Ebook Sleepy or sleepless - Clinical approach to the sleep patient: Part 2

(BQ) Part 2 book Sleepy or sleepless - Clinical approach to the sleep patient presents the following contents: Key history and physical examination findings for the sleepless or restless patient, assessment and management of insomnia, the parasomnias, the sleepless child, sleeplessness during and after pregnancy,...

The Sleepless or Restless Patient

© Springer International Publishing Switzerland 2015

R.K Malhotra (ed.), Sleepy or Sleepless, DOI 10.1007/978-3-319-18054-0_8

Key History and Physical Examination

Findings for the Sleepless or Restless Patient

John Harrington and Kelly Marie Newton

Sleeplessness, restlessness at night, and insomnia are a common clinical complaint for the primary care patient Patients may present with insomnia as the chief com-plaint, but insomnia will commonly be present as part of another illness or com-plaint Insomnia has been reported and is observed worldwide In the adult population, 33–50 % will complain of insomnia in their lifetime, and 10–15 % will associate these symptoms with distress or impairment Identifi able risk factors include increasing age, female sex, comorbid disorders, shift work, and potentially lower socioeconomic status [ 1 , 2 ] Patients with psychiatric and chronic pain disor-ders have insomnia rates that are reported to be as high as 50–75 % [ 2 ] Insomnia is often chronic; over the course of several years, 50–85 % of individuals will report persistence in symptoms [ 2 ]

The International Classifi cation of Sleep Disorders, Third Edition, defi nes nia as repeated diffi culty with sleep initiation, duration, consolidation, or quality that occurs despite adequate sleep opportunity, a persistent sleep diffi culty, and associ-ated daytime dysfunction [ 1 ] Patients often complain of extended periods of noctur-nal wakefulness or insuffi cient sleep that are associated with daytime symptoms of fatigue, decreased mood, irritability, malaise, or some kind of cognitive impairment

insom-to include impaired concentration and memory [ 1 ] Table 8.1 lists some common consequences and impairments associated with insomnia

Division of Pulmonary/Critical Care/Sleep/Allergy ,

985990 Nebraska Medical Center , Omaha , NE 68198-5990 , USA

K M Newton

Division of Critical Care and Hospital Medicine, Department of Medicine ,

National Jewish Health , 1400 Jackson Street , Denver , CO 80206 , USA

Patient History

The evaluation of the patient complaining of sleeplessness begins with a careful history and physical exam that addresses both sleep and waking behaviors The history should include questions designed to evaluate the possibility of common medical, psychiatric and medication, or substance abuse-related issues [ 2 ] Taking a good history from a patient with sleeplessness or restless sleep can be time consuming, but

is critical to making a correct diagnosis and in guiding the treatment plan

A good sleep history includes characterizing the insomnia complaints such as the type of complaint (falling asleep, staying asleep, early morning wakings, or non- restorative sleep), severity, impact on daytime functioning, frequency (how many nights a week), duration (how long has this been occurring), type of course (inter-mittent or progressive), aggravating or ameliorating symptoms, treatment attempts, and response to therapy [ 2 ] Discussing the patient’s bedtime behaviors such as characterizing the sleeping environment, the patient’s emotional state, and whether the patient senses dread regarding sleep and sleep behaviors can provide insight [ 2 ] Understanding the patients’ sleep-wake cycle to include sleep latency (time to fall asleep), number of awakenings, length of awakenings, sleep duration, and napping can all provide clues to the patient’s insomnia Day-to-day variability should also

be examined [ 2 ] Patterns of sleep can be ascertained which may provide clues to circadian rhythm disorders, and assessing the amount of sleep can provide clues that the patient has too much or too little sleep opportunity [ 2 ]

In assessing insomnia, it is important to screen for comorbid sleep disorders such

as restless leg syndrome, obstructive sleep apnea, and parasomnias (sleep walking/sleep talking) [ 2 ] Comorbid medical complaints such as chronic pain, untreated refl ux, uncontrolled nocturnal asthma, headaches, and paroxsysmal nocturnal dyspnea may contribute to the patient’s complaint of insomnia [ 2 ]

A complete insomnia history includes medical, psychiatric, medication/substance,

psychiatric illnesses often comorbid or even causative for insomnia, but direct effects

Table 8.1 Consequences of

concentration, memory issues) Poor work or school performance Mood disturbance or irritability Daytime sleepiness

Decreased work performance Lack of motivation or initiative reduction Errors or accidents at work or while driving Muscle tension

Headaches

GI upset

of prescription or over-the-counter medications may impact sleep and daytime functioning [ 2 ] For example, a patient taking an over-the-counter sleep headache remedy containing caffeine may be sabotaging their ability to fall asleep A careful evaluation of their caffeine intake and smoking/tobacco history can be illuminating Many patients with insomnia use cigarettes before bed as a way to “relax,” yet few patients realize the simulating effects of the nicotine Alcohol is commonly used prior to bed to help initiate sleep by many suffering with insomnia, without realizing that alcohol can cause frequent and prolonged nighttime awakenings Finally, evalu-ating and offering suggestions regarding waking and bedtime behaviors may improve symptoms For example, the light from using electronic devices in bed is counterpro-ductive to sleep and may cause or perpetuate insomnia.

Physical Examination

There are no specifi c features of the physical exam associated with insomnia or restless sleep However, a thorough physical exam may provide clues to comorbid conditions The physical exam should evaluate for risk factors for sleep apnea to include

Table 8.2 Topics to cover when taking a patient history for compliant of insomnia

Time the patient tries to go sleep How long it takes to fall asleep Frequency and cause of nighttime awakenings How long it takes to return to sleep after waking Time of fi nal awaking

Time the patient gets out of bed for the day Frequency and timing of daytime naps How many says per week insomnia occurs

Activities in bed besides sleep and sex

Note amount and time

of day used

Tobacco use Alcohol use Recreational drug use

Current and past psychiatric disorders Medication/supplement

use

Note doses and timing of administration Note any prescription or nonprescription sleep aids that have been tried

Comfort of bed and surrounding Disruption from bed partner, children, pets

Life and social stressors at time of insomnia onset

obesity, increased neck circumference, and a crowded airway [ 2 ] The practitioner should look for signs of comorbid medical conditions to include pulmonary disease (cyanosis, clubbing, hypoxemia), cardiac (clubbing, heart murmur, crackles, peripheral edema), rheumatologic, endocrine (thyroid), and/or gastrointestinal symptoms The mental status exam should include an insight to mood, anxiety, memory, concentration, and alertness [ 2 ]

Additional Tools

There are other tools that can be utilized to form a working differential diagnosis for the etiology of insomnia A dedicated prospective sleep log can help identify issues such as insuffi cient sleep and circadian rhythm disorders such as advanced or delayed sleep phase A standardized scale such as an Epworth can provide insight to how severe the impact on daily functioning is [ 2 3 ] Patients who may have a pre-test probability of obstructive sleep apnea or periodic limb movement disorder may

be appropriate for polysomnogram

Differential Diagnosis

Conceptually, chronic insomnia can be grouped into three categories: (1) insomnia associated with other sleep disorders, particularly sleep-disordered breathing, move-ment disorders, or circadian rhythm disorders; (2) comorbid medical or psychiatric illnesses to include medications/substances; and (3) primary insomnia [ 2 ] (Table 8.3 )

(continued)

Table 8.3 Causes of transient and chronic insomnia

Causes of transient insomnia

Acute life stresses,

Adjustment sleep disorder Jet lag

Shift work sleep disorder

Causes of chronic insomnia

sleep, medical, neurologic, or psychiatric disorder, nor due to substance abuse or withdrawal

Idiopathic insomnia Paradoxical insomnia (sleep state misperception)

Psychophysiologic insomnia Alterations in

circadian rhythms

Insomnia is related to disorders

of the timing of sleep periods secondary to desynchrony between endogenous circadian rhythms and the environment

Advanced sleep-phase syndrome Delayed sleep-phase syndrome Irregular sleep-wake pattern Non-24-h sleep-wake syndrome

Etiology Characteristics Sleep disorders

behaviors that are arousing and not conducive to sleep

Inadequate sleep hygiene Limit-setting sleep disorder Sleep-onset association disorder Nocturnal eating/drinking syndrome Environmental

factors

Insomnia is due to environmental conditions or external factors that are not conducive to sleep

