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Managing Sleep Health in Primary Care

1


Paul P. Doghramji, MD, FAAFP

Family Practice Physician

Collegeville Family Practice & Pottstown Medical Specialists, Inc.

Medical Director of Health Services, Ursinus College – Collegeville, PA

Attending Family Practice Physician, Pottstown Memorial Medical Center – Pottstown, PA

Learning Objectives

▪ Communicate risk factors associated with not getting

enough sleep

▪ Explain the sleep/wake cycle and circadian rhythms

▪ Identify common sleep disorders in primary care

▪ Use appropriate diagnostic tools to assess patients’

sleep health


2

Agenda

▪ What is sleep?

▪ Sleep stages

▪ Sleep physiology

▪ Dreaming

▪ Sleepiness

▪ Sleep disorders

▪ Insomnia and comorbidities

Sleep Perspectives

▪ Behavioral

▪ Reversible

▪ Perceptual disengagement from, and unresponsiveness to, the environment

▪ Neurophysiological

▪ Two distinct states: REM sleep and NREM

▪ Actively produced, not a result of passive inactivity

▪ Highly regulated by homeostatic and circadian processes

▪ Produces changes in the entire organism, not just the CNS

▪ Teleological

▪ Necessary for survival; deprivation leads to functional impairments and eventual death

▪ Important for clearance of neurotoxic waste products (e.g., beta amyloid) that accumulate in

the brain during wakefulness

NREM = non-rapid eye movement

Carskadon MA, Dement WC (2005), Normal human sleep: an overview. In: Principles and Practice of Sleep Medicine, 4th ed., Kryger MH et al., eds. Philadelphia: Elsevier/Saunders, pp13-23. Science vol 342, 18 Oct 2013.


3

Why is sleep important?

▪ Cognition and performance

▪ Mood regulation

▪ Mental health

▪ Physical health

▪ Safety

Fig. 4 Aβ plaque deposition after chronic sleep restriction and chronic orexin receptor blockade in transgenic mice (A) Mice that underwent chronic sleep restriction for 21 days showed significantly greater Aβ plaque deposition in multiple subregions of the cortex compared to age-matched control mice.

The glymphatic system supports interstitial solute and fluid clearance from the brain.

Sci Transl Med 2012;4:147ra111


4

Sleep Stages

SLEEP REST


5

Two States of Sleep

Rapid eye movement (REM) sleep

▪ When dreaming occurs

▪ “Active brain in a paralyzed body”

Hours 1

N 1

& REM

N 2

N3

2 3 4 5 6 7 8

Non-REM sleep

▪ 3 stages

▪ Based primarily on EEG

Typical Sleep Architectural Pattern of a Young Human Adult

Adapted from Hauri P. The Sleep Disorders. Kalamazoo, Mich: Upjohn;1982:8.

Stage I & REM sleep (red) are graphed on the same level because their EEG patterns are very similar

Sleep Architecture

▪ Sleep is entered through stage N1

▪ Orderly progression from stage N1 to N3 and, typically within 90

minutes of sleep onset, to the 1st REM period

▪ 90-minute cycle of REM-NREM repeats throughout sleep

▪ As the night progresses

▪ REM periods increase in duration and density of eye movements

▪ N3 sleep becomes less prominent in the 2nd half of the night


6

Sleep Stage Characteristics

NREM REM

Heart rate Steady Variable

Blood pressure Steady Labile

Respirations Regular Irregular

Skeletal muscle tone Normal Decreased

Thermoregulation Waking modes Decreased

Penile tumescence Infrequent Frequent

Mental activity Limited Dreaming

Brain O2 consumption Decreased Waking level

Lee-Chiong T, ed. Sleep: A Comprehensive Handbook. Hoboken, NJ: Wiley & Sons; 2006.

Sleep Across the Life Span

0

100

200

300

400

500

600

700

Tota

l Sle

ep

Tim

e (

min

)

Age (years)

Total Time in Bed

Awake in Bed

NREM N 1

REM

NREM N 2

NREM N 3

10 20 30 40 50 60 70 8050

Adapted from Williams RL, et al. Electroencephalography of Human Sleep: Clinical Applications. New York, NY: John Wiley & Sons; 1974.


