BRAIN INJURY professional vol. 14 issue 4
Sleep Disorders and TRAUMATIC
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vol. 14 issue 4
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Editor in Chief Message Guest Editor’s Message BIP Expert Interview
Sleep Apnea and Traumatic Brain Injury
Effectiveness of Cognitive Behavioral Therapy for Treating Insomnia in Healthy Individuals and Those with Brain Injury
Risa Nakase-Richardson, PhD, FACRM • Daniel J. Schwartz, MD
Marie Dahdah, PhD • Kathleen Bell, MD • Anthony Lequerica, PhD Amber Merfeld, MPH-PAPH
Circadian Rhythms: Disruptions and Treatments in Acute Traumatic Brain Injury Jamie M. Zeitzer, PhD • Eric M Watson, PhD • Erin Holcomb, PhD
Sleep Hygiene: A Novel, Nonpharmacological Approach to Treating Sleep-Wake Cycle Disturbance after Moderate to Severe Brain Injury on an Inpatient Rehabilitation Unit Kimberley R. Monden, PhD • Don Gerber, PhD Jody Newman, MA, CCC-SLP • Angie Philippus, BA Jennifer Biggs, BA, RN, MSN, CNRN • Heidi Schneider, RN, CNRN Eric Spier, MD • Alan Weintraub, MD • Michael Makley, MD
Recommended Sleep Duration for Adults and Children: An American Academy of Sleep Medicine and Sleep Research Society Consensus Statement Sagarika Nallu, MD
What is Polysomnography and Why are There Different Types? Sagarika Nallu, MD
Brain Injury Professional is a membership benefit of the North American Brain Injury Society and the International Brain Injury Association
NORTH AMERICAN BRAIN INJURY SOCIETY CHAIRMAN Mariusz Ziejewski, PhD VICE CHAIR Debra Braunling-McMorrow, PhD IMMEDIATE PAST CHAIR Ronald C. Savage, EdD TREASURER Bruce H. Stern, Esq. FAMILY LIAISON Skye MacQueen EXECUTIVE DIRECTOR/ADMINISTRATION Margaret J. Roberts EXECUTIVE DIRECTOR/OPERATIONS J. Charles Haynes, JD MARKETING MANAGER Megan Bell-Johnston GRAPHIC DESIGNER Kristin Odom
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PUBLISHER J. Charles Haynes, JD EDITOR IN CHIEF Debra Braunling-McMorrow, PhD EDITOR IN CHIEF Nathan Zasler, MD EDITOR EMERITUS Ronald C. Savage, EdD EDITOR, LEGISLATIVE ISSUES Susan L. Vaughn EDITOR, LITERATURE REVIEW Debra Braunling-McMorrow, PhD EDITOR, TECHNOLOGY Tina Trudel, PhD FOUNDING EDITOR Donald G. Stein, PhD DESIGN AND LAYOUT Kristin Odom ADVERTISING SALES Megan Bell-Johnston
EDITORIAL ADVISORY BOARD Michael Collins, PhD Walter Harrell, PhD Chas Haynes, JD Cindy Ivanhoe, MD Ronald Savage, EdD Elisabeth Sherwin, PhD Donald Stein, PhD Sherrod Taylor, Esq. Tina Trudel, PhD Robert Voogt, PhD Mariusz Ziejewski, PhD
Managing Editor Brain Injury Professional PO Box 131401, Houston, TX 77219-1401 Tel 713.526.6900 Website: www.nabis.org Email: email@example.com
Megan Bell-Johnston Brain Injury Professional HDI Publishers PO Box 131401, Houston, TX 77219-1401 Tel 713.526.6900 Email: firstname.lastname@example.org
North American Brain Injury Society PO Box 1804, Alexandria, VA 22313 Tel 703.960.6500 / Fax 703.960.6603 Website: www.nabis.org ISSN 2375-5210 Brain Injury Professional is a quarterly publication published jointly by the North American Brain Injury Society and HDI Publishers. © 2018 NABIS/HDI Publishers. All rights reserved. No part of this publication may be reproduced in whole or in part in any way without the written permission from the publisher. For reprint requests, please contact, Managing Editor, Brain Injury Professional, PO Box 131401, Houston, TX 77219-1400, Tel 713.526.6900, Fax 713.526.7787, e-mail email@example.com.
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Children’s Healthcare of Atlanta has CARF-accredited pediatric rehab services We offer: • CARF-accredited inpatient and day rehab services with specialty recognition in spinal cord system of care, brain injury specialty program and pediatric specialty program • Care for patients big and small, from birth to age 21 • Board-certified pediatric physiatrists • 28 private rooms • Therapy seven days a week • Day rehab program for follow-up care
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editor in chief
As an Editor in Chief for the Brain Injury Professional, we provide a special edition on chronic sleep disturbances that many with brain injury experience.
Debra Braunling-McMorrow, PhD
Dr. Risa Nakase-Richardson brings our attention to the often cascading consequences of chronic sleep disturbances that many with brain injury experience. Accurately assessing and treating sleep disturbances may then add to the complexity of the course of rehabilitation or life-long living for those with brain injury. One of my goals for the BIP is to bring the reader’s attention to literature typically outside of their professional domain but relevant to the brain injury rehabilitation world. In this edition, Dr. NakaseRichardson has attempted to merge the research and literature in sleep rehabilitation with the brain injury sleep research and best practices. This includes suggesting guidelines for clinicians to better recognize, assess and treat sleep disturbances. The rate of sleep disturbance issues and the costs associated with sleep disturbances in the US is staggering. This edition is as helpful for all our readers for their own sleep hygiene as it is to enhance their clinical practice. I hope you will find this issue of great interest. Once again, be sure to mark your calendars for the upcoming North American Brain Injury Society Medical and Legal Issues in Brain Injury Conference, Brain Injury Across the Age Spectrum: Improving Outcomes for Children and Adults, March 14-17, 2018 in Houston, TX. Brain Injury Across the Age Spectrum: Improving Outcomes for Children and Adults is co-sponsored by both the North American Brain Injury Society and the National Collaborative on Children’s Brain Injury. This educational event is designed to present the latest scientific and clinical advances in the area of brain injury. Emphasis will be placed on a multidisciplinary approach in the management of patients with brain injury from acute care through to community re-entry and beyond. An internationally recognized faculty will present on a broad range of brain injury topics relating to the development of effective treatment interventions and restoring children and adults with brain injury to optimal levels of functioning. In addition to the myriad of invited talks from luminaries in the field, participants will have opportunity to present their work through the Call for Abstracts process. Accepted abstracts will be published in the Journal of Head Trauma Rehabilitation and presented as oral sessions, panels and scientific posters. The 5th PINK Concussions Summit on Female Brain Injury aka ‘PINK 5 Houston’ will be hosted by NABIS on Friday, March 16, as a full day track. The summit will feature top experts presenting evidenced-based research on sex and gender differences in female brain injury as well as panels of women sharing their personal experience of brain injury including concussions from sport, domestic violence, accidents or military service. See you in Houston!
Author Bio Debra Braunling-McMorrow, PhD, is the President and CEO of Learning Services. She serves on the board of the North American Brain Injury Society as Vice Chair. She has served as a chair of the American Academy for the Certification of Brain Injury Specialists (AACBIS), board of executive directors of Brain Injury Association of America, and several national committees, editorial boards, and peer review panels She is a published author and lecturer in the field of brain injury rehabilitation for over 30 years. To contact Dr. McMorrow, please email firstname.lastname@example.org.
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Proven Experience, Exceptional Care Tree of Life Services has been helping persons with acquired brain injury optimize their functional outcomes for over 15 years under the leadership of Nathan D. Zasler, MD, internationally recognized brain injury neurorehabilitation physician. We provide transitional rehabilitation and long-term assisted living services in home-like settings in our community. We strive to optimize clientâ&#x20AC;&#x2122;s functional outcomes by utilizing evidence based medical and neurorehabilitation assessment and treatment strategies along with close medical oversight. Our competitive, individualized per diem rates make us a cost effective choice given our scope of services , quality of care, and beautiful living environments.
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Improving the Recognition and Treatment of Sleep Disorders in Neurorehabilitation Risa Nakase-Richardson, PhD, FACRM
References 1. Zepelin H, Siegel JM, Tobler I. Mammalian sleep. Principles and practice of sleep medicine. 2005;4:91-100. 2. Van Someren EJW, Riemersma-Van Der Lek RF. LIve to the rhythem, slave to the rhythm. Sleep Medicine Reviews. 2007;11(6):465-484. 3. Horne JA. Sleep function, with particular reference to sleep deprivation. Annals of clinical research. 1985;17(5):199-208. 4. Dinges DF, Pack F, Williams K, et al. Cumulative sleepiness, mood disturbance, and psychomotor vigilance performance decrements during a week of sleep restricted to 4-5 hours per night. Sleep. Apr 1997;20(4):267-277. 5. Mathias JL, Alvaro PK. Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: a meta-analysis. Sleep medicine. Aug 2012;13(7):898-905. 6. Dash MB, Douglas CL, Vyazovskiy VV, Cirelli C, Tononi G. Long-term homeostasis of extracellular glutamate in the rat cerebral cortex across sleep and waking states. Journal of Neuroscience. 2009;29(3):620629. 7. Longordo F, Kopp C, Lüthi A. Consequences of sleep deprivation on neurotransmitter receptor expression and function. European Journal of Neuroscience. 2009;29(9):1810-1819. 8. McDermott CM, LaHoste GJ, Chen C, Musto A, Bazan NG, Magee JC. Sleep deprivation causes behavioral, synaptic, and membrane excitability alterations in hippocampal neurons. Journal of Neuroscience. 2003;23(29):9687-9695. 9. Walker MP. The role of sleep in cognition and emotion. Annals of the New York Academy of Sciences. 2009;1156(1):168197. 10. Zunzunegui C, Gao B, Cam E, Hodor A, Bassetti CL. Sleep disturbance impairs stroke recovery in the rat. Sleep. 2011;34(9):12611269. 11. Xie L, Kang H, Xu Q, et al. Sleep drives metabolite clearance from the adult brain. science. 2013;342(6156):373-377. 12. Rutherford GW, Corrigan JD. (2011). Long-term consequences of traumatic brain injury. J Head Trauma Rehabil. 2009: 24, 421-423. 13. McCarty DE. Beyond Ockham’s Razor: Redefining Problem-Solving in Clinical Sleep Medicine using a “Five-Finger” Approach. J Clinical Sleep Medicine 2010; 6:292-6 14. Larson EB, Zollman FS. The effect of sleep medications on cognitive recovery from traumatic brain injury. J Head Trauma Rehabil 2010; 25:61-7. 15. Clinical Trials Registration for Comparison of Sleep Apnea Assessment Strategies to Maximize TBI Rehabilitation Particpation and Outcome (C-SAS). https:// www.clinicaltrials.gov/ct2/show/NCT03033 901?term=TBI&cond=Sleep+Apnea&rank=1. Website accessed on October 24, 2017. 16. Flanagan S, Bell K, Dams-O’Connor K, Arciniegas D, Hammond F, Fann J, Watanabe T, Nakase-Richardson R. Developing a medical surveillance for traumatic brain injury. Brain Injury Professional. 2015; 12, 8-11.
It is well-established that sleep is a critical and an essential behavioral state for almost all animal species.1 Cognitive impairment, behavioral disruption, and emotional changes are common with mild disruption of the 24-hour sleep-wake cycle.2 The effects of sleep disruption on cognition are dosedependent and resolve once normal sleep patterns have returned.3 However, chronic sleep dysfunction contributes to persistent impairments in cognitive functioning.3,4 Sleep disruption and disorders are prevalent following traumatic brain injury (TBI).5 Animal studies highlight the critical role that restorative sleep plays in facilitating mechanisms of neural repair following brain injury6-10 and early neurodegeneration.11 In a review published by the Institute of Medicine, TBI was found to be associated with many chronic health conditions and accelerated aging.12 Further, management of comorbidities has become an increasing focus for optimizing TBI outcomes. As such, improving the recognition and treatment of sleep disorders in TBI should be a central focus of rehabilitation efforts.
