Current Psychiatry

General psychiatry practitioners such as myself traditionally have relied on writing case reports to describe our clinical experience. One obstacle to getting cases published is that many research journals require submitted articles to include large samples and rating scales as measures of change in the conditions of patients being studied.

I have published articles about my clinical experiences using patient data collected with the Clinical Global Impressions (CGI) scale and other standardized tests. Research instruments such as the CGI can gather empiric data and are easy to use in clinical practice.¹

This article describes how routine standardized testing provides useful data for research and improves diagnostic accuracy—and patient outcomes—even before I meet my patients for the first time.

Why use standardized tests?

Benefits. All my new patients undergo screening before their first face-to-face meeting with a psychiatrist. This registration visit takes about 2 hours, after which they are scheduled for an appointment based on clinical urgency. We charge no fee for the screening visit; the benefits of gathering a comprehensive database before the clinical evaluation outweigh the cost of the tests, software, and staff time.

Along with completing insurance and biographical paperwork, patients perform self-administered psychosocial and medical histories and a battery of standardized tests. This information allows me to focus on interpersonal issues—rather than fact-finding—during the first interview. It also ensures a comprehensive patient history.

Box 1

Limitations. One limitation to using rating scales to publish experiences in clinical practice is that clinical need, rather than a research protocol, determines the frequency of visits. Another is that we ask patients to rate symptoms they experience in the week before office visits. Thus, the data do not capture changes that occurred in other weeks.

Standardized tests we use

Except for the Quick Inventory of Depressive Symptomatology (QIDS), I selected the tests I use in the late 1980s because of:

• their ease of use and affordability
  
• my familiarity with them from my academic work
  
• their suitability for a mood disorder clinical practice such as mine.
  

Psychosocial history. Patients use an office computer to complete a questionnaire about family and developmental history, financial and employment history, education, health, alcohol and drug history, current stressors, and the presenting problem. Software from Multi-Health Systems (See Related Resources) allows me to add or remove questions as needed.

To ensure privacy when the next patient uses the computer, each patient’s report is deleted after it is printed. I receive the printed report, which details all responses and flags those that may require clarification.

Medical history. A standardized form asks patients about whether they have had most common medical conditions, their present symptoms, and family members’ health. An additional form inquires into psychiatric treatment, family history of psychiatric illnesses, and present medications.

Mini-SCID. The Mini-SCID has several advantages over the Structured Clinical Interview for DSM (SCID):

• Patients self-administer the test on a computer at the office.
  
• For research purposes, Mini-SCID results are protected from clinician biases because patients are interviewed using uniform questions and circumstances.
  

Box 2

Symptom Checklist-90 (SCL-90). This tool adds another layer of support for bipolar illness diagnosis (Box 1). It also is useful in conjunction with rating scales specific to other diagnostic categories, such as depression and anxiety.

The SCL-90³ consists of 90 statements that measure the severity of 9 dimensions of psychopathology: somatization, obsession-compulsion, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoid ideation, and psychoticism. Using a scale of 0 (not at all) to 4 (a great deal), patients rate how much they are bothered by the feelings expressed in each statement.

In its standard scoring, the SCL-90 returns a score for 9 scales. Hunter et al⁴ developed an alternate set of 8 scales that uses SCL-90 questions to screen for depression, mania, schizophrenia, antisocial personality disorder, somatization disorder, obsessive-compulsive disorder, panic disorder, and agoraphobia. These SCL-90 diagnostic scales showed good reliability as an aid to the Mini-SCID in identifying diagnoses among 1,457 adult psychiatric outpatients.

Clinical Global Impressions scale. The CGI uses a 7-point Likert scale to describe the clinician’s impression of change in a patient’s condition. This scale:

• transcends symptom checklists by incorporating knowledge of the patient’s history, symptoms, and behaviors
  
• lends itself easily to repeated measures of change and severity of the condition being rated.¹
  

Every office visit

At the screening visit and before every office visit, my patients complete 2 depression rating tests to document changes between visits and over time: a visual analog scale (VAS) and the QIDS.

The VAS’ 10-cm line with the left side marked “worst ever” and the right side marked “best ever” is a simple tool. It captures patients’ subjective impressions of their mood states in answer to the question, “How do you feel today?” I used the VAS as an outcome measure in a study of modafinil augmentation of antidepressant therapy.⁷

The QIDS is a 16-item screen that measures 9 depressive symptoms.⁸ It has been validated against the Hamilton Depression Rating Scale (HAM-D)⁹ and was used as the outcome measure in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial.¹⁰ The QIDS-16 is available online for free use in many languages (see Related Resources).¹¹

Until recently, our office performed routine depression screening with the 52-item Carroll Depression Rating Scale (CDRS),¹³ a self-administered inventory designed to mirror results from the HAM-D. I published articles using the CDRS as the primary outcome measure in a chart review of long-term effectiveness of antidepressant monotherapy (Box 3)^13,14 and in a study of modafinil’s effectiveness as adjunctive therapy in patients with unipolar depression.⁷

Box 3

Logistical concerns

Patient feedback. Although some patients complain about having to complete depression rating scales at every visit, most accept this as equivalent to having routine blood pressure measurements. Many become interested in tracking their improvement by test scores in addition to subjective feelings.

Related resources

• Multi-Health Systems. Publishers of mental health assessment tools. www.mhs.com.
  
• Inventory of Depressive Symptomatology (IDS) and Quick Inventory of Depressive Symptomatology (QIDS). www.ids-qids.org.
  

• Modafinil • Provigil
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  

Dr. Nasr is a speaker for Takeda Pharmaceutical Company, Pfizer Inc, Eli Lilly and Company, Bristol-Myers Squibb, Forest Pharmaceuticals, and GlaxoSmithKline.

Acknowledgment

Dr. Nasr acknowledges the contribution of research assistant Burdette J. Wendt, who collects and analyzes the data referenced above and helped prepare this manuscript.

HIPAA. The Health Insurance Portability and Accountability Act (HIPAA) allows publication of large-scale studies that do not identify patients individually. We also obtained permission from the local Institutional Review Board to disseminate non-identifying cumulative data.

General psychiatry practitioners such as myself traditionally have relied on writing case reports to describe our clinical experience. One obstacle to getting cases published is that many research journals require submitted articles to include large samples and rating scales as measures of change in the conditions of patients being studied.

I have published articles about my clinical experiences using patient data collected with the Clinical Global Impressions (CGI) scale and other standardized tests. Research instruments such as the CGI can gather empiric data and are easy to use in clinical practice.¹

This article describes how routine standardized testing provides useful data for research and improves diagnostic accuracy—and patient outcomes—even before I meet my patients for the first time.

Why use standardized tests?

Benefits. All my new patients undergo screening before their first face-to-face meeting with a psychiatrist. This registration visit takes about 2 hours, after which they are scheduled for an appointment based on clinical urgency. We charge no fee for the screening visit; the benefits of gathering a comprehensive database before the clinical evaluation outweigh the cost of the tests, software, and staff time.

Along with completing insurance and biographical paperwork, patients perform self-administered psychosocial and medical histories and a battery of standardized tests. This information allows me to focus on interpersonal issues—rather than fact-finding—during the first interview. It also ensures a comprehensive patient history.

Box 1

Limitations. One limitation to using rating scales to publish experiences in clinical practice is that clinical need, rather than a research protocol, determines the frequency of visits. Another is that we ask patients to rate symptoms they experience in the week before office visits. Thus, the data do not capture changes that occurred in other weeks.

Standardized tests we use

Except for the Quick Inventory of Depressive Symptomatology (QIDS), I selected the tests I use in the late 1980s because of:

• their ease of use and affordability
  
• my familiarity with them from my academic work
  
• their suitability for a mood disorder clinical practice such as mine.
  

Psychosocial history. Patients use an office computer to complete a questionnaire about family and developmental history, financial and employment history, education, health, alcohol and drug history, current stressors, and the presenting problem. Software from Multi-Health Systems (See Related Resources) allows me to add or remove questions as needed.

To ensure privacy when the next patient uses the computer, each patient’s report is deleted after it is printed. I receive the printed report, which details all responses and flags those that may require clarification.

Medical history. A standardized form asks patients about whether they have had most common medical conditions, their present symptoms, and family members’ health. An additional form inquires into psychiatric treatment, family history of psychiatric illnesses, and present medications.

Mini-SCID. The Mini-SCID has several advantages over the Structured Clinical Interview for DSM (SCID):

• Patients self-administer the test on a computer at the office.
  
• For research purposes, Mini-SCID results are protected from clinician biases because patients are interviewed using uniform questions and circumstances.
  

Box 2

Symptom Checklist-90 (SCL-90). This tool adds another layer of support for bipolar illness diagnosis (Box 1). It also is useful in conjunction with rating scales specific to other diagnostic categories, such as depression and anxiety.

The SCL-90³ consists of 90 statements that measure the severity of 9 dimensions of psychopathology: somatization, obsession-compulsion, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoid ideation, and psychoticism. Using a scale of 0 (not at all) to 4 (a great deal), patients rate how much they are bothered by the feelings expressed in each statement.

In its standard scoring, the SCL-90 returns a score for 9 scales. Hunter et al⁴ developed an alternate set of 8 scales that uses SCL-90 questions to screen for depression, mania, schizophrenia, antisocial personality disorder, somatization disorder, obsessive-compulsive disorder, panic disorder, and agoraphobia. These SCL-90 diagnostic scales showed good reliability as an aid to the Mini-SCID in identifying diagnoses among 1,457 adult psychiatric outpatients.

Clinical Global Impressions scale. The CGI uses a 7-point Likert scale to describe the clinician’s impression of change in a patient’s condition. This scale:

• transcends symptom checklists by incorporating knowledge of the patient’s history, symptoms, and behaviors
  
• lends itself easily to repeated measures of change and severity of the condition being rated.¹
  

Every office visit

At the screening visit and before every office visit, my patients complete 2 depression rating tests to document changes between visits and over time: a visual analog scale (VAS) and the QIDS.

The VAS’ 10-cm line with the left side marked “worst ever” and the right side marked “best ever” is a simple tool. It captures patients’ subjective impressions of their mood states in answer to the question, “How do you feel today?” I used the VAS as an outcome measure in a study of modafinil augmentation of antidepressant therapy.⁷

The QIDS is a 16-item screen that measures 9 depressive symptoms.⁸ It has been validated against the Hamilton Depression Rating Scale (HAM-D)⁹ and was used as the outcome measure in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial.¹⁰ The QIDS-16 is available online for free use in many languages (see Related Resources).¹¹

Until recently, our office performed routine depression screening with the 52-item Carroll Depression Rating Scale (CDRS),¹³ a self-administered inventory designed to mirror results from the HAM-D. I published articles using the CDRS as the primary outcome measure in a chart review of long-term effectiveness of antidepressant monotherapy (Box 3)^13,14 and in a study of modafinil’s effectiveness as adjunctive therapy in patients with unipolar depression.⁷

Box 3

Logistical concerns

Patient feedback. Although some patients complain about having to complete depression rating scales at every visit, most accept this as equivalent to having routine blood pressure measurements. Many become interested in tracking their improvement by test scores in addition to subjective feelings.

Related resources

• Multi-Health Systems. Publishers of mental health assessment tools. www.mhs.com.
  
• Inventory of Depressive Symptomatology (IDS) and Quick Inventory of Depressive Symptomatology (QIDS). www.ids-qids.org.
  

• Modafinil • Provigil
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  

Dr. Nasr is a speaker for Takeda Pharmaceutical Company, Pfizer Inc, Eli Lilly and Company, Bristol-Myers Squibb, Forest Pharmaceuticals, and GlaxoSmithKline.

Acknowledgment

Dr. Nasr acknowledges the contribution of research assistant Burdette J. Wendt, who collects and analyzes the data referenced above and helped prepare this manuscript.

HIPAA. The Health Insurance Portability and Accountability Act (HIPAA) allows publication of large-scale studies that do not identify patients individually. We also obtained permission from the local Institutional Review Board to disseminate non-identifying cumulative data.

General psychiatry practitioners such as myself traditionally have relied on writing case reports to describe our clinical experience. One obstacle to getting cases published is that many research journals require submitted articles to include large samples and rating scales as measures of change in the conditions of patients being studied.

I have published articles about my clinical experiences using patient data collected with the Clinical Global Impressions (CGI) scale and other standardized tests. Research instruments such as the CGI can gather empiric data and are easy to use in clinical practice.¹

This article describes how routine standardized testing provides useful data for research and improves diagnostic accuracy—and patient outcomes—even before I meet my patients for the first time.

Why use standardized tests?

Benefits. All my new patients undergo screening before their first face-to-face meeting with a psychiatrist. This registration visit takes about 2 hours, after which they are scheduled for an appointment based on clinical urgency. We charge no fee for the screening visit; the benefits of gathering a comprehensive database before the clinical evaluation outweigh the cost of the tests, software, and staff time.

Along with completing insurance and biographical paperwork, patients perform self-administered psychosocial and medical histories and a battery of standardized tests. This information allows me to focus on interpersonal issues—rather than fact-finding—during the first interview. It also ensures a comprehensive patient history.

