You are leaving Medscape Education
Cancel Continue
Log in to save activities Your saved activities will show here so that you can easily access them whenever you're ready. Log in here CME & Education Log in to keep track of your credits.
 

CME / ABIM MOC / CE

Are Sleep Disorders in Athletes a Sign of CTE?

  • Authors: News Author: Megan Brooks; CME Author: Charles P. Vega, MD
  • CME / ABIM MOC / CE Released: 12/16/2020
  • THIS ACTIVITY HAS EXPIRED
  • Valid for credit through: 12/16/2021
Start Activity


Target Audience and Goal Statement

This article is intended for primary care physicians, neurologists, sleep medicine specialists, nurses, and other physicians who treat and manage patients at risk for chronic traumatic encephalopathy.

The goal of this activity is to provide medical news to primary care clinicians and other healthcare professionals in order to enhance patient care.

Upon completion of this activity, participants will be able to:

  • Describe the pathology of rapid eye movement sleep behavior disorder
  • Assess any association between rapid eye movement sleep behavior disorder and chronic traumatic encephalopathy based on symptoms and neuropathological findings
  • Outline implications for the healthcare team


Disclosures

As an organization accredited by the ACCME, Medscape, LLC, requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest.

Medscape, LLC, encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.


News Author

  • Megan Brooks

    Freelance writer, Medscape

    Disclosures

    Disclosure: Megan Brooks has disclosed no relevant financial relationships.

CME Author

  • Charles P. Vega, MD

    Health Sciences Clinical Professor of Family Medicine
    University of California, Irvine School of Medicine
    Irvine, California

    Disclosures

    Disclosure: Charles P. Vega, MD, has disclosed the following relevant financial relationships:
    Served as an advisor or consultant for: GlaxoSmithKline

Editor/Nurse Planner

  • Stephanie Corder, ND, RN, CHCP

    Associate Director, Accreditation and Compliance
    Medscape, LLC

    Disclosures

    Disclosure: Stephanie Corder, ND, RN, CHCP, has disclosed no relevant financial relationships.  

CME Reviewer

  • Hazel Dennison, DNP, RN, FNP, CPHQ, CNE

    Associate Director, Accreditation and Compliance, Medscape, LLC

    Disclosures

    Disclosure: Hazel Dennison, DNP, RN, FNP, CPHQ, CNE, has disclosed no relevant financial relationships.

Medscape, LLC staff have disclosed that they have no relevant financial relationships.


Accreditation Statements



In support of improving patient care, Medscape, LLC is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.


This activity was planned by and for the healthcare team, and learners will receive 0.25 Interprofessional Continuing Education (IPCE) credit for learning and change.

    For Physicians

  • Medscape, LLC designates this enduring material for a maximum of 0.25 AMA PRA Category 1 Credit(s)™ . Physicians should claim only the credit commensurate with the extent of their participation in the activity.

    Successful completion of this CME activity, which includes participation in the evaluation component, enables the participant to earn up to 0.25 MOC points in the American Board of Internal Medicine's (ABIM) Maintenance of Certification (MOC) program. Participants will earn MOC points equivalent to the amount of CME credits claimed for the activity. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting ABIM MOC credit.

    Contact This Provider

    For Nurses

  • Awarded 0.25 contact hour(s) of continuing nursing education for RNs and APNs; none of these credits is in the area of pharmacology.

    Contact This Provider

For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact [email protected]


Instructions for Participation and Credit

There are no fees for participating in or receiving credit for this online educational activity. For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page. To receive AMA PRA Category 1 Credit™, you must receive a minimum score of 75% on the post-test.

Follow these steps to earn CME/CE credit*:

  1. Read the target audience, learning objectives, and author disclosures.
  2. Study the educational content online or printed out.
  3. Online, choose the best answer to each test question. To receive a certificate, you must receive a passing score as designated at the top of the test. We encourage you to complete the Activity Evaluation to provide feedback for future programming.

You may now view or print the certificate from your CME/CE Tracker. You may print the certificate but you cannot alter it. Credits will be tallied in your CME/CE Tracker and archived for 6 years; at any point within this time period you can print out the tally as well as the certificates from the CME/CE Tracker.

