Focal EEG Abnormalities

Thoru Yamada

Elizabeth Meng

General Characteristics of Focal EEG Abnormalities

Focal EEG abnormalities were first described in 1936 by Gray Walter in brain tumor patients.¹ The abnormalities were characterized by localized slow waves, which he termed “delta waves.” Since then, EEG has served as an important, noninvasive diagnostic tool for localized cerebral lesions. However, this has changed with the advent of computerized tomography (CT) and magnetic resonance imaging (MRI) as these studies proved to be more accurate in the anatomical localization of lesions. However, EEG has remained an important tool for functional assessment of localized cerebral lesions. The potential for improved anatomical/spatial accuracy of EEG lies with the use of computerized quantitative methods. Although positron emission tomography (PET) scan and functional MRI can reveal functional alterations of the brain, EEG is superior in its temporal resolution. For example, focal cerebral dysfunction can be revealed almost instantaneously after the clamping of a carotid artery during endarterectomy surgery if the hemisphere on the side of clamped carotid artery encounters a risk of ischemia (see Video 11-1). Poor spatial resolution of scalp-recorded EEG is in part due to the distortion by volume conductors that lie between the cortex and scalp, that is, CSF (cerebrospinal fluid), dura, skull, and scalp. By the time the electrical activity reaches the scalp, the current is attenuated and distorted. Combining computerized EEG data and MRI will provide more accurate anatomical localization. The more accurate anatomical assessment of electrical source of interest from the brain can be made by MEG (magnetoencephalography). Focal EEGs are represented by the following findings:

Focal/unilateral amplitude depression or slowing of basic background activity (alpha, beta waves) without an increase in theta-delta slow waves (Fig. 12-1)
Focal/unilateral amplitude depression or slowing of basic background activity associated with an increase in theta-delta slow waves (Fig. 12-2)
Focal/unilateral theta-delta slow waves with preserved basic background activity (Fig. 12-3)
Focal/unilateral enhancement of basic background activity with or without associated slow waves (Fig. 12-4)
Focal/unilateral epileptiform activity with or without associated slow waves (Fig. 12-5)

ALTERATION OF BACKGROUND ACTIVITY

EEG recorded directly from the surface of a brain tumor shows no EEG activity. Slow waves appear some distance from the tumor location. Recorded from the scalp, depression, slowing, and disruption of the background rhythm are common findings near a lesion. In evaluating focal abnormalities, the EEG should be examined for symmetry of amplitude and frequency, continuity, and reactivity of the background activity between homologous areas. An amplitude asymmetry alone, without frequency asymmetry, should be treated cautiously as technical errors (i.e., unequal interelectrode distances between homologous electrode pairs or cancelation effect due to equipotential distribution between two electrodes) must be considered (see “Technical Pitfalls and Errors,” Chapter 15; see also Figs. 15-47 and 15-48). The destructive lesions or lesions involving cortex and white matter tend to show attenuated background activity associated with delta activity (see Fig. 12-2). Slowed background rhythm with preservation of amplitude tends to occur in chronic lesions (see Fig. 12-3). Slowing of the alpha rhythm may occur in lesions not necessarily involving the occipital lobe. Slowing of background rhythm often accompanies theta-delta waves, disrupting normal continuity of background rhythm. Focal delta slow waves in a preserved background activity may be seen in subcortical lesions.

Focal or unilateral depression of beta rhythm, either intrinsic or drug induced, is also an important parameter in interpretation of a focal abnormality (Fig. 12-6). Beta depression is a sensitive indicator for cerebral ischemia. Beta depression may also be seen in the region of an epileptic focus. In sleep, unilateral depression of sleep spindles, vertex sharp waves, or other sleep patterns may be present on the side of a lesion (Figs. 12-7A and B and 12-8A and B). When EEG shows bilateral slowing, the side of slower frequency and/or decreased background activity is the worse hemisphere irrespective of amplitude asymmetry (Fig. 12-9).

