Michele G. Sullivan

VIENNA — Pesticide exposure might increase the risk of later dementia by as much as 70%.

“Exposure to pesticides may have long-term damaging effects on the nervous system that contribute to the development of Alzheimer's or other dementias,” Kathleen M. Hayden, Ph.D., said at the International Conference on Alzheimer's Disease.

“We need more research to fully characterize the increased risks associated with different types of pesticides, and the duration of their use,” she added.

Dr. Hayden of Duke University Medical Center, Durham, N.C., based her study on data from the Cache County Study of Memory, Health, and Aging. The ongoing study began in 1995, and includes 5,092 subjects, who are assessed every 3 years.

The study participants were given a questionnaire that focused on pesticide exposure.

The study population was a good one for examining the impact of pesticides, Dr. Hayden said, because the subjects live in a rural area, the economy of which relies heavily on growing wheat, soybeans, apples, corn, and hay.

Dr. Hayden and her colleagues assessed the risk of new-onset dementia and Alzheimer's disease in 4,012 of these subjects who were free of dementia at baseline.

Their logistic regression analysis was based on 6 years of follow-up, and controlled for age, sex, education, and ApoE4 status.

At baseline, the subjects were a mean of 75 years old. Pesticide exposure had occurred in 19% (743). The exposed group was primarily male (89%).

After 6 years of follow-up, there were 412 new cases of dementia; 85 of these subjects (21%) reported having had some degree of pesticide exposure on their baseline assessment.

The analysis found consistent significant relationships between new-onset dementia and exposure to both organophosphates and organochlorines. Any exposure to pesticide was associated with a 56% increase in the risk of dementia and Alzheimer's disease.

Exposure to organophosphate compounds increased the risk of dementia by 36% and increased the risk of Alzheimer's disease by 59%. Exposure to organochlorines increased the risk of dementia by 60% and increased the risk of Alzheimer's disease by 70%, the investigators found.

The study did not take into account the duration or extent of exposure, and does not prove a causal link between pesticides and dementia, Dr. Hayden cautioned. But the findings do suggest that more study is necessary, especially in light of the ever-increasing use of such chemicals.

“Some pesticides do alter the level of neurotransmitters, and their use has increased drastically in the past 50 years,” Dr. Hayden said.

“According to the Environmental Protection Agency, there are more than 18,000 pesticides licensed for use in the U.S., and each year, more than 2 million pounds are applied to our crops, parks, homes, and forests,” she said.

Any pesticide exposure increased the risk of dementia and Alzheimer's disease by 56%. More study is needed in light of the ever-increasing use of such chemicals.

Source ©4loops/iStockphoto.com

VIENNA — Pesticide exposure might increase the risk of later dementia by as much as 70%.

“Exposure to pesticides may have long-term damaging effects on the nervous system that contribute to the development of Alzheimer's or other dementias,” Kathleen M. Hayden, Ph.D., said at the International Conference on Alzheimer's Disease.

“We need more research to fully characterize the increased risks associated with different types of pesticides, and the duration of their use,” she added.

Dr. Hayden of Duke University Medical Center, Durham, N.C., based her study on data from the Cache County Study of Memory, Health, and Aging. The ongoing study began in 1995, and includes 5,092 subjects, who are assessed every 3 years.

The study participants were given a questionnaire that focused on pesticide exposure.

The study population was a good one for examining the impact of pesticides, Dr. Hayden said, because the subjects live in a rural area, the economy of which relies heavily on growing wheat, soybeans, apples, corn, and hay.

Dr. Hayden and her colleagues assessed the risk of new-onset dementia and Alzheimer's disease in 4,012 of these subjects who were free of dementia at baseline.

Their logistic regression analysis was based on 6 years of follow-up, and controlled for age, sex, education, and ApoE4 status.

At baseline, the subjects were a mean of 75 years old. Pesticide exposure had occurred in 19% (743). The exposed group was primarily male (89%).

After 6 years of follow-up, there were 412 new cases of dementia; 85 of these subjects (21%) reported having had some degree of pesticide exposure on their baseline assessment.

The analysis found consistent significant relationships between new-onset dementia and exposure to both organophosphates and organochlorines. Any exposure to pesticide was associated with a 56% increase in the risk of dementia and Alzheimer's disease.

Exposure to organophosphate compounds increased the risk of dementia by 36% and increased the risk of Alzheimer's disease by 59%. Exposure to organochlorines increased the risk of dementia by 60% and increased the risk of Alzheimer's disease by 70%, the investigators found.

The study did not take into account the duration or extent of exposure, and does not prove a causal link between pesticides and dementia, Dr. Hayden cautioned. But the findings do suggest that more study is necessary, especially in light of the ever-increasing use of such chemicals.

“Some pesticides do alter the level of neurotransmitters, and their use has increased drastically in the past 50 years,” Dr. Hayden said.

“According to the Environmental Protection Agency, there are more than 18,000 pesticides licensed for use in the U.S., and each year, more than 2 million pounds are applied to our crops, parks, homes, and forests,” she said.

Any pesticide exposure increased the risk of dementia and Alzheimer's disease by 56%. More study is needed in light of the ever-increasing use of such chemicals.

Source ©4loops/iStockphoto.com

VIENNA — Pesticide exposure might increase the risk of later dementia by as much as 70%.

“Exposure to pesticides may have long-term damaging effects on the nervous system that contribute to the development of Alzheimer's or other dementias,” Kathleen M. Hayden, Ph.D., said at the International Conference on Alzheimer's Disease.

“We need more research to fully characterize the increased risks associated with different types of pesticides, and the duration of their use,” she added.

Dr. Hayden of Duke University Medical Center, Durham, N.C., based her study on data from the Cache County Study of Memory, Health, and Aging. The ongoing study began in 1995, and includes 5,092 subjects, who are assessed every 3 years.

The study participants were given a questionnaire that focused on pesticide exposure.

The study population was a good one for examining the impact of pesticides, Dr. Hayden said, because the subjects live in a rural area, the economy of which relies heavily on growing wheat, soybeans, apples, corn, and hay.

Dr. Hayden and her colleagues assessed the risk of new-onset dementia and Alzheimer's disease in 4,012 of these subjects who were free of dementia at baseline.

Their logistic regression analysis was based on 6 years of follow-up, and controlled for age, sex, education, and ApoE4 status.

At baseline, the subjects were a mean of 75 years old. Pesticide exposure had occurred in 19% (743). The exposed group was primarily male (89%).

After 6 years of follow-up, there were 412 new cases of dementia; 85 of these subjects (21%) reported having had some degree of pesticide exposure on their baseline assessment.

The analysis found consistent significant relationships between new-onset dementia and exposure to both organophosphates and organochlorines. Any exposure to pesticide was associated with a 56% increase in the risk of dementia and Alzheimer's disease.

Exposure to organophosphate compounds increased the risk of dementia by 36% and increased the risk of Alzheimer's disease by 59%. Exposure to organochlorines increased the risk of dementia by 60% and increased the risk of Alzheimer's disease by 70%, the investigators found.

The study did not take into account the duration or extent of exposure, and does not prove a causal link between pesticides and dementia, Dr. Hayden cautioned. But the findings do suggest that more study is necessary, especially in light of the ever-increasing use of such chemicals.

“Some pesticides do alter the level of neurotransmitters, and their use has increased drastically in the past 50 years,” Dr. Hayden said.

“According to the Environmental Protection Agency, there are more than 18,000 pesticides licensed for use in the U.S., and each year, more than 2 million pounds are applied to our crops, parks, homes, and forests,” she said.

Any pesticide exposure increased the risk of dementia and Alzheimer's disease by 56%. More study is needed in light of the ever-increasing use of such chemicals.

Source ©4loops/iStockphoto.com

PHILADELPHIA — About 20% of soldiers returning from Iraq or Afghanistan develop chronic daily headache after blast exposure or concussion, according to a preliminary study.

Dr. Brett Theeler and his colleagues found that newly returned soldiers who were exposed to blast explosions within 60 feet and those who suffered concussion injuries with or without loss of consciousness were likely to develop headache within 1 week of their experience. Chronic daily headache (CDH) was defined as headaches occurring at least 15 days per month.

