Paradoxical insomnia

Sleep Disorders

Updated 07.07.2024
Released 09.06.1995
Expires For CME 07.07.2027

Paradoxical insomnia

Authors: Lynn Kataria MD, Swathi Charya DO

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Editor: Bradley V Vaughn MD

Paradoxical insomnia

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Introduction

Overview

Paradoxical insomnia (previously called sleep state misperception) is characterized by complaints of little or no sleep over long periods of time without the level of impairment expected with such a level of sleep deprivation. Patients often describe heightened awareness of their surroundings when lying down to sleep. Sleep study reveals normal sleep architecture with normal sleep-onset latency and sleep efficiency, but with subjective patient reports indicating prolonged sleep-onset latency and poor sleep efficiency. Emerging literature has suggested that underestimation of one’s total sleep time has been linked to cases of subjective total insomnia, and sleep wake misperception is relatively common across various sleep wake diagnoses. Treatment of paradoxical insomnia usually involves patient reassurance. Behavioral therapy and sedative hypnotics have also been tried.

Key points

	• Paradoxical insomnia should be considered in patients with insomnia who complain of severe insomnia, with little or no sleep but without objective evidence of consequences commensurate with the described level of sleep deprivation.
	• Patients show evidence of overestimation of sleep onset latency and underestimation of sleep efficiency.
	• Subjective overestimation of sleep onset latency is more common than underestimation in insomnia patients.
	• Patients do not show other evidence of malingering or psychopathology.
	• Polysomnographic recordings do not show evidence of sleep disorder, and sleep parameters such as sleep efficiency and sleep onset latency are within normal limits.

Historical note and terminology

Sleep state misperception (paradoxical insomnia) is a diagnostic term adopted in the International Classification of Sleep Disorders (04) to replace two previously used diagnostic categories of sleep disorders: subjective insomnia complaint without objective findings and subjective sleepiness complaint without objective findings. In the ICSD-3 edition, the term sleep state misperception was replaced with “paradoxical insomnia” and will be used where appropriate herein (02). The American Academy of Sleep Medicine developed Research and Diagnostic Criteria (RDC) for insomnia (03). The RDC criteria also provided three subclassifications of primary insomnia: psychophysiologic insomnia, paradoxical insomnia, and idiopathic insomnia. Other terms used in the past to describe patients with this disorder include subjective insomnia, pseudo-insomnia, subjective sleepiness, and sleep hypochondriasis. The ICSD-3 classifies paradoxical insomnia as a clinical and pathophysiological subtype of a chronic insomnia disorder, and symptoms must be present for at least 3 months.

Paradoxical insomnia implies a significant and persistent symptom, either insomnia or sleepiness, which is not documented on objective testing (nocturnal polysomnography and daytime multiple sleep latency test). Paradoxical insomnia is characterized by discrepancy between subjective and objective assessments of sleep measure and can be challenging to diagnose and to treat. Furthermore, most studies use a single night of polysomnographic recording to objectively measure sleep onset latency and sleep efficiency, which may not accurately measure an individual’s typical sleep due to high night-to-night variability.

A review of this concept of sleep state misperception addressed a different subset of individuals who seem to overestimate the amount of time spent in sleep compared to that captured on polysomnography. For extensive reviews, please see (28; 10).

Clinical manifestations

Presentation and course

	• Paradoxical insomnia should be considered in patients with subjective feelings of insomnia who complain of little or no sleep but without objective evidence of the described level of sleep deprivation on sleep study data.
	• Patients can have various presentations, including overestimation of sleep onset latency, underestimation of total sleep time, or overestimation of total sleep time.
	• Subjective overestimation of sleep onset latency is more common than underestimation in insomnia patients. Patients do not show other evidence of malingering or psychopathology.

The diagnosis of paradoxical insomnia requires that the patient complain of a sleep-related symptom, either insomnia or excessive daytime sleepiness, that is not documented by standard evaluation with nocturnal polysomnography and the multiple sleep latency test. These symptoms cannot be better explained by other psychiatric or medical conditions. Additionally, the symptom must be present during the evaluation. In either case, the symptom must be long-standing and result in a disturbance of occupational or social function that the patient believes will improve with successful treatment of the symptom. The diagnosis does not apply to cases of malingering or to symptoms directly secondary to a diagnosed psychiatric disorder.

Longer sleep latency contributes to subjective feelings of underestimation of total sleep time, whereas shorter sleep onset latency predisposes to subjective overestimation of total sleep time.

The misperception of the sleep state is typically described by patients as many years of short sleep, no sleep, or nonrestorative sleep. Patients may also report constant or near constant awareness of environmental stimuli throughout most nights. They may also complain of constant thoughts or rumination through most of the night as they lay recumbent. Some patients report that pharmacological or behavioral treatment improved symptoms, in some cases for prolonged periods of time. In other cases, treatment was not effective, or was effective only briefly, and then the symptoms returned. After the sleep evaluation, no abnormality is found, leading to the diagnosis of paradoxical insomnia.

