LONDON—A dynamic model based on long-term observations and a statistical modeling approach can help neurologists predict the future disability trajectory of a new patient with primary progressive multiple sclerosis (MS), according to a study presented at the 32nd Congress of the European Committee for Treatment and Research in MS (ECTRIMS). The existence of heterogeneous classes of patients should be considered in the design of future clinical trials in primary progressive MS that have time-to-reach-disability milestones as their primary end points, said the researchers.

Several natural history studies of patients with primary progressive MS have been reported from international registries over the past decades. This population had a consistently heterogeneous rate of disability accumulation. Time to reach the milestone of an Expanded Disability Status Scale (EDSS) score of 6 ranged between seven and 14 years from disease onset.

Alessio Signori, PhD, postdoctoral researcher in biostatistics at the University of Genoa, Italy, and colleagues sought to identify subgroups of patients with primary progressive MS who had similar longitudinal EDSS trajectories over time. The investigators included in their analysis all patients with primary progressive MS in the MSBase international registry who had their first EDSS assessment within five years of disease onset. Longitudinal EDSS scores were modeled by a latent class mixed model (LCMM) using a nonlinear function of time from onset. LCMM is an advanced statistical approach that models heterogeneity between patients by classifying them into unobserved groups (ie, latent classes) that have similar characteristics.

A total of 853 participants with primary progressive MS (51.7% female) from 24 countries with a mean age at onset of 42.4, a median baseline EDSS score of 4, and 2.4 years of disease duration were included. LCMM detected three distinct subgroups of patients with a mild (n = 143; 16.8%), a moderate (n = 378; 44.3%), and a severe (n = 332; 38.9%) disability trajectory, respectively. Time from disease onset to diagnosis was shortest for the severe group. Median time to an EDSS score of 4 was 14, five, and 3.7 years for the three groups, respectively. The probability of reaching an EDSS score of 6 at 10 years was 0%, 46.5%, and 83.1%, respectively. Increasing severity of the disability time course was related to a decreasing frequency of patients with at least one relapse during follow-up (ie, from 47.6% to 36.5%).

“Using this modeling approach, it is possible to predict the future disease course of a subject with primary progressive MS using early EDSS assessments,” said Dr. Signori. “By using only one year of EDSS monitoring, 73% of patients are correctly classified in their disability trajectory group (mild, moderate, or severe). After three years, this proportion is 87%, and after five years, it is 92%.”

LONDON—A dynamic model based on long-term observations and a statistical modeling approach can help neurologists predict the future disability trajectory of a new patient with primary progressive multiple sclerosis (MS), according to a study presented at the 32nd Congress of the European Committee for Treatment and Research in MS (ECTRIMS). The existence of heterogeneous classes of patients should be considered in the design of future clinical trials in primary progressive MS that have time-to-reach-disability milestones as their primary end points, said the researchers.

Several natural history studies of patients with primary progressive MS have been reported from international registries over the past decades. This population had a consistently heterogeneous rate of disability accumulation. Time to reach the milestone of an Expanded Disability Status Scale (EDSS) score of 6 ranged between seven and 14 years from disease onset.

Alessio Signori, PhD, postdoctoral researcher in biostatistics at the University of Genoa, Italy, and colleagues sought to identify subgroups of patients with primary progressive MS who had similar longitudinal EDSS trajectories over time. The investigators included in their analysis all patients with primary progressive MS in the MSBase international registry who had their first EDSS assessment within five years of disease onset. Longitudinal EDSS scores were modeled by a latent class mixed model (LCMM) using a nonlinear function of time from onset. LCMM is an advanced statistical approach that models heterogeneity between patients by classifying them into unobserved groups (ie, latent classes) that have similar characteristics.

A total of 853 participants with primary progressive MS (51.7% female) from 24 countries with a mean age at onset of 42.4, a median baseline EDSS score of 4, and 2.4 years of disease duration were included. LCMM detected three distinct subgroups of patients with a mild (n = 143; 16.8%), a moderate (n = 378; 44.3%), and a severe (n = 332; 38.9%) disability trajectory, respectively. Time from disease onset to diagnosis was shortest for the severe group. Median time to an EDSS score of 4 was 14, five, and 3.7 years for the three groups, respectively. The probability of reaching an EDSS score of 6 at 10 years was 0%, 46.5%, and 83.1%, respectively. Increasing severity of the disability time course was related to a decreasing frequency of patients with at least one relapse during follow-up (ie, from 47.6% to 36.5%).

“Using this modeling approach, it is possible to predict the future disease course of a subject with primary progressive MS using early EDSS assessments,” said Dr. Signori. “By using only one year of EDSS monitoring, 73% of patients are correctly classified in their disability trajectory group (mild, moderate, or severe). After three years, this proportion is 87%, and after five years, it is 92%.”

LONDON—A dynamic model based on long-term observations and a statistical modeling approach can help neurologists predict the future disability trajectory of a new patient with primary progressive multiple sclerosis (MS), according to a study presented at the 32nd Congress of the European Committee for Treatment and Research in MS (ECTRIMS). The existence of heterogeneous classes of patients should be considered in the design of future clinical trials in primary progressive MS that have time-to-reach-disability milestones as their primary end points, said the researchers.

Several natural history studies of patients with primary progressive MS have been reported from international registries over the past decades. This population had a consistently heterogeneous rate of disability accumulation. Time to reach the milestone of an Expanded Disability Status Scale (EDSS) score of 6 ranged between seven and 14 years from disease onset.

Alessio Signori, PhD, postdoctoral researcher in biostatistics at the University of Genoa, Italy, and colleagues sought to identify subgroups of patients with primary progressive MS who had similar longitudinal EDSS trajectories over time. The investigators included in their analysis all patients with primary progressive MS in the MSBase international registry who had their first EDSS assessment within five years of disease onset. Longitudinal EDSS scores were modeled by a latent class mixed model (LCMM) using a nonlinear function of time from onset. LCMM is an advanced statistical approach that models heterogeneity between patients by classifying them into unobserved groups (ie, latent classes) that have similar characteristics.

A total of 853 participants with primary progressive MS (51.7% female) from 24 countries with a mean age at onset of 42.4, a median baseline EDSS score of 4, and 2.4 years of disease duration were included. LCMM detected three distinct subgroups of patients with a mild (n = 143; 16.8%), a moderate (n = 378; 44.3%), and a severe (n = 332; 38.9%) disability trajectory, respectively. Time from disease onset to diagnosis was shortest for the severe group. Median time to an EDSS score of 4 was 14, five, and 3.7 years for the three groups, respectively. The probability of reaching an EDSS score of 6 at 10 years was 0%, 46.5%, and 83.1%, respectively. Increasing severity of the disability time course was related to a decreasing frequency of patients with at least one relapse during follow-up (ie, from 47.6% to 36.5%).

“Using this modeling approach, it is possible to predict the future disease course of a subject with primary progressive MS using early EDSS assessments,” said Dr. Signori. “By using only one year of EDSS monitoring, 73% of patients are correctly classified in their disability trajectory group (mild, moderate, or severe). After three years, this proportion is 87%, and after five years, it is 92%.”

A new way to track the progression of Parkinson’s disease could help evaluate experimental treatments aimed at slowing or stopping the disease’s progression. “We provide evidence using task-based functional MRI (fMRI) for cortical and striatal functional deterioration in Parkinson’s disease over a one-year period,” researchers reported in the August 16 issue of Neurology.

Study results also describe unique patterns of functional changes in patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) that are more widespread, compared with those in Parkinson’s disease, suggesting that distinctive rates of disease progression in parkinsonian disorders may assist in future clinical studies of disease-modifying therapies.

While current treatments focus on controlling symptoms, biomarkers provide a quantifiable way to measure how medications address not just symptoms, but the neurologic changes behind them. Previous studies have used imaging techniques that require the injection of a drug that crosses the blood–brain barrier. “Our technique does not rely upon the injection of a drug. Not only is it noninvasive, it is much less expensive,” said senior study author David Vaillancourt, PhD, a Professor in the Department of Applied Physiology and Kinesiology at the University of Florida, Gainesville.

A total of 112 individuals were scanned at baseline and at one year while preforming a unimanual grip force task. The study cohort included 46 patients with Parkinson’s disease, 13 patients with MSA, 19 patients with PSP, and 34 healthy controls. The outcome measure was percent signal change in the prespecified brain regions.

A year after the baseline study, the 46 patients with Parkinson’s disease showed declining function in the primary motor cortex and putamen, compared with controls. Changes after one year in patients with MSA were exclusively extrastriatal and included a reduction in functional activity in the primary motor cortex, supplementary motor area, and superior cerebellum. In patients with PSP, all regions of interest were less active at one year, compared with baseline. Functional activity of the brain regions in the control group did not change during the study.

“Collectively, these findings point to disease-specific noninvasive progression markers of sensorimotor brain regions in parkinsonian disorders,” the researchers said.

The present findings build on two 2015 studies that used fMRI to document progressive deterioration from Parkinson’s disease, MSA, and PSP.

Suggested Reading

Burciu RG, Chung JW, Shukla P, et al. Functional MRI of disease progression in Parkinson disease and atypical parksonian syndromes. Neurology. 2016;87(7):709-717.