In the cohort of 5,270 soldiers who completed a 13-question headache survey, 957 screened positive for any of the risk factors: 196 were classified as having CDH and 761 did not The mean headache frequency was 23 days per month for the CDH group and 5 days per month for the non-CDH group. Headaches were migraine type in 66% of soldiers with CDH and 48% of soldiers without CDH. Most of those with CDH (55%) developed headaches within 1 week of having had a concussion, compared with 33% of those without CDH, Dr. Theeler reported at the International Headache Congress.

Soldiers with CDH were also exposed to more blasts on average than those without CDH (six vs. five, respectively). Although the average difference in blast exposure was small, there was a very wide range of exposures among those with CDH, “leading us to consider that there may be a dose-response relationship between blast exposure and headache,” said Dr. Theeler, a neurologist and U.S. Army captain at William Beaumont Army Medical Center, El Paso, Tex.

More than twice as many solders with CDH also screened positive for posttraumatic stress disorder (40% vs. 17%).

Dr. Theeler said his data were preliminary. However, he published a recent article suggesting that a history of mild head trauma consistent with blast exposure was present in 50% of soldiers who screened positive for headache (Headache 2009;49:529-34).

The International Headache Society and the American Headache Society sponsored the congress.

PHILADELPHIA — About 20% of soldiers returning from Iraq or Afghanistan develop chronic daily headache after blast exposure or concussion, according to a preliminary study.

Dr. Brett Theeler and his colleagues found that newly returned soldiers who were exposed to blast explosions within 60 feet and those who suffered concussion injuries with or without loss of consciousness were likely to develop headache within 1 week of their experience. Chronic daily headache (CDH) was defined as headaches occurring at least 15 days per month.

In the cohort of 5,270 soldiers who completed a 13-question headache survey, 957 screened positive for any of the risk factors: 196 were classified as having CDH and 761 did not The mean headache frequency was 23 days per month for the CDH group and 5 days per month for the non-CDH group. Headaches were migraine type in 66% of soldiers with CDH and 48% of soldiers without CDH. Most of those with CDH (55%) developed headaches within 1 week of having had a concussion, compared with 33% of those without CDH, Dr. Theeler reported at the International Headache Congress.

Soldiers with CDH were also exposed to more blasts on average than those without CDH (six vs. five, respectively). Although the average difference in blast exposure was small, there was a very wide range of exposures among those with CDH, “leading us to consider that there may be a dose-response relationship between blast exposure and headache,” said Dr. Theeler, a neurologist and U.S. Army captain at William Beaumont Army Medical Center, El Paso, Tex.

More than twice as many solders with CDH also screened positive for posttraumatic stress disorder (40% vs. 17%).

Dr. Theeler said his data were preliminary. However, he published a recent article suggesting that a history of mild head trauma consistent with blast exposure was present in 50% of soldiers who screened positive for headache (Headache 2009;49:529-34).

The International Headache Society and the American Headache Society sponsored the congress.

PHILADELPHIA — About 20% of soldiers returning from Iraq or Afghanistan develop chronic daily headache after blast exposure or concussion, according to a preliminary study.

Dr. Brett Theeler and his colleagues found that newly returned soldiers who were exposed to blast explosions within 60 feet and those who suffered concussion injuries with or without loss of consciousness were likely to develop headache within 1 week of their experience. Chronic daily headache (CDH) was defined as headaches occurring at least 15 days per month.

In the cohort of 5,270 soldiers who completed a 13-question headache survey, 957 screened positive for any of the risk factors: 196 were classified as having CDH and 761 did not The mean headache frequency was 23 days per month for the CDH group and 5 days per month for the non-CDH group. Headaches were migraine type in 66% of soldiers with CDH and 48% of soldiers without CDH. Most of those with CDH (55%) developed headaches within 1 week of having had a concussion, compared with 33% of those without CDH, Dr. Theeler reported at the International Headache Congress.

Soldiers with CDH were also exposed to more blasts on average than those without CDH (six vs. five, respectively). Although the average difference in blast exposure was small, there was a very wide range of exposures among those with CDH, “leading us to consider that there may be a dose-response relationship between blast exposure and headache,” said Dr. Theeler, a neurologist and U.S. Army captain at William Beaumont Army Medical Center, El Paso, Tex.

More than twice as many solders with CDH also screened positive for posttraumatic stress disorder (40% vs. 17%).

Dr. Theeler said his data were preliminary. However, he published a recent article suggesting that a history of mild head trauma consistent with blast exposure was present in 50% of soldiers who screened positive for headache (Headache 2009;49:529-34).

The International Headache Society and the American Headache Society sponsored the congress.

PHILADELPHIA — Migraine with aura seems to be a risk factor for cervical artery dissection, Dr. Ville Artto concluded in a poster presented at the International Headache Congress.

His study of 626 subjects found that migraine and migraine with aura were significantly more common among both men and women who had experienced a cervical artery dissection than among control subjects.

The pathophysiologic link between migraine and cervical artery dissection remains unclear, Dr. Artto said. More than 60% of the patients who had active migraines at the time of their dissections, however, reported that their migraines were alleviated after the incident.

Patients with migraine and cervical artery dissection may represent a link between ischemic stroke and migraine, wrote Dr. Artto of the Helsinki (Finland) University Central Hospital. “This connection may represent common pathophysiological or genetic background, or both,” he wrote.

The study included 313 patients, mean age 46 years, with cervical artery dissection and 313 age-matched controls. Cases were significantly more likely to smoke than were controls (37% vs. 23%), and female cases were significantly more likely than female controls to be using oral contraceptives (36% vs. 25%).

Migraine was present in 36% of cases and in 23% of controls. Migraine with aura was present in 23% of cases and 12% of controls. Both differences were significant. In women, migraine was present in 54% of cases and 35% of controls; migraine with aura was present in 35% of cases and 18% of controls. Among men, migraine was present in 27% of cases and 16% of controls; migraine with aura was present in 16% of cases and 0.4% of controls.

When the investigators compared the characteristics of the dissection between patients with and without migraines, they found similar rates of vertebrobasilar dissection, bilateral dissection, occlusion, and intracranial dissection. The National Institutes of Health Stroke Scale score was not different at onset (3 in migraineurs and 4 in nonmigraineurs). The Rankin score was similar at 3 months (1 in both groups). The rate of ischemic stoke was 68% in migraineurs and 73% in nonmigraineurs, which was not a significant difference.

The International Headache Society and the American Headache Society sponsored the congress. Dr. Artto did not report any relevant conflicts of interest.

PHILADELPHIA — Migraine with aura seems to be a risk factor for cervical artery dissection, Dr. Ville Artto concluded in a poster presented at the International Headache Congress.

His study of 626 subjects found that migraine and migraine with aura were significantly more common among both men and women who had experienced a cervical artery dissection than among control subjects.

The pathophysiologic link between migraine and cervical artery dissection remains unclear, Dr. Artto said. More than 60% of the patients who had active migraines at the time of their dissections, however, reported that their migraines were alleviated after the incident.

Patients with migraine and cervical artery dissection may represent a link between ischemic stroke and migraine, wrote Dr. Artto of the Helsinki (Finland) University Central Hospital. “This connection may represent common pathophysiological or genetic background, or both,” he wrote.

The study included 313 patients, mean age 46 years, with cervical artery dissection and 313 age-matched controls. Cases were significantly more likely to smoke than were controls (37% vs. 23%), and female cases were significantly more likely than female controls to be using oral contraceptives (36% vs. 25%).

Migraine was present in 36% of cases and in 23% of controls. Migraine with aura was present in 23% of cases and 12% of controls. Both differences were significant. In women, migraine was present in 54% of cases and 35% of controls; migraine with aura was present in 35% of cases and 18% of controls. Among men, migraine was present in 27% of cases and 16% of controls; migraine with aura was present in 16% of cases and 0.4% of controls.

When the investigators compared the characteristics of the dissection between patients with and without migraines, they found similar rates of vertebrobasilar dissection, bilateral dissection, occlusion, and intracranial dissection. The National Institutes of Health Stroke Scale score was not different at onset (3 in migraineurs and 4 in nonmigraineurs). The Rankin score was similar at 3 months (1 in both groups). The rate of ischemic stoke was 68% in migraineurs and 73% in nonmigraineurs, which was not a significant difference.

The International Headache Society and the American Headache Society sponsored the congress. Dr. Artto did not report any relevant conflicts of interest.

PHILADELPHIA — Migraine with aura seems to be a risk factor for cervical artery dissection, Dr. Ville Artto concluded in a poster presented at the International Headache Congress.

