Current Psychiatry

Schizophrenia prodrome is an early or prepsychotic state that is a deviation from an individual’s usual behavior and experience.¹ Prepsychotic patients can differentiate reality from fantasy but gradually lose this ability as their illness progresses.² Therefore, early identification and treatment of prepsychotic adolescents and those with early psychosis can reduce social withdrawal, isolation, and psychosocial morbidity and mortality.

Detective work

Probing for possible paranoia and psychotic symptoms in adolescents who do not present with these complaints can be challenging. Maintain rapport as you probe for unusual thought content and delusional ideas by inquiring about your patient’s “experiences” rather than the more pejorative term “problems.” Some prodromal patients may be at imminent risk of conversion to psychosis and continued deterioration. The following questions that are based on prodrome assessment scales^1,3 can help detect emerging psychosis.

Thinking can be evaluated by asking:

• Do you feel that you or people around you have changed in a way you can’t explain?
  
• Do people seem alien or evil?
  
• Have you been confused about whether something is real or imaginary?
  
• Do you daydream a lot?
  
• Are you preoccupied with stories or ideas?
  

• How are others treating you?
  
• Do you feel that people think about you in a negative way?
  
• Do you feel singled out?
  
• Do you feel that you must be vigilant around others to be safe?
  

• How do you spend your free time?
  
• How often do you talk with friends and family?
  
• What groups do you participate in?
  
• How friendly are others at school or work?
  

Ask your patient about computer use, especially favorite Web sites and electronic games. Some alienated and schizoid adolescents may be heavily involved in role-playing fantasy electronic games.⁴ Loners may fill their free time in cyberspace.

Perceptual abnormalities and hallucinations can be determined by asking:

• Do you ever feel your mind plays tricks on you?
  
• Do you hear unusual sounds?
  
• Do you ever hear your name being called when no one is there?
  
• Do you feel a presence around you?
  
• Do you ever see people or things but realize they may not be real?
  

• Do you feel numb?
  
• Do you feel disconnected from yourself or your life, as if you are a spectator?
  
• Do you lack rapport with others?
  
• Are you bored?
  

Estimate deteriorating role functioning by inquiring about problems completing assignments and impaired tolerance of normal stress.

• Do you avoid or feel overwhelmed by situations that previously you could deal with?
  
• Is it harder to get through the day?
  
• Are you easily thrown off by unexpected events?
  

Schizophrenia prodrome is an early or prepsychotic state that is a deviation from an individual’s usual behavior and experience.¹ Prepsychotic patients can differentiate reality from fantasy but gradually lose this ability as their illness progresses.² Therefore, early identification and treatment of prepsychotic adolescents and those with early psychosis can reduce social withdrawal, isolation, and psychosocial morbidity and mortality.

Detective work

Probing for possible paranoia and psychotic symptoms in adolescents who do not present with these complaints can be challenging. Maintain rapport as you probe for unusual thought content and delusional ideas by inquiring about your patient’s “experiences” rather than the more pejorative term “problems.” Some prodromal patients may be at imminent risk of conversion to psychosis and continued deterioration. The following questions that are based on prodrome assessment scales^1,3 can help detect emerging psychosis.

Thinking can be evaluated by asking:

• Do you feel that you or people around you have changed in a way you can’t explain?
  
• Do people seem alien or evil?
  
• Have you been confused about whether something is real or imaginary?
  
• Do you daydream a lot?
  
• Are you preoccupied with stories or ideas?
  

• How are others treating you?
  
• Do you feel that people think about you in a negative way?
  
• Do you feel singled out?
  
• Do you feel that you must be vigilant around others to be safe?
  

• How do you spend your free time?
  
• How often do you talk with friends and family?
  
• What groups do you participate in?
  
• How friendly are others at school or work?
  

Ask your patient about computer use, especially favorite Web sites and electronic games. Some alienated and schizoid adolescents may be heavily involved in role-playing fantasy electronic games.⁴ Loners may fill their free time in cyberspace.

Perceptual abnormalities and hallucinations can be determined by asking:

• Do you ever feel your mind plays tricks on you?
  
• Do you hear unusual sounds?
  
• Do you ever hear your name being called when no one is there?
  
• Do you feel a presence around you?
  
• Do you ever see people or things but realize they may not be real?
  

• Do you feel numb?
  
• Do you feel disconnected from yourself or your life, as if you are a spectator?
  
• Do you lack rapport with others?
  
• Are you bored?
  

Estimate deteriorating role functioning by inquiring about problems completing assignments and impaired tolerance of normal stress.

• Do you avoid or feel overwhelmed by situations that previously you could deal with?
  
• Is it harder to get through the day?
  
• Are you easily thrown off by unexpected events?
  

Schizophrenia prodrome is an early or prepsychotic state that is a deviation from an individual’s usual behavior and experience.¹ Prepsychotic patients can differentiate reality from fantasy but gradually lose this ability as their illness progresses.² Therefore, early identification and treatment of prepsychotic adolescents and those with early psychosis can reduce social withdrawal, isolation, and psychosocial morbidity and mortality.

Detective work

Probing for possible paranoia and psychotic symptoms in adolescents who do not present with these complaints can be challenging. Maintain rapport as you probe for unusual thought content and delusional ideas by inquiring about your patient’s “experiences” rather than the more pejorative term “problems.” Some prodromal patients may be at imminent risk of conversion to psychosis and continued deterioration. The following questions that are based on prodrome assessment scales^1,3 can help detect emerging psychosis.

Thinking can be evaluated by asking:

• Do you feel that you or people around you have changed in a way you can’t explain?
  
• Do people seem alien or evil?
  
• Have you been confused about whether something is real or imaginary?
  
• Do you daydream a lot?
  
• Are you preoccupied with stories or ideas?
  

• How are others treating you?
  
• Do you feel that people think about you in a negative way?
  
• Do you feel singled out?
  
• Do you feel that you must be vigilant around others to be safe?
  

• How do you spend your free time?
  
• How often do you talk with friends and family?
  
• What groups do you participate in?
  
• How friendly are others at school or work?
  

Ask your patient about computer use, especially favorite Web sites and electronic games. Some alienated and schizoid adolescents may be heavily involved in role-playing fantasy electronic games.⁴ Loners may fill their free time in cyberspace.

Perceptual abnormalities and hallucinations can be determined by asking:

• Do you ever feel your mind plays tricks on you?
  
• Do you hear unusual sounds?
  
• Do you ever hear your name being called when no one is there?
  
• Do you feel a presence around you?
  
• Do you ever see people or things but realize they may not be real?
  

• Do you feel numb?
  
• Do you feel disconnected from yourself or your life, as if you are a spectator?
  
• Do you lack rapport with others?
  
• Are you bored?
  

Estimate deteriorating role functioning by inquiring about problems completing assignments and impaired tolerance of normal stress.

• Do you avoid or feel overwhelmed by situations that previously you could deal with?
  
• Is it harder to get through the day?
  
• Are you easily thrown off by unexpected events?
  

Prevailing wisdom says it takes 3 to 4 weeks for an antidepressant to show clinical effect. Historically, patients who improve in the first 2 weeks have been labeled “placebo responders.”¹ Several recent studies, however, demonstrate a real, drug-based response in many patients as early as the first week of treatment, depending on the medication (Table).^2-5 In practical terms, these studies raise the question of how long you should wait for an antidepressant to “work.”

