Five studies used one of the newer non-benzodiazepine hypnotics.One large level 1 study 63 found that zolpidem 10 mg administeredat bedtime for 3–4 nights following eastward travel across 5–9time zones improved self-reported total sleep time and sleep quality,and reduced awakenings from sleep; however daytime symptomsof JLD were not addressed. Another level 2 study 65 found thatzopiclone 7.5 mg given at bedtime improved sleep duration (measuredby actigraphy) for the four post-flight days following a 5-hourwestward flight. Daytime activity was also greater, but subjectiveJLD scores were not improved (<strong>com</strong>pared to placebo).Two studies <strong>com</strong>pared a non-benzodiazepine hypnotic withmelatonin or placebo following eastward travel. One large level1 study 52 found that zolpidem 10 mg administered during a nightflight and for 4 days after arrival following eastward travel across6–9 time zones was significantly better than melatonin 5 mg (orplacebo) in counteracting JLD symptoms, and better at achievingself-reported sleep duration and self-reported sleep quality (butnot verified by actigraphy). In this study, a group receiving zolpidemplus melatonin did not report better sleep or better JLD scoresthan the zolpidem alone group. Another level 1 study 60 found thatzopiclone 15 mg (<strong>com</strong>pared to melatonin 2 mg or placebo) administeredfor one night only after arrival found that zopicloneand melatonin were equally effective at improving both subjectiveand objective (actigraphy) sleep duration and quality. Othersymptoms of JLD were not assessed.One small level 2 study of simulated eastward 8 hour timeshift 67 <strong>com</strong>pared zolpidem 10 mg (versus placebo) given at thenew bedtime on the first two nights following the shift with the effectsof continuous bright light exposure (versus dim light) uponawakening on the day of the advance and the following day. Totalsleep times (by polysomnography) did not differ between treatments,though sleep efficiency improved with zolpidem (on thenight of the shift only) or with bright light (on the night after shiftonly). No other symptoms of JLD were reported.Thus, these agents are in general effective for treatment of theinsomnia of JLD, but of unproved benefit for the daytime symptoms.In addition, some caution is warranted in the use of hypnoticsfor JLD, since adverse effects have been reported, includingglobal amnesia, 70 and at least one study reporting a much higherrate of adverse events with a hypnotic (zolpidem) <strong>com</strong>pared toother treatment groups. 523.2.2.6 Caffeine is indicated as a way to counteract jet lag-inducedsleepiness, but may also disrupt nighttime sleep. [7.4.2.4] (Option)Two level 2 studies tested the use of slow-release caffeine aftertravel across times zones. One level 2 study found that eitherslow-release caffeine 300 mg daily for 5 days after flight or melatonin5 mg daily starting on the day of travel to 3 days post flightfollowing eastward travel across 7 time zones (<strong>com</strong>pared to placebo)was associated with faster entrainment of circadian rhythmsas measured by salivary cortisol levels. 62 In another level 2 studyutilizing the same protocol, 61 slow-release caffeine resulted in lessdaytime sleepiness (<strong>com</strong>pared to melatonin or placebo) by objectivebut not subjective measures, but also reported longer sleeponset and more awakenings at night. The benefit of improveddaytime sleepiness must be weighed against disrupted nocturnalsleep. Additionally, information was lacking on the effect of caffeineon other daytime symptoms of jet lag. Individualized therapyand clinical follow-up is re<strong>com</strong>mended.SLEEP, Vol. 30, No. 11, 2007 14513.2.3 Advanced Sleep Phase DisorderAdvanced sleep phase disorder (ASPD) is defined as a sleeppattern scheduled several hours earlier than is usual or desired.There is no standard for how much earlier a sleep schedule needsto be in order to qualify as pathological. Diagnosis