

Limitations and caveats

Clinical work with DPD patients traditionally has focused on diminishing problematic dependency. Recent research suggests, however, that expressing dependency strivings in a flexible, situation-appropriate manner can strengthen interpersonal ties and facilitate adaptation and healthy psychological functioning.^2,5 Thus, the most effective interventions emphasize replacing unhealthy, maladaptive dependency with flexible, adaptive dependency.

Beyond the strategies summarized in Table 3, several other considerations—such as setting limits—are important in managing DPD and in minimizing therapeutic obstacles and impasses.

Set firm limits on after-hours contact early in treatment. Unless you set firm limits at the outset of therapy, dependent patients tend to have a higher-than-average number of “pseudo-emergencies” and make frequent requests for between-sessions contact.

In inpatient settings, patients with DPD receive more consultations and psychotropic medications than do non-DPD patients with similar demographic and diagnostic profiles, and their treatment costs can become excessive.²¹

Shift responsibility. When you provide adequate structure early in treatment, the dependent patient will feel secure enough to open up and disclose troubling thoughts and feelings. Then, as therapy progresses, help the patient experience autonomy and competence within the therapeutic milieu by gradually requiring him or her to take on increasing responsibility for structuring treatment.¹⁰

Beware of countertransference. Many therapists infantilize dependent patients, and exploitation or abuse—financial or sexual—may follow. You must acknowledge and confront these problematic feelings when they occur, either in formal clinical supervision or in informal consultation with other mental health professionals.^4,21

Two countertransference reactions are particularly common (and problematic) in therapeutic work with dependent patients:

• the fantasy of insatiability (believing that no matter how much support and reassurance the patient receives, it will never be enough)
  
• the fantasy of permanence (believing the patient will become so comfortable in therapy’s protective cocoon that he or she will never leave treatment).
  

Because some studies suggest that dependent patients may be at increased risk for suicide, monitor them continuously for negative indicators.^8,9 Five danger signs (Table 4) suggest an increased risk of self-destructive behavior in dependent patients.

Table 4

5 warning signs of self-destructive behavior in dependent patients

Because dependent persons often construct interpersonal milieus that foster and propagate their dependency, concurrent marital and/or family therapy may be warranted to disrupt entrenched dysfunctional patterns.^16,17 Examine the rewards dependent patients obtain for behaving helpless and vulnerable and ways in which their dependency may reward friends, family members, and coworkers.

Related resources

• Baltes MM. The many faces of dependency in old age. Cambridge, UK: Cambridge University Press; 1996.
  
• Bornstein RF. The dependent personality: developmental, social, and clinical perspectives. Psychol Bull 1992;112(1):3-23.
  
• Millon T. Disorders of personality: DSM-IV and beyond. New York: Wiley; 1996.
  

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

Mr. K, age 34, has been hospitalized 4 times in 5 years for acute exacerbations of schizophrenia caused by medication nonadherence. This time he reports he discontinued antipsychotic therapy because he was “tired of taking medications every day.”

He spent 2 weeks in the acute inpatient psychiatric unit and restarted olanzapine—titrated to 15 mg/d—to which he responded well. When he presented to our outpatient clinic for follow-up, Mr. K reported adhering to his medications and denied positive symptoms. He complained of mild daytime sedation but no other side effects.

Schizophrenia patients spend most of their lives stable, rather than hospitalized for acute psychotic episodes. While stable, they continue to require close attention, and medical issues are particularly important during this time. Outpatient maintenance—such as optimizing antipsychotic therapy, offering psychosocial interventions, and monitoring physical health and well-being—provides opportunities to improve the course of illness for patients such as Mr. K.

This article describes a 7-point checkup to keep schizophrenia outpatients stable. It can help you maintain or improve patients’ function, prevent relapse, and monitor for adverse effects (Table 1).

Table 1

7-point checkup for assessing the stable schizophrenia patient

1. Symptom clusters

For several years, Mr. K worked as a research technician in a university lab, maintained an apartment, and attended to activities of daily living while taking olanzapine, 15 mg nightly. After discontinuing his medication, he reported auditory hallucinations, paranoid delusions, ideas of reference, and grossly disorganized thinking and behavior. He also was using marijuana daily, which exacerbated his psychotic symptoms and paranoia.

Addressing schizophrenia’s symptom clusters (Table 2) is key to improving patients’ social and occupational function and quality of life. Mr. K no longer has hallucinations, delusions, or disorganized thinking or behavior, but our evaluation shows his improvements are limited to schizophrenia’s positive symptoms.

Table 2

Schizophrenia’s 4 symptom clusters*

Cognitive symptoms. Mr. K’s concentration, attention, and memory are impaired, which interferes with his work. His ability to abstract is not impaired.