Burciu RG, Ofori E, Shukla P, et al. Distinct patters of brain activity in progressive supranuclear palsy and Parkinson’s disease. Mov Disord. 2015;30(9):1248-1258.

Oh M, Kim JS, Kim JY, et al. Subregional patterns of preferential striatal dopamine transporter loss differ in Parkinson disease, progressive supranuclear palsy, and multiple system atrophy. J Nucl Med. 2012;53(3):399-406.

Planetta PJ, Kurani AS, Shukla P, et al. Distinct functional and macrostructural brain changes in Parkinson’s disease and multiple system atrophy. Human Brain Mapp. 2015;36(3):1165-1179.

A new way to track the progression of Parkinson’s disease could help evaluate experimental treatments aimed at slowing or stopping the disease’s progression. “We provide evidence using task-based functional MRI (fMRI) for cortical and striatal functional deterioration in Parkinson’s disease over a one-year period,” researchers reported in the August 16 issue of Neurology.

Study results also describe unique patterns of functional changes in patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) that are more widespread, compared with those in Parkinson’s disease, suggesting that distinctive rates of disease progression in parkinsonian disorders may assist in future clinical studies of disease-modifying therapies.

While current treatments focus on controlling symptoms, biomarkers provide a quantifiable way to measure how medications address not just symptoms, but the neurologic changes behind them. Previous studies have used imaging techniques that require the injection of a drug that crosses the blood–brain barrier. “Our technique does not rely upon the injection of a drug. Not only is it noninvasive, it is much less expensive,” said senior study author David Vaillancourt, PhD, a Professor in the Department of Applied Physiology and Kinesiology at the University of Florida, Gainesville.

A total of 112 individuals were scanned at baseline and at one year while preforming a unimanual grip force task. The study cohort included 46 patients with Parkinson’s disease, 13 patients with MSA, 19 patients with PSP, and 34 healthy controls. The outcome measure was percent signal change in the prespecified brain regions.

A year after the baseline study, the 46 patients with Parkinson’s disease showed declining function in the primary motor cortex and putamen, compared with controls. Changes after one year in patients with MSA were exclusively extrastriatal and included a reduction in functional activity in the primary motor cortex, supplementary motor area, and superior cerebellum. In patients with PSP, all regions of interest were less active at one year, compared with baseline. Functional activity of the brain regions in the control group did not change during the study.

“Collectively, these findings point to disease-specific noninvasive progression markers of sensorimotor brain regions in parkinsonian disorders,” the researchers said.

The present findings build on two 2015 studies that used fMRI to document progressive deterioration from Parkinson’s disease, MSA, and PSP.

Suggested Reading

Burciu RG, Chung JW, Shukla P, et al. Functional MRI of disease progression in Parkinson disease and atypical parksonian syndromes. Neurology. 2016;87(7):709-717.

Burciu RG, Ofori E, Shukla P, et al. Distinct patters of brain activity in progressive supranuclear palsy and Parkinson’s disease. Mov Disord. 2015;30(9):1248-1258.

Oh M, Kim JS, Kim JY, et al. Subregional patterns of preferential striatal dopamine transporter loss differ in Parkinson disease, progressive supranuclear palsy, and multiple system atrophy. J Nucl Med. 2012;53(3):399-406.

Planetta PJ, Kurani AS, Shukla P, et al. Distinct functional and macrostructural brain changes in Parkinson’s disease and multiple system atrophy. Human Brain Mapp. 2015;36(3):1165-1179.

A new way to track the progression of Parkinson’s disease could help evaluate experimental treatments aimed at slowing or stopping the disease’s progression. “We provide evidence using task-based functional MRI (fMRI) for cortical and striatal functional deterioration in Parkinson’s disease over a one-year period,” researchers reported in the August 16 issue of Neurology.

Study results also describe unique patterns of functional changes in patients with multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) that are more widespread, compared with those in Parkinson’s disease, suggesting that distinctive rates of disease progression in parkinsonian disorders may assist in future clinical studies of disease-modifying therapies.

While current treatments focus on controlling symptoms, biomarkers provide a quantifiable way to measure how medications address not just symptoms, but the neurologic changes behind them. Previous studies have used imaging techniques that require the injection of a drug that crosses the blood–brain barrier. “Our technique does not rely upon the injection of a drug. Not only is it noninvasive, it is much less expensive,” said senior study author David Vaillancourt, PhD, a Professor in the Department of Applied Physiology and Kinesiology at the University of Florida, Gainesville.

A total of 112 individuals were scanned at baseline and at one year while preforming a unimanual grip force task. The study cohort included 46 patients with Parkinson’s disease, 13 patients with MSA, 19 patients with PSP, and 34 healthy controls. The outcome measure was percent signal change in the prespecified brain regions.

A year after the baseline study, the 46 patients with Parkinson’s disease showed declining function in the primary motor cortex and putamen, compared with controls. Changes after one year in patients with MSA were exclusively extrastriatal and included a reduction in functional activity in the primary motor cortex, supplementary motor area, and superior cerebellum. In patients with PSP, all regions of interest were less active at one year, compared with baseline. Functional activity of the brain regions in the control group did not change during the study.

“Collectively, these findings point to disease-specific noninvasive progression markers of sensorimotor brain regions in parkinsonian disorders,” the researchers said.

The present findings build on two 2015 studies that used fMRI to document progressive deterioration from Parkinson’s disease, MSA, and PSP.

Suggested Reading

Burciu RG, Chung JW, Shukla P, et al. Functional MRI of disease progression in Parkinson disease and atypical parksonian syndromes. Neurology. 2016;87(7):709-717.

Burciu RG, Ofori E, Shukla P, et al. Distinct patters of brain activity in progressive supranuclear palsy and Parkinson’s disease. Mov Disord. 2015;30(9):1248-1258.

Oh M, Kim JS, Kim JY, et al. Subregional patterns of preferential striatal dopamine transporter loss differ in Parkinson disease, progressive supranuclear palsy, and multiple system atrophy. J Nucl Med. 2012;53(3):399-406.

Planetta PJ, Kurani AS, Shukla P, et al. Distinct functional and macrostructural brain changes in Parkinson’s disease and multiple system atrophy. Human Brain Mapp. 2015;36(3):1165-1179.

SAN DIEGO—A behavioral intervention for comorbid insomnia in people with chronic migraine may reduce headache frequency by approximately 50%, according to research presented at the 58th Annual Scientific Meeting of the American Headache Society. Improvements in headache frequency and sleep efficiency continue after the intervention ends, as is the case with many behavioral therapies.

More than 38% of migraineurs sleep less than six hours per night, compared with about 10% of the general population. In addition, the prevalence of insomnia is much higher among individuals with headache than among the general population. “Most people who present for treatment of migraine have insomnia, and that’s true even of episodic migraineurs,” said Todd Smitherman, PhD, Associate Professor of Clinical Psychology at the University of Mississippi in Oxford.

Treatment Included Stimulus Control

Dr. Smitherman and colleagues conducted a randomized controlled pilot trial to study whether a behavioral intervention for comorbid insomnia could improve sleep and headache in adults with chronic migraine. The researchers enrolled 31 individuals in the study who met the diagnostic criteria for chronic migraine and insomnia. People with medication overuse were excluded from the study. Participants were randomized to cognitive behavioral therapy for insomnia (CBTi) administered in three 30-minute sessions, or to sham treatment.

Both groups received training in five skills. Participants who received CBTi were advised to adhere to a consistent bedtime that allowed eight hours in bed, to avoid other activities while in bed (eg, reading or watching TV), and to discontinue naps. These participants also were instructed to get out of bed and engage temporarily in quiet activity if they were unable to fall asleep after 30 minutes (ie, stimulus control). Finally, this group also underwent sleep restriction.

The control group received instructions to maintain a consistent liquid intake, to eat a serving of protein in the morning, to perform acupressure near the elbow, to practice range-of-motion exercises in the morning, and to eat dinner at a consistent time every evening. The same therapist administered both treatments to reduce allegiance effects.

All participants maintained daily headache diaries, completed self-report measures, and underwent actigraphy. The study’s primary outcome was reduction in headache frequency at two weeks post-treatment and at six-week follow-up.

CBTi Improved Sleep and Headache

The control group had a slightly lower headache frequency at baseline (20.5 days/month) than did the active group (22.7 days/month). The population’s mean age was 30.8, 90.3% of the sample was female, and 80.6% were Caucasian.

At two weeks post treatment, headache frequency was reduced by 26.9% for participants who received CBTi and by 36.2% for controls. At six weeks, headache frequency was reduced by 48.9% for the CBTi group and by 25.0% for controls. At six weeks, people who received CBTi also were 60% less likely to have headache, compared with controls. Individuals who received CBTi continued to improve after the intervention ended, said Dr. Smitherman. In contrast, individuals in the control group regressed toward their baseline conditions.

Participants’ insomnia symptoms were significantly correlated with the probability of headache, as well as with changes in disability. The actigraphy data indicated that CBTi produced significantly larger increases in total sleep time and sleep efficiency than sham treatment. CBTi also was associated with greater reductions in self-reported insomnia severity, compared with sham treatment.

