The normal adult EEG

Alpha Activity

Hans Berger, the Berlin psychiatrist who in 1929 recorded the first EEG in humans, described a rhythm in the alpha frequency (8 to <13 Hz) in the posterior regions of the head. This is the posterior dominant rhythm (PDR) ( Figure 2-1 ). The PDR is of maximal amplitude in the occipital regions and attenuates with eye opening. It is best seen when the person is in the relaxed, waking state with eyes closed. Note that waves in the alpha frequency may be found in various locations and in various states (e.g., alpha coma or during a seizure). Such waves are not the PDR as described earlier.

The PDR is in the alpha frequency in a normal adult. However, it may be slower in children or in the presence of diffuse disease processes. In normal adults, the PDR should be above 8.5 Hz, as the PDR of 8 Hz is only seen in <1% of normal adults at any age.

In assessing the PDR, look for the patient's best – that is, the highest posterior frequency achieved during the most alert state. Slower posterior rhythms in the theta range or theta waves admixed with the alpha may be due to mild drowsiness and thus have no pathological significance.

The PDR is usually symmetric but may be of higher amplitude over the non-dominant hemisphere. In that case a 2 : 1 ratio is acceptable. If greater than 2 : 1, it may be related to an abnormality, but it also could be the result of incorrect electrode placement. The latter is more likely if the lower-amplitude alpha is well organized and equally persistent as that on the opposite side. Consideration should be given to the possible presence of an insulating process between the scalp electrodes and the cerebral cortex, as might be seen with a subdural collection. In that case the alpha on the affected side may either be markedly depressed in amplitude, or absent.

The PDR, while usually maximal in the occipital regions, often distributes to the adjacent parietal and posterior temporal areas. Moreover, this may be variable over the course of the recording.

If the PDR increases in frequency when the patient opens his or her eyes and persists with the eyes open, or appears only during eye-opening, drowsiness is a likely cause. When the frequency transiently increases immediately after eye closure, it is called alpha squeak. Some people have little or no PDR during the resting state. This finding has no clinical significance and occurs in perhaps 5% of individuals. If the patient is tense, the PDR may not be recorded. In such cases, the PDR may appear as the patient becomes more relaxed.

Take note of processes that may lead to a decline in PDR frequency. These include (but are not limited to) effect of medication(s) such as phenytoin or valproic acid, early dementias, increased intracranial pressure, hypothyroidism, and other metabolic disorders such as hepatic insufficiency.

The absence of the PDR on one side is always pathological. In older subjects this asymmetry is often due to remote infarction. In younger subjects the cause is more likely to be brain damage such as congenital hemiatrophy. If a record contains alpha frequency and looks relatively normal, save for the fact that the alpha frequency is equally prominent in the frontal regions, interpretation depends on the state of the patient and the presence of reactivity. In a comatose patient (e.g., after cardio­pulmonary arrest), with widespread alpha activity that does not react to eye movements or undergo state change, it is termed alpha coma and carries a poor prognosis.

Beta Activity

Beta activity is defined as a frequency of 13–30 Hz and is present in the background of most subjects. If completely absent it may represent an abnormality depending on other features of the EEG. Maximal beta amplitude is usually in the frontocentral regions, but it may be widespread. It does not respond to eye opening, as does the PDR. During drowsiness, beta may seem to increase in amplitude. This appears to be a function of amplitude diminution of other background frequencies and thus is more apparent than real.

Beta activity increases in amplitude and abundance by various drugs (e.g., barbiturates, chloral hydrate, benzodiazepines, and tricyclic antidepressants). In these circumstances, the beta activity is usually between 14–16 Hz ( Figure 2-2 ).

Perhaps the most important finding when analyzing beta activity is interhemispheric asymmetry. In particular, the side of reduced amplitude usually points to the pathological hemisphere. Examples include acute and remote infarct, subdural collections, and porencephaly. By the same token, beta amplitude may be unilaterally increased. This occurs in the setting of a previous craniotomy (so-called breach artifact). In this case breach refers to an opening or rift (i.e., “Captain, there is a breach in the hull” versus “doctor, the baby is breech.”) Lower impedances from the lack of skull continuity result in higher amplitudes of beta activity. Brain abscess, stroke, tumors, vascular malformations, and cortical dysplasia can be associated with either a focal decrease or an enhancement of beta activity. Beta asymmetry, if present, should always be considered in concert with asymmetry of other background frequencies.

Theta Activity

Theta activity (4–8 Hz) is often present in the waking adult EEG, although it may be completely absent. It tends to be somewhat more evident in the midline and temporal derivations. Approximately 35% of normal young adults show intermittent theta rhythm during relaxed wakefulness that is maximal in the frontocentral head regions. Also, intermittent theta frequency in temporal leads, either bilateral or unilateral (usually left more than right), can be seen in the asymptomatic elderly population with an incidence of about 35%.

