AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

Until the past 3 decades, localization of brain tumors and other focal lesions was difficult. Neuroimaging techniques consisted of skull radiography, which was usually negative, and pneumoencephalograms, which were invasive, painful, and often uninformative. In 1936, Walter, who introduced the term "delta waves," first identified the association between localized slow waves on EEG and tumors of the cerebral hemispheres. This established EEG as an important tool for localizing brain tumors. For the next 4 decades, electroencephalographers mounted an enormous effort to improve accuracy of localization and to seek clues to underlying pathological processes.

Experience has shown EEG to be somewhat reliable in localizing lesions involving superficial accessible portions of the cerebral hemispheres, though it is of limited value in deep-seated lesions, especially posterior fossa tumors. The role of EEG in detecting focal cerebral disturbances has undergone a significant change since the development of CT scan and MRI. Today EEG is used primarily to complement these studies by evaluating functional changes in the patient's condition; it demonstrates aspects of brain physiology that are not reflected in structural neuroimaging. Functional neuroimaging techniques, such as positron emission tomography (PET), single-photon emission computed tomography (SPECT), and functional MRI (fMRI), can exhibit physiologic changes but not with the temporal resolution of EEG. Furthermore, EEG provides the only continuous measure of cerebral function over time.

This article reviews the major EEG changes that occur with different brain tumors, as determined by location, histologic type, associated complications, and surgical and nonsurgical treatments. For excellent patient education resources, visit eMedicine's Cancer and Tumors Center and Procedures Center. Also, see eMedicine's patient education articles Brain Cancer and Electroencephalography (EEG).

BACKGROUND

Section 3 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

Classification

Intracranial tumors have been classified by location and histology.

Classification by location, modified from Merritt (1991), is as follows:

I. Tumors of the skull

A. Metastatic tumors
B. Eosinophilic granuloma

II. Tumors of the meninge

A. Meningioma
B. Meningeal carcinomatosis

III. Tumors of the cranial nerve

A. Acoustic neuromas
B. Trigeminal neuromas

IV. Neuroectodermal tumor

A. Cerebral

1. Astrocytoma
2. Oligodendroglioma
3. Glioblastoma

B. Cerebellar

1. Medulloblastoma
2. Astrocytoma

C. Brain stem

1. Glioma
2. Ependymoma

V. Other primary tumor

A. Pituitary adenoma
B. Pinealoma
C. Congenital tumors (eg, craniopharyngioma)
D. Granulomas

VI. Metastatic

A. Parenchymal tumors

The 1993 World Health Organization classification is based on histology. A simplified version is as follows:

I. Tumors of neuroepithelial origin

A. Astrocytic tumors

1. Astrocytoma
2. Anaplastic (malignant) astrocytoma
3. Glioblastoma

B. Oligodendroglial tumors
C. Ependymal tumors
D. Mixed gliomas
E. Choroid plexus tumors
F. Neuroepithelial tumors of uncertain origin
G. Neuronal and mixed neuronal-glial tumors

1. Dysembryoplastic neuroepithelial tumor
2. Ganglioglioma

H. Pineal parenchymal tumors

II. Embryonal tumors

III. Tumors of cranial and spinal nerves

IV. Tumors of the meninge

A. Meningioma and its variants
B. Malignant neoplasms (eg, chondrosarcoma)

V. Lymphomas and hematopoietic neoplasms

VI. Germ cell tumors

VII. Cysts and tumorlike lesion

A. Colloid cyst of the third ventricle
B. Hypothalamic hamartoma

VIII. Tumors of the sellar region

A. Pituitary adenoma
B. Craniopharyngioma

IX. Local extension from regional tumors

X. Metastatic tumors

XI. Unclassified tumors

Epidemiology

One estimate states that in the United States, approximately 35,000 new cases of primary brain tumor are diagnosed each year, corresponding to an incidence of 8-19 cases per 100,000 population. Metastatic brain tumors are 3-4-fold more common, estimated at 110,000-140,000 new cases per year in the United States.

The following characteristics apply to primary brain tumors:

• Second most common cause of cancer death in children and adults aged 34 years and younger
• Third most common cause of cancer death in men aged 35-54 years
• Represent approximately 1.8% of all cancer deaths

The various types of brain tumors occur with different frequencies in children and in adults.