Box 1

Limitations. One limitation to using rating scales to publish experiences in clinical practice is that clinical need, rather than a research protocol, determines the frequency of visits. Another is that we ask patients to rate symptoms they experience in the week before office visits. Thus, the data do not capture changes that occurred in other weeks.

Standardized tests we use

Except for the Quick Inventory of Depressive Symptomatology (QIDS), I selected the tests I use in the late 1980s because of:

• their ease of use and affordability
  
• my familiarity with them from my academic work
  
• their suitability for a mood disorder clinical practice such as mine.
  

Psychosocial history. Patients use an office computer to complete a questionnaire about family and developmental history, financial and employment history, education, health, alcohol and drug history, current stressors, and the presenting problem. Software from Multi-Health Systems (See Related Resources) allows me to add or remove questions as needed.

To ensure privacy when the next patient uses the computer, each patient’s report is deleted after it is printed. I receive the printed report, which details all responses and flags those that may require clarification.

Medical history. A standardized form asks patients about whether they have had most common medical conditions, their present symptoms, and family members’ health. An additional form inquires into psychiatric treatment, family history of psychiatric illnesses, and present medications.

Mini-SCID. The Mini-SCID has several advantages over the Structured Clinical Interview for DSM (SCID):

• Patients self-administer the test on a computer at the office.
  
• For research purposes, Mini-SCID results are protected from clinician biases because patients are interviewed using uniform questions and circumstances.
  

Box 2

Symptom Checklist-90 (SCL-90). This tool adds another layer of support for bipolar illness diagnosis (Box 1). It also is useful in conjunction with rating scales specific to other diagnostic categories, such as depression and anxiety.

The SCL-90³ consists of 90 statements that measure the severity of 9 dimensions of psychopathology: somatization, obsession-compulsion, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoid ideation, and psychoticism. Using a scale of 0 (not at all) to 4 (a great deal), patients rate how much they are bothered by the feelings expressed in each statement.

In its standard scoring, the SCL-90 returns a score for 9 scales. Hunter et al⁴ developed an alternate set of 8 scales that uses SCL-90 questions to screen for depression, mania, schizophrenia, antisocial personality disorder, somatization disorder, obsessive-compulsive disorder, panic disorder, and agoraphobia. These SCL-90 diagnostic scales showed good reliability as an aid to the Mini-SCID in identifying diagnoses among 1,457 adult psychiatric outpatients.

Clinical Global Impressions scale. The CGI uses a 7-point Likert scale to describe the clinician’s impression of change in a patient’s condition. This scale:

• transcends symptom checklists by incorporating knowledge of the patient’s history, symptoms, and behaviors
  
• lends itself easily to repeated measures of change and severity of the condition being rated.¹
  

Every office visit

At the screening visit and before every office visit, my patients complete 2 depression rating tests to document changes between visits and over time: a visual analog scale (VAS) and the QIDS.

The VAS’ 10-cm line with the left side marked “worst ever” and the right side marked “best ever” is a simple tool. It captures patients’ subjective impressions of their mood states in answer to the question, “How do you feel today?” I used the VAS as an outcome measure in a study of modafinil augmentation of antidepressant therapy.⁷

The QIDS is a 16-item screen that measures 9 depressive symptoms.⁸ It has been validated against the Hamilton Depression Rating Scale (HAM-D)⁹ and was used as the outcome measure in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial.¹⁰ The QIDS-16 is available online for free use in many languages (see Related Resources).¹¹

Until recently, our office performed routine depression screening with the 52-item Carroll Depression Rating Scale (CDRS),¹³ a self-administered inventory designed to mirror results from the HAM-D. I published articles using the CDRS as the primary outcome measure in a chart review of long-term effectiveness of antidepressant monotherapy (Box 3)^13,14 and in a study of modafinil’s effectiveness as adjunctive therapy in patients with unipolar depression.⁷

Box 3

Logistical concerns

Patient feedback. Although some patients complain about having to complete depression rating scales at every visit, most accept this as equivalent to having routine blood pressure measurements. Many become interested in tracking their improvement by test scores in addition to subjective feelings.

Related resources

• Multi-Health Systems. Publishers of mental health assessment tools. www.mhs.com.
  
• Inventory of Depressive Symptomatology (IDS) and Quick Inventory of Depressive Symptomatology (QIDS). www.ids-qids.org.
  

• Modafinil • Provigil
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  

Dr. Nasr is a speaker for Takeda Pharmaceutical Company, Pfizer Inc, Eli Lilly and Company, Bristol-Myers Squibb, Forest Pharmaceuticals, and GlaxoSmithKline.

Acknowledgment

Dr. Nasr acknowledges the contribution of research assistant Burdette J. Wendt, who collects and analyzes the data referenced above and helped prepare this manuscript.

HIPAA. The Health Insurance Portability and Accountability Act (HIPAA) allows publication of large-scale studies that do not identify patients individually. We also obtained permission from the local Institutional Review Board to disseminate non-identifying cumulative data.

Sexual disorders such as premature ejaculation, erectile dysfunction (ED), and low libido reduce quality of life in patients with depression, anxiety, and other psychiatric illnesses. In addition, sexual dysfunction is a side effect of many drugs used to treat psychiatric disorders.¹

Psychiatry—with its biopsychosocial model—can easily assume the evaluation and treatment of sexual disorders. To inform your practice, this article provides an update on pharmacotherapy for the 3 most common sexual disorders. Its emphasis on biologic treatment is not intended to minimize the importance of psychological interventions.

Premature ejaculation

Premature ejaculation is one of the most common male sexual complaints. In some surveys, approximately 30% of men express concern about ejaculating too rapidly.² Behavioral therapy often is effective (Box 1), but in my experience most male patients prefer a pharmacologic approach to sexual problems.

Anesthetic creams. Locally applied anesthetic creams—such as prilocaine, lidocaine mixtures, and creams consisting of natural herbs—can increase ejaculatory latency by approximately 7 to 10 minutes. The major side effect of these preparations is penile hypoanesthesia. The man also must use a condom or wash off the cream before vaginal penetration to minimize vaginal absorption.³

Box 1

Among the SSRIs, paroxetine appears to have the greatest effect on ejaculatory latency (Table 1).⁵ Most trials have found that the dose needed to delay ejaculation is similar to the dose necessary to treat depressive disorders.

Some case reports suggest that phosphodiesterase type 5 inhibitors (PDE-5 inhibitors) may help to delay ejaculation, but this effect has not been borne out in double-blind studies.⁶

Table 1

Drug treatment options for premature ejaculation

Erectile dysfunction

Men with major depressive disorder, anxiety disorders, and psychotic disorders have higher rates of ED, compared with the general male population. ED also can be a side effect of—and adversely affect adherence to—antidepressant and antipsychotic therapy.⁷ Restored erectile function can positively affect patients’ self-esteem and sense of personal efficacy and may facilitate recovery from depression.⁸

PDE-5 inhibitors. Nitric oxide release triggers the production of cyclic guanosine monophosphate, which leads to decreased intracellular calcium, smooth muscle relaxation, and penile erection. All available PDE-5 inhibitors work by inhibiting the degradation of cyclic guanosine monophosphate. They are highly specific, vary somewhat in selectivity for other phosphodiesterase enzyme types, and differ in duration of action (Table 2).

Common side effects include dyspepsia, stuffy nose, and headache. The use of PDE-5 inhibitors with nitrates is contraindicated because of the risk of severe hypotension. Use PDE-5 inhibitors cautiously:

• with alpha blockers because of the risk of hypotension
  
• in men with aortic stenosis, recent myocardial infarction, unstable angina, heart failure, arrhythmias, degenerative retinal disease, or poorly controlled hypertension.⁹
  

Table 2

Duration of action of PDE-5 inhibitors

Other options. Other accepted options for treating ED include intracavernosal injection of vasoactive substances such as phentolamine or prostaglandin E1, or intraurethral insertion of prostaglandins.¹² Since the advent of PDE-5 inhibitors, these approaches are rarely used.

Cabergoline. Off-label use of dopaminergic agents such as cabergoline may be moderately effective in treating ED in men who do not respond adequately to PDE-5 inhibitors. Cabergoline is a dopamine D2 receptor agonist used to treat hyperprolactinemia and Parkinson’s disease.

In a randomized, double-blind, placebo- controlled study, 402 men who did not respond to sildenafil received cabergoline, 0.5 to 1 mg weekly for 6 months. Among the 370 men (92%) who completed the trial, mean weekly intercourse episodes increased from 1.4 to 2.2, compared with 1.2 to 1.4 in men who received placebo.¹³

Cabergoline also improved erectile function and sexual satisfaction in a randomized, double-blind, placebo-controlled trial of 50 men with psychogenic erectile dysfunction.¹⁴

Treatment outcomes. Most studies report positive psychological responses to ED reversal in men using PDE-5 inhibitors. Successful therapy has been associated with increased self-esteem, satisfaction, and sexual satisfaction.⁸ Some studies have found increased sexual satisfaction in the partner as well.¹⁵

Approximately 50% of PDE-5 inhibitor prescriptions are not refilled, however, and some case reports suggest that restored erectile function can result in:

• divorce and marital discord
  
• no change in partner-related activity.¹⁶
  

Hypoactive sexual desire

PDE-5 inhibitors. The success of PDE-5 inhibitors in treating ED led to investigations into whether these agents also could treat female sexual disorders. Large multisite trials using sildenafil failed to find evidence of efficacy in treating female hypoactive sexual desire or arousal disorders, however.¹⁸ Similarly, trials of topical prostaglandin E1 and alpha blockers were unsuccessful in women.

Some small studies suggested that PDE-5 inhibitors might be useful in:

• women with normal libido but decreased arousal¹⁹
  
• young women with normal libido and inability to reach orgasm.²⁰
  

More recently, Shifren et al²² showed in a randomized, placebo-controlled trial that transdermal testosterone, 150 or 300 micrograms/day for 12 weeks, improved sexual function and psychological wellbeing in women age 31 to 56 after surgical menopause. Since then, numerous large, multisite, double-blind studies have demonstrated the efficacy of transdermal testosterone in treating low sexual desire in surgically menopausal women.²³ Transdermal testosterone has been approved for this indication in the European Union but not in the United States.

Testosterone also has been reported to increase sexual desire in women who experienced natural menopause and in normal premenopausal women.²⁴ The study of the relationship of testosterone to libido in women is complicated by numerous factors, however (Box 2).^23,24

Other agents. Recent research has focused on centrally active compounds’ effect on libido. One agent in development is flibanserin, a serotonergic 5HT2 antagonist and a 5HT1a agonist. Data from large, multisite studies indicates that this compound increases libido in women with low sexual desire.

Box 2

The investigational compound bremelanotide—a synthetic version of melanocytes stimulating hormone—is administered intranasally and appears to acutely influence libido in women.²⁶ Trials have been delayed because of this agent’s effects on blood pressure.

Herbal compounds. Some herbal compounds are being sold for low-desire complaints. Web sites for 2 herbal compounds, Ziti and Alibi, cite unpublished double-blind studies attesting to their efficacy. Because these studies are unpublished, one cannot evaluate their methodologies.

One double-blind study of the herbal compound ArginMax—which contains ginseng, ginkgo, damiana, L-arginine, and multivitamins—suggests efficacy in a small group of women with poorly specified sexual problems.²⁷ Zestra, a topical herbal compound, has been evaluated in large multisite studies and found to be effective in increasing female sexual responsiveness.²⁸

Other approaches. Some clinicians advocate using the testosterone precursor dehydroepiandrosterone (DHEA) for low sexual desire, although evidence does not support its efficacy.²⁹

A battery-operated device is FDA -approved for treating sexual dysfunction in women. The clitoral vacuum increases vaginal engorgement and various indices of sexual responsiveness. This device’s target population is not clearly defined.³⁰

When medication side effects are causing hypoactive sexual desire, consider substituting another drug or using antidotes such as buspirone or bupropion. Unfortunately, however, most sexual desire problems are idiopathic.

Testosterone therapy has been shown to improve libido, although it is not FDA-approved for this indication. Considerable off-label use occurs, but long-term safety is unknown.

Related resource

• Medline Plus. Sexual problems overview. www.nlm.nih.gov/medlineplus/ency/article/001951.htm.
  

• Bupropion • Wellbutrin
  
• Buspirone • BuSpar
  
• Cabergoline • Dostinex
  
• Clomipramine • Anafranil
  
• Fluoxetine • Prozac
  
• Lorazepam • Ativan
  
• Paroxetine • Paxil
  
• Phentolamine • Regitine
  
• Prostaglandin E1 • Liprostin
  
• Sertraline • Zoloft
  
• Sildenafil • Viagr
  
• Tadalafil • Cialis
  
• Vardenafil • Levitra
  

Dr. Segraves receives grant/research support from Pfizer, Boehringer Ingelheim, AstraZeneca, Bristol-Myers Squibb, and Novartis and is a consultant to Eli Lilly and Company, GlaxoSmithKline, Boehringer Ingelheim, and Bristol-Myers Squibb.

