SAPIENT SLEEP SOLUTIONS
From Sleep, Sleep Disorders and Depression, and Current Issues in Perinatal Mood Disorders, sponsored by the
University of Michigan Medical School
| SLEEP AND DEPRESSION —Roseanne Armitage, PhD, Professor, Department of Psychiatry; Director, Sleep and
Chronophysiology Laboratory; and Adjunct Professor, Department of Psychology, University of Michigan Medical
School, Ann Arbor
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| Take-home message: likelihood of sleep problems remitting with treatment of depression alone extremely low, given
nature of antidepressants used most frequently (ie, selective serotonin reuptake inhibitors [SSRIs] and selective norepinephrine
reuptake inhibitors [SNRIs])
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| Functions of sleep: slow-wave sleep—deep restorative, high-amplitude, non-rapid eye movement (REM) sleep that
reflects basic sleep homeostasis, maintaining energy balance; provides rest and recovery from daytime activities; period
when most body- and blood-cell repair done and function of immune system recovered and regulated; entrainment
of circadian rhythms maintained; stage 2 sleep—where individual spends most of night; associated with trying
to maintain vigilance but still remain asleep (“if there’s a big environmental event with teeth that’s about to bite you,
you’re able to wake up and get out of its way”); thought that important part of stage 2 sleep is being able to poll environment
for relevant stimuli to which individual needs to respond; REM sleep—associated with memory consolidation
and development of neural connections
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| Why is sleep important to depression? >80% of patients with major depressive disorder report sleep disturbances;
thought that patients with bipolar depression have similar experience, but seem to lean more toward hypersomnia
rather than toward other sleep disturbances; not much published data on sleep disturbances in bipolar mania (“it’s
very hard to do overnight sleep studies in people who sleep less than an hour a night”); depressed patients, especially
men, often present with complaint of sleep disturbance rather than admitting to having psychiatric disorder; sleep
disturbances >2 wk in duration increase lifetime risk for psychiatric illness, and for depression in particular; in patients
who have already experienced episode of depression, persistent sleep disturbance associated with risk for relapse
and recurrence and for suicide
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| Relationship between sleep and course of illness in depression: in community sample of >700 children, those who
had trouble sleeping 7 times more likely than good sleepers to have symptoms of depression and anxiety; those who
had trouble sleeping at 6 yr of age twice as likely to have full-blown depression by 11 yr of age; in sample of >1900
depressed adults, having had sleep problems as child predictive of more episodes of depression in adulthood; published
studies of sleep disturbances in depression indicate no single sleep variable differentiates depressed patients
from those with other psychiatric disorders, but rather cluster of sleep disturbances associated with major depressive
disorders, and subclassifications of major depression associated with each of these sleep profiles; prolonged sleep latency
profiles insomnia; short latency to first REM sleep period found in ≈40% of symptomatic, unmedicated depressed
patients; ≈65% of depressed patients show increased sleep fragmentation; other features common in
depression include increased stage 1 sleep, decreased deep restorative slow-wave sleep, and reduced total sleep time;
30% to 40% of depressed patients have hypersomnia, sleeping 12 to 14 hr per night and having trouble arousing in
morning
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| Antidepressants: consider nature of sleep disturbance in selecting antidepressant (eg, soporific or sedating antidepressant
ill-advised in patient with hypersomnia); ask patient how he or she sleeps before starting antidepressant and during
antidepressant therapy; most antidepressants potent suppressors of REM sleep, which should be therapeutic;
monoamine oxidase inhibitors (MAOIs) most potent REM suppressors, then tricyclic antidepressants (TCAs), followed
by SSRIs; SNRIs least potent REM suppressors; tetracyclic antidepressants bupropion and nefazodone do not
suppress REM sleep, and some evidence suggests trazodone also does not; increased time awake most dramatic with
SSRIs, and ≈80% of depressed patients report more wakefulness at night on SSRI than at baseline when they were
symptomatic and unmedicated; also SSRIs exacerbate restless leg syndrome and periodic limb movements in almost
100% of patients who already have those conditions; difficult to enhance deep restorative slow-wave sleep because it requires
antidepressant so sedating that it may impair daytime performance and decrease cognitive function; few studies
published on using combination therapy to manage depression and sleep disturbances
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| Circadian rhythm and biologic clocks: circadian rhythms pervasive in physiology, mood, behavior, and performance,
and entrained to 24-hr cycle of light and dark; master clock in human brain as exquisitely sensitive to light as
those of other mammals; prolonged disturbance in circadian rhythm associated with same impairment in performance
as that of chronic sleep loss
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| Research questions about circadian rhythm and biologic clocks: 1) what is their role in depression? 2) will exposure
to bright light and more regularized rest, activity, and sleep cycles re-entrain circadian rhythm? 3) is disturbance
of circadian rhythm consequence of therapy? 4) does gender matter? 5) is there critical period in development where
circadian rhythms become regularized in humans? (thought to be 4 to 6 mo of age) 6) is there some impairment in
initial entrainment of circadian rhythm in infants who later develop depression? 7) will it be possible to identify prospectively
children at high risk of developing depression?