*The credit that you receive is based on your user profile.

CME / ABIM MOC / CE

Are Sleep Disorders in Athletes a Sign of CTE?

Authors: News Author: Megan Brooks; CME Author: Charles P. Vega, MDFaculty and Disclosures
THIS ACTIVITY HAS EXPIRED

CME / ABIM MOC / CE Released: 12/16/2020

Valid for credit through: 12/16/2021

processing....

Clinical Context

Rapid eye movement (REM) sleep is an important part of healthy sleep, and it is the phase of sleep during which most dreams occur. The brain usually creates muscle atony during REM sleep, which protects humans from acting out our dreams. However, approximately 1% of the population has rapid eye movement sleep behavior disorder (RBD), in which this protective atonia is lost during REM sleep. The authors of the current study describe that dysfunction of GABA-based neuronal mechanisms contributes to RBD, and therefore antidepressants and benzodiazepines can be used to treat RBD. The monoaminergic dorsal and median raphe nuclei are particularly implicated in the pathology of RBD.

RBD may be a precursor for other serious neurologic conditions, including parkinsonism and dementia. The current study analyzes a potential link between RBD and chronic traumatic encephalopathy (CTE).

Study Synopsis and Perspective

RBD is surprisingly common in athletes and may signal CTE caused by brainstem tau and Lewy body pathologies, new research suggests.

CTE is a neurodegenerative disorder linked to years of repetitive head impacts from playing professional football and other contact sports.

"Repetitive head impacts may damage sleep-relevant brainstem nuclei and lead to REM sleep behavior disorder," senior author Thor Stein, MD, PhD, a neuropathologist at VA Boston Healthcare, Massachusetts, said in a webinar hosted by the Concussion Legacy Foundation.

"This is something both athletes and their doctors need to be aware of," added Dr Stein, assistant professor of pathology and laboratory medicine at Boston University School of Medicine.

The findings were published September 17 in Acta Neuropathologica.

Surprising Findings

In RBD, the paralysis that normally occurs during REM sleep is incomplete or absent, causing people to act out their dreams by talking, flailing their arms and legs, punching, kicking, and other behaviors while asleep.

"The disorder often comes to medical attention when there is an injury or potential for injury to the individual or the individual's bed partner," Dr Stein noted.

To investigate ties between CTE and RBD, the researchers analyzed the brains of 247 deceased male contact sports athletes that were donated to the Veterans Affairs-Boston University-Concussion Legacy Foundation (VA-BU-CLF) Brain Bank.

The athletes died at a mean age of 63 years. They all had a neuropathological diagnosis of CTE. Their relatives provided information on sleep.

Nearly one third of these athletes (n=80, 32%) with CTE displayed symptoms characteristic of RBD when they were alive. "That really surprised us," said Dr Stein. "This is about 30 times more than what's reported in the general population, where it has been estimated to be present in about 1% of people," he noted.

In addition, there was a clear dose-response effect. Athletes with CTE and RBD had played contact sports for significantly more years than their peers without RBD (18.3 vs 15.1 years; P=.02).

"The odds of reporting RBD symptoms increased about 4% per year of play," first author Jason Adams, an MD/PhD student now at the University of California, San Diego, said in a statement.

New Insight

The results also point to a potential cause for RBD.

Compared with who have CTE and no RBD, those who have CTE and RBD were nearly 4 times more likely to have tau pathology within brainstem nuclei involved in REM sleep (odds ratio [OR], 3.96; 95% confidence interval [CI], 1.43-10.96; P=.008). Athletes with CTE and RBD were also more likely to have Lewy body pathology (OR, 2.36; 95% CI, 1.18-4.72; P=.02).

"Contrary to our expectations, tau pathology in the raphe nuclei was more strongly associated with RBD than Lewy body pathology, suggesting that tau pathology is more likely to lead to sleep dysfunction in CTE," Dr Stein said.

Christopher John Nowinski, PhD, cofounder and chief executive officer of the Concussion Legacy Foundation, said this study is important because it identifies a potential cause of RBD.

Dr Nowinski, a former professional wrestler, developed RBD after suffering years of concussions and still suffers from the disorder today.

