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How to talk to patients about religion and spirituality
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In the midst of turmoil and suffering, patients often search for meaning and interpret their circumstances in the context of their religious or spiritual (R/S) beliefs. National polling data show that most Americans identify themselves as R/S, and inpatient and outpatient studies demonstrate that patients want clinicians to inquire about their R/S beliefs.1 In addition, R/S beliefs can benefit patients as a source of well-being, hope, purpose, higher self-esteem, coping, and social support.2 Given the importance of R/S to patients, psychiatrists should seek to understand their patient’s distress in the context of their beliefs.
Why is it hard for psychiatrists to bring up the subject? Psychiatrists might be hesitant to discuss R/S beliefs with patients because of personal discomfort, limited training opportunities during residency and in clinical practice, or time or economic constraints.3 Psychiatrists tend to be less R/S than the general population4 and may fear that they are being perceived as overly intrusive or offensive.
When should we inquire about spirituality and religion? Take an R/S history during each new patient evaluation and when admitting a patient for hospitalization, and include this information in the social history.5 Doing so could lead to a chaplain referral when appropriate. Questions about R/S beliefs usually are not perceived as intrusive if asked along with other questions that focus on patients’ social support system and may help identify barriers to self-harm or harm to others.
How do we start the conversation? There are several ways to start the discussion about R/S that are engaging, efficient, respectful, and caring. Start with simple questions, such as “Is R/S an important part of your life?” or “Do you rely on your faith during a difficult time like this?”
If your patient answers yes to these questions, consider exploring:
- How does your patient use R/S? Does he or she use it to cope with mental illness, or is it a source of distress? Is it both?
- How would your patient like you to address R/S in your work together?
- Is your patient a member of an R/S community, and if so, is it a source of support for him or her?
- Is your patient interested in working collaboratively with an R/S provider—eg, clergy, pastoral counselor?
If your patients say R/S is not important to them or they do not rely on faith, ask if R/S has been important to them in the past. Also, have them consider what gives their life meaning and hope, what is sacred to them, and who or what will help them cope during a difficult time.
Disclosure
Dr. Clark and the Reverend Doctor King report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. Harrison is a consultant to the Samaritan Center of Puget Sound, Seattle, WA.
Acknowledgement
The authors thank J. Gary Trantham, MD, for his assistance with this article.
1. Puchalski C. Spiritual assessment in clinical practice. Psychiatr Ann. 2006;36(3):150-155.
2. Moreira-Almeida A, Neto FL, Koenig HG. Religiousness and mental health: a review. Rev Bras Psiquiatr. 2006;28(3):242-250.
3. Griffith JL. Managing religious countertransference in clinical settings. Psychiatr Ann. 2006;36(3):196-204.
4. Curlin FA, Lawrence RE, Odell S, et al. Religion, spirituality, and medicine: psychiatrists’ and other physicians’ differing observations, interpretations, and clinical approaches. Am J Psychiatry. 2007;164(12):1825-1831.
5. Koenig HG. Spirituality in patient care: why how, when, and what. West Conshohocken, PA: Templeton Press; 2007.
Discuss this article at www.facebook.com/CurrentPsychiatry
In the midst of turmoil and suffering, patients often search for meaning and interpret their circumstances in the context of their religious or spiritual (R/S) beliefs. National polling data show that most Americans identify themselves as R/S, and inpatient and outpatient studies demonstrate that patients want clinicians to inquire about their R/S beliefs.1 In addition, R/S beliefs can benefit patients as a source of well-being, hope, purpose, higher self-esteem, coping, and social support.2 Given the importance of R/S to patients, psychiatrists should seek to understand their patient’s distress in the context of their beliefs.
Why is it hard for psychiatrists to bring up the subject? Psychiatrists might be hesitant to discuss R/S beliefs with patients because of personal discomfort, limited training opportunities during residency and in clinical practice, or time or economic constraints.3 Psychiatrists tend to be less R/S than the general population4 and may fear that they are being perceived as overly intrusive or offensive.
When should we inquire about spirituality and religion? Take an R/S history during each new patient evaluation and when admitting a patient for hospitalization, and include this information in the social history.5 Doing so could lead to a chaplain referral when appropriate. Questions about R/S beliefs usually are not perceived as intrusive if asked along with other questions that focus on patients’ social support system and may help identify barriers to self-harm or harm to others.
How do we start the conversation? There are several ways to start the discussion about R/S that are engaging, efficient, respectful, and caring. Start with simple questions, such as “Is R/S an important part of your life?” or “Do you rely on your faith during a difficult time like this?”
If your patient answers yes to these questions, consider exploring:
- How does your patient use R/S? Does he or she use it to cope with mental illness, or is it a source of distress? Is it both?
- How would your patient like you to address R/S in your work together?
- Is your patient a member of an R/S community, and if so, is it a source of support for him or her?
- Is your patient interested in working collaboratively with an R/S provider—eg, clergy, pastoral counselor?
If your patients say R/S is not important to them or they do not rely on faith, ask if R/S has been important to them in the past. Also, have them consider what gives their life meaning and hope, what is sacred to them, and who or what will help them cope during a difficult time.
Disclosure
Dr. Clark and the Reverend Doctor King report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. Harrison is a consultant to the Samaritan Center of Puget Sound, Seattle, WA.
Acknowledgement
The authors thank J. Gary Trantham, MD, for his assistance with this article.
Discuss this article at www.facebook.com/CurrentPsychiatry
In the midst of turmoil and suffering, patients often search for meaning and interpret their circumstances in the context of their religious or spiritual (R/S) beliefs. National polling data show that most Americans identify themselves as R/S, and inpatient and outpatient studies demonstrate that patients want clinicians to inquire about their R/S beliefs.1 In addition, R/S beliefs can benefit patients as a source of well-being, hope, purpose, higher self-esteem, coping, and social support.2 Given the importance of R/S to patients, psychiatrists should seek to understand their patient’s distress in the context of their beliefs.
Why is it hard for psychiatrists to bring up the subject? Psychiatrists might be hesitant to discuss R/S beliefs with patients because of personal discomfort, limited training opportunities during residency and in clinical practice, or time or economic constraints.3 Psychiatrists tend to be less R/S than the general population4 and may fear that they are being perceived as overly intrusive or offensive.
When should we inquire about spirituality and religion? Take an R/S history during each new patient evaluation and when admitting a patient for hospitalization, and include this information in the social history.5 Doing so could lead to a chaplain referral when appropriate. Questions about R/S beliefs usually are not perceived as intrusive if asked along with other questions that focus on patients’ social support system and may help identify barriers to self-harm or harm to others.
How do we start the conversation? There are several ways to start the discussion about R/S that are engaging, efficient, respectful, and caring. Start with simple questions, such as “Is R/S an important part of your life?” or “Do you rely on your faith during a difficult time like this?”
If your patient answers yes to these questions, consider exploring:
- How does your patient use R/S? Does he or she use it to cope with mental illness, or is it a source of distress? Is it both?
- How would your patient like you to address R/S in your work together?
- Is your patient a member of an R/S community, and if so, is it a source of support for him or her?
- Is your patient interested in working collaboratively with an R/S provider—eg, clergy, pastoral counselor?
If your patients say R/S is not important to them or they do not rely on faith, ask if R/S has been important to them in the past. Also, have them consider what gives their life meaning and hope, what is sacred to them, and who or what will help them cope during a difficult time.
Disclosure
Dr. Clark and the Reverend Doctor King report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Dr. Harrison is a consultant to the Samaritan Center of Puget Sound, Seattle, WA.
Acknowledgement
The authors thank J. Gary Trantham, MD, for his assistance with this article.
1. Puchalski C. Spiritual assessment in clinical practice. Psychiatr Ann. 2006;36(3):150-155.
2. Moreira-Almeida A, Neto FL, Koenig HG. Religiousness and mental health: a review. Rev Bras Psiquiatr. 2006;28(3):242-250.
3. Griffith JL. Managing religious countertransference in clinical settings. Psychiatr Ann. 2006;36(3):196-204.
4. Curlin FA, Lawrence RE, Odell S, et al. Religion, spirituality, and medicine: psychiatrists’ and other physicians’ differing observations, interpretations, and clinical approaches. Am J Psychiatry. 2007;164(12):1825-1831.
5. Koenig HG. Spirituality in patient care: why how, when, and what. West Conshohocken, PA: Templeton Press; 2007.
1. Puchalski C. Spiritual assessment in clinical practice. Psychiatr Ann. 2006;36(3):150-155.
2. Moreira-Almeida A, Neto FL, Koenig HG. Religiousness and mental health: a review. Rev Bras Psiquiatr. 2006;28(3):242-250.
3. Griffith JL. Managing religious countertransference in clinical settings. Psychiatr Ann. 2006;36(3):196-204.
4. Curlin FA, Lawrence RE, Odell S, et al. Religion, spirituality, and medicine: psychiatrists’ and other physicians’ differing observations, interpretations, and clinical approaches. Am J Psychiatry. 2007;164(12):1825-1831.
5. Koenig HG. Spirituality in patient care: why how, when, and what. West Conshohocken, PA: Templeton Press; 2007.
Reducing CYP450 drug interactions caused by antidepressants
Most psychiatrists are aware that some antidepressants can cause clinically significant drug interactions, especially through the cytochrome P450 (CYP450) hepatic enzyme system. Antidepressants’ potential for drug interactions is especially important for patients who take >1 other medication, including cardiovascular agents.1
Unfortunately, drug interactions can be difficult to remember and are commonly missed. One strategy to help remember a list of antidepressants with a relatively low potential for CYP450 drug interactions is to use the mnemonic Various Medicines Definitely Commingle Very Easily (VMDCVE) to recall venlafaxine, mirtazapine, desvenlafaxine,2 citalopram, vilazodone,3 and escitalopram. The order in which these medications are listed does not indicate a preference for any of the 6 antidepressants. Bupropion and duloxetine are not included in this list because they are moderately potent inhibitors of the 2D6 isoenzyme.4,5
A few caveats
There are some important caveats in using this mnemonic:
- None of these antidepressants is completely devoid of effects on the CYP450 system. However, compared with the antidepressants included in this mnemonic, fluoxetine, paroxetine, fluvoxamine, duloxetine, bupropion, and nefazodone are more likely to have clinically significant effects on CYP450.4,5
- Although sertraline has a lower potential for CYP450-mediated drug interactions at low doses, it is not included in this mnemonic because it may have greater effects on 2D6 inhibition in some patients, especially at higher doses, such as ≥150 mg/d.5 Also, sertraline may significantly increase lamotrigine levels through a different mechanism: inhibition of uridine 5’-diphosphate glucuronosyltransferase 1A4.4
- Antidepressants also may be the substrates for CYP450 drug interactions caused by other medications.
- This mnemonic refers only to CYP450-mediated drug interactions. Antidepressants included in this mnemonic may have a high potential for drug interactions mediated by displacement from carrier proteins— eg, with digoxin or warfarin.
- Pharmacodynamic drug interactions also are possible—eg, serotonin syndrome as a result of combining a selective serotonin reuptake inhibitor with another serotonergic medication.
To remain vigilant for drug-drug interactions, routinely use a drug interaction software, in addition to this mnemonic.
Disclosure
Dr. Mago receives grant/research, support from Bristol-Myers Squibb, Eli Lilly and Company, and NARSAD.
1. Williams S, Wynn G, Cozza K, et al. Cardiovascular medications. Psychosomatics. 2007;48(6):537-547.
2. Nichols AI, Tourian KA, Tse SY, et al. Desvenlafaxine for major depressive disorder: incremental clinical benefits from a second-generation serotonin-norepinephrine reuptake inhibitor. Expert Opin Drug Metab Toxicol. 2010;6(12):1565-1574.
3. Laughren TP, Gobburu J, Temple RJ, et al. Vilazodone: clinical basis for the US Food and Drug Administration’s approval of a new antidepressant. J Clin Psychiatry. 2011;72(9):1166-1173.
4. Sandson NB, Armstrong SC, Cozza KL. An overview of psychotropic drug-drug interactions. Psychosomatics. 2005;46(5):464-494.
5. Spina E, Santoro V, D’Arrigo C. Clinically relevant pharmacokinetic drug interactions with second-generation antidepressants: an update. Clin Ther. 2008;30(7):1206-1227.