Although amplitude depression and paucity of background activity are common findings of focal abnormality, higher-thannormal alpha rhythm amplitude on the side of a lesion may be seen in some cases, especially in slowly progressive or chronic lesions (Fig. 12-10A and B). Similarly, beta rhythm, mu rhythm, or sleep spindles may be augmented ipsilateral to the side of a lesion (Fig. 12-11).²,³,⁴,⁵,⁶ Both ends of the spectrum, either depression or accentuation of sleep spindles, have been reported in

patients with Sturge-Weber syndrome (Fig. 12-12).⁵ Similarly, marked attenuation or accentuation of beta rhythm has been reported on the side of a porencephalic cyst.⁷

FIGURE 12-1 | A 6-year-old boy with a history of focal seizures involving left arm. There was depression and intermittent slowing of alpha rhythm over the right hemisphere but without significant focal delta-theta slow.

FIGURE 12-2 | A 62-year-old woman with acute aphasia and right-sided weakness secondary to left middle cerebral artery infarct. EEG showed decreased background activity along with more or less continuous polymorphic delta activity over the left hemisphere, while EEG on the right side is entirely normal.

FIGURE 12-3 | A 27-year-old woman with a history of partial complex seizures secondary to arachnoid cystic lesion in right frontal lobe. Note polymorphic delta from right anterior temporal region, but with preserved symmetric background alpha rhythm. A portion of this example is shown in the box.

FIGURE 12-4 | A 49-year-old man with a history of right subdural hematoma and status post craniotomy on the right. EEG showed increased amplitude of background activity as well as underlying polymorphic delta slow waves over the right hemisphere. Increased background amplitude over the right is likely secondary to skull defect. A portion of this example is shown in the box.

FIGURE 12-5 | A 6-year-old boy with a history of focal seizure with secondary generalization. Note spike maximum at C3 or P3 electrode along with irregular delta activity from left hemisphere (shown in boxes).

FIGURE 12-6 | A 19-year-old man with left frontal intraparenchymal hemorrhage secondary to head trauma. EEG showed bilaterally diffuse and bifrontal dominant delta-theta activity. There was consistent depression of beta activity over the left frontal region and this was the only lateralizing EEG finding (compare the channels shown by the box and oval circle).

FIGURE 12-7 | A 47-year-old woman with a left chronic subdural hematoma. EEG showed only minimal slowing on left side (shown by rectangular boxes) (A), but sleep record showed consistent depression of V wave (shown by rectangular box) over the left hemisphere (B).

FIGURE 12-8 | A 46-year-old man with partial complex seizures secondary to left frontoparietal infarct 13 years ago. Awake EEG showed only decreased amplitude of background activity (A). Sleep record showed consistent depression of sleep spindles and POSTs (shown by rectangular box) (B).

FIGURE 12-9 | A 6-year-old boy with developmental delay and right hemiparesis. EEG showed bilateral delta activity with slower and lower amplitude delta over the left hemisphere, indicating that left hemisphere is worse than right.

FIGURE 12-10 | Patient was a 60-year-old man presenting with sudden onset of slurred speech and right facial droop. MRI showed large parietal mass lesion with small hemorrhagic extending from posterior periventricular region (A). EEG in awake showed left>right alpha rhythm without significant slow waves (A). In sleep, there were irregular delta slow waves focused at left posterior head region (B, shown by rectangular box). This case illustrates very unusual EEG features showing enhanced alpha on the side of lesion (in common sense, right side should be considered abnormal side). Sleep record, however, showed delta slow waves in left posterior quadrant corresponding to the site of legion (B). This is also unusual since focal slow waves are usually more clear in awake than in sleep record (see Fig. 12-14). (This patient did not have skull defect or craniotomy at the time of this EEG recording.)

FIGURE 12-10 | (Continued)

FIGURE 12-11 | An 11-year-old boy with a history of stable cyst in right frontal region. EEG showed focal polymorphic delta in right frontal region. Note increased beta activity in the same region (shown in boxes). There was no skull defect in this patient.

FIGURE 12-12 | A 26-year-old man with a history of closed head injury and left epidural hematoma, and status post craniotomy 6 months prior to the EEG. Note increased beta and “spiky” alpha and enhanced mu rhythm over the left central and midtemporal region (breach rhythm).

