EEG Basics

The electroencephalogram is the oldest functional test in clinical neurology and still one of the most informative. For roughly a tenth of a second's worth of brain activity it gives you a window onto cortical physiology in real time — something no scan can match. The catch is that the EEG speaks its own language: a vocabulary of frequencies, a grammar of montages, and a small dictionary of patterns that map onto specific clinical states. This page builds that vocabulary from the ground up: what the squiggles actually represent, the four classic frequency bands and what they mean, the normal architecture of wakefulness and sleep, the epileptiform and periodic abnormalities you must recognize, and the clinical questions an EEG is uniquely suited to answer.

What the EEG actually measures

A common misconception is that EEG records action potentials — the spikes that fire down axons. It does not. The scalp EEG is too far away and the events too brief and asynchronous. What it records instead are the summated excitatory and inhibitory postsynaptic potentials of cortical pyramidal neurons. These large neurons are arranged in palisades perpendicular to the cortical surface, so their extracellular currents add up coherently and create dipoles strong enough to be detected through skull and scalp. Because of this geometry, a visible scalp deflection requires a synchronized patch of cortex on the order of several square centimeters; deep or small generators may be electrically silent at the scalp.

• Electrodes: Standard placement follows the International 10–20 system, in which electrodes sit at 10% or 20% increments of the measured distances between bony landmarks (nasion, inion, preauricular points). This makes recordings reproducible across labs and over time, with odd-numbered electrodes on the left, even on the right, and "z" along the midline.
• Montages: The EEG is the voltage difference between pairs of electrodes, and how those pairs are arranged is the montage. A bipolar montage links adjacent electrodes in chains; the abnormality is localized by phase reversal, where adjacent channels deflect toward each other. A referential montage compares each electrode against a common reference; here the channel with the largest deflection sits over the source. Reading both is routine — each shows things the other can obscure.

The frequency bands

Frequency is the heart of EEG interpretation. The same waveform can be perfectly normal in one state and frankly pathologic in another — context is everything. The four classic bands, from slowest to fastest:

• Delta (<4 Hz): The slowest rhythm. Delta is normal in deep (N3) sleep and in infancy, but pathologic in an awake adult. Focal delta over one region suggests an underlying structural lesion; generalized delta points to a diffuse encephalopathy.
• Theta (4–7 Hz): Normal in drowsiness, sleep, and in children. Excess theta in an awake, alert adult is a mild, nonspecific sign of cerebral dysfunction.
• Alpha (8–13 Hz): The signature rhythm of relaxed wakefulness. The posterior dominant rhythm is the alpha seen over the occipital regions when a relaxed patient closes the eyes; it attenuates with eye opening and with mental effort.
• Beta (>13 Hz): Fast, low-amplitude activity, maximal frontally, associated with alertness and active concentration. Beta is markedly enhanced by benzodiazepines and barbiturates, so a diffuse beta excess should prompt a look at the medication list.

Normal awake, drowsy, and sleep architecture

A normal EEG is not static — it evolves predictably as the patient transitions from alert wakefulness through drowsiness into sleep. Recognizing the normal landmarks is what keeps you from over-calling benign features as disease.

• Awake: A well-formed, reactive posterior dominant rhythm in the alpha range with eyes closed, attenuating on eye opening, plus low-amplitude frontal beta.
• Drowsy: The posterior rhythm slows and fragments, beta and theta increase, and slow lateral eye movements appear.
• Sleep: The hallmarks of N2 sleep are sleep spindles (brief 11–16 Hz bursts), K-complexes (large biphasic sharp-and-slow transients), and vertex (V) waves (sharp negative transients at the midline central region). Deeper N3 sleep brings high-amplitude delta. These are all normal — confusing a vertex wave or a K-complex for an epileptiform discharge is a classic beginner's error.

Epileptiform abnormalities

Epileptiform discharges are the EEG findings that carry the strongest association with a tendency toward seizures. The core morphologies are the spike (a sharply contoured transient lasting roughly 20–70 ms) and the sharp wave (70–200 ms), each standing out from the background and typically followed by a slow wave. Interictal discharges occur between seizures and support a diagnosis of epilepsy; ictal patterns are the rhythmic, evolving discharges of a seizure itself.

