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Jack Adams
Jack Adams

Atlas Of EEG Patterns

Organized by EEG pattern, the Atlas orients you to the basics of EEG, helps the reader identify the characteristic EEG wave features and leads you to the EEG diagnosis through a table that organizes all of the EEG patterns according to their wave features. The Atlas includes the full range of EEG patterns from the common rhythms to the rare findings, and it also includes numerous examples of artifacts.

Atlas of EEG Patterns


Delirium, also known as encephalopathy, is a reversible generalized confusional state induced by a systemic disorder. The clinical phenomena of confusion in a delirious state may closely resemble a complex partial or atypical absence seizure, involving blank staring with disorientation, inattention, and variable responsiveness, stupor with reduced vigilance, and unusual movements including myoclonic jerks. Encephalopathic patients may have acute symptomatic seizures, resulting in diagnostic confusion. EEG in a delirious patient may show either diffuse nonspecific nonepileptiform background slowing, or even epileptiform-appearing patterns such as triphasic waveforms (see Figure 56 for triphasic wave pattern), which are most common in patients with underlying associated hepatic or renal impairment or both, and resultant encephalopathy, although similar patterns may be induced by drug intoxication or adverse effects or other nonlesional causes of severe generalized cerebral dysfunction.

Coma is a clinical state of eyes closed, irreversible unresponsiveness (at least temporarily), as opposed to sleep in which the unresponsive state is readily reversible to wakefulness. The hallmark of coma patterns is their lack of variability and relative (or absolute) lack of reactivity. Reactivity of the background (background frequency speeding up, or changing in reaction to physical or auditory stimuli) is a sign of relative integrity and considered relatively more favorable.

Several common EEG coma patterns have been described. The two patterns that are considered to have the worst prognosis for recovery following anoxic-ischemic encephalopathy are burst suppression (see Figure 59) and alpha coma, with other patterns considered intermediate (theta coma, Figure 60) or even favorable (spindle coma). However, prognostication should certainly not rely upon EEG alone, as the findings must be integrated into the clinical context and other ancillary tests such as neuroimaging.

  • processing.... Drugs & Diseases > Neurology Encephalopathic EEG Patterns Updated: May 11, 2018 Author: Selim R Benbadis, MD; Chief Editor: Helmi L Lutsep, MD more...

Share Email Print Feedback Close Facebook Twitter LinkedIn WhatsApp webmd.ads2.defineAd(id: 'ads-pos-421-sfp',pos: 421); Sections Encephalopathic EEG Patterns Sections Encephalopathic EEG Patterns Overview Generalized Slowing More Severe EEG Patterns Less Common EEG Patterns Patient Education Show All Media Gallery References Overview Overview Since the EEG is a test of cerebral function, diffuse (generalized) abnormal patterns are by definition indicative of diffuse brain dysfunction (ie, diffuse encephalopathy). [1, 2, 3, 4]

More severe patterns: These patterns are generally considered the next level of severity beyond generalized slowing. They include periodic patterns (such as burst-suppression), background suppression, and electrocerebral inactivity (ECI).

Periodic patterns: Discharges occur at regular intervals (ie, periodicity). The discharges are typically complex and multiphasic and are often epileptiform in morphology. [5, 6] Thus, they are like periodic lateralizing epileptiform discharges (PLEDs), except instead of being lateralized, they are generalized. They are sometimes referred to as generalized periodic epileptiform discharges (GPEDs). Their periodicity rather than their morphology sets them apart as a unique and clinically useful entity (as is true for PLEDs). By contrast, the term bi-PLEDs usually refers to periodic discharges that are bihemispheric but asynchronous (ie, independent).

As usual, these severe encephalopathic patterns are completely nonspecific as to etiology but represent extremely severe degrees of diffuse encephalopathy. Because sedative medications can cause or aggravate these abnormalities, careful interpretation is warranted when reading these patterns. These patterns are indicative of very severe brain dysfunction if sedative medications can be excluded with certainty as their cause. [8]

Periodic patterns, including burst-suppression patterns, are somewhat more common in anoxic injuries than in other systemic disturbances. Periodic patterns can be induced by high doses of sedatives such as barbiturates, benzodiazepines, or propofol. In fact, burst-suppression pattern is typically the goal and the method used to titrate doses of anesthetics for treatment of refractory status epilepticus.

