Issues in brainmapping...Nonspecific EEG patterns

Version 17 A Monthly Publication presented by Professor Yasser Metwally January 2010

NONSPECIFIC ABNORMAL EEG PATTERNS
Electroencephalogram (EEG) abnormalities can be divided into three descriptive categories:

a) Distortion and disappearance of normal patterns,
b) Appearance and increase of abnormal patterns, and
c) Disappearance of all patterns.

The description of the above EEG abnormalities can be further expanded by identifying their spatial extent (local or widespread, unilateral or
bilateral) and their temporal persistence (brief and intermittent or prolonged and persistent). The intermittent abnormalities characterized by the
sudden appearance and disappearance of a pattern are called "paroxysmal."

The above classification of EEG abnormalities is purely descriptive. In addition to descriptive categorization, EEG abnormalities can be
subdivided on the basis of their usual clinical correlations. Most abnormal patterns, whether persistent or intermittent, are nonspecific because
they are not associated with a specific pathological condition or etiology. However, some patterns usually occurring paroxysmally with distinctive
wave forms (such as spike, spike and wave, sharp wave, seizure pattern, or periodic complexes) are specific in that they are frequently associated
with specific pathophysiological reactions (such as epilepsy) or a specific disease process (such as SSPE or Jakob- Creutzfeldt). This chapter will
deal with the nonspecific abnormalities.

In spite of the fact that nonspecific abnormalities are not related to a specific pathophysiologic reaction or a specific disease process, they
nonetheless can be divided into three basic categories based on their usual association with different types of cerebral disturbances. These three
basic categories are:

1. Widespread intermittent slow abnormalities, often associated with an active (improving, worsening, or fluctuating) cerebral disturbance;
2. Bilateral persistent EEG findings, usually associated with impaired conscious purposeful responsiveness; and
3. Focal persistent EEG findings, usually associated with focal cerebral disturbance.

The above division s are based on the usual clinical correlates, but it is important to realize that these correlations are statistical and not absolute.
The best intuitive grasp of the somewhat variable relationship between EEG abnormalities and clinical or other laboratory evidence of central
nervous system (CNS) disturbance is obtained when the EEG is viewed as an extension of the neurologic examination. When viewed from this
perspective, the EEG studies electrical signs of neurologic function, whereas the neurologic examination studies physical signs. In any one
patient, depending on the nature and location of the pathology, abnormalities may be found in both EEG and clinical examination, in only one
examination, or in neither, just as abnormalities may be found in one, both, or neither of two subsets on the clinical examination (such as reflex
and sensory examination). Furthermore, the results of both EEG and clinical evaluation may be normal although the patient has anatomic
abnormalities detectable by contrast studies or computerized tomography. The opposite also holds, in that both the EEG and clinical examination
may show distinct abnormalities when radiographic studies are normal. An intelligent integration of the results of functional tests (such as the
EEG and clinical examination) with radiographic tests which study anatomy (such as contrast studies or computerized tomography) requires an
understanding of the value and limitation of each test, as well as the overall clinical field of neurology. With this conceptual background,
nonspecific EEG abnormalities will be discussed based on the three general categories of clinical correlation.

WIDESPREAD INTERMITTENT SLOW ACTIVITY ASSOCIATED WITH AN ACTIVE CEREBRAL DISTURBANCE

Description

Morphologically, this type of abnormality is characterized by intermittent rhythmic slow activity often in the delta frequency range, thus
accounting for its descriptive acronym, IRDA (intermittent rhythmic delta activity). When in the delta frequency range, it is often composed of
runs of sinusoidal or sawtoothed waves with more rapid ascending than descending phases with mean frequencies close to 2.5 Hz. The waves are
relatively stereotyped in form and frequency and occur in short bursts. This pattern usually demonstrates reactivity; it is attenuated by alerting
and eye opening and accentuated with eye closure, hyperventilation, or drowsiness (stage 1, nonREM sleep). With the onset of stage 2 and deeper
levels of nonREM sleep, the abnormal IRDA disappears. However, in REM sleep the abnormal IRDA may again become apparent.

Intermittent rhythmic delta activity is usually bilateral and widespread in distribution, with peak localization strongly influenced by age. In
adults, the peak amplitude of the pattern is usually localized
over the frontal area, thus giving rise to the acronym,
FIRDA (frontal IRDA), whereas in children the peak
amplitude frequently develops over the occipital or posterior
head regions, giving the acronym, OIRDA (occipital IRDA).
This difference in location from adults to children is not
related to difference in pathological processes, but simply
reflects an age-determined variation in what is an otherwise
similar, nonspecific reaction to a wide variety of changing
pathological processes.

