EEG is a high yield topic for resident and board exams, so take the time to review this topic carefully! This chapter will teach you to read EEG: from normal findings to epileptiform discharges to associated clinical syndromes. You will also learn commonly tested EEG artifacts. Complete with real EEG tracing examples. Test your skills at the end with a practice quiz! Of note, medical students are not expected to know how to read EEG for exam purposes.

Authors: Brian Hanrahan MD, Steven Gangloff MD

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EEG Basics

  • EEG measures the potential difference between two electrodes on the scalp.
  • The electrical fields that generate EEG signals are the result of inhibitory and excitatory postsynaptic potentials (IPSPs and EPSPs) on the apical dendrites of cortical neurons. (Figure 1).
    • The EEG does not measure single action potentials. It measures a summation of postsynaptic potentials.
  • The region of the brain with the lowest threshold to electrical stimulation is the hippocampus.

Figure 1: Postsynaptic Potential Summation

EEG review
The result of the summation of postsynaptic potentials is the overall change in the membrane potential. At point A, several different excitatory postsynaptic potentials (EPSPs) add up to a large depolarization. At point B, a mix of excitatory and inhibitory postsynaptic potentials result in a different result for the membrane potential. Licensed under a Creative Commons Attribution 4.0 International License. Download the image for free here.

EEG Patterns Throughout Development

Preterm EEG

  • <32 weeks: Tracé discontinu is seen, which is a discontinuous background pattern that resembles burst suppression. There are bursts of mixed frequency activity lasting <15 seconds followed by long periods of low voltage generalized background suppression.
    • There is no difference in the EEG background with state changes.
  • >32 weeks: Trace alternant replaces trace discontinu; High-voltage bursts are separated by low-amplitude voltage waves. Other findings include delta brushes, frontal sharp transients, and theta bursts.

Term and pediatric EEG

  • Term (40 weeks): Frontal sharp waves can be seen during sleep.
    • All pre-term findings resolve by the 42nd-44th week.
  • 44 weeks: Sleep spindles form. They can be asynchronous until 2 years of age.
  • 46 weeks: Vertex transients can be seen.
  • 1 year: Theta frequency posterior dominant rhythm develops.
  • 8-10 years old: Alpha rhythms of 9 Hz to 10 Hz become the predominant frequency.

Preterm and pediatric EEG findings

Background Rhythms

  • Delta activity (<4 Hz): When generalized it is Indicative of generalized cerebral dysfunction/encephalopathy produced by processes involving subcortical white matter. If focal, it can represent focal cerebral lesions such as a tumor, cerebral infarction, or cerebral abscess.
  • Theta activity (4-8 Hz): Can be seen normally in drowsiness or pathologically in patients with increased intracranial pressures or mild encephalopathy.

EEG review theta of drowsiness

  • Alpha activity (8-12 Hz): At rest, a quiet awake individual has a posterior (occipital) dominant background alpha activity of 8.5-12 Hz.
    • Alpha activity can be suppressed with eye-opening.
Review EEG normal awake EEG
Average montage. Normal Awake (alpha range waves) EEG
Normal PDR on EEG
Normal Awake PDR on EEG
Normal PDR by Age
  • Beta activity (13-30 Hz): Can be seen normally in adults, but more often seen secondary to medications like benzodiazepines, barbiturates, drug toxicity, or anesthesia.
    • Increases in drowsiness and light sleep.
EEG review Beta range activity in the frontal head
Beta-range activity in the frontal (left>right) head regions

States on EEG

Wakefulness

  • A posterior dominant rhythm (PDR) is seen. This is present in the posterior leads.
  • Eye blinks are often seen.
  • You may see muscle artifacts, indicating the patient is moving.

Drowsiness

  • There is background fragmentation (breaking up of the well-formed PDR).
  • Mild theta slowing activity may be seen in the temporal leads (Rhythmic Mid-temporal Theta of Drowsiness, RMTD). 

N1 Sleep

  • Vertex waves appear.
  • The patient is no longer blinking.
  • Less background muscle artifact.

N2 Sleep

  • Sleep spindles and K complexes appear.

N3 Sleep

  • Slow waves of sleep are seen.

REM Sleep

  • Rapid eye movements are seen, evidenced by lateral eye movement artifact and lateral rectus spike artifact.

Provoking Actions

  • Provoking actions can be performed to elicit ictal/interictal activity in patients with generalized epilepsy. These actions can also provoke non-epileptic spells (PNES/NEBS) in some patients.
    • Photic stimulation: A light is placed in front of the patient that flashes at various frequencies (3-30 Hz). It is performed to assess the occipital driving response and susceptibility to photosensitive seizures.
    • Hyperventilation: Rapid deep breathing can provoke epileptiform discharges and seizures.
      • A decrease in amplitude is commonly seen in healthy adults and is benign.
      • Hypoglycemia can enhance slowing.
      • 3 Hz spike-and-waves can be triggered by hyperventilation in absence seizure patients (see below).
      • 3 Hz waves seen in children during hyperventilation can be normal.

