Introduction
An electroencephalogram (EEG) is an essential tool that studies the brain's electrical activity. Despite developing more advanced imaging techniques, EEG remains the essential paraclinical tool for seizure evaluation. It is primarily used to assess seizures and conditions that may mimic seizures. It is also useful to classify seizure types, assess comatose patients in the intensive care unit, and evaluate encephalopathies, among other indications. The electrical properties of the brain were first discovered by an English scientist, Richard Caton, in 1875, and about 50 years later, the German psychiatrist Hans Berger recorded the first human EEG.[1][2]
Anatomy and Physiology
Register For Free And Read The Full Article
- Search engine and full access to all medical articles
- 10 free questions in your specialty
- Free CME/CE Activities
- Free daily question in your email
- Save favorite articles to your dashboard
- Emails offering discounts
Learn more about a Subscription to StatPearls Point-of-Care
Anatomy and Physiology
The EEG recording electrodes are placed over the scalp. They measure the absolute electrical potentials generated by the neurons of the underlying cerebral cortex. An estimated cortical area of 10 cm2 discharging synchronously is required to generate a deflection on scalp EEG.[3] The pyramidal cell bodies are mostly present in layers 3 and 5 of the cerebral cortex.[4] Following the release of neurotransmitters at the endplate, excitatory or inhibitory postsynaptic potentials (EPSP/IPSP) are generated secondary to neuronal depolarization (in the case of EPSP with intracellular sodium influx resulting in extracellular negativity) or hyperpolarization (in the case of IPSP intracellular negativity). The summation of EPSPs and IPSPs over a selected cortical region with synchronous discharge creates an electrical field with positive and negative ends (dipole). The dipole is typically parallel to the pyramidal cell orientation. The EEG measures this summation.[5][6]
The cortical neurons and the subcortical structures are systematically connected through well-developed feedback linkages.[7] During the resting or relaxed state, the EEG records a sinusoidal rhythmic activity called the posterior dominant rhythm that is believed to be due to oscillatory interaction between the cortex (visual cortex in this instance) and subcortical structures (thalamus).[8][9] During activation, the cortical activity desynchronizes, and the oscillatory activity is replaced with lower amplitude and faster frequency activity. In the event of a seizure, a large super-synchronous neuronal discharge is created from an abnormal brain network. EEG evaluation provides important information about the localization and the spread of such discharges.
The commonly encountered waveform frequencies in EEGs are alpha (8 to 12 Hz), beta (13 to 30 Hz), theta (4 to 7 Hz), and delta (less than 4 Hz). The predominance of waveforms in an EEG varies based on the individual's age and state of wakefulness. The EEG waveforms start with discontinuous backgrounds during the prenatal phase and mature to be continuous at a later age. The normal adult resting posterior dominant rhythm of 8.5 Hz in the posterior head regions is noted after 8 years. The slower waveforms are less during the wakeful state and dominate during later stages of sleep. There is also an anterior-to-posterior distribution of waveforms with faster frequencies in the anterior and slower frequencies in the posterior head regions. Sleep spindles and K-complexes are other notable components/waveforms that appear during the first year of life and are useful to differentiate sleep stages. One should learn several benign EEG variants and artifacts to avoid reporting a false-positive test.[10]
Indications
There are several indications for an EEG.[11][12][13] A brief list of various indications includes:
- To classify the type of seizure and localize the onset of seizures[14][10]
- Sodium amobarbital or Wada test to determine the hemisphere dominance for language and memory[15]
- Management of status epilepticus and inducing therapeutic coma[16][17][16]
- Patients with altered mental status from various etiologies like toxic metabolic encephalopathies[18][19]
- Encephalopathic patients with unexplained etiologies to assess the degree of encephalopathy[20]
- Syncope or symptoms of loss of consciousness with a negative cardiac workup[21]
- Comatose patients in the intensive care unit with impaired or persistent confusion or decreased responsiveness[22][23]
- Prognostication after cardiac arrest[24]
- Identify delayed ischemic changes after subarachnoid and intracranial hemorrhage[25][26]
- Anesthetic procedures to monitor the depth of anesthesia[27]
- Brain death determination[28][29]
Contraindications
