Blume's Atlas of Pediatric and Adult Electroencephalography, 1st Edition

Chapter 5

Nonepileptiform Abnormalities

Posterior and Diffuse Delta Activity

Arrhythmic unilateral or bilateral delta usually represents an acute or subacute process. In children, such may be accentuated or confined to the posterior head regions. This regionality does not necessarily connote a permanent posterior structural lesion. Posterior reversible encephalopathy syndrome (PRES) may be one association.

Focal Delta

Focal delta represents a physiologically acute process in that area. Trauma, acute infarct, abscess or tumor are possible etiologies. A focal seizure may produce a gradually resolving delta postictally. Prominent regional or hemispheric delta may occur with hemiplegic migraine, and this resolves over several days. A ventricular shunt tube produces persistent parietal delta in children.

Delta activity is more prominent in young children in terms of greater persistence, lower frequency, higher amplitude, and larger field. Delta abundance in the acute phase has no prognostic significance.

Excessive Beta

Petersen and Eeg Olofsson (1971) found small quantities of beta activity in all their 743 children; amplitude exceeded 20 µV in only 1%. Benzodiazepines and barbiturates augment beta prominence in both children and adults, with accompanying diffuse theta. Unmedicated children with chronic encephalopathies may also have prominent beta (Spit & Storm van Leeuwen, 1963).

Triphasic Waves

In adults whose metabolic encephalopathies impair awareness, triphasic waves may transiently appear. These bilaterally synchronous and symmetrical waves initiate and terminate with small upward deflections surrounding a prominent downward deflection. They appear maximally frontally (Fp1,2) and may have anterior–posterior or posterior–anterior lags in their expression. Although most popularly associated with hepatic coma, they may represent other metabolic encephalopathies, epileptic encephalopathy (Sundaram & Blume, 1987), and dementia (Rae-Grant et al., 1987).

Abnormal Sleep Potentials

A wide variety of conditions can decrease sleep potentials, particularly spindles, and especially if association cortices or the thalamus is involved. Bilateral or unilateral attenuation may occur depending upon the process. Paradoxically, extreme spindles, more widespread and persistent than normal spindles, are associated with diffuse encephalopathies of childhood (Gibbs & Gibbs, 1964).

Nonepileptiform Abnormalities


Diffuse and Posterior Delta (Figs. 5-1 to 5-13)

  • Delta in childhood, compared with that in adults, has the following characteristics:
  1. Higher voltage and lower frequency for same insult.
  2. Quantity and location more variable during recording and more dependent on state of alertness.
  3. Posterior delta more likely reflects a diffuse insult in children than in adults.
  4. Eye opening may accentuate, diminish, or not affect posterior delta.


Focal Delta (Figs. 5-14 to 5-21, 5-25, 5-30, and 5-31)

  • In children less than 5 years
  1. Lower frequency and higher voltage in younger children than in older.
  2. Persists during wakefulness and sleep.
  • In older children and adults:
  1. 0.5 to 3 Hz, arrhythmic.
  2. Always associated with theta and/or diminished background activity.

Hypoactivity (Figs. 5-22 to 5-24, 5-26, 5-29)

  • Absent or minimal normal activity of any type except low-voltage arrhythmic delta.
  • Diffuse, hemispheric, or regional.
  • If diffuse, poor prognosis for recovery for an acute illness unless:
  1. A substantial amount of sedative medication present.
  2. Metabolic or electrolytic abnormalities present.
  3. Immediately postictal.
  • If hemispheric or regional, poor prognosis for recovery of related functioning unless immediately postictal.

Absent Alpha Bilaterally (Fig. 5-27)

  • Associated with blindness from birth.
  • Occipital spikes common.

Oligorhythmia (Fig. 5-28)

  • Lack of normal rich mixture of waveforms of childhood.
  • Dominant activity is theta.
  • An awake (not drowsy) pattern.
  • Associated with a severe, diffuse, nonprogressive encephalopathy.

Beta (Figs. 5-32 and 5-33)

  • Usually related to medication.
  • If no medication, abnormal if exceeding 20 µV.
  • In absence of medication, associated with chronic encephalopathy.
  • Maximal posteriorly in children less than 5 years of age.
  • Maximal anteriorly after 6 years.

Spindle Asymmetry (Figs. 5-34 and 5-35)

  • Consistent, therefore nonshifting asymmetry.
  • Best assessed on ipsilateral ear, bipolar montage.

Absent Spindles (Fig. 5-36)

  • No spindles in any stage of sleep.
  • Associated with diffuse encephalopathy-degenerative (e.g. Alzheimer's disease) or metabolic.

Extreme Spindles (Figs. 5-37 and 5-38)

  • Widespread.
  • Persistent.
  • High voltage.
  • Cognitive impairment.


Abnormal Alpha and Photic Driving Symmetry (Figs. 5-39 to 5-41)

  • Lower side <50% of higher side.
  • Persistent throughout recording.
  • Assessed on ipsilateral ear or common average referential montages.
  • Scrutinize for frequency asymmetry; lower is abnormal side.
  • Scrutinize for reactivity asymmetry; less reactive is abnormal side.

Mu and Beta Asymmetries (Fig. 5-42)

  • Mu asymmetry indicates dysfunction of the lower side if no skull defect, persistent, and associated beta reduction.
  • Persistent beta asymmetry usuallyindicates dysfunction of lower side.

Regional Attenuation (Figs. 5-39, 5-43 to 5-51)

  • Overlies the center of dysfunction or lesion.
  • Better localizing feature than associated delta.
  • Represents more severe dysfunction than regional delta.
  • Often unapparent on scalp EEG.
  • More difficult to assess in areas whose normal rhythms are low-voltage—i.e., frontally.

Asymmetrical Sleep Spindles

  • Distinguish persistent (abnormal) from shifting (normal) asymmetry.
  • Less than 50% lower indicates ipsilateral dysfunction of thalamocortical pathway.



Skull Defect Effects: Breach Rhythm (Figs. 5-52 to 5-55)

  • Accentuates beta and theta rhythms in central, parietal, and frontal regions.
  • Central rhythms attenuate to extremity movement, like mu.
  • Steeply sloped field, thus accentuated on bipolar montages.
  • Apiculate negative phases of waves.
  • Alpha amplitude enhanced if defect posterior.

