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How often should women be screened for breast cancer?
- Starting at age 20, women should undergo clinical breast exam every 3 years and be counseled about awareness of breast changes.
- Average risk women should undergo clinical breast examination and screening mammography annually starting at age 40.
- Health care providers should inform women about the benefits and limitations of mammography and the potential for false positives.
- Women at high risk include those with inherited susceptibility to breast cancer or chest radiation at a young age. They should be screened with mammography and breast MRI annually starting at age 30.
Breast cancer is the most widespread cancer effecting women in the United States.1 The high prevalence and inherent “cost” of breast cancer mandates physicians to be aware of effective screening tools, existing guidelines, and potential adverse effects.
Mammography screening and improvements in breast cancer treatments have contributed to improved survival rates, but2,3 mammography screening has declined since 2000. Potential reasons for this decrease include:
- poor access to medical care
- fear of radiation exposure
- concern of undesirable test results
- anticipated pain
- misconceptions of cancer risk
- changes in recommendations regarding mammography screening.
Patients with psychiatric illnesses are less likely to receive mammography screening.4,5 Cancer patients with schizophrenia, particularly women with breast cancer, have an increased risk of mortality.6
Risk assessment
Age, genetic predisposition, and factors that affect endogenous estrogen exposure such as early menarche, late menopause, and nulliparity are among the most important breast cancer risk factors (Table 1). Explore these and other risk factors with your patient before making screening recommendations.
Tools such as the Breast Cancer Risk Assessment Tool (BCRAT) can assist in stratifying your patient’s risk. The BCRAT, available at www.cancer.gov/bcrisktool, takes into account, age, race, family history, and previous breast abnormalities. Women at average risk for breast cancer include those with an estimated lifetime risk of <15%. Women with an estimated lifetime risk of 15% to 20% are at moderate risk. Women >20% are at high risk and should consider more intensive screening (Table 2).7,8
Other examples of high-risk features include chest radiation therapy (eg, for Hodgkin’s lymphoma) between age 10 to 30 or a breast cancer 1, early onset (BRCA1) or breast cancer 2, early onset (BRCA2) mutation carried by the patient or a first-degree family member, which can leave patients more susceptible to breast cancer.
Table 1
Breast cancer risk factors
Female sex |
Older age |
Genetic risk factors (eg, BRCA1 and BRCA2 gene mutation)–5% to 10% of breast cancers |
Family history of breast cancer |
Personal history of breast cancer |
Race (eg, Whites have highest incidence, African Americans have highest mortality) |
Certain benign breast diseases (eg, atypical hyperplasia) |
Early menarche, late menopause |
Prior chest radiation (eg, for Hodgkin’s lymphoma; especially age 10 to 30) |
Nulliparity, late child-bearing |
Oral contraceptive use |
Hormone replacement therapy (combined estrogen/progesterone) |
Not breastfeeding |
Alcohol (2 to 5 drinks daily increases risk 1.5 times) |
Obesity |
BRCA1: breast cancer 1, early onset; BRCA2: breast cancer 2, early onset Source: Adapted from the American Cancer Society; available at www.cancer.org |
Breast cancer screening
Choice of screening is guided by an individualized risk assessment. For women with average risk for breast cancer, the major components of breast cancer screening are clinical breast examination (CBE) and screening mammography.
Breast self-examination is not routinely recommended by expert groups. The American Cancer Society (ACS) recommends that clinicians discuss the benefits and limitations of breast self-exam with patients. The National Comprehensive Cancer Network (NCCN) recommends that women maintain breast health awareness but no longer advocates instruction in self-examination.
CBE by a trained provider, when coupled to routine screening mammography, may add modest benefit in terms of detecting cancer. The ACS and the NCCN suggest CBE along with annual mammography for all women starting at age 40.
Mammography has been to shown to reduce breast cancer mortality.8 A United States Preventive Services Task Force (USPSTF) review found statistically significant reductions in breast cancer mortality for women age 39 to 69.9
Because the USPSTF found a small net benefit of screening mammography in women age 40 to 49, their recent guidelines recommend against routine mammograms for this age group. Instead, the USPSTF suggests that screening be based on individualized risk assessment and discussion of the benefits and risks (false positive tests, overdiagnosis, and psychological harms) of screening.10 Other groups continue to recommend annual mammography starting at age 40 for women at average risk (Table 2).
MRI is more sensitive screening than mammography and the combination of MRI and routine mammograms is more sensitive than either test alone. In 2007, the ACS recommended annual breast MRI screening in addition to mammogram for women at high risk for breast cancer (Table 2). For women with moderately increased risk (15% to 20% lifetime) there is insufficient evidence to recommend for or against MRI for screening, but one may consider it on a case-by-case basis; for example, for women with personal history of breast cancer, atypical hyperplasia, or with mammographically dense breasts.
Table 2
American Cancer Society breast cancer screening recommendations
Women at average risk* | Women at high risk* | |
---|---|---|
Breast self-exam | Not routinely recommended. Discuss the benefits and limitations starting with patients in their 20s. Emphasize the importance of reporting new breast symptoms to a health care provider | |
Clinical breast exam | At least every 3 years for women in their 20s and 30s. Annually starting at age 40 | Annually, starting at age 30 |
Mammography | Annually, starting at age 40 | Annually, starting at age 30 |
Breast MRI | Not recommended | Annually, starting at age 30, along with mammogram |
*Women at average risk for breast cancer include those with an estimated lifetime risk of <15%. Women with an estimated lifetime risk of 15% to 20% are at moderate risk. Women >20% are at high risk and should consider more intensive screening | ||
Source: References 7,8, American Cancer Society (www.cancer.org) |
Potential harms
Potential mammography harms include the possibility of a false positive result, anxiety as one awaits the test result, and anticipation of discomfort associated with the procedure. There also is the potential for “overdiagnosis” or detection of a cancer that would not have adversely impacted the patient if it had not been discovered. There is also a small risk of radiation exposure from repeated mammograms, but this has not been firmly established in the literature.
False-positive results—an abnormal finding on mammogram that does not result in a breast cancer diagnosis—is a significant issue. One study estimated that 11% of screening mammograms return abnormal findings that lead to additional workup, the majority (90%) of which ultimately result in benign diagnoses.11 Workup often leads to additional mammograms, ultrasound, breast MRI, and invasive procedures such as needle biopsies. False-positive mammograms have been associated with increased symptoms of depression and anxiety.12 Patients may be more apprehensive about breast cancer following a false-positive result, but this does not appear to lead to chronic anxiety.13
The vulnerability of patients experiencing psychiatric illness coupled with the potential psychological consequences of breast cancer make it imperative that psychiatrists remain up-to-date on breast cancer screening guidelines. Reported poor adherence to screening recommendations for mammography may increase the burden of illness and mortality from breast cancer in individuals with mental illness.
Conversations about health maintenance measures always should include careful discussion of the benefits and potential harms associated with the recommended screening tools. Because psychiatrists work closely with patients who may be less likely to undergo mammography, it is important to provide support and advocate for access to health care screening.
Related Resource
- National Cancer Institute. www.cancer.gov.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Table 3
Number needed to screen (NNS) with mammography to prevent 1 breast cancer death
Age | NNS |
---|---|
39 to 49 | 1,904 |
50 to 59 | 1,339 |
60 to 69 | 337 |
Source: Reference 9 |
1. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2009. CA Cancer J Clin. 2009;59:225-249.
2. Chu KC, Tarone RE, Kessler LG, et al. Recent trends in U. S. breast cancer incidence, survival, and mortality rates. J Natl Cancer Inst. 1996;88:1571-1579.
3. Berry DA, Cronin KA, Plevritis SK, et al. Effect of screening and adjuvant therapy on mortality from breast cancer. N Eng J Med. 2005;353:1784-1792.
4. Ludman EJ, Ichikawa LE, Simon GE, et al. Breast and cervical cancer screening specific effects of depression and obesity. Am J Prev Med. 2010;38:303-310.
5. Lindamer LA, Wear E, Robins-Sadler G. Mammography stages of change in middle-aged women with schizophrenia: an exploratory analysis. BMC Psychiatry. 2006;6:49.-
6. Tran E, Rouillon F, Loze JY, et al. Cancer mortality in patients with schizophrenia: an 11-year prospective cohort study. Cancer. 2009;15:3555-3562.
7. Smith RA, Cokkinides V, Brooks D, et al. Cancer screening in the United States, 2010: a review of current American Cancer Society guidelines and issues in cancer screening. CA Cancer J Clin. 2010;60(2):99-119.
8. Saslow D, Boetes C, Burke W, et al. American Cancer Society guidelines for screening with MRI as an adjunct to mammography. CA Cancer J Clin. 2007;57:75-89.
9. Nelson HD, Tyne K, Naik A, et al. Screening for breast cancer: an update from the U.S. Preventive Services Task Force. Ann Intern Med. 2009;151:727-737W237-W242.
10. US Preventive Services Task Force. Screening for breast cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2009;151:716-726W236.-
11. Brown ML, Houn F, Sickles EA, et al. Screening mammography in community practice: positive predictive value of abnormal findings and yield of follow-up diagnostic procedures. AJR Am J Roentgenol. 1995;165:1373-1377.
12. Jatoi I, Zhu K, Shah M, et al. Psychological distress in U.S. women who have experienced false-positive mammograms. Breast Cancer Res Treat. 2006;100:191-200.
13. Brewer NT, Salz T, Lillie SE, et al. Systematic review: the long-term effects of false-positive mammograms. Ann Intern Med. 2007;146:502-510.
- Starting at age 20, women should undergo clinical breast exam every 3 years and be counseled about awareness of breast changes.
- Average risk women should undergo clinical breast examination and screening mammography annually starting at age 40.
- Health care providers should inform women about the benefits and limitations of mammography and the potential for false positives.
- Women at high risk include those with inherited susceptibility to breast cancer or chest radiation at a young age. They should be screened with mammography and breast MRI annually starting at age 30.
Breast cancer is the most widespread cancer effecting women in the United States.1 The high prevalence and inherent “cost” of breast cancer mandates physicians to be aware of effective screening tools, existing guidelines, and potential adverse effects.
Mammography screening and improvements in breast cancer treatments have contributed to improved survival rates, but2,3 mammography screening has declined since 2000. Potential reasons for this decrease include:
- poor access to medical care
- fear of radiation exposure
- concern of undesirable test results
- anticipated pain
- misconceptions of cancer risk
- changes in recommendations regarding mammography screening.
Patients with psychiatric illnesses are less likely to receive mammography screening.4,5 Cancer patients with schizophrenia, particularly women with breast cancer, have an increased risk of mortality.6
Risk assessment
Age, genetic predisposition, and factors that affect endogenous estrogen exposure such as early menarche, late menopause, and nulliparity are among the most important breast cancer risk factors (Table 1). Explore these and other risk factors with your patient before making screening recommendations.
Tools such as the Breast Cancer Risk Assessment Tool (BCRAT) can assist in stratifying your patient’s risk. The BCRAT, available at www.cancer.gov/bcrisktool, takes into account, age, race, family history, and previous breast abnormalities. Women at average risk for breast cancer include those with an estimated lifetime risk of <15%. Women with an estimated lifetime risk of 15% to 20% are at moderate risk. Women >20% are at high risk and should consider more intensive screening (Table 2).7,8
Other examples of high-risk features include chest radiation therapy (eg, for Hodgkin’s lymphoma) between age 10 to 30 or a breast cancer 1, early onset (BRCA1) or breast cancer 2, early onset (BRCA2) mutation carried by the patient or a first-degree family member, which can leave patients more susceptible to breast cancer.
Table 1
Breast cancer risk factors
Female sex |
Older age |
Genetic risk factors (eg, BRCA1 and BRCA2 gene mutation)–5% to 10% of breast cancers |
Family history of breast cancer |
Personal history of breast cancer |
Race (eg, Whites have highest incidence, African Americans have highest mortality) |
Certain benign breast diseases (eg, atypical hyperplasia) |
Early menarche, late menopause |
Prior chest radiation (eg, for Hodgkin’s lymphoma; especially age 10 to 30) |
Nulliparity, late child-bearing |
Oral contraceptive use |
Hormone replacement therapy (combined estrogen/progesterone) |
Not breastfeeding |
Alcohol (2 to 5 drinks daily increases risk 1.5 times) |
Obesity |
BRCA1: breast cancer 1, early onset; BRCA2: breast cancer 2, early onset Source: Adapted from the American Cancer Society; available at www.cancer.org |
Breast cancer screening
Choice of screening is guided by an individualized risk assessment. For women with average risk for breast cancer, the major components of breast cancer screening are clinical breast examination (CBE) and screening mammography.
Breast self-examination is not routinely recommended by expert groups. The American Cancer Society (ACS) recommends that clinicians discuss the benefits and limitations of breast self-exam with patients. The National Comprehensive Cancer Network (NCCN) recommends that women maintain breast health awareness but no longer advocates instruction in self-examination.
CBE by a trained provider, when coupled to routine screening mammography, may add modest benefit in terms of detecting cancer. The ACS and the NCCN suggest CBE along with annual mammography for all women starting at age 40.
Mammography has been to shown to reduce breast cancer mortality.8 A United States Preventive Services Task Force (USPSTF) review found statistically significant reductions in breast cancer mortality for women age 39 to 69.9
Because the USPSTF found a small net benefit of screening mammography in women age 40 to 49, their recent guidelines recommend against routine mammograms for this age group. Instead, the USPSTF suggests that screening be based on individualized risk assessment and discussion of the benefits and risks (false positive tests, overdiagnosis, and psychological harms) of screening.10 Other groups continue to recommend annual mammography starting at age 40 for women at average risk (Table 2).
MRI is more sensitive screening than mammography and the combination of MRI and routine mammograms is more sensitive than either test alone. In 2007, the ACS recommended annual breast MRI screening in addition to mammogram for women at high risk for breast cancer (Table 2). For women with moderately increased risk (15% to 20% lifetime) there is insufficient evidence to recommend for or against MRI for screening, but one may consider it on a case-by-case basis; for example, for women with personal history of breast cancer, atypical hyperplasia, or with mammographically dense breasts.
Table 2
American Cancer Society breast cancer screening recommendations
Women at average risk* | Women at high risk* | |
---|---|---|
Breast self-exam | Not routinely recommended. Discuss the benefits and limitations starting with patients in their 20s. Emphasize the importance of reporting new breast symptoms to a health care provider | |
Clinical breast exam | At least every 3 years for women in their 20s and 30s. Annually starting at age 40 | Annually, starting at age 30 |
Mammography | Annually, starting at age 40 | Annually, starting at age 30 |
Breast MRI | Not recommended | Annually, starting at age 30, along with mammogram |
*Women at average risk for breast cancer include those with an estimated lifetime risk of <15%. Women with an estimated lifetime risk of 15% to 20% are at moderate risk. Women >20% are at high risk and should consider more intensive screening | ||
Source: References 7,8, American Cancer Society (www.cancer.org) |
Potential harms
Potential mammography harms include the possibility of a false positive result, anxiety as one awaits the test result, and anticipation of discomfort associated with the procedure. There also is the potential for “overdiagnosis” or detection of a cancer that would not have adversely impacted the patient if it had not been discovered. There is also a small risk of radiation exposure from repeated mammograms, but this has not been firmly established in the literature.
False-positive results—an abnormal finding on mammogram that does not result in a breast cancer diagnosis—is a significant issue. One study estimated that 11% of screening mammograms return abnormal findings that lead to additional workup, the majority (90%) of which ultimately result in benign diagnoses.11 Workup often leads to additional mammograms, ultrasound, breast MRI, and invasive procedures such as needle biopsies. False-positive mammograms have been associated with increased symptoms of depression and anxiety.12 Patients may be more apprehensive about breast cancer following a false-positive result, but this does not appear to lead to chronic anxiety.13
The vulnerability of patients experiencing psychiatric illness coupled with the potential psychological consequences of breast cancer make it imperative that psychiatrists remain up-to-date on breast cancer screening guidelines. Reported poor adherence to screening recommendations for mammography may increase the burden of illness and mortality from breast cancer in individuals with mental illness.
Conversations about health maintenance measures always should include careful discussion of the benefits and potential harms associated with the recommended screening tools. Because psychiatrists work closely with patients who may be less likely to undergo mammography, it is important to provide support and advocate for access to health care screening.