There are no clear contraindications to performing an EEG. However, electrode placement could be challenging following a craniotomy and in case of breaches in the skull or open wounds. The EEG should be performed after a detailed history and if there are concerns for seizures or epilepsy. Activation procedures should be omitted in individuals with certain underlying conditions. For example, hyperventilation is a relative contraindication in patients with a history of strokes, myocardial infarction, surgeries (transplants), acute respiratory distress syndrome, asthma, Moyamoya disease, and sickle cell anemia.[30][31]
Equipment
The basic equipment includes electrodes (silver/silver-chloride electrodes are the most widely used), an amplifier, and an EEG system (monitor and processor). Previously, mechanical pen and paper recording devices were used to plot the EEG recordings (analog recording). In current clinical practice, a standard EEG system can obtain information from at least 128 channels, with a greater than 10 kHz sampling rate from all the channels, along with a 24-bit resolution at each amplifier.[5] Other important components of the electrode placement are the gel and salts that are applied to improve the scalp conductivity and thereby record waveforms. Nowadays, dry electrodes are also used to improve and hasten scalp preparation.[32]
Personnel
The EEG is performed by the EEG technician/technologist, who is a trained professional with appropriate undergraduate education and training. They undergo rigorous training and certification process. Once a study is completed, the recordings are reviewed, and a report is generated by the clinical neurophysiologist, who is typically a board-certified/eligible neurologist who undergoes additional subspecialty training in EEG/epilepsy.[33] The EEG performance in the ICU and the epilepsy monitoring units requires the participation of additional trained staff (nurses, support staff, monitor technicians, and others) to provide proper and safe evaluation and care of all patients.[34]
Preparation
When the EEG is performed in an outpatient setting, clear instructions are provided to the patients before their EEG appointment. They are recommended not to use conditioners or other substances that might affect the recording quality (electrode impedance). The scalp is usually cleaned well to obtain proper recording with low impedance.[35] Typically, the impedance should be lower than 5 kohm. Several measures are typically taken for ICU patients to reduce the disturbances from various medical instruments, devices, and lines used. Mechanical restraints and not chemical restraints might sometimes be necessary to ensure a proper EEG recording.
Technique or Treatment
A routine EEG is performed in a quiet room with controllable lighting levels. The test should be performed by an EEG technician with appropriate and relevant training. The 10 to 20 international system is widely used for scalp electrode placement.[36] Typically, at least 21 electrodes are placed on an adult scalp, including a reference and ground electrodes. Once the electrodes are placed, the impedance of all electrodes should be measured and ensured that it is less than 5 kohms. Calibration should be performed before beginning the study. These include recording a square wave signal and biological calibration. Various activation procedures are performed during the recording to trigger epileptiform abnormalities and other EEG changes. These include eye-opening and closure, hyperventilation, and photic stimulation. The recordings of drowsiness and sleep are important components of any EEG procedure. Sleep deprivation is also used as a provocative technique.[37]
The EEG channels are displayed following different montages, and each channel records the electrical potential difference between the 2 components (electrodes) of each channel. EEGs should be reviewed using different types of montages (mainly bipolar and referential montages) to isolate and localize abnormal discharges accurately.[38] The digitalization of EEG has significantly improved the ease of reformatting and re-montaging per the electroencephalographer's requirements for interpretation purposes.[39] Commonly used montages are:
- Referential montages (eg ear reference, average reference)
- Bipolar montages (longitudinal and transverse)
- Laplacian montages[40][41]
Referential Montages
The channels display the potential difference between the recording/active electrode and a preselected reference (another electrode over a body area or the average of a certain number of selected electrodes).
Bipolar Montages
The longitudinal or transverse channels display the potential difference between 2 contiguous electrodes. These montages easily detect asymmetry between the 2 brain hemispheres.
