Guide to Recognizing and Treating Sleep Disturbances in the Nursing Home
Case 2
An 85-year-old man with history of Alzheimer’s disease, major depression and arthritis, reports insomnia and “tingling in my legs” at bedtime. The patient cannot identify when the symptoms started but reports that his legs often jerk during sleep. He consumes a cup of coffee daily and has a previous 20 pack-year smoking history (he quit 40 years ago). On review of systems, he endorses fatigue. His current medication list includes fluoxetine, donepezil hydrochloride, ibuprofen as needed for arthritic pain, and a multivitamin. His examination was unremarkable, with a BMI of 26, neck circumference < 16, no tonsillar enlargement, normal (noncrowded) oropharynx, lungs clear to auscultation bilaterally, heart sounds demonstrating a normal S1 and S2, and legs without edema.
Case 2 Reflection: Restless Legs Syndrome/Willis-Ekbom Disease
Restless legs syndrome (RLS) also known as Willis-Ekbom disease, affects approximately 10 million adults in the United States alone [22]. RLS is a sensorimotor disorder that must satisfy the following 5 primary diagnostic criteria: (1) urge to move the legs with or without dysesthesias; (2) onset or exacerbation with rest or inactivity; (3) relief with movement; (4) symptoms are worse in the evening or at night (circadian component); (5) symptoms cannot be solely accounted for as consequence of another medical or behavioral condition. Other supporting clinical features can alert a clinician to the likelihood of a RLS diagnosis; these include positive family history, response to dopaminergic therapy, lack of profound daytime sleepiness, and presence of periodic limb movements during sleep (PLMS) [23–26]. In younger individuals, the symptoms present insidiously whereas older adults (> 50 years of age) will usually present with sudden onset [27].
Not only do patients lack the restorative sleep needed to ward off fatigue and restfulness, but patients also demonstrate higher rates of comorbidities (eg, anxiety, hypertension, depression) as well as large economic burden secondary to absenteeism and decreased on-the-job effectiveness [28,29]. As a results, patients with RLS experience significant reductions in quality of life related to this sensorimotor disorder [28].
No confirmatory laboratory test exists to diagnose RLS; however, patients suspected of having RLS should be evaluated with a basic metabolic panel, iron studies, and a thorough neurologic examination, as iron deficiency, kidney failure, uremia and peripheral neuropathy can lead to secondary RLS [30,31]. Evidence shows that RLS is common in NH residents [32] and may account for problematic behaviors, such as late night pacing [7]. Forty-five percent of community dwelling individuals over 65 years old exhibit a PLMS index (leg kicks per hour) of greater than 5 [33]. PLMS, while not a disorder in and of itself, can serve as a marker for potential disease. PLMS are characterized by intermittent episodes of stereotyped leg movements. PLMS typically do not awaken the patient from sleep and therefore do not contribute to insomnia or daytime sleepiness, representing a key clinical difference from RLS. It is important to note that PLMS are nonspecific and may be common in older adults that do not meet the diagnostic criteria for RLS.
Treatment of RLS is based on the frequency of symptoms and the level of functional impairment caused by the syndrome. RLS treatment recommendations should always espouse nonpharmacological interventions that include improving sleep practices, engagement in daily physical activity, targeted placement of sedentary activity in the morning when symptoms are less prominent, and concerted efforts to avoid the use of RLS-exacerbating medications (eg, selective serotonin reuptake inhibitor (SSRIs), neuroleptic agents, antihistamines) [28]. If there is an underlying condition contributing to RLS, such as metabolic disturbance or iron deficiency, then these conditions should be corrected before initiating RLS medications. Several medications are FDA-approved for treatment of RLS, including dopamine agonists (eg, ropinirole, rotigotine, pramipexole), dopamine precursor (eg, levodopa), glutamate-related (eg, gabapentin), benzodiazepines (eg, temazepam, clonazepam). Augmentation, the worsening of RLS symptoms, can occur in patients taking dopamine agonists. If this occurs, dopamine agents should be discontinued or switched to other agents (such as a long-acting dopamine agonist, gabapentin encarbil, as well as non-FDA approved therapies such as opioids). However, it is important to note that weaning off dopamine agents may result in mild but in most cases moderate and/or severe withdrawal from the medication, so counseling and close monitoring should be done.