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| TREATING INSOMNIA AND INSUFFICIENT SLEEP —Todd Arnedt, PhD, Assistant Professor, Department of
Psychiatry; and Director, Behavioral Sleep Medicine Program, Sleep and Chronophysiology Laboratory, University of
Michigan Medical School, Ann Arbor
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| Introduction: Americans getting less sleep, and that sleep of poorer quality; self-selected sleep deprivation most common
form of sleep loss; studies show sleep deprivation increases risk for psychiatric disorders; sleep loss as early as
5 to 6 yr of age independently predicts development of alcohol and substance abuse in adolescence
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| Insomnia: subjective complaint that consists of taking long time to fall asleep (>30 min considered problematic), difficulty
staying asleep, waking and having difficulty returning to sleep, and/or early morning awakening or not feeling
rested in morning; difficulty staying asleep most common complaint; patients with insomnia describe impaired daytime
functioning associated with their insomnia; fatigue most common complaint, and patients differentiate fatigue
from sleepiness (fatigue consists of tiredness, lassitude, and lack of energy; sleepiness is ability to lie down and fall
asleep); other common complaints include mood and cognitive effects, difficulty with memory, and work and interpersonal
difficulties; to be clinically relevant, insomnia must occur ≥3 times per week; if it lasts <1 mo, called acute,
1 to 6 mo, subacute, and >6 mo, chronic, with treatment implications for each category
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 | Ramifications of insomnia: poor quality of life; lack of work productivity; absenteeism; cost (estimated $1.1 billion
per year); if left untreated, insomnia does not get better; in study, when disorders such as depression with insomnia
treated, insomnia persistent and most common residual symptom, even after depression remitted; sleep disturbance
increases risk for relapse and recurrence of depression and for suicide
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| Treating patient with insomnia: goal is to identify underlying cause of insomnia and treat that; history and physical
examination usually unveil major causes of insomnia and laboratory studies seldom needed; several tools, including
sleep diaries and sleep questionnaires, available for determining cause of insomnia; once underlying cause
identified, important to treat it; possible causes of insomnia include depression, stress, medical disorders, and medications;
consider supplementing primary therapy with sleep therapy; acute phase of insomnia often triggered by
precipitating factor; in early stages, medications appropriate and indicated
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| Early stages of insomnia: people tend to engage in behaviors, such as going to bed early or sleeping late, that compensate
for lost sleep; they may try to will themselves to sleep, drink more caffeine during daytime, get more stimulation
during day, use hypnotic agent at bedtime; these behaviors eventually perpetuate insomnia for years, even
in absence of obvious precipitating event, and treatment should take them into account
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| Cognitive behavioral treatment for insomnia (CBTI): in studies, 75% of patients who undergo CBTI do better relative
to controls; however, no single treatment alone solves problem of insomnia, and treatment approach should include
at least stimulus control, paradoxical intention, and progressive muscle relaxation; other modalities
identified as probably efficacious include sleep restriction, education about sleep hygiene, CBTI, and biofeedback
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| Stimulus control: goal to get patient to reassociate bed and bedroom with sleep; patient instructions include going to
bed only when sleepy, using bed and bedroom for only sleep and sex, leaving bedroom if patient cannot sleep
within 15 to 20 min, staying out of bed until very, very sleepy, then returning to bed, and not falling asleep outside
of bed or bedroom; important that patient avoid daytime napping
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| Sleep restriction: have patient keep baseline sleep diary for 2 wk without intervention, then compute average
amount of time he or she actually sleeps (not amount of time in bed) per night; collaborate with patient on schedule
that he or she can follow every night of week, including weekends; initially allow 5 hr of sleep per night (no
matter what patient’s actual sleep time is); when patient returns 1 wk later, if sleep efficiency ≥85%, give him or
her 15 min more sleep per night (at beginning of sleep period), and repeat procedure; may be necessary to convince
