Ischemia Algorithm Could Reduce the Need for Stress Tests

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SAN FRANCISCO — In some patients being evaluated for chest pain, stress tests might be avoided through the use of an algorithm designed to predict the probability of cardiac ischemia, David D. Moyer-Diener and his associates said at the annual meeting of the American College of Emergency Physicians.

In a prospective, observational cohort study of consecutive patients evaluated at a chest pain center, investigators obtained Acute Coronary Ischemia-Time Insensitive Predictive Instrument (ACI-TIPI) scores and conventional chest pain work-ups on 1,478 low- or intermediate-risk patients for whom acute myocardial ischemia had been ruled out. The treating physicians were blinded to the ACI-TIPI scores, and patients underwent conventional evaluations including serial enzyme tests and provocative cardiac testing.

Among 400 patients who had ACI-TIPI scores of 20 or less, 265 were men younger than age 35 years or women younger than age 45 years, and 217 underwent provocative cardiac testing. None of the 265 patients developed an acute coronary syndrome within 30 days, as determined by phone calls to patients and reviews of records and the Social Security Death Index.

If clinicians had used an ACI-TIPI score of 20 or less in these subsets of young patients to exclude provocative cardiac testing and had sent these patients home, 15% of all stress tests in the study cohort could have been avoided without causing any harm, said Mr. Moyer-Diener, a medical student at the University of Michigan, Ann Arbor, who conducted the study with Michael G. Mikhail, M.D., and associates at the university.

At the meeting, physicians on a separate panel discussing cutting-edge research both praised and criticized the study.

“There's been a lot of debate about just how useful” an ACI-TIPI score is, said Charles V. Pollack Jr., M.D., chair of emergency medicine at Pennsylvania Hospital, Philadelphia. Many emergency physicians would rather not have a quantitative number related to the risk of ischemia on a patient's chart, he said, because if the case sparks a lawsuit, they would rather defend their clinical impression that the patient didn't have ischemia.

The ACI-TIPI was designed to predict the probability of cardiac ischemia on a 0− to 100-point scale, to serve as support or a “second opinion” in clinical decision making. The way ACI-TIPI was used in the study to identify patients who don't need further tests “is not really the use for which it was designed,” but the idea is intriguing, Dr. Pollack said.

Jerome R. Hoffman, M.D., lauded the investigators for trying to identify a strategy to cut down on the many unnecessary tests performed for chest pain evaluation that are not backed by evidence-based medicine. “It's very hard to get us out of that rut,” said Dr. Hoffman, professor of emergency medicine at the University of California, Los Angeles.

In practical terms, however, physicians are unlikely to adopt these criteria for avoiding stress tests. An ACI-TIPI score of 20 or less is associated with a 19% risk of acute myocardial ischemia, Dr. Hoffman explained. For medicolegal reasons, physicians will not feel comfortable sending patients home if that number appears on a patient's chart.

“That, more than anything, makes me question the value of an ACI-TIPI— other than as a research tool,” Dr. Hoffman said.

Previous studies have shown that physicians were from two to three times more likely to admit patients if given an ACI-TIPI score to include in the patient's chart, said Ian G. Stiell, M.D., of the University of Ottawa. On the other hand, it's “refreshing” to hear skepticism about widespread use in the United States of stress tests, chest pain units, and prolonged cardiac monitoring, he added.

Dr. Pollack noted that the current study claimed to exclude patients with acute myocardial ischemia. “I think that's a dangerous statement,” he said, “because ordinarily that is done in a chest pain center by measuring serial troponin levels, which excludes only necrosis. It doesn't exclude ischemia.”

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SAN FRANCISCO — In some patients being evaluated for chest pain, stress tests might be avoided through the use of an algorithm designed to predict the probability of cardiac ischemia, David D. Moyer-Diener and his associates said at the annual meeting of the American College of Emergency Physicians.

In a prospective, observational cohort study of consecutive patients evaluated at a chest pain center, investigators obtained Acute Coronary Ischemia-Time Insensitive Predictive Instrument (ACI-TIPI) scores and conventional chest pain work-ups on 1,478 low- or intermediate-risk patients for whom acute myocardial ischemia had been ruled out. The treating physicians were blinded to the ACI-TIPI scores, and patients underwent conventional evaluations including serial enzyme tests and provocative cardiac testing.

Among 400 patients who had ACI-TIPI scores of 20 or less, 265 were men younger than age 35 years or women younger than age 45 years, and 217 underwent provocative cardiac testing. None of the 265 patients developed an acute coronary syndrome within 30 days, as determined by phone calls to patients and reviews of records and the Social Security Death Index.

If clinicians had used an ACI-TIPI score of 20 or less in these subsets of young patients to exclude provocative cardiac testing and had sent these patients home, 15% of all stress tests in the study cohort could have been avoided without causing any harm, said Mr. Moyer-Diener, a medical student at the University of Michigan, Ann Arbor, who conducted the study with Michael G. Mikhail, M.D., and associates at the university.

At the meeting, physicians on a separate panel discussing cutting-edge research both praised and criticized the study.

“There's been a lot of debate about just how useful” an ACI-TIPI score is, said Charles V. Pollack Jr., M.D., chair of emergency medicine at Pennsylvania Hospital, Philadelphia. Many emergency physicians would rather not have a quantitative number related to the risk of ischemia on a patient's chart, he said, because if the case sparks a lawsuit, they would rather defend their clinical impression that the patient didn't have ischemia.

The ACI-TIPI was designed to predict the probability of cardiac ischemia on a 0− to 100-point scale, to serve as support or a “second opinion” in clinical decision making. The way ACI-TIPI was used in the study to identify patients who don't need further tests “is not really the use for which it was designed,” but the idea is intriguing, Dr. Pollack said.

Jerome R. Hoffman, M.D., lauded the investigators for trying to identify a strategy to cut down on the many unnecessary tests performed for chest pain evaluation that are not backed by evidence-based medicine. “It's very hard to get us out of that rut,” said Dr. Hoffman, professor of emergency medicine at the University of California, Los Angeles.

In practical terms, however, physicians are unlikely to adopt these criteria for avoiding stress tests. An ACI-TIPI score of 20 or less is associated with a 19% risk of acute myocardial ischemia, Dr. Hoffman explained. For medicolegal reasons, physicians will not feel comfortable sending patients home if that number appears on a patient's chart.

“That, more than anything, makes me question the value of an ACI-TIPI— other than as a research tool,” Dr. Hoffman said.

Previous studies have shown that physicians were from two to three times more likely to admit patients if given an ACI-TIPI score to include in the patient's chart, said Ian G. Stiell, M.D., of the University of Ottawa. On the other hand, it's “refreshing” to hear skepticism about widespread use in the United States of stress tests, chest pain units, and prolonged cardiac monitoring, he added.

Dr. Pollack noted that the current study claimed to exclude patients with acute myocardial ischemia. “I think that's a dangerous statement,” he said, “because ordinarily that is done in a chest pain center by measuring serial troponin levels, which excludes only necrosis. It doesn't exclude ischemia.”

SAN FRANCISCO — In some patients being evaluated for chest pain, stress tests might be avoided through the use of an algorithm designed to predict the probability of cardiac ischemia, David D. Moyer-Diener and his associates said at the annual meeting of the American College of Emergency Physicians.

In a prospective, observational cohort study of consecutive patients evaluated at a chest pain center, investigators obtained Acute Coronary Ischemia-Time Insensitive Predictive Instrument (ACI-TIPI) scores and conventional chest pain work-ups on 1,478 low- or intermediate-risk patients for whom acute myocardial ischemia had been ruled out. The treating physicians were blinded to the ACI-TIPI scores, and patients underwent conventional evaluations including serial enzyme tests and provocative cardiac testing.

Among 400 patients who had ACI-TIPI scores of 20 or less, 265 were men younger than age 35 years or women younger than age 45 years, and 217 underwent provocative cardiac testing. None of the 265 patients developed an acute coronary syndrome within 30 days, as determined by phone calls to patients and reviews of records and the Social Security Death Index.

If clinicians had used an ACI-TIPI score of 20 or less in these subsets of young patients to exclude provocative cardiac testing and had sent these patients home, 15% of all stress tests in the study cohort could have been avoided without causing any harm, said Mr. Moyer-Diener, a medical student at the University of Michigan, Ann Arbor, who conducted the study with Michael G. Mikhail, M.D., and associates at the university.

At the meeting, physicians on a separate panel discussing cutting-edge research both praised and criticized the study.

“There's been a lot of debate about just how useful” an ACI-TIPI score is, said Charles V. Pollack Jr., M.D., chair of emergency medicine at Pennsylvania Hospital, Philadelphia. Many emergency physicians would rather not have a quantitative number related to the risk of ischemia on a patient's chart, he said, because if the case sparks a lawsuit, they would rather defend their clinical impression that the patient didn't have ischemia.

The ACI-TIPI was designed to predict the probability of cardiac ischemia on a 0− to 100-point scale, to serve as support or a “second opinion” in clinical decision making. The way ACI-TIPI was used in the study to identify patients who don't need further tests “is not really the use for which it was designed,” but the idea is intriguing, Dr. Pollack said.

Jerome R. Hoffman, M.D., lauded the investigators for trying to identify a strategy to cut down on the many unnecessary tests performed for chest pain evaluation that are not backed by evidence-based medicine. “It's very hard to get us out of that rut,” said Dr. Hoffman, professor of emergency medicine at the University of California, Los Angeles.

In practical terms, however, physicians are unlikely to adopt these criteria for avoiding stress tests. An ACI-TIPI score of 20 or less is associated with a 19% risk of acute myocardial ischemia, Dr. Hoffman explained. For medicolegal reasons, physicians will not feel comfortable sending patients home if that number appears on a patient's chart.

“That, more than anything, makes me question the value of an ACI-TIPI— other than as a research tool,” Dr. Hoffman said.

Previous studies have shown that physicians were from two to three times more likely to admit patients if given an ACI-TIPI score to include in the patient's chart, said Ian G. Stiell, M.D., of the University of Ottawa. On the other hand, it's “refreshing” to hear skepticism about widespread use in the United States of stress tests, chest pain units, and prolonged cardiac monitoring, he added.

Dr. Pollack noted that the current study claimed to exclude patients with acute myocardial ischemia. “I think that's a dangerous statement,” he said, “because ordinarily that is done in a chest pain center by measuring serial troponin levels, which excludes only necrosis. It doesn't exclude ischemia.”

