Abstract
Insomnia is one of the most common sleep concerns raised by patients both to primary care as well as sleep specialists. Chronic insomnia has a lifetime prevalence of approximately 30% in the general population, resulting in roughly $100 billion dollars healthcare expenditures annually. Given the complexity of insomnia this can become burdensome for primary care providers. In this article we will highlight the main issues and how to manage these individuals in the primary care clinic.
Introduction
Insomnia is defined as a persistent difficulty to fall or maintain sleep and linked with dissatisfaction, concern, or perceived daytime impairment.1 There are three subtypes of insomnia, often overlooked or under-treated, affecting all ages and being disruptive on mental as well as physical health. Treatment requires a collaborative effort between the patient and physician. We will discuss the impact on health, definition, subtypes, manifestations, testing, and treatment for insomnia.
Impact on Health
Chronic Insomnia, untreated or unrecognized, can have detrimental effects on mental and physical health, with an increased risk of depression, suicide and other psychiatric disorders.2 Patients with insomnia with short sleep duration are at increased risk for developing hypertension and impaired sleep events can also adversely impact patient’s perception of pain.3,4 This can cause patients with chronic pain as well as fibromyalgia to have a predisposition to developing insomnia as well. It has also been shown that patients with objective short sleep duration are associated with high risk of diabetes and mortality.5
Subtypes and Definations
Due to difficulty of initiation or maintenance of sleep, patients with insomnia frequently perceive daytime impairment (i.e. fatigue, decreased mood, irritability, general malaise, or cognitive impairment).1 Currently insomnia has been subcategorized into three subtypes by International Classification of Sleep Disorders 3rd edition Text Revision (ICSD-3-TR): chronic insomnia disorder, short term insomnia disorder, and other insomnia disorder.
Chronic Insomnia
Chronic insomnia affects about 10% of the population more common with female subjects and individuals with medical, psychiatric, substance abuse disorders, advanced age and lower socioeconomic status (Figure 1).1,6,7 To establish the diagnosis, criteria A-F must be met.8
Figure 1.
Chronic insomnia affects about 10% of the population more common with female subjects and individuals with medical, psychiatric substance abuse disorders, advanced age and lower socioeconomic status.
A) One of the following must be present: difficulty initiating sleep, difficulty maintaining sleep, final awakening earlier than desired, resistance to going to bed on an appropriate schedule, or difficulty sleeping without caregivers presence or intervention (in adults with cognitive dysfunction).
B) The patient or caregiver notices at least one of the following in relation to night time sleeping difficulty: 1) fatigue, 2) impaired attention, concentration or memory, 3) impaired social, family, occupational, or academic performance, 4) mood disturbance or irritability, 5) subjective daytime sleepiness, 6) behavioral problems (e.g. hyperactivity, impulsivity, aggression), 7) reduced motivation/energy/initiative, 8) proneness for errors/accidents, 9) concerns about/dissatisfaction with sleep.
C) Reported sleep/wake complaints cannot be explained purely by inadequate opportunity or inadequate circumstances for sleep.
D) The sleep disturbance and associated daytime symptoms occur ≥ three times per week.
E) Symptoms have been present for ≥3 months. (Although some patients with chronic insomnia may show recurrent episodes lasting for several weeks at a time over several years but not meeting the three months in each time)
F) The sleep disturbance and associated daytime symptoms are not solely due to another current sleep disorder, medical disorder, mental disorder, or medication/substance use.
There are some essential features for chronic insomnia that help delineate individuals with insomnia versus unrealistic expectations about sleep and they are as follows.8 Sleep onset insomnia if it takes >30 minutes to fall asleep. Sleep maintenance insomnia if the period of wakefulness during sleep is >30 minutes or, early morning awakenings typically >30 minutes before desired rising time as well as an overall reduction in total sleep time.
Short term insomnia disorder is acute insomnia is also a relatively common disorder. In adults the one year prevalence is 15–20% and it’s more common in women and older individuals.8 The main difference obviously is the duration, acute <3 months. In acute insomnia, the patient usually can identify the inciting event or circumstance that became the catalyst for onset.