patient that he or she does not need 8 hr of sleep per night, that quality of sleep more important than quantity;
advise patient that things eventually will get better, but not in “a couple of days,” and that “it takes
consistent, concerted effort”
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| Education about sleep hygiene: will not work or will have only minimal gains if done as sole treatment; goal to educate
patient about things that hurt and help sleep; advise patient to regularize his or her daily schedule, including
sleep and meals; have prebedtime snack and develop bedtime routine; get daily exposure to light; wind down before
bed; create sleep-conducive environment; never take daytime naps, watch clock, exercise late at night, or use
any substances close to bedtime
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| Cognitive components: “if you have repeated bad nights of sleep you start to worry about sleep [and] about
how you’re going to function during the daytime”; use treatment approach that allows patient to explore attitudes
and beliefs about sleep, including dysfunctional ones; displace dysfunctional attitudes with more appropriate ones;
most patients have misconceptions about causes of insomnia; many have unrealistic idea about how much sleep
they need every day; many feel sleep has diminished control and predictability; many have faulty beliefs about
sleep-promoting practices; recent evidence suggests many patients do not adhere to guidelines of sleep hygiene
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| Adjunctive techniques: relaxation techniques to reduce physiologic or cognitive arousal; light therapy; paradoxical
intentions
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| Cognitive behavioral treatment of insomnia: not long-term regimen (usually takes 4 to 10 therapy sessions over
course of 3 to 5 mo); first session, do intake and provide treatment overview; second session, start behavioral
strategies, including sleep restriction and stimulus control; third session, education about sleep hygiene; fourth
session, use cognitive therapy; fifth through seventh sessions, continue cognitive therapy, adjust sleep schedule,
and use adjunctive strategies; at end, talk about how to maintain gains and prevent relapse
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| Large-scale results: summary of several meta-analyses shows CBTI produces medium to large effects on sleep latency,
waking after sleep onset, and frequency of nighttime awakenings; relatively small effects on total sleep time
but large effect on sleep quality; these studies used patients with primary insomnia, but more recent studies show
results also hold true in patients with secondary insomnia
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| CBTI vs pharmacotherapy: in acute phase, effects essentially same, although pharmacotherapy works faster; recent
study found that most effective way of combining CBTI and pharmacotherapy is starting both treatments together,
stopping medication, and continuing with CBTI; no long-term studies for pharmacotherapy, but studies of CBTI
show that people usually maintain gains over at least 2 yr
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| Conclusions: insufficient sleep very common problem associated with significant morbidity; most patients have never
been asked about sleep by their physicians; insomnia adversely affects functioning; CBTI as efficacious as medications
in treatment of insomnia
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Educational Objectives
| The goal of this program is to educate the listener about the relationship between sleep and depression and about strategies
for treating insomnia and sleep insufficiency. After hearing and assimilating this program, the clinician will be
better able to:
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| 1. Describe various sleep disturbances and the role they play in depression.
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| 2. Discuss which antidepressants might be most helpful in treating each type of sleep disturbance.
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| 3. Define insomnia and state the effects it has on people.
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| 4. Formulate a strategy for treating insomnia and sleep insufficiency that incorporates cognitive behavioral therapy
for insomnia (CBTI).
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| 5. Compare CBTI with pharmacotherapy in the treatment of insomnia and sleep insufficiency.
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Suggested Reading
Argyropoulos SV, Wilson SJ: Sleep disturbances in depression and the effects of antidepressants. Int Rev Psychiatry
17:237, 2005; Armitage R et al: Effects of clozapine on sleep in bipolar and schizoaffective disorders. Prog Neuropsychopharmacol
Biol Psychiatry 28:1065, 2004; Armitage R et al: Rest-activity cycles in childhood and adolescent depression.