Most psychiatrists are aware that some antidepressants can cause clinically significant drug interactions, especially through the cytochrome P450 (CYP450) hepatic enzyme system. Antidepressants’ potential for drug interactions is especially important for patients who take >1 other medication, including cardiovascular agents.1
Unfortunately, drug interactions can be difficult to remember and are commonly missed. One strategy to help remember a list of antidepressants with a relatively low potential for CYP450 drug interactions is to use the mnemonic Various Medicines Definitely Commingle Very Easily (VMDCVE) to recall venlafaxine, mirtazapine, desvenlafaxine,2 citalopram, vilazodone,3 and escitalopram. The order in which these medications are listed does not indicate a preference for any of the 6 antidepressants. Bupropion and duloxetine are not included in this list because they are moderately potent inhibitors of the 2D6 isoenzyme.4,5
A few caveats
There are some important caveats in using this mnemonic:
- None of these antidepressants is completely devoid of effects on the CYP450 system. However, compared with the antidepressants included in this mnemonic, fluoxetine, paroxetine, fluvoxamine, duloxetine, bupropion, and nefazodone are more likely to have clinically significant effects on CYP450.4,5
- Although sertraline has a lower potential for CYP450-mediated drug interactions at low doses, it is not included in this mnemonic because it may have greater effects on 2D6 inhibition in some patients, especially at higher doses, such as ≥150 mg/d.5 Also, sertraline may significantly increase lamotrigine levels through a different mechanism: inhibition of uridine 5’-diphosphate glucuronosyltransferase 1A4.4
- Antidepressants also may be the substrates for CYP450 drug interactions caused by other medications.
- This mnemonic refers only to CYP450-mediated drug interactions. Antidepressants included in this mnemonic may have a high potential for drug interactions mediated by displacement from carrier proteins— eg, with digoxin or warfarin.
- Pharmacodynamic drug interactions also are possible—eg, serotonin syndrome as a result of combining a selective serotonin reuptake inhibitor with another serotonergic medication.
To remain vigilant for drug-drug interactions, routinely use a drug interaction software, in addition to this mnemonic.
Disclosure
Dr. Mago receives grant/research, support from Bristol-Myers Squibb, Eli Lilly and Company, and NARSAD.
Most psychiatrists are aware that some antidepressants can cause clinically significant drug interactions, especially through the cytochrome P450 (CYP450) hepatic enzyme system. Antidepressants’ potential for drug interactions is especially important for patients who take >1 other medication, including cardiovascular agents.1
Unfortunately, drug interactions can be difficult to remember and are commonly missed. One strategy to help remember a list of antidepressants with a relatively low potential for CYP450 drug interactions is to use the mnemonic Various Medicines Definitely Commingle Very Easily (VMDCVE) to recall venlafaxine, mirtazapine, desvenlafaxine,2 citalopram, vilazodone,3 and escitalopram. The order in which these medications are listed does not indicate a preference for any of the 6 antidepressants. Bupropion and duloxetine are not included in this list because they are moderately potent inhibitors of the 2D6 isoenzyme.4,5
A few caveats
There are some important caveats in using this mnemonic:
- None of these antidepressants is completely devoid of effects on the CYP450 system. However, compared with the antidepressants included in this mnemonic, fluoxetine, paroxetine, fluvoxamine, duloxetine, bupropion, and nefazodone are more likely to have clinically significant effects on CYP450.4,5
- Although sertraline has a lower potential for CYP450-mediated drug interactions at low doses, it is not included in this mnemonic because it may have greater effects on 2D6 inhibition in some patients, especially at higher doses, such as ≥150 mg/d.5 Also, sertraline may significantly increase lamotrigine levels through a different mechanism: inhibition of uridine 5’-diphosphate glucuronosyltransferase 1A4.4
- Antidepressants also may be the substrates for CYP450 drug interactions caused by other medications.
- This mnemonic refers only to CYP450-mediated drug interactions. Antidepressants included in this mnemonic may have a high potential for drug interactions mediated by displacement from carrier proteins— eg, with digoxin or warfarin.
- Pharmacodynamic drug interactions also are possible—eg, serotonin syndrome as a result of combining a selective serotonin reuptake inhibitor with another serotonergic medication.
To remain vigilant for drug-drug interactions, routinely use a drug interaction software, in addition to this mnemonic.
Disclosure
Dr. Mago receives grant/research, support from Bristol-Myers Squibb, Eli Lilly and Company, and NARSAD.
1. Williams S, Wynn G, Cozza K, et al. Cardiovascular medications. Psychosomatics. 2007;48(6):537-547.
2. Nichols AI, Tourian KA, Tse SY, et al. Desvenlafaxine for major depressive disorder: incremental clinical benefits from a second-generation serotonin-norepinephrine reuptake inhibitor. Expert Opin Drug Metab Toxicol. 2010;6(12):1565-1574.
3. Laughren TP, Gobburu J, Temple RJ, et al. Vilazodone: clinical basis for the US Food and Drug Administration’s approval of a new antidepressant. J Clin Psychiatry. 2011;72(9):1166-1173.
4. Sandson NB, Armstrong SC, Cozza KL. An overview of psychotropic drug-drug interactions. Psychosomatics. 2005;46(5):464-494.
5. Spina E, Santoro V, D’Arrigo C. Clinically relevant pharmacokinetic drug interactions with second-generation antidepressants: an update. Clin Ther. 2008;30(7):1206-1227.
1. Williams S, Wynn G, Cozza K, et al. Cardiovascular medications. Psychosomatics. 2007;48(6):537-547.
2. Nichols AI, Tourian KA, Tse SY, et al. Desvenlafaxine for major depressive disorder: incremental clinical benefits from a second-generation serotonin-norepinephrine reuptake inhibitor. Expert Opin Drug Metab Toxicol. 2010;6(12):1565-1574.
3. Laughren TP, Gobburu J, Temple RJ, et al. Vilazodone: clinical basis for the US Food and Drug Administration’s approval of a new antidepressant. J Clin Psychiatry. 2011;72(9):1166-1173.
4. Sandson NB, Armstrong SC, Cozza KL. An overview of psychotropic drug-drug interactions. Psychosomatics. 2005;46(5):464-494.
5. Spina E, Santoro V, D’Arrigo C. Clinically relevant pharmacokinetic drug interactions with second-generation antidepressants: an update. Clin Ther. 2008;30(7):1206-1227.
Sleep terrors in adults: How to help control this potentially dangerous condition
Sleep terrors (STs)—also known as night terrors—are characterized by sudden arousal accompanied by a piercing scream or cry in the first few hours after falling asleep. These parasomnias arise out of slow-wave sleep (stages 3 and 4 of nonrapid eye movement [non-REM] sleep) and affect approximately 5% of adults.1 The condition is twice as common in men than women, and usually affects children but may not develop until adulthood.1
During STs, a patient may act scared, afraid, agitated, anxious, or panicky without being fully aware of his or her surroundings. The episode may last 30 seconds to 5 minutes; most patients don’t remember the event the next morning. STs may leave individuals feeling exhausted and perplexed the next day. Verbalization during the episode is incoherent and a patient’s perception of the environment seems altered. Tachycardia, tachypnea, sweating, flushed skin, or mydriasis are prominent. When ST patients walk, they may do so violently and can cause harm to themselves or others.
The differential diagnosis of STs includes posttraumatic stress disorder; nocturnal seizures characterized by excessive motor activity and organic CNS lesions; REM sleep behavior disorder; sleep choking syndrome; and nocturnal panic attacks. Patients with STs report high rates of stressful events—eg, divorce or bereavement—in the previous year. They are more likely to have a history of mood and anxiety disorders and high levels of depression, anxiety, and obsessive-compulsive and phobic traits. One study found patients with STs were 4.3 times more likely to have had a car accident in the past year.2
Evaluating and treating STs
Rule out comorbid conditions such as obstructive sleep apnea and periodic limb movement disorder. Encourage your patient to improve his or her sleep hygiene by maintaining a regular sleep/wake cycle, exercising, and limiting caffeine and alcohol and exposure to bright light before bedtime.
Self-help techniques. To avoid injury, encourage your patient to remove dangerous objects from their sleeping area. Suggest locking the doors to the room or home, and putting medications in a secure place. Patients also may consider keeping their mattress close to the floor to limit the risk of injury.
Pharmacotherapy and psychotherapy. Along with counseling and support, your patient may benefit from cognitive-behavioral therapy, relaxation therapy, or hypnosis.3 Anticipatory arousal therapy may help by interrupting the altered underlying electrophysiology of partial arousal.
If your patient is concerned about physical injury during STs, consider prescribing clonazepam, temazepam, or diazepam.4 Trazodone and selective serotonin reuptake inhibitors such as paroxetine5 also have been used to treat STs.
Disclosure
Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Crisp AH. The sleepwalking/night terrors syndrome in adults. Postgrad Med J. 1996;72(852):599-604.
2. Oudiette D, Leu S, Pottier M, et al. Dreamlike mentations during sleepwalking and sleep terrors in adults. Sleep. 2009;32(12):1621-1627.
3. Lowe P, Humphreys C, Williams SJ. Night terrors: women’s experiences of (not) sleeping where there is domestic violence. Violence Against Women. 2007;13(6):549-561.
4. Schenck CH, Mahowald MW. Long-term nightly benzodiazepine treatment of injurious parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med. 1996;100(3):333-337.
5. Lillywhite AR, Wilson SJ, Nutt DJ. Successful treatment of night terrors and somnambulism with paroxetine. Br J Psychiatry. 1994;164(4):551-554.
Sleep terrors (STs)—also known as night terrors—are characterized by sudden arousal accompanied by a piercing scream or cry in the first few hours after falling asleep. These parasomnias arise out of slow-wave sleep (stages 3 and 4 of nonrapid eye movement [non-REM] sleep) and affect approximately 5% of adults.1 The condition is twice as common in men than women, and usually affects children but may not develop until adulthood.1
During STs, a patient may act scared, afraid, agitated, anxious, or panicky without being fully aware of his or her surroundings. The episode may last 30 seconds to 5 minutes; most patients don’t remember the event the next morning. STs may leave individuals feeling exhausted and perplexed the next day. Verbalization during the episode is incoherent and a patient’s perception of the environment seems altered. Tachycardia, tachypnea, sweating, flushed skin, or mydriasis are prominent. When ST patients walk, they may do so violently and can cause harm to themselves or others.
The differential diagnosis of STs includes posttraumatic stress disorder; nocturnal seizures characterized by excessive motor activity and organic CNS lesions; REM sleep behavior disorder; sleep choking syndrome; and nocturnal panic attacks. Patients with STs report high rates of stressful events—eg, divorce or bereavement—in the previous year. They are more likely to have a history of mood and anxiety disorders and high levels of depression, anxiety, and obsessive-compulsive and phobic traits. One study found patients with STs were 4.3 times more likely to have had a car accident in the past year.2
Evaluating and treating STs
Rule out comorbid conditions such as obstructive sleep apnea and periodic limb movement disorder. Encourage your patient to improve his or her sleep hygiene by maintaining a regular sleep/wake cycle, exercising, and limiting caffeine and alcohol and exposure to bright light before bedtime.
Self-help techniques. To avoid injury, encourage your patient to remove dangerous objects from their sleeping area. Suggest locking the doors to the room or home, and putting medications in a secure place. Patients also may consider keeping their mattress close to the floor to limit the risk of injury.
Pharmacotherapy and psychotherapy. Along with counseling and support, your patient may benefit from cognitive-behavioral therapy, relaxation therapy, or hypnosis.3 Anticipatory arousal therapy may help by interrupting the altered underlying electrophysiology of partial arousal.
If your patient is concerned about physical injury during STs, consider prescribing clonazepam, temazepam, or diazepam.4 Trazodone and selective serotonin reuptake inhibitors such as paroxetine5 also have been used to treat STs.
Disclosure
Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Sleep terrors (STs)—also known as night terrors—are characterized by sudden arousal accompanied by a piercing scream or cry in the first few hours after falling asleep. These parasomnias arise out of slow-wave sleep (stages 3 and 4 of nonrapid eye movement [non-REM] sleep) and affect approximately 5% of adults.1 The condition is twice as common in men than women, and usually affects children but may not develop until adulthood.1
During STs, a patient may act scared, afraid, agitated, anxious, or panicky without being fully aware of his or her surroundings. The episode may last 30 seconds to 5 minutes; most patients don’t remember the event the next morning. STs may leave individuals feeling exhausted and perplexed the next day. Verbalization during the episode is incoherent and a patient’s perception of the environment seems altered. Tachycardia, tachypnea, sweating, flushed skin, or mydriasis are prominent. When ST patients walk, they may do so violently and can cause harm to themselves or others.
