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Normal Sleep EEG Author: Selim R Benbadis, MD; Chief Editor: Helmi L Lutsep, MD more...

Updated: Mar 8, 2010

Overview

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 4stages (stage I, stage II, stage III, stage IV). NREM and REM occur in alternating cycles, each lasting approximately90-100 minutes, with a total of 4-6 cycles. In general, in the healthy young adult NREM sleep accounts for 75-90% ofsleep time (3-5% stage I, 50-60% stage II, and 10-20% stages III and IV). REM sleep accounts for 10-25% of sleeptime.

Total sleep time in the healthy young adult approximates 7.5-8 hours. In the full-term newborn, sleep cycles lastapproximately 60 minutes (50% NREM, 50% REM, alternating through a 3-4 h interfeeding period). The newbornsleeps approximately 16-20 hours per day; these numbers decline to a mean of 10 hours during childhood.

Stage I Sleep

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

The earliest indication of transition from wakefulness to stage I sleep (drowsiness) is shown here and usually consists of acombination of (1) drop out of alpha activity and (2) slow rolling eye movements.

Slow rolling (lateral) eye movements during stage I sleep. Like faster lateral eye movements, slow ones are best seen at the F7and F8 electrodes, with the corneal positivity indicating the side of gaze.

Normal Sleep EEG http://emedicine.medscape.com/article/1140322-overview

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On this transverse montage, typical vertex sharp transients are seen. In contrast to K complexes, these are narrow (brief) andmore focal, with a maximum negativity at the mid line (Cz and to a lesser degree Fz). These are seen in sleep stages I and II.

Vertex waves are focal sharp transients typically best seen on transverse montages (through the midline) and would be missed onthis longitudinal bipolar montage if it did not include midline channels (Fz-Cz-Pz). Vertex waves are seen in sleep stages I and II.

Positive occipital sharp transients of sleep (POSTS) are seen in both occipital regions, with their typical characteristics containedin their name. They also have morphology classically described as "reverse check mark" and often occur in consecutive runs ofseveral seconds, as shown here.

Waveform descriptions

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 similarto eye movements in general (see EEG Artifacts). However, they are slow (ie, typically 0.25-0.5 Hz). SREMsdisappear in stage II and deeper sleep stages.Attenuation (drop out) of the alpha rhythm: Drop out of alpha activity typically occurs together with or nearbySREM. The alpha rhythm gradually becomes slower, less prominent, and fragmented.Central or frontocentral theta activityEnhanced beta activityPositive 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 age50 years. POSTS are seen very commonly on EEG and have been said to be more common during daytimenaps than during nocturnal sleep. Most characteristics of POSTS are contained in their name. They have apositive maximum at the occiput, are contoured sharply, and occur in early sleep (stages I and II). Theirmorphology is classically described as "reverse check mark," and their amplitude is 50-100 µV. They typicallyoccur in runs of 4-5 Hz and are bisynchronous, although they may be asymmetric. They persist in stage IIsleep but usually disappear in subsequent stages.Vertex sharp transients: Also called vertex waves or V waves, these transients are almost universal. Althoughthey are often grouped together with K complexes, strictly speaking, vertex sharp transients are distinct fromK complexes. Like K complexes, vertex waves are maximum at the vertex (central midline placement ofelectrodes [Cz]), so that, depending on the montage, they may be seen on both sides, usually symmetrically.


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Their amplitude is 50-150 µV. They can be contoured sharply and occur in repetitive runs, especially inchildren. 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[2] ) is awell-recognized normal variant of drowsiness in children aged 3 months to 13 years. This is described asparoxysmal bursts (3-5 Hz) of high-voltage (as high as 350 µV) sinusoidal waves, maximally expressed in theprefrontal-central areas, that brake after the cerebral activity amplitude drops during drowsiness.

Clinical correlation

The importance of normal sleep patterns is that they should not be mistaken for pathologic sharp waves. Severalnormal 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 Sleep

Stage II is the predominant sleep stage during a normal night's sleep. The distinct and principal EEG criterion toestablish stage II sleep is the appearance of sleep spindles or K complexes. The presence of sleep spindles isnecessary and sufficient to define stage II sleep. Another characteristic finding of stage II sleep is the appearance ofK complexes, but since K complexes are typically associated with a spindle, spindles are the defining features ofstage 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.

This shows a K complex, typically a high-amplitude long-duration biphasic waveform with overriding spindle. This is a transversemontage, which shows the typical maximum (manifested by a "phase reversal") at the midline.

Typical sleep spindles with short-lived waxing and waning 15-Hz activity maximum in the frontocentral regions. Note theassociated slow (theta) activity that also characterizes stage II sleep.


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Vertex sharp transients. This transverse montage illustrates the maximum negativity (manifested by a negative phase reversal) atthe midline. The location is similar to that of K complexes, but these are shorter (narrower) and more localized.

K complex, with its typical characteristics: high-amplitude, widespread, broad, diphasic slow transient with overriding spindle. Onthe longitudinal montage (left), the K complex appears to be generalized. However, the transverse montage clearly shows that themaximum (phase reversal) is at the midline (Fz and Cz).