7

Sleep Physiology


8

Brainstem Mechanisms Underlying Sleep and Arousal

Orexin = Hypocretin

▪ Hypothalamic peptides (OX1 and OX2)

▪ Localized in the dorsolateral hypothalamus

▪ Wide projections throughout brain and spinal column

▪ Peptide neurotransmitters involved in

▪ Arousal

▪ Locomotion

▪ Metabolism (energy and appetite control)

▪ Increase blood pressure & heart rate

Peyron et al. J Neurosci. 1998;18:9996. Moore et al. Arch Ital Biol. 2001;139:195. Silber & Rye. Neurology. 2001;56:1616.


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Flip Flop Switch Model of Arousal and Sleep

Awake Sleep

Modified from Saper CB, et al. Nature. 2005;437(7063):1257-1263.

Dreaming


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When do we dream?

▪ Dreaming occurs in all stages of sleep

▪ 80% of persons who are awakened during REM sleep and

sleep onset (N1 & N2)

▪ 40% of persons who are awakened from a deep sleep

Foulkes D. Dreaming: a cognitive-psychological analysis. Hillsdale, N.J.: Erlbaum, 1985.

N1 & N2 N3 REM

Simpler, shorter

and have fewer

associations

than REM sleep

dreams

More diffuse

(e.g., about a

color or an

emotion)

Tend to be

bizarre and

detailed, with

storyline plot

associations

Highest recall during sleep stages with EEG patterns

most like those in the waking state

D

R

E

A

M

S

REM and Non-REM Dreams


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Frightening Dreams

TYPE OF

DREAMINCIDENCE SYMPTOMS SLEEP STAGE

ASSOCIATED

FACTORSFrequent

nightmares in

children

20% to 30%,

declines with age

Frightening, detailed plots

Difficult return to sleep

REM sleep, usually

late in sleep (4 - 6

a.m.)

Usually no pathology

Frequent

nightmares in

adults

5% to 8%

Increased awakenings

Daytime memory

impairment and anxiety

REM sleep

“Thin-boundary” / creative

personality

May have associated

psychopathology

PTSD

8% - 68% of

veterans

>25% of trauma

victims

Stereotypic dreams of the

trauma

Intense rage, fear, grief

REM sleep and sleep

onset

Significant trauma

Daytime hyper-

arousability & anxiety

REM sleep

behavior

disorder

Most common in

late middle age and

in men

Acting out of dreams

Nocturnal injuries

REM sleep

REM EMG tone

Degenerative neurologic

illness in 50%

Night terrors

1% to 4% of

children

Declines with age

Rare in adults

Blood-curdling screams

Autonomic discharge

Limited recall

Deep sleep, early

(1- 3 a.m.)

Stages 3 & 4

arousals on PSG

No pathology in children

Psychiatric & neurologic

disorders in adults

PAGEL JF, Nightmares and Disorders of Dreaming. Am Fam Physician. 2000 Apr 1;61(7):2037-2042.

REM = rapid eye movement; EMG = electromyography

Sleepiness


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Sleepiness: How do patients describe it?

▪ “I’m tired all the time”

▪ “I have no energy”

▪ “I feel fatigued”

▪ “I feel depressed”

▪ “I don’t feel rested”

▪ “I don’t sleep well”

The International Classification of Sleep Disorders: Diagnostic and Coding Manual. 2nd ed. Westchester, IL: American Academy of Sleep Medicine; 2005.

Chervin RD. Chest 2000;118:372-379. Shen J, et al. Sleep Med Rev 2006;10:63-76.

Patients Also Mean Other Things“TIRED”

Sleepiness FatigueLack of

motivation

Tendency to fall

asleep or inability

to stay awake

Sensation of

weariness,

tiredness,

exhaustion,

loss of energy;

the desire to rest

“I don’t feel like

doing anything…”

Improved by sleep Improved by rest,

exertion makes it

worse


13

Sleepiness in America

37%

16%

0%

10%

20%

30%

40%

At least a few days per month At least a few days per week

% of US Adults Reporting that They Are So Sleepyit Interferes with Their Daily Activities

National Sleep Foundation. “Sleep in America” Poll. March 2002.

