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Abstract
As it can be seen, sleep problems in elderly are very common. This takes the form of difficulties in sleep initiation or maintenance, complain of longer sleep latency, frequent awakenings at night, insufficient sleeping time, and excessive daytime sleepiness. Also the prevalence of primary sleep disorders, periodic leg movements in sleep, and restless sleep syndrome starts to increase significantly in the middle years of life. Sleep disturbance in the elderly is linked tightly with the deterioration of circadian rhythm system. There is a higher incidence of sleep disorders among elderly subjects than among individuals of any other age group.
Older adults report high rates of sleeping problems .Poor sleep quality or lack of consolidated sleep adversely affects daytime mental performance and motor function. This contributes to the significantly higher rate of automobile and other accidents of people with chronic insomnia, as well as to memory impairment, failure to accomplish daily tasks, diminished ability to concentrate, and interpersonal difficulties. In older adults, untreated sleep problems are a strong predictor of nursing home placement.
Behaviorally, sleep is defined as a reversible behavioral state of perceptual disengagement from and unresponsiveness to the environment. Sleep is a brain process, but is not a unitary process, and some sleep processes are active, involving significant cortical activation. Sleep is primarily studied through the use of overnight continuous electroencephalogram (EEG) sleep recordings which is referred to as polysomnography (PSG). In addition, electrooculograms (EOG) are included to measure eye movements and electromylograms (EMG) are used to record muscle activity. Two separate sleep states have been identified, non-rapid eye movement (NREM) and rapid eye movement (REM). NREM sleep has been divided into Stages 1-4. Thus during sleep individual 30 second recording periods (one epoch) are categorized as wakefulness (W or Stage 0) or Stage 1, 2, 3, or 4, or REM. It is also been found that W, NREM and REM sleep are not mutually exclusive with elements of one or more of these states appearing simultaneously.
During NREM sleep the brain is relatively inactive. The 4 NREM stages roughly parallel a depth of sleep continuum, with arousal thresholds generally lowest in Stage 1 and highest in Stage 4 sleep. Stages 3 and 4 (referred to as slow wave sleep [SWS]) occur when there is 20-50% and greater than 50% delta wave activity, respectively. In contrast to NREM sleep, REM sleep is defined by EEG activation, muscle atonia, and episodic bursts of rapid eye movements. The mental activity of REM sleep is associated with dreaming.
Other physiologic activities may accompany REM sleep including middle ear muscle activity, periorbital integrated potentials, and in males, sleep-related erections. There are two phases of REM sleep referred to as ”phasic REM sleep” and ”tonic REM sleep”. Phasic REM sleep occurs when REM and other phasic activity are high, and tonic REM sleep occurs when REM background activity is present but there is very little phasic activity.
Onset of sleep is not easily defined but is considered to occur with EEG changes from W to Stage 1 with the presence of slow eye movements. With a normal pattern of sleep, humans progress through NREM sleep (stages 1-4) with some fluctuation before entering REM sleep. NREM and REM sleep alternate in a cyclical fashion. The normal pattern is 90 - 120 minute long cycles of NREM and REM sleep. Sleep onset typically occurs in less than 15 minutes and nocturnal awakening are few and brief. Stage 1 represents a very small portion of the total sleep time, 1-5%, with Stage 2 accounting for the largest portion, approximately half the nights sleep. REM sleep is greatest in the latter third of the night usually making up 20% to 25% of total sleep. Generally, there are 4-6 episodes of REM sleep with the latter episodes becoming progressively longer. The remaining sleep time is made up of SWS, i.e. Stages 3 and 4. SWS predominates in the first third of the night.
Sleep patterns are driven by circadian rhythm. Anything that disrupts this rhythm can affect sleep. For example, REM sleep can occur earlier, essentially reversing the sleep pattern. This can be seen in shift workers or frequent flyers. Human sleep should be viewed as a component of the 24-hour sleep-wake cycle rather than a discrete entity.
The precise neurophysiologic basis for the sleep-wake cycle is not known. Brain function is supported by activating and inhibitory processes. Brain activation is high during waking, decreases during NREM sleep, and increases again during REM sleep. This involves nearly all structures of the brain. Neurotransmitters involved include γ-aminobutyric acid (GABA), glutamate, acetylcholine, norepinephrine, serotonin, dopamine, histamine, hypocretin and others.
Sleep patterns can be different based on a number of factors. With increasing age, there is a gradual decline in total sleep associated with fragmentation or greater wakefulness intermixed with sleep. Elderly people typically spend more time in bed but less time sleeping. Sleep patterns will also be different depending on prior sleep history. Following sleep loss on previous nights, recovery sleep occurs which is usually prolonged and deeper.
