A comprehensive, curated atlas of electroencephalographic patterns for clinical neurophysiology education. Spanning neonatal through adult recordings, with dedicated critical care EEG nomenclature following ACNS 2021 standardized terminology.
EEG patterns from premature infants (< 29 weeks CA) through full-term neonates (38–42 weeks CA), including both normal maturational patterns and pathological findings.
Age-dependent maturational patterns from premature to full-term neonates
The neonatal EEG matures in parallel with brain anatomical development. It is essential to evaluate neonatal EEGs in the context of the infant's conceptional age (CA), as patterns that are normal at one age may be abnormal at another. The EEG should be interpreted along with behavioral state (active sleep, quiet sleep, wakefulness) for accurate assessment.
At less than 29 weeks CA, the EEG is continuously discontinuous, consisting of bursts of medium-to-high amplitude waveforms (maximal over posterior regions) interrupting a nearly flat background. Periods of EEG activity are brief (< 15 s) and interburst intervals average 8–12 s but may last up to 25–30 s. Interhemispheric synchrony is well developed at this age (90–100%).
Delta brushes consist of medium-to-high voltage (25–200 µV) 0.3–1.5 Hz delta waves with superimposed 10–150 µV rhythmic fast activity (8–22 Hz). First appearing at ~26 weeks CA over the central head region, they become abundant between 32–34 weeks CA and decline until disappearing at ~40 weeks CA, lastly over temporal/occipital regions.
A distinctive age-specific finding at 29–31 weeks CA, consisting of brief bursts of theta activity over the temporal regions. This pattern is characteristic of this maturational stage and should not be confused with epileptiform activity. Behavioral states begin to differentiate at this age, with more prominent variations between quiescence and body motility.
Replaces tracé discontinu at 34–37 weeks CA. A less strikingly discontinuous pattern in which inter-burst periods have more activity and are shorter in duration. EEG reactivity to stimulation is present in all states. Delta brushes begin to decline. Well-formed frontal sharp transients (encoches frontales) appear. Interhemispheric synchrony increases to 70–85% at 35–36 weeks and > 90% at 38 weeks CA.
At term, 4 basic EEG patterns are established: (a) Low Voltage Irregular (LVI) — seen in wakefulness and active sleep; (b) Mixed Voltage (MV) — wakefulness and active sleep; (c) High Voltage Slow (HVS) — continuous 25–150 µV delta in quiet sleep; (d) Tracé Alternant (TA) — dominates quiet sleep. Nearly 100% interhemispheric synchrony. Frontal sharp transients and monorhythmic frontal delta persist.
Biphasic, sharply contoured waveforms maximal over frontal and mid-frontal head regions. First seen at 34–35 weeks CA, occur most often during sleep and transitions between active and quiet sleep. May be unilateral, asymmetric, or bilateral and synchronous. They are commonly seen up to 41 weeks CA and are rarely seen after 46 weeks CA.
Sporadic multifocal sharp transients in either wakefulness or sleep in a 28–42 week CA infant are a normal finding. Most abundant between 32–34 weeks CA. They decrease after 40 weeks CA but rare (2–3/hour) multifocal spikes in any state are considered normal up to 46 weeks CA. An abnormal increase represents a non-specific response to encephalopathy.
Short runs of bilateral, monomorphic or rhythmic 2–4 Hz, 50–150 µV activity occurring frequently at 34–37 weeks CA and persisting into the perinatal period. This normal pattern should not be confused with abnormal patterns or neonatal epileptiform activity.
Pathological neonatal patterns including seizure discharges and encephalopathic backgrounds
Almost always focal or lateralized in onset. Consist of rhythmical monomorphic waveforms or repetitive spikes/sharp waves with buildup that evolves in repetition rate and morphology. Duration usually < 1 min but can exceed 30 min. Frequently multifocal and may overlap in time. Poor correlation between specific ictal patterns and clinical manifestations.
A severely abnormal pattern in neonates consisting of high-amplitude bursts alternating with periods of marked suppression or inactivity. Unlike normal tracé discontinu, burst-suppression lacks reactivity to stimulation and is invariant across behavioral states. Seen in early infantile epileptic encephalopathy (Ohtahara syndrome) and early myoclonic encephalopathy.
