Electroencephalograph (EEG) changes sensitively along with the state of consciousness in both physiological and pathological states. The alpha rhythm slows down in physiological sleep states and pathologically stuporous states. As the stage of sleep deepens or consciousness becomes more impaired, theta and then delta activities predominate. The EEG also changes dramatically with age, especially during infancy and early childhood, and there are many age-specific EEG patterns. There are also many inter- and intraindividual variables in both normal and abnormal states. Deciding whether the EEG is abnormal or normal depends on the qualitative and quantitative deviation from the normal state. The ordinary EEG interpretation by visual analysis, therefore, relies largely on the electroencephalographer’s (EEGer) experience, knowledge, and subjective as well as objective judgment.

EEG interpretation is based on systematic visual inspection and multifactorial analyses of background activity and abnormal patterns by incidence, frequency, amplitude, morphology, topography, and reactivity and by their relationship to age and level of consciousness. Abnormalities may occur within the background activity alone, or with the appearance of abnormal patterns, or both. The abnormal EEG consists of slowing of the background (alpha) rhythm, the appearance of slow waves, paroxysmal activity, and/or varieties of specific patterns. These abnormalities may be (i) focal, (ii) bilaterally diffuse, or (iii) unilateral or lateralized. In a broad sense, slow background activity and slow waves imply cerebral dysfunction, whereas paroxysmal activity suggests an underlying seizure tendency. However, any EEG abnormality is rarely pathognomonic or specific for a certain diagnosis. Under certain clinical conditions, however, some EEG abnormalities help narrow the diagnostic possibilities.

Background activity slower than 8 Hz during the fully awake state is abnormal in any age except for children less than 3 years old. When the alpha rhythm is replaced by slower rhythms, the background activity may be diffuse rather than the more typical occipital dominant pattern. Bilaterally diffuse or focally dominant slow background activity, even without another abnormality, is a sensitive indicator of cortical dysfunction (see Fig. 6-10 and Fig. 11-1). In a focal cerebral lesion, however, the slower or depressed background activity is often associated with delta slow waves (Fig. 8-1; see also Fig. 6-11).

Amplitude asymmetry between homologous regions should be approached cautiously. This may be due to technical factors such as unequal interelectrode distance between the two homologous electrode pairs, especially, if this appears only in one bipolar montage but not in other montages (see Fig. 15-48A and B). An amplitude asymmetry noted on a bipolar recording must be confirmed by referential montage (see Fig. 15-47). Localized scalp edema, subgaleal collection of fluid, or a skull defect (i.e., craniotomy) can also cause amplitude asymmetry. This should be documented by the technologist.

Consistent amplitude asymmetry of the alpha rhythm greater than 50% may be clinically significant, especially when the amplitude is lower on the right side (since the alpha rhythm is generally of higher amplitude on the right in normal subjects). A subdural hematoma may have depressed background activity without accompanying other abnormalities (see Fig. 6-9). This is explained by the longer distance to the electrode from the cortex by the depressed cortex and increased impedance due to fluid collection. Amplitude accentuation ipsilateral to the lesion is rare, but this may occur with a brain tumor situated close to the cortex.¹ Focal accentuation of alpha and beta activities is a common finding in a patient with a skull defect (Breach rhythm) (see Fig. 7-20; see also Fig. 12-12).

The unilateral failure of alpha attenuation with eye opening is a rare finding and is termed Bancaud’s phenomenon, which may be seen in a localized hemispheric lesion.² Although abnormal alpha rhythm without other abnormalities primarily represents cortical dysfunction, unilateral reduction of the alpha rhythm has been reported in patients with unilateral thalamic tumor³ and subcortical cerebral infarct.⁴

Frequency asymmetry of background activity or alpha rhythm with or without amplitude depression is a more reliable finding than amplitude asymmetry alone, indicating focal pathology. Irrespective of amplitude difference, the side with slower frequencies is (more) abnormal (see Fig. 6-12).