depends onthe amount of distress the patient expresses about being unableto conform to a more conventional sleep schedule after ruling outother causes of sleep maintenance insomnia.3.2.3.1 There is insufficient evidence to re<strong>com</strong>mend the use of theMorningness-Eveningness Questionnaire (MEQ) for the routinediagnosis of ASPD. [11.3.2] (Option)This parameter is based upon <strong>com</strong>mittee consensus. There weretwo level 2 studies 71,72 that found ASPD patients scored high onthe MEQ indicating morning-lark traits. A third study (level 3) 73also found high MEQ scores in subjects presumed to have ASPD.However, there were no studies that evaluated the sensitivity orspecificity of this questionnaire as a diagnostic tool in sleep clinicor general populations. The MEQ can serve a confirmatory rolefor ASPD diagnosis but may not by itself serve as a basis for thisdiagnosis.3.2.3.2 Polysomnography is not routinely indicated for thediagnosis of ASPD. [11.3.3] (Standard)This is a reiteration of the prior practice parameter paper providedregarding indications for PSG. 10 Regarding ASPD, no studiesretrieved for review utilized PSG to make this diagnosis. One level2 study 72 found the expected advance in the time of sleep onset inASPD subjects; on the other hand, another level 2 study 74 foundfairly standard bedtimes in ICSD-ASPD diagnosed subjects.3.2.3.3 There is insufficient evidence to re<strong>com</strong>mend the use ofcircadian markers for the routine diagnosis of ASPD. [11.3.4](Option)There were two level 2 studies 71,72 using DLMO as a circadianmarker and one level 3 study 73 using urinary 6-sulfatoxy melatonin(MT6) acrophase which found advanced melatonin secretionin presumed ASPD subjects. Three level 2 studies 74-76 and one level4 study 77 found early core body temperature minima in patientswith ASPD, sleep maintenance or terminal insomnia. The reviewindicated that the available data are limited by heterogeneity ofsubjects. Additionally, none of the studies evaluated the use ofcircadian markers as diagnostic aids (no measures of the sensitivityor specificity of the tests). Thus, although the results of suchmeasures are generally consistent with advanced circadian timing,measuring circadian markers can not yet be re<strong>com</strong>mended asdiagnostic aids.3.2.3.4 Prescribed sleep/wake scheduling, timed light exposure,or timed melatonin administration are indicated as treatments forpatients with ASPD. [11.4] (Option)This re<strong>com</strong>mendation is based on available evidence and<strong>com</strong>mittee consensus. One level 4 study 78 achieved sleep advancewith sleep scheduling. There have been six studies usingscheduled bright light as a treatment. One level 3 study 73 foundPractice Parameters for the Clinical Evaluation of CRSD—Morgenthaler et al
evening light exposure no more effective than placebo in shiftingcircadian phase. A level 2 study 79 succeeded in reducing time inbed after awakening in the morning. Another level 2 study 74 thatused ICSD criteria to determine ASPD presence succeeded inimproving sleep variables but another level 2 replication of thisstudy 75 did not. One level 4 77 and one level 2 study 76 achievedpost-treatment DLMO phase delays and improved sleep qualityin patients with <strong>com</strong>plaints of terminal insomnia. Although thereis a rationale for using melatonin for ASPD, there is no reportedevidence in support of this treatment. Overall, the evidence forefficacy of these interventions is weak or conflicting, but therisks and costs entailed are low. As there are few alternatives, anindividualized approach using one or more of these treatmentswith follow up to ascertain efficacy or side effects may be appropriate.3.2.4 Delayed Sleep Phase DisorderDelayed sleep phase disorder (DSPD) is characterized by a stabledelay of the habitual nocturnal sleep period. Individuals with DSPDare often unable to fall asleep until the early morning hours and unableto awaken until