Sexual disorders such as premature ejaculation, erectile dysfunction (ED), and low libido reduce quality of life in patients with depression, anxiety, and other psychiatric illnesses. In addition, sexual dysfunction is a side effect of many drugs used to treat psychiatric disorders.¹

Psychiatry—with its biopsychosocial model—can easily assume the evaluation and treatment of sexual disorders. To inform your practice, this article provides an update on pharmacotherapy for the 3 most common sexual disorders. Its emphasis on biologic treatment is not intended to minimize the importance of psychological interventions.

Premature ejaculation

Premature ejaculation is one of the most common male sexual complaints. In some surveys, approximately 30% of men express concern about ejaculating too rapidly.² Behavioral therapy often is effective (Box 1), but in my experience most male patients prefer a pharmacologic approach to sexual problems.

Anesthetic creams. Locally applied anesthetic creams—such as prilocaine, lidocaine mixtures, and creams consisting of natural herbs—can increase ejaculatory latency by approximately 7 to 10 minutes. The major side effect of these preparations is penile hypoanesthesia. The man also must use a condom or wash off the cream before vaginal penetration to minimize vaginal absorption.³

Box 1

Among the SSRIs, paroxetine appears to have the greatest effect on ejaculatory latency (Table 1).⁵ Most trials have found that the dose needed to delay ejaculation is similar to the dose necessary to treat depressive disorders.

Some case reports suggest that phosphodiesterase type 5 inhibitors (PDE-5 inhibitors) may help to delay ejaculation, but this effect has not been borne out in double-blind studies.⁶

Table 1

Drug treatment options for premature ejaculation

Erectile dysfunction

Men with major depressive disorder, anxiety disorders, and psychotic disorders have higher rates of ED, compared with the general male population. ED also can be a side effect of—and adversely affect adherence to—antidepressant and antipsychotic therapy.⁷ Restored erectile function can positively affect patients’ self-esteem and sense of personal efficacy and may facilitate recovery from depression.⁸

PDE-5 inhibitors. Nitric oxide release triggers the production of cyclic guanosine monophosphate, which leads to decreased intracellular calcium, smooth muscle relaxation, and penile erection. All available PDE-5 inhibitors work by inhibiting the degradation of cyclic guanosine monophosphate. They are highly specific, vary somewhat in selectivity for other phosphodiesterase enzyme types, and differ in duration of action (Table 2).

Common side effects include dyspepsia, stuffy nose, and headache. The use of PDE-5 inhibitors with nitrates is contraindicated because of the risk of severe hypotension. Use PDE-5 inhibitors cautiously:

• with alpha blockers because of the risk of hypotension
  
• in men with aortic stenosis, recent myocardial infarction, unstable angina, heart failure, arrhythmias, degenerative retinal disease, or poorly controlled hypertension.⁹
  

Table 2

Duration of action of PDE-5 inhibitors

Other options. Other accepted options for treating ED include intracavernosal injection of vasoactive substances such as phentolamine or prostaglandin E1, or intraurethral insertion of prostaglandins.¹² Since the advent of PDE-5 inhibitors, these approaches are rarely used.

Cabergoline. Off-label use of dopaminergic agents such as cabergoline may be moderately effective in treating ED in men who do not respond adequately to PDE-5 inhibitors. Cabergoline is a dopamine D2 receptor agonist used to treat hyperprolactinemia and Parkinson’s disease.

In a randomized, double-blind, placebo- controlled study, 402 men who did not respond to sildenafil received cabergoline, 0.5 to 1 mg weekly for 6 months. Among the 370 men (92%) who completed the trial, mean weekly intercourse episodes increased from 1.4 to 2.2, compared with 1.2 to 1.4 in men who received placebo.¹³

Cabergoline also improved erectile function and sexual satisfaction in a randomized, double-blind, placebo-controlled trial of 50 men with psychogenic erectile dysfunction.¹⁴

Treatment outcomes. Most studies report positive psychological responses to ED reversal in men using PDE-5 inhibitors. Successful therapy has been associated with increased self-esteem, satisfaction, and sexual satisfaction.⁸ Some studies have found increased sexual satisfaction in the partner as well.¹⁵

Approximately 50% of PDE-5 inhibitor prescriptions are not refilled, however, and some case reports suggest that restored erectile function can result in:

• divorce and marital discord
  
• no change in partner-related activity.¹⁶
  

Hypoactive sexual desire

PDE-5 inhibitors. The success of PDE-5 inhibitors in treating ED led to investigations into whether these agents also could treat female sexual disorders. Large multisite trials using sildenafil failed to find evidence of efficacy in treating female hypoactive sexual desire or arousal disorders, however.¹⁸ Similarly, trials of topical prostaglandin E1 and alpha blockers were unsuccessful in women.

Some small studies suggested that PDE-5 inhibitors might be useful in:

• women with normal libido but decreased arousal¹⁹
  
• young women with normal libido and inability to reach orgasm.²⁰
  

More recently, Shifren et al²² showed in a randomized, placebo-controlled trial that transdermal testosterone, 150 or 300 micrograms/day for 12 weeks, improved sexual function and psychological wellbeing in women age 31 to 56 after surgical menopause. Since then, numerous large, multisite, double-blind studies have demonstrated the efficacy of transdermal testosterone in treating low sexual desire in surgically menopausal women.²³ Transdermal testosterone has been approved for this indication in the European Union but not in the United States.

Testosterone also has been reported to increase sexual desire in women who experienced natural menopause and in normal premenopausal women.²⁴ The study of the relationship of testosterone to libido in women is complicated by numerous factors, however (Box 2).^23,24

Other agents. Recent research has focused on centrally active compounds’ effect on libido. One agent in development is flibanserin, a serotonergic 5HT2 antagonist and a 5HT1a agonist. Data from large, multisite studies indicates that this compound increases libido in women with low sexual desire.

Box 2

The investigational compound bremelanotide—a synthetic version of melanocytes stimulating hormone—is administered intranasally and appears to acutely influence libido in women.²⁶ Trials have been delayed because of this agent’s effects on blood pressure.

Herbal compounds. Some herbal compounds are being sold for low-desire complaints. Web sites for 2 herbal compounds, Ziti and Alibi, cite unpublished double-blind studies attesting to their efficacy. Because these studies are unpublished, one cannot evaluate their methodologies.

One double-blind study of the herbal compound ArginMax—which contains ginseng, ginkgo, damiana, L-arginine, and multivitamins—suggests efficacy in a small group of women with poorly specified sexual problems.²⁷ Zestra, a topical herbal compound, has been evaluated in large multisite studies and found to be effective in increasing female sexual responsiveness.²⁸

Other approaches. Some clinicians advocate using the testosterone precursor dehydroepiandrosterone (DHEA) for low sexual desire, although evidence does not support its efficacy.²⁹

A battery-operated device is FDA -approved for treating sexual dysfunction in women. The clitoral vacuum increases vaginal engorgement and various indices of sexual responsiveness. This device’s target population is not clearly defined.³⁰

When medication side effects are causing hypoactive sexual desire, consider substituting another drug or using antidotes such as buspirone or bupropion. Unfortunately, however, most sexual desire problems are idiopathic.

Testosterone therapy has been shown to improve libido, although it is not FDA-approved for this indication. Considerable off-label use occurs, but long-term safety is unknown.

Related resource

• Medline Plus. Sexual problems overview. www.nlm.nih.gov/medlineplus/ency/article/001951.htm.
  

• Bupropion • Wellbutrin
  
• Buspirone • BuSpar
  
• Cabergoline • Dostinex
  
• Clomipramine • Anafranil
  
• Fluoxetine • Prozac
  
• Lorazepam • Ativan
  
• Paroxetine • Paxil
  
• Phentolamine • Regitine
  
• Prostaglandin E1 • Liprostin
  
• Sertraline • Zoloft
  
• Sildenafil • Viagr
  
• Tadalafil • Cialis
  
• Vardenafil • Levitra
  

Dr. Segraves receives grant/research support from Pfizer, Boehringer Ingelheim, AstraZeneca, Bristol-Myers Squibb, and Novartis and is a consultant to Eli Lilly and Company, GlaxoSmithKline, Boehringer Ingelheim, and Bristol-Myers Squibb.

Sexual disorders such as premature ejaculation, erectile dysfunction (ED), and low libido reduce quality of life in patients with depression, anxiety, and other psychiatric illnesses. In addition, sexual dysfunction is a side effect of many drugs used to treat psychiatric disorders.¹

Psychiatry—with its biopsychosocial model—can easily assume the evaluation and treatment of sexual disorders. To inform your practice, this article provides an update on pharmacotherapy for the 3 most common sexual disorders. Its emphasis on biologic treatment is not intended to minimize the importance of psychological interventions.

Premature ejaculation

Premature ejaculation is one of the most common male sexual complaints. In some surveys, approximately 30% of men express concern about ejaculating too rapidly.² Behavioral therapy often is effective (Box 1), but in my experience most male patients prefer a pharmacologic approach to sexual problems.

Anesthetic creams. Locally applied anesthetic creams—such as prilocaine, lidocaine mixtures, and creams consisting of natural herbs—can increase ejaculatory latency by approximately 7 to 10 minutes. The major side effect of these preparations is penile hypoanesthesia. The man also must use a condom or wash off the cream before vaginal penetration to minimize vaginal absorption.³

Box 1

Among the SSRIs, paroxetine appears to have the greatest effect on ejaculatory latency (Table 1).⁵ Most trials have found that the dose needed to delay ejaculation is similar to the dose necessary to treat depressive disorders.

Some case reports suggest that phosphodiesterase type 5 inhibitors (PDE-5 inhibitors) may help to delay ejaculation, but this effect has not been borne out in double-blind studies.⁶

Table 1

Drug treatment options for premature ejaculation

Erectile dysfunction

Men with major depressive disorder, anxiety disorders, and psychotic disorders have higher rates of ED, compared with the general male population. ED also can be a side effect of—and adversely affect adherence to—antidepressant and antipsychotic therapy.⁷ Restored erectile function can positively affect patients’ self-esteem and sense of personal efficacy and may facilitate recovery from depression.⁸

PDE-5 inhibitors. Nitric oxide release triggers the production of cyclic guanosine monophosphate, which leads to decreased intracellular calcium, smooth muscle relaxation, and penile erection. All available PDE-5 inhibitors work by inhibiting the degradation of cyclic guanosine monophosphate. They are highly specific, vary somewhat in selectivity for other phosphodiesterase enzyme types, and differ in duration of action (Table 2).

Common side effects include dyspepsia, stuffy nose, and headache. The use of PDE-5 inhibitors with nitrates is contraindicated because of the risk of severe hypotension. Use PDE-5 inhibitors cautiously:

• with alpha blockers because of the risk of hypotension
  
• in men with aortic stenosis, recent myocardial infarction, unstable angina, heart failure, arrhythmias, degenerative retinal disease, or poorly controlled hypertension.⁹
  

Table 2

Duration of action of PDE-5 inhibitors

Other options. Other accepted options for treating ED include intracavernosal injection of vasoactive substances such as phentolamine or prostaglandin E1, or intraurethral insertion of prostaglandins.¹² Since the advent of PDE-5 inhibitors, these approaches are rarely used.

Cabergoline. Off-label use of dopaminergic agents such as cabergoline may be moderately effective in treating ED in men who do not respond adequately to PDE-5 inhibitors. Cabergoline is a dopamine D2 receptor agonist used to treat hyperprolactinemia and Parkinson’s disease.

In a randomized, double-blind, placebo- controlled study, 402 men who did not respond to sildenafil received cabergoline, 0.5 to 1 mg weekly for 6 months. Among the 370 men (92%) who completed the trial, mean weekly intercourse episodes increased from 1.4 to 2.2, compared with 1.2 to 1.4 in men who received placebo.¹³

Cabergoline also improved erectile function and sexual satisfaction in a randomized, double-blind, placebo-controlled trial of 50 men with psychogenic erectile dysfunction.¹⁴

Treatment outcomes. Most studies report positive psychological responses to ED reversal in men using PDE-5 inhibitors. Successful therapy has been associated with increased self-esteem, satisfaction, and sexual satisfaction.⁸ Some studies have found increased sexual satisfaction in the partner as well.¹⁵

Approximately 50% of PDE-5 inhibitor prescriptions are not refilled, however, and some case reports suggest that restored erectile function can result in:

• divorce and marital discord
  
• no change in partner-related activity.¹⁶
  

Hypoactive sexual desire

PDE-5 inhibitors. The success of PDE-5 inhibitors in treating ED led to investigations into whether these agents also could treat female sexual disorders. Large multisite trials using sildenafil failed to find evidence of efficacy in treating female hypoactive sexual desire or arousal disorders, however.¹⁸ Similarly, trials of topical prostaglandin E1 and alpha blockers were unsuccessful in women.