Figure 1. Frontal intermittent rhythmic delta
activity (FIRDA) associated with widespread
polymorphic delta activity produced by drug
intoxication.

Etiologic Nonspecificity of IRDA

IRDA is not specific for a single etiology and can occur in response to systemic toxic or metabolic disturbances as well as diffuse or focal
intracranial diseases . This may be due to diverse etiologies, such as infectious, inflammatory, degenerative, traumatic, vascular, or neoplastic
disorders.

IRDA is also the nonspecific type of slowing that
occurs in normal individuals in response to
hyperventilation. In such cases, it should not be
interpreted as an abnormality, but rather as the
response of a normal CNS to the stress of an acutely
changing pCO.

Figure 2. Occipital intermittent rhythmic delta
activity (OIRDA) associated with right cerebellar
astrocytoma, the posterior maximum of the OIRDA
is age-dependant and not related to the location of
the pathology .

Nonlocalizing Nature of IRDA

Since IRDA may occur in response to systemic toxic or metabolic disturbances, diffuse intracranial pathology, or focal intracranial pathology, its
localizing value obviously is limited. Even when it is due to a focal expanding lesion, the peak localization of the IRDA tends to be age-dependent
(maximal frontal in adults and maximal posterior in children. It is independent of the localization of the lesion, which may be at some distance,
either in the supra- or infratentorial space, from the maximum expression of the IRDA. The recognition that IRDA is a nonlocalizing rhythm,
even when associated with an intracranial lesion, led to its earlier designation as a "projected" or "distant" rhythm. Such a designation, however,
can be misleading because it encourages the misconception that the IRDA, associated with a "distant" lesion, is morphologically distinct from
IRDA due to diffuse intracranial disease or a systemic toxic or metabolic disturbance.
Although frequently bilateral, IRDA may occur predominantly unilaterally. Even when it occurs unilaterally in association with a lateralized
supratentorial lesion, the lateralization of the IRDA, although usually ipsilateral, may even be contralateral to the focal lesion. Therefore, when
IRDA is present, determining whether it is due to a focal lesion (and if so, the location of the focal lesion) is best based on persistent localizing
signs discussed later and not on the morphology or even the laterality of IRDA.

Mechanisms Responsible for IRDA

The mechanisms responsible for the genesis of IRDA are only partially understood. Earlier studies investigated the mechanisms of IRDA-
associated lesions producing increased intracranial pressure. It was recognized early that with benign intracranial hypertension (pseudotumor
cerebri), IRDA was not present. However, in increased intracranial pressure with tumor or aqueductal stenosis, IRDA is frequently present. Based
on this, earlier workers related the appearance of IRDA to increased intraventricular pressure within the third ventricle tending to produce an
acute or subacute dilatation of the third ventricle. Later studies investigated the appearance of IRDA in diffuse encephalopathies with documented
post mortem histopathological changes. Based on these studies, it was concluded that the main correlate of IRDA was diffuse gray matter disease,
both in cortical and subcortical locations. Finally, any comprehensive theory about the origin of IRDA must not only take into account that IRDA
is found in diverse systemic and intracranial processes, but must also take into consideration that IRDA is more likely to appear during the course
of an active (fluctuating, progressing, or resolving) cerebral disturbance and less likely to be associated with a chronic, stable, cerebral

disturbance. Clinically, the earliest correlate of the appearance of IRDA, especially in an otherwise normal EEG, is a subtle, fluctuating
impairment of attention and arousal. As the condition progresses, often leading to more persistent, bilateral abnormalities, frank alteration in
consciousness appropriate to the degree of persistent, bilateral abnormalities usually appear.

In summary, IRDA is nonspecific in that it can be seen in association with a wide variety of pathological processes varying from systemic toxic or
metabolic disturbances to focal intracranial lesions. Even when associated with a focal lesion, IRDA by itself is nonlocalizing. The common
denominator in the wide variety of pathological processes producing IRDA is that, when such an abnormality appears, it is likely to be associated
with the development of widespread CNS dysfunction; the earliest clinical correlates are fluctuating levels of alertness and attention. With focal
lesions, one mechanism may be an increased transventricular pressure with secondary disturbances at both the subcortical and cortical levels.
With primary intracranial encephalopathies, it appears to be due to widespread involvement of the gray matter at subcortical and cortical levels.