• The most common childhood tumors are astrocytoma, medulloblastoma, and ependymoma.
• The most common adult tumors are metastatic brain tumors (from lung, breast, melanoma, and other primary tumors), glioblastoma, and anaplastic astrocytoma.

Brain tumors presenting with seizures

Seizures occur in 40-60% of patients with supratentorial tumors and are the presenting symptom in 10-40%. When seizures start in adulthood, neoplasms are the cause in 2-20% of patients. In general, the more slowly a tumor grows, the more likely it is to present with a seizure. For example, as many as 92% of oligodendrogliomas are associated with seizures, and in most patients they are the presenting symptom. Similar or higher percentages apply to gangliogliomas and dysembryoplastic neuroepithelial tumors.

Location is also important in determining the likelihood of seizures. Perirolandic cortex is believed to be most epileptogenic, although this impression may reflect in part the ease of diagnosing seizures in the presence of prominent motor activity. Medial temporal structures are probably the next most epileptogenic, followed by other areas of frontal, temporal, and parietal lobes, with occipital lobe the least likely to produce seizures. Subcortical tumors, such as those in the thalamus and particularly the posterior fossa, rarely cause seizures.

TYPES OF EEG ABNORMALITIES ASSOCIATED WITH BRAIN TUMORS

Section 4 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

EEG abnormalities in brain tumors depend on the stage at which the patient presents for evaluation. EEG changes observed with tumors result mainly from disturbances in bordering brain parenchyma, since tumor tissue is electrically silent (with the possible exception of tumors containing neuronal elements, such as gangliogliomas). For this reason, EEG localization often is misleading, although lateralization is generally reliable.

The following are common findings:

• Polymorphic delta activity (PDA)
• Intermittent rhythmic delta activity (IRDA)
• Diffuse or localized theta activity
• Localized loss of activity over the area of the tumor
• Asymmetric beta activity
• Disturbance of the alpha rhythm
• Spikes, sharp waves, or spike-wave discharges

Activation procedures are usually of limited value in patients with tumors, although hyperventilation occasionally can accentuate focal slowing. Asymmetries of photic driving can be useful at times, although they also can be misleading.

Slow wave activity

Focal delta activity is the classic electrographic sign of a local disturbance in cerebral function. A structural lesion is strongly suggested if the delta activity is continuously present; shows variability in waveform amplitude, duration, and morphology (polymorphic); and persists during changes in physiologic states, such as sleep or alerting procedures. When focal delta is found without a corresponding imaging abnormality, it is usually in the setting of acute seizures (especially postictally), nonhemorrhagic infarction, or trauma.

Clinical and experimental observations indicate that PDA results primarily from lesions affecting cerebral white matter; involvement of superficial cortex is not essential, and lesions restricted to the cortical mantle generally do not produce significant delta activity. Functional deafferentation of cortex likely is critical.

Delta activity that fails to persist into sleep or attenuates significantly with arousal or eye opening is less indicative of structural pathology, as is rhythmic or sinusoidal delta. The latter usually occurs intermittently and is termed IRDA. It is usually bilateral and of high amplitude and is typically maximal occipitally (OIRDA) in children and frontally (FIRDA) in adults. Unlike PDA, IRDA increases in drowsiness and attenuates with arousal. IRDA often is observed without structural pathology, as in metabolic encephalopathies, but it also can occur with diencephalic or other deep lesions; in this situation, an amplitude asymmetry can be present, with higher amplitude ipsilateral to the lesion.

As in other clinical settings, theta activity is indicative of less severe localized or diffuse dysfunction than delta activity and is observed more commonly with functional disturbances than with structural disturbances. When unaccompanied by delta activity, theta is less likely to indicate a lesion that produces a focal neurological deficit or seizures.

Localized loss and asymmetries of background activity

Since tumor tissue probably does not generate electrical activity detectable with conventional recording techniques, electrical silence is the best localizing sign of a cerebral tumor. However, it is a rare finding, occurring only when the tumor involves significant cortical areas with minimal subcortical disruption. Incomplete loss of activity, especially faster normal rhythms, is observed more commonly and is diagnostically helpful.