Table

Variables in antidepressant response

Early indications. Here are some tips for gauging antidepressant response, depending on what you see in the first 2 to 4 weeks:

• Obtain a pretreatment score on the Beck Depression Inventory or other depression rating scale, and repeat the assessment at least once between days 7 and 10 of treatment. If there is little or no improvement, consider a modest dosage increase.
  
• Don’t assume that a patient who responds to an antidepressant during the first 2 weeks is experiencing a placebo effect. It may be a drug-mediated response. Some patients will retain and build on this early response, whereas others’ response may wane over subsequent weeks.
  
• No response to an antidepressant during weeks 1 through 4 does not bode well for most patients,^5,6 although the data do not support giving up on an antidepressant after 1 to 2 weeks of nonresponse. Responses will “accumulate” during weeks 3 to 5 of treatment.⁷
  
• Patients who show little response during the first 2 weeks of treatment but experience some improvement during weeks 3 and 4 may be late responders. However, if the patient shows no improvement by week 3 or 4, consider switching to a different antidepressant, perhaps one from a different chemical class.⁸
  
• Different neurovegetative signs and symptoms of depression may improve at different rates, with some requiring >8 weeks of treatment. Insight, for example, may not improve until the second month of treatment.⁹
  
• Individualize treatment. Many treatment-refractory depressed patients—who failed to respond to 1 or more adequate drug trials—may require longer and more intensive treatment (>3 months) beffore showing a robust response.¹⁰
  
• “Onset of response” does not equal “clinical recovery,” nor is an improved Hamilton Depression Scale score a proxy for “high quality of life.” Patients may need ≥2 months for clinically significant improvement in interpersonal, social, and vocational function.¹¹
  

Acknowledgement

The author expresses his appreciation to Michael Posternak, MD, Andrew Nierenberg, MD, and Alex J. Mitchell, MD, for their helpful comments on an early draft of this article.

Prevailing wisdom says it takes 3 to 4 weeks for an antidepressant to show clinical effect. Historically, patients who improve in the first 2 weeks have been labeled “placebo responders.”¹ Several recent studies, however, demonstrate a real, drug-based response in many patients as early as the first week of treatment, depending on the medication (Table).^2-5 In practical terms, these studies raise the question of how long you should wait for an antidepressant to “work.”

Table

Variables in antidepressant response

Early indications. Here are some tips for gauging antidepressant response, depending on what you see in the first 2 to 4 weeks:

• Obtain a pretreatment score on the Beck Depression Inventory or other depression rating scale, and repeat the assessment at least once between days 7 and 10 of treatment. If there is little or no improvement, consider a modest dosage increase.
  
• Don’t assume that a patient who responds to an antidepressant during the first 2 weeks is experiencing a placebo effect. It may be a drug-mediated response. Some patients will retain and build on this early response, whereas others’ response may wane over subsequent weeks.
  
• No response to an antidepressant during weeks 1 through 4 does not bode well for most patients,^5,6 although the data do not support giving up on an antidepressant after 1 to 2 weeks of nonresponse. Responses will “accumulate” during weeks 3 to 5 of treatment.⁷
  
• Patients who show little response during the first 2 weeks of treatment but experience some improvement during weeks 3 and 4 may be late responders. However, if the patient shows no improvement by week 3 or 4, consider switching to a different antidepressant, perhaps one from a different chemical class.⁸
  
• Different neurovegetative signs and symptoms of depression may improve at different rates, with some requiring >8 weeks of treatment. Insight, for example, may not improve until the second month of treatment.⁹
  
• Individualize treatment. Many treatment-refractory depressed patients—who failed to respond to 1 or more adequate drug trials—may require longer and more intensive treatment (>3 months) beffore showing a robust response.¹⁰
  
• “Onset of response” does not equal “clinical recovery,” nor is an improved Hamilton Depression Scale score a proxy for “high quality of life.” Patients may need ≥2 months for clinically significant improvement in interpersonal, social, and vocational function.¹¹
  

Acknowledgement

The author expresses his appreciation to Michael Posternak, MD, Andrew Nierenberg, MD, and Alex J. Mitchell, MD, for their helpful comments on an early draft of this article.

Prevailing wisdom says it takes 3 to 4 weeks for an antidepressant to show clinical effect. Historically, patients who improve in the first 2 weeks have been labeled “placebo responders.”¹ Several recent studies, however, demonstrate a real, drug-based response in many patients as early as the first week of treatment, depending on the medication (Table).^2-5 In practical terms, these studies raise the question of how long you should wait for an antidepressant to “work.”

Table

Variables in antidepressant response

Early indications. Here are some tips for gauging antidepressant response, depending on what you see in the first 2 to 4 weeks:

• Obtain a pretreatment score on the Beck Depression Inventory or other depression rating scale, and repeat the assessment at least once between days 7 and 10 of treatment. If there is little or no improvement, consider a modest dosage increase.
  
• Don’t assume that a patient who responds to an antidepressant during the first 2 weeks is experiencing a placebo effect. It may be a drug-mediated response. Some patients will retain and build on this early response, whereas others’ response may wane over subsequent weeks.
  
• No response to an antidepressant during weeks 1 through 4 does not bode well for most patients,^5,6 although the data do not support giving up on an antidepressant after 1 to 2 weeks of nonresponse. Responses will “accumulate” during weeks 3 to 5 of treatment.⁷
  
• Patients who show little response during the first 2 weeks of treatment but experience some improvement during weeks 3 and 4 may be late responders. However, if the patient shows no improvement by week 3 or 4, consider switching to a different antidepressant, perhaps one from a different chemical class.⁸
  
• Different neurovegetative signs and symptoms of depression may improve at different rates, with some requiring >8 weeks of treatment. Insight, for example, may not improve until the second month of treatment.⁹
  
• Individualize treatment. Many treatment-refractory depressed patients—who failed to respond to 1 or more adequate drug trials—may require longer and more intensive treatment (>3 months) beffore showing a robust response.¹⁰
  
• “Onset of response” does not equal “clinical recovery,” nor is an improved Hamilton Depression Scale score a proxy for “high quality of life.” Patients may need ≥2 months for clinically significant improvement in interpersonal, social, and vocational function.¹¹
  

Acknowledgement

The author expresses his appreciation to Michael Posternak, MD, Andrew Nierenberg, MD, and Alex J. Mitchell, MD, for their helpful comments on an early draft of this article.

In “Dangers of stimulant patch misuse” (Current Psychiatry, March 2007) Dr. A. Preston West raises concerns about potential toxic increases in methylphenidate levels if a transdermal patch is not used as directed or if it is scratched or re-attached during use. In support of his argument, Dr. West refers to a transdermal preparation of clonidine, an antihypertensive medication.¹ However, his concerns are based upon the assumption that methylphenidate and clonidine patches use the same technology and have the same pharmacologic properties. There are substantial differences between these delivery systems and their pharmacologic mechanisms.

