Interpretation of an EEG (or scoring an epoch of sleep in a PSG) begins by analyzing whether a DPR is present, bilateral, symmetric, and within the expected normal frequency range for age and state. The DPR (also called the dominant alpha rhythm or the alpha rhythm) is probably the most important EEG pattern and rhythm. The alpha rhythm is often of highest amplitude over the occipital, posterior temporal, and parietal scalp regions. In one-third of healthy adults, the alpha rhythm extends into the temporal and central regions, which results in the DPR equally seen in the frontal, central, and occipital channels linked to the mastoid references when recording EEG during a routine PSG (Fig. 1).

Fig. 1 Diffuse alpha activity. Example of diffusely distributed alpha rhythm caused by alpha activity extending to the temporal and central regions. A 30-second PSG epoch shows an example of diffusely distributed alpha rhythm caused by alpha activity extending to the temporal and central regions in a 41-year-old awake man.

(Courtesy of M. Grigg-Damberger.)

The alpha rhythm is usually best seen with eyes closed during periods of physical relaxation and relative mental inactivity; it attenuates or is blocked by eye opening and attention, especially visual and mental effort (Fig. 2). This attribute is called reactivity of the alpha rhythm, and can vary from complete suppression of the activity to varying degrees of attenuation with voltage reduction. Reactivity of the DPR may be transient, or appear and then fade with continued eye closure. Some have a DPR that is nonreactive; absent reactivity of an alpha rhythm is only abnormal if it is distinctly asymmetric.

Fig. 2 Dominant posterior alpha rhythm. Normal symmetric reactivity of the DPR to eye opening. Note how the 10- to 10.5-Hz dominant posterior alpha rhythm over the posterior regions (P3-O1, P4-O2, P7-O1, and P8-O2) appears with eye closure in this 12-year-old child. The alpha rhythm is usually best seen with eyes closed during periods of physical relaxation and relative mental inactivity; it attenuates or is blocked by eye opening and attention (especially visual and mental effort).

(Courtesy of M. Grigg-Damberger.)

The frequency of the DPR in normal adults ranges from 8 Hz to 13 Hz or more. Most normal adults and adolescents have an alpha rhythm between 9 and 11 Hz, and only 5% have a DPR of 11.5 Hz or more.² The mean DPR in 500 normal adult subjects was 10.2 ± 0.9 Hz, 10.5 Hz in those adults younger than age 24 years, and 10.4 Hz in those 24 to 47 years old.³ The DPR remains greater than 8.5 Hz even in healthy octogenarians.

In approximately 25% of normal adults, the alpha rhythm is poorly visualized, with 6% to 7% of normal adults demonstrating voltages of less than 15 Hz.⁴ Because of this, the bilateral absence of a DPR is not considered abnormal. The frequency of alpha rhythm is only measured when the patient is awake and not drowsy because it decreases by 1 to 2 Hz with drowsiness. In the baseline calibration period of a PSG, the DPR is best measured and assessed during periods of eye opening and closure.

DPRs first appear in infants 3 to 4 months’ term as irregular, relatively high-amplitude (50–100 μV or greater), reactive 3.5- to 4.5-Hz activity over the occipital regions. Many infants achieve 5 to 6 Hz by 5 to 6 months of age, 70% have 5- to 6-Hz alpha-like activity by 12 months’ term, and 82% have a mean occipital frequency of 8 Hz (range 7.5–9.5 Hz) by 36 months of age.⁵ Most children have a 9- to 11-Hz posterior alpha rhythm by 8 years of age, and normal adult occipital alpha frequencies are typically reached by 13 years. The mean posterior alpha frequency is 9 Hz in 65% of the 9-year-olds and 10 Hz in 65% of normal children by age 15.

