Chapter 028. Sleep Disorders (Part 14) Shift-Work Disorder: Treatment Caffeine is frequently used to promote wakefulness. However, it cannot forestall sleep indefinitely, and it does not shield users from sleep-related performance lapses. Postural changes, exercise, and strategic placement of nap opportunities can sometimes temporarily reduce the risk of fatigue-related performance lapses. Properly timed exposure to bright light can facilitate rapid adaptation to night-shift work. While many techniques (e.g., light treatment) used to facilitate adaptation to night shift work may help patients with this disorder, modafinil is the only therapeutic intervention that has ever been evaluated as a treatment for this specific patient population. Modafinil (200 mg, taken 30–60 min before the start of each night shift) is approved by the U.S. Food and Drug Administration as a treatment for the excessive sleepiness during night work in patients with SWD. Although treatment with modafinil significantly increases sleep latency and reduces the risk of lapses of attention during night work, SWD patients remain excessively sleepy at night, even while being treated with modafinil. Safety programs should promote education about sleep and increase awareness of the hazards associated with night work. The goal should be to minimize both sleep deprivation and circadian disruption. Work schedules should be designed to minimize: (1) exposure to night work, (2) the frequency of shift rotation so that shifts do not rotate more than once every 2–3 weeks, (3) the number of consecutive night shifts, and (4) the duration of night shifts. Shift durations of >16 h should be universally recognized as increasing the risk of sleep- related errors and performance lapses to a level that is unacceptable in nonemergency circumstances. Delayed Sleep Phase Disorder Delayed sleep phase disorder is characterized by: (1) reported sleep onset and wake times intractably later than desired, (2) actual sleep times at nearly the same clock hours daily, and (3) essentially normal all-night polysomnography except for delayed sleep onset. Patients exhibit an abnormally delayed endogenous circadian phase, with the temperature minimum during the constant routine occurring later than normal. This delayed phase could be due to: (1) an abnormally long, genetically determined intrinsic period of the endogenous circadian pacemaker; (2) an abnormally reduced phase-advancing capacity of the pacemaker; or (3) an irregular prior sleep-wake schedule, characterized by frequent nights when the patient chooses to remain awake well past midnight (for social, school, or work reasons). In most cases, it is difficult to distinguish among these factors, since patients with an abnormally long intrinsic period are more likely to "choose" such late-night activities because they are unable to sleep at that time. Patients tend to be young adults. This self-perpetuating condition can persist for years and does not usually respond to attempts to reestablish normal bedtime hours. Treatment methods involving bright-light phototherapy during the morning hours or melatonin administration in the evening hours show promise in these patients, although the relapse rate is high. Advanced Sleep Phase Disorder Advanced sleep phase disorder (ASPD) is the converse of the delayed sleep phase syndrome. Most commonly, this syndrome occurs in older people, 15% of whom report that they cannot sleep past 5 A.M., with twice that number complaining that they wake up too early at least several times per week. Patients with ASPD experience excessive daytime sleepiness during the evening hours, when they have great difficulty remaining awake, even in social settings. Typically, patients awaken from 3–5 A.M. each day, often several hours before their desired wake times. In addition to age-related ASPD, an early-onset familial variant of this condition has also been reported. In one such family, autosomal dominant ASPD was due to a missense mutation in a circadian clock component (PER2, as shown in Fig. 28-2) that altered the circadian period. Patients with ASPD may benefit from bright-light phototherapy during the evening hours, designed to reset the circadian pacemaker to a later hour. Non-24-Hour Sleep-Wake Disorder This condition can occur when the maximal phase-advancing capacity of the circadian pacemaker is not adequate to accommodate the difference between the 24-h geophysical day and the intrinsic period of the pacemaker in the patient. Alternatively, patients' self-selected exposure to artificial light may drive the circadian pacemaker to a >24-h schedule. Affected patients are not able to maintain a stable phase relationship between the output of the pacemaker and the 24-h day. Such patients typically present with an incremental pattern of successive delays in sleep onsets and wake times, progressing in and out of phase with local time. When the patient's endogenous rhythms are out of phase with the local environment, insomnia coexists with excessive daytime sleepiness. Conversely, when the endogenous rhythms are in phase with the local environment, symptoms remit. The intervals between symptomatic periods may last several weeks to several months. Blind individuals unable to perceive light are particularly susceptible to this disorder. Nightly low-dose (0.5 mg) melatonin administration has been reported to improve sleep and, in some cases, to induce synchronization of the circadian pacemaker. . Chapter 028. Sleep Disorders (Part 14) Shift-Work Disorder: Treatment Caffeine is frequently used to promote wakefulness. However, it cannot forestall sleep indefinitely,. increasing the risk of sleep- related errors and performance lapses to a level that is unacceptable in nonemergency circumstances. Delayed Sleep Phase Disorder Delayed sleep phase disorder is. patients, although the relapse rate is high. Advanced Sleep Phase Disorder Advanced sleep phase disorder (ASPD) is the converse of the delayed sleep phase syndrome. Most commonly, this syndrome