Laplacian Montages
In this montage, the reference is a combined weighted average of the potentials surrounding a particular electrode or region of interest. It is typically useful to study or assess focal discharges with minimal field.[42]
Complications
Unexpected complications can occur if due diligence is not performed while screening patients before performing the activation or provocative procedures like hyperventilation in certain individuals, as mentioned previously. Long-term EEG monitoring in epilepsy monitoring units and intensive care units is associated with skin injury, and appropriate care needs to be provided.[43]
Clinical Significance
EEG is an important tool for investigating central nervous system pathologies associated with seizures and altered mental status in routine practice. It is a complementary test to the more advanced imaging studies. EEG is widely used in the evaluation of epilepsy patients, altered mental status or altered consciousness, parasomnias, encephalopathies secondary to various metabolic and toxic derangements, dementias, and strokes presenting as seizures. EEG is also useful to assess for prognostication in patients with anoxic brain injury, traumatic brain injuries, determining brain death, and drug toxicities. EEG is fundamentally a universal tool for assessing interictal brain wave activity and understanding underlying progress in an unresponsive or comatose individual. It better is also useful to assess patients with behavioral or psychogenic spells that appear to be similar to seizures.[11][12][13]
The activation procedures help or facilitate capturing abnormal discharges that are useful to classify the areas of the brain involved in focal epilepsies or determine if the individual has a genetic or primary type of epilepsy. Long-term EEGs with video are useful to capture seizures and characterize their semiology. From a diagnostic and treatment standpoint, this information would be useful for presurgical work with curative intent if the patient's seizures tend to be medically intractable. The more invasive form of EEGs using the grid and depth electrodes is applied to assess the brain's electrical activity from the surface of the cortex and subcortical white matter, respectively.[44][45]
Enhancing Healthcare Team Outcomes
An interprofessional team is essential for managing patients who require a diagnostic EEG. A team of well-trained EEG technicians, nurses, clinical neurophysiologists, and neurologists is required to appropriately screen the patients and ensure a proper test is performed safely and interpreted correctly based on guidelines, thus facilitating the best treatment decision to be made by the treating providers.[46] The EEG interpreting physicians should be board-certified and follow the guidelines provided by the appropriate clinical neurophysiology society for EEG reporting.[47][48]
References
Haas LF. Hans Berger (1873-1941), Richard Caton (1842-1926), and electroencephalography. Journal of neurology, neurosurgery, and psychiatry. 2003 Jan:74(1):9 [PubMed PMID: 12486257]
Tudor M, Tudor L, Tudor KI. [Hans Berger (1873-1941)--the history of electroencephalography]. Acta medica Croatica : casopis Hravatske akademije medicinskih znanosti. 2005:59(4):307-13 [PubMed PMID: 16334737]
COOPER R, WINTER AL, CROW HJ, WALTER WG. COMPARISON OF SUBCORTICAL, CORTICAL AND SCALP ACTIVITY USING CHRONICALLY INDWELLING ELECTRODES IN MAN. Electroencephalography and clinical neurophysiology. 1965 Feb:18():217-28 [PubMed PMID: 14255050]
DeFelipe J,Fariñas I, The pyramidal neuron of the cerebral cortex: morphological and chemical characteristics of the synaptic inputs. Progress in neurobiology. 1992 Dec; [PubMed PMID: 1410442]