The clonidine patch uses first-generation patch technology that contains active medication dissolved in a liquid reservoir separated from the skin by a rate-controlling membrane and an adhesive layer.¹ Medication delivery to the skin is determined by the rate-controlling membrane.¹ This creates the possibility of increased administration of medication if the rate-controlling layer is broken.

In comparison, Daytrana (methylphenidate transdermal system) utilizes a dot matrix patch technology. Methylphenidate is mixed with acrylic and then combined with silicone, holding the drug in the patch and skin, respectively.² The drug’s adhesive design leads to a semi-solid suspension of microscopic concentrated drug cells evenly dispersed through an uncompromised silicone adhesive.² The rate of medication delivery is based on the components in the matrix. Therefore, this technology decreases the risk of increased doses of medication when patch integrity is violated.

In terms of pharmacologic effects, clonidine works by stimulation of alpha-2 adrenergic receptors in the brain. Methylphenidate is a stimulant and is thought to act by blocking the reuptake of dopamine and norepinephrine.^1,3 These 2 chemicals have different pharmacologic properties and different adverse event profiles.

Of course, it is possible to misuse the methylphenidate patch by taking more than the prescribed amount, which could result in adverse events. However, inappropriate usage can be monitored, and patients should be advised of the risks of taking too much stimulant medication.

As with all drugs, take care to choose the most appropriate medication and delivery system for your patient. Although not every patient is a candidate for a transdermal delivery system, it can be an effective means for delivering methylphenidate to treat ADHD symptoms.

Lenard Adler, MD
Associate professor of psychiatry
Director, adult ADHD program
New York University Medical Center
New York

Anthony Rostain, MD, MA
Associate professor of psychiatry and pediatrics
University of Pennsylvania School of Medicine
Philadelphia

In “Dangers of stimulant patch misuse” (Current Psychiatry, March 2007) Dr. A. Preston West raises concerns about potential toxic increases in methylphenidate levels if a transdermal patch is not used as directed or if it is scratched or re-attached during use. In support of his argument, Dr. West refers to a transdermal preparation of clonidine, an antihypertensive medication.¹ However, his concerns are based upon the assumption that methylphenidate and clonidine patches use the same technology and have the same pharmacologic properties. There are substantial differences between these delivery systems and their pharmacologic mechanisms.

The clonidine patch uses first-generation patch technology that contains active medication dissolved in a liquid reservoir separated from the skin by a rate-controlling membrane and an adhesive layer.¹ Medication delivery to the skin is determined by the rate-controlling membrane.¹ This creates the possibility of increased administration of medication if the rate-controlling layer is broken.

In comparison, Daytrana (methylphenidate transdermal system) utilizes a dot matrix patch technology. Methylphenidate is mixed with acrylic and then combined with silicone, holding the drug in the patch and skin, respectively.² The drug’s adhesive design leads to a semi-solid suspension of microscopic concentrated drug cells evenly dispersed through an uncompromised silicone adhesive.² The rate of medication delivery is based on the components in the matrix. Therefore, this technology decreases the risk of increased doses of medication when patch integrity is violated.

In terms of pharmacologic effects, clonidine works by stimulation of alpha-2 adrenergic receptors in the brain. Methylphenidate is a stimulant and is thought to act by blocking the reuptake of dopamine and norepinephrine.^1,3 These 2 chemicals have different pharmacologic properties and different adverse event profiles.

Of course, it is possible to misuse the methylphenidate patch by taking more than the prescribed amount, which could result in adverse events. However, inappropriate usage can be monitored, and patients should be advised of the risks of taking too much stimulant medication.

As with all drugs, take care to choose the most appropriate medication and delivery system for your patient. Although not every patient is a candidate for a transdermal delivery system, it can be an effective means for delivering methylphenidate to treat ADHD symptoms.

Lenard Adler, MD
Associate professor of psychiatry
Director, adult ADHD program
New York University Medical Center
New York

Anthony Rostain, MD, MA
Associate professor of psychiatry and pediatrics
University of Pennsylvania School of Medicine
Philadelphia

In “Dangers of stimulant patch misuse” (Current Psychiatry, March 2007) Dr. A. Preston West raises concerns about potential toxic increases in methylphenidate levels if a transdermal patch is not used as directed or if it is scratched or re-attached during use. In support of his argument, Dr. West refers to a transdermal preparation of clonidine, an antihypertensive medication.¹ However, his concerns are based upon the assumption that methylphenidate and clonidine patches use the same technology and have the same pharmacologic properties. There are substantial differences between these delivery systems and their pharmacologic mechanisms.

The clonidine patch uses first-generation patch technology that contains active medication dissolved in a liquid reservoir separated from the skin by a rate-controlling membrane and an adhesive layer.¹ Medication delivery to the skin is determined by the rate-controlling membrane.¹ This creates the possibility of increased administration of medication if the rate-controlling layer is broken.

In comparison, Daytrana (methylphenidate transdermal system) utilizes a dot matrix patch technology. Methylphenidate is mixed with acrylic and then combined with silicone, holding the drug in the patch and skin, respectively.² The drug’s adhesive design leads to a semi-solid suspension of microscopic concentrated drug cells evenly dispersed through an uncompromised silicone adhesive.² The rate of medication delivery is based on the components in the matrix. Therefore, this technology decreases the risk of increased doses of medication when patch integrity is violated.

In terms of pharmacologic effects, clonidine works by stimulation of alpha-2 adrenergic receptors in the brain. Methylphenidate is a stimulant and is thought to act by blocking the reuptake of dopamine and norepinephrine.^1,3 These 2 chemicals have different pharmacologic properties and different adverse event profiles.

Of course, it is possible to misuse the methylphenidate patch by taking more than the prescribed amount, which could result in adverse events. However, inappropriate usage can be monitored, and patients should be advised of the risks of taking too much stimulant medication.

As with all drugs, take care to choose the most appropriate medication and delivery system for your patient. Although not every patient is a candidate for a transdermal delivery system, it can be an effective means for delivering methylphenidate to treat ADHD symptoms.

Lenard Adler, MD
Associate professor of psychiatry
Director, adult ADHD program
New York University Medical Center
New York

Anthony Rostain, MD, MA
Associate professor of psychiatry and pediatrics
University of Pennsylvania School of Medicine
Philadelphia

Dr. Menahem Krakowski’s article “Violent behavior: Choosing antipsychotic and other agents” (Current Psychiatry, April 2007) did not discuss violent behavior triggered by posttraumatic re-enactments, which often are dissociated experiences. Patients’ past trauma experiences may be triggered in settings such as inpatient and residential facilities and cause intense rage and assaults. Not recognizing them and using intramuscular medication—although producing rapid sedation—can intensify and lower the threshold for repeated re-enactments in these restricted settings.

In the adolescent residential facility where I work, posttraumatic rages are the most common form of aggression. Recent work at Massachusetts General Hospital with patients having suppressed rape memories found that propranolol may be the most effective pharmacologic agent to decrease the intensity of re-enactment experiences.

The association between aggression and posttraumatic experiences is described in a well-known case book.¹ Effective treatment requires clinicians to recognize that the aggression benefits from an abreaction context and correction-based therapy.²

Traumatic behavior in inpatient and residential settings may be overlooked or mislabeled as aggression. For this reason, whenever aggressive behavior is raised as a clinical issue, it should simultaneously raise the possibility that posttraumatic re-enactment is driving its presentation.