In the appropriate clinical context, certain periodic patterns can suggest and support the diagnoses of Creutzfeldt-Jakob disease (CJD) and subacute sclerosing panencephalitis (SSPE). Classically, the periodicity for CJD is approximately 1-2 seconds, whereas it is much longer in SSPE (approximately 4-10 s).

Rhythmicity or periodicity is one of the hallmarks of electrographic seizures; thus, periodic patterns quite often are observed in the context of nonconvulsive status epilepticus. [9] Often the decision whether to consider a periodic pattern ictal must rely on clinical information or the response to anticonvulsant treatment.

To be classified as one of these patterns, the activity should be frankly excessive in amplitude or in spatial distribution (ie, widespread), appear in unusual spatial distribution, or appear excessive in amount (ie, near continuous). Although some investigators classify these patterns as abnormal even if the pattern is reactive, unreactive activity is preferred. The most important criterion is patient coma at the time of clinical recording.

Alpha coma, beta coma, and spindle coma are infrequent. They are, like all the encephalopathic patterns, nonspecific in regard to etiology, although anoxia often is associated with alpha coma and drugs with beta coma. They are generally indicative of a severe degree of encephalopathy. Reactivity is a good prognostic factor. In fact, some investigators, including the author, do not classify a record as alpha or spindle coma if it is reactive.

Triphasic waves classically are associated with hepatic encephalopathy. However, they are not specific and can be observed in uremic encephalopathy and even other types of metabolic derangements. Many other patterns can have a triphasic morphology. Like periodic patterns, triphasic waves quite often are observed in the context of nonconvulsive status epilepticus. Often the decision whether to consider triphasic waves ictal must rely on the clinical information or the response to anticonvulsant treatment.

This EEG atlas is based on the Cleveland Classification, developed by Professor Hans Lüders (Lüders and Noachtar, atlas and classification of electroencephalography, 2000). This classification allows for an objective description of the EEG that is reproducible, redundancy free, avoids subjective terms and correlates the electrographic findings to their clinical significance.

Organized by wave features rather than pattern names, this atlas helps guide the reader to an EEG interpretation even when the waveform is unfamiliar. The first section takes the reader through the process of characterizing EEG waves by their features. The second section organizes EEG patterns by their features, so provides EEG waveform differential diagnoses. The third section is organized alphabetically by pattern name with each pattern described in a way that allows the reader to distinguish it from similarly appearing patterns. Examples of the patterns also are provided.

After the major section on EEG patterns from both a basic and advanced viewpoint, there is an extensive section on prolonged continuous digital EEG monitoring, including data reduction, screening, and trending techniques such as compressed spectral array. These techniques can aid efficient recognition of seizures, ischemia, and other neurologic events, and can help visualize long-term trends.

This atlas is written for practitioners, fellows and residents in critical care medicine, neurology, epilepsy and clinical neurophysiology, and is essential reading for anyone getting involved in EEG monitoring in the intensive care unit.

Free to use without a subscription, Dr David Strayhorn established this website to serve as an extensive atlas of different normal and abnormal EEGs. Don't forget to test your reading skills using the included EEG archive!

Despite over 65 years of electroencephalography (EEG) in newborn infants, our understanding of the rhythmic cortical activity patterns associated with normal development and brain injury remains largely speculative. The long term goal of the current project is to create a developmental activity atlas in which abberant EEG patterns in the at-risk newborn are matched to specific disruptions in brain areas and neuronal types. A first step towards this goal requires an un-anesthetized preclinical model with demonstrated homology to fetal and neonatal human cortical activity in which cells can be genetically manipulated and the underlying effects on cortical circuits rigorously probed. By measuring activity in vivo through the depth of cortex and corresponding thalamic networks in developing neonatal rodents, we will provide insight into the circuit changes that may underlie human fetal thalamo-cortical development to inform future studies of subcortical injury in infants and non-human primates. By manipulating the activity of thalamic neurons we will assay the distinct contributions of the thalamic relay and inhibitory neurons to the maturation of specific features of the EEG common to developing humans and rodents. Given the challenges of imaging and diagnosis in the fragile at-risk newborn, EEG has the potential to be a valuable and inexpensive bedside diagnostic tool. An improved understanding of the control of cortical activity development will inform diagnosis after neonatal brain injury and improve targeting of treatments for the cognitive and intellectual disability that often results. 041b061a72


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