Younger age has been shown to be an independent risk factor for overestimation of sleep onset latency and underestimation of total sleep time. Younger people are dealing with greater challenges in both work and private life as well as societal peer pressures and, thus, can react more emotionally to disturbed sleep. Due to high-functioning demand during the day, fear of reduced functioning from poor sleep likely enhances the perception of wakefulness at night. This, in turn, makes this population more prone to underestimation of total sleep time and sleep state misperception (07). Patients may also present with a complaint of chronic disabling sleepiness; nevertheless, during polysomnographic evaluation no sleep disorder is found, and the level of physiological sleepiness is not abnormal. Thus, as in the case of insomnia, the sleep state is misperceived.

Prognosis and complications

The prognosis of this patient group is not clearly delineated. The condition appears to be chronic with persistent attempts to obtain relief of symptoms. A major complication is drug dependence, as the patients often receive hypnotics or stimulants from physicians. Chronic use of either type of drug can be associated with drug dependence.

Clinical vignette

A 42-year-old married Asian-American woman was referred to the sleep disorders center for the evaluation of difficulty initiating and maintaining sleep for the past 1.5 years. The sleep problem began when the patient and her husband had moved to New York City in connection with their business. The patient had gained 20 lbs during the onset of the insomnia. She consulted an internist, who recommended weight loss, and the patient then began experiencing fainting spells and weakness that increased her distress. She then consulted a psychiatrist who prescribed fluoxetine, which worsened her sleep and other symptoms. The medication was discontinued, and clonazepam was prescribed (0.25 mg), which improved her symptoms. Another move occurred about 1 year after the sleep complaint began. She consulted an internist in her new location; her cholesterol was mildly elevated, but no other medical diagnoses were found, and the medication was continued.

This physician referred her to the sleep disorders center. In the sleep consultation, she said her goal was 6 hours of undisturbed sleep each night without the use of medication. She used the medication every night over the past year and estimated about 3 to 4 hours of sleep. Further history revealed that her weight was stable over the past 1.5 years after the 20-lb gain (5 feet 2 inches and 135 lbs). Her husband was concerned about her snoring and occasional pauses in her breathing while apparently asleep. She used no alcohol, caffeine, tobacco, or illicit drugs. Other than infertility, there was no history of other medical symptoms or disorders. The patient underwent one night of polysomnography at her usual bedtime with monitoring of respiration in addition to the usual polysomnographic parameters. Her medication had been discontinued for 10 days prior to the recording and the patient complained of very little sleep during that period. The morning after the sleep recording, she stated that she had slept 5 or 10 minutes during the 8 hours in bed. The polysomnography found about 6 hours of sleep with normal sleep stages, and only five apnea episodes with mild intermittent snoring. The sleep disorders physician met with the patient as well as with the patient and her husband several times. A copy of her sleep study was provided in detail for review and reassurance. The focus of these discussions was a description of the physiological normality of her sleep different than her perception. Sleep hygiene was emphasized as treatment. It was emphasized that physically her sleep was adequate and restorative. The patient agreed to stop the medication and adopt more regular sleep habits and decrease her work hours. This plan was successful in the short term, but the patient was lost to follow-up.

Biological basis

Etiology and pathogenesis

The etiology of paradoxical insomnia is not known, and the neurophysiological mechanisms of paradoxical insomnia still require further investigation (28). Some attribute the insomnia complaint to presleep cognition that imparts an impression of not sleeping. Others theorize that excessive mentation or rumination in sleep gives the patient the impression of not sleeping although, in fact, the mentation is in the sleep state. Sleep state discrepancy has been associated with certain personality traits, such as neuroticism and hypochondriasis, which can increase feelings of anxiety and arousal. This has typically been seen in paradoxical insomnia where polysomnography findings are normal (31). Paradoxical insomnia and psychophysiological factors have overlapping symptoms as well as similarly elevated adrenocorticotropic hormone and cortisol levels as measured in a small study comparing the two groups (22).

In a similar vein, the disorder is seen as an extreme example of the tendency of most insomnia patients to exaggerate or misreport their sleep problem. Insomnia patients, including cases of subjective insomnia, tend to underestimate their total sleep duration (32). Individuals with insomnia can be more prone to sleep fragmentation and may need longer periods of continuous sleep (greater than 30 minutes) to perceive they were asleep (07).

Investigators have hypothesized that there are differences in brain anatomy and function in patients with paradoxical insomnia compared to healthy subjects. Researchers have reported that patients with paradoxical insomnia were found to have regional shrinkage in specific areas of the brain, including the caudate, nucleus accumbens, putamen, hippocampus, thalamus, and amygdala (13). The direction of causality of these findings is unclear; their relationship to the estimation of sleep has yet to be explained.

Psychological distress from certain personality traits may influence perception of sleep, which is supported by the finding that elevated scores on the Psychasthenia scale of the Minnesota Multiphasic Personality Inventory correlate positively with sleep time underestimation. Others speculate that there are certain neurophysiological mechanisms of sleep misperception in these individuals, including abnormal neuronal circuitry and increased cortical arousals (29). For instance, it has been shown that auditory stimuli sufficient to increase arterial blood pressure or heart rate without signs of arousal on the EEG can result in increased sleepiness. Actigraphy has shown increased movement in paradoxical insomnia patients, providing some support for this hypothesis. In addition, certain personality profiles have been linked to paradoxical insomnia, such as anxiety, rumination, intrusive thoughts, and depressed mood. Pathological traits, including neuroticism, excessive body dissatisfaction, or histrionic somatization, have been seen in insomnia patients. Patients with paradoxical insomnia display anxiety and subjective uneasiness about their sleep, which could eventually lead to sleep difficulties viewed objectively. Therefore, the results of the Minnesota Multiphasic Personality Inventory may actually differ if administered when symptoms of insomnia first appear compared to later on (29).