Level 3 (low-level) evidenceBiasiucci A, Franceschiello B, Murray MM. Electroencephalography. Current biology : CB. 2019 Feb 4:29(3):R80-R85. doi: 10.1016/j.cub.2018.11.052. Epub [PubMed PMID: 30721678]
Kirschstein T, Köhling R. What is the source of the EEG? Clinical EEG and neuroscience. 2009 Jul:40(3):146-9 [PubMed PMID: 19715175]
Babiloni C, Binetti G, Cassarino A, Dal Forno G, Del Percio C, Ferreri F, Ferri R, Frisoni G, Galderisi S, Hirata K, Lanuzza B, Miniussi C, Mucci A, Nobili F, Rodriguez G, Luca Romani G, Rossini PM. Sources of cortical rhythms in adults during physiological aging: a multicentric EEG study. Human brain mapping. 2006 Feb:27(2):162-72 [PubMed PMID: 16108018]
Goldman RI,Stern JM,Engel J Jr,Cohen MS, Simultaneous EEG and fMRI of the alpha rhythm. Neuroreport. 2002 Dec 20; [PubMed PMID: 12499854]
Sauseng P, Klimesch W, Stadler W, Schabus M, Doppelmayr M, Hanslmayr S, Gruber WR, Birbaumer N. A shift of visual spatial attention is selectively associated with human EEG alpha activity. The European journal of neuroscience. 2005 Dec:22(11):2917-26 [PubMed PMID: 16324126]
Ramakrishnan S, Asuncion RMD, Rayi A. Localization-Related Epilepsies on EEG. StatPearls. 2024 Jan:(): [PubMed PMID: 32491577]
Herman ST, Abend NS, Bleck TP, Chapman KE, Drislane FW, Emerson RG, Gerard EE, Hahn CD, Husain AM, Kaplan PW, LaRoche SM, Nuwer MR, Quigg M, Riviello JJ, Schmitt SE, Simmons LA, Tsuchida TN, Hirsch LJ, Critical Care Continuous EEG Task Force of the American Clinical Neurophysiology Society. Consensus statement on continuous EEG in critically ill adults and children, part I: indications. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2015 Apr:32(2):87-95. doi: 10.1097/WNP.0000000000000166. Epub [PubMed PMID: 25626778]
Level 3 (low-level) evidencePrimavera A,Audenino D,Cocito L, Emergent EEG: Indications and diagnostic yield. Neurology. 2004 Mar 23; [PubMed PMID: 15037727]
Level 3 (low-level) evidenceVarelas PN, Spanaki MV, Hacein-Bey L, Hether T, Terranova B. Emergent EEG: indications and diagnostic yield. Neurology. 2003 Sep 9:61(5):702-4 [PubMed PMID: 12963769]
Modur PN, Rigdon B. Diagnostic yield of sequential routine EEG and extended outpatient video-EEG monitoring. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2008 Jan:119(1):190-6 [PubMed PMID: 18042424]
Gotman J, Bouwer MS, Jones-Gotman M. Intracranial EEG study of brain structures affected by internal carotid injection of amobarbital. Neurology. 1992 Nov:42(11):2136-43 [PubMed PMID: 1436524]
Privitera M,Hoffman M,Moore JL,Jester D, EEG detection of nontonic-clonic status epilepticus in patients with altered consciousness. Epilepsy research. 1994 Jun; [PubMed PMID: 7957038]
Level 2 (mid-level) evidenceClaassen J, Hirsch LJ, Emerson RG, Bates JE, Thompson TB, Mayer SA. Continuous EEG monitoring and midazolam infusion for refractory nonconvulsive status epilepticus. Neurology. 2001 Sep 25:57(6):1036-42 [PubMed PMID: 11571331]
Kaplan PW, Rossetti AO. EEG patterns and imaging correlations in encephalopathy: encephalopathy part II. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2011 Jun:28(3):233-51. doi: 10.1097/WNP.0b013e31821c33a0. Epub [PubMed PMID: 21633250]
Malhotra K, Rayi A. Gyriform Infarction in Cerebral Air Embolism: Imaging Mimicker of Status Epilepticus. Annals of Indian Academy of Neurology. 2017 Jul-Sep:20(3):313-315. doi: 10.4103/aian.AIAN_94_17. Epub [PubMed PMID: 28904468]
Kaplan PW. The EEG in metabolic encephalopathy and coma. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2004 Sep-Oct:21(5):307-18 [PubMed PMID: 15592005]
Brenner RP. Electroencephalography in syncope. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 1997 May:14(3):197-209 [PubMed PMID: 9244159]