Figure 3. The intermittent rhythmic delta activity [left
image] and the the polymorphic slow wave activity [right
image]

FOCAL PERSISTENT EEG FINDINGS ASSOCIATED WITH FOCAL CEREBRAL LESIONS

As was done in the preceding section on bilateral persistent EEG findings, focal persistent EEG abnormalities can be divided into the following
general descriptive types. These are a) distortion and disappearance of normal patterns, b) appearance and increase of abnormal patterns, and c)
disappearance of all patterns.

There is some overlap in the first two types of abnormalities, since abnormal rhythms may be related to the distortion of previously recognized
normal rhythms. Disappearance of all rhythms in a focal area can seldom be seen at the cerebral cortex, although they may be detected with
electrocorticography.

The focal distortion of normal rhythms may produce an asymmetry of amplitude, frequency, or reactivity of the rhythm. Amplitude asymmetries
alone, unless extreme, are the least reliable finding. Amplitude may be increased or decreased on the side of focal abnormality. However, if there
is focal slowing of physiologic rhythms (for example, the alpha rhythm) by 1 Hz or more, this usually identifies reliably the side of focal
abnormality, whether or not the amplitude of the rhythm is increased or decreased. The unilateral loss of reactivity of a physiologic rhythm, such
as the loss of reactivity of the alpha rhythm to eye opening or to mental alerting, also reliably identifies the focal side of abnormality. Because of
shifting asynchronies and asymmetries of the mu rhythm, the exact limits of normal asymmetry become more difficult to define; however, the
asymmetrical slowing of the central mu rhythm by 1 Hz or more, usually associated with an increase in amplitude, is a reliable sign of focal
abnormality often of a chronic nature.

In addition to the waking rhythms discussed above, the normal activity of sleep inducing spindles and vertex waves may be distorted or lost by a
focal lesion in the appropriate distribution.

As normal rhythms are distorted, focal abnormalities may produce focal persistent polymorphic delta activity (PPDA), one of the most reliable
findings of a focal cerebral disturbance. The more persistent, the less reactive, and the more polymorphic such focal slowing, the more reliable
an indicator it becomes for the presence of a focal cerebral disturbance.
Intermittent rhythmic delta activity (IRDA) may be seen with a focal cerebral disturbance but, as mentioned earlier, it is both nonspecific as far
as etiology and nonlocalizing. When present in association with a focal cerebral lesion, it usually implies that the pathological process is
beginning to produce an active cerebral disturbance of the type that is likely to become associated with changing (fluctuating or progressive)
impairment of attention and alertness.

Focal epileptiform abnormality may occur in association with focal cerebral abnormalities, but since they have a relatively specific association
with additional symptomatology such as epilepsy.

Etiologic Nonspecificity

The above abnormalities do not reflect the underlying etiology but simply reflect that a pathological process is present. Similar abnormalities
may occur, whether they result from focal inflammation, trauma, vascular disease, brain tumor, or almost any other cause of focal cortical
disturbance, including an asymmetrical onset of CNS degenerative diseases.

Persistent Focal Abnormalities and Other Evidence of Focal Cerebral Disease

In general, no matter what the etiology, there is a rough correlation between the EEG evidence of focal cerebral disturbance and clinical as well
as radiographic evidence of focal cerebral disturbance. However, in spite of this rough relationship, there are striking examples of lack of
correlation in both directions. Some of this lack of correlation is understandable. For instance, a small infarct in the internal capsule is likely to
be missed both by radiographic studies and EEG studies, in spite of the fact that its presence may be readily detected by significant abnormalities
on clinical examination. On the other hand, both the clinical examination and the EEG may be strikingly normal in spite of the fact that the
computed tomography (CT, MRI) scan shows evidence of a well-described cystic or calcified lesion in the silent area of the brain, which may
have been present in a relatively nonprogressive form for a long period of time. Finally, the EEG may show major abnormalities in spite of a
normal clinical examination with positive CT findings, provided the lesion is in a clinically silent area, such as one temporal or frontal lobe.
With a transient ischemic attack, it is common for the clinical examination, the radiographic studies, and the EEG to be normal within attacks.
Nonetheless, in our experience, there are a small percentage of patients who have transient ischemic attacks likely on a hemodynamic basis,
rather than on the more common embolic basis, who retain a major EEG abnormality in spite of the fact that their CT scan/MRI are normal and
their neurologic examination has returned to normal after the transient attack. The exact mechanism responsible for this is uncertain, but it is
interesting to note that another apparent hemodynamic cause of transient neurologic deficit in complicated migraine also may be associated with
a marked residual EEG abnormality even when the neurologic examination has returned to normal and even when the CT scan is normal.
Finally, it is not uncommon for the EEG to show clear-cut abnormalities and focal lesions without neurologic deficit without CT abnormalities
when there is an associated epileptogenic process.