Regional Delta Activity (Figs. 5-56 to 5-76, 5-79 to 5-81)

  • Arrhythmic 0.5- to 3-Hz waves.
  • Near lesion slowest, least reactive, no superimposed faster frequency.
  • Variable persistence, greater with acute lesion.
  • Posterior delta more attenuated with eye opening than anterior delta.
  • Almost always with abnormal background rhythms in same region—attenuation or excess theta. If not, suspect artifact.
  • Posterior delta disrupts alpha more than does anterior delta.
  • May appear only in drowsiness, light sleep, or with hyperventilation.

Bioccipital Delta (Fig. 5-77)

  • Postictal effect of generalized tonic–clonic seizure.
  • Alpha preserved or minimally slowed.

Intermittent Rhythmic Delta Activity (IRDA) (Figs. 5-67, 5-76, 5-78 to 5-81)

  • Rhythmic 1- to 3-Hz delta.
  • Bursts or brief runs.
  • Widely distributed.
  • Usually anterior maximum.
  • Appears with diffuse encephalopathies, including postictal states.
  • Not localizing but more common with anterior lesions than posterior ones.
  • Regional or focal delta may coexist.

Focal and Regional Theta (Figs. 5-82 to 5-86)

  • Persistently lateralized to one hemisphere or localized to one region indicates regional dysfunction.
  • Disrupts background less than regional delta.
  • May not react to eye opening or alerting.
  • May appear only in repose and drowsiness.

Slow Background and Diffuse Theta

  • Exclude drowsiness as cause.
  • 7 to 8 Hz posterior rhythm.
  • Diffuse theta increases.
  • Slight accentuation of theta in left temporal region occurs commonly with diffuse increase; does not imply focal lesion.
  • Medication, metabolic abnormality most common causes.
  • Often with diffuse excess beta medication effect.

Medication Effect (Beta) (Fig. 5-87)

  • Benzodiazepines and barbiturates.
  • Combines with background to produce apiculate waveforms.
  • Epileptiform discharges may be produced by drugs such as clozapine, lithium.

Diffuse and Bilateral Arrhythmic Delta (Figs. 5-88 and 5-89)

  • Continuous arrhythmic 0.5 to 3 Hz diffuse waves.
  • Theta replaces alpha as highest-frequency background rhythm.
  • Severity inversely proportional to: delta frequency, reactivity to afferent stimuli and background frequency.
  • Severity and/or acuteness directly proportional to persistence.

Triphasic Waves and Diffuse Delta (Fig. 5-90)

  • Metabolic encephalopathy.
  • Dementia.

Dementia (Figs. 5-89, 5-91 to 5-97)

  • Diffuse delta.
  • Spikes: multifocal, bisynchronous, periodic, or aperiodic.
  • Triphasic waves.
  • Rapidity of cognitive decline correlates with prominence of EEG abnormalities.

Fig. 5-1. Generalized delta. Patient's age, 3 years. Slightly drowsy. This recording was carried out 4 h after a generalized seizure of unknown duration. Prominent generalized delta activity may persist for several hours after a generalized seizure in younger children. It persists in diminishing amounts up to 7 to 10 days thereafter. The quantity and persistence of postictal delta activity is greater in infants and in younger children than in older children and adults. Such 1 to 1.5 Hz delta without theta activity is abnormal in drowsiness at any age beyond the first few months of life. Calibration signal 1 s, 300 µV.


Fig. 5-2. Effect of alerting on quantity of delta. Patient's age, 16 months. Awake. Delta activity can be augmented as well as attenuated by alerting procedures (c). In this instance, the mechanism by which passive eye closure augmented the delta is more likely that of alerting the patient instead of passive eye closure per se, as the delta decreases while passive eye closure is maintained and he ceases to struggle (right segment). The augmentation is too abrupt for hyperventilation to play a role here. Such variability of delta quantity with state of alertness is important to consider when sequential recordings are compared. Calibration signal 1 s, 200 µV.


Fig. 5-3. Diffuse rhythmic delta. Patient's age, 7 months. Awake. There is an excessive amount of high-voltage rhythmic delta activity over both hemispheres in this patient, whose posterior fossa tumor was partially removed 3 weeks prior to the recording. The right ventriculoperitoneal shunt, inserted 1 week before his posterior fossa decompression because of hydrocephalus, was not functioning. This likely accounts for the excess delta activity. Muscle artifact is seen in channels 1, 2, 5, and 6. Calibration signal 1 s, 100 µV.


Fig. 5-4. Diffuse rhythmic delta. Patient's age, 7 months. Drowsy. Same recording as in Fig. 5-3. The abnormal rhythmic delta activity persists into drowsiness. In itself, this would be an abnormal drowsy pattern because (a) its average frequency is too low for the more persistent medium to high-voltage drowsy patterns, which are at 4 to 5 Hz, and (b) this train of delta lasts too long to be the burst pattern of drowsiness. A slight increase in low-voltage delta at this frequency normally may be seen in drowsiness at this age. Calibration signal 1 s, 150 µV.


Fig. 5-5a. Delta and hypoactivity. Patient's age, 5 years. Obtunded. In addition to excess delta activity for age, there is a paucity of other rhythms. Both the Haemophilus influenzae meningoencephalitis and the 1-min grand mal seizure the patient had likely contribute to these findings. Calibration signal 1 s, 100 µV.


Fig. 5-5b. Diffuse delta: effect of arousal. Patient's age, 5 years. Obtunded. Same recording as in Fig. 5-5a. Note again how alerting the patient (c) augments the quantity of delta activity. Calibration signal 1 s, 100 µV.


Fig. 5-6. Four weeks later. Patient's age, 5 years. Awake. Eyes closed. Same patient as previous illustration. The patient had improved clinically but functioned at a 3 year level. Both legs displayed increased tone. The EEG has improved remarkably but the background activity is slow and there is mild excess theta diffusely, maximum bifrontally. Calibration signal 1 s, 70 µV.


