Electroencephalography

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30 Electroencephalography

Chapter Summary

Neurophysiological basis of the EEG

CLINICAL PANELS

The EEG is an important neurological tool, for three main reasons:

1 It is central to the study of the physiology of sleep and the pathophysiology of sleep disorders.

2 It is essential for analysis of seizures and for monitoring progress during their treatment.

3 It is a valuable aid to localization of space-occupying lesions including brain tumors.

We suggest you review the amino acid transmitters in Chapter 8 before reading about drug therapy in the Clinical Panels.

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. Burst firing excites the reticular nucleus, which in turn causes the relay neurons to become hyperpolarized by opening the GIRK potassium channels (Figure 8.11).

The rhythmic waxing and waning of thalamic neurons is attributed to a pulsatile discharge pattern inherent to the cells of the reticular nucleus. Exaggeration of the normal spike and wave pattern is found in a common form of epilepsy known as ‘absence’ seizures (see later).

After about an hour’s sleep the stage 2 wave pattern is repeated and is succeeded by a longer period of slow wave sleep. Up to a minute may then be spent in REM sleep, a dream state accompanied by:

• visual imagery

• rapid eye movements generated by the extraocular muscle contractions

• electromyographic silence in the musculature of trunk and limbs

• an EEG beta rhythm characteristic of the waking state – hence the term paradoxical sleep.

REM sleep is the dominant state during the final two cycles in the 8 hours spent in bed. Although the significance of dreams is a matter of endless debate, activation of the visual cortex is brought about by the PGO pathway, from pontine reticular formation to lateral geniculate body to occipital cortex. In individuals blind from birth, dreams have a purely auditory content, perhaps associated with activation of the lateral geniculate body.

In the clinic, because of the brief time that an EEG is recorded, a patient does not often cycle through REM sleep patterns. It should be noted that in normal circumstances REM sleep almost never occurs during the first descent into sleep. Should it do so, the strange sleep disorder called narcolepsy should come to mind (Clinical Panel 30.1).

Clinical Panel 30.1 Narcolepsy

Narcolepsy (Gr. ‘sleep seizure’) is a sleep disorder characterized by daytime sleep attacks. These attacks form part of the narcoleptic syndrome. The complete syndrome has characteristic features:

• An irresistable desire to sleep, for periods of up an hour, several times during the day. This is accompanied by sleep paralysis, at either the beginning or the end of an attack, where the patient is in a state of complete awareness but is unable to even open the eyes, for 1–2 minutes.

• Hypnogogic (Gr. ‘accompanying sleep’) hallucinations at sleep onset, characterized by striking visual imagery.The hallucinations are a distorted version of REM sleep.

• During the awake state, there occur brief episodes of muscle paralysis, known as cataplexy, a term used to signify sudden paralysis, triggered by emotion, notably by surprise of any kind. Cataplexy occurs in three out of four patients and may range from mild (e.g. dropping the head or jaw, dropping something held in the hand) to severe, with collapse due to flaccid paralysis of the trunk and limbs with consciousness fully preserved. Occasionally, cataplexy may be the only presenting symptom.

The ‘distorted REM’ nature of narcolepsy appears obvious from the occurrence of the two kinds of paralysis during the awake state rather than during the vivid dream period. Narcolepsy has a familial incidence and may be an immune disorder. It can be very distressing: the patient may be accused of laziness or incompetence at work and is at risk of accidents when driving a car or merely crossing the street.

The key problem is a diminution of gray matter in the walls of the hypothalamus associated with scant production of the excitatory peptide orexin (hypocretin) by a group of neurons in the lateral hypothalamus. Orexin receptors are normally present on the histaminergic neurons of the tuberomammillary nucleus (TMN). As mentioned in Chapter 26, the TMN projects widely to the cerebral cortex and maintains the awake state by activating H₁ receptors on cortical neurons. The drug modafinil is now a medication used to treat narcolepsy, perhaps by decreasing GABA-mediated neurotransmission. The current conventional approach is to reduce sleep attacks by means of noradrenergic drugs such as amphetamine in low dosage, and/or monoamine oxidase inhibitors; both of these prolong the action of norepinephrine released by the cerulean nucleus, and reduce REM sleep.