Altitude insomnia Environmental sleep disorder Food allergy insomnia Toxin-induced sleep disorder

sleep-related breathing disorders

or parasomnias

Central sleep apnea Obstructive sleep apnea Parasomnias

Confusional arousals Sleep terrors Sleepwalking Rhythmic movement disorder Sleep starts

Nocturnal leg cramps Nightmares

REM sleep behavior disorder

limb movements of sleep may be associated with arousals, awakenings, and sleep disruption Restless legs syndrome can give rise to sleep-onset insomnia

Periodic limb movement disorder Restless legs syndrome

physiologic alterations involving the respiratory, cardiac, gastrointestinal, and musculoskeletal systems

Respiratory disorders Asthma

COPD Central alveolar hypoventilation syndrome

Cardiac disorders Nocturnal angina Congestive heart failure Pain syndromes

Gastrointestinal syndromes GERD

Peptic ulcer disease Sleep-related abnormal swallowing

Dermatologic syndromes Pruritus

Cancer Infectious disorders

(continued)

Table 8.3 (continued)

Summary

Insomnia remains a common and pervasive problem in the adult population with a signifi cant impact on health, well-being, and daytime functioning A careful history and physical exam can provide valuable clues into the etiology of the insomnia and therefore guidance regarding the treatment plan

Neurologic disorders Neurologic disorders can prevent

sleep onset and disrupt its continuity

Cerebral degenerative disorders Dementia

Fatal familial insomnia Nocturnal paroxysmal dystonia Parkinson’s disease

Sleep-related headaches Sleep-related seizures

an underlying psychiatric disorder Conversely, among this patient group, there is an increased risk of developing a new psychiatric illness

Alcoholism Anxiety disorders Mood disorders Panic disorders Personality disorders Psychoses

Somatoform disorders Menstruation and

pregnancy

Both pregnancy and the menstrual cycle can produce insomnia among women

Menstrual-associated sleep disorder Pregnancy-associated sleep disorder Medication and

substance abuse

The use and abuse of hypnotic agents, stimulants, and alcohol are important causes of insomnia

Alcohol-dependent sleep disorder

The effects of these and other medications are also infl uenced

by the possible development of tolerance, withdrawal symptoms, and drug interactions

Hypnotic-dependent sleep disorder Stimulant-dependent sleep disorder

Adapted with permission from Lee-Chiong, Teofi lo Sleep Medicine Essentials 2008 New York, New York: Oxford University Press, USA, 2008, with permission

© Springer International Publishing Switzerland 2015

R.K Malhotra (ed.), Sleepy or Sleepless, DOI 10.1007/978-3-319-18054-0_9

Diagnostic Tools and Testing in the Sleepless and Restless Patient

Fouad Reda

In addition to a thorough history and physical, there are a variety of tools available for the clinician to evaluate a patient who comes in with complaints of insomnia, sleeplessness, or restless sleep

Sleep Diaries

Sleep diaries are valuable tools in assessing sleepless or restless patients (Fig 9.1a )

A sleep diary is designed to get the information about a patient’s sleep pattern It has the potential of reducing recall or report bias The patient self-monitors his/her sleep every night and records it This helps in the initial assessment as well as in tracking treatment effect of different interventions It provides valuable information which includes some or all of the following:

• Bedtime

• Sleep onset latency (SOL)—time taken to fall asleep following bedtime

• Wake after sleep onset (WASO)—sum of wake times from sleep onset to fi nal awakening

• Time in bed (TIB)—time from bedtime to getting out of bed

• The presumed cause, number, time, and length of any nighttime awakenings and activities during these moments

• Total sleep time (TST)—time in bed minus SL and minus WASO

• Sleep effi ciency (SE)—TST divided by TIB times 100

• Wake up time

F Reda , M.D (*)

SLUCare Sleep Disorders Center, Department of Neurology and Psychiatry ,

St Louis University School of Medicine , 1465 S Grand Blvd , St Louis , MO 63104 , USA

Fig 9.1 Example of a sleep diary ( a ) and actigraphy ( b ) for patient with insomnia due to delayed

sleep phase disorder

• Whether the person woke up spontaneously, by an alarm clock, or because of other (specifi ed) disturbance

• Quality of sleep

• Nap times (frequency, timing, and duration)

• A few words about how the person felt during the day (mood, tiredness, etc.)

• The name, dosage, and time of any drugs used including medication, sleep aids, caffeine, and alcohol

• The time and type/heaviness of evening meal

• Activities the last hour before bedtime, such as meditation, watching TV, playing games

• Stress level before bedtime

A study done on 50 subjects (25 narcoleptics and 25 matched control subjects) comparing the sleep diary and polysomnography found out that the sleep diary is reliable with high sensitivity and specifi city (92.3 and 95.6 %) [ 1 ]

Actigraphy

Actigraphy utilizes a wristwatch-like portable device which contains an ter, a clock, internal memory, and a photo sensor It records the rest/activity cycle which may correspond to the sleep/wake cycle It may assist to determine the sleep patterns in normal healthy adult population, to evaluate patients suspected of advanced sleep phase syndrome (ASPS), delayed sleep phase syndrome (DSPS), shift work sleep disorder, and other circadian sleep disorders including jet lag and non-24 h sleep/wake syndrome It is used to determine the circadian rhythm patterns in patients with insomnia (including insomnia associated with depression) and hypersomnia When sleep diaries are used in conjunction with actigraphy, more information can

accelerome-be obtained in regard to sleep/wake cycle of the subject accelerome-being studied But there may

be discrepancy between both these studies especially in young males whose graphic estimates of wake after sleep onset (WASO) were substantially greater than sleep diary estimates (74 min actigraphy vs 7 min sleep diary) [ 2 ] In children, acti-graphic estimates of total sleep time is substantially less than sleep diary and parental report (6 h 51 min actigraphy vs 8 h 16 min sleep diary v 8 h 51 min parent report)

Questionnaires

Insomnia Severity Index

The insomnia severity index assesses the patient’s perception of insomnia in a seven-item questionnaire Less than or equal to seven is considered normal The full

https://www.myhealth.va.gov/mhv-portal- web/anonymous.portal?_nfpb=true&_pageLabel=healthyLiving&contentPage=healthy_living/sleep_insomnia_index.htm

Pittsburg Sleep Quality Index

The Pittsburg Sleep Quality Index is a self-reported questionnaire assessing sleep quality over 1 month interval consisting of 19 items which generate seven

“component” scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep effi ciency, sleep disturbances, use of sleeping medication, and daytime dys-function [ 3 ] A global PSQI score of >5 is considered poor sleep (diagnostic sensi-tivity of 89.6 % and specifi city of 86.5 %)

Epworth Sleepiness Scale

The Epworth Sleepiness Scale is a self-reported questionnaire to assess the

sleepi-ness of the patient by assessing the patient’s tendency to fall asleep in specifi c

situ-ations [ 4 ] It is valuable in assessing sleepless patient because typically insomniacs are not usually “sleepy” individuals However, when sleepless patients face a sig-nifi cant reduction in the overall hours of sleep, a resultant sleep restriction and day-time sleepiness might occur This questionnaire has eight items each scored from 0

to 3 A score of 0–9 is considered normal and is expected to be seen in a typical insomniac patient A score of 16 or above indicates high level of daytime sleepiness

as seen in severe obstructive sleep apnea or narcolepsy It can be found at http://epworthsleepinessscale.com/epworth-sleepiness-scale.pdf

Beck Depression Inventory and Beck Anxiety Inventory

Among other depression and anxiety scales, these are crucial in identifying primary mood or anxiety problem that can be contributing to patient’s overall hyperarousal state Beck Depression Inventory (BDI) and Beck Anxiety Inventory (BAI) are self- reported 21-item questionnaires to measure depression and anxiety, respectively

A BDI score of less than 10 indicates no or minimum depression A BDI score of more than 18 is moderate to severe depression A BAI score of 0–7 indicates mini-mal level of anxiety; 8–15, mild anxiety; 16–25, moderate anxiety; and 26–63, severe anxiety