Assessment Options: Sleep Parameters

▪ Subjective: based on self-report

▪Epworth

▪ Insomnia Severity Scale

▪Diaries

▪Often do not reflect objective sleep measures

▪ Objective: Sleep lab or home sleep monitor

▪ Wearable technology (eg, Fitbit) increasingly capable of more

objective sleep assessment: eg, total sleep time, slow wave sleep,

REM sleep

▪Not reimbursable, not validated in clinical practice


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Epworth Sleepiness Scale

Johns MW. Sleep. 1991;14:540-545.

Rate the chances of dozing in sedentary situations

Never Slight Moderate High

Sitting and reading 0 1 2 3

Watching television 0 1 2 3

Sitting, inactive in a public place (eg, a movie theater or a meeting)

0 1 2 3

As a passenger in a car for an hour without a break

0 1 2 3

Lying down to rest in the afternoon when circumstances permit

0 1 2 3

Sitting and talking to someone 0 1 2 3

Sitting quietly after lunch without alcohol

0 1 2 3

In a car, while stopped for a few minutes in the traffic

0 1 2 3

Score >=10 Prompts Further Evaluation

US women 20.8%,US men 29.7%2

South Africa1 24.5%

Japan1 12.4%

China1 6.2%

Austria1 17.5%

Belgium1 17.5%

Brazil1 14.3%

Germany1 7.2%

Portugal1 18.3%

Slovakia1 13.7%

Spain1 12.7%

Norway3 17.7%

N=35,327 survey respondents aged 39 ± 15.3 years.1

ESS, Epworth Sleepiness Scale

1. Soldatos CR, et al. Sleep Med. 2005;6:5-13; 2. Baldwin CM, et al. Sleep. 2004;27:305-311; 3. Pallesen S, et al. Sleep. 2007;30:619-624.

Worldwide Prevalence of ESS Scores >10


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Categories of Sleepiness

▪ Insufficient sleep

▪ Factitious

▪ Insomnia

▪ Poor quality sleep

▪ Obstructive sleep apnea

▪ Restless Legs Syndrome

▪ Disturbed timing of sleep

▪ Circadian rhythm disorders

▪ Medications and substances

▪ Rx, OTC, herbals

▪ Illicit drugs, alcohol

▪ Brain “damage”

▪ MS, Parkinson’s, TBI, stroke,

Alzheimer's

▪ Narcolepsy

Sleep Disorders


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Restless Legs Syndrome6

10%-15%

Comorbid Insomnias4

6%

Narcolepsy5

0.06%†

Obstructive Sleep Apnea1

3%-28%

Sleep-Wake Disorders: Prevalence in Adults

*Among night and rotating shift workers; †Prevalence of hypersomnias such as narcolepsy without cataplexy may be higher.

1. Young T, et al. Am J Respir Crit Care Med. 2002;165:1217-1239. 4. Ohayon MM. Sleep Med Rev. 2002;6:97-111.2. Drake CL, et al. Sleep. 2004;27:1453-1462. 5. Silber MH, et al. Sleep. 2002;25:197-202.3. Strine DP, et al. Sleep Med. 2005;6:23-27. 6. Merlino G et al. Neurol Sci. 2007;28:S37-S46. †Mignot E, et al. Brain. 2006;129:1609-1623. †Singh M, et al. Sleep. 2006;29:890-895.

Shift Work Disorder2

8%-32%* Insufficient Sleep

Syndrome3

26%

How to Diagnose the Cause of Sleepiness

▪ Get detailed sleep/wake history

▪ Determine whether sleepy, fatigue, or depression

▪ Quantify degree of sleepiness: ESS

▪ Start probing for the causes, looking for clues

▪ Insufficient Sleep Syndrome: doesn’t get enough sleep

▪ OSA: loud snoring, waking up choking, witnesses apneas, waking with

sore throat, headache, enuresis, nocturia

▪ RLS: uncomfortable feelings in legs prevent sleep, need to move them to

relieve symptoms

▪ PLMD: no clues except excessive sleepiness

▪ Narcolepsy: hypnogogic/hypnopompic hallucinations, sleep paralysis,

cataplexy


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Obstructive Sleep Apnea

Symptoms

▪ Loud Snoring

▪ Gasping, choking

▪ Witnessed apneas

▪ Morning headaches, sore throat

▪ Enuresis/nocturia

Physical Findings

▪ Large neck

▪ Crowded pharynx

▪ Obesity

▪ Micrognathia, short chin

Treatment

▪ CPAP/BiPAP/Auto-AP

▪ Oral appliance

▪ Surgery

▪ Weight loss

▪ Positioning

▪ “Provent”