Affective symptoms. Mr. K denies signs or symptoms of depression, mania, hopelessness, or thoughts of wanting to hurt himself or anyone else.

Because antipsychotics do not adequately treat negative and cognitive symptoms, we will address these symptom clusters with psychosocial interventions.

2. Adherence

Nonadherence to medication is the most common cause of relapse and rehospitalization for patients with schizophrenia.¹ We find the following strategies helpful when encouraging, maintaining, and monitoring adherence to medications.

Normalize adherence and enlist patient participation.

We inform Mr. K that most patients have trouble taking medications every day and ask how he remembers. Brainstorming with patients on ways to remember to take medications increases their likelihood of participating.

Try reminder strategies. Recommend pillboxes, alarms, and other aids. Consider enlisting family members to help patients remember to take their medications every day.

Monitor prescriptions. We limit Mr. K’s prescription to 1 month so that we can assess the timeliness and consistency of refills.

Educate. Emphasize the link between adherence and wellness, and nonadherence and relapse-—which Mr. K has clearly demonstrated. We repeat this lesson on multiple visits and counsel any involved family members as well, so that everyone understands the importance of adherence to the patient’s continued well-being.

Look for signs of nonadherence. Because Mr. K discontinued his medications without telling his physician, we remain vigilant for signs of nonadherence—such as reemergence of hallucinations, delusions, paranoia, or ideas of reference—or sudden disappearance of a side effect—such as daytime sedation, which he has consistently reported with olanzapine.

Discontinuation rates in the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) suggest that many stable schizophrenia outpatients are dissatisfied with their medications. Most patients in all treatment groups changed their medications during the 18-month National Institute of Mental Health-sponsored trial.²

SGAs versus FGAs. Schizophrenia patients may be more likely to tolerate second-generation antipsychotics (SGAs) than first-generation antipsychotics (FGAs) because of FGAs’ higher risk of movement side effects such as akathisia. Some data suggest that patients find SGAs more tolerable overall, leading to lower discontinuation rates.³

Recent evidence, however, has cast doubt on the idea that SGAs are clinically superior to FGAs. The CUtLASS trial,⁴ for example, found no quality-of-life differences in patients using either class. Both FGAs and SGAs reduce the risk of relapse in stable patients, although SGAs may have an advantage over FGAs in preventing relapse. An analysis by Leucht et al⁵ found lower relapse/treatment failure rates in 6 placebo-controlled SGA trials (total 983 patients), compared with 11 FGA trials (total 2,032 patients).

Although the data comparing SGAs with FGAs are controversial, SGAs seem to have lower EPS potential. Regardless of the type of antipsychotic, however, studies have shown that patients who relapse while taking antipsychotics have less-severe episodes than those who relapse after discontinuing their medications.

For patients who frequently forget or incorrectly take oral medications, long-acting depot antipsychotics may increase adherence and decrease relapse rates during the stable phase.⁶

3. Weight gain, cardiovascular risk

Cardiovascular disease is the leading cause of death among persons with schizophrenia,^7,8 whose life span is 10 to 20 years shorter than the population at large.⁹ Schizophrenia patients may be genetically predisposed to cardiovascular disease and metabolic syndrome (Table 3),¹⁰ exacerbated by typically sedentary lifestyles, high smoking rates, and poor diets. Certain SGAs add to the risk of weight gain and metabolic abnormalities.¹¹

Table 3

Does your patient have metabolic syndrome?

Table 4

Monitoring protocol for patients taking second-generation antipsychotics*

• using treatments that do not increase the risk for cardiovascular disease
  
• switching to agents with less weight gain liability if a patient’s weight increases >7% or his or her body mass index (BMI) increases 1 unit during antipsychotic therapy.
  

Mr. K remained stable on olanzapine for several years, but his blood glucose, cholesterol, and triglycerides have risen dramatically and he has gained 40 lbs. Although we were concerned that he might not respond as well to another SGA, we reviewed the risks and benefits with specific concern about his cardiovascular health. As a result, we switched him to aripiprazole, 15 mg/d, with close monitoring and supervision for signs of relapse.

SGAs’ heterogeneity. The ADA/APA statement and multiple clinical trials support differential risks of weight gain and metabolic abnormalities with SGAs (Table 5). Patients in CATIE phase 1 who were randomly assigned to olanzapine experienced greater total weight gain and monthly weight gain (mean +2 lb/month) than patients taking any other antipsychotic.¹³ In an analysis of change from baseline to last observation, 30% of patients in the olanzapine group gained >7% of their baseline weight, compared with 7% to 16% of patients taking other antipsychotics.