Skull defect or burr hole secondary to craniotomy or head injury causes local enhancement of underlying EEG activity, especially beta rhythm. The focal amplitude accentuation secondary to skull defect is referred to as “breach rhythm” and is usually discreetly localized to one or two electrodes near the skull defect or burr hole site (Fig. 12-13; see also Fig. 7-20). This beta enhancement may result in a “spiky”-appearing activity, which includes “spike-like” or “sharp-like” transients. In fact, these are often difficult to differentiate from true spike or sharp discharges. If the “spiky” discharge is disproportionately larger or wider spread than the breach rhythm, it is likely true spike.

FOCAL DELTA ACTIVITY

Delta activity can be divided into two types by morphological characteristics, one is arrhythmic (polymorphic) and the other is rhythmic (monomorphic or monorhythmic). Arrhythmic delta activity (ADA) consists of serial waves of irregular shape with variable duration and amplitude, which occur continuously or intermittently. ADA reacts little to eye opening or alerting stimuli. Focal ADA is usually most evident in the awake state and becomes less distinct in non-REM sleep (Fig. 12-14A and B).

Focal ADA usually indicates a lesion involving subcortical white matter. Greater irregularity in waveforms, slower frequency, greater persistence, and less amount of superimposed or intermixed fast activity generally indicate a more severe and acute lesion. In determining the most affected area, the same rule applies. The region of slower frequency and lower amplitude delta activity is more severely affected (see Fig. 12-9). Faster and higher amplitude delta, often mixed with alpha or theta, is more common at a distance further from the lesion.

Continuous ADA, especially when associated with loss of background activity, correlates highly with acute or rapidly progressive destructive lesions (see Fig. 12-2). Intermittent or less continuous ADA intermingled with theta or alpha background activity may be a sign of a chronic lesion or may occur during the recovery process of focal damage (see Fig. 12-3).

In contrast to the irregularly formed ADA, intermittent rhythmic delta activity (IRDA) or RDA^* has a rhythmic sinusoidal waveform occurring as bursts or paroxysms. Classically, IRDA/RDA^* was thought to represent a projected rhythm, thus correlating with deep midline lesions such as tumors in the thalamus, hypothalamus, or brainstem. IRDA/RDA^* is now recognized to occur more commonly in toxic/metabolic encephalopathy than in focal intrinsic brain lesions. IRDA/RDA^* has two characteristic distributions, one is frontally predominant RDA^*/(FIRDA) and the other is occipitally predominant RDA (OIRDA). FIRDA/frontally predominant RDA^* is usually seen in adult patients (see Fig. 6-3; see also Fig. 8-14), whereas OIRDA/occipitally predominant RDA^* occurs more commonly in children (see Fig. 8-15, see also Video 10-6).

Although IRDA is more common in metabolic, toxic, encephalopathy, it can occur in infratentorial lesions and is usually bilaterally symmetrical or shows shifting asymmetries. With supratentorial lesions, IRDA may be asymmetric, usually with greater amplitude on the side of the lesion.⁸,⁹

Unlike ADA which is resistant to reactivity, IRDA/RDA^* tends to be augmented by eyes closing or hyperventilation and is attenuated by alerting stimuli.

FIGURE 12-13 | A 5-year-old boy with diagnosis of Sturge-Weber syndrome and history of seizures. MRI showed atrophy of left frontal, parietal, and occipital lobes, enlarged left lateral ventricle, and left frontal calcification. This sleep EEG showed consistent depression of sleep spindles, V waves, and beta activity over the left hemisphere.

FIGURE 12-14 | A 44-year-old woman with right spastic hemiparesis secondary to head injury 11 years ago. MRI showed encephalomalacia on left temporal lobe and enlarged left lateral ventricle. EEG in awake state showed intermittent delta waves and decreased alpha rhythm over the left hemisphere (A). In sleep, delta waves appear bilaterally and focal delta activity noted in awake state becomes unclear (B).

FIGURE 12-14 | (Continued)

Focal or lateralized IRDA (LRDA^*) implies potential seizure activity rather than focal structural lesion (see Chapter 10, section “Indication for CCEEG.” See also Fig. 13-2A and B, Video 13-4).

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