Spikes with positive polarity occurring over the rolandic and parasagittal head regions that clearly stand out from the background. When accompanied by other EEG abnormalities, they are associated with periventricular leukomalacia (often a consequence of intraventricular hemorrhage). Their presence should raise the question of underlying structural abnormality.
Interburst intervals exceeding normal limits for gestational age are abnormal. At < 29 weeks, intervals > 30 s are concerning; at 32+ weeks, they should not exceed 15 s. Prolonged intervals (> 30 s at any age) often indicate cerebral hypoxia or severe encephalopathy. The presence of featureless (isoelectric) intervals is always pathological after 34 weeks CA.
Characterized by continuous or nearly continuous electrographic seizure activity, with seizure discharges alternating between hemispheres. May present as rhythmical waves of 6–7 Hz appearing on one side, then shifting to the other hemisphere. Commonly follows anoxic episodes at birth. Carries significant prognostic implications.
EEG patterns from infancy through adolescence, including age-dependent normal variants and epilepsy syndromes of childhood.
Age-dependent maturational changes from infancy through adolescence
Between 3–4 months of age, ~75% of normal infants demonstrate a 3–4 Hz occipital rhythm during wakefulness that is activated by passive eye closure and attenuated by passive eye opening. This is the precursor of the alpha rhythm. It progressively increases: ~5 Hz by 12 months, ~6–7 Hz by 24 months, ~8 Hz by 3 years, reaching adult frequency (8–13 Hz) by mid-childhood.
Appear in rudimentary form at 40 weeks CA, consistently seen by 2–3 months. They present as 12–14 Hz runs over central/parasagittal regions lasting 3–5 s. In the first 3 years, they have a characteristic comb-shaped morphology (negative phase sharply contoured, positive phase rounded). Frequently asynchronous over the two hemispheres until ~8 months; persistent unilateral spindles are abnormal at any age.
Considered to be formed from the alpha rhythm, sharing the same distribution and reactivity to eye opening. Most commonly seen between ages 8–14 years but occur between 2–21 years. Each waveform spans 3–6 combined alpha waves with characteristic fused alpha wave morphology. Normal slow waves rarely exceed 1.5× the alpha rhythm amplitude and should attenuate with the alpha rhythm during alerting.
A normal drowsiness pattern seen predominantly in children ages 3 months to 13 years. Characterized by high-amplitude, rhythmic, bisynchronous 3–5 Hz theta activity with maximal amplitude over the central and frontal head regions during transitions into drowsiness and light sleep. Often very high amplitude (200–350 µV).
In children, runs of posterior rhythmic delta activity can be seen as a normal variant during hyperventilation or drowsiness. OIRDA in the context of idiopathic generalized epilepsy (particularly childhood absence epilepsy) is seen in 21–30% of cases and may have a notchy morphology. In isolation without epileptiform discharges, it may represent a normal age-dependent response to hyperventilation.
EEG correlates of childhood epilepsy syndromes and developmental epileptic encephalopathies
A chaotic, high-amplitude pattern consisting of disorganized, asynchronous, high-voltage (often > 200 µV) slow waves with multifocal spikes and sharp waves arising from multiple brain regions. Characteristic of infantile epileptic spasms syndrome (IESS / West syndrome). The ictal EEG correlate is typically an electrodecremental response. Hypsarrhythmia may be modified (asymmetric, with burst-suppression features).
Two mandatory EEG patterns: (A) Generalized slow spike-and-wave (≤ 2.5 Hz) — spikes (< 70 ms) or sharp waves (70–200 ms) followed by high-voltage negative slow waves, bilaterally synchronous, anterior predominant, occurring in runs. (B) Generalized paroxysmal fast activity — bursts of diffuse 10+ Hz activity during sleep. Background shows diffuse theta-delta slowing. The slow SW pattern wanes in adolescence/adulthood.
Regular 3 Hz (2.5–4 Hz) generalized spike-and-wave discharges at onset of absence seizures. Background is normal. Discharges provoked by hyperventilation in 87% of untreated patients. Photic stimulation triggers GSW in 21%. OIRDA with notchy morphology seen in 21–30%. Duration 5–30 s. Fragmented GSW may appear focal/multifocal in sleep but morphology resembles GSW.