late morning or early afternoon. During theirpreferred sleep schedules, sleep duration and quality are generallynormal. However, sleep-onset insomnia and morning sleepiness occurif sleep and waking are attempted at an earlier time.3.2.4.1 Polysomnography is not indicated in the routineassessment of DSPD. [12.3.5] (Standard)This is a reiteration of the indications for PSG practice parameters.10 In the present review, one study using PSG in patientswith DSPD that <strong>com</strong>pared conventional and habitual sleepschedules demonstrated differences in sleep duration and sleeparchitecture. Nevertheless, PSG rarely provides additional informationfrom that obtained from sleep history and sleep logs,and no new studies addressed the use of PSG as a diagnostic aidin DSPD.This re<strong>com</strong>mendation for chronotherapy is based only on twolevel 4 case report studies 82,83 and <strong>com</strong>mittee consensus; there areno controlled trials supporting its efficacy or safety. Longer lastingand more practical alternatives are needed given that <strong>com</strong>pliancewith the treatment is difficult and lasting benefit has not beendemonstrated.3.2.4.4 Properly timed melatonin administration is indicated as atherapy for DSPD. [12.4.3] (Guideline)This re<strong>com</strong>mendation is supported by one level 1 84 two level2 85,86 and one level 4 87 studies. Afternoon or evening administrationof melatonin shifts circadian rhythms (indicated by dim lightmelatonin onset [DLMO] and core body temperature minimum,[CBTmin]) to an earlier time. Compared to placebo, melatonintreatment reduced sleep onset latency, but there was no changein total sleep time or subjective daytime alertness. As with otherstudies involving melatonin, the optimal timing and dosing ofmelatonin administration are not established. In the reviewedstudies, three used 5 mg 84,85,87 while one 86 used two strengths (0.3mg and 3 mg). Effective times of administration varied between1.5 and 6 hours prior to the habitual bedtime.3.2.4.5. Vitamin B12 is not indicated in the treatment for DSPD.[12.4.4] (Guideline)This re<strong>com</strong>mendation is based on one level 1 88 multicenterstudy in which no benefit <strong>com</strong>pared to placebo was noted followingadministration of vitamin B12 (1 mg) three times a day to 50subjects for four weeks.3.2.4.6 There is insufficient evidence supporting the use ofhypnotic medications to promote sleep or the use of stimulantmedications to promote alertness for DSPD. [12.4.5; 12.4.6](Option)This parameter is based on <strong>com</strong>mittee consensus. There wasonly one level 4 report 83 indicating some benefit, but sufficientevidence to support this practice is lacking.3.2.5 Free-Running Circadian Rhythm Sleep Disorder3.2.4.2 Morning light exposure is indicated in the treatment ofDSPD. Optimal timing, duration, and dosing of morning lighttreatment for DSPD remain to be determined. [12.4.2] (Guideline)One level 1 80 and one level 2 81 study demonstrated that properlytimed morning light exposure causes a phase advance of sleeponset time and circadian rhythms (CBTmin), and increases objectivelydetermined daytime alertness. In the reviewed studies, 2500lux for 2-3 hours prior to or at rise time was used. The effects oflower doses, blue light wavelengths, or other timings are not yetknown. The treatments were generally well tolerated and of somebeneficial effect, but more potent and less difficult to follow treatmentsare needed.3.2.4.3. Chronotherapy (i.e., prescribed progressive delay in theschedule of sleep time until the desired sleep schedule is reached)may be useful for DSPD. [12.4.1] (Option)SLEEP, Vol. 30, No. 11, 2007 1452Patients with free-running (FRD) rhythms are thought to reflecta failure of entrainment. This condition is most <strong>com</strong>mon inblind individuals (about 50% of whom have FRD) and is highlyunusual in sighted individuals. Because of this, as noted in the ac<strong>com</strong>panyingreview, most studies are level 4 single case reports.Roughly one-fourth of sighted individuals with FRD have relatedpsychiatric diagnoses.3.2.5.1 Sleep logs are useful for assessment in FRD patients.