Insomnia and Bipolar Disorder

Sleep restriction is not recommended for patients with bipolar disorder because it can promote manic episodes, said Dr. Smitherman. Alternatives for these patients include training in progressive muscle relaxation or referral to a provider for behavioral therapy.

Neurologists need larger and longer studies of behavioral therapy, Dr. Smitherman added. “We need to isolate the mechanisms of action.” One of the mechanisms appears to be that changes in sleep improve migraine, given the associations that data analyses reveal.

Suggested Reading

Calhoun AH, Ford S. Behavioral sleep modification may revert transformed migraine to episodic migraine. Headache. 2007;47(8):1178-1183.

Rains JC, Poceta JS. Headache and sleep disorders: review and clinical implications for headache management. Headache. 2006;46(9):1344-1363.

Smitherman TA, Walters AB, Davis RE, et al. Randomized controlled pilot trial of behavioral insomnia treatment for chronic migraine with comorbid insomnia. Headache. 2016;56(2):276-291.

SAN DIEGO—A behavioral intervention for comorbid insomnia in people with chronic migraine may reduce headache frequency by approximately 50%, according to research presented at the 58th Annual Scientific Meeting of the American Headache Society. Improvements in headache frequency and sleep efficiency continue after the intervention ends, as is the case with many behavioral therapies.

More than 38% of migraineurs sleep less than six hours per night, compared with about 10% of the general population. In addition, the prevalence of insomnia is much higher among individuals with headache than among the general population. “Most people who present for treatment of migraine have insomnia, and that’s true even of episodic migraineurs,” said Todd Smitherman, PhD, Associate Professor of Clinical Psychology at the University of Mississippi in Oxford.

Treatment Included Stimulus Control

Dr. Smitherman and colleagues conducted a randomized controlled pilot trial to study whether a behavioral intervention for comorbid insomnia could improve sleep and headache in adults with chronic migraine. The researchers enrolled 31 individuals in the study who met the diagnostic criteria for chronic migraine and insomnia. People with medication overuse were excluded from the study. Participants were randomized to cognitive behavioral therapy for insomnia (CBTi) administered in three 30-minute sessions, or to sham treatment.

Both groups received training in five skills. Participants who received CBTi were advised to adhere to a consistent bedtime that allowed eight hours in bed, to avoid other activities while in bed (eg, reading or watching TV), and to discontinue naps. These participants also were instructed to get out of bed and engage temporarily in quiet activity if they were unable to fall asleep after 30 minutes (ie, stimulus control). Finally, this group also underwent sleep restriction.

The control group received instructions to maintain a consistent liquid intake, to eat a serving of protein in the morning, to perform acupressure near the elbow, to practice range-of-motion exercises in the morning, and to eat dinner at a consistent time every evening. The same therapist administered both treatments to reduce allegiance effects.

All participants maintained daily headache diaries, completed self-report measures, and underwent actigraphy. The study’s primary outcome was reduction in headache frequency at two weeks post-treatment and at six-week follow-up.

CBTi Improved Sleep and Headache

The control group had a slightly lower headache frequency at baseline (20.5 days/month) than did the active group (22.7 days/month). The population’s mean age was 30.8, 90.3% of the sample was female, and 80.6% were Caucasian.

At two weeks post treatment, headache frequency was reduced by 26.9% for participants who received CBTi and by 36.2% for controls. At six weeks, headache frequency was reduced by 48.9% for the CBTi group and by 25.0% for controls. At six weeks, people who received CBTi also were 60% less likely to have headache, compared with controls. Individuals who received CBTi continued to improve after the intervention ended, said Dr. Smitherman. In contrast, individuals in the control group regressed toward their baseline conditions.

Participants’ insomnia symptoms were significantly correlated with the probability of headache, as well as with changes in disability. The actigraphy data indicated that CBTi produced significantly larger increases in total sleep time and sleep efficiency than sham treatment. CBTi also was associated with greater reductions in self-reported insomnia severity, compared with sham treatment.

Insomnia and Bipolar Disorder

Sleep restriction is not recommended for patients with bipolar disorder because it can promote manic episodes, said Dr. Smitherman. Alternatives for these patients include training in progressive muscle relaxation or referral to a provider for behavioral therapy.

Neurologists need larger and longer studies of behavioral therapy, Dr. Smitherman added. “We need to isolate the mechanisms of action.” One of the mechanisms appears to be that changes in sleep improve migraine, given the associations that data analyses reveal.

Suggested Reading

Calhoun AH, Ford S. Behavioral sleep modification may revert transformed migraine to episodic migraine. Headache. 2007;47(8):1178-1183.

Rains JC, Poceta JS. Headache and sleep disorders: review and clinical implications for headache management. Headache. 2006;46(9):1344-1363.

Smitherman TA, Walters AB, Davis RE, et al. Randomized controlled pilot trial of behavioral insomnia treatment for chronic migraine with comorbid insomnia. Headache. 2016;56(2):276-291.

SAN DIEGO—A behavioral intervention for comorbid insomnia in people with chronic migraine may reduce headache frequency by approximately 50%, according to research presented at the 58th Annual Scientific Meeting of the American Headache Society. Improvements in headache frequency and sleep efficiency continue after the intervention ends, as is the case with many behavioral therapies.

More than 38% of migraineurs sleep less than six hours per night, compared with about 10% of the general population. In addition, the prevalence of insomnia is much higher among individuals with headache than among the general population. “Most people who present for treatment of migraine have insomnia, and that’s true even of episodic migraineurs,” said Todd Smitherman, PhD, Associate Professor of Clinical Psychology at the University of Mississippi in Oxford.

Treatment Included Stimulus Control

Dr. Smitherman and colleagues conducted a randomized controlled pilot trial to study whether a behavioral intervention for comorbid insomnia could improve sleep and headache in adults with chronic migraine. The researchers enrolled 31 individuals in the study who met the diagnostic criteria for chronic migraine and insomnia. People with medication overuse were excluded from the study. Participants were randomized to cognitive behavioral therapy for insomnia (CBTi) administered in three 30-minute sessions, or to sham treatment.

Both groups received training in five skills. Participants who received CBTi were advised to adhere to a consistent bedtime that allowed eight hours in bed, to avoid other activities while in bed (eg, reading or watching TV), and to discontinue naps. These participants also were instructed to get out of bed and engage temporarily in quiet activity if they were unable to fall asleep after 30 minutes (ie, stimulus control). Finally, this group also underwent sleep restriction.

The control group received instructions to maintain a consistent liquid intake, to eat a serving of protein in the morning, to perform acupressure near the elbow, to practice range-of-motion exercises in the morning, and to eat dinner at a consistent time every evening. The same therapist administered both treatments to reduce allegiance effects.

All participants maintained daily headache diaries, completed self-report measures, and underwent actigraphy. The study’s primary outcome was reduction in headache frequency at two weeks post-treatment and at six-week follow-up.

CBTi Improved Sleep and Headache

The control group had a slightly lower headache frequency at baseline (20.5 days/month) than did the active group (22.7 days/month). The population’s mean age was 30.8, 90.3% of the sample was female, and 80.6% were Caucasian.

At two weeks post treatment, headache frequency was reduced by 26.9% for participants who received CBTi and by 36.2% for controls. At six weeks, headache frequency was reduced by 48.9% for the CBTi group and by 25.0% for controls. At six weeks, people who received CBTi also were 60% less likely to have headache, compared with controls. Individuals who received CBTi continued to improve after the intervention ended, said Dr. Smitherman. In contrast, individuals in the control group regressed toward their baseline conditions.

Participants’ insomnia symptoms were significantly correlated with the probability of headache, as well as with changes in disability. The actigraphy data indicated that CBTi produced significantly larger increases in total sleep time and sleep efficiency than sham treatment. CBTi also was associated with greater reductions in self-reported insomnia severity, compared with sham treatment.

Insomnia and Bipolar Disorder

Sleep restriction is not recommended for patients with bipolar disorder because it can promote manic episodes, said Dr. Smitherman. Alternatives for these patients include training in progressive muscle relaxation or referral to a provider for behavioral therapy.

Neurologists need larger and longer studies of behavioral therapy, Dr. Smitherman added. “We need to isolate the mechanisms of action.” One of the mechanisms appears to be that changes in sleep improve migraine, given the associations that data analyses reveal.

Suggested Reading

Calhoun AH, Ford S. Behavioral sleep modification may revert transformed migraine to episodic migraine. Headache. 2007;47(8):1178-1183.

Rains JC, Poceta JS. Headache and sleep disorders: review and clinical implications for headache management. Headache. 2006;46(9):1344-1363.

Smitherman TA, Walters AB, Davis RE, et al. Randomized controlled pilot trial of behavioral insomnia treatment for chronic migraine with comorbid insomnia. Headache. 2016;56(2):276-291.

Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.

The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.

Take your pick of candidates, but don't expect a difference in your practice "hassle factor"—or paycheck.

Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.¹ These programs have bipartisan support and are not going away.

In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.

What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign² (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.

In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.

Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.

The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.

Take your pick of candidates, but don't expect a difference in your practice "hassle factor"—or paycheck.

Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.¹ These programs have bipartisan support and are not going away.