His study of 626 subjects found that migraine and migraine with aura were significantly more common among both men and women who had experienced a cervical artery dissection than among control subjects.

The pathophysiologic link between migraine and cervical artery dissection remains unclear, Dr. Artto said. More than 60% of the patients who had active migraines at the time of their dissections, however, reported that their migraines were alleviated after the incident.

Patients with migraine and cervical artery dissection may represent a link between ischemic stroke and migraine, wrote Dr. Artto of the Helsinki (Finland) University Central Hospital. “This connection may represent common pathophysiological or genetic background, or both,” he wrote.

The study included 313 patients, mean age 46 years, with cervical artery dissection and 313 age-matched controls. Cases were significantly more likely to smoke than were controls (37% vs. 23%), and female cases were significantly more likely than female controls to be using oral contraceptives (36% vs. 25%).

Migraine was present in 36% of cases and in 23% of controls. Migraine with aura was present in 23% of cases and 12% of controls. Both differences were significant. In women, migraine was present in 54% of cases and 35% of controls; migraine with aura was present in 35% of cases and 18% of controls. Among men, migraine was present in 27% of cases and 16% of controls; migraine with aura was present in 16% of cases and 0.4% of controls.

When the investigators compared the characteristics of the dissection between patients with and without migraines, they found similar rates of vertebrobasilar dissection, bilateral dissection, occlusion, and intracranial dissection. The National Institutes of Health Stroke Scale score was not different at onset (3 in migraineurs and 4 in nonmigraineurs). The Rankin score was similar at 3 months (1 in both groups). The rate of ischemic stoke was 68% in migraineurs and 73% in nonmigraineurs, which was not a significant difference.

The International Headache Society and the American Headache Society sponsored the congress. Dr. Artto did not report any relevant conflicts of interest.

PHILADELPHIA — The psychiatric comorbidities of anxiety and depression may not portend poorer outcome in patients being treated for severe migraine, according to an analysis of results from a randomized, controlled trial.

In fact, compared with patients who did not have anxiety or depression, patients with those disorders actually experienced greater improvement in their headache-related disability scores over a 16-month period, said Elizabeth Seng, a doctoral student in the department of psychology at Ohio University, Athens.

The results seem to belie conventional clinical wisdom, which suggests that patients with psychiatric comorbidities don't respond to headache therapy as well as others, Ms. Seng said at a poster session during the International Headache Congress. But clinician perception, rather than clinical response, is probably the root of this belief, she said in an interview.

“In this study, participants who had comorbid depression and anxiety actually changed more over treatment,” reaching the same end points as those without depression or anxiety, Ms. Seng said.

She extracted her results from the unpublished Treatment of Severe Migraine trial, led by Kenneth Holroyd, Ph.D., also of Ohio University. The trial randomized 232 patients with severe migraine. Everyone received optimal acute therapy. Patients were then assigned to one of four treatment arms: placebo, beta-blocker, behavioral management plus placebo, or behavioral management plus beta-blocker.

The trial consisted of a 4-month run-in period and 12 months of treatment. Behavioral management consisted of clinic visits, telephone calls, and homework. The homework focused on relaxation, migraine warning signs, effective medication use, stress management or thermal biofeedback, and establishing an individual migraine management plan.

The cohort was 79% women, with a mean age of 38 years. They had an average of five headaches a month, with a 15-year headache history.

At baseline, patients with either anxiety or depression showed worse average scores on the Headache Disability Inventory (HDI) than did patients without those disorders (56 vs. 41, respectively). They also showed worse scores on the Migraine-Specific Quality of Life (MSQOL) Questionnaire (43 vs. 37).

After 1 year of treatment, both groups improved significantly and similarly on both scales. On the HDI, those with comorbidities decreased an average of 33 points, to a score of 23; those without comorbidities dropped an average of 21 points, to a score of 20, Ms. Seng reported at the congress, which was sponsored by the International Headache Society and the American Headache Society.

On the MSQOL, the group with comorbidities dropped an average of 22 points to a final score of 21. The group without comorbidities dropped an average of 15 points to a final score of 22.

The study was supported by the National Institutes of Health. Merck and GlaxoSmithKline provided the study medication. Ms. Seng had no relevant disclosures to report.

'In this study, participants who had comorbid depression and anxiety actually changed more over treatment.'

Source MS. SENG

PHILADELPHIA — The psychiatric comorbidities of anxiety and depression may not portend poorer outcome in patients being treated for severe migraine, according to an analysis of results from a randomized, controlled trial.

In fact, compared with patients who did not have anxiety or depression, patients with those disorders actually experienced greater improvement in their headache-related disability scores over a 16-month period, said Elizabeth Seng, a doctoral student in the department of psychology at Ohio University, Athens.

The results seem to belie conventional clinical wisdom, which suggests that patients with psychiatric comorbidities don't respond to headache therapy as well as others, Ms. Seng said at a poster session during the International Headache Congress. But clinician perception, rather than clinical response, is probably the root of this belief, she said in an interview.

“In this study, participants who had comorbid depression and anxiety actually changed more over treatment,” reaching the same end points as those without depression or anxiety, Ms. Seng said.

She extracted her results from the unpublished Treatment of Severe Migraine trial, led by Kenneth Holroyd, Ph.D., also of Ohio University. The trial randomized 232 patients with severe migraine. Everyone received optimal acute therapy. Patients were then assigned to one of four treatment arms: placebo, beta-blocker, behavioral management plus placebo, or behavioral management plus beta-blocker.

The trial consisted of a 4-month run-in period and 12 months of treatment. Behavioral management consisted of clinic visits, telephone calls, and homework. The homework focused on relaxation, migraine warning signs, effective medication use, stress management or thermal biofeedback, and establishing an individual migraine management plan.

The cohort was 79% women, with a mean age of 38 years. They had an average of five headaches a month, with a 15-year headache history.

At baseline, patients with either anxiety or depression showed worse average scores on the Headache Disability Inventory (HDI) than did patients without those disorders (56 vs. 41, respectively). They also showed worse scores on the Migraine-Specific Quality of Life (MSQOL) Questionnaire (43 vs. 37).

After 1 year of treatment, both groups improved significantly and similarly on both scales. On the HDI, those with comorbidities decreased an average of 33 points, to a score of 23; those without comorbidities dropped an average of 21 points, to a score of 20, Ms. Seng reported at the congress, which was sponsored by the International Headache Society and the American Headache Society.

On the MSQOL, the group with comorbidities dropped an average of 22 points to a final score of 21. The group without comorbidities dropped an average of 15 points to a final score of 22.

The study was supported by the National Institutes of Health. Merck and GlaxoSmithKline provided the study medication. Ms. Seng had no relevant disclosures to report.

'In this study, participants who had comorbid depression and anxiety actually changed more over treatment.'

Source MS. SENG

PHILADELPHIA — The psychiatric comorbidities of anxiety and depression may not portend poorer outcome in patients being treated for severe migraine, according to an analysis of results from a randomized, controlled trial.

In fact, compared with patients who did not have anxiety or depression, patients with those disorders actually experienced greater improvement in their headache-related disability scores over a 16-month period, said Elizabeth Seng, a doctoral student in the department of psychology at Ohio University, Athens.

The results seem to belie conventional clinical wisdom, which suggests that patients with psychiatric comorbidities don't respond to headache therapy as well as others, Ms. Seng said at a poster session during the International Headache Congress. But clinician perception, rather than clinical response, is probably the root of this belief, she said in an interview.

“In this study, participants who had comorbid depression and anxiety actually changed more over treatment,” reaching the same end points as those without depression or anxiety, Ms. Seng said.

She extracted her results from the unpublished Treatment of Severe Migraine trial, led by Kenneth Holroyd, Ph.D., also of Ohio University. The trial randomized 232 patients with severe migraine. Everyone received optimal acute therapy. Patients were then assigned to one of four treatment arms: placebo, beta-blocker, behavioral management plus placebo, or behavioral management plus beta-blocker.

The trial consisted of a 4-month run-in period and 12 months of treatment. Behavioral management consisted of clinic visits, telephone calls, and homework. The homework focused on relaxation, migraine warning signs, effective medication use, stress management or thermal biofeedback, and establishing an individual migraine management plan.

The cohort was 79% women, with a mean age of 38 years. They had an average of five headaches a month, with a 15-year headache history.