Polysomnography

Polysomnography is not routinely used in the assessment of insomnia It is cated when the insomnia complaint is more so related to poor sleep quality, rather than diffi culty with sleep initiation or maintenance [ 5 ] In this case, it serves in identifying common disrupters of sleep quality, i.e., sleep-related breathing disorder

indi-or periodic limb movement disindi-order It provides valuable infindi-ormation when sleep state misperception or paradoxical insomnia is suspected It is also indicated when initial diagnosis is uncertain, the treatment fails, or precipitous arousals occur with violent or injurious behavior

Multiple Sleep Latency Test

It is an EEG-based clinical tool to assess sleep tendency during daytime after a standard night sleep in the laboratory and provides supportive evidence in the diag-nosis of narcolepsy/hypersomnia [ 6 ] It is important to remember that narcoleptics, and despite their daytime sleepiness, has a common complain of insomnia and spe-cifi cally middle insomnia and with frequent nighttime awakening It is usually done after previous night polysomnogram The subject is given a series of 4–5 nap oppor-tunities The MSLT is used to evaluate patients with suspected narcolepsy and also suspected idiopathic hypersomnia, but not routinely indicated in the initial evalua-tion and diagnosis of obstructive sleep apnea syndrome, or in assessment of change following treatment with nasal continuous positive airway pressure (CPAP) The MSLT is not routinely indicated for evaluation of sleepiness in medical and neuro-logical disorder (other than narcolepsy), insomnia, or circadian rhythm disorders

4 Johns MW A new method for measuring daytime sleepiness: the Epworth sleepiness scale Sleep 1991;14(6):540–5

5 Littner M, Hirshkowitz M, Kramer M, Kapen S, Anderson WM, Bailey D, Berry RB, Davila D, Johnson S, Kushida C, Loube DI, Wise M, Woodson BT Practice parameters for using poly- somnography to evaluate insomnia: an update Sleep 2003;26(6):754–60

6 Littner MR, Kushida C, Wise M, Davila DG, Morgenthaler T, Lee-Chiong T, Hirshkowitz M, Daniel LL, Bailey D, Berry RB, Kapen S, Kramer M Practice parameters for clinical use of the multiple sleep latency test and the maintenance of wakefulness test Sleep 2005;28(1): 113–21

© Springer International Publishing Switzerland 2015

R.K Malhotra (ed.), Sleepy or Sleepless, DOI 10.1007/978-3-319-18054-0_10

Assessment and Management of Insomnia

Edward D Huntley and J Todd Arnedt

Insomnia is a common disorder characterized by persistent sleep diffi culties despite adequate opportunity and circumstances for sleep accompanied by impairment in daytime functioning This chapter reviews assessment procedures for insomnia with

an emphasis on insomnia as a diagnostic entity that is a subjective and 24-h disorder diagnosed through clinical observations of symptoms In addition, this chapter reviews the clinical management of insomnia discussing both non-pharmacological and pharmacological interventions The effi cacy, durability, and limitations of these interventions are also reviewed

Prevalence rates for insomnia vary according to diagnostic criteria applied [ 1 ] with approximately 30 % of the US general population [ 2 ] reporting clinically sig-nifi cant symptoms of insomnia These estimates are higher in primary care popula-tions with up to 50 % reporting insomnia symptoms; however, only approximately

5 % of these patients seek treatment [ 3 ] Diffi culty maintaining sleep (e.g., diffi culty returning to sleep after awakenings) is the most common insomnia symptom, reported in approximately 35 % of the general population However, a combination

of symptoms is the most common clinical presentation [ 6 8 ], and those with bined symptoms tend to have the greatest impairment [ 4 ] The prevalence rate of insomnia based on a frequency of symptoms of 3 or more days a week with at least

com-a 1-month durcom-ation is com-approximcom-ately 15 %, com-and this rcom-ate decrecom-ases to 11 % com-after accounting for daytime impairment (e.g., fatigue, impaired work performance,

Sleep and Chronophysiology Laboratory, Behavioral Sleep Medicine Program, Department

of Psychiatry and Neurology , University of Michigan Health System ,

4250 Plymouth Road , Ann Arbor , MI 48109-2700 , USA

cognitive complaints, emotional disturbance, and social/relationship dysfunction) and decreases further to 6 % when based on DSM-IV diagnostic criteria [ 5 ] Insomnia is associated with signifi cant societal costs including reduced quality

of life, decrements in perceived health, impaired role functioning, increased risk for new psychiatric and substance use disorders, and exacerbation of comorbid health conditions [ 6 10 ]

The economic impact of chronic insomnia is also signifi cant In the place, the association of insomnia with presenteeism (low on-the-job work per-formance) is equivalent to 11.3 work days annually, and insomnia increases the risk of both workplace and non-workplace injuries [ 11 , 12 ] Workers with insom-nia also miss work twice as often, have a threefold greater risk of serious road accidents, and report lower work effi ciency and job satisfaction than good sleeper controls [ 13 ] Moreover, the average 6-month direct and indirect costs for adults with untreated insomnia are estimated to be at least $1,100 greater than for adults without insomnia [ 14 ]

work-Sociodemographic characteristics are associated with insomnia prevalence, symptom profi les, and use of prescription medications to treat insomnia Women report higher rates of insomnia relative to men, are twice as likely to be diagnosed with insomnia [ 1 ], and are more likely to report using prescription medication to treat their symptoms [ 15 , 16 ] Insomnia prevalence is relatively stable from the

years and older reporting more sleep maintenance problems and decreased time impairment compared to younger age groups Daytime consequences of insomnia may be underreported in retired individuals, disabled individuals, or individuals who live alone because impairments are less likely to be noticed and commented on by others Adults 65 years or older also tend to report greater use

day-of prescription medication for insomnia [ 15 , 16 ] Taken together these data cate that women and adults who are middle aged or older are likely to be seen in consultation for insomnia

Psychiatric and chronic health conditions are associated with the prevalence of insomnia symptoms and highlight the importance of completing a comprehensive medical and psychiatric history as part of an insomnia evaluation Preexisting depression, anxiety, and chronic pain predict insomnia at 3-year follow-up with relative risks of 3.8, 2.6, and 1.8, respectively Moreover, preexisting insomnia pre-dicts anxiety and depression at 3-year follow-up with relative risks of 2.1 and 1.9, respectively [ 17 ] Individuals experiencing depression and insomnia generally fare worse than people with depression only, and it is common for patients to continue

to report insomnia after successful treatment of their depression [ 18 ] Therefore, insomnia is a signifi cant risk factor for new onset [ 19 ], relapse, and recurrence of depression [ 20 ] These data highlight the bidirectional relationships of insomnia with other health conditions and suggest that insomnia may be a residual symptom that puts individuals at greater risk of relapse

Models of Insomnia

There are several models of insomnia including behavioral [ 21 , 22 ], psychological [ 23 , 24 ], and neurobiological [ 25 ], but the most widely used heuristic is Spielman’s 3-P model of insomnia [ 26 ] This model posits that genetic, physiological, or psycho-

Identifi ed inherent characteristics considered predisposing factors include a familial history of light or disrupted sleep and psychological characteristics such as a ten-dency to worry excessively and disproportionate concern with personal health or

well-being Precipitating factors include environmental, physiological, or

psycho-logical stressors that exceed a hypothetical threshold of insomnia symptom severity

to initiate an acute episode of insomnia Some examples of precipitating conditions include physical stressors (e.g., acute illness, pain), psychiatric stressors (clinical depression, mania), or social stressors (either positive or negative) Once insomnia

has been initiated, environmental, physiological, or psychological factors perpetuate

and maintain insomnia symptoms over time, even after the original precipitating

event has resolved or has been effectively managed The perpetuating factors that have received most attention include the practice of nonsleep activities in the bed-room (e.g., use of electronic media in bed, eating in bed), the tendency to stay in bed while awake, and the tendency to spend excessive amounts of time in bed (i.e., sleep extension by going to bed earlier or getting out of bed later or napping); efforts to deal with the consequences of insomnia (e.g., excessive caffeine intake); and pre-sleep cognitive arousal including negative sleep-related beliefs and attitudes (e.g., worry about inability to sleep and daytime consequences as a result of sleep loss, unrealistic sleep expectations) Clinical research has primarily focused on developing interventions targeting perpetuating factors, with sleep restriction addressing exces-sive time spent in bed, cognitive therapy addressing cognitive arousal, and stimulus control targeting nonsleep activities in the bedroom and time awake in bed The 3-P model is a useful heuristic that can be used to provide patients with a rationale for psychological interventions and to identify potential targets for intervention