EEG Normal Variants

  • Benign EEG variants are commonly seen in the setting of drowsiness or early sleep. A review of normal sleep EEG findings can be found here. Being able to differentiate between benign and epileptiform phenomena is integral to prevent the misdiagnosis of epilepsy.
Table of benign EEG findings
Benign EEG Findings

EEG Artifacts

 
Table of Common EEG artifacts
Table of Common EEG Artifacts
  • Some artifacts can be removed using filters. The notch filter, for example, can remove the ambient electrical artifacts from outlets, lights, etc. in the room. In the U.S., standard electrical current cycles at 60 Hz, so a 60 Hz notch filter can be used. In the UK, a 50 Hz filter is used.

Rhythmic Epileptiform Discharges

Generalized rhythmic delta activity (GRDA)

  • Generalized in all leads, GRDA typically signifies global cerebral dysfunction, such as in a severe encephalopathy, but is not felt to be a risk factor for seizure or seizure tendency.
  • Frontal predominant GRDA can be seen with a variety of pathologies including posterior fossa lesions, intracranial lesions, and increased intraventricular pressure.
EEG review GRDA generalized rhythmic delta activity
Generalized rhythmic delta activity (GRDA)

Lateralized rhythmic delta (LRDA)

  • Can be seen with focal lesions such as hemorrhage, tumor, or stroke.
  • LRDA is associated with increased seizure risk/ seizure tendency.
EEG with Left posterior lateralized rhythmic delta activity (LRDA)
Left posterior lateralized rhythmic delta activity (LRDA)

Periodic Epileptiform Discharges

Lateralized periodic discharges (LPDs)

  • Often seen with focal acute or subacute cerebral dysfunction, such as with herpes simplex encephalitis, stroke, abscess, or subdural hematoma.
  • Formerly known as periodic lateralized epileptiform discharges (PLEDs).

Generalized periodic discharges

  • Felt to have the highest seizure tendency of the “ictal-interictal” patterns.
  • If seen clinically with rapidly progressive dementia it can be strongly suggestive of Creutzfeldt-Jakob disease.
  • Formerly known as generalized periodic epileptiform discharges (GPEDs).

Periodic discharges

Disease-related Discharges

  • Hepatic encephalopathy: Patients with end-stage liver disease can present with hyperammonemia and generalized periodic waves with triphasic morphology. They are bilaterally synchronous and usually frontally predominant and exhibit three phases (i.e. negative, positive, negative). Triphasic waves can also be seen in ESRD and other forms of metabolic encephalopathy.