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2004 in Review

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The revelation in September that the popular arthritis drug rofecoxib (Vioxx) more than doubles the risk of myocardial infarction led to its withdrawal by Merck and to a reevaluation of the safety of other cyclooxygenase-2 inhibitors. In the aftermath, many have questioned why the Food and Drug Administration and Merck had not paid more attention to earlier results that also raised safety concerns.

Regardless of the conclusions reached by the various investigators, “More safety experience is going to be required, and there may be more cautionary labels not for what has been seen but for what is not known.

“The issues brought forth by Vioxx will ultimately drip down to almost everything we do. But we mustn't overlook the fact that a huge number of patients have taken the drug and been exposed to increased risk,” Barry Massie, M.D., chief of cardiology at the Veterans Affairs Medical Center, San Francisco, told CARDIOLOGY NEWS.

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The revelation in September that the popular arthritis drug rofecoxib (Vioxx) more than doubles the risk of myocardial infarction led to its withdrawal by Merck and to a reevaluation of the safety of other cyclooxygenase-2 inhibitors. In the aftermath, many have questioned why the Food and Drug Administration and Merck had not paid more attention to earlier results that also raised safety concerns.

Regardless of the conclusions reached by the various investigators, “More safety experience is going to be required, and there may be more cautionary labels not for what has been seen but for what is not known.

“The issues brought forth by Vioxx will ultimately drip down to almost everything we do. But we mustn't overlook the fact that a huge number of patients have taken the drug and been exposed to increased risk,” Barry Massie, M.D., chief of cardiology at the Veterans Affairs Medical Center, San Francisco, told CARDIOLOGY NEWS.

The revelation in September that the popular arthritis drug rofecoxib (Vioxx) more than doubles the risk of myocardial infarction led to its withdrawal by Merck and to a reevaluation of the safety of other cyclooxygenase-2 inhibitors. In the aftermath, many have questioned why the Food and Drug Administration and Merck had not paid more attention to earlier results that also raised safety concerns.

Regardless of the conclusions reached by the various investigators, “More safety experience is going to be required, and there may be more cautionary labels not for what has been seen but for what is not known.

“The issues brought forth by Vioxx will ultimately drip down to almost everything we do. But we mustn't overlook the fact that a huge number of patients have taken the drug and been exposed to increased risk,” Barry Massie, M.D., chief of cardiology at the Veterans Affairs Medical Center, San Francisco, told CARDIOLOGY NEWS.

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Low-Molecular-Weight Heparin Aids in Acute MI : Reviparin's protective effects extended to 30 days from the start of treatment in the multinational study.

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Low-Molecular-Weight Heparin Aids in Acute MI : Reviparin's protective effects extended to 30 days from the start of treatment in the multinational study.

NEW ORLEANS — Antithrombotic treatment, in the form of the low-molecular-weight heparin reviparin, has been shown for the first time to safely improve the outcomes of patients with an acute MI.

“Although heparin is often routinely used to treat patients with an acute myocardial infarction, the incremental benefit from heparin or newer antithrombotics has been poorly defined,” Jeffrey L. Anderson, M.D., said at the annual scientific sessions of the American Heart Association.

The new findings show that reviparin “clearly improves the outcomes of patients who undergo thrombolysis with streptokinase or urokinase,” said Dr. Anderson, associate chief of the division of cardiology at LDS Hospital in Salt Lake City.

But the value of adding reviparin or a similar agent remains in doubt when patients are treated with the fibrin-specific drugs most often used for thrombolysis in the United States, such as alteplase (tissue plasminogen activator), reteplase, and tenecteplase. That's because this new trial, conducted in India, China, Pakistan, and several South American countries and involving 15,570 patients, included only about 100 patients treated with a fibrin-specific thrombolytic drug. Close to 80% of the patients received acute treatment to clear their coronary thrombus, but this treatment was primarily streptokinase in about 50% of patients, urokinase in about 23% of patients, and primary percutaneous intervention in about 6% of patients.

Despite this limitation, the results showed that “reviparin is a simple, inexpensive therapy that is globally applicable for treating acute myocardial infarction,” said Salim Yusuf, D.Phil., director of the division of cardiology at McMaster University in Hamilton, Canada, and lead investigator for the study.

Reviparin is marketed by Abbott Pharmaceuticals under the name Clivarine in several countries in Europe and Asia, but is not approved for U.S. use. Abbott provided the reviparin, but otherwise, the study had no commercial funding.

The study enrolled patients with ST-segment-elevation MI or new bundle branch block who presented within 12 hours of symptom onset. All patients were to be treated with aspirin, and they could also be treated with a regimen designed to produce reperfusion in their blocked coronary arteries. The average age of the patients was 59 years, and the average time from symptom onset to treatment was 4.8 hours, with 61% of patients treated within 6 hours. Aspirin was used on 97% of patients, 72% received an ACE inhibitor, 66% received a lipid-lowering drug, 60% received a β-blocker, and 55% received a thienopyridine, most commonly clopidogrel.

Patients were randomized to treatment with reviparin or placebo by subcutaneous injection b.i.d for 7 days; 76% of patients received the full 7-day course.

The study's primary end point was the incidence of death, repeat MI, or stroke during the 7 days of treatment. The rate of these outcomes was 11.0% in the placebo group and 9.6% in the reviparin group—a statistically significant relative reduction of 13%, Dr. Yusuf reported. Patients treated with reviparin also had a 13% relative reduction in the study's secondary end point, which included death, repeat MI, stroke, or ischemic ECG changes. Treatment with reviparin was also associated with a significant 11% relative reduction in death alone.

The protective effect from reviparin treatment extended to 30 days after the start of treatment. At that time, the rate of death, repeat MI, or stroke was 13.6% in the placebo group and 11.8% in the reviparin group, again a statistically significant 13% relative reduction. These results showed that “stopping therapy after 7 days was not associated with any rebound,” Dr. Yusuf said.

Like all antithrombotic drugs, reviparin boosted the rate of bleeding events. The rate of life-threatening or major bleeds not included in the primary outcomes after 7 days of treatment was 0.1% in the placebo group, compared with 0.2% in the reviparin group. The increased risk of important bleeding events was small, compared with the overall benefit, he noted.

Another noteworthy finding was that the faster treatment with reviparin started the greater the benefit. Patients who started treatment within 2 hours of symptom onset had a 30% relative drop in the primary end point. This relative benefit fell to 20% when treatment began 2–4 hours and to 15% when treatment began within 4–8 hours. The benefit completely disappeared when treatment was delayed beyond 8 hours.

An inevitable question is whether treatment with the low-molecular-weight heparins approved for use in the United States would confer the same benefits. “It's a tricky issue, because low-molecular-weight heparins are very heterogeneous compounds. You need to know the exact dosage to use.” Dr. Yusuf said.

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NEW ORLEANS — Antithrombotic treatment, in the form of the low-molecular-weight heparin reviparin, has been shown for the first time to safely improve the outcomes of patients with an acute MI.

“Although heparin is often routinely used to treat patients with an acute myocardial infarction, the incremental benefit from heparin or newer antithrombotics has been poorly defined,” Jeffrey L. Anderson, M.D., said at the annual scientific sessions of the American Heart Association.

The new findings show that reviparin “clearly improves the outcomes of patients who undergo thrombolysis with streptokinase or urokinase,” said Dr. Anderson, associate chief of the division of cardiology at LDS Hospital in Salt Lake City.

But the value of adding reviparin or a similar agent remains in doubt when patients are treated with the fibrin-specific drugs most often used for thrombolysis in the United States, such as alteplase (tissue plasminogen activator), reteplase, and tenecteplase. That's because this new trial, conducted in India, China, Pakistan, and several South American countries and involving 15,570 patients, included only about 100 patients treated with a fibrin-specific thrombolytic drug. Close to 80% of the patients received acute treatment to clear their coronary thrombus, but this treatment was primarily streptokinase in about 50% of patients, urokinase in about 23% of patients, and primary percutaneous intervention in about 6% of patients.

Despite this limitation, the results showed that “reviparin is a simple, inexpensive therapy that is globally applicable for treating acute myocardial infarction,” said Salim Yusuf, D.Phil., director of the division of cardiology at McMaster University in Hamilton, Canada, and lead investigator for the study.

Reviparin is marketed by Abbott Pharmaceuticals under the name Clivarine in several countries in Europe and Asia, but is not approved for U.S. use. Abbott provided the reviparin, but otherwise, the study had no commercial funding.

The study enrolled patients with ST-segment-elevation MI or new bundle branch block who presented within 12 hours of symptom onset. All patients were to be treated with aspirin, and they could also be treated with a regimen designed to produce reperfusion in their blocked coronary arteries. The average age of the patients was 59 years, and the average time from symptom onset to treatment was 4.8 hours, with 61% of patients treated within 6 hours. Aspirin was used on 97% of patients, 72% received an ACE inhibitor, 66% received a lipid-lowering drug, 60% received a β-blocker, and 55% received a thienopyridine, most commonly clopidogrel.

Patients were randomized to treatment with reviparin or placebo by subcutaneous injection b.i.d for 7 days; 76% of patients received the full 7-day course.

The study's primary end point was the incidence of death, repeat MI, or stroke during the 7 days of treatment. The rate of these outcomes was 11.0% in the placebo group and 9.6% in the reviparin group—a statistically significant relative reduction of 13%, Dr. Yusuf reported. Patients treated with reviparin also had a 13% relative reduction in the study's secondary end point, which included death, repeat MI, stroke, or ischemic ECG changes. Treatment with reviparin was also associated with a significant 11% relative reduction in death alone.

The protective effect from reviparin treatment extended to 30 days after the start of treatment. At that time, the rate of death, repeat MI, or stroke was 13.6% in the placebo group and 11.8% in the reviparin group, again a statistically significant 13% relative reduction. These results showed that “stopping therapy after 7 days was not associated with any rebound,” Dr. Yusuf said.

Like all antithrombotic drugs, reviparin boosted the rate of bleeding events. The rate of life-threatening or major bleeds not included in the primary outcomes after 7 days of treatment was 0.1% in the placebo group, compared with 0.2% in the reviparin group. The increased risk of important bleeding events was small, compared with the overall benefit, he noted.