Be advised that a young child does not close the eyes until drowsy, so the frequency of the posterior rhythm when a young child’s eyes spontaneously close often represents drowsiness. As seen in adults, during drowsiness the DPR is often 1 to 2 Hz slower than the child’s actual DPR. Reactivity of the DPR to passive eye closure can be first seen as early as 3 months of age, and is usually first present by 5 to 6 months.^6,7

In general, bilateral slowing of the DPR is most often caused by conditions that slow brain metabolism. Some are transient (associated with acute toxic or metabolic encephalopathies) whereas others are chronic (including dementias, cerebral atrophy, or bilateral cerebral lesions such as bilateral strokes). Bilateral slowing of the DPR is a sign of encephalopathy, and its degree often reflects the severity of the cerebral dysfunction, that is, the more the slowing, the more severe the cerebral dysfunction. The most common conditions associated with a bilaterally slowed DPR are metabolic disorders and dementias or, less often, bilateral cortical lesions (such as bilateral strokes). Bilateral absence of an alpha rhythm with bilateral occipital needle-like spikes can be seen in patients with congenital or early-acquired binocular blindness.

A unilateral slowed or absent DPR can be seen with: (1) ipsilateral damage to the occipital cortex (ie, stroke, contusion, and tumor); (2) ipsilateral damage to thalamus; (3) transient ischemic attacks; (4) milder head injuries; and (5) following a seizure or migraine. Fig. 3 shows a significantly slower and poorly sustained DPR on the left. Unilateral failure of the DPR to attenuate (react) with eye opening or mental concentration is called the Bancaud phenomenon, and is seen with ipsilateral temporal or parietal cortical lesions such as tumors or infarcts.¹⁰ However, asymmetries in frequencies of the posterior rhythm occasionally are falsely lateralizing when the dominant generator of the posterior rhythm involves the medial surface of one cerebral hemisphere and projects contralaterally.

Fig. 3 Asymmetric dominant posterior rhythm. A significantly slower and poorly sustained DPR on the left (arrow). Note the asymmetric dominant posterior rhythm in this 10-second EEG fragment recorded in a 36-year-old man who had a left occipital ischemic stroke in the past. The dominant posterior rhythm is 10 Hz over P4-O2 (arrow); 7 to 8 Hz intermixed with 3 to 5 Hz over P3-O1.

(Courtesy of M. Grigg-Damberger.)

Beta activity are EEG frequencies greater than 13 Hz. Beta activity is most often seen over the frontal and central scalp regions, usually at a frequency of 18 to 25 Hz, less often at 14 to 16 Hz, and rarely at 35 Hz. Beta activity may become more prominent or accentuated by mental, lingual, or cognitive efforts. Beta activity typically has a voltage of 5 to 20 μV. The voltage of beta activity in 98% of adults is less than 20 μV, and beta voltages greater than 25 μV are considered abnormal.⁸

Beta activity often increases with drowsiness. In very young children, prominent beta activity appears in NREM 1 sleep, which may be maximal posteriorly. The abrupt onset of prominent 20- to 25-Hz beta activity typically maximal over the central and postcentral regions heralds drowsiness in some children and sometimes persists during NREM 1 and 2 sleep, first seen at 5 to 6 months of age and rarely after age 7 years.

Excessive prominent augmentation of 15- to 25-Hz beta activity during wakefulness and drowsiness in an older child or an adult is most often the result of a medication effect, particularly seen with benzodiazepines and barbiturates.¹¹ Benzodiazepines, barbiturates, and chloral hydrate are potent activators of beta activity, often increasing beta activity in the 14- to 16-Hz bandwidth. Increased theta activity may accompany excessive beta activity in some cases.

Central nervous system stimulants such as methylphenidate, amphetamines, cocaine, tricyclic antidepressants, and levothyroxine also increase beta activity, but such activity is often low in voltage.¹² Withdrawal from alcohol or barbiturates may produce a similar low-voltage EEG with beta activity.^12,13 The beta-inducing effects of medications on the EEG are more pronounced in children compared with adults, and in acute rather than chronic use.¹² Fig. 4 shows increased beta activity on a PSG, caused by clonazepam.

Fig. 4 Increased beta activity in a PSG, due to clonazepam. A 15-second fragment of EEG recorded in a 12-year-old boy in NREM 2 sleep shows excessive medium to high beta activity maximal bianteriorly (arrows).