Sleep disruption and disorders are prevalent following traumatic brain injury. This topical issue on TBI and sleep promotes the use of the “five-finger” approach to sleep management in TBI which attributes sleep disturbance to five source domains (circadian misalignment, pharmacologic factors, medical factors, psychological factors, and primary sleep medicine diagnoses).13 Empirically derived guidelines for evaluation and management of specific sleep disorders are made readily accessible by the American Academy of Sleep Medicine (AASM; www.aasm.org); however, their implementation in routine TBI clinical care is poorly understood. More concerning, failure to select the right treatment for the underlying mechanism of disordered sleep may result in disease progression. Without understanding the underlying etiology, treatment of sleep symptoms may be futile. Rehabilitation provider’s primary mode of treatment for sleep complaints is pharmacologic intervention without understanding of underlying formal sleep disorders.14 Emphasized in this issue is a description of major sleep disorders (sleep apnea, insomnia, and circadian rhythm disorder) experienced by TBI patients as well as informational pieces to promote greater awareness of efforts led by the AASM and Sleep Research Society (SRS) to promote healthy sleep and increase access to effective treatments. The first article is an abbreviated review of sleep apnea, consequences of under-recognition, and information for stakeholders to promote access to diagnostics and rationale for treatment. At the time of this writing, a Patient-Centered Outcomes Research Institute (PCORI) funded multi-center study15 utilizing the VA and NIDILRR TBI Model System research infrastructure is underway to compare sleep apnea screening and diagnostic tools during acute inpatient rehabilitation. This unprecedented study utilizing various methods of assessment (questionnaires, actigraphy, polysomnography) will help inform clinician choices for screening and diagnostic tools to promote earlier recognition of sleep apnea following TBI. This was a recommendation endorsed by the clinicians and scientists at the 2014 Galveston Brain Injury Conference.16 Study authors are the contributors to this special issue. Other articles include outstanding summaries of insomnia and circadian rhythm disorders with evidence based treatments that are poorly understood and utilized in rehabilitation settings. A novel approach to environmental management during inpatient rehabilitation at Craig Hospital is also summarized. My recent site visit to Craig Hospital’s Sleep-Centric Unit left me awe-struck seeing the culture change in daily practice across all disciplines to promote healthy sleep in a hospital environment. Their experience is a model for all rehabilitation units. Finally, awareness of important sleep promoting efforts underway are highlighted in side-bar articles. Among them is a summary of a recent position statement by the AASM and SRS indicating (for the first time) sleep duration targets for all age groups. We look forward to your feedback on this special issue.
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Sleep Apnea and Traumatic Brain Injury • Risa Nakase-Richardson, PhD, FACRM • Daniel J. Schwartz, MD
What is sleep apnea? Sleep apnea is a sleep-related breathing disorder that is characterized by repeated cessation (i.e., apnea) or near cessation (i.e., hypopnea) of ventilation during sleep. Subtypes of sleep apnea include obstructive, central or mixed type. Obstructive sleep apnea (OSA) is diagnosed when there is repetitive collapse or obstruction of the airway resulting in oxygen desaturation (hypoxemia) and/ or disturbance of sleep (arousals [<15 seconds] or awakenings [>15 seconds]) resulting in sleep fragmentation and non-restorative sleep. OSA is the more prevalent form of sleep apnea that is felt to be under-recognized in the general population. Central sleep apnea (CSA) is less common and occurs when there is temporal failure of the physiological mechanisms that drive breathing rhythm. This typically occurs with medical disorders (such as CHF), high altitude, brainstem insult or more commonly pharmacologic side-effect from medications that depress respiratory effort (e.g., opioids). Both are diagnosed with polysomnography (see sidebar article, “What is polysomnography?”) with American Academy of Sleep Medicine (AASM) endorsed practice guidelines for treatment.1,2
Sleep Apnea is Theorized to Impact Neural Repair and Neurodegeneration in Brain Injury. Animal and human studies have shown that sleep-wake cycle disturbances may alter neurotransmitters and receptor systems, neuronal activation and related signaling molecules, as well as physical functioning, mood, cognition and behavior.3-6 Zunzunegu and colleagues demonstrated the moderating effects of sleep on several endogenous brain repair mechanisms in an animal model of brain injury.7 Following lesion placement, an experimental group was deprived of sleep during recovery and performed significantly
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worse on behavioral tasks (a proxy for cognition) compared to a control group allowed to sleep during recovery.7 Following autopsy, the group deprived of sleep had significantly lower amounts of indices of brain repair including axonal sprouting, synaptogenesis, and vasogenesis compared to the control group allowed to sleep.7 In a review paper on sleep and TBI, O’Hara, Zeitzer and colleagues proposed that in addition to sleep loss and fragmentation, sleep apnea may also be associated with hypoxemia that may contribute to the early neurodegeneration observed in those with TBI.8 The benefits of continuous sleep were highlighted by a recent animal study showing insufficient sleep lead to greater accumulation of beta-amyloid proteins and other neurotoxins, associated with neurodegenerative disorders.9 In this study, decreased beta-amyloid proteins were found during continuous sleep due to the glymphatic system expanding space around neuronal structures to increase flow of cerebrospinal fluid to flush out toxins accumulated during waking hours.9 Collectively, chronic nightly hypoxemia and frequent arousals and awakenings (disturbing the continuity of sleep) due to cessation of breathing in sleep apnea reducing total sleep time may serve as mechanisms to explain earlier cognitive decline at younger ages in chronic TBI relative to persons with non-TBI.8 These mechanisms may contribute to the worse cognitive outcomes observed for those with sleep apnea and TBI.
Sleep Apnea is Under-Recognized Sleep apnea is thought to occur in one-third of those with TBI.10,11 This number may be an underestimate given that sleep apnea may be largely undiagnosed and untreated in both the general and TBI populations.12 The higher incidence of sleep apnea in TBI is poorly understood. However, large population-based studies suggest that sleep apnea may increase risk for TBI.
Studies conducted on large samples demonstrate that the ill-effects of sleep apnea were detectable several years prior to the clinical diagnosis being made and are associated with behaviors which increase the risk of TBI including work injuries and motor-vehicle accidents.13,14 For example, Young and colleagues conducted a national survey with 913 non-clinic based, employed individuals and reported severe sleep apnea was associated with a 7-fold increased risk of multiple auto-accidents in the five years prior to diagnosis.14 One Canadian study attributed 810,000 collisions and 1,400 fatalities to sleep apnea for a total cost of $15.9 billion.15 When the indirect costs are considered, expanded sleep apnea screening and APAP treatment have the potential to save billions of dollars.16-18 These findings are consistent with a recent white paper commissioned by the AASM entitled “Hidden Health Crisis Costing Billions,” which summarized the economic impact for all stakeholders.19 Highlights include the economic impact of sleep apnea in a single fiscal year in the United States. Modeling estimates of the cost of obstructive sleep apnea (the more prevalent form) diagnosis and treatment was 12.4 billion in the general population in 2015. However, the burden of undiagnosed obstructive sleep apnea was 149.6 billion in 2015 primarily due to lost productivity, absenteeism, costs of comorbidities due to OSA sequelae (e.g., hypertension, cardiovascular disease), motor-vehicle, and workplace accidents. They estimated that the cost to diagnose and treat every U.S. Adult with undiagnosed OSA would be 49.5 billion; however, it would result in a projected savings of 100.1 billion dollars.19 These findings are key in arguing for improved access to diagnostic and treatment modalities in our healthcare environments including rehabilitation settings.
There is growing evidence of early cognitive decline following sleep apnea diagnosis with a recent large-scale epidemiologic study in Taiwan demonstrating a 1.7 times greater risk of developing dementia within 5 years of diagnosis compared to non-sleep apnea controls matched for age and gender and adjustment for other common covariates (e.g., hypertension, hyperlipidemia, stroke, diabetes).27,28 In sum, the negative consequences of sleep apnea across health, functioning, disability, and economic outcomes are well documented and may contribute to chronic health outcomes following TBI.15,16,29-31
Why is sleep apnea prevalent in TBI?
Leveraging the existing TBI Model System (TBIMS) partnership, a new study funded by the Patient-Centered Outcomes Research Institute (PCORI) is underway to promote earlier diagnosis and management of sleep apnea in neurorehabilitation. When completed, the six center PCORI-funded study, Comparison of Sleep Apnea Screening and Diagnostic Tools (C-SAS) will identify the best tests for screening and diagnosing sleep apnea in moderate to severe TBI in-patients undergoing neurorehabilitation. See sidebar article on different types of polysomnography. The combination of early diagnostics and longitudinal data available in the NIDILRR and VA TBI Model Systems will be an invaluable research resource to answer many important questions about the long-term effect of sleep apnea in TBI. To date, the Agency for Healthcare Research and Quality has published 44 Future Research Needs Papers32 and two address sleep apnea diagnosis (Paper 11)33 and treatment (Paper 12)34 as high priority future research needs.
The increased risk for injury associated with sleep apnea may explain the higher incidence in TBI. Epidemiologic studies support that sleep apnea may serve as a comorbidity that increases risk for TBI.20-23 TBI can also affect the control of breathing during sleep. As studies show a preponderance of OSA after TBI, neurologic alterations in pharyngeal muscle coordination could contribute, considering the prevalence of various forms of dysphagia after TBI. Alternatively, medications commonly prescribed after TBI could influence the occurrence of sleep apnea. Sedatives, hypnotics, opioids, and other drugs with muscle relaxant properties might alter the pliability of the hypopharyngeal musculature and/or the central nervous response to obstruction. This has the possibility of increasing the risk for sleep apnea though two prior studies examining TBI in acute rehabilitation settings did not find an association between medications and sleep apnea diagnosis.10,11
Presence of Sleep Apnea is Underexplored as a Mediator of TBI Outcome. Sleep apnea is associated with poor physical health, impaired cognition, depression, and dementia. Multiple nightly stresses on the heart and brain are associated with systemic hypertension, atherosclerosis, increased insulin resistance, and increased risk of cardiac arrhythmias, heart attack, and stroke.20-23 Sleep apnea has been identified as a significant risk factor for stroke, independent of hypertension.21 In addition, individuals with sleep apnea are more likely to have poor physical health resulting in increased resource utilization and medical cost compared to matched non-apnea patients.24-26 Stresses on the neurological system may explain the well-established impairments in memory, sustained attention, and emotional disturbances including depression.24
To date, only Wilde and colleagues have compared a sleep apnea group (n=19) to a non-sleep apnea control group (n=17) in the post-acute stages of TBI recovery and found significant differences in concurrent memory functioning and sustained attention.31 The effect of treatment on outcome was not examined. Limitations of this study included the cross-sectional design, mixed injury severity, and correlational nature of analyses. Our own data from Veterans and service-members with TBI reveal that sleep apnea is among the most common sleep disorders in consecutive rehabilitation admissions, consistent with civilian samples.10,11 The differential effect of sleep apnea on post-TBI cognition is consistent with the theoretical model proposed by O’Hara, Zeitzer and colleagues that sleep apnea is a potential mechanism for persistent cognitive dysfunction after TBI and early development of dementia.8 As such, the chronicity of sleep apnea after TBI is a critical gap in knowledge that can inform clinical management to possibly mitigate the contribution of sleep apnea to poor chronic health and outcome in TBI.
Treatment of Sleep Apnea Improves Outcome in the General Population. Positive Airway Pressure (PAP) therapy is the American Academy of Sleep Medicine’s first line of therapy for sleep apnea; however, noncompliance can be up to 55% in the general population.35,36 Medicare arbitrarily defines the minimum criterion for treatment as 4 hours/night for greater than 70% of nights.36 Sustained use of PAP has been shown to slow deterioration of cognition, preserve sleep quality, and enhance mood in older dementia patients with sleep apnea.35 A dose-response relationship has been demonstrated between treatment and outcomes in non-TBI sleep apnea.37,38 Partial exposure to PAP enhances outcomes relative to no treatment.37,38 Patients who used PAP at least 4 hours/night showed a variety of positive outcomes: lowered blood pressure, better cardiovascular disease risk profile, better insulin resistance profile, and reduction in markers of inflammation and oxidative stress.39
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Non-adhering patients do not experience these beneficial outcomes.38 At the time of this article, the American Academy of Sleep Medicine posted updated guidelines for public comment40 that have a strong recommendation for educational interventions when initiating positive airway pressure therapy.
14. Young T, Blustein J, Finn L, Palta M. Sleep-disordered breathing and motor vehicle accidents in a population-based sample of employed adults. Sleep. 1997;20(8):608-613.
Much of the information in this article can be used to help elucidate the significance of complying with treatment for those with comorbid sleep apnea and brain injury.
18. Medicine AAoS. Cost justification for diagnosis and treatment of obstructive sleep apnea. Position statement of the American Academy of Sleep Medicine. Sleep. 2000;23(8):1017-1018.
15. Sassani A, Findley LJ, Kryger M, Goldlust E, George C, Davidson TM. Reducing motor-vehicle collisions, costs, and fatalities by treating obstructive sleep apnea syndrome. Sleep. 2004;27(3):453-458. 16. Hillman DR, Murphy AS, Antic R, Pezzullo L. The economic cost of sleep disorders. Sleep. 2006;29(3):299305. 17. Watson NF. Health care savings: the economic value of diagnostic and therapeutic care for obstructive sleep apnea. Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine. 2016;12(8):1075.
19. Medicine AAoS. Hidden health crisis costing America billions. Underdiagnosing and undertreating obstructive sleep apnea draining healthcare system Mountain View, CA: Frost & Sullivan. 2016. 20. Peppard P, Young T, Palta M, et al. Population-based study of sleep-disordered breathing as a risk factor for hypertension. Archives of internal medicine. 2000;157(15):1746-1752. 21. Redline S, Yenokyan G, Gottlieb DJ, et al. Obstructive sleep apnea–hypopnea and incident stroke: the sleep heart health study. American journal of respiratory and critical care medicine. 2010;182(2):269-277. 22. Shahar E, Whitney CW, REdline S, et al. Sleep-disordered breathing and cardiovascular disease: crosssectional results of the Sleep Heart Health Study. American journal of respiratory and critical care medicine. 2001;163(1):19-25. 23. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. American journal of respiratory and critical care medicine. 2002;165(9):1217-1239.