Another noteworthy finding was that the faster treatment with reviparin started the greater the benefit. Patients who started treatment within 2 hours of symptom onset had a 30% relative drop in the primary end point. This relative benefit fell to 20% when treatment began 2–4 hours and to 15% when treatment began within 4–8 hours. The benefit completely disappeared when treatment was delayed beyond 8 hours.

An inevitable question is whether treatment with the low-molecular-weight heparins approved for use in the United States would confer the same benefits. “It's a tricky issue, because low-molecular-weight heparins are very heterogeneous compounds. You need to know the exact dosage to use.” Dr. Yusuf said.

NEW ORLEANS — Antithrombotic treatment, in the form of the low-molecular-weight heparin reviparin, has been shown for the first time to safely improve the outcomes of patients with an acute MI.

“Although heparin is often routinely used to treat patients with an acute myocardial infarction, the incremental benefit from heparin or newer antithrombotics has been poorly defined,” Jeffrey L. Anderson, M.D., said at the annual scientific sessions of the American Heart Association.

The new findings show that reviparin “clearly improves the outcomes of patients who undergo thrombolysis with streptokinase or urokinase,” said Dr. Anderson, associate chief of the division of cardiology at LDS Hospital in Salt Lake City.

But the value of adding reviparin or a similar agent remains in doubt when patients are treated with the fibrin-specific drugs most often used for thrombolysis in the United States, such as alteplase (tissue plasminogen activator), reteplase, and tenecteplase. That's because this new trial, conducted in India, China, Pakistan, and several South American countries and involving 15,570 patients, included only about 100 patients treated with a fibrin-specific thrombolytic drug. Close to 80% of the patients received acute treatment to clear their coronary thrombus, but this treatment was primarily streptokinase in about 50% of patients, urokinase in about 23% of patients, and primary percutaneous intervention in about 6% of patients.

Despite this limitation, the results showed that “reviparin is a simple, inexpensive therapy that is globally applicable for treating acute myocardial infarction,” said Salim Yusuf, D.Phil., director of the division of cardiology at McMaster University in Hamilton, Canada, and lead investigator for the study.

Reviparin is marketed by Abbott Pharmaceuticals under the name Clivarine in several countries in Europe and Asia, but is not approved for U.S. use. Abbott provided the reviparin, but otherwise, the study had no commercial funding.

The study enrolled patients with ST-segment-elevation MI or new bundle branch block who presented within 12 hours of symptom onset. All patients were to be treated with aspirin, and they could also be treated with a regimen designed to produce reperfusion in their blocked coronary arteries. The average age of the patients was 59 years, and the average time from symptom onset to treatment was 4.8 hours, with 61% of patients treated within 6 hours. Aspirin was used on 97% of patients, 72% received an ACE inhibitor, 66% received a lipid-lowering drug, 60% received a β-blocker, and 55% received a thienopyridine, most commonly clopidogrel.

Patients were randomized to treatment with reviparin or placebo by subcutaneous injection b.i.d for 7 days; 76% of patients received the full 7-day course.

The study's primary end point was the incidence of death, repeat MI, or stroke during the 7 days of treatment. The rate of these outcomes was 11.0% in the placebo group and 9.6% in the reviparin group—a statistically significant relative reduction of 13%, Dr. Yusuf reported. Patients treated with reviparin also had a 13% relative reduction in the study's secondary end point, which included death, repeat MI, stroke, or ischemic ECG changes. Treatment with reviparin was also associated with a significant 11% relative reduction in death alone.

The protective effect from reviparin treatment extended to 30 days after the start of treatment. At that time, the rate of death, repeat MI, or stroke was 13.6% in the placebo group and 11.8% in the reviparin group, again a statistically significant 13% relative reduction. These results showed that “stopping therapy after 7 days was not associated with any rebound,” Dr. Yusuf said.

Like all antithrombotic drugs, reviparin boosted the rate of bleeding events. The rate of life-threatening or major bleeds not included in the primary outcomes after 7 days of treatment was 0.1% in the placebo group, compared with 0.2% in the reviparin group. The increased risk of important bleeding events was small, compared with the overall benefit, he noted.

Another noteworthy finding was that the faster treatment with reviparin started the greater the benefit. Patients who started treatment within 2 hours of symptom onset had a 30% relative drop in the primary end point. This relative benefit fell to 20% when treatment began 2–4 hours and to 15% when treatment began within 4–8 hours. The benefit completely disappeared when treatment was delayed beyond 8 hours.

An inevitable question is whether treatment with the low-molecular-weight heparins approved for use in the United States would confer the same benefits. “It's a tricky issue, because low-molecular-weight heparins are very heterogeneous compounds. You need to know the exact dosage to use.” Dr. Yusuf said.

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Interventional cardiology gained ground this year as an alternative to coronary artery bypass graft surgery, as drug-eluting stents were shown to reduce restenosis rates. This and other advances in devices, such carotid stents with distal protection, could have a far-reaching impact on the health care system (including costs) as more patients undergo percutaneous interventions. For example, drug-eluting stents have “thrown a monkey wrench in the hospitals economic projections about their angioplasty business because there is a higher cost up front to acquire these stents, and with reduced amounts of restenosis, they have less repeat business,” John M. Flack, M.D., of Wayne State University, Detroit, told CARDIOLOGY NEWS.

With new devices and technologies, boundaries between interventional cardiologists, interventional radiologists, vascular surgeons, and neurologists are disappearing, leading specialty societies to establish competency requirements to protect patients as well as turf. Even the Food and Drug Administration is getting into the act, with training criteria physicians must meet before they can implant Guidant's Acculink carotid stent.

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Interventional cardiology gained ground this year as an alternative to coronary artery bypass graft surgery, as drug-eluting stents were shown to reduce restenosis rates. This and other advances in devices, such carotid stents with distal protection, could have a far-reaching impact on the health care system (including costs) as more patients undergo percutaneous interventions. For example, drug-eluting stents have “thrown a monkey wrench in the hospitals economic projections about their angioplasty business because there is a higher cost up front to acquire these stents, and with reduced amounts of restenosis, they have less repeat business,” John M. Flack, M.D., of Wayne State University, Detroit, told CARDIOLOGY NEWS.

With new devices and technologies, boundaries between interventional cardiologists, interventional radiologists, vascular surgeons, and neurologists are disappearing, leading specialty societies to establish competency requirements to protect patients as well as turf. Even the Food and Drug Administration is getting into the act, with training criteria physicians must meet before they can implant Guidant's Acculink carotid stent.

Interventional cardiology gained ground this year as an alternative to coronary artery bypass graft surgery, as drug-eluting stents were shown to reduce restenosis rates. This and other advances in devices, such carotid stents with distal protection, could have a far-reaching impact on the health care system (including costs) as more patients undergo percutaneous interventions. For example, drug-eluting stents have “thrown a monkey wrench in the hospitals economic projections about their angioplasty business because there is a higher cost up front to acquire these stents, and with reduced amounts of restenosis, they have less repeat business,” John M. Flack, M.D., of Wayne State University, Detroit, told CARDIOLOGY NEWS.

With new devices and technologies, boundaries between interventional cardiologists, interventional radiologists, vascular surgeons, and neurologists are disappearing, leading specialty societies to establish competency requirements to protect patients as well as turf. Even the Food and Drug Administration is getting into the act, with training criteria physicians must meet before they can implant Guidant's Acculink carotid stent.

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U.S. Lags Behind Europe in Transfer Time to PCI

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NEW ORLEANS — Just 4% of U.S. acute MI patients transferred from one hospital to another for primary percutaneous intervention are treated within 90 minutes as recommended in recent guidelines, Brahmajee K. Nallamothu, M.D., reported at the annual scientific sessions of the American Heart Association.

This finding from the large National Registry of Myocardial Infarction (NRMI) database indicates an urgent need for improved process-of-care systems in order to minimize time delays for transferred MI patients, said Dr. Nallamothu of the University of Michigan, Ann Arbor.

PCI, when performed expeditiously, yields outcomes clearly superior to thrombolytic therapy. But at present, only about 20% of U.S. acute care hospitals have the capacity to perform primary PCI.

When a patient presents to a hospital without such capacity, the only options are on-site thrombolysis or immediate transfer to another facility for the procedure.

The pro-transfer argument is bolstered by several favorable European randomized controlled trials. However, these trials were conducted in countries with better-organized care and shorter transfer distances than are the norm in the United States. As a result, total door-to-balloon times in the randomized trials was only about 90 minutes. And the great majority of transferred American patients don't even come close to that speed of care.

Dr. Nallamothu's analysis of the NRMI-3 and −4 cohorts underscores that point. Of 4,278 consecutive acute MI patients transferred for primary PCI at 419 hospitals participating in the registry, only 4.2% had a door-to-balloon time of 90 minutes or less, as recommended in the recently issued AHA/American College of Cardiology guidelines (J. Am. Coll. Cardiol. 2004;44:671–719). The median door-to-balloon time was 180 minutes. Only 16.2% of transferred patients had a door-to-balloon time of 120 minutes or less, as recommended in earlier AHA/ACC guidelines. The great bulk of the time delay occurred because of prolonged transit times. More than 50% of transferred patients had transfer times in excess of 120 minutes.

NRMI is an ongoing project funded by Genentech. Dr. Nallamothu's study was supported by the National Heart, Lung, and Blood Institute.

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NEW ORLEANS — Just 4% of U.S. acute MI patients transferred from one hospital to another for primary percutaneous intervention are treated within 90 minutes as recommended in recent guidelines, Brahmajee K. Nallamothu, M.D., reported at the annual scientific sessions of the American Heart Association.

This finding from the large National Registry of Myocardial Infarction (NRMI) database indicates an urgent need for improved process-of-care systems in order to minimize time delays for transferred MI patients, said Dr. Nallamothu of the University of Michigan, Ann Arbor.

PCI, when performed expeditiously, yields outcomes clearly superior to thrombolytic therapy. But at present, only about 20% of U.S. acute care hospitals have the capacity to perform primary PCI.

When a patient presents to a hospital without such capacity, the only options are on-site thrombolysis or immediate transfer to another facility for the procedure.

The pro-transfer argument is bolstered by several favorable European randomized controlled trials. However, these trials were conducted in countries with better-organized care and shorter transfer distances than are the norm in the United States. As a result, total door-to-balloon times in the randomized trials was only about 90 minutes. And the great majority of transferred American patients don't even come close to that speed of care.