Case 2 Outcome
Given the patient’s history of dementia, opioids, benzodiazepines and other delirium-inducing medications should be avoided. His antidepressive regimen, fluoxetine, should be re-evaluated as these medications have been associated with RLS exacerbation. In addition to SSRIs, medications associated with RLS are MAO inhibitors (selegeline, phenelzine), antipsychotics (risperdone, olanzapine), tricyclic antidepressants (mirtazapine), antihistamines (diphenhydramine, cimetidine), calcium channel blockers (verapamil, nifedipine, diltiazem), and phenytoin [34,35]. His treatment began with behavioral, nonpharmacological management, and blood testing for iron studies. His low iron level prompted initiation of oral supplementation, and he was asked to follow up in 3 months for reevaluation and possible initiation of low-dose dopamine agonists.
Case 3
A 73-year-old man with dementia is found to have very irregular sleep wake patterns with a variable bedtime and awakening time, often missing breakfast. He is found dozing off often during the day, particularly during times of inactivity. He has frequent awakenings during the night often calling for the staff to guide him back to bed. He has had some falls secondary to walking around his room. He has been prescribed various hypnotics without much benefit and instead, has suffered from some confusion while on these medications. His room is very dark and has no windows.
Case 3 Reflection: Circadian Rhythm Sleep-Wake Disorders
Circadian rhythm sleep-wake disorders (CRSWDs) are characterized by an individual’s natural propensity to want to go to sleep and be awake during a period that is undesirable personally and/or socially [36]. CRSWDs can be a result of the desynchronization of the 2 sleep processes: (1) homeostatic drive (regulates sleep intensity) and (2) circadian rhythm (maintains daytime alertness); [36]. CRSWDs can also be due to an individual’s naturally occurring sleep drives becoming misaligned with their social/personal sleep-wake demands (eg, employment schedule and socializing opportunities with family/friends). With increasing age, the circadian rhythm becomes less adept at functioning in a desynchronized pattern [7], which can result in daytime sleepiness and night time sleep fragmentation [7,37]. CRSWDs are highly prevalent in individuals with dementia [7,36]. As dementia progresses, the ability to maintain a balance of the 2 sleep process becomes more impaired [7]. As a result, individuals with dementia, particularly Alzheimer’s disease, are likely to experience agitation, irritability, and/or confusion during the evening and night, a behavioral problem referred to as “sundowning” [38].
There are several types of CRSWDs, including delayed sleep-phase syndrome, advanced sleep-phase syndrome, irregular sleep-wake disorder, non–24-hour sleep-wake disorder, shift work sleep disorder, and jet lag sleep disorder. However, the most common type of CRSWDs observed in older adults is advanced sleep-phase syndrome [39]. Due to excessive sleepiness in the early evening, affected individuals may report a need to shift to earlier and earlier bedtimes (~6 to 7 pm) and wake times (~3 to 4 am) [36]. For older affected adults, this can cause distress and frustration, particularly if their sleep phase prevents them from participating in evening activities (eg, socializing with family/friends) [36].
In the assessment of patients with suspected CRSWDs, sleep diaries (self-reported or caregiver) daily account of sleep and wake times over at least 1 week) and actigraphy (wrist-worn accelerometer designed to measure activity and inactivity at night) can be used, particularly in older adults with dementia [40,41].
CRSWD treatment may include behavioral modifications and/or pharmacological intervention. Behavioral modifications can consist of chronotherapy, relaxation training, and/or bright light therapy. Chronotherapy involves making gradual shifts in an individual’s sleep time to meet his/her desired sleep schedule. Relaxation training involves implementing behaviors/activities that reduce tension and enhance the smooth transition into sleep. Bright light therapy involves exposure to an appropriate intensity and duration of light, which is an important environmental cue to help the synchrony of the sleep-wake cycle [7]. Previous studies have observed that NH residents are exposed to a restricted amount of bright light during the daytime [42,43], but higher levels of artificial light at night (eg, hallway lighting) [7]. NH residents’ exposure to artificial bright light during the daytime has not only improved the residents’ sleep [44–46], but also has improved their cognitive functioning and reduced their depressive symptoms [47]. Thus, steps towards targeted light exposure in sync with the typical sleep-wake cycle (eg, mandated time in well-lit rooms during the day and during meals) for NH residents, particularly those with CRSWDs, could prove to be beneficial across several social, behavioral and neurocognitive domains. Lastly, NH residents exposed to at least 30 minutes of outdoor daylight and at least 3 occasions of low intensity physical activities for 10 to 15 minutes daily can potentially improve sleep-wake patterns [48]. Thus, it may be beneficial to have an intervention that couples bright light exposure and physical activity in the NH setting.