Approximately 10% of normal subjects show a low-voltage (<20 µV) background pattern that is difficult to measure.⁵ There is some evidence that genetic factors play a role in determining the voltage pattern in a healthy person.⁶ In some cases, it is difficult to differentiate if the low-voltage activity is abnormally
suppressed or simply a normal variant. In some normal people, the background activity is low voltage initially but may show measurable alpha rhythm in the latter portion of the recording. The measurable alpha rhythm may also appear during hyperventilation. The normal low-voltage background pattern also tends to show well-defined and prominent photic driving responses with high-frequency photic stimulation. In some cases, it is not possible to determine the normality or abnormality unless a previous EEG is available for comparison. One clinical correlation of the low-voltage EEG pattern is Huntington chorea in which progressive voltage decline likely correlates with loss of cortical activity rather than indicating a desynchronized background that would be seen in normal people⁷ (see Fig. 11-19).

A diffuse increase of beta activity is a common finding secondary to sedative, hypnotic, or anxiolytic drug effect (Fig. 8-2; see also Fig. 7-21A and B). The most common medications are benzodiazepines or barbiturates. The medication’s effect is usually more prominent and distinct in sleep, characteristically showing abundant sleep spindles with a paucity of vertex sharp waves or K complexes (Fig. 8-3). The degree of beta accentuation varies considerably from one individual to another and is not dependent on the dose of medication; this alone should not be considered an abnormal finding. A prominent and diffuse beta activity in the form of sleep spindles can be seen in semicomatose or comatose patients after overdose or therapeutically induced by the hypnotic or anxiolytic drugs (Fig. 8-4). This may be referred to as “spindle coma” (see “Spindle Coma,” Chapter 11; see also Fig. 11-16).

An unusually prominent diffuse or localized beta activity may be seen in patients with grossly anomalous brain such as agyria (lissencephaly) or cortical dysplasia.⁸ Unilateral or focal depression of beta activity is a reliable and sensitive indicator of focal cortical dysfunction (Fig. 8-5; see also Fig. 12-6).⁹ This asymmetry may be accentuated when the patient is on a sedative or hypnotic drug, that is, the intact cortex can produce beta activity, while the impaired cortex cannot.

Beta and alpha activities can be focally enhanced in a patient who has a burr hole or skull defect, resulting in a “breach rhythm”¹⁰ with a characteristic mu-shaped waveform (see Fig. 7-20; see also Fig. 12-12). This commonly occurs in central and midtemporal electrodes. The breach rhythm alone should not be regarded as abnormal because it is due to a physical effect, not cortical injury. In addition, EEG activity near the burr hole has a “sharper” or more “spiky” appearance than the activities from other areas. It is best to be conservative in determining these as spike discharges.

Focal or diffuse beta may signify the onset of an ictal event, which often shows progressive changes from low-voltage, faster- to slower-frequency waves with increasing amplitude as the seizure evolves (Fig. 8-6; see Fig. 10-7).

An unusual accentuation of fast activity in the form of sleep spindles is termed “extreme spindle.” This is characterized by very frequent and high-amplitude (often >200 µV) sleep spindles, seen in children (<12 years old) with intellectual disability or cerebral palsy.¹¹ The spindle activity may be seen even in the awake state (Fig. 8-7).

Activity with frequency faster than 30 Hz (gamma rhythm) is relatively rare in routine scalp EEG recordings but can be seen at the onset of seizure events (Fig. 8-8). Gamma rhythm recorded from intracranial subdural electrodes could demonstrate an accurate localization of seizure onset zone (Fig. 8-9).¹² Fast-frequency activity (close to gamma frequency) in association with rhythmic delta waves has been recognized as a unique diagnostic EEG pattern for patients with anti-NMDA (N-methyl D-aspartate) receptor encephalitis¹³ (Fig. 8-10; see also Chapter 11 Fig. 11-21A and B).