Dr. Nallamothu's analysis of the NRMI-3 and −4 cohorts underscores that point. Of 4,278 consecutive acute MI patients transferred for primary PCI at 419 hospitals participating in the registry, only 4.2% had a door-to-balloon time of 90 minutes or less, as recommended in the recently issued AHA/American College of Cardiology guidelines (J. Am. Coll. Cardiol. 2004;44:671–719). The median door-to-balloon time was 180 minutes. Only 16.2% of transferred patients had a door-to-balloon time of 120 minutes or less, as recommended in earlier AHA/ACC guidelines. The great bulk of the time delay occurred because of prolonged transit times. More than 50% of transferred patients had transfer times in excess of 120 minutes.

NRMI is an ongoing project funded by Genentech. Dr. Nallamothu's study was supported by the National Heart, Lung, and Blood Institute.

NEW ORLEANS — Just 4% of U.S. acute MI patients transferred from one hospital to another for primary percutaneous intervention are treated within 90 minutes as recommended in recent guidelines, Brahmajee K. Nallamothu, M.D., reported at the annual scientific sessions of the American Heart Association.

This finding from the large National Registry of Myocardial Infarction (NRMI) database indicates an urgent need for improved process-of-care systems in order to minimize time delays for transferred MI patients, said Dr. Nallamothu of the University of Michigan, Ann Arbor.

PCI, when performed expeditiously, yields outcomes clearly superior to thrombolytic therapy. But at present, only about 20% of U.S. acute care hospitals have the capacity to perform primary PCI.

When a patient presents to a hospital without such capacity, the only options are on-site thrombolysis or immediate transfer to another facility for the procedure.

The pro-transfer argument is bolstered by several favorable European randomized controlled trials. However, these trials were conducted in countries with better-organized care and shorter transfer distances than are the norm in the United States. As a result, total door-to-balloon times in the randomized trials was only about 90 minutes. And the great majority of transferred American patients don't even come close to that speed of care.

Dr. Nallamothu's analysis of the NRMI-3 and −4 cohorts underscores that point. Of 4,278 consecutive acute MI patients transferred for primary PCI at 419 hospitals participating in the registry, only 4.2% had a door-to-balloon time of 90 minutes or less, as recommended in the recently issued AHA/American College of Cardiology guidelines (J. Am. Coll. Cardiol. 2004;44:671–719). The median door-to-balloon time was 180 minutes. Only 16.2% of transferred patients had a door-to-balloon time of 120 minutes or less, as recommended in earlier AHA/ACC guidelines. The great bulk of the time delay occurred because of prolonged transit times. More than 50% of transferred patients had transfer times in excess of 120 minutes.

NRMI is an ongoing project funded by Genentech. Dr. Nallamothu's study was supported by the National Heart, Lung, and Blood Institute.

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Women Wait Longer for Emergency Angioplasty

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Women who presented to Michigan hospitals with acute ST-segment elevation myocardial infarction waited significantly longer than men to undergo emergency angioplasty—and even men waited too long according to Mauro Moscucci, M.D., the lead, investigator in the study.

“We have an ideal target for quality improvement, something we can easily try to correct,” said Dr. Moscucci, who presented the data at the scientific sessions of the American Heart Association and discussed the findings in a later interview. “If we can improve our treatment times, we can substantially reduce the risk of death.”

Dr. Moscucci and his associates analyzed data collected on 1,551 patients who had primary percutaneous coronary intervention for acute ST-segment elevation during a 20-month period ending in June 2004. Patients had the procedure at 1 of the 16 hospitals participating in the regional Blue Cross Blue Shield of Michigan Cardiovascular Consortium.

The investigators found that only 26% of the 442 women who had an emergency angioplasty—and 34% of the 1,069 men—had the procedure within the 90-minute time frame recommended by the American Heart Association and the American College of Cardiology.

On average, women waited more than 118 minutes before treatment began, compared with 106 minutes for men.

Patients of both sexes whose angioplasty began within 90 minutes of arrival at the hospital had a 50% lower risk of dying in the hospital than those who waited longer, said Dr. Moscucci, director of interventional cardiology at the University of Michigan Cardiovascular Center, Ann Arbor.

“Since there's been such a focus on angioplasty recently, we wondered whether the recommended door-to-balloon time of 90 minutes was still significant in terms of survival,” he said. “We found that it's still an important predictor of in-hospital mortality, and that perhaps we're not doing as well as we should.”

Women in the study were more than twice as likely as men to die in the hospital; their mortality rate was about 7%, compared with about 3% in men. When the investigators adjusted for the average older age of women and the higher frequency of comorbidities, they still found higher in-hospital mortality rates for women, Dr. Moscucci said.

The gender-difference findings augment a growing body of research showing that women with heart attacks seek care later, present more often with atypical symptoms and comorbidities such as severe diabetes, and face delays in treatment, he said.

In addition to the greater delays in treatment, the Michigan study showed that it takes longer for women to get to an emergency department in the first place. Women reported that their symptoms started an average of 105 minutes before they got to the emergency department; the average time for men was 85 minutes.

Dr. Moscucci said that hospital procedures for activating cardiac catheterization labs vary significantly. Labs could be activated faster—which, along with faster diagnosis, would help hasten door-to-balloon times—if more ambulances had the capability to automatically read or transmit ECGs and if more hospitals allowed emergency physicians and not just cardiologists to activate the labs directly, he said.

A recent survey of more than 1,000 women older than 35 years showed that only 47% of women who had head, neck, back, and jaw pain—typical heart attack symptoms— would call their doctor, and just 35% would call 911 or visit an emergency department.

“Women and their families still need a great deal of education. Their symptoms can be very atypical—perhaps only weakness, difficulty breathing, or dizziness,” said Michael J. Bresler, M.D., professor of emergency medicine at Stanford (Calif.) University. Women in whom heart attack is diagnosed “should be rushed to the cath lab or quickly given a lytic drug if immediate catheterization isn't available,” he said.

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Women who presented to Michigan hospitals with acute ST-segment elevation myocardial infarction waited significantly longer than men to undergo emergency angioplasty—and even men waited too long according to Mauro Moscucci, M.D., the lead, investigator in the study.

“We have an ideal target for quality improvement, something we can easily try to correct,” said Dr. Moscucci, who presented the data at the scientific sessions of the American Heart Association and discussed the findings in a later interview. “If we can improve our treatment times, we can substantially reduce the risk of death.”

Dr. Moscucci and his associates analyzed data collected on 1,551 patients who had primary percutaneous coronary intervention for acute ST-segment elevation during a 20-month period ending in June 2004. Patients had the procedure at 1 of the 16 hospitals participating in the regional Blue Cross Blue Shield of Michigan Cardiovascular Consortium.

The investigators found that only 26% of the 442 women who had an emergency angioplasty—and 34% of the 1,069 men—had the procedure within the 90-minute time frame recommended by the American Heart Association and the American College of Cardiology.

On average, women waited more than 118 minutes before treatment began, compared with 106 minutes for men.

Patients of both sexes whose angioplasty began within 90 minutes of arrival at the hospital had a 50% lower risk of dying in the hospital than those who waited longer, said Dr. Moscucci, director of interventional cardiology at the University of Michigan Cardiovascular Center, Ann Arbor.

“Since there's been such a focus on angioplasty recently, we wondered whether the recommended door-to-balloon time of 90 minutes was still significant in terms of survival,” he said. “We found that it's still an important predictor of in-hospital mortality, and that perhaps we're not doing as well as we should.”

Women in the study were more than twice as likely as men to die in the hospital; their mortality rate was about 7%, compared with about 3% in men. When the investigators adjusted for the average older age of women and the higher frequency of comorbidities, they still found higher in-hospital mortality rates for women, Dr. Moscucci said.

The gender-difference findings augment a growing body of research showing that women with heart attacks seek care later, present more often with atypical symptoms and comorbidities such as severe diabetes, and face delays in treatment, he said.

In addition to the greater delays in treatment, the Michigan study showed that it takes longer for women to get to an emergency department in the first place. Women reported that their symptoms started an average of 105 minutes before they got to the emergency department; the average time for men was 85 minutes.

Dr. Moscucci said that hospital procedures for activating cardiac catheterization labs vary significantly. Labs could be activated faster—which, along with faster diagnosis, would help hasten door-to-balloon times—if more ambulances had the capability to automatically read or transmit ECGs and if more hospitals allowed emergency physicians and not just cardiologists to activate the labs directly, he said.

A recent survey of more than 1,000 women older than 35 years showed that only 47% of women who had head, neck, back, and jaw pain—typical heart attack symptoms— would call their doctor, and just 35% would call 911 or visit an emergency department.

“Women and their families still need a great deal of education. Their symptoms can be very atypical—perhaps only weakness, difficulty breathing, or dizziness,” said Michael J. Bresler, M.D., professor of emergency medicine at Stanford (Calif.) University. Women in whom heart attack is diagnosed “should be rushed to the cath lab or quickly given a lytic drug if immediate catheterization isn't available,” he said.

Women who presented to Michigan hospitals with acute ST-segment elevation myocardial infarction waited significantly longer than men to undergo emergency angioplasty—and even men waited too long according to Mauro Moscucci, M.D., the lead, investigator in the study.

“We have an ideal target for quality improvement, something we can easily try to correct,” said Dr. Moscucci, who presented the data at the scientific sessions of the American Heart Association and discussed the findings in a later interview. “If we can improve our treatment times, we can substantially reduce the risk of death.”

Dr. Moscucci and his associates analyzed data collected on 1,551 patients who had primary percutaneous coronary intervention for acute ST-segment elevation during a 20-month period ending in June 2004. Patients had the procedure at 1 of the 16 hospitals participating in the regional Blue Cross Blue Shield of Michigan Cardiovascular Consortium.

The investigators found that only 26% of the 442 women who had an emergency angioplasty—and 34% of the 1,069 men—had the procedure within the 90-minute time frame recommended by the American Heart Association and the American College of Cardiology.

On average, women waited more than 118 minutes before treatment began, compared with 106 minutes for men.

Patients of both sexes whose angioplasty began within 90 minutes of arrival at the hospital had a 50% lower risk of dying in the hospital than those who waited longer, said Dr. Moscucci, director of interventional cardiology at the University of Michigan Cardiovascular Center, Ann Arbor.

“Since there's been such a focus on angioplasty recently, we wondered whether the recommended door-to-balloon time of 90 minutes was still significant in terms of survival,” he said. “We found that it's still an important predictor of in-hospital mortality, and that perhaps we're not doing as well as we should.”