Reference

Kim SJ, Lyoo IK, Lee YS, Lee J-Y, Yoon SJ, Kim JE, Kim JH, Hong SJ, Jeong D.-U. Gray matter deficits in young adults with narcolepsy. Acta Neurol Scand. 2009;119:61-67.

It should also be mentioned that volunteers awakened during REM sleep do not invariably report a dream; and that dreaming occasionally happens during NREM sleep.

EEG activation procedures

In order to check for susceptibility to seizures, a routine EEG includes a brief period of hyperventilation and another of photic stimulation using strobe (flickering) light at varying frequencies (Figure 30.7).

Figure 30.7 In normal subjects, stroboscopic lighting induces matching spikes in occipital recordings. Many epileptic patients are at risk of generalized tonic-clonic seizures caused by forward spread of strobe effects.

(Adapted from Binnie, 1988.)

Maturation of wave format

Accurate interpretation of printouts necessitates familiarity on the part of the electroencephalographer with those patterns which are age-specific and hence represent normal maturational stages of development. Earliest recordings, from premature babies, show only imtermittent electrical activity which is asynchronous between the hemispheres. Continuous symmetrical activity emerges during childhood, with increasingly distinctive wakeful and sleeping patterns. During early teenage years the adult EEG pattern is established.

Figure 30.8 Bipolar montage illustrating focal slowing. Printouts from right lateral frontal areas display delta waves in this 60-year-old female suffering from headache and drowsiness for several months without overt physical signs. Coronal MRI slices showed compression of the right lateral ventricle. Surgery revealed the cause to have been an astrocytoma. (Analogous tracings from the left frontal area are normal.)

Focal spike or sharp wave discharges may show a patch of phase reversal between adjacent electrodes (Figure 30.9). In the frontal or parietal regon, this is suggestive of an ictal focus; in the occipital it is associated with visual impairment.

Figure 30.9 Phase reversal. This patient suffered from primary focal seizures. Phase reversal between the T8 and P8 electrodes suggests an ictal focus located in the right posterior temporal lobe.

Clinical Panel 30.2 Seizures

Next to cerebrovascular disease, seizures (epileptic attacks) are the most common group of problems encountered in clinical neurology. Some 3% of the population suffer two or more attacks during their lifetime.

The term ‘seizure’ or ‘ictus’ refers to a transient alteration of behavior brought about by abnormal burst-firing of neurons in the cerebral cortex. The ‘interictal period’ is the time interval between seizures.

Seizures are categorized as follows:

A complex seizure has an ictal focus of origin, usually in the temporal lobe. It spreads to induce a secondarily generalized tonic-clonic seizure. In this context, seizures that are generalized from the start are called primary generalized tonic-clonic seizures.

Generalized seizures

Generalized, tonic–clonic seizures (formerly known as grand mal seizures) are characterized by sudden onset of unconsciousness. The individual is ‘struck down’. The body stiffens, for up to a minute (tonic stage), and then exhibits jerky movements of all four limbs, and chewing movements of the mouth for about another minute (clonic stage). Usually, a third minute is spent in more relaxed unconsciousness. EEG recordings taken at the onset of this kind of ictus (attack) show simultaneous bilateral burst-firing all over the cortex (Figure CP 30.2.1).

In those at risk, hyperventilation, or photic stimulation by strobe lighting (Figure 30.7), can precipitate tonic-clonic attacks.

Absence seizures (formerly, petit mal) are characterized by a generalized, 3 Hz spike-and-wave activity (Figure CP 30.2.2). These seizures usually occur between the ages of 4 and 14.

The typical case is a child who, upon relaxing after some physical or mental activity, passes through ‘blank’ periods (absences) of 10–30 seconds, usually with detectable twitching of muscles of the face or fingers. Dozens of such episodes may occur over a period of several hours, often so mild that low-level activities such as walking are not interrupted. The child is unaware of individual episodes, which may occur a hundred or more times in one day. The ‘blank’ periods are brought about by prolonged inhibitory postsynaptic potentials on sensory thalamic relay neurons generated by thalamic reticular neurons made hyperactive by corticothalamic excitatory discharges.

Focal (partial) seizures

Note: The term ‘partial’ refers to seizure origin in a particular lobe (focus) of the brain and not to seizures confined to one part of the body. Complex partial seizures can become generalized.