Assessment

Clinical assessment of insomnia should consist of a comprehensive review of the patient’s sleep history and medical and psychiatric history to establish the course of insomnia including predisposing, precipitating, and perpetuating factors as well as medical and psychiatric comorbidities The patient’s sleep history should character-ize specifi c insomnia complaints (e.g., onset, duration, frequency, severity), pre-sleep conditions (e.g., presleep activities, bedroom environment), an evaluation of sleep-wake patterns, daytime impairment, and other sleep-related symptoms [ 27 ]

A thorough history of alcohol and drug use as well as prescribed and counter medications is necessary Given that psychiatric comorbidities are common

over-the-in over-the-insomnia presentations, the timover-the-ing and dose of psychiatric medications is necessary to be determined because psychiatric medications taken at night may increase arousal and subsequently interfere with sleep initiation

Sleep diaries are critical for characterizing the subjective experiences of nia patients who generally overestimate sleep onset latency and underreport total sleep time relative to polysomnography [ 28 ] Sleep diaries completed prospectively

insom-by patients are essential tools for both pretreatment evaluation of the nature of insomnia complaints and for monitoring insomnia treatment progress (Fig 10.1 ) Consensus recommendations for standardizing the format of sleep diaries, instruc-tions to patients, and key variables have recently been proposed [ 29 ] Generally 2 weeks of baseline sleep diary data will help to identify sleep-wake patterns and associated variability, and these data can be used to guide appropriate interventions [ 30 ] Although sleep diaries provide an abundance of critical data, clinicians should

be aware they do not provide a complete description of patient-relevant sleep plaints and should be supplemented with additional dimensional measures

Symptom inventories provide clinicians with dimensional measures of frequency and severity, which provide necessary information to inform accurate diagnosis and assessment of response to clinical intervention Insomnia symptom severity can be quantifi ed by using the Insomnia Severity Index (ISI) [ 23 ], a seven-item self-report inventory that reliably identifi es clinically signifi cant symptoms of insomnia (i.e., cutoff scores of 10, 11, and 14 have been identifi ed for community, clinical, and

Fig 10.1 Example of a typical sleep diary

primary care populations, respectively) [ 31 , 32 ], and it can be used to monitor clinically signifi cant change over the course of treatment (i.e., seven-point reduction indicates the minimally important difference to be considered moderately improved; scores ≤7 indicate remission) [ 32 ] The addition of qualitative measures of sleep-

quantify functional impairment and may potentially identify comorbid sleep ders that cause daytime sleepiness Inclusion of brief self-report instruments to

Symptomatology [ 36 ]), anxiety (Generalized Anxiety Disorder scale [GAD-7] [ 37 ]

or the trait subscale of the State Trait Anxiety Inventory [ 38 ]), and PTSD (Life Events Checklist [ 39 ] and the PTSD Checklist [ 40 ]) is warranted given the high rate

of co-occurrence of these disorders with insomnia

Polysomnographic (PSG) testing and actigraphy monitoring are not considered routine assessments for an insomnia evaluation PSG in particular generally does not provide relevant information for confi rming or excluding the presence of insom-nia [ 41 ] However, for patients with a primary complaint of nonrestorative sleep or sleep maintenance insomnia with collateral information from a bed partner regard-ing observations of sleep-disordered breathing, periodic limb movements during sleep, or excessive daytime somnolence, consideration of a PSG is warranted Actigraphy may be helpful in ruling out a circadian rhythm sleep disorder, monitor-ing adherence to treatment recommendations, and assessing objective sleep dura-

actigraphy may be useful in cases of sleep state misperception (also known as doxical insomnia), a condition characterized by objectively normal sleep duration, continuity, and architecture despite patient complaints of gross sleep disturbances and minimal daytime impairment It is noteworthy that individuals with insomnia generally underestimate sleep duration and overestimate sleep onset latency and awakenings relative to good sleepers In addition, individuals with insomnia fre-quently have normal daytime alertness and longer sleep latencies on the multiple sleep latency test [ 43 , 44 ] Taken together these data support the role of physiologi-cal hyperarousal in insomnia

Diagnosis

Diagnostic classifi cation systems are necessary for defi ning criteria used in the diagnosis and treatment of insomnia, facilitate communication between providers, and provide a basis for billing Variability between sleep-wake nosologies refl ects the idiosyncratic nature of classifi cation systems in general and a need to standard-ize a uniform diagnostic classifi cation system Contemporary nosologies describing

sleep-wake disorders (e.g., Diagnostic and Statistical Manual of Mental Disorders , 5th edition (DSM-5) [ 45 ], International Classifi cation of Diseases (ICD-10) [ 46 ],

and International Classifi cation of Sleep Disorders , 3rd edition (ICSD-3) [ 47 ])

characterize insomnia as global sleep dissatisfaction associated with diffi culty initiating or maintaining sleep despite adequate opportunity (e.g., enough time allotted for sleep) and circumstances (e.g., suitable sleep environment) for sleep with clinically signifi cant daytime impairment (e.g., daytime fatigue, psychological distress, cognitive impairment, concerns/worry about sleep) In children, these sleep diffi culties are often reported by a caregiver and may include observations of bed-time resistance or diffi culty sleeping independently (i.e., sleep onset association) without caregiver intervention [ 48 ] Inclusion of an adequate opportunity and cir-cumstances for sleep differentiates insomnia from sleep deprivation Epidemiological and longitudinal studies support the DSM-5 and ICSD-3 specifi cation of sleep dif-

fi culties occurring with a frequency of at least three nights a week [ 5 , 49 ] with additional temporal specifi ers included for duration of symptoms including epi-sodic/short- term insomnia (symptoms lasting ≥1 month but <3 months) and persis-

history of recurrent episodes over several years would be subsumed under the sistent/chronic diagnosis given the duration of symptoms It is noteworthy that ear-lier classifi cation systems included nonrestorative sleep (e.g., sleep that is of poor quality or unrefreshing) as an independent insomnia criterion, but these complaints alone do not suffi ce as the sole sleep complaint in current nosologies

Historically within clinical practice insomnia subtypes have been characterized

by the nature of their sleep complaints as early, middle, and late based on perceived diffi culty with sleep initiation, sleep maintenance diffi culty during the night, and sleep maintenance diffi culty at the end of the night, respectively Additional catego-rization schemes of primary versus secondary age of onset (i.e., childhood vs adult) have served as useful heuristics, but they are categorizations of convenience lacking empirical support or biological basis and have yielded low diagnostic reliability [ 51 ,

52 ] Classifi cation of insomnia based on objective sleep duration has yielded haps a viable means of distinguishing insomnia subtypes Insomnia with objective short sleep duration (i.e., <5–6 h of objective sleep) is associated with cognitive- emotional, cortical, and physiological hyperarousal and health problems including diabetes, hypertension, increased mortality, and neuropsychological defi cits [ 53 ] relative to insomnia with longer sleep duration (i.e., >6 h of objective sleep) It is noteworthy from a clinical perspective that individuals reporting short sleep dura-tions of 4 h or less are at high risk for early termination of group or individual therapy [ 54 ]

sleep phase type, are characterized by sleep diffi culties arising from misalignment between preferred sleep schedules and the endogenous circadian rhythm Delayed sleep phase type is differentiated from insomnia because individuals with insomnia feel sleepy at their desired bedtime but are unable to sleep regardless of their bed and rise times whereas an individual with delayed sleep phase type will report nor-mal sleep duration with little to no sleep initiation or maintenance complaints when allowed to sleep on their internally preferred schedule Delayed sleep phase type is more common among adolescents and young adults Individuals with insomnia report sleep maintenance problems and early morning rise times regardless of sleep schedule whereas sleep duration and continuity is normal for an individual with advanced sleep phase type when sleeping in phase (i.e., early bed and wake time) Advanced sleep phase type is more common in older adults than children or young adults A differential diagnosis may be enhanced by having patients complete self-reported circadian rhythm characteristics such as the Horne and Östberg