The differential diagnosis of STs includes posttraumatic stress disorder; nocturnal seizures characterized by excessive motor activity and organic CNS lesions; REM sleep behavior disorder; sleep choking syndrome; and nocturnal panic attacks. Patients with STs report high rates of stressful events—eg, divorce or bereavement—in the previous year. They are more likely to have a history of mood and anxiety disorders and high levels of depression, anxiety, and obsessive-compulsive and phobic traits. One study found patients with STs were 4.3 times more likely to have had a car accident in the past year.2
Evaluating and treating STs
Rule out comorbid conditions such as obstructive sleep apnea and periodic limb movement disorder. Encourage your patient to improve his or her sleep hygiene by maintaining a regular sleep/wake cycle, exercising, and limiting caffeine and alcohol and exposure to bright light before bedtime.
Self-help techniques. To avoid injury, encourage your patient to remove dangerous objects from their sleeping area. Suggest locking the doors to the room or home, and putting medications in a secure place. Patients also may consider keeping their mattress close to the floor to limit the risk of injury.
Pharmacotherapy and psychotherapy. Along with counseling and support, your patient may benefit from cognitive-behavioral therapy, relaxation therapy, or hypnosis.3 Anticipatory arousal therapy may help by interrupting the altered underlying electrophysiology of partial arousal.
If your patient is concerned about physical injury during STs, consider prescribing clonazepam, temazepam, or diazepam.4 Trazodone and selective serotonin reuptake inhibitors such as paroxetine5 also have been used to treat STs.
Disclosure
Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Crisp AH. The sleepwalking/night terrors syndrome in adults. Postgrad Med J. 1996;72(852):599-604.
2. Oudiette D, Leu S, Pottier M, et al. Dreamlike mentations during sleepwalking and sleep terrors in adults. Sleep. 2009;32(12):1621-1627.
3. Lowe P, Humphreys C, Williams SJ. Night terrors: women’s experiences of (not) sleeping where there is domestic violence. Violence Against Women. 2007;13(6):549-561.
4. Schenck CH, Mahowald MW. Long-term nightly benzodiazepine treatment of injurious parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med. 1996;100(3):333-337.
5. Lillywhite AR, Wilson SJ, Nutt DJ. Successful treatment of night terrors and somnambulism with paroxetine. Br J Psychiatry. 1994;164(4):551-554.
1. Crisp AH. The sleepwalking/night terrors syndrome in adults. Postgrad Med J. 1996;72(852):599-604.
2. Oudiette D, Leu S, Pottier M, et al. Dreamlike mentations during sleepwalking and sleep terrors in adults. Sleep. 2009;32(12):1621-1627.
3. Lowe P, Humphreys C, Williams SJ. Night terrors: women’s experiences of (not) sleeping where there is domestic violence. Violence Against Women. 2007;13(6):549-561.
4. Schenck CH, Mahowald MW. Long-term nightly benzodiazepine treatment of injurious parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med. 1996;100(3):333-337.
5. Lillywhite AR, Wilson SJ, Nutt DJ. Successful treatment of night terrors and somnambulism with paroxetine. Br J Psychiatry. 1994;164(4):551-554.
When to treat subthreshold hypomanic episodes
According to DSM-IV-TR, the minimal duration of a hypomanic episode is 4 days.1 Should we treat patients for hypomanic symptoms that last <4 days? Could antidepressants’ high failure rate2 be because many depressed patients have untreated “subthreshold hypomanic episodes”? Aripiprazole, quetiapine, and lithium all have been shown to alleviate depression when added to an antidepressant.3-5 Is it possible that these medications are treating subthreshold hypomanic episodes rather than depression?
The literature does not answer these questions. To further confuse matters, a subthreshold hypomanic episode may not be a discrete episode. In such episodes, hypomanic symptoms may overlap at some point and the duration of each symptom may vary.
When I administer the Mood Disorder Questionnaire,6,7 I ask patients about 13 hypomanic symptoms. Patient responses to questions about 7 of these symptoms—increased energy, irritability, talking, and activity, feeling “hyper,” racing thoughts, and decreased need for sleep—can help demonstrate the variability of symptom duration. For example, a patient may complain of increased energy and irritability for 3 days, increased activity and feeling “hyper” for 2 days, increased talking and a decreased need to sleep for 1 day, and racing thoughts every day.
Alternative criteria
Considering this variation, I often use the following criteria when considering whether to treat subthreshold hypomanic symptoms:
- ≥4 symptoms must last ≥2 consecutive days
- ≥3 symptoms must overlap at some point, and
- ≥2 of the symptoms must be increased energy, increased activity, or racing thoughts.
However, some patients have hypomanic symptoms that do not meet these relaxed criteria but require treatment.8 I also need to know when these episodes started, how frequently they occur, and how much of a problem they cause in the patient’s life. I often treat subthreshold hypomanic episodes with an antipsychotic or a mood stabilizer. As with all patients I see, I consider the patient’s reliability, substance abuse history, and mental status during the interview.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Pigott HE, Leventhal AM, Alter GS, et al. Efficacy and effectiveness of antidepressants: current status of research. Psychother Psychosom. 2010;79(5):267-279.
3. Nelson JC, Pikalov A, Berman RM. Augmentation treatment in major depressive disorder: focus on aripiprazole. Neuropsychiatr Dis Treat. 2008;4(5):937-948.
4. Daly EJ, Trivedi MH. A review of quetiapine in combination with antidepressant therapy in patients with depression. Neuropsychiatr Dis Treat. 2007;3(6):855-867.
5. Price LH, Carpenter LL, Tyrka AR. Lithium augmentation for refractory depression: a critical reappraisal. Prim Psychiatry. 2008;15(11):35-42.
6. Hirschfeld RM, Williams JB, Spitzer RL, et al. Development and validation of a screening instrument for bipolar spectrum disorder: the Mood Disorder Questionnaire. Am J Psychiatry. 2000;157(11):1873-1875.
7. The Mood Disorder Questionnaire. http://www.drpaddison.com/mood.pdf. Accessed June 20 2012.
8. Angst J, Azorin JM, Bowden CL, et al. Prevalence and characteristics of undiagnosed bipolar disorders in patients with a major depressive episode: the BRIDGE study. Arch Gen Psychiatry. 2011;68(8):791-798.
According to DSM-IV-TR, the minimal duration of a hypomanic episode is 4 days.1 Should we treat patients for hypomanic symptoms that last <4 days? Could antidepressants’ high failure rate2 be because many depressed patients have untreated “subthreshold hypomanic episodes”? Aripiprazole, quetiapine, and lithium all have been shown to alleviate depression when added to an antidepressant.3-5 Is it possible that these medications are treating subthreshold hypomanic episodes rather than depression?
The literature does not answer these questions. To further confuse matters, a subthreshold hypomanic episode may not be a discrete episode. In such episodes, hypomanic symptoms may overlap at some point and the duration of each symptom may vary.
When I administer the Mood Disorder Questionnaire,6,7 I ask patients about 13 hypomanic symptoms. Patient responses to questions about 7 of these symptoms—increased energy, irritability, talking, and activity, feeling “hyper,” racing thoughts, and decreased need for sleep—can help demonstrate the variability of symptom duration. For example, a patient may complain of increased energy and irritability for 3 days, increased activity and feeling “hyper” for 2 days, increased talking and a decreased need to sleep for 1 day, and racing thoughts every day.
Alternative criteria
Considering this variation, I often use the following criteria when considering whether to treat subthreshold hypomanic symptoms:
- ≥4 symptoms must last ≥2 consecutive days
- ≥3 symptoms must overlap at some point, and
- ≥2 of the symptoms must be increased energy, increased activity, or racing thoughts.
However, some patients have hypomanic symptoms that do not meet these relaxed criteria but require treatment.8 I also need to know when these episodes started, how frequently they occur, and how much of a problem they cause in the patient’s life. I often treat subthreshold hypomanic episodes with an antipsychotic or a mood stabilizer. As with all patients I see, I consider the patient’s reliability, substance abuse history, and mental status during the interview.
According to DSM-IV-TR, the minimal duration of a hypomanic episode is 4 days.1 Should we treat patients for hypomanic symptoms that last <4 days? Could antidepressants’ high failure rate2 be because many depressed patients have untreated “subthreshold hypomanic episodes”? Aripiprazole, quetiapine, and lithium all have been shown to alleviate depression when added to an antidepressant.3-5 Is it possible that these medications are treating subthreshold hypomanic episodes rather than depression?
The literature does not answer these questions. To further confuse matters, a subthreshold hypomanic episode may not be a discrete episode. In such episodes, hypomanic symptoms may overlap at some point and the duration of each symptom may vary.
When I administer the Mood Disorder Questionnaire,6,7 I ask patients about 13 hypomanic symptoms. Patient responses to questions about 7 of these symptoms—increased energy, irritability, talking, and activity, feeling “hyper,” racing thoughts, and decreased need for sleep—can help demonstrate the variability of symptom duration. For example, a patient may complain of increased energy and irritability for 3 days, increased activity and feeling “hyper” for 2 days, increased talking and a decreased need to sleep for 1 day, and racing thoughts every day.
Alternative criteria
Considering this variation, I often use the following criteria when considering whether to treat subthreshold hypomanic symptoms:
- ≥4 symptoms must last ≥2 consecutive days
- ≥3 symptoms must overlap at some point, and
- ≥2 of the symptoms must be increased energy, increased activity, or racing thoughts.
However, some patients have hypomanic symptoms that do not meet these relaxed criteria but require treatment.8 I also need to know when these episodes started, how frequently they occur, and how much of a problem they cause in the patient’s life. I often treat subthreshold hypomanic episodes with an antipsychotic or a mood stabilizer. As with all patients I see, I consider the patient’s reliability, substance abuse history, and mental status during the interview.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Pigott HE, Leventhal AM, Alter GS, et al. Efficacy and effectiveness of antidepressants: current status of research. Psychother Psychosom. 2010;79(5):267-279.
3. Nelson JC, Pikalov A, Berman RM. Augmentation treatment in major depressive disorder: focus on aripiprazole. Neuropsychiatr Dis Treat. 2008;4(5):937-948.
4. Daly EJ, Trivedi MH. A review of quetiapine in combination with antidepressant therapy in patients with depression. Neuropsychiatr Dis Treat. 2007;3(6):855-867.
5. Price LH, Carpenter LL, Tyrka AR. Lithium augmentation for refractory depression: a critical reappraisal. Prim Psychiatry. 2008;15(11):35-42.
6. Hirschfeld RM, Williams JB, Spitzer RL, et al. Development and validation of a screening instrument for bipolar spectrum disorder: the Mood Disorder Questionnaire. Am J Psychiatry. 2000;157(11):1873-1875.
7. The Mood Disorder Questionnaire. http://www.drpaddison.com/mood.pdf. Accessed June 20 2012.
8. Angst J, Azorin JM, Bowden CL, et al. Prevalence and characteristics of undiagnosed bipolar disorders in patients with a major depressive episode: the BRIDGE study. Arch Gen Psychiatry. 2011;68(8):791-798.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Pigott HE, Leventhal AM, Alter GS, et al. Efficacy and effectiveness of antidepressants: current status of research. Psychother Psychosom. 2010;79(5):267-279.
3. Nelson JC, Pikalov A, Berman RM. Augmentation treatment in major depressive disorder: focus on aripiprazole. Neuropsychiatr Dis Treat. 2008;4(5):937-948.
4. Daly EJ, Trivedi MH. A review of quetiapine in combination with antidepressant therapy in patients with depression. Neuropsychiatr Dis Treat. 2007;3(6):855-867.
5. Price LH, Carpenter LL, Tyrka AR. Lithium augmentation for refractory depression: a critical reappraisal. Prim Psychiatry. 2008;15(11):35-42.
6. Hirschfeld RM, Williams JB, Spitzer RL, et al. Development and validation of a screening instrument for bipolar spectrum disorder: the Mood Disorder Questionnaire. Am J Psychiatry. 2000;157(11):1873-1875.
7. The Mood Disorder Questionnaire. http://www.drpaddison.com/mood.pdf. Accessed June 20 2012.
8. Angst J, Azorin JM, Bowden CL, et al. Prevalence and characteristics of undiagnosed bipolar disorders in patients with a major depressive episode: the BRIDGE study. Arch Gen Psychiatry. 2011;68(8):791-798.