Simple focal seizures are almost always motor or sensory. Loci of origin are as shown in Table CP 30.2.1.

A jacksonian seizure (named after neurologist John Hughlings Jackson) involves sequential activation of adjacent areas of the motor cortex, e.g ankle, knee, hip, shoulder, elbow, hand, lips, tongue, larynx. A jacksonian seizure may be followed by weakness/paralysis of the affected limb(s) for a period of hours or days; it is known as Todd’s paralysis.

Benign rolandic epilepsy, a relatively common disorder in childhood, has an ictal focus of origin in front of or behind the fissure of Rolando (central sulcus). Motor attacks originate in front of the rolandic fissure and usually involve only the contralateral arm or leg or face, although some become jacksonian. Somatosensory attacks (Figure CP 30.2.3) originate behind the fissure and are described in Table CP 30.2.1.

A diagnosis of benign rolandic epilepsy requires EEG confirmation while the child is quietly asleep during an interictal period. Here, a normal background montage is interrupted by high-voltage spikes that occur at short intervals in the area of the ictal focus. Frequency of attacks dwindles during maturation and the EEG becomes normal by the 16th year.

Complex focal seizures are synonymous with temporal lobe epilepsy. They will be taken up in Chapter 34 following a description there of the relevant areas of the temporal lobe.

Drug therapy

Anticonvulsant drugs, administered in appropriate amounts, control about half of all seizures completely and another quarter almost completely. The drugs are of a broadly predictable nature. Most of them either reduce glutamatergic activity or enhance GABA-mediated inhibitory processes. For tonic-clonic and complex partial seizures, some current drugs of choice are:

• Glutamate antagonists: phenytoin and carbamazepine (Tegretol), reduce high-frequency repetitive firing by blocking glutamate ionotropic receptors (Ch. 8), making their ion channels less permeable to sodium and/or calcium.

• GABA agonists: benzodiazepines and barbiturates enhance the hyperpolarizing effect of GABA on glutamate neurons, as illustrated in Figure 8.7. Sodium valproate blocks the transaminase enzyme which converts GABA to glutamate within adjacent astrocytes (Ch. 8), thereby extending GABA’s time in the synaptic cleft.

The most widely used and most effective drug for absence seizures is ethosuximide. Ethosuximide is a specific T-channel blocker. At appropriate dosage, excitability of thalamic relay neurons is sufficiently reduced to prevent them entering burst-firing mode.

References

Dichter MA. Emerging concepts in the pathogenesis of epilepsy and eleptogenesis. Arch Neurol. 2009;66:443-447.

Oliviero A, Della Marca G, Tonali PA, Pilato E, Saturno E, Dileone M, Versace V, Mennuni G, Di Lazzaro V. Functional involvement of the cerebral cortex in human narcolepsy. J Neurol. 2005;252:56-61.

Smith SJM. EEG in the diagnosis, classification, and management of patients with epilepsy. J Neurol Neurosurg Psychiatry. 2005;76(Suppl II):ii2-ii7.

Steriade M. Sleep, epilepsy and thalamic reticular nucleus. Trends Neurosci. 2005;28:317-324.

Figure CP 30.2.1 Characteristic ‘frenzied’ pattern of a tonic-clonic seizure.

(A) End of interictal period.

(B) Generalized seizure pattern involving all electrode positions.

(C) In less than 1 second, the seizure pattern is ‘scribbled’ by generalized tonic muscle spasm.

(D) Immediate postictal period, with slow waveform pattern throughout.

(E) Resumption of normal waveforms.

Figure CP 30.2.2 (A) Absence seizure. This episode was recorded over a period of 4 seconds. The spike-and-slow wave pattern is bilateral and generalized. In this patient the pattern is rather faster than usual. (B) The spike-and-slow-wave prototype.

Table CP 30.2.1 Loci of origin of simple focal seizures

Motor	Movement of any part of the motor homunculus, sometimes with aphasia
Somatosensory	Contralateral nunbness/tingling of face, fingers or toes
Primary visual cortex	Flashes of light or patches of darkness in contralateral visual field
Visual association cortex	Twinkling-light images in contralateral visual field
Basal occipitotemporal junction	Formed visual images of people or places, sometimes accompanied by sounds
Superior temporal gyrus (unusual)	Tinnitus, sometimes garbled word sounds