The last subtype of insomnia is “Other Insomnia Disorder,” reserved for individuals who have difficulty either starting or maintaining sleep but don’t meet the full criteria for short or chronic insomnia disorder.8 This may be assigned to an individual on a provisional basis when further information is needed to be obtained to establish a diagnosis. This diagnosis should be used scarcely given its non-specific name.
Differential Diagnosis
There are several disorders that can mimic insomnia making it difficult to differentiate the true cause when a proper history and physical is overlooked. Such disorders include but not limited to: Circadian rhythm sleep wake disorders, excessive time in bed, short sleeper, sleep disruptive environmental circumstances, chronic insufficient sleep syndrome, narcolepsy, sleep related breathing disorders, and movement disorders.
There are several different Circadian rhythm sleep-wake disorders (CRSWD) that can mimic insomnia. Four of them may mimic chronic and two mimic short term insomnia disorder. The mimickers of chronic insomnia are delayed sleep wake phase disorder (DSWPD), advanced sleep wake phase disorder (ASWPD), irregular sleep wake rhythm disorder (ISWRD), and non-24-hour sleep wake rhythm disorder (N24SWD).
DSWPD is a sleep initiation problem typically seen in teenagers and young adults. These individuals consistently have sleep initiation that is later than desired, or due to social norms, required timing.9 This is due to a delayed endogenous circadian rhythm. Patients with DSWPD are able to fall asleep with less difficulty and acquire a normal duration of sleep, if they’re allowed to sleep on their preferred time, and feel rested and productive throughout their day.
On the opposite side of the spectrum is ASWPD that may be mistaken as sleep maintenance insomnia. Patients with ASWPD will have a consistent earlier than desired sleep initiation timing and will wake up earlier than social normal due to their endogenous circadian rhythm being more advanced.10 Their total sleep time is sufficient and are able to carry out their daily activities without difficulties.
ISWRD is a CRSWD in which there is lack of clearly defined circadian rhythm of sleep and wake.11 In these individuals the sleep wake pattern is temporally disorganized with significant variability of sleep and wake episodes throughout the 24 hour cycle leading to fragmented sleep wake episodes.11 These individuals will have their longest sleep episode < 4 hours. They nap throughout the day, total sleep time through the day may be normal for the given age.
N24SWD is a CRSWD where the intrinsic circadian pacemaker is not attuned to a 24-hour light-dark cycle.12 Patients typically display sleep wake patterns that have a progressive delay or advancement depending on the length of time than their endogenous circadian rhythm.12 Given this pattern it can cause an individual to have sleep onset or sleep maintenance insomnia. It can also cause the patient to be hypersomnolent. This is typically seen in blind individuals and rarely in sighted individuals. The cause for this CRSWD in sighted individuals is still unknown. For this disorder, a diagnosis requires a 14 day sleep diary/actigraphy documenting progressively shifting sleep wake times.12
CRSWD mimickers of acute insomnia include Shift work disorder and jet lag caused by a mismatch between the endogenous circadian rhythm and desired or required sleep wake schedule. These then cause one to complain about their sleep as their inner circadian rhythm has been manipulated for certain needs required at that time.
There are two other factors/disorders that are related to environmental or social events that mimic insomnia. Environmental changes can disrupt sleep, including noise, light, extreme temperatures and safety, ex: watching TV, working on computers, reading in bed, due to light from electronic devices reaching the retina inhibiting melatonin release.13 This type of behavior conditions the brain to not associate the bed as a place of rest. Patients will report that the “mind is racing” when not using electronic devices. In addition, concerns for one’s safety will also heightene a sense of arousal, inhibiting sleep.