Related Resource
- National Cancer Institute. www.cancer.gov.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Table 3
Number needed to screen (NNS) with mammography to prevent 1 breast cancer death
Age | NNS |
---|---|
39 to 49 | 1,904 |
50 to 59 | 1,339 |
60 to 69 | 337 |
Source: Reference 9 |
- Starting at age 20, women should undergo clinical breast exam every 3 years and be counseled about awareness of breast changes.
- Average risk women should undergo clinical breast examination and screening mammography annually starting at age 40.
- Health care providers should inform women about the benefits and limitations of mammography and the potential for false positives.
- Women at high risk include those with inherited susceptibility to breast cancer or chest radiation at a young age. They should be screened with mammography and breast MRI annually starting at age 30.
Breast cancer is the most widespread cancer effecting women in the United States.1 The high prevalence and inherent “cost” of breast cancer mandates physicians to be aware of effective screening tools, existing guidelines, and potential adverse effects.
Mammography screening and improvements in breast cancer treatments have contributed to improved survival rates, but2,3 mammography screening has declined since 2000. Potential reasons for this decrease include:
- poor access to medical care
- fear of radiation exposure
- concern of undesirable test results
- anticipated pain
- misconceptions of cancer risk
- changes in recommendations regarding mammography screening.
Patients with psychiatric illnesses are less likely to receive mammography screening.4,5 Cancer patients with schizophrenia, particularly women with breast cancer, have an increased risk of mortality.6
Risk assessment
Age, genetic predisposition, and factors that affect endogenous estrogen exposure such as early menarche, late menopause, and nulliparity are among the most important breast cancer risk factors (Table 1). Explore these and other risk factors with your patient before making screening recommendations.
Tools such as the Breast Cancer Risk Assessment Tool (BCRAT) can assist in stratifying your patient’s risk. The BCRAT, available at www.cancer.gov/bcrisktool, takes into account, age, race, family history, and previous breast abnormalities. Women at average risk for breast cancer include those with an estimated lifetime risk of <15%. Women with an estimated lifetime risk of 15% to 20% are at moderate risk. Women >20% are at high risk and should consider more intensive screening (Table 2).7,8
Other examples of high-risk features include chest radiation therapy (eg, for Hodgkin’s lymphoma) between age 10 to 30 or a breast cancer 1, early onset (BRCA1) or breast cancer 2, early onset (BRCA2) mutation carried by the patient or a first-degree family member, which can leave patients more susceptible to breast cancer.
Table 1
Breast cancer risk factors
Female sex |
Older age |
Genetic risk factors (eg, BRCA1 and BRCA2 gene mutation)–5% to 10% of breast cancers |
Family history of breast cancer |
Personal history of breast cancer |
Race (eg, Whites have highest incidence, African Americans have highest mortality) |
Certain benign breast diseases (eg, atypical hyperplasia) |
Early menarche, late menopause |
Prior chest radiation (eg, for Hodgkin’s lymphoma; especially age 10 to 30) |
Nulliparity, late child-bearing |
Oral contraceptive use |
Hormone replacement therapy (combined estrogen/progesterone) |
Not breastfeeding |
Alcohol (2 to 5 drinks daily increases risk 1.5 times) |
Obesity |
BRCA1: breast cancer 1, early onset; BRCA2: breast cancer 2, early onset Source: Adapted from the American Cancer Society; available at www.cancer.org |
Breast cancer screening
Choice of screening is guided by an individualized risk assessment. For women with average risk for breast cancer, the major components of breast cancer screening are clinical breast examination (CBE) and screening mammography.
Breast self-examination is not routinely recommended by expert groups. The American Cancer Society (ACS) recommends that clinicians discuss the benefits and limitations of breast self-exam with patients. The National Comprehensive Cancer Network (NCCN) recommends that women maintain breast health awareness but no longer advocates instruction in self-examination.
CBE by a trained provider, when coupled to routine screening mammography, may add modest benefit in terms of detecting cancer. The ACS and the NCCN suggest CBE along with annual mammography for all women starting at age 40.
Mammography has been to shown to reduce breast cancer mortality.8 A United States Preventive Services Task Force (USPSTF) review found statistically significant reductions in breast cancer mortality for women age 39 to 69.9
Because the USPSTF found a small net benefit of screening mammography in women age 40 to 49, their recent guidelines recommend against routine mammograms for this age group. Instead, the USPSTF suggests that screening be based on individualized risk assessment and discussion of the benefits and risks (false positive tests, overdiagnosis, and psychological harms) of screening.10 Other groups continue to recommend annual mammography starting at age 40 for women at average risk (Table 2).
MRI is more sensitive screening than mammography and the combination of MRI and routine mammograms is more sensitive than either test alone. In 2007, the ACS recommended annual breast MRI screening in addition to mammogram for women at high risk for breast cancer (Table 2). For women with moderately increased risk (15% to 20% lifetime) there is insufficient evidence to recommend for or against MRI for screening, but one may consider it on a case-by-case basis; for example, for women with personal history of breast cancer, atypical hyperplasia, or with mammographically dense breasts.
Table 2
American Cancer Society breast cancer screening recommendations
Women at average risk* | Women at high risk* | |
---|---|---|
Breast self-exam | Not routinely recommended. Discuss the benefits and limitations starting with patients in their 20s. Emphasize the importance of reporting new breast symptoms to a health care provider | |
Clinical breast exam | At least every 3 years for women in their 20s and 30s. Annually starting at age 40 | Annually, starting at age 30 |
Mammography | Annually, starting at age 40 | Annually, starting at age 30 |
Breast MRI | Not recommended | Annually, starting at age 30, along with mammogram |
*Women at average risk for breast cancer include those with an estimated lifetime risk of <15%. Women with an estimated lifetime risk of 15% to 20% are at moderate risk. Women >20% are at high risk and should consider more intensive screening | ||
Source: References 7,8, American Cancer Society (www.cancer.org) |
Potential harms
Potential mammography harms include the possibility of a false positive result, anxiety as one awaits the test result, and anticipation of discomfort associated with the procedure. There also is the potential for “overdiagnosis” or detection of a cancer that would not have adversely impacted the patient if it had not been discovered. There is also a small risk of radiation exposure from repeated mammograms, but this has not been firmly established in the literature.
False-positive results—an abnormal finding on mammogram that does not result in a breast cancer diagnosis—is a significant issue. One study estimated that 11% of screening mammograms return abnormal findings that lead to additional workup, the majority (90%) of which ultimately result in benign diagnoses.11 Workup often leads to additional mammograms, ultrasound, breast MRI, and invasive procedures such as needle biopsies. False-positive mammograms have been associated with increased symptoms of depression and anxiety.12 Patients may be more apprehensive about breast cancer following a false-positive result, but this does not appear to lead to chronic anxiety.13
The vulnerability of patients experiencing psychiatric illness coupled with the potential psychological consequences of breast cancer make it imperative that psychiatrists remain up-to-date on breast cancer screening guidelines. Reported poor adherence to screening recommendations for mammography may increase the burden of illness and mortality from breast cancer in individuals with mental illness.
Conversations about health maintenance measures always should include careful discussion of the benefits and potential harms associated with the recommended screening tools. Because psychiatrists work closely with patients who may be less likely to undergo mammography, it is important to provide support and advocate for access to health care screening.
Related Resource
- National Cancer Institute. www.cancer.gov.
Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Table 3
Number needed to screen (NNS) with mammography to prevent 1 breast cancer death
Age | NNS |
---|---|
39 to 49 | 1,904 |
50 to 59 | 1,339 |
60 to 69 | 337 |
Source: Reference 9 |
1. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2009. CA Cancer J Clin. 2009;59:225-249.
2. Chu KC, Tarone RE, Kessler LG, et al. Recent trends in U. S. breast cancer incidence, survival, and mortality rates. J Natl Cancer Inst. 1996;88:1571-1579.
3. Berry DA, Cronin KA, Plevritis SK, et al. Effect of screening and adjuvant therapy on mortality from breast cancer. N Eng J Med. 2005;353:1784-1792.
4. Ludman EJ, Ichikawa LE, Simon GE, et al. Breast and cervical cancer screening specific effects of depression and obesity. Am J Prev Med. 2010;38:303-310.
5. Lindamer LA, Wear E, Robins-Sadler G. Mammography stages of change in middle-aged women with schizophrenia: an exploratory analysis. BMC Psychiatry. 2006;6:49.-
6. Tran E, Rouillon F, Loze JY, et al. Cancer mortality in patients with schizophrenia: an 11-year prospective cohort study. Cancer. 2009;15:3555-3562.
7. Smith RA, Cokkinides V, Brooks D, et al. Cancer screening in the United States, 2010: a review of current American Cancer Society guidelines and issues in cancer screening. CA Cancer J Clin. 2010;60(2):99-119.
8. Saslow D, Boetes C, Burke W, et al. American Cancer Society guidelines for screening with MRI as an adjunct to mammography. CA Cancer J Clin. 2007;57:75-89.
9. Nelson HD, Tyne K, Naik A, et al. Screening for breast cancer: an update from the U.S. Preventive Services Task Force. Ann Intern Med. 2009;151:727-737W237-W242.
10. US Preventive Services Task Force. Screening for breast cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2009;151:716-726W236.-
11. Brown ML, Houn F, Sickles EA, et al. Screening mammography in community practice: positive predictive value of abnormal findings and yield of follow-up diagnostic procedures. AJR Am J Roentgenol. 1995;165:1373-1377.
12. Jatoi I, Zhu K, Shah M, et al. Psychological distress in U.S. women who have experienced false-positive mammograms. Breast Cancer Res Treat. 2006;100:191-200.
13. Brewer NT, Salz T, Lillie SE, et al. Systematic review: the long-term effects of false-positive mammograms. Ann Intern Med. 2007;146:502-510.
1. Jemal A, Siegel R, Ward E, et al. Cancer statistics, 2009. CA Cancer J Clin. 2009;59:225-249.
2. Chu KC, Tarone RE, Kessler LG, et al. Recent trends in U. S. breast cancer incidence, survival, and mortality rates. J Natl Cancer Inst. 1996;88:1571-1579.
3. Berry DA, Cronin KA, Plevritis SK, et al. Effect of screening and adjuvant therapy on mortality from breast cancer. N Eng J Med. 2005;353:1784-1792.
4. Ludman EJ, Ichikawa LE, Simon GE, et al. Breast and cervical cancer screening specific effects of depression and obesity. Am J Prev Med. 2010;38:303-310.
5. Lindamer LA, Wear E, Robins-Sadler G. Mammography stages of change in middle-aged women with schizophrenia: an exploratory analysis. BMC Psychiatry. 2006;6:49.-
6. Tran E, Rouillon F, Loze JY, et al. Cancer mortality in patients with schizophrenia: an 11-year prospective cohort study. Cancer. 2009;15:3555-3562.
7. Smith RA, Cokkinides V, Brooks D, et al. Cancer screening in the United States, 2010: a review of current American Cancer Society guidelines and issues in cancer screening. CA Cancer J Clin. 2010;60(2):99-119.
8. Saslow D, Boetes C, Burke W, et al. American Cancer Society guidelines for screening with MRI as an adjunct to mammography. CA Cancer J Clin. 2007;57:75-89.
9. Nelson HD, Tyne K, Naik A, et al. Screening for breast cancer: an update from the U.S. Preventive Services Task Force. Ann Intern Med. 2009;151:727-737W237-W242.
10. US Preventive Services Task Force. Screening for breast cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. 2009;151:716-726W236.-
11. Brown ML, Houn F, Sickles EA, et al. Screening mammography in community practice: positive predictive value of abnormal findings and yield of follow-up diagnostic procedures. AJR Am J Roentgenol. 1995;165:1373-1377.
12. Jatoi I, Zhu K, Shah M, et al. Psychological distress in U.S. women who have experienced false-positive mammograms. Breast Cancer Res Treat. 2006;100:191-200.
13. Brewer NT, Salz T, Lillie SE, et al. Systematic review: the long-term effects of false-positive mammograms. Ann Intern Med. 2007;146:502-510.
Small Study Highlights Olfactory Reference Syndrome
Major Finding: Most patients with olfactory reference syndrome (85%) have concurrent major depressive disorder, and 44% have sought nonpsychiatric medical treatment for their perceived odor.
Data Source: A study of 20 patients with olfactory reference syndrome.
Disclosures: Dr. Phillips disclosed that she has received grant and research support from the American Foundation for Suicide Prevention and the National Institute of Mental Health.
Patients with olfactory reference syndrome have high rates of clinical depression and other comorbid psychiatric disorders, and nearly half of them do not seek psychiatric treatment for their perceived order.
Those are key findings from a small, novel study discussed during a press briefing sponsored by the American Psychiatric Association.
Olfactory reference syndrome (ORS) is a preoccupation with the belief that one emits a foul or offensive body odor that is not perceived by other people, said lead study investigator Dr. Katharine A. Phillips, of the department of psychiatry at Rhode Island Hospital/Brown University, Providence.
The few reports about ORS that have been published in the last century “suggest that it is clinically important,” she said. “Patients suffer tremendously as a result of this false belief, and they appear to be very impaired in terms of their functioning and to have high rates of suicidality.”
In an effort to better understand the clinical features of ORS, the researchers used semistructured measurement tools to assess 20 patients with the syndrome, including the Structured Clinical Interview for DSM-IV (SCID) to assess comorbidity, the Brown Assessment of Beliefs Scale to assess insight/delusionality and referential thinking, and a slightly modified version of the Yale-Brown Obsessive Compulsive Scale to assess ORS severity. The mean age of patients was 33 years, 60% were female, and the mean age of onset was 16 years.
Patients reported being preoccupied with their perceived body odor for 3-8 hours per day, mostly the mouth (75%), armpits (60%), and genitals (35%). Bad breath was the most common odor description reported (75%), followed by sweat (65%).
Most patients (85%) reported being completely convinced that their belief about the odor was accurate, and 77% reported thinking “that other people take special notice of them in a negative way because they smell so bad,” Dr. Phillips said. In addition, 85% of patients reported that they actually smelled the odor (an olfactory hallucination).
All of the patients reported practicing repetitive behaviors in an effort to camouflage the perceived odor, mostly with perfume or scented powder (90%), chewing gum (60%), deodorant (55%), and mints (55%).
“Some patients actually drank perfume,” she said. “Some of them constantly chewed gum, ate mints, or reapplied deodorant over and over throughout the day [and] used prescription strength mouthwashes frequently. Some patients showered for hours a day, using an entire bar of soap, trying to remove the odor they perceived.”
In addition, 74% reported that ORS symptoms led to avoidance of social interactions “because they felt so ashamed,” she said. “They worried that other people thought badly of them because they felt they stank.”
More than a third of the patients (40%) said that symptoms were so bad that they were housebound for at least 1 week. “They didn't leave the house at all because they felt too embarrassed [or] ashamed,” she said.
More than two-thirds of the patients (68%) had a history of suicidal ideation, 32% had attempted suicide, and 53% had been hospitalized in a psychiatric unit. The most common lifetime comorbid disorder was major depressive disorder (85%), followed by social phobia (65%), and substance use disorders (50%).
Dr. Phillips also reported that 44% of patients had sought nonpsychiatric medical treatment for the perceived odor. “They went to dentists if they thought they had bad breath, [to] dermatologists if they thought they had smelly sweat,” she said. “One participant in our study had their tonsils removed because they thought their tonsils were causing their breath to be bad.”
About one-third of patients received nonpsychiatric treatment for the perceived odor “but in no case did this treatment diminish the worry about the perceived body odor.”
Dr. Phillips concluded her remarks by noting that ORS “appears to be very under-recognized, and we certainly need more research on this area of study.”
The study also was presented during a poster session at the APA's annual meeting in New Orleans.
Patients 'appear to be very impaired in terms of their functioning and to have high rates of suicidality.'
Source DR. PHILLIPS
Major Finding: Most patients with olfactory reference syndrome (85%) have concurrent major depressive disorder, and 44% have sought nonpsychiatric medical treatment for their perceived odor.
Data Source: A study of 20 patients with olfactory reference syndrome.
Disclosures: Dr. Phillips disclosed that she has received grant and research support from the American Foundation for Suicide Prevention and the National Institute of Mental Health.