Alpha rhythm

By the time the patient presents with focal or diffuse neurological symptoms and signs, disturbance of the alpha rhythm may be observed. Slowing of the alpha rhythm ipsilateral to a tumor is more common and significant than asymmetry of amplitude. However, disturbance of alpha rhythm depends on the site of the tumor. The more posterior the location, the more the alpha tends to be slowed, nonpersistent, or disturbed by admixed theta waves. The alpha rhythm also may fail to block to eye opening on the side of the neoplasm (ie, Bancaud phenomenon).

Beta activity

Abnormalities of beta activity usually are limited to voltage asymmetries. To be considered unequivocally abnormal, a persistent amplitude difference of one third or greater (expressed as a fraction of the higher voltage) should be present. Diminished beta activity results either from cortical dysfunction, as in parenchymal tumors, or from an increase in resistance of the medium-separating cortex from scalp-recording electrodes, as in meningiomas or subdural collections. Focally increased beta activity usually is associated with a skull defect.

Interictal epileptiform discharges

Isolated discharges

Spikes, sharp waves, or spike-wave complexes occurring with consistent localization are observed uncommonly early in the course of brain tumors. In one study predating the CT scan era, such discharges appeared with only 3% of gliomas and metastatic tumors at the time of craniotomy. However, they were more common either as early findings of slowly growing neoplasms associated with seizures or later after focal slowing had developed.

Periodic lateralized epileptiform discharges

Patients with tumors may exhibit periodic lateralized epileptiform discharges (PLEDs) at times, particularly after a series of seizures. In a study of 282 patients with typical PLEDs, tumor was present in 18%. Most patients with this EEG finding have had or will have seizures, if they are observed sufficiently closely and persistently; the pattern likely represents a transitional state between ictal and interictal epileptiform discharges. Aggressiveness of treatment depends in part on whether the discharges are resolving (ie, becoming less sharp, more localized, and further apart) or the opposite.

Seizure patterns

When electrographic seizures are recorded during a routine EEG, status epilepticus should be suspected. Clinical accompaniments may be subtle, as in aphasic or other forms of nonconvulsive status, particularly when the patient's baseline condition has been compromised by the tumor, its treatment, or complications.

EEG CHANGES IN TUMORS BY LOCATION

Section 5 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

Since EEG reflects activity of cortical neurons, hemispheric tumors affect EEG most consistently and prominently. In older studies, a normal EEG occurred in approximately 5% of hemispheric, 25% of deep or basal, and 25% of infratentorial tumors. The overall figure now may be 50% or higher, given the earlier diagnosis allowed by modern neuroimaging. Location is an important determinant of the likelihood and nature of EEG abnormalities.

Frontal lobe tumors

• Frontal lobe tumors characteristically cause focal PDA, which accurately localizes the lesion.
• In approximately one third of patients, slow waves are bilateral and may be IRDA rather than PDA. This occurs most often when deep structures such as the corpus callosum are involved (eg, butterfly glioma).
• IRDA is more frequent with frontal tumors than with tumors in other hemispheric locations, even in children in whom the IRDA is often maximal occipitally (OIRDA).
• The slow wave abnormality may be only in the theta range, particularly in small, slowly growing tumors.
• The alpha rhythm usually is preserved, although it may be disrupted with large lesions.
• Parasagittal tumors, particularly meningiomas, may cause decreased beta activity on the side of the tumor or runs of ipsilateral alpha and theta activity.
• Sharp waves and spikes are most likely in slow-growing neoplasms and may be bilateral; occasionally, frontally predominant spike-wave complexes mimicking those of idiopathic epilepsies may be produced.

Temporal lobe tumors

Temporal gliomas are generally the easiest to localize on EEG, since PDA occurs over the tumor site in more than 80% of patients. Tumors in other locations, such as the thalamus, also may produce temporal delta; however, focal delta is more reliably localizing when background rhythms also are attenuated.

Anterior temporal

• When tumors are in this location, a well-preserved alpha rhythm occurs.
• PDA is well localized.
• EEG from the contralateral hemisphere is often virtually normal.
• Since these tumors often are associated with seizures, they may demonstrate interictal epileptiform discharges. These discharges may be identical to those associated with nonneoplastic lesions such as mesial temporal sclerosis, especially when the tumor is located medially, as is often the case with very slow-growing tumors, such as gangliogliomas and dysembryoplastic neuroepithelial tumors.

Posterior temporal

• Tumors in this location are characterized by PDA and usually disturbance of the ipsilateral alpha rhythm.
• The alpha rhythm will show slowing or disorganization with intermixed theta.
• Occasionally, alpha amplitude is decreased markedly rather than slowed.