Kim J. Masters, MD
Medical director
Three Rivers Midlands Residential Treatment Center
West Columbia, SC
Clinical assistant professor
Medical University of South Carolina
Charleston

Dr. Menahem Krakowski’s article “Violent behavior: Choosing antipsychotic and other agents” (Current Psychiatry, April 2007) did not discuss violent behavior triggered by posttraumatic re-enactments, which often are dissociated experiences. Patients’ past trauma experiences may be triggered in settings such as inpatient and residential facilities and cause intense rage and assaults. Not recognizing them and using intramuscular medication—although producing rapid sedation—can intensify and lower the threshold for repeated re-enactments in these restricted settings.

In the adolescent residential facility where I work, posttraumatic rages are the most common form of aggression. Recent work at Massachusetts General Hospital with patients having suppressed rape memories found that propranolol may be the most effective pharmacologic agent to decrease the intensity of re-enactment experiences.

The association between aggression and posttraumatic experiences is described in a well-known case book.¹ Effective treatment requires clinicians to recognize that the aggression benefits from an abreaction context and correction-based therapy.²

Traumatic behavior in inpatient and residential settings may be overlooked or mislabeled as aggression. For this reason, whenever aggressive behavior is raised as a clinical issue, it should simultaneously raise the possibility that posttraumatic re-enactment is driving its presentation.

Kim J. Masters, MD
Medical director
Three Rivers Midlands Residential Treatment Center
West Columbia, SC
Clinical assistant professor
Medical University of South Carolina
Charleston

Dr. Menahem Krakowski’s article “Violent behavior: Choosing antipsychotic and other agents” (Current Psychiatry, April 2007) did not discuss violent behavior triggered by posttraumatic re-enactments, which often are dissociated experiences. Patients’ past trauma experiences may be triggered in settings such as inpatient and residential facilities and cause intense rage and assaults. Not recognizing them and using intramuscular medication—although producing rapid sedation—can intensify and lower the threshold for repeated re-enactments in these restricted settings.

In the adolescent residential facility where I work, posttraumatic rages are the most common form of aggression. Recent work at Massachusetts General Hospital with patients having suppressed rape memories found that propranolol may be the most effective pharmacologic agent to decrease the intensity of re-enactment experiences.

The association between aggression and posttraumatic experiences is described in a well-known case book.¹ Effective treatment requires clinicians to recognize that the aggression benefits from an abreaction context and correction-based therapy.²

Traumatic behavior in inpatient and residential settings may be overlooked or mislabeled as aggression. For this reason, whenever aggressive behavior is raised as a clinical issue, it should simultaneously raise the possibility that posttraumatic re-enactment is driving its presentation.

Kim J. Masters, MD
Medical director
Three Rivers Midlands Residential Treatment Center
West Columbia, SC
Clinical assistant professor
Medical University of South Carolina
Charleston

I enjoyed Dr. Henry A. Nasrallah’s editorial (“3 Types of ‘EBM’: Which do you practice?” Current Psychiatry, April 2007), which reminded me of a rough guide to clinical prescribing that I often refer to when teaching residents. According to a bell-shaped curve, approximately 80% of your patients should be on “normal” doses and medication combinations. However 10% should be on abnormally low or high doses, or an unusual combination of medications. If all your patients are on similar standard or FDA-approved doses, seek consultation.

Obviously, this guideline does not apply to clinicians working with atypical patient populations.

James H. Thomas, MD
Cincinnati, OH

Dr. Nasrallah responds

Dr. Thomas’ dose distribution guideline would also correlate with the slow, regular, and rapid cytochrome metabolism found in the general population.

Henry A. Nasrallah, MD
Professor of psychiatry, neurology,
and neuroscience
University of Cincinnati College of Medicine

I enjoyed Dr. Henry A. Nasrallah’s editorial (“3 Types of ‘EBM’: Which do you practice?” Current Psychiatry, April 2007), which reminded me of a rough guide to clinical prescribing that I often refer to when teaching residents. According to a bell-shaped curve, approximately 80% of your patients should be on “normal” doses and medication combinations. However 10% should be on abnormally low or high doses, or an unusual combination of medications. If all your patients are on similar standard or FDA-approved doses, seek consultation.

Obviously, this guideline does not apply to clinicians working with atypical patient populations.

James H. Thomas, MD
Cincinnati, OH

Dr. Nasrallah responds

Dr. Thomas’ dose distribution guideline would also correlate with the slow, regular, and rapid cytochrome metabolism found in the general population.

Henry A. Nasrallah, MD
Professor of psychiatry, neurology,
and neuroscience
University of Cincinnati College of Medicine

I enjoyed Dr. Henry A. Nasrallah’s editorial (“3 Types of ‘EBM’: Which do you practice?” Current Psychiatry, April 2007), which reminded me of a rough guide to clinical prescribing that I often refer to when teaching residents. According to a bell-shaped curve, approximately 80% of your patients should be on “normal” doses and medication combinations. However 10% should be on abnormally low or high doses, or an unusual combination of medications. If all your patients are on similar standard or FDA-approved doses, seek consultation.

Obviously, this guideline does not apply to clinicians working with atypical patient populations.

James H. Thomas, MD
Cincinnati, OH

Dr. Nasrallah responds

Dr. Thomas’ dose distribution guideline would also correlate with the slow, regular, and rapid cytochrome metabolism found in the general population.

Henry A. Nasrallah, MD
Professor of psychiatry, neurology,
and neuroscience
University of Cincinnati College of Medicine

Missing from Dr. Bruce Sutor’s excellent article about negotiating the managed care maze (“Avoiding managed care’s pitfalls and pratfalls,” Current Psychiatry, March 2007) is a detailed discussion of “hold harmless” clauses that are often inserted into contracts that physicians must sign. These clauses aim to protect the managed care company from legal liability in certain situations. This manipulative and dishonest displacement of responsibility for service denial onto the practitioner’s shoulders is a major factor in clinician dissatisfaction.

Richard C. Heckmann, MD
Staff psychiatrist
Veterans Administration Medical Center Fayetteville
Fayetteville, AR

Dr. Sutor responds

There are 2 common forms of “hold harmless” agreements in managed care contracts. The first typically states that if the managed care company become insolvent or otherwise unable to pay claims, the provider will not bill the patient for the unpaid fees. Beyond negotiating this clause out of the contract—an unlikely event—the best way for practitioners to minimize potential losses is to submit claims in a timely fashion.

The second type states that providers will hold the managed care company harmless if a patient sues a provider. If the patient also sues the managed care company, the provider could be liable for expenses incurred by the managed care company, regardless of the suit’s outcome. Practitioners can protect themselves by confirming that their malpractice insurance covers such expenses. Many contract attorneys and managed care consultants strongly recommend against signing contracts containing this type of clause.

Bruce Sutor, MD
Assistant professor
Department of psychiatry and psychology
Mayo Clinic College of Medicine
Rochester, MN

Missing from Dr. Bruce Sutor’s excellent article about negotiating the managed care maze (“Avoiding managed care’s pitfalls and pratfalls,” Current Psychiatry, March 2007) is a detailed discussion of “hold harmless” clauses that are often inserted into contracts that physicians must sign. These clauses aim to protect the managed care company from legal liability in certain situations. This manipulative and dishonest displacement of responsibility for service denial onto the practitioner’s shoulders is a major factor in clinician dissatisfaction.