In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.

What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign² (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.

In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.

Health care has not been at the top of the agenda in this presidential campaign, but it remains a highly contentious political issue. Because the Affordable Care Act (aka Obamacare) was all about expanding health care coverage and not much about cost containment, it is not surprising that health care insurance costs continue to escalate.

The Accountable Care Organization demonstrations around the country have shown that some, but not all, health care organizations are able to bend the steep cost incline downward using incentives, bundled payments, excellent primary care access, and care coordination. But we are once again seeing large increases in insurance premiums, and no one is happy about that.

Take your pick of candidates, but don't expect a difference in your practice "hassle factor"—or paycheck.

Practical solutions are scarce. Good solutions for controlling rising health care costs are difficult to come by in the United States. There are a variety of suggestions and approaches favored by one party or the other that will be decided through political and administrative channels. The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA), the Merit-based Incentive Payment System (MIPS), and alternative payment models (APMs) are the federal government’s new programs that have been set out to encourage quality, while controlling costs in outpatient settings.¹ These programs have bipartisan support and are not going away.

In addition, each state is reorganizing Medicaid in an attempt to improve quality and reduce costs. Usually these cost control/quality improvement programs are foisted on us by federal or state governments (which pay for about 64% of health care costs in the United States), by insurers, or both. Fortunately, the American Academy of Family Physicians has been putting the interests of family physicians in front of legislators and policy makers to try to ease the pain as much as possible.

What can YOU do? If you have the time and the stomach for it, join forces with AAFP to become involved in the politics of health care reform and speak up for family medicine and primary care. In your own office or clinic, put the “Choosing Wisely” campaign² (from the American Board of Internal Medicine) into practice: Focus on reducing unnecessary tests and treatments.

In the end, no matter which party occupies the White House for the next 4 years, health care payment reform is inevitable. Both parties agree that the steep rise in health care costs is unsustainable. So take your pick of presidential candidates, but don’t expect that choice to make a lot of difference in your practice “hassle factor”—or paycheck.

MUNICH – A group of 12 genes that influence blood sugar appears to help drive the risk of heart disease, independent of type 2 diabetes.

The genome-wide association study determined that every 1 mmol/L increase in fasting glucose associated with these genes increased the risk of coronary heart disease by 43%, Jordi Merino, PhD, said at the annual meeting of the European Association for the Study of Diabetes.

“Our results quantify the causal relationship between isolated, genetically increased fasting glucose and heart disease risk beyond the genetic effect of type 2 diabetes,” said Dr. Merino of Massachusetts General Hospital, Boston. “They suggest that modulating glycemia may provide cardiovascular benefit.”

©Gio_tto/Thinkstock

It’s known that patients with type 2 diabetes have a higher incidence of coronary heart disease, even after accounting for traditional cardiovascular risk factors, he said. But five large prospective randomized studies – including the much-vaunted ACCORD – failed to find convincing evidence that managing blood glucose in patients with diabetes exerts any benefit on cardiovascular outcomes. In fact, patients assigned to intensive management (blood glucose targeted to below 6%) had a relative increase in all-cause mortality of 22% and an absolute increase of 1%, without any differences in cardiovascular mortality (5% vs. 4%; hazard ratio, 1.22) (N Engl J Med. 2008;358:2545-59).

However, a 2014 subanalysis of ACCORD found that outcomes for ischemic heart disease were significantly better in the intensively managed group. There was a 20% reduction in the risk of heart attack; a 19% reduction in a combined endpoint of heart attack; and similar reductions in the risk of coronary revascularization and unstable angina (Lancet. 2014;384:1936-41).

“We believed genetics might help to answer the question about this discrepancies in findings,” Dr. Merino said.

To investigate this, he and his colleagues plumbed the largest meta-analyses of genome-wide association studies of glucose and insulin regulation. MAGIC (the Meta-Analyses of Glucose and Insulin-related traits Consortium) is a collaborative effort that has combined genetic data from 55 studies.

MAGIC investigators have identified dozens of loci that influence levels of fasting glucose, fasting insulin, and hemoglobin A_1c. The project includes data on 133,000 subjects without type 2 diabetes.

They used these data to conduct a Mendelian randomization analysis – a way of establishing causality between a specific gene and a specific clinical trait. Such an analysis is valid only when there are no other functional pathways between the genetic variant and the outcome and when confounding factors that could also affect the outcome can be controlled for.

MAGIC found 234 genetic variants that influence fasting glucose. Some of these also increase the risk of type 2 diabetes; after excluding those, Dr. Merino was left with 107 candidate genes. A disequilibrium analysis further pruned the group, leaving 12 genes that are independently associated with fasting glucose regulation.

He and his colleagues then applied data from the CARDIoGRAMplusC4D Consortium, which is searching for multiple risk loci for coronary artery disease and myocardial infarction in several large genetic studies. They created a five-level risk score for the glycemia-modulating genes and used to it determine how much genetically driven glucose variability affected the risk of heart disease in 5,000 subjects included in the Framingham Heart Study. The analysis controlled for lipids, blood pressure, and body mass index, he noted.

In a model that included all 12 of the variants, the investigators found that every 1 mmol/L increase in fasting glucose was associated with a significant 43% increase in the risk of heart disease.

A second analysis excluded one of the genes, but the significant association with increased risk of heart disease was preserved, at 34% per 1 mmol/L increase in fasting glucose. Individually, 10 of the genes raised the risk of coronary heart disease from a low of 6% (OR 1.06) to a high of almost 400% (OR 3.8).

The final pleiotropic analysis excluded all genes that could have more than one effect on heart disease; five genes survived to this level. Overall, they raised the risk of heart disease by 33%. Individually, the relative increased risks ranged from a low of 12% (odds ratio, 1.12) to a high of 87% (OR, 1.87). One gene was associated with a 25% risk reduction.

Dr. Merino had no financial disclosures.

msullivan@frontlinemedcom.com

MUNICH – A group of 12 genes that influence blood sugar appears to help drive the risk of heart disease, independent of type 2 diabetes.

The genome-wide association study determined that every 1 mmol/L increase in fasting glucose associated with these genes increased the risk of coronary heart disease by 43%, Jordi Merino, PhD, said at the annual meeting of the European Association for the Study of Diabetes.

“Our results quantify the causal relationship between isolated, genetically increased fasting glucose and heart disease risk beyond the genetic effect of type 2 diabetes,” said Dr. Merino of Massachusetts General Hospital, Boston. “They suggest that modulating glycemia may provide cardiovascular benefit.”

©Gio_tto/Thinkstock

It’s known that patients with type 2 diabetes have a higher incidence of coronary heart disease, even after accounting for traditional cardiovascular risk factors, he said. But five large prospective randomized studies – including the much-vaunted ACCORD – failed to find convincing evidence that managing blood glucose in patients with diabetes exerts any benefit on cardiovascular outcomes. In fact, patients assigned to intensive management (blood glucose targeted to below 6%) had a relative increase in all-cause mortality of 22% and an absolute increase of 1%, without any differences in cardiovascular mortality (5% vs. 4%; hazard ratio, 1.22) (N Engl J Med. 2008;358:2545-59).

However, a 2014 subanalysis of ACCORD found that outcomes for ischemic heart disease were significantly better in the intensively managed group. There was a 20% reduction in the risk of heart attack; a 19% reduction in a combined endpoint of heart attack; and similar reductions in the risk of coronary revascularization and unstable angina (Lancet. 2014;384:1936-41).

“We believed genetics might help to answer the question about this discrepancies in findings,” Dr. Merino said.

To investigate this, he and his colleagues plumbed the largest meta-analyses of genome-wide association studies of glucose and insulin regulation. MAGIC (the Meta-Analyses of Glucose and Insulin-related traits Consortium) is a collaborative effort that has combined genetic data from 55 studies.

MAGIC investigators have identified dozens of loci that influence levels of fasting glucose, fasting insulin, and hemoglobin A_1c. The project includes data on 133,000 subjects without type 2 diabetes.

They used these data to conduct a Mendelian randomization analysis – a way of establishing causality between a specific gene and a specific clinical trait. Such an analysis is valid only when there are no other functional pathways between the genetic variant and the outcome and when confounding factors that could also affect the outcome can be controlled for.

MAGIC found 234 genetic variants that influence fasting glucose. Some of these also increase the risk of type 2 diabetes; after excluding those, Dr. Merino was left with 107 candidate genes. A disequilibrium analysis further pruned the group, leaving 12 genes that are independently associated with fasting glucose regulation.

He and his colleagues then applied data from the CARDIoGRAMplusC4D Consortium, which is searching for multiple risk loci for coronary artery disease and myocardial infarction in several large genetic studies. They created a five-level risk score for the glycemia-modulating genes and used to it determine how much genetically driven glucose variability affected the risk of heart disease in 5,000 subjects included in the Framingham Heart Study. The analysis controlled for lipids, blood pressure, and body mass index, he noted.

In a model that included all 12 of the variants, the investigators found that every 1 mmol/L increase in fasting glucose was associated with a significant 43% increase in the risk of heart disease.