Table 5

Differential risks of weigh gain and metabolic abnormalities with SGAs

Mr. K remains free of positive symptoms after taking aripiprazole for several months. He complains less of daytime sedation and has lost >10 lbs. We are awaiting repeat glucose, cholesterol, and triglyceride serum levels. We will continue to monitor his weight and metabolic values and ensure that he receives primary care follow-up.

4. Eps and tardive dyskinesia

Compared with FGAs, SGAs may be associated with a lower incidence of tardive dyskinesia (TD) and extrapyramidal symptoms (EPS). Even so, routine screening for EPS and TD remains necessary, according to the Mount Sinai consensus conference on physical health monitoring of patients with schizophrenia.¹⁶ At every visit, we observe Mr. K for:

• facial movements (excessive blinking, puckering, lip smacking, sucking, or grimacing)
  
• decreased arm swing while walking or choreoathetoid-like or writhing limb or trunk movements.
  

In addition to screening for metabolic syndrome, EPS, and movement disorders, the Mount Sinai consensus conference¹⁶ offers guidelines for monitoring prolactin, cardiac, and ocular changes in patients taking antipsychotics.

5. Mood disorders, substance abuse

Screen schizophrenia outpatients for signs of anxiety, depression, mania, and substance abuse at every visit. An antidepressant trial is recommended for depressive episodes even if antipsychotic therapy has adequately reduced positive psychotic symptoms.¹⁷ This strategy can prevent depressive relapses and might help prevent psychotic relapse as well.¹⁸ Also consider adjunctive therapy such as:

• mood stabilizers for affective instability
  
• benzodiazepines for short-term anxiety or agitation
  
• tricyclics or selective serotonin reuptake inhibitors for comorbid anxiety disorders such as obsessive-compulsive or panic disorder.¹⁹
  

Because of Mr. K’s history of marijuana abuse, we tell him we will use random urine toxicology screens. We also order urine toxicology if patients behave abnormally or appear impaired. We counsel patients and families about the link between substance use and psychotic decompensation, which Mr. K has demonstrated several times.

We emphasize that the goal of repeated questioning and screening is to ensure Mr. K’s well-being. If he is using substances, we will refer him to the help he needs.

6. Prodromal signs of relapse

Mr. K has reported decreased sleep, increased irritability, increased social isolation, and some agitation before his acute psychotic decompensations. These symptoms form his prodrome for relapse, which we routinely assess at follow-up visits.

We question him about sleep, social contacts, irritability, and agitation; assess psychotic symptoms; and observe thought processes and behaviors. If a patient endorses or displays prodromal signs of relapse, we consider:

• Is he taking the medication?
  
• Is he abusing substances?
  
• Does a change in dosage (actual or a cytochrome P450-mediated drug-drug interaction) explain a decrease in efficacy?
  
• Is he under stress and need an increased antipsychotic dosage?
  
• Might psychosocial interventions (support groups, cognitive-behavioral therapy, family involvement, etc.) help him deal with symptoms, decrease stress, or avoid an exacerbation?
  
• Has medication been optimized (correct dosing, long enough duration), or does the patient need an increased dosage or a different antipsychotic?
  

7. Psychosocial interventions

Combining medications with psychosocial programs is most effective for maintaining remission and improving patients’ social and occupational functioning.¹⁷ For Mr. K we recommend these interventions:

Social skills training. Mr. K now meets with other schizophrenia patients and a moderator to set long-term goals and smaller, attainable goals as homework assignments each week. Patients get feedback, positive reinforcement, and the opportunity to practice new skills. Mr. K is working on improving family relationships, furthering his career, and improving his interpersonal skills.

Family therapy and education. We have met with Mr. K’s mother several times, and she now visits him regularly and speaks with him on the phone at least once a week. She attends Support and Family Education and National Alliance on Mental Illness meetings to increase her understanding of her son’s illness.

Alcoholics Anonymous/Marijuana Anonymous. We refer Mr. K to AA/MA groups; he attends 2 to 3 times per week and has a sponsor. He is not sober yet but has dramatically cut back his substance use and continues to express motivation to quit.

Related resources

• Torrey EF. Surviving schizophrenia: a manual for families, patients, and providers, 5th ed. New York: Harper Collins; 2006.
  
• Mueser KT, Gingerich S. The complete family guide to schizophrenia: helping your loved one get the most out of life. New York: Guilford Press; 2006.
  
• National Alliance on Mental Illness. Resources for schizophrenia patients and their families. www.nami.org.
  

• Aripiprazole • Abilify
  
• Clozapine • Clozaril
  
• Haloperidol • Haldol
  
• Olanzapine • Zyprexa
  
• Perphenazine • Trilafon
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Thioridazine • Mellaril
  
• Ziprasidone • Geodon
  

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

Dr. Marder receives research/grant support from Janssen Pharmaceutica and Eli Lilly and Co. and is a consultant or speaker for Bristol-Myers Squibb Co., Otsuka America Pharmaceutical, Pfizer, Solvay Pharmaceuticals, Merck and Co., and Roche.