Ultimately, treatment of this comorbidity after TBI may help improve outcomes at a cellular and functional level unlike management of other comorbidities which could change the trajectory of both acute and chronic outcomes after TBI.
24. Jennum P, Kjellberg J. Health, social and economical consequences of sleep-disordered breathing: a controlled national study. Thorax. 2011;66(7):560-566.
27. Chang W-P, Liu M-E, Chang W-C, et al. Sleep apnea and the risk of dementia: a population-based 5-year follow-up study in Taiwan. PloS one. 2013;8(10):e78655.
1. Aurora RN, Chowdhuri S, Ramar K, et al. The treatment of central sleep apnea syndromes in adults: practice parameters with an evidence-based literature review and meta-analyses. Sleep. 2012;35(1):17-40. 2. Force AOSAT, Medicine AAoS. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine. 2009;5(3):263.
25. Sivertsen B, Øverland S, Glozier N, Bjorvatn B, Mæland JG, Mykletun A. The effect of OSAS on sick leave and work disability. European Respiratory Journal. 2008;32(6):1497-1503. 26. Sjösten N, Kivimäki M, Oksanen T, et al. Obstructive sleep apnoea syndrome as a predictor of work disability. Respiratory medicine. 2009;103(7):1047-1055.
28. Kim H, Yun C-H, Thomas RJ, et al. Obstructive sleep apnea as a risk factor for cerebral white matter change in a middle-aged and older general population. Sleep. 2013;36(5):709-715. 29. Bahammam A, Delaive K, Ronald J, Manfreda J, Roos L, Kryger MH. Health care utilization in males with obstructive sleep apnea syndrome two years after diagnosis and treatment. Sleep. 1999;22(6):740-747.
3. Dash MB, Douglas CL, Vyazovskiy VV, Cirelli C, Tononi G. Long-term homeostasis of extracellular glutamate in the rat cerebral cortex across sleep and waking states. Journal of Neuroscience. 2009;29(3):620-629.
30. Fischer J, Raschke F. Economic and medical significance of sleep-related breathing disorders. Respiration. 1997;64(Suppl. 1):39-44.
4. Longordo F, Kopp C, Lüthi A. Consequences of sleep deprivation on neurotransmitter receptor expression and function. European Journal of Neuroscience. 2009;29(9):1810-1819.
31. Wilde MC, Castriotta RJ, Lai JM, Atanasov S, Masel BE, Kuna ST. Cognitive impairment in patients with traumatic brain injury and obstructive sleep apnea. Archives of physical medicine and rehabilitation. 2007;88(10):1284-1288.
5. McDermott CM, LaHoste GJ, Chen C, Musto A, Bazan NG, Magee JC. Sleep deprivation causes behavioral, synaptic, and membrane excitability alterations in hippocampal neurons. Journal of Neuroscience. 2003;23(29):9687-9695.
32. Future Research Needs Projects. Future Research Needs Projects 2010; https://effectivehealthcare.ahrq. gov/topics/future-research-needs-projects/overview/, 2017.
6. Walker MP. The role of sleep in cognition and emotion. Annals of the New York Academy of Sciences. 2009;1156(1):168-197.
33. Science JMECfCDaC. Comparative Effectiveness of Diagnosis and Treatment of Obstructive Sleep Apnea in Adults. 2011; https://effectivehealthcare.ahrq.gov/topics/future-research-needs-projects/overview/.
7. Zunzunegui C, Gao B, Cam E, Hodor A, Bassetti CL. Sleep disturbance impairs stroke recovery in the rat. Sleep. 2011;34(9):1261-1269.
34. Balk EM, Chung M, Moorthy D, et al. Future Research Needs for Diagnosis of Obstructive Sleep Apnea. 2012.
8. Luzon A, Hubbard J. Sleep apnea, apolipoprotein epsilon 4 allele, and TBI: mechanism for cognitive dysfunction and development of dementia. Journal of rehabilitation research and development. 2009;46(6):837.
35. Cooke JR, Ayalon L, Palmer BW, et al. Sustained use of CPAP slows deterioration of cognition, sleep, and mood in patients with Alzheimer’s disease and obstructive sleep apnea: a preliminary study. Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine. 2009;5(4):305.
9. Xie L, Kang H, Xu Q, et al. Sleep drives metabolite clearance from the adult brain. science. 2013;342(6156):373-377.
36. Raj R, Hirshkowitz M. Effect of the new Medicare guideline on patient qualification for positive airway pressure therapy. Sleep medicine. 2003;4(1):29-33.
10. Holcomb EM, Schwartz DJ, McCarthy M, Thomas B, Barnett SD, Nakase-Richardson R. Incidence, Characterization, and Predictors of Sleep Apnea in Consecutive Brain Injury Rehabilitation Admissions. The Journal of head trauma rehabilitation. 2016;31(2):82-100.
37. Marcus CL, Radcliffe J, Konstantinopoulou S, et al. Effects of positive airway pressure therapy on neurobehavioral outcomes in children with obstructive sleep apnea. American journal of respiratory and critical care medicine. 2012;185(9):998-1003.
11. Webster JB, Bell KR, Hussey JD, Natale TK, Lakshminarayan S. Sleep apnea in adults with traumatic brain injury: a preliminary investigation. Archives of physical medicine and rehabilitation. 2001;82(3):316-321.
38. Weaver TE, Maislin G, Dinges DF, et al. Relationship between hours of CPAP use and achieving normal levels of sleepiness and daily functioning. Sleep. 2007;30(6):711-719.
12. Mathias J, Alvaro P. Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: a meta-analysis. Sleep medicine. 2012;13(7):898-905.
39. Vrints H, Shivalkar B, Heuten H, et al. Cardiovascular mechanisms and consequences of obstructive sleep apnoea. Acta Clinica Belgica. 2013;68(3):169-178.
13. Sjösten N, Vahtera J, Salo P, et al. Increased risk of lost workdays prior to the diagnosis of sleep apnea. CHEST Journal. 2009;136(1):130-136.
40. Practice Guidelines. Practice Standards 2017; https://aasm.org/clinical-resources/practice-standards/ practice-guidelines/, 2017.
Author Bios Risa Nakase-Richardson, PhD, FACRM, is a Clinical Research Neuropsychologist in Mental Health and Behavioral Sciences, the VA HSR&D Center for Innovation and Disability Rehabilitation Research and Defense and Veterans Brain Injury Center at the James A. Haley Veterans Hospital Polytrauma Rehabilitation Center. She is an Associate Professor in the College of Medicine, Pulmonary and Sleep Medicine Section, at the University of South Florida. She has worked in neuro-rehabilitation in both clinical and research capacities since 1998. She is a Fellow of the American Congress of Rehabilitation Medicine and National Academy of Neuropsychology. She has over 70 publications in peer-reviewed journals and over 200 presentations at scientific meetings. She has served as PI or Investigator on 13 grants funded by various federal agencies and private organizations including VA, DOD, PCORI, NIDILRR, and NAN. She is the Principal Investigator for the PCORI-funded multicenter center study entitled, Comparison of Sleep Apnea Assessment Strategies to Maximize TBI Rehabilitation Participation and Outcome (C-SAS) whose investigators provided the informational content for this special issue. Her interests include rehabilitation outcome for persons with brain injury with a more recent emphasis on the role of sleep in management of brain injury. She has established an objective sleep monitoring program using actigraphy and polysomnography in the management of sleep in acute rehabilitation and recently edited a special issue in the Journal of Head Trauma and Rehabilitation on the topic. She supervises trainees in rehabilitation medicine, sleep medicine, and psychology in both clinical and research topics related to post-traumatic sleep disturbances and severe brain injury. Email: Risa.Richardson@va.gov. Daniel J. Schwartz, MD, is an Associate Professor in the College of Medicine at the University of South Florida and Directs the Sleep Laboratory at James A. Haley Veterans Hospital in Tampa, Florida. His interests are in sleep apnea and its impact on outcome. He is currently a funded investigator on VA and PCORI grants examining sleep in traumatic brain injury survivors.
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Effectiveness of Cognitive Behavioral Therapy for Treating Insomnia in Healthy Individuals and Those with Brain Injury • Marie Dahdah, PhD • Kathleen Bell, MD • Anthony Lequerica, PhD • Amber Merfeld, MPH-PAPH The contents of this manuscript were developed under a contract with the Patient Centered Outcomes Research Institute (PCORI Project CER1511-33005). The statements presented in this presentation are solely the responsibility of the author(s) and do not necessarily represent the views of the Patient-Centered Outcomes Research Institute (PCORI), its Board of Governors or Methodology Committee. The authors declare no conflicts of interest.
In the United States, about 30% of the healthy population suffers from insomnia symptoms, though this number is thought to vary from 4.7-30% across studies.1,2 These rates vary even more widely for individuals with brain injury. Prevalence rates of post-TBI sleep disturbances range from 30-84%. In a meta-analytic study by Mathias and Alvaro (2012), traumatic brain injury (TBI) survivors were three times more likely to suffer from diagnosed insomnia than large-scale community samples.3 Rates across insomnia studies vary according to the stringency of diagnostic criteria across studies. Clinical guidelines developed by an AASM-delegated expert panel for the evaluation and management of chronic in¬somnia in adults and the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-V) indicate that clinical distress or impairment in social, occupational, or other important areas of functioning must accompany a diagnosis of insomnia.4,5 Despite its high prevalence, insomnia is thought to be underdiagnosed and undertreated.6,7
The lower end of these estimates is purportedly conservative because this estimate includes direct costs, such as medical costs, lost productivity, depression directly associated with insomnia, and alcohol abuse.2 In fact, indirect costs due to absenteeism from work/ school, insomnia-related work accidents, and increased health care costs are thought to make up nearly 47% of the cost of insomnia to the individual and to society.1 This is disconcerting as some individuals with insomnia continue to struggle with significant sleep disturbance for over a decade.1,8 Cognitive behavioral treatment for insomnia (CBTi) is 1.7 times less costly than treatment with sedative-hypnotics, regardless of format (individual, group, internet, community-based workshop) and it lowers healthcare utilization.1,9,10
Cost of Insomnia
Insomnia is known to be associated with multiple somatic and mental health illnesses, particularly hypertension, cardiovascular disease, cerebrovascular disease, diabetes, depression, and anxiety.2,11,12 Secondary insomnia comprises nearly 90% of insomnia cases.13
The estimated cost associated with insomnia is $92 to $175 billion annually, making up nearly 1% of the U.S. gross domestic product.