Emerging research and neurophysiologic studies have shown altered EEG frequency bands and event-related potentials in nonrapid eye movement sleep in patients with paradoxical insomnia (31). This could be indirectly linked to increased microarousals in these patients, which could contribute to subjective feelings of sleepiness and decreased total sleep time.

In some patients with subjective sleepiness, misperception or mislabeling of another bodily state such as fatigue or depression probably accounts for the symptom. For instance, in two studies, both nefazodone and fluoxetine alleviated depression and resulted in improvements in subjective sleep quality, although patients given fluoxetine showed significant declines in objective sleep characteristics such as an increased number of awakenings and decreased sleep efficiency. No group difference in sleep diary measures of sleep quality was seen between patients given nefazodone or the antidepressant paroxetine, despite the declines in objective sleep measures observed in patients given paroxetine. Others may attribute such daytime dysfunction as trouble concentrating or memory problems to sleepiness when in fact sleepiness is not present. Alternatively, the usual changes in alertness that are related to the circadian rhythm can be perceived as abnormal somnolence by some patients when those are expected changes in the levels of sleepiness.

Studies now show that sleep-wake estimation inaccuracy is a common feature throughout sleep-wake diagnoses (32).

Patients with sleep apnea are found to overestimate sleep onset latency and underestimate total sleep time (11). In a large sample of patients with obstructive sleep apnea (n=405), perception of total sleep time improved when the patient underwent a CPAP titration study (11). These reports support the concept of paradoxical insomnia in somnolent patients. In the above cited reports, the authors conclude that marked discrepancies between patient reports and objective measures are not limited to insomnia patients. The subjective state of sleepiness is correlated with, but different than, physiological sleepiness or sleep propensity as measured by the multiple sleep latency test.

The essential aspects of paradoxical insomnia are that physiological measurement of the sleep-wake system is intact, despite the complaint of sleep-related symptoms. The pathogenesis and pathophysiology for the perception of sleep and sleepiness remains unclear. An attempt has been made to correlate multiple EEG measures such as sleep stage, sleep onset latency, waking time and arousal frequency, total sleep time, EEG frequency, and sleep spindle density with the perception of sleep. It is clear that no single factor or combination of EEG factors completely explains the subjective perception of sleep. Likewise, the pathogenesis and pathophysiology for the misperception is unknown. However, some progress has been made in terms of the role of sleep spindles in paradoxical insomnia. Normand and colleagues suggest that a deficiency in sleep spindles might account, at least in part, for the sleep state misperception that occurs in paradoxical insomnia (24). Sleep spindle characteristics for 17 patients with paradoxical insomnia, 29 good sleepers, and 24 patients with psychophysiological insomnia were compared. Relative to the other groups, paradoxical insomniacs had the shortest sleep spindles on night 3 of 4 in the laboratory. The study highlights a need for additional studies on spindle length and its role in perception of sleep.

A study by Senel and colleagues looked at the role of sleep spindles in paradoxical insomnia (06). The study looked at sleep spindle characteristics in 20 patients with paradoxical insomnia versus 20 healthy control subjects. Additionally, certain personality traits were assessed via several questionnaires, including neuroticism or extroversion (Eysenck Personality Questionnaire), somatic perceptions (Somatization Scale), uncontrollable anxiety (Penn State Worry Questionnaire), tendency for ruminative thinking (Ruminative Thought Style Questionnaire), and depressive symptoms (Beck Depression Inventory). A significant difference was observed in the density of sleep spindles between the two groups of patients, with lower density spindles observed in patients with paradoxical insomnia. Additionally, the duration of spindles showed a positive correlation in patients with notable scores of extroversion (EPQR-A) and uncontrollable anxiety (PSWQ). It was noted that the frequency of spindles was the same between the healthy controls and the patients with paradoxical insomnia. This study further confirmed that certain sleep protective mechanisms are disrupted in paradoxical insomnia, as seen by the lower density of sleep spindles in these patients. Furthermore, fast sleep spindle activity can be observed with certain personality traits, as seen in those with increased levels of anxiety, therefore, leading to sleep state misperception.

Perception of being asleep or awake in insomnia patients differs from the perception in normal sleepers, and this is independent of age, sex, or laboratory versus ambulatory recording setting (31). In Trimmel and colleagues’ study, n = 303 patients with insomnia underestimated total sleep in the sleep laboratory by an average of 46 minutes. Paradoxical insomnia was not specifically studied in these reports, but these findings may point to a unique perceptual difference in insomnia patients. One study compared REM sleep macrostructure and microstructure as well as clinical interviews between good sleepers, psychophysiological insomnia, and paradoxical insomnia. Participants underwent four consecutive polysomnograhies in the laboratory. The paradoxical insomnia group was distinguished by higher number of wake intrusions in REM, and there was a relationship between REM duration and dream imagery activity (26).