Some small studies suggested that PDE-5 inhibitors might be useful in:

• women with normal libido but decreased arousal¹⁹
  
• young women with normal libido and inability to reach orgasm.²⁰
  

More recently, Shifren et al²² showed in a randomized, placebo-controlled trial that transdermal testosterone, 150 or 300 micrograms/day for 12 weeks, improved sexual function and psychological wellbeing in women age 31 to 56 after surgical menopause. Since then, numerous large, multisite, double-blind studies have demonstrated the efficacy of transdermal testosterone in treating low sexual desire in surgically menopausal women.²³ Transdermal testosterone has been approved for this indication in the European Union but not in the United States.

Testosterone also has been reported to increase sexual desire in women who experienced natural menopause and in normal premenopausal women.²⁴ The study of the relationship of testosterone to libido in women is complicated by numerous factors, however (Box 2).^23,24

Other agents. Recent research has focused on centrally active compounds’ effect on libido. One agent in development is flibanserin, a serotonergic 5HT2 antagonist and a 5HT1a agonist. Data from large, multisite studies indicates that this compound increases libido in women with low sexual desire.

Box 2

The investigational compound bremelanotide—a synthetic version of melanocytes stimulating hormone—is administered intranasally and appears to acutely influence libido in women.²⁶ Trials have been delayed because of this agent’s effects on blood pressure.

Herbal compounds. Some herbal compounds are being sold for low-desire complaints. Web sites for 2 herbal compounds, Ziti and Alibi, cite unpublished double-blind studies attesting to their efficacy. Because these studies are unpublished, one cannot evaluate their methodologies.

One double-blind study of the herbal compound ArginMax—which contains ginseng, ginkgo, damiana, L-arginine, and multivitamins—suggests efficacy in a small group of women with poorly specified sexual problems.²⁷ Zestra, a topical herbal compound, has been evaluated in large multisite studies and found to be effective in increasing female sexual responsiveness.²⁸

Other approaches. Some clinicians advocate using the testosterone precursor dehydroepiandrosterone (DHEA) for low sexual desire, although evidence does not support its efficacy.²⁹

A battery-operated device is FDA -approved for treating sexual dysfunction in women. The clitoral vacuum increases vaginal engorgement and various indices of sexual responsiveness. This device’s target population is not clearly defined.³⁰

When medication side effects are causing hypoactive sexual desire, consider substituting another drug or using antidotes such as buspirone or bupropion. Unfortunately, however, most sexual desire problems are idiopathic.

Testosterone therapy has been shown to improve libido, although it is not FDA-approved for this indication. Considerable off-label use occurs, but long-term safety is unknown.

Related resource

• Medline Plus. Sexual problems overview. www.nlm.nih.gov/medlineplus/ency/article/001951.htm.
  

• Bupropion • Wellbutrin
  
• Buspirone • BuSpar
  
• Cabergoline • Dostinex
  
• Clomipramine • Anafranil
  
• Fluoxetine • Prozac
  
• Lorazepam • Ativan
  
• Paroxetine • Paxil
  
• Phentolamine • Regitine
  
• Prostaglandin E1 • Liprostin
  
• Sertraline • Zoloft
  
• Sildenafil • Viagr
  
• Tadalafil • Cialis
  
• Vardenafil • Levitra
  

Dr. Segraves receives grant/research support from Pfizer, Boehringer Ingelheim, AstraZeneca, Bristol-Myers Squibb, and Novartis and is a consultant to Eli Lilly and Company, GlaxoSmithKline, Boehringer Ingelheim, and Bristol-Myers Squibb.

Principal Source: Nishimura K, Sugiyama D, Kogata Y, et al. Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis. Ann Intern Med 2007;146:797-808.

Discussant: Robert M. McCarron, DO

Dr. McCarron is assistant professor, departments of internal medicine and psychiatry and behavioral sciences, University of California, Davis. He is CURRENTPSYCHIATRY’Ssection editor for medicine/psychiatry interface.

Up to 70% of patients with rheumatoid arthritis (RA) have a comorbid depressive or anxiety disorder, and depression is estimated to be 2 to 3 times more prevalent in RA patients than in the general population.¹ Until recently, rheumatoid factor (RF)—an antibody directed against a specific portion of immunoglobulin G—was the only serologic test for RA. Although included in American College of Rheumatology diagnostic criteria, RF has a relatively low specificity for RA (85%).

A new test—the anti-cyclic citrullinated peptide antibody (anti-CCP)—is highly specific for RA (96%) and thus less likely than RF to give a false-positive result. RF often is detected in non-RA patients, including the elderly and persons with hepatitis C, Sjögren syndrome, and systemic lupus erythematosus. The anti-CCP test’s sensitivity (67%) is roughly equal to that of RF (69%).

Anti-CCP can rule out other conditions that might mimic RA² —such as osteoarthritis ( Table 1 )—and is a key diagnostic tool to identify early-onset RA. Early detection of RA can lead to a timely primary care referral, use of disease-modifying medications, and improved clinical outcome.

Table 1

Is joint pain rheumatoid arthritis (RA) or osteoarthritis (OA)?

A single test result is not a definitive RA diagnosis ( Table 2 ). A variety of physical, laboratory, and radiologic findings are required to make the diagnosis and initiate therapy. If your patient’s pain is consistent with RA, however, consider ordering a serum RF and anti-CCP to assist the primary care practitioner with prompt diagnosis and treatment. Both erythrocyte sedimentation rate and C-reactive protein have low specificity for RA and should not be included as part of the diagnostic workup.

RA diagnosis. RA is an autoimmune disorder that causes joint pain and deformity, multiple extra-articular manifestations, and disability. It affects 1% to 2% of Americans and 3 times as many women as men. Most adult RA patients initially present with joint swelling and pain between ages 35 to 55.³

Consider screening for RA if your patient complains of joint pain or stiffness that is worse in the morning or after several hours of inactivity. Although atypical presentations occur, the presence of these RA characteristics warrant further inquiry:⁴

• a first-degree relative with RA
• symmetrical joint involvement
• peripheral joint involvement such as metacarpophalangeal (MCP) joints
• proximal interphalangeal (PIP) or wrist joints involvement
• age >35 years.

Table 2

American College of Rheumatology
diagnostic criteria for rheumatoid arthritis (RA)*

Osteoarthritis (OA) is characterized by bony hypertrophy, whereas with RA affected joints tend to feel slightly warm, soft or “boggy,” and are painful to the touch. Patients with OA usually do not have PIP joint pain but instead experience tenderness over the distal interphalangeal (DIP) joints.

Related resources

• American College of Rheumatology. www.rheumatology.org.
• Arthritis National Research Foundation. www.curearthritis.org.

Disclosure

Dr. McCarron is a consultant to Eli Lilly and Company.

Principal Source: Nishimura K, Sugiyama D, Kogata Y, et al. Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis. Ann Intern Med 2007;146:797-808.

Discussant: Robert M. McCarron, DO

Dr. McCarron is assistant professor, departments of internal medicine and psychiatry and behavioral sciences, University of California, Davis. He is CURRENTPSYCHIATRY’Ssection editor for medicine/psychiatry interface.

Up to 70% of patients with rheumatoid arthritis (RA) have a comorbid depressive or anxiety disorder, and depression is estimated to be 2 to 3 times more prevalent in RA patients than in the general population.¹ Until recently, rheumatoid factor (RF)—an antibody directed against a specific portion of immunoglobulin G—was the only serologic test for RA. Although included in American College of Rheumatology diagnostic criteria, RF has a relatively low specificity for RA (85%).

A new test—the anti-cyclic citrullinated peptide antibody (anti-CCP)—is highly specific for RA (96%) and thus less likely than RF to give a false-positive result. RF often is detected in non-RA patients, including the elderly and persons with hepatitis C, Sjögren syndrome, and systemic lupus erythematosus. The anti-CCP test’s sensitivity (67%) is roughly equal to that of RF (69%).

Anti-CCP can rule out other conditions that might mimic RA² —such as osteoarthritis ( Table 1 )—and is a key diagnostic tool to identify early-onset RA. Early detection of RA can lead to a timely primary care referral, use of disease-modifying medications, and improved clinical outcome.

Table 1

Is joint pain rheumatoid arthritis (RA) or osteoarthritis (OA)?

A single test result is not a definitive RA diagnosis ( Table 2 ). A variety of physical, laboratory, and radiologic findings are required to make the diagnosis and initiate therapy. If your patient’s pain is consistent with RA, however, consider ordering a serum RF and anti-CCP to assist the primary care practitioner with prompt diagnosis and treatment. Both erythrocyte sedimentation rate and C-reactive protein have low specificity for RA and should not be included as part of the diagnostic workup.

RA diagnosis. RA is an autoimmune disorder that causes joint pain and deformity, multiple extra-articular manifestations, and disability. It affects 1% to 2% of Americans and 3 times as many women as men. Most adult RA patients initially present with joint swelling and pain between ages 35 to 55.³

Consider screening for RA if your patient complains of joint pain or stiffness that is worse in the morning or after several hours of inactivity. Although atypical presentations occur, the presence of these RA characteristics warrant further inquiry:⁴

• a first-degree relative with RA
• symmetrical joint involvement
• peripheral joint involvement such as metacarpophalangeal (MCP) joints
• proximal interphalangeal (PIP) or wrist joints involvement
• age >35 years.

Table 2

American College of Rheumatology
diagnostic criteria for rheumatoid arthritis (RA)*

Osteoarthritis (OA) is characterized by bony hypertrophy, whereas with RA affected joints tend to feel slightly warm, soft or “boggy,” and are painful to the touch. Patients with OA usually do not have PIP joint pain but instead experience tenderness over the distal interphalangeal (DIP) joints.

Related resources

• American College of Rheumatology. www.rheumatology.org.
• Arthritis National Research Foundation. www.curearthritis.org.

Disclosure

Dr. McCarron is a consultant to Eli Lilly and Company.

Principal Source: Nishimura K, Sugiyama D, Kogata Y, et al. Meta-analysis: diagnostic accuracy of anti-cyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis. Ann Intern Med 2007;146:797-808.

Discussant: Robert M. McCarron, DO

Dr. McCarron is assistant professor, departments of internal medicine and psychiatry and behavioral sciences, University of California, Davis. He is CURRENTPSYCHIATRY’Ssection editor for medicine/psychiatry interface.

Up to 70% of patients with rheumatoid arthritis (RA) have a comorbid depressive or anxiety disorder, and depression is estimated to be 2 to 3 times more prevalent in RA patients than in the general population.¹ Until recently, rheumatoid factor (RF)—an antibody directed against a specific portion of immunoglobulin G—was the only serologic test for RA. Although included in American College of Rheumatology diagnostic criteria, RF has a relatively low specificity for RA (85%).

A new test—the anti-cyclic citrullinated peptide antibody (anti-CCP)—is highly specific for RA (96%) and thus less likely than RF to give a false-positive result. RF often is detected in non-RA patients, including the elderly and persons with hepatitis C, Sjögren syndrome, and systemic lupus erythematosus. The anti-CCP test’s sensitivity (67%) is roughly equal to that of RF (69%).

Anti-CCP can rule out other conditions that might mimic RA² —such as osteoarthritis ( Table 1 )—and is a key diagnostic tool to identify early-onset RA. Early detection of RA can lead to a timely primary care referral, use of disease-modifying medications, and improved clinical outcome.

Table 1

Is joint pain rheumatoid arthritis (RA) or osteoarthritis (OA)?

A single test result is not a definitive RA diagnosis ( Table 2 ). A variety of physical, laboratory, and radiologic findings are required to make the diagnosis and initiate therapy. If your patient’s pain is consistent with RA, however, consider ordering a serum RF and anti-CCP to assist the primary care practitioner with prompt diagnosis and treatment. Both erythrocyte sedimentation rate and C-reactive protein have low specificity for RA and should not be included as part of the diagnostic workup.

RA diagnosis. RA is an autoimmune disorder that causes joint pain and deformity, multiple extra-articular manifestations, and disability. It affects 1% to 2% of Americans and 3 times as many women as men. Most adult RA patients initially present with joint swelling and pain between ages 35 to 55.³

Consider screening for RA if your patient complains of joint pain or stiffness that is worse in the morning or after several hours of inactivity. Although atypical presentations occur, the presence of these RA characteristics warrant further inquiry:⁴

• a first-degree relative with RA
• symmetrical joint involvement
• peripheral joint involvement such as metacarpophalangeal (MCP) joints
• proximal interphalangeal (PIP) or wrist joints involvement
• age >35 years.

Table 2

American College of Rheumatology
diagnostic criteria for rheumatoid arthritis (RA)*

Osteoarthritis (OA) is characterized by bony hypertrophy, whereas with RA affected joints tend to feel slightly warm, soft or “boggy,” and are painful to the touch. Patients with OA usually do not have PIP joint pain but instead experience tenderness over the distal interphalangeal (DIP) joints.

Related resources

• American College of Rheumatology. www.rheumatology.org.
• Arthritis National Research Foundation. www.curearthritis.org.

Disclosure

Dr. McCarron is a consultant to Eli Lilly and Company.