Mr. K, age 34, has been hospitalized 4 times in 5 years for acute exacerbations of schizophrenia caused by medication nonadherence. This time he reports he discontinued antipsychotic therapy because he was “tired of taking medications every day.”

He spent 2 weeks in the acute inpatient psychiatric unit and restarted olanzapine—titrated to 15 mg/d—to which he responded well. When he presented to our outpatient clinic for follow-up, Mr. K reported adhering to his medications and denied positive symptoms. He complained of mild daytime sedation but no other side effects.

Schizophrenia patients spend most of their lives stable, rather than hospitalized for acute psychotic episodes. While stable, they continue to require close attention, and medical issues are particularly important during this time. Outpatient maintenance—such as optimizing antipsychotic therapy, offering psychosocial interventions, and monitoring physical health and well-being—provides opportunities to improve the course of illness for patients such as Mr. K.

This article describes a 7-point checkup to keep schizophrenia outpatients stable. It can help you maintain or improve patients’ function, prevent relapse, and monitor for adverse effects (Table 1).

Table 1

7-point checkup for assessing the stable schizophrenia patient

1. Symptom clusters

For several years, Mr. K worked as a research technician in a university lab, maintained an apartment, and attended to activities of daily living while taking olanzapine, 15 mg nightly. After discontinuing his medication, he reported auditory hallucinations, paranoid delusions, ideas of reference, and grossly disorganized thinking and behavior. He also was using marijuana daily, which exacerbated his psychotic symptoms and paranoia.

Addressing schizophrenia’s symptom clusters (Table 2) is key to improving patients’ social and occupational function and quality of life. Mr. K no longer has hallucinations, delusions, or disorganized thinking or behavior, but our evaluation shows his improvements are limited to schizophrenia’s positive symptoms.

Table 2

Schizophrenia’s 4 symptom clusters*

Cognitive symptoms. Mr. K’s concentration, attention, and memory are impaired, which interferes with his work. His ability to abstract is not impaired.

Affective symptoms. Mr. K denies signs or symptoms of depression, mania, hopelessness, or thoughts of wanting to hurt himself or anyone else.

Because antipsychotics do not adequately treat negative and cognitive symptoms, we will address these symptom clusters with psychosocial interventions.

2. Adherence

Nonadherence to medication is the most common cause of relapse and rehospitalization for patients with schizophrenia.¹ We find the following strategies helpful when encouraging, maintaining, and monitoring adherence to medications.

Normalize adherence and enlist patient participation.

We inform Mr. K that most patients have trouble taking medications every day and ask how he remembers. Brainstorming with patients on ways to remember to take medications increases their likelihood of participating.

Try reminder strategies. Recommend pillboxes, alarms, and other aids. Consider enlisting family members to help patients remember to take their medications every day.

Monitor prescriptions. We limit Mr. K’s prescription to 1 month so that we can assess the timeliness and consistency of refills.

Educate. Emphasize the link between adherence and wellness, and nonadherence and relapse-—which Mr. K has clearly demonstrated. We repeat this lesson on multiple visits and counsel any involved family members as well, so that everyone understands the importance of adherence to the patient’s continued well-being.

Look for signs of nonadherence. Because Mr. K discontinued his medications without telling his physician, we remain vigilant for signs of nonadherence—such as reemergence of hallucinations, delusions, paranoia, or ideas of reference—or sudden disappearance of a side effect—such as daytime sedation, which he has consistently reported with olanzapine.

Discontinuation rates in the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) suggest that many stable schizophrenia outpatients are dissatisfied with their medications. Most patients in all treatment groups changed their medications during the 18-month National Institute of Mental Health-sponsored trial.²

SGAs versus FGAs. Schizophrenia patients may be more likely to tolerate second-generation antipsychotics (SGAs) than first-generation antipsychotics (FGAs) because of FGAs’ higher risk of movement side effects such as akathisia. Some data suggest that patients find SGAs more tolerable overall, leading to lower discontinuation rates.³

Recent evidence, however, has cast doubt on the idea that SGAs are clinically superior to FGAs. The CUtLASS trial,⁴ for example, found no quality-of-life differences in patients using either class. Both FGAs and SGAs reduce the risk of relapse in stable patients, although SGAs may have an advantage over FGAs in preventing relapse. An analysis by Leucht et al⁵ found lower relapse/treatment failure rates in 6 placebo-controlled SGA trials (total 983 patients), compared with 11 FGA trials (total 2,032 patients).