Women in the study were more than twice as likely as men to die in the hospital; their mortality rate was about 7%, compared with about 3% in men. When the investigators adjusted for the average older age of women and the higher frequency of comorbidities, they still found higher in-hospital mortality rates for women, Dr. Moscucci said.

The gender-difference findings augment a growing body of research showing that women with heart attacks seek care later, present more often with atypical symptoms and comorbidities such as severe diabetes, and face delays in treatment, he said.

In addition to the greater delays in treatment, the Michigan study showed that it takes longer for women to get to an emergency department in the first place. Women reported that their symptoms started an average of 105 minutes before they got to the emergency department; the average time for men was 85 minutes.

Dr. Moscucci said that hospital procedures for activating cardiac catheterization labs vary significantly. Labs could be activated faster—which, along with faster diagnosis, would help hasten door-to-balloon times—if more ambulances had the capability to automatically read or transmit ECGs and if more hospitals allowed emergency physicians and not just cardiologists to activate the labs directly, he said.

A recent survey of more than 1,000 women older than 35 years showed that only 47% of women who had head, neck, back, and jaw pain—typical heart attack symptoms— would call their doctor, and just 35% would call 911 or visit an emergency department.

“Women and their families still need a great deal of education. Their symptoms can be very atypical—perhaps only weakness, difficulty breathing, or dizziness,” said Michael J. Bresler, M.D., professor of emergency medicine at Stanford (Calif.) University. Women in whom heart attack is diagnosed “should be rushed to the cath lab or quickly given a lytic drug if immediate catheterization isn't available,” he said.

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A guide to assessing decision-making capacity

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Epidural steroids for back and leg pain: Mechanism of action and efficacy

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Coping with the influenza vaccine shortage

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Help children and teens stop impulsive hair pulling

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Trichotillomania (TTM) is distressing to pediatric patients who pull their hair and to their parents who feel helpless to stop the destructive behavior. Hair-pulling with psychiatric comorbidity requires comprehensive assessment and treatment, but we have found that cognitive-behavioral therapy (CBT) alone can help children and adolescents with uncomplicated TTM.

This article describes a typical patient with adolescent-onset mild-to-moderate TTM and the three-step CBT approach—awareness training, stimulus control, and habit reversal—that we find effective in reducing pediatric hair pulling.

Jane, age 12, was referred to our clinic by her primary doctor after an 8-week trial of fluoxetine, 80 mg/d, failed to stop her hair pulling. Jane, who is right-handed, has been pulling her hair for 2 years, mostly in the right front scalp. Her shame over the hair loss makes her reluctant to participate in social activities. A dermatologist found no medical cause for her behavior, such as alopecia or folliculitis.

Jane’s parents say she has no history of a major mood disorder or anxiety. Her hair pulling causes significant “tension and stress” for all family members.

WHY DO PATIENTS PULL HAIR?

Cognitive-behavioral theory suggests that chronic TTM originates as a normal response to stress that often escapes personal and social awareness but gradually increases in frequency and severity (Box).1-8 Thus, hair pulling becomes associated with internal and external cues through conditioning and is maintained primarily by positive reinforcement. Hair-pulling urges that are reinforced by pulling intensify the need to pull, perpetuating the behavioral cycle.

A genetic link? Familial research has associated TTM with increased rates of obsessive-compulsive disorder (OCD) or other excessive habits—such as nail biting or skin picking—among first-degree relatives.6,9,10 Neuroimaging of persons with TTM has shown hyperactivity in the left cerebellum and right superior parietal lobe11 as well as possible structural abnormalities in the left putamen,12 left inferior frontal gyrus, and right cluneal cortex.13

These findings do not necessarily indicate pre-existing brain pathology, however. Perhaps TTM leads to changes in brain structure or function, or both TTM and the brain abnormalities may be caused by another as-yet-unknown variable.

Decreased pain sensitivity. Patients with TTM often report that hair pulling is not painful,2 though we suspect that persons without TTM would disagree and derive no pleasure from it. Changes in pain sensitivity may influence the reinforcing quality of pulling behavior. One possible mechanism for such alterations is upregulation of the endogenous opioid system; some intriguing evidence suggests that opioid receptor antagonists such as naltrexone may reduce pulling.14

Box

Hair-pulling tends to begin early

Trichotillomania (TTM) is an impulse control disorder characterized by repetitive hair pulling,1 which typically emerges during adolescence. In a large clinical sample of adult hair pullers, mean age of onset was 13.2 Very-early onset (before age 5) may be a more benign form of TTM that tends to abate spontaneously and requires little or no therapeutic intervention.3

Despite the absence of body hair in prepubertal children, their pulling patterns are consistent with those of adults. The scalp is the most common pulling site, followed by eyelashes and eyebrows.4

Psychiatric comorbidity. In two studies evaluating psychiatric comorbidity in pediatric clinical samples, 60% to 70% of children and teens with TTM had at least one comorbid axis I disorder.5,6 Disruptive behavior disorders were most common in one study,6 whereas overanxious disorder was most common in the other.5 In a large clinical sample of adults with TTM, 51% met criteria for comorbid depression.2

Early identification and treatment of TTM are recommended because of the disorder’s distressing nature and social stigma. Early interventions also may help prevent later adult psychiatric comorbidity and functional impairment, although no studies have been done to demonstrate this benefit.7,8

Pain tolerance at the preferred pulling site has not been studied, however. For patients who feel pain from hair pulling, the pain itself may reinforce the behavior by distracting the individual from negative emotional or physiologic states.15

CASE CONTINUED: COUNTING THE WAYS

Jane and her parents agree that she pulls her hair 5 to 8 times daily, one hair at a time with her right index finger and thumb while doing homework or watching TV. The trigger, she says, is “an itch” on her scalp; “sometimes pulling relieves the itch.” She fails to resist pulling her hair 9 out of 10 times.

Table 1

Defining hair pulling: What to ask the pediatric patient

Response descriptionHow many times do you pull your hair each day?
How many hairs do you pull each time?
From what body areas do you pull hair?
What are all the steps involved in pulling (Touching the head before pulling? Pulling one hair at a time with the thumb and index finger)?
Response detectionUnder what circumstances do you sense the urge to pull?
How strong is the urge on a scale of 1 to 10, with 10 being the greatest intensity you ever felt?
How do you try to resist and overcome the urge to pull?
PrecursorsExternal cues (Do you pull when you look at yourself in a mirror?)
Internal cues (Do you pull when you are nervous?)
High-risk situationsWhat are you usually doing when you get the urge to pull? (reading, talking on the telephone, watching TV, using a computer, etc.)
Consequences that reinforce the behaviorDo you pull to reduce physical sensations (such as itching) at the site of pulling?
Does pulling relieve sadness or worry about problems at home or in school?
Do you pull to create a more even hairline?
 

 

Psychiatric comorbidity is common—if not the norm—in adults with TTM. Although axis I comorbidity is also seen in children and adolescents, their hair pulling is frequently uncomplicated. Jane meets criteria for TTM, as determined by the Trichotillomania Diagnostic Interview,16 but her history does not support a comorbid disorder. After discussing the diagnosis with Jane and her parents, the psychiatrist begins treatment with CBT alone.

MEDICATION OR CBT?

SSRIs. Literature on TTM pharmacotherapy is very limited and equivocal. Medications that have helped adults with TTM have been described,17 but the lack of a single, randomized, controlled trial in pediatric TTM severely limits treatment recommendations for children.

Selective serotonin reuptake inhibitors (SSRIs) have shown efficacy for treating anger and other impulse control problems but not for TTM. Some practitioners use SSRIs for TTM because of the belief that TTM is a variant of OCD. However, TTM may be maintained by positive reinforcement rather than compulsive tendencies and thus may not respond to SSRIs.

CBT. Evidence on CBT justifies cautious recommendations for pediatric TTM. In randomized trials, CBT reduced hair pulling in adults and was more effective than SSRIs or placebo.18,19

REDUCING THE URGE

Obtain detailed information about a child or adolescent’s hair-pulling episodes (Table 1), as recognizing triggers and reactions is vital to effective CBT. Explain to the patient that:

  • the pleasure or satisfaction she derives from pulling reinforces the urge to pull
  • she can reduce the urge by learning and using awareness training, stimulus control, and habit reversal (Table 2).

Awareness training involves patient self-monitoring to gain awareness of urges to pull and of pulling behavior. The child must become alert to every hair pulled and to response precursors, such as placing her hand on her head. For a patient such as Jane, a useful technique is to post reminders on the TV and school notebook and in the bedroom and bathroom—wherever pulling typically occurs.

A “PULLING CALENDAR”

Jane begins a daily “pulling calendar” in which she records each time she pulls a hair while watching TV or doing homework. She is asked to include the total number of hairs pulled and the intensity of the “itch to pull” on a scale of 1 to 10.

Stimulus control. Most patients can identify high-risk situations, such as time in the bathroom, talking on the phone, watching TV, driving, reading, or while falling asleep. Boredom, frustration, anxiety, and sadness may serve as pulling cues.

With stimulus control, the patient tries to reduce her ability to freely engage in pulling behavior in high-risk situations. For instance, you might encourage a child who pulls hairs while doing homework to stick Band-Aid®-type adhesive strips on her thumb and index finger tips before she starts studying as an impediment to gripping hairs. Such “speed bumps” may allow her to delay pulling and reach for tools that assist in habit reversal.

TREATMENT THAT APPEALS

Jane agrees to apply adhesive strips to her fingers and understands why. Because she is a fan of Peter Pan, we place Peter Pan stickers on her books and notebooks and on the TV remote control as reminders not to pull.

Table 2

CBT strategies to reduce the hair-pulling urge

Awareness trainingIncreases patient’s awareness of pulling
Stimulus controlEstablishes an environment less conducive to pulling
Habit reversal/ responsePatient develops alternate activities that provide competing positive reinforcement comparable to that gained from pulling

Habit reversal and competing response procedures provide pleasurable physical stimulation as an alternative to pulling. The most effective methods engage the same motions as used in hair pulling. Examples include sculpting with clay, hulling sunflower seeds, and playing with Koosh® balls—small rubbery balls filled with a jellylike plasma and covered with hundreds of soft “tentacles.”

‘CALMER, HAPPIER’

We explain habit reversal to Jane and instruct her to use the Koosh ball a few times a day. She enjoys pulling its rubber strands, an action that uses the same muscles as hair pulling. Because she will need Koosh balls during all identified high-risk situations, we instruct her to buy one for her book bag and to leave one near the couch where she watches TV.