High-amplitude, stereotyped centrotemporal (rolandic) spikes with horizontal dipole, typically activated in drowsiness and sleep. Background is normal. Spikes may shift location and laterality. May evolve to DEE-SWAS in some children. Onset 3–13 years with remission by adolescence. The most common childhood focal epilepsy syndrome.
Marked sleep potentiation of epileptiform activity in NREM sleep with near-continuous spike-and-wave during sleep (spike-wave index > 50–85%). Associated with developmental regression. May evolve from SeLECTS or structural focal epilepsies. Etiologies include unknown, genetic (e.g., GRIN2A), and early developmental lesions such as cortical malformations (polymicrogyria) or vascular insults (40–60% in CSWS, rare in LKS).
EEG may be initially normal. Over time, generalized and multifocal epileptiform discharges emerge. Characterized by generalized spike-wave and polyspike-wave, focal/multifocal discharges, and photoparoxysmal response. Background may show progressive slowing. SCN1A pathogenic variants found in > 80% of cases. Refractory epilepsy with neurodevelopmental decline and risk of SUDEP.
Background shows normal, age-appropriate posterior dominant rhythm at onset. Characteristic monomorphic biparietal theta rhythms (not seen in all patients). With increased seizure frequency, generalized background slowing appears. Interictal: generalized 2–6 Hz spike-and-wave or polyspike-and-wave complexes in 2–6 s bursts. 5% have GLUT1 deficiency (SLC2A1).
Normal and abnormal EEG patterns in adults, including wakefulness, sleep, benign variants, and epilepsy-related findings.
Wakefulness, sleep, and benign variant patterns in the adult EEG
The hallmark of the normal adult EEG. A sinusoidal 8–13 Hz rhythm maximal over the posterior head regions that is blocked by eye opening and disappears in drowsiness/sleep. Stable 8–12 Hz even during normal aging. Alpha rhythm is poorly visualized in ~25% of normal adults. Voltage asymmetry > 50% is abnormal (especially left > right). Frequency difference > 1 Hz between hemispheres is abnormal.
Frequencies > 13 Hz, commonly in the 18–25 Hz range. Normal voltage < 20 µV in 98% of adults. Three types: frontal beta (most common, blocks with contralateral movement), widespread beta, and posterior beta (fast alpha variant at ~2× alpha frequency). Voltages > 25 µV are abnormal. Benzodiazepines, barbiturates, and chloral hydrate are potent beta activators.
Centrally located arciform alpha frequency rhythm (usually 8–10 Hz) representing the sensorimotor cortex at rest. Blocks not with eye opening but with contralateral movement of an extremity. May be seen only on one side and may be quite asymmetric and asynchronous without underlying structural lesion. When persistent, unreactive, and associated with focal slowing, mu-like frequencies are abnormal.
Positive sharp transients occurring over the occipital regions during visual scanning of a picture or complex visual scene. They are triggered by saccadic eye movements and are abolished by elimination of the visual stimulus (closing eyes or fixation). Recognized by their characteristic shape, posterior distribution, and specific precipitating mechanism.
Rhythms of 3.5–6.5 Hz representing approximately half the frequency of the surrounding alpha rhythm. Appears over the posterior head regions, alternates with the usual alpha rhythm, and shares the same distribution and reactivity (blocks with eye opening). Rare but normal. Should not be confused with intermittent occipital slow waves or pathological theta activity.
Sleep EEG differs completely from waking EEG. Elements include: vertex sharp transients and slow waves (N1), K-complexes and sleep spindles (N2), high-amplitude delta activity (N3), and sawtooth waves with low-voltage mixed frequency (REM). POSTs (positive occipital sharp transients of sleep) are seen in N1–N2. Sleep cycles consist of progressive deepening through stages with periodic REM episodes.
No activity over 20 µV in recordings from any part of the head. At high gain, a wide range of frequencies including beta, theta, some delta, and sometimes posterior alpha is distinguishable. Not seen in normal children but becomes more common with advancing age. May also be seen in tense subjects who show normal amplitude when relaxed. Very low voltage (< 10 µV) is more likely abnormal.