A second analysis excluded one of the genes, but the significant association with increased risk of heart disease was preserved, at 34% per 1 mmol/L increase in fasting glucose. Individually, 10 of the genes raised the risk of coronary heart disease from a low of 6% (OR 1.06) to a high of almost 400% (OR 3.8).

The final pleiotropic analysis excluded all genes that could have more than one effect on heart disease; five genes survived to this level. Overall, they raised the risk of heart disease by 33%. Individually, the relative increased risks ranged from a low of 12% (odds ratio, 1.12) to a high of 87% (OR, 1.87). One gene was associated with a 25% risk reduction.

Dr. Merino had no financial disclosures.

msullivan@frontlinemedcom.com

MUNICH – A group of 12 genes that influence blood sugar appears to help drive the risk of heart disease, independent of type 2 diabetes.

The genome-wide association study determined that every 1 mmol/L increase in fasting glucose associated with these genes increased the risk of coronary heart disease by 43%, Jordi Merino, PhD, said at the annual meeting of the European Association for the Study of Diabetes.

“Our results quantify the causal relationship between isolated, genetically increased fasting glucose and heart disease risk beyond the genetic effect of type 2 diabetes,” said Dr. Merino of Massachusetts General Hospital, Boston. “They suggest that modulating glycemia may provide cardiovascular benefit.”

©Gio_tto/Thinkstock

It’s known that patients with type 2 diabetes have a higher incidence of coronary heart disease, even after accounting for traditional cardiovascular risk factors, he said. But five large prospective randomized studies – including the much-vaunted ACCORD – failed to find convincing evidence that managing blood glucose in patients with diabetes exerts any benefit on cardiovascular outcomes. In fact, patients assigned to intensive management (blood glucose targeted to below 6%) had a relative increase in all-cause mortality of 22% and an absolute increase of 1%, without any differences in cardiovascular mortality (5% vs. 4%; hazard ratio, 1.22) (N Engl J Med. 2008;358:2545-59).

However, a 2014 subanalysis of ACCORD found that outcomes for ischemic heart disease were significantly better in the intensively managed group. There was a 20% reduction in the risk of heart attack; a 19% reduction in a combined endpoint of heart attack; and similar reductions in the risk of coronary revascularization and unstable angina (Lancet. 2014;384:1936-41).

“We believed genetics might help to answer the question about this discrepancies in findings,” Dr. Merino said.

To investigate this, he and his colleagues plumbed the largest meta-analyses of genome-wide association studies of glucose and insulin regulation. MAGIC (the Meta-Analyses of Glucose and Insulin-related traits Consortium) is a collaborative effort that has combined genetic data from 55 studies.

MAGIC investigators have identified dozens of loci that influence levels of fasting glucose, fasting insulin, and hemoglobin A_1c. The project includes data on 133,000 subjects without type 2 diabetes.

They used these data to conduct a Mendelian randomization analysis – a way of establishing causality between a specific gene and a specific clinical trait. Such an analysis is valid only when there are no other functional pathways between the genetic variant and the outcome and when confounding factors that could also affect the outcome can be controlled for.

MAGIC found 234 genetic variants that influence fasting glucose. Some of these also increase the risk of type 2 diabetes; after excluding those, Dr. Merino was left with 107 candidate genes. A disequilibrium analysis further pruned the group, leaving 12 genes that are independently associated with fasting glucose regulation.

He and his colleagues then applied data from the CARDIoGRAMplusC4D Consortium, which is searching for multiple risk loci for coronary artery disease and myocardial infarction in several large genetic studies. They created a five-level risk score for the glycemia-modulating genes and used to it determine how much genetically driven glucose variability affected the risk of heart disease in 5,000 subjects included in the Framingham Heart Study. The analysis controlled for lipids, blood pressure, and body mass index, he noted.

In a model that included all 12 of the variants, the investigators found that every 1 mmol/L increase in fasting glucose was associated with a significant 43% increase in the risk of heart disease.

A second analysis excluded one of the genes, but the significant association with increased risk of heart disease was preserved, at 34% per 1 mmol/L increase in fasting glucose. Individually, 10 of the genes raised the risk of coronary heart disease from a low of 6% (OR 1.06) to a high of almost 400% (OR 3.8).

The final pleiotropic analysis excluded all genes that could have more than one effect on heart disease; five genes survived to this level. Overall, they raised the risk of heart disease by 33%. Individually, the relative increased risks ranged from a low of 12% (odds ratio, 1.12) to a high of 87% (OR, 1.87). One gene was associated with a 25% risk reduction.

Dr. Merino had no financial disclosures.

msullivan@frontlinemedcom.com

In this interview, Dr Bosserman and Dr Zon talk aboout the ins and outs of the upcoming implementation of MACRA, the Medicare Access and CHIP Reauthorization Act of 2015. The legislation will usher in the switch from volume- to value- and performance-based Medicare payments. It goes into effect in January 2019, but the measurements will be based on 2017 performance. Dr Zon lists five steps for preparing for MACRA: first, participate in the three 2016 quality-reporting programs – PQRS, meaningful use, and VBM – to avoid 2018 penalties; second, review your Quality and Resource Use Reports, or QRUR, which are available online; third, focus on performance by reviewing quality  benchmarks and implementing strategies and workflows to ensure above-average performance; fourth, ensure data and information accuracy, eg, physician specialty and practice address; and fifth, audit and educate your practice on proper use of the International Classification of Diseases, Revision 10 coding.

For more, listen to the podcast below, or click on the PDF icon at the top of this introduction to read a transcript of the interveiw.

In this interview, Dr Bosserman and Dr Zon talk aboout the ins and outs of the upcoming implementation of MACRA, the Medicare Access and CHIP Reauthorization Act of 2015. The legislation will usher in the switch from volume- to value- and performance-based Medicare payments. It goes into effect in January 2019, but the measurements will be based on 2017 performance. Dr Zon lists five steps for preparing for MACRA: first, participate in the three 2016 quality-reporting programs – PQRS, meaningful use, and VBM – to avoid 2018 penalties; second, review your Quality and Resource Use Reports, or QRUR, which are available online; third, focus on performance by reviewing quality  benchmarks and implementing strategies and workflows to ensure above-average performance; fourth, ensure data and information accuracy, eg, physician specialty and practice address; and fifth, audit and educate your practice on proper use of the International Classification of Diseases, Revision 10 coding.

For more, listen to the podcast below, or click on the PDF icon at the top of this introduction to read a transcript of the interveiw.

In this interview, Dr Bosserman and Dr Zon talk aboout the ins and outs of the upcoming implementation of MACRA, the Medicare Access and CHIP Reauthorization Act of 2015. The legislation will usher in the switch from volume- to value- and performance-based Medicare payments. It goes into effect in January 2019, but the measurements will be based on 2017 performance. Dr Zon lists five steps for preparing for MACRA: first, participate in the three 2016 quality-reporting programs – PQRS, meaningful use, and VBM – to avoid 2018 penalties; second, review your Quality and Resource Use Reports, or QRUR, which are available online; third, focus on performance by reviewing quality  benchmarks and implementing strategies and workflows to ensure above-average performance; fourth, ensure data and information accuracy, eg, physician specialty and practice address; and fifth, audit and educate your practice on proper use of the International Classification of Diseases, Revision 10 coding.

For more, listen to the podcast below, or click on the PDF icon at the top of this introduction to read a transcript of the interveiw.

Federal health officials are advising men who have possibly been exposed to Zika virus to practice safe sex and delay plans for conception for at least 6 months after exposure.

The Centers for Disease Control and Prevention updated its recommendations for preventing sexual transmission of the Zika virus and its preconception guidance, extending the time frame that men should abstain from unprotected sex to prevent transmission.

Previously, only symptomatic men were advised to wait 6 months before trying to conceive a child, while asymptomatic men had to wait only 8 weeks from last possible exposure. Now, men who have been exposed to the virus should either abstain from sex or use a condom to prevent sexual transmission of the disease for at least 6 months, even if they are asymptomatic. Men who are trying to have a child with their partner should also wait at least 6 months.

For now, recommendations for women have not been changed. Women who have been exposed to Zika virus should wait at least 8 weeks after symptom onset (if symptomatic) or last possible exposure to the virus before attempting to conceive. Women who do not plan to become pregnant but live in, or travel to, Zika-endemic regions should either abstain from sex or use the best possible protection available to them (MMWR. 2016 Sep 30. doi: 10.15585/mmwr.mm6539e1).

“Two new reports describe one presumed and one more definitive case of sexual transmission from men with asymptomatic Zika virus infection to female sex partners,” Emily E. Peterson, MD, of the CDC’s Zika response team, and her colleagues wrote in the Morbidity and Mortality Weekly Report. “Among reported cases of sexually transmitted Zika virus infection, the longest reported period between sexual contact that might have transmitted Zika virus and symptom onset was 32-41 days (based on an incubation period of 3-12 days).”

Zika virus can be transmitted through either vaginal, anal, or oral sexual intercourse. While Zika virus RNA decreases over time after the infection passes, it can linger in semen for as long as 188 days after symptom onset, according to the CDC.

For nonpregnant women, Zika virus RNA has been detected in serum for up to 13 days post-onset of symptoms, and for 58 days in whole blood samples. For pregnant women, it can be detected in serum for as long as 10 weeks after the onset of symptoms.