Although the data comparing SGAs with FGAs are controversial, SGAs seem to have lower EPS potential. Regardless of the type of antipsychotic, however, studies have shown that patients who relapse while taking antipsychotics have less-severe episodes than those who relapse after discontinuing their medications.

For patients who frequently forget or incorrectly take oral medications, long-acting depot antipsychotics may increase adherence and decrease relapse rates during the stable phase.⁶

3. Weight gain, cardiovascular risk

Cardiovascular disease is the leading cause of death among persons with schizophrenia,^7,8 whose life span is 10 to 20 years shorter than the population at large.⁹ Schizophrenia patients may be genetically predisposed to cardiovascular disease and metabolic syndrome (Table 3),¹⁰ exacerbated by typically sedentary lifestyles, high smoking rates, and poor diets. Certain SGAs add to the risk of weight gain and metabolic abnormalities.¹¹

Table 3

Does your patient have metabolic syndrome?

Table 4

Monitoring protocol for patients taking second-generation antipsychotics*

• using treatments that do not increase the risk for cardiovascular disease
  
• switching to agents with less weight gain liability if a patient’s weight increases >7% or his or her body mass index (BMI) increases 1 unit during antipsychotic therapy.
  

Mr. K remained stable on olanzapine for several years, but his blood glucose, cholesterol, and triglycerides have risen dramatically and he has gained 40 lbs. Although we were concerned that he might not respond as well to another SGA, we reviewed the risks and benefits with specific concern about his cardiovascular health. As a result, we switched him to aripiprazole, 15 mg/d, with close monitoring and supervision for signs of relapse.

SGAs’ heterogeneity. The ADA/APA statement and multiple clinical trials support differential risks of weight gain and metabolic abnormalities with SGAs (Table 5). Patients in CATIE phase 1 who were randomly assigned to olanzapine experienced greater total weight gain and monthly weight gain (mean +2 lb/month) than patients taking any other antipsychotic.¹³ In an analysis of change from baseline to last observation, 30% of patients in the olanzapine group gained >7% of their baseline weight, compared with 7% to 16% of patients taking other antipsychotics.

Table 5

Differential risks of weigh gain and metabolic abnormalities with SGAs

Mr. K remains free of positive symptoms after taking aripiprazole for several months. He complains less of daytime sedation and has lost >10 lbs. We are awaiting repeat glucose, cholesterol, and triglyceride serum levels. We will continue to monitor his weight and metabolic values and ensure that he receives primary care follow-up.

4. Eps and tardive dyskinesia

Compared with FGAs, SGAs may be associated with a lower incidence of tardive dyskinesia (TD) and extrapyramidal symptoms (EPS). Even so, routine screening for EPS and TD remains necessary, according to the Mount Sinai consensus conference on physical health monitoring of patients with schizophrenia.¹⁶ At every visit, we observe Mr. K for:

• facial movements (excessive blinking, puckering, lip smacking, sucking, or grimacing)
  
• decreased arm swing while walking or choreoathetoid-like or writhing limb or trunk movements.
  

In addition to screening for metabolic syndrome, EPS, and movement disorders, the Mount Sinai consensus conference¹⁶ offers guidelines for monitoring prolactin, cardiac, and ocular changes in patients taking antipsychotics.

5. Mood disorders, substance abuse

Screen schizophrenia outpatients for signs of anxiety, depression, mania, and substance abuse at every visit. An antidepressant trial is recommended for depressive episodes even if antipsychotic therapy has adequately reduced positive psychotic symptoms.¹⁷ This strategy can prevent depressive relapses and might help prevent psychotic relapse as well.¹⁸ Also consider adjunctive therapy such as:

• mood stabilizers for affective instability
  
• benzodiazepines for short-term anxiety or agitation
  
• tricyclics or selective serotonin reuptake inhibitors for comorbid anxiety disorders such as obsessive-compulsive or panic disorder.¹⁹
  

Because of Mr. K’s history of marijuana abuse, we tell him we will use random urine toxicology screens. We also order urine toxicology if patients behave abnormally or appear impaired. We counsel patients and families about the link between substance use and psychotic decompensation, which Mr. K has demonstrated several times.

We emphasize that the goal of repeated questioning and screening is to ensure Mr. K’s well-being. If he is using substances, we will refer him to the help he needs.

6. Prodromal signs of relapse

Mr. K has reported decreased sleep, increased irritability, increased social isolation, and some agitation before his acute psychotic decompensations. These symptoms form his prodrome for relapse, which we routinely assess at follow-up visits.

We question him about sleep, social contacts, irritability, and agitation; assess psychotic symptoms; and observe thought processes and behaviors. If a patient endorses or displays prodromal signs of relapse, we consider:

• Is he taking the medication?
  
