Sleep Disorders in Other Medical Conditions

Sleep Disorders in Other Medical Conditions

A sleep disorder due to a general medical condition is defined in DSM-IV-TR as a prominent disturbance in sleep severe enough to warrant independent clinical attention. Subtypes include in-somnia, hypersomnia, parasomnia and mixed types. As a gen-eral rule, any disease or disorder that causes pain, discomfort, or a heightened state of arousal in the waking state is capable of disrupting or interfering with sleep. Examples of this phe-nomenon include pain syndromes of any sort, arthritic and other rheumatological disorders, prostatism and other causes of uri-nary frequency or urgency, chronic obstructive lung disease and other pulmonary conditions. Many of these conditions increase in prevalence with advancing age, suggesting at least one reason that sleep disorders are more likely to be seen in senior popu-lations. The following include disorders known to cause distur-bances in sleep: rheumatoid arthritis, fibromyalgia, chronic ob-structive pulmonary conditions, congestive heart failure, peptic ulcer disease, GERD, rectal urgency, Parkinson’s disease, Hunt-ington’s chorea, advanced Alzheimer’s disease and hereditary progressive dystonia.

Sleep in Elderly with Dementia

The sleep of older adults with dementia is extremely disturbed, with severely fragmented sleep, often to the extent that there is not a single hour in a 24-hour day that is spent fully awake or asleep. Patients with mild to moderate dementia have extremely fragmented sleep at night, while those with severe dementia are extremely sleepy during both the day and night. Sleep stages also change with dementia, with significantly lower amounts of stages 3, 4 and REM sleep, and significantly more awakenings, as well as more time spent awake during the night. This results in increased stage 1 sleep and decreased sleep efficiency. It has also been shown that there is a high prevalence of sleep apnea in patients with dementia, with as many as 80% having symptoms that meet the criteria for diagnosis. The sleep changes and dis-ruption seen are likely due to the neuronal degeneration found in Alzheimer’s disease. Neuronal structures damaged in patients with dementia include the basal forebrain and the reticular for-mation of the brain stem, the same structures implicated in sleep regulation.

The nocturnal awakenings seen in dementia patients are often accompanied by agitation, confusion and wandering. These behaviors have been referred to as “sundowning” as it was believedthat they typically occurred as the sun set. A recent study (Martin et al., 2000) challenged the idea of sundowning by showing that peak levels of agitation occur during various times of the day, but more often in the afternoon, rather than in the evening or night.

It has been suggested that agitation or sundowning may be a circadian rhythm disorder. Sleep disruption in demented individuals may be amenable to treatment using bright light ex-posure. Others have tested this theory by exposing patients with dementia to bright light. The results have been mixed, but in general support the theory that increased light exposure, whether during the morning or evening, will improve both sleep and be-havior to some extent.

Substance-induced Sleep Disorder

An important aspect of the evaluation of any patient, particularly those with sleep disorders, is the review of medications and other substances (including prescription, over-the-counter and recrea-tional drugs, as well as alcohol, stimulants, narcotics, coffee and caffeine, and nicotine) and exposure to toxins, heavy metals, and so forth. These substances may affect sleep and wakefulness dur-ing either ingestion or withdrawal, causing most commonly in-somnia, hypersomnia, or, less frequently, parasomnia or mixed types of difficulties. On the basis of DSM-IV-TR criteria, a di-agnosis of substance-induced sleep disorder may be made if the disturbance of sleep is sufficiently severe to warrant independent clinical attention and is judged to result from the direct physi-ological effects of a substance. Substance-induced sleep disorder cannot result from mental disorder or occur during delirium. If appropriate, the context for the development of sleep symptoms may be indicated by specifying with onset during intoxication or with onset during withdrawal.

The recognition of substance-related sleep disturbances usually depends on active searching by the psychiatrist, begin-ning with a careful history, physical examination, laboratory and toxicological testing, and information (with permission) from former health care providers or friends and relatives. Patients may not know what prescription medications they are taking or the doses, and may forget to mention over-the-counter medications, coffee, occupational or environmental toxins, and so forth. In the case of alcohol and drugs of abuse, they may deny to themselves and others their use, or quantity, or frequency of use. Substance dependence and abuse is often associated with other psychiatric diagnoses or symptoms. When comorbidity does exist, it is im-portant to establish, if possible, whether the sleep disturbance is primary or secondary, that is, whether the sleep disturbance is substance-induced (secondary) or whether the substance use functions as a form of “self-medication” for sleep disturbance, in which the sleep disturbance would be considered primary. Many patients with alcoholism experience secondary depression dur-ing the first few weeks of withdrawal from alcohol and exhibit short REM latency and other sleep changes similar to those re-ported in primary depression. This secondary depression usu-ally remits spontaneously. Likewise, about one-third of patients with unipolar depression and about three-fifths of patients with bipolar disorder, manic type, have a substance use pattern that meets diagnostic criteria for alcoholism or substance abuse at some point. Prognosis and treatment may be altered in comorbid states, depending on whether the sleep disturbance is primary or secondary. In general, treatment should be aimed at the primary diagnosis after management of any acute withdrawal condition that may exist.