New research has further shown that although there may be no overt changes to the overall macrostructure of sleep in patients with paradoxical insomnia, there may be changes to the underlying microstructure of sleep. Studying components, such as microarousals or cyclic alternating pattern (CAP), in patients with paradoxical insomnia are facets of microstructure that can offer more detail and convey the physiologic abnormalities that may be missed by studying overall sleep macrostructure. In a study published by Wenjing and colleagues, PSG microstructure findings of 89 patients with paradoxical insomnia were compared with 41 healthy control subjects without sleep-related complaints. There was a noticeable increase of spontaneous arousals during rapid eye movement (REM) sleep in patients with paradoxical insomnia when compared to healthy controls. This was not observed with non-rapid eye movement sleep. As REM sleep is important for subjective sleep quality and fulfilment of rest, these increased instances of microarousals and REM sleep instability can form some of the foundation for insomnia-related complaints in patients with paradoxical insomnia (27).

A study by Yoon and colleagues studied factors associated with negative and positive sleep state misperception (35). As sleep duration can be underestimated (negative state misperception) as well as overestimated (positive state misperception), sleep state misperception should fall under a “continuum of sleep perception.” The patients were divided into two groups based on the misperception index, which gives a numerical value to the discrepancy between self-reported total sleep time and objective total sleep time as measured by nocturnal polysomnography reading. A positive misperception index value (> 0) indicated underestimation of total sleep time, whereas a negative misperception value (< 0) indicated overestimation of total sleep time. The patients with a positive misperception index value were categorized into the Positive Sleep State Misperception (PSSM) group, whereas those with a negative misperception index value were placed into the Negative Sleep State Misperception (NSSM) group. Of the 150 patients, 76.7% were sorted into the NSSM group, and 23.3% were categorized into the PSSM group. It was noted that patients with negative sleep state misperception were significantly older than patients with positive sleep state misperception. Polysomnographic recording showed that the PSSM group displayed larger quantities of N3 or slow-wave sleep. Slow-wave sleep is linked with the perception of adequate sleep duration and accurate sleep time estimation. Therefore, patients with inadequate slow-wave sleep may be more prone to underestimate their sleep duration. This suggests that quality of sleep can be poorer in older individuals when subjectively measured. Addressing these misperceptions of sleep with a cognitive approach could be beneficial for these patients to correct dysfunctional beliefs surrounding sleep.

Alpha-delta sleep (A-DS), which is an electroencephalographic (EEG) feature characterized by presence of alpha waves and low voltage fast activity representing relaxed wakefulness, superimposed on delta waves, characteristic of deep nonrapid eye movement (NREM) sleep, has long been associated with light sleep sensation. The literature regarding A-DS and sleep time misperception has been equivocal. However, in one study, investigators prospectively analyzed polysomnograms of about 5000 patients referred to a sleep laboratory and showed significant correlation between the discrepancy in subjective and objective sleep duration and perception of light sleep with degree of A-DS ranked from 1 to 4, especially in patients without obstructive sleep apnea and insomnia (21).

EEG spectral analyses of polysomnography recordings in insomnia patients have been explored in a number of studies. A study by Lecci and colleagues looked into electroencephalographic patterns, specifically whether spectral power changes that are not routinely present in polysomnography monitoring could explain why some patients feel awake during parts of the night and, therefore, underestimate their total sleep time, such as in paradoxical insomnia (20). Subjects underwent home sleep testing and estimated their total sleep time the next day. Patients who underestimated or overestimated their sleep time were separated from those who accurately or almost accurately estimated their total sleep time. Ten patients with paradoxical insomnia underwent supervised high-density EEG sleep recording in the laboratory to evaluate spectral power EEG changes and further distinguish the under-and overestimators from those who accurately estimated their total sleep time. The study found that those who underestimated their total sleep time had increased EEG activation over the central electrodes in both non-REM and REM sleep, which included a shift from lower to higher frequency power, thus, displaying a “wake”-like pattern. These findings were not linked to age, medications, or testing setting (home versus in lab). This increased activation in the central areas of the cortex is thought to play a role in increased feelings of wakefulness as these areas have an abundance of noradrenaline.

On the contrary, those with overestimation of total sleep time showed lower frequency power and decreased activation of EEG in REM sleep. An imprint of NREM sleep is EEG frequencies in the delta range, constituting slow-wave sleep. Oppositely, neuronal firing is represented by high frequencies, representing the brain to be in a more “wake”-like state. Beta power correlates with autonomic arousal. Therefore, the results of this study suggest that underestimation of total sleep time is linked to high frequencies and, thus, EEG activation, leading to feelings of wakefulness and underestimation of total sleep time. Conversely, those who overestimated their sleep showed increases in lower frequencies of EEG; however, this was only during the REM stage of sleep, which usually judges subjective sleep quality (20). This study suggests that slow frequency activity in REM sleep can contribute to overestimating sleep time. The findings from this study step away from generalizing misperception of sleep state and shift gears towards evidence that insomnia patients may actually be perceiving subtle changes from “sleep to wake-like brain activity,” which are not usually encompassed in the standard polysomnography montage.

