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Any treatment for insomnia should accomplish3 goals: induce sleep, maintain sleep, and pro-mote functionality the next day. Insomnia treat-ments include behavioral, cognitive, orpharmacotherapy, alone or in combination. Ingeneral, behavioral and/or cognitive therapy

should be part of any first-line approach. Beforeany treatment is administered, it is necessary todetermine the type of insomnia (eg, trouble fallingasleep or trouble staying asleep) in addition toensuring commitment from the patient to makesleep a priority and offer commitment from thehealthcare practitioner to be available for the longterm. This article reviews the available behavioraland cognitive therapies for which there is evi-dence of their benefit (ie, relaxation training, stim-ulus control therapy, sleep restriction, sleephygiene education, and cognitive therapy). Manybehavioral therapies can be conducted by a pri-

mary care practitioner. The article also reviews the3 treatment strategies for pharmacotherapy (ie,antihistamines, -aminobutyric acid receptor ago-nists, and melatonin receptor agonists). A briefdiscussion of newer drug therapies also is includ-ed. The nurse practitioners role is vital in estab-lishing the impact of insomnia on mental andphysical health. Assessing sleep at each visit willcreate a standard that the patient will identify asimperative as other vital signs.(Adv Stud Med. 2006;6(10D):S1033-S1039)

The goal of any treatment for insomniais, essentially, to go to sleep, stay asleep,and feel good the next day. To deter-mine the best treatment for a particularpatient, it is necessary to determine the

type of insomnia (eg, trouble falling asleep or troublestaying asleep), which is best measured by using a sleep

diary for 2 weeks.Insomnia treatments include behavioral, cognitive,

or pharmacotherapy, alone or in combination. In gener-al, behavioral and/or cognitive therapy should be part ofany first-line approach, because not every patient wantsor is willing to take medication for insomnia, and phar-macotherapy may be contraindicated for some patients.Also, as will be discussed, although pharmacotherapy isespecially useful for treating acute insomnia, behavioraland cognitive therapies not only increase the chances oftreatment success but also are more effective at prevent-ing future insomnia episodes.

BEHAVIORALTHERAPY

Behavioral therapy is designed to tighten the rela-tionship between sleep behavior and bedtime. It isaccomplished through establishing rituals that pro-mote better sleep. The disadvantage with behavioraltherapy is that it can take up to 12 weeks or longer toaffect sleep quality.

For a patient to extract the most benefit, behavioraltherapy requires a commitment by the patient to makesleep a priority, specifically to take stock of his or her per-

sonal sleep needs, face up to his or her sleep problems,learn to manage sleep crises, take age into account(because sleep needs differ throughout life), and adopt asleep-smart lifestyle.1 The best and most effective way toimprove sleep hygiene is to adopt a regular schedule, inparticular maintaining a regular sleep schedule 7 days perweek. This can even be written as a prescription for thepatient. Other more regimented therapies include sleeprestriction, stimulus control, and relaxation training.

PROCEEDINGS

TREATMENT OF INSOMNIA*

Nancy Nadolski, FNP, MSN, MEd, RN

*Based on a presentation at a symposium held at the2006 National Conference of the American Academy ofNurse Practitioners, Grapevine, Texas, June 21, 2006.

Nurse Practitioner, Foothills Foundation, Boise, Idaho.Address correspondence to: Nancy Nadolski, FNP,

MSN, MEd, RN, Nurse Practitioner, Foothills Foundation,223 West State Street, Boise, ID 83702.E-mail: nancy@nancynadolski.com.

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Sleep restriction ensures that time in bed is equal totime asleep. This will avoid the anxiety of lying awake inbed, worrying about sleep, and increasing the associationof sleep as an unpleasant or stressful experience. Sleep

restriction usually starts by asking the patient to identifyhow many hours of sleep he or she is getting.Maintaining a sleep diary may be necessary to accurate-ly determine this. If the patient says, Im only sleeping5 hours a night, restrict bedtime to only 5 hours (eg,going to bed at midnight and waking at 5:00 AM). Thisinitially creates a sleep debt and the patient will be verytired the first few days, but often it also relieves anxietyabout going to sleep. Also, because patients with insom-nia mistakenly spend extra time in bed trying to fallasleep, sleep restriction ensures that the sleep debt accu-mulates to such a degree that sleep will more easily fol-

low. The allotment of restricted sleep time (which shouldnot be less than 5 hours) can then be added to by 15 to30 minutes per week, until it builds up to a sleep dura-tion that is best for the patient. Although it produces themost rapid changes in sleep patterns, some patients maynot be motivated to pursue this type of therapy.2