Questionnaire (MCTQ) [ 56 ] Insuffi cient sleep syndrome is differentiated from insomnias by the presence of excessive daytime somnolence, which is not typical in chronic insomnia In addition, the chronic sleep restriction associated with insuffi -cient sleep syndrome is volitional whereas those with chronic insomnia have reduced total sleep times due to sleep initiation and maintenance problems in the context of adequate opportunity and circumstances for sleep Finally, as discussed above, other sleep disorders including sleep-disordered breathing and periodic limb movement disorder may manifest as sleep maintenance problems, and restless legs syndrome may contribute to sleep initiation or maintenance complaints

Treatment

Pharmacological Interventions

Nationally representative samples of adults in the USA indicate use of prescription medication to treat insomnia has increased over time [ 15 , 57 ] with approximately

3 % of adults reporting the use of medication to treat insomnia symptoms [ 15 ] and

Hypnotics remain fi rst-line treatments for chronic insomnia in primary care because they are widely available, are easy to prescribe, provide immediate symptomatic relief, and are effi cacious in the short term [ 58 ] When addressed in primary care settings, insomnia is typically treated with FDA-approved hypnotics including ben-zodiazepine receptor agonists, nonbenzodiazepine receptor agonists, melatonin receptor agonists, antihistamines, and antidepressants [ 59 – 64 ] (Table 10.1 ) Benzodiazepine and nonbenzodiazepine receptor agonists generally have similar effi cacy on PSG and sleep diary outcomes [ 65 ] Several medications with sedating properties used to treat anxiety, depression, and seizures are commonly used off-label to treat insomnia, however, effi cacy data is limited [ 59 ] Patients often seek

over-the- counter medications containing antihistamines or natural products (e.g., melatonin, L -tryptophan, valerian), but the FDA does not regulate herbs and supple-ments; therefore, patients may be unaware that the dose and purity of a given product

is not monitored Over-the-counter medications and supplements are generally not recommended due to limited effi cacy and safety data [ 27 ] Available data on antihis-tamines suggests that tolerance to these medications likely develops quickly [ 66 ]; therefore, use should be short term The limited evidence for evaluating exogenous melatonin for insomnia indicates relatively modest benefi t as refl ected in relatively small effect sizes for reductions in sleep onset latency and increased sleep effi ciency and total sleep time relative to benzodiazepine and nonbenzodiazepine receptor ago-nists [ 60 ] Nonbenzodiazepine receptor agonists (1.23 % of the US population) are the most commonly prescribed medications for insomnia followed by trazodone (0.97 %), benzodiazepines (0.40 %), quetiapine (0.32 %), and doxepin (0.12 %) It is not uncommon to be prescribed additional sedative medications, with one study indi-cating that up to 55 % of patients take an additional sedative hypnotic (e.g., opioid or benzodiazepine) and 10 % take three or more [ 15 ] It is noteworthy that there is no medication prescribed in the USA with FDA approval for use in pediatric patients for the treatment of insomnia, but pediatric patients frequently are prescribed medica-tions off-label to treat insomnia, with antihistamines (33 %), benzodiazepine (26 %), alpha-2 agonists (e.g., clonidine, guanfacine; 15 %), and antidepressants (6 %) com-monly recommended [ 67 ] The timing of medication is also critical for optimal treat-ment, with minimal side effects occurring when taken within close proximity to bedtime However, estimates indicate that up to 20 % of individuals use their hyp-notic medication in the middle of the night [ 68 ] This practice can be quite problem-atic given that an adequate opportunity to sleep is recommended when using hypnotics given their long half-life (e.g., 1.5–100 h for benzodiazepines and 1–6 h for nonbenzodiazepine receptor agonists) Individuals utilizing medication in the middle of the night are vulnerable to next-day hangover effects, including cognitive impairment and psychomotor impairment Furthermore, benzodiazepines carry the risk of tolerance, dependence, and withdrawal effects such as rebound insomnia [ 69 ] Relative to placebo, nonbenzodiazepine receptor agonists and sedating antide-pressants are associated with higher rates of headache, somnolence, dizziness, and

associated with complex sleep-related behaviors such as sleep walking, aggressive behavior, eating, and driving Therefore, care is required in coordinating pharmaco-logical interventions to minimize potentially sedating side effects, which may increase risk of injury

In the short term hypnotics serve as an appropriate measure for treating insomnia complaints However, insomnia is often chronic, making short-term use of hypnotics

a less favorable treatment option In addition, there is limited evidence to support the long-term use of hypnotics with many placebo-controlled studies lasting for only 4 weeks or less in non-elderly adults [ 65 , 70 ] and very few studies lasting 12 months [ 71 – 73 ] Hypnotics may be contraindicated in individuals with medical histories including alcohol or sedative abuse/dependence and untreated sleep apnea [ 74 ] Many patients report a strong desire to discontinue use of hypnotic medications

[ 75 ], and this should be done gradually (e.g., 25 % reduction/week) under the vision of a physician to minimize withdrawal effects (e.g., rebound insomnia)

Non-pharmacological Interventions

Non-pharmacological interventions for insomnia are intended to promote greater control over sleep, reduce emotional distress, reduce variability in sleep schedules, consolidate sleep, and enhance sleep effi ciency These interventions have well- established short-term and long-term effi cacy [ 76 , 77 ] and seem to have fewer side effects [ 78 ] than pharmacological interventions for insomnia Behavioral strategies including sleep restriction therapy and stimulus control therapy (Table 10.2 ) meet established “standard” treatment criteria as defi ned by the American Psychological Association criteria for empirically validated treatments [ 79 ] or consensus recom-mendations made by the American Academy of Sleep Medicine as effective and evidenced-based interventions for insomnia [ 80 ] These strategies are typically combined and supplemented with cognitive therapy and sleep education as a multi-component cognitive behavioral therapy for insomnia (CBT-I), which is often con-

effi cacy of non-pharmacological interventions has been reviewed in several meta- analyses [ 76 , 77 , 82 – 85 ] which have consistently indicated that 50–70 % of treated patients benefi t from intervention with medium to large effect sizes observed for sleep onset latency, wake time after sleep onset, sleep effi ciency, and sleep quality ratings (Fig 10.2 ) Effect sizes for total sleep time at the end of intervention are small but improve during follow-up periods with medium effect sizes [ 82 , 84 , 85 ] Initial treatment gains maintained during follow-up periods for as long as 2–3 years [ 78 , 86 , 87 ] Although CBT-I yields effective changes in sleep, categorical response and remission treatment outcomes are diffi cult to determine because no universally accepted criteria have been established [ 30 ] Several trials have utilized the ISI [ 88 – 90 ], sleep effi ciency >85 % [ 87 ], or a combination of sleep effi ciency and sleep quality ratings [ 91 ], with overall report of response rates of 52–65 % and remission rates of 32–55 % [ 89 – 91 ] Indeed the establishment of guidelines will guide clinical practice and future effectiveness trials The evaluation of treatment outcomes has also unfortunately focused primarily on sleep-related variables rather than daytime functioning, a cardinal feature of insomnia and a principal factor infl uencing those seeking treatment It is critical to evaluate daytime functioning to further assess response and remission, and the use of an instrument like the PROMIS Sleep- Related Impairment questionnaire may help evaluate response and remission multidimensionally

The effi cacy and safety of CBT-I have been documented not only in numerous controlled trials of patients with primary insomnia but also in patients with insom-nia and co-occurring conditions commonly seen in primary care, such as depression and other psychiatric disorders [ 92 , 93 ], chronic pain [ 94 – 96 ], breast cancer [ 97 ,

98 ], and hypnotic dependence [ 75 ] Head-to-head comparisons of CBT-I and

Table 10.2 Non-pharmacological interventions for insomnia

Technique

Recommended

the bed/sleep environment with sleep rather than sleep-incompatible behaviors (e.g., boredom, frustration, or worry at not being able to sleep) and

to reestablish a consistent sleep/wake schedule

patient’s time in bed is limited to the total sleep time derived from 1 to 2 weeks of sleep diary Time

in bed is subsequently titrated up or down based on response to intervention, and minimum time in bed

is generally never less than 5 h and is applied

fl exibly based on acceptance and adherence to treatment Prohibits naps at times other than the assigned time in bed

