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Improving Sleep Management in the Elderly

  • Fri, 9/5/08 - 4:54pm
  • 0 Comments
  • 4611 reads
Author(s): 

Cathleen A. Bergeron, RN, CDONA/LTC, MSHA, Charles A. Crecelius, MD, PhD, FACP, CMD, Robert Murphy, RN, Sharon Roth Maguire, MS, APRN-BC, GNP, APNP, Dan Osterweil, MD, MscED, CMD, William Simonson, PharmD, FASCP, CGP, Barney S. Spivack, MD, CMD, FACP, Brian D. Stwalley, PharmD, CGP, FASCP, Phyllis C. Zee, MD, PhD

This supplement is sponsored by Takeda Pharmaceuticals North America, Inc.

Improving Sleep Management in the Elderly

“If sleep does not serve an absolutely vital function, then it is the biggest mistake the evolutionary process ever made.”
--Alan Rechschaffen, University of Chicago

Introduction
Sleep, which occupies a third of our lives, is a vital function that affects cognition and performance, as reflected by mental and physical health. The problem of insomnia in older adults living in long-term care (LTC) settings is multifactorial, involving aging biology, sleep physiology, behavior, and environment. All of these factors can feed on each other to create a vicious cycle of little sleep and high stress. This white paper is a practical guide for the management of insomnia in LTC settings, which include skilled nursing and assisted living facilities. The purpose of this guide is to help clinicians more effectively recognize, assess, treat, and monitor insomnia in the elderly residing in LTC. Specific objectives include:

•Explain the nature of normal sleep and insomnia
•Describe the prevalence of insomnia in older adults
•Identify the clinical, economic, and regulatory implications of insomnia
•Examine the impact of new regulations and guidelines
•Summarize practical methods to recognize, evaluate, treat, and monitor insomnia

The Nature of Insomnia
Insomnia may be defined as complaints of disturbed sleep in the presence of adequate opportunity and circumstance for sleep.1 While people who reside in long-term care facilities are residents, we use the term “patient(s)” throughout this document since we are addressing individuals within the context of treating a medical condition.

Classification of Insomnia
The American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV)™ lists the main characteristics of insomnia as recurring, difficulty falling asleep, difficulty maintaining sleep, and nonrefreshing sleep, accompanied by impairment of function.2 All or some of these should be present at the time of diagnosis. Patients may express dissatisfaction with sleep quantity or quality. The impact of insomnia is significant and includes distress (eg, fatigue, moodiness) and impairment in social or emotional areas, decreased quality of life (QOL), or impairment of daily functioning.

Insomnia may be characterized as acute or chronic depending on its duration. Acute insomnia (also called transient insomnia) is often caused by emotional or physical discomfort and is marked by individual episodes that do not last longer than several weeks.1 If left untreated, acute insomnia may develop into chronic insomnia. By definition, chronic insomnia lasts a minimum of 30 days, but some clinicians assert that it has to last 3 months or longer to be classified as being chronic.1 Chronic insomnia is characterized by 1 or more of the following symptoms: difficulty falling asleep, difficulty maintaining sleep, and waking up too early.

Primary Versus Comorbid Insomnia
In addition to duration, insomnia can also be classified as primary or comorbid (formerly referred to as secondary insomnia) (Table 1).3 By definition, the term primary insomnia implies no other known cause of sleep disturbance. Subgroups of primary insomnia include idiopathic and psychophysiologic insomnia.4 Patients with primary insomnia exhibit unique patterns of cognitive hyperarousal and physiological arousal.5-8 In the laboratory, the biological mechanisms of primary insomnia have been associated with increased global cerebral glucose metabolism during sleep and while awake, as well as a reduced relative metabolism in the prefrontal cortex while awake. Furthermore, there is evidence of hypothalamic-adrenal hyperactivity.

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