Distinguishing between adult ADHD and mild cognitive impairment
There is considerable overlap between symptoms of adult attention-deficit/hyperactivity disorder (ADHD) and mild cognitive impairment (MCI), including problems with sustained attention or concentration, anterograde memory, and executive functioning. Differentiating these clinical syndromes based on symptomatic presentation alone can be difficult, but considering the following factors can help you make a more informed diagnosis:
Neurodevelopmental disorder history. DSM-IV-TR stipulates onset for some ADHD symptoms by age 7, although a DSM-5 Work Group is considering symptom onset as late as age 12.1 Initial onset or a dramatic worsening of longstanding ADHD symptoms in middle-age or older adults is atypical for this neurodevelopmental disorder.
Detailed self-diagnosed symptoms. Patients with ADHD usually can give a satisfactory history of their symptoms. Patients with MCI often are less able to provide a useful history because they have prominent difficulties with anterograde memory, which may be associated with emerging anosognosia.
Educational learning difficulties. Patients with ADHD frequently have comorbid learning difficulties and substance abuse disorders, which are uncommon in MCI.
Rating scales. When in doubt, use rating scales to assess for ADHD.2 Ask your patient to complete the rating scale based on how he or she remembers behaving in elementary through middle school, most of their adult life after age 20, and since symptom onset. Obtain collateral ratings from a reliable informant based on his or her knowledge of the patient’s long-term behavioral functioning.
Worsening symptoms. The typical ADHD patient will have a “positive” screen for symptoms, but will report fewer and less severe symptoms from childhood or adolescence through young adulthood and into middle and older age. Suspect MCI when your patient or an informant reports a clear worsening of symptoms in recent months or years despite a lack of evidence of a significant intervening psychiatric disorder.
Psychopharmacotherapy. Patients with MCI usually do not benefit from medications for ADHD. Patients with ADHD often report improvement in at least some of their symptoms with psychopharmacologic treatment.
When your patient’s history, rating scale assessment, and medication trials do not allow you to make a confident differential diagnosis, consider referring him or her for psychological or neuropsychological testing.
There can be overlap in psychometric test findings of middle-age and older adults with a history of ADHD and those who may have MCI. Still, MCI patients’ cognitive difficulties usually are more concerning and dramatic, including problems with spontaneous recall as well as “recognition memory.”
When findings from psychometric testing are equivocal because of possible co-occurrence, retesting in 12 to 18 months usually will help you make a reliable differential diagnosis. Specifically, progression of cognitive dysfunction—including evidence of worsening anterograde memory—is common in MCI but not in ADHD.
Current symptoms of major depressive disorder may further “muddy the waters.” However, parameters such as response to adequate medication trials, progression of cognitive dysfunction, and worsening of test-based cognitive or neuropsychological deficits over time can be useful in reaching a satisfactory differential diagnosis.
Disclosure
Dr. Pollak reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
There is considerable overlap between symptoms of adult attention-deficit/hyperactivity disorder (ADHD) and mild cognitive impairment (MCI), including problems with sustained attention or concentration, anterograde memory, and executive functioning. Differentiating these clinical syndromes based on symptomatic presentation alone can be difficult, but considering the following factors can help you make a more informed diagnosis:
Neurodevelopmental disorder history. DSM-IV-TR stipulates onset for some ADHD symptoms by age 7, although a DSM-5 Work Group is considering symptom onset as late as age 12.1 Initial onset or a dramatic worsening of longstanding ADHD symptoms in middle-age or older adults is atypical for this neurodevelopmental disorder.
Detailed self-diagnosed symptoms. Patients with ADHD usually can give a satisfactory history of their symptoms. Patients with MCI often are less able to provide a useful history because they have prominent difficulties with anterograde memory, which may be associated with emerging anosognosia.
Educational learning difficulties. Patients with ADHD frequently have comorbid learning difficulties and substance abuse disorders, which are uncommon in MCI.
Rating scales. When in doubt, use rating scales to assess for ADHD.2 Ask your patient to complete the rating scale based on how he or she remembers behaving in elementary through middle school, most of their adult life after age 20, and since symptom onset. Obtain collateral ratings from a reliable informant based on his or her knowledge of the patient’s long-term behavioral functioning.
Worsening symptoms. The typical ADHD patient will have a “positive” screen for symptoms, but will report fewer and less severe symptoms from childhood or adolescence through young adulthood and into middle and older age. Suspect MCI when your patient or an informant reports a clear worsening of symptoms in recent months or years despite a lack of evidence of a significant intervening psychiatric disorder.
Psychopharmacotherapy. Patients with MCI usually do not benefit from medications for ADHD. Patients with ADHD often report improvement in at least some of their symptoms with psychopharmacologic treatment.
When your patient’s history, rating scale assessment, and medication trials do not allow you to make a confident differential diagnosis, consider referring him or her for psychological or neuropsychological testing.
There can be overlap in psychometric test findings of middle-age and older adults with a history of ADHD and those who may have MCI. Still, MCI patients’ cognitive difficulties usually are more concerning and dramatic, including problems with spontaneous recall as well as “recognition memory.”
When findings from psychometric testing are equivocal because of possible co-occurrence, retesting in 12 to 18 months usually will help you make a reliable differential diagnosis. Specifically, progression of cognitive dysfunction—including evidence of worsening anterograde memory—is common in MCI but not in ADHD.
Current symptoms of major depressive disorder may further “muddy the waters.” However, parameters such as response to adequate medication trials, progression of cognitive dysfunction, and worsening of test-based cognitive or neuropsychological deficits over time can be useful in reaching a satisfactory differential diagnosis.
Disclosure
Dr. Pollak reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
There is considerable overlap between symptoms of adult attention-deficit/hyperactivity disorder (ADHD) and mild cognitive impairment (MCI), including problems with sustained attention or concentration, anterograde memory, and executive functioning. Differentiating these clinical syndromes based on symptomatic presentation alone can be difficult, but considering the following factors can help you make a more informed diagnosis:
Neurodevelopmental disorder history. DSM-IV-TR stipulates onset for some ADHD symptoms by age 7, although a DSM-5 Work Group is considering symptom onset as late as age 12.1 Initial onset or a dramatic worsening of longstanding ADHD symptoms in middle-age or older adults is atypical for this neurodevelopmental disorder.
Detailed self-diagnosed symptoms. Patients with ADHD usually can give a satisfactory history of their symptoms. Patients with MCI often are less able to provide a useful history because they have prominent difficulties with anterograde memory, which may be associated with emerging anosognosia.
Educational learning difficulties. Patients with ADHD frequently have comorbid learning difficulties and substance abuse disorders, which are uncommon in MCI.
Rating scales. When in doubt, use rating scales to assess for ADHD.2 Ask your patient to complete the rating scale based on how he or she remembers behaving in elementary through middle school, most of their adult life after age 20, and since symptom onset. Obtain collateral ratings from a reliable informant based on his or her knowledge of the patient’s long-term behavioral functioning.
Worsening symptoms. The typical ADHD patient will have a “positive” screen for symptoms, but will report fewer and less severe symptoms from childhood or adolescence through young adulthood and into middle and older age. Suspect MCI when your patient or an informant reports a clear worsening of symptoms in recent months or years despite a lack of evidence of a significant intervening psychiatric disorder.
Psychopharmacotherapy. Patients with MCI usually do not benefit from medications for ADHD. Patients with ADHD often report improvement in at least some of their symptoms with psychopharmacologic treatment.
When your patient’s history, rating scale assessment, and medication trials do not allow you to make a confident differential diagnosis, consider referring him or her for psychological or neuropsychological testing.
There can be overlap in psychometric test findings of middle-age and older adults with a history of ADHD and those who may have MCI. Still, MCI patients’ cognitive difficulties usually are more concerning and dramatic, including problems with spontaneous recall as well as “recognition memory.”
When findings from psychometric testing are equivocal because of possible co-occurrence, retesting in 12 to 18 months usually will help you make a reliable differential diagnosis. Specifically, progression of cognitive dysfunction—including evidence of worsening anterograde memory—is common in MCI but not in ADHD.
Current symptoms of major depressive disorder may further “muddy the waters.” However, parameters such as response to adequate medication trials, progression of cognitive dysfunction, and worsening of test-based cognitive or neuropsychological deficits over time can be useful in reaching a satisfactory differential diagnosis.
Disclosure
Dr. Pollak reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Trichotillomania: Targeting the root of the disorder
An estimated 1% of Americans have trichotillomania (TTM), an impulse-control disorder in which patients experience pleasure or gratification from recurrently pulling out their own hair, resulting in noticeable hair loss.1,2 This disorder is more commonly diagnosed in women, likely reflecting treatment-seeking bias; women may be more likely to seek care for TTM because of social stigma associated with hair loss.2 Avulsion of hair usually occurs at the scalp, but also can be seen in multiple sites, including eyebrows, eyelashes, beards, and pubic regions; the number of sites typically increases with the patient’s age.3
The lifetime prevalence of comorbid axis I disorders in patients with TTM is 82%.3 Because of this, TTM often is first encountered in a psychiatric setting. Psychiatrists should have knowledge of TTM diagnosis and treatment because they may be the only point of care for TTM patients. When considering a TTM diagnosis, be aware that in some cultures rending hair is a mourning ritual or a rite of passage.3
Evidence for cognitive therapies
Behavioral models suggest TTM behaviors are learned and maintained by both classical and operant conditioning. Therapies that target the cognitive processes that trigger urges to pull, the avulsion of hair, and recognizing the consequences have the best empirical support.3
Habit reversal training (HRT) is considered the most effective treatment for TTM.3 One trial found a single 2-hour HRT intervention resulted in greater reductions in hair pulling episodes and higher remission rates compared with placebo.3 HRT trains patients to create a competing response, such as fist clenching, that is incompatible and blocks the undesired response.
Other therapeutic approaches to TTM include acceptance and commitment therapy, cognitive-behavioral therapy (CBT), and dialectical behavioral therapy-enhanced HRT. Evidence is most robust for CBT-HRT; randomized controlled trials found a statistically significant reduction in TTM in patients receiving CBT-HRT.3 One review suggests CBT-HRT should be considered first-line therapy for TTM.3
Pharmacologic options
Although no medications are FDA-approved for treating TTM, options include clomipramine, olanzapine, fluoxetine, pimozide, inositol, naltrexone, and N-acetylcysteine.2,3 The most robust trials of pharmacotherapy monotherapy were for N-acetylcysteine and naltrexone; both medications had significantly greater reduction in hair-pulling symptoms compared with placebo.3 Some evidence suggests combined pharmacotherapy and psychotherapy might be an effective approach.2,3
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Woods DW, Flessner C, Franklin ME, et al. Understanding and treating trichotillomania: what we know and what we don’t know. Psychiatr Clin North Am. 2006;29(2):487-501, ix.
3. Duke DC, Keeley ML, Geffken GR, et al. Trichotillomania: a current review. Clin Psychol Rev. 2010;30(2):181-193.
An estimated 1% of Americans have trichotillomania (TTM), an impulse-control disorder in which patients experience pleasure or gratification from recurrently pulling out their own hair, resulting in noticeable hair loss.1,2 This disorder is more commonly diagnosed in women, likely reflecting treatment-seeking bias; women may be more likely to seek care for TTM because of social stigma associated with hair loss.2 Avulsion of hair usually occurs at the scalp, but also can be seen in multiple sites, including eyebrows, eyelashes, beards, and pubic regions; the number of sites typically increases with the patient’s age.3
The lifetime prevalence of comorbid axis I disorders in patients with TTM is 82%.3 Because of this, TTM often is first encountered in a psychiatric setting. Psychiatrists should have knowledge of TTM diagnosis and treatment because they may be the only point of care for TTM patients. When considering a TTM diagnosis, be aware that in some cultures rending hair is a mourning ritual or a rite of passage.3
Evidence for cognitive therapies
Behavioral models suggest TTM behaviors are learned and maintained by both classical and operant conditioning. Therapies that target the cognitive processes that trigger urges to pull, the avulsion of hair, and recognizing the consequences have the best empirical support.3
Habit reversal training (HRT) is considered the most effective treatment for TTM.3 One trial found a single 2-hour HRT intervention resulted in greater reductions in hair pulling episodes and higher remission rates compared with placebo.3 HRT trains patients to create a competing response, such as fist clenching, that is incompatible and blocks the undesired response.