A teenager who doesn’t trust you can become resistant, leave the room, clam up, or become verbally hostile during a psychiatric interview.¹ Our group has identified techniques that may help you develop rapport with teen athletes or other adolescents.

Be a Good Sport

The department of psychiatry at Cooper University Hospital in Camden, NJ, established a program at an urban high school to evaluate student athletes for stress, anxiety, depression, trauma, and substance abuse. The assessment takes place in the high school’s athletic department after an initial screening. Because the assessment program and psychiatrists were new to the school, many of the boys and girls were not forthcoming when talking with clinicians.

Our resident psychiatrists and medical students used Sports Illustrated covers and popular films to break the ice with these teenagers. This approach—which we used during group and individual psychotherapy— often puts teens at ease.

For example, the psychiatrist would bring to the session an issue of Sports Illustrated featuring a well-known athlete with a psychiatric disorder—such as substance abuse, depression, or steroid abuse. The teens quickly became more relaxed and talkative. They seemed interested in giving opinions about the athlete on the magazine cover and his or her issues.

The teens also responded to discussion of the popular sports movie Friday Night Lights, which portrays a small town’s obsession with winning another state football championship. Many of the film’s characters exhibit psychopathology, including the running back’s narcissistic traits, the fullback’s substance abuse, and the quarterback’s lingering effects of having a mentally ill mother. The plot raises questions about the stress and pressure of football; does it exacerbate the development of psychopathology, adequately prepare athletes for life’s uncertainties, or encourage an unrealistic view of society?

Psychiatrists with a sports background often could relate well to the students’ experiences. A therapist with a good understanding of the sport the teen plays can talk about shared experiences, such as dealing with winning or losing. This shared knowledge allows you and the athlete to speak the same language and helps the teen identify with you.

Dress the part

By wearing neat casual attire, you can put a student athlete at ease. A modest polo shirt with the school’s or hospital’s logo—rather than a suit—is appropriate for male and female psychiatrists when interviewing an adolescent athlete at high school. In our experience, teens begin to view psychiatrists as down-to-earth people to whom they can relate, as opposed to overly formal physicians who ask difficult questions.

A teenager who doesn’t trust you can become resistant, leave the room, clam up, or become verbally hostile during a psychiatric interview.¹ Our group has identified techniques that may help you develop rapport with teen athletes or other adolescents.

Be a Good Sport

The department of psychiatry at Cooper University Hospital in Camden, NJ, established a program at an urban high school to evaluate student athletes for stress, anxiety, depression, trauma, and substance abuse. The assessment takes place in the high school’s athletic department after an initial screening. Because the assessment program and psychiatrists were new to the school, many of the boys and girls were not forthcoming when talking with clinicians.

Our resident psychiatrists and medical students used Sports Illustrated covers and popular films to break the ice with these teenagers. This approach—which we used during group and individual psychotherapy— often puts teens at ease.

For example, the psychiatrist would bring to the session an issue of Sports Illustrated featuring a well-known athlete with a psychiatric disorder—such as substance abuse, depression, or steroid abuse. The teens quickly became more relaxed and talkative. They seemed interested in giving opinions about the athlete on the magazine cover and his or her issues.

The teens also responded to discussion of the popular sports movie Friday Night Lights, which portrays a small town’s obsession with winning another state football championship. Many of the film’s characters exhibit psychopathology, including the running back’s narcissistic traits, the fullback’s substance abuse, and the quarterback’s lingering effects of having a mentally ill mother. The plot raises questions about the stress and pressure of football; does it exacerbate the development of psychopathology, adequately prepare athletes for life’s uncertainties, or encourage an unrealistic view of society?

Psychiatrists with a sports background often could relate well to the students’ experiences. A therapist with a good understanding of the sport the teen plays can talk about shared experiences, such as dealing with winning or losing. This shared knowledge allows you and the athlete to speak the same language and helps the teen identify with you.

Dress the part

By wearing neat casual attire, you can put a student athlete at ease. A modest polo shirt with the school’s or hospital’s logo—rather than a suit—is appropriate for male and female psychiatrists when interviewing an adolescent athlete at high school. In our experience, teens begin to view psychiatrists as down-to-earth people to whom they can relate, as opposed to overly formal physicians who ask difficult questions.

A teenager who doesn’t trust you can become resistant, leave the room, clam up, or become verbally hostile during a psychiatric interview.¹ Our group has identified techniques that may help you develop rapport with teen athletes or other adolescents.

Be a Good Sport

The department of psychiatry at Cooper University Hospital in Camden, NJ, established a program at an urban high school to evaluate student athletes for stress, anxiety, depression, trauma, and substance abuse. The assessment takes place in the high school’s athletic department after an initial screening. Because the assessment program and psychiatrists were new to the school, many of the boys and girls were not forthcoming when talking with clinicians.

Our resident psychiatrists and medical students used Sports Illustrated covers and popular films to break the ice with these teenagers. This approach—which we used during group and individual psychotherapy— often puts teens at ease.

For example, the psychiatrist would bring to the session an issue of Sports Illustrated featuring a well-known athlete with a psychiatric disorder—such as substance abuse, depression, or steroid abuse. The teens quickly became more relaxed and talkative. They seemed interested in giving opinions about the athlete on the magazine cover and his or her issues.

The teens also responded to discussion of the popular sports movie Friday Night Lights, which portrays a small town’s obsession with winning another state football championship. Many of the film’s characters exhibit psychopathology, including the running back’s narcissistic traits, the fullback’s substance abuse, and the quarterback’s lingering effects of having a mentally ill mother. The plot raises questions about the stress and pressure of football; does it exacerbate the development of psychopathology, adequately prepare athletes for life’s uncertainties, or encourage an unrealistic view of society?

Psychiatrists with a sports background often could relate well to the students’ experiences. A therapist with a good understanding of the sport the teen plays can talk about shared experiences, such as dealing with winning or losing. This shared knowledge allows you and the athlete to speak the same language and helps the teen identify with you.

Dress the part

By wearing neat casual attire, you can put a student athlete at ease. A modest polo shirt with the school’s or hospital’s logo—rather than a suit—is appropriate for male and female psychiatrists when interviewing an adolescent athlete at high school. In our experience, teens begin to view psychiatrists as down-to-earth people to whom they can relate, as opposed to overly formal physicians who ask difficult questions.

Lithium is making a comeback for good reason. Aside from its tried and true efficacy for bipolar disorder, lithium has neuroprotective effects and antisuicide properties.^1,2

Psychiatry residents who were taught to use divalproex and atypical antipsychotics to treat bipolar disorder are discovering lithium’s benefits. However, all psychiatrists might need a refresher—outlined by the mnemonic LITHIUM—on the fundamentals of this “old school” medication.

Levels between 0.6 and 1.0 mEq/L are sufficient to maintain most bipolar patients, although acute manic patients might require higher levels.^2,3 Some patients who cannot tolerate lithium’s side effects might benefit from lower levels near 0.4 to 0.5 mEq/L. Remember, lithium levels are standardized in 12-hour trough plasma concentrations.

Interactions. Nonsteroidal anti-inflammatory drugs (except aspirin and sulindac), angiotensin-converting enzyme inhibitors, thiazide and loop diuretics, verapamil, and diltiazem can increase lithium concentration.⁴ Caffeine, theophylline, sodium bicarbonate, and dialysis could decrease lithium levels. Be careful when adding lithium to anticonvulsants or antipsychotics because of increased neurotoxicity risk.

Toxicity can lead to coma, seizures, cardiovascular collapse, and death, especially when serum concentrations exceed 3.5 mEq/L.^2,4,5 Be alert to early toxicity symptoms such as drowsiness, confusion, coarse hand tremor, worsening gastrointestinal complaints, dysarthria, impaired consciousness, cogwheel rigidity, and ataxia. Lithium’s narrow therapeutic index requires prudent monitoring. Some patients could experience toxicity at low plasma concentrations, such as 1.0 to 1.5 mEq/L.

Half-life varies depending on the patient’s renal function. Steady state is usually reached within 5 days² but can take up to 10 days because of prolonged half-life in elderly and renally impaired patients (Table). Drawing lithium levels too early could lead to lithium toxicity in these patients, who require modified dosing regimens and monitoring.

Table

Renal metabolism of lithium

Indications. Lithium is FDA-approved for acute mania and bipolar maintenance, but it also has been used for bipolar depression, antidepressant augmentation, schizoaffective disorder, and mixed manic states.³ Consider combining lithium with an atypical antipsychotic for inpatients with severe bipolar mania with psychotic features. Also consider lithium therapy for patients with recurrent unipolar depression who have been successfully treated with antidepressants but then relapse.

Urinary excretion. Order creatinine measurements every 2 to 3 months for the first 6 months of therapy, then every 6 to 12 months. Although lithium is not a first-line mood-stabilizing drug for patients with renal impairment, it can be used safely in patients with hepatic dysfunction.^2,4 Dehydration and a low-sodium diet can cause lithium accumulation, so evaluate patients’ sodium and water balance at the beginning of and throughout lithium therapy. Encourage patients to keep their sodium and water intake as consistent as possible to avoid fluctuations in lithium levels.

Managing side effects is essential to maximize lithium’s effectiveness. Consider switching to a slow-release preparation if your patient cannot tolerate various side effects of regular lithium. If the patient continues to have side effects, consider lowering the dose in 300-mg increments or as clinically indicated. Closely monitor the patient for improved side effects while aiming to maintain an appropriate therapeutic level. Also, moving the entire lithium dose to bedtime could minimize side effects. If these strategies are not adequate, consider adding:

• thyroid replacement to manage elevated thyroid stimulating hormone or frank hypothyroidism
  
• propranolol, 40 to 100 mg/d in divided doses, for tremor
  
• amiloride, 5 to 10 mg/d, for polyuria
  
• loperamide as needed for diarrhea.^2,5
  

Educate your patients on potential side effects, and encourage them to report any unwanted effects. Developing a good patient-provider relationship is essential to maximizing treatment adherence.

Lithium is making a comeback for good reason. Aside from its tried and true efficacy for bipolar disorder, lithium has neuroprotective effects and antisuicide properties.^1,2

Psychiatry residents who were taught to use divalproex and atypical antipsychotics to treat bipolar disorder are discovering lithium’s benefits. However, all psychiatrists might need a refresher—outlined by the mnemonic LITHIUM—on the fundamentals of this “old school” medication.

Levels between 0.6 and 1.0 mEq/L are sufficient to maintain most bipolar patients, although acute manic patients might require higher levels.^2,3 Some patients who cannot tolerate lithium’s side effects might benefit from lower levels near 0.4 to 0.5 mEq/L. Remember, lithium levels are standardized in 12-hour trough plasma concentrations.

Interactions. Nonsteroidal anti-inflammatory drugs (except aspirin and sulindac), angiotensin-converting enzyme inhibitors, thiazide and loop diuretics, verapamil, and diltiazem can increase lithium concentration.⁴ Caffeine, theophylline, sodium bicarbonate, and dialysis could decrease lithium levels. Be careful when adding lithium to anticonvulsants or antipsychotics because of increased neurotoxicity risk.

Toxicity can lead to coma, seizures, cardiovascular collapse, and death, especially when serum concentrations exceed 3.5 mEq/L.^2,4,5 Be alert to early toxicity symptoms such as drowsiness, confusion, coarse hand tremor, worsening gastrointestinal complaints, dysarthria, impaired consciousness, cogwheel rigidity, and ataxia. Lithium’s narrow therapeutic index requires prudent monitoring. Some patients could experience toxicity at low plasma concentrations, such as 1.0 to 1.5 mEq/L.

Half-life varies depending on the patient’s renal function. Steady state is usually reached within 5 days² but can take up to 10 days because of prolonged half-life in elderly and renally impaired patients (Table). Drawing lithium levels too early could lead to lithium toxicity in these patients, who require modified dosing regimens and monitoring.

Table

Renal metabolism of lithium

Indications. Lithium is FDA-approved for acute mania and bipolar maintenance, but it also has been used for bipolar depression, antidepressant augmentation, schizoaffective disorder, and mixed manic states.³ Consider combining lithium with an atypical antipsychotic for inpatients with severe bipolar mania with psychotic features. Also consider lithium therapy for patients with recurrent unipolar depression who have been successfully treated with antidepressants but then relapse.

Urinary excretion. Order creatinine measurements every 2 to 3 months for the first 6 months of therapy, then every 6 to 12 months. Although lithium is not a first-line mood-stabilizing drug for patients with renal impairment, it can be used safely in patients with hepatic dysfunction.^2,4 Dehydration and a low-sodium diet can cause lithium accumulation, so evaluate patients’ sodium and water balance at the beginning of and throughout lithium therapy. Encourage patients to keep their sodium and water intake as consistent as possible to avoid fluctuations in lithium levels.