Over time, Jane reports a gradual decrease of hair pulling with the use of awareness training and stimulus control techniques. Using the Koosh ball (habit reversal) helps her improve. By the 10th week, Jane and her parents report a 70% decrease in hair pulling, based on the pulling calendar entries and other objective evidence of treatment response. All report feeling “calmer and happier.”

CONCLUSION

Cognitive and behavioral strategies are useful and safe for treating pediatric TTM. Enlisting the parents and patient in identifying problem situations and applying creative solutions may increase the chances of success.

 

 

Follow-up is important for maintaining new cognitive and behavioral patterns. We recommend that you see patients monthly for at least 3 months, depending on how the patient feels about additional sessions. We encourage families to call and report on progress or relapses. Booster CBT sessions can help deal with setbacks.

Related resources

  • Trichotillomania Learning Center, Inc.; devoted to improving TTM understanding and providing access to treatments and support groups. www.trich.org. Accessed Sept. 17, 2004.
  • Golomb RG, Vavrichek SM. The hair pulling “habit” and you: how to solve the trichotillomania puzzle (rev ed). Silver Spring, MD: Writer’s Cooperative of Greater Washington; 2000. Book for children and teenagers.

Drug brand names

  • Fluoxetine • Prozac
  • Naltrexone • Depade, ReVia

Disclosure

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

Acknowledgment

Preparation of this article was supported in part by a grant from the National Institute of Mental Health (MH61457).

References

1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed., text rev. Washington, DC: American Psychiatric Association Press; 2000;674-7.

2. Christenson GA, Mackenzie TB, Mitchell JE. Characteristics of 60 adult chronic hairpullers. Am J Psychiatry 1991;148:365-70.

3. Swedo SE, Leonard HL. Trichotillomania: an obsessive compulsive spectrum disorder? Psychiatr Clin North Am 1992;15:777-90.

4. Reeve E. Hair pulling in children and adolescents. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Association Press, 1999;201-24.

5. Reeve EA, Bernstein GA, Christenson GA. Clinical characteristics and psychiatric comorbidity in children with trichotillomania. J Am Acad Child Adolesc Psychiatry 1992;31:132-8.

6. King RA, Scahill L, Vitulano LA, et al. Childhood trichotillomania: clinical phenomenology, comorbidity, and family genetics. J Am Acad Child Adolesc Psychiatry 1995;34:1451-9.

7. Franklin ME, Bux DA, Foa EB. Pediatric trichotillomania: conceptualization and treatment implications. In: Orvashel H, Faust J, Hersen M, eds. Handbook of conceptualization and treatment of child psychopathology. Oxford, UK: Elsevier Science; 2001;379-98.

8. Keuthen NJ, Franklin ME. Trichotillomania: psychopathology and treatment development [presentation]. Reno, NV: Association for the Advancement of Behavior Therapy annual meeting, 2002.

9. Bienvenu OJ, Samuels JF, Riddle MA, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: results from a family study. Biol Psychiatry 2000;48:287-93.

10. Lenane MC, Swedo SE, Rapoport JL, et al. Rates of obsessive compulsive disorder in first degree relatives of patients with trichotillomania: a research note. J Child Psychol Psychiatry 1992;33:925-33.

11. Swedo SE, Rapoport JL, Leonard HL, et al. Regional cerebral glucose metabolism of women in trichotillomania. Arch Gen Psychiatry 1991;48:828-33.

12. O’Sullivan RL, Rauch SL, Breiter HC, et al. Reduced basal ganglia volumes in trichotillomania measured via morphometric magnetic resonance imaging. Biol Psychiatry 1997;42:39-45.

13. Grachev ID. MRI-based morphometric topographic parcellation of human neocortex in trichotillomania. Psychiatry Clin Neurosci 1997;51:315-21.

14. Carrion VG. Naltrexone for the treatment of trichotillomania: a case report. J Clin Psychopharmacol 1995;15:444-5.

15. Christenson GA, Mansueto CS. Trichotillomania: descriptive characteristics and phenomenology. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Press, 1999;1-41.

16. Rothbaum BO, Ninan PT. The assessment of trichotillomania. Behav Res Ther 1994;32(6):651-62.

17. Lundt LP. Trichotillomania: a heads-up on severe cases. Current Psychiatry 2004;3(5):89-105.

18. Ninan PT, Rothbaum BO, Marsteller FA, et al. A placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillomania. J Clin Psychiatry. 2000;61:47-50.

19. Azrin NH, Nunn RG, Frantz SE. Treatment of hairpulling (trichotillomania): a comparative study of habit reversal and negative practice training. J Behav Ther Exp Psychiatry 1980;11:13-20.

Author and Disclosure Information

Dodanid Cardona, MD
Fellow, child and adolescent psychiatry Children’s Hospital of Philadelphia

Martin E. Franklin, PhD
Associate professor of clinical psychology in psychiatry Department of psychiatry University of Pennsylvania School of Medicine Philadelphia

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Dodanid Cardona, MD
Fellow, child and adolescent psychiatry Children’s Hospital of Philadelphia

Martin E. Franklin, PhD
Associate professor of clinical psychology in psychiatry Department of psychiatry University of Pennsylvania School of Medicine Philadelphia

Author and Disclosure Information

Dodanid Cardona, MD
Fellow, child and adolescent psychiatry Children’s Hospital of Philadelphia

Martin E. Franklin, PhD
Associate professor of clinical psychology in psychiatry Department of psychiatry University of Pennsylvania School of Medicine Philadelphia

Trichotillomania (TTM) is distressing to pediatric patients who pull their hair and to their parents who feel helpless to stop the destructive behavior. Hair-pulling with psychiatric comorbidity requires comprehensive assessment and treatment, but we have found that cognitive-behavioral therapy (CBT) alone can help children and adolescents with uncomplicated TTM.

This article describes a typical patient with adolescent-onset mild-to-moderate TTM and the three-step CBT approach—awareness training, stimulus control, and habit reversal—that we find effective in reducing pediatric hair pulling.

Jane, age 12, was referred to our clinic by her primary doctor after an 8-week trial of fluoxetine, 80 mg/d, failed to stop her hair pulling. Jane, who is right-handed, has been pulling her hair for 2 years, mostly in the right front scalp. Her shame over the hair loss makes her reluctant to participate in social activities. A dermatologist found no medical cause for her behavior, such as alopecia or folliculitis.

Jane’s parents say she has no history of a major mood disorder or anxiety. Her hair pulling causes significant “tension and stress” for all family members.

WHY DO PATIENTS PULL HAIR?

Cognitive-behavioral theory suggests that chronic TTM originates as a normal response to stress that often escapes personal and social awareness but gradually increases in frequency and severity (Box).1-8 Thus, hair pulling becomes associated with internal and external cues through conditioning and is maintained primarily by positive reinforcement. Hair-pulling urges that are reinforced by pulling intensify the need to pull, perpetuating the behavioral cycle.

A genetic link? Familial research has associated TTM with increased rates of obsessive-compulsive disorder (OCD) or other excessive habits—such as nail biting or skin picking—among first-degree relatives.6,9,10 Neuroimaging of persons with TTM has shown hyperactivity in the left cerebellum and right superior parietal lobe11 as well as possible structural abnormalities in the left putamen,12 left inferior frontal gyrus, and right cluneal cortex.13

These findings do not necessarily indicate pre-existing brain pathology, however. Perhaps TTM leads to changes in brain structure or function, or both TTM and the brain abnormalities may be caused by another as-yet-unknown variable.

Decreased pain sensitivity. Patients with TTM often report that hair pulling is not painful,2 though we suspect that persons without TTM would disagree and derive no pleasure from it. Changes in pain sensitivity may influence the reinforcing quality of pulling behavior. One possible mechanism for such alterations is upregulation of the endogenous opioid system; some intriguing evidence suggests that opioid receptor antagonists such as naltrexone may reduce pulling.14

Box

Hair-pulling tends to begin early

Trichotillomania (TTM) is an impulse control disorder characterized by repetitive hair pulling,1 which typically emerges during adolescence. In a large clinical sample of adult hair pullers, mean age of onset was 13.2 Very-early onset (before age 5) may be a more benign form of TTM that tends to abate spontaneously and requires little or no therapeutic intervention.3

Despite the absence of body hair in prepubertal children, their pulling patterns are consistent with those of adults. The scalp is the most common pulling site, followed by eyelashes and eyebrows.4

Psychiatric comorbidity. In two studies evaluating psychiatric comorbidity in pediatric clinical samples, 60% to 70% of children and teens with TTM had at least one comorbid axis I disorder.5,6 Disruptive behavior disorders were most common in one study,6 whereas overanxious disorder was most common in the other.5 In a large clinical sample of adults with TTM, 51% met criteria for comorbid depression.2

Early identification and treatment of TTM are recommended because of the disorder’s distressing nature and social stigma. Early interventions also may help prevent later adult psychiatric comorbidity and functional impairment, although no studies have been done to demonstrate this benefit.7,8

Pain tolerance at the preferred pulling site has not been studied, however. For patients who feel pain from hair pulling, the pain itself may reinforce the behavior by distracting the individual from negative emotional or physiologic states.15

CASE CONTINUED: COUNTING THE WAYS

Jane and her parents agree that she pulls her hair 5 to 8 times daily, one hair at a time with her right index finger and thumb while doing homework or watching TV. The trigger, she says, is “an itch” on her scalp; “sometimes pulling relieves the itch.” She fails to resist pulling her hair 9 out of 10 times.

Table 1

Defining hair pulling: What to ask the pediatric patient

Response descriptionHow many times do you pull your hair each day?
How many hairs do you pull each time?
From what body areas do you pull hair?
What are all the steps involved in pulling (Touching the head before pulling? Pulling one hair at a time with the thumb and index finger)?
Response detectionUnder what circumstances do you sense the urge to pull?
How strong is the urge on a scale of 1 to 10, with 10 being the greatest intensity you ever felt?
How do you try to resist and overcome the urge to pull?
PrecursorsExternal cues (Do you pull when you look at yourself in a mirror?)
Internal cues (Do you pull when you are nervous?)
High-risk situationsWhat are you usually doing when you get the urge to pull? (reading, talking on the telephone, watching TV, using a computer, etc.)
Consequences that reinforce the behaviorDo you pull to reduce physical sensations (such as itching) at the site of pulling?
Does pulling relieve sadness or worry about problems at home or in school?
Do you pull to create a more even hairline?
 