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Insomnia’s Impact on Cognitive and Physical Health
Although insomnia does not directly cause mortality, it is associated with an increased risk of mortality due to other causes and with cardiovascular events.14
The 3-P Model and Development of Insomnia A convenient way to conceptualize external forces affecting presentation of insomnia is the 3-P Model. The 3 P’s include: Predisposing, precipitating and perpetuating factors.15 Predispositional factors precede the onset of insomnia and represent a variety of trait-based characteristics that increase vulnerability to sleep disorders, but are insufficient by themselves to cause onset of insomnia. These factors range across demographic (e.g., older age), socioeconomic (e.g., lower SES), biological (e.g., hyperarousal), and psychological (e.g., mental health disorders) domains.16-18 In the context of predispositional factors lowering the threshold for onset of sleep disturbance, acute insomnia onset occurs in the presence of one or more precipitating factors, often stressful life events (e.g., illness, life transition, heart attack, loss of a loved one).19 According to AASM practice parameters, acute insomnia is typically short-lived, and remits within a month.13,20 When symptoms persist for greater than 6 months and affect function, insomnia is classified as chronic. Poor sleep patterns are now being perpetuated via maladaptive cognitive and behavioral coping strategies that unintentionally condition physical and mental arousal and promote learning of negative sleep behaviors and cognitions.13,21 Examples include, changes in daytime behaviors, such as increased caffeine, nicotine, or other stimulant consumption, or daytime naps which can both affect sleep drive. Some may make compensatory changes in their sleep/wake schedule that potentially modify one’s circadian rhythm.13,21 CBTi is a multifaceted treatment, which addresses these perpetuating factors.22,23
Cognitive Behavioral Therapy for Insomnia The number of systematic reviews and meta-analyses demonstrating the effectiveness of CBTi has served as the impetus for clinicians, researchers, the National Institute on Health (NIH), American Academy of Sleep Medicine (AASM), and the American College of Physicians to recommend CBTi as the first-line treatment for chronic insomnia in adults.1,2,24 CBTi has also been demonstrated to be effective in treating insomnia comorbid with medical and psychiatric conditions.1 TABLE 1 summarizes the components of CBTi.13 Use of stimulus control therapy, relaxation training, and CBT interventions are supported as practice standards by the AASM.25 Implementing multiple approaches and techniques may make CBTi more effective and long-lasting in its benefits than implementation of singular techniques.26
Pharmacotherapeutic Treatment for Insomnia There is “no single reliable pharmacologic method to treat insomnia”.13,28 Yet, there are numerous classes of medications indicated for the treatment of insomnia: sedative-hypnotics, antidepressants, melatonin, and benzodiazepine receptor agonists. Herbal preparations may also be utilized such as chamomile, kava, or valerian. Medications are recommended for short-term use, acute bouts of insomnia, whereas CBTi is felt to be beneficial for chronic insomnia.29 In addition, CBTi does not come with the risk of side effects, dependence, and tolerance that may be associated with medications.11
Brain Injury and CBT Few studies have examined CBTi in brain injured populations. Most publications include cases reports. However, one randomized controlled trial (RCT) of CBT (n=13) versus usual care (n=11) in a TBI sample found 70% of individuals reporting improvements in sleep (sleep quality, insomnia severity) and depression, which were maintained 2 months following conclusion of treatment.30 Adaptations included repetition of manualized content, increased structure, efforts at making concepts concrete, providing visual handouts, and electronic reminders to accommodate cognitive deficits.30 Similar adaptations and outcomes were observed in one pilot stroke RCT.31
Implications and Future Directions Insomnia has been linked to increased risk of cardiac and cerebrovascular diseases; cognitive impairments; decline in emotional well-being; and greater health care utilization. Chronic insomnia remains largely underdiagnosed in medical populations, creating a missed opportunity for implementation of evidencebased treatment. Despite AASM practice parameters supporting CBTi as a first-line, standard of care treatment for insomnia, pharmacologic interventions are commonplace and adversely impact cognition during brain injury recovery.32
TABLE 1: Components of CBTi CBTi%Intervention%Component%%
% Sleep%Hygiene% % Stimulus%Control% %
Sleep%Restriction% % Contraindicated%for%individuals%with%a%history%of%bipolar% 1,11 disorder%with%mania,%significant%anxiety,%and%seizures. %
Increasing%behaviors%and%environmental%conditions%that% promote%sleep,%and%eliminate%behaviors%or%conditions%that% interfere%with%sleep.%% Aims%to%strengthen%the%association%between%the% bed/bedroom%and%sleep,%while%weakening%associations%with% 11 arousing%activities%that%interfere%with%sleep. %Improves%SOL% and%sleep%efficiency%up%to%1%year%postDintervention.%%% Reduces%the%amount%of%time%spent%in%bed%and%designates%a% sleep%goal%that%better%resembles%the%actual%amount%of%time% 11 an%individual%is%sleeping. %Induces%partial%sleep%deprivation% to%build%sleep%debt%and%activate%sleep%drive.%Improves%SOL,% TST,%and%sleep%efficiency.%%
Addresses%anxiety%or%worry%that%promotes%sleepDdisruptive% arousal.%Helps%individuals%identify%and%replace%maladaptive% 11 sleepDrelated%beliefs. %Includes%discussion%of%sleep%hygiene.%%
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Though additional longitudinal studies are needed to determine the sustained effectiveness of CBTi, at least one study has shown sustained benefits for up to 3 years utilizing internet delivery of CBTi.33 CBTi has effectively treated insomnia in a variety of medical populations and in individuals across the developmental life span, regardless of delivery format. It is more cost effective than medication and, when successful, poses fewer adverse risks to individuals.
Traumatic brain injury survivors were three times more likely to suffer from diagnosed insomnia than large-scale community samples. References 1. Reynolds SA, Ebben MR. The Cost of Insomnia and the Benefit of Increased Access to Evidence-Based Treatment: Cognitive Behavioral Therapy for Insomnia. Sleep Med Clin 2017;12:39-46. doi: 10.1016/j. jsmc.2016.10.011. 2. van Straten A, van der Zweerde T, Kleiboer A, Cuijpers P, Morin CM, Lancee J. Cognitive and behavioral therapies in the treatment of insomnia: A meta-analysis. Sleep Med Rev 2017. Epub Ahead of Print. doi: 10.1016/j.smrv.2017.02.001. 3. Mathias JL, Alvaro PK. Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: A meta-analysis. Sleep Med 2012;13:898-905. 4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (5th ed). Washington DC: American Psychiatric Association; 2013. 5. Schutte-Rodin S, Broch L, Buysse D, Dorsey C, Sateia M. Clinical guideline for the evaluation and management of chronic insomnia in adults. J Clin Sleep Med 2008;4(5): 487-504. 6. Navarro-Bravo B, Párraga-Martínez I, López-Torres Hidalgo J, Andrés-Pretel F, Rabanales-Sotos J. Group cognitive behavioral therapy for insomnia: a meta-analysis. An Psicol-Spain 2015;31(1):8-18. doi: 10.6018/ analesps.31.1.168641. 7. Ram S, Seirawan H, Kumar SKS, Clark GT. Prevalence and impact of sleep disorders and sleep habits in the United States. Sleep Breath 2010;14:63-70. doi: 10.1007/s11325-009-0281-3. 8. Shahly V, Berglund PA, Coulouvrat C, et al. The associations of insomnia with costly workplace accidents and errors: results from the America Insomnia Survey. Arch Gen Psychiatry 2012;69(10):1054-1063.
12. Davidson JR, Dawson S, Krsmanovic A. Effectiveness of Group Cognitive Behavioral Therapy for Insomnia (CBT-I) in a Primary Care Setting. Behav Sleep Med 2017. Epub Ahead of Print. doi: 10.1080/15402002.2017.1318753. 13. Williams J, Roth A, Vatthauer K, McCrae CS. Cognitive Behavioral Treatment of Insomnia. CHEST 2013;143(2):554-565. doi: 10.1378/chest.12-0731. 14. Chien KL, Chen PC, Hsu HC, et al. Habitual sleep duration and insomnia and the risk of cardiovascular events and all-cause death: report from a community-based cohort. SLEEP 2010;33(2):177-184. 15. Spielman AJ, Glovinsky P. The varied nature of insomnia. In: Hauri PJ (ed), Case studies of insomnia. New York: Plenum Press; 1991. 16. Ohayon MM, Lemoine P. A connection between insomnia and psychiatric disorders in the French general population. Encephale 2002;28(5):420-428. 17. Riemann, D. Hyperarousal and insomnia: state of the science. Sleep Med Rev 2010;14(1):17. doi:10.1016/j.smrv.2009.09.002. 18. Riemann D, Spiegelhalder K, Feige B, et al. The hyperarousal model of insomnia: a review of the concept and its evidence. Sleep Med Rev 2010;14(1):19-31. doi:10.1016/j.smrv.2009.04.002. 19. Vahtera J, Kivimaki M, Hublin C, et al. Liability to anxiety and severe life events as predictors of new-onset sleep disturbances. SLEEP 2007;30(11):1537-1546. 20. Morgenthaler K, Aless C, Friedman L, et al. Practice Parameters for the Psychological and Behavioral Treatment of Insomnia: An Update. An American Academy of Sleep Medicine Report. SLEEP 2006;29(11):1415-1419. 21. Siebern AT, Manber R. New developments in cognitive behavioral therapy as the first-line treatment of insomnia. Psychol Res Behav Manag 2011;4:21-28. doi:10.2147/PRBM.S10041. 22. Spielman A. Assessment of insomnia. Clin Psychol Rev 1986;6(1):11-25. 23. Morin CM, Stone J, Trinkle D, Mercer J, Remsberg S. Dysfunctional beliefs and attitudes about sleep among older adults with and without insomnia complaints. Psychol Aging 1993;8(3):463-467. 24. McCrae CS. Incorporating psychologists into your practice. Paper presented at: The Business of Sleep Medicine; February 20-21, 2011; La Jolla, CA. 25. Redeker NS, Jeon S, Muench U, Campbell D, Walsleben J, Rapoport DM. Insomnia symptoms and daytime function in stable heart failure. SLEEP 2010;33(9):1210-1216. 26. Edinger JD, Sampson WS. A primary care “friendly” cognitive behavioral insomnia therapy. SLEEP 2003;26(2):177-182. 27. Ram S, Seirawan H, Kumar SKS, Clark GT. Prevalence and impact of sleep disorders and sleep habits in the United States. Sleep Breath 2010;14:63-70. doi: 10.1007/s11325-009-0281-3. 28. Sateia M, Buysse D, eds. Insomnia: Diagnosis and Treatment. London, England: Informa Healthcare; 2010. 29. American Academy of Sleep Medicine. Choosing Wisely: An initiative of the ABIM Foundation 2014. http://www.choosingwisely.org/societies/american-academy-of-sleep-medicine/. Accessed September 28, 2017. 30. Nguyen S, McKay A, Wong D, Rajaratnam SM, Spitz G, Williams G, Mansfield D, Ponsford JL. Cognitive Behavior Therapy to Treat Sleep Disturbance and Fatigue After Traumatic Brain Injury: A Pilot Randomized Controlled Trial. Arch Phys Med Rehabil 2017;98:1508-1517. doi: 10.1016/j.apmr.2017.02.031.
9. Blom K, Jernelöv S, Rück C, et al. Three-year follow-up of insomnia and hypnotics after controlled internet treatment for insomnia. SLEEP 2016;39(6):1267-1274.
31. Nguyen S, Wong D, McKay A, Rajaratnam SMW, Spitz G, Williams G, Mansfield D, Ponsford JL. Cognitive behavioural therapy for post-stroke fatigue and sleep disturbance: a pilot randomised controlled trial with blind assessment. Neuropsychol Rehabil 2017. Epub Ahead of Print. doi: 10.1080/09602011.2017.1326945.
10. Bonin EM, Beecham J, Swift N, et al. Psycho-educational CBT-Insomnia workshops in the community. A cost-effectiveness analysis alongside a randomized controlled trial. Behav Res Ther 2014;55:40-47.
32. Larson EB, Zollman FS. The effect of sleep medications on cognitive recovery from traumatic brain injury. J Head Trauma Rehabil 2010;25(1):61-67.
11. Koffel EA, Koffel JB, Gehrman PR. A meta-analysis of Group Cognitive Behavioral Therapy for Insomnia. Sleep Med Rev 2015;19:6-16. doi: 10.1016/j.smrv.2014.05.001.
33. Backhaus J, Hohagen F, Voderholzer U, et al. Longterm effectiveness of a short-term cognitive-behavioral group treatment for primary insomnia. Eur Arch Psychiatry Clin Neurosci 2001;251(1):35-41.
Author Bios Marie N. Dahdah, PhD, is a clinical neuropsychologist who has worked in neurorehabilitation for 15 years with a primary focus in concussion/traumatic brain injury. Dr. Dahdah’s published and ongoing research examines cognitive and psychosocial outcomes following traumatic brain injury, with special interest in dysexecutive changes following neurological compromise. She is a site principal investigator for the PCORI-funded comparative effectiveness study of sleep apnea screening and diagnostic tools in acute TBI rehabilitation. Kathleen Bell, MD, is a Professor and Chair of the PM&R Department at the University of Texas Southwestern and a nationally recognized leader in rehabilitation medicine, with specific expertise in TBI/concussion and stroke. She has conducted numerous research studies examining sleep disorders and fatigue following TBI, including the impact of phototherapy, exercise, and telephone problem-solving treatment to improve sleep quality and fatigue. She serves as a content expert and consultant for the PCORI-funded comparative effectiveness study of sleep apnea screening and diagnostic tools in acute TBI rehabilitation. Anthony H. Lequerica, PhD, is a Neuropsychologist with extensive experience in quantitative methods and psychometrics. He has written over 35 peerreviewed publications and has given presentations and lectures at conferences at the local, national, and international level. Dr. Lequerica has strong research interests in sleep/wake disorders after acquired brain injury, and has received grant funding from the New Jersey Commission on Brain Injury Research for studies examining sleep after TBI. Amber Merfeld, MPH-PAPH, has worked as a Health Educator with the National Diabetes Prevention Program (DPP) and is a Certified DPP Lifestyle Coach. She is a coordinator on the Group Lifestyle Balance(GLB-AIM) project at Baylor Institute for Rehabilitation, a study examining the feasibility and effectiveness of an existing weight-loss approach adapted for individuals with spinal cord injury, multiple sclerosis, amputation, or musculoskeletal issues. She is a research coordinator for the PCORI-funded comparative effectiveness study of sleep apnea screening and diagnostic tools in acute TBI rehabilitation.