  • Subdural hematoma: Hemispheric asymmetry with the lower amplitude discharges localizing to the affected hemisphere.
  • HSV encephalitis: Due to the predilection for the temporal lobes, patients will present with lateralized periodic discharges (LPDs) most prominent in temporal leads.
EEG review lateralized periodic discharges LPDs
Lateralized periodic discharges (LPDs) in HSV Encephalitis
  • Stroke: Shows focal irregular theta/delta activity with LRDA or LPDs.
EEG review frontal irregular delta activity from right MCA stroke
Right frontal irregular delta activity secondary to a right MCA stroke
  • NMDA encephalitis: Generalized rhythmic delta activity with superimposed beta activity, called a delta brush pattern.
Ipsilateral ear reference montage showing a delta burst pattern secondary to NMDA encephalitis By Tomotaka Mizoguchi, Makoto Hara, Satoshi Hirose, and Hideto Nakajima – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8885512/, CC BY 4.0, https://commons.wikimedia.org/w/index.php?curid=118188149
  • Creutzfeldt-Jakob disease: A disorganized background with generalized periodic discharges (GPDs) at 0.5 to 1 Hz with myoclonic jerks that are worsened by stimulation (startle myoclonus).
  • Fatal familial insomnia (FFI): Loss of sleep spindles.
  • Subacute sclerosing panencephalitis: High-amplitude bisynchronous delta waves, frontal rhythmic delta activity, high-amplitude and low-frequency generalized periodic discharges (once every 5-7 seconds), with periods of electrodecrement following EEG complexes, and focal spike and slow-waves.
  • Landau-Kleffner syndrome: Abundant epileptic activity activated by the transition to NREM sleep, and typically meeting criteria for Developmental/Epileptic Encephalopathy with Spike Wave Activation In Sleep (DEE-SWAS), formerly known as electrical status epilepticus during slow sleep (ESES).
  • Tay-Sachs disease: Slow background with or without multifocal epileptiform discharges.
  • Alzheimer’s disease: Decrease or loss of alpha and beta activity at an earlier stage than other dementias.
  • Angelman syndrome: Notched delta activity.
    • The specificity of this is relatively high, about 40%, and when seen with the classic phenotypic features, it is a powerful detection tool.
    • Also has pseudo-hypsarrythmia (hypsarrythmia that doesn’t have fragmentation in sleep).
Average montage EEG showing diffuse high voltage (100-200 μV) 1.5–2 Hz rhythmic delta waves with ill-defined spike and sharp waves in the anterior regions, characteristic for a notched delta pattern
  • Lithium toxicity: Generalized delta/theta activity with multifocal spikes.
EEG review lithium toxicity encephalopathy with multifocal sharps
Moderate to severe encephalopathy with multifocal sharps from lithium toxicity
  • Hypoxic-ischemic encephalopathy: Can present secondary to cardiac arrest, drug overdose, drowning, etc.
    • EEG can have a variable pattern.
    • Favorable prognostic EEG findings include background variability, reactivity to external stimuli, and if sleep patterns are present.
    • Poor prognostic EEG findings are burst suppression, monorhythmic patterns, alpha coma (unless in the setting of reversible cause for coma such as metabolic dysfunction, sedative drugs, etc.), generalized periodic discharges, and electrocerebral inactivity (ECI).
      • ECI is defined as no EEG activity with the sensitivity set at 2 microvolts.
      • Burst suppression represents a severe disturbance of cerebral function which can also be seen with aggressive anesthesia.
Burst suppression EEG pattern Secondary to Prolonged Cardiac Arrest
Burst Suppression Secondary to Prolonged Cardiac Arrest
  • After anoxic insult patients can develop a type of myoclonic epilepsy called Lance-Adams syndrome (LAS).
  • Treatment: Clonazepam, sodium valproate, and levetiracetam.

ECI & Brain Death

  • Electrocerebral inactivity (ECI) is defined as no EEG activity over 2 uV with scalp electrode pairs 10 or more cm apart, and requires a specific technique to conclude, beyond a standard EEG.

  • ECI is a poor prognostic finding but is no longer used as part of the criteria for brain death.

  • Similarly, while EEG is helpful for prognostication in those with cortical injury, it is no longer used in the diagnosis of brain death. At this time, the diagnosis of brain death relied on brainstem reflex testing and cardiopulmonary tests.

References

  1. Louis, Erik St., et al. “Electroencephalography (EEG): An Introductory Text and Atlas of Normal and Abnormal Findings in Adults, Children, and Infants.” 2016, doi:10.5698/978-0-9979756-0-4.
  2. OpenStax College, Anatomy & Physiology. OpenStax CNX. Nov 7, 2014 http://cnx.org/contents/[email protected].
  3. Schomer D.L. (2007) The Normal EEG in an Adult. In: Blum A.S., Rutkove S.B. (eds) The Clinical Neurophysiology Primer. Humana Press.
  4. “Sleep: A Comprehensive Handbook.” Apr. 2005, doi:10.1002/0471751723.
  5. Wieser, H, et al. “EEG in Creutzfeldt–Jakob Disease.” Clinical Neurophysiology, vol. 117, no. 5, 2006, pp. 935–951., doi:10.1016/j.clinph.2005.12.007.
  6. Korff, Christian M., Kent R. Kelley, and Douglas R. Nordli Jr. “Notched delta, phenotype, and Angelman syndrome.” Journal of clinical neurophysiology 22.4 (2005): 238-243.
  7. R. Cooper, A.L. Winter, H.J. Crow, W.G. Walter. “Comparison of subcortical, cortical and scalp activity using chronically indwelling electrodes in man”. Electroencephalogr Clin Neurophysiol, 18 (1965), pp. 217-228.
  8. Markand, O. N., & Panszi, J. G. (1975). The electroencephalogram in subacute sclerosing panencephalitis. Archives of neurology, 32(11), 719-726.
  9. Wijdicks EFM, Varelas PN, Gronseth GS, Greer DM. Evidence-based guideline update: Determining brain death in adults. Report of the Quality Standards Subcommittee of the American Academy of Neurology 2010;74:1911-1918.
  10. Samanta, Debopam. “Epilepsy in Angelman syndrome: A scoping review.” Brain and Development 43.1 (2021): 32-44.
  11. Pearl PL, Carrazana EJ, Holmes GL. The Landau-Kleffner Syndrome. Epilepsy Curr. 2001;1(2):39-45. doi:10.1046/j.1535-7597.2001.00012.

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