This can be summarised as:
1. Decreased total sleep time
2. Changes in NREM sleep
3. Increased nimber of arousals
4. Reduction in deep sleep
5. Changes in REM sleep
Pharmacotherapy commonly affects the sleep state distribution. Taking advantage of this, pharmacologic treatments have been developed for the treatment of sleep disorders, e.g. benzodiazepines. Most pertinent to this review, many antidepressants are known to cause disruption of sleep and the sleep pattern.
Sleep is affected by pathology. There are a number of disorders which are specifically related to sleep such as narcolepsy, sleep apnea, restless leg syndrome and parasomnias (undesirable behavioral or experiential phenomena occurring during sleep). Many medical conditions can affect sleep and most psychiatric conditions affect sleep.
Sleep disorders lead to one of two primary complaints: (a) an inability to initiate or maintain sleep at night (insomnia) or (b) an inability to maintain wakefulness during the day (excessive daytime sleepiness). Some patients have both complaints, but usually one of these predominates. As both complaints suggest a heterogeneous set of underlying disorders, a specific diagnosis is needed before the appropriate treatment approach can be determined. Much less common types of sleep complaints are sleepwalking, violent movements during sleep, or acting out of dreams (parasomnias). Although these latter problems are rare relative to insomnia, they should be taken seriously because of the increased risk of injury once a sleeping person has left the bed.
There are known risk factors for sleep disturbances in elderly, of which:
1. Gender; it is found to be more reported in older women than older men.
2. Menopause; as a result of the hormonal disturbance, sleep disturbance is much more common in post-menopausal women, and improve very well with hormonal replacement therapy.
3. Nocturia; causes frequent awakenings in the elderly.
4. Co-morbid medical diseases and drug treatment.
5. Psychological and psychosocial factors.
6. Age-related disturbance of homeostatic sleep process.
7. Age related disturbance of circadian rhythm.
8. Disturbance of thermo-regulation.
9. Stress and cortisol effect.
10. Abnormality in the pineal gland and melatonin.
Causes of sleep disturbance in elderly
Important risk factors for poor sleep in older adults can be divided into two categories: (a) those associated with aging that are unique to older adults and (b) those that cause poor sleep in people of all ages but occur more commonly in older adults. Most identified precipitants of poor sleep are similar for younger and older adults. Primary sleep disorders, pain, medical conditions that decrease respiratory stability, neurodegenerative disorders, medication effects, depression, and cardiopulmonary disorders (e.g., chronic obstructive pulmonary disease [COPD], congestive heart failure [CHF]) are all examples of conditions that often contribute to sleep disturbance. Older adults are at increased risk for poor sleep primarily because of the increased prevalence of these well-documented causes of poor sleep. In fact, many older adults will have more than one such risk factor.
Evaluation of Sleep Disturbance in the Elderly
Most patients with disturbed sleep do not report this problem. As with other medical symptoms, interviewing the patient about his or her sleep is the first step. Much can be learned from just a few interview questions for the interview questions. The goal of such an interview is to assess whether referral for additional medical evaluation, psychiatric evaluation, or sleep specialist evaluation is indicated.
The specific areas for assessment are as follows: (a) identification of the presence or absence of sleep disturbance, (b) characterization of the type of sleep disturbance, (c) assessment of the type and degree of daytime impairment, and (d) assessment of the outcome of past evaluations or treatments for the sleep disturbance. For evaluation of complaints of insomnia, sleep logs are very helpful to assess potential contributing factors, as well as evaluating the severity and variability of the symptoms. Additionally, patients’ self-monitoring of medication, alcohol, and caffeine use may provide insight into potential contributing factors for poor sleep.
Polysomnography, or sleep study, is needed to definitively diagnose a primary sleep disorder such as OSA syndrome or PLMD. Polysomnography consists of overnight monitoring of 12 or more channels of physiological data. These channels include at least 2 EEG measures (electro-oculogram [EOG], to measure eye movements for scoring REM sleep, and chin electromyogram [EMG], to detect the muscle atonia that accompanies REM sleep), respiratory effort, airflow, oxygen saturation (with oximetry measured with a finger sensor), electrocardiogram (ECG), and EMG of the anterior tibialis to monitor for limb movements diagnostic of PLMD. Patients are studied for about 8 hr during the time of their usual sleep period. Most sleep centers are hospital based.
Management of sleep disorders
Medical Care: Evaluate patients for other primary sleep disorders (e.g., sleep apnea) and for underlying medical, psychiatric, and substance abuse disorders, and institute appropriate treatment. Sleep hygiene and behavioral strategies are used in combination with medication to treat insomnia, particularly primary insomnia.