Other therapeutic approaches to TTM include acceptance and commitment therapy, cognitive-behavioral therapy (CBT), and dialectical behavioral therapy-enhanced HRT. Evidence is most robust for CBT-HRT; randomized controlled trials found a statistically significant reduction in TTM in patients receiving CBT-HRT.3 One review suggests CBT-HRT should be considered first-line therapy for TTM.3
Pharmacologic options
Although no medications are FDA-approved for treating TTM, options include clomipramine, olanzapine, fluoxetine, pimozide, inositol, naltrexone, and N-acetylcysteine.2,3 The most robust trials of pharmacotherapy monotherapy were for N-acetylcysteine and naltrexone; both medications had significantly greater reduction in hair-pulling symptoms compared with placebo.3 Some evidence suggests combined pharmacotherapy and psychotherapy might be an effective approach.2,3
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
An estimated 1% of Americans have trichotillomania (TTM), an impulse-control disorder in which patients experience pleasure or gratification from recurrently pulling out their own hair, resulting in noticeable hair loss.1,2 This disorder is more commonly diagnosed in women, likely reflecting treatment-seeking bias; women may be more likely to seek care for TTM because of social stigma associated with hair loss.2 Avulsion of hair usually occurs at the scalp, but also can be seen in multiple sites, including eyebrows, eyelashes, beards, and pubic regions; the number of sites typically increases with the patient’s age.3
The lifetime prevalence of comorbid axis I disorders in patients with TTM is 82%.3 Because of this, TTM often is first encountered in a psychiatric setting. Psychiatrists should have knowledge of TTM diagnosis and treatment because they may be the only point of care for TTM patients. When considering a TTM diagnosis, be aware that in some cultures rending hair is a mourning ritual or a rite of passage.3
Evidence for cognitive therapies
Behavioral models suggest TTM behaviors are learned and maintained by both classical and operant conditioning. Therapies that target the cognitive processes that trigger urges to pull, the avulsion of hair, and recognizing the consequences have the best empirical support.3
Habit reversal training (HRT) is considered the most effective treatment for TTM.3 One trial found a single 2-hour HRT intervention resulted in greater reductions in hair pulling episodes and higher remission rates compared with placebo.3 HRT trains patients to create a competing response, such as fist clenching, that is incompatible and blocks the undesired response.
Other therapeutic approaches to TTM include acceptance and commitment therapy, cognitive-behavioral therapy (CBT), and dialectical behavioral therapy-enhanced HRT. Evidence is most robust for CBT-HRT; randomized controlled trials found a statistically significant reduction in TTM in patients receiving CBT-HRT.3 One review suggests CBT-HRT should be considered first-line therapy for TTM.3
Pharmacologic options
Although no medications are FDA-approved for treating TTM, options include clomipramine, olanzapine, fluoxetine, pimozide, inositol, naltrexone, and N-acetylcysteine.2,3 The most robust trials of pharmacotherapy monotherapy were for N-acetylcysteine and naltrexone; both medications had significantly greater reduction in hair-pulling symptoms compared with placebo.3 Some evidence suggests combined pharmacotherapy and psychotherapy might be an effective approach.2,3
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Woods DW, Flessner C, Franklin ME, et al. Understanding and treating trichotillomania: what we know and what we don’t know. Psychiatr Clin North Am. 2006;29(2):487-501, ix.
3. Duke DC, Keeley ML, Geffken GR, et al. Trichotillomania: a current review. Clin Psychol Rev. 2010;30(2):181-193.
1. Diagnostic and statistical manual of mental disorders, 4th ed, text rev. Washington DC: American Psychiatric Association; 2000.
2. Woods DW, Flessner C, Franklin ME, et al. Understanding and treating trichotillomania: what we know and what we don’t know. Psychiatr Clin North Am. 2006;29(2):487-501, ix.
3. Duke DC, Keeley ML, Geffken GR, et al. Trichotillomania: a current review. Clin Psychol Rev. 2010;30(2):181-193.
‘Bugs in my skin’: What you should know about delusional infestation
Patients with delusional infestation (DI) falsely believe that they are infested with tiny infectious agents—typically vermin, insects, or small animals—that crawl on, in, or under their skin, leaving marks and building nests.1 Patients often describe the pathogens on the skin of hands, arms, feet, lower legs, scalp, or genital areas. They state the pathogen is difficult to diagnose and usually is contracted by human contact. Most patients with DI engage in intensive, repetitive, and often dangerous self-cleansing to get rid of the pathogens, which results in skin lesions.1 Less often, patients believe they are infested with bacteria or viruses.1
The typical DI patient is a middle age or older female with few social contacts, no psychiatric history, and normal cognitive and social function.1 Geriatric patients with dementia and vision or hearing impairment who live in a nursing home may develop DI; it also may be seen in geriatric patients with vascular encephalopathy.
What to consider
First rule out a genuine infestation by referring your patient for dermatologic and microbiologic testing. Order basic laboratory tests to assess inflammation markers—complete blood cell count, erythrocyte sedimentation rate, C-reactive protein, electrolytes, liver function, thyroid-stimulating hormone, and fasting glucose.1 Suggest a cranial MRI to rule out a brain disorder. Also, perform a urinalysis for cocaine, amphetamines, or cannabinoids, which can cause DI.1 Rule out medical conditions that are associated with pruritus and psychiatric symptoms, including endocrine, renal, hepatic, rheumatoid, and nutritional conditions.
Treating DI patients
Collaborate with a dermatologist, microbiologist, and primary care physician because these clinicians can deliver medical interventions, such as treating skin lesions and prescribing non-sedating antihistamines to alleviate pruritus. The Table1 offers other suggestions for managing DI patients.
Pharmacotherapy. Although high-quality evidence supporting antipsychotics for treating DI is lacking, olanzapine and risperidone are considered first-line agents; haloperidol and perphenazine also are recommended.1 Response and remission rates are similar with typical and atypical antipsychotics and the median onset of efficacy with antipsychotics is approximately 1.5 weeks.1,2 Antidepressants—including escitalopram, sertraline, mirtazapine, and venlafaxine—have been shown to effectively treat DI.3 In treatment-resistant cases, pimozide and electroconvulsive therapy have been used.1
Psychotherapy is effective for only 10% of DI patients.4
Table
Treating patients with DI: What to do and what to avoid
| Do’s | Don’t |
|---|---|
| Do acknowledge and empathize with your patient’s concerns | Don’t try to convince your patient he or she is wrong about the self-diagnosis |
| Do perform a thorough physical exam and diagnostic investigation | Don’t use words such as “delusional” or “psychotic” |
| Do paraphrase symptoms as “sensations” or “crawling” instead of reinforcing or questioning them | Don’t start psychopharmacology until you establish rapport with your patient |
| Do indicate that symptoms could be secondary to overactivity of the nervous system or “unexplained dermopathy” | |
| Do suggest that antipsychotics may help reduce your patient’s distress and itching | |
| DI: delusional infestation Source: Adapted from reference 1 | |
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Freudenmann RW, Lepping P. Delusional infestation. Clin Microbiol Rev. 2009;22(4):690-732.
2. Freudenmann RW, Lepping P. Second-generation antipsychotics in primary and secondary delusional parasitosis: outcome and efficacy. J Clin Psychopharmacol. 2008;28(5):500-508.
3. Cipriani A, Furukawa TA, Salanti G, et al. Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis. Lancet. 2009;373(9665):746-758.
4. Wykoff RF. Delusions of parasitosis: a review. Rev Infect Dis. 1987;9(3):433-437.
Patients with delusional infestation (DI) falsely believe that they are infested with tiny infectious agents—typically vermin, insects, or small animals—that crawl on, in, or under their skin, leaving marks and building nests.1 Patients often describe the pathogens on the skin of hands, arms, feet, lower legs, scalp, or genital areas. They state the pathogen is difficult to diagnose and usually is contracted by human contact. Most patients with DI engage in intensive, repetitive, and often dangerous self-cleansing to get rid of the pathogens, which results in skin lesions.1 Less often, patients believe they are infested with bacteria or viruses.1
The typical DI patient is a middle age or older female with few social contacts, no psychiatric history, and normal cognitive and social function.1 Geriatric patients with dementia and vision or hearing impairment who live in a nursing home may develop DI; it also may be seen in geriatric patients with vascular encephalopathy.
What to consider
First rule out a genuine infestation by referring your patient for dermatologic and microbiologic testing. Order basic laboratory tests to assess inflammation markers—complete blood cell count, erythrocyte sedimentation rate, C-reactive protein, electrolytes, liver function, thyroid-stimulating hormone, and fasting glucose.1 Suggest a cranial MRI to rule out a brain disorder. Also, perform a urinalysis for cocaine, amphetamines, or cannabinoids, which can cause DI.1 Rule out medical conditions that are associated with pruritus and psychiatric symptoms, including endocrine, renal, hepatic, rheumatoid, and nutritional conditions.
Treating DI patients
Collaborate with a dermatologist, microbiologist, and primary care physician because these clinicians can deliver medical interventions, such as treating skin lesions and prescribing non-sedating antihistamines to alleviate pruritus. The Table1 offers other suggestions for managing DI patients.
Pharmacotherapy. Although high-quality evidence supporting antipsychotics for treating DI is lacking, olanzapine and risperidone are considered first-line agents; haloperidol and perphenazine also are recommended.1 Response and remission rates are similar with typical and atypical antipsychotics and the median onset of efficacy with antipsychotics is approximately 1.5 weeks.1,2 Antidepressants—including escitalopram, sertraline, mirtazapine, and venlafaxine—have been shown to effectively treat DI.3 In treatment-resistant cases, pimozide and electroconvulsive therapy have been used.1
Psychotherapy is effective for only 10% of DI patients.4
Table
Treating patients with DI: What to do and what to avoid
| Do’s | Don’t |
|---|---|
| Do acknowledge and empathize with your patient’s concerns | Don’t try to convince your patient he or she is wrong about the self-diagnosis |
| Do perform a thorough physical exam and diagnostic investigation | Don’t use words such as “delusional” or “psychotic” |
| Do paraphrase symptoms as “sensations” or “crawling” instead of reinforcing or questioning them | Don’t start psychopharmacology until you establish rapport with your patient |
| Do indicate that symptoms could be secondary to overactivity of the nervous system or “unexplained dermopathy” | |
| Do suggest that antipsychotics may help reduce your patient’s distress and itching | |
| DI: delusional infestation Source: Adapted from reference 1 | |
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Patients with delusional infestation (DI) falsely believe that they are infested with tiny infectious agents—typically vermin, insects, or small animals—that crawl on, in, or under their skin, leaving marks and building nests.1 Patients often describe the pathogens on the skin of hands, arms, feet, lower legs, scalp, or genital areas. They state the pathogen is difficult to diagnose and usually is contracted by human contact. Most patients with DI engage in intensive, repetitive, and often dangerous self-cleansing to get rid of the pathogens, which results in skin lesions.1 Less often, patients believe they are infested with bacteria or viruses.1
The typical DI patient is a middle age or older female with few social contacts, no psychiatric history, and normal cognitive and social function.1 Geriatric patients with dementia and vision or hearing impairment who live in a nursing home may develop DI; it also may be seen in geriatric patients with vascular encephalopathy.
What to consider
First rule out a genuine infestation by referring your patient for dermatologic and microbiologic testing. Order basic laboratory tests to assess inflammation markers—complete blood cell count, erythrocyte sedimentation rate, C-reactive protein, electrolytes, liver function, thyroid-stimulating hormone, and fasting glucose.1 Suggest a cranial MRI to rule out a brain disorder. Also, perform a urinalysis for cocaine, amphetamines, or cannabinoids, which can cause DI.1 Rule out medical conditions that are associated with pruritus and psychiatric symptoms, including endocrine, renal, hepatic, rheumatoid, and nutritional conditions.
Treating DI patients
Collaborate with a dermatologist, microbiologist, and primary care physician because these clinicians can deliver medical interventions, such as treating skin lesions and prescribing non-sedating antihistamines to alleviate pruritus. The Table1 offers other suggestions for managing DI patients.