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Circadian Rhythms: Disruptions and Treatments in Acute Traumatic Brain Injury • Jamie M. Zeitzer, PhD • Eric M Watson, PhD • Erin Holcomb, PhD Circadian Rhythms and the Sleep-Wake Cycle Circadian rhythms are near 24-hour oscillations that occur in nearly all living organisms. These fundamental rhythms allow for the temporal organization of physiologic events, as well as the anticipation of external events that occur on a regular daily, monthly, or yearly basis. In humans, the hypothalamic suprachiasmatic nucleus (SCN) acts as the central circadian pacemaker, both keeping the internal circadian clock synchronized with the outside world and synchronizing the activity of 24-hour oscillators that can be found in nearly all tissue types (e.g., liver, kidney, skin). The synchronization of the internal clock with the external world occurs through regular exposure to light. Unlike conscious visual perception, light reaches the SCN through intrinsically photosensitive retinal ganglion cells (ipRGC); this circuit is part of the so-called non-image forming (NIF) system. ipRGC integrate information from both the rod/cone system as well as its own photosensitive pigment, melanopsin. The ipRGC primarily respond to information about the intensity of the light exposure, broadly integrating light exposure over both time1 and space2. Given the peak sensitivity of melanopsin to blue light3, the NIF system is more sensitive to blue light (as opposed to the maximal sensitivity to green light found in conscious perception of light), especially as the duration of the light exposure extends beyond a few minutes4.
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The NIF system also responds to light in a relative manner such that bright light exposure during the daytime mitigates the impact of light exposure at night5-7. Regular light exposure, especially in the morning, will keep the circadian system properly aligned with a desired sleep-wake schedule8. The circadian system runs, on average, at 24 hours and 12 minutes9, meaning that there is a daily advance of 12 minutes necessary to keep the slightly longer than 24-hour clock synchronized with the 24 hour day. One of the more observable influences of the human circadian clock is in its contribution to the timing of sleep. Humans are one of the few mammalian species that consolidate sleep and wake into singular daily bouts. This consolidation process is controlled by two separate mechanisms – a homeostat and the circadian clock. The biological underpinning of the former is unknown, though hypothesized to be adenosinergic in origin10, and represents a simple appetitive process such that the longer one is awake, the more tired they get and the longer one sleeps, the less tired they become. The circadian alertness signal, arising from the SCN and possibly being mediated through hypocretin release 11, has a strong signal for wake at the end of the normal waking day, thereby offsetting the increased homeostatic pressure and allowing for consolidation of wake12. Likewise, the SCN has a strong signal for sleep at the end of the normal sleep period, thereby offsetting the decreased homeostatic pressure and allowing for the consolidation of sleep12.
Sleep-Wake Cycle Disruption and Traumatic Brain Injury (TBI) General disruption of the sleep-wake cycle is common following moderate to severe TBI13, 14. This is especially true in inpatient rehabilitation units, when receipt of optimal sleep may be most critical for neuronal repair and recovery15. Clinically, changes in the sleep-wake cycle during the acute stages of recovery have been associated with return of consciousness16, trajectory of cognitive recovery17, and participation in therapies18. Thus, consolidation of the sleep-wake cycle may represent a means for optimizing outcome for individuals with brain injury. The reason for a higher rate of sleep-wake cycle disruption in those with TBI compared to the general population is not entirely understood. Research from non-human mammals indicates there might be TBI-related damage to the circadian clock19 or potentially its output pathways. While the neural etiology of the disruption is unknown, phenomenologically, the lack of consolidation of sleep is frequently observed. One contributing factor might be the lack of regular light exposure. The lack of proper daytime light exposure can occur for several reasons, including interventions to manage behavioral agitation (a common post-traumatic symptom) through offering low stimulation (and low light) environments, patient complaints of photophobia, napping, and reduced exposure to outdoor environments and sunlight. Aberrant light exposure at night is also common due to mid-sleep awakenings secondary to regular nursing checks and procedures, aspects of the medical condition (e.g., pain, fever, inflammation) and treatment of the condition (i.e., sleep-disrupting medications or procedures), as well as comorbid conditions with known changes in sleep patterns (e.g., anxiety, depression). The lack of regular light exposure will result in a clock that has both a lower amplitude and an unpredictable phase (timing)20. General changes to scheduling in the hospital setting, including absence or loss of meal timing (e.g., with continuous tube feeds) and disruption of rest-activity cycles may also contribute general changes in sleep-wake patterns.
Circadian Rhythm Sleep Disorders – Assessment and Diagnosis There are several recognized sleep disorders that have putative circadian dysregulation as the underlying mechanism21, 22. In post-acute patients with TBI undergoing rehabilitation, the most commonly observed circadian rhythm sleep disorders are Delayed Sleep-Wake Phase Disorder (DSWPD) and Irregular Sleep-Wake Rhythm Disorder (ISWRD)23-24. DSWPD is a condition in which the timing of sleep is very late as compared to that which is socially-acceptable or appropriate. ISWRD is characterized by non-consolidated sleep – that is sleep that occurs throughout the day and night with no obvious 24-hour organization. Both of these may be self-resolving disorders associated with the injury itself or with the hospitalization and appear to decrease with severity over time 23, 24, 25. Neither of these are inherently pathological; they are, however, inconvenient from both a social and medical perspective. As direct examination of the SCN is not possible in humans, monitoring of the “hands” of the clock (i.e., variables that are strongly influenced by the SCN) is required. From a practical standpoint, measurement of sleep timing is a proxy for the timing of the circadian clock, despite significant interpretive limitations. Although polysomnography is a gold-standard for recording sleep, limitations exist for monitoring of circadian rhythm.
Wrist actigraphy has been used for many years as a proxy for determining sleep patterns26, and has been validated for use in individuals with TBI27. Wrist actigraphy depends on the collection of tri-axial accelerometry data from a device worn on non-dominant wrist. Automated, standardized algorithms (e.g., see28) can be used to approximate the occurrence of sleep. As such, sleep patterns over weeks or months are readily collectable. In the hospitalized patient recovering from a TBI, ISWRD and DSWPD may appear phenotypically using wrist actigraphy23-24. The latter is often described as patients being unable to go to sleep at the scheduled time of lights-off, while the former is often described as patients having poor sleep at night and napping frequently during the daytime. It is important to exclude alternate sleep pathologies before arriving at the conclusion that the observed sleep problem is of circadian origins – just because a sleep pattern is later than normal or is irregular does not necessitate that there is an underlying disruption to the circadian clock. There are many possibly pathologies that could result in the phenotype of ISWRD. Sleep apnea (discussed elsewhere in this volume), a condition in which there are frequent awakenings secondary to hypoxic events, can cause excessive daytime somnolence and subsequent daytime napping. As there is a finite amount of sleep an individual can have, daytime sleeping can lead to fragmentation of night sleep. As stated above, medications, pain, and nursing schedules can also lead to nocturnal sleep disruptions and subsequent daytime naps. All of these would result in sleep that is highly fragmented and could be mistaken for being a circadian (ISWRD) sleep disorder. There have been limited studies examining if there are any pathologies of the underlying circadian clock in those with TBI 29,30 . These have mostly indicated that there may be a disruption of circadian timing, but that this disruption is brief (days), occurring in the acute post-TBI period, self-resolving and likely due to the hospital environment rather than a consequence of the TBI. As the treatment for these non-circadian causes would be quite different from the treatment for a circadian disorder, ruling out non-circadian causes for an irregular sleep phenotype would be of paramount importance.
Treatment Approaches Once other causes of an irregular sleep pattern have been excluded, the treatment for an underlying circadian cause can be initiated. Irregular sleep with a putative circadian etiology is observed in many older individuals, especially those with dementia31. The common treatment for such a sleep disruption in this population is phototherapy, though meta-analyses have found phototherapy to have mixed effectiveness32-34. There are many parameters of phototherapy that can be varied (timing, color, intensity, and duration of the light exposure). A typical session might be 30 minutes of 3,000 lux broad spectrum light administered soon after awakening every day, continuing even after stabilization of the sleep schedule. In addition to phototherapy, enhancing daytime lighting and minimizing night time light exposure can be beneficial for treating ISWRD. It has been theorized that this regularization and enhancement of light exposure will enhance the amplitude of the circadian clock, thereby increasing the strength of the circadian derived sleep- and wakepromoting signals and subsequent consolidation of sleep and wake. The treatment of DSWPD is similar to that of ISWRD. A typical regimen would include phototherapy in the morning (as described above) followed by enhanced lighting during the day and light avoidance in the evening, especially before bedtime.
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Low dose melatonin (0.3 mg) can also be administered in the evening to support the phototherapy38. Both morning light exposure and low dose evening melatonin administration cause phase advances (i.e., the circadian clock signals earlier on subsequent days). This phase advance helps to offset the phase delay occurring in these patients. While the melatonin and light therapies can help to change the underlying biological cause of the delayed sleep, adjunctive behavioral therapies may be useful to align the sleep behavior with that of the biological proclivity (i.e., convince the patient to attempt to go to sleep earlier).
The gold standard for adjusting sleep behavior is Cognitive Behavioral Therapy for Insomnia (CBT-I). ! !
CBT-I is discussed elsewhere in this volume35. Preliminary studies indicate that CBT-I in combination with light may be effective in DSWPD in both adolescents and older adults36-37 without TBI. An outstanding question is to address which components of CBT-I would be most impactful in those with TBI, especially in conditions in which cognition is impaired or otherwise altered (FIGURE 1). Whatever the cause of the sleep disruption, treatment is imperative in hospitalized patients with a TBI. Fragmentation or loss of nocturnal sleep not only diminishes the restorative aspects of sleep, but also leads to daytime sleepiness subsequent difficulties engaging in rehabilitation. While treatment of circadian rhythm sleep disorders is mostly benign, failure to correctly identify the etiology of the sleep disruption can lead to significant disruptions in recovery from a TBI. Critical research is needed to provide better tools to adequately and rapidly diagnose disruptions of the circadian system in this population.
! ! !
!Stimulus! ! Control!
Cognitive! Sleep! Restructuring! Restriction!
! Figure'1.!Standard!therapy!for!both!Delayed!Sleep!Wake!Phase!Disorder!(DSWPD)!and!Irregular!Sleep!Wake!Rhythm!Disorder!(ISWRD)!includes!morning!phototherapy!and! cognitive!behavioral!therapy!for!insomnia!(CBTBI).!Addition!of!low!dose!melatonin!(0.3!mg)!in!the!evening!may!also!be!useful!for!DSWPD.!CBTBI!is!a!useful!adjunctive!therapy!to! increase!the!patient's!desire!to!get!good!sleep!and!to!follow!their!biology,!which!the!phototherapy!aims!at!aligning!to!a!more!proper!time.!There!are!several!components!to!CBTB I!that!require!active!patient!participation!and!may!be!inappropriate!in!an!individual!following!a!TBI!(e.g.,!cognitive!restructuring).!Several!of!the!hygiene!components,!however,! may!be!implemented!by!the!nursing!staff!or!family!members!in!attendance!(43).!These!include!establishing!a!set!wake!time,!abstaining!from!caffeine!in!the!afternoon,! implementing!a!stimulus!control!protocol!(i.e.,!limiting!the!number!of!activities!in!the!room),!reducing!distractions!in!the!room,!decreasing!volume!levels!in!and!out!of!the!room,! discouraging!use!of!electronics!in!the!evening,!reinforcing!a!sleepBpromoting!bedtime!routine!(e.g.,!relaxation!exercises,!soothing!music,!enjoyable!decaffeinated!hot!beverage,! or!other!patient!preferred!sleepBpromoting!activities),!and!providing!psychoeducation!about!sleep!hygiene.!
! References !
14. Mathias JL, Alvaro PK. Prevalence of sleep disturbances, disorders, and problems following traumatic brain injury: a meta-analysis. Sleep Med. 2012;13(7):898-905.
! JJ, Lu J, Chou TC, Scammell T, Saper CB. Melanopsin ! 2. Gooley in cells of origin of the retinohypothalamic tract. Nature Neurosci. 2001;4(12):1165-.
16. Duclos C, Dumont M, Arbour C, Paquet J, Blais H, Menon DK, et al. Parallel recovery of consciousness and sleep in acute traumatic brain injury. Neurology. 2017;88(3):268-75.
3. Newman LA, Walker MT, Brown RL, Cronin TW, Robinson PR. Melanopsin forms a functional shortwavelength photopigment. Biochem. 2003;42:12734-8.
17. Holcomb EM, Towns S, Kamper JE, Barnett SD, Sherer M, Evans C, et al. The relationship between sleep-wake cycle disturbance and trajectory of cognitive recovery during acute traumatic brain injury. J Head Trauma Rehabil. 2016;31(2):108-16.
1. Nelson DE, Takahashi JS. Sensitivity and integration in a visual pathway for circadian entrainment in the hamster (Mesocricetus auratus). J Physiol. 1991;439:115-45.
4. Gooley JJ, Rajaratnam SM, Brainard GC, Kronauer RE, Czeisler CA, Lockley SW. Spectral responses of the human circadian system depend on the irradiance and duration of exposure to light. Sci Transl Med. 2010;2(31):31ra3. 5. Chang AM, Scheer FA, Czeisler CA. The human circadian system adapts to prior photic history. J Physiol. 2011;589:1095-102. 6. Zeitzer JM, Friedman L, Yesavage JA. Effectiveness of evening phototherapy for insomnia is reduced by bright daytime light exposure. Sleep Med. 2011;12:805-7. 7. Smith KA, Schoen MW, Czeisler CA. Adaptation of human pineal melatonin suppression by recent photic history. J Clin Endo Metab. 2004;89:3610-4. 8. Khalsa SBS, Jewett ME, Cajochen C, Czeisler CA. A phase-response curve to single bright light pulses in human subjects. J Physiol. 2003;549:945-52. 9. Czeisler CA, Duffy JF, Shanahan TL, Brown EN, Mitchell JF, Rimmer DW, et al. Stability, precision, and near24-hour period of the human circadian pacemaker. Science. 1999;284(5423):2177-81.