Cyclic alternating pattern (CAP) is an EEG pattern characterized by sequences of electrocortical events of non-REM sleep distinct from background activity and recurring with a periodicity of 20 to 40 seconds. This has been reported to correlate with poor sleep quality. Patients with paradoxical insomnia had significantly higher CAP rate overall, which increased before subjective sleep onset time compared to normal controls (25). These findings were supported in a study that compared CAPs in 10 individuals with paradoxical insomnia to 10 individuals with psychophysiological insomnia and to 10 normal controls. Differences mostly concerned increases in A3 and B3, and especially B3 in stage 2, in both psychophysiological insomnia and paradoxical insomnia. The authors attributed these findings to the level of hyperarousal. Moreover, although CAP rate was similar between the insomnia subtypes, the overall CAP time was increased in the paradoxical insomnia subgroup (12).

Misperceptions of sleep can occur in normal healthy volunteers. In a sample of 44 participants, all were asked to sleep at their normal nighttime schedule on their first night in the laboratory. Then they had a 12-hour nighttime sleep opportunity as well as a 4-hour daytime nap opportunity without access to time cues. The extended night sleep opportunities and long daytime naps were designed to induce an “insomnia” with substantial time awake during scheduled sleep. Results showed that sleep estimations were accurate when participants sleep according to their normal night’s schedule. Participants underestimated sleep time in the 12-hour sleep opportunity, and this was inversely correlated with stage 2 sleep. Participants overestimated sleep in the 4-hour daytime nap opportunity, and this was correlated with REM and stage 3 sleep. The study suggests that sleep misperceptions may be related in part to the presence or absence of time cues and time of day (08).

Another study by Te Lindert and colleagues looked at sleep state misperception accounting for night-to-night variability using seven nights of sleep diaries and actigraphy recordings of 181 patients with insomnia and 55 people without sleep complaints (30). In this study, good sleepers tended to accurately estimate or overestimate their sleep time. However, actigraphy data suggested objectively longer time spent asleep compared to subjective self-reported shorter time asleep. The data revealed three subtypes of the subjective features of sleep leading to sleep state misperception: one’s shortest reported sleep duration and the mean and standard deviation of misperception. These characteristics showed differences across days, suggesting that night-to-night variability should be considered with this diagnosis. In future studies, insomnia patients can hopefully be assigned to one of these subtypes. Further studies could also look at the response of these subtypes to cognitive and pharmacologic therapy.

Certain patient populations may be more prone to underestimation or overestimation of sleep times. Patients with posttraumatic stress disorder underestimate total sleep time and sleep efficiency compared to objective sleep measured by actigraphy (16). Patients with mild traumatic brain injury have been shown to perceive that they sleep a bit less than they actually do on polysomnography. A sample of 37 patients reported they slept 342 minutes in the lab when they actually slept 382 minutes on average (34).

Further studies are needed for better understanding of the underlying pathophysiology of paradoxical insomnia, which should include, but not be limited to, quantitative EEG analysis, neurophysiological, and objective psychological variables. Evaluating the impact of various stimuli on cortical measures such as examining event-related potentials (ERPs) to study hyperarousal is also recommended (05). By the same token, more patients evaluated for subjective complaints of excessive sleepiness or perceived insomnia should be evaluated with polysomnogram studies and multiple sleep latency tests in order to correctly identify paradoxical insomnia.

Differential diagnosis

Confusing conditions

• Anxiety
• Delayed sleep phase
• Depression
• Idiopathic hypersomnia
• Idiopathic insomnia
• Insomnia (sleep onset, sleep maintenance)
• Narcolepsy
• Obstructive sleep apnea
• Paradoxical insomnia

Associated or underlying disorders

Whether paradoxical insomnia should be considered a distinct subtype of insomnia or lumped under primary insomnia has been an area of considerable debate and review. Paradoxical insomnia typically includes a complaint of either insomnia or daytime sleepiness. Insomnia can be associated with difficulty initiating sleep, maintaining sleep, or with a sensation of nonrestorative sleep. With paradoxical insomnia, daytime symptoms associated with the sensation of lack of restoration are endorsed more frequently than the nighttime complaints. The critical difference between paradoxical insomnia and other insomnia categories (psychophysiologic, idiopathic) is that these patients have physiologically normal sleep on polysomnographic evaluation. Criteria for other diagnostic entities related to insomnia require the presence of disturbed sleep that is related to the cause of the insomnia. In most cases of insomnia, there is a degree of misperception of the sleep problem; however, in paradoxical insomnia this is the major finding, and the diagnosis is utilized only after completion of the sleep disorder evaluation. Over-reliance on polysomnographic data may increase the number of patients classified as having paradoxical insomnia as one night of polysomnography may be an inaccurate representation of one’s typical sleep due to high night-to-night variability.

Perception of sleep may also be influenced by psychiatric comorbidities. When 211 patients completed both the Pittsburgh Sleep Quality Index (PSQI) and sleep diary–derived sleep quality measures, the patients who endorsed more psychiatric comorbidities had a weaker correlation between these two measures (P = .047) (17).