Fig. 5-7. Confusional migraine with recovery. Patient's age, 13 years. Awake. Eyes closed. The top eight channels record his confused state, with migraine headache creating diffuse delta activity, maximum posteriorly. The bottom eight channels, recorded 7 weeks later, illustrate a normal EEG with complete clinical recovery. Calibration signal 1 s, 70 µV.


Fig. 5-8. Posterior delta. Patient's age, 3 years. Awake. Both the generalized seizure occurring 16 h prior to the recording and the mild head injury that occurred 1 week earlier may have contributed to this abnormal delta activity, as seen bilaterally in the posterior head regions. The slightly greater extension anteriorly on the left may reflect the fact that the grand mal seizure began with right-sided jerking. It is not uncommon for children to have posteriorly situated or posteriorly accentuated delta activity consequent to processes that affect the brain diffusely. Therefore, in the acute phase, such delta, when bilateral, does not necessarily indicate lesions in the posterior head regions. Calibration signal 1 s, 150 µV.


Fig. 5-9. Posterior delta. Patient's age, 3 years. Light sleep. Same recording as in Fig. 5-8. The posterior delta activity is augmented, constituting an abnormal light sleep pattern. Also abnormal is the absence of any additional alteration in the recording from wakefulness to light sleep, such as V waves or spindles; this absence reflects the diffuseness of the process. Calibration signal 1 s, 100 µV.


Fig. 5-10. Posterior delta. Patient's age, 9 years. Awake. Eyes open. Excessive posterior delta in an older child. Calibrations 1 s, 100 µV.


Fig. 5-11. Posterior delta: accentuation with eye closure. Patient's age, 9 years. Posterior abnormalities may be more prominent with the eyes closed as indicated by eye closure artifact in frontal–polar leads. Calibration signal 1 s, 100 µV.


Fig. 5-12. Posterior rhythmic waves. Patient's age, 8 years. Awake. Eye closure. As such rhythmic waves have been described in normal children (Eeg-Olofsson, 1971), these data give only slight support to a clinical impression that the patient's staring spells represent seizures. Such rhythmic waves may represent spike–waves, and these latter should be sought by an ipsilateral ear montage, hyperventilation, photic stimulation, and sleep. The rhythmic morphology of these slow waves and the normal alpha activity for age suggest that their greater appearance on the left does not represent a focal lesion. Calibration signal 1 s, 200 µV.


Fig. 5-13a. Normal posterior delta: augments with eye opening (c). Patient's age, 7 years. Awake. In some children, delta activity is not only more apparent when alpha attenuates but actually increases then. Calibration signal 1 s, 100 µV.


Fig. 5-13b. Normal delta and slow-wave transient (*). Patient's age, 7 years. Awake. Posterior delta activity appears with the eyes open (↑); its increase is immediately preceded by a posterior slow-wave transient, a normal phenomenon associated with eye movements in children. Less defined forms of such transients appear to contribute to the delta activity with the eyes open. Calibrations signal 1 s, 100 µV.


Fig. 5-14. Left central parietal and diffuse delta. Patient's age, 15 years. Semicomatose. Rhythmic 0.5 to 1 Hz, medium-voltage left central–parietal (C3,P3) delta activity with low-voltage diffuse delta. Calibration signal 1 s, 50 µV.


Fig. 5-15. Left temporal delta. Patient's age, 15 years. Awake. Eyes closed. Delta activity appears very principally at F7–T3 with minimal spread parasagittally. Note the preservation of alpha activity bilaterally, suggesting that the process does not extend posteriorly. Calibration signal 1 s, 100 µV.


Fig. 5-16. Low frequency filter (LFF) change enhances right occipital–parietal–central delta. Patient's age, 9 years. Eyes closed. The top eight channels are recorded with the LFF 1.0 Hz. Lowering the LFF to 0.3 Hz (bottom eight channels) enhances minimally the display of this focal delta. Calibration signal 1 s, 150 µV.


Fig. 5-17. Left parietal–temporal–occipital delta. Patient's age, 22 months. Drowsy. Abnormal delta and theta occupy the left hemisphere posteriorly in this patient, who had a 3 hour seizure involving the right side of his body 4 days prior to the recording. The activity in the right hemisphere is normal. Calibration signal 1 s, 200 µV.


Fig. 5-18. Left hemispheric and diffuse delta. Patient's age, 11 months. Awake. The left hemispheric delta is accompanied by left posterior temporal–parietal and left frontal spikes. The quantity of right hemispheric delta slightly exceeds normal limits. Calibration signal 1 s, 150 µV.


Fig. 5-19. Effect of eye opening on delta field. Patient's age, 8 years. Awake. Although the anterior spread on the left is greater, the delta with eyes closed is bioccipital. Eye opening (*) restricted the delta to left occipital with slight anterior spread. Low voltage; left occipital and left central spikes appear. Calibration signal 1 s, 200 µV.


Fig. 5-20. Effect of eye opening on focal abnormality. Patient's age, 7 years. Awake. The principal abnormality is loss of left occipital alpha, which indicates left occipital involvement of the dysfunction. The greater quantity of excess theta and delta in channel 4 than in channel 3 indicates more left occipital than left parietal involvement. Eye opening attenuates left-sided theta and produces normal right occipital delta. Nonetheless, the major abnormality resides on the left, posteriorly. Calibration signal 1 s, 150 µV.


Fig. 5-21. Right posterior temporal–parietal–occipital delta. Patient's age, 4 years. Awake. Right posterior temporal–parietal–occipital abnormality in a recording done 2 days after a seizure that began with leftward ocular deviation. Calibration signal 1 s, 150 µV.


Figs. 5-22. Loss of left central activity and excess left temporal–occipital theta. Patient's age, 14 years. Awake. Eyes closed. Occasionally, the principal abnormality is rhythms that are absent as opposed to abnormally present. In this instance, the left central (C3) activity is minimal in comparison with the normal 10 Hz right central rhythm. Less severe is the slight increase in left occipital (O1) and left temporal (F7,T3,T5) theta. Note the normal quantity of right “posterior slow of youth.” Calibration signal 1 s, 70 µV.