15. Zunzunegui C, Gao B, Cam E, Hodor A, Bassetti CL. Sleep disturbance impairs stroke recovery in the rat. Sleep. 2011;34(9):1261-9.
18. Silva MA, Nakase-Richardson R, Sherer M, Barnett SD, Evans CC, Yablon SA. Posttraumatic confusion predicts patient cooperation during traumatic brain injury rehabilitation. Am J Phys Med Rehabil. 2012;91(10):890-3. 19. Boone DR, Sell SL, Micci MA, Crookshanks JM, Parsley M, Uchida T, et al. Traumatic brain injury-induced dysregulation of the circadian clock. PLoS One. 2012;7(10):e46204. 20. Jewett ME, Kronauer RE, Czeisler CA. Phase-amplitude resetting of the human circadian pacemaker via bright light: a further analysis. J Biol Rhythms. 1994;9(3-4):295-314. 21. AASM. International Classification of Sleep Disorders. s ed. Darien, IL: American Academy of Sleep Medicine; 2014. 22. Association AP. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington DC: American Psychiatric Association; 2013 2013.
10. Porkka-Heiskanen T, Strecker RE, Thakkar M, Bjorkum AA, Greene RW, McCarley RW. Adenosine: a mediator of the sleep-inducing effects of prolonged wakefulness. Science. 1997;276:1265-8.
23. Nakase-Richardson R, Sherer M, Barnett SD, Yablon SA, Evans CC, Kretzmer T, et al. Prospective evaluation of the nature, course, and impact of acute sleep abnormality after traumatic brain injury. Arch Phys Med Rehabil. 2013;94(5):875-82.
11. Zeitzer JM, Buckmaster CL, Parker KJ, Hauck CM, Lyons DM, Mignot E. Circadian and homeostatic regulation of hypocretin in a primate model: implications for the consolidation of wakefulness. J Neurosci. 2003;23(8):3555-60.
24. Duclos C, Dumont M, Blais H, Paquet J, Laflamme E, de Beaumont L, et al. Rest-activity cycle disturbances in the acute phase of moderate to severe traumatic brain injury. Neurorehabil Neural Repair. 2014;28(5):47282.
12. Dijk D-J, Czeisler CA. Paradoxical timing of the circadian rhythm of sleep propensity serves to consolidate sleep and wakefulness in humans. Neurosci Letters. 1994;166:63-8. 13. Castriotta RJ, Wilde MC, Lai JM, Atanasov S, Masel BE, Kuna ST. Prevalence and consequences of sleep disorders in traumatic brain injury. J Clin Sleep Med. 2007;3(4):349-56.
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25. Baumann CR, Werth E, Stocker R, Ludwig S, Bassetti CL. Sleep-wake disturbances 6 months after traumatic brain injury: a prospective study. Brain. 2007;130:1873-83. 26. Ancoli-Israel S, Cole R, Alessi C, Chambers M, Moorcroft W, Pollack CP. The role of actigraphy in the study of sleep and circadian rhythms. Sleep. 2003;26(3):342-92.
27. Kamper JE, Garofano J, Schwartz DJ, Silva MA, Zeitzer J, Modarres M, et al. Concordance of actigraphy with polysomnography in traumatic brain injury neurorehabilitation admissions. J Head Trauma Rehabil. 2016;31(2):117-25. 28. Cole RJ, Kripke DF, Gruen W, Mullaney DJ, Gillin JC. Automatic sleep/wake identification from wrist activity. Sleep. 1992;15(5):461-9. 29. Frieboes R-M, Müller U, Murck H, von Cramon DY, Holsboer F, Steiger A. Nocturnal hormone secretion and the sleep EEG in patients several months after traumatic brain injury. Journal of Neuropsychiatry and Clinical Neurosciences. 1999;11(3):354-60. 30. Seifman MA, Gomes K, Nguyen PN, Bailey M, Rosenfeld JV, Cooper DJ, et al. Measurement of serum melatonin in intensive care unit patients: changes in traumatic brain injury, trauma, and medical conditions. Front Neurol. 2014;5:237. 31. Sack RL, Auckley D, Auger RR, Carskadon MA, Wright KP, Jr., Vitiello MV, et al. Circadian rhythm sleep disorders: part II, advanced sleep phase disorder, delayed sleep phase disorder, free-running disorder, and irregular sleep-wake rhythm. An American Academy of Sleep Medicine review. Sleep. 2007;30(11):1484-501. 32. van Maanen A, Meijer AM, van der Heijden KB, Oort FJ. The effects of light therapy on sleep problems: A systematic review and meta-analysis. Sleep Med Rev. 2016;29:52-62. 33. Forbes D, Blake CM, Thiessen EJ, Peacock S, Hawranik P. Light therapy for improving cognition, activities of daily living, sleep, challenging behaviour, and psychiatric disturbances in dementia. Cochrane Database Syst Rev. 2014(2):CD003946. 34. Auger RR, Burgess HJ, Emens JS, Deriy LV, Thomas SM, Sharkey KM. Clinical practice guideline for the treatment of intrinsic circadian rhythm sleep-wake disorders: Advanced Sleep-Wake Phase Disorder (ASWPD), Delayed Sleep-Wake Phase Disorder (DSWPD), Non-24-Hour Sleep-Wake Rhythm Disorder (N24SWD), and Irregular Sleep-Wake Rhythm Disorder (ISWRD). An update for 2015: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2015;11(10):1199-236. 35. Qaseem A, Kansagara D, Forciea MA, Cooke M, Denberg TD, Clinical Guidelines Committee of the American College of P. Management of chronic insomnia disorder in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2016;165(2):125-33. 36. Gradisar M, Dohnt H, Gardner G, Paine S, Starkey K, Menne A, et al. A randomized controlled trial of cognitive-behavior therapy plus bright light therapy for adolescent delayed sleep phase disorder. Sleep. 2011;34(12):1671-80. 37. McCurry SM, Gibbons LE, Logsdon RG, Vitiello MV, Teri L. Nighttime insomnia treatment and education for Alzheimer’s disease: a randomized, controlled trial. J Am Geriatr Soc. 2005;53(5):793-802.
Author Bios Jamie M. Zeitzer, PhD, is an Associate Professor of Psychiatry and Behavioral Sciences in the Division of Sleep Sciences and Medicine at Stanford University and a Health Science Specialist in the Mental Illness Research Education and Clinical Center at the VA Palo Alto Health Care System. Dr. Zeitzer is human physiologist specializing in understanding the biological underpinnings of disruptions in both sleep and circadian rhythms and in the development of novel countermeasures to these disruptions. He received his undergraduate degree in biology from Vassar College, PhD in neurobiology from Harvard University, and completed postdoctoral fellowships in neurology at the University of California, Los Angeles and in psychiatry at Stanford University. He serves as a co-investigator on the PCORI-funded comparative effectiveness study of screening and diagnostic tools for sleep apnea in acute TBI rehabilitation. Email: email@example.com.
Erin Holcomb, PhD, is an Assistant Professor at Baylor College of Medicine with an interest in clinical research on sleep disruption in acute TBI. She is a consulting neuropsychologist at TIRR Memorial Hermann and completed her post-doctoral fellowship at the VA Polytrauma Rehabilitation Center at James A. Haley Veterans Hospital. Her focus is on standardization of assessment and treatment techniques within an inpatient rehabilitation unit.
Eric Watson, PhD, is currently in his 2nd year of a twoyear postdoctoral fellowship in clinical neuropsychology and rehabilitation research within the Department of Rehabilitation Medicine at the Icahn School of Medicine at Mount Sinai. His clinical and research interests include aging, cognitive rehabilitation, behavioral sleep medicine, applied electroencephalography, and health interventions for cognitively impaired populations (e.g., medication adherence, weight management, and chronic pain).
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Sleep Hygiene: A Novel, Nonpharmacological Approach to Treating Sleep-Wake Cycle Disturbance after Moderate to Severe Brain Injury on an Inpatient Rehabilitation Unit • Kimberley R. Monden, PhD • Don Gerber, PhD • Jody Newman, MA, CCC-SLP • Angie Philippus, BA • Jennifer Biggs, BA, RN, MSN, CNRN • Heidi Schneider, RN, CNRN • Eric Spier, MD • Alan Weintraub, MD • Michael Makley, MD
The Role of Sleep Hygiene Clinical studies of sleep after TBI have historically focused on pharmacological interventions, but many of the sleep medications commonly used in non-TBI populations have side effects that may exacerbate the cognitive impairments experienced by individuals with TBI.1 As a result, nonpharmacological, sleep hygiene approaches may be more feasible for treating sleep disturbance after TBI. Sleep hygiene consists for 4 key domains: 1. sleep homeostatic factors (e.g., regular exercise), 2. circadian factors (e.g., increased exposure to bright light), 3. medication and drug effects (e.g., restrict alcohol and caffeine consumption), and 4. arousal in the sleep setting (e.g., stress management during the day, bedtime ritual).2
As part of unit based practice, all individuals with TBI routinely undergo 72 hours of sleep monitoring with actigraphy (Actiwatch, Philips-Respironics) to obtain estimates of sleep quantity and quality. Actigraphy is a non-invasive method of determining rest-activity cycles using a wristwatch-like accelerometer to monitor gross movement. The Philips Actiware software generates an algorithm to determine whether the movements reach a threshold associated with either wake-like behavior or sleep, thereby providing a surrogate indicator of sleep. After 72 hours, nursing removes the Actiwatch, uploads the data, and places the clinical report in the patient’s chart. These reports are used by the physicians to guide treatment. Study personnel also use this information to screen patients who are eligible to participate in the pilot study. The sleep hygiene intervention was developed and based on the work of Morin,5 employing concepts of both sleep restriction and stimulus control. The sleep hygiene protocol consists of five principle components:
Preliminary studies have shown the benefits of blue light therapy for decreasing daytime sleepiness and improving sleep quality, cognitive function, and mood.3,4 Despite this knowledge, there has been minimal effort across inpatient rehabilitation facilities to provide environmental and behavioral treatments to support improved sleep-wake regulation.
1. improved nighttime sleep environment,
Developing a Sleep Centric TBI Unit
To improve the sleep environment, participants are moved to specially modified rooms to provide a dark, quiet sleep environment with light blocking shades and dimming lights. They are asked to engage in 30 minutes of pre-sleep quiet time during which light and sound is reduced and use of technology (TV, laptop, cell phone) is restricted. Nursing tracks their patients’ sleep using an observational scale (the Makley Sleep Scale) and attempt to minimize contact that might disrupt sleep.
Over the past year and a half, Craig Hospital has been conducting a pilot study to treat disrupted sleep with a sleep hygiene intervention on our inpatient TBI unit. The primary purpose of the study is to test the processes, resources, management, and scientific basis of the study, and the overall feasibility of implementing a sleep hygiene intervention on a TBI rehabilitation unit.
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2. increased daytime activation, 3. enhanced circadian stimuli, 4. consistent morning wake time and ADL routines each day, and 5. no caffeine intake after 12:00pm.
To increase daytime activation therapeutic recreation conducts an evaluation to identify meaningful activities for the participant to engage in during the day when not in scheduled therapies. Attempts are made to keep participants out of bed during the day and daytime naps are limited to 30 minutes at a time. Ambient room lighting is kept at >100 lux while participants are resting during the day. Circadian stimuli are enhanced by ensuring a well-lit wake environment during daytime and a dark environment for sleep. Participants receive 30 minutes of blue light therapy each morning. A minimum of 100 lux is targeted during the day by keeping the lights on and the blackout shade up. A maximum of 100 lux is targeted during the night by keeping the lights off and shades down for the duration of the rest period. Activities of daily living (ADL) routines are adjusted based on the participant’s sleep history and clinical presentation. ADL morning routines also occur at a consistent time seven days a week. Finally, participants in the sleep hygiene intervention have restricted caffeine intake – dieticians provide specialized dietary menus that restrict caffeine intake after noon.