Pharmacotherapy. Although high-quality evidence supporting antipsychotics for treating DI is lacking, olanzapine and risperidone are considered first-line agents; haloperidol and perphenazine also are recommended.1 Response and remission rates are similar with typical and atypical antipsychotics and the median onset of efficacy with antipsychotics is approximately 1.5 weeks.1,2 Antidepressants—including escitalopram, sertraline, mirtazapine, and venlafaxine—have been shown to effectively treat DI.3 In treatment-resistant cases, pimozide and electroconvulsive therapy have been used.1
Psychotherapy is effective for only 10% of DI patients.4
Table
Treating patients with DI: What to do and what to avoid
| Do’s | Don’t |
|---|---|
| Do acknowledge and empathize with your patient’s concerns | Don’t try to convince your patient he or she is wrong about the self-diagnosis |
| Do perform a thorough physical exam and diagnostic investigation | Don’t use words such as “delusional” or “psychotic” |
| Do paraphrase symptoms as “sensations” or “crawling” instead of reinforcing or questioning them | Don’t start psychopharmacology until you establish rapport with your patient |
| Do indicate that symptoms could be secondary to overactivity of the nervous system or “unexplained dermopathy” | |
| Do suggest that antipsychotics may help reduce your patient’s distress and itching | |
| DI: delusional infestation Source: Adapted from reference 1 | |
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Freudenmann RW, Lepping P. Delusional infestation. Clin Microbiol Rev. 2009;22(4):690-732.
2. Freudenmann RW, Lepping P. Second-generation antipsychotics in primary and secondary delusional parasitosis: outcome and efficacy. J Clin Psychopharmacol. 2008;28(5):500-508.
3. Cipriani A, Furukawa TA, Salanti G, et al. Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis. Lancet. 2009;373(9665):746-758.
4. Wykoff RF. Delusions of parasitosis: a review. Rev Infect Dis. 1987;9(3):433-437.
1. Freudenmann RW, Lepping P. Delusional infestation. Clin Microbiol Rev. 2009;22(4):690-732.
2. Freudenmann RW, Lepping P. Second-generation antipsychotics in primary and secondary delusional parasitosis: outcome and efficacy. J Clin Psychopharmacol. 2008;28(5):500-508.
3. Cipriani A, Furukawa TA, Salanti G, et al. Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis. Lancet. 2009;373(9665):746-758.
4. Wykoff RF. Delusions of parasitosis: a review. Rev Infect Dis. 1987;9(3):433-437.
Strategies for managing patients with chronic subjective dizziness
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Chronic subjective dizziness (CSD) is characterized by persistent (>3 months) dizziness, lightheadedness, or unsteadiness, without vertigo or ataxia. Symptoms often are worse in highly stimulating visual environments (eg, busy malls or grocery stores) or settings with indistinct visual orientation cues (eg, large open areas, heavy fog). Neuro-otologic examination and laboratory testing reveal no active vestibular deficits.1
CSD is not a psychiatric illness, but exists at the interface of psychiatry and neuro-otology. For example, anxiety and depressive disorders often accompany CSD, but are not an integral part of it. Treatment outcomes are good and prognosis for full function is high.
Conditions that cause dizziness
Vertigo—a sensation of rotation or linear movement of self or surroundings—occurs in discrete attacks that typically have an acute onset and are caused by neuro-otologic conditions.2 Symptoms may last for seconds (benign paroxysmal positional vertigo [BPPV]), hours (Meniere’s disease), minutes to days (vestibular migraine), or weeks (vestibular neuronitis). Unsteadiness, a swaying or rocking sensation, dizziness, and a disturbed sense of spatial orientation without illusory movement may be acute, subacute, or chronic. These symptoms may accompany vertigo or occur independently.2 Psychiatric disorders (panic), dysautonomias (vasovagal spells), and cardiovascular conditions (dysrhythmias) may cause episodic unsteadiness and dizziness, but not vertigo. Several illnesses can cause persistent unsteadiness and dizziness, including bilateral peripheral vestibular deficits, central vestibular lesions (strokes), proprioceptive or visual loss (neuropathies), and generalized anxiety disorder.
Up to 30% of patients who experience episodic balance problems develop persistent unsteadiness or dizziness (ie, CSD).3 Clinical history, exam, and laboratory tests may be normal or identify previous triggering events (eg, past vestibular insults), but transient conditions cannot explain patients’ persistent symptoms. Often, patients describe a transition from episodic vertigo and ataxia to chronic, often daily unsteadiness and dizziness. In this situation, the illness that started the problem often is not the one that continues to be distressing. Rather, patients develop hypersensitivity to motion stimuli (visual, vestibular, and proprioceptive inputs) and hypervigilance about motion environments that last long after the trigger event has resolved. These CSD features are thought to arise from threat-related failure of postural control systems to return to normal functioning after shifting into high-risk strategies during the acute events that disrupted balance.
5 strategies for managing CSD
1. Develop a common language among other clinicians you work with. The concept of CSD will be new to most patients and their referring clinicians, so they will need to hear about it more than once. From a neuro-otologic standpoint, make a point of separating past and present problems (ie, not the vestibular neuronitis, BPPV, etc., that the patient previously had, but the CSD they presently have). From a psychological standpoint, talk in behavioral terms—hypersensitivity to motion, hypervigilance about motion environments, use of safety maneuvers (eg, touching a wall when walking), and avoiding situations that provoke dizziness. These are reflexive, fear-driven symptoms, but patients understand them better in terms of dizziness and unsteadiness.
2. Keep in mind that dizziness is the chief complaint. As patients go from primary care to otolaryngology, audiology, vestibular rehabilitation, and psychiatry, the problem is dizziness. You may find anxiety or depression along the way, but dizziness comes first for these patients.
3. Educate patients and referring physicians. Give patients and their referring physicians materials that define CSD and its differential diagnosis.3 Check off patients’ symptoms in the diagnostic list and circle their medical comorbidities, if present. For psychiatrists, this is a good point to start discussing behavioral morbidity and treatment.
4. Screen for coexisting medical-psychiatric diagnoses (eg, Meniere’s disease, panic disorder) or primarily psychiatric problems (conversion disorder). In addition to the otologic exam for vestibular diseases, patients should be screened for migraine, traumatic brain injury, dysautonomia, and dysrhythmias. Ask patients to complete symptom self-reports, including the Patient Health Questionnaire-9 (for depression) and Generalized Anxiety Disorder-7 (for anxiety).
5. Treat the patient’s primary problem (eg, CSD, vertigo, ataxia, or headache) first. If headache and balance symptoms are intertwined, use venlafaxine or combine a selective serotonin reuptake inhibitor (SSRI) with a separate migraine prophylactic agent.
Treatment options
Pharmacotherapy. Five open-label studies found SSRIs are effective for CSD even for patients without psychiatric comorbidity.3 Use a “start low, go slow” strategy to avoid aggravating symptoms. Final doses usually are in the lower half of the therapeutic range. Full treatment response may take 8 to 12 weeks. Vestibular suppressants such as meclizine work reasonably well for acute vertigo, but have no role in treating CSD.
Vestibular and balance rehabilitation therapy (VBRT) is an exercise program performed at home by patients but overseen by specially trained physical therapists. It is an excellent habituation/desensitization program that can be integrated with medication and psychotherapy. All patients with CSD should undergo VBRT.
Cognitive-behavioral therapy may be helpful for treating psychiatric morbidity (anxiety, depression, phobic avoidance) in patients with CSD, but it appears to be less effective for physical symptoms of dizziness.3
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Staab JP, Ruckenstein MJ. Expanding the differential diagnosis of chronic dizziness. Arch Otolaryngol Head Neck Surg. 2007;133(2):170-176.
2. Bisdorff A, Von Brevern M, Lempert T, et al. Classification of vestibular symptoms: towards an international classification of vestibular disorders. J Vestib Res. 2009;19(1-2):1-13.
3. Staab JP. Psychological aspects of vestibular disorders. In: Eggers SD Zee DS, eds Vertigo and imbalance: clinical neurophysiology of the vestibular system. Boston, MA: Elsevier. 2010;502-522.
Discuss this article at www.facebook.com/CurrentPsychiatry
Chronic subjective dizziness (CSD) is characterized by persistent (>3 months) dizziness, lightheadedness, or unsteadiness, without vertigo or ataxia. Symptoms often are worse in highly stimulating visual environments (eg, busy malls or grocery stores) or settings with indistinct visual orientation cues (eg, large open areas, heavy fog). Neuro-otologic examination and laboratory testing reveal no active vestibular deficits.1
CSD is not a psychiatric illness, but exists at the interface of psychiatry and neuro-otology. For example, anxiety and depressive disorders often accompany CSD, but are not an integral part of it. Treatment outcomes are good and prognosis for full function is high.
Conditions that cause dizziness
Vertigo—a sensation of rotation or linear movement of self or surroundings—occurs in discrete attacks that typically have an acute onset and are caused by neuro-otologic conditions.2 Symptoms may last for seconds (benign paroxysmal positional vertigo [BPPV]), hours (Meniere’s disease), minutes to days (vestibular migraine), or weeks (vestibular neuronitis). Unsteadiness, a swaying or rocking sensation, dizziness, and a disturbed sense of spatial orientation without illusory movement may be acute, subacute, or chronic. These symptoms may accompany vertigo or occur independently.2 Psychiatric disorders (panic), dysautonomias (vasovagal spells), and cardiovascular conditions (dysrhythmias) may cause episodic unsteadiness and dizziness, but not vertigo. Several illnesses can cause persistent unsteadiness and dizziness, including bilateral peripheral vestibular deficits, central vestibular lesions (strokes), proprioceptive or visual loss (neuropathies), and generalized anxiety disorder.
Up to 30% of patients who experience episodic balance problems develop persistent unsteadiness or dizziness (ie, CSD).3 Clinical history, exam, and laboratory tests may be normal or identify previous triggering events (eg, past vestibular insults), but transient conditions cannot explain patients’ persistent symptoms. Often, patients describe a transition from episodic vertigo and ataxia to chronic, often daily unsteadiness and dizziness. In this situation, the illness that started the problem often is not the one that continues to be distressing. Rather, patients develop hypersensitivity to motion stimuli (visual, vestibular, and proprioceptive inputs) and hypervigilance about motion environments that last long after the trigger event has resolved. These CSD features are thought to arise from threat-related failure of postural control systems to return to normal functioning after shifting into high-risk strategies during the acute events that disrupted balance.
5 strategies for managing CSD
1. Develop a common language among other clinicians you work with. The concept of CSD will be new to most patients and their referring clinicians, so they will need to hear about it more than once. From a neuro-otologic standpoint, make a point of separating past and present problems (ie, not the vestibular neuronitis, BPPV, etc., that the patient previously had, but the CSD they presently have). From a psychological standpoint, talk in behavioral terms—hypersensitivity to motion, hypervigilance about motion environments, use of safety maneuvers (eg, touching a wall when walking), and avoiding situations that provoke dizziness. These are reflexive, fear-driven symptoms, but patients understand them better in terms of dizziness and unsteadiness.
2. Keep in mind that dizziness is the chief complaint. As patients go from primary care to otolaryngology, audiology, vestibular rehabilitation, and psychiatry, the problem is dizziness. You may find anxiety or depression along the way, but dizziness comes first for these patients.
3. Educate patients and referring physicians. Give patients and their referring physicians materials that define CSD and its differential diagnosis.3 Check off patients’ symptoms in the diagnostic list and circle their medical comorbidities, if present. For psychiatrists, this is a good point to start discussing behavioral morbidity and treatment.
4. Screen for coexisting medical-psychiatric diagnoses (eg, Meniere’s disease, panic disorder) or primarily psychiatric problems (conversion disorder). In addition to the otologic exam for vestibular diseases, patients should be screened for migraine, traumatic brain injury, dysautonomia, and dysrhythmias. Ask patients to complete symptom self-reports, including the Patient Health Questionnaire-9 (for depression) and Generalized Anxiety Disorder-7 (for anxiety).
5. Treat the patient’s primary problem (eg, CSD, vertigo, ataxia, or headache) first. If headache and balance symptoms are intertwined, use venlafaxine or combine a selective serotonin reuptake inhibitor (SSRI) with a separate migraine prophylactic agent.
Treatment options
Pharmacotherapy. Five open-label studies found SSRIs are effective for CSD even for patients without psychiatric comorbidity.3 Use a “start low, go slow” strategy to avoid aggravating symptoms. Final doses usually are in the lower half of the therapeutic range. Full treatment response may take 8 to 12 weeks. Vestibular suppressants such as meclizine work reasonably well for acute vertigo, but have no role in treating CSD.