At baseline, patients with either anxiety or depression showed worse average scores on the Headache Disability Inventory (HDI) than did patients without those disorders (56 vs. 41, respectively). They also showed worse scores on the Migraine-Specific Quality of Life (MSQOL) Questionnaire (43 vs. 37).

After 1 year of treatment, both groups improved significantly and similarly on both scales. On the HDI, those with comorbidities decreased an average of 33 points, to a score of 23; those without comorbidities dropped an average of 21 points, to a score of 20, Ms. Seng reported at the congress, which was sponsored by the International Headache Society and the American Headache Society.

On the MSQOL, the group with comorbidities dropped an average of 22 points to a final score of 21. The group without comorbidities dropped an average of 15 points to a final score of 22.

The study was supported by the National Institutes of Health. Merck and GlaxoSmithKline provided the study medication. Ms. Seng had no relevant disclosures to report.

'In this study, participants who had comorbid depression and anxiety actually changed more over treatment.'

Source MS. SENG

A new phase II trial will test the safety and efficacy of the pandemic influenza A(H1N1) vaccine in patients with mild, moderate, and severe asthma.

Although the vaccine has already been approved as safe and effective in the general population, additional studies are necessary to confirm its effect on those with asthma—especially those who take glucocorticoid medications, Dr. Anthony Fauci said in a statement.

“People with severe asthma often take high doses of glucocorticoids that can suppress their immune system, placing them at greater risk for infection and possibly serious disease caused by 2009 H1N1 influenza virus,” said Dr. Fauci, director of the National Institute of Allergy and Infectious Disease (NIAID). “We need to determine the optimal dose of 2009 H1N1 influenza vaccine that can be safely administered to this at-risk population and whether one or two doses are needed.”

The study, sponsored by NIAID and the National Heart, Lung, and Blood Institute, plans to enroll 350-400 healthy subjects aged 12 years and older with mild, moderate, or severe asthma. Participants will be stratified into two groups: those with mild to moderate versus those with severe asthma. All participants will be randomly assigned to receive either high-dose (30 mcg) or low-dose (15 mcg) H1N1 vaccine. In addition to studying adverse events and immune response, researchers will look for any effect the vaccine may have on asthma indicators.

The study will last 34 weeks, and will be conducted in Georgia, Missouri, Ohio, North Carolina, Pennsylvania, Virginia, and Wisconsin.

A new phase II trial will test the safety and efficacy of the pandemic influenza A(H1N1) vaccine in patients with mild, moderate, and severe asthma.

Although the vaccine has already been approved as safe and effective in the general population, additional studies are necessary to confirm its effect on those with asthma—especially those who take glucocorticoid medications, Dr. Anthony Fauci said in a statement.

“People with severe asthma often take high doses of glucocorticoids that can suppress their immune system, placing them at greater risk for infection and possibly serious disease caused by 2009 H1N1 influenza virus,” said Dr. Fauci, director of the National Institute of Allergy and Infectious Disease (NIAID). “We need to determine the optimal dose of 2009 H1N1 influenza vaccine that can be safely administered to this at-risk population and whether one or two doses are needed.”

The study, sponsored by NIAID and the National Heart, Lung, and Blood Institute, plans to enroll 350-400 healthy subjects aged 12 years and older with mild, moderate, or severe asthma. Participants will be stratified into two groups: those with mild to moderate versus those with severe asthma. All participants will be randomly assigned to receive either high-dose (30 mcg) or low-dose (15 mcg) H1N1 vaccine. In addition to studying adverse events and immune response, researchers will look for any effect the vaccine may have on asthma indicators.

The study will last 34 weeks, and will be conducted in Georgia, Missouri, Ohio, North Carolina, Pennsylvania, Virginia, and Wisconsin.

A new phase II trial will test the safety and efficacy of the pandemic influenza A(H1N1) vaccine in patients with mild, moderate, and severe asthma.

Although the vaccine has already been approved as safe and effective in the general population, additional studies are necessary to confirm its effect on those with asthma—especially those who take glucocorticoid medications, Dr. Anthony Fauci said in a statement.

“People with severe asthma often take high doses of glucocorticoids that can suppress their immune system, placing them at greater risk for infection and possibly serious disease caused by 2009 H1N1 influenza virus,” said Dr. Fauci, director of the National Institute of Allergy and Infectious Disease (NIAID). “We need to determine the optimal dose of 2009 H1N1 influenza vaccine that can be safely administered to this at-risk population and whether one or two doses are needed.”

The study, sponsored by NIAID and the National Heart, Lung, and Blood Institute, plans to enroll 350-400 healthy subjects aged 12 years and older with mild, moderate, or severe asthma. Participants will be stratified into two groups: those with mild to moderate versus those with severe asthma. All participants will be randomly assigned to receive either high-dose (30 mcg) or low-dose (15 mcg) H1N1 vaccine. In addition to studying adverse events and immune response, researchers will look for any effect the vaccine may have on asthma indicators.

The study will last 34 weeks, and will be conducted in Georgia, Missouri, Ohio, North Carolina, Pennsylvania, Virginia, and Wisconsin.

PHILADELPHIA — Sumatriptan and naratriptan do not appear to significantly raise the risk of major congenital malformations in fetuses that are exposed to the drugs in utero, according to the latest analysis of an international pregnancy registry.

Established in 1996, the GlaxoSmithKline registry has accumulated data on 849 pregnancies exposed to the drugs. Birth defects occurred in 4.5% of infants exposed in the first trimester or during all of their gestation, which was not significantly higher than that previously identified for women with migraines.

Major congenital malformations are known to occur in the offspring of women with migraines at a slightly higher rate than in the general population (3.4% vs. 2%-3%, respectively), Marianne C. Cunnington, Ph.D, of GlaxoSmithKline in Harlow, England, reported in a poster at the International Headache Congress.

The registry relies on a voluntary reporting strategy that encourages health care providers to submit information on exposed pregnancies as early as possible. Retrospective case reporting also is accepted. Pregnancy outcome is ascertained by medical records that the provider forwards after birth, or by medical records confirming other outcomes, including fetal demise or abortion.

At the outset, the registry collects data on the timing, dosage, duration, indication, and administration of the drugs; maternal demographics; expected date of delivery; and any prenatal testing. At follow-up, there is a review of the pregnancy outcome, drug exposure during pregnancy, and the women's headache history during pregnancy.

So far, the registry has amassed information on 761 pregnancies exposed to sumatriptan and 88 exposed to naratriptan. Outcomes are known for 570 of the sumatriptan-exposed pregnancies and 57 of the naratriptan-exposed pregnancies. Twenty-one sumatriptan-exposed pregnancies and 31 naratriptan-exposed pregnancies are pending delivery. The rest have been lost to follow-up, Dr. Cunnington noted in the poster at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Among the sumatriptan-exposed pregnancies, there were 23 birth defects, 4 fetal deaths, 32 spontaneous fetal losses, and 11 induced abortions.

The malformations that occurred in infants who were exposed to sumatriptan in the first trimester included abnormal head circumference, single palmar crease and systolic murmur; moderate craniosynostosis; cerebral abnormality with developmental delay; partial cleft lip; ventricular septal defects; biliary atresia; diaphragmatic hernia; pyloric stenosis; anterior displacement of anus; hip dysplasia; polydactyly; malformation of left hand; and Down syndrome.

No data were available for the three birth defects that occurred in infants who were exposed to sumatriptan after the first trimester.

Among fetuses exposed to naratriptan, there were five spontaneous losses, one induced abortion, and one live infant with a 2.5-mm ventricular septal defect that was expected to close spontaneously.

Dr. Cunnington noted that five additional independent studies, including a Swedish study of more than 2,000 sumatriptan recipients, have failed to find an increase in birth defects associated with in utero exposure. “While its use in pregnancy cannot be encouraged,” she and her colleague Sara A. Ephross, Ph.D., wrote, “there is consistent evidence that sumatriptan is not associated with a substantial increase in the risk of major congenital malformations following exposure.”

To report pregnancies exposed to sumatriptan, naratriptan, or the sumatriptan/naproxen combination, North American physicians can call 800–336-2176, and international physicians can call 910-256-0549.

The report was published online in Headache (doi: 10.1111/j.1526-4610.2009.01529.x).

PHILADELPHIA — Sumatriptan and naratriptan do not appear to significantly raise the risk of major congenital malformations in fetuses that are exposed to the drugs in utero, according to the latest analysis of an international pregnancy registry.