Patients with olfactory reference syndrome have high rates of clinical depression and other comorbid psychiatric disorders, and nearly half of them do not seek psychiatric treatment for their perceived order.
Those are key findings from a small, novel study discussed during a press briefing sponsored by the American Psychiatric Association.
Olfactory reference syndrome (ORS) is a preoccupation with the belief that one emits a foul or offensive body odor that is not perceived by other people, said lead study investigator Dr. Katharine A. Phillips, of the department of psychiatry at Rhode Island Hospital/Brown University, Providence.
The few reports about ORS that have been published in the last century “suggest that it is clinically important,” she said. “Patients suffer tremendously as a result of this false belief, and they appear to be very impaired in terms of their functioning and to have high rates of suicidality.”
In an effort to better understand the clinical features of ORS, the researchers used semistructured measurement tools to assess 20 patients with the syndrome, including the Structured Clinical Interview for DSM-IV (SCID) to assess comorbidity, the Brown Assessment of Beliefs Scale to assess insight/delusionality and referential thinking, and a slightly modified version of the Yale-Brown Obsessive Compulsive Scale to assess ORS severity. The mean age of patients was 33 years, 60% were female, and the mean age of onset was 16 years.
Patients reported being preoccupied with their perceived body odor for 3-8 hours per day, mostly the mouth (75%), armpits (60%), and genitals (35%). Bad breath was the most common odor description reported (75%), followed by sweat (65%).
Most patients (85%) reported being completely convinced that their belief about the odor was accurate, and 77% reported thinking “that other people take special notice of them in a negative way because they smell so bad,” Dr. Phillips said. In addition, 85% of patients reported that they actually smelled the odor (an olfactory hallucination).
All of the patients reported practicing repetitive behaviors in an effort to camouflage the perceived odor, mostly with perfume or scented powder (90%), chewing gum (60%), deodorant (55%), and mints (55%).
“Some patients actually drank perfume,” she said. “Some of them constantly chewed gum, ate mints, or reapplied deodorant over and over throughout the day [and] used prescription strength mouthwashes frequently. Some patients showered for hours a day, using an entire bar of soap, trying to remove the odor they perceived.”
In addition, 74% reported that ORS symptoms led to avoidance of social interactions “because they felt so ashamed,” she said. “They worried that other people thought badly of them because they felt they stank.”
More than a third of the patients (40%) said that symptoms were so bad that they were housebound for at least 1 week. “They didn't leave the house at all because they felt too embarrassed [or] ashamed,” she said.
More than two-thirds of the patients (68%) had a history of suicidal ideation, 32% had attempted suicide, and 53% had been hospitalized in a psychiatric unit. The most common lifetime comorbid disorder was major depressive disorder (85%), followed by social phobia (65%), and substance use disorders (50%).
Dr. Phillips also reported that 44% of patients had sought nonpsychiatric medical treatment for the perceived odor. “They went to dentists if they thought they had bad breath, [to] dermatologists if they thought they had smelly sweat,” she said. “One participant in our study had their tonsils removed because they thought their tonsils were causing their breath to be bad.”
About one-third of patients received nonpsychiatric treatment for the perceived odor “but in no case did this treatment diminish the worry about the perceived body odor.”
Dr. Phillips concluded her remarks by noting that ORS “appears to be very under-recognized, and we certainly need more research on this area of study.”
The study also was presented during a poster session at the APA's annual meeting in New Orleans.
Patients 'appear to be very impaired in terms of their functioning and to have high rates of suicidality.'
Source DR. PHILLIPS
Major Finding: Most patients with olfactory reference syndrome (85%) have concurrent major depressive disorder, and 44% have sought nonpsychiatric medical treatment for their perceived odor.
Data Source: A study of 20 patients with olfactory reference syndrome.
Disclosures: Dr. Phillips disclosed that she has received grant and research support from the American Foundation for Suicide Prevention and the National Institute of Mental Health.
Patients with olfactory reference syndrome have high rates of clinical depression and other comorbid psychiatric disorders, and nearly half of them do not seek psychiatric treatment for their perceived order.
Those are key findings from a small, novel study discussed during a press briefing sponsored by the American Psychiatric Association.
Olfactory reference syndrome (ORS) is a preoccupation with the belief that one emits a foul or offensive body odor that is not perceived by other people, said lead study investigator Dr. Katharine A. Phillips, of the department of psychiatry at Rhode Island Hospital/Brown University, Providence.
The few reports about ORS that have been published in the last century “suggest that it is clinically important,” she said. “Patients suffer tremendously as a result of this false belief, and they appear to be very impaired in terms of their functioning and to have high rates of suicidality.”
In an effort to better understand the clinical features of ORS, the researchers used semistructured measurement tools to assess 20 patients with the syndrome, including the Structured Clinical Interview for DSM-IV (SCID) to assess comorbidity, the Brown Assessment of Beliefs Scale to assess insight/delusionality and referential thinking, and a slightly modified version of the Yale-Brown Obsessive Compulsive Scale to assess ORS severity. The mean age of patients was 33 years, 60% were female, and the mean age of onset was 16 years.
Patients reported being preoccupied with their perceived body odor for 3-8 hours per day, mostly the mouth (75%), armpits (60%), and genitals (35%). Bad breath was the most common odor description reported (75%), followed by sweat (65%).
Most patients (85%) reported being completely convinced that their belief about the odor was accurate, and 77% reported thinking “that other people take special notice of them in a negative way because they smell so bad,” Dr. Phillips said. In addition, 85% of patients reported that they actually smelled the odor (an olfactory hallucination).
All of the patients reported practicing repetitive behaviors in an effort to camouflage the perceived odor, mostly with perfume or scented powder (90%), chewing gum (60%), deodorant (55%), and mints (55%).
“Some patients actually drank perfume,” she said. “Some of them constantly chewed gum, ate mints, or reapplied deodorant over and over throughout the day [and] used prescription strength mouthwashes frequently. Some patients showered for hours a day, using an entire bar of soap, trying to remove the odor they perceived.”
In addition, 74% reported that ORS symptoms led to avoidance of social interactions “because they felt so ashamed,” she said. “They worried that other people thought badly of them because they felt they stank.”
More than a third of the patients (40%) said that symptoms were so bad that they were housebound for at least 1 week. “They didn't leave the house at all because they felt too embarrassed [or] ashamed,” she said.
More than two-thirds of the patients (68%) had a history of suicidal ideation, 32% had attempted suicide, and 53% had been hospitalized in a psychiatric unit. The most common lifetime comorbid disorder was major depressive disorder (85%), followed by social phobia (65%), and substance use disorders (50%).
Dr. Phillips also reported that 44% of patients had sought nonpsychiatric medical treatment for the perceived odor. “They went to dentists if they thought they had bad breath, [to] dermatologists if they thought they had smelly sweat,” she said. “One participant in our study had their tonsils removed because they thought their tonsils were causing their breath to be bad.”
About one-third of patients received nonpsychiatric treatment for the perceived odor “but in no case did this treatment diminish the worry about the perceived body odor.”
Dr. Phillips concluded her remarks by noting that ORS “appears to be very under-recognized, and we certainly need more research on this area of study.”
The study also was presented during a poster session at the APA's annual meeting in New Orleans.
Patients 'appear to be very impaired in terms of their functioning and to have high rates of suicidality.'
Source DR. PHILLIPS
Ask Pain Patients About Self-Perceived Burden
Major Finding: Perceived burdensomeness was independently associated with suicidal ideation among patients with chronic pain, and a model including this measure correctly classified 95% of patients as to the presence or absence of suicidal ideation.
Data Source: A retrospective study of 109 patients in a military population with chronic pain referred to a psychology clinic.
Disclosures: Dr. Kanzler reported that she had no conflicts of interest related to the study.
SEATTLE – Asking patients with chronic pain a single question – “Do you believe it would be better for everyone involved if you were to die?” – can determine whether he or she is having suicidal thoughts or wishes, findings from a retrospective study suggest.
Among 109 patients with chronic pain, patients' perceptions that they were a burden to others as assessed with this question was the sole independent predictor of suicidal ideation even after depression and hopelessness were taken into account.
A model including perceived burdensomeness, in addition to conventional risk factors, correctly classified 95% of the patients regarding the presence or absence of suicidal ideation.
“It's important to consider perceived burdensomeness in the patients that you see,” advised lead investigator Kathryn E. Kanzler, Psy.D., who is a captain in the U.S. Air Force and a psychologist at Lackland Air Force Base in San Antonio. “Just one question – that's all it takes to get kind of a quick snapshot of what's going on.”
Patients with chronic conditions may be uniquely attuned to the impact of their health on their caregivers, Dr. Kanzler told attendees of the annual meeting of the Society of Behavioral Medicine. “Research has found that self-perceived burden … can have a direct impact on significant medical decision making,” she said, such as choosing to reduce or entirely skip dialysis.
In the study, she and her colleagues retrospectively reviewed the medical records of 109 outpatients with chronic pain who were referred to a psychology clinic for evaluation and possible behavioral and psychosocial interventions. All were active or retired military personnel, or their dependents or family members.
The patients were age 42 years on average. The majority were married (72%), female (65%), and white (66%).
The leading primary cause of pain was headache/migraine (seen in 28% of patients), followed by chronic low back pain (16%), fibromyalgia (13%), temporomandibular or myofascial pain (9%), arthritis (3%), and complex regional pain syndrome (1%). The remaining patients (30%) had pain due to other conditions, such as cancer or orthopedic injuries.
The investigators used responses on the Beck Depression Inventory–Second Edition (BDI-II) to assess patients' hopelessness, suicidal ideation, and depression.
Perceived burdensomeness was assessed from responses to a single statement, “It would be better for everyone involved if I were to die,” with possible response options ranging from 1 (never or none of the time) to 5 (always or a great many times).
Overall, 7% of patients were found to have suicidal ideation, Dr. Kanzler reported. A logistic regression model including age, sex, race, marital status, depression, and hopelessness improved the ability to predict suicidal ideation above a null model.
Adding patients' perceived burdensomeness to this model further improved the ability to predict suicidal ideation and also improved model fit.
When controlling for depression and hopelessness, perceived burdensomeness was the sole independent predictor of suicidal ideation.
There was no difference in the findings between patients who did and did not have an identified caregiver, a finding that corroborated those from other studies suggesting that perceived burdensomeness may apply to the people who are important in one's life generally.
Perceived burdensomeness performed better at correctly classifying patients without suicidal ideation (98%) than at correctly classifying those with suicidal ideation (63%).
“We hope this study adds to the understanding of the really complex relationship between chronic pain and suicide ideation,” Dr. Kanzler said. “Perceived burdensomeness as a risk factor might help explain high rates of suicide ideation beyond the types of things that definitely, immediately come to mind.”
Importantly, she noted, perceived burdensomeness is modifiable, in contrast to many of the other risk factors for suicidal ideation, such as age and sex. “Some kind of a cognitive intervention might be useful,” she proposed, such as intervening to change the meaning of the cognition of perceived burdensomeness or to challenge the cognition itself.
Encouraging increased communication with the key people in a patient's life may also be beneficial, according to Dr. Kanzler. “Sometimes, especially in our population, there is not necessarily an identified caregiver, but this perceived burdensomeness kind of affects the whole group that surrounds that person,” she explained. “So that type of intervention might also be useful, going beyond the individual patient.”
Major Finding: Perceived burdensomeness was independently associated with suicidal ideation among patients with chronic pain, and a model including this measure correctly classified 95% of patients as to the presence or absence of suicidal ideation.
Data Source: A retrospective study of 109 patients in a military population with chronic pain referred to a psychology clinic.
Disclosures: Dr. Kanzler reported that she had no conflicts of interest related to the study.
SEATTLE – Asking patients with chronic pain a single question – “Do you believe it would be better for everyone involved if you were to die?” – can determine whether he or she is having suicidal thoughts or wishes, findings from a retrospective study suggest.
Among 109 patients with chronic pain, patients' perceptions that they were a burden to others as assessed with this question was the sole independent predictor of suicidal ideation even after depression and hopelessness were taken into account.
A model including perceived burdensomeness, in addition to conventional risk factors, correctly classified 95% of the patients regarding the presence or absence of suicidal ideation.
“It's important to consider perceived burdensomeness in the patients that you see,” advised lead investigator Kathryn E. Kanzler, Psy.D., who is a captain in the U.S. Air Force and a psychologist at Lackland Air Force Base in San Antonio. “Just one question – that's all it takes to get kind of a quick snapshot of what's going on.”
Patients with chronic conditions may be uniquely attuned to the impact of their health on their caregivers, Dr. Kanzler told attendees of the annual meeting of the Society of Behavioral Medicine. “Research has found that self-perceived burden … can have a direct impact on significant medical decision making,” she said, such as choosing to reduce or entirely skip dialysis.
In the study, she and her colleagues retrospectively reviewed the medical records of 109 outpatients with chronic pain who were referred to a psychology clinic for evaluation and possible behavioral and psychosocial interventions. All were active or retired military personnel, or their dependents or family members.
The patients were age 42 years on average. The majority were married (72%), female (65%), and white (66%).
The leading primary cause of pain was headache/migraine (seen in 28% of patients), followed by chronic low back pain (16%), fibromyalgia (13%), temporomandibular or myofascial pain (9%), arthritis (3%), and complex regional pain syndrome (1%). The remaining patients (30%) had pain due to other conditions, such as cancer or orthopedic injuries.
The investigators used responses on the Beck Depression Inventory–Second Edition (BDI-II) to assess patients' hopelessness, suicidal ideation, and depression.
Perceived burdensomeness was assessed from responses to a single statement, “It would be better for everyone involved if I were to die,” with possible response options ranging from 1 (never or none of the time) to 5 (always or a great many times).
Overall, 7% of patients were found to have suicidal ideation, Dr. Kanzler reported. A logistic regression model including age, sex, race, marital status, depression, and hopelessness improved the ability to predict suicidal ideation above a null model.
Adding patients' perceived burdensomeness to this model further improved the ability to predict suicidal ideation and also improved model fit.
When controlling for depression and hopelessness, perceived burdensomeness was the sole independent predictor of suicidal ideation.
There was no difference in the findings between patients who did and did not have an identified caregiver, a finding that corroborated those from other studies suggesting that perceived burdensomeness may apply to the people who are important in one's life generally.
Perceived burdensomeness performed better at correctly classifying patients without suicidal ideation (98%) than at correctly classifying those with suicidal ideation (63%).
“We hope this study adds to the understanding of the really complex relationship between chronic pain and suicide ideation,” Dr. Kanzler said. “Perceived burdensomeness as a risk factor might help explain high rates of suicide ideation beyond the types of things that definitely, immediately come to mind.”
Importantly, she noted, perceived burdensomeness is modifiable, in contrast to many of the other risk factors for suicidal ideation, such as age and sex. “Some kind of a cognitive intervention might be useful,” she proposed, such as intervening to change the meaning of the cognition of perceived burdensomeness or to challenge the cognition itself.
Encouraging increased communication with the key people in a patient's life may also be beneficial, according to Dr. Kanzler. “Sometimes, especially in our population, there is not necessarily an identified caregiver, but this perceived burdensomeness kind of affects the whole group that surrounds that person,” she explained. “So that type of intervention might also be useful, going beyond the individual patient.”
Major Finding: Perceived burdensomeness was independently associated with suicidal ideation among patients with chronic pain, and a model including this measure correctly classified 95% of patients as to the presence or absence of suicidal ideation.
Data Source: A retrospective study of 109 patients in a military population with chronic pain referred to a psychology clinic.
Disclosures: Dr. Kanzler reported that she had no conflicts of interest related to the study.
SEATTLE – Asking patients with chronic pain a single question – “Do you believe it would be better for everyone involved if you were to die?” – can determine whether he or she is having suicidal thoughts or wishes, findings from a retrospective study suggest.
Among 109 patients with chronic pain, patients' perceptions that they were a burden to others as assessed with this question was the sole independent predictor of suicidal ideation even after depression and hopelessness were taken into account.
A model including perceived burdensomeness, in addition to conventional risk factors, correctly classified 95% of the patients regarding the presence or absence of suicidal ideation.