Sleep hygiene, a nonpharmacological approach to treatment of disrupted sleep, offers many benefits for patients with TBI including potentially minimizing the use of centrally acting medications which could slow the recovery process.1 Craig Hospital’s sleep hygiene intervention has been well received by patients, families, and staff. For clinical settings considering a sleep hygiene intervention, the institutional support and multidisciplinary effort necessary to successfully implement such an environment must be considered. Successful implementation of a sleep centric TBI rehabilitation unit requires participation from nursing, dietary, physicians, and family. References 1. Flanagan SR, Greenwald B, Wieber S. Pharmacological treatment of insomnia for indivdiuals with brain injury. Journal of Head Trauma Rehabilitation. 2007;22(1):67-70. 2. Bogdanov S, Naismith S, Lah S. Sleep outcomes following sleep-hygiene-related interventions for individuals with traumatic brain injury: A systematic review. Brain Injury. Mar 22 2017:1-12. 3. Brooks M. Bright light therapy improves sleep, cognitive in mild TBI. 2013. www.medscape.com/ viewarticle/805547. 4. Sinclair KL, Ponsford JL, Taffe J, Lockley SW, Rajaratnam SMW. Randomized controlled trial of light therapy for fatigue following traumatic brain injury. Neurorehabil Neural Repair. 2014;28(4):303-313. 5. Morin CM. Insomnia: Psychological assessment and management. New York, USA: Guilford Press; 1993.
Author Bios Kimberley R. Monden, PhD, is a Principal Investigator in the Research Department at Craig Hospital. After completing her Bachelor’s degree in Psychology and Master’s degrees in Counseling Psychology, with a focus on positive psychology, Dr. Monden earned her Doctoral degree in Counseling Psychology at the University of Kansas in 2009. She completed her pre-doctoral internship in Clinical Psychology at the University of Kansas Medical Center in Kansas City, KS and Post-Doctoral Fellowship in Health Psychology and Integrated Primary Care at the University of Wisconsin Hospital and Clinics and Access Community Health Centers in Madison, Wisconsin. Dr. Monden is a Licensed Psychologist with clinical experience in health and rehabilitation psychology. She serves on the Executive Committee of Division 22 (Rehabilitation Psychology) of the American Psychological Association as Treasurer and Past Chair of the Communications Committee. Dr. Monden has research funding support for NIDILLR and the Craig Hospital Foundation. She studies perceptions of injustice and resilience following traumatic injury with an interest in improving quality of life and long-term psychosocial outcomes after injury. Email: KMonden@craighospital. Don Gerber, PsyD, ABPP-RP, is a rehabilitation neuropsychologist and principal investigator at Craig Hospital. He primarily works with individuals who have sustained traumatic brain injuries. His research focus is developing clinical research pilot studies. Jody Newman, MA, CCC-SLP, is a speech-language pathologist who has been working in the field of brain injury rehabilitation since 1977. She is the co-author of Group Interactive Structured Treatment–GIST, an evidence-based social competence treatment for individuals with brain injury. Currently, she works as a research clinician and study coordinator at Craig Hospital, and also co-leads GIST groups for outpatients. Angela Philippus, BA, Research Assistant, received her Bachelor’s Degree in Psychology from Metropolitan State University in 2009. Currently, Ms. Philippus is the research assistant for a randomized controlled pilot trial, “Optimized Sleep after Brain Injury: A Pilot Study” and a multi-center prospective observational cohort study, “Comparison of Sleep Apnea Assessment Strategies to Maximize Traumatic Brain Injury Rehabilitation Participation and Outcome”. Jennifer Biggs, RN, MSN, CNRN, NEA-BC, has worked at Craig Hospital in the Nursing Department for 14 years. She has a BSN from Regis University and MSN in Nursing Leadership from Regis University. She is certified in neuroscience and is a board certified advanced nurse executive. Heidi Schneider, RN, is a certified neuroscience-registered nurse and a lead nurse for Craig Hospital’s traumatic brain injury unit. She has an interest in sleep disruption after brain injury. Eric T. Spier, MD, joined the medical staff at Craig Hospital in 2016 after building and serving as the Medical Director for Mentis El Paso, a 24 bed post-acute neuro rehabilitation program that served the West Texas/New Mexico and surrounding areas. Dr. Spier earned his medical degree from The University of Texas Medical School in Houston and completed his residency at The Yale School of Medicine in New Haven and the Baylor College of Medicine in Houston. He is boarded in Physical Medicine & Rehabilitation and Brain Injury Medicine. He serves on multiple national boards including the Board of Governors for the Academy of Certification of Brain Injury Specialists, the Association of Academic Physical Medicine and Rehabilitation’s Health and Legislation Committee and a panel member for the BIAA/Mt. Sinai investigation to develop guidelines for the Rehabilitation and Disease Management of Adults with Moderate to Severe TBIs. Alan Weintraub, MD, has been Medical Director of the Brain Injury Program at Craig Hospital since 1986 and is an Associate Clinical Professor at the University Of Colorado School Of Medicine. His specific research and clinical interests are in neuroimaging biomarkers, neuropharmacology, access to rehabilitation and the long-term consequences of brain injury afflicting individuals and their families. Michael Makley, MD, is a neurologist and inventor with more than 20 years of experience taking care of patients with brain injury and stroke. He is the Director of the Sleep in Early Brain Injury Recovery [SEIBER] Project at Craig Hospital in Englewood Colorado and the Principle Investigator of the Optimized Sleep after Brain Injury [OSABI] Trial which recently completed phase one patient recruitment.
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Recommended Sleep Duration for Adults and Children: An American Academy of Sleep Medicine and Sleep Research Society Consensus Statement1,2 • Sagarika Nallu, MD
Sleep is vital to human health, and a good night’s sleep is essential to overall physical, cognitive, and emotional well-being. Sleep loss causes issues with memory, attention, mood regulation, complex thought, motor responses to stimuli, and performance at work or school. Sleep loss may also disrupt thermoregulation and increase the risk of various physical and mental disorders. Short and long sleep duration is associated with up to a two-fold increased risk of obesity, diabetes, hypertension, incident cardiovascular disease, stroke, depression, substance abuse, and increased death rates in multiple studies. In addition, an estimated 100,000 motor vehicle accidents each year are believed to be the result of drivers’ drowsiness or fatigue behind the wheel.
Despite the physiological need, nearly 70 percent of high school adolescents sleep less than the recommended 8-9 hours a night. An insufficient amount of sleep in this age group is associated with suicide risk, obesity, depression, mood problems, low grades, and delinquent behavior. The Centers for Disease Control and Prevention (CDC) in the United States has declared insufficient sleep a “public health problem.” more than a third of American adults and children are not getting enough sleep on a regular basis. Our behaviors during the day, and especially before bedtime, can have a major impact on your sleep.
They can promote healthy sleep or contribute to sleeplessness. The National Sleep Foundation recommends a relaxing bedtime ritual and winding down before bed. Our sleep cycle is defined by five stages and two distinct parts-rapid eye movement (REM) and non-REM sleep-that work to promote not only the quantity of sleep but also the quality of sleep, which impacts overall health. Each stage of sleep is influenced by various neurochemical actions among the brain regions. Sleep patterns evolve across the normal aging process. The American Academy of Sleep Medicine and Sleep Research Society developed two consensus recommendations1-2 for the amount of sleep that adults, teens, and children require for optimal health and functioning (see TABLE 2) which was also endorsed by the American Academy of Pediatrics. References 1. Watson NF, Badr MS, Belenky G, Bliwise DL, et. al. Recommended amount of sleep for a healthy adult: a joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society. J Clin Sleep Med 2015;11(6):591–592 2. Paruthi S, Brooks LJ, D’Ambrosio C, Hall WA, et. al. Recommended amount of sleep for pediatric populations: a consensus statement of the American Academy of Sleep Medicine. J Clin Sleep Med 2016;12(6):785–786.
TABLE 2: Recommended Amount of Sleep Per 24 Hours By Age Table'Y.'Recommended'Amount'of'Sleep'Per'24'Hours'By'Age' Infants!aged!4B12!months!
Sagarika Nallu, MD, is an Assistant Professor in the Morsani College of Medicine with appointments in Sleep Medicine, Neurology, and Pediatrics.
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2002 – 2005. He is also the author of two novels on brain injury, Crashing Minds and Concussion is Forever.
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Concussion, Mild, Moderate and Severe Brain Injury Complex Cases. Outcomes that work. Neurorehabilitation Neurobehavioral Rehabilitation and Supported Living Supported Living Outpatient, Home and Community Services Assessment and Evaluation Services
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For information or to make a referral www.remed.com ◊ firstname.lastname@example.org ◊ 800-84ReMed ◊ 484-595-9300 BRAIN INJURY professional 23
What is Polysomnography and Why are There Different Types? • Sagarika Nallu, MD
Polysomnography (PSG) is present reference or “gold” standard for evaluation of sleep and sleep related breathing disorders.1 The evaluation should include a thorough sleep history and a physical examination that includes the respiratory, cardiovascular, and neurologic systems.2 Access to polysomnography (PSG) in a timely manner may be limited or delayed in some locales and health care systems, and this circumstance has prompted the use of simpler limited channel sleep monitoring for the diagnosis of OSA.3 Limited channel monitoring is also known as portable monitoring (PM), home monitoring (HM), home sleep testing (HST), or out of center sleep testing (OCST).3
3. Level 3 polysomnography is a portable study, which can be performed at patient’s home and does not include EEG or overnight monitoring by a RSPGT and has a minimum of 7 diagnostic channels. 4. Level 4 polysomnography includes use of one or two variables typically arterial oxygen and airflow. The American Academy of Sleep Medicine has published practice parameters for routine use of polysomnography that distinguishes these levels of evaluation in the diagnostic workup and indication for follow-up testing.1-3
There are four levels of Polysomnography based on the number of diagnostic channels used, presence and involvement of certified respiratory polysomnography technician (RPSGT) and portability. 1 Classification of polysomnography testing are summarized in TABLE 3.1
The practice parameters stated that unattended portable monitoring for the assessment of OSA is an acceptable alternative to PSG only in the following situations:
1. Level 1 polysomnography includes administering the test in a sleep‐laboratory with full EEG montage and RSPGT monitoring throughout the night (Level 1 PSG).
2. patients are unable to be studied in the sleep laboratory (safety or immobility), and
2. Level 2 polysomnography includes all of the same parameters except for overnight monitoring of a RPSGT (unattended or ambulatory PSG). ! References 1. Kapur VK, Auckley DH, Chowdhuri S, Kuhlmann DC, Mehra R, Ramar K, Harrod CG. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(3):479–504.
3. as a follow-up study when the diagnosis of OSA was previously established by PSG, and the intent of testing is to evaluate the response to therapy (weight loss, surgery, or oral appliance).2-3
! TABLE 3: Classification of Sleep Testing
2. Epstein LJ, Kristo D, Strollo PJ, Friedman N, Malhotra A, Patil SP, Ramar K, Rogers R, Schwab RJ, Weaver EM, Weinstein MD. Clinical guideline for the evaluation, management, and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009; 5: 263-276. 3. Collop NA; Tracy SL; Kapur V; Mehra R; Kuhlmann D; Fleishman SA; Ojile JM. Obstructive sleep apnea devices for out-of-center (OOC) testing: technology evaluation. J Clin Sleep Med 2011;7(5):531-548.
1. severe clinical symptoms are indicative of OSA, and initiation of treatment is urgent, and PSG is not readily available,
Table'Z'B'CLASSIFICATION'OF'SLEEP'TESTING' ! Level!I!(type!1)!
Minimum!of!! seven!channels!! including!EEG,!! EOG,!chin!EMG,!! ECG,!airflow,!! respiratory!effort,!! oxygen!saturation!!!!
Minimum!of!! seven!channels!! including!EEG,!! EOG,!chin!EMG,!! ECG!or!heart!! rate,!airflow,!! respiratory!effort,!! oxygen!saturation!!!!
Minimum!of!four!! including!ventilation!! (at!least!two!channels!! of!respiratory!! movement!or!! respiratory!! movement!and!! airflow),!heart!rate!! or!ECG,!and!oxygen!! saturation!!!!
Level!IV!(type!4)! ! Continuous!! single!or!dual!! bioBparameter!! recording! Minimum!of!one!! oxygen!saturation,!! flow,!or!chest! movement! !
Author Bio Sagarika Nallu, MD, is an Assistant Professor in the Morsani College of Medicine with appointments in Sleep Medicine, Neurology, and Pediatrics.
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4.875 x 4.875.qxp_front 11/1/17 12:02 Page 1
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with Mark Aloia, PhD
Mark Aloia, PhD
Mark Aloia is the Global Lead for Behavior Change at Philips HealthTech and an Associate Professor of Medicine at National Jewish Health in Denver, CO. He has also been on the faculty at the University of Rochester and at Brown University as a prominent health researcher. Dr. Aloia has studied health behavior change for the past 20 years and maintains NIH funding through his academic work, with over $15M in funding to study health behavior change. He serves as an NIH grant reviewer and has published over 50 scientific papers in high quality journals. Dr. Aloia has also served on the Editorial Boards of the journals Sleep, Health Psychology, and Behavioral Sleep Medicine. He has edited a book on Behavioral Treatment for Sleep Disorders that has been translated into multiple languages. He is a regular blogger on Healthy Living for the Huffington Post. Dr. Aloia’s focus on behavioral methods to improve adherence to treatment has made significant contributions to the sleep and health psychology fields. His studies include a strong focus on promoting positive health behaviors using theoretical models of behavior change and bringing theory into practice by incorporating these ideas into mobile applications and new sensor technology. His work at Philips has resulted in products and services that have demonstrated effects on health outcomes and help differentiate the company as a developer with empirically tested health outcomes.
