Chapter 028. Sleep Disorders (Part 8) pot

Chapter 028. Sleep Disorders
(Part 8)

Insomnia Associated with Neurologic Disorders
A variety of neurologic diseases result in sleep disruption through both
indirect, nonspecific mechanisms (e.g., pain in cervical spondylosis or low back
pain) or by impairment of central neural structures involved in the generation and
control of sleep itself. For example, dementia from any cause has long been
associated with disturbances in the timing of the sleep-wake cycle, often
characterized by nocturnal wandering and an exacerbation of symptomatology at
night (so-called sundowning).
Epilepsy may rarely present as a sleep complaint (Chap. 363). Often the
history is of abnormal behavior, at times with convulsive movements during sleep.
The differential diagnosis includes REM sleep behavior disorder, sleep apnea
syndrome, and periodic movements of sleep (see above). Diagnosis requires
nocturnal polysomnography with a full EEG montage. Other neurologic diseases
associated with abnormal movements, such as Parkinson's disease, hemiballismus,
Huntington's chorea, and Tourette syndrome (Chap. 366), are also associated with
disrupted sleep, presumably through secondary mechanisms. However, the
abnormal movements themselves are greatly reduced during sleep. Headache
syndromes (migraine or cluster headache) may show sleep-associated
exacerbations (Chap. 15) by unknown mechanisms.
Fatal familial insomnia is a rare hereditary disorder caused by degeneration
of anterior and dorsomedial nuclei of the thalamus. Insomnia is a prominent early
symptom. Patients develop progressive autonomic dysfunction, followed by
dysarthria, myoclonus, coma, and death. The pathogenesis is a mutation in the
prion gene (Chap. 378).

Insomnia Associated with Other Medical Disorders

A number of medical conditions are associated with disruptions of sleep.

The association is frequently nonspecific, e.g., sleep disruption due to chronic pain
from rheumatologic disorders. Attention to this association is important in that
sleep-associated symptoms are often the presenting or most bothersome complaint.
Treatment of the underlying medical problem is the most useful approach. Sleep
disruption can also result from the use of medications such as glucocorticoids (see
below).
One prominent association is between sleep disruption and asthma. In
many asthmatics there is a prominent daily variation in airway resistance that
results in marked increases in asthmatic symptoms at night, especially during
sleep. In addition, treatment of asthma with theophylline-based compounds,
adrenergic agonists, or glucocorticoids can independently disrupt sleep. When
sleep disruption is a side effect of asthma treatment, inhaled glucocorticoids (e.g.,
beclomethasone) that do not disrupt sleep may provide a useful alternative.
Cardiac ischemia may also be associated with sleep disruption. The
ischemia itself may result from increases in sympathetic tone as a result of sleep
apnea. Patients may present with complaints of nightmares or vivid, disturbing
dreams, with or without awareness of the more classic symptoms of angina or of
the sleep disordered breathing. Treatment of the sleep apnea may substantially
improve the angina and the nocturnal sleep quality. Paroxysmal nocturnal dyspnea
can also occur as a consequence of sleep-associated cardiac ischemia that causes
pulmonary congestion exacerbated by the recumbent posture.
Chronic obstructive pulmonary disease is also associated with sleep
disruption, as is cystic fibrosis, menopause, hyperthyroidism, gastroesophageal
reflux, chronic renal failure, and liver failure.[newpage]
Medication-, Drug-, or Alcohol-Dependent Insomnia
Disturbed sleep can result from ingestion of a wide variety of agents.
Caffeine is perhaps the most common pharmacologic cause of insomnia. It
produces increased latency to sleep onset, more frequent arousals during sleep,
and a reduction in total sleep time for up to 8–14 h after ingestion. Even small
amounts of coffee can significantly disturb sleep in some patients; therefore, a 1-

to 2-month trial without caffeine should be attempted in patients with these
symptoms. Similarly, alcohol and nicotine can interfere with sleep, despite the fact
that many patients use them to relax and promote sleep. Although alcohol can
increase drowsiness and shorten sleep latency, even moderate amounts of alcohol
increase awakenings in the second half of the night. In addition, alcohol ingestion
prior to sleep is contraindicated in patients with sleep apnea because of the
inhibitory effects of alcohol on upper airway muscle tone. Acutely, amphetamines
and cocaine suppress both REM sleep and total sleep time, which return to normal
with chronic use. Withdrawal leads to a REM sleep rebound. A number of
prescribed medications can produce insomnia. Antidepressants,
sympathomimetics, and glucocorticoids are common causes. In addition, severe
rebound insomnia can result from the acute withdrawal of hypnotics, especially
following the use of high doses of benzodiazepines with a short half-life. For this
reason, hypnotic doses should be low to moderate and prolonged drug tapering is
encouraged.