J Am Acad Child Adolesc Psychiatry 43:761, 2004; Armitage R et al: Sleep microarchitecture as a predictor
of recurrence in children and adolescents with depression. Int J Neuropsychopharmacol 5:217 2002; Armitage R et al:
Slow-wave activity in NREM sleep: sex and age effects in depressed outpatients and healthy controls. Psychiatry Res
95:201, 2000; Armitage R, Hoffmann RF: Sleep EEG, depression and gender. Sleep Med Rev 5:237, 2001; Armitage
R. The effects of antidepressants on sleep in patients with depression. Can J Psychiatry 45:803, 2000; Bouchard S,
Bastien C, Morin CM: Self-efficacy and adherence to cognitive-behavioral treatment of insomnia. Behav Sleep Med.
1:187, 2003; Brunello N, Armitage R et al: Depression and sleep disorders: clinical relevance, economic burden, and
pharmacological treatment. Neuropsychobiology 42:107, 2000; Cahn SC et al: Predictors of interest in psychological
treatment for insomnia among older primary care patients with disturbed sleep. Behav Sleep Med 3:87, 2005; Edinger
JD, Means MK: Cognitive-behavioral therapy for primary insomnia. Clin Psychol Rev 25:539, 2005; Erman MK:
Therapeutic options in the treatment of insomnia. J Clin Psychiatry 66(Suppl 9):18, 2005; Gooneratne NS et al: Functional
outcomes of excessive daytime sleepiness in older adults. J Am Geriatr Soc 51:642, 2003; Harvey AG, Tang
NK, Browning L: Cognitive approaches to insomnia. Clin Psychol Rev 25:593, 2005; Hasler G et al: Excessive daytime
sleepiness in young adults: a 20-year prospective community study. J Clin Psychiatry 66:521, 2005; Jansson M,
Linton SJ: Cognitive-behavioral group therapy as an early intervention for insomnia: a randomized controlled trial. J
Occup Rehabil 15:177, 2005; Lindberg E et al: Role of snoring and daytime sleepiness in occupational accidents. Am J
Respir Crit Care Med 164:2031, 2001; Melamed S, Oksenberg A: Excessive daytime sleepiness and risk of occupational
injuries in non-shift daytime workers. Sleep 25:315, 2002; Morin CM: Cognitive-behavioral approaches to the
treatment of insomnia. J Clin Psychiatry 65(Suppl 16):33, 2004; Nelson JC, Portera L, Leon AC. Residual symptoms
in depressed patients after treatment with fluoxetine or reboxetine. J Clin Psychiatry 66:1409, 2005; Roth T: Prevalence,
associated risks, and treatment patterns of insomnia. J Clin Psychiatry 66(SUPPL 9):10, 2005; Saxena AD,
George CF: Sleep and motor performance in on-call internal medicine residents. Sleep 28:1386, 2005; Silber MH:
Clinical practice. Chronic insomnia. N Engl J Med 353:803, 2005; Staner L: Sleep disturbances, psychiatric disorders,
and psychotropic drugs. Dialogues Clin Neurosci 7:323, 2005; Stepanski EJ: Behavioral sleep medicine: a historical
perspective. Behav Sleep Med 1:4, 2003; Vallieres A et al: Sequential treatment for chronic insomnia: a pilot study. Behav
Sleep Med 2:94, 2004; Vallieres A, Morin CM, Guay B: Sequential combinations of drug and cognitive behavioral
therapy for chronic insomnia: an exploratory study. Behav Res Ther 43:1611, 2005; Winkelman J: A novel
combination therapy for primary insomnia? Sleep 27:604, 2004.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue,
the faculty reported nothing to disclose.
Drs. Armitage and Arnedt were recorded at Sleep, Sleep Disorders and Depression, and Current Issues in Perinatal
Mood Disorders, held November 10-11, 2005, in Ann Arbor, Michigan, and sponsored by the University of Michigan
Medical School. The Audio-Digest Foundation thanks the speakers and the University of Michigan Medical School for
their cooperation in the production of this program.
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