“It's important to consider perceived burdensomeness in the patients that you see,” advised lead investigator Kathryn E. Kanzler, Psy.D., who is a captain in the U.S. Air Force and a psychologist at Lackland Air Force Base in San Antonio. “Just one question – that's all it takes to get kind of a quick snapshot of what's going on.”
Patients with chronic conditions may be uniquely attuned to the impact of their health on their caregivers, Dr. Kanzler told attendees of the annual meeting of the Society of Behavioral Medicine. “Research has found that self-perceived burden … can have a direct impact on significant medical decision making,” she said, such as choosing to reduce or entirely skip dialysis.
In the study, she and her colleagues retrospectively reviewed the medical records of 109 outpatients with chronic pain who were referred to a psychology clinic for evaluation and possible behavioral and psychosocial interventions. All were active or retired military personnel, or their dependents or family members.
The patients were age 42 years on average. The majority were married (72%), female (65%), and white (66%).
The leading primary cause of pain was headache/migraine (seen in 28% of patients), followed by chronic low back pain (16%), fibromyalgia (13%), temporomandibular or myofascial pain (9%), arthritis (3%), and complex regional pain syndrome (1%). The remaining patients (30%) had pain due to other conditions, such as cancer or orthopedic injuries.
The investigators used responses on the Beck Depression Inventory–Second Edition (BDI-II) to assess patients' hopelessness, suicidal ideation, and depression.
Perceived burdensomeness was assessed from responses to a single statement, “It would be better for everyone involved if I were to die,” with possible response options ranging from 1 (never or none of the time) to 5 (always or a great many times).
Overall, 7% of patients were found to have suicidal ideation, Dr. Kanzler reported. A logistic regression model including age, sex, race, marital status, depression, and hopelessness improved the ability to predict suicidal ideation above a null model.
Adding patients' perceived burdensomeness to this model further improved the ability to predict suicidal ideation and also improved model fit.
When controlling for depression and hopelessness, perceived burdensomeness was the sole independent predictor of suicidal ideation.
There was no difference in the findings between patients who did and did not have an identified caregiver, a finding that corroborated those from other studies suggesting that perceived burdensomeness may apply to the people who are important in one's life generally.
Perceived burdensomeness performed better at correctly classifying patients without suicidal ideation (98%) than at correctly classifying those with suicidal ideation (63%).
“We hope this study adds to the understanding of the really complex relationship between chronic pain and suicide ideation,” Dr. Kanzler said. “Perceived burdensomeness as a risk factor might help explain high rates of suicide ideation beyond the types of things that definitely, immediately come to mind.”
Importantly, she noted, perceived burdensomeness is modifiable, in contrast to many of the other risk factors for suicidal ideation, such as age and sex. “Some kind of a cognitive intervention might be useful,” she proposed, such as intervening to change the meaning of the cognition of perceived burdensomeness or to challenge the cognition itself.
Encouraging increased communication with the key people in a patient's life may also be beneficial, according to Dr. Kanzler. “Sometimes, especially in our population, there is not necessarily an identified caregiver, but this perceived burdensomeness kind of affects the whole group that surrounds that person,” she explained. “So that type of intervention might also be useful, going beyond the individual patient.”
Shorter Sleep Duration Predicts Distress
Young adults who report sleeping fewer hours per night on average than do their counterparts are at elevated risk for persistent or new-onset psychological distress, according to results of a large, prospective cohort study.
Researchers found a linear correlation – a 14% greater risk for higher psychological distress for each hour slept fewer than 8, on average, per night – after they controlled for possible confounders. Sleeping 8-9 hours per night is recommended.
A total of 19,648 Australians (aged 17-24 years) reported their sleep hours for the previous month in a survey of registered drivers. Researchers found almost one-third (32.5%) had high baseline levels of psychological distress (defined as a score greater than 21 on the K10 (Kessler Psychological Distress Scale), a 10-item instrument that screens for feeling “tired out for no reason,” nervous, hopeless, restless, or depressed during the previous 4 weeks.
Psychological distress was most acute among the less than 2% of young adults who reported sleeping an average 5 hours or fewer per night, representing a group that might benefit the most from an intervention to improve their sleep routine. Another 18% reported sleeping an average 7 hours or fewer per night, and 30% reported sleeping 7-8 hours each night.
The full findings of the study were published in the September issue of the journal Sleep (2010;33:1139-45).
Lead researcher Dr. Nicholas Glozier and his associates also resurveyed a random sample of 2,937 respondents 12-18 months later. They found that high levels of distress persisted for 32% of the 945 who were initially distressed at baseline. In addition, 12% of those with no initial elevated distress (239 of 1992 respondents) had new-onset distress 1 year later, reported Dr. Glozier, who is on the psychological medicine faculty at the Brain and Mind Research Institute at the University of Sydney.
Again, a linear association was found between shorter sleep duration and likelihood for onset of psychological distress (relative risk, 1.12). Risk was most pronounced among those reporting an average 5 hours or fewer of sleep (RR, 3.25), compared with other participants.
This is the first prospective study to link shorter sleep duration in young adults with increased psychological distress, the researchers noted. Interestingly, there was no increased risk of psychological distress at any time in the study among those who reported sleeping an average 9 hours or more per night.
Based on these findings, clinicians could potentially identify young adults who are at elevated risk for persistent or new onset psychological distress by asking about sleep duration. Also, because young adulthood is a time when elevated psychological distress could develop into depression and many other psychiatric conditions, short sleep duration could be an important marker for early intervention, the authors wrote.
The authors acknowledged the difficulty associated with any populationwide effort to improve sleep (such as reducing late-night television viewing, computer gaming, and Internet use). Instead, they recommend that clinicians identify and focus their efforts on young adults who are at highest risk: those who report current distress or extremely short sleep duration. Other researchers demonstrated an association between short sleep duration and later bedtimes with depressed mood and suicidal ideation among adolescents (Sleep 2010;33:97-106).
Disclosures: There was no industry support for the study. Dr. Glozier is a member of the Sanofi-Aventis advisory board and is a speaker for CSL Laboratories. Dr. Ian Hickie, one of the investigators, formerly served as chief executive officer and clinical adviser for Beyondblue, the Australian National Depression Initiative, and has led projects supported by numerous drug industry partners. The other authors reported no relevant disclosures.
Young adults who report sleeping fewer hours per night on average than do their counterparts are at elevated risk for persistent or new-onset psychological distress, according to results of a large, prospective cohort study.
Researchers found a linear correlation – a 14% greater risk for higher psychological distress for each hour slept fewer than 8, on average, per night – after they controlled for possible confounders. Sleeping 8-9 hours per night is recommended.
A total of 19,648 Australians (aged 17-24 years) reported their sleep hours for the previous month in a survey of registered drivers. Researchers found almost one-third (32.5%) had high baseline levels of psychological distress (defined as a score greater than 21 on the K10 (Kessler Psychological Distress Scale), a 10-item instrument that screens for feeling “tired out for no reason,” nervous, hopeless, restless, or depressed during the previous 4 weeks.
Psychological distress was most acute among the less than 2% of young adults who reported sleeping an average 5 hours or fewer per night, representing a group that might benefit the most from an intervention to improve their sleep routine. Another 18% reported sleeping an average 7 hours or fewer per night, and 30% reported sleeping 7-8 hours each night.
The full findings of the study were published in the September issue of the journal Sleep (2010;33:1139-45).
Lead researcher Dr. Nicholas Glozier and his associates also resurveyed a random sample of 2,937 respondents 12-18 months later. They found that high levels of distress persisted for 32% of the 945 who were initially distressed at baseline. In addition, 12% of those with no initial elevated distress (239 of 1992 respondents) had new-onset distress 1 year later, reported Dr. Glozier, who is on the psychological medicine faculty at the Brain and Mind Research Institute at the University of Sydney.
Again, a linear association was found between shorter sleep duration and likelihood for onset of psychological distress (relative risk, 1.12). Risk was most pronounced among those reporting an average 5 hours or fewer of sleep (RR, 3.25), compared with other participants.
This is the first prospective study to link shorter sleep duration in young adults with increased psychological distress, the researchers noted. Interestingly, there was no increased risk of psychological distress at any time in the study among those who reported sleeping an average 9 hours or more per night.
Based on these findings, clinicians could potentially identify young adults who are at elevated risk for persistent or new onset psychological distress by asking about sleep duration. Also, because young adulthood is a time when elevated psychological distress could develop into depression and many other psychiatric conditions, short sleep duration could be an important marker for early intervention, the authors wrote.
The authors acknowledged the difficulty associated with any populationwide effort to improve sleep (such as reducing late-night television viewing, computer gaming, and Internet use). Instead, they recommend that clinicians identify and focus their efforts on young adults who are at highest risk: those who report current distress or extremely short sleep duration. Other researchers demonstrated an association between short sleep duration and later bedtimes with depressed mood and suicidal ideation among adolescents (Sleep 2010;33:97-106).
Disclosures: There was no industry support for the study. Dr. Glozier is a member of the Sanofi-Aventis advisory board and is a speaker for CSL Laboratories. Dr. Ian Hickie, one of the investigators, formerly served as chief executive officer and clinical adviser for Beyondblue, the Australian National Depression Initiative, and has led projects supported by numerous drug industry partners. The other authors reported no relevant disclosures.
Young adults who report sleeping fewer hours per night on average than do their counterparts are at elevated risk for persistent or new-onset psychological distress, according to results of a large, prospective cohort study.
Researchers found a linear correlation – a 14% greater risk for higher psychological distress for each hour slept fewer than 8, on average, per night – after they controlled for possible confounders. Sleeping 8-9 hours per night is recommended.
A total of 19,648 Australians (aged 17-24 years) reported their sleep hours for the previous month in a survey of registered drivers. Researchers found almost one-third (32.5%) had high baseline levels of psychological distress (defined as a score greater than 21 on the K10 (Kessler Psychological Distress Scale), a 10-item instrument that screens for feeling “tired out for no reason,” nervous, hopeless, restless, or depressed during the previous 4 weeks.
Psychological distress was most acute among the less than 2% of young adults who reported sleeping an average 5 hours or fewer per night, representing a group that might benefit the most from an intervention to improve their sleep routine. Another 18% reported sleeping an average 7 hours or fewer per night, and 30% reported sleeping 7-8 hours each night.
The full findings of the study were published in the September issue of the journal Sleep (2010;33:1139-45).
Lead researcher Dr. Nicholas Glozier and his associates also resurveyed a random sample of 2,937 respondents 12-18 months later. They found that high levels of distress persisted for 32% of the 945 who were initially distressed at baseline. In addition, 12% of those with no initial elevated distress (239 of 1992 respondents) had new-onset distress 1 year later, reported Dr. Glozier, who is on the psychological medicine faculty at the Brain and Mind Research Institute at the University of Sydney.
Again, a linear association was found between shorter sleep duration and likelihood for onset of psychological distress (relative risk, 1.12). Risk was most pronounced among those reporting an average 5 hours or fewer of sleep (RR, 3.25), compared with other participants.
This is the first prospective study to link shorter sleep duration in young adults with increased psychological distress, the researchers noted. Interestingly, there was no increased risk of psychological distress at any time in the study among those who reported sleeping an average 9 hours or more per night.
Based on these findings, clinicians could potentially identify young adults who are at elevated risk for persistent or new onset psychological distress by asking about sleep duration. Also, because young adulthood is a time when elevated psychological distress could develop into depression and many other psychiatric conditions, short sleep duration could be an important marker for early intervention, the authors wrote.
The authors acknowledged the difficulty associated with any populationwide effort to improve sleep (such as reducing late-night television viewing, computer gaming, and Internet use). Instead, they recommend that clinicians identify and focus their efforts on young adults who are at highest risk: those who report current distress or extremely short sleep duration. Other researchers demonstrated an association between short sleep duration and later bedtimes with depressed mood and suicidal ideation among adolescents (Sleep 2010;33:97-106).
Disclosures: There was no industry support for the study. Dr. Glozier is a member of the Sanofi-Aventis advisory board and is a speaker for CSL Laboratories. Dr. Ian Hickie, one of the investigators, formerly served as chief executive officer and clinical adviser for Beyondblue, the Australian National Depression Initiative, and has led projects supported by numerous drug industry partners. The other authors reported no relevant disclosures.
Psoriasis Tied to Increased Risk of Psychiatric Disorders in Kids
Major Finding: Psoriasis patients were particularly more likely to be diagnosed with depression (3%) or anxiety (1.8%), compared with controls (2.4% and 1.4%, respectively).
Data Source: A large, retrospective, case-control study of 7,404 children with psoriasis under age 18 years and 37,020 controls.
Disclosures: Abbott Laboratories sponsored the study.
MIAMI – Children with psoriasis have a significantly greater risk of developing a psychiatric disorder than do those without psoriasis, according to findings from a large, retrospective, case-control study.
Nationally representative health plan data for 7,404 children with psoriasis aged younger than 18 years found that 5.1% were diagnosed with or treated for a psychiatric disorder after health plan enrollment, compared with 4.1% of 37,020 controls. Psoriasis patients were particularly more likely to be diagnosed with depression (3%) or anxiety (1.8%), compared with controls (2.4% and 1.4%, respectively), Carol Bao, Ph.D., reported during a poster discussion session at the meeting.
For children with psoriasis, the estimated hazard ratio for developing any psychiatric disorder was 1.25, for developing depression was 1.23, and for developing anxiety was 1.32, said Dr. Bao, a senior manager at Abbott Laboratories, Chicago.
The investigators also looked at prescriptions for psychotropic medications in assessing risk for development of psychiatric disorders. Prescriptions can be a marker for a diagnosis in cases where the prescribing physician may be hesitant to refer the patient or make a diagnosis, Dr. Bao explained, noting that this helped correct for possible underestimation of the development of psychiatric disorders and provided a risk estimate range.
When both diagnoses and prescriptions were considered, psoriasis patients had 25%-47% greater risk of developing a psychiatric disorder, 23%-62% greater risk of developing depression, and 32%-250% greater risk of developing anxiety, compared with controls, she said.
Patients included in the study had a mean age of 11.4 years. They were selected from a database of health plan participants who were enrolled in a plan at least 6 months before and after the first psoriasis diagnosis date (the index date), and who were followed from the index date until they were first diagnosed with any psychiatric disorder or were prescribed a drug used for the treatment of a psychiatric disorder. Any plan participant with a preenrollment psychiatric diagnosis or prescription was excluded.
Controls were matched to patients based on age, sex, and index date.
The findings of an increased risk of developing psychiatric disorders in case patients remained significant after controlling for age, sex, health plan, region of residence, and comorbidities, Dr. Bao noted.
The study is limited by the potential for coding and reporting errors in the data used and by lack of information on the severity of the psychiatric disorders. However, the findings do suggest that the psychiatric impact of psoriasis on children must be addressed because of the potential for both short- and long-term adverse effects.
“If we put these data in perspective, the development of psychiatric disorders at a young age can have a great impact in future adult life,” she said.
Major Finding: Psoriasis patients were particularly more likely to be diagnosed with depression (3%) or anxiety (1.8%), compared with controls (2.4% and 1.4%, respectively).
Data Source: A large, retrospective, case-control study of 7,404 children with psoriasis under age 18 years and 37,020 controls.
Disclosures: Abbott Laboratories sponsored the study.
MIAMI – Children with psoriasis have a significantly greater risk of developing a psychiatric disorder than do those without psoriasis, according to findings from a large, retrospective, case-control study.
Nationally representative health plan data for 7,404 children with psoriasis aged younger than 18 years found that 5.1% were diagnosed with or treated for a psychiatric disorder after health plan enrollment, compared with 4.1% of 37,020 controls. Psoriasis patients were particularly more likely to be diagnosed with depression (3%) or anxiety (1.8%), compared with controls (2.4% and 1.4%, respectively), Carol Bao, Ph.D., reported during a poster discussion session at the meeting.
For children with psoriasis, the estimated hazard ratio for developing any psychiatric disorder was 1.25, for developing depression was 1.23, and for developing anxiety was 1.32, said Dr. Bao, a senior manager at Abbott Laboratories, Chicago.
The investigators also looked at prescriptions for psychotropic medications in assessing risk for development of psychiatric disorders. Prescriptions can be a marker for a diagnosis in cases where the prescribing physician may be hesitant to refer the patient or make a diagnosis, Dr. Bao explained, noting that this helped correct for possible underestimation of the development of psychiatric disorders and provided a risk estimate range.