Richard C. Heckmann, MD
Staff psychiatrist
Veterans Administration Medical Center Fayetteville
Fayetteville, AR

Dr. Sutor responds

There are 2 common forms of “hold harmless” agreements in managed care contracts. The first typically states that if the managed care company become insolvent or otherwise unable to pay claims, the provider will not bill the patient for the unpaid fees. Beyond negotiating this clause out of the contract—an unlikely event—the best way for practitioners to minimize potential losses is to submit claims in a timely fashion.

The second type states that providers will hold the managed care company harmless if a patient sues a provider. If the patient also sues the managed care company, the provider could be liable for expenses incurred by the managed care company, regardless of the suit’s outcome. Practitioners can protect themselves by confirming that their malpractice insurance covers such expenses. Many contract attorneys and managed care consultants strongly recommend against signing contracts containing this type of clause.

Bruce Sutor, MD
Assistant professor
Department of psychiatry and psychology
Mayo Clinic College of Medicine
Rochester, MN

Missing from Dr. Bruce Sutor’s excellent article about negotiating the managed care maze (“Avoiding managed care’s pitfalls and pratfalls,” Current Psychiatry, March 2007) is a detailed discussion of “hold harmless” clauses that are often inserted into contracts that physicians must sign. These clauses aim to protect the managed care company from legal liability in certain situations. This manipulative and dishonest displacement of responsibility for service denial onto the practitioner’s shoulders is a major factor in clinician dissatisfaction.

Richard C. Heckmann, MD
Staff psychiatrist
Veterans Administration Medical Center Fayetteville
Fayetteville, AR

Dr. Sutor responds

There are 2 common forms of “hold harmless” agreements in managed care contracts. The first typically states that if the managed care company become insolvent or otherwise unable to pay claims, the provider will not bill the patient for the unpaid fees. Beyond negotiating this clause out of the contract—an unlikely event—the best way for practitioners to minimize potential losses is to submit claims in a timely fashion.

The second type states that providers will hold the managed care company harmless if a patient sues a provider. If the patient also sues the managed care company, the provider could be liable for expenses incurred by the managed care company, regardless of the suit’s outcome. Practitioners can protect themselves by confirming that their malpractice insurance covers such expenses. Many contract attorneys and managed care consultants strongly recommend against signing contracts containing this type of clause.

Bruce Sutor, MD
Assistant professor
Department of psychiatry and psychology
Mayo Clinic College of Medicine
Rochester, MN

The article “Hypnotics and driving: FDA action and clinical trials show need for precautions” (Current Psychiatry, April 2007) was superb in its thoroughness on sedative hypnotics’ risks. However, it lacked any comparative data and discussion about the risks associated with other commonly used sleep medications such as trazodone, ramelteon, or quetiapine. It also does not provide enough comparative information on driving impairment from diminished sleep. As for informed consent, a useful strategy is to find out if someone else shares the patient’s bed or bedroom, and to make sure he or she knows the risks of sedative hypnotics.

Finally, care should be taken when making a diagnostic assessment before using sedative hypnotics. Rule out other medical causes of poor sleep—such as sleep apnea—because I’ve observed that such patients use more sleep medication than necessary because the condition diminishes the drugs’ effectiveness. Of course, sleep hygiene techniques should be tried first.

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

Drs. Freeman and Buckland respond

We agree with Dr. Moffic that a more comprehensive comparison of hypnotics would be useful. Sleep problems are almost always multifactorial, and behavioral manipulation—not medication—often is the first and best intervention. We know that a driver’s reaction time decreases as fatigue and sleepiness increase,¹ an important consideration when developing a treatment plan, especially when treating a patient who drives for a living. Physicians should investigate medical disorders such as sleep apnea and ensure that patients employ sleep hygiene principles before beginning any medication. Safety issues detailed in the article need to be part of the informed consent.

Enlisting the help of others close to the patient increases the detection of side effects and complications. This support can be applied to any medication or intervention used to treat our patients. The sedative hypnotics can be helpful to patients but also quite damaging. Any treatment plan must consider safety first.

Bradley Freeman, MD
Fourth-year resident

J. Jason Buckland, DO
Department of neuropsychiatry and
behavioral science
University of South Carolina School
of Medicine, Columbia

The article “Hypnotics and driving: FDA action and clinical trials show need for precautions” (Current Psychiatry, April 2007) was superb in its thoroughness on sedative hypnotics’ risks. However, it lacked any comparative data and discussion about the risks associated with other commonly used sleep medications such as trazodone, ramelteon, or quetiapine. It also does not provide enough comparative information on driving impairment from diminished sleep. As for informed consent, a useful strategy is to find out if someone else shares the patient’s bed or bedroom, and to make sure he or she knows the risks of sedative hypnotics.

Finally, care should be taken when making a diagnostic assessment before using sedative hypnotics. Rule out other medical causes of poor sleep—such as sleep apnea—because I’ve observed that such patients use more sleep medication than necessary because the condition diminishes the drugs’ effectiveness. Of course, sleep hygiene techniques should be tried first.

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

Drs. Freeman and Buckland respond

We agree with Dr. Moffic that a more comprehensive comparison of hypnotics would be useful. Sleep problems are almost always multifactorial, and behavioral manipulation—not medication—often is the first and best intervention. We know that a driver’s reaction time decreases as fatigue and sleepiness increase,¹ an important consideration when developing a treatment plan, especially when treating a patient who drives for a living. Physicians should investigate medical disorders such as sleep apnea and ensure that patients employ sleep hygiene principles before beginning any medication. Safety issues detailed in the article need to be part of the informed consent.

Enlisting the help of others close to the patient increases the detection of side effects and complications. This support can be applied to any medication or intervention used to treat our patients. The sedative hypnotics can be helpful to patients but also quite damaging. Any treatment plan must consider safety first.

Bradley Freeman, MD
Fourth-year resident

J. Jason Buckland, DO
Department of neuropsychiatry and
behavioral science
University of South Carolina School
of Medicine, Columbia

The article “Hypnotics and driving: FDA action and clinical trials show need for precautions” (Current Psychiatry, April 2007) was superb in its thoroughness on sedative hypnotics’ risks. However, it lacked any comparative data and discussion about the risks associated with other commonly used sleep medications such as trazodone, ramelteon, or quetiapine. It also does not provide enough comparative information on driving impairment from diminished sleep. As for informed consent, a useful strategy is to find out if someone else shares the patient’s bed or bedroom, and to make sure he or she knows the risks of sedative hypnotics.

Finally, care should be taken when making a diagnostic assessment before using sedative hypnotics. Rule out other medical causes of poor sleep—such as sleep apnea—because I’ve observed that such patients use more sleep medication than necessary because the condition diminishes the drugs’ effectiveness. Of course, sleep hygiene techniques should be tried first.