Managing side effects is essential to maximize lithium’s effectiveness. Consider switching to a slow-release preparation if your patient cannot tolerate various side effects of regular lithium. If the patient continues to have side effects, consider lowering the dose in 300-mg increments or as clinically indicated. Closely monitor the patient for improved side effects while aiming to maintain an appropriate therapeutic level. Also, moving the entire lithium dose to bedtime could minimize side effects. If these strategies are not adequate, consider adding:

• thyroid replacement to manage elevated thyroid stimulating hormone or frank hypothyroidism
  
• propranolol, 40 to 100 mg/d in divided doses, for tremor
  
• amiloride, 5 to 10 mg/d, for polyuria
  
• loperamide as needed for diarrhea.^2,5
  

Educate your patients on potential side effects, and encourage them to report any unwanted effects. Developing a good patient-provider relationship is essential to maximizing treatment adherence.

Lithium is making a comeback for good reason. Aside from its tried and true efficacy for bipolar disorder, lithium has neuroprotective effects and antisuicide properties.^1,2

Psychiatry residents who were taught to use divalproex and atypical antipsychotics to treat bipolar disorder are discovering lithium’s benefits. However, all psychiatrists might need a refresher—outlined by the mnemonic LITHIUM—on the fundamentals of this “old school” medication.

Levels between 0.6 and 1.0 mEq/L are sufficient to maintain most bipolar patients, although acute manic patients might require higher levels.^2,3 Some patients who cannot tolerate lithium’s side effects might benefit from lower levels near 0.4 to 0.5 mEq/L. Remember, lithium levels are standardized in 12-hour trough plasma concentrations.

Interactions. Nonsteroidal anti-inflammatory drugs (except aspirin and sulindac), angiotensin-converting enzyme inhibitors, thiazide and loop diuretics, verapamil, and diltiazem can increase lithium concentration.⁴ Caffeine, theophylline, sodium bicarbonate, and dialysis could decrease lithium levels. Be careful when adding lithium to anticonvulsants or antipsychotics because of increased neurotoxicity risk.

Toxicity can lead to coma, seizures, cardiovascular collapse, and death, especially when serum concentrations exceed 3.5 mEq/L.^2,4,5 Be alert to early toxicity symptoms such as drowsiness, confusion, coarse hand tremor, worsening gastrointestinal complaints, dysarthria, impaired consciousness, cogwheel rigidity, and ataxia. Lithium’s narrow therapeutic index requires prudent monitoring. Some patients could experience toxicity at low plasma concentrations, such as 1.0 to 1.5 mEq/L.

Half-life varies depending on the patient’s renal function. Steady state is usually reached within 5 days² but can take up to 10 days because of prolonged half-life in elderly and renally impaired patients (Table). Drawing lithium levels too early could lead to lithium toxicity in these patients, who require modified dosing regimens and monitoring.

Table

Renal metabolism of lithium

Indications. Lithium is FDA-approved for acute mania and bipolar maintenance, but it also has been used for bipolar depression, antidepressant augmentation, schizoaffective disorder, and mixed manic states.³ Consider combining lithium with an atypical antipsychotic for inpatients with severe bipolar mania with psychotic features. Also consider lithium therapy for patients with recurrent unipolar depression who have been successfully treated with antidepressants but then relapse.

Urinary excretion. Order creatinine measurements every 2 to 3 months for the first 6 months of therapy, then every 6 to 12 months. Although lithium is not a first-line mood-stabilizing drug for patients with renal impairment, it can be used safely in patients with hepatic dysfunction.^2,4 Dehydration and a low-sodium diet can cause lithium accumulation, so evaluate patients’ sodium and water balance at the beginning of and throughout lithium therapy. Encourage patients to keep their sodium and water intake as consistent as possible to avoid fluctuations in lithium levels.

Managing side effects is essential to maximize lithium’s effectiveness. Consider switching to a slow-release preparation if your patient cannot tolerate various side effects of regular lithium. If the patient continues to have side effects, consider lowering the dose in 300-mg increments or as clinically indicated. Closely monitor the patient for improved side effects while aiming to maintain an appropriate therapeutic level. Also, moving the entire lithium dose to bedtime could minimize side effects. If these strategies are not adequate, consider adding:

• thyroid replacement to manage elevated thyroid stimulating hormone or frank hypothyroidism
  
• propranolol, 40 to 100 mg/d in divided doses, for tremor
  
• amiloride, 5 to 10 mg/d, for polyuria
  
• loperamide as needed for diarrhea.^2,5
  

Educate your patients on potential side effects, and encourage them to report any unwanted effects. Developing a good patient-provider relationship is essential to maximizing treatment adherence.

Principal Source: Harris R, Lohr KN. Screening for prostate cancer: an update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2002; 137(11):917-29.

Discussant: Weber Chen, MD

Dr. Chen is an oncologist and hematologist in Los Angeles, CA.

All men age >65—including psychiatric patients—are at higher risk for prostate cancer. The prostate-specific antigen (PSA) blood test can detect prostate cancer early and decrease mortality but often returns a false positive. Because this can increase a patient’s anxiety and lead to unnecessary procedures, consider the psychological impact of waiting for PSA test results as well as possible risk factors for prostate cancer (Table 5).¹ Refer patients at high risk or those with elevated PSA levels to primary care physicians for evaluation.

PSA testing. The PSA blood test is the screening method of choice for detecting prostate cancer. Before the test’s release in 1992, most prostate cancers were identified at an advanced and incurable state. Because early-stage prostate cancer has few signs or symptoms, PSA screening can identify localized and potentially curable disease.

Despite its benefits, PSA screening in prostate cancer is controversial.

• Detection of clinically insignificant cancers may lead to unnecessary treatments.
• An elevated PSA lacks specificity. Despite an increased likelihood of prostate cancer in men with moderately elevated PSA (4 to 10 ng/ml), biopsy usually reveals benign prostatic hyperplasia (BPH) rather than prostate cancer.
• No randomized studies have confirmed that PSA screening decreases prostate cancer mortality. It is not clear that early detection and treatment changes the natural history and outcome of the disease.²

Table 5

Risk factors for prostate cancer

PSA originally was introduced as a tumor marker to detect cancer recurrence or disease progression after treatment. However, it became an important cancer screening tool by the early 1990s and led to a spike in the incidence of prostate cancer, peaking in 1992.³ Most of these newly diagnosed cancers were clinically localized or organ confined, which led to an increase in radical prostatectomy and radiation therapy.

PSA and cancer risk. PSA is a glycoprotein produced by prostate epithelial cells. The upper limit of normal PSA levels is 4 ng/ml. The positive predictive value for prostate cancer at PSA levels between 4 and 10 ng/ml is approximately 25% but increases to 42% to 64% at PSA levels >10 ng/ml.⁴ Nearly 75% of cancers detected within the “gray zone”—PSA values between 4 and 10.0 ng/ml—are organ confined and potentially curable. At PSA values >10 ng/ml less than half of cancers detected are organ-confined.¹

Studies show that PSA elevations precede clinical disease by an average of 5 years.⁵ PSA elevations may occur with other benign conditions particularly BPH and prostatitis. Digital rectal exams (DRE), ejaculation, prostate biopsy, and acute urinary retention also can cause elevated PSA levels.

Should your patient be tested? The American Cancer Society recommends PSA screening and DRE for men age ≥50 who have ≥10 years life expectancy. Men at higher risk, such as African-Americans and those with a family history of prostate cancer, should begin testing between ages 40 and 45.

Prostate cancer is the most frequently diagnosed cancer in men in the United States. Each year more than 200,000 cases are diagnosed, and approximately 25,000 prostate cancer patients die. Prostate cancer is the second leading cause of cancer death in men after lung cancer and is usually diagnosed in men age 6

Related resources

• National Cancer Institute. Prostate Cancer. www.cancer.gov/cancertopics/types/prostate.
• Emedicine.com. Prostate cancer. www.emedicine.com/urology/index.shtml#prostate.
• National Comprehensive Cancer Network. www.nccn.org.

Disclosure

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

Principal Source: Harris R, Lohr KN. Screening for prostate cancer: an update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2002; 137(11):917-29.

Discussant: Weber Chen, MD

Dr. Chen is an oncologist and hematologist in Los Angeles, CA.

All men age >65—including psychiatric patients—are at higher risk for prostate cancer. The prostate-specific antigen (PSA) blood test can detect prostate cancer early and decrease mortality but often returns a false positive. Because this can increase a patient’s anxiety and lead to unnecessary procedures, consider the psychological impact of waiting for PSA test results as well as possible risk factors for prostate cancer (Table 5).¹ Refer patients at high risk or those with elevated PSA levels to primary care physicians for evaluation.

PSA testing. The PSA blood test is the screening method of choice for detecting prostate cancer. Before the test’s release in 1992, most prostate cancers were identified at an advanced and incurable state. Because early-stage prostate cancer has few signs or symptoms, PSA screening can identify localized and potentially curable disease.

Despite its benefits, PSA screening in prostate cancer is controversial.

• Detection of clinically insignificant cancers may lead to unnecessary treatments.
• An elevated PSA lacks specificity. Despite an increased likelihood of prostate cancer in men with moderately elevated PSA (4 to 10 ng/ml), biopsy usually reveals benign prostatic hyperplasia (BPH) rather than prostate cancer.
• No randomized studies have confirmed that PSA screening decreases prostate cancer mortality. It is not clear that early detection and treatment changes the natural history and outcome of the disease.²

Table 5

Risk factors for prostate cancer

PSA originally was introduced as a tumor marker to detect cancer recurrence or disease progression after treatment. However, it became an important cancer screening tool by the early 1990s and led to a spike in the incidence of prostate cancer, peaking in 1992.³ Most of these newly diagnosed cancers were clinically localized or organ confined, which led to an increase in radical prostatectomy and radiation therapy.

PSA and cancer risk. PSA is a glycoprotein produced by prostate epithelial cells. The upper limit of normal PSA levels is 4 ng/ml. The positive predictive value for prostate cancer at PSA levels between 4 and 10 ng/ml is approximately 25% but increases to 42% to 64% at PSA levels >10 ng/ml.⁴ Nearly 75% of cancers detected within the “gray zone”—PSA values between 4 and 10.0 ng/ml—are organ confined and potentially curable. At PSA values >10 ng/ml less than half of cancers detected are organ-confined.¹

Studies show that PSA elevations precede clinical disease by an average of 5 years.⁵ PSA elevations may occur with other benign conditions particularly BPH and prostatitis. Digital rectal exams (DRE), ejaculation, prostate biopsy, and acute urinary retention also can cause elevated PSA levels.

Should your patient be tested? The American Cancer Society recommends PSA screening and DRE for men age ≥50 who have ≥10 years life expectancy. Men at higher risk, such as African-Americans and those with a family history of prostate cancer, should begin testing between ages 40 and 45.

Prostate cancer is the most frequently diagnosed cancer in men in the United States. Each year more than 200,000 cases are diagnosed, and approximately 25,000 prostate cancer patients die. Prostate cancer is the second leading cause of cancer death in men after lung cancer and is usually diagnosed in men age 6

Related resources

• National Cancer Institute. Prostate Cancer. www.cancer.gov/cancertopics/types/prostate.
• Emedicine.com. Prostate cancer. www.emedicine.com/urology/index.shtml#prostate.
• National Comprehensive Cancer Network. www.nccn.org.

Disclosure

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

Principal Source: Harris R, Lohr KN. Screening for prostate cancer: an update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2002; 137(11):917-29.

Discussant: Weber Chen, MD

Dr. Chen is an oncologist and hematologist in Los Angeles, CA.

All men age >65—including psychiatric patients—are at higher risk for prostate cancer. The prostate-specific antigen (PSA) blood test can detect prostate cancer early and decrease mortality but often returns a false positive. Because this can increase a patient’s anxiety and lead to unnecessary procedures, consider the psychological impact of waiting for PSA test results as well as possible risk factors for prostate cancer (Table 5).¹ Refer patients at high risk or those with elevated PSA levels to primary care physicians for evaluation.

PSA testing. The PSA blood test is the screening method of choice for detecting prostate cancer. Before the test’s release in 1992, most prostate cancers were identified at an advanced and incurable state. Because early-stage prostate cancer has few signs or symptoms, PSA screening can identify localized and potentially curable disease.

Despite its benefits, PSA screening in prostate cancer is controversial.

• Detection of clinically insignificant cancers may lead to unnecessary treatments.
• An elevated PSA lacks specificity. Despite an increased likelihood of prostate cancer in men with moderately elevated PSA (4 to 10 ng/ml), biopsy usually reveals benign prostatic hyperplasia (BPH) rather than prostate cancer.
• No randomized studies have confirmed that PSA screening decreases prostate cancer mortality. It is not clear that early detection and treatment changes the natural history and outcome of the disease.²

Table 5

Risk factors for prostate cancer

PSA originally was introduced as a tumor marker to detect cancer recurrence or disease progression after treatment. However, it became an important cancer screening tool by the early 1990s and led to a spike in the incidence of prostate cancer, peaking in 1992.³ Most of these newly diagnosed cancers were clinically localized or organ confined, which led to an increase in radical prostatectomy and radiation therapy.