“Detection of Zika virus RNA in blood might not indicate the presence of infectious virus, and thus the potential risk for maternal-fetal Zika virus transmission periconceptionally is unknown,” the researchers wrote.

dchitnis@frontlinemedcom.com

Federal health officials are advising men who have possibly been exposed to Zika virus to practice safe sex and delay plans for conception for at least 6 months after exposure.

The Centers for Disease Control and Prevention updated its recommendations for preventing sexual transmission of the Zika virus and its preconception guidance, extending the time frame that men should abstain from unprotected sex to prevent transmission.

Previously, only symptomatic men were advised to wait 6 months before trying to conceive a child, while asymptomatic men had to wait only 8 weeks from last possible exposure. Now, men who have been exposed to the virus should either abstain from sex or use a condom to prevent sexual transmission of the disease for at least 6 months, even if they are asymptomatic. Men who are trying to have a child with their partner should also wait at least 6 months.

For now, recommendations for women have not been changed. Women who have been exposed to Zika virus should wait at least 8 weeks after symptom onset (if symptomatic) or last possible exposure to the virus before attempting to conceive. Women who do not plan to become pregnant but live in, or travel to, Zika-endemic regions should either abstain from sex or use the best possible protection available to them (MMWR. 2016 Sep 30. doi: 10.15585/mmwr.mm6539e1).

“Two new reports describe one presumed and one more definitive case of sexual transmission from men with asymptomatic Zika virus infection to female sex partners,” Emily E. Peterson, MD, of the CDC’s Zika response team, and her colleagues wrote in the Morbidity and Mortality Weekly Report. “Among reported cases of sexually transmitted Zika virus infection, the longest reported period between sexual contact that might have transmitted Zika virus and symptom onset was 32-41 days (based on an incubation period of 3-12 days).”

Zika virus can be transmitted through either vaginal, anal, or oral sexual intercourse. While Zika virus RNA decreases over time after the infection passes, it can linger in semen for as long as 188 days after symptom onset, according to the CDC.

For nonpregnant women, Zika virus RNA has been detected in serum for up to 13 days post-onset of symptoms, and for 58 days in whole blood samples. For pregnant women, it can be detected in serum for as long as 10 weeks after the onset of symptoms.

“Detection of Zika virus RNA in blood might not indicate the presence of infectious virus, and thus the potential risk for maternal-fetal Zika virus transmission periconceptionally is unknown,” the researchers wrote.

dchitnis@frontlinemedcom.com

Federal health officials are advising men who have possibly been exposed to Zika virus to practice safe sex and delay plans for conception for at least 6 months after exposure.

The Centers for Disease Control and Prevention updated its recommendations for preventing sexual transmission of the Zika virus and its preconception guidance, extending the time frame that men should abstain from unprotected sex to prevent transmission.

Previously, only symptomatic men were advised to wait 6 months before trying to conceive a child, while asymptomatic men had to wait only 8 weeks from last possible exposure. Now, men who have been exposed to the virus should either abstain from sex or use a condom to prevent sexual transmission of the disease for at least 6 months, even if they are asymptomatic. Men who are trying to have a child with their partner should also wait at least 6 months.

For now, recommendations for women have not been changed. Women who have been exposed to Zika virus should wait at least 8 weeks after symptom onset (if symptomatic) or last possible exposure to the virus before attempting to conceive. Women who do not plan to become pregnant but live in, or travel to, Zika-endemic regions should either abstain from sex or use the best possible protection available to them (MMWR. 2016 Sep 30. doi: 10.15585/mmwr.mm6539e1).

“Two new reports describe one presumed and one more definitive case of sexual transmission from men with asymptomatic Zika virus infection to female sex partners,” Emily E. Peterson, MD, of the CDC’s Zika response team, and her colleagues wrote in the Morbidity and Mortality Weekly Report. “Among reported cases of sexually transmitted Zika virus infection, the longest reported period between sexual contact that might have transmitted Zika virus and symptom onset was 32-41 days (based on an incubation period of 3-12 days).”

Zika virus can be transmitted through either vaginal, anal, or oral sexual intercourse. While Zika virus RNA decreases over time after the infection passes, it can linger in semen for as long as 188 days after symptom onset, according to the CDC.

For nonpregnant women, Zika virus RNA has been detected in serum for up to 13 days post-onset of symptoms, and for 58 days in whole blood samples. For pregnant women, it can be detected in serum for as long as 10 weeks after the onset of symptoms.

“Detection of Zika virus RNA in blood might not indicate the presence of infectious virus, and thus the potential risk for maternal-fetal Zika virus transmission periconceptionally is unknown,” the researchers wrote.

dchitnis@frontlinemedcom.com

A good way to survive an acute myocardial infarction is to go to the best hospital.

Some patients seem to have found out where those are. For those of us who want to know where to go and what to look for, a recent analysis of 800,000 Medicare patients admitted with acute myocardial infarction (AMI) and heart failure in 10,000 hospitals between 2008 and 2009 provides some reassuring news (National Bureau of Economic Research Working Paper 21603). Its findings indicated that in an era when health care choice is seemingly influenced by testimonial TV ads and the creation of hospitals that look like hotels, technical medical quality outranks all the glitz and bricks. Quality was measured by hospital mortality, 30-day readmissions, adherence to well-established guidelines, and patient satisfaction questionnaires. The investigators measured the effect that medical quality and the “comfort quotient” had on the growth of hospital patient volume through the emergency departments and interhospital referrals.

Hospital admissions increased in hospitals with the highest-quality performance. Over the 2-year period, the hospitals with the highest-quality performance had increases in hospital volume. Hospitals with a 1% improvement in the adjusted AMI mortality had a 17% increase in market share and a 1.5 % growth rate.

The authors estimated that patients with an AMI (or their family) were willing to travel an additional 1.8 miles for an ED admission to a hospital with a higher survival rate, and 34 miles further for a transfer to a hospital with a higher survival rate. When patients had the option to choose a hospital to be transferred to for further care, quality of care measures had an even greater impact on choice. Postdischarge evaluation of patient satisfaction had little or no effect on growth.

Patients admitted through the ED have the least chance for hospital choice, but even in these patients knowledge about quality influenced the choice of the hospital and the long-term hospital growth rate. Considering the fact that there is scant information available either to patients or even doctors about quality measures, there appears to be a choice process either by patient family, doctor, or ambulance driver to direct patients to the hospital with the best survival rate.

How they made those decisions is not clear. Comparative hospital survival data are rarely transmitted to staff physicians and are not widely available to the public. I have never seen any data like these in the multitude of hospital TV ads, yet somehow those numbers, real or perceived, affected admission and transfer. Maybe it’s just reputation; we all know about that. If you are really interested, you can find hospital medical quality and patient experience data at Medicare’s Hospital Compare site.

All this is good. Medical quality wins. Other studies, however, suggest that usually the “comfort quotient” and measures of medical quality are more closely linked. It has also been suggested that volume is the driving force for the improvement in both quality measures by providing the resources and logistics for better care. Whatever the mechanism, it seems that high-quality medical care is not a bad way to choose which neighborhood hospital to go to in order to survive an AMI.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

A good way to survive an acute myocardial infarction is to go to the best hospital.

Some patients seem to have found out where those are. For those of us who want to know where to go and what to look for, a recent analysis of 800,000 Medicare patients admitted with acute myocardial infarction (AMI) and heart failure in 10,000 hospitals between 2008 and 2009 provides some reassuring news (National Bureau of Economic Research Working Paper 21603). Its findings indicated that in an era when health care choice is seemingly influenced by testimonial TV ads and the creation of hospitals that look like hotels, technical medical quality outranks all the glitz and bricks. Quality was measured by hospital mortality, 30-day readmissions, adherence to well-established guidelines, and patient satisfaction questionnaires. The investigators measured the effect that medical quality and the “comfort quotient” had on the growth of hospital patient volume through the emergency departments and interhospital referrals.

Hospital admissions increased in hospitals with the highest-quality performance. Over the 2-year period, the hospitals with the highest-quality performance had increases in hospital volume. Hospitals with a 1% improvement in the adjusted AMI mortality had a 17% increase in market share and a 1.5 % growth rate.

The authors estimated that patients with an AMI (or their family) were willing to travel an additional 1.8 miles for an ED admission to a hospital with a higher survival rate, and 34 miles further for a transfer to a hospital with a higher survival rate. When patients had the option to choose a hospital to be transferred to for further care, quality of care measures had an even greater impact on choice. Postdischarge evaluation of patient satisfaction had little or no effect on growth.

Patients admitted through the ED have the least chance for hospital choice, but even in these patients knowledge about quality influenced the choice of the hospital and the long-term hospital growth rate. Considering the fact that there is scant information available either to patients or even doctors about quality measures, there appears to be a choice process either by patient family, doctor, or ambulance driver to direct patients to the hospital with the best survival rate.

How they made those decisions is not clear. Comparative hospital survival data are rarely transmitted to staff physicians and are not widely available to the public. I have never seen any data like these in the multitude of hospital TV ads, yet somehow those numbers, real or perceived, affected admission and transfer. Maybe it’s just reputation; we all know about that. If you are really interested, you can find hospital medical quality and patient experience data at Medicare’s Hospital Compare site.