The other disorder is Chronic insufficient sleep syndrome where there is inadequate sleep duration secondary to work, personal requirements or social/recreational schedules. This will lead to daytime sleepiness and fatigue, however given sufficient sleep time, they are able to initiate and maintain sleep without difficulty for normal duration.14
Other normal variants of sleep schedules are individuals with excessive time spent in bed and short sleepers. These individuals may express prolonged sleep latency or long periods of wakefulness during the night without complaints of insomnia or daytime impairment.8 In adults, without cognitive impairments, this is most common in non-complaining individuals who allocate more time in bed than required. Unemployed individuals could be at risk of developing inefficient sleep habits by spending excessive time in bed, as they lack a structuring activity.15 Short sleepers are individuals who commonly obtain <6 hours of sleep and have no sleep/wake complaints or daytime dysfunction.16 For these individuals the short average sleep period is not from intentional prolonged sleep restriction but rather their constitutional disposition for reduced sleep requirement.16
There are multiple disorders that cause or mimic insomnia if not properly evaluated. These disorders include, but not limited to: sleep-related breathing disorders, movement disorders, chronic pain with fibromyalgia, and narcolepsy. With sleep related breathing disorders, most commonly obstructive sleep apnea (OSA), there can be frequent night time awakenings, mimicking sleep maintenance insomnia, due to the fragmented sleep occurring with the arousals after obstructive events. These can fully awaken patients making it difficult/frustrating for the patient regain sleep. Movement disorders such as restless leg syndrome (RLS) and periodic limb movement disorder (PLMD) can lead to insomnia. RLS is a sensorimotor disorder in which the individual will complain of a strong, irresistible urge to move the limbs. The sensations occur predominantly in the evening with inactivity.17 Resolution of the symptoms when moving or walk around is a hallmark feature. The term RLS is a misnomer as some patients will also describe some arm sensations.17 These sensations make it difficult for individuals to fall asleep for which patients present as sleep initiation insomnia. PLMD is characterized by periodic episodes of repetitive, stereotype limb movements during sleep which then leads to clinical sleep disturbance or daytime impairment that cannot be explained by another sleep disorder or etiology. This can lead to frequent awakening during the night mimicking sleep maintenance insomnia. In patients who have under-treated chronic pain or fibromyalgia, insomnia will occur 50–80% of the time.4 Under-treated pain or uncontrolled fibromyalgia can lead to sleep initiation insomnia. Narcolepsy, a rare central disorder of hyper-somnolence, can also be mistaken for insomnia. Narcolepsy can be mistaken for sleep maintenance insomnia as these patients have high arousal states when asleep causing fragmentation and frequent nocturnal awakenings.
Testing
Routine and detailed testing is not indicated in the evaluation of insomnia unless required to exclude other sleep disorders based on history or exam. A useful tool to assist in differentiating sleep disorders and insomnia includes a two-week sleep diary.2 Using sleep diaries can also help differentiate whether the individual has a CRSWD as well as possible habits that are perpetuating their symptoms, such as drinking caffeine at night. Another beneficial tool is actigraphy, a device that is typically worn on the wrist and detects motion. Lack of movement suggests sleep and useful in individuals, not sure or unable to recall their sleep pattern.18 With concerns of insomnia, polysomnography (PSG) is indicated when the history suggest an underlying sleep disorder such as OSA or PLMs. In lab PSGs are indicated. In regard to a multiple sleep latency test (MSLT) this test is only indicated if the individual has hypersomnolence for who narcolepsy is of concern.18 With insomnia, the history is paramount in differentiating the problem. See Figure 2 for a list of questions that can help differentiate the type and underlying cause to their sleep difficulty.
Figure 2.
- How long have you had insomnia?
- Anything specific started the insomnia?
- Stresses, medications?
- What time do you go to bed?
- Are you sleepy when you go to bed?
- How long does it take you to fall asleep?
- What do you do during this time?
- Anything prevent you from falling asleep?
- Racing mind, noises, leg symptoms, other?
- Do you wake up in the middle of the night?
- What wakes you up?
- How long do you take to fall asleep?
- What time do you wake up in the morning?
- Do you wake up with an alarm or by yourself?
- Do you take naps and how long?
- Do you drink any caffeine, alcohol, or drugs?