Relaxation

training

intrusive thoughts at bedtime interfering with sleep Common techniques include diaphragmatic breathing, progressive muscle relaxation, meditation, mindfulness, and imagery Cognitive

behavioral

therapy for

insomnia (CBT-I)

sleep restriction, relaxation) and cognitive interventions

Paradoxical

intention

preoccupation with the effort and ability to sleep that is believed to precipitate an aroused state incompatible with sleep Patients are instructed to remain passively awake without any effort to fall asleep rather than trying to fall asleep This strategy

is repeated as necessary if patient awakens during the night

to help patients learn to control a physiological parameter (e.g., muscle tension, EEG) to reduce somatic arousal

Cognitive therapy No recommendation Strategies aimed at challenging and changing

dysfunctional attitudes and beliefs, misconceptions about sleep, and beliefs about insomnia and its perceived daytime consequences that contribute to emotional distress and further sleep problems Sleep hygiene

therapy

No recommendation Guidelines about healthy sleep practices (e.g., diet,

exercise, substance use) and environmental factors (e.g., light, noise, temperature) that may promote or interfere with sleep Typically includes

psychoeducation about normative sleep and changes in sleep patterns associated with aging

macotherapy found that ratings of sleep quality were equivalent or better for CBT-I treated patients at posttreatment and superior 1 and 6 months following treatment [ 78 , 99 ] Although smaller in magnitude, improvements in objective sleep quality measured by actigraphy [ 91 ] and polysomnography [ 87 , 90 ] have also been consis-tently found with CBT-I CBT-I offers several potential advantages over pharmaco-therapy, including greater patient preference [ 81 , 100 ], equal to superior outcomes after 6–8 weeks of therapy [ 78 , 99 , 101 ], more evidence of sustained treatment effi cacy (e.g., [ 86 , 87 ]), fewer adverse side effects and contraindications, and no concerns about drug interactions However, sleep restriction therapy, a common component of CBT-I, may increase somnolence and decrease psychomotor vigilance [ 102 ] Therefore, it is recommended that providers advise patients to exercise cau-tion when engaging in sleep-sensitive tasks (e.g., driving, operating machinery) Moreover, providers are also encouraged to consider the limitations of CBT-I’s pri-mary behavioral components, sleep restriction, and stimulus control for individuals with conditions that may be exacerbated by sleep resection, including bipolar disor-der, epilepsy, parasomnias, and psychotic disorders Also stimulus control may not

be appropriate for individuals who are disabled, cannot get out of bed easily sisted, or are at risk of accidental injury

Despite several strengths, dissemination of CBT-I is limited by the dearth of clinicians trained to deliver these interventions [ 103 ], access to sleep disorders cen-ters, and cost Relative to pharmacotherapy, CBT for insomnia is perceived to be more burdensome, with a typical course requiring 5–6 face-to-face sessions over a 6–7-week period [ 77 ] Another signifi cant barrier is that providers trained to deliver CBT-I are typically not located in primary care Instead, patients who prefer CBT-I over hypnotics must fi nd one of the few qualifi ed providers in the country (fewer

0.0

Post treatment Follow up

0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9

Fig 10.2 Mean effect size estimates (Cohen’s d ) of sleep diary parameters derived from meta-

effects, respectively SOL indicates sleep onset latency, FNA indicates frequency of nocturnal awakenings, WASO indicates wake after sleep onset time, TST indicates total sleep time, and SE

indicates sleep effi ciency

than 200 providers are certifi ed in Behavioral Sleep Medicine nationwide [ http://www.absm.org/BSMSpecialists.aspx ], a designation that denotes expertise in CBT for insomnia), most of whom are located in departments of psychology/psychiatry

or affi liated with sleep disorders centers in major urban areas Finally, CBT-I

is often criticized as being more costly than pharmacotherapy Using 2002 reimbursement rates, one study estimated that 8 weeks of group (4–6 patients) CBT-I costs $279.92 compared with $255.30 for 100 tablets of zolpidem 10 mg These estimates predate the availability of zolpidem in generic form, meaning that short-term medication costs are substantially lower On the other hand, they also fail

to consider that CBT-I is time limited whereas hypnotic use frequently exceeds 8

analyses of available insomnia therapies despite the importance of such information [ 105 ] Addressing these major barriers—treatment modality, provider, and cost—is likely critical for CBT-I to be adopted as a fi rst-line insomnia therapy

Efforts to increase CBT-I have focused primarily on altering treatment modality and, in some cases, reducing treatment length For example, Buysse and colleagues [ 91 ] found that a behaviorally focused intervention administered during two face-to- face sessions and two telephone calls produced a 67 % response rate and 55 % remission rate among a sample of older adults with chronic insomnia Treatment gains were maintained at 6-month follow-up Alternate CBT-I modalities studied include written materials [ 106 – 109 ], telephone [ 88 ], television- and video-delivered therapy [ 110 ], and Internet-based interventions [ 111 – 114 ] Written and media- based interventions without therapist involvement have generally produced small to moderate sleep and daytime symptom improvements in community-dwelling adults with chronic insomnia [ 107 , 108 , 115 ] One exception is a recent study that found telephone-delivered therapist support of bibliotherapy resulted in a 61 % insomnia remission rate for adults with insomnia, compared to 24 % for bibliotherapy alone [ 109 ] Telephone-delivered CBT produces effect sizes on sleep and daytime symp-toms equivalent to face-to-face randomized controlled CBT trials [ 77 , 82 , 88 , 101 ]

of adults with chronic insomnia Several recent studies have evaluated Internet- delivered CBT-based insomnia treatments [ 111 – 114 , 116 – 119 ] One study randomized 164 adults with chronic insomnia to a six-session CBT-based web pro-gram, imagery relief therapy (active control), or treatment as usual More than half

of CBT-I participants completed treatment with a sleep effi ciency index above 85 % (within normal limits), compared to only 17 % and 8 % of the imagery rehearsal therapy and treatment as usual participants, respectively Posttreatment effects of CBT-I on daytime symptoms relative to the two control conditions were more mod-

est (Cohen’s d = 0.32–0.72) Sleep treatment gains were sustained at 8-week

up Findings from other studies of web-based insomnia interventions have been mixed for both sleep and daytime measures, some have suffered from high attrition [ 111 ], and web-based interventions may be more appropriate for less severe patients and those without comorbid disorders [ 120 ] In addition, web-based treatment pro-grams are likely to pose challenges to integrate fully into primary care practices There has been increasing recognition of the importance of economic data to evaluate the impact of untreated insomnia and the potential cost savings with treat-

ment [ 58 , 104 , 121 – 123 ] To date, very few studies have considered the cost- effectiveness of insomnia treatment [ 124 – 127 ] Only one UK-based study conducted

a cost utility analysis of CBT for insomnia Two hundred and nine patients with chronic insomnia who were chronic hypnotic users (mean = 13.4 years) received a six-session CBT-I treatment and were followed up at 3, 6, and 12 months posttreatment Using 1999/2000 pricing, the mean incremental cost per quality-adjusted life- year (QALY) after 6 months was £3,418 (equivalent to US$5,527 in 1999), a fi gure that is easily within the range considered to represent good value

In addition, the total cost of service provision was £154.40 (USD $249.68 in 1999) per patient [ 127 ] The study did not include an active control group, so no conclu-sions can be reached about the relative value of CBT-I treatment compared to other available treatments

Future Directions

Insomnia is a common health concern that is often underdiagnosed and subsequently treated This chapter reviewed the range of effective pharmacological and non- pharmacological treatments currently available Future research charactering the effectiveness of these interventions and mechanisms associated with therapeutic effects will likely continue to infl uence clinical practice To that end, dismantling studies evaluating individual components of CBT-I may help to match individual treatment components to patient populations One example of this in older adults found that stimulus control alone, sleep restriction alone, and multicomponent behav-ioral therapy were equally effi cacious [ 89 ] This study highlights the utility of single components as well and combined approaches for older adults with insomnia Similar studies are clearly needed in larger, more diverse samples to help move insomnia treatment away from a one-size-fi ts-all approach to a more personalized one