In sleep state misperception of sleepiness, the essential difference from other diagnostic categories is the lack of corroboration of the sleepiness by the multiple sleep latency test (MSLT), a series of nap opportunities across the daytime following a nocturnal polysomnography. However, misperception of whether sleep has occurred on the MSLT has been documented in older adults (> 60 years old) with cognitive impairment. With a criterion of misperceiving at least two nap opportunities, patients who scored lower on the mini mental status examination and lower on the Epworth Sleepiness scale tended to “underperceive” naps (23). Other factors often associated with daytime sleepiness, such as sleep apnea syndrome or disturbed nocturnal sleep, are not present.

Diagnostic workup

	• The diagnostic workup for paradoxical insomnia includes polysomnographic testing with standard montage; a multiple sleep latency test can be included for those with complaints of excessive sleepiness.
	• Actigraphy data are also useful in observing differences between subjective and objective sleep onset latency and sleep efficiency and are a good tool to gain an understanding of usual sleep habits in one’s own environment.

To establish the diagnosis of paradoxical insomnia requires that the patient's complaint of persistent insomnia is not verified by polysomnography, even though the patient feels that the evaluation night was representative of usual sleep.

Polysomnography should include routine sleep stage monitoring, a requirement not sustained in the International Classification of Sleep Disorders, third edition, as well as monitoring of respiration (airflow, effort, oximetry), ECG, leg movements, and continuous video observation (02). The RDC criteria for paradoxical insomnia suggest sleep efficiencies greater than 85% to 90% and a total sleep time (TST) greater than 6.5 hours on recorded nocturnal polysomnography. The MSLT is necessary in patients with a complaint of sleepiness. The assessment should also include a psychiatric evaluation to determine if depression or malingering accounts for the patient's sleep complaint.

Actigraphy is another useful tool in documenting the discrepancy between subjective and objective sleep duration and latency. These evaluations can also be used to reassure the patient regarding good sleep efficiency noted on multiple nights in the usual sleep environment. According to the AASM (American Academy of Sleep Medicine) practice parameters, no specific recommendations were made with regards to use of actigraphy for paradoxical insomnia. Its use for insomnia in general is regarded as “guideline” (this is a patient care strategy that reflects a moderate degree of clinical certainty).

Management

	• Although there is no one specific treatment for paradoxical insomnia, psychoeducation and behavioral therapy have been helpful in this patient population.
	• Sedative medications should be used with caution, and benefit versus risk should be assessed in all patients.

There is no standard treatment for paradoxical insomnia. Management of paradoxical insomnia requires an adequate evaluation leading to accurate diagnosis and appropriate medical care.

Nonpharmacological treatments of paradoxical insomnia may include psychoeducation and behavioral experiments to test misperceptions of sleep. The clinician can use other objective methods available, such as comparing evidence of sleep on the polysomnogram or inactivity on actigraphy to sleep diaries with the patient. In one method developed by Geyer and colleagues, patients receive sleep education specifically for paradoxical insomnia (14). They are shown their polysomnogram waveforms and a video of themselves sleeping in the sleep lab. The patient is asked to indicate when on the video sleep onset occurred. Follow-up sessions include discussions about the discrepancy between objective sleep onset latency and subjective sleep onset latency. This method plus behavioral treatments (sleep education, sleep hygiene, progressive muscle relaxation, and stimulus control) was tested in four individuals with paradoxical insomnia. Post-treatment sessions were conducted 4 and 5 months after baseline. Two of the four patients who received sleep education for paradoxical insomnia had self-reported improvements in insomnia severity, sleep latency, and total sleep time. The other two patients who did not improve had elevated N1% sleep (15).

Other strategies include having the patient use a counter during the night to count the number of awakenings they experience. Patients often report that they press the counter fewer times than they thought they might have. Cognitive therapy is also used to address the patient’s difficulty in perceiving sleep reliably. Patients are reminded that time influences our perception of sleep and that sleep is essentially defined by the absence of memories (18).

In other cases, symptomatic treatment with sedative hypnotics is beneficial; however, these medications should be used with caution. There are case reports of patients who developed paradoxical insomnia as a result of taking zolpidem and other hypnotic medications, such as quetiapine (01; 33).

The authors in a case report describe a patient with paradoxical insomnia and severe depression who responded to electroconvulsive therapy (ECT) treatments (09). The patient had severe insomnia that was causing major depression with suicidal ideation. She reported sleeping for only 35 hours in a month and had no response to multiple sedatives including zolpidem, zaleplon, temazepam, trazodone, chloral hydrate, and oxazepam. She was also started on antidepressants, including mirtazapine and venlafaxine. Actigraphy recordings showed consolidated periods of apparent sleep. Patient underwent ECT treatments three times a week, and following the very first treatment, she reported sleeping 7 hours. The improvement persisted for up to 24 months postdischarge.

Another study examined 29 Iranian patients with paradoxical insomnia who were randomized to receive either olanzapine or risperidone daily for 8 weeks. A Pittsburgh Sleep Quality Index (PSQI) was completed before and after therapy. Patients on olanzapine showed significantly greater improvements in sleep compared to those who received risperidone (19).

Outcomes

In paradoxical insomnia with a complaint of sleepiness, CNS stimulants temporarily improve the symptom, especially if fatigue or a latent mood disorder underlies the complaint. The physician must be concerned about an increased risk of drug dependence when prescribing sedatives or stimulants to this patient population as there is little reason to expect a physiological benefit despite symptomatic improvement.