Alcohol

Alcohol is probably the most commonly self-administered “sleep-ing aid”. Although it may be sedating, especially in middle-aged or elderly or sleep-deprived persons, its usefulness as a hypnotic is limited by potential disinhibiting and arousing effects, gastric irri-tation, falling blood-alcohol levels in the early part of the night with mild withdrawal symptoms and sleep fragmentation at the end of the night, morning headaches and hangover effects, tolerance with repeated use, and exacerbation of BRSDs such as apnea.

Virtually any type of sleep disturbance has been attributed to the effects of alcohol or alcohol withdrawal in patients with al-cohol abuse or dependence. Insomnia may occur during episodes of drinking and acute and chronic withdrawal. Complaints of in-somnia and objective disruption of sleep continuity and stages 3 and 4 sleep have been reported for up to several years in some ab-stinent patients. Hypersomnia may occur during heavy bouts of drinking, sometimes with peripheral compression neuropathies, or as “terminal hypersomnia” after delirium tremens. Circadian sleep disturbances may also occur during bouts of drinking, in-cluding periods of short polyphasic sleep–wake episodes. Paras-omnias include sleepwalking and enuresis.

Because alcohol may temporarily improve the poor sleep of the chronic alcoholic individual, sleep disturbance may be a factor in relapse. Treatment of the sleep disturbances of the chronic but abstinent alcoholic individual is difficult. Nonphar-macological approaches include sleep hygiene and sleep restric-tion, as well as attention to general nutrition, physical health and psychosocial supports. Use of benzodiazepines or other hypnot-ics is not generally recommended because of cross-tolerance or deliberate or inadvertent overdose.

Nicotine

Aside from medical complications, such as coughing that may interfere with sleep, smoking has been associated with both dif-ficulty in falling asleep and getting up in the morning suggesting that nicotine may phase delay the circadian oscillator. Further-more, compared with nonsmokers, men who smoked reported more nightmares, women who smoked reported more daytime sleepiness. Furthermore, as blood-nicotine levels fall during the night, smokers go into relative withdrawal and start craving a cigarette. One of the best measures of nicotine dependence is how long the smoker can wait in the morning for the first smoke. Ab-stinence from smoking is associated with lighter and more frag-mented sleep, daytime sleepiness on the Multiple Sleep Latency Test, irritability, craving and other subjective emotional distress.

Amphetamines, Cocaine and Caffeine

Stimulants initially prolong sleep onset and reduce REM sleep, sleep continuity, and sleep duration, but tolerance usually devel-ops. During acute withdrawal, hypersomnia and excessive REM sleep occur for the first week or so but may be followed by a few days of insomnia.

Like the stimulants, caffeine usually promotes arousal and delays sleep, but withdrawal may be associated with hypersomnia. It is probably the most commonly self-administered stimulant, for example, the morning cup of coffee to “get going”. Caffeine has some benefits as a mild stimulant to overcome sleepiness.

Opiates

Short-term use of opiates may increase sleep and subjective sleep quality and reduce REM sleep, especially in patients who need an analgesic for relief of pain, but these drugs may also disrupt sleep. Tolerance usually develops with repeated administration. Withdrawal may be associated with hypersomnia or the “nods”.

Sedatives, Hypnotics and Anxiolytics

Tolerance usually develops with repeated administration of the sedating effects of barbiturates, chloral hydrate and even ben-zodiazepines. This is true especially with short half-life agents, with the possible exception of zaleplon. As mentioned earlier, 1 or 2 days of withdrawal insomnia may occur after a few days of administration of short half-life benzodiazepines, such as triazolam, but not with the newer nonbenzodiazepine hypnotics, such as zolpidem and zaleplon.

Potential side effects associated with sedating medications during the sleep period include falls and fractures, difficulty arousing to the telephone or the crying infant, amnesia, impair-ment of cognitive and motor skills, drug-induced sleepwalking, and possibly, BRSDs.

Other Substances

Many medications produce sleep disturbance, including those with central or autonomic nervous system effects, like adren-ergic agonists and antagonists, dopamine agonists and antago-nists, cholinergic agonists and antagonists, antihistamines and steroids. Among the prescription drugs associated frequently with sleep disorders are the SSRIs, which have been connected with overarousal and insomnia in some patients and, more com-monly, sedation in other patients. Coadministration of trazodone at night has been shown, in a double-blind, placebo-controlled study, to be effective in managing fluoxetine-induced insomnia in depressed patients (Nierenberg et al., 1994). Additional sleep-related disturbances occasionally associated with the SSRIs in-clude sleepwalking, REM sleep behavior disorder and rapid eye movements during non-REM sleep.