Similar to younger adults with key differences: alpha rhythm may be slower (mean ~9 Hz in 60+, 8–9 Hz in centenarians), less persistent, and less reactive. Beta activity often more prominent. Sporadic generalized slow waves may be slightly more common. Intermittent temporal slow waves appear in some normal elderly subjects, especially on the left side. Alpha < 8 Hz is generally abnormal even in elderly.
Epileptiform discharges, focal abnormalities, and generalized patterns in adult epilepsies
Typical age at onset 10–24 years. EEG shows generalized 3–6 Hz polyspike-and-wave and spike-and-wave complexes, often with frontal predominance. Background is normal. Myoclonic seizures correlate with polyspike-wave bursts. Sleep deprivation is a common trigger. Photic stimulation may provoke discharges. SCBs (sodium channel blockers) aggravate myoclonic and absence seizures in JME.
Interictal epileptiform discharges (IEDs) include spikes (< 70 ms) and sharp waves (70–200 ms) that stand out from background, have a disrupting quality, and show an after-going slow wave. Focal IEDs indicate a cortical irritative zone and are found in temporal (most common), frontal, parietal, or occipital locations. They support a clinical diagnosis of epilepsy but may be seen in 0.5–2% of healthy individuals.
Diffuse slowing of background activity indicates bilateral cerebral dysfunction. Ranges from mild (intermittent theta) to severe (continuous polymorphic delta). Etiologies include metabolic/toxic encephalopathy, medication effects, infection, dementia, and post-ictal state. The degree of slowing generally correlates with the severity of cerebral dysfunction. An alpha rhythm that never exceeds 8 Hz in an awake adult is abnormal.
Continuous, irregular (polymorphic) delta activity localizing to a specific brain region, indicating underlying structural pathology (tumor, stroke, abscess, contusion). It is persistent, unresponsive to eye opening, and may be associated with attenuation of faster frequencies over the same region. The most reliable EEG indicator of a focal structural lesion in the corresponding brain region.
Sinusoidal alpha-frequency (7–8 Hz) waves occurring in comatose patients, differing from normal alpha in being widespread without posterior predominance, lacking spontaneous variability, and typically showing no reactivity to stimulation. May occur with theta frequencies (alpha-theta coma). Causes include pontine lesions, severe head injury, and anoxic encephalopathy. Often associated with poor prognosis except in beta coma pattern.
Ictal EEG pattern showing rhythmic, evolving activity arising from a focal brain region. Typically begins with low-amplitude fast activity or rhythmic theta/alpha that evolves in frequency, amplitude, and distribution. The pattern spreads regionally and may become generalized (bilateral tonic-clonic). The absence of ictal activity on scalp EEG does not rule out seizures, particularly simple partial seizures.
Following ACNS 2021 Standardized Critical Care EEG Terminology — periodic patterns, rhythmic patterns, and ictal-interictal continuum.
The American Clinical Neurophysiology Society (ACNS) published standardized critical care EEG terminology to ensure consistent description of EEG patterns encountered in critically ill patients. Main terms are organized into two axes: periodic discharges (PDs) and rhythmic delta activity (RDA), each classified by location (generalized, lateralized, bilateral independent, or multifocal) with modifiers for morphology, prevalence, frequency, duration, and additional features (+F = fast activity, +R = rhythmic, +S = sharp).
Periodic complexes occurring throughout the brain in a symmetric and synchronized manner. Independently associated with poor outcome in ~90%. Etiologies include severe anoxic encephalopathy, post-status epilepticus, toxic/metabolic encephalopathy, drug-induced (lithium, baclofen), and Creutzfeldt-Jakob disease. Whether GPDs represent an EEG pattern of status epilepticus remains debated — many believe they represent brain damage rather than ongoing seizures.
Lateralized to one hemisphere. Sharp waves, spikes, or more complex waveforms occurring at periodic intervals (every 0.5–4 s), especially in temporal or posterior head regions. Considered more interictal than ictal, but often resistant to AEDs. Up to 70% of patients with LPDs are found to have experienced NCSE on cEEG monitoring. Etiologies: acute stroke, tumors, CNS infection, hemorrhage, TBI, PRES, familial hemiplegic migraine.
Formerly known as BiPLEDs. Periodic discharges occurring independently and asynchronously in both hemispheres. Each hemisphere shows its own periodic pattern with independent timing. This pattern is highly associated with severe bilateral brain injury and carries a very poor prognosis. Most commonly seen in anoxic injury, herpes simplex encephalitis, and Creutzfeldt-Jakob disease.
