Normal Sleep EEG

Normal Sleep EEG

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Loomis provided the earliest detailed description of various stages of sleep in the mid-1930s, and in the early 1950s, Aserinsky and Kleitman identified rapid eye movement (REM) sleep [1] . Sleep is generally divided into 2 broad types: nonrapid eye movement (NREM) sleep and REM sleep. Based on EEG changes, NREM is divided further into 4 stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each lasting approximately 90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM sleep accounts for 75-90% of sleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM sleep accounts for 10-25% of sleep time.

According to the National Sleep Foundation, the appropriate sleep duration for newborns is between 14 and 17 hours, sleep cycles last approximately 60 minutes (50% NREM, 50% REM, alternating through a 3-4 hour interfeeding period); these numbers decline to a mean of 10 hours during childhood. Recommended sleep for infants is between 12 and 15 hours, toddlers between 11 and 14 hours, preschoolers between 10 and 13 hours, and school-aged children between 9 and 11 hours. For teenagers, 8 to 10 hours is considered appropriate, 7 to 9 hours for young adults and adults, and 7 to 8 hours of sleep for older adults. [2]

Stage I sleep is also referred to as drowsiness or presleep and is the first or earliest stage of sleep. Representative EEG waveforms are shown in the images below.

The features of drowsiness are as follows:

Slow rolling eye movements (SREMs): SREMs are usually the first evidence of drowsiness seen on the EEG. SREMs of drowsiness are most often horizontal but can be vertical or oblique, and their distribution is similar to eye movements in general (see EEG Artifacts). However, they are slow (ie, typically 0.25-0.5 Hz). SREMs disappear in stage II and deeper sleep stages.

Attenuation (drop out) of the alpha rhythm: Drop out of alpha activity typically occurs together with or nearby SREM. The alpha rhythm gradually becomes slower, less prominent, and fragmented.

Central or frontocentral theta activity

Enhanced beta activity

Positive occipital sharp transients of sleep (POSTS): POSTS start to occur in healthy people at age 4 years, become fairly common by age 15 years, remain common through age 35 years, and start to disappear by age 50 years. POSTS are seen very commonly on EEG and have been said to be more common during daytime naps than during nocturnal sleep. Most characteristics of POSTS are contained in their name. They have a positive maximum at the occiput, are contoured sharply, and occur in early sleep (stages I and II). Their morphology is classically described as “reverse check mark,” and their amplitude is 50-100 µV. They typically occur in runs of 4-5 Hz and are bisynchronous, although they may be asymmetric. They persist in stage II sleep but usually disappear in subsequent stages.

Vertex sharp transients: Also called vertex waves or V waves, these transients are almost universal. Although they are often grouped together with K complexes, strictly speaking, vertex sharp transients are distinct from K complexes. Like K complexes, vertex waves are maximum at the vertex (central midline placement of electrodes [Cz]), so that, depending on the montage, they may be seen on both sides, usually symmetrically. Their amplitude is 50-150 µV. They can be contoured sharply and occur in repetitive runs, especially in children. They persist in stage II sleep but usually disappear in subsequent stages. Unlike K complexes, vertex waves are narrower and more focal and by themselves do not define stage II.

Hypnagogic hypersynchrony: Hypnagogic hypersynchrony (first described by Gibbs and Gibbs, 1950 [3] ) is a well-recognized normal variant of drowsiness in children aged 3 months to 13 years. This is described as paroxysmal bursts (3-5 Hz) of high-voltage (as high as 350 µV) sinusoidal waves, maximally expressed in the prefrontal-central areas, that brake after the cerebral activity amplitude drops during drowsiness.

The importance of normal sleep patterns is that they should not be mistaken for pathologic sharp waves. Several normal stage I patterns easily can be mistaken for epileptic sharp waves or spikes, including vertex sharp transients, POSTS, and even fragments of alpha rhythm as it drops out.

Stage II is the predominant sleep stage during a normal night’s sleep. The distinct and principal EEG criterion to establish stage II sleep is the appearance of sleep spindles or K complexes. The presence of sleep spindles is necessary and sufficient to define stage II sleep. Another characteristic finding of stage II sleep is the appearance of K complexes, but since K complexes are typically associated with a spindle, spindles are the defining features of stage II sleep. Except for slow rolling eye movements, all patterns described under stage I persist in stage II sleep. Representative examples of the waveforms described here are shown in the images below.

Sleep spindles normally first appear in infants aged 6-8 weeks and are bilaterally asynchronous. These become well-formed spindles and bilaterally synchronous by the time the individual is aged 2 years. Sleep spindles have a frequency of 12-16 Hz (typically 14 Hz) and are maximal in the central region (vertex), although they occasionally predominate in the frontal regions. They occur in short bursts of waxing and waning spindlelike (fusiform) rhythmic activity. Amplitude is usually 20-100 µV. Extreme spindles (described by Gibbs and Gibbs) are unusually high-voltage (100-400 µV) and prolonged (>20 s) spindles located over the frontal regions.

K complexes (initially described by Loomis) are high amplitude (>100 µV), broad (>200 ms), diphasic, and transient and are often associated with sleep spindles. Location is frontocentral, with a typical maximum at the midline (central midline placement of electrodes [Cz] or frontal midline placement of electrodes [Fz]). They occur spontaneously and are elicited as an arousal response. They may have an association with blood pressure fluctuation during sleep.