Vestibular and balance rehabilitation therapy (VBRT) is an exercise program performed at home by patients but overseen by specially trained physical therapists. It is an excellent habituation/desensitization program that can be integrated with medication and psychotherapy. All patients with CSD should undergo VBRT.
Cognitive-behavioral therapy may be helpful for treating psychiatric morbidity (anxiety, depression, phobic avoidance) in patients with CSD, but it appears to be less effective for physical symptoms of dizziness.3
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Discuss this article at www.facebook.com/CurrentPsychiatry
Chronic subjective dizziness (CSD) is characterized by persistent (>3 months) dizziness, lightheadedness, or unsteadiness, without vertigo or ataxia. Symptoms often are worse in highly stimulating visual environments (eg, busy malls or grocery stores) or settings with indistinct visual orientation cues (eg, large open areas, heavy fog). Neuro-otologic examination and laboratory testing reveal no active vestibular deficits.1
CSD is not a psychiatric illness, but exists at the interface of psychiatry and neuro-otology. For example, anxiety and depressive disorders often accompany CSD, but are not an integral part of it. Treatment outcomes are good and prognosis for full function is high.
Conditions that cause dizziness
Vertigo—a sensation of rotation or linear movement of self or surroundings—occurs in discrete attacks that typically have an acute onset and are caused by neuro-otologic conditions.2 Symptoms may last for seconds (benign paroxysmal positional vertigo [BPPV]), hours (Meniere’s disease), minutes to days (vestibular migraine), or weeks (vestibular neuronitis). Unsteadiness, a swaying or rocking sensation, dizziness, and a disturbed sense of spatial orientation without illusory movement may be acute, subacute, or chronic. These symptoms may accompany vertigo or occur independently.2 Psychiatric disorders (panic), dysautonomias (vasovagal spells), and cardiovascular conditions (dysrhythmias) may cause episodic unsteadiness and dizziness, but not vertigo. Several illnesses can cause persistent unsteadiness and dizziness, including bilateral peripheral vestibular deficits, central vestibular lesions (strokes), proprioceptive or visual loss (neuropathies), and generalized anxiety disorder.
Up to 30% of patients who experience episodic balance problems develop persistent unsteadiness or dizziness (ie, CSD).3 Clinical history, exam, and laboratory tests may be normal or identify previous triggering events (eg, past vestibular insults), but transient conditions cannot explain patients’ persistent symptoms. Often, patients describe a transition from episodic vertigo and ataxia to chronic, often daily unsteadiness and dizziness. In this situation, the illness that started the problem often is not the one that continues to be distressing. Rather, patients develop hypersensitivity to motion stimuli (visual, vestibular, and proprioceptive inputs) and hypervigilance about motion environments that last long after the trigger event has resolved. These CSD features are thought to arise from threat-related failure of postural control systems to return to normal functioning after shifting into high-risk strategies during the acute events that disrupted balance.
5 strategies for managing CSD
1. Develop a common language among other clinicians you work with. The concept of CSD will be new to most patients and their referring clinicians, so they will need to hear about it more than once. From a neuro-otologic standpoint, make a point of separating past and present problems (ie, not the vestibular neuronitis, BPPV, etc., that the patient previously had, but the CSD they presently have). From a psychological standpoint, talk in behavioral terms—hypersensitivity to motion, hypervigilance about motion environments, use of safety maneuvers (eg, touching a wall when walking), and avoiding situations that provoke dizziness. These are reflexive, fear-driven symptoms, but patients understand them better in terms of dizziness and unsteadiness.
2. Keep in mind that dizziness is the chief complaint. As patients go from primary care to otolaryngology, audiology, vestibular rehabilitation, and psychiatry, the problem is dizziness. You may find anxiety or depression along the way, but dizziness comes first for these patients.
3. Educate patients and referring physicians. Give patients and their referring physicians materials that define CSD and its differential diagnosis.3 Check off patients’ symptoms in the diagnostic list and circle their medical comorbidities, if present. For psychiatrists, this is a good point to start discussing behavioral morbidity and treatment.
4. Screen for coexisting medical-psychiatric diagnoses (eg, Meniere’s disease, panic disorder) or primarily psychiatric problems (conversion disorder). In addition to the otologic exam for vestibular diseases, patients should be screened for migraine, traumatic brain injury, dysautonomia, and dysrhythmias. Ask patients to complete symptom self-reports, including the Patient Health Questionnaire-9 (for depression) and Generalized Anxiety Disorder-7 (for anxiety).
5. Treat the patient’s primary problem (eg, CSD, vertigo, ataxia, or headache) first. If headache and balance symptoms are intertwined, use venlafaxine or combine a selective serotonin reuptake inhibitor (SSRI) with a separate migraine prophylactic agent.
Treatment options
Pharmacotherapy. Five open-label studies found SSRIs are effective for CSD even for patients without psychiatric comorbidity.3 Use a “start low, go slow” strategy to avoid aggravating symptoms. Final doses usually are in the lower half of the therapeutic range. Full treatment response may take 8 to 12 weeks. Vestibular suppressants such as meclizine work reasonably well for acute vertigo, but have no role in treating CSD.
Vestibular and balance rehabilitation therapy (VBRT) is an exercise program performed at home by patients but overseen by specially trained physical therapists. It is an excellent habituation/desensitization program that can be integrated with medication and psychotherapy. All patients with CSD should undergo VBRT.
Cognitive-behavioral therapy may be helpful for treating psychiatric morbidity (anxiety, depression, phobic avoidance) in patients with CSD, but it appears to be less effective for physical symptoms of dizziness.3
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Staab JP, Ruckenstein MJ. Expanding the differential diagnosis of chronic dizziness. Arch Otolaryngol Head Neck Surg. 2007;133(2):170-176.
2. Bisdorff A, Von Brevern M, Lempert T, et al. Classification of vestibular symptoms: towards an international classification of vestibular disorders. J Vestib Res. 2009;19(1-2):1-13.
3. Staab JP. Psychological aspects of vestibular disorders. In: Eggers SD Zee DS, eds Vertigo and imbalance: clinical neurophysiology of the vestibular system. Boston, MA: Elsevier. 2010;502-522.
1. Staab JP, Ruckenstein MJ. Expanding the differential diagnosis of chronic dizziness. Arch Otolaryngol Head Neck Surg. 2007;133(2):170-176.
2. Bisdorff A, Von Brevern M, Lempert T, et al. Classification of vestibular symptoms: towards an international classification of vestibular disorders. J Vestib Res. 2009;19(1-2):1-13.
3. Staab JP. Psychological aspects of vestibular disorders. In: Eggers SD Zee DS, eds Vertigo and imbalance: clinical neurophysiology of the vestibular system. Boston, MA: Elsevier. 2010;502-522.
How to respond to an in-flight emergency
Discuss this article at www.facebook.com/CurrentPsychiatry
Requests for a physician to assist during in-flight medical emergencies are becoming more common as travelers age and more people have access to air travel.1 Yet in this age of medical specialization, all physicians are not created equal, particularly in providing acute care. Responding to in-flight medical emergencies can be stressful, particularly for specialists who may doubt their skill base in a medical crisis.
The in-flight medical consulting service Medlink reported that only 3.5% of calls it receives are related to psychiatric emergencies.2 This means that psychiatrists who answer an in-flight distress call will almost invariably find themselves confronting a medical issue.
Discomfort with possibly having to deliver acute or invasive medical care may deter psychiatrists from responding. However, psychiatrists should be familiar with many medical problems and their basic management, particularly if their institution requires up-to-date advanced cardiac life support certification. Understanding your role and conceptualizing a general approach before you find yourself in the midst of an in-flight medical emergency can be helpful. We suggest the following principles for responding to in-flight emergencies:
- Respond to a call only if you are a licensed, currently practicing physician.
- Defer to other physicians present who may have more experience delivering acute medical care.3
- If you have been drinking alcohol, do not respond unless there are no other health care providers on board. If you do respond, know your limitations and make them known to the air crew and patient.
- Identify yourself to the patient. Give him or her your name and tell the patient that you are a psychiatrist. If the chief complaint is not something you regularly deal with, tell the patient and crew.
- Perform the best history and physical exam you can, given the setting. Obtain vital signs. Document your findings for your records and for medical personnel who may later assume patient care.
- Do not attempt procedures you are unfamiliar with or not qualified to perform (eg, starting an IV, intubations). Administer only treatments you are comfortable with.
- If you are concerned the patient may face significant morbidity or death, advise the crew to divert the flight to the closest hospital.
- Realize that it is not your role to take leadership of the situation, unless you are the only physician present. Do not be afraid to ask for help from other physicians or health care providers—including nurses or emergency medical technicians—who may not have heard or acknowledged the call or a ground-based medical consulting service. Also, once another physician has taken over, you still can contribute by stabilizing the ill patient’s emotions and behavior.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article of with manufacturers of competing products.
1. Gendreau MA, DeJohn C. Responding to medical events during commercial airline flights. N Engl J Med. 2002;346(14):1067-1073.
2. Matsumoto K, Goebert D. In-flight psychiatric emergencies. Aviat Space Environ Med. 2001;72(10):919-923.
3. Macleod S. “If there is a doctor aboard this flight…”: issues and advice for the passenger-psychiatrist. Australas Psychiatry. 2008;16(4):233-237.
Discuss this article at www.facebook.com/CurrentPsychiatry
Requests for a physician to assist during in-flight medical emergencies are becoming more common as travelers age and more people have access to air travel.1 Yet in this age of medical specialization, all physicians are not created equal, particularly in providing acute care. Responding to in-flight medical emergencies can be stressful, particularly for specialists who may doubt their skill base in a medical crisis.
The in-flight medical consulting service Medlink reported that only 3.5% of calls it receives are related to psychiatric emergencies.2 This means that psychiatrists who answer an in-flight distress call will almost invariably find themselves confronting a medical issue.
Discomfort with possibly having to deliver acute or invasive medical care may deter psychiatrists from responding. However, psychiatrists should be familiar with many medical problems and their basic management, particularly if their institution requires up-to-date advanced cardiac life support certification. Understanding your role and conceptualizing a general approach before you find yourself in the midst of an in-flight medical emergency can be helpful. We suggest the following principles for responding to in-flight emergencies:
- Respond to a call only if you are a licensed, currently practicing physician.
- Defer to other physicians present who may have more experience delivering acute medical care.3
- If you have been drinking alcohol, do not respond unless there are no other health care providers on board. If you do respond, know your limitations and make them known to the air crew and patient.
- Identify yourself to the patient. Give him or her your name and tell the patient that you are a psychiatrist. If the chief complaint is not something you regularly deal with, tell the patient and crew.
- Perform the best history and physical exam you can, given the setting. Obtain vital signs. Document your findings for your records and for medical personnel who may later assume patient care.
- Do not attempt procedures you are unfamiliar with or not qualified to perform (eg, starting an IV, intubations). Administer only treatments you are comfortable with.
- If you are concerned the patient may face significant morbidity or death, advise the crew to divert the flight to the closest hospital.
- Realize that it is not your role to take leadership of the situation, unless you are the only physician present. Do not be afraid to ask for help from other physicians or health care providers—including nurses or emergency medical technicians—who may not have heard or acknowledged the call or a ground-based medical consulting service. Also, once another physician has taken over, you still can contribute by stabilizing the ill patient’s emotions and behavior.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article of with manufacturers of competing products.
Discuss this article at www.facebook.com/CurrentPsychiatry
Requests for a physician to assist during in-flight medical emergencies are becoming more common as travelers age and more people have access to air travel.1 Yet in this age of medical specialization, all physicians are not created equal, particularly in providing acute care. Responding to in-flight medical emergencies can be stressful, particularly for specialists who may doubt their skill base in a medical crisis.
The in-flight medical consulting service Medlink reported that only 3.5% of calls it receives are related to psychiatric emergencies.2 This means that psychiatrists who answer an in-flight distress call will almost invariably find themselves confronting a medical issue.
Discomfort with possibly having to deliver acute or invasive medical care may deter psychiatrists from responding. However, psychiatrists should be familiar with many medical problems and their basic management, particularly if their institution requires up-to-date advanced cardiac life support certification. Understanding your role and conceptualizing a general approach before you find yourself in the midst of an in-flight medical emergency can be helpful. We suggest the following principles for responding to in-flight emergencies:
- Respond to a call only if you are a licensed, currently practicing physician.