All this is good. Medical quality wins. Other studies, however, suggest that usually the “comfort quotient” and measures of medical quality are more closely linked. It has also been suggested that volume is the driving force for the improvement in both quality measures by providing the resources and logistics for better care. Whatever the mechanism, it seems that high-quality medical care is not a bad way to choose which neighborhood hospital to go to in order to survive an AMI.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

A good way to survive an acute myocardial infarction is to go to the best hospital.

Some patients seem to have found out where those are. For those of us who want to know where to go and what to look for, a recent analysis of 800,000 Medicare patients admitted with acute myocardial infarction (AMI) and heart failure in 10,000 hospitals between 2008 and 2009 provides some reassuring news (National Bureau of Economic Research Working Paper 21603). Its findings indicated that in an era when health care choice is seemingly influenced by testimonial TV ads and the creation of hospitals that look like hotels, technical medical quality outranks all the glitz and bricks. Quality was measured by hospital mortality, 30-day readmissions, adherence to well-established guidelines, and patient satisfaction questionnaires. The investigators measured the effect that medical quality and the “comfort quotient” had on the growth of hospital patient volume through the emergency departments and interhospital referrals.

Hospital admissions increased in hospitals with the highest-quality performance. Over the 2-year period, the hospitals with the highest-quality performance had increases in hospital volume. Hospitals with a 1% improvement in the adjusted AMI mortality had a 17% increase in market share and a 1.5 % growth rate.

The authors estimated that patients with an AMI (or their family) were willing to travel an additional 1.8 miles for an ED admission to a hospital with a higher survival rate, and 34 miles further for a transfer to a hospital with a higher survival rate. When patients had the option to choose a hospital to be transferred to for further care, quality of care measures had an even greater impact on choice. Postdischarge evaluation of patient satisfaction had little or no effect on growth.

Patients admitted through the ED have the least chance for hospital choice, but even in these patients knowledge about quality influenced the choice of the hospital and the long-term hospital growth rate. Considering the fact that there is scant information available either to patients or even doctors about quality measures, there appears to be a choice process either by patient family, doctor, or ambulance driver to direct patients to the hospital with the best survival rate.

How they made those decisions is not clear. Comparative hospital survival data are rarely transmitted to staff physicians and are not widely available to the public. I have never seen any data like these in the multitude of hospital TV ads, yet somehow those numbers, real or perceived, affected admission and transfer. Maybe it’s just reputation; we all know about that. If you are really interested, you can find hospital medical quality and patient experience data at Medicare’s Hospital Compare site.

All this is good. Medical quality wins. Other studies, however, suggest that usually the “comfort quotient” and measures of medical quality are more closely linked. It has also been suggested that volume is the driving force for the improvement in both quality measures by providing the resources and logistics for better care. Whatever the mechanism, it seems that high-quality medical care is not a bad way to choose which neighborhood hospital to go to in order to survive an AMI.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The clinical course of postnatally acquired Zika virus disease in children younger than 18 years is mild and rarely results in severe illness or death, reported Alyson Goodman, MD, and her associates at the Centers for Disease Control and Prevention (CDC), Atlanta.

There were a total of 158 confirmed or probable postnatally acquired Zika virus disease cases among children younger than 18 years reported to the CDC in the United States between January 2015 and July 2016, wrote researchers in a case series that described the epidemiology, clinical findings, and outcomes of the cases (MMWR. 2016 Sep 30;65:1-4).

©Devonyu/Thinkstock

The cases were reported in 30 d ifferent states, and the states with the highest numbers of reported cases were Florida (23%), New York (11%), and California (9%). All patients acquired Zika virus infections during travel to a location where mosquito-borne transmission had been documented, according to researchers.

The median patient age was 14 years, the majority of the patients were female (56%), and five patients were pregnant.

Of Zika’s four primary clinical signs and symptoms, 82% of the pediatric population had a rash, 55% had a fever, 29% had conjunctivitis, and 28% had arthralgia, with 70% of the children presenting with two or more of these symptoms.

Only two children were hospitalized because of their infections. No children were reported to have meningitis, encephalitis, or Guillain-Barré syndrome, and no patients with Zika virus infection died, researchers reported.

This data “corroborates previously published reports suggesting that the clinical course of Zika virus disease is typically mild in children, as it is in adults,” Dr. Goodman and her associates wrote.

Severe disease and death in children with postnatally acquired Zika virus infection are rare, the researchers pointed out, but they encouraged physicians to consider a Zika virus disease diagnosis for children with the four common symptoms and who reside in or traveled to an area with active Zika virus transmission. All Zika virus disease cases should be reported to state health departments.

jcraig@frontlinemedcom.com

On Twitter @jessnicolecraig

The clinical course of postnatally acquired Zika virus disease in children younger than 18 years is mild and rarely results in severe illness or death, reported Alyson Goodman, MD, and her associates at the Centers for Disease Control and Prevention (CDC), Atlanta.

There were a total of 158 confirmed or probable postnatally acquired Zika virus disease cases among children younger than 18 years reported to the CDC in the United States between January 2015 and July 2016, wrote researchers in a case series that described the epidemiology, clinical findings, and outcomes of the cases (MMWR. 2016 Sep 30;65:1-4).

©Devonyu/Thinkstock

The cases were reported in 30 d ifferent states, and the states with the highest numbers of reported cases were Florida (23%), New York (11%), and California (9%). All patients acquired Zika virus infections during travel to a location where mosquito-borne transmission had been documented, according to researchers.

The median patient age was 14 years, the majority of the patients were female (56%), and five patients were pregnant.

Of Zika’s four primary clinical signs and symptoms, 82% of the pediatric population had a rash, 55% had a fever, 29% had conjunctivitis, and 28% had arthralgia, with 70% of the children presenting with two or more of these symptoms.

Only two children were hospitalized because of their infections. No children were reported to have meningitis, encephalitis, or Guillain-Barré syndrome, and no patients with Zika virus infection died, researchers reported.

This data “corroborates previously published reports suggesting that the clinical course of Zika virus disease is typically mild in children, as it is in adults,” Dr. Goodman and her associates wrote.

Severe disease and death in children with postnatally acquired Zika virus infection are rare, the researchers pointed out, but they encouraged physicians to consider a Zika virus disease diagnosis for children with the four common symptoms and who reside in or traveled to an area with active Zika virus transmission. All Zika virus disease cases should be reported to state health departments.

jcraig@frontlinemedcom.com

On Twitter @jessnicolecraig

The clinical course of postnatally acquired Zika virus disease in children younger than 18 years is mild and rarely results in severe illness or death, reported Alyson Goodman, MD, and her associates at the Centers for Disease Control and Prevention (CDC), Atlanta.

There were a total of 158 confirmed or probable postnatally acquired Zika virus disease cases among children younger than 18 years reported to the CDC in the United States between January 2015 and July 2016, wrote researchers in a case series that described the epidemiology, clinical findings, and outcomes of the cases (MMWR. 2016 Sep 30;65:1-4).

©Devonyu/Thinkstock

The cases were reported in 30 d ifferent states, and the states with the highest numbers of reported cases were Florida (23%), New York (11%), and California (9%). All patients acquired Zika virus infections during travel to a location where mosquito-borne transmission had been documented, according to researchers.

The median patient age was 14 years, the majority of the patients were female (56%), and five patients were pregnant.

Of Zika’s four primary clinical signs and symptoms, 82% of the pediatric population had a rash, 55% had a fever, 29% had conjunctivitis, and 28% had arthralgia, with 70% of the children presenting with two or more of these symptoms.

Only two children were hospitalized because of their infections. No children were reported to have meningitis, encephalitis, or Guillain-Barré syndrome, and no patients with Zika virus infection died, researchers reported.

This data “corroborates previously published reports suggesting that the clinical course of Zika virus disease is typically mild in children, as it is in adults,” Dr. Goodman and her associates wrote.

Severe disease and death in children with postnatally acquired Zika virus infection are rare, the researchers pointed out, but they encouraged physicians to consider a Zika virus disease diagnosis for children with the four common symptoms and who reside in or traveled to an area with active Zika virus transmission. All Zika virus disease cases should be reported to state health departments.

jcraig@frontlinemedcom.com

On Twitter @jessnicolecraig

MRI-guided focused ultrasound thalamotomy reduces hand tremor in patients with essential tremor, according to data published August 25 in the New England Journal of Medicine. The technique also reduces disability and improves self-reported quality of life, said the researchers.

“We are excited to have this new noninvasive treatment option for patients who struggle every day with this debilitating neurologic disorder,” said Howard M. Eisenberg, MD, the R.K. Thompson Professor and Chair of Neurosurgery at the University of Maryland School of Medicine in Baltimore and an author of the study. “We saw an impressive reduction in tremors in hands and arms and an improvement in quality of life in patients who experienced no relief from medication.”

Dr. Eisenberg and colleagues randomized 76 patients with moderate to severe essential tremor that had not responded to at least two trials of medical therapy to unilateral focused ultrasound thalamotomy or a sham procedure. The investigators administered the Clinical Rating Scale for Tremor (CRST) and the Quality of Life in Essential Tremor (QUEST) questionnaire to participants at baseline and at one, three, six, and 12 months. Videotaped tremor assessments were rated by an independent group of neurologists who were blinded to the treatment assignments. After three months, patients in the sham-procedure group were allowed to cross over to active treatment.