Fig. 5-23. Left hemispheric hypoactivity. Patient's age, 2 years. Awake, eyes open. The voltage of the left hemispheric activity is abnormally low, whereas the right hemispheric activity is normal for this age. This patient has a left ventriculoperitoneal shunt. Three days prior to recording, he had a 20 min seizure involving his right arm and leg. Calibration signal 1 s, 150 µV.


Fig. 5-24. Decreased potentials, left hemisphere. Patient's age, 10 months. Drowsy. Not only is the quantity of activity in the left hemisphere abnormally decreased but that which is present is abnormally slow for this age and state of alertness. Normal drowsy pattern, right hemisphere. Calibration signal 1 s, 100 µV.


Fig. 5-25. Excess right hemispheric delta. Patient's age, 7 years. Sleep. Note also the reduced beta activity on the right as compared to the left and the bilateral lack of V waves and spindles, which should appear at this level of sleep. Calibration signal 1 s, 100 µV.


Fig. 5-26. Left frontal–temporal attenuation and excess bilateral posterior delta. Patient's age, 3 months. Obtunded. The excess arrhythmic delta activity predominates but further visual inspection discloses an attenuation at FP1–C3–T3–F7. At this age, the normally low anterior potentials make identification of abnormal attenuation particularly difficult, but their asymmetry in this instance identifies the left frontal–temporal areas as distinctly abnormal. Note the rare T5–O1 spikes. Calibration signal 1 s, 100 µV.


Fig. 5-27. Absent alpha. Patient's age, 12 years. Awake, eyes closed. There is no alpha rhythm in this patient, who has been blind since birth because of retrolental fibroplasia. Likewise, occipital spikes may occur in patients with anterior visual system lesions dating from early life; they do not necessarily indicate a primary insult to the occipital lobe. Note the central rhythm seen principally on the right. Calibration signal 1 s, 70 µV.


Fig. 5-28. Oligorhythmia. Patient's age, 12 months. Awake. Although monorhythmic waves at 5 Hz might be considered normal in drowsiness, they constitute a severe abnormality when seen alone in an awake child of any age. The chief abnormality is an absence of competing rhythms (oligorhythmia), so that the unopposed theta appears almost sinusoidal. This rhythm characteristically persists throughout the entire recording; there may be a minimal alteration with sleep. Infants such as this patient, have a severe generalized nonprogressive encephalopathy. Calibration signal 1 s, 100 µV.


Fig. 5-29. Decreased left alpha. Patient's age, 6 years. Awake. Eyes closed. The principal abnormality is a relative paucity of left-sided alpha activity as compared with the right. A slight excess of theta/delta activity appears diffusely, slightly more in the left hemisphere. Calibration signal 1 s, 150 µV.


Fig. 5-30. Posterior delta, maximal on the right. Patient's age, 15 years. Awake. Eyes closed. The waveforms closely resemble the normal “posterior slow of youth”; but their abundance, particularly on the right, is unusual. That alpha activity is also more abundant on the right raises the possibility that this quantity of “posterior slow of youth” lies within the extent of normality. Calibration signal 1 s, 150 µV.


Fig. 5-31. Passive eye closure elicits abnormal posterior rhythms, principally on the right. Patient's age, 5 years. Awake. Passive eye closure (*) discloses a 3 to 5 Hz rhythm at O2–T6–P4 and a 4–5 Hz left posterior background activity. The right hemispheric abnormality is more abnormal for age, although the rhythm on each side is abnormally slow. Calibration signal 1 s, 200 µV.


Fig. 5-32. Excess beta and theta. Patient's age, 8 years. Awake. Medication, such as benzodiazepines and barbiturates, augment both beta and theta in otherwise normal children and adults. Calibration signal 1 s, 100 µV.


Fig. 5-33. Normal beta. Patient's age, 8 years. Awake. A small amount of beta is a normal component of childhood EEGs: the quantity varies from patient to patient; it is relatively prominent in this normal child. Benzodiazepines and barbiturates may produce this beta quantity, but other patients apparently take no medication. Calibration signal 1 s, 70 µV.


Fig. 5-34. Several asymmetries. Patient's age, 10 months. Sleep. The most severe abnormality in this sleep recording is a paucity of potentials in the left temporal–frontal–central areas. Even more widespread dysfunction is indicated by the lack of left hemispheric spindles. Spindles appear normally in the right hemisphere. Delta activity of sleep is normal in the right hemisphere and clearly suppressed on the left. The normal posteriorly accentuated delta activity in sleep in also decreased on the left. Calibration signal 1 s, 150 µV.


Fig. 5-35. Asymmetry of sleep potentials, reduced on the left. Patient's age, 18 months. Sleep. To identify a clear reduction of sleep potentials requires evaluation over several minutes' recording, as normal shifts in amplitude between the hemispheres often occur, particularly in youth. The V waves and spindles remain consistently lower on the left during this recording. Such abnormal asymmetry of sleep potentials may be the only abnormality of a recording made during wakefulness and sleep. Calibration signal 1 s, 200 µV.


Fig. 5-36. Absent spindles. Patient's age, 5 months. Sleep. Low-voltage or absent spindles in light to moderate sleep at this age almost always reflects a diffuse, moderately severe encephalopathy. Calibration signal 1 s, 150 µV.


Fig. 5-37. Extreme spindles. Patient's age, 9 years. Sleep. These spindles conform to the Gibbs (1964) description of extreme spindles except for voltage, which they gave as 200 to 400 µV. These spindles are considerably more diffuse and continuous than normal spindles. As is typical for this waveform when bilateral, this patient has been severely cognitively impaired all her life. Calibration signal 1 s, 70 µV.


Fig. 5-38. Extreme spindles. Patient's age, 9 years. Sleep. Same phenomenon as shown in Fig. 5-37, viewed on a coronal montage. Calibration signal 1 s, 70 µV.


Fig. 5-39. Right alpha reduction with occipital delta. Patient's age, 21 years. Awake. Eyes closed. Although the right-sided alpha voltage would equate with that of many normal individuals, in this patient it is significantly lower than that of the left and is frequently interrupted by delta and theta activity at O2. Calibration signal 1 s, 70 µV.