A growing line of research has evaluated the combination of pharmacological and non-pharmacological interventions [ 87 , 90 , 128 ] with data indicating that add-ing medication to CBT-I produces faster improvement in total sleep time, wake after sleep onset, and sleep effi ciency than CBT-I alone in the acute treatment phase [ 128 ] Although the faster treatment response did not predict a better clinical out-come, there may be several reasons to consider augmenting CBT-I with medication Medication in the acute phase of treatment may provide quicker symptom relief by reducing nightly variability in sleep This benefi t may in turn increase the accept-ability of behavioral interventions that are often challenging to implement in the early stages of treatment Considering medication and CBT-I may be particularly relevant for individuals with objective short sleep durations who are at increased risk for signifi cant medical sequelae [ 129 ] and early treatment termination [ 54 ] The durability of such a combined approach is unknown, and studies with longer treat-ment follow-up intervals (e.g., 6 and 12 months) are needed Caution with this approach is warranted as it is possible that the addition of a hypnotic medication

may increase daytime somnolence and decrease psychomotor vigilance when bined with sleep restriction

Although current data indicate that a majority of patients with insomnia will respond and remit to non-pharmacological interventions, clearly a signifi cant pro-portion of patients fail to respond This reality indicates a need for novel strategies

to augment existing interventions Likewise increased focus on daytime functioning

is warranted, and the use of activity monitors like the Fitbit ® , which can interface with smartphone or web-based applications, has the potential to cost-effectively monitor 24-h activity and provide valuable information to clinicians and patients

Integration of such a device has the potential to augment CBT-I by providing a means to extend data collection, reduce patient burden, and increase access to certi-

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© Springer International Publishing Switzerland 2015

R.K Malhotra (ed.), Sleepy or Sleepless, DOI 10.1007/978-3-319-18054-0_11

Sleepless Patient: Circadian Rhythm

Sleep–Wake Disorders

Hallie Kendis and Phyllis C Zee

Multiple factors, including genetics, behavior, environment, and specifi c sleep disorders, can contribute to sleeplessness and excessive sleepiness in patients Thus,

it is essential to inquire about sleep habits, sleep and work environments, tions, medical comorbidities, and specifi c sleep disorders such as insomnia, sleep apnea, restless legs syndrome, and disorders of the circadian system Disturbance in circadian timing can have profound effects on the quality and quantity of sleep across the 24-h day

This chapter will focus on approach to the diagnosis and management of dian rhythm sleep–wake disorders (CRSWDs) CRSWDs demonstrate a chronic sleep and wake disturbance due to alterations of the circadian timekeeping system

circa-or misalignment between the endogenous circadian rhythm and exogenous factcirca-ors that affect the timing or duration of sleep Common symptoms include insomnia during the attempted sleep period, excessive sleepiness during periods of required wakefulness, or a combination of the two Work and/or home responsibilities, per-formance, participation in social activities, safety, and health suffer due to the

behavioral and environmental factors affect the clinical manifestation of these orders Figure 11.1 shows a schematic representation of the primary CRSWDs Circadian rhythms are endogenous and genetically regulated and persist in the absence of external time cues with a period of approximately 24 h A central pace-maker located in the paired suprachiasmatic nuclei (SCN) of the anterior hypothala-mus regulates and coordinates the timing of nearly all physiological processes

H Kendis , M.D

Northwestern University Feinberg School of Medicine , Chicago , IL USA

P C Zee , M.D., Ph.D (*)

Sleep Disorders Center, Center for Circadian and Sleep Medicine,

Northwestern University Feinberg School of Medicine , 710 North Lake Shore Drive,

Suite 520 , Chicago , IL 60611 , USA

Information from the suprachiasmatic nucleus is sent to other areas of the brain and peripheral organs to synchronize the function of the peripheral oscillators located in these tissues In addition to the sleep–wake cycle, the SCN regulates and coordi-nates nearly all physiologic and behavioral processes Therefore, when there is a disruption of the circadian system and/or misalignment between the timing of the endogenous rhythm and external environment, not only are sleep disturbances apparent, but metabolic, cardiovascular, immunological, hormonal, gastrointestinal, cognitive functions can be impaired [ 2 ]

The light–dark cycle is the strongest synchronizing agent for the circadian tem The SCN receives afferent light input primarily from the melanopsin contain-ing retinal ganglion cells of the retina via the retino-hypothalamic tract [ 3 , 4 ]

sys-In humans, light exposure prior to the core body temperature minimum (evening) produces delays, while light pulses after the core body temperature minimum (early morning) produce advances [ 5 ] In addition to light, the SCN also receives internal signals from the pineal gland, via the nocturnal release of melatonin Endogenous melatonin release begins to rise 2–3 h before sleep onset and peaks in the middle of the night Opposite to the effects of light, melatonin during the early morning induces delays in circadian rhythms, while melatonin during the early evening induces advances [ 6 , 7 ] Normal release of melatonin involves a projection from the hypothalamus, through the cervical spinal cord, and back to the pineal Through timed activation by these synchronizing or entraining agents, the circadian clock can make daily adjustments to maintain synchronization (entrainment) with the external light–dark cycle and social and work schedules

Fig 11.1 Schematic representation of the primary CRSWDs

Circadian Rhythm Sleep–Wake Disorders

General Evaluation

Evaluation of patients with suspected CRSWD requires a thorough sleep and medical history Evaluation of sleep–wake patterns with sleep diary and actigraphy monitoring is recommended for all CRSWDs for at least 1–2 weeks Longer moni-toring may be helpful when the sleep–wake rhythm is unstable In addition, in patients in which the diagnosis is unclear or who have extreme sleep and wake times, more accurate biomarkers of circadian timing, such as the rhythm of endog-enous melatonin, are recommended when possible

Melatonin can be measured via plasma, saliva, or urine, though commercially available salivary kits are the most practical method in the clinical setting [ 8 ] Because bright light exposure can suppress melatonin secretion, sampling has to be done in dim light or dark conditions starting 5–6 h before habitual sleep onset time The timing of dim light melatonin onset (DLMO) is an excellent marker for the tim-ing of circadian rhythms There are different methods for determining DLMO The most common are fi xed thresholds of 3 pg/mL in salivary samples or 10 pg/mL in serum samples Using a relative threshold that is two standard deviations above the baseline may be more accurate as baseline melatonin levels can vary from one per-son to another [ 9 ] Figure 11.2 shows a general approach to the evaluation of patients with CRSWDs

Fig 11.2 Symptoms of insomnia or excessive daytime sleepiness

General Treatment Approach

The overall goal of treatment of CRSWD is to improve sleep quality, daytime formance, health, and safety of patients by utilizing a multimodal program that involves behavioral, environmental, and pharmacologic approaches aimed to syn-chronize the endogenous rhythm with that of the external environment All patients should be educated on good sleep hygiene practices, including structuring sleep and wake times and maintaining a dark sleep environment In addition, timed exposure

per-to light and dark, as well as administration of exogenous melaper-tonin, can reset the timing of circadian rhythms It is important to keep in mind that depending on the time of exposure, these agents can advance or delay the phase of circadian rhythms, for example, melatonin given in the late afternoon to early evening (5–6 h before DLMO will advance circadian rhythms [ 7 , 10 , 11 ]) In contrast to melatonin, expo-sure to bright light in the evening (prior to DLMO) will delay circadian rhythms, and exposure in the morning will advance the rhythm Table 11.1 shows a summary

of the treatment approaches for CRSWDs

Table 11.1 Circadian rhythm sleep disorders and their treatments

• Oral melatonin dosed 5–7 h prior to habitual bed time

• Bright light therapy for 1–2 h prior to habitual wake time Advanced

• Blind: oral melatonin 1 h prior to bed time

• Sighted: morning bright light therapy in addition to evening melatonin Irregular

sleep–wake

rhythm disorder

(ISWRD)

• Increase daytime light and activity

• Avoid nighttime light

• Children: oral melatonin in the evening

• Elderly: combination of evening melatonin and morning bright light therapy

Shift work

disorder (SWD)

• Naps before night shift or during shift if possible

• Bright light, intermittent caffeine, modafi nil/armodafi nil at the beginning of the shift

• Avoid bright light at the end of the shift and during the commute home

• Melatonin in the morning and/or hypnotics prior to sleep time

in the mid to late morning; oral melatonin in the evening

• Westward travel: bright light exposure in the early evening, avoid bright light in the morning