Established in 1996, the GlaxoSmithKline registry has accumulated data on 849 pregnancies exposed to the drugs. Birth defects occurred in 4.5% of infants exposed in the first trimester or during all of their gestation, which was not significantly higher than that previously identified for women with migraines.

Major congenital malformations are known to occur in the offspring of women with migraines at a slightly higher rate than in the general population (3.4% vs. 2%-3%, respectively), Marianne C. Cunnington, Ph.D, of GlaxoSmithKline in Harlow, England, reported in a poster at the International Headache Congress.

The registry relies on a voluntary reporting strategy that encourages health care providers to submit information on exposed pregnancies as early as possible. Retrospective case reporting also is accepted. Pregnancy outcome is ascertained by medical records that the provider forwards after birth, or by medical records confirming other outcomes, including fetal demise or abortion.

At the outset, the registry collects data on the timing, dosage, duration, indication, and administration of the drugs; maternal demographics; expected date of delivery; and any prenatal testing. At follow-up, there is a review of the pregnancy outcome, drug exposure during pregnancy, and the women's headache history during pregnancy.

So far, the registry has amassed information on 761 pregnancies exposed to sumatriptan and 88 exposed to naratriptan. Outcomes are known for 570 of the sumatriptan-exposed pregnancies and 57 of the naratriptan-exposed pregnancies. Twenty-one sumatriptan-exposed pregnancies and 31 naratriptan-exposed pregnancies are pending delivery. The rest have been lost to follow-up, Dr. Cunnington noted in the poster at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Among the sumatriptan-exposed pregnancies, there were 23 birth defects, 4 fetal deaths, 32 spontaneous fetal losses, and 11 induced abortions.

The malformations that occurred in infants who were exposed to sumatriptan in the first trimester included abnormal head circumference, single palmar crease and systolic murmur; moderate craniosynostosis; cerebral abnormality with developmental delay; partial cleft lip; ventricular septal defects; biliary atresia; diaphragmatic hernia; pyloric stenosis; anterior displacement of anus; hip dysplasia; polydactyly; malformation of left hand; and Down syndrome.

No data were available for the three birth defects that occurred in infants who were exposed to sumatriptan after the first trimester.

Among fetuses exposed to naratriptan, there were five spontaneous losses, one induced abortion, and one live infant with a 2.5-mm ventricular septal defect that was expected to close spontaneously.

Dr. Cunnington noted that five additional independent studies, including a Swedish study of more than 2,000 sumatriptan recipients, have failed to find an increase in birth defects associated with in utero exposure. “While its use in pregnancy cannot be encouraged,” she and her colleague Sara A. Ephross, Ph.D., wrote, “there is consistent evidence that sumatriptan is not associated with a substantial increase in the risk of major congenital malformations following exposure.”

To report pregnancies exposed to sumatriptan, naratriptan, or the sumatriptan/naproxen combination, North American physicians can call 800–336-2176, and international physicians can call 910-256-0549.

The report was published online in Headache (doi: 10.1111/j.1526-4610.2009.01529.x).

PHILADELPHIA — Sumatriptan and naratriptan do not appear to significantly raise the risk of major congenital malformations in fetuses that are exposed to the drugs in utero, according to the latest analysis of an international pregnancy registry.

Established in 1996, the GlaxoSmithKline registry has accumulated data on 849 pregnancies exposed to the drugs. Birth defects occurred in 4.5% of infants exposed in the first trimester or during all of their gestation, which was not significantly higher than that previously identified for women with migraines.

Major congenital malformations are known to occur in the offspring of women with migraines at a slightly higher rate than in the general population (3.4% vs. 2%-3%, respectively), Marianne C. Cunnington, Ph.D, of GlaxoSmithKline in Harlow, England, reported in a poster at the International Headache Congress.

The registry relies on a voluntary reporting strategy that encourages health care providers to submit information on exposed pregnancies as early as possible. Retrospective case reporting also is accepted. Pregnancy outcome is ascertained by medical records that the provider forwards after birth, or by medical records confirming other outcomes, including fetal demise or abortion.

At the outset, the registry collects data on the timing, dosage, duration, indication, and administration of the drugs; maternal demographics; expected date of delivery; and any prenatal testing. At follow-up, there is a review of the pregnancy outcome, drug exposure during pregnancy, and the women's headache history during pregnancy.

So far, the registry has amassed information on 761 pregnancies exposed to sumatriptan and 88 exposed to naratriptan. Outcomes are known for 570 of the sumatriptan-exposed pregnancies and 57 of the naratriptan-exposed pregnancies. Twenty-one sumatriptan-exposed pregnancies and 31 naratriptan-exposed pregnancies are pending delivery. The rest have been lost to follow-up, Dr. Cunnington noted in the poster at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Among the sumatriptan-exposed pregnancies, there were 23 birth defects, 4 fetal deaths, 32 spontaneous fetal losses, and 11 induced abortions.

The malformations that occurred in infants who were exposed to sumatriptan in the first trimester included abnormal head circumference, single palmar crease and systolic murmur; moderate craniosynostosis; cerebral abnormality with developmental delay; partial cleft lip; ventricular septal defects; biliary atresia; diaphragmatic hernia; pyloric stenosis; anterior displacement of anus; hip dysplasia; polydactyly; malformation of left hand; and Down syndrome.

No data were available for the three birth defects that occurred in infants who were exposed to sumatriptan after the first trimester.

Among fetuses exposed to naratriptan, there were five spontaneous losses, one induced abortion, and one live infant with a 2.5-mm ventricular septal defect that was expected to close spontaneously.

Dr. Cunnington noted that five additional independent studies, including a Swedish study of more than 2,000 sumatriptan recipients, have failed to find an increase in birth defects associated with in utero exposure. “While its use in pregnancy cannot be encouraged,” she and her colleague Sara A. Ephross, Ph.D., wrote, “there is consistent evidence that sumatriptan is not associated with a substantial increase in the risk of major congenital malformations following exposure.”

To report pregnancies exposed to sumatriptan, naratriptan, or the sumatriptan/naproxen combination, North American physicians can call 800–336-2176, and international physicians can call 910-256-0549.

The report was published online in Headache (doi: 10.1111/j.1526-4610.2009.01529.x).

BANGKOK, THAILAND — Serum levels of N-acetyl aspartate are significantly higher among patients with relapsing-remitting multiple sclerosis and clinical syndromes suggestive of MS than they are in patients with neuromyelitis optica, and might be a valid biomarker to help distinguish the disorders.

In her study of 176 subjects, Dr. Carla Tortorella found that serum N-acetyl aspartate (NAA) levels were about 14 times higher in those with MS or a clinically isolated syndrome suggestive of MS (CIS) than they were in those with neuromyelitis optica (NMO). In fact, said Dr. Tortorella of the University of Bari, Italy, levels in NMO patients were the same as they were in age-matched healthy controls.

NAA is normally synthesized in neural mitochondria and leaves the cell by several methods, Dr. Tortorella said at the World Congress of Neurology: passing from neurons to oligodendrocytes where it is catabolized; passing through the astrocytes into the extracellular space and thus into the bloodstream; and passing into the cerebrospinal fluid. This process is abnormal in patients with MS, leading to increased serum NAA levels, but no studies have compared these levels in patients with MS and those with NMO.

Dr. Tortorella examined serum and CSF levels of NAA in 48 patients with relapsing-remitting MS, 20 with CIS, and 32 with NMO. She also included 76 age-matched healthy controls for comparison.

There were some baseline differences between the groups. Those with NMO were older (median 43 years) than those with CIS (28 years) or MS (38 years). Disease duration was also different: CIS, 6 months; MS, 6 years; NMO, 5 years.

The Expanded Disability Status Scale score was 1.5 in the CIS group, 2 in the MS group, and 4.6 in the NMO group. None of the MS or CIS patients were taking disease-modifying drugs, while 10 of the NMO patients were taking immunosuppressants.

All patients submitted serum NAA samples. The levels were similarly high in those with CIS and MS (1.7 mM/L in each group). These were significantly higher than the levels found in those with NMO and among healthy controls (0.12 mM/L each).

While all of the MS and CIS patients had CSF levels available for testing, only eight of the NMO patients did, and there were no CSF samples from healthy controls. “Nevertheless, the CSF NAA levels were markedly and consistently higher in the CIS and MS patients [0.68 and 0.76 mM/L] than they were in the NMO patients [0.05 mM/L],” Dr. Tortorella said.