A morphological descriptor within the ACNS framework for generalized periodic discharges with triphasic morphology. Historically associated with metabolic encephalopathy (especially hepatic). However, triphasic morphology and anterior-posterior lag are NOT specific and can be seen during or after seizures and status epilepticus. Morphology and frequency of periodic discharges vary in the same patient, appearing epileptiform at one time and not at others.
Ongoing electrographic seizure activity without prominent motor manifestations. In comatose patients, it is often difficult to distinguish ictal, interictal, and non-ictal patterns. GPDs at 1–2 Hz can be seen in metabolic encephalopathy and post-anoxic coma, as well as during or after NCSE. GPDs associated with seizures tend to be sharper and appear on a lower-amplitude interdischarge background, but significant overlap exists.
Bursts of irregular or rhythmic slow waves (with intermixed faster components) separated by low-amplitude delta or electrocerebral silence. Bursts last 1–3 s with inter-burst intervals of 2–10 s. Seen in comatose patients with reversible (general anesthesia) or irreversible (cardiopulmonary arrest) conditions. Not responsive to stimuli. The duration of intervals increases as condition worsens until electrocerebral silence supervenes.
A distinctive pattern characterized by periodic delta waves with stereotyped fast activity at the crest and downslope of each delta wave. Using ACNS terminology: 1-Hz GPDs+F of blunt morphology with delta wave discharges and superimposed fast activity. Classically associated with anti-NMDA receptor encephalitis but not pathognomonic. If abundant or continuous = definite EDB; if occasional or frequent = possible EDB.
A spectrum of EEG findings from clearly interictal to potentially ictal, with no abrupt transition. Demonstrated by QEEG trends (Color Density Spectral Array) showing gradual reduction of power across frequencies. Includes patterns such as GPDs+FR (fast and rhythmic) that may represent probable NCSE, gradually transitioning to sporadic epileptiform discharges. The cutoff between "highly epileptiform" and "interictal" is not easily defined.
All EEG patterns and descriptions are derived from the following authoritative clinical neurophysiology references. All images are placeholders to be replaced by the Saudi EEG database.
1. Ebersole JS, Pedley TA. Current Practice of Clinical Electroencephalography, 3rd Edition. Lippincott Williams & Wilkins, 2003.
2. Tatum WO IV, Husain AM, Benbadis SR, Kaplan PW. Normal Adult EEG and Patterns of Uncertain Significance. J Clin Neurophysiol 2006;23:194–207.
3. Hirsch LJ, Brenner RP. Atlas of EEG in Critical Care. Wiley-Blackwell, London, 2010.
4. ACNS Standardized Critical Care EEG Terminology, 2021 Revision.
5. Epilepsy — CSCN EEG Review, May 30, 2025 (Dr. Hanin presentation).
6. The Abnormal EEG: Interictal and Ictal Patterns — NERC 2025 Lecture.
7. NICE NG217: Epilepsies in Children, Young People and Adults (2025).
8. Werner SS, Stockard JE, Bickford RG. Atlas of Neonatal EEG. Raven Press, New York, 1977.
9. Lombroso CT. Neonatal polygraphy in full-term and premature infants. J Clin Neurophysiol, 1979; 1985; 1993.
10. Specchio N et al. International League Against Epilepsy classification and definition of epilepsy syndromes. Epilepsia, 2022.
11. EEG Examples Atlas — ACNS Standardized Critical Care EEG Terminology 2021 (with legends).
12. Pitfalls in Ictal EEG Interpretation, LTM EEG and Intracranial EEG (Hirsch LJ et al.).
13. DEE-SWAS / ESES / CSWS / LKS presentation (Hanin).
14. Channelopathies in Epilepsy: Clinical Presentations, Pathogenic Mechanisms, and Therapeutic Insights. J Neurology.
All EEG image placeholders in this atlas are intended to be replaced by de-identified EEG recordings from the Saudi clinical neurophysiology database. Each entry includes the full literature citation for the pattern description, which will be retained alongside the Saudi EEG exemplars. This atlas is designed as a collaborative educational resource for Saudi board trainees, clinical neurophysiologists, and EEG technologists.