When both diagnoses and prescriptions were considered, psoriasis patients had 25%-47% greater risk of developing a psychiatric disorder, 23%-62% greater risk of developing depression, and 32%-250% greater risk of developing anxiety, compared with controls, she said.
Patients included in the study had a mean age of 11.4 years. They were selected from a database of health plan participants who were enrolled in a plan at least 6 months before and after the first psoriasis diagnosis date (the index date), and who were followed from the index date until they were first diagnosed with any psychiatric disorder or were prescribed a drug used for the treatment of a psychiatric disorder. Any plan participant with a preenrollment psychiatric diagnosis or prescription was excluded.
Controls were matched to patients based on age, sex, and index date.
The findings of an increased risk of developing psychiatric disorders in case patients remained significant after controlling for age, sex, health plan, region of residence, and comorbidities, Dr. Bao noted.
The study is limited by the potential for coding and reporting errors in the data used and by lack of information on the severity of the psychiatric disorders. However, the findings do suggest that the psychiatric impact of psoriasis on children must be addressed because of the potential for both short- and long-term adverse effects.
“If we put these data in perspective, the development of psychiatric disorders at a young age can have a great impact in future adult life,” she said.
Major Finding: Psoriasis patients were particularly more likely to be diagnosed with depression (3%) or anxiety (1.8%), compared with controls (2.4% and 1.4%, respectively).
Data Source: A large, retrospective, case-control study of 7,404 children with psoriasis under age 18 years and 37,020 controls.
Disclosures: Abbott Laboratories sponsored the study.
MIAMI – Children with psoriasis have a significantly greater risk of developing a psychiatric disorder than do those without psoriasis, according to findings from a large, retrospective, case-control study.
Nationally representative health plan data for 7,404 children with psoriasis aged younger than 18 years found that 5.1% were diagnosed with or treated for a psychiatric disorder after health plan enrollment, compared with 4.1% of 37,020 controls. Psoriasis patients were particularly more likely to be diagnosed with depression (3%) or anxiety (1.8%), compared with controls (2.4% and 1.4%, respectively), Carol Bao, Ph.D., reported during a poster discussion session at the meeting.
For children with psoriasis, the estimated hazard ratio for developing any psychiatric disorder was 1.25, for developing depression was 1.23, and for developing anxiety was 1.32, said Dr. Bao, a senior manager at Abbott Laboratories, Chicago.
The investigators also looked at prescriptions for psychotropic medications in assessing risk for development of psychiatric disorders. Prescriptions can be a marker for a diagnosis in cases where the prescribing physician may be hesitant to refer the patient or make a diagnosis, Dr. Bao explained, noting that this helped correct for possible underestimation of the development of psychiatric disorders and provided a risk estimate range.
When both diagnoses and prescriptions were considered, psoriasis patients had 25%-47% greater risk of developing a psychiatric disorder, 23%-62% greater risk of developing depression, and 32%-250% greater risk of developing anxiety, compared with controls, she said.
Patients included in the study had a mean age of 11.4 years. They were selected from a database of health plan participants who were enrolled in a plan at least 6 months before and after the first psoriasis diagnosis date (the index date), and who were followed from the index date until they were first diagnosed with any psychiatric disorder or were prescribed a drug used for the treatment of a psychiatric disorder. Any plan participant with a preenrollment psychiatric diagnosis or prescription was excluded.
Controls were matched to patients based on age, sex, and index date.
The findings of an increased risk of developing psychiatric disorders in case patients remained significant after controlling for age, sex, health plan, region of residence, and comorbidities, Dr. Bao noted.
The study is limited by the potential for coding and reporting errors in the data used and by lack of information on the severity of the psychiatric disorders. However, the findings do suggest that the psychiatric impact of psoriasis on children must be addressed because of the potential for both short- and long-term adverse effects.
“If we put these data in perspective, the development of psychiatric disorders at a young age can have a great impact in future adult life,” she said.
Chronotherapeutics Corrects Circadian Rhythms
AMSTERDAM – Circadian dysfunction can greatly affect brain function – impairing behavior, cognition, and affect – and can be improved with a “chronotherapeutic” approach, according to Anna Wirz-Justice, Ph.D., one of the leading researchers in the field.
Dr. Wirz-Justice, professor emeritus at the center for chronobiology at Psychiatric University Clinics in Basel, Switzerland, coauthored the treatment manual, “Chronotherapeutics for Affective Disorders: A Clinician's Manual for Light and Wake Therapy” (Basel: Karger, 2009).
“In the treatment of affective disorders, chronotherapeutics offers a new synthesis of nonpharmacologic interventions designed to accelerate remission. Combining it with concomitant or follow-up medications shows great promise,” said Dr. Wirz-Justice, who has led numerous investigative studies in the field and lectured on the role of circadian rhythms in affective disorders at the congress.
Circadian rhythms are directed by a master biological block in the suprachiasmatic nucleus (SCN) as well as circadian oscillators in all brain regions and peripheral tissues. The SCN is synchronized daily by environmental signals, mainly light. Receiving information on lighting conditions directly from the retina, the SCN drives secretion of melatonin and regulates peripheral “clocks,” whose outputs modulate the SCN through feedback or feed-forward effects.
Specific circadian genes such as CLOCK, BMAL1, and PER are responsible for the main SCN “clock-working” machinery.
New interest in the role of circadian dysregulation in psychiatric disorders has arisen from the finding that a mutation in a core circadian clock gene induces hyperactivity, decreased sleep, and mania-like behavior in mice.
“Animal studies were the key development that brought the field to its present exciting position, by suggesting that 'clock genes' are directing the circadian rhythms in all physiological processes,” Dr. Wirz-Justice said.
Clinical Impact on Disorders
In healthy individuals, physiological and biochemical variables such as body temperature, cortisol and melatonin, thyroid-stimulating hormone, norepinephrine and serotonin exhibit circadian rhythms.
However, in patients who have affective disorders, many of these rhythms are disturbed in phase and amplitude.
For instance, in major depressive disorder (MDD), most patients present with sleep disturbances and altered circadian rhythms, including hormonal secretion, cardiac function, and body temperature.
Sleep disruption is a major symptom in depression and is often the factor prompting depressed persons to seek medical help.
Synchronizing impaired circadian rhythms through “chronotherapeutics” – improving sleep or paradoxically staying awake most of the night – can be extremely helpful in treating patients with MDD and bipolar disorder, Dr. Wirz-Justice said, but the approach is not limited to depression.
In addition to major depression (seasonal and nonseasonal), chronotherapeutics indications include bipolar disorder, premenstrual dysphoric disorder and depression during pregnancy, bulimia nervosa, attention-deficit/hyperactivity disorder, dementia, Parkinson's disease, and shift-work and jet-lag disturbances, according to Dr. Wirz-Justice.
“Light therapy has been used to resynchronize disturbed sleep schedules back to a more normal pattern. Light is also an effective antidepressant, acting on many of the same neurotransmitter systems and brain structures as antidepressant drugs,” she said.
“The new message is that light therapy is not just for seasonal affective disorder but for all forms of depression and for many other disorders,” she added.
“As an adjuvant to antidepressants in unipolar depressive patients or to lithium in bipolar patients, morning light hastens and potentiates the antidepressant response. Light therapy shows benefit even for patients with chronic depression of 2 years or more and provides a viable alternative for patients who refuse, resist, or cannot tolerate medication,” Dr. Wirz-Justice said.
Elements of chronotherapy include light therapy, dark therapy or blue-blocking sunglasses, wake therapy (total or partial sleep deprivation in the second half of the night), phase advance of the sleep-wake cycle, and exogenously administered melatonin.
Sleep Deprivation and Dark Therapy
A 1-night sleep deprivation, or “wake therapy,” is the most rapid antidepressant known, according to Dr. Wirz-Justice. A single night's sleep deprivation induces brain changes similar to those that result from many weeks of antidepressant drugs (Curr. Pharm. Des. 2009;15:2637-49).
“Approximately 60% of patients, independent of diagnostic subtypes, respond with marked improvement within hours,” she said. “Mostly, however, they relapse after recovery sleep, which indicates how important wakefulness must be. We have found you can prevent relapse by combining daily light therapy with antidepressants or lithium or a short phase advance of sleep over 3 days.”
Dark therapy (defined as keeping patients in a dark setting and extending rest-sleep for periods of 10-14 hours) has yielded positive results in controlling symptoms in acute mania and calming rapid-cycling bipolar patients in the manic phase, she said.
Since this approach is impractical, an alternative that is being investigated is the use of blue-blocking sunglasses. Blue is the wavelength to which the circadian system is particularly sensitive. Thus, by blocking this range in the light spectrum one can induce “circadian darkness” while not impairing vision, she explained.
Dr. Wirz-Justice is advocating wider use of these techniques in psychiatry and their incorporation into residency programs. “In clinical practice, there is still r
“In clinical practice, there is still rather widespread ignorance about circadian sleep disturbances and chronotherapeutics in spite of the significant evidence base,” she said.
“Enterprising doctors should try this out, and the techniques should be taught in residency programs.”
Disclosures: Dr. Wirz-Justice reported no potential conflicts of interest.
For more information on chronotherapeutics, check out the Center for Environmental Therapeutics' Web site at
AMSTERDAM – Circadian dysfunction can greatly affect brain function – impairing behavior, cognition, and affect – and can be improved with a “chronotherapeutic” approach, according to Anna Wirz-Justice, Ph.D., one of the leading researchers in the field.
Dr. Wirz-Justice, professor emeritus at the center for chronobiology at Psychiatric University Clinics in Basel, Switzerland, coauthored the treatment manual, “Chronotherapeutics for Affective Disorders: A Clinician's Manual for Light and Wake Therapy” (Basel: Karger, 2009).
“In the treatment of affective disorders, chronotherapeutics offers a new synthesis of nonpharmacologic interventions designed to accelerate remission. Combining it with concomitant or follow-up medications shows great promise,” said Dr. Wirz-Justice, who has led numerous investigative studies in the field and lectured on the role of circadian rhythms in affective disorders at the congress.
Circadian rhythms are directed by a master biological block in the suprachiasmatic nucleus (SCN) as well as circadian oscillators in all brain regions and peripheral tissues. The SCN is synchronized daily by environmental signals, mainly light. Receiving information on lighting conditions directly from the retina, the SCN drives secretion of melatonin and regulates peripheral “clocks,” whose outputs modulate the SCN through feedback or feed-forward effects.
Specific circadian genes such as CLOCK, BMAL1, and PER are responsible for the main SCN “clock-working” machinery.
New interest in the role of circadian dysregulation in psychiatric disorders has arisen from the finding that a mutation in a core circadian clock gene induces hyperactivity, decreased sleep, and mania-like behavior in mice.
“Animal studies were the key development that brought the field to its present exciting position, by suggesting that 'clock genes' are directing the circadian rhythms in all physiological processes,” Dr. Wirz-Justice said.
Clinical Impact on Disorders
In healthy individuals, physiological and biochemical variables such as body temperature, cortisol and melatonin, thyroid-stimulating hormone, norepinephrine and serotonin exhibit circadian rhythms.
However, in patients who have affective disorders, many of these rhythms are disturbed in phase and amplitude.
For instance, in major depressive disorder (MDD), most patients present with sleep disturbances and altered circadian rhythms, including hormonal secretion, cardiac function, and body temperature.
Sleep disruption is a major symptom in depression and is often the factor prompting depressed persons to seek medical help.
Synchronizing impaired circadian rhythms through “chronotherapeutics” – improving sleep or paradoxically staying awake most of the night – can be extremely helpful in treating patients with MDD and bipolar disorder, Dr. Wirz-Justice said, but the approach is not limited to depression.
In addition to major depression (seasonal and nonseasonal), chronotherapeutics indications include bipolar disorder, premenstrual dysphoric disorder and depression during pregnancy, bulimia nervosa, attention-deficit/hyperactivity disorder, dementia, Parkinson's disease, and shift-work and jet-lag disturbances, according to Dr. Wirz-Justice.
“Light therapy has been used to resynchronize disturbed sleep schedules back to a more normal pattern. Light is also an effective antidepressant, acting on many of the same neurotransmitter systems and brain structures as antidepressant drugs,” she said.
“The new message is that light therapy is not just for seasonal affective disorder but for all forms of depression and for many other disorders,” she added.
“As an adjuvant to antidepressants in unipolar depressive patients or to lithium in bipolar patients, morning light hastens and potentiates the antidepressant response. Light therapy shows benefit even for patients with chronic depression of 2 years or more and provides a viable alternative for patients who refuse, resist, or cannot tolerate medication,” Dr. Wirz-Justice said.
Elements of chronotherapy include light therapy, dark therapy or blue-blocking sunglasses, wake therapy (total or partial sleep deprivation in the second half of the night), phase advance of the sleep-wake cycle, and exogenously administered melatonin.
Sleep Deprivation and Dark Therapy
A 1-night sleep deprivation, or “wake therapy,” is the most rapid antidepressant known, according to Dr. Wirz-Justice. A single night's sleep deprivation induces brain changes similar to those that result from many weeks of antidepressant drugs (Curr. Pharm. Des. 2009;15:2637-49).
“Approximately 60% of patients, independent of diagnostic subtypes, respond with marked improvement within hours,” she said. “Mostly, however, they relapse after recovery sleep, which indicates how important wakefulness must be. We have found you can prevent relapse by combining daily light therapy with antidepressants or lithium or a short phase advance of sleep over 3 days.”
Dark therapy (defined as keeping patients in a dark setting and extending rest-sleep for periods of 10-14 hours) has yielded positive results in controlling symptoms in acute mania and calming rapid-cycling bipolar patients in the manic phase, she said.
Since this approach is impractical, an alternative that is being investigated is the use of blue-blocking sunglasses. Blue is the wavelength to which the circadian system is particularly sensitive. Thus, by blocking this range in the light spectrum one can induce “circadian darkness” while not impairing vision, she explained.
Dr. Wirz-Justice is advocating wider use of these techniques in psychiatry and their incorporation into residency programs. “In clinical practice, there is still r
“In clinical practice, there is still rather widespread ignorance about circadian sleep disturbances and chronotherapeutics in spite of the significant evidence base,” she said.
“Enterprising doctors should try this out, and the techniques should be taught in residency programs.”
Disclosures: Dr. Wirz-Justice reported no potential conflicts of interest.
For more information on chronotherapeutics, check out the Center for Environmental Therapeutics' Web site at
AMSTERDAM – Circadian dysfunction can greatly affect brain function – impairing behavior, cognition, and affect – and can be improved with a “chronotherapeutic” approach, according to Anna Wirz-Justice, Ph.D., one of the leading researchers in the field.
Dr. Wirz-Justice, professor emeritus at the center for chronobiology at Psychiatric University Clinics in Basel, Switzerland, coauthored the treatment manual, “Chronotherapeutics for Affective Disorders: A Clinician's Manual for Light and Wake Therapy” (Basel: Karger, 2009).
“In the treatment of affective disorders, chronotherapeutics offers a new synthesis of nonpharmacologic interventions designed to accelerate remission. Combining it with concomitant or follow-up medications shows great promise,” said Dr. Wirz-Justice, who has led numerous investigative studies in the field and lectured on the role of circadian rhythms in affective disorders at the congress.
Circadian rhythms are directed by a master biological block in the suprachiasmatic nucleus (SCN) as well as circadian oscillators in all brain regions and peripheral tissues. The SCN is synchronized daily by environmental signals, mainly light. Receiving information on lighting conditions directly from the retina, the SCN drives secretion of melatonin and regulates peripheral “clocks,” whose outputs modulate the SCN through feedback or feed-forward effects.
Specific circadian genes such as CLOCK, BMAL1, and PER are responsible for the main SCN “clock-working” machinery.
New interest in the role of circadian dysregulation in psychiatric disorders has arisen from the finding that a mutation in a core circadian clock gene induces hyperactivity, decreased sleep, and mania-like behavior in mice.
“Animal studies were the key development that brought the field to its present exciting position, by suggesting that 'clock genes' are directing the circadian rhythms in all physiological processes,” Dr. Wirz-Justice said.