 

Psychiatric comorbidity is common—if not the norm—in adults with TTM. Although axis I comorbidity is also seen in children and adolescents, their hair pulling is frequently uncomplicated. Jane meets criteria for TTM, as determined by the Trichotillomania Diagnostic Interview,16 but her history does not support a comorbid disorder. After discussing the diagnosis with Jane and her parents, the psychiatrist begins treatment with CBT alone.

MEDICATION OR CBT?

SSRIs. Literature on TTM pharmacotherapy is very limited and equivocal. Medications that have helped adults with TTM have been described,17 but the lack of a single, randomized, controlled trial in pediatric TTM severely limits treatment recommendations for children.

Selective serotonin reuptake inhibitors (SSRIs) have shown efficacy for treating anger and other impulse control problems but not for TTM. Some practitioners use SSRIs for TTM because of the belief that TTM is a variant of OCD. However, TTM may be maintained by positive reinforcement rather than compulsive tendencies and thus may not respond to SSRIs.

CBT. Evidence on CBT justifies cautious recommendations for pediatric TTM. In randomized trials, CBT reduced hair pulling in adults and was more effective than SSRIs or placebo.18,19

REDUCING THE URGE

Obtain detailed information about a child or adolescent’s hair-pulling episodes (Table 1), as recognizing triggers and reactions is vital to effective CBT. Explain to the patient that:

  • the pleasure or satisfaction she derives from pulling reinforces the urge to pull
  • she can reduce the urge by learning and using awareness training, stimulus control, and habit reversal (Table 2).

Awareness training involves patient self-monitoring to gain awareness of urges to pull and of pulling behavior. The child must become alert to every hair pulled and to response precursors, such as placing her hand on her head. For a patient such as Jane, a useful technique is to post reminders on the TV and school notebook and in the bedroom and bathroom—wherever pulling typically occurs.

A “PULLING CALENDAR”

Jane begins a daily “pulling calendar” in which she records each time she pulls a hair while watching TV or doing homework. She is asked to include the total number of hairs pulled and the intensity of the “itch to pull” on a scale of 1 to 10.

Stimulus control. Most patients can identify high-risk situations, such as time in the bathroom, talking on the phone, watching TV, driving, reading, or while falling asleep. Boredom, frustration, anxiety, and sadness may serve as pulling cues.

With stimulus control, the patient tries to reduce her ability to freely engage in pulling behavior in high-risk situations. For instance, you might encourage a child who pulls hairs while doing homework to stick Band-Aid®-type adhesive strips on her thumb and index finger tips before she starts studying as an impediment to gripping hairs. Such “speed bumps” may allow her to delay pulling and reach for tools that assist in habit reversal.

TREATMENT THAT APPEALS

Jane agrees to apply adhesive strips to her fingers and understands why. Because she is a fan of Peter Pan, we place Peter Pan stickers on her books and notebooks and on the TV remote control as reminders not to pull.

Table 2

CBT strategies to reduce the hair-pulling urge

Awareness trainingIncreases patient’s awareness of pulling
Stimulus controlEstablishes an environment less conducive to pulling
Habit reversal/ responsePatient develops alternate activities that provide competing positive reinforcement comparable to that gained from pulling

Habit reversal and competing response procedures provide pleasurable physical stimulation as an alternative to pulling. The most effective methods engage the same motions as used in hair pulling. Examples include sculpting with clay, hulling sunflower seeds, and playing with Koosh® balls—small rubbery balls filled with a jellylike plasma and covered with hundreds of soft “tentacles.”

‘CALMER, HAPPIER’

We explain habit reversal to Jane and instruct her to use the Koosh ball a few times a day. She enjoys pulling its rubber strands, an action that uses the same muscles as hair pulling. Because she will need Koosh balls during all identified high-risk situations, we instruct her to buy one for her book bag and to leave one near the couch where she watches TV.

Over time, Jane reports a gradual decrease of hair pulling with the use of awareness training and stimulus control techniques. Using the Koosh ball (habit reversal) helps her improve. By the 10th week, Jane and her parents report a 70% decrease in hair pulling, based on the pulling calendar entries and other objective evidence of treatment response. All report feeling “calmer and happier.”

CONCLUSION

Cognitive and behavioral strategies are useful and safe for treating pediatric TTM. Enlisting the parents and patient in identifying problem situations and applying creative solutions may increase the chances of success.

 

 

Follow-up is important for maintaining new cognitive and behavioral patterns. We recommend that you see patients monthly for at least 3 months, depending on how the patient feels about additional sessions. We encourage families to call and report on progress or relapses. Booster CBT sessions can help deal with setbacks.

Related resources

  • Trichotillomania Learning Center, Inc.; devoted to improving TTM understanding and providing access to treatments and support groups. www.trich.org. Accessed Sept. 17, 2004.
  • Golomb RG, Vavrichek SM. The hair pulling “habit” and you: how to solve the trichotillomania puzzle (rev ed). Silver Spring, MD: Writer’s Cooperative of Greater Washington; 2000. Book for children and teenagers.

Drug brand names

  • Fluoxetine • Prozac
  • Naltrexone • Depade, ReVia

Disclosure

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

Acknowledgment

Preparation of this article was supported in part by a grant from the National Institute of Mental Health (MH61457).

Trichotillomania (TTM) is distressing to pediatric patients who pull their hair and to their parents who feel helpless to stop the destructive behavior. Hair-pulling with psychiatric comorbidity requires comprehensive assessment and treatment, but we have found that cognitive-behavioral therapy (CBT) alone can help children and adolescents with uncomplicated TTM.

This article describes a typical patient with adolescent-onset mild-to-moderate TTM and the three-step CBT approach—awareness training, stimulus control, and habit reversal—that we find effective in reducing pediatric hair pulling.

Jane, age 12, was referred to our clinic by her primary doctor after an 8-week trial of fluoxetine, 80 mg/d, failed to stop her hair pulling. Jane, who is right-handed, has been pulling her hair for 2 years, mostly in the right front scalp. Her shame over the hair loss makes her reluctant to participate in social activities. A dermatologist found no medical cause for her behavior, such as alopecia or folliculitis.

Jane’s parents say she has no history of a major mood disorder or anxiety. Her hair pulling causes significant “tension and stress” for all family members.

WHY DO PATIENTS PULL HAIR?

Cognitive-behavioral theory suggests that chronic TTM originates as a normal response to stress that often escapes personal and social awareness but gradually increases in frequency and severity (Box).1-8 Thus, hair pulling becomes associated with internal and external cues through conditioning and is maintained primarily by positive reinforcement. Hair-pulling urges that are reinforced by pulling intensify the need to pull, perpetuating the behavioral cycle.

A genetic link? Familial research has associated TTM with increased rates of obsessive-compulsive disorder (OCD) or other excessive habits—such as nail biting or skin picking—among first-degree relatives.6,9,10 Neuroimaging of persons with TTM has shown hyperactivity in the left cerebellum and right superior parietal lobe11 as well as possible structural abnormalities in the left putamen,12 left inferior frontal gyrus, and right cluneal cortex.13

These findings do not necessarily indicate pre-existing brain pathology, however. Perhaps TTM leads to changes in brain structure or function, or both TTM and the brain abnormalities may be caused by another as-yet-unknown variable.

Decreased pain sensitivity. Patients with TTM often report that hair pulling is not painful,2 though we suspect that persons without TTM would disagree and derive no pleasure from it. Changes in pain sensitivity may influence the reinforcing quality of pulling behavior. One possible mechanism for such alterations is upregulation of the endogenous opioid system; some intriguing evidence suggests that opioid receptor antagonists such as naltrexone may reduce pulling.14

Box

Hair-pulling tends to begin early

Trichotillomania (TTM) is an impulse control disorder characterized by repetitive hair pulling,1 which typically emerges during adolescence. In a large clinical sample of adult hair pullers, mean age of onset was 13.2 Very-early onset (before age 5) may be a more benign form of TTM that tends to abate spontaneously and requires little or no therapeutic intervention.3

Despite the absence of body hair in prepubertal children, their pulling patterns are consistent with those of adults. The scalp is the most common pulling site, followed by eyelashes and eyebrows.4

Psychiatric comorbidity. In two studies evaluating psychiatric comorbidity in pediatric clinical samples, 60% to 70% of children and teens with TTM had at least one comorbid axis I disorder.5,6 Disruptive behavior disorders were most common in one study,6 whereas overanxious disorder was most common in the other.5 In a large clinical sample of adults with TTM, 51% met criteria for comorbid depression.2

Early identification and treatment of TTM are recommended because of the disorder’s distressing nature and social stigma. Early interventions also may help prevent later adult psychiatric comorbidity and functional impairment, although no studies have been done to demonstrate this benefit.7,8

Pain tolerance at the preferred pulling site has not been studied, however. For patients who feel pain from hair pulling, the pain itself may reinforce the behavior by distracting the individual from negative emotional or physiologic states.15

CASE CONTINUED: COUNTING THE WAYS

Jane and her parents agree that she pulls her hair 5 to 8 times daily, one hair at a time with her right index finger and thumb while doing homework or watching TV. The trigger, she says, is “an itch” on her scalp; “sometimes pulling relieves the itch.” She fails to resist pulling her hair 9 out of 10 times.

Table 1

Defining hair pulling: What to ask the pediatric patient

Response descriptionHow many times do you pull your hair each day?
How many hairs do you pull each time?
From what body areas do you pull hair?
What are all the steps involved in pulling (Touching the head before pulling? Pulling one hair at a time with the thumb and index finger)?
Response detectionUnder what circumstances do you sense the urge to pull?
How strong is the urge on a scale of 1 to 10, with 10 being the greatest intensity you ever felt?
How do you try to resist and overcome the urge to pull?
PrecursorsExternal cues (Do you pull when you look at yourself in a mirror?)
Internal cues (Do you pull when you are nervous?)
High-risk situationsWhat are you usually doing when you get the urge to pull? (reading, talking on the telephone, watching TV, using a computer, etc.)
Consequences that reinforce the behaviorDo you pull to reduce physical sensations (such as itching) at the site of pulling?
Does pulling relieve sadness or worry about problems at home or in school?
Do you pull to create a more even hairline?
 