- Defer to other physicians present who may have more experience delivering acute medical care.3
- If you have been drinking alcohol, do not respond unless there are no other health care providers on board. If you do respond, know your limitations and make them known to the air crew and patient.
- Identify yourself to the patient. Give him or her your name and tell the patient that you are a psychiatrist. If the chief complaint is not something you regularly deal with, tell the patient and crew.
- Perform the best history and physical exam you can, given the setting. Obtain vital signs. Document your findings for your records and for medical personnel who may later assume patient care.
- Do not attempt procedures you are unfamiliar with or not qualified to perform (eg, starting an IV, intubations). Administer only treatments you are comfortable with.
- If you are concerned the patient may face significant morbidity or death, advise the crew to divert the flight to the closest hospital.
- Realize that it is not your role to take leadership of the situation, unless you are the only physician present. Do not be afraid to ask for help from other physicians or health care providers—including nurses or emergency medical technicians—who may not have heard or acknowledged the call or a ground-based medical consulting service. Also, once another physician has taken over, you still can contribute by stabilizing the ill patient’s emotions and behavior.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article of with manufacturers of competing products.
1. Gendreau MA, DeJohn C. Responding to medical events during commercial airline flights. N Engl J Med. 2002;346(14):1067-1073.
2. Matsumoto K, Goebert D. In-flight psychiatric emergencies. Aviat Space Environ Med. 2001;72(10):919-923.
3. Macleod S. “If there is a doctor aboard this flight…”: issues and advice for the passenger-psychiatrist. Australas Psychiatry. 2008;16(4):233-237.
1. Gendreau MA, DeJohn C. Responding to medical events during commercial airline flights. N Engl J Med. 2002;346(14):1067-1073.
2. Matsumoto K, Goebert D. In-flight psychiatric emergencies. Aviat Space Environ Med. 2001;72(10):919-923.
3. Macleod S. “If there is a doctor aboard this flight…”: issues and advice for the passenger-psychiatrist. Australas Psychiatry. 2008;16(4):233-237.
Implementing a smoking ban: Tips for success
Discuss this article at www.facebook.com/CurrentPsychiatry
The prevalence of tobacco use among psychiatric patients is up to 4 times greater than that of the general population.1 Increasing numbers of psychiatric facilities have implemented policies that ban smoking to eliminate secondhand smoke, achieve a cleaner environment, encourage healthier lifestyles for patients and staff, and reduce patient smoke breaks, which allows more time for treatment.2 The potential benefits of tobacco-free psychiatric institutions has led some clinicians to call for the total exclusion of tobacco from psychiatric and addiction settings.3
New Hampshire Hospital is a 152-bed acute inpatient psychiatric facility that has approximately 2,400 patient admissions per year. Most patients have psychotic or mood disorders, often with a co-occurring substance use or personality disorder. We report our experience in planning and implementing a campus-wide “total” smoking ban—a ban on all tobacco products in the hospital building and on hospital grounds.
Implementation and results
Our hospital’s interdisciplinary Tobacco-Free Campus Task Force developed specific recommendations and a timeline for implementing the total smoking ban. Hospital staff voiced concerns that banning smoking would lead to increased episodes of aggressive behavior. We reviewed data on the use of seclusion and restraints, patient assaults, and smoking contraband before and after initiating the total smoking ban. We found no evidence of an increase in the use of seclusion or restraints or in patient assaults with staff injury after implementing the smoking ban. However, we did see an initial increase in smoking contraband. These rates peaked and then tapered to pre-smoking ban rates within 2 years.
Why we succeeded
Several factors contributed to the successful implementation of our total smoking ban:
- Hospital administration supported having a smoke-free campus, and executive leadership allowed staff to develop strategies, programs, treatment options, and groups to maximize the possibility of success.
- Extensive communication with outside agencies, advocacy groups, and care providers allowed for discussion of potential difficulties, such as concerns regarding individuals not having access to tobacco during their hospital stay and how this could affect their treatment.
- The hospital’s Tobacco-Free Campus Task Force helped develop strategies that allowed for an effective transition to a smoke-free campus, such as increasing the number of smoking cessation groups for patients and staff and eliminating the sale of tobacco products at the hospital’s visitor shop.
- Extensive preparation, clear timelines, and achievable goals created a positive climate for a “culture of change.”
Recommendations
If you are considering a total smoking ban at your facility, we recommend the following steps:
- set a clear target date
- allow adequate time for hospital staff and administration to develop strategies for implementation
- make sure hospital administration is supportive
- involve all hospital disciplines—psychiatry, nursing, rehabilitation, psychology, social work, etc.
- address staff concerns regarding patient and staff safety
- ensure adequate nicotine replacement therapy options for patients and staff
- anticipate an initial increase in smoking-related contraband
- understand there may be differing opinions regarding the smoking ban, but remain committed to the change.
Dr. Folks is a consultant to Independent Medical Experts Consulting Services and Medical Care Management Corporation.
Drs. de Nesnera and Rauter report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Morisano D, Bacher I, Audrain-McGovern J, et al. Mechanisms underlying the comorbidity of tobacco use in mental health and addictive disorders. Can J Psychiatry. 2009;54(6):356-367.
2. Etter M, Khan AN, Etter JF. Acceptability and impact of a partial smoking ban followed by a total smoking ban in a psychiatric hospital. Prev Med. 2008;46(6):572-578.
3. Moss TG, Weinberger AH, Vessicchio JC, et al. A tobacco reconceptualization in psychiatry: toward the development of tobacco-free psychiatric facilities. Am J Addict. 2010;19(4):293-311.
Discuss this article at www.facebook.com/CurrentPsychiatry
The prevalence of tobacco use among psychiatric patients is up to 4 times greater than that of the general population.1 Increasing numbers of psychiatric facilities have implemented policies that ban smoking to eliminate secondhand smoke, achieve a cleaner environment, encourage healthier lifestyles for patients and staff, and reduce patient smoke breaks, which allows more time for treatment.2 The potential benefits of tobacco-free psychiatric institutions has led some clinicians to call for the total exclusion of tobacco from psychiatric and addiction settings.3
New Hampshire Hospital is a 152-bed acute inpatient psychiatric facility that has approximately 2,400 patient admissions per year. Most patients have psychotic or mood disorders, often with a co-occurring substance use or personality disorder. We report our experience in planning and implementing a campus-wide “total” smoking ban—a ban on all tobacco products in the hospital building and on hospital grounds.
Implementation and results
Our hospital’s interdisciplinary Tobacco-Free Campus Task Force developed specific recommendations and a timeline for implementing the total smoking ban. Hospital staff voiced concerns that banning smoking would lead to increased episodes of aggressive behavior. We reviewed data on the use of seclusion and restraints, patient assaults, and smoking contraband before and after initiating the total smoking ban. We found no evidence of an increase in the use of seclusion or restraints or in patient assaults with staff injury after implementing the smoking ban. However, we did see an initial increase in smoking contraband. These rates peaked and then tapered to pre-smoking ban rates within 2 years.
Why we succeeded
Several factors contributed to the successful implementation of our total smoking ban:
- Hospital administration supported having a smoke-free campus, and executive leadership allowed staff to develop strategies, programs, treatment options, and groups to maximize the possibility of success.
- Extensive communication with outside agencies, advocacy groups, and care providers allowed for discussion of potential difficulties, such as concerns regarding individuals not having access to tobacco during their hospital stay and how this could affect their treatment.
- The hospital’s Tobacco-Free Campus Task Force helped develop strategies that allowed for an effective transition to a smoke-free campus, such as increasing the number of smoking cessation groups for patients and staff and eliminating the sale of tobacco products at the hospital’s visitor shop.
- Extensive preparation, clear timelines, and achievable goals created a positive climate for a “culture of change.”
Recommendations
If you are considering a total smoking ban at your facility, we recommend the following steps:
- set a clear target date
- allow adequate time for hospital staff and administration to develop strategies for implementation
- make sure hospital administration is supportive
- involve all hospital disciplines—psychiatry, nursing, rehabilitation, psychology, social work, etc.
- address staff concerns regarding patient and staff safety
- ensure adequate nicotine replacement therapy options for patients and staff
- anticipate an initial increase in smoking-related contraband
- understand there may be differing opinions regarding the smoking ban, but remain committed to the change.
Dr. Folks is a consultant to Independent Medical Experts Consulting Services and Medical Care Management Corporation.
Drs. de Nesnera and Rauter report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Discuss this article at www.facebook.com/CurrentPsychiatry
The prevalence of tobacco use among psychiatric patients is up to 4 times greater than that of the general population.1 Increasing numbers of psychiatric facilities have implemented policies that ban smoking to eliminate secondhand smoke, achieve a cleaner environment, encourage healthier lifestyles for patients and staff, and reduce patient smoke breaks, which allows more time for treatment.2 The potential benefits of tobacco-free psychiatric institutions has led some clinicians to call for the total exclusion of tobacco from psychiatric and addiction settings.3
New Hampshire Hospital is a 152-bed acute inpatient psychiatric facility that has approximately 2,400 patient admissions per year. Most patients have psychotic or mood disorders, often with a co-occurring substance use or personality disorder. We report our experience in planning and implementing a campus-wide “total” smoking ban—a ban on all tobacco products in the hospital building and on hospital grounds.
Implementation and results
Our hospital’s interdisciplinary Tobacco-Free Campus Task Force developed specific recommendations and a timeline for implementing the total smoking ban. Hospital staff voiced concerns that banning smoking would lead to increased episodes of aggressive behavior. We reviewed data on the use of seclusion and restraints, patient assaults, and smoking contraband before and after initiating the total smoking ban. We found no evidence of an increase in the use of seclusion or restraints or in patient assaults with staff injury after implementing the smoking ban. However, we did see an initial increase in smoking contraband. These rates peaked and then tapered to pre-smoking ban rates within 2 years.
Why we succeeded
Several factors contributed to the successful implementation of our total smoking ban:
- Hospital administration supported having a smoke-free campus, and executive leadership allowed staff to develop strategies, programs, treatment options, and groups to maximize the possibility of success.
- Extensive communication with outside agencies, advocacy groups, and care providers allowed for discussion of potential difficulties, such as concerns regarding individuals not having access to tobacco during their hospital stay and how this could affect their treatment.
- The hospital’s Tobacco-Free Campus Task Force helped develop strategies that allowed for an effective transition to a smoke-free campus, such as increasing the number of smoking cessation groups for patients and staff and eliminating the sale of tobacco products at the hospital’s visitor shop.
- Extensive preparation, clear timelines, and achievable goals created a positive climate for a “culture of change.”
Recommendations
If you are considering a total smoking ban at your facility, we recommend the following steps:
- set a clear target date
- allow adequate time for hospital staff and administration to develop strategies for implementation
- make sure hospital administration is supportive
- involve all hospital disciplines—psychiatry, nursing, rehabilitation, psychology, social work, etc.
- address staff concerns regarding patient and staff safety
- ensure adequate nicotine replacement therapy options for patients and staff
- anticipate an initial increase in smoking-related contraband
- understand there may be differing opinions regarding the smoking ban, but remain committed to the change.
Dr. Folks is a consultant to Independent Medical Experts Consulting Services and Medical Care Management Corporation.
Drs. de Nesnera and Rauter report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Morisano D, Bacher I, Audrain-McGovern J, et al. Mechanisms underlying the comorbidity of tobacco use in mental health and addictive disorders. Can J Psychiatry. 2009;54(6):356-367.
2. Etter M, Khan AN, Etter JF. Acceptability and impact of a partial smoking ban followed by a total smoking ban in a psychiatric hospital. Prev Med. 2008;46(6):572-578.
3. Moss TG, Weinberger AH, Vessicchio JC, et al. A tobacco reconceptualization in psychiatry: toward the development of tobacco-free psychiatric facilities. Am J Addict. 2010;19(4):293-311.
1. Morisano D, Bacher I, Audrain-McGovern J, et al. Mechanisms underlying the comorbidity of tobacco use in mental health and addictive disorders. Can J Psychiatry. 2009;54(6):356-367.
2. Etter M, Khan AN, Etter JF. Acceptability and impact of a partial smoking ban followed by a total smoking ban in a psychiatric hospital. Prev Med. 2008;46(6):572-578.
3. Moss TG, Weinberger AH, Vessicchio JC, et al. A tobacco reconceptualization in psychiatry: toward the development of tobacco-free psychiatric facilities. Am J Addict. 2010;19(4):293-311.