"Living through this, I can tell you, this is not a benign symptom by any stretch of the imagination," said Dr Nowinski, who moderated the webinar. "You are a danger to yourself; you are a danger to others. Hopefully, this study will help us better understand treatment going forward," he said.

Reached for comment on the study, Carmela Tartaglia, MD, Marion and Gerald Soloway Chair in Brain Injury and Concussion Research at the University of Toronto, Canada, said sleep studies are "the most important" factor that needs to be considered when making a diagnosis of probable RBD.

"It is very important to do sleep studies, as it is often difficult to rely on informants, since nightmares and talking in sleep is often misreported as RBD. A polysomnography is the gold standard," Dr Tartaglia told Medscape Medical News.

Another factor is the use of medications. "Although the authors mention antidepressants and benzodiazepines can cause sleep changes, acetylcholinesterase inhibitors (used to treat Alzheimer's disease) are often associated with nightmares and so could be playing an even larger role in misdiagnosis of RBD," Dr Tartaglia said.

In her view, the results of increased brainstem tau pathology associated with RBD should be "pondered in light of recent findings that brainstem tau pathology is an early finding in Alzheimer's disease and that is an illness not associated with RBD."

Summing up, Dr Tartaglia said "changes in sleep are increasingly recognized in concussion and should be studied in prospective studies that include polysomnography so that an accurate diagnosis of RBD can be made. It would be interesting to see the replication of these results in a cohort of such patients."

Support for the study was provided by the Department of Veterans Affairs, the Alzheimer's Association, the National Institutes of Health, Concussion Legacy Foundation, Andlinger Foundation, and World Wrestling Entertainment. Adams and Dr Stein have disclosed no relevant financial relationships.

Acta Neuropathol. Published September 17, 2020.[1]

Study Highlights

  • Study subjects were former athletes who donated their brains for research. All autopsy participants had a history of repeated head injury.
  • Participants with a history of corticobasal degeneration, progressive supranuclear palsy, or other motor neuron disease were excluded from analysis.
  • The study team queried individuals who knew the decedents about their history of head injury and any diagnosis or symptoms of RBD.
  • The brains of subjects were reviewed for neuropathological findings, including an immunohistochemical analysis.
  • The main study outcome was the relationship between RBD and neuropathological findings associated with CTE.
  • 247 men provided data for analysis. The mean age at death was 63 years, and most men had a history of dementia. The mean duration of cognitive impairment was nearly 10 years.
  • 32% of the study cohort was found to have a probable history of RBD.
  • Most characteristics between subjects with probable RBD and no RBD were similar. Rates of dementia, sleep apnea, and parkinsonism were not statistically different between these groups, as were the ages of incident cognitive decline and death.
  • However, subjects with probable RBD had a longer duration of sports participation vs. non-RBD subjects (mean, 18.3 vs 15.1 years, respectively).
  • Neocortical Lewy body disease was found in 33% of probable RBD subjects compared with 17% of non-RBD subjects (P=.005).
  • The presence of probable RBD did not affect CTE stage or severity of Alzheimer's disease or vascular pathology.
  • The prevalence of p-tau neurofibrillary tangles (NFTs) in the probable RBD and non-RBD groups were 84% and 66%, respectively (P=.02). The odds ratio for NFTs in the dorsal and median raphe nuclei associated with probable RBD was 3.96 (95% CI, 1.43-10.96).
  • The odds ratio for Lewy body pathology in the dorsal and median raphe nuclei associated with probable RBD was 3.96 (95% CI, 1.43-10.96).

Clinical Implications

  • RBD is associated with the loss of muscle atony during REM sleep. Dysfunction of GABA-based neuronal mechanisms contributes to RBD, and monoaminergic dorsal and median raphe nuclei are particularly implicated in the pathology of RBD.
  • In the current study, 32% of men with a history of repeated head injuries were found to have probable RBD. Probable RBD was not associated with rates of cognitive decline or age at death, but men with RBD were more likely to have NFTs and Lewy body pathology in the dorsal and median raphe nuclei.
  • Implications for the Healthcare Team: The healthcare team should obtain a history of head injury among patients with suspected RBD and work to ensure protection against future head trauma. Including discussing any findings at team meetings and educating the individual patient about the risks of RBD.

Earn Credit

  • Print