 

Psychiatric comorbidity is common—if not the norm—in adults with TTM. Although axis I comorbidity is also seen in children and adolescents, their hair pulling is frequently uncomplicated. Jane meets criteria for TTM, as determined by the Trichotillomania Diagnostic Interview,16 but her history does not support a comorbid disorder. After discussing the diagnosis with Jane and her parents, the psychiatrist begins treatment with CBT alone.

MEDICATION OR CBT?

SSRIs. Literature on TTM pharmacotherapy is very limited and equivocal. Medications that have helped adults with TTM have been described,17 but the lack of a single, randomized, controlled trial in pediatric TTM severely limits treatment recommendations for children.

Selective serotonin reuptake inhibitors (SSRIs) have shown efficacy for treating anger and other impulse control problems but not for TTM. Some practitioners use SSRIs for TTM because of the belief that TTM is a variant of OCD. However, TTM may be maintained by positive reinforcement rather than compulsive tendencies and thus may not respond to SSRIs.

CBT. Evidence on CBT justifies cautious recommendations for pediatric TTM. In randomized trials, CBT reduced hair pulling in adults and was more effective than SSRIs or placebo.18,19

REDUCING THE URGE

Obtain detailed information about a child or adolescent’s hair-pulling episodes (Table 1), as recognizing triggers and reactions is vital to effective CBT. Explain to the patient that:

  • the pleasure or satisfaction she derives from pulling reinforces the urge to pull
  • she can reduce the urge by learning and using awareness training, stimulus control, and habit reversal (Table 2).

Awareness training involves patient self-monitoring to gain awareness of urges to pull and of pulling behavior. The child must become alert to every hair pulled and to response precursors, such as placing her hand on her head. For a patient such as Jane, a useful technique is to post reminders on the TV and school notebook and in the bedroom and bathroom—wherever pulling typically occurs.

A “PULLING CALENDAR”

Jane begins a daily “pulling calendar” in which she records each time she pulls a hair while watching TV or doing homework. She is asked to include the total number of hairs pulled and the intensity of the “itch to pull” on a scale of 1 to 10.

Stimulus control. Most patients can identify high-risk situations, such as time in the bathroom, talking on the phone, watching TV, driving, reading, or while falling asleep. Boredom, frustration, anxiety, and sadness may serve as pulling cues.

With stimulus control, the patient tries to reduce her ability to freely engage in pulling behavior in high-risk situations. For instance, you might encourage a child who pulls hairs while doing homework to stick Band-Aid®-type adhesive strips on her thumb and index finger tips before she starts studying as an impediment to gripping hairs. Such “speed bumps” may allow her to delay pulling and reach for tools that assist in habit reversal.

TREATMENT THAT APPEALS

Jane agrees to apply adhesive strips to her fingers and understands why. Because she is a fan of Peter Pan, we place Peter Pan stickers on her books and notebooks and on the TV remote control as reminders not to pull.

Table 2

CBT strategies to reduce the hair-pulling urge

Awareness trainingIncreases patient’s awareness of pulling
Stimulus controlEstablishes an environment less conducive to pulling
Habit reversal/ responsePatient develops alternate activities that provide competing positive reinforcement comparable to that gained from pulling

Habit reversal and competing response procedures provide pleasurable physical stimulation as an alternative to pulling. The most effective methods engage the same motions as used in hair pulling. Examples include sculpting with clay, hulling sunflower seeds, and playing with Koosh® balls—small rubbery balls filled with a jellylike plasma and covered with hundreds of soft “tentacles.”

‘CALMER, HAPPIER’

We explain habit reversal to Jane and instruct her to use the Koosh ball a few times a day. She enjoys pulling its rubber strands, an action that uses the same muscles as hair pulling. Because she will need Koosh balls during all identified high-risk situations, we instruct her to buy one for her book bag and to leave one near the couch where she watches TV.

Over time, Jane reports a gradual decrease of hair pulling with the use of awareness training and stimulus control techniques. Using the Koosh ball (habit reversal) helps her improve. By the 10th week, Jane and her parents report a 70% decrease in hair pulling, based on the pulling calendar entries and other objective evidence of treatment response. All report feeling “calmer and happier.”

CONCLUSION

Cognitive and behavioral strategies are useful and safe for treating pediatric TTM. Enlisting the parents and patient in identifying problem situations and applying creative solutions may increase the chances of success.

 

 

Follow-up is important for maintaining new cognitive and behavioral patterns. We recommend that you see patients monthly for at least 3 months, depending on how the patient feels about additional sessions. We encourage families to call and report on progress or relapses. Booster CBT sessions can help deal with setbacks.

Related resources

  • Trichotillomania Learning Center, Inc.; devoted to improving TTM understanding and providing access to treatments and support groups. www.trich.org. Accessed Sept. 17, 2004.
  • Golomb RG, Vavrichek SM. The hair pulling “habit” and you: how to solve the trichotillomania puzzle (rev ed). Silver Spring, MD: Writer’s Cooperative of Greater Washington; 2000. Book for children and teenagers.

Drug brand names

  • Fluoxetine • Prozac
  • Naltrexone • Depade, ReVia

Disclosure

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

Acknowledgment

Preparation of this article was supported in part by a grant from the National Institute of Mental Health (MH61457).

References

1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed., text rev. Washington, DC: American Psychiatric Association Press; 2000;674-7.

2. Christenson GA, Mackenzie TB, Mitchell JE. Characteristics of 60 adult chronic hairpullers. Am J Psychiatry 1991;148:365-70.

3. Swedo SE, Leonard HL. Trichotillomania: an obsessive compulsive spectrum disorder? Psychiatr Clin North Am 1992;15:777-90.

4. Reeve E. Hair pulling in children and adolescents. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Association Press, 1999;201-24.

5. Reeve EA, Bernstein GA, Christenson GA. Clinical characteristics and psychiatric comorbidity in children with trichotillomania. J Am Acad Child Adolesc Psychiatry 1992;31:132-8.

6. King RA, Scahill L, Vitulano LA, et al. Childhood trichotillomania: clinical phenomenology, comorbidity, and family genetics. J Am Acad Child Adolesc Psychiatry 1995;34:1451-9.

7. Franklin ME, Bux DA, Foa EB. Pediatric trichotillomania: conceptualization and treatment implications. In: Orvashel H, Faust J, Hersen M, eds. Handbook of conceptualization and treatment of child psychopathology. Oxford, UK: Elsevier Science; 2001;379-98.

8. Keuthen NJ, Franklin ME. Trichotillomania: psychopathology and treatment development [presentation]. Reno, NV: Association for the Advancement of Behavior Therapy annual meeting, 2002.

9. Bienvenu OJ, Samuels JF, Riddle MA, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: results from a family study. Biol Psychiatry 2000;48:287-93.

10. Lenane MC, Swedo SE, Rapoport JL, et al. Rates of obsessive compulsive disorder in first degree relatives of patients with trichotillomania: a research note. J Child Psychol Psychiatry 1992;33:925-33.

11. Swedo SE, Rapoport JL, Leonard HL, et al. Regional cerebral glucose metabolism of women in trichotillomania. Arch Gen Psychiatry 1991;48:828-33.

12. O’Sullivan RL, Rauch SL, Breiter HC, et al. Reduced basal ganglia volumes in trichotillomania measured via morphometric magnetic resonance imaging. Biol Psychiatry 1997;42:39-45.

13. Grachev ID. MRI-based morphometric topographic parcellation of human neocortex in trichotillomania. Psychiatry Clin Neurosci 1997;51:315-21.

14. Carrion VG. Naltrexone for the treatment of trichotillomania: a case report. J Clin Psychopharmacol 1995;15:444-5.

15. Christenson GA, Mansueto CS. Trichotillomania: descriptive characteristics and phenomenology. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Press, 1999;1-41.

16. Rothbaum BO, Ninan PT. The assessment of trichotillomania. Behav Res Ther 1994;32(6):651-62.

17. Lundt LP. Trichotillomania: a heads-up on severe cases. Current Psychiatry 2004;3(5):89-105.

18. Ninan PT, Rothbaum BO, Marsteller FA, et al. A placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillomania. J Clin Psychiatry. 2000;61:47-50.

19. Azrin NH, Nunn RG, Frantz SE. Treatment of hairpulling (trichotillomania): a comparative study of habit reversal and negative practice training. J Behav Ther Exp Psychiatry 1980;11:13-20.

References

1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed., text rev. Washington, DC: American Psychiatric Association Press; 2000;674-7.

2. Christenson GA, Mackenzie TB, Mitchell JE. Characteristics of 60 adult chronic hairpullers. Am J Psychiatry 1991;148:365-70.

3. Swedo SE, Leonard HL. Trichotillomania: an obsessive compulsive spectrum disorder? Psychiatr Clin North Am 1992;15:777-90.

4. Reeve E. Hair pulling in children and adolescents. In: Stein DJ, Christenson GA, Hollander E, eds. Trichotillomania. Washington, DC: American Psychiatric Association Press, 1999;201-24.

5. Reeve EA, Bernstein GA, Christenson GA. Clinical characteristics and psychiatric comorbidity in children with trichotillomania. J Am Acad Child Adolesc Psychiatry 1992;31:132-8.

6. King RA, Scahill L, Vitulano LA, et al. Childhood trichotillomania: clinical phenomenology, comorbidity, and family genetics. J Am Acad Child Adolesc Psychiatry 1995;34:1451-9.

7. Franklin ME, Bux DA, Foa EB. Pediatric trichotillomania: conceptualization and treatment implications. In: Orvashel H, Faust J, Hersen M, eds. Handbook of conceptualization and treatment of child psychopathology. Oxford, UK: Elsevier Science; 2001;379-98.

8. Keuthen NJ, Franklin ME. Trichotillomania: psychopathology and treatment development [presentation]. Reno, NV: Association for the Advancement of Behavior Therapy annual meeting, 2002.

9. Bienvenu OJ, Samuels JF, Riddle MA, et al. The relationship of obsessive-compulsive disorder to possible spectrum disorders: results from a family study. Biol Psychiatry 2000;48:287-93.

10. Lenane MC, Swedo SE, Rapoport JL, et al. Rates of obsessive compulsive disorder in first degree relatives of patients with trichotillomania: a research note. J Child Psychol Psychiatry 1992;33:925-33.

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Current Psychiatry - 03(12)
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Current Psychiatry - 03(12)
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68-76
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Help children and teens stop impulsive hair pulling
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