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

Drs. Freeman and Buckland respond

We agree with Dr. Moffic that a more comprehensive comparison of hypnotics would be useful. Sleep problems are almost always multifactorial, and behavioral manipulation—not medication—often is the first and best intervention. We know that a driver’s reaction time decreases as fatigue and sleepiness increase,¹ an important consideration when developing a treatment plan, especially when treating a patient who drives for a living. Physicians should investigate medical disorders such as sleep apnea and ensure that patients employ sleep hygiene principles before beginning any medication. Safety issues detailed in the article need to be part of the informed consent.

Enlisting the help of others close to the patient increases the detection of side effects and complications. This support can be applied to any medication or intervention used to treat our patients. The sedative hypnotics can be helpful to patients but also quite damaging. Any treatment plan must consider safety first.

Bradley Freeman, MD
Fourth-year resident

J. Jason Buckland, DO
Department of neuropsychiatry and
behavioral science
University of South Carolina School
of Medicine, Columbia

Where do you turn for help in dosing an antidepressant for a child with major depressive disorder? You might be misinformed if you rely on methods used in multicenter, randomized, placebo-controlled trials, according to Robert L. Findling, MD, an expert in child and adolescent pharmacokinetics (PK).

In a recent review,¹ Dr. Findling and colleagues at University Hospitals, Case Medical Center, and Case Western Reserve University concluded that:

• Data from PK studies do not support the dosing strategies used in many placebo-controlled efficacy trials of antidepressants in children and adolescents
• Excessively low or high dosages may explain—at least in part—why antidepressants failed to show efficacy or were associated with agitation, hostility, or increased suicidality among depressed pediatric patients in some studies.

To provide Current Psychiatry readers with more information on this topic, Section Editor Robert A. Kowatch, MD, PhD, interviewed Dr. Findling about pediatric PK studies and what they can tell clinicians about dosing antidepressants and antipsychotics in children and adolescents.

Not ‘small adults’

Dr. Kowatch: Warnings about a risk of suicidality in young people taking antidepressants have increased physicians’ concern about accurate dosing for children. How do pediatric pharmacokinetic parameters differ from those of adults?

Dr. Findling: Children and adolescents are not, of course, simply small adults. Significant differences in absorption rate, volume of distribution, and elimination affect PK parameters, such as half-life, throughout the life cycle.²

Dr. Kowatch: What determines these differences? Are they based on factors such as weight, age, puberty, or gender?

Dr. Findling: In general, PK differences observed with antidepressants have been dependent on the patient’s age or weight, rather than on gender differences or sexual maturation. To assume that drug exposure is weight-proportional across the life cycle is fraught with peril and is not true for many compounds, including psychotropics.

Dr. Kowatch: In which age groups would clinicians see the greatest differences in drug exposure?

Dr. Findling: It depends on the compound. Exposure to lithium, for example, is determined by the glomerular filtration rate, which often is much higher and necessitates higher weight-adjusted dosing in a younger child than in a teenager or adult. Drug exposure becomes more complicated with more complex compounds, with differing volumes of distribution, absorption rates, and perhaps multiple enzymes involved in bio-disposition.

Factors that affect dosing

Dr. Kowatch: Clinically, what’s the best way to determine safe, effective psychotropic dosing in children?

Dr. Findling: The short answer is to study the literature, and unfortunately most people find PK studies just about as interesting as watching paint dry. But a good PK study provides insight into a very important parameter, which is dosing.

Ultimately, we can’t talk about a medicine’s effectiveness or safety as a fixed statement. You can’t say drug “x” is effective for this condition or drug “y” is associated with this rate of side effects because tolerability and effectiveness are dose-dependent. And if you don’t know how to dose a medicine, you can’t characterize its pharmacodynamic properties when prescribing it to a youngster.

So you have to know the literature; what happens at different doses is terribly important.

Dr. Kowatch: In children with psychiatric disorders, what does the literature say about whether the diagnosis determines the dose?

Dr. Findling: With children, dosing may be diagnosis-dependent for the same medications within the same age groups. For example, Tourette’s syndrome or conduct disorder in children and adolescents can be managed with lower antipsychotic doses than those required for major psychotic illnesses or mania. Unfortunately, we see youngsters with major psychotic illnesses or mania who have been prescribed the lower antipsychotic doses used to treat conduct disorder, and we see youngsters with conduct disorder who have been given 2 or 3 times the recommended antipsychotic dosages for that condition.

As you increase the dose you get higher exposure, and with higher exposure you have more side effects. Across the 3 antipsychotics we’ve studied—risperidone, quetiapine, and aripiprazole—youngsters with conduct disorder need about half or less of the medication needed by those with psychotic illness or mania.

Dr. Kowatch: What about dosing selective serotonin reuptake inhibitor (SSRI) antidepressants?

Dr. Findling: For some SSRIs, daily weight-adjusted doses are similar across the life cycle. However, there are exceptions. With paroxetine, for example, you get greater drug exposure in young people than in adults, even if you control for weight differences. And paroxetine has nonlinear kinetics in adults and in young patients; when you double the dose, you more than double the exposure.

Exposure and half-life

Dr. Kowatch: Can you talk more about nonlinear kinetics?

Where do you turn for help in dosing an antidepressant for a child with major depressive disorder? You might be misinformed if you rely on methods used in multicenter, randomized, placebo-controlled trials, according to Robert L. Findling, MD, an expert in child and adolescent pharmacokinetics (PK).

In a recent review,¹ Dr. Findling and colleagues at University Hospitals, Case Medical Center, and Case Western Reserve University concluded that:

• Data from PK studies do not support the dosing strategies used in many placebo-controlled efficacy trials of antidepressants in children and adolescents
• Excessively low or high dosages may explain—at least in part—why antidepressants failed to show efficacy or were associated with agitation, hostility, or increased suicidality among depressed pediatric patients in some studies.

To provide Current Psychiatry readers with more information on this topic, Section Editor Robert A. Kowatch, MD, PhD, interviewed Dr. Findling about pediatric PK studies and what they can tell clinicians about dosing antidepressants and antipsychotics in children and adolescents.

Not ‘small adults’

Dr. Kowatch: Warnings about a risk of suicidality in young people taking antidepressants have increased physicians’ concern about accurate dosing for children. How do pediatric pharmacokinetic parameters differ from those of adults?

Dr. Findling: Children and adolescents are not, of course, simply small adults. Significant differences in absorption rate, volume of distribution, and elimination affect PK parameters, such as half-life, throughout the life cycle.²

Dr. Kowatch: What determines these differences? Are they based on factors such as weight, age, puberty, or gender?

Dr. Findling: In general, PK differences observed with antidepressants have been dependent on the patient’s age or weight, rather than on gender differences or sexual maturation. To assume that drug exposure is weight-proportional across the life cycle is fraught with peril and is not true for many compounds, including psychotropics.

Dr. Kowatch: In which age groups would clinicians see the greatest differences in drug exposure?

Dr. Findling: It depends on the compound. Exposure to lithium, for example, is determined by the glomerular filtration rate, which often is much higher and necessitates higher weight-adjusted dosing in a younger child than in a teenager or adult. Drug exposure becomes more complicated with more complex compounds, with differing volumes of distribution, absorption rates, and perhaps multiple enzymes involved in bio-disposition.

Factors that affect dosing

Dr. Kowatch: Clinically, what’s the best way to determine safe, effective psychotropic dosing in children?