References

01: Abba-Aji A, Bardoloi P. Paradoxical insomnia in a patient taking zopiclone. BMJ Case Rep 2017;2017. PMID 28104722
02: American Academy of Sleep Medicine. International classification of sleep disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine, 2014.
03: American Academy of Sleep Medicine. ICSD-2 – International classification of sleep disorders, 2nd ed. Diagnostic and coding manual. Westchester, IL: American Academy of Sleep Medicine, 2005.
04: American Sleep Disorders Association. International classification of sleep disorders: diagnostic and coding manual. Rochester (MN): American Sleep Disorders Association, 1990.
05: Bastien CH, Ceklic T, St-Hilaire P, et al. Insomnia and sleep misperception. Pathol Biol (Paris) 2014;62(5):241-51. PMID 25179115
06: Senel GB, Aydın Ö, Aydin ET, Bayar MR, Karadeniz D. Changes in sleep structure and sleep spindles are associated with neuropsychiatric profile in paradoxical insomnia. Int J Psychophysiol 2021;168:27-32. PMID 34331959
07: Bensen-Boakes DB, Lovato N, Meaklim H, Bei B, Scott H. “Sleep-wake state discrepancy”: toward a common understanding and standardized nomenclature. Sleep 2022;45(10):zsac187. PMID 35972329
08: Bianchi MT, Wang W, Klerman EB. Sleep misperception in healthy adults: implications for insomnia diagnosis. J Clin Sleep Med 2012;8(5):547-54. PMID 23066367
09: Case K, Hurwitz TD, Kim SW, Cramer-Bornemann M, Schenck CH. A case of extreme paradoxical insomnia responding selectively to electroconvulsive therapy. J Clin Sleep Med 2008;4(1):62-3. PMID 18350965
10: Castelnovo A, Ferri R, Punjabi NM, et al. The paradox of paradoxical insomnia: a theoretical review towards a unifying evidence-based definition. Sleep Med Rev 2019;44:70-82. PMID 30731262
11: Castillo J, Goparaju B, Bianchi MT. Sleep-wake misperception in sleep apnea patients undergoing diagnostic versus titration polysomnography. J Psychosom Res 2014;76(5):361-7. PMID 24745776
12: Chouvarda I, Grassi A, Mendez MO, et al. Insomnia types and sleep microstructure dynamics. Conf Proc IEEE Eng Med Biol Soc 2013;2013:6167-70. PMID 24111148
13: Emamian F, Mahdipour M, Noori K, et al. Alterations of subcortical brain structures in paradoxical and psychophysiological insomnia disorder. Front Psychiatry 2021;12:661286. PMID 34025484
14: Geyer JD, Lichstein KL, Carney PR, Dillard SC. Paradoxical Insomnia. In: Winkelman JW, Henderson JH, Kotaga S, et al., editors. Case Book of Sleep Medicine: A Learning Companion to the International Classification of Sleep Disorders, Diagnostic and Coding Manual. 2nd ed. Westchester, IL: American Academy of Sleep Medicine, 2008:25-8.
15: Geyer JD, Lichstein KL, Ruiter ME, Ward, LC, Carney PR, Dillard SC. Sleep education for paradoxical insomnia. Behav Sleep Med 2011;9:266-72. PMID 22003980
16: Ghadami MR, Khaledi-Paveh B, Nasouri M, Khazaie H. PTSD-related paradoxical insomnia: an actigraphic study among veterans with chronic PTSD. J Inj Violence Res 2015;7(2):54-8. PMID 25590695
17: Hartmann JA, Carney CE, Lachowski A, Edinger JD. Exploring the construct of subjective sleep quality in patients with insomnia. J Clin Psychiatry 2015;76(6):e768-73. PMID 26132684
18: Harvey AG, Talbot LS. Intervention to reduce misperception. In: Perlis, Aloia, and Kuhn, editors. Behavioral Treatments for Sleep Disorders: A Comprehensive Primer of Behavioral Sleep Medicine Interventions. London, UK: Academic Press, Elsevier, 2011.
19: Khazaie H, Rezaie L, Darvish F, Najafi F, Avis K. Treatment of paradoxical insomnia with atypical antipsychotic drugs. A comparison of olanzapine and risperidone. Neurosciences (Riyadh) 2013;18(1):64-9. PMID 23291800
20: Lecci S, Cataldi J, Betta M, Bernardi G, Heinzer R, Siclari F. Electroencephalographic changes associated with subjective under- and overestimation of sleep duration. Sleep 2020;12;43(11):zsaa094. PMID 32409833
21: Martinez D, Breitenbach TC, Lenz Mdo C. Light sleep and sleep time misperception-relationship to alpha-delta sleep. Clin Neurophysiol 2010;121(5):704-11. PMID 20153688
22: Mohammadi H, Rezaei M, Amiri SM, Rahimi Z, Mansouri K, Khazaie H. Sleep architecture and hypothalamic-pituitary-adrenal activity in paradoxical and psychophysiological insomnia. Basic Clin Neurosci 2018;9(6):397-407. PMID 30719254
23: Nguyen-Michel VH, Lévy PP, Pallanca O, et al. Underperception of naps in older adults referred for a sleep assessment: an insomnia trait and a cognitive problem? J Am Geriatr Soc 2015;63(10):2001-7. PMID 26415517
24: Normand MP, St-Hilaire P, Bastien CH. Sleep spindles characteristics in insomnia sufferers and their relationship with sleep misperception. Neural Plast 2016;2016:6413473. PMID 27478648
25: Parrino L, Milioli G, De Paolis F, Grassi A, Terzano MG. Paradoxical insomnia: the role of CAP and arousals in sleep misperception. Sleep Med 2009;10(10):1139-45. PMID 19595628
26: Perusse AD, Pedneault-Drolet M, Rancourt C, Turcotte I, St-Jean G, Bastien CH. REM sleep as a potential indicator or hyperarousal in psychophysiological and paradoxical insomnia sufferers. Int J Psychophysiol 2015;95(3):372-8. PMID 25596383
27: Ren W, Zhang N, Sun Y, et al. The REM microarousal and REM duration as the potential indicator in paradoxical insomnia. Sleep Med 2023;109:110-7. PMID 37429109
28: Rezaie L, Fobian AD, McCall WV, Khazaie H. Paradoxical insomnia and subjective-objective sleep discrepancy: a review. Sleep Med Rev 2018;40:196-202. PMID 29402512
29: Rezaie L, Vakili-Amini Y, Paschall E, Khazaie H. Personality profiles in paradoxical insomnia: a case-control study. Sleep Sci 2020;13(4):242-8. PMID 33564371
30: Te Lindert BHW, Blanken TF, van der Meijden WP, et al. J Sleep Res 2020;29(1):e12937. PMID 31674088
31: Trimmel K, Eder HG, Böck M, Stefanic-Kejik A, Klösch G, Seidel S. The (mis)perception of sleep: factors influencing the discrepancy between self-reported and objective sleep parameters. J Clin Sleep Med 2021;17(5):917-24. PMID 33393901
32: Valko PO, Hunziker S, Graf K, Werth E, Baumann CR. Sleep-wake misperception. A comprehensive analysis of a large sleep lab cohort. Sleep Med 2021;88:96-103. PMID 34742039
33: Wasey W, Saleh S, Abernathy K, Sapra A, Bhandari P. Paradoxical insomnia in a frustrated patient treated with hypnotics for ten years. Cureus 2021;13(7): e16234. PMID 34367831
34: Yang TLC, Colantonio A, Mollayeva T. Misperception of sleep duration in mild traumatic brain injury/concussion: a preliminary report. Brain Inj 2021;35(2):189-99. PMID 33459073
35: Yoon G, Lee MH, Oh SM, Choi JW, Yoon SY, Lee YJ. J Clin Sleep Med 2022;18(7):1789-95. PMID 35383568