• Is he abusing substances?
  
• Does a change in dosage (actual or a cytochrome P450-mediated drug-drug interaction) explain a decrease in efficacy?
  
• Is he under stress and need an increased antipsychotic dosage?
  
• Might psychosocial interventions (support groups, cognitive-behavioral therapy, family involvement, etc.) help him deal with symptoms, decrease stress, or avoid an exacerbation?
  
• Has medication been optimized (correct dosing, long enough duration), or does the patient need an increased dosage or a different antipsychotic?
  

7. Psychosocial interventions

Combining medications with psychosocial programs is most effective for maintaining remission and improving patients’ social and occupational functioning.¹⁷ For Mr. K we recommend these interventions:

Social skills training. Mr. K now meets with other schizophrenia patients and a moderator to set long-term goals and smaller, attainable goals as homework assignments each week. Patients get feedback, positive reinforcement, and the opportunity to practice new skills. Mr. K is working on improving family relationships, furthering his career, and improving his interpersonal skills.

Family therapy and education. We have met with Mr. K’s mother several times, and she now visits him regularly and speaks with him on the phone at least once a week. She attends Support and Family Education and National Alliance on Mental Illness meetings to increase her understanding of her son’s illness.

Alcoholics Anonymous/Marijuana Anonymous. We refer Mr. K to AA/MA groups; he attends 2 to 3 times per week and has a sponsor. He is not sober yet but has dramatically cut back his substance use and continues to express motivation to quit.

Related resources

• Torrey EF. Surviving schizophrenia: a manual for families, patients, and providers, 5th ed. New York: Harper Collins; 2006.
  
• Mueser KT, Gingerich S. The complete family guide to schizophrenia: helping your loved one get the most out of life. New York: Guilford Press; 2006.
  
• National Alliance on Mental Illness. Resources for schizophrenia patients and their families. www.nami.org.
  

• Aripiprazole • Abilify
  
• Clozapine • Clozaril
  
• Haloperidol • Haldol
  
• Olanzapine • Zyprexa
  
• Perphenazine • Trilafon
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Thioridazine • Mellaril
  
• Ziprasidone • Geodon
  

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

Dr. Marder receives research/grant support from Janssen Pharmaceutica and Eli Lilly and Co. and is a consultant or speaker for Bristol-Myers Squibb Co., Otsuka America Pharmaceutical, Pfizer, Solvay Pharmaceuticals, Merck and Co., and Roche.

Mr. K, age 34, has been hospitalized 4 times in 5 years for acute exacerbations of schizophrenia caused by medication nonadherence. This time he reports he discontinued antipsychotic therapy because he was “tired of taking medications every day.”

He spent 2 weeks in the acute inpatient psychiatric unit and restarted olanzapine—titrated to 15 mg/d—to which he responded well. When he presented to our outpatient clinic for follow-up, Mr. K reported adhering to his medications and denied positive symptoms. He complained of mild daytime sedation but no other side effects.

Schizophrenia patients spend most of their lives stable, rather than hospitalized for acute psychotic episodes. While stable, they continue to require close attention, and medical issues are particularly important during this time. Outpatient maintenance—such as optimizing antipsychotic therapy, offering psychosocial interventions, and monitoring physical health and well-being—provides opportunities to improve the course of illness for patients such as Mr. K.

This article describes a 7-point checkup to keep schizophrenia outpatients stable. It can help you maintain or improve patients’ function, prevent relapse, and monitor for adverse effects (Table 1).

Table 1

7-point checkup for assessing the stable schizophrenia patient

1. Symptom clusters

For several years, Mr. K worked as a research technician in a university lab, maintained an apartment, and attended to activities of daily living while taking olanzapine, 15 mg nightly. After discontinuing his medication, he reported auditory hallucinations, paranoid delusions, ideas of reference, and grossly disorganized thinking and behavior. He also was using marijuana daily, which exacerbated his psychotic symptoms and paranoia.

Addressing schizophrenia’s symptom clusters (Table 2) is key to improving patients’ social and occupational function and quality of life. Mr. K no longer has hallucinations, delusions, or disorganized thinking or behavior, but our evaluation shows his improvements are limited to schizophrenia’s positive symptoms.

Table 2

Schizophrenia’s 4 symptom clusters*

Cognitive symptoms. Mr. K’s concentration, attention, and memory are impaired, which interferes with his work. His ability to abstract is not impaired.

Affective symptoms. Mr. K denies signs or symptoms of depression, mania, hopelessness, or thoughts of wanting to hurt himself or anyone else.

Because antipsychotics do not adequately treat negative and cognitive symptoms, we will address these symptom clusters with psychosocial interventions.