Case 1 A 20-year-old female college student has nearly daily diffi culty falling asleep for the past 2 years, but has become more pronounced about 6 months ago She reports that most nights she goes to bed by midnight, but lies in bed for 2–4 h before falling asleep Once asleep, however, she sleeps uninterrupted until her alarm goes off for class at 8 am She hits the snooze button several times as she has signifi -cant diffi culty getting up this early She is very sleepy and often dozes on and off during her fi rst two classes She is struggling in school and has had to drop out of two classes last semester On weekends and when she visited her parents during winter break, she would go to bed about 2 am and would generally be asleep by 3 am and would wake up between 10 am–noon Although she felt a lot better, she was unproductive She had tried melatonin which only sometimes helped her fall asleep

Delayed Sleep–Wake Phase Disorder

Defi nition

Delayed sleep–wake phase disorder (DSWPD) is an alteration in the circadian rhythm in which the phase of the major sleep period is delayed in relation to the required sleep and wake times This is manifested by a chronic or recurrent com-plaint of inability to fall asleep at a desired conventional clock time together with the inability to awaken at a desired and socially acceptable time for at least 3 months When able to choose their preferred schedule, patients generally exhibit normal sleep quality and duration and maintain stably delayed sleep and wake times Lastly the sleep disturbance is not better explained by another sleep disorder, medical or neurological disorder, mental disorder, medication use, or substance use disorder [ 1 ]

In addition to alterations in sleep timing, comorbidities including anxiety and sion, increased substance use, and lower grades in school have been reported [ 12 ]

polymorphisms in the hPer3 gene, involved in control of the circadian rhythm, have been associated with a delayed sleep phase [ 14 ] Alterations in response to light, resulting in increased sensitivity during the evening or a decreased sensitivity in the morning, can result in a chronic delay in the phase of circadian rhythms Most impor-tantly behaviors may exacerbate these changes as an individual with DSWPD will likely have increased exposure to light at night as they remain awake later and low levels of morning light as their wake time is delayed [ 12 , 15 , 16 ] These self- selected light and dark cycles can exacerbate and help perpetuate the delayed sleep phase The sleep architecture of DSWPD subjects who sleep at their preferred times is thought to be normal for age However, the delayed phase alters the timing of both REM sleep and slow wave sleep, making it more diffi cult to awaken for early morn-ing commitments [ 12 ]

Diagnosis

Diagnosis is made based primarily on a careful clinical history of chronic inability

to fall asleep at night and diffi culty waking up in the morning that interferes with daytime functioning In addition, documentation of a delayed sleep–wake rhythm

by at least 7 days (preferably for 14 days) of sleep log and actigraphy monitoring (if available) is required Questionnaires can also be helpful to delineate an individual’s circadian chronotype Patients with DSWPD are typically evening types If the sleep log or actigraphy does not clearly document a delayed pattern, other biomark-ers, such as salivary melatonin, can be collected for more objective data to confi rm the delayed circadian phase

Treatment

Treatment should be individualized to the patient depending on the magnitude of the phase delay as well as the timing of morning and early evening responsibilities First-line therapy includes improving sleep hygiene, adherence to a structured sleep and wake schedule (including on nonwork days), avoiding bright light in the eve-ning, and increasing light exposure in the morning [ 17 ] However, behavioral and

DSWPD Due to the comorbidity with depression and anxiety disorders, it is tant to consider the contribution of mood disorders in the treatment plan

The fi rst documented successful specifi c treatment was chronotherapy This entailed delaying sleep by 3 h nightly until the patient reached the goal bedtime Although this is effi cacious, it is diffi cult to maintain More practical treatments include a combination of timed bright light therapy and oral low-dose melatonin intake Bright light exposure shortly upon awakening in the morning can help advance the timing of sleep and wake cycles, whereas exogenous melatonin in the evening has been shown to advance sleep onset time and wake time Timing of the

melatonin dose is important in infl uencing the effect size [ 10 ] For a larger advance, the dose should be taken about 5–6 h prior to DLMO or 7 h before sleep onset time [ 7 , 18 , 19 ] For example, in the case presented, the patient falls asleep between 2 and

3 am and wakes up naturally between 10 am and noon Light exposure should begin

at approximately 9 am, and then the timing can be advanced gradually over 1–2 weeks until the desired wake up time is achieved If melatonin treatment is chosen for this patient, low dose between 0.5 and 3 mg should be administered at approxi-mately 8 pm Combined therapy with bright light and melatonin may be more effec-tive than alone and also reduce subjective sleepiness, fatigue, and cognitive dysfunction over time [ 17 ]

Case 2 A 66-year-old female presents to her physician for chronic early morning awakening that is now signifi cantly reducing her sleep duration and leading to day-time impairment She continues to teach and has to be at school from 7:30 am until

4 pm She needs to wake up by 6 am to have time to prepare, but for the past 7 months, she wakes up naturally between 3 and 4 am She will try and lie in bed and

go back to sleep Most of the time, she will just get up after an hour of trying to fall asleep or if able to fall back to sleep, sleep is very light She is getting on an average week about 4–5 h of sleep at night In the evenings, she is exhausted and can prob-ably fall asleep after dinner (7 pm), but forces herself to stay up to spend time with her husband until about 10:30 pm She has no diffi culties falling asleep On non-work days, she takes a nap at 1 pm for about an hour She denies snoring or gasping arousals, witnessed apneas, discomfort in her legs, or any abnormal behaviors in sleep She does not endorse any symptoms of depression

Advanced Sleep–Wake Phase Disorder

Defi nition

In contrast to DSWPD, patients with advanced sleep–wake phase disorder (ASWPD) demonstrate a stable sleep schedule that is several hours earlier than desired sleep time and interferes with their daytime responsibilities Sleep disturbances include diffi culty staying awake until the desired bedtime and diffi culty maintaining sleep until desired wake time for at least 3 months Similar to individuals with DSWPD, when able to sleep during the preferred sleep times, sleep quality and duration are typically normal [ 1 ]

Prevalence

ASWPD is less common than DSWPD, but may be underreported, as these viduals are less likely to experience occupational disruptions Although the preva-lence in the general population is low, ASWPD is more common among older adults

Pathophysiology

A genetic basis for some familial forms of ASWPD has been identifi ed

These familial cases have polymorphisms in hPer2 and casein kinase 1 delta

genes that shorten the circadian period [ 20 , 21 ] In addition, behavioral and mental exposures can also result in an earlier circadian phase For example, a person with ASWPD is awake during the early morning hours and is more likely to be exposed to early morning light, which advances the timing of the sleep and wake rhythm and perpetuates the problem

Diagnosis

The diagnosis is primarily based on a clinical history of early evening sleepiness and early morning awakening that is associated with impairment in functioning However, if individuals are allowed to sleep during their preferred schedule, the sleep quality and duration are normal for age, but with a stable advanced phase

In addition, current diagnostic criteria require demonstrating an advance in the ing of the major sleep period in relation to the desired sleep and wake times Either sleep logs alone or in conjunction with actigraphy monitoring when possible for at least 7 days (preferably 14 days) are recommended to confi rm the diagnosis The monitoring demonstrates a stable advanced sleep pattern, usually with individual sleep onset time between 6 and 9 pm and rise time between 2 and 5 am Measurement

tim-of the DLMO can also be used to confi rm the diagnosis [ 1 ]

Treatment

The goal of treatment is to improve sleep quality and daytime function by delaying the timing of the sleep–wake cycle to the desired or required schedule General sleep hygiene education, structuring the timing of sleep and wake, and light expo-sure are essential Specifi cally, patients should be advised to avoid exposure to early bright morning light by wearing sunglasses (amber colored to block blue light) until midmorning and increase exposure to evening bright light between 7 and 9 pm (either outdoor natural light or artifi cial indoor light-emitting devices) Although evening bright light (2,500–10,000 lx) therapy is the most common treatment, there

is limited data regarding its effectiveness in patient populations [ 8 22 ] Melatonin

in the morning can delay the phase of circadian rhythms, but evidence is lacking regarding its effectiveness and safety in patients with ASWPD Melatonin can have

a hypnotic effect and caution needs to be used if given in the morning [ 23 ]

Case 3 An 18-year-old male with history of signifi cant anxiety and social phobia ents for evaluation of sleeping diffi culties that have been ongoing for the past 3 years