The stigmata of stage II sleep, spindles and K complexes, are usually easy to identify and are less subject to overinterpretation or misinterpretation than the patterns of stage I sleep.

Stages III and IV sleep are usually grouped together as “slow wave sleep” or “delta sleep.” Slow wave sleep (SWS) is usually not seen during routine EEG, which is too brief a recording. However, it is seen during prolonged (>24 h) EEG monitoring. Representative examples of SWS EEGs are shown in the images below.

Men aged 20-29 years spend about 21% of their total sleep in SWS, those aged 40-49 years spend about 8% in SWS, and those aged 60-69 spend about 2% in SWS. [4] Notably, elderly people’s sleep comprises only a small amount of deep sleep (virtually no stage IV sleep and scant stage III sleep). Their total sleep time approximates 6.5 hours.

SWS is characterized by relative body immobility, although body movement artifacts may be registered on electromyogram (EMG) toward the end of SWS.

SWS, or delta sleep, is characterized, as the name implies, by delta activity. This is typically generalized and polymorphic or semirhythmic. By strict sleep staging criteria on polysomnography, SWS is defined by the presence of such delta activity for more than 20% of the time, and an amplitude criterion of at least 75 µV is often applied.

The distinction between stage III and stage IV sleep is only a quantitative one that has to do with the amount of delta activity. Stage III is defined by delta activity that occupies 20-50% of the time, whereas in stage IV, delta activity represents greater than 50% of the time. Sleep spindles and K complexes may persist in stage III and even to some degree in stage IV, but they are not prominent.

As already mentioned, SWS is usually not seen during routine EEG, which is too brief a recording. However, it is seen during prolonged EEG monitoring. One important clinical aspect of SWS is that certain parasomnias occur specifically out of this stage and must be differentiated from seizures. These slow wave sleep parasomnias include confusional arousals, night terrors (pavor nocturnus), and sleepwalking (somnambulism).

REM sleep normally is not seen on routine EEGs, because the normal latency to REM sleep (100 min) is well beyond the duration of routine EEG recordings (approximately 20-30 min). The appearance of REM sleep during a routine EEG is referred to as sleep-onset REM period (SOREMP) and is considered an abnormality. While not observed on routine EEG, REM sleep commonly is seen during prolonged (>24 h) EEG monitoring. Representative examples of waveforms described here can be seen in the images below.

By strict sleep staging criteria on polysomnography, REM sleep is defined by (1) rapid eye movements, (2) muscle atonia, and (3) EEG desynchronization (compared to slow wave sleep). Thus, 2 of the 3 defining characteristics are not cerebral waves and theoretically require monitoring of eye movements (electro-oculogram [EOG]) and muscle tone (electromyelogram [EMG]). Fortunately, muscle activity and eye movements can be evaluated on EEG; thus, REM sleep is usually not difficult to identify. In addition to the 3 features already named, “saw tooth” waves also are seen in REM sleep.

EEG desynchronization: The EEG background activity changes from that seen in slow wave sleep (stage III or IV) to faster and lower voltage activity (theta and beta), resembling wakefulness. Saw tooth waves are a special type of central theta activity that has a notched morphology resembling the blade of a saw and usually occurs close to rapid eye movements (ie, phasic REM). They are only rarely clearly identifiable.

Rapid eye movements: These are saccadic, predominantly horizontal, and occur in repetitive bursts.

Despite the lack of a dedicated EMG channel, the muscle atonia that characterizes REM sleep is usually apparent as a general sense of “quiet” muscle artifacts compared to wakefulness.

The duration of REM sleep increases progressively with each cycle and tends to predominate late in the sleep period into early morning. The occurrence of REM too soon after sleep onset, referred to as SOREMP, is considered pathological. However, newborns and infants enter REM more rapidly and spend a higher proportion of sleep in REM (this is true in most species and supports the theory that REM sleep is involved in brain development).

For excellent patient education resources, see eMedicineHealth’s patient education articles Sleep: Understanding the Basics and Electroencephalography (EEG).


What is normal sleep EEG?

How is stage I sleep defined on normal sleep EEG?

What are the EEG waveform features of drowsiness in stage I sleep?

How is stage II sleep defined on normal EEG?

What are the EEG waveform features of stage II sleep?

How are stage III and IV sleep defined on normal sleep EEG?

What are the EEG waveform features of stage III and IV sleep?

How is rapid eye movement (REM) sleep defined on normal sleep EEG?

What are EEG waveform features of rapid eye movement (REM) sleep?

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Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Acorda, Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion, Upsher-Smith.<br/>Serve(d) as a speaker or a member of a speakers bureau for: Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion.<br/>Received research grant from: Acorda, Livanova, Greenwich, Lundbeck, Sepracor, Sunovion, UCB, Upsher-Smith.

Diego Antonio Rielo, MD Staff Physician, Department of Neurology, Memorial Hospital West, Memorial Healthcare

Diego Antonio Rielo, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Norberto Alvarez, MD Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children’s Hospital; Medical Director, Wrentham Developmental Center

Norberto Alvarez, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Nothing to disclose.

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Executive Committee for the NINDS-funded DEFUSE3 Trial; Physician Advisory Board for Coherex Medical.

Normal Sleep EEG

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