Chronic widespread hemispheric disease, such as Sturge-Weber syndrome or infantile hemiplegia, characteristically produces widespread voltage
attenuation over the abnormal hemisphere. In one study, this electrographic accompaniment was seen in every patient with Sturge-Weber disease
even when there was no associated focal neurologic deficit. These asymmetries were noted even in young children prior to the development of the
characteristic intracranial calcifications. Finally, local contusion or inflammatory disease may produce a dramatic and marked EEG change
without CT accompaniment and with or without accompanying focal clinical deficit, depending on the location and intensity of the abnormality.
However, even when the EEG picks up subclinical abnormalities not associated with roentgenographic changes, the abnormalities in general are
quite nonspecific and require close correlation with the clinical
history and other information before arriving at a specific
diagnosis.

Figure 4. Polymorphic slow wave activity in a patient with
subcortical glioma, notice the marked variability in wave shape
morphology, frequency and amplitude.

Mechanisms Responsible for EEG Findings
Associated With Focal Cerebral Disturbance

In the absence of a clear-cut understanding of the mechanisms
responsible for the generation of normal EEG activity, an
accurate explanation of how focal cerebral disturbances result in distortion in the amplitude, frequency, and reactivity of normal scalp-recorded
rhythms is not possible. However, in general, these distortions occur because focal abnormalities may alter the interconnections, number,
frequency, synchrony, voltage output, and axis orientation of individual neuronal generators, as well as the size and location and integrity of the
cortical area containing the individual generators giving rise to the total signal ultimately detected on the scalp.

There is general agreement among various workers that focal pathology in the underlying white matter is commonly associated with PPDA . In
these cases, it is postulated that the white matter lesions produce PPDA by deafferenting the overlying cortex from its underlying white matter
input.

If so, this theory could also be extended to explain focal PPDA occurring post-ictally. Although it would not be reasonable to explain post-ictal
focal PPDA on the basis of a primary white matter disturbance, it is reasonable to assume that the postictal state, either by exhaustion or
inhibition, may functionally deafferent the cortex from its underlying white matter input. Finally, even if deafferentation of the cerebral cortex
from its underlying white matter is the primary mechanism responsible for PPDA, whether focal or generalized, additional factors such as the
acuteness or changing nature of the deafferentation would have to be postulated as an additional important factor, inasmuch as PPDA is more
commonly associated with acute, active disturbances and less commonly seen in chronic, stable disturbances.