Singh J, Thakur G, Alexander J, Rayi A, Peng J, Bell W, Britton J. Predictors of Nonconvulsive Seizure and Their Effect on Short-term Outcome. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2021 May 1:38(3):221-225. doi: 10.1097/WNP.0000000000000687. Epub [PubMed PMID: 32141985]
Sutter R, Fuhr P, Grize L, Marsch S, Rüegg S. Continuous video-EEG monitoring increases detection rate of nonconvulsive status epilepticus in the ICU. Epilepsia. 2011 Mar:52(3):453-7. doi: 10.1111/j.1528-1167.2010.02888.x. Epub 2011 Jan 4 [PubMed PMID: 21204818]
Level 2 (mid-level) evidenceSivaraju A, Gilmore EJ, Wira CR, Stevens A, Rampal N, Moeller JJ, Greer DM, Hirsch LJ, Gaspard N. Prognostication of post-cardiac arrest coma: early clinical and electroencephalographic predictors of outcome. Intensive care medicine. 2015 Jul:41(7):1264-72. doi: 10.1007/s00134-015-3834-x. Epub 2015 May 5 [PubMed PMID: 25940963]
Vespa PM, Nuwer MR, Juhász C, Alexander M, Nenov V, Martin N, Becker DP. Early detection of vasospasm after acute subarachnoid hemorrhage using continuous EEG ICU monitoring. Electroencephalography and clinical neurophysiology. 1997 Dec:103(6):607-15 [PubMed PMID: 9546487]
Claassen J, Hirsch LJ, Kreiter KT, Du EY, Connolly ES, Emerson RG, Mayer SA. Quantitative continuous EEG for detecting delayed cerebral ischemia in patients with poor-grade subarachnoid hemorrhage. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2004 Dec:115(12):2699-710 [PubMed PMID: 15546778]
Level 2 (mid-level) evidenceZhang XS, Roy RJ, Jensen EW. EEG complexity as a measure of depth of anesthesia for patients. IEEE transactions on bio-medical engineering. 2001 Dec:48(12):1424-33 [PubMed PMID: 11759923]
Kompanje EJ, Epker JL, de Groot Y, Wijdicks EF, van der Jagt M. [Determination of brain death in organ donation: is EEG required?]. Nederlands tijdschrift voor geneeskunde. 2013:157(42):A6444 [PubMed PMID: 24128600]
Young GB, Shemie SD, Doig CJ, Teitelbaum J. Brief review: the role of ancillary tests in the neurological determination of death. Canadian journal of anaesthesia = Journal canadien d'anesthesie. 2006 Jun:53(6):620-7 [PubMed PMID: 16738299]
Level 1 (high-level) evidenceKane N, Grocott L, Kandler R, Lawrence S, Pang C. Hyperventilation during electroencephalography: safety and efficacy. Seizure. 2014 Feb:23(2):129-34. doi: 10.1016/j.seizure.2013.10.010. Epub 2013 Nov 1 [PubMed PMID: 24252807]
Matheja P, Weckesser M, Debus O, Franzius Ch, Löttgen J, Schober O, Kurlemann G. Moyamoya syndrome: impaired hemodynamics on ECD SPECT after EEG controlled hyperventilation. Nuklearmedizin. Nuclear medicine. 2002 Feb:41(1):42-6 [PubMed PMID: 11917348]
Lopez-Gordo MA, Sanchez-Morillo D, Pelayo Valle F. Dry EEG electrodes. Sensors (Basel, Switzerland). 2014 Jul 18:14(7):12847-70. doi: 10.3390/s140712847. Epub 2014 Jul 18 [PubMed PMID: 25046013]
Herman ST, Abend NS, Bleck TP, Chapman KE, Drislane FW, Emerson RG, Gerard EE, Hahn CD, Husain AM, Kaplan PW, LaRoche SM, Nuwer MR, Quigg M, Riviello JJ, Schmitt SE, Simmons LA, Tsuchida TN, Hirsch LJ, Critical Care Continuous EEG Task Force of the American Clinical Neurophysiology Society. Consensus statement on continuous EEG in critically ill adults and children, part II: personnel, technical specifications, and clinical practice. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2015 Apr:32(2):96-108. doi: 10.1097/WNP.0000000000000165. Epub [PubMed PMID: 25626777]
Level 3 (low-level) evidenceShafer PO, Buelow JM, Noe K, Shinnar R, Dewar S, Levisohn PM, Dean P, Ficker D, Pugh MJ, Barkley GL. A consensus-based approach to patient safety in epilepsy monitoring units: recommendations for preferred practices. Epilepsy & behavior : E&B. 2012 Nov:25(3):449-56. doi: 10.1016/j.yebeh.2012.07.014. Epub 2012 Sep 20 [PubMed PMID: 22999858]