2. Adherence

Nonadherence to medication is the most common cause of relapse and rehospitalization for patients with schizophrenia.¹ We find the following strategies helpful when encouraging, maintaining, and monitoring adherence to medications.

Normalize adherence and enlist patient participation.

We inform Mr. K that most patients have trouble taking medications every day and ask how he remembers. Brainstorming with patients on ways to remember to take medications increases their likelihood of participating.

Try reminder strategies. Recommend pillboxes, alarms, and other aids. Consider enlisting family members to help patients remember to take their medications every day.

Monitor prescriptions. We limit Mr. K’s prescription to 1 month so that we can assess the timeliness and consistency of refills.

Educate. Emphasize the link between adherence and wellness, and nonadherence and relapse-—which Mr. K has clearly demonstrated. We repeat this lesson on multiple visits and counsel any involved family members as well, so that everyone understands the importance of adherence to the patient’s continued well-being.

Look for signs of nonadherence. Because Mr. K discontinued his medications without telling his physician, we remain vigilant for signs of nonadherence—such as reemergence of hallucinations, delusions, paranoia, or ideas of reference—or sudden disappearance of a side effect—such as daytime sedation, which he has consistently reported with olanzapine.

Discontinuation rates in the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) suggest that many stable schizophrenia outpatients are dissatisfied with their medications. Most patients in all treatment groups changed their medications during the 18-month National Institute of Mental Health-sponsored trial.²

SGAs versus FGAs. Schizophrenia patients may be more likely to tolerate second-generation antipsychotics (SGAs) than first-generation antipsychotics (FGAs) because of FGAs’ higher risk of movement side effects such as akathisia. Some data suggest that patients find SGAs more tolerable overall, leading to lower discontinuation rates.³

Recent evidence, however, has cast doubt on the idea that SGAs are clinically superior to FGAs. The CUtLASS trial,⁴ for example, found no quality-of-life differences in patients using either class. Both FGAs and SGAs reduce the risk of relapse in stable patients, although SGAs may have an advantage over FGAs in preventing relapse. An analysis by Leucht et al⁵ found lower relapse/treatment failure rates in 6 placebo-controlled SGA trials (total 983 patients), compared with 11 FGA trials (total 2,032 patients).

Although the data comparing SGAs with FGAs are controversial, SGAs seem to have lower EPS potential. Regardless of the type of antipsychotic, however, studies have shown that patients who relapse while taking antipsychotics have less-severe episodes than those who relapse after discontinuing their medications.

For patients who frequently forget or incorrectly take oral medications, long-acting depot antipsychotics may increase adherence and decrease relapse rates during the stable phase.⁶

3. Weight gain, cardiovascular risk

Cardiovascular disease is the leading cause of death among persons with schizophrenia,^7,8 whose life span is 10 to 20 years shorter than the population at large.⁹ Schizophrenia patients may be genetically predisposed to cardiovascular disease and metabolic syndrome (Table 3),¹⁰ exacerbated by typically sedentary lifestyles, high smoking rates, and poor diets. Certain SGAs add to the risk of weight gain and metabolic abnormalities.¹¹

Table 3

Does your patient have metabolic syndrome?

Table 4

Monitoring protocol for patients taking second-generation antipsychotics*

• using treatments that do not increase the risk for cardiovascular disease
  
• switching to agents with less weight gain liability if a patient’s weight increases >7% or his or her body mass index (BMI) increases 1 unit during antipsychotic therapy.
  

Mr. K remained stable on olanzapine for several years, but his blood glucose, cholesterol, and triglycerides have risen dramatically and he has gained 40 lbs. Although we were concerned that he might not respond as well to another SGA, we reviewed the risks and benefits with specific concern about his cardiovascular health. As a result, we switched him to aripiprazole, 15 mg/d, with close monitoring and supervision for signs of relapse.

SGAs’ heterogeneity. The ADA/APA statement and multiple clinical trials support differential risks of weight gain and metabolic abnormalities with SGAs (Table 5). Patients in CATIE phase 1 who were randomly assigned to olanzapine experienced greater total weight gain and monthly weight gain (mean +2 lb/month) than patients taking any other antipsychotic.¹³ In an analysis of change from baseline to last observation, 30% of patients in the olanzapine group gained >7% of their baseline weight, compared with 7% to 16% of patients taking other antipsychotics.

Table 5

Differential risks of weigh gain and metabolic abnormalities with SGAs

Mr. K remains free of positive symptoms after taking aripiprazole for several months. He complains less of daytime sedation and has lost >10 lbs. We are awaiting repeat glucose, cholesterol, and triglyceride serum levels. We will continue to monitor his weight and metabolic values and ensure that he receives primary care follow-up.