(Courtesy of M. Grigg-Damberger.)

Beta activity is usually symmetric. Persistently reduced voltages of beta activity greater than 50% suggest a cortical gray abnormality within the lower amplitude hemisphere. Lesser intermittent voltage asymmetries may simply reflect normal physiologic skull asymmetries.⁸ A persistent focal suppression or attenuation of beta activity over a scalp region or hemisphere is a reliable localizing sign, and a hallmark of a structural lesion involving the underlying cerebral cortex or from an extradural fluid collection (such as a subdural hematoma). Focal attenuation of faster activities on the side of the lesion is most commonly associated with occlusive vascular disease.¹⁴

A marked focal increase in beta activity is most often caused by an underlying skull defect (most often a craniotomy or burr hole). Known as a breach rhythm, this pattern is characterized by sharply contoured waveforms with beta activity that is often threefold higher than that seen over other scalp regions (Fig. 5).¹⁵ Misidentifying the sharply contoured waveforms evident in the region of the breach rhythm because of interictal epileptiform discharges (IEDs) is a common perilous pitfall in EEG interpretation.¹⁶ The defect in the skull (most often a craniotomy, burr hole, or fracture) creates a low-resistance pathway for EEG currents, resulting in a localized increase in beta activity that is maximal near the margins of the skull defect. The amplitude of underlying theta and alpha activity is similarly enhanced through the defect, and this leads to the sharply contoured waveforms being misidentified as discharges.¹⁷ Of note, focal delta slowing over a skull defect is not caused by the skull defect, but reflects the acute or chronic underlying focal structural lesion. Asymmetric eye movements can be seen in patients with frontal skull defects. On rare occasions, beta activity is increased on the scalp region overlying a brain tumor or a focal cortical dysplastic lesion.¹⁴

Fig. 5 Breach rhythm caused by an underlying skull defect. Note the prominent fast activity over the right anterior temporal (F8) and to a lesser extent over the right frontal (F4) electrodes (arrows). This activity was caused by a skull defect, the EEG pattern being called a breach rhythm.

(Courtesy of M. Grigg-Damberger.)

Abnormalities of the distinctive PSG markers of sleep, such as sleep spindles and vertex waves, may be seen in PSG recording using standard and expanded EEG montages. Sleep spindles first appear in NREM 2, and may persist in early NREM 3 sleep. Sleep spindles most often occur at a frequency of 12 to 14 Hz (but range from 10 to 16 Hz), and recur at a frequency of 3 to 6 bursts per minute in stable undisturbed NREM 2 sleep. Sleep spindles first appear 3 to 4 weeks’ term (43–44 weeks conceptional age) over the midline central (vertex, Cz) region. The absence of sleep spindles by 3 months’ term is considered abnormal. At 3 and 6 months’ term, 50% of sleep spindles are synchronous, shifting at times from side to side. Sleep spindles are synchronous by 12 months in 70% of cases. By age 2 years, sleep spindles appear synchronously over both hemispheres and are approximately symmetric.¹⁸

The unilateral absence, decreased amplitude, or decreased frequency of sleep spindles is associated with an underlying ipsilateral pathologic condition, which can be found within the cortex or along the thalamocortical axis.¹⁹ Fig. 6 shows an example of asymmetric sleep spindles caused by a unilateral thalamic stroke. Sleep-spindle activity may be influenced by various hypnotic-sedative drugs.²⁰ Benzodiazepines and barbiturates also increase sleep-spindle activity. Bilateral prolonged spindles have been seen in recordings of patients with chronic and/or excessive benzodiazepines and barbiturate use.²⁰ An uncommon pattern of almost continuous sleep spindles during NREM 2 (called extreme spindles) has been observed in individuals with severe intellectual disability.^21,22

Fig. 6 Asymmetric sleep spindles caused by a thalamic stroke. Note the asymmetric sleep spindles in this 10-second EEG fragment. Sleep spindles were present on the left (arrow) (maximal C3, Cz) and absent on the right. The loss of sleep spindles on the right was caused by a thalamic stroke.

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