- Do you currently or have you taken any medications for insomnia?
Management
The goal in the treatment of insomnia is to improve the patients experience in initiating and maintaining sleep, improving the quality of life without introducing unnecessary harm.18 When insomnia is due to an underlying medical condition, treating that condition is the first step. If there is no responsible underlying medical or psychiatric condition, the first line treatment is always to ensure proper sleep hygiene, cognitive behavioral therapy, followed by pharmacological therapy.
Sleep hygiene should be assessed whenever an individual has a complaint about their sleep quality. The environment is a dark, quiet, cool room in a safe environment, void of distractions and used only for sleep and intimacy. Patients should be discouraged from naps, avoid late consumption of caffeine, alcohol or smoking or exercise prior to intended sleep.18 A sleep schedule should also be established for continuity.
Cognitive Behavioral Therapy for Insomnia (CBT-I) is considered the first line of treatment.19 CBT-I is a multi-component treatment that targets behavioral, cognitive, and physiological factors that perpetuate insomnia and aims to modify and alter maladaptive behaviors and distorted beliefs about sleep and insomnia.19 CBT-I is led by trained therapist that covers stimulus control, sleep restriction, relaxation techniques, cognitive therapy, and sleep hygiene education.19 This form of therapy can be delivered in multiple formats such as face to face, tele-visit, or group therapy. CBT-I has been shown to improve sleep as efficacious as medication in the short term but its effects are more sustainable in the long term.19 One study showed that between 70–80% of patients had improvement in their insomnia, 50% achieved clinically meaningful outcomes (sleep latency was < 30 minutes, and reduction in hypnotic use) and 33% became good sleepers after undergoing CBT-I.20,21 CBT-I has also been shown to help individuals slow or reverse cortical gray matter atrophy in patients with comorbid fibromyalgia.4 CBT-I has also been found to be beneficial for individuals with insomnia with comorbid conditions such as depression, posttraumatic stress disorder (PTSD), anxiety, alcohol dependence, chronic pain, and cancer.19 Benefits from CBT-I compared to medications is an elimination of dependency on “medication” and avoiding potential drug side effects.
Hypnotic medications can improve sleep only modestly with the evidence of low quality and 60% of the benefit attributed to a placebo effect.18,22 Five classes of medications are approved by the FDA to be used for insomnia. Some assist with sleep onset, others for sleep maintenance or both. Examples are
Benzodiazepine receptor agonists (Z-drugs), Orexin receptor antagonists, Melatonin receptor agonists, Tricyclic antidepressants, and Benzodiazepines. Benzodiazepine receptor agonists (Z-drugs) used for insomnia are Zolpidem, Zaleplon, and Eszopiclone that attach to the GABA receptor.23 A black box warning exist on these agents due to case reports of complex sleep behaviors, including sleepwalking, driving, cooking and sexual acts during sleep. Eszopiclone and Zolpidem are approved to treat both sleep onset and maintenance insomnia.22 Zaleplon is recommended only for sleep onset insomnia.
Orexin receptor antagonists can be used in insomnia by blocking the Orexin receptor. There are currently three FDA approved Orexin receptor antagonists: Suvorexant, Lemborexant, and Daridorexant.24 These medications are contraindicated in patients with narcolepsy. These three medications are used to treat sleep maintenance insomnia and do not have a limit on duration of use.18
The third class is melatonin receptor agonists such as Ramelteon a synthetic tricyclic analog of melatonin and binds to MT1 and MT2 receptors in the suprachiasmatic nucleus.23 Ramelteon is used to treat sleep onset insomnia.18
The fourth class of medications are Tricyclic antidepressants, such as Doxepin, has a high affinity for H1 receptor (approximately 100 times more than that of nor-epinephrine and serotonin receptors) which given the antagonism in the TMN nucleus inhibits the arousal pathway thus producing its hypnotic action.25 Doxepin is indicated for sleep maintenance insomnia as the onset of the medication is slow and the duration of the effects are long.18 Frequently in the primary care setting Trazodone is given for insomnia due to the sedating side effects. However, the risk/benefit assessment suggest greater harm and its use should be discouraged.22
The last class of medication is benzodiazepines, two of which are Temazepam and Triazolam. They work by binding to the GABA receptors and cause release of the inhibitory neurotransmitter GABA which then induces sedative and hypnotic effect.23 Both of these medications are indicated for sleep onset insomnia but only Temazepam is indicated for the treatment of sleep maintenance insomnia as well. While considered safer, recommendations remain for a limited period of use to avoid dependency.