A mixture of spindles (ie, bicentral short-lived rhythmic 14 Hz bursts) and positive occipital sharp transients of sleep (POSTS) canbe seen. POSTS occur in stage I, but the presence of spindles is "diagnostic" of stage II.

A mixture of positive occipital sharp transients of sleep (POSTS) and spindles (fronto-central short-lived rhythmic 14-Hz bursts)can be seen.


Sleep spindles normally first appear in infants aged 6-8 weeks and are bilaterally asynchronous. These becomewell-formed spindles and bilaterally synchronous by the time the individual is aged 2 years. Sleep spindles have afrequency of 12-16 Hz (typically 14 Hz) and are maximal in the central region (vertex), although they occasionallypredominate in the frontal regions. They occur in short bursts of waxing and waning spindlelike (fusiform) rhythmicactivity. Amplitude is usually 20-100 µV. Extreme spindles (described by Gibbs and Gibbs) are unusuallyhigh-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 transientand are often associated with sleep spindles. Location is frontocentral, with a typical maximum at the midline (centralmidline placement of electrodes [Cz] or frontal midline placement of electrodes [Fz]). They occur spontaneously andare elicited as an arousal response. They may have an association with blood pressure fluctuation during sleep.


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

Stage III and IV 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.

Slow wave sleep with predominantly delta activity, especially in the first half.

Slow wave sleep with predominantly delta activity.

Men aged 20-29 years spend about 21% of their total sleep in SWS, those aged 40-49 years spend about 8% inSWS, and those aged 60-69 spend about 2% in SWS.[3] Notably, elderly people's sleep comprises only a smallamount of deep sleep (virtually no stage IV sleep and scant stage III sleep). Their total sleep time approximates 6.5hours.

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


SWS, or delta sleep, is characterized, as the name implies, by delta activity. This is typically generalized andpolymorphic or semirhythmic. By strict sleep staging criteria on polysomnography, SWS is defined by the presence ofsuch 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 deltaactivity. Stage III is defined by delta activity that occupies 20-50% of the time, whereas in stage IV, delta activityrepresents greater than 50% of the time. Sleep spindles and K complexes may persist in stage III and even to somedegree in stage IV, but they are not prominent.



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

REM Sleep

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

Rapid eye movement sleep with rapid (saccadic) eye movements. While muscle "atonia" cannot be proven without a dedicatedelectromyogram (EMG) channel, certainly EMG artifact is absent with a "quiet" recording. Also, no alpha rhythm is present thatwould suggest wakefulness.

Typical saccadic eye movements of rapid eye movement sleep are shown, with lateral rectus "spikes" seen just preceding thelateral abducting eye movements.

In addition to rapid eye movements, this rapid eye movement sleep record is characterized by brief fragments of alpha rhythm(first half) and central saw tooth waves (second half).


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This is a good example of saw tooth waves seen in rapid eye movement sleep and their "notched" morphology.

This is a good example of saw tooth waves seen in rapid eye movement sleep and their "notched" morphology, best seen here inthe Cz-Pz (last) channel.

This illustrates the typical appearance of saw tooth waves on a polysomnogram (PSG) display, equivalent to 1 cm/s.


By strict sleep staging criteria on polysomnography, REM sleep is defined by (1) rapid eye movements, (2) muscleatonia, and (3) EEG desynchronization (compared to slow wave sleep). Thus, 2 of the 3 defining characteristics arenot cerebral waves and theoretically require monitoring of eye movements (electro-oculogram [EOG]) and muscletone (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 areseen in REM sleep.

EEG desynchronization: The EEG background activity changes from that seen in slow wave sleep (stage IIIor IV) to faster and lower voltage activity (theta and beta), resembling wakefulness. Saw tooth waves are aspecial type of central theta activity that has a notched morphology resembling the blade of a saw and usuallyoccurs 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 asa 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 periodinto early morning. The occurrence of REM too soon after sleep onset, referred to as SOREMP, is consideredpathological. 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).


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Patient Education

For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patienteducation articles Sleep: Understanding the Basics and Electroencephalography (EEG).

Contributor Information and DisclosuresAuthorSelim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology andNeurosurgery, University of South Florida School of Medicine, Tampa General Hospital

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,and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; CyberonicsHonoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Ortho McNeil HonorariaSpeaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Speaking, consulting

Coauthor(s)Diego Rielo, MD Staff Physician, Department of Neurology, Memorial Hospital West, Memorial Healthcare

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

Disclosure: Nothing to disclose.

Specialty Editor BoardLeslie Huszar, MD Consulting Staff, Department of Neurology, Indian River Memorial Hospital

Leslie Huszar, MD is a member of the following medical societies: American Academy of Neurology, AmericanAssociation for the Advancement of Science, and American Medical Electroencephalographic Association


Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

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,Wrentham, MA

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


Chief EditorHelmi L Lutsep, MD Professor, Department of Neurology, Oregon Health & Science University; AssociateDirector, Oregon Stroke Center

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

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel


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membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Reviewpanel membership; Abbott Consulting fee Consulting; Sanofi Consulting fee Consulting

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Normal Sleep EEG - We Got This! – ryansrallyryansrally.org/wp-content/uploads/2011/10/Normal-Sleep-EEG.pdf · Normal Sleep EEG Author: Selim R Benbadis, MD; ... Loomis provided