With stimulus control, the patient must examinenot only the environment in which he or she sleeps, butalso the environment that he or she is letting go of whensuccumbing to sleep. Depending on the patient, thismay involve removing reminders of insomnia (eg, aclock), removing any physical stimuli that can prevent

sleep onset or duration (eg, a snoring spouse, a pet, or atelevision), using the bed only for sleeping and sexualrelations (ie, no paying bills, working, eating, or watch-ing television in bed), and sleeping only in bed (with nonapping). Stimulus control also tightens the relation-ship between going to bed and going to sleep by requir-ing the patient to get up and out of bed if he or she isunable to fall asleep in 15 to 20 minutes and doingsomething until the patient is tired again. This can berepeated as often as necessary. Finally, the patient shouldavoid any activity that may stimulate the mind beforebedtime, such as checking e-mail, watching the news, or

discussing a topic that causes anger or angst.In the place of these stimuli are relaxation techniques

that help to quiet the mind, relax the body, and createbedtime rituals, which also help to foster sleep hygiene.These techniques can include reading, listening tomusic, praying or meditating, a hot bath, comfortablepajamas (or sleeping nude, if that is a patient preference)and linens, cooler bedroom temperature, and being onlyslightly hungry. Because these techniques can sometimes

induce performance anxiety, the selected techniqueshould be started during the day, when there is no pres-sure or expectation of sleep, and practiced regularly.2

The other possible advantage with relaxation tech-

niques is that they can be self-taught, which can lowerhealthcare costs. A recent small study by Morin et al3

illustrated the benefit with this type of program. A totalof 192 patients with insomnia were randomized to notreatment or a self-help program, which consisted of 6educational booklets mailed weekly. The booklets pro-vided information on insomnia, healthy sleep practices,behavioral sleep scheduling, and cognitive strategies.After 6 months of follow-up, the intervention effectivelyimproved all measured insomnia symptoms. Theimprovements were statistically significant, but clinicallymodest. The authors note that the study had several lim-

itations, including poor compliance (43%62%) and achanging patient population (ie, approximately 50% ofpatients had a different sleep status between study selec-tion and randomization). The authors note that it isplausible then that additional social support, feedback,and reinforcement throughout intervention, perhapsthrough telephone consultations, could improve bothcompliance and outcomes.3 Nurse practitioners (NP)are ideally suited for this but, ironically, are not reim-bursed by insurance companies for this type of care.

COGNITIVETHERAPY

Sleep behavior is learned. Our attitudes and beliefsabout sleep were instilled in us from our parents.Therefore, the first step in cognitive therapy for insomniais to determine how the patient perceives sleep (eg, Issleep a priority? How much sleep do you think youneed?). Many patients misjudge how much sleep is opti-mal for them, perhaps thinking they only need 6 hoursof sleep when they need more or focusing on getting 8hours of sleep when they may not need that much. Othercommon misconceptions about sleep include myths (eg,the best sleep is before midnight) or fear of going crazy

or becoming psychotic or dying without sleep. In fact, ithas never clearly been shown that lack of sleep causes psy-chosis. Cognitive therapy involves restructuring (ie, chal-lenging and replacing) anxiety-producing and erroneousbeliefs about sleep and sleep loss. Cognitive therapy isusually administered by a mental health professional or aclinician who specializes in sleep disorders.