Conclusion
Insomnia remains a complex and burdensome disease, common in the general population and easily mistaken for other disease states. Due to the complexity of the disorder, these processes can be difficult to manage in the primary care setting. Referral to a sleep medicine specialist may be warranted in patients with insomnia, who do no not respond to basic behavioral therapy and have persistent and distressing symptoms.
Footnotes
Jason Zweig, MD, is a Sleep Medicine Fellow; Ashraf Gohar, MD, FCCP, FAASM, is Professor of Medicine; and Abid Bhat, MD, MBA, (pictured), is Professor of Medicine; all are at University Health Hospital, University of Missouri-Kansas City, Kansas City, Missouri.
Disclosure: No financial disclosures reported. Artificial intelligence was not used in the study, research, preparation, or writing of this manuscript.
References
- 1.Levenson JC, Kay DB, Buysse DJ. The pathophysiology of insomnia. Chest. 2015;147(4) doi: 10.1378/chest.14-1617. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Schutte-Rodin SL, Broch L, Buysee D, Dorsey C, Sateia M. Clinical guideline for the evaluation and management of chronic insomnia in adults. Journal of Clinical Sleep Medicine. 2008;4(5) [PMC free article] [PubMed] [Google Scholar]
- 3.Dai Y, Chen B, Chen L, et al. Insomnia with objective, but not subjective, short sleep duration is associated with increased risk of incident hypertension: the Sleep Heart Health Study. Journal of Clinical Sleep Medicine. 2023;19(8) doi: 10.5664/jcsm.10570. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.McCrae CS, Mundt JM, Curtis AF, et al. Gray matter changes following cognitive behavioral therapy for patients with comorbid fibromyalgia and insomnia: A pilot study. Journal of Clinical Sleep Medicine. 2018;14(9) doi: 10.5664/jcsm.7344. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5.Fernandez-Mendoza J, Vgontzas AN. Insomnia and its impact on physical and mental health. Curr Psychiatry Rep. 2013;15(12) doi: 10.1007/s11920-013-0418-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Bonnet MH, Burton GG, Arand DL. Physiological and medical findings in insomnia: Implications for diagnosis andcare. Sleep Med Rev. 2014;18(2) doi: 10.1016/j.smrv.2013.02.003. [DOI] [PubMed] [Google Scholar]
- 7.Baglioni C, Regen W, Teghen A, et al. Sleep changes in the disorder of insomnia: A meta-analysis of polysomnographic studies. Sleep Med Rev. 2014;18(3) doi: 10.1016/j.smrv.2013.04.001. [DOI] [PubMed] [Google Scholar]
- 8.American Academy of Sleep Medicine. International Classification of Sleep Disorders. 3rd, Text revision ed. Darien, IL: American Academy of Sleep Medicine; 2023. [Google Scholar]
- 9.Saxvig IW, Pallesen S, Wilhelmsen-Langeland A, Molde H, Bjorvatn B. Prevalence, and correlates of delayed sleep phase in high school students. Sleep Med. 2012;13(2) doi: 10.1016/j.sleep.2011.10.024. [DOI] [PubMed] [Google Scholar]