References
1. Aoki, Y., and Lombroso, C. 1973. Prognostic value of electroencephalography in Reye's syndrome. Neurology (Minneap.), 23:333-343.
2. Bancaud, J., Hdcaen, H., and Lairy, G.C. 1955. Modifications de la reactivite E.E.G., troubles des fonctions symboliques et troubles
confusionnels dans Jes ldsions hemisphdriques localisdes. Electroenceph. Clin. Neurophysiol., 7:179.
3. Beecher, H.K. 1968. A definition of irreversible coma. Report of the Ad Hoc Committee of the Harvard Medical School to examine the
definition of brain death. J.A.M.A., 205:337.
4. Bergamasco, B., Bergamini, L., Doriguzzi, T., and Fabiani, D. 1968. EEG sleep patterns as a prognostic criterion in posttraumatic coma.
Electroenceph. Clin. Neurophysiol., 24:374-377.
5. Boddie, H., Banna, M., and Bradley, W.G. 1974. "Benign" intracranial hypertension. Brain, 97:313-326.
6. Brenner, R., Schwartzman, R., and Richey, E. 1975. Prognostic significance of episodic low amplitude or relatively isoelectric EEG patterns.
Dis. Nerv. Syst., 36:582.
7. Brenner, R., and Sharbrough, F. 1976. Electroencephalographic evaluation in Sturge-Weber syndrome. Neurology, 26:629-632.
8. Carroll, W., and Mastaglia, F. 1979. Alpha and beta coma in drug intoxication uncomplicated by cerebral hypoxia. Electroenceph. Clin.
Neurophysiol., 46:95-105.
9. Chase, T., Moretti, L., and Prensky, A. 1968. Clinical and electroencephalographic manifestations of vascular lesions of the pons.
Neurology, 18:357.
10. Chatrian, G. 1980. Electrophysiologic Evaluation of Brain Death: A Critical Appraisal. In Aminoff, M. (ed.): Electrodiagnosis in Clinical
Neurology. New York, Churchill Livingstone, 600 P.
11. Chatrian, G., White, L., Jr., and Daly, D. 1963. Electroencephalographic patterns resembling those of sleep in certain comatose states after
injuries to the head. Electroenceph. Clin. Neurophysiol., 15:272-280.
12. Cobb, W. (ed.). 1976. Part B. EEG interpretation in clinical medicine. In Remond, A. (editor-in-chieo: Handbook of Electroencephalography
and Clinical Neurophysiology. Vol. 11. Amsterdam, Elsevier Scientific Publishing Co.
13. Cobb, W., Guiloff, R., and Cast, J. 1979. Breach rhythm: The EEG related to skull defects. Electroenceph. Clin. Neurophysiol., 47:251-271.
14. Cobb, W., and Muller, G. 1954. Parietal focal theta rhythm. Electroenceph. Clin. Neurophysiol., 6:455.
15. Daly, D. 1968. The effect of sleep upon the electroencephalogram in patients with brain tumors. Electroenceph. Clin. Neurophysiol., 25:521-
529.
16. Daly, D., Whelan, J., Bickford, R., and McCarthy, C. 1953. The electroencephalogram in cases of tumors of the posterior fossa and third
ventricle. Electroenceph. Clin. Neurophysiol., 5:203-216.
17. Faure, J., Drooglever-Fortuyn, J., Gastaut, H., Larramendi, L., Martin, P., Passouant, P., Rdmond, A., Titeca, J., and Walter, W.G. 1951. De
la gense et de la signification des rythmes recucillis distance dans les cas de tumeurs cerebrales. Electroenceph. Clin. Neurophysiol., 3:429-
434.
18. Gloor, P., Ball, G., and Schaul, N. 1977. Brain lesions that produce delta waves in the EEG. Neurology (Minneap.), 27:326-333.
19. Gloor, P., Kalabay, O., and Giard, N. 1968. The electroencephalogram in diffuse encephalopathies: Electroencephalographic correlates of
grey and white matter lesions. Brain, 91:779-802.
20. Grindal, A., Suter, C., Martinez, A. 1977. Alpha-pattern coma: 24 cases with 9 survivors. Annals of Neurol., 1:371-377.
21. Guidelines in EEG No. 1. 1976. Minimal technical standards for EEG recording in suspected cerebral death. Willoughby, Ohio, American
EEG Society.
22. Hess, R. (ed.). 1975. Part C. Brain tumors and other space occupying processes. In Remond, A. (editor-in-chief): Handbook of
Electroencephalography and Clinical Neurophysiology. Vol. 14. Amsterdam, Elsevier Scientific Publishing Co.
23. Klass, D., and Daly, D. (eds.). 1979. Current Practice of Clinical Electroencephalography. First edition. New York, Raven Press.
24. Kooi, K., Tucker, R., and Marshall, R. 1978. Fundamentals of Electroencephalography. Second edition. Hagerstown, Harper & Row.
25. Markand, 0. 1976. Electroencephalogram in "locked-in" syndrome. Electroenceph. Clin. Neurophysiol., 40:529.
26. Martinius, J., Matthes, A., and Lombroso, C. 1968. Electroencephalographic features in posterior fossa tumors in children. Electroenceph.
Clin. Neurophysiol., 25:128-139.
27. Scollo-Lavizzari, A. 1970. The effect of sleep on EEG abnormalities at a distance from the lesion: All night study of 30 cases. Eur. Neurol.,
3:65-87.
28. Sidell, A., and Daly, D. 1961. The electroencephalogram in cases of benign intracranial hypertension. Neurology (Minneap.), 11:413-417.
29. Voukydis, P. 1974. Effect of intracranial blood on the electrocardiogram. New England J. Med., 291:612.
30. Walker, A.E. 1977. An appraisal of the criteria of cerebral death. A summary statement. A collaboration study. J.A.M.A., 237:982.
31. Westmoreland, B., and Klass, D. 1971. Asymmetrical attenuation of alpha activity with arithmetical attention. Electroenceph. Clin.
Neurophysiol., 31:634-635 (abstract).
32. Westmoreland, B., Klass, D., Sharbrough, F., and Reagan, T. 1975. Alpha coma: EEG, clinical, pathologic and etiologic correlations. Arch.
Neurol., 32:713.

The author,
Professor Yasser Metwally
Professor of clinical neurology, Ain Shams university, Cairo, Egypt.
www.yassermetwally.com

A new version of this publication is uploaded in my web site every month
Follow the following link to download the current version:
http://brainmapping.yassermetwally.com/map.pdf

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Issues in brainmapping...Nonspecific EEG patterns

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