75: Clinical Neurophysiology and Electroencephalography

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CHAPTER 75 Clinical Neurophysiology and Electroencephalography


The history of the encephalogram (EEG) may be traced back to the 1700s when Luigi Galvani demonstrated that electrical stimulation of a peripheral nerve in a frog caused contraction. In the mid-nineteenth century, Carlo Matteucci and Emil DuBoid-Reymond established the field of electrophysiology. In 1929, the German neuropsychiatrist Hans Berger demonstrated the Elektrenkephalogramm as a graphical representation of electrical activity in the human brain. In 1935, Frederic and Erna Gibbs with William Lennox recorded the EEG in patients in epilepsy and demonstrated its clinical utility.1 The synaptic origin of the EEG was demonstrated by Renshaw in the 1940.2 Starting in the 1950s, intracranial implantation of EEG electrodes was used for evaluation of epilepsy surgery. During this period, systematic description of sleep architecture with the EEG was also described. Computerized EEG acquisition and analysis have been possible since the 1970s.3 Long-term recording of simultaneous video and EEG tracings revolutionized the evaluation of epilepsy on many fronts.

The EEG records low-voltage electrical activity produced by the brain. Recordings are often characteristic of certain ages and states of consciousness. Although primarily used to detect epileptic abnormalities, it is possible to recognize generalized malfunction of the brain, sleep disturbances, and other localized or paroxysmal abnormalities. The EEG has excellent temporal resolution but relatively poor spatial resolution; it can detect rapid changes in function, but it has difficulty localizing abnormalities.

Most commonly, the EEG is recorded from the scalp with small surface electrodes. However, other electrodes are sometimes used under special circumstances. Intracranial electrodes may be placed in the subdural or epidural space, or deep in the brain (as depth electrodes in patients with epilepsy). These are used to record electrical signals with much greater spatial resolution and sensitivity than can be achieved with surface electrodes; in addition, electrical signals may be applied to the electrodes to perform brain mapping.

Although the precise origin of the electrical activity is unknown, EEG activity recorded from the scalp is believed to originate from the postsynaptic potential of the neurons of the cortical pyramidal layer of the cortex. These charges form an electrical dipole, with a positive charge on one end and a negative charge on the other; this creates an electrical field. The summation of the electrical fields may be recorded by surface electrodes.4

The EEG records differences in electric fields, rather than a single action potential. As such, the voltage difference between two electrodes is measured by an amplifier; it is impossible to record from a single electrode. Each pair of electrodes outputs the difference between their potentials through a single channel, which may be graphically displayed on paper or on a computer monitor. The typical EEG machine connects a minimum of 21 electrodes and can display 16 (or more) channels. Electrical activity is recorded from a variety of standard sites on the scalp, according to a standard layout scheme (called the 10-20 International System of Electrode Placement) that can be easily replicated in all laboratories.5 Careful calibration of the signal intensity needs to be performed before each recording.

Because of the low amplitude of electrical signals from the brain, artifacts frequently contaminate the EEG. These may include eye movements, muscle movements, electrode “noise,” and sweating, as well as others. A major challenge in the interpretation of EEGs is to distinguish artifact from brain signals. Filters are routinely used to reduce noise, in both the high- and low-frequency domains. A special “60-Hz” filter may be used to attenuate artifacts from electrical devices that use alternating current.

Considerable attention must be given to the selection of montages (or derivations), for example, determining the combination of pairs of electrodes to be recorded. Two different montages are currently in use. In the referential (or monopolar) montage, each of the electrodes is measured against the same reference electrode, which is presumed to be relatively electrically inactive. Commonly used reference points are the ears, other noncephalic regions, or the average of all other electrodes. In bipolar montages, electrodes in a line along an anatomical region are recorded serially as successive pairs. The first channel would be from the first and second electrodes, the second channel would be from the second and third electrodes, and so forth. The most popular bipolar montage is the anteroposterior “double banana” montage. Creation of different montages gives various views of the electrical activity at different parts of the brain. All EEGs are analyzed using multiple montages over the same recording, including both referential and bipolar montages.

