Neurophysiological Basis of the EEG

Since its initial development, EEG has remained a unique tool for the study of cortical function and a valuable supplement to history, physical examination, and information gained by radiological studies.

When small metallic disc electrodes are placed on the surface of the scalp, oscillating currents of 20–100 µV can be detected and are referred to as an electroencephalogram (EEG). Their origin is a direct consequence of the additive effect of groups of cortical pyramidal neurons being arranged in radial (outward-directed) columns. The columns relevant here are those beneath the surface of the cortical gyri. As the membrane potentials of these columns fluctuate, an electrical dipole (adjacent areas of opposite charge) develops. The dipole results in an electrical field potential as current flows through the adjacent extracellular space as well as intracellularly through the neurons (Figure 30.1). It is the extracellular component of this current that is recorded in the EEG and variations in both the strength and density of the current loops result in its characteristic sinusoidal waveform.

Figure 30.1 Diagram illustrating the contribution of individual excitatory and inhibitory synaptic currents to the extracellular field potentials. Micropipettes are being used to sample intracellular and extracellular events. (A) Intracelluar recordings show that the excitatory synapse generates a rapid EPSP (excitatory postsynaptic potential) at the synaptic site on the dendrite and a slower and smaller EPSP at the soma. Extracellular recordings show that the source (positive) of excitatory synaptic current flows outward through the membrane of proximal dendrite and soma, and inward (the sink) at the synaptic site. (B) An inhibitory synapse is seen to have the opposite effect. The IPSP (inhibitory postsynaptic potential) is associated with a current source at the synaptic site and a sink along the proximal dendrite and soma.

The oscillations of the EEG, measured in microvolts (µV) are thought to be generated by reciprocal excitatory and inhibitory interactions of neighboring cortical cell columns.

Technique

After careful preparation of the skin of the scalp to ensure good contact, electrodes are affixed in a placement that is in conformity with the 10–20 International System of Electrode Placement, when the scalp is divided into a grid in accordance with Figure 30.2.

Figure 30.2 Deployment of surface electrodes on the scalp. Letters: Fp, frontopolar; F, frontal; T, temporal; P, parietal; C, coronal; O, occipital; Z, midline. Numbers: Odd numbers, left side; even numbers, right side. A1, A2 are reference electrode positions (see text).

By defining a consistent placement of electrodes, direct comparison to follow-up studies is feasible, as is a method to compensate for differences in head size. Each electrode placement allows it to preferentially record over a cortical surface area of approximately 6 cm². The nomenclature employed to define each electrode position combines a letter with a number, as shown in the figure.

Actual EEG recordings are made from all sites simultaneously. The potential difference between electrode pairs is recorded (as a rule) and this is displayed as a separate individual graph or channel. Often other physiological recordings are performed at the same time (e.g. an electrocardiograph and/or a surface EMG).

If varying pairs of electrodes are used, the montage (output) is termed bipolar (Figure 30.3A). If they have one recording site in common (auricle, or mastoid area), it is called referential (Figure 30.3B).

Figure 30.3 (A) Bipolar recording. A succession of adjacent pairs of electrodes is used. Only four sample tracings are shown. (B) Referential recording. The reference electrode is attached to the ear in this example. Again only four sample tracings are shown.

Figure 30.4 provides a complete set of normal tracings.

Figure 30.4 A complete set of normal tracings is shown, tagged in accordance with the nomenclature in Figure 30.2. (An electrocardiogram [EKG] has been taken simultaneously.) Note the low amplitude of the waves (20 µV or less) and their high frequency in this 2-second sample.

Types of Pattern

Normal EEG rhythms

Awake state EEG

The EEG demonstrates prominent changes both with the level of alertness and during the various stages of sleep. Each of these patterns is specific and is taken into account during the EEG interpretation. A routine EEG study will usually take 30–45 minutes and will include recordings made during wakefulness and during early stages of sleep, since specific abnormalities (especially epileptiform ones) may only be detected during the sleep portion of the recording.

In the alert awake state (Figure 30.5A), the pattern is described as desynchronized because the waveforms are quite irregular. The background frequency is usually around 9.5 Hz. A beta frequency of more than 14 Hz may be superimposed over anterior head regions.

Figure 30.5 EEG in the awake state. (A) Subject is alert with eyes open. Beta waves are seen in Fp2–F4 and F4–C4. (B) Subject is relaxed with eyes closed. An eyeblink artifact is seen in the Fp2–F4 tracing. Alpha waves are seen in P4–O2. The beta waves are characterized by low amplitude and high frequency, the alpha waves by rhythmic waxing and waning.

In a relaxed state with the eyes closed, rhythmic waveforms appear in the alpha frequency (8–14 Hz), notably over the parieto-occipital area (Figure 30.5B).

Normal sleep EEG

Glossary

• REM sleep Dreamy light sleep accompanied by rapid eye movements; also called paradoxical sleep because of EEG resemblance to the awake state.

• NREM sleep Non–rapid eye movement sleep (stages 1–3); stage 3 is also called slow wave sleep.

People normally pass through three to five sleep cycles per night. The sequence of events is summarized in Figure 30.5. Alpha rhythm becomes apparent (on occipital leads) during quiet rest with eyes closed.

By general agreement, sleep proper is associated with slow-wave patterns in the EEG. There is a rapid descent through stage 1, characterized by a steady theta rhythm, into stage 2, characterized by theta waves interrupted by sinusoidal waveforms called sleep spindles, and by occasional K complex spikes. Stage 3 is characterized by slow, delta waves – hence the term slow wave sleep for that stage (Figure 30.6).

Figure 30.6 Typical 8-hour sleep and EEG patterns. Note that the REM (rapid eye movement) period (in pink) is not one of the official four sleep stages despite being routinely referred to as REM sleep. The EMG trace shows that skeletal muscles are ‘paralyzed’ during REM sleep.

It is generally agreed that the waxing and waning of cortical activity during slow wave sleep has its origin in the thalamus, where the relay nuclei projecting to the cortex also enter a rhythmic discharge mode during slow wave sleep. This rhythm is characterized by a succession of hyperpolarized states alternating with depolarized states exhibiting bursts of firing. The vigorous firing is triggered by momentary opening of voltage gated calcium channels. The transient (momentary) opening accounts for the term T-channels applied to these.

As described in Chapter 27, thalamocortical projections pass through an inhibitory shell in the form of the thalamic reticular nucleus, with reciprocal connections to parent relay cells as shown in Figure 27.4

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