Dr. Findling: The short answer is to study the literature, and unfortunately most people find PK studies just about as interesting as watching paint dry. But a good PK study provides insight into a very important parameter, which is dosing.

Ultimately, we can’t talk about a medicine’s effectiveness or safety as a fixed statement. You can’t say drug “x” is effective for this condition or drug “y” is associated with this rate of side effects because tolerability and effectiveness are dose-dependent. And if you don’t know how to dose a medicine, you can’t characterize its pharmacodynamic properties when prescribing it to a youngster.

So you have to know the literature; what happens at different doses is terribly important.

Dr. Kowatch: In children with psychiatric disorders, what does the literature say about whether the diagnosis determines the dose?

Dr. Findling: With children, dosing may be diagnosis-dependent for the same medications within the same age groups. For example, Tourette’s syndrome or conduct disorder in children and adolescents can be managed with lower antipsychotic doses than those required for major psychotic illnesses or mania. Unfortunately, we see youngsters with major psychotic illnesses or mania who have been prescribed the lower antipsychotic doses used to treat conduct disorder, and we see youngsters with conduct disorder who have been given 2 or 3 times the recommended antipsychotic dosages for that condition.

As you increase the dose you get higher exposure, and with higher exposure you have more side effects. Across the 3 antipsychotics we’ve studied—risperidone, quetiapine, and aripiprazole—youngsters with conduct disorder need about half or less of the medication needed by those with psychotic illness or mania.

Dr. Kowatch: What about dosing selective serotonin reuptake inhibitor (SSRI) antidepressants?

Dr. Findling: For some SSRIs, daily weight-adjusted doses are similar across the life cycle. However, there are exceptions. With paroxetine, for example, you get greater drug exposure in young people than in adults, even if you control for weight differences. And paroxetine has nonlinear kinetics in adults and in young patients; when you double the dose, you more than double the exposure.

Exposure and half-life

Dr. Kowatch: Can you talk more about nonlinear kinetics?

Where do you turn for help in dosing an antidepressant for a child with major depressive disorder? You might be misinformed if you rely on methods used in multicenter, randomized, placebo-controlled trials, according to Robert L. Findling, MD, an expert in child and adolescent pharmacokinetics (PK).

In a recent review,¹ Dr. Findling and colleagues at University Hospitals, Case Medical Center, and Case Western Reserve University concluded that:

• Data from PK studies do not support the dosing strategies used in many placebo-controlled efficacy trials of antidepressants in children and adolescents
• Excessively low or high dosages may explain—at least in part—why antidepressants failed to show efficacy or were associated with agitation, hostility, or increased suicidality among depressed pediatric patients in some studies.

To provide Current Psychiatry readers with more information on this topic, Section Editor Robert A. Kowatch, MD, PhD, interviewed Dr. Findling about pediatric PK studies and what they can tell clinicians about dosing antidepressants and antipsychotics in children and adolescents.

Not ‘small adults’

Dr. Kowatch: Warnings about a risk of suicidality in young people taking antidepressants have increased physicians’ concern about accurate dosing for children. How do pediatric pharmacokinetic parameters differ from those of adults?

Dr. Findling: Children and adolescents are not, of course, simply small adults. Significant differences in absorption rate, volume of distribution, and elimination affect PK parameters, such as half-life, throughout the life cycle.²

Dr. Kowatch: What determines these differences? Are they based on factors such as weight, age, puberty, or gender?

Dr. Findling: In general, PK differences observed with antidepressants have been dependent on the patient’s age or weight, rather than on gender differences or sexual maturation. To assume that drug exposure is weight-proportional across the life cycle is fraught with peril and is not true for many compounds, including psychotropics.

Dr. Kowatch: In which age groups would clinicians see the greatest differences in drug exposure?

Dr. Findling: It depends on the compound. Exposure to lithium, for example, is determined by the glomerular filtration rate, which often is much higher and necessitates higher weight-adjusted dosing in a younger child than in a teenager or adult. Drug exposure becomes more complicated with more complex compounds, with differing volumes of distribution, absorption rates, and perhaps multiple enzymes involved in bio-disposition.

Factors that affect dosing

Dr. Kowatch: Clinically, what’s the best way to determine safe, effective psychotropic dosing in children?

Dr. Findling: The short answer is to study the literature, and unfortunately most people find PK studies just about as interesting as watching paint dry. But a good PK study provides insight into a very important parameter, which is dosing.

Ultimately, we can’t talk about a medicine’s effectiveness or safety as a fixed statement. You can’t say drug “x” is effective for this condition or drug “y” is associated with this rate of side effects because tolerability and effectiveness are dose-dependent. And if you don’t know how to dose a medicine, you can’t characterize its pharmacodynamic properties when prescribing it to a youngster.

So you have to know the literature; what happens at different doses is terribly important.

Dr. Kowatch: In children with psychiatric disorders, what does the literature say about whether the diagnosis determines the dose?

Dr. Findling: With children, dosing may be diagnosis-dependent for the same medications within the same age groups. For example, Tourette’s syndrome or conduct disorder in children and adolescents can be managed with lower antipsychotic doses than those required for major psychotic illnesses or mania. Unfortunately, we see youngsters with major psychotic illnesses or mania who have been prescribed the lower antipsychotic doses used to treat conduct disorder, and we see youngsters with conduct disorder who have been given 2 or 3 times the recommended antipsychotic dosages for that condition.

As you increase the dose you get higher exposure, and with higher exposure you have more side effects. Across the 3 antipsychotics we’ve studied—risperidone, quetiapine, and aripiprazole—youngsters with conduct disorder need about half or less of the medication needed by those with psychotic illness or mania.

Dr. Kowatch: What about dosing selective serotonin reuptake inhibitor (SSRI) antidepressants?

Dr. Findling: For some SSRIs, daily weight-adjusted doses are similar across the life cycle. However, there are exceptions. With paroxetine, for example, you get greater drug exposure in young people than in adults, even if you control for weight differences. And paroxetine has nonlinear kinetics in adults and in young patients; when you double the dose, you more than double the exposure.

Exposure and half-life

Dr. Kowatch: Can you talk more about nonlinear kinetics?