She found no significant association between NAA levels and age, disease duration, or disease activity. However, among those with MS, she found a significant correlation between increasing NAA levels and worsening Expanded Disability Status Scale scores.

Because the correlation between serum NAA and MS is so much stronger than it is with NMO, Dr. Tortorella suggested that NAA might be a useful way not only to help distinguish between the disorders but to measure the progression of MS, particularly in the early phase of the disease.

The findings make sense in light of the pathology of the various disorders, she said. “One theory is that NAA is higher in MS and CIS because there is more extensive and less focal impairment than there is in NMO, suggesting axonal damage that extends beyond the enhancing lesion. There also could be a defective NAA metabolism in the oligodendrocytes, which are really damaged in MS.”

Dr. Tortorella did not have any conflicts of interest to declare.

BANGKOK, THAILAND — Serum levels of N-acetyl aspartate are significantly higher among patients with relapsing-remitting multiple sclerosis and clinical syndromes suggestive of MS than they are in patients with neuromyelitis optica, and might be a valid biomarker to help distinguish the disorders.

In her study of 176 subjects, Dr. Carla Tortorella found that serum N-acetyl aspartate (NAA) levels were about 14 times higher in those with MS or a clinically isolated syndrome suggestive of MS (CIS) than they were in those with neuromyelitis optica (NMO). In fact, said Dr. Tortorella of the University of Bari, Italy, levels in NMO patients were the same as they were in age-matched healthy controls.

NAA is normally synthesized in neural mitochondria and leaves the cell by several methods, Dr. Tortorella said at the World Congress of Neurology: passing from neurons to oligodendrocytes where it is catabolized; passing through the astrocytes into the extracellular space and thus into the bloodstream; and passing into the cerebrospinal fluid. This process is abnormal in patients with MS, leading to increased serum NAA levels, but no studies have compared these levels in patients with MS and those with NMO.

Dr. Tortorella examined serum and CSF levels of NAA in 48 patients with relapsing-remitting MS, 20 with CIS, and 32 with NMO. She also included 76 age-matched healthy controls for comparison.

There were some baseline differences between the groups. Those with NMO were older (median 43 years) than those with CIS (28 years) or MS (38 years). Disease duration was also different: CIS, 6 months; MS, 6 years; NMO, 5 years.

The Expanded Disability Status Scale score was 1.5 in the CIS group, 2 in the MS group, and 4.6 in the NMO group. None of the MS or CIS patients were taking disease-modifying drugs, while 10 of the NMO patients were taking immunosuppressants.

All patients submitted serum NAA samples. The levels were similarly high in those with CIS and MS (1.7 mM/L in each group). These were significantly higher than the levels found in those with NMO and among healthy controls (0.12 mM/L each).

While all of the MS and CIS patients had CSF levels available for testing, only eight of the NMO patients did, and there were no CSF samples from healthy controls. “Nevertheless, the CSF NAA levels were markedly and consistently higher in the CIS and MS patients [0.68 and 0.76 mM/L] than they were in the NMO patients [0.05 mM/L],” Dr. Tortorella said.

She found no significant association between NAA levels and age, disease duration, or disease activity. However, among those with MS, she found a significant correlation between increasing NAA levels and worsening Expanded Disability Status Scale scores.

Because the correlation between serum NAA and MS is so much stronger than it is with NMO, Dr. Tortorella suggested that NAA might be a useful way not only to help distinguish between the disorders but to measure the progression of MS, particularly in the early phase of the disease.

The findings make sense in light of the pathology of the various disorders, she said. “One theory is that NAA is higher in MS and CIS because there is more extensive and less focal impairment than there is in NMO, suggesting axonal damage that extends beyond the enhancing lesion. There also could be a defective NAA metabolism in the oligodendrocytes, which are really damaged in MS.”

Dr. Tortorella did not have any conflicts of interest to declare.

BANGKOK, THAILAND — Serum levels of N-acetyl aspartate are significantly higher among patients with relapsing-remitting multiple sclerosis and clinical syndromes suggestive of MS than they are in patients with neuromyelitis optica, and might be a valid biomarker to help distinguish the disorders.

In her study of 176 subjects, Dr. Carla Tortorella found that serum N-acetyl aspartate (NAA) levels were about 14 times higher in those with MS or a clinically isolated syndrome suggestive of MS (CIS) than they were in those with neuromyelitis optica (NMO). In fact, said Dr. Tortorella of the University of Bari, Italy, levels in NMO patients were the same as they were in age-matched healthy controls.

NAA is normally synthesized in neural mitochondria and leaves the cell by several methods, Dr. Tortorella said at the World Congress of Neurology: passing from neurons to oligodendrocytes where it is catabolized; passing through the astrocytes into the extracellular space and thus into the bloodstream; and passing into the cerebrospinal fluid. This process is abnormal in patients with MS, leading to increased serum NAA levels, but no studies have compared these levels in patients with MS and those with NMO.

Dr. Tortorella examined serum and CSF levels of NAA in 48 patients with relapsing-remitting MS, 20 with CIS, and 32 with NMO. She also included 76 age-matched healthy controls for comparison.

There were some baseline differences between the groups. Those with NMO were older (median 43 years) than those with CIS (28 years) or MS (38 years). Disease duration was also different: CIS, 6 months; MS, 6 years; NMO, 5 years.

The Expanded Disability Status Scale score was 1.5 in the CIS group, 2 in the MS group, and 4.6 in the NMO group. None of the MS or CIS patients were taking disease-modifying drugs, while 10 of the NMO patients were taking immunosuppressants.

All patients submitted serum NAA samples. The levels were similarly high in those with CIS and MS (1.7 mM/L in each group). These were significantly higher than the levels found in those with NMO and among healthy controls (0.12 mM/L each).

While all of the MS and CIS patients had CSF levels available for testing, only eight of the NMO patients did, and there were no CSF samples from healthy controls. “Nevertheless, the CSF NAA levels were markedly and consistently higher in the CIS and MS patients [0.68 and 0.76 mM/L] than they were in the NMO patients [0.05 mM/L],” Dr. Tortorella said.

She found no significant association between NAA levels and age, disease duration, or disease activity. However, among those with MS, she found a significant correlation between increasing NAA levels and worsening Expanded Disability Status Scale scores.

Because the correlation between serum NAA and MS is so much stronger than it is with NMO, Dr. Tortorella suggested that NAA might be a useful way not only to help distinguish between the disorders but to measure the progression of MS, particularly in the early phase of the disease.

The findings make sense in light of the pathology of the various disorders, she said. “One theory is that NAA is higher in MS and CIS because there is more extensive and less focal impairment than there is in NMO, suggesting axonal damage that extends beyond the enhancing lesion. There also could be a defective NAA metabolism in the oligodendrocytes, which are really damaged in MS.”

Dr. Tortorella did not have any conflicts of interest to declare.

PHILADELPHIA — Sumatriptan and naratriptan do not appear to significantly raise the risk of major congenital malformations in fetuses that are exposed to the drugs in utero, according to the latest analysis of an international pregnancy registry.

Established in 1996, the GlaxoSmithKline registry has accumulated data on 849 pregnancies exposed to the drugs. Birth defects occurred in 4.5% of infants exposed in the first trimester or during all of their gestation, which was not significantly higher than that previously identified for women with migraines. Major congenital malformations are known to occur in the offspring of women with migraines at a slightly higher rate than in the general population (3.4% vs. 2%-3%, respectively), Marianne C. Cunnington, Ph.D., and her colleague Sara A. Ephross, Ph.D., reported in a poster at the International Headache Congress. Both are employees of GlaxoSmithKline.

The registry relies on a voluntary reporting strategy that encourages health care providers to submit information on exposed pregnancies as early as possible. Retrospective case reporting also is accepted. Pregnancy outcome is ascertained by medical records that the provider forwards after birth, or by medical records confirming other outcomes, including fetal demise or abortion.

So far, the registry has amassed information on 761 pregnancies exposed to sumatriptan and 88 exposed to naratriptan. Outcomes are known for 570 of the sumatriptan-exposed pregnancies and 57 of the naratriptan-exposed pregnancies. Twenty-one sumatriptan-exposed pregnancies and 31 naratriptan-exposed pregnancies are pending delivery. The rest have been lost to follow-up, the investigators noted in their poster at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Among the sumatriptan-exposed pregnancies, there were 23 birth defects, 4 fetal deaths, 32 spontaneous fetal losses, and 11 induced abortions.