Clinical Impact on Disorders
In healthy individuals, physiological and biochemical variables such as body temperature, cortisol and melatonin, thyroid-stimulating hormone, norepinephrine and serotonin exhibit circadian rhythms.
However, in patients who have affective disorders, many of these rhythms are disturbed in phase and amplitude.
For instance, in major depressive disorder (MDD), most patients present with sleep disturbances and altered circadian rhythms, including hormonal secretion, cardiac function, and body temperature.
Sleep disruption is a major symptom in depression and is often the factor prompting depressed persons to seek medical help.
Synchronizing impaired circadian rhythms through “chronotherapeutics” – improving sleep or paradoxically staying awake most of the night – can be extremely helpful in treating patients with MDD and bipolar disorder, Dr. Wirz-Justice said, but the approach is not limited to depression.
In addition to major depression (seasonal and nonseasonal), chronotherapeutics indications include bipolar disorder, premenstrual dysphoric disorder and depression during pregnancy, bulimia nervosa, attention-deficit/hyperactivity disorder, dementia, Parkinson's disease, and shift-work and jet-lag disturbances, according to Dr. Wirz-Justice.
“Light therapy has been used to resynchronize disturbed sleep schedules back to a more normal pattern. Light is also an effective antidepressant, acting on many of the same neurotransmitter systems and brain structures as antidepressant drugs,” she said.
“The new message is that light therapy is not just for seasonal affective disorder but for all forms of depression and for many other disorders,” she added.
“As an adjuvant to antidepressants in unipolar depressive patients or to lithium in bipolar patients, morning light hastens and potentiates the antidepressant response. Light therapy shows benefit even for patients with chronic depression of 2 years or more and provides a viable alternative for patients who refuse, resist, or cannot tolerate medication,” Dr. Wirz-Justice said.
Elements of chronotherapy include light therapy, dark therapy or blue-blocking sunglasses, wake therapy (total or partial sleep deprivation in the second half of the night), phase advance of the sleep-wake cycle, and exogenously administered melatonin.
Sleep Deprivation and Dark Therapy
A 1-night sleep deprivation, or “wake therapy,” is the most rapid antidepressant known, according to Dr. Wirz-Justice. A single night's sleep deprivation induces brain changes similar to those that result from many weeks of antidepressant drugs (Curr. Pharm. Des. 2009;15:2637-49).
“Approximately 60% of patients, independent of diagnostic subtypes, respond with marked improvement within hours,” she said. “Mostly, however, they relapse after recovery sleep, which indicates how important wakefulness must be. We have found you can prevent relapse by combining daily light therapy with antidepressants or lithium or a short phase advance of sleep over 3 days.”
Dark therapy (defined as keeping patients in a dark setting and extending rest-sleep for periods of 10-14 hours) has yielded positive results in controlling symptoms in acute mania and calming rapid-cycling bipolar patients in the manic phase, she said.
Since this approach is impractical, an alternative that is being investigated is the use of blue-blocking sunglasses. Blue is the wavelength to which the circadian system is particularly sensitive. Thus, by blocking this range in the light spectrum one can induce “circadian darkness” while not impairing vision, she explained.
Dr. Wirz-Justice is advocating wider use of these techniques in psychiatry and their incorporation into residency programs. “In clinical practice, there is still r
“In clinical practice, there is still rather widespread ignorance about circadian sleep disturbances and chronotherapeutics in spite of the significant evidence base,” she said.
“Enterprising doctors should try this out, and the techniques should be taught in residency programs.”
Disclosures: Dr. Wirz-Justice reported no potential conflicts of interest.
For more information on chronotherapeutics, check out the Center for Environmental Therapeutics' Web site at
TNF Blockade May Lower Risk of Depression in Arthritis
DESTIN, FLA. – The benefits of tumor necrosis factor blockade extend beyond the joints to the hearts and minds of rheumatoid arthritis patients, Dr. Iain McInnes reported at the congress.
Findings from two studies suggest anti-TNF treatment can inhibit the cytokine-induced chain of events that leads to the increased risk of cardiovascular disease and clinical depression in RA.
Along with lead investigator Dr. Mike J.L. Peters of VU University Medical Center in Amsterdam, Dr. McInnes and colleagues at the University of Glasgow (Scotland) have shown, for the first time, that anti-TNF-alpha therapy lowers circulating levels of the cardiac neurohormone N-terminal prohormone brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis (RA) who do not have evident heart failure.
Previously identified as a clinically relevant biomarker for heart failure, NT-proBNP is independently associated with cardiovascular risk in individuals with and without preexisting cardiovascular disease. Thus, the observed reduction in NT-proBNP suggests a “potential beneficial effect of [TNF-alpha] blockers with respect to vascular risk and ventricular function in rheumatoid arthritis,” Dr. McInnes said.
The study measured serum NT-proBNP at baseline and after 16 weeks of biweekly adalimumab treatment in 171 consecutive RA patients without heart failure (Ann. Rheum. Dis. 2010 April 7 [doi:10.1136/ard.2009.119412]).
After week 16, the investigators observed an approximately 18% reduction in NT-proBNP levels, providing biological evidence that TNF-alpha blockade does not worsen ventricular function in patients with RA who do not have prevalent heart failure, and supporting epidemiologic findings that indicate it may reduce overall cardiovascular risks in these patients, said Dr. McInnes.
The results also add weight to the accumulating evidence that implicates TNF-alpha in the cardiovascular events associated with RA, and support the beneficial effect that blocking TNF-alpha has on surrogate vascular markers, he said.
In a separate study, Dr. McInnes and colleagues sought to assess the functional effects of anti-TNF-alpha therapy on the brains of depressed patients with RA, and determined that TNF-alpha blockade mediates altered serotonin transporter availability and induces an improvement in depression measures.
“This is critically important,” Dr. McInnes stressed. “I think we as rheumatologists underappreciate the prevalence and impact of depression on our patients,” he said, referring to a 2006 report suggesting that the prevalence of major depressive disorder exceeds 40% and that of suicidal ideation is up to 11% in RA patients (Rheumatology [Oxford] 2006;45:1325-7).
Findings from earlier research have shown that proinflammatory cytokines can increase the density and activity of the serotonin transporter (SERT), a primary target for antidepressant therapy. On that basis, Dr. McInnes and his associates hypothesized that TNF blockade might be associated with altered SERT activity in RA patients, he said. They tested this hypothesis in a clinical, proof-of-concept study by measuring SERT density using SPECT (single-photon emission CT) in six patients with seropositive RA 2 weeks before the initiation of adalimumab therapy and 4 days after the last treatment, he said.
After anti-TNF-alpha therapy, “there was a significant decrease in the [SERT] density in all of the patients.” Along with that came overall improvements in physical and mental functioning, as measured by the Hamilton Rating Scale for Depression, the Social Functioning 36-item scale, the Hospital Anxiety and Depression Scale, and the composite 28 joint count Disease Activity Score, Dr. McInnes reported.
Although it is yet unclear whether the observed SERT alterations are specific to RA or are related to cytokine action in general, “the findings provide important insight into the biology linking clinical depression and rheumatoid arthritis.” If confirmed in larger studies, the findings may offer guidance for developing treatment strategies, according to Dr. McInnes.
Disclosures: Dr. McInnes has received research support or honoraria from Schering-Plough, Roche, Bristol-Myers Squibb Co., and Wyeth and has served as a consultant for Schering-Plough and Roche.
'I think we as rheumatologists underappreciate the prevalence and impact of depression on our patients.'
Source DR. MCINNES
DESTIN, FLA. – The benefits of tumor necrosis factor blockade extend beyond the joints to the hearts and minds of rheumatoid arthritis patients, Dr. Iain McInnes reported at the congress.
Findings from two studies suggest anti-TNF treatment can inhibit the cytokine-induced chain of events that leads to the increased risk of cardiovascular disease and clinical depression in RA.
Along with lead investigator Dr. Mike J.L. Peters of VU University Medical Center in Amsterdam, Dr. McInnes and colleagues at the University of Glasgow (Scotland) have shown, for the first time, that anti-TNF-alpha therapy lowers circulating levels of the cardiac neurohormone N-terminal prohormone brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis (RA) who do not have evident heart failure.
Previously identified as a clinically relevant biomarker for heart failure, NT-proBNP is independently associated with cardiovascular risk in individuals with and without preexisting cardiovascular disease. Thus, the observed reduction in NT-proBNP suggests a “potential beneficial effect of [TNF-alpha] blockers with respect to vascular risk and ventricular function in rheumatoid arthritis,” Dr. McInnes said.
The study measured serum NT-proBNP at baseline and after 16 weeks of biweekly adalimumab treatment in 171 consecutive RA patients without heart failure (Ann. Rheum. Dis. 2010 April 7 [doi:10.1136/ard.2009.119412]).
After week 16, the investigators observed an approximately 18% reduction in NT-proBNP levels, providing biological evidence that TNF-alpha blockade does not worsen ventricular function in patients with RA who do not have prevalent heart failure, and supporting epidemiologic findings that indicate it may reduce overall cardiovascular risks in these patients, said Dr. McInnes.
The results also add weight to the accumulating evidence that implicates TNF-alpha in the cardiovascular events associated with RA, and support the beneficial effect that blocking TNF-alpha has on surrogate vascular markers, he said.
In a separate study, Dr. McInnes and colleagues sought to assess the functional effects of anti-TNF-alpha therapy on the brains of depressed patients with RA, and determined that TNF-alpha blockade mediates altered serotonin transporter availability and induces an improvement in depression measures.
“This is critically important,” Dr. McInnes stressed. “I think we as rheumatologists underappreciate the prevalence and impact of depression on our patients,” he said, referring to a 2006 report suggesting that the prevalence of major depressive disorder exceeds 40% and that of suicidal ideation is up to 11% in RA patients (Rheumatology [Oxford] 2006;45:1325-7).
Findings from earlier research have shown that proinflammatory cytokines can increase the density and activity of the serotonin transporter (SERT), a primary target for antidepressant therapy. On that basis, Dr. McInnes and his associates hypothesized that TNF blockade might be associated with altered SERT activity in RA patients, he said. They tested this hypothesis in a clinical, proof-of-concept study by measuring SERT density using SPECT (single-photon emission CT) in six patients with seropositive RA 2 weeks before the initiation of adalimumab therapy and 4 days after the last treatment, he said.
After anti-TNF-alpha therapy, “there was a significant decrease in the [SERT] density in all of the patients.” Along with that came overall improvements in physical and mental functioning, as measured by the Hamilton Rating Scale for Depression, the Social Functioning 36-item scale, the Hospital Anxiety and Depression Scale, and the composite 28 joint count Disease Activity Score, Dr. McInnes reported.
Although it is yet unclear whether the observed SERT alterations are specific to RA or are related to cytokine action in general, “the findings provide important insight into the biology linking clinical depression and rheumatoid arthritis.” If confirmed in larger studies, the findings may offer guidance for developing treatment strategies, according to Dr. McInnes.
Disclosures: Dr. McInnes has received research support or honoraria from Schering-Plough, Roche, Bristol-Myers Squibb Co., and Wyeth and has served as a consultant for Schering-Plough and Roche.
'I think we as rheumatologists underappreciate the prevalence and impact of depression on our patients.'
Source DR. MCINNES
DESTIN, FLA. – The benefits of tumor necrosis factor blockade extend beyond the joints to the hearts and minds of rheumatoid arthritis patients, Dr. Iain McInnes reported at the congress.
Findings from two studies suggest anti-TNF treatment can inhibit the cytokine-induced chain of events that leads to the increased risk of cardiovascular disease and clinical depression in RA.
Along with lead investigator Dr. Mike J.L. Peters of VU University Medical Center in Amsterdam, Dr. McInnes and colleagues at the University of Glasgow (Scotland) have shown, for the first time, that anti-TNF-alpha therapy lowers circulating levels of the cardiac neurohormone N-terminal prohormone brain natriuretic peptide (NT-proBNP) in patients with rheumatoid arthritis (RA) who do not have evident heart failure.
Previously identified as a clinically relevant biomarker for heart failure, NT-proBNP is independently associated with cardiovascular risk in individuals with and without preexisting cardiovascular disease. Thus, the observed reduction in NT-proBNP suggests a “potential beneficial effect of [TNF-alpha] blockers with respect to vascular risk and ventricular function in rheumatoid arthritis,” Dr. McInnes said.
The study measured serum NT-proBNP at baseline and after 16 weeks of biweekly adalimumab treatment in 171 consecutive RA patients without heart failure (Ann. Rheum. Dis. 2010 April 7 [doi:10.1136/ard.2009.119412]).
After week 16, the investigators observed an approximately 18% reduction in NT-proBNP levels, providing biological evidence that TNF-alpha blockade does not worsen ventricular function in patients with RA who do not have prevalent heart failure, and supporting epidemiologic findings that indicate it may reduce overall cardiovascular risks in these patients, said Dr. McInnes.
The results also add weight to the accumulating evidence that implicates TNF-alpha in the cardiovascular events associated with RA, and support the beneficial effect that blocking TNF-alpha has on surrogate vascular markers, he said.
In a separate study, Dr. McInnes and colleagues sought to assess the functional effects of anti-TNF-alpha therapy on the brains of depressed patients with RA, and determined that TNF-alpha blockade mediates altered serotonin transporter availability and induces an improvement in depression measures.
“This is critically important,” Dr. McInnes stressed. “I think we as rheumatologists underappreciate the prevalence and impact of depression on our patients,” he said, referring to a 2006 report suggesting that the prevalence of major depressive disorder exceeds 40% and that of suicidal ideation is up to 11% in RA patients (Rheumatology [Oxford] 2006;45:1325-7).
Findings from earlier research have shown that proinflammatory cytokines can increase the density and activity of the serotonin transporter (SERT), a primary target for antidepressant therapy. On that basis, Dr. McInnes and his associates hypothesized that TNF blockade might be associated with altered SERT activity in RA patients, he said. They tested this hypothesis in a clinical, proof-of-concept study by measuring SERT density using SPECT (single-photon emission CT) in six patients with seropositive RA 2 weeks before the initiation of adalimumab therapy and 4 days after the last treatment, he said.
After anti-TNF-alpha therapy, “there was a significant decrease in the [SERT] density in all of the patients.” Along with that came overall improvements in physical and mental functioning, as measured by the Hamilton Rating Scale for Depression, the Social Functioning 36-item scale, the Hospital Anxiety and Depression Scale, and the composite 28 joint count Disease Activity Score, Dr. McInnes reported.
Although it is yet unclear whether the observed SERT alterations are specific to RA or are related to cytokine action in general, “the findings provide important insight into the biology linking clinical depression and rheumatoid arthritis.” If confirmed in larger studies, the findings may offer guidance for developing treatment strategies, according to Dr. McInnes.
Disclosures: Dr. McInnes has received research support or honoraria from Schering-Plough, Roche, Bristol-Myers Squibb Co., and Wyeth and has served as a consultant for Schering-Plough and Roche.
'I think we as rheumatologists underappreciate the prevalence and impact of depression on our patients.'
Source DR. MCINNES
Zolpidem Relieves Middle-of-Night Insomnia
Major Finding: Persons who received a new formulation of low-dose sublingual zolpidem for middle-of-the-night insomnia showed no potential for abuse of the drug in the form of dependency, tolerance, or rebound potential, compared with placebo recipients.
Data Source: A 4-week outpatient study of 146 subjects.
Disclosures: Dr. Roth has served as a consultant to Transept Pharmaceuticals Inc., the manufacturer of the sublingual formulation of zolpidem tartrate. He has also received research support from and had other relationships with numerous pharmaceutical companies.
AMSTERDAM – A sublingual 3.5-mg formulation of zolpidem tartrate is effective for middle-of-the-night insomnia, producing no tolerance, rebound, or increase in use over 4 weeks, investigators reported at the congress.
“Awakening during the night with difficulty falling back to sleep is a prevalent condition, and a p.r.n. treatment for this is needed as it may decrease overall drug exposure,” said the study's coinvestigator, Thomas Roth, Ph.D., of Henry Ford Hospital, Detroit.