▪ “Inspire”

Screening for OSA: STOP-BANG Method

STOP Questionnaire*

▪ Snoring

▪ Tiredness (daytime)

▪ Observed you stop

breathing during sleep

▪ High blood Pressure

BANG†

▪ BMI > 35

▪ Age > 50 years

▪ Neck circumference

> 40 cm (~ 16 in)

▪ Gender: Male

* High risk = Yes to > 2 of 4 STOP items

† High risk = Yes to > 3 of 8 STOP-BANG items

Chung F, et al. Anesthesiology 2008;108:812-821.


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Airway Assessment: OSA Mallampati Scale

Nuckton TJ, et al. Sleep. 2006;29:903-908.

Odds of OSA increase >2-fold for every 1-point increase

Class I Class II Class III Class IV

Restless Leg Syndrome (RLS)

Symptoms

▪ Irresistible urge to move legs usually with unpleasant sensations

▪ Relief with movement

▪ Worse at night

▪ Worse with rest

Etiology

▪ Dopaminergic dysfunction

▪ Iron deficiency

▪ Renal insufficiencies

▪ Peripheral neuropathies

▪ 25% secondary

Treatment

▪ Dopaminergic agents

▪ Iron if deficient

▪ Sedative hypnotics

▪ Anticonvulsants

▪ Opiates

▪ Sleep hygiene

Allen RP, Sleep Med, 2003.


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Periodic Limb Movement Disorder (PLMD) vs. RLS

▪ Substantial overlap

▪ Up to 85% of RLS patients have PLMD

▪ 30% of PLMD patients have RLS

▪ RLS diagnosis is made clinically

▪ PLMD diagnosis is made via PSG

▪ No other daytime clues, just sleepiness

▪ Treatments are the same

Insomnia and Comorbidities


20

Insomnia

As a disorder:

▪ Trouble getting to sleep and/or

▪ Trouble staying asleep and/or

▪ Waking up too early and/or

▪ Occurring more days of the week than not

▪ Ongoing for over 3 months

Why Should PCP’s be Proactive about Insomnia?

▪ Very prevalent in primary care

▪ But patients don’t tell you

▪ Serious consequences

▪ Day to day life

▪ Poor outcome on mental and

physical health

▪ Insomnia is a clue

▪ Most insomnia is co-morbid

▪ Easy to identify

Treatment

▪ Relieves an upsetting symptom

▪ Improves next day

consequences

▪ Improves outcome of

co-morbidity

▪ Psychiatric

▪ Medical

▪ Majority is done by PCP


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Insomnia Risk Factors

▪ Age (older)

▪ Sex (especially post-1 and perimenopausal2 females)

▪ Divorce / separation / widowhood

▪ Psychiatric illness (mood and anxiety disorders)

▪ Medical conditions

▪ Cigarette smoking

▪ Alcohol and coffee consumption

▪ Certain prescription drugs

1. NIH Consens State Sci Statements. 2005;22:1-30.

2. Young T, et al. Sleep. 2003;26:667-672.

Insomnia Screening and Follow-up

▪ Sleep Schedule: Do you have trouble getting to sleep, staying asleep, or waking

up too early?

▪ Daytime consequences: Do you feel like you have slept well throughout the day?

▪ Sleep timing: When do you go to bed? …Wake up? …Middle of the night

awakening? …How long does it take you to fall back to sleep?

▪ Treatments: What remedies have you tried? Any previous Rx’s?

▪ Sleep hygiene/lifestyle issues: Alcohol? Smoking? Exercise? Medications that

cause insomnia?

▪ Duration, frequency, prior: How long has this been going on?...How often?...

Have you had it before?...

Sateia MJ, Doghramji K, Hauri PJ, Morin MM. Sleep. 2000;23:1-66.

Erman MK. In: Sleep Disorders: Diagnosis and Treatment. Totowa, NY: Humana Press; 1998:21-51.


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How Frequent are Comorbidities?

Terzano MG, et al. Sleep Med. 2004;5:67-75. Katz DA, McHorney CA. (1998).

Clinical correlates of insomnia in patients with chronic illness. Arch Intern Med 158(10):1099-1107.