Fig. 5-40. Eyes closed disclose alpha asymmetry. Patient's age, 18 years. Awake. Eyes closed. The side of the lower and slower alpha voltage almost always indicates that of the principal abnormality. In this instance, such asymmetry appears only with the eyes closed as a reduction in voltage on right. Calibration signal 1 s, 70 µV.


Fig. 5-41. Asymmetrical photic driving with a cause. Patient's age, 41 years. Awake. Eyes closed. As photic driving may commonly be asymmetrical with a tendency to be higher on the right, in this instance its impairment on the left relates to low voltage O1–T5 delta activity. The latter is caused by a left occipital tumor. Calibration signal 1 s, 70 µV.


Fig. 5-42. Beta asymmetry. Patient's age, 71 years. In addition to a mild alpha asymmetry (lower right), the beta activity is moderately less abundant on the right as compared to the left. The assessment should include an ear reference montage to exclude cancellation effects. As beta may be up to 35% lower on one side in normal subjects (Zifkin, 1990), a beta asymmetry should be at least moderate and persistent before it is given clinical significance. This patient had a previous right hemispheric stroke. Calibration signal 1 s, 50 µV.


Fig. 5-43. More delta in healthier hemisphere. Patient's age, 74 years. The principal abnormality is a reduction in potentials in the right hemisphere, which “allows” an abnormal delta activity to be better expressed on the healthier left. Calibration signal 1 s, 50 µV.


Fig. 5-44. Right hemispheric attenuation and delta. Patient's age, 36 years. Awake. Eyes closed. Higher-frequency background activity of the left hemisphere appears minimally in the right hemisphere. The right temporal region may be the most abnormal because of the attenuation of higher frequencies and relative monorhythmicity of its delta. In contrast, the right parasagittal region has shown an ability to develop a rich mixture of waveforms and, therefore, is healthier than the right temporal region. Note the rare spikes at T3, reflecting the frequent bihemispheric participation in any process severely damaging one hemisphere. A F4 spike occurs in the first second. Calibration signal 1 s, 150 µV.


Fig. 5-45. Left-hemispheric attenuation and delta. Patient's age, 67 years. Awake. Eyes closed. Activity at all normal frequencies is attenuated in the left hemisphere, which contains excessive delta throughout. Note the lack of any right hemispheric abnormality. Calibration signal 1 s, 100 µV.


Fig. 5-46. Left hemispheric delta and attenuation. Patient's age, 51 years. Awake. Eyes closed. Remarkably, the prominent left hemispheric arrhythmic delta activity propagates minimally to the right hemisphere; this may help in assessing patients whose delta activity appears bilaterally but maximally on one side. Note the decreased left central–parietal background as compared with the right. Calibration signal 1 s, 100 µV.


Fig. 5-47. Hemiplegic migraine. Patient's age, 30 years. Arousal. EEG in the acute phase of hemiplegic migraine showing alpha and central rhythm background reduction in the left hemisphere together with diffuse left hemispheric delta and bihemispheric delta bursts. The clinical deficits and EEG both subsequently resolved completely. Calibration signal 1 s, 100 µV.


Fig. 5-48. Left hemispheric suppression and delta. Patient's age, 53 years. Awake. Eyes closed. The principal feature is a relative paucity of left hemispheric potentials diffusely together with persistent, arrhythmic delta activity. On this montage, the latter appears principally anteriorly. In contrast is the rhythmic 2 to 4 Hz delta burst whose diffuse presence is likely impeded on the left by the same process that attenuated ongoing left hemispheric activity. Intermittent rhythmic 2 to 4 Hz delta has limited localizing significance and usually signifies a relatively recent or evolving process. Calibration signal 1 s, 70 µV.


Fig. 5-49. Left hemispheric attenuation in sleep. Patient's age, 20 years. The principal attenuation appears in the left occipital (O1) and left parietal (P3) regions, with moderate attenuation in the left posterior mid-temporal regions (T3,T5). In assessing the distribution of attenuation, remember that, unlike localization of other waveforms, both components of a derivation are responsible for the attenuation. There is no aspect of this recording suggesting an electrical cancellation of background rhythms in the left posterior region, such as might occur with synchronous rhythmic activity. The attenuation extends diffusely throughout the left hemisphere as a moderate spindle attenuation. As usual, V waves are the waveforms most resistant to unilateral dysfunction. Calibration signal 1 s, 70 µV.


Fig. 5-50. Posterior and diffuse attenuation—less than apparent? Patient's age, 60 years. A paucity of parietal–occipital activity appears on this bipolar recording, whose most obvious feature is anterior delta with poorly formed triphasic waves. Posterior scalp edema may attenuate potentials in a supine, comatose patient. Calibration signal 1 s, 30 µV.


Fig. 5-51. More abundant activity revealed by referential montage. Patient's age, 60 years. Recording at the same time with the same settings as the previous illustration demonstrates considerably more abundant posterior activity, even though the references (A1, A2) may have contributed somewhat to the potentials in posterior derivations. Nonetheless, the montages taken together do reveal a loss of posterior activity, but not as complete as suggested by the bipolar montage. Calibration signal 1 s, 30 µV.


Fig. 5-52. Skull defect, left. Patient's age, 16 years. Awake. Eyes closed. A skull defect augments potentials of any frequency—most prominently central and occipital rhythms, as seen in this normal segment. Calibration signal 1 s, 70 µV.


Fig. 5-53. Mu rhythm and alpha with skull defect on coronal montage. Patient's age, 30 years. Wiggling the right thumb with the eyes remaining closed (*) attenuated the higher left mu rhythm at C3, revealing that the unattenuated 8 Hz rhythm in the T5–P3 derivation is alpha activity. This higher alpha activity and the undercurrent delta activity at T3 and minimally at T5 are probably not related to the central (C3) skull defect and suggest dysfunction in the left temporal region (T5, T3). Calibration signal 1 s, 50 µV.


Fig. 5-54. Prominent mu rhythm with skull defect. Patient's age, 30 years. Eye opening in the fourth second blocked the alpha rhythm, revealing a more ample left mu rhythm (breach rhythm) than that of the right as a consequence of the skull defect (Cobb, 1979). Wiggling the right thumb (*) abolished this mu rhythm. Calibration signal 1 s, 50 µV.


