Health Articles

Parkinson’s disease compromises both initiation and maintenance of sleep. The effects of levodopa on REM and deep sleep vary, depending on dosage, and the drug can cause nightmares. Amantadine improves quantitative sleep.

Sleepiness during the day and decreased functional capacity are prominent symptoms of hypothyroidism. Stages 3 and 4 sleep are reduced significantly but return to normal with thyroid replacement. Hyperthyroidism increases stages 3 and 4 sleep to almost 70% of total sleep time (25% is normal), but hyperthyroid patients often complain of insomnia. When a euthyroid state returns, sleep stages become normal.

Patients undergoing renal dialysis experience chronic sleep disturbances. In uremic patients, long awakenings from all stages of sleep are common, deep sleep time is proportionally shorter, and total sleep time is decreased. Elevated BUN levels correlate with the severity of the disturbance; dialysis alleviates the disturbance, increasing stages 3 and 4 sleep.

Acid secretion increases during the night, which can awaken patients with ulcer disease or cause difficulty initiating sleep. Recent studies support nocturnal use of Hb-receptor blockers, although some (eg, cimetidine) can penetrate the CNS and cause side effects. Esophageal reflux, which can cause discomfort, may be prevented by elevating the head of the bed.

Chronic obstructive pulmonary disease can cause frequent awakenings, increase the amount of time spent in lighter (stage 1) sleep, markedly reduce stages 3 and 4 and REM sleep, and decrease total sleep time. Sympathomimetic bronchodilatqrs (the mainstay of treatment for reversible bronchospasm) are CNS stimulants that can exacerbate insomnia.

Many drugs for hypertension can adversely affect sleep. Diuretics can awaken a person to urinate, who then may have difficulty resuming sleep, β-lilockers, clonidine, reserpine, and α-methyldopa act on the CNS, altering sleep physiology. Patients who have insomnia related to antihypertensive use may need to have their drug regimens altered. Heart failure can lead to orthopnea; demented patients with orthopnea may be unable to explain their complaint, becoming agitated instead. Angina pectoris can prolong sleep latency, reducing the deep sleep of stages 3 and 4. This disruption of sleep integrity can lead to chronic insomnia and dependency on hypnotics.

Medical illnesses and their drug treatments can adversely affect sleep. Drugs can blunt nocturnal breathing, exacerbate or cause apnea, produce unwanted arousals, and otherwise alter sleep physiology. In addition, some disease symptoms are worse during sleep.
Musculoskeletal disorders: Patients with osteoarthritis may awaken with stiffness and pain, then have difficulty falling asleep again. Fibro-myositis, polymyalgia rheumatica, recent fractures, and flexion contractures all can cause pain and impair sleep. Treatment consists of effecting behavioral change with the judicious use of analgesics, exercise, and other forms of physical activity.

Reversible causes of sleep disorders associated with dementia, such as drug-related toxicity, infections, dehydration, drug-drug interactions, pressure necrosis, malnutrition, and anemia, should be sought. Commonly used pharmacologic treatment includes benzodiazepines and antipsychotics. No drug has been shown to be particularly effective, and antipsychotics have many adverse effects. Nonpharmacologic treatment includes scheduling activities at a time when the patient seems to be affected by sundowning. Napping during the day may help consolidate the sleep schedule, but a long nap may interfere with nighttime sleep. Other approaches include manipulating the environment (eg, providing adequate light and temperature), evaluating and treating pain, correcting hearing and visual deficits, and treating metabolic illnesses.

The suprachiasmatic nucleus and other neuroanatomic areas involved in the control of sleep (eg, the locus ceruleus and the nucleus basalis of Meynert) are affected by Alzheimer’s disease. Patients with Alzheimer’s disease have low sleep efficiency, spend a high percentage of sleep time in stage 1 and less time in stages 3 and 4 sleep, and experience more arousals and awakenings, all of which parallel the severity of dementia. The percentage of REM sleep (as compared with total sleep time) decreases, the reduction becoming more pronounced as dementia progresses. Many persons with Alzheimer’s disease or multi-infarct dementia also have sleep-related respiratory disturbances.
Sundowning, a poorly understood phenomenon associated with dementia, has been defined as the nocturnal exacerbation of disruptive behaviors in which agitation is a prominent feature. Between 12% and 14% of demented nursing home patients demonstrate agitated behavior (eg, pacing and verbal aggression) more often at night than during the day. Demented patients are unlikely to sleep between 3 and 7 PM, the time such agitation usually occurs during winter months in northern regions when the sun sets earlier.

In advanced sleep phase syndrome, the onset and awakening times of habitual sleep occur earlier than desired, leading to an inability to adhere to a standard sleep schedule. Although this syndrome does not meet the strict criteria of a disabling sleep disorder, sufferers complain of fatigue during the day and tend to use excessive amounts of hypnotics or alcohol. In the elderly, this syndrome may be more sociologic than physiologic.
Treatment includes all aspects of sleep hygiene (see TABLE 11-1), especially gradually reducing the total time spent in bed and avoiding chronic use of hypnotics. Contributory factors (eg, depression, concomitant medical illness, drugs that alter sleep physiology) should be ruled out or dealt with.