PSA and cancer risk. PSA is a glycoprotein produced by prostate epithelial cells. The upper limit of normal PSA levels is 4 ng/ml. The positive predictive value for prostate cancer at PSA levels between 4 and 10 ng/ml is approximately 25% but increases to 42% to 64% at PSA levels >10 ng/ml.⁴ Nearly 75% of cancers detected within the “gray zone”—PSA values between 4 and 10.0 ng/ml—are organ confined and potentially curable. At PSA values >10 ng/ml less than half of cancers detected are organ-confined.¹

Studies show that PSA elevations precede clinical disease by an average of 5 years.⁵ PSA elevations may occur with other benign conditions particularly BPH and prostatitis. Digital rectal exams (DRE), ejaculation, prostate biopsy, and acute urinary retention also can cause elevated PSA levels.

Should your patient be tested? The American Cancer Society recommends PSA screening and DRE for men age ≥50 who have ≥10 years life expectancy. Men at higher risk, such as African-Americans and those with a family history of prostate cancer, should begin testing between ages 40 and 45.

Prostate cancer is the most frequently diagnosed cancer in men in the United States. Each year more than 200,000 cases are diagnosed, and approximately 25,000 prostate cancer patients die. Prostate cancer is the second leading cause of cancer death in men after lung cancer and is usually diagnosed in men age 6

Related resources

• National Cancer Institute. Prostate Cancer. www.cancer.gov/cancertopics/types/prostate.
• Emedicine.com. Prostate cancer. www.emedicine.com/urology/index.shtml#prostate.
• National Comprehensive Cancer Network. www.nccn.org.

Disclosure

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

Principal Source: Omalu BI, Ives DG, Buhari AM, et al. Death rates and causes of death after bariatric surgery for Pennsylvania residents, 1995 to 2004. Arch Surg 2007; 142(10):923-8.

Discussant: Glen L. Xiong, MD

Dr. Xiong is assistant clinical professor, departments of internal medicine and psychiatry and behavioral sciences, University of California, Davis.

Many obese patients suffer from depression, bipolar disorder, panic disorder, personality disorders, or other psychiatric conditions.¹ Morbidly obese patients searching for a lasting solution to their weight problems might seek a psychiatric evaluation for bariatric surgery. However, before giving the green light for the procedure, consider that a recent study questions if bariatric surgery decreases mortality in obese patients.

Most bariatric surgery practice guidelines require evaluation and treatment of comorbid psychiatric conditions such as eating disorders, depression, and substance use disorder, which can worsen postoperative outcomes. Indications for bariatric surgery include a body mass index (BMI) ≥40 kg/m² or ≥35 kg/m² with significant obesity-related comorbid medical conditions, such as diabetes ( Table 3 ).

A large-scale epidemiologic study found that bariatric surgery patients had a higher long-term risk of dying from coronary artery disease and suicide than the general population ( Table 4 ).² Bariatric surgery patients also have a higher mortality rate than the general population, although they may have an absolute 1% survival advantage over closely matched obese patients who do not have the surgery.³ This advantage might disappear when selection bias is controlled, however, because patients who undergo surgery are more motivated to improve their health than patients who remain obese.

Table 3

Body mass index (BMI) values

Of 16,683 bariatric operations performed in Pennsylvania over 10 years, 440 (2.6%) patients died. Nearly 1% of these deaths occurred within 30 days. The total death rate was approximately 1% per year and almost 6% at 5 years. In addition to the medical causes, 45 bariatric patients died from traumatic causes:

• 16 suicides (4%)
• 14 drug overdoses (3%)
• 10 motor vehicle accidents (2%)
• 3 homicides (0.7%)
• 2 falls (0.5%).

Women accounted for 10 of the 16 suicides (62.5%) and 12 of the 14 (85.7%) drug overdoses.

Treatment options. When treating obese patients, choose medications with a low risk for weight gain, which may include switching to a medication in the same class that is less likely to cause weight gain. Also, give patients educational handouts and resources about dietary and exercise regimens that focus on behavioral reinforcement. Although important, lifestyle modification and medication management produce nonsustained and modest results for most obese patients. Benefits are even more limited in morbidly obese patients with BMI ≥40 kg/m².

Bariatric surgery is an emerging treatment option for obese patients, although its use has been limited by safety concerns, availability, and lack of coverage by many insurance companies. Among obesity treatments, only bariatric surgery has demonstrated enduring weight loss and reduced medical comorbidities such as diabetes.⁴

Table 4

Leading medical causes of death after bariatric surgery

A new epidemic. The prevalence of obesity—nearly 1 in 3 Americans—has increased dramatically over the last few decades for reasons that include dietary indiscretion and sedentary lifestyle.⁵ Obesity is associated with decreased life expectancy,⁶ reduced quality of life, and higher incidence of diabetes, hypertension, arthritis, cardiovascular disease, sleep apnea, gastroesophageal reflux disease, and other chronic medical conditions. In addition, metabolic side effects of some psychotropic medications—especially antipsychotics—can exacerbate weight gain.

Related resources

• American Society for Bariatric Surgery. Pre-surgical psychological assessment of bariatric surgery candidates. www.asbs.org/html/pdf/PsychPreSurgicalAssessment.pdf.
• National Heart Lung and Blood Institute. Body mass index calculator. www.nhlbisupport.com/bmi/bmicalc.htm.
• Torpy JM, Burke A, Glass RM. JAMA patient page. Bariatric surgery. JAMA 2005;294;(15):1986. Available at: http://jama.ama-assn.org/cgi/reprint/294/15/1986.pdf.

Disclosure

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

Principal Source: Omalu BI, Ives DG, Buhari AM, et al. Death rates and causes of death after bariatric surgery for Pennsylvania residents, 1995 to 2004. Arch Surg 2007; 142(10):923-8.

Discussant: Glen L. Xiong, MD

Dr. Xiong is assistant clinical professor, departments of internal medicine and psychiatry and behavioral sciences, University of California, Davis.

Many obese patients suffer from depression, bipolar disorder, panic disorder, personality disorders, or other psychiatric conditions.¹ Morbidly obese patients searching for a lasting solution to their weight problems might seek a psychiatric evaluation for bariatric surgery. However, before giving the green light for the procedure, consider that a recent study questions if bariatric surgery decreases mortality in obese patients.

Most bariatric surgery practice guidelines require evaluation and treatment of comorbid psychiatric conditions such as eating disorders, depression, and substance use disorder, which can worsen postoperative outcomes. Indications for bariatric surgery include a body mass index (BMI) ≥40 kg/m² or ≥35 kg/m² with significant obesity-related comorbid medical conditions, such as diabetes ( Table 3 ).

A large-scale epidemiologic study found that bariatric surgery patients had a higher long-term risk of dying from coronary artery disease and suicide than the general population ( Table 4 ).² Bariatric surgery patients also have a higher mortality rate than the general population, although they may have an absolute 1% survival advantage over closely matched obese patients who do not have the surgery.³ This advantage might disappear when selection bias is controlled, however, because patients who undergo surgery are more motivated to improve their health than patients who remain obese.

Table 3

Body mass index (BMI) values

Of 16,683 bariatric operations performed in Pennsylvania over 10 years, 440 (2.6%) patients died. Nearly 1% of these deaths occurred within 30 days. The total death rate was approximately 1% per year and almost 6% at 5 years. In addition to the medical causes, 45 bariatric patients died from traumatic causes:

• 16 suicides (4%)
• 14 drug overdoses (3%)
• 10 motor vehicle accidents (2%)
• 3 homicides (0.7%)
• 2 falls (0.5%).

Women accounted for 10 of the 16 suicides (62.5%) and 12 of the 14 (85.7%) drug overdoses.

Treatment options. When treating obese patients, choose medications with a low risk for weight gain, which may include switching to a medication in the same class that is less likely to cause weight gain. Also, give patients educational handouts and resources about dietary and exercise regimens that focus on behavioral reinforcement. Although important, lifestyle modification and medication management produce nonsustained and modest results for most obese patients. Benefits are even more limited in morbidly obese patients with BMI ≥40 kg/m².

Bariatric surgery is an emerging treatment option for obese patients, although its use has been limited by safety concerns, availability, and lack of coverage by many insurance companies. Among obesity treatments, only bariatric surgery has demonstrated enduring weight loss and reduced medical comorbidities such as diabetes.⁴

Table 4

Leading medical causes of death after bariatric surgery

A new epidemic. The prevalence of obesity—nearly 1 in 3 Americans—has increased dramatically over the last few decades for reasons that include dietary indiscretion and sedentary lifestyle.⁵ Obesity is associated with decreased life expectancy,⁶ reduced quality of life, and higher incidence of diabetes, hypertension, arthritis, cardiovascular disease, sleep apnea, gastroesophageal reflux disease, and other chronic medical conditions. In addition, metabolic side effects of some psychotropic medications—especially antipsychotics—can exacerbate weight gain.

Related resources

• American Society for Bariatric Surgery. Pre-surgical psychological assessment of bariatric surgery candidates. www.asbs.org/html/pdf/PsychPreSurgicalAssessment.pdf.
• National Heart Lung and Blood Institute. Body mass index calculator. www.nhlbisupport.com/bmi/bmicalc.htm.
• Torpy JM, Burke A, Glass RM. JAMA patient page. Bariatric surgery. JAMA 2005;294;(15):1986. Available at: http://jama.ama-assn.org/cgi/reprint/294/15/1986.pdf.

Disclosure

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

Principal Source: Omalu BI, Ives DG, Buhari AM, et al. Death rates and causes of death after bariatric surgery for Pennsylvania residents, 1995 to 2004. Arch Surg 2007; 142(10):923-8.

Discussant: Glen L. Xiong, MD

Dr. Xiong is assistant clinical professor, departments of internal medicine and psychiatry and behavioral sciences, University of California, Davis.

Many obese patients suffer from depression, bipolar disorder, panic disorder, personality disorders, or other psychiatric conditions.¹ Morbidly obese patients searching for a lasting solution to their weight problems might seek a psychiatric evaluation for bariatric surgery. However, before giving the green light for the procedure, consider that a recent study questions if bariatric surgery decreases mortality in obese patients.

Most bariatric surgery practice guidelines require evaluation and treatment of comorbid psychiatric conditions such as eating disorders, depression, and substance use disorder, which can worsen postoperative outcomes. Indications for bariatric surgery include a body mass index (BMI) ≥40 kg/m² or ≥35 kg/m² with significant obesity-related comorbid medical conditions, such as diabetes ( Table 3 ).

A large-scale epidemiologic study found that bariatric surgery patients had a higher long-term risk of dying from coronary artery disease and suicide than the general population ( Table 4 ).² Bariatric surgery patients also have a higher mortality rate than the general population, although they may have an absolute 1% survival advantage over closely matched obese patients who do not have the surgery.³ This advantage might disappear when selection bias is controlled, however, because patients who undergo surgery are more motivated to improve their health than patients who remain obese.

Table 3

Body mass index (BMI) values

Of 16,683 bariatric operations performed in Pennsylvania over 10 years, 440 (2.6%) patients died. Nearly 1% of these deaths occurred within 30 days. The total death rate was approximately 1% per year and almost 6% at 5 years. In addition to the medical causes, 45 bariatric patients died from traumatic causes:

• 16 suicides (4%)
• 14 drug overdoses (3%)
• 10 motor vehicle accidents (2%)
• 3 homicides (0.7%)
• 2 falls (0.5%).

Women accounted for 10 of the 16 suicides (62.5%) and 12 of the 14 (85.7%) drug overdoses.

Treatment options. When treating obese patients, choose medications with a low risk for weight gain, which may include switching to a medication in the same class that is less likely to cause weight gain. Also, give patients educational handouts and resources about dietary and exercise regimens that focus on behavioral reinforcement. Although important, lifestyle modification and medication management produce nonsustained and modest results for most obese patients. Benefits are even more limited in morbidly obese patients with BMI ≥40 kg/m².

Bariatric surgery is an emerging treatment option for obese patients, although its use has been limited by safety concerns, availability, and lack of coverage by many insurance companies. Among obesity treatments, only bariatric surgery has demonstrated enduring weight loss and reduced medical comorbidities such as diabetes.⁴

Table 4

Leading medical causes of death after bariatric surgery

A new epidemic. The prevalence of obesity—nearly 1 in 3 Americans—has increased dramatically over the last few decades for reasons that include dietary indiscretion and sedentary lifestyle.⁵ Obesity is associated with decreased life expectancy,⁶ reduced quality of life, and higher incidence of diabetes, hypertension, arthritis, cardiovascular disease, sleep apnea, gastroesophageal reflux disease, and other chronic medical conditions. In addition, metabolic side effects of some psychotropic medications—especially antipsychotics—can exacerbate weight gain.

Related resources

• American Society for Bariatric Surgery. Pre-surgical psychological assessment of bariatric surgery candidates. www.asbs.org/html/pdf/PsychPreSurgicalAssessment.pdf.
• National Heart Lung and Blood Institute. Body mass index calculator. www.nhlbisupport.com/bmi/bmicalc.htm.
• Torpy JM, Burke A, Glass RM. JAMA patient page. Bariatric surgery. JAMA 2005;294;(15):1986. Available at: http://jama.ama-assn.org/cgi/reprint/294/15/1986.pdf.