Fig. 5-55. Bursts of spike-like waves with a skull defect. Patient's age, 49 years. These apiculate waves are not spikes because of their rhythmic nature and the lack of an aftercoming slow wave of the same polarity. Note that the lower-voltage bursts (*), similar in morphology to the apiculate higher-voltage ones, do not resemble spikes. Calibration signal 1 s, 50 µV.


Fig. 5-56. Left temporal–central–parietal delta activity. Patient's age, 16 years. Awake. Eyes closed. Same patient as in Fig.5-52. The left temporal–central–parietal delta activity in this segment of the recording exceeds that which could be ascribed to the aforementioned skull defect. Calibration signal 1 s, 70 µV.


Fig. 5-57. Transient left anterior–midtemporal delta. Patient's age, 39 years. Although prominent, this temporal delta (F7–T3) appears principally during light drowsiness, as evidenced by loss of alpha. Arousal (last seconds) attenuates this delta. Calibration signal 1 s, 50 µV.


Fig. 5-58. Right temporal delta and theta. Patient's age, 42 years. Awake. Eyes closed. The 2 to 3 Hz delta mixes with theta to create the irregularity seen at F8–T4, with relative “cancellation” of potentials in the F8–T4 derivation. Calibration signal 1 s, 70 µV.


Fig. 5-59. Pulse artifact and delta activity. Patient's age, 38 years. Scrutiny of this recording will reveal arrhythmic delta activity involving F8, T4, and M2 (mandibular notch electrode), which is unrelated to the ECG as recorded by the mandibular notch electrodes (M1–M2). In contrast, the rhythmic delta at T6 is time locked to the ECG and is a pulse artifact. Calibration signal 1 s, 70 µV.


Fig. 5-60. Marked “activation” of left temporal delta in light sleep. Patient's age, 29 years. Prominent and persistent delta activity appears at F7–T3 during light sleep (right), whereas none is present in wakefulness (left). The prominent delta in the T3–T5 derivation indicates no spread to T5. Note the left-sided small sharp spike (*); this is a normal phenomenon. Calibration signal 1 s, 50 µV.


Fig. 5-61. Monophasic 1-Hz left temporal delta and central theta. Patient's age, 73 years. Awake. Eyes closed. This post-stroke recording contains better background activity over the involved hemisphere than that of the light sleep portion of the previous illustration. The intermittent nature of the left temporal delta contrasts with the more persistent delta of the previous segment. However, both the severity and location of the stroke may influence the post-stroke evolution. Calibration signal 1 s, 70 µV.


Fig. 5-62. Intermittent temporal delta activity. Patient's age, 55 years. Rarely, focal delta activity can appear intermittently, as in this example. Arenas et al. (1986) found temporal delta to occur rarely in the normal elderly and slightly more so in the left temporal region compared with the right. Therefore this abnormality, occurring in approximately the incidence of the sample depicted here, would indicate a clear focal right temporal abnormality at virtually any age. Calibration signal 1 s, 100 µV.


Fig. 5-63. State-dependent left temporal delta. Patient's age, 29 years. This left temporal (F7–T3) delta activity, minimally evident during wakefulness (first 4 s), is prominently seen during early drowsiness (subsequent 6 s), only to recede as drowsiness persists. Calibration signal 1 s, 50 µV.


Fig. 5-64. Right temporal delta only on coronal montage. Patient's age, 18 years. Awake. Eyes closed. The top eight channels disclose delta activity at F8–T4, which does not appear in the simultaneously recorded bipolar anterior–posterior montage. Eye movements complicate the assessment. Calibration signal 1 s, 70 µV.


Fig. 5-65. More than left temporal delta. Patient's age, 67 years. Awake. Eyes closed. In addition to the evident run of F7–T3 delta activity, scrutiny discloses a less regulated alpha at O1 as opposed to O2 and a low-voltage delta activity there as well. Calibration signal 1 s, 70 µV.


Fig. 5-66. Left temporal and left frontal deltas. Patient's age, 73 years. Drowsy. Eyes closed. Arrhythmic delta, the more localizing, occurs at F7–T3, whereas rhythmic delta, less localizing, appears at FP1 with spread to F3 and F7. The right hemisphere is normal. Calibration signal 1 s, 70 µV.


Fig. 5-67. Bitemporal persistent delta and IRDA. Patient's age 66 years. Two bursts of intermittent rhythmic delta activity (IRDA) are superimposed upon the bitemporally accentuated, more persistent delta activity. Calibration signal 1 s, 50 µV.


Fig. 5-68. Right hemispheric delta. Patient's age, 73 years. Awake. Eyes closed. As this ill-localized, right hemispheric delta activity is associated with a distinctly lower right-sided alpha, involvement of the right occipital–parietal region is assured. However, a coronal montage or a left ear montage would assess its anterior extent. Calibration signal 1 s, 70 µV.


Fig. 5-69. Left hemispheric delta and eye movements. Patient's age, 19 years. Eye movements can partially obscure frontal delta activity, which in this instance is best revealed in the last 3 s, which are free of eye movements. Such delta is also revealed by comparing F3–C3 versus F4–C4 and C3–P3 versus the C4–P4 derivations, which illustrate left anterior delta activity. The left-sided alpha activity is slightly disrupted by this left hemisphere process. A possible left frontal–central spike appears in the third second, but any downward deflection in the Fp1–F3 derivation is “lost” in an eyeblink. Calibration signal 1 s, 50 µV.


Fig. 5-70. Focal and diffuse delta. Patient's age, 31 years. In this instance, persistent 1 Hz delta activity in the right central–parietal region (F4–C4, C4–P4, and P4–O2 derivations) can be discerned despite the diffuse bursts of intermittent 400 to 600 ms, medium-voltage waves. The C4 and P4 delta is that which is indicative of regional dysfunction because of its lower frequency and persistence. The intermittent delta does not have localizing significance even though it is accentuated posteriorly. Calibration signal 1 s, 50 µV.