4. Eps and tardive dyskinesia

Compared with FGAs, SGAs may be associated with a lower incidence of tardive dyskinesia (TD) and extrapyramidal symptoms (EPS). Even so, routine screening for EPS and TD remains necessary, according to the Mount Sinai consensus conference on physical health monitoring of patients with schizophrenia.¹⁶ At every visit, we observe Mr. K for:

• facial movements (excessive blinking, puckering, lip smacking, sucking, or grimacing)
  
• decreased arm swing while walking or choreoathetoid-like or writhing limb or trunk movements.
  

In addition to screening for metabolic syndrome, EPS, and movement disorders, the Mount Sinai consensus conference¹⁶ offers guidelines for monitoring prolactin, cardiac, and ocular changes in patients taking antipsychotics.

5. Mood disorders, substance abuse

Screen schizophrenia outpatients for signs of anxiety, depression, mania, and substance abuse at every visit. An antidepressant trial is recommended for depressive episodes even if antipsychotic therapy has adequately reduced positive psychotic symptoms.¹⁷ This strategy can prevent depressive relapses and might help prevent psychotic relapse as well.¹⁸ Also consider adjunctive therapy such as:

• mood stabilizers for affective instability
  
• benzodiazepines for short-term anxiety or agitation
  
• tricyclics or selective serotonin reuptake inhibitors for comorbid anxiety disorders such as obsessive-compulsive or panic disorder.¹⁹
  

Because of Mr. K’s history of marijuana abuse, we tell him we will use random urine toxicology screens. We also order urine toxicology if patients behave abnormally or appear impaired. We counsel patients and families about the link between substance use and psychotic decompensation, which Mr. K has demonstrated several times.

We emphasize that the goal of repeated questioning and screening is to ensure Mr. K’s well-being. If he is using substances, we will refer him to the help he needs.

6. Prodromal signs of relapse

Mr. K has reported decreased sleep, increased irritability, increased social isolation, and some agitation before his acute psychotic decompensations. These symptoms form his prodrome for relapse, which we routinely assess at follow-up visits.

We question him about sleep, social contacts, irritability, and agitation; assess psychotic symptoms; and observe thought processes and behaviors. If a patient endorses or displays prodromal signs of relapse, we consider:

• Is he taking the medication?
  
• Is he abusing substances?
  
• Does a change in dosage (actual or a cytochrome P450-mediated drug-drug interaction) explain a decrease in efficacy?
  
• Is he under stress and need an increased antipsychotic dosage?
  
• Might psychosocial interventions (support groups, cognitive-behavioral therapy, family involvement, etc.) help him deal with symptoms, decrease stress, or avoid an exacerbation?
  
• Has medication been optimized (correct dosing, long enough duration), or does the patient need an increased dosage or a different antipsychotic?
  

7. Psychosocial interventions

Combining medications with psychosocial programs is most effective for maintaining remission and improving patients’ social and occupational functioning.¹⁷ For Mr. K we recommend these interventions:

Social skills training. Mr. K now meets with other schizophrenia patients and a moderator to set long-term goals and smaller, attainable goals as homework assignments each week. Patients get feedback, positive reinforcement, and the opportunity to practice new skills. Mr. K is working on improving family relationships, furthering his career, and improving his interpersonal skills.

Family therapy and education. We have met with Mr. K’s mother several times, and she now visits him regularly and speaks with him on the phone at least once a week. She attends Support and Family Education and National Alliance on Mental Illness meetings to increase her understanding of her son’s illness.

Alcoholics Anonymous/Marijuana Anonymous. We refer Mr. K to AA/MA groups; he attends 2 to 3 times per week and has a sponsor. He is not sober yet but has dramatically cut back his substance use and continues to express motivation to quit.

Related resources

• Torrey EF. Surviving schizophrenia: a manual for families, patients, and providers, 5th ed. New York: Harper Collins; 2006.
  
• Mueser KT, Gingerich S. The complete family guide to schizophrenia: helping your loved one get the most out of life. New York: Guilford Press; 2006.
  
• National Alliance on Mental Illness. Resources for schizophrenia patients and their families. www.nami.org.
  

• Aripiprazole • Abilify
  
• Clozapine • Clozaril
  
• Haloperidol • Haldol
  
• Olanzapine • Zyprexa
  
• Perphenazine • Trilafon
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Thioridazine • Mellaril
  
• Ziprasidone • Geodon
  

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

Dr. Marder receives research/grant support from Janssen Pharmaceutica and Eli Lilly and Co. and is a consultant or speaker for Bristol-Myers Squibb Co., Otsuka America Pharmaceutical, Pfizer, Solvay Pharmaceuticals, Merck and Co., and Roche.