Cognitive therapy is an important treatment optionbecause it offers both short- and long-term benefits,

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particularly when combined with behavioral therapy(Figure 1).4-6 Therefore, it also can prevent futureepisodes of insomnia or better prepare the patient inhandling these episodes when they do occur. Cognitive

therapy also can help distinguish cases of true insomniafrom age-related sleep changes and to reduce the emo-tional distress that insomnia ultimately inflicts.5

COGNITIVE-BEHAVIORALTREATMENT

Cognitive and behavioral treatments can be adminis-tered separately, but most clinical research has focused ontheir combination: cognitive-behavioral therapy (CBT).CBT is especially useful in addressing perpetuating fac-tors that contribute to insomnia. In chronic insomnia,the patient inadvertently creates a vicious cycle of

impaired sleep, fatigue, worry about sleep, excessive timein bed or napping to make up for the sleep debt, andultimately creating physical and emotional arousal,which further inhibits sleep.2 Pharmacotherapy is oftenbest used to break this cycle of sleep debt, whereas CBTis used long-term to prevent recurrence, as evidenced byseveral studies.4,7,8Although most of the discussion herehas focused on primary insomnia, CBT also benefitspatients with secondary insomnia.9-17 However, little isknown about its usefulness for insomnia caused by jetlag, acute stress, or shift work.2

THENURSEPRACTITIONERSROLE INCBTA key component in CBT is for NPs to monitor

patterns of the patient and the bed partner. CBTrequires making sleep a high priority for all sleepers inthe household. Educating the patient about sleeparchitecture and what it means for better sleep out-comes is very important. Also, seeing the patient on aweekly basis while therapy is being employed allowsfor feedback and support and the chance for thepatient to develop insight and judgment about barriersto getting to sleep and staying asleep.

PHARMACOTHERAPY

By the time many patients with insomnia present to ahealthcare practitioner (HCP), they usually are desperatefor a quick fix, saying, Just knock me out. Im so tiredof being tired. For patients unwilling to pursue behav-ioral and/or cognitive therapy, or in whom the insomniais not resolved, there are several medication choices.However, the specific medication must produce sleep that

is of the same quality and consistency as a normal nightssleepthat is, the patient should be able to fall asleep eas-ily, stay asleep, and be functional the next day.

There are many neurotransmitters involved in the

sleep-wake cycle: sleep promoting (ie, adenosine, mela-tonin, galanin, and -aminobutyric acid [GABA]) andwakefulness-promoting (ie, norepinephrine, orexin,

75

60

45

30

15

0

CBT Med Comb Placebo

Wakeaftersleeponset,min

Pre

Post

FU3

FU12

FU24

Improvem

ent

Figure 1. Long-term Outcomes with CBT vs

Medication for Insomnia

In this study, 78 adults with chronic primary insomnia were randomized to

receive CBT (ie, stimulus control, sleep restriction, sleep hygiene, and cog-

nitive therapy), pharmacotherapy, both (Comb), or placebo. Outpatient

treatment lasted 8 weeks and follow-ups continued at 3, 12, and 24 months.

Efficacy is defined as a decrease in the number of minutes awake after sleep

onset, which is the sum of the duration of all awakenings between sleep

onset and final wake-up time.

CBT = cognitive-behavioral therapy; Comb = CBT and pharmacotherapy;FU = follow-up.

Adapted with permission from Morin et al.JAMA.1999;281:991-999.4

Trazodone*

Zolpidem

Amitriptyline*

Mirtazapine*

TemazepamQuetiapine*

Zaleplon

Clonazepam

Hydroxyzine*

0 1 2 3

Occurences, millions

AntidepressantBZRA

BZD

Atypical antipsychotic

Antihistamine

Figure 2. Drugs Used to Treat Insomnia

*Not approved by the US Food and Drug Administration for this use.BZD = benzodiazepine; BZRA = benzodiazepine-receptor agonist.

Adapted with permission from Walsh. Sleep. 2004;27:1441-1442.18

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acetylcholine, dopamine, and histamine). Medicationsprescribed for insomnia work primarily by affecting 1of 3 neurotransmitters: histamine, GABA, and mela-tonin. Although many drugs frequently are prescribed

in the attempt to treat insomnia (Figure 2),18

most donot have a US Food and Drug Administration (FDA)indication for this use.18