• Educating the patient on good sleep practices is essential for the effective treatment of insomnia. Cognitive behavior therapy (CBT) targeted at debunking myths and misconceptions about sleep and sleep loss has been proven to be as effective as pharmacotherapy in the treatment of acute insomnia.
• Use the bed for sleep and sex only (no television watching or reading in bed).
• Do not watch the clock while in bed. Practice relaxation techniques before bedtime. Avoid stimulating activities during the 3 hours before bedtime, such as heavy exercise, tense or thrilling reading or television, or arguments.
• Maintain a regular schedule for bedtime and wakening; avoid naps. Early to rise and early to bed is the most effective schedule. A ”night owl” schedule is poor sleep hygiene.
• Avoid struggling to fall asleep in bed. Instead, get up and spend quiet time out of bed until sleep comes.
• Light-phase shift therapy is useful for sleep disturbances associated with circadian rhythm abnormalities. Patients may be exposed to bright light, from either a light box or natural sunlight, to help normalize the sleep schedule.
Diet: No special diet is needed to treat insomnia, but large meals and spicy foods should be avoided in the 3 hours before bedtime.
• Patients should avoid sleep-disturbing substances such as alcohol, nicotine, and caffeine. Alcohol creates the illusion of good sleep, but sleep architecture is affected adversely. Nicotine and caffeine are stimulating and should be avoided in the second half of the day, from late afternoon on.
• Consumption of tryptophan-containing foods may help induce sleep. The classic example is warm milk.
• Strenuous exercise during the day may promote better sleep, but this same exercise during the 3 hours before bedtime can cause initial insomnia.
• Stimulating activities should be avoided 3 hours before bedtime. Examples include tense movies, exciting novels, thrilling television shows, arguments, and vigorous physical exercise other than coitus.
Pharmacotherapy:
Many agents are useful in treating insomnia. Short-term drug therapy is preferred to restore a normal sleep pattern. Generally, hypnotic drugs are approved for 2 weeks or less of continuous use. In chronic insomnia, longer courses may be indicated, which require long-term monitoring to ensure ongoing appropriate use of the medication.
Barbiturates and chloral hydrate are seldom used now because of safety concerns related to their undesirably low therapeutic indexes.
Drugs that block the histamine type 1 receptor are used primarily in over-the-counter preparations, are inexpensive, and are helpful to some patients. However, in view of the anticholinergic properties of these agents, caution should be exercised in their use with older patients and with those who have disorders such as prostatic hypertrophy, cognitive disorders, and constipation. In addition, most of these drugs have a long duration of action, and their sedative effects may persist well into the following day.
Zolpidem (Ambien) and zaleplon (Sonata) are the newest and, arguably, the safest agents that are US Food and Drug Administration (FDA) approved for short-term hypnotic use. Zolpidem (Ambien CR) has recently released an extended-release version that lasts slightly longer than the original preparation. In addition, the FDA recently approved the new agent eszopiclone (Lunesta) as the first agent for long-term use in the management of chronic insomnia.
Drug Category: Benzodiazepines -- Benzodiazepine receptor agonists are the mainstay in treatment of insomnia. Flurazepam, temazepam, quazepam, estazolam, and triazolam are the benzodiazepines that are approved by the US Food and Drug Administration as hypnotics.
These drugs bind to a special benzodiazepine site on the GABA receptor complex, enhancing activity of this neurotransmitter. All have variable half-lives and different metabolites that affect their onset and duration of action. This class of drugs suppresses REM sleep and reduces stages 3 and 4 sleep while increasing stage 2 sleep. The drug described here, temazepam, is only one example of this class of medications. A more detailed discussion of the other agents in this class can be found elsewhere in the text.
Imidazopyridine -- Zolpidem is the sole member of this class of medications. It binds at a benzodiazepine receptor subtype (omega I). Found more in CNS more than in peripheral nervous system, which helps to account for hypnotic effect with no significant muscle-relaxant properties. Unlike benzodiazepines, normal sleep architecture not suppressed.
Pyrazolopyrimidine -- Zaleplon is the sole agent in this class of nonbenzodiazepine hypnotics.
Pyrrolopyrazine -- This is another nonbenzodiazepine sedative/hypnotic drug class indicated to improve sleep onset and maintenance
Melatonin receptor agonist -- Ramelteon is the first and only nonscheduled insomnia medication with a novel mechanism of action
Antidepressants - Although no antidepressants are approved specifically for use in the treatment of sleep disorders, a cyclic antidepressant, trazodone (Desyrel), is used routinely for this purpose.