35

28

19 17 15 1411

0

10

20

30

40

50

30

47

37 39

50

3842

106

17

2522

1215

0

10

20

30

40

50

InsomniaSevere insomnia

Pre

vale

nce

%

Medical Conditions in Primary

Care Patients with InsomniaInsomnia with Medical Conditions

How Does Inadequate Sleep Increase CVD?

▪ Total sleep time (TST) < 5 hours compared to TST > 5 hours

▪ Higher glucose & cortisol levels

▪ HPA-associated endocrine & metabolic imbalances

▪ Hypercholesterolemia even after controlling for other risk factors

▪ Night time BP: Nighttime SBP higher and day-to-night SBP dipping was lower

(-8% vs -15%, P < 0.01) in insomniacs

▪ Atherosclerosis: Total sleep time (P = 0.005), and sleep quality (P = 0.05)

contributed to increased carotid intima-media thickness

▪ Inflammation: Serum CRP levels higher and increased at a steeper rate

Lanfranchi, PA, et al. (2009). Nighttime blood pressure in normotensive subjects with chronic insomnia: implications for cardiovascular risk. Sleep 32(6): 760-766.

Nakazaki, C, et al. (2012). Association of insomnia and short sleep duration with atherosclerosis risk in the elderly."Am J Hypertens 25(11): 1149-1155. Parthasarathy,

S, et al. (2015). Persistent insomnia is associated with mortality risk. Am J Med 128(3): 268-275 e262. Lin, CL, et al. (2016). The relationship between insomnia with short

sleep duration is associated with hypercholesterolemia: a cross-sectional study. J Adv Nurs 72(2): 339-347. Farina, B., et al. (2014). Heart rate and heart rate variability

modification in chronic insomnia patients. Behav Sleep Med 12(4): 290-306. de Zambotti, M., et al. (2011). Sleep onset and cardiovascular activity in primary insomnia.

J Sleep Res 20(2): 318-325.


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Does insomnia contribute to development of hypertension?

Lewis, P. E., et al. (2014). Risk of type II diabetes and hypertension associated with chronic insomnia among active component, U.S. Armed Forces,

1998-2013. MSMR 21(10): 6-13.

Prospective Follow-up

▪ Active duty in US Military

▪ Excluded: Chronic

insomnia prior to

1/1/1998

▪ Without hypertension at

baseline

▪ Chronic insomnia led to

higher risk of

hypertension (aHR 2.00)

Rate of Developing

Hypertension(per 10,000 person-years)

46.2

95.6

0

20

40

60

80

100

Controls Insomnia

Does Insomnia Increase Risk of CVDs?

1.681.85

1.4 1.3

0

0.5

1

1.5

2

aOR of CV Event

0.961.35

4.53

0

1

2

3

4

5

1 2 3

aOR for CHF

1st CV Event

# Insomnia Symptoms

Hsu, CY, et al. (2015). The Association Between Insomnia and Increased Future Cardiovascular Events: A Nationwide Population-Based Study.

Psychosom Med 77(7): 743-751. Laugsand, LE, et al. (2014). Insomnia and the risk of incident heart failure: a population study. Eur Heart J 35(21):

1382-1393. Canivet, C, et al. (2014). Insomnia increases risk for cardiovascular events in women and in men with low SES: a longitudinal, register-

based study. J Psychosom Res 76(4): 292-299.


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How Much Does Insomnia Contribute to CV Mortality?

Health Professionals Follow-Up Study

▪ US men free of cancer

▪ Insomnia symptoms in 2004, followed through 2010

▪ Adjusted for age, lifestyle factors, and common chronic conditions

Metaanalysis of 13 Prospective Studies

▪ 122,501 subjects followed for 3-20 yrs

▪ Insomnia increased risk by 45% of developing or dying from CVD ▪ (RR 1.45, 1.29-1.62; p < 0.00001)

Li, Y, et al. (2014). "Association between insomnia symptoms and mortality: a prospective

study of U.S. men." Circulation 129(7): 737-746. Sofi, F, et al. (2014). Insomnia and risk of

cardiovascular disease: a meta-analysis. Eur J Prev Cardiol 21(1): 57-64.