Zolpidem sublingual tablets 3.5 mg and 1.75 mg were developed for the treatment of insomnia that is characterized by difficulty returning to sleep after middle-of-the-night (MOTN) awakening. The compound is formulated with binary buffers to promote buccal absorption of a portion of the drug. This facilitates bioavailability, resulting in a rapid return to sleep. Previous studies have found that sublingual zolpidem significantly reduces sleep latency after MOTN dosing. In a sleep laboratory study, sleep latency time was approximately 28 minutes with placebo but just 10 minutes with zolpidem 3.5 mg (Sleep 2008;31:1277-84).
“This is a reduced dose of zolpidem, and importantly it is a sublingual formulation so you achieve much faster blood levels to help you fall back asleep but you reduce the total blood level as compared to taking it prophylactically. The concern is that over time, people take more and more of the medication,” Dr. Roth said.
The drug is currently under review by the Food and Drug Administration for MOTN awakening.
In a study designed to address possible abuse liability associated with p.r.n. use of the drug, 75 outpatients received zolpidem and 71 patients received placebo; all were assessed for latency to sleep onset after MOTN dosing across a 4-week treatment period. For a check of rebound potential, outcomes also were observed on the first night of nondosing after 1 or more nights of medication use.
The study found no evidence of residual sleepiness after MOTN dosing with zolpidem. Patients who received the drug actually reported greater alertness compared with baseline. On a scale of 1-9 (with 9 being most alert), the mean score was 4.9 at baseline, increasing to 5.7 after zolpidem dosing. Scores in the placebo arm were 4.7 and 5.2, respectively.
Sleep quality also improved significantly. Mean scores were 4.7 at baseline and 5.8 with zolpidem, vs. 4.5 and 5.2, respectively, with placebo.
The study found no evidence for the development of tolerance to zolpidem's efficacy. Latency to sleep onset improved over the first 2 weeks, and apparently stabilized by week 3, for both the active-treatment and placebo groups, suggesting a nonspecific trend toward improvement in outcome over time.
The response to the medication did not change across the entire treatment period, and drug use was not different between treatment and placebo groups. In fact, drug use during week 4bwas significantly lower than during week 1 in both the active and placebo arms.
There was no evidence of rebound effects on sleep initiation or total sleep time on nondosing nights, regardless of the number of nights of continuous use. On average, for nights during which zolpidem was not dosed, total sleep time was similar for the active and placebo groups.
Dr. Roth noted that the improvement over placebo of about 20 minutes is clinically meaningful. “It doesn't sound impressive, but try sleeping 20 minutes less every night for 3 months – you'll be in a coma. The effect is cumulative. It's about 2 hours a week.”
Sublingual zolpidem helped patients get back to sleep, with no evidence of residual sleepiness.
Source ©iStockphoto/redmonkey8
Major Finding: Persons who received a new formulation of low-dose sublingual zolpidem for middle-of-the-night insomnia showed no potential for abuse of the drug in the form of dependency, tolerance, or rebound potential, compared with placebo recipients.
Data Source: A 4-week outpatient study of 146 subjects.
Disclosures: Dr. Roth has served as a consultant to Transept Pharmaceuticals Inc., the manufacturer of the sublingual formulation of zolpidem tartrate. He has also received research support from and had other relationships with numerous pharmaceutical companies.
AMSTERDAM – A sublingual 3.5-mg formulation of zolpidem tartrate is effective for middle-of-the-night insomnia, producing no tolerance, rebound, or increase in use over 4 weeks, investigators reported at the congress.
“Awakening during the night with difficulty falling back to sleep is a prevalent condition, and a p.r.n. treatment for this is needed as it may decrease overall drug exposure,” said the study's coinvestigator, Thomas Roth, Ph.D., of Henry Ford Hospital, Detroit.
Zolpidem sublingual tablets 3.5 mg and 1.75 mg were developed for the treatment of insomnia that is characterized by difficulty returning to sleep after middle-of-the-night (MOTN) awakening. The compound is formulated with binary buffers to promote buccal absorption of a portion of the drug. This facilitates bioavailability, resulting in a rapid return to sleep. Previous studies have found that sublingual zolpidem significantly reduces sleep latency after MOTN dosing. In a sleep laboratory study, sleep latency time was approximately 28 minutes with placebo but just 10 minutes with zolpidem 3.5 mg (Sleep 2008;31:1277-84).
“This is a reduced dose of zolpidem, and importantly it is a sublingual formulation so you achieve much faster blood levels to help you fall back asleep but you reduce the total blood level as compared to taking it prophylactically. The concern is that over time, people take more and more of the medication,” Dr. Roth said.
The drug is currently under review by the Food and Drug Administration for MOTN awakening.
In a study designed to address possible abuse liability associated with p.r.n. use of the drug, 75 outpatients received zolpidem and 71 patients received placebo; all were assessed for latency to sleep onset after MOTN dosing across a 4-week treatment period. For a check of rebound potential, outcomes also were observed on the first night of nondosing after 1 or more nights of medication use.
The study found no evidence of residual sleepiness after MOTN dosing with zolpidem. Patients who received the drug actually reported greater alertness compared with baseline. On a scale of 1-9 (with 9 being most alert), the mean score was 4.9 at baseline, increasing to 5.7 after zolpidem dosing. Scores in the placebo arm were 4.7 and 5.2, respectively.
Sleep quality also improved significantly. Mean scores were 4.7 at baseline and 5.8 with zolpidem, vs. 4.5 and 5.2, respectively, with placebo.
The study found no evidence for the development of tolerance to zolpidem's efficacy. Latency to sleep onset improved over the first 2 weeks, and apparently stabilized by week 3, for both the active-treatment and placebo groups, suggesting a nonspecific trend toward improvement in outcome over time.
The response to the medication did not change across the entire treatment period, and drug use was not different between treatment and placebo groups. In fact, drug use during week 4bwas significantly lower than during week 1 in both the active and placebo arms.
There was no evidence of rebound effects on sleep initiation or total sleep time on nondosing nights, regardless of the number of nights of continuous use. On average, for nights during which zolpidem was not dosed, total sleep time was similar for the active and placebo groups.
Dr. Roth noted that the improvement over placebo of about 20 minutes is clinically meaningful. “It doesn't sound impressive, but try sleeping 20 minutes less every night for 3 months – you'll be in a coma. The effect is cumulative. It's about 2 hours a week.”
Sublingual zolpidem helped patients get back to sleep, with no evidence of residual sleepiness.
Source ©iStockphoto/redmonkey8
Major Finding: Persons who received a new formulation of low-dose sublingual zolpidem for middle-of-the-night insomnia showed no potential for abuse of the drug in the form of dependency, tolerance, or rebound potential, compared with placebo recipients.
Data Source: A 4-week outpatient study of 146 subjects.
Disclosures: Dr. Roth has served as a consultant to Transept Pharmaceuticals Inc., the manufacturer of the sublingual formulation of zolpidem tartrate. He has also received research support from and had other relationships with numerous pharmaceutical companies.
AMSTERDAM – A sublingual 3.5-mg formulation of zolpidem tartrate is effective for middle-of-the-night insomnia, producing no tolerance, rebound, or increase in use over 4 weeks, investigators reported at the congress.
“Awakening during the night with difficulty falling back to sleep is a prevalent condition, and a p.r.n. treatment for this is needed as it may decrease overall drug exposure,” said the study's coinvestigator, Thomas Roth, Ph.D., of Henry Ford Hospital, Detroit.
Zolpidem sublingual tablets 3.5 mg and 1.75 mg were developed for the treatment of insomnia that is characterized by difficulty returning to sleep after middle-of-the-night (MOTN) awakening. The compound is formulated with binary buffers to promote buccal absorption of a portion of the drug. This facilitates bioavailability, resulting in a rapid return to sleep. Previous studies have found that sublingual zolpidem significantly reduces sleep latency after MOTN dosing. In a sleep laboratory study, sleep latency time was approximately 28 minutes with placebo but just 10 minutes with zolpidem 3.5 mg (Sleep 2008;31:1277-84).
“This is a reduced dose of zolpidem, and importantly it is a sublingual formulation so you achieve much faster blood levels to help you fall back asleep but you reduce the total blood level as compared to taking it prophylactically. The concern is that over time, people take more and more of the medication,” Dr. Roth said.
The drug is currently under review by the Food and Drug Administration for MOTN awakening.
In a study designed to address possible abuse liability associated with p.r.n. use of the drug, 75 outpatients received zolpidem and 71 patients received placebo; all were assessed for latency to sleep onset after MOTN dosing across a 4-week treatment period. For a check of rebound potential, outcomes also were observed on the first night of nondosing after 1 or more nights of medication use.
The study found no evidence of residual sleepiness after MOTN dosing with zolpidem. Patients who received the drug actually reported greater alertness compared with baseline. On a scale of 1-9 (with 9 being most alert), the mean score was 4.9 at baseline, increasing to 5.7 after zolpidem dosing. Scores in the placebo arm were 4.7 and 5.2, respectively.
Sleep quality also improved significantly. Mean scores were 4.7 at baseline and 5.8 with zolpidem, vs. 4.5 and 5.2, respectively, with placebo.
The study found no evidence for the development of tolerance to zolpidem's efficacy. Latency to sleep onset improved over the first 2 weeks, and apparently stabilized by week 3, for both the active-treatment and placebo groups, suggesting a nonspecific trend toward improvement in outcome over time.
The response to the medication did not change across the entire treatment period, and drug use was not different between treatment and placebo groups. In fact, drug use during week 4bwas significantly lower than during week 1 in both the active and placebo arms.
There was no evidence of rebound effects on sleep initiation or total sleep time on nondosing nights, regardless of the number of nights of continuous use. On average, for nights during which zolpidem was not dosed, total sleep time was similar for the active and placebo groups.
Dr. Roth noted that the improvement over placebo of about 20 minutes is clinically meaningful. “It doesn't sound impressive, but try sleeping 20 minutes less every night for 3 months – you'll be in a coma. The effect is cumulative. It's about 2 hours a week.”
Sublingual zolpidem helped patients get back to sleep, with no evidence of residual sleepiness.
Source ©iStockphoto/redmonkey8
Allergen-Specific IgE Linked to Depression
Major Finding: IgE levels predicted worsening of depressive symptoms during high pollen season in patients with recurrent mood disorders.
Data Source: A blinded study of 100 patients.
Disclosures: The National Institute of Mental Health funded the study. The researchers had no relevant financial disclosures to make.
Allergen-specific immunoglobulin E and allergy symptoms are associated with worsening of depression scores in patients with mood disorders who are exposed to seasonal pollen peaks, preliminary results from a novel study suggest.
“We already know that depression is a very common disorder, but allergy is even more common,” Dr. Partam Manalai of the mood and anxiety program in the department of psychiatry at the University of Maryland School of Medicine, Baltimore, said at a press briefing.
“One in every two people might have some kind of sensitivity to some allergen, and one in five people may have allergic rhinitis. During exacerbations of allergic rhinitis, people experience worsening of mood, cognition, and overall well-being.”
Dr. Manalai went on to note that there is a spring peak in pollen count that corresponds with tree pollen, while there is a somewhat smaller fall peak in pollen count, which corresponds with ragweed and grass pollen. At the same time, he said, several previously published studies have found a peak in the rate of completed suicides in the spring, and a somewhat smaller peak in the fall.
“To our knowledge, this is the first report of a biological marker of allergic sensitization (allergen-specific IgE) predicting worsening in depressive symptoms during the high pollen season,” Dr. Manalai said.
“In a group of patients with allergy and depression, prophylactic treatment of these conditions may prevent worsening of mood during peak allergen season. Our findings may be conducive to research on new preventative and therapeutic targets in the management of mood disorders.”
In the study, researchers blinded to the patients' IgE status evaluated 100 patients from Baltimore and Washington, with diagnoses of recurrent mood disorder– once during a low pollen period and once during the preceding or subsequent peak high pollen period.
Patients taking antihistamines and decongestants were included in the analysis, but those with active substance-related or psychotic disorders were excluded, as were those taking montelukast or intranasal corticosteroids.
The researchers administered the Structured Interview Guide for the Hamilton Depression Rating Scale-Seasonal Affective Disorder Version and the Allergy Symptom Severity Assessment and compared the scores during the low and high pollen periods.
As recommended by the National Allergy Bureau, they conducted volumetric sampling for pollen in grains/m
The mean age of patients was 44 years, and 60 were men. Nearly half (47) were IgE positive for tree and/or ragweed pollen, while the rest (53) were IgE negative.
Dr. Manalai reported that changes in typical depression scores were significantly related to worsening of allergy symptoms (P = .008) while changes in atypical depression scores were significantly related to allergy-specific IgE positivity (P = .033), but not to worsening of allergy symptoms.
“The worse the allergy symptoms, the worse the depression scores,” Dr. Manalai said.
Specifically, during low pollen season, the mean SIGH-SAD score for those in the allergen-specific IgE-positive group who had typical depression was 11.77, compared with a mean score of 9.8 for their counterparts in the allergen-specific IgE negative group. The SIGH-SAD score was also higher for those in the allergen-specific IgE-positive group who had atypical depression (a mean of 5.27, compared with a mean of 4.37 for their counterparts in the allergen-specific IgE negative group).
During high pollen season, the mean SIGH-SAD score for those in the allergen-specific IgE-positive group who had typical depression was 11.54, compared with a mean score of 9.76 for their counterparts in the allergen-specific IgE negative group.
The SIGH-SAD score was also higher for those in the allergen-specific IgE-positive group who had atypical depression (a mean of 6.9, compared with 5.13 for their counterparts in the allergen-specific IgE negative group).
In a later interview, lead author Dr. Teodor T. Postolache, who directs the University of Maryland psychiatry department's mood and anxiety program, pointed out that these mean scores “need to be adjusted for C-reactive protein. C-reactive protein changes were used in the models to adjust for and minimize the masking effects of nonallergic inflammation during the duration of the study (such as virus infections, sinus infections, to name a few).”
Major Finding: IgE levels predicted worsening of depressive symptoms during high pollen season in patients with recurrent mood disorders.
Data Source: A blinded study of 100 patients.
Disclosures: The National Institute of Mental Health funded the study. The researchers had no relevant financial disclosures to make.
Allergen-specific immunoglobulin E and allergy symptoms are associated with worsening of depression scores in patients with mood disorders who are exposed to seasonal pollen peaks, preliminary results from a novel study suggest.
“We already know that depression is a very common disorder, but allergy is even more common,” Dr. Partam Manalai of the mood and anxiety program in the department of psychiatry at the University of Maryland School of Medicine, Baltimore, said at a press briefing.
“One in every two people might have some kind of sensitivity to some allergen, and one in five people may have allergic rhinitis. During exacerbations of allergic rhinitis, people experience worsening of mood, cognition, and overall well-being.”
Dr. Manalai went on to note that there is a spring peak in pollen count that corresponds with tree pollen, while there is a somewhat smaller fall peak in pollen count, which corresponds with ragweed and grass pollen. At the same time, he said, several previously published studies have found a peak in the rate of completed suicides in the spring, and a somewhat smaller peak in the fall.
“To our knowledge, this is the first report of a biological marker of allergic sensitization (allergen-specific IgE) predicting worsening in depressive symptoms during the high pollen season,” Dr. Manalai said.
“In a group of patients with allergy and depression, prophylactic treatment of these conditions may prevent worsening of mood during peak allergen season. Our findings may be conducive to research on new preventative and therapeutic targets in the management of mood disorders.”
In the study, researchers blinded to the patients' IgE status evaluated 100 patients from Baltimore and Washington, with diagnoses of recurrent mood disorder– once during a low pollen period and once during the preceding or subsequent peak high pollen period.
Patients taking antihistamines and decongestants were included in the analysis, but those with active substance-related or psychotic disorders were excluded, as were those taking montelukast or intranasal corticosteroids.
The researchers administered the Structured Interview Guide for the Hamilton Depression Rating Scale-Seasonal Affective Disorder Version and the Allergy Symptom Severity Assessment and compared the scores during the low and high pollen periods.
As recommended by the National Allergy Bureau, they conducted volumetric sampling for pollen in grains/m
The mean age of patients was 44 years, and 60 were men. Nearly half (47) were IgE positive for tree and/or ragweed pollen, while the rest (53) were IgE negative.
Dr. Manalai reported that changes in typical depression scores were significantly related to worsening of allergy symptoms (P = .008) while changes in atypical depression scores were significantly related to allergy-specific IgE positivity (P = .033), but not to worsening of allergy symptoms.