HISTAMINE

Histamine is an excitatory neurotransmitter, there-fore, antihistamines cause sleepiness. Antihistaminesare the second most commonly used drug in theUnited States to treat insomnia (after alcohol).Antihistamines can be obtained over-the-counter(OTC) or by prescription, but they do not have USFDA approval for treating insomnia. Diphen-

hydramine is probably the most well-known antihista-mine, but many patients also take Tylenol PM, whichis 25-mg diphenhydramine and 500-mg aceta-minophen. These antihistamines are relatively inex-pensive and, because they have no abuse potential,they are not scheduled by the US Drug EnforcementAdministration (DEA). However, many patients mis-takenly think that because these drugs are OTC, theycan safely take virtually limitless quantities for insom-nia. However, these medications have an 8- to 15-hourhalf-life, which leads to daytime sedation and potentialdanger of overdose. Patients also can develop a toler-

ance to them over time.Several antidepressants also have histamine as a sec-

ondary binding characteristic; these include trazodone(used frequently to treat insomnia), paroxetine, mir-tazapine, fluvoxamine, and, in general, tricyclic anti-depressants (eg, clomipramine, amitriptyline, andnortriptyline).19 However, these drugs also lack USFDA approval for treating insomnia and also havepotential for side effects, which should be weighedwhen creating a long-term treatment strategy forinsomnia. This is especially important in elderlypatients.

-AMINOBUTYRICACID

Drugs that activate GABAergic neurotransmissionhave been studied extensively, and several drugs withthis mechanism of action have indications for thetreatment of insomnia. Virtually all of these drugsenhance GABAAreceptor activity and are referred to assedative-hypnotics. Sedatives decrease activity, moder-ate excitement, and calm the recipient; hypnotics pro-

duce drowsiness and facilitate the onset and mainte-nance of natural-type sleep (ie, the person can be easi-ly awakened and electroencephalography recordingsare similar to those with naturally occurring sleep).20

Barbiturates were the first drugs found to affectGABAergic neurotransmission; however, the mostfrequently prescribed and well known are the benzo-diazepines. Most benzodiazepines are quicklyabsorbed. The primary differences between them liein their relative elimination half-lives, which canrange from less than 4 hours to more than 1 week(Figure 3).21-23 The variety of half-lives with thesedrugs makes them especially useful for managing dif-ferent types of insomnia, but also highlights theimportance of carefully documenting insomnia symp-toms, such as difficulty falling asleep versus difficulty

staying asleep. Patients having trouble falling sleepshould use drugs with short half-lives, whereaspatients waking up after only a few hours would farebetter with intermediate to longer half-life drugs.Patients often report increased total sleep time as thelitmus test for a good nights sleep (eg, I slept 8 hourslast night or I didnt wake up once last night). The

Triazolam*

Flurazepam*

Quazepam*

Estazolam*

Temazepam*

Zolpidem

Zaleplon

Eszopiclone

Half-life, hrs

1

2

3

6

11

10 24

39

74

Figure 3. Benzodiazepines and Nonbenzodiazepines Have

a Wide Range of Half-lives

*Benzodiazepines.Several commonly used benzodiazepine and nonbenzodiazepine -aminobu-tyric acid agonists and their half-lives are shown. Half-lives can extend to beyond1 week for some drugs, such as medazepam, nordazepam, and prazepam.Data from Dikeos and Soldatos.22

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longer the medications half-life, the greater theopportunity for increasing total sleep time, and thereis less chance of wake after sleep onset. However, cor-rect timing of the dose is important and requires close

patient monitoring to minimize the risk of driving (orworking) drowsy in the morning.

In fact, there are several limitations with using ben-zodiazepine and nonbenzodiazepine GABA receptoragonists. For example, all of these medications are clas-sified as schedule IV controlled substances by the USDEA. Also, some of the side effects associated withtheir use include psychomotor impairment, depressedrespiration, and amnesia. Patients taking these drugsover a long period of time also can suffer fromrebound insomnia when the medication is stoppedand/or tolerance to the drugs over time. Also, overdose

is a potential danger with these drugs.Nonbenzodiazepines are the most recently avail-

able drugs in this class. They include eszopiclone (indi-cated for sleep onset and maintenance, and the firsthypnotic to be approved without a short-term use lim-itation), zaleplon (indicated for sleep onset, but suffi-ciently short-acting to be taken late during the night),and zolpidem (indicated for improving sleep onset andtotal sleep time). Controlled-release zolpidem isapproved for treating insomnia associated with diffi-culty initiating and maintaining sleep.