The study’s primary outcome was the between-group difference in the change from baseline to three months in hand tremor, rated on Parts A and B of the CRST. Secondary outcomes included functional limitations in daily activities, measured according to eight items in the disability subsection of the CRST; quality of life, assessed with the QUEST at three months; and the durability of the reduction in hand tremor at 12 months.

Hand-tremor scores improved by 8.5 points in the intervention group and by 0.2 points among controls. Improvement occurred in the hand contralateral to the thalamotomy. The between-group difference in the mean change was 8.3 points. The improvement in the thalamotomy group was maintained at 12 months (change from baseline, 7.2 points). Focused ultrasound thalamotomy also improved total disability score by 62% at three months, compared with 3% among controls, and the improvement was sustained at 12 months. Patients’ self-rated quality of life improved by 46% at three months in the intervention group and by 3% among controls.

Adverse events of thalamotomy included gait disturbance (36% of patients) and paresthesias or numbness (38% of patients). These adverse events persisted at 12 months in 9% and 14% of patients, respectively.

In an accompanying editorial, Elan D. Louis, MD, Chief of the Division of Movement Disorders at Yale University in New Haven, Connecticut, said that the study results are promising, particularly since the procedure, unlike traditional thalamotomy, does not require entering the skull with a probe. “Nevertheless,” he added, “there are several important concerns.” The first concern is the limited follow-up period. The sustained benefit beyond one year is not known. “This is particularly important because of tachyphylaxis, which is the second concern,” Dr. Louis wrote. Tremor score in the group that underwent focused ultrasound thalamotomy increased from 8.84 at one month to 10.89 at 12 months, an increase of 23%. A third concern is that the procedure did not achieve large improvements in everyone; the percentage change in tremor was less than 20% in nine of 56 patients. “Even with these concerns,” Dr. Louis said, “the procedure will take its place among other surgical procedures for medically refractory essential tremor.”

—Erik Greb and Glenn Williams

Suggested Reading

Elias WJ, Lipsman N, Ondo WG, et al. A randomized trial of focused ultrasound thalamotomy for essential tremor. N Engl J Med. 2016;375(8):730-739.

Louis ED. Treatment of medically refractory essential tremor. N Engl J Med. 2016;375(8):792-793.

MRI-guided focused ultrasound thalamotomy reduces hand tremor in patients with essential tremor, according to data published August 25 in the New England Journal of Medicine. The technique also reduces disability and improves self-reported quality of life, said the researchers.

“We are excited to have this new noninvasive treatment option for patients who struggle every day with this debilitating neurologic disorder,” said Howard M. Eisenberg, MD, the R.K. Thompson Professor and Chair of Neurosurgery at the University of Maryland School of Medicine in Baltimore and an author of the study. “We saw an impressive reduction in tremors in hands and arms and an improvement in quality of life in patients who experienced no relief from medication.”

Dr. Eisenberg and colleagues randomized 76 patients with moderate to severe essential tremor that had not responded to at least two trials of medical therapy to unilateral focused ultrasound thalamotomy or a sham procedure. The investigators administered the Clinical Rating Scale for Tremor (CRST) and the Quality of Life in Essential Tremor (QUEST) questionnaire to participants at baseline and at one, three, six, and 12 months. Videotaped tremor assessments were rated by an independent group of neurologists who were blinded to the treatment assignments. After three months, patients in the sham-procedure group were allowed to cross over to active treatment.

The study’s primary outcome was the between-group difference in the change from baseline to three months in hand tremor, rated on Parts A and B of the CRST. Secondary outcomes included functional limitations in daily activities, measured according to eight items in the disability subsection of the CRST; quality of life, assessed with the QUEST at three months; and the durability of the reduction in hand tremor at 12 months.

Hand-tremor scores improved by 8.5 points in the intervention group and by 0.2 points among controls. Improvement occurred in the hand contralateral to the thalamotomy. The between-group difference in the mean change was 8.3 points. The improvement in the thalamotomy group was maintained at 12 months (change from baseline, 7.2 points). Focused ultrasound thalamotomy also improved total disability score by 62% at three months, compared with 3% among controls, and the improvement was sustained at 12 months. Patients’ self-rated quality of life improved by 46% at three months in the intervention group and by 3% among controls.

Adverse events of thalamotomy included gait disturbance (36% of patients) and paresthesias or numbness (38% of patients). These adverse events persisted at 12 months in 9% and 14% of patients, respectively.

In an accompanying editorial, Elan D. Louis, MD, Chief of the Division of Movement Disorders at Yale University in New Haven, Connecticut, said that the study results are promising, particularly since the procedure, unlike traditional thalamotomy, does not require entering the skull with a probe. “Nevertheless,” he added, “there are several important concerns.” The first concern is the limited follow-up period. The sustained benefit beyond one year is not known. “This is particularly important because of tachyphylaxis, which is the second concern,” Dr. Louis wrote. Tremor score in the group that underwent focused ultrasound thalamotomy increased from 8.84 at one month to 10.89 at 12 months, an increase of 23%. A third concern is that the procedure did not achieve large improvements in everyone; the percentage change in tremor was less than 20% in nine of 56 patients. “Even with these concerns,” Dr. Louis said, “the procedure will take its place among other surgical procedures for medically refractory essential tremor.”

—Erik Greb and Glenn Williams

Suggested Reading

Elias WJ, Lipsman N, Ondo WG, et al. A randomized trial of focused ultrasound thalamotomy for essential tremor. N Engl J Med. 2016;375(8):730-739.

Louis ED. Treatment of medically refractory essential tremor. N Engl J Med. 2016;375(8):792-793.

MRI-guided focused ultrasound thalamotomy reduces hand tremor in patients with essential tremor, according to data published August 25 in the New England Journal of Medicine. The technique also reduces disability and improves self-reported quality of life, said the researchers.

“We are excited to have this new noninvasive treatment option for patients who struggle every day with this debilitating neurologic disorder,” said Howard M. Eisenberg, MD, the R.K. Thompson Professor and Chair of Neurosurgery at the University of Maryland School of Medicine in Baltimore and an author of the study. “We saw an impressive reduction in tremors in hands and arms and an improvement in quality of life in patients who experienced no relief from medication.”

Dr. Eisenberg and colleagues randomized 76 patients with moderate to severe essential tremor that had not responded to at least two trials of medical therapy to unilateral focused ultrasound thalamotomy or a sham procedure. The investigators administered the Clinical Rating Scale for Tremor (CRST) and the Quality of Life in Essential Tremor (QUEST) questionnaire to participants at baseline and at one, three, six, and 12 months. Videotaped tremor assessments were rated by an independent group of neurologists who were blinded to the treatment assignments. After three months, patients in the sham-procedure group were allowed to cross over to active treatment.

The study’s primary outcome was the between-group difference in the change from baseline to three months in hand tremor, rated on Parts A and B of the CRST. Secondary outcomes included functional limitations in daily activities, measured according to eight items in the disability subsection of the CRST; quality of life, assessed with the QUEST at three months; and the durability of the reduction in hand tremor at 12 months.

Hand-tremor scores improved by 8.5 points in the intervention group and by 0.2 points among controls. Improvement occurred in the hand contralateral to the thalamotomy. The between-group difference in the mean change was 8.3 points. The improvement in the thalamotomy group was maintained at 12 months (change from baseline, 7.2 points). Focused ultrasound thalamotomy also improved total disability score by 62% at three months, compared with 3% among controls, and the improvement was sustained at 12 months. Patients’ self-rated quality of life improved by 46% at three months in the intervention group and by 3% among controls.

Adverse events of thalamotomy included gait disturbance (36% of patients) and paresthesias or numbness (38% of patients). These adverse events persisted at 12 months in 9% and 14% of patients, respectively.

In an accompanying editorial, Elan D. Louis, MD, Chief of the Division of Movement Disorders at Yale University in New Haven, Connecticut, said that the study results are promising, particularly since the procedure, unlike traditional thalamotomy, does not require entering the skull with a probe. “Nevertheless,” he added, “there are several important concerns.” The first concern is the limited follow-up period. The sustained benefit beyond one year is not known. “This is particularly important because of tachyphylaxis, which is the second concern,” Dr. Louis wrote. Tremor score in the group that underwent focused ultrasound thalamotomy increased from 8.84 at one month to 10.89 at 12 months, an increase of 23%. A third concern is that the procedure did not achieve large improvements in everyone; the percentage change in tremor was less than 20% in nine of 56 patients. “Even with these concerns,” Dr. Louis said, “the procedure will take its place among other surgical procedures for medically refractory essential tremor.”

—Erik Greb and Glenn Williams

Suggested Reading

Elias WJ, Lipsman N, Ondo WG, et al. A randomized trial of focused ultrasound thalamotomy for essential tremor. N Engl J Med. 2016;375(8):730-739.

Louis ED. Treatment of medically refractory essential tremor. N Engl J Med. 2016;375(8):792-793.