Normal Awake EEG

Normal Awake EEG

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This article describes the most common features of the normal awake EEG. The images at the end of the article show representative examples of the features discussed here. [1, 10]

The alpha rhythm is the most prominent feature of the normal mature EEG. It typically is identified first during the review.

Beta activity refers to a frequency band rather than a distinct (specific) rhythm such as alpha or mu. Beta activity is commonly present in the EEG of healthy people. However, it is often difficult to see because of its low amplitude.

Gastaut initially described the mu rhythm in 1952. This morphologically distinct activity is observed in approximately 17-19% of young adults. [11]

The normal alpha rhythm has the following characteristics:

Frequency of 8-12 Hz – Lower limit of normal generally accepted in adults and children older than 8 years is 8 Hz

Location – Posterior dominant; occasionally, the maximum may be a little more anterior, and it may be more widespread

Morphology – Rhythmic, regular, and waxing and waning

Amplitude – Generally 20-100 mV

Reactivity – Best seen with eyes closed; attenuates with eye opening

Normal beta activity has the following characteristics:

Frequency (by definition) greater than 13 Hz – Common 18-25 Hz, less common 14-16 Hz, and rare 35-40 Hz [2]

Location – Mostly frontocentral but somewhat variable; some describe various types according to location and reactivity: generalized, precentral, and posterior

Morphology – Usually rhythmic, waxing and waning, and symmetric

Amplitude – Usually range of 5-20 mV

Reactivity – Most common 18- to 25-Hz beta activity enhanced during stages I and II sleep and tends to decrease during deeper sleep stages; central beta activity may be reactive (attenuates) to voluntary movements and proprioceptive stimuli; in infants older than 6 months, onset of sleep marked by increased beta activity in central and postcentral regions [3]

Characteristics of the mu rhythms are as follows:

Frequency of 7-11 Hz – Generally in alpha frequency band (8-12 Hz)

Location – Centroparietal area

Morphology – Archlike shape or like an “m”; most often asymmetric and asynchronous between the 2 sides and may be unilateral

Amplitude – Generally low to medium and comparable to that of the alpha rhythm

Reactivity – Most characteristic feature defining the mu rhythm; mu rhythm attenuates with contralateral extremity movement, the thought of a movement, or tactile stimulation; contrary to the alpha rhythm, does not react to eye opening and closing

The mu rhythm has been documented on subdural recording of both sensory and motor cortex and shows the same characteristics as that seen on surface EEG, including distribution, morphology, and reactivity. [4] Furthermore, some correspondence exists between functional mapping of sensorimotor function and somatotopic distribution of mu reactivity. [3, 5, 6]

Occasionally the alpha rhythm is of very low amplitude or even not identifiable. This is not abnormal. In addition to amplitude, other characteristics can vary somewhat without being abnormal, including morphology (eg, spiky), distribution (eg, widespread), and harmonic frequency (eg, slow or fast alpha variant).

In healthy individuals, beta activity commonly can be mildly different (< 35%) in amplitude between the 2 hemispheres, which may be caused by differences in skull thickness. Definite focal, regional, or hemispheric difference (at least 50%) in amplitude may be significant and may suggest either skull defect (side with higher amplitude) or a structural lesion (side with lower amplitude). [7] The amount and voltage of beta activity is enhanced by commonly used sedative medications (benzodiazepines, barbiturates).

Asymmetry, unilaterality, or asynchrony of the mu rhythm is generally not abnormal unless associated with other abnormalities. Very high-voltage mu activity may be recorded in the central regions over skull defects and may become sharp in configuration, and thus can be mistaken for epileptiform discharges. [8] When mu rhythm is detected in an EEG, it should be verified by testing its reactivity.

For excellent patient education resources, see eMedicineHealth’s patient education article Electroencephalography (EEG).

Benbadis SR. Introduction to EEG. Lee-Chiong T, ed. Sleep: A Comprehensive Handbook. Hoboken, NJ: Wiley & Sons; 2006. 989-1024.

Pfurtscheller G, Stancak A Jr, Edlinger G. On the existence of different types of central beta rhythms below 30 Hz. Electroencephalogr Clin Neurophysiol. 1997 Apr. 102(4):316-25. [Medline].

McFarland DJ, Miner LA, Vaughan TM, et al. Mu and beta rhythm topographies during motor imagery and actual movements. Brain Topogr. 2000 Spring. 12(3):177-86. [Medline].

Arroyo S, Lesser RP, Gordon B, et al. Functional significance of the mu rhythm of human cortex: an electrophysiologic study with subdural electrodes. Electroencephalogr Clin Neurophysiol. 1993 Sep. 87(3):76-87. [Medline].

Pfurtscheller G, Neuper C, Krausz G. Functional dissociation of lower and upper frequency mu rhythms in relation to voluntary limb movement. Clin Neurophysiol. 2000 Oct. 111(10):1873-9. [Medline].

Pineda JA, Allison BZ, Vankov A. The effects of self-movement, observation, and imagination on mu rhythms and readiness potentials (RP’s): toward a brain-computer interface (BCI). IEEE Trans Rehabil Eng. 2000 Jun. 8(2):219-22. [Medline].

Benbadis SR. Focal disturbances of brain function. Levin KH, Luders HO, eds. Comprehensive Clinical Neurophysiology. Philadelphia, Pa: WB Saunders; 2000. 457-67.

Smith SJ. EEG in the diagnosis, classification, and management of patients with epilepsy. J Neurol Neurosurg Psychiatry. 2005 Jun. 76 Suppl 2:ii2-7. [Medline].

Smith SJ. EEG in neurological conditions other than epilepsy: when does it help, what does it add?. J Neurol Neurosurg Psychiatry. 2005 Jun. 76 Suppl 2:ii8-12. [Medline].

Kamarajan C, Porjesz B. Advances in Electrophysiological Research. Alcohol Res. 2015. 37 (1):53-87. [Medline].

Thorpe SG, Cannon EN, Fox NA. Spectral and source structural development of mu and alpha rhythms from infancy through adulthood. Clin Neurophysiol. 2015 Mar 20. [Medline].

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 Awake EEG

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