A routine EEG is recorded for at least 20 minutes. However, it is possible to record from electrodes that are glued onto the scalp; these will record the patient’s EEG for hours, days, and even weeks, if clinically necessary.

Before the 1980s, the EEG was recorded on paper through an “analog” system. Today, nearly all EEGs are recorded “digitally” and displayed on a computer monitor. The major advantage of digital recording is that the EEG can be reformatted and flexibly reviewed in any montage, allowing the development of automated seizure detection algorithms. Benefits of other quantitative tools remain to be realized (see Quantitative EEG, later in this chapter).6


The electrical activity from any electrode pair can be described in terms of amplitude and frequency (Figure 75-1). Amplitude ranges from 5 μV to 200 μV. The frequency of EEG activity ranges from 0 Hz to about 20 Hz. The frequencies are described by Greek letters: delta (0 to 3 Hz), theta (4 to 7 Hz), alpha (8 to 13 Hz), and beta (more than 13 Hz).

In the normal awake adult (with eyes closed), alpha rhythm predominates in the posterior part of the head. The amplitude of the alpha waves falls off anteriorly, and it is often replaced by low-voltage beta activity. Often, some low-voltage theta activity can be seen in frontocentral or temporal regions. The alpha rhythm, which is prominent posteriorly, disappears (or is blocked) when the eyes open. This reactivity to eye opening/closure is an important aspect of a normal EEG, and is often attenuated with many pathologies.

When a normal adult becomes drowsy, the alpha rhythm gradually disappears, frontocentral beta activity may become more prominent, and frontocentrotemporal theta activity becomes predominant. Drowsiness is stage I sleep. As sleep becomes deeper, high-voltage single or complex theta or delta waves, called vertex sharp waves, appear centrally. Stage II sleep is characterized by increased numbers of vertex sharp waves, and runs of sinusoidal 12- to 14-Hz beta activity, called sleep spindles, occur. Deeper sleep (Stage III, “slow wave” sleep), characterized by progressively more and higher-voltage delta activity, is not usually seen in routine EEG recordings.

In routine EEG studies, some “activation” procedures are carried out to enhance or elicit normal or abnormal EEG activity. These procedures, such as hyperventilation, photic stimulation, sleep, sleep deprivation, and, rarely, the use of drugs, are useful in bringing out epileptic activity.7 The most common activation procedures are 3 minutes of hyperventilation and a flashing strobe light (at frequencies between 5 and 30 Hz). The normal response to hyperventilation ranges from no change from baseline to a buildup of high-amplitude delta waves. A hyperventilation response is particularly marked in children and young adults. The most specific abnormal response to hyperventilation is the production of generalized spike-wave discharges of a typical absence seizure. Photic stimulation with a stroboscope may produce a driving response, or occipital discharges at a frequency that is a harmonic multiple of the flash frequency. In a small number of epileptic patients, photic stimulation may elicit electrographic epileptiform activity, or even frank seizures.8 The use of an activating procedure in patients monitored on video-EEG for nonepileptic psychogenic seizures is controversial. On the one hand, procedures (such as saline injection or placement of a vibrating tuning fork on the patient) to elicit psychogenic seizures are easy, safe, and potentially diagnostic. However, others believe that the deception involved undermines the care of the patient. Some have proposed using only standard activating procedures (e.g., hyperventilation and photic stimulation) to elicit psychogenic seizures.9


The EEG background is dramatically different in neonates, infants, and children. The EEG plays an important role in the evaluation of preterm infants, as stereotyped EEG changes are seen in the maturing brain.10 The EEG may be discontinuous and asynchronous in premature infants. Sharp activity, not indicative of epileptic activity, may be seen up to age 1 month. Posterior background rhythms increase from 5 to 6 Hz at age 1 to the normal 9 to 11 Hz by age 15.11 Alpha background decreases with age, but should not drop below 8 Hz.12


Abnormalities of the EEG are either focal (involving only one area of the brain) or generalized (involving the entire brain). Additionally, abnormalities are either continuous or intermittent. An abnormality that appears and disappears suddenly is called paroxysmal.