[13.3.1] (Option)This re<strong>com</strong>mendation is based on <strong>com</strong>mittee consensus andclinical practice rather than data. Sleep logs have been found usefulin determining sleep patterns in people with FRD.3.2.5.2 Circadian phase markers are useful to determine circadianphase and confirm the diagnosis of FRD in sighted and unsightedpatients. [13.3.4] (Option)This parameter is supported by evidence presented in the ac<strong>com</strong>panyingreview and by <strong>com</strong>mittee consensus. There are one level 2 89and seven level 4 studies 90-96 that have used the melatonin rhythmPractice Parameters for the Clinical Evaluation of CRSD—Morgenthaler et al
- Page 1 and 2:
Practice Management Tips ForSHIFT W
- Page 3 and 4:
Patient QuestionnaireDo you often f
- Page 5 and 6:
Sleep/Wake LogIn bedOut of bedLight
- Page 7 and 8:
PHQ-9 QUICK DEPRESSION ASSESSMENTFo
- Page 9 and 10:
Insomnia Severity IndexPlease answe
- Page 11 and 12:
Take-Away PointsSHIFT WORK DISORDER
- Page 13 and 14:
SHIFT WORKDISORDERBright Light Ther
- Page 40 and 41:
PrimarycareScreeningfor depressioni
- Page 42 and 43:
PrimarycareThescreening questionnai
- Page 44 and 45:
Shift-work disorderContents and Fac
- Page 46 and 47:
Shift-work disorderThe diagnosis of
- Page 48 and 49:
Shift-work disorderas heightened le
- Page 50 and 51:
Shift-work disorderFigure 1 Risk ra
- Page 52 and 53:
Shift-work disorderare not function
- Page 54 and 55:
The characterization andpathology o
- Page 56 and 57:
Shift-work disorderFigure 2 Sleep/w
- Page 58 and 59:
Shift-work disorderFigure 3 Blood p
- Page 60 and 61:
Recognition of shift-workdisorder i
- Page 62 and 63:
Shift-work disorderThe timing of sh
- Page 64 and 65:
Shift-work disorderthe other potent
- Page 66 and 67:
Managing the patient withshift-work
- Page 68 and 69:
Shift-work disorderFigure 3 Optimal
- Page 70 and 71:
Shift-work disorderfor a motor vehi
- Page 72 and 73:
Shift-work disordermoderate caffein
- Page 74 and 75:
Supplement toAvailable at jfponline
- Page 76 and 77: Armodafinil for Treatment of Excess
- Page 78 and 79: Armodafinil for Treatment of Excess
- Page 80 and 81: Armodafinil for Treatment of Excess
- Page 82 and 83: Armodafinil for Treatment of Excess
- Page 84 and 85: Armodafinil for Treatment of Excess
- Page 86 and 87: Armodafinil for Treatment of Excess
- Page 88 and 89: Armodafinil for Treatment of Excess
- Page 90 and 91: Armodafinil for Treatment of Excess
- Page 92 and 93: Armodafinil for Treatment of Excess
- Page 94 and 95: Armodafinil for Treatment of Excess
- Page 96 and 97: Armodafinil for Treatment of Excess
- Page 98 and 99: The Epidemiology and Diagnosis of I
- Page 100 and 101: The Epidemiology and Diagnosis of I
- Page 102 and 103: The Epidemiology and Diagnosis of I
- Page 120 and 121: CIRCADIAN RHYTHM SLEEP DISORDERSPra
- Page 122 and 123: Table 2— AASM Levels of Recommend
- Page 124 and 125: 3.2.1.1 Both the Morningness-Evenin
- Page 128 and 129: as an indicator of phase in sighted
- Page 130 and 131: 4.4 Advanced Sleep Phase DisorderBe
- Page 132 and 133: 45. Walsh, JK, Randazzo, AC, Stone,
- Page 134: 123. Van Someren, EJ, Kessler, A, M
- Page 142 and 143: Table 1—Subject Demographicsn M:F
- Page 144 and 145: Scale. 28 The simple reaction time
- Page 146 and 147: Median RT (msec)1600A14001200100080
- Page 148 and 149: 10Mentally AExhaustedSharpScore8642
- Page 150 and 151: Current Treatment Options in Neurol
- Page 152 and 153: 398 Sleep Disordersand sleep loss,
- Page 154 and 155: 400 Sleep DisordersTable 1. Treatme
- Page 156 and 157: 402 Sleep DisordersStandard dosageC
- Page 158 and 159: 404 Sleep DisordersStandard procedu
- Page 160 and 161: 406 Sleep DisordersCaffeineMelatoni
- Page 162 and 163: 408 Sleep DisordersWake-promoting a
- Page 164 and 165: 410 Sleep Disordersnight shift: ada