The malformations that occurred in infants who were exposed to sumatriptan in the first trimester included abnormal head circumference, single palmar crease, and systolic murmur; moderate craniosynostosis; cerebral abnormality with developmental delay; partial cleft lip; ventricular septal defects (4); biliary atresia; diaphragmatic hernia; pyloric stenosis (3); anterior displacement of anus; hip dysplasia; polydactyly; malformation of left hand; and Down syndrome (3).

No data were available for the three birth defects that occurred in infants who were exposed to sumatriptan after the first trimester.

Among fetuses exposed to naratriptan, there were five spontaneous losses, one induced abortion, and one live infant with a 2.5-mm ventricular septal defect that was expected to close spontaneously.

The pregnancy registry did not contain any data on the exposure to the combination of sumatriptan and naproxen. The full report was published online in Headache (doi: 10.1111/j.1526-4610.2009.01529.x).

PHILADELPHIA — Sumatriptan and naratriptan do not appear to significantly raise the risk of major congenital malformations in fetuses that are exposed to the drugs in utero, according to the latest analysis of an international pregnancy registry.

Established in 1996, the GlaxoSmithKline registry has accumulated data on 849 pregnancies exposed to the drugs. Birth defects occurred in 4.5% of infants exposed in the first trimester or during all of their gestation, which was not significantly higher than that previously identified for women with migraines. Major congenital malformations are known to occur in the offspring of women with migraines at a slightly higher rate than in the general population (3.4% vs. 2%-3%, respectively), Marianne C. Cunnington, Ph.D., and her colleague Sara A. Ephross, Ph.D., reported in a poster at the International Headache Congress. Both are employees of GlaxoSmithKline.

The registry relies on a voluntary reporting strategy that encourages health care providers to submit information on exposed pregnancies as early as possible. Retrospective case reporting also is accepted. Pregnancy outcome is ascertained by medical records that the provider forwards after birth, or by medical records confirming other outcomes, including fetal demise or abortion.

So far, the registry has amassed information on 761 pregnancies exposed to sumatriptan and 88 exposed to naratriptan. Outcomes are known for 570 of the sumatriptan-exposed pregnancies and 57 of the naratriptan-exposed pregnancies. Twenty-one sumatriptan-exposed pregnancies and 31 naratriptan-exposed pregnancies are pending delivery. The rest have been lost to follow-up, the investigators noted in their poster at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Among the sumatriptan-exposed pregnancies, there were 23 birth defects, 4 fetal deaths, 32 spontaneous fetal losses, and 11 induced abortions.

The malformations that occurred in infants who were exposed to sumatriptan in the first trimester included abnormal head circumference, single palmar crease, and systolic murmur; moderate craniosynostosis; cerebral abnormality with developmental delay; partial cleft lip; ventricular septal defects (4); biliary atresia; diaphragmatic hernia; pyloric stenosis (3); anterior displacement of anus; hip dysplasia; polydactyly; malformation of left hand; and Down syndrome (3).

No data were available for the three birth defects that occurred in infants who were exposed to sumatriptan after the first trimester.

Among fetuses exposed to naratriptan, there were five spontaneous losses, one induced abortion, and one live infant with a 2.5-mm ventricular septal defect that was expected to close spontaneously.

The pregnancy registry did not contain any data on the exposure to the combination of sumatriptan and naproxen. The full report was published online in Headache (doi: 10.1111/j.1526-4610.2009.01529.x).

PHILADELPHIA — Sumatriptan and naratriptan do not appear to significantly raise the risk of major congenital malformations in fetuses that are exposed to the drugs in utero, according to the latest analysis of an international pregnancy registry.

Established in 1996, the GlaxoSmithKline registry has accumulated data on 849 pregnancies exposed to the drugs. Birth defects occurred in 4.5% of infants exposed in the first trimester or during all of their gestation, which was not significantly higher than that previously identified for women with migraines. Major congenital malformations are known to occur in the offspring of women with migraines at a slightly higher rate than in the general population (3.4% vs. 2%-3%, respectively), Marianne C. Cunnington, Ph.D., and her colleague Sara A. Ephross, Ph.D., reported in a poster at the International Headache Congress. Both are employees of GlaxoSmithKline.

The registry relies on a voluntary reporting strategy that encourages health care providers to submit information on exposed pregnancies as early as possible. Retrospective case reporting also is accepted. Pregnancy outcome is ascertained by medical records that the provider forwards after birth, or by medical records confirming other outcomes, including fetal demise or abortion.

So far, the registry has amassed information on 761 pregnancies exposed to sumatriptan and 88 exposed to naratriptan. Outcomes are known for 570 of the sumatriptan-exposed pregnancies and 57 of the naratriptan-exposed pregnancies. Twenty-one sumatriptan-exposed pregnancies and 31 naratriptan-exposed pregnancies are pending delivery. The rest have been lost to follow-up, the investigators noted in their poster at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Among the sumatriptan-exposed pregnancies, there were 23 birth defects, 4 fetal deaths, 32 spontaneous fetal losses, and 11 induced abortions.

The malformations that occurred in infants who were exposed to sumatriptan in the first trimester included abnormal head circumference, single palmar crease, and systolic murmur; moderate craniosynostosis; cerebral abnormality with developmental delay; partial cleft lip; ventricular septal defects (4); biliary atresia; diaphragmatic hernia; pyloric stenosis (3); anterior displacement of anus; hip dysplasia; polydactyly; malformation of left hand; and Down syndrome (3).

No data were available for the three birth defects that occurred in infants who were exposed to sumatriptan after the first trimester.

Among fetuses exposed to naratriptan, there were five spontaneous losses, one induced abortion, and one live infant with a 2.5-mm ventricular septal defect that was expected to close spontaneously.

The pregnancy registry did not contain any data on the exposure to the combination of sumatriptan and naproxen. The full report was published online in Headache (doi: 10.1111/j.1526-4610.2009.01529.x).

PHILADELPHIA — OnabotulinumtoxinA appears to be a safe, effective, and well-tolerated headache prophylactic for patients with chronic migraine.

Two large randomized controlled trials showed that the toxin reduced migraine frequency and improved headache-related disability over 24 weeks, Dr. David W. Dodick said at the International Headache Congress.

The studies—PREEMPT 1 and 2—were conducted at 22 centers in North America and Europe, and included 1,384 patients (average age 41 years). Each trial consisted of a 4-week baseline period, during which patients kept a daily headache diary, followed by 24 weeks of treatment during which patients received two injection cycles of either placebo or onabotulinumtoxinA (Botox), which has not been approved by the Food and Drug Administration for migraine prophylaxis. For 24-56 weeks, there was an open-label trial consisting of three injection cycles of the study drug, said Dr. Dodick of the Mayo Clinic Arizona, Phoenix.

At baseline, patients reported a mean of 20 headache days per month, 19 of which were considered migraine days, with a mean of 290 cumulative headache hours. The mean score on the Headache Impact Test-6 (HIT-6) survey was 65, indicating severe impact. Most of the patients (93%) also reported severe headache-related disability, and 65% were overusing acute pain medications.

During the double-blind phase, patients randomized to the treatment group received two injection cycles (one every 12 weeks) of onabotulinumtoxinA 155 U. The medication was injected at 31 sites across seven muscle areas in the head and neck. At the physicians' discretion, an additional 40 units could be injected among three additional muscle groups.

The study's main end point was frequency of headache days; secondary end points were frequency of migraine days, moderate/severe headache days, monthly headache hours, and proportion of patients with a severe HIT-6 score.

At 24 weeks, patients in the active group had a significantly greater reduction in headache days and migraine days than those taking placebo (—8 vs. —6, respectively). The HIT-6 score also declined significantly more among the active group (—5 points vs. —2 points). Patients receiving the study drug experienced a greater decrease in cumulative headache hours per month (—120 vs. —80 hours), Dr. Dodick said at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Adverse events occurred in 62% of those taking the study drug and 52% of those taking placebo—a significant difference. The study was sponsored by Allergan Inc. Dr. Dodick reported having received honoraria from the company.

Patients receiving the study drug experienced a greater decrease in cumulative headache hours per month.

Source DR. DODICK

PHILADELPHIA — OnabotulinumtoxinA appears to be a safe, effective, and well-tolerated headache prophylactic for patients with chronic migraine.