Fig. 5-71. Right central–parietal theta and delta. Patient's age, 81 years. Background activity in the right central–parietal regions (C4 and P4) is slightly interrupted by 5 to 7 Hz theta and very low voltage (approximately 1 Hz) delta activity. The latter can be realized by viewing the tracing from a greater distance. Its minimal presence in the left parietal (P3) region does not indicate an additional abnormality there. The relatively normal alpha activity suggests that the process does not engulf the right occipital lobe. None of the sharply contoured waves is a spike, as they are simply combinations of background rhythms. Calibration signal 1 s, 70 µV.


Fig. 5-72. Eye opening elicits delta. Patient's age, 23 years. Awake. Eye opening attenuated alpha normally and is associated with the enhancement of bifrontal delta activity, principally at FP1–F3. The eye-movement field (FP1,2) is not that of the delta activity. Calibration signal 1 s, 70 µV.


Fig. 5-73. Eye blinks galore. Patient's age, 91 years. IOL and IOR = left and right infraorbital leads. Confused. Prominent “phase reversals” between infraorbital leads (negative) and FP1,2 (positive). Calibration signal 1 s, 100 µV.


Fig. 5-75. Frontal delta and eye blink. Patient's age, 91 years. Confused. Eyes closed. The eye blink (9th second), produces a “phase reversal” between the infraorbital leads as referred to CZ and the frontal leads in contradistinction to the ongoing delta activity where no phase reversal occurs. Calibration signal 1 s, 100 µV.


Fig. 5-74. No eye movements. Patient's age, 91 years. Confused. Eyes closed. IOL and IOR = left and right infraorbital leads. The lack of “phase reversals” between the left and right infraorbital leads and FP1,2, F3,4 as referred to CZ indicate that the slow waves represent bifrontal delta activity. Note the greater involvement of infraorbital leads by the rhythmic delta (first 2 s) than the arrhythmic delta (last 3 s). Calibration signal 1 s, 70 µV.


Fig. 5-76. Right frontal IRDA and more persistent delta. Patient's age, 69 years. The IRDA is followed by lower-voltage, longer-duration, and more persistent delta waves in the right frontal region (FP2, F8, F4). The very slow waves in the F7–A1 derivation are slow eye movements. Calibration signal 1 s, 50 µV.


Fig. 5-77. Bioccipital delta. Patient's age, 42 years. Sleep. The prominent bioccipital delta activity in sleep is abnormal for this age. It may represent the posterior reversible encephalopathy syndrome (PRES), which occurs in acute cerebral illness. Calibration signal 1 s, 100 µV.


Fig. 5-78. Intermittent rhythmic delta activity (IRDA). Patient's age, 49 years. Awake. Eyes closed. Such bisynchronous rhythmic delta activity can be seen in the first weeks after a generalized tonic–clonic seizure but may represent other conditions. Note the interruption of normal background rhythms at the time of the rhythmic delta, aiding the distinction from glossokinetic artifact. Calibration signal 1 s, 100 µV.


Fig. 5-79. Rhythmic and arrhythmic delta. Two patients: (1) top eight channels, 49 years, awake; (2) bottom eight channels, 85 years, state undetermined. Persistent arrhythmic delta activity should be sought in patients with bursts of rhythmic delta activity. No arrhythmic delta appears in the first patient, whereas the two asynchronous delta bursts of the second patient are linked by persistent bifrontal delta. Calibration signal 1 s, 100 µV.


Fig. 5-80. Rhythmic and arrhythmic deltas. Patient's age, 23 years. Awake. Eyes open. The prominence of one phenomenon should not occlude another. The left, arrhythmic, persistent delta has more lateralizing and localizing value than the more prominent, more rhythmic delta seen in the center of the illustration. Calibration signal 1 s, 70 µV.


Fig. 5-81. Two deltas. Patient's age, 35 years. Confused. Eyes closed. Rhythmic delta represents an acute or subacute diffuse cerebral process but is not specific for any etiology. Note that the posteriorly situated delta is slower than the anterior one. A1 and A2 are unlikely to be involved: if they were, the delta at FP1,2 would not be so rhythmic. Calibration signal 1 s, 100 µV.


Fig. 5-82. Focal left temporal theta activity. Patient's age, 35 years. The small amount of right temporal theta activity is normal, but that in the left temporal region (F7–T3) is too abundant in incidence and amplitude to be considered normal. Unfortunately, assessing the quantity of theta activity in the left temporal region is more difficult than on the right because of its normally greater quantity on the left. While this quantity of theta activity is clearly abnormal at age 35 years, it would be abnormal even in the seventh decade; Calibration signal 1 s, 70 µV.


Fig. 5-83. Focal and diffuse theta. Patient's age, 29 years. A focal abnormality within a diffuse abnormality is discerned by comparing homologous derivations for the persistence of any excess theta or delta activity in one area throughout most of the tracing. The 6 Hz diffuse theta does not obscure the persistent focal 3 to 6 Hz theta at C4 and P4. Calibration signal 1 s, 70 µV.


Fig. 5-84. Right central–parietal theta. Patient's age, 29 years. Here, 3 to 7 Hz theta appears in the right central–parietal (C4–P4) regions. Its minimal expression in homologous areas of the left does not indicate bilateral abnormality. Note the very low voltage subtle delta activity underlying such moderately prominent theta, also at C4–P4. Calibration signal 1 s, 100 µV.


Fig. 5-85. Excess diffuse theta. Patient's age, 30 years. Arousal. Although the ongoing background rhythms are normal, the drowsy portion contains excess theta and possibly a preceding delta rhythm. Calibration signal 1 s, 50 µV.


Fig. 5-86. Apiculate waves, no spikes. Patient's age, 23 years. Awake. Eyes closed. All of the theta bursts in this recording contain sharply contoured apiculate waves and none is distinctly a spike. Calibration signal 1 s, 100 µV.


Fig. 5-87. Excess beta and theta, medication effect. Patient's age, 42 years. Awake. Eyes closed. Excess beta almost always represents a medication effect by benzodiazepines or barbiturates and other drugs. Although the quantity of theta activity exceeds normal, it is also a medication effect. Calibration signal 1 s, 100 µV.