Nonepileptic EEG Abnormalities

The most common focal EEG abnormality consists of slow wave activity. Increased “slow activity” (i.e., theta and delta activity in a waking record) is virtually always abnormal. Almost all conditions that diffusely affect the brain increase slow activity.

In particular, focal delta activity is usually irregular in configuration and is termed polymorphic delta activity (PDA) (Figure 75-2). PDA is usually indicative of a focal brain lesion (such as tumor, stroke, hemorrhage, or abscess).13 Before the advent of modern neuroimaging, focal delta abnormalities were used to localize cerebral lesions. Focal cerebral lesions may also cause asymmetric slowing of the background alpha waves or asymmetric beta activity.

The EEG may also show generalized abnormalities, particularly in encephalopathies. As a general rule, the EEG is a sensitive, though nonspecific, test for encephalopathies. The most common pattern with metabolic encephalopathies is generalized moderate- to high-amplitude theta and delta activity without an alpha resting background.14 Another common pattern observed with hepatic and renal encephalopathies is the presence of triphasic delta waves.15 These are high-voltage, diffuse periodic discharges, and are at times difficult to differentiate from epileptiform generalized spike/sharp-slow wave discharges.16 In infectious encephalopathies, particularly in encephalitides, an admixture of slow activity and epileptogenic activity is often seen.

Intermittent rhythmic delta activity may be seen focally or diffusely. Such activity is frequently confined to the frontal region in adults, and is called frontal intermittent rhythmic delta activity (FIRDA); in children, this pattern is most often located posteriorly. Although initially believed to have been a sign of increased intracranial pressure in young people, these monomorphic high-amplitude waves are most often seen in diffuse encephalopathies.17

In hypoxic encephalopathies, low-amplitude slow waves are typically observed.18 In more severe cases, one may observe a burst-suppression pattern, in which a voltage-suppressed background is interrupted by generalized high-amplitude sharp activity. In most severe cases of coma, generalized suppression of amplitude (i.e., electrocerebral silence) on the EEG in the absence of possible modifying factors (e.g., medications and hypothermia) is an ancillary test to confirm brain death.19

EEG Abnormalities in Seizure Disorders

The EEG has been particularly useful in the analysis of patients with seizure disorders. Paroxysmal abnormalities are common between overt seizures (i.e., interictally), as well as during seizures (ictally). Paroxysmal abnormalities include the spike and the sharp wave. A spike is a single wave that stands out from the background activity and has a duration of less than 70 ms. A sharp wave is similar with a duration between 70 and 200 ms. A spike or sharp wave has an asymmetric up-phase and down-phase and is often followed by a slow wave. The existence of a spike or sharp wave is highly specific; a single sharp wave in the proper clinical context may be sufficient to confirm a seizure disorder. However, such findings are insensitive; the EEG is frequently normal and devoid of such discharges even in patients known to have epilepsy. Multiple recordings may be required to capture an abnormality and to make a diagnosis.20

Epileptic paroxysmal abnormalities can be either generalized or focal. The classic generalized abnormality is the 3-Hz spike and wave pattern that underlies the petit mal absence attack (Figure 75-3). A typical focal abnormality is a focal single spike followed by a slow wave. This abnormality can be seen interictally in focal epilepsy, such as temporal lobe epilepsy (TLE). EEG recorded during a seizure may show a variety of patterns, including repetitive spikes/sharp waves, spike–slow wave complexes, rhythmic theta activity, and others. After a seizure (postictally), the EEG most frequently shows pronounced slow waves. Scalp EEGs are notoriously unreliable for the detection of simple partial seizures.

The relationship of any of these abnormalities to the particular patient is complex. For example, paroxysmal activity on an EEG may (or may not) mean that the patient’s problem is related to epilepsy; the final determination typically rests on the overall clinical picture and on the results of a therapeutic trial. One should resist the temptation to consider the EEG independently. In particular, a normal EEG does not exclude epilepsy, since the EEG may be normal during a focal seizure that is observed clinically.


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