Recent studies are highlighting high rates of sleep apnea after TBI and stroke, and CPAP therapy is the front-line treatment in practice guidelines.
What is CPAP therapy and why do so many patients refuse to use it? CPAP is a device that operates like a splint in the upper airway. You see, the airway closes at night with apnea and CPAP blows air into the airway which, when your mouth is closed and you most is covered, holds the airway open. You can still breathe out, bit the pressure applied by CPAP keeps your airway from collapsing. Some people absolutely love treatment. They use it whenever they sleep and they feel great because of it. Others find treatment odd or uncomfortable. Some never even give it much of a chance. It can be odd to change your sleeping environment like that and sometimes, when we struggle making a change, the struggle gets to us enough that our motivation decreases and we give up.
What has your research shown to be effective for improving compliance with CPAP therapies? Mainly, we apply psychological techniques that have been used for decades to help people get through the struggles associated with making a change. We’ve found that this can help tremendously.
Is there a critical window to improve compliance? Most people think that the first week is critical, but that does not mean we can’t change things later.
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What do you suggest as modifications to improving sleep apnea treatment compliance for persons with cognitive impairment? It can be more difficult with this population, especially if the impairment is moderate to severe. My advice would depend on the type of impairment and the degree. What has been your experience? Interviewer Comment: For more severe impairments, I have found it critical to work with family members and the medical staff to link the importance of sleep apnea treatment compliance to brain health. For those with less severe injuries, we can also engage the patient in the discussion. We also try to work on desensitization to the treatment at times other than bedtime. This allows acclimation during times when they are distracted with other things such as watching TV – even if it is initially 10 minutes. It may make going to sleep with the mask on much easier over time.
Tell us about your Dream Mapper program that you designed for Phillips? We built a mobile app and website that uses our behavioral techniques in a friendly way. It also gives feedback on your nightly usage and allows you to set achievable goals. It has been dramatically helpful, improving adherence by over 20% in 170,000 patients. We now have over 500,000 people using it and it gets great reviews.
What is on the frontier as alternative treatments for sleep apnea?
In the context of mild sleep apnea and acute brain injury, what are your thoughts about the need to treat mild OSA?
Many companies have been trying to develop other treatments. I’m not terribly informed about this, but I believe that treatment Drugs, oral appliances, implants and other things are all being cannot hurt and may help if the patient can use it. If not, I would Canoeing main campus inapnea Loretto, Minnesota studied. It may be more about finding the right intervention for the at Vinland’s reassess as time passes to see if the resolves with time, but I right type of apnea. Apnea is not likely a single thing. suspect this would not be the predominant case.
drug & alcohol treatment for adults with disabilities
About the Interviewer
Risa Nakase-Richardson, PhD, FACRM, is a Clinical Research Neuropsychologist in Mental Health and Behavioral Sciences, the VA HSR&D Center for Innovation and Disability Rehabilitation Research and Defense and Veterans Brain Injury Center at the James A. Haley Vinland Veterans Hospital Polytrauma Rehabilitation Center. Shealcohol is an Associate Professor in thefor College of Medicine, Center provides drug and treatment adults with Pulmonary and Sleep Medicine Section, at the University of South Florida. She has worked in neuro-rehabilitation in both cognitive disabilities, including traumatic brain injury, fetal alcohol clinical and research capacities since 1998. She is a Fellow of the American Congress of Rehabilitation Medicine and National Academy of Neuropsychology. has over 70and publications in peer-reviewed journals and over 200 presentations at scientific spectrumShe disorder learning disabilities. We make all possible meetings. She has served as PI or Investigator on 13 grants funded by various federal agencies and private organizations including for cognitive deficits and individual learning styles. VA, DOD, PCORI,accommodations NIDILRR, and NAN. She is the Principal Investigator for the PCORI-funded multicenter center study entitled, Comparison of Sleep Apnea Assessment Strategies to Maximize TBI Rehabilitation Participation and Outcome (C-SAS) whose Located Loretto, just 20outcome milesforwest investigators provided the informational content for thisin special issue. HerMinnesota interests include — rehabilitation personsof withMinneapolis. brain injury with a more recent emphasis on the role of sleep in management of brain injury. She has established an objective sleep monitoring program using actigraphy and polysomnography in the management of sleep in acute rehabilitation and recently edited a special issue in the Journal of Head Trauma and Rehabilitation on the topic. She supervises trainees in rehabilitation medicine, sleep medicine, and psychology in both clinical and research topics related to posttraumatic sleep disturbances and severe brain injury. Email: Risa.Richardson@va.gov.
(763)479-3555 • VinlandCenter.org
Restore Neurobehavioral Center is a residential, post acute healthcare organization dedicated exclusively to serving adults with acquired brain injury who also present with moderate to severe behavioral problems. Services range from intensive inpatient neuro-rehabilitation and transitional community re-entry services to long term supported living services. Restore Neurobehavioral Center, located in a suburb north of Atlanta, is the site of our inpatient post acute neuro-rehabilitation program as well as one of our supported living sites. We operate two other community living sites, Restore-Lilburn (GA) and Restore-Ragland (AL).
www.restorehealthgroup.com 800-437-7972 ext 8251 BRAIN INJURY PROFESSIONAL
BRAIN INJURY professional 27
literature review Crashing Through Walls By Janis Ruoff, PhD
Crashing Through Walls is a gripping account of a “typical” American family initially concerned about day to day matters, their loves and losses and their dreams for the future. Everything changes in an instant when Jeff, just 18 years of age, is involved in a motor vehicle crash which brings into sharp focus the frailty of life. His mother touchingly recounts; “on Friday Jeff, my baby, had a head on collision with a van and now he lies there in a coma”. The journey of Jeff’s recovery from a severe traumatic brain injury (TBI) is told through the eyes of his mother Janis, who also expertly weaves poignant reflections about the recovery process through the eyes of her son.
Of the impact of the injury Jeff writes; “About my TBI, imagine that there is a person with a GIANT paintbrush who follows me through life, EVERY time I have an experience this person waits until it is over and quickly paints over it”.
This quote brilliantly captures the challenges for a person with TBI struggling to comprehend situations where clarity of perception is always just beyond reach, it hints at the frustration of families who fight to understand why experience does not lead to a change in behaviour for the person with TBI, and who hold on to the hope that the person they once knew will re-emerge. Throughout the book Janis shares personal reflections that are touching, and at time sad, but with humour and determination that helped her overcome the almost insurmountable challenges that her family faced. In the end, the story Janis and her family share is about making a fresh future, different from the one they imagined, but still full of hope and joy. Many of the challenges and frustration related in the book will be familiar to others who have been through a similar experience and would be of great value to families who are beginning their own journey supporting a loved one following a TBI. I believe the book should be on recommended reading lists for those professionals working with families and individuals with TBI, as it provides a unique and valuable understanding of the enormous impact of these injuries which painfully reverberate across time and situations.
About the Author Audrey McKinlay, is a Senior Lecturer in the Clinical Psychology training programme in the Melbourne School of Psychological Sciences at the University of Melbourne in Victoria, Australia. Audrey’s research expertise is in traumatic brain injury, with a particular focus on early childhood injuries, and the long term and adult outcomes of childhood mild TBI. Dr. McKinlay leads a number of large funded projects investigating outcomes for children and young people following TBI, conducted in both Australia and New Zealand, where she is an Adjunct Research Fellow at the University of Canterbury in Christchurch, New Zealand. Audrey is also investigating the support needs of educators working with children who have experienced a TBI, and collaborates with colleagues in the US and UK on this work. Older people’s health is also a focus of Audrey’s research, with a particular interest in TBI and Parkinson’s disease. Audrey is a registered psychologist in both Australia and New Zealand, and endorsed in both Clinical Psychology and Neuro Psychology, where she works with children and young people who have experienced TBI, and their families. Dr. McKinlay is a founding board member for the International Paediatric Brain Injury Society.
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A Unique Conference Organized by the National Collaborative on Childrenâ&#x20AC;&#x2122;s Brain Injury and the North American Brain Injury Society
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Jonathan M. Silver, MD Conference Chair Roberta DePompei, PhD Pediatric Co-Chair
Ann Glang, PhD Pediatric Co-Chair
Sharon Grandinette, MS Ed Pediatric Co-Chair
Mariusz Ziejewski, PhD Scientific Abstract Chair
Brain Injury Across the Age Spectrum Improving Outcomes for Children, Adolescents, & Adults March 14-17, 2018 Hyatt Regency Hotel Houston, Texas
See you in Houston!
Sleep Disorders and
TRAUMATIC BRAIN INJURY Acknowledgement The contents of this special issue were developed under a contract with the Patient Centered Outcomes Research Institute (PCORI Project CER-1511-33005), Subcontract from General Dynamics Health Solutions (W91YTZ-13-C-0015) from the Defense and Veterans Brain Injury Center, National Institute on Disability, Independent Living, and Rehabilitation Research (90DP0045-01-0 [PI: Shafi & Womack]; 90DP0028 [PI: Sherer], 90DPTB0009-01-00 [PI: Oâ&#x20AC;&#x2122;Conner], 90DPTB0007-01-00 [Harrison-Felix]) and U.S. Department of Veterans Affairs Health Services Research and Development COIN grant (1 I50 HX001233-01; CINDRR). The statements presented in this special issue are solely the responsibility of the authors and do not necessarily represent the views of the Patient-Centered Outcomes Research Institute (PCORI), nor its Board of Governors or Methodology Committee. Views also do not represent the Departments of Defense, Veterans Affairs, or Health and Human Services (ACL, NIDILRR). The authors of this special issue declare no conflicts of interest.
The National Healthy Sleep Awareness Project was established by the Centers for Disease Control and Prevention and the American Academy of Sleep Medicine, to increase public awareness of the importance of healthy sleep. It also promotes the treatment and prevention of sleep disorders.
Learn more from the National Healthy Sleep Awareness Project: sleepeducation.org/healthysleep
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New 3rd Edition!
U B I
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n io t a it il b a h e R ic g Neurolo riends or family & f f e d i u g l a n o an educati
Neurologic Rehabilitation This New Edition features a comprehensive section on Neuropharmacology as well as a detailed section for family adjustment, tips for caregivers, and commonly asked questions and answers. A valuable resource for patients, families, and professionals.
Print version availiable NOW @ www.FINR.net www.finr.net 800-697-5390
To schedule a Continuing Education Inservice, Facility Tour, or to request additional educational materials please call Ana Aguilar at 1-800-697-5390 ext. 4420
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Madison Schwartz, Stanford Law, Randall H. Scarlett, Randall A. Scarlett, Ronnie Pang, Olga Rios, Mary Anne Scarlett, and Brendan D. Nay.
SCARLETT LAW GROUP Scarlett Law Group is a premier California personal injury law firm that in two decades has become one of the state’s go-to practices for large-scale personal injury and wrongful death cases, particularly those involving traumatic brain injuries. With his experienced team of attorneys and support staff, founder Randall Scarlett has built a highly selective plaintiffs’ firm that is dedicated to improving the quality of life of its injured clients. “I live to assist people who have sustained traumatic brain injury or other catastrophic harms,” Scarlett says. “There is simply no greater calling than being able to work in a field where you can help people obtain the treatment they so desperately need.” To that end, Scarlett and his firm strive to achieve maximum recovery for their clients, while also providing them with the best medical experts available. “As a firm, we ensure that our clients receive both
the litigation support they need and the cutting-edge medical treatments that can help them regain independence,” Scarlett notes. Scarlett’s record-setting verdicts for clients with traumatic brain injuries include $10.6 million for a 31-year-old man, $49 million for a 23-year-old man, $26 million for a 7-year-old, and $22.8 million for a 52-year-old woman. In addition, his firm regularly obtains eight-figure verdicts for clients who have endured spinal cord injuries, automobile accidents, big rig trucking accidents, birth injuries, and wrongful death. Most recently, Scarlett secured an $18.6 million consolidated case jury verdict in February 2014 on behalf of the family of a woman who died as a result of the negligence of a trucking company and the dangerous condition of a roadway in Monterey, Calif. The jury awarded $9.4 million to Scarlett’s clients, which ranks as
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one of the highest wrongful death verdicts rendered in recent years in the Monterey County Superior Court. “Having successfully tried and resolved cases for decades, we’re prepared and willing to take cases to trial when offers of settlement are inadequate, and I think that’s ultimately what sets us apart from many other personal injury law firms,” observes Scarlett, who is a Diplomate of the American Board of Professional Liability Attorneys. In 2015, Mr. Scarlett obtained a $13 million jury verdict for the family of a one year old baby who suffered permanent injuries when a North Carolina Hospital failed to diagnose and properly treat bacterial meningitis that left the child with severe neurological damage. Then, just a month later, Scarlett secured an $11 million settlement for a 28-year-old Iraq War veteran who was struck by a vehicle in a crosswalk, rendering her brain damaged.