1.25

1.091.04

1

1.25

1.5

Total Mortality CVD MortalityDifficulty Initiating & Nonrestorative

Difficulty initiatingDifficulty maintainingEarly-morning awakenings

1.55 (1.19-2.04)

1.32 (1.02-1.72)

Health Professionals Follow-Up Study

Adjusted Hazards Ratio

How Does Insomnia Contribute to Diabetes Risk?

Insulin Resistance Associated with

Subjective Sleep Complaints In

Those without Diabetes

ORs

Adjusted

for

InsomniaDaytime

Sleepiness

Sex and age1.68

(1.09–2.58)

1.80

(1.22–2.66)

Fully*1.24

(0.74–2.09)

1.75

(1.10–2.77)

*Adjusting for sex, age, alcohol consumption,

smoking, exercise, occupational status, BMI,

and family history of diabetes

Pykkönen A-J, et al. (2012) Subjective Sleep Complaints Are

Associated With Insulin Resistance in Individuals Without Diabetes.

Diabetes Care 35:2271–8.

aORs for HbA1c >= 6.0%

6.79

3.96

2.33

0

2

4

6

8

Kachi, Y., et al. (2011). Association between insomnia symptoms and

hemoglobin A1c level in Japanese men. PLoS One 6(7): e21420.

Males 22-69 years old with no hx of diabetes

Difficulty maintaining

sleep

Lasting 2+wks

Early AM

awakening

Some-times

Some-times

Japanese company annual health check-up


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Does Treating Insomnia Lower Blood Pressure?

Standard BP treatment + estazolam

vs.

Standard BP treatment + placebo

▪ Insomnia treatment efficacy

▪ Estazolam: 67.3% (P < 0.001)

▪ Placebo: 14.0%

▪ Goal BP(< 140/90 mmHg)

▪ Estazolam: 74.8% (P < 0.001)

▪ Placebo: 50.5%

Li, Y, et al. (2017). "The impact of the improvement of insomnia on blood

pressure in hypertensive patients." J Sleep Res 26(1): 105-114.

Blood Pressure Reduction

from Baseline

-2.6 -2.8-2.5

-3.4

0

-2.3-2

-2.5 -2.7

-0.7

-2.8

-5

-7.1

0

-2.5

-3.7

-5.4

-8

-6

-4

-2

07 14 21 28 7 14 21 28

Placebo Estazolam

Systolic Diastolic

N = 202N = 200

Days of Treatment

Does Insomnia Increase Risk of Psychiatric Disorders?

31.1

35.9

30

14.4

5

21

18

10

0

5

10

15

20

25

30

35

40

Pati

en

ts (%

)

Incidence (%) over 3.5 years

Insomnia (n=240)

No Insomnia (n=739)

Breslau N, Roth T, Rosenthal L, Andreski P. Sleep disturbance and psychiatric disorders: a longitudinal epidemiological study of young adults. Biol Psychiatry. 1996;39:411-418.


26

Does Treating Insomnia Improve Comorbidities?

0

20

40

60

80

100

4 Months 16 Months

Poor Good

0

20

40

60

80

100

4 Months 16 MonthsControl Tai Chi

By Sleep Quality

%

4 months

CBT .21 (.03-1.47) p<.10

TCC NS

16 months

CBT .06 (.005-.669) p<.01

TCC .10 (.008-1.29) p<.05

ORs of Remaining

at High Risk

2-hour group sessions

weekly for 4 mo with a

16-mo evaluationRisk score based on 8 biomarkers: HDL, LDL, triglycerides,

C-reactive protein, fibrinogen, HA1c, glucose, insulin• High risk = 4 or more abnormal

By Intervention

% Remaining at High Risk

Carroll, JE, et al. (2015). Improved sleep quality in older adults with insomnia reduces biomarkers of disease risk: pilot results from a randomized controlled comparative

efficacy trial. Psychoneuroendocrinology 55: 184-192.

How is Insomnia Best Conceptualized to Guide Treatment?

▪ Genetic: heritability 42% - 57% in chronic insomnia

▪ Final common pathway: Autonomic and CNS hyperarousal

▪ Greater whole-brain metabolism during both sleep and wake periods

▪ Increased secretion of corticotropin and cortisol throughout sleep-wake cycle

▪ Sleep-wake regulation imbalance

▪ Overactivity of arousal systems

▪ Hypoactivity of sleep-inducing systems

▪ Both

▪ Failure of wake-promoting structures to deactivate during the transition

from waking to sleep states

Riemann D., et al. (2015). The neurobiology, investigation, and treatment of chronic insomnia. Lancet Neurol 14(5): 547-558. Vgontzas, AN, et al. (2013).