COMPLEMENTARYMEDICINEAlthough an HCP need not endorse or reject com-

plementary medicines for the treatment of insomnia,it is important to be aware of what patients are con-suming or even reading about these products. Forexample, valerian root and kava kava are commonlytouted as insomnia treatments. The biggest potentialhazard with these treatments is lack of standardizationin their production (noted in a July 2001 New YorkTimes article by Nagourney).24 Both HCPs and con-sumers can check to see if a particular product hasbeen tested for content (www.consumerlab.com).

MELATONINAGONIST

Recall that melatonin is one of the critical regula-tors of the circadian rhythm. Its secretion is controlledby the suprachiasmatic nuclei (SCN), increasing asdrowsiness sets in, with maximal levels at approxi-mately 3:00 AM to 4:00 AM.25,26 Melatonin has beenused to shift the sleep-wake cycle in people sufferingfrom jet lag or shift work insomnia. It is available as a

dietary supplement. Ramelteon is a potent and selec-tive melatonin receptor agonist and received US FDAapproval in July 2005 for sleep onset insomnia.Importantly, it is not a scheduled drug by the US

DEA, it carries no risk of abuse or tolerance, and itdoes not impact GABA or histaminic neurotransmis-sion. It is the first drug in 35 years to act outside ofthose 2 neurotransmitter systems.

Ramelteon acts on melatonin 1 (MT1) and mela-tonin 2 (MT2) receptors, which are heavily concen-trated in the SCN.27 Given the key role of the SCN insleep regulation, agents with high affinity and selectiv-ity for MT1 and MT2 receptors are rational targets inthe treatment of insomnia.27 Specifically, binding toMT1 receptors could decrease SCN stimulatory out-put (the alerting signal). These effects are in addition

to the melatonin already available and active in thebody. With the alerting mechanism inhibited, thesleep switch is able to turn on. Agonism of the MT2receptors may help to entrain the circadian clockthrough phase shifting, which could help adjust thetiming of sleep.27,28 To date, the most common sideeffects observed are sleepiness, dizziness, and fatigue.As with any other medication for the treatment ofinsomnia, patients should avoid driving or operatingmachinery for a few days until they know how thedrug will affect them the next day.

DRUGSUNDERINVESTIGATIONAlso under investigation are several other new

drugs. Gaboxadol is GABA receptor agonist, but itacts only on certain types of GABA receptors (ie, out-side synaptic junctions of thalamic and cortical neu-rons), which are thought to play an importantregulatory role in the onset, maintenance, and depthof the sleep process.29Also in phase III clinical trials arelow-dose doxepin (a tricyclic antidepressant) andindiplon (a short-acting benzodiazepine receptor ago-nist hypnotic).30-35

THENURSEPRACTITIONERSROLE INPRESCRIBING

The NPs role in prescribing any of these medica-tions is to match the insomnia symptom with the mostappropriate treatment option. However, each state hasits own prescriptive authority guidelines for NPsregarding scheduled medications. Once the medicationis started, consistent follow-up is important to ensurethat the dosage meets the specific needs of the patientand that behavioral interventions also are employed.

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CONCLUSIONS

Behavioral therapy focuses on sleep restriction,stimulus control, relaxation, and sleep hygiene educa-

tion, whereas cognitive therapy restructures anxiety-producing or erroneous beliefs about sleep.Medications treat 3 targets in sleep regulation: GABA,histamine, and melatonin. A multifaceted approach totreating insomnia appears to be most effectiveonethat can provide immediate relief, allay patient fearsand anxiety that may have developed over sleeping,and maintain these benefits over the long term.Studies have shown that CBT is beneficial for prima-ry and secondary insomnia, maintains benefits longterm, and when used with pharmacotherapy canimprove patient outcomes even further. The NPs role

is to monitor and educate the patient and the bed part-ner, to ensure that sleep is a high priority in the house-hold, and to maintain close follow-up. If medication isrequired, the NP will ensure that the medicationmatches the insomnia symptoms. Given the strengthof data regarding insomnia treatments, future researchquestions include the timing of CBT versus pharma-cotherapy (eg, concurrently or sequentially), optimaltreatment dosage (ie, timing and frequency of follow-up consultations), and whether maintenance treat-ment will enhance long-term outcomes.2,36

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