“The worse the allergy symptoms, the worse the depression scores,” Dr. Manalai said.
Specifically, during low pollen season, the mean SIGH-SAD score for those in the allergen-specific IgE-positive group who had typical depression was 11.77, compared with a mean score of 9.8 for their counterparts in the allergen-specific IgE negative group. The SIGH-SAD score was also higher for those in the allergen-specific IgE-positive group who had atypical depression (a mean of 5.27, compared with a mean of 4.37 for their counterparts in the allergen-specific IgE negative group).
During high pollen season, the mean SIGH-SAD score for those in the allergen-specific IgE-positive group who had typical depression was 11.54, compared with a mean score of 9.76 for their counterparts in the allergen-specific IgE negative group.
The SIGH-SAD score was also higher for those in the allergen-specific IgE-positive group who had atypical depression (a mean of 6.9, compared with 5.13 for their counterparts in the allergen-specific IgE negative group).
In a later interview, lead author Dr. Teodor T. Postolache, who directs the University of Maryland psychiatry department's mood and anxiety program, pointed out that these mean scores “need to be adjusted for C-reactive protein. C-reactive protein changes were used in the models to adjust for and minimize the masking effects of nonallergic inflammation during the duration of the study (such as virus infections, sinus infections, to name a few).”
Major Finding: IgE levels predicted worsening of depressive symptoms during high pollen season in patients with recurrent mood disorders.
Data Source: A blinded study of 100 patients.
Disclosures: The National Institute of Mental Health funded the study. The researchers had no relevant financial disclosures to make.
Allergen-specific immunoglobulin E and allergy symptoms are associated with worsening of depression scores in patients with mood disorders who are exposed to seasonal pollen peaks, preliminary results from a novel study suggest.
“We already know that depression is a very common disorder, but allergy is even more common,” Dr. Partam Manalai of the mood and anxiety program in the department of psychiatry at the University of Maryland School of Medicine, Baltimore, said at a press briefing.
“One in every two people might have some kind of sensitivity to some allergen, and one in five people may have allergic rhinitis. During exacerbations of allergic rhinitis, people experience worsening of mood, cognition, and overall well-being.”
Dr. Manalai went on to note that there is a spring peak in pollen count that corresponds with tree pollen, while there is a somewhat smaller fall peak in pollen count, which corresponds with ragweed and grass pollen. At the same time, he said, several previously published studies have found a peak in the rate of completed suicides in the spring, and a somewhat smaller peak in the fall.
“To our knowledge, this is the first report of a biological marker of allergic sensitization (allergen-specific IgE) predicting worsening in depressive symptoms during the high pollen season,” Dr. Manalai said.
“In a group of patients with allergy and depression, prophylactic treatment of these conditions may prevent worsening of mood during peak allergen season. Our findings may be conducive to research on new preventative and therapeutic targets in the management of mood disorders.”
In the study, researchers blinded to the patients' IgE status evaluated 100 patients from Baltimore and Washington, with diagnoses of recurrent mood disorder– once during a low pollen period and once during the preceding or subsequent peak high pollen period.
Patients taking antihistamines and decongestants were included in the analysis, but those with active substance-related or psychotic disorders were excluded, as were those taking montelukast or intranasal corticosteroids.
The researchers administered the Structured Interview Guide for the Hamilton Depression Rating Scale-Seasonal Affective Disorder Version and the Allergy Symptom Severity Assessment and compared the scores during the low and high pollen periods.
As recommended by the National Allergy Bureau, they conducted volumetric sampling for pollen in grains/m
The mean age of patients was 44 years, and 60 were men. Nearly half (47) were IgE positive for tree and/or ragweed pollen, while the rest (53) were IgE negative.
Dr. Manalai reported that changes in typical depression scores were significantly related to worsening of allergy symptoms (P = .008) while changes in atypical depression scores were significantly related to allergy-specific IgE positivity (P = .033), but not to worsening of allergy symptoms.
“The worse the allergy symptoms, the worse the depression scores,” Dr. Manalai said.
Specifically, during low pollen season, the mean SIGH-SAD score for those in the allergen-specific IgE-positive group who had typical depression was 11.77, compared with a mean score of 9.8 for their counterparts in the allergen-specific IgE negative group. The SIGH-SAD score was also higher for those in the allergen-specific IgE-positive group who had atypical depression (a mean of 5.27, compared with a mean of 4.37 for their counterparts in the allergen-specific IgE negative group).
During high pollen season, the mean SIGH-SAD score for those in the allergen-specific IgE-positive group who had typical depression was 11.54, compared with a mean score of 9.76 for their counterparts in the allergen-specific IgE negative group.
The SIGH-SAD score was also higher for those in the allergen-specific IgE-positive group who had atypical depression (a mean of 6.9, compared with 5.13 for their counterparts in the allergen-specific IgE negative group).
In a later interview, lead author Dr. Teodor T. Postolache, who directs the University of Maryland psychiatry department's mood and anxiety program, pointed out that these mean scores “need to be adjusted for C-reactive protein. C-reactive protein changes were used in the models to adjust for and minimize the masking effects of nonallergic inflammation during the duration of the study (such as virus infections, sinus infections, to name a few).”
Aneurysmal Coiling Often Leads to Acute Headache
Major Finding: Postprocedural headaches occurred in 72% of patients who underwent intracranial endovascular aneurysmal coiling.
Data Source: A retrospective chart review of 263 patients who underwent intracranial endovascular aneurysmal coiling.
Disclosures: Dr. Baron had no relevant disclosures.
CARLSBAD, CALIF. – Nearly three quarters of patients had an acute headache after endovascular coiling of cerebral aneurysms in a review of a 3-year period at a single center.
The postprocedural headaches occurred significantly more often in women, smokers, and patients with a preprocedural history of headache or anxiety and depression, according to Dr. Eric P. Baron.
“Optimized risk-factor management prior to coiling may help decrease the occurrence of postcoiling headache.
“The presence of these risk factors may also help predict those more likely to complain of postcoiling headache and help guide clinical decisions of neuroimaging or other testing.
However, good clinical judgment should always supersede in these decisions,” said Dr. Baron, a neurologist who is affiliated with the Center for Headache and Pain at the Cleveland Clinic Neurological Institute.
Although urgent diagnostic procedures to evaluate postcoiling headaches proved unhelpful, Dr. Baron and his colleagues found that triptans or dihydroergotamine (DHE) safely treated both pre- and postcoiling headaches in a small group of migraineurs.
Headache was also common in aneurysm patients before coiling, both for those who underwent emergent and elective coiling. Coiling resolved headaches in a small proportion of these patients, he noted.
“Triptans and DHE may not necessarily be a contraindication in all migraineurs with pre- and postcoiling headache, and aneurysmal coiling may actually resolve preexisting headaches in a select group of patients, but at this time, predicting that group of patients is unclear.
“Ultimately, further prospective studies are necessary to better evaluate all of these trends,” Dr. Baron said.
The investigators reviewed the records of 263 adult patients (200 women and 63 men) who underwent either emergent or elective intracranial endovascular coiling for aneurysm treatment between July 2006 and June 2009.
Patients with skull defects, ventricular shunt placement, cranial trauma, extracranial procedures, and intracranial neoplasms or infections were excluded.
Most (76%) of the aneurysms were located in the anterior circulation; 24% were in the posterior circulation. A headache developed following coiling in 189 (72%) patients.
A significantly greater percentage of patients with headaches were women (81%).
More women overall also developed postcoiling headache than did men (77% vs. 57%).
Smoking was a significant risk factor for postprocedural headache. A majority of patients (56%) with postcoiling headaches were smokers, and 85% of all smokers developed postcoiling headache.
The incidence of postcoiling headache was higher in women who smoked than it was in men who smoked (90% vs. 70%, respectively).
Postcoiling headaches also affected 86% of patients with either anxiety or depression.
Postprocedural headaches were significantly more likely to occur among patients who experienced headaches prior to undergoing endovascular coiling, regardless of the length of time they had had them, the review found.
Headache complaints spurred 118 urgent diagnostic procedures, including 69 noncontrast CTs, 7 CT angiograms, 29 MR scans (including angiography and venography), 5 cerebral angiograms, and 8 lumbar punctures. All were negative for an acute process that was felt to be the cause of the headache.
“Excessive diagnostic testing is often obtained in patients with prior intracranial endovascular coiling. Results are frequently low yield and may lead to unnecessary risks and costs,” Dr. Baron said.
Pre- and postcoiled aneurysms often are considered a contraindication for the use of triptans or ergots such as DHE to treat headaches in migraineurs, according to Dr. Baron. But in this cohort, triptans were used without incident in 10 cases before coiling and in 10 cases after coiling; DHE was used for one patient after coiling.
Headaches resolved after coiling in a small proportion of patients, including 27% of patients who underwent emergency coiling, 16% of patients who had headaches for less than 1 year before elective coiling, and 11% of patients who had headaches for 1 year or longer before elective coiling.
Major Finding: Postprocedural headaches occurred in 72% of patients who underwent intracranial endovascular aneurysmal coiling.
Data Source: A retrospective chart review of 263 patients who underwent intracranial endovascular aneurysmal coiling.
Disclosures: Dr. Baron had no relevant disclosures.
CARLSBAD, CALIF. – Nearly three quarters of patients had an acute headache after endovascular coiling of cerebral aneurysms in a review of a 3-year period at a single center.
The postprocedural headaches occurred significantly more often in women, smokers, and patients with a preprocedural history of headache or anxiety and depression, according to Dr. Eric P. Baron.
“Optimized risk-factor management prior to coiling may help decrease the occurrence of postcoiling headache.
“The presence of these risk factors may also help predict those more likely to complain of postcoiling headache and help guide clinical decisions of neuroimaging or other testing.
However, good clinical judgment should always supersede in these decisions,” said Dr. Baron, a neurologist who is affiliated with the Center for Headache and Pain at the Cleveland Clinic Neurological Institute.
Although urgent diagnostic procedures to evaluate postcoiling headaches proved unhelpful, Dr. Baron and his colleagues found that triptans or dihydroergotamine (DHE) safely treated both pre- and postcoiling headaches in a small group of migraineurs.
Headache was also common in aneurysm patients before coiling, both for those who underwent emergent and elective coiling. Coiling resolved headaches in a small proportion of these patients, he noted.
“Triptans and DHE may not necessarily be a contraindication in all migraineurs with pre- and postcoiling headache, and aneurysmal coiling may actually resolve preexisting headaches in a select group of patients, but at this time, predicting that group of patients is unclear.
“Ultimately, further prospective studies are necessary to better evaluate all of these trends,” Dr. Baron said.
The investigators reviewed the records of 263 adult patients (200 women and 63 men) who underwent either emergent or elective intracranial endovascular coiling for aneurysm treatment between July 2006 and June 2009.
Patients with skull defects, ventricular shunt placement, cranial trauma, extracranial procedures, and intracranial neoplasms or infections were excluded.
Most (76%) of the aneurysms were located in the anterior circulation; 24% were in the posterior circulation. A headache developed following coiling in 189 (72%) patients.
A significantly greater percentage of patients with headaches were women (81%).
More women overall also developed postcoiling headache than did men (77% vs. 57%).
Smoking was a significant risk factor for postprocedural headache. A majority of patients (56%) with postcoiling headaches were smokers, and 85% of all smokers developed postcoiling headache.
The incidence of postcoiling headache was higher in women who smoked than it was in men who smoked (90% vs. 70%, respectively).
Postcoiling headaches also affected 86% of patients with either anxiety or depression.
Postprocedural headaches were significantly more likely to occur among patients who experienced headaches prior to undergoing endovascular coiling, regardless of the length of time they had had them, the review found.
Headache complaints spurred 118 urgent diagnostic procedures, including 69 noncontrast CTs, 7 CT angiograms, 29 MR scans (including angiography and venography), 5 cerebral angiograms, and 8 lumbar punctures. All were negative for an acute process that was felt to be the cause of the headache.
“Excessive diagnostic testing is often obtained in patients with prior intracranial endovascular coiling. Results are frequently low yield and may lead to unnecessary risks and costs,” Dr. Baron said.
Pre- and postcoiled aneurysms often are considered a contraindication for the use of triptans or ergots such as DHE to treat headaches in migraineurs, according to Dr. Baron. But in this cohort, triptans were used without incident in 10 cases before coiling and in 10 cases after coiling; DHE was used for one patient after coiling.
Headaches resolved after coiling in a small proportion of patients, including 27% of patients who underwent emergency coiling, 16% of patients who had headaches for less than 1 year before elective coiling, and 11% of patients who had headaches for 1 year or longer before elective coiling.
Major Finding: Postprocedural headaches occurred in 72% of patients who underwent intracranial endovascular aneurysmal coiling.
Data Source: A retrospective chart review of 263 patients who underwent intracranial endovascular aneurysmal coiling.
Disclosures: Dr. Baron had no relevant disclosures.
CARLSBAD, CALIF. – Nearly three quarters of patients had an acute headache after endovascular coiling of cerebral aneurysms in a review of a 3-year period at a single center.
The postprocedural headaches occurred significantly more often in women, smokers, and patients with a preprocedural history of headache or anxiety and depression, according to Dr. Eric P. Baron.
“Optimized risk-factor management prior to coiling may help decrease the occurrence of postcoiling headache.
“The presence of these risk factors may also help predict those more likely to complain of postcoiling headache and help guide clinical decisions of neuroimaging or other testing.
However, good clinical judgment should always supersede in these decisions,” said Dr. Baron, a neurologist who is affiliated with the Center for Headache and Pain at the Cleveland Clinic Neurological Institute.
Although urgent diagnostic procedures to evaluate postcoiling headaches proved unhelpful, Dr. Baron and his colleagues found that triptans or dihydroergotamine (DHE) safely treated both pre- and postcoiling headaches in a small group of migraineurs.
Headache was also common in aneurysm patients before coiling, both for those who underwent emergent and elective coiling. Coiling resolved headaches in a small proportion of these patients, he noted.
“Triptans and DHE may not necessarily be a contraindication in all migraineurs with pre- and postcoiling headache, and aneurysmal coiling may actually resolve preexisting headaches in a select group of patients, but at this time, predicting that group of patients is unclear.
“Ultimately, further prospective studies are necessary to better evaluate all of these trends,” Dr. Baron said.
The investigators reviewed the records of 263 adult patients (200 women and 63 men) who underwent either emergent or elective intracranial endovascular coiling for aneurysm treatment between July 2006 and June 2009.
Patients with skull defects, ventricular shunt placement, cranial trauma, extracranial procedures, and intracranial neoplasms or infections were excluded.
Most (76%) of the aneurysms were located in the anterior circulation; 24% were in the posterior circulation. A headache developed following coiling in 189 (72%) patients.
A significantly greater percentage of patients with headaches were women (81%).
More women overall also developed postcoiling headache than did men (77% vs. 57%).
Smoking was a significant risk factor for postprocedural headache. A majority of patients (56%) with postcoiling headaches were smokers, and 85% of all smokers developed postcoiling headache.
The incidence of postcoiling headache was higher in women who smoked than it was in men who smoked (90% vs. 70%, respectively).
Postcoiling headaches also affected 86% of patients with either anxiety or depression.
Postprocedural headaches were significantly more likely to occur among patients who experienced headaches prior to undergoing endovascular coiling, regardless of the length of time they had had them, the review found.
Headache complaints spurred 118 urgent diagnostic procedures, including 69 noncontrast CTs, 7 CT angiograms, 29 MR scans (including angiography and venography), 5 cerebral angiograms, and 8 lumbar punctures. All were negative for an acute process that was felt to be the cause of the headache.
“Excessive diagnostic testing is often obtained in patients with prior intracranial endovascular coiling. Results are frequently low yield and may lead to unnecessary risks and costs,” Dr. Baron said.
Pre- and postcoiled aneurysms often are considered a contraindication for the use of triptans or ergots such as DHE to treat headaches in migraineurs, according to Dr. Baron. But in this cohort, triptans were used without incident in 10 cases before coiling and in 10 cases after coiling; DHE was used for one patient after coiling.
Headaches resolved after coiling in a small proportion of patients, including 27% of patients who underwent emergency coiling, 16% of patients who had headaches for less than 1 year before elective coiling, and 11% of patients who had headaches for 1 year or longer before elective coiling.