Insomnia with objective short sleep duration: the most biologically severe phenotype of the disorder. Sleep Med Rev 17(4): 241-254. Vgontzas et al.

Nofzinger et al. Am J of Psychiatry. 2004;161:2126-2128.


27

1. Kupfer DJ, Reynolds CF III. N Engl J Med. 1997;336:341-346.

2. Consensus Conference. JAMA. 1984;251:2410-2414.

Stepwise Approach for Managing Insomnia

Discuss With

Patient How They Sleep

Diagnosis1, 2

Education,

Including

Good Sleep

Practices1, 2

Nonpharma-

cologic

and/or

Pharma-

cologic

Therapy1, 2

Referral to

Sleep

Specialist

(In Cases of

Treatment

Failure)1

Patient Education: Most Powerful Tool

▪ Inform WHY management is so important

▪ Consequences

▪ Emphasize keeping regimented sleep schedule

▪ Wake up same time every day

▪ Naps usually not a good idea

▪ Emphasize sleeping long enough

▪ Can’t catch up on weekends

▪ Emphasize lifestyle measures

▪ Alcohol, exercise, smoking, caffeine, diet (no large meals)


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Treatments: CBT and/or Medications?

▪ Address the co-morbid condition as well as the insomnia

▪ Discuss with patient pros and cons of meds and CBT

▪ Medications:

▪ Which are best applicable?

▪ Habit forming?

▪ How long to use?

▪ Side effects?

▪ CBT: at your discretion—ability, time, interest

▪ Allow patient to voice his/her concerns, fears, and needs

How Does Cognitive Behavioral Therapy Compare To Pharmacotherapy?

Adapted from: Jacobs GD, et al. Arch Intern Med. 2004;164:1888-1896.

Schutte-Rodin S et al. J Clin Sleep Med. 2008;4(5):487-504. Morin CM, et al. Sleep 1999;22:1134-56.

CBT-I Components

▪ Sleep hygiene education

▪ Cognitive therapy

▪ Sleep restriction therapy

▪ Stimulus control therapy

▪ Relaxation training

Sleep Hygiene

▪ Regular wake time

▪ Limit time awake and in bed

▪ Limit napping during the day

▪ Avoid clock watching if awake

▪ Avoid caffeine (after 2 PM),

alcohol after dinner, or eating

dinner just before bedtime

▪ Avoid stressful activities in

the evening


29

Treating Insomnia: Choosing the Right Pharmacotherapy

▪ Trouble with sleep initiation only: rapid and short acting

▪ Ramelteon, triazolam, zaleplon, zolpidem

▪ Trouble staying asleep with sleep initiation problems: rapid and long acting

▪ Eszopiclone, temazepam, zolpidem ER, zolpidem (if awakes early in evening), suvorexant

▪ Trouble staying asleep withOUT sleep initiation problems

▪ Doxepin (taken at sleep onset), sublingual zolpidem (taken if one awakens)

▪ Issues with controlled substances: both of these unscheduled

▪ Ramelteon, doxepin

▪ Generic medications

▪ Temazepam, triazolam, zaleplon, zolpidem, eszopiclone

When to Consider Referral to a Sleep Expert

▪ Suspected obstructive sleep apnea or narcolepsy1-3

▪ Violent behaviors or unusual parasomnias1-3

▪ Daytime tiredness (sleepiness) that you can’t figure out1

▪ Insomnia fails to respond to behavioral and/or pharmacologic

therapy after an appropriate interval1,3

▪ You don’t feel comfortable treating the condition

1. Doghramji P. J Clin Psychiatry. 2001;62(suppl 10):18-26.

2. Sateia MJ, Owens J, Dube C, Goldberg R. Sleep. 2000;23:243-308.

3. Kushida CA, Littner MR, Morgenthaler T, et al. Sleep. 2005;28:499-521.


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Additional Resources

▪ For additional resources, visit:

▪ Sleepfoundation.org

▪ Sleep.org

▪ Sleephealthjournal.org

http://www.sleepfoundation.org/

http://www.sleep.org/

http://www.sleephealthjournal.org/

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