• Focal epileptiform discharges (focal spikes or sharp waves) localize the irritable cortical zone and point toward a focal (localization-related) epilepsy — for example, anterior temporal spikes in mesial temporal lobe epilepsy.
• 3-Hz generalized spike-and-wave is the classic, beautifully regular pattern of childhood absence epilepsy, often provoked by hyperventilation and accompanied by a behavioral arrest.
• Generalized polyspike-and-wave (often 4–6 Hz) is characteristic of juvenile myoclonic epilepsy and correlates with the myoclonic jerks.
• Hypsarrhythmia is a chaotic, disorganized, very high-amplitude pattern of multifocal spikes and slow waves — the interictal signature of infantile spasms (West syndrome).

Periodic patterns

Periodic patterns are recurring complexes at a quasi-regular interval. Modern ACNS critical-care terminology has renamed several older eponyms, and the new terms are worth using.

• Lateralized periodic discharges (LPDs) — formerly PLEDs — are periodic complexes confined to one hemisphere. They flag acute focal cerebral injury: classic associations are herpes simplex encephalitis and recent (acute) stroke. LPDs sit on the ictal–interictal continuum and warrant close attention to seizure risk.
• Generalized periodic discharges (GPDs) are bilateral, synchronous periodic complexes seen in diffuse processes, including severe metabolic encephalopathy and anoxic injury.
• Triphasic waves are blunt, generalized, frontally predominant complexes with a characteristic three-phase morphology, classically described in hepatic and other metabolic encephalopathies. They are suggestive but not specific — they appear in a range of toxic-metabolic states and can be difficult to distinguish from GPDs.

Slowing: focal versus generalized

Slowing is the most common abnormality on EEG and follows a simple logic. Focal slowing — delta or theta confined to one region — implies a localized disturbance of the underlying cortex or white matter, typically a structural lesion (tumor, infarct, abscess, contusion). Diffuse or generalized slowing indicates a global disturbance of brain function — an encephalopathy from metabolic derangement, toxins, hypoxia, or a diffuse process — and its degree tracks loosely with the severity of the encephalopathy.

Status epilepticus and the role of continuous EEG

EEG is indispensable in the critically ill. Many comatose ICU patients seize without any outward movement — nonconvulsive status epilepticus — and the only way to detect it is to look at the brain electrically. Continuous EEG (cEEG) monitoring is therefore standard in evaluating unexplained altered consciousness after convulsive status, after cardiac arrest, and in any patient whose mental status is worse than their imaging explains. cEEG also guides titration of anesthetic infusions to a target such as burst-suppression in refractory status.

Activation procedures

Routine EEG includes maneuvers designed to provoke latent abnormalities that the resting record may miss.

• Hyperventilation: Three to five minutes of overbreathing induces hypocapnic cerebral vasoconstriction. It reliably provokes the 3-Hz spike-and-wave of absence epilepsy and may bring out focal slowing.
• Photic stimulation: A strobe flashed at a range of frequencies can elicit a photoparoxysmal (photoconvulsive) response — generalized epileptiform discharges driven by the light — most often in the genetic generalized epilepsies.

What EEG is used for

• Classifying seizures and epilepsy syndromes — distinguishing focal from generalized, and pinning down syndromes (absence, JME, West syndrome) by their signature discharges.
• Evaluating encephalopathy and coma — gauging severity and identifying patterns such as triphasic waves.
• Detecting nonconvulsive seizures and status in the ICU via continuous monitoring.
• Brain death / death by neurologic criteria — historical only: EEG was once used as an ancillary test demonstrating electrocerebral inactivity (no cerebral activity above 2 µV). It is no longer an acceptable ancillary test: the 2023 AAN/AAP/CNS/SCCM consensus guideline removed EEG (and evoked potentials) because they do not assess brainstem function. The acceptable adult ancillary tests are now cerebral blood-flow / perfusion studies — four-vessel catheter angiography, radionuclide cerebral blood-flow scan, and transcranial Doppler (adults only).
• Prognostication after cardiac arrest — patterns such as suppression, burst-suppression with identical bursts, and unreactive backgrounds carry prognostic weight as part of a multimodal assessment.

Quick reference: the rhythms