- 10.Curtis BJ, Ashbrook LH, Young T, et al. Extreme morning chronotypes are often familial and not exceedingly rare: The estimated prevalence of advanced sleep phase, familial advanced sleep phase, and advanced sleep-wake phase disorder in a sleep clinic population. Sleep. 2019;42(10) doi: 10.1093/sleep/zsz148. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Zee PC, Vitiello MV. Circadian Rhythm Sleep Disorder: Irregular Sleep Wake Rhythm. Sleep Med Clin. 2009;4(2):213–218. doi: 10.1016/j.jsmc.2009.01.009. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Auger RR, Burgess HJ, Emens JS, Deriy LV, Thomas SM, Sharkey KM. Clinical practice guideline for the treatment of intrinsic circadian rhythm sleep-wake disorders: Advanced Sleep-Wake Phase Disorder (ASWPD), Delayed Sleep-Wake Phase Disorder (DSWPD), Non-24-Hour Sleep-Wake Rhythm Disorder (N24SWD), and Irregular Sleep-Wake Rhythm Disorder (ISWRD). an update for 2015. Journal of Clinical Sleep Medicine. 2015;11(10) doi: 10.5664/jcsm.5100. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 13.Caddick ZA, Gregory K, Arsintescu L, Flynn-Evans EE. A review of the environmental parameters necessary for an optimal sleep environment. Build Environ. 2018;132 [Google Scholar]
- 14.Mader EC, Mader ACL, Singh P. Insufficient Sleep Syndrome: A Blind Spot in Our Vision of Healthy Sleep. Cureus. 2022 doi: 10.7759/cureus.30928. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Greissl S, Mergl R, Sander C, Hensch T, Engel C, Hegerl U. Is unemployment associated with inefficient sleep habits? A cohort study using objective sleep measurements. J Sleep Res. 2022;31(3) doi: 10.1111/jsr.13516. [DOI] [PubMed] [Google Scholar]
- 16.Skiba V, Hershner S. Short Sleeper. AASM Sleep Education [Google Scholar]
- 17.Nanayakkara B, Di Michiel J, Yee BJ. Restless legs syndrome. Aust J Gen Pract. 2023;52(9) doi: 10.31128/AJGP-02-23-6722. [DOI] [PubMed] [Google Scholar]
- 18.Sutton EL. Insomnia. Ann Intern Med. 2021;174(3) doi: 10.7326/AITC202103160. [DOI] [PubMed] [Google Scholar]
- 19.Chan NY, Chan JWY, Li SX, Wing YK. Non-pharmacological Approaches for Management of Insomnia. Neurotherapeutics. 2021;18(1) doi: 10.1007/s13311-021-01029-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Morin CM, Hauri PJ, Espie CA, Spielman AJ, Buysse DJ, Bootzin RR. Nonpharmacologic treatment of chronic insomnia. Sleep. 1999;22(8) doi: 10.1093/sleep/22.8.1134. [DOI] [PubMed] [Google Scholar]
- 21.Morin CM, Jarrin DC. Epidemiology of Insomnia. Sleep Med Clin. 2022;17(2) doi: 10.1016/j.jsmc.2022.03.003. [DOI] [PubMed] [Google Scholar]
- 22.Sateia MJ, Buysse DJ, Krystal AD, Neubauer DN, Heald JL. Clinical Practice Guideline for the Pharmacologic Treatment of Chronic Insomnia in Adults: An American academy of sleep medicine clinical practice guideline. Journal of Clinical Sleep Medicine. 2017;13(2) doi: 10.5664/jcsm.6470. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Brunton L, Chabner B, Knollman B. Goodman and Gilman’s The Pharmacological Basis of Therapeutics. Twelfth Edition. 2011. [Accessed May 3, 2015]. http://books.google.de/books/about/Goodman_and_Gilman_s_The_Pharmacological.html?id=e_yAOpyyaowC&pgis=1 .
- 24.Monkemeyer N, Thomas SV, Hilleman DE, Malesker MA. Insomnia Treatment Update with a Focus on Orexin Receptor Antagonists. 5 Vol. 47. US Pharmacist; 2022. [Google Scholar]
- 25.Katwala J, Kumar AK, Sejpal JJ, Terrence M, Mishra M. Therapeutic rationale for low dose doxepin in insomnia patients. Asian Pac J Trop Dis. 2013;3(4) [Google Scholar]