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Lynn Kataria MD

Dr. Kataria of the Washington DC Veterans Affairs Medical Center has no relevant financial relationships to disclose.
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Swathi Charya DO

Dr. Charya of George Washington University has no relevant financial relationships to disclose.
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Editor

Bradley V Vaughn MD

Dr. Vaughn of UNC Hospital Chapel Hill and University of North Carolina School of Medicine has no relevant financial relationships to disclose.
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Former Authors

Frank Zorick MD
Stephen P Duntley MD
Daniela N Minecan MD
Sunita Kumar MD
Deirdre A Conroy PhD
Antonio Culebras MD FAAN FAHA FAASM

Patient Profile

Age range of presentation: 19 to 65+ years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Nonorganic insomnia: F51.0

Nonorganic sleep disorder, unspecified: F51.9
ICD-11: Insomnia disorders, unspecified: 7A0Z

Sleep-wake disorders, unspecified: 7B2Z

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Paradoxical insomnia

Associated Disorders

memory problems
psychophysiological insomnia
sleep fragmentation
sleep state
trouble concentrating

Differential Diagnosis

anxiety
delayed sleep phase
depression
idiopathic hypersomnia
idiopathic insomnia
- insomnia (sleep onset, sleep maintenance)
- narcolepsy
- obstructive sleep apnea
- paradoxical insomnia

Also Relevant

Delayed sleep phase syndrome
Idiopathic insomnia
Inadequate sleep hygiene
Insufficient sleep syndrome
Irregular sleep-wake rhythm disorder
- Pharmacological treatment of insomnia
- Psychophysiological insomnia
- Sleep disorders

Clinical Categories

Sleep Disorders

Patient Handouts

Problem sleepiness

Web References

Clinical Trials

NIH: Sleep Disorders

	• Surveys of the general adult population have found that at least 15% to 20% complain of insomnia-type symptoms. Around 5% to 10% of those with these complaints or subjective sleepiness could be categorized as having paradoxical insomnia.
	• General symptoms of insomnia are relatively common throughout adult society; however, based on objective polysomnographic data, paradoxical insomnia is relatively rare.

Paradoxical insomnia

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

Anesthesia

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Questions or Comment?

Also in This Category

Hypersomnolence

Fatal familial insomnia

Central sleep apnea

Sleep and mental disorders

Sleep paralysis

Sleep and epilepsy

Narcolepsy

Confusional arousal

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