Level 2 (mid-level) evidenceFerree TC, Luu P, Russell GS, Tucker DM. Scalp electrode impedance, infection risk, and EEG data quality. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2001 Mar:112(3):536-44 [PubMed PMID: 11222977]
Level 2 (mid-level) evidenceHoman RW, Herman J, Purdy P. Cerebral location of international 10-20 system electrode placement. Electroencephalography and clinical neurophysiology. 1987 Apr:66(4):376-82 [PubMed PMID: 2435517]
Sinha SR, Sullivan L, Sabau D, San-Juan D, Dombrowski KE, Halford JJ, Hani AJ, Drislane FW, Stecker MM. American Clinical Neurophysiology Society Guideline 1: Minimum Technical Requirements for Performing Clinical Electroencephalography. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2016 Aug:33(4):303-7. doi: 10.1097/WNP.0000000000000308. Epub [PubMed PMID: 27482788]
Foldvary N, Caruso AC, Mascha E, Perry M, Klem G, McCarthy V, Qureshi F, Dinner D. Identifying montages that best detect electrographic seizure activity during polysomnography. Sleep. 2000 Mar 15:23(2):221-9 [PubMed PMID: 10737339]
Halford JJ, Sabau D, Drislane FW, Tsuchida TN, Sinha SR. American Clinical Neurophysiology Society Guideline 4: Recording Clinical EEG on Digital Media. The Neurodiagnostic journal. 2016:56(4):261-265. doi: 10.1080/21646821.2016.1245563. Epub [PubMed PMID: 28436799]
Acharya JN, Hani AJ, Thirumala P, Tsuchida TN. American Clinical Neurophysiology Society Guideline 3: A Proposal for Standard Montages to Be Used in Clinical EEG. The Neurodiagnostic journal. 2016:56(4):253-260. doi: 10.1080/21646821.2016.1245559. Epub [PubMed PMID: 28436788]
Acharya JN, Hani AJ, Thirumala PD, Tsuchida TN. American Clinical Neurophysiology Society Guideline 3: A Proposal for Standard Montages to Be Used in Clinical EEG. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2016 Aug:33(4):312-6. doi: 10.1097/WNP.0000000000000317. Epub [PubMed PMID: 27482795]
Gordon R, Rzempoluck EJ. Introduction to Laplacian montages. American journal of electroneurodiagnostic technology. 2004 Jun:44(2):98-102 [PubMed PMID: 15328706]
Drees C, Makic MB, Case K, Mancuso MP, Hill A, Walczak P, Limon S, Biesecker K, Frey L. Skin Irritation during Video-EEG Monitoring. The Neurodiagnostic journal. 2016:56(3):139-150. doi: 10.1080/21646821.2016.1202032. Epub [PubMed PMID: 28436772]
Level 3 (low-level) evidenceBehrens E, Zentner J, van Roost D, Hufnagel A, Elger CE, Schramm J. Subdural and depth electrodes in the presurgical evaluation of epilepsy. Acta neurochirurgica. 1994:128(1-4):84-7 [PubMed PMID: 7847148]
Level 2 (mid-level) evidenceWellmer J,von der Groeben F,Klarmann U,Weber C,Elger CE,Urbach H,Clusmann H,von Lehe M, Risks and benefits of invasive epilepsy surgery workup with implanted subdural and depth electrodes. Epilepsia. 2012 Aug; [PubMed PMID: 22708979]
Level 2 (mid-level) evidenceTsuchida TN, Acharya JN, Halford JJ, Kuratani JD, Sinha SR, Stecker MM, Tatum WO, Drislane FW. American Clinical Neurophysiology Society: EEG Guidelines Introduction. The Neurodiagnostic journal. 2016:56(4):231-234. doi: 10.1080/21646821.2016.1245513. Epub [PubMed PMID: 28436786]
Tatum WO, Olga S, Ochoa JG, Munger Clary H, Cheek J, Drislane F, Tsuchida TN. American Clinical Neurophysiology Society Guideline 7: Guidelines for EEG Reporting. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2016 Aug:33(4):328-32. doi: 10.1097/WNP.0000000000000319. Epub [PubMed PMID: 27482790]
Kane N, Acharya J, Benickzy S, Caboclo L, Finnigan S, Kaplan PW, Shibasaki H, Pressler R, van Putten MJAM. A revised glossary of terms most commonly used by clinical electroencephalographers and updated proposal for the report format of the EEG findings. Revision 2017. Clinical neurophysiology practice. 2017:2():170-185. doi: 10.1016/j.cnp.2017.07.002. Epub 2017 Aug 4 [PubMed PMID: 30214992]