Two large randomized controlled trials showed that the toxin reduced migraine frequency and improved headache-related disability over 24 weeks, Dr. David W. Dodick said at the International Headache Congress.

The studies—PREEMPT 1 and 2—were conducted at 22 centers in North America and Europe, and included 1,384 patients (average age 41 years). Each trial consisted of a 4-week baseline period, during which patients kept a daily headache diary, followed by 24 weeks of treatment during which patients received two injection cycles of either placebo or onabotulinumtoxinA (Botox), which has not been approved by the Food and Drug Administration for migraine prophylaxis. For 24-56 weeks, there was an open-label trial consisting of three injection cycles of the study drug, said Dr. Dodick of the Mayo Clinic Arizona, Phoenix.

At baseline, patients reported a mean of 20 headache days per month, 19 of which were considered migraine days, with a mean of 290 cumulative headache hours. The mean score on the Headache Impact Test-6 (HIT-6) survey was 65, indicating severe impact. Most of the patients (93%) also reported severe headache-related disability, and 65% were overusing acute pain medications.

During the double-blind phase, patients randomized to the treatment group received two injection cycles (one every 12 weeks) of onabotulinumtoxinA 155 U. The medication was injected at 31 sites across seven muscle areas in the head and neck. At the physicians' discretion, an additional 40 units could be injected among three additional muscle groups.

The study's main end point was frequency of headache days; secondary end points were frequency of migraine days, moderate/severe headache days, monthly headache hours, and proportion of patients with a severe HIT-6 score.

At 24 weeks, patients in the active group had a significantly greater reduction in headache days and migraine days than those taking placebo (—8 vs. —6, respectively). The HIT-6 score also declined significantly more among the active group (—5 points vs. —2 points). Patients receiving the study drug experienced a greater decrease in cumulative headache hours per month (—120 vs. —80 hours), Dr. Dodick said at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Adverse events occurred in 62% of those taking the study drug and 52% of those taking placebo—a significant difference. The study was sponsored by Allergan Inc. Dr. Dodick reported having received honoraria from the company.

Patients receiving the study drug experienced a greater decrease in cumulative headache hours per month.

Source DR. DODICK

PHILADELPHIA — OnabotulinumtoxinA appears to be a safe, effective, and well-tolerated headache prophylactic for patients with chronic migraine.

Two large randomized controlled trials showed that the toxin reduced migraine frequency and improved headache-related disability over 24 weeks, Dr. David W. Dodick said at the International Headache Congress.

The studies—PREEMPT 1 and 2—were conducted at 22 centers in North America and Europe, and included 1,384 patients (average age 41 years). Each trial consisted of a 4-week baseline period, during which patients kept a daily headache diary, followed by 24 weeks of treatment during which patients received two injection cycles of either placebo or onabotulinumtoxinA (Botox), which has not been approved by the Food and Drug Administration for migraine prophylaxis. For 24-56 weeks, there was an open-label trial consisting of three injection cycles of the study drug, said Dr. Dodick of the Mayo Clinic Arizona, Phoenix.

At baseline, patients reported a mean of 20 headache days per month, 19 of which were considered migraine days, with a mean of 290 cumulative headache hours. The mean score on the Headache Impact Test-6 (HIT-6) survey was 65, indicating severe impact. Most of the patients (93%) also reported severe headache-related disability, and 65% were overusing acute pain medications.

During the double-blind phase, patients randomized to the treatment group received two injection cycles (one every 12 weeks) of onabotulinumtoxinA 155 U. The medication was injected at 31 sites across seven muscle areas in the head and neck. At the physicians' discretion, an additional 40 units could be injected among three additional muscle groups.

The study's main end point was frequency of headache days; secondary end points were frequency of migraine days, moderate/severe headache days, monthly headache hours, and proportion of patients with a severe HIT-6 score.

At 24 weeks, patients in the active group had a significantly greater reduction in headache days and migraine days than those taking placebo (—8 vs. —6, respectively). The HIT-6 score also declined significantly more among the active group (—5 points vs. —2 points). Patients receiving the study drug experienced a greater decrease in cumulative headache hours per month (—120 vs. —80 hours), Dr. Dodick said at the congress, which was sponsored by the International Headache Society and the American Headache Society.

Adverse events occurred in 62% of those taking the study drug and 52% of those taking placebo—a significant difference. The study was sponsored by Allergan Inc. Dr. Dodick reported having received honoraria from the company.

Patients receiving the study drug experienced a greater decrease in cumulative headache hours per month.

Source DR. DODICK

A new phase II trial will test the safety and efficacy of the pandemic influenza A(H1N1) vaccine on patients with mild to severe asthma.

Although the vaccine has already been approved as safe and effective in the general population, additional studies are necessary to confirm its effect on those with asthma—especially those who take glucocorticoid medications, Dr. Anthony Fauci said in a statement.

“People with severe asthma often take high doses of glucocorticoids that can suppress their immune system, placing them at greater risk for infection and possibly serious disease caused by 2009 H1N1 influenza virus,” said Dr. Fauci, director of the National Institute of Allergy and Infectious Disease (NIAID). “We need to determine the optimal dose of 2009 H1N1 influenza vaccine that can be safely administered to this at-risk population and whether one or two doses are needed to provide an immune response that is predictive of protection.”

The study, sponsored by NIAID and the National Heart, Lung, and Blood Institute, plans to enroll 350-400 healthy subjects aged 12 years and older with mild, moderate, or severe asthma. Participants will be stratified into two groups: those with mild to moderate versus those with severe asthma. All participants will be randomly assigned to receive either a high-dose (30 mcg) or low-dose (15 mcg) H1N1 vaccine. Both vaccine dosages will be administered in two intramuscular injections 21 days apart. Participants assigned to the higher dose (30 mcg) will receive two injections of the 15-mcg vaccine at each administration.

A new phase II trial will test the safety and efficacy of the pandemic influenza A(H1N1) vaccine on patients with mild to severe asthma.

Although the vaccine has already been approved as safe and effective in the general population, additional studies are necessary to confirm its effect on those with asthma—especially those who take glucocorticoid medications, Dr. Anthony Fauci said in a statement.

“People with severe asthma often take high doses of glucocorticoids that can suppress their immune system, placing them at greater risk for infection and possibly serious disease caused by 2009 H1N1 influenza virus,” said Dr. Fauci, director of the National Institute of Allergy and Infectious Disease (NIAID). “We need to determine the optimal dose of 2009 H1N1 influenza vaccine that can be safely administered to this at-risk population and whether one or two doses are needed to provide an immune response that is predictive of protection.”

The study, sponsored by NIAID and the National Heart, Lung, and Blood Institute, plans to enroll 350-400 healthy subjects aged 12 years and older with mild, moderate, or severe asthma. Participants will be stratified into two groups: those with mild to moderate versus those with severe asthma. All participants will be randomly assigned to receive either a high-dose (30 mcg) or low-dose (15 mcg) H1N1 vaccine. Both vaccine dosages will be administered in two intramuscular injections 21 days apart. Participants assigned to the higher dose (30 mcg) will receive two injections of the 15-mcg vaccine at each administration.

A new phase II trial will test the safety and efficacy of the pandemic influenza A(H1N1) vaccine on patients with mild to severe asthma.

Although the vaccine has already been approved as safe and effective in the general population, additional studies are necessary to confirm its effect on those with asthma—especially those who take glucocorticoid medications, Dr. Anthony Fauci said in a statement.

“People with severe asthma often take high doses of glucocorticoids that can suppress their immune system, placing them at greater risk for infection and possibly serious disease caused by 2009 H1N1 influenza virus,” said Dr. Fauci, director of the National Institute of Allergy and Infectious Disease (NIAID). “We need to determine the optimal dose of 2009 H1N1 influenza vaccine that can be safely administered to this at-risk population and whether one or two doses are needed to provide an immune response that is predictive of protection.”

The study, sponsored by NIAID and the National Heart, Lung, and Blood Institute, plans to enroll 350-400 healthy subjects aged 12 years and older with mild, moderate, or severe asthma. Participants will be stratified into two groups: those with mild to moderate versus those with severe asthma. All participants will be randomly assigned to receive either a high-dose (30 mcg) or low-dose (15 mcg) H1N1 vaccine. Both vaccine dosages will be administered in two intramuscular injections 21 days apart. Participants assigned to the higher dose (30 mcg) will receive two injections of the 15-mcg vaccine at each administration.