If theta activity is consistently found in only one location, or is predominant over one hemisphere, it is likely to reflect underlying structural disease. The lesion, however, is usually less malignant, or extensive, than in the case of delta-range focality. Examples are meningioma, low-grade glioma, and remote infarction.

Diffuse theta is usual in children. In the young, theta abundance is quite variable, and one should be flexible when determining whether the theta is excessive or not. When in doubt, err on the side of normality. In comatose patients who have suffered catastrophic brain damage, rhythmic theta may be found diffusely. This finding is termed theta coma.

Delta Activity

Delta activity (<4 Hz) was described in 1936 by W. Gray Walter, a young English physiologist. He gathered his bulky EEG apparatus in an operating room where a patient was undergoing neurosurgery for a malignant tumor. Electrodes placed over the involved area recorded very slow, high-voltage potentials that were slower in frequency than previously reported waveforms. Walter termed these potentials delta waves. Since that time, focal delta activity has proved a reliable indicator of localized disease of the brain.

As a rule, delta waves are not present in the adult during wakefulness. It follows that their presence in wake implies cerebral dysfunction. Delta waves are a normal and important component of adult sleep.

There are other circumstances wherein delta is a normal component of the EEG. For instance, delta is prominent in infants and young children and is common in adolescents in the posterior head regions (posterior slow waves of youth).

Excessive diffuse delta is abnormal and indicates encephalopathy of non-specific etiology. Focal polymorphic delta activity usually indicates a structural lesion involving the white matter, especially when it is continuously seen. Focal rhythmic delta activity can involve the ipsilateral gray matter and be indicative of underlying cerebral hyperexcitability.

Features of Sleep

The recording of sleep is one of the most powerful diagnostic adjuncts in electroencephalography. Relatively minor abnormalities on the routine EEG may be amplified during sleep, and new abnormalities may appear. This is particularly the case with epileptiform activity. Most patients become drowsy at some point during a routine recording, and many actually sleep spontaneously for variable periods. Focal spike or sharp wave discharges often appear or are increased during stage I (drowsiness) and stage II sleep.

Likewise, focal slow wave abnormalities may be exaggerated during these stages. With deeper sleep (slow-wave sleep, SWS) there is a tendency for epileptiform activity and focal slowing to become less obvious.

Stage I sleep is characterized by slowing, fragmentation (increasing irregularity), and ultimate disappearance of the PDR. The background may appear to be generally of lower voltage (due to absence of the PDR), and beta activity may be more obvious. Diffuse theta activity appears and increases in abundance. Vertex waves, which appear during stage I sleep, are synchronous, episodic, sharply contoured potentials (<200 ms in duration) that are maximal over the central regions. They may assume a very sharp, spike-like configuration; are variable in amplitude; and sometimes occur in rhythmic runs. In addition, positive occipital sharp transients of sleep (POSTs) may be quite prominent. These potentials have the appearance of sharp waves, are electropositive at the occipital electrodes, and may be mono- or biphasic in configuration. Do not be surprised to find long rhythmic runs of POSTs that could be mistaken for an ictal discharge by the unwary ( Figure 2-3 ). Both vertex waves and POSTs may persist into stage II sleep.

Stage II sleep arrives with the appearance of well-defined sleep spindles and K-complexes ( Figure 2-4 ). Sleep spindles are synchronous, sinusoidal waves at 12–14 (± 2) Hz with a potential maximum in the central regions. If spindles are only fragmentary or very brief, the patient is not considered to be firmly in Stage II. K-complexes are high-voltage, synchronous bi- or triphasic slow potentials (>500 ms) usually with a central or bifrontal preponderance, often (but not invariably) in close association with sleep spindles. A K-complex can be evoked by a sudden auditory stimulus (Knock).

SWS is characterized by increasing amounts of diffuse delta activity, occupying variable amounts of the background ( Figure 2-5 ). At the same time there is a progressive decline in sleep spindles – in fact, they may disappear. The delta may reach very high voltage without clinical signifi­cance. In adults, SWS is seldom encountered during routine recording.

Rapid eye movement (REM) sleep is characterized by rapid eye movements and loss of muscle tone ( Figure 2-6 ). The EEG background consists of low-voltage theta activity, and eye channels demonstrate irregular vertical and horizontal eye movements. Epileptiform discharges are seldom present in REM sleep. Non-REM sleep and REM sleep alternate in cycles 4–6 times during normal sleep, with increasing REM sleep in the last third of the night. Recall that the first REM period usually occurs about 90 minutes after sleep onset, and patients with narcolepsy experience REM onset sleep. However, a routine EEG with REM may reflect sleep deprivation and does not necessarily mean a sleep disorder such as narcolepsy.