Disclosure

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

I work in a state-run, long-term care facility for mentally ill patients in northern Minnesota that is scheduled to close within a few weeks. I have seen the results of the transition to community-based services and the effects it has on mentally ill patients. The Minnesota governor calls it “mental health redesign.” The state’s Department of Human Services commissioner cites the U.S. Supreme Court case know as the Olmsted decision as the reason these institutions must be closed. The court ruled that the unnecessary segregation of individuals with disabilities in institutions may constitute discrimination based on disability. On one hand the lawmakers use the Olmstead decision to promote their policies, but ignore the conditions that are set forth in that decision [treatment professionals must have determined that community placement is appropriate, the transfer is not opposed by the affected individual, and the placement can be reasonably accommodated, taking into account the resources available to the state and the needs of others with mental disabilities]. I doubt if the lawmakers who endorsed this legislation have read the Olmsted decision.

In his editorial, Dr. Nasrallah states that he is perplexed that there is no public outrage about the misery of the seriously mentally ill. Many of us are outraged. However, as residents of our communities, we are guilty of trusting the integrity of our elected and appointed officials. We believe what we are led to believe. Furthermore it is human nature to be frightened by what we do not understand and avoid what scares us.

Many people believe that there is a stigma associated with being in a psychiatric institution, but I believe the stigma lies with mental illness itself.

I have spent 24 years caring for the mentally ill as a nurses’ aid. For the last 5 years I have tried repeatedly to raise the awareness of state lawmakers about the hidden costs and consequences of deinstitutionalization, but without success. Many people do not know that community-based services are 3 to 4 times more costly than institutional care. However, I believe that the driving force behind this trend lies in the federal IMD (institution for mental disease) exclusion. Persons living in a psychiatric institution do not qualify for Medicaid dollars, but the same patients who live in the community do qualify. In Minnesota we are told that it is all about the client, but in fact it is all about the dollar.

I fear that the situation will not change until there is a major event that really raises the public’s hackles. Policies will not change until the right person has to live through the tragic consequences related to deinstitutionalization. Eventually the pendulum will swing the other way, but at what cost?

Lisa K. Lemke
Laporte, MN

I work in a state-run, long-term care facility for mentally ill patients in northern Minnesota that is scheduled to close within a few weeks. I have seen the results of the transition to community-based services and the effects it has on mentally ill patients. The Minnesota governor calls it “mental health redesign.” The state’s Department of Human Services commissioner cites the U.S. Supreme Court case know as the Olmsted decision as the reason these institutions must be closed. The court ruled that the unnecessary segregation of individuals with disabilities in institutions may constitute discrimination based on disability. On one hand the lawmakers use the Olmstead decision to promote their policies, but ignore the conditions that are set forth in that decision [treatment professionals must have determined that community placement is appropriate, the transfer is not opposed by the affected individual, and the placement can be reasonably accommodated, taking into account the resources available to the state and the needs of others with mental disabilities]. I doubt if the lawmakers who endorsed this legislation have read the Olmsted decision.

In his editorial, Dr. Nasrallah states that he is perplexed that there is no public outrage about the misery of the seriously mentally ill. Many of us are outraged. However, as residents of our communities, we are guilty of trusting the integrity of our elected and appointed officials. We believe what we are led to believe. Furthermore it is human nature to be frightened by what we do not understand and avoid what scares us.

Many people believe that there is a stigma associated with being in a psychiatric institution, but I believe the stigma lies with mental illness itself.

I have spent 24 years caring for the mentally ill as a nurses’ aid. For the last 5 years I have tried repeatedly to raise the awareness of state lawmakers about the hidden costs and consequences of deinstitutionalization, but without success. Many people do not know that community-based services are 3 to 4 times more costly than institutional care. However, I believe that the driving force behind this trend lies in the federal IMD (institution for mental disease) exclusion. Persons living in a psychiatric institution do not qualify for Medicaid dollars, but the same patients who live in the community do qualify. In Minnesota we are told that it is all about the client, but in fact it is all about the dollar.

I fear that the situation will not change until there is a major event that really raises the public’s hackles. Policies will not change until the right person has to live through the tragic consequences related to deinstitutionalization. Eventually the pendulum will swing the other way, but at what cost?

Lisa K. Lemke
Laporte, MN

I work in a state-run, long-term care facility for mentally ill patients in northern Minnesota that is scheduled to close within a few weeks. I have seen the results of the transition to community-based services and the effects it has on mentally ill patients. The Minnesota governor calls it “mental health redesign.” The state’s Department of Human Services commissioner cites the U.S. Supreme Court case know as the Olmsted decision as the reason these institutions must be closed. The court ruled that the unnecessary segregation of individuals with disabilities in institutions may constitute discrimination based on disability. On one hand the lawmakers use the Olmstead decision to promote their policies, but ignore the conditions that are set forth in that decision [treatment professionals must have determined that community placement is appropriate, the transfer is not opposed by the affected individual, and the placement can be reasonably accommodated, taking into account the resources available to the state and the needs of others with mental disabilities]. I doubt if the lawmakers who endorsed this legislation have read the Olmsted decision.

In his editorial, Dr. Nasrallah states that he is perplexed that there is no public outrage about the misery of the seriously mentally ill. Many of us are outraged. However, as residents of our communities, we are guilty of trusting the integrity of our elected and appointed officials. We believe what we are led to believe. Furthermore it is human nature to be frightened by what we do not understand and avoid what scares us.

Many people believe that there is a stigma associated with being in a psychiatric institution, but I believe the stigma lies with mental illness itself.

I have spent 24 years caring for the mentally ill as a nurses’ aid. For the last 5 years I have tried repeatedly to raise the awareness of state lawmakers about the hidden costs and consequences of deinstitutionalization, but without success. Many people do not know that community-based services are 3 to 4 times more costly than institutional care. However, I believe that the driving force behind this trend lies in the federal IMD (institution for mental disease) exclusion. Persons living in a psychiatric institution do not qualify for Medicaid dollars, but the same patients who live in the community do qualify. In Minnesota we are told that it is all about the client, but in fact it is all about the dollar.

I fear that the situation will not change until there is a major event that really raises the public’s hackles. Policies will not change until the right person has to live through the tragic consequences related to deinstitutionalization. Eventually the pendulum will swing the other way, but at what cost?

Lisa K. Lemke
Laporte, MN

I could not agree more with Dr. Nasrallah’s editorial on deinstitutionalization. My opinion is based on >50 years experience in psychiatry.

I started my career in l954 at Eastern State Hospital in Williamsburg, VA. As a first-year resident, I was ordered to assist Dr. Walter Freeman in performing transorbital lobotomies. I also administered hundreds of electroconvulsive treatments. After completing my training in child psychiatry and obtaining board certification, I spent 13 years training in psychoanalysis at the Washington Psychoanalytic Institute in Washington, DC. Today I am semi-retired but still give lectures to medical students and evaluate patients for possible involuntary commitment.

In the 1950s when I evaluated patients for inpatient commitment in Richmond, VA, we used completely different criteria than are used today. For example, persons needing treatment for psychiatric disorders that would endanger their health such as alcoholism were sent to a state hospital. Today patients are sent to state hospitals only if they present an imminent danger of suicide or homicide or are incapable of self-care.

Now we are treating patients who have a variety of conditions and are released as soon as they are not suicidal or homicidal and have a protective environment. Many stop taking medication or decompensate and are repeatedly brought back for assessment.

Psychiatry has changed thanks to pharmaceuticals and insurance companies. Today, psychiatrists establish a diagnosis at the phenomenological level following the DSM-IV-TR and then prescribe the latest medication. There is no time for psychodynamic formulation or another treatment approach. Social workers, not psychiatrists, perform psychotherapy because it costs less for the insurance companies. The courts buy into the idea that sociopsychiatric problems can be solved with medication. Because of the high cost of hospitalization, as soon as a patient can function he or she is discharged.

In the 1950s the idea was that patients have a right to treatment and therefore were hospitalized in state facilities. Today patients have the right to civil liberties as long as they do not present an imminent danger to society. Although I can remember some cases when patients stayed in state hospitals longer than was strictly necessary, often for the convenience of the patient and family, today I see many more cases when the patient would be better treated in state hospitals at a lower cost to the taxpayers.

Manuel Hernandez, MD
McLean, VA

I could not agree more with Dr. Nasrallah’s editorial on deinstitutionalization. My opinion is based on >50 years experience in psychiatry.

I started my career in l954 at Eastern State Hospital in Williamsburg, VA. As a first-year resident, I was ordered to assist Dr. Walter Freeman in performing transorbital lobotomies. I also administered hundreds of electroconvulsive treatments. After completing my training in child psychiatry and obtaining board certification, I spent 13 years training in psychoanalysis at the Washington Psychoanalytic Institute in Washington, DC. Today I am semi-retired but still give lectures to medical students and evaluate patients for possible involuntary commitment.

In the 1950s when I evaluated patients for inpatient commitment in Richmond, VA, we used completely different criteria than are used today. For example, persons needing treatment for psychiatric disorders that would endanger their health such as alcoholism were sent to a state hospital. Today patients are sent to state hospitals only if they present an imminent danger of suicide or homicide or are incapable of self-care.

Now we are treating patients who have a variety of conditions and are released as soon as they are not suicidal or homicidal and have a protective environment. Many stop taking medication or decompensate and are repeatedly brought back for assessment.

Psychiatry has changed thanks to pharmaceuticals and insurance companies. Today, psychiatrists establish a diagnosis at the phenomenological level following the DSM-IV-TR and then prescribe the latest medication. There is no time for psychodynamic formulation or another treatment approach. Social workers, not psychiatrists, perform psychotherapy because it costs less for the insurance companies. The courts buy into the idea that sociopsychiatric problems can be solved with medication. Because of the high cost of hospitalization, as soon as a patient can function he or she is discharged.

In the 1950s the idea was that patients have a right to treatment and therefore were hospitalized in state facilities. Today patients have the right to civil liberties as long as they do not present an imminent danger to society. Although I can remember some cases when patients stayed in state hospitals longer than was strictly necessary, often for the convenience of the patient and family, today I see many more cases when the patient would be better treated in state hospitals at a lower cost to the taxpayers.

Manuel Hernandez, MD
McLean, VA

I could not agree more with Dr. Nasrallah’s editorial on deinstitutionalization. My opinion is based on >50 years experience in psychiatry.

I started my career in l954 at Eastern State Hospital in Williamsburg, VA. As a first-year resident, I was ordered to assist Dr. Walter Freeman in performing transorbital lobotomies. I also administered hundreds of electroconvulsive treatments. After completing my training in child psychiatry and obtaining board certification, I spent 13 years training in psychoanalysis at the Washington Psychoanalytic Institute in Washington, DC. Today I am semi-retired but still give lectures to medical students and evaluate patients for possible involuntary commitment.

In the 1950s when I evaluated patients for inpatient commitment in Richmond, VA, we used completely different criteria than are used today. For example, persons needing treatment for psychiatric disorders that would endanger their health such as alcoholism were sent to a state hospital. Today patients are sent to state hospitals only if they present an imminent danger of suicide or homicide or are incapable of self-care.

Now we are treating patients who have a variety of conditions and are released as soon as they are not suicidal or homicidal and have a protective environment. Many stop taking medication or decompensate and are repeatedly brought back for assessment.

Psychiatry has changed thanks to pharmaceuticals and insurance companies. Today, psychiatrists establish a diagnosis at the phenomenological level following the DSM-IV-TR and then prescribe the latest medication. There is no time for psychodynamic formulation or another treatment approach. Social workers, not psychiatrists, perform psychotherapy because it costs less for the insurance companies. The courts buy into the idea that sociopsychiatric problems can be solved with medication. Because of the high cost of hospitalization, as soon as a patient can function he or she is discharged.

In the 1950s the idea was that patients have a right to treatment and therefore were hospitalized in state facilities. Today patients have the right to civil liberties as long as they do not present an imminent danger to society. Although I can remember some cases when patients stayed in state hospitals longer than was strictly necessary, often for the convenience of the patient and family, today I see many more cases when the patient would be better treated in state hospitals at a lower cost to the taxpayers.

Manuel Hernandez, MD
McLean, VA

I enjoyed reading Dr. Nasrallah’s editorial in the March issue. The article was well written and I agree with his opinions completely. Also, I congratulate Dr. Nasrallah as I suspect it took quite a bit of bravery to espouse the position he took on this issue.

Todd Baughman, PA-C
Shonto, AZ

I enjoyed reading Dr. Nasrallah’s editorial in the March issue. The article was well written and I agree with his opinions completely. Also, I congratulate Dr. Nasrallah as I suspect it took quite a bit of bravery to espouse the position he took on this issue.

Todd Baughman, PA-C
Shonto, AZ

I enjoyed reading Dr. Nasrallah’s editorial in the March issue. The article was well written and I agree with his opinions completely. Also, I congratulate Dr. Nasrallah as I suspect it took quite a bit of bravery to espouse the position he took on this issue.

Todd Baughman, PA-C
Shonto, AZ