The slaying of 32 Virginia Tech University students and faculty by a mentally ill student sparked a national dialogue about mental illness on college campuses. The April 16 rampage—in which the shooter also killed himself—raises many questions about mental health care and the stigma of psychiatric illness:

• Why did TV commentators assume the crime was caused by “evil” and “psychopathy,” instead of a medical illness in a young man with many psychiatric manifestations?
• Why do most people assume that a psychotic individual driven by delusions is too “incompetent” or “confused” to plan and carry out a complex series of deadly assaults?
• Why did the mentally ill student receive no follow-up care before the crimes, even though he had received psychiatric treatment?
• Do medical record requirements in the Health Insurance Portability and Accountability Act (HIPAA) protect individual privacy at the expense of public safety if a patient is seriously mentally ill?
• If the university administration had known about the student’s psychiatric disorder, would he have received better treatment and supervision? Or would he have been stigmatized or expelled, whether or not he responded well to medications and counseling?
• How can roommates or teachers receive adequate information to help a mentally ill student or monitor for treatment adherence when HIPAA rules prevent even families from knowing details of mentally ill adults’ diagnosis or treatment?
• Can laws prohibiting gun sales to persons with a history of serious mental illness be made foolproof, or will guns remain accessible from underground sources?
• Because the home-to-college transition can be very stressful, should colleges require freshman courses on how to recognize distress and seek help?
• Given that schizophrenia, bipolar mania, and psychotic depression often emerge between ages 18 and 25, why have colleges and universities not adopted early screening and intervention?
• Are mentally ill persons more dangerous than the general population, or is that perception based on highly dramatized media reports of isolated incidents?
• When will the public understand that patients with serious mental illness who adhere to treatment often have positive outcomes?
• Why are alcohol and substance abuse—which cause morbidity and death among college students—not “feared” as much as mental illness?
• When will health insurance cover brain diseases that manifest as thought disorders or behavioral aberrations, such as schizophrenia or obsessive-compulsive disorder, in parity with brain diseases that manifest as muscle paralysis, such as stroke or multiple sclerosis?
• Given that >25% of the U.S. population has a diagnosable and treatable mental disorder, why is our mental health system so fragmented, so inadequate, and so underfunded? And why is there no public outcry to fix it?

Virginia Tech’s tragedy has thrust these questions and many more into the public consciousness. To address them, the medical establishment, public health officials, teachers, education administrators, and advocacy groups have a lot of work to do, and regrettably—given past patterns—more bloodshed may occur before answers emerge.

Finally, as a parent and husband, I have one last question: how can we console the bereaved families of the Virginia Tech students and faculty who suddenly lost a son or daughter, husband or wife in the prime of life? For them, improvements in mental health care on our college campuses will come too late.

See related article: Does this patient have prodromal psychosis?

The slaying of 32 Virginia Tech University students and faculty by a mentally ill student sparked a national dialogue about mental illness on college campuses. The April 16 rampage—in which the shooter also killed himself—raises many questions about mental health care and the stigma of psychiatric illness:

• Why did TV commentators assume the crime was caused by “evil” and “psychopathy,” instead of a medical illness in a young man with many psychiatric manifestations?
• Why do most people assume that a psychotic individual driven by delusions is too “incompetent” or “confused” to plan and carry out a complex series of deadly assaults?
• Why did the mentally ill student receive no follow-up care before the crimes, even though he had received psychiatric treatment?
• Do medical record requirements in the Health Insurance Portability and Accountability Act (HIPAA) protect individual privacy at the expense of public safety if a patient is seriously mentally ill?
• If the university administration had known about the student’s psychiatric disorder, would he have received better treatment and supervision? Or would he have been stigmatized or expelled, whether or not he responded well to medications and counseling?
• How can roommates or teachers receive adequate information to help a mentally ill student or monitor for treatment adherence when HIPAA rules prevent even families from knowing details of mentally ill adults’ diagnosis or treatment?
• Can laws prohibiting gun sales to persons with a history of serious mental illness be made foolproof, or will guns remain accessible from underground sources?
• Because the home-to-college transition can be very stressful, should colleges require freshman courses on how to recognize distress and seek help?
• Given that schizophrenia, bipolar mania, and psychotic depression often emerge between ages 18 and 25, why have colleges and universities not adopted early screening and intervention?
• Are mentally ill persons more dangerous than the general population, or is that perception based on highly dramatized media reports of isolated incidents?
• When will the public understand that patients with serious mental illness who adhere to treatment often have positive outcomes?
• Why are alcohol and substance abuse—which cause morbidity and death among college students—not “feared” as much as mental illness?
• When will health insurance cover brain diseases that manifest as thought disorders or behavioral aberrations, such as schizophrenia or obsessive-compulsive disorder, in parity with brain diseases that manifest as muscle paralysis, such as stroke or multiple sclerosis?
• Given that >25% of the U.S. population has a diagnosable and treatable mental disorder, why is our mental health system so fragmented, so inadequate, and so underfunded? And why is there no public outcry to fix it?

Virginia Tech’s tragedy has thrust these questions and many more into the public consciousness. To address them, the medical establishment, public health officials, teachers, education administrators, and advocacy groups have a lot of work to do, and regrettably—given past patterns—more bloodshed may occur before answers emerge.

Finally, as a parent and husband, I have one last question: how can we console the bereaved families of the Virginia Tech students and faculty who suddenly lost a son or daughter, husband or wife in the prime of life? For them, improvements in mental health care on our college campuses will come too late.

See related article: Does this patient have prodromal psychosis?

The slaying of 32 Virginia Tech University students and faculty by a mentally ill student sparked a national dialogue about mental illness on college campuses. The April 16 rampage—in which the shooter also killed himself—raises many questions about mental health care and the stigma of psychiatric illness:

• Why did TV commentators assume the crime was caused by “evil” and “psychopathy,” instead of a medical illness in a young man with many psychiatric manifestations?
• Why do most people assume that a psychotic individual driven by delusions is too “incompetent” or “confused” to plan and carry out a complex series of deadly assaults?
• Why did the mentally ill student receive no follow-up care before the crimes, even though he had received psychiatric treatment?
• Do medical record requirements in the Health Insurance Portability and Accountability Act (HIPAA) protect individual privacy at the expense of public safety if a patient is seriously mentally ill?
• If the university administration had known about the student’s psychiatric disorder, would he have received better treatment and supervision? Or would he have been stigmatized or expelled, whether or not he responded well to medications and counseling?
• How can roommates or teachers receive adequate information to help a mentally ill student or monitor for treatment adherence when HIPAA rules prevent even families from knowing details of mentally ill adults’ diagnosis or treatment?
• Can laws prohibiting gun sales to persons with a history of serious mental illness be made foolproof, or will guns remain accessible from underground sources?
• Because the home-to-college transition can be very stressful, should colleges require freshman courses on how to recognize distress and seek help?
• Given that schizophrenia, bipolar mania, and psychotic depression often emerge between ages 18 and 25, why have colleges and universities not adopted early screening and intervention?
• Are mentally ill persons more dangerous than the general population, or is that perception based on highly dramatized media reports of isolated incidents?
• When will the public understand that patients with serious mental illness who adhere to treatment often have positive outcomes?
• Why are alcohol and substance abuse—which cause morbidity and death among college students—not “feared” as much as mental illness?
• When will health insurance cover brain diseases that manifest as thought disorders or behavioral aberrations, such as schizophrenia or obsessive-compulsive disorder, in parity with brain diseases that manifest as muscle paralysis, such as stroke or multiple sclerosis?
• Given that >25% of the U.S. population has a diagnosable and treatable mental disorder, why is our mental health system so fragmented, so inadequate, and so underfunded? And why is there no public outcry to fix it?

Virginia Tech’s tragedy has thrust these questions and many more into the public consciousness. To address them, the medical establishment, public health officials, teachers, education administrators, and advocacy groups have a lot of work to do, and regrettably—given past patterns—more bloodshed may occur before answers emerge.

Finally, as a parent and husband, I have one last question: how can we console the bereaved families of the Virginia Tech students and faculty who suddenly lost a son or daughter, husband or wife in the prime of life? For them, improvements in mental health care on our college campuses will come too late.

See related article: Does this patient have prodromal psychosis?