Fig. 5-88. Diffuse delta with hydrocephalus. Patient's age, 50 years. Awake. Eyes closed. The diffuse high-voltage, arrhythmic, persistent delta activity suggests a blocked shunt in a patient with hydrocephalus. The EEG may revert to normal with shunt revision. Calibration signal 1 s, 200 µV.


Fig. 5-89. Diffuse delta with dementia. Patient's age, 76 years. In this awake recording, background activity is disorganized and largely replaced by diffuse delta and theta. This pattern is not characteristic of any specific type of encephalopathy: a metabolic encephalopathy or primary dementing process could produce it. Calibration signal 1 s, 100 µV.


Fig. 5-90. Triphasic waves and diffuse delta. Patient's age 68 years. This referential montage depicts the frontally predominant triphasic waves together with diffuse delta activity. The low-voltage apiculate waves at A2 may represent ECG. Calibration 1 s, 100 µV.


Fig. 5-91. Jakob–Creutzfeldt disease without diffuse discharges. Patient's age, 65 years. Although the patient is awake with eyes closed, the background is slow and disorganized; excess theta and some delta activity appear diffusely. Potentials are generally lower in the left hemisphere compared with the right, but this asymmetry may be seen in some patients with degenerative conditions. This constellation of findings does not distinguish Alzheimer's disease from Jakob–Creutzfeldt disease and can be found in encephalopathies from other causes. However, the low-voltage spike in the left parietal–central (P3, C3) region is a feature seen less commonly in Alzheimer's disease than in Jakob–Creutzfeldt disease (Burger et al., 1952). Calibration signal 1 s, 70 µV.


Fig. 5-92. Jakob–Creutzfeldt disease with diffuse discharges. Same patient as previous illustration. Diffuse delta activity has augmented considerably, and bilaterally synchronous spike and slow-wave complexes have appeared. This finding would favor Jakob–Creutzfeldt disease as the etiology of the dementia. Calibration signal 1 s, 70 µV.


Fig. 5-93. Periodic spikes and diffuse delta; Jakob–Creutzfeldt disease. Ear reference montage. Same patient as previous 2 illustrations. These periodic discharges share some characteristics of triphasic waves and therefore could represent rapidly progressive Alzheimer's disease. Note the diffuse delta and the right frontal (FP2, F4) accentuation of the periodic discharges. Calibration signal 1 s, 100 µV.


Fig. 5-94. Periodic spikes in Jakob–Creutzfeldt disease. Same recording as in previous 3 illustrations. Disorganized background, diffuse delta activity, and periodic broad spikes are all characteristic of this rapidly developing dementia. Such discharges may be asymmetrical or predominate over one region, the right frontal area in this instance. This patient was normal until 1 month prior to the recording, when forgetfulness, disorientation, apathy, and synchronous twitching of the arms began. Calibration signal 1 s, 100 µV.


Fig. 5-95. Jakob–Creutzfeldt disease: asymmetry of background potentials. Patient's age, 58 years. The background activity is disorganized and there is an excess amount of diffuse delta activity. As may occur with dementing illness, one hemisphere may be more affected than another; in this instance the background potentials are considerably more attenuated in the left hemisphere than in the right. A clue to the etiology of the dementia is the frequent multifocal spikes, some of which are synchronous and which repeat at a fairly regular rate. Such discharges suggest Jakob–Creutzfeldt disease, because epileptiform discharges are an unusual feature of Alzheimer's disease. This patient had a 1 month history of memory impairment, right-side visual neglect, and left–right confusion. Calibration signal 1 s, 70 µV.


Fig. 5-96. Diffuse periodic spike–waves and delta activity; Jakob–Creutzfeldt disease. Same patient as in previous illustration. Drowsy. Referential A1/A2 montage. The spikes and spike–waves in drowsiness have become more evidently periodic and are more diffuse. Calibration signal 1 s, 70 µV.


Fig. 5-97. Attenuation with afferent stimuli; Jakob–Creutzfeldt disease. Patient's age, 76 years. This patient became confused and ataxic 1 month prior to this recording. At the time of this awake recording, she was severely demented. Background activity is disorganized and there is diffuse excess delta activity. Afferent stimuli (*) attenuated the recording diffusely; right central (C4) and left superior–frontal (F3) spikes occurred. In severe encephalopathies in adulthood, the EEGs may revert in some respects to those of earlier ages. For example, the attenuation with afferent stimuli is similar to that which appears in newborns. Calibration signal 1 s, 100 µV.


Arenas AM, Brenner RP, Reynolds CF III. Temporal slowing in the elderly revisited. AM J EEG Technol. 1986;26:105–114.

Burger LJ, Rowan AJ, Goldensohn ES. Creutzfeldt–Jakob disease. Arch Neurol. 1972;26:428–433.



Cobb WA, Guiloff RJ, Cast J. Breach rhythm. The EEG related to skull defects. Electroencephalogr Clin Neurophysiol 1979;47:251–271.

Eeg-Olofsson O. The development of the electroencephalogram in normal children from the age of 1 through 15 years. Neuropadiatrie. 1971;2:405–426.

Gibbs FA, Gibbs EL. Atlas of Electroencephalography. Vol 3. Reading, PA: Addison Wesley; 1964;12–14.

Petersen I, Eeg Olofsson O. Development of the EEG in normal children from age 1 to 15 years. Neuropadiatrie. 1971;2:247–304.

Rae-Grant A, Blume W, Lau C, et al. The electroencephalogram in Alzheimer-type dementia: A sequential study correlating the electroencephalogram with psychometric and quantitative pathological data. Arch Neurol. 1987;44:50–54.

Spit JM, Storm van Leeuwen W. The relation between beta activity and cerebral atrophy. Electroencephalogr Clin Neurophysiol. 1963;15:344(P).

Sundaram M, Blume WT. Triphasic waves: Clinical correlates and morphology. Can J Neurol Sci. 1987;14(2):136–140.

Zifkin BG, Cracco RQ. An orderly approach to the abnormal EEG. In: Daly DD, Pedley TA, eds. Current Practice of Clinical Electroencephalography. New York: Raven Press, 1990:253–267.