Parietal lobe tumors

• Tumors in this region less often produce localized slowing; PDA usually is lateralized but often not clearly localized. When phase reversals are present, they may be temporal or frontal rather than parietal.

• PDA is often slow (<2 Hz), but it is usually of lower amplitude than with frontal or temporal tumors.
• The alpha background generally is disturbed either ipsilaterally or bilaterally.
• Theta rather than delta activity may occur in meningiomas, low-grade gliomas, and small metastases.
• In centroparietal tumors, mu rhythms may be attenuated ipsilaterally but occasionally may be more persistent and of higher amplitude.
• Since seizures are common in patients with tumors in perirolandic areas, ipsilateral epileptiform discharges may be present; at times, they may be difficult to distinguish from mu, especially after craniotomy.

Occipital lobe tumors

• Most occipital gliomas produce focal changes, especially PDA, which spreads variably to more anterior and contralateral locations. Occipital meningiomas, mainly of the tentorium, can cause more focal EEG changes.
• The background alpha rhythm is rarely normal and may be impaired either ipsilaterally or bilaterally.
• Interictal epileptiform discharges are rare.

Deep hemispheric tumors

Deep hemispheric tumors include those than impinge on the lateral and third ventricle and surrounding structures, including the diencephalon, basal ganglia, and corpus callosum. Neuroimaging has led to earlier diagnosis of smaller tumors that may be associated with normal EEGs. When abnormalities are observed, the following apply:

• The typical EEG finding is IRDA. This finding classically has been associated with hydrocephalus or increased intracranial pressure, but this assumption may be incorrect, since IRDA is uncommon in hydrocephalus of nonneoplastic origin and is not present in benign intracranial hypertension.
• PDA typically does not occur, although asymmetric IRDA is relatively common.
• Especially in older patients, rhythmic delta may be more continuous than intermittent.
• Alpha rhythm and sleep spindles may be disrupted ipsilateral to the lesion.
• Epileptiform discharges are very rare.

Intraventricular and sellar tumors

Lateral ventricle (ependymoma, meningioma)

• EEG may exhibit PDA over the ipsilateral temporal lobe.
• Theta and sharp waves may be present temporally.

Third ventricle (colloid cyst, epidermoid, craniopharyngioma, hypothalamic hamartoma)

• EEG is usually normal unless the lesion is large.
• Slowing may be bifrontal or diffuse.
• Runs of theta may be observed.
• In hypothalamic hamartomas, ictal and interictal EEG discharges may be seen over the frontal or temporal lobe, depending on whether anterior or posterior hypothalamus is involved.

Sellar region

• EEG is usually normal.
• If present, slowing is usually bitemporal.

Infratentorial tumors

Brain stem and cerebellum

• EEG is more often abnormal in children.
• If present, slowing is most often posterior and bilateral.
• IRDA may be observed, especially if hydrocephalus is present.

Cerebellopontine angle (acoustic neuroma)

• EEG is usually normal, especially with small tumors.
• When present, slowing is usually temporal or temporal occipital.
• Slowing is often intermittent and usually but not always ipsilateral; it may be bilateral or even predominantly contralateral.

TUMOR TYPE AND EEG

Section 6 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

EEG patterns are not specific for tumor pathology, but some general correlations exist.

• Slowly growing extraaxial tumors, such as meningiomas, produce the mildest EEG disturbances, whereas rapidly growing intraaxial tumors, such as glioblastomas, cause the most marked abnormalities.
• Benign intraaxial tumors, such as astrocytomas or oligodendrogliomas, are intermediate in their effects on the EEG.
• Interictal discharges most commonly are observed initially in slowly growing tumors and often are observed later in the course of higher-grade lesions.

Meningiomas

Being extraaxial, meningiomas compress the brain but cause little destruction of brain tissue. Therefore, meningiomas of the anterior or middle cranial fossa, unless large, infrequently alter EEGs. Convexity meningiomas are more likely to cause EEG changes. With rolandic or parasagittal meningiomas, common EEG changes include the following:

• Focal theta activity
• FIRDA
• Diminished, or less often, augmented beta activity
• Focal PDA that is usually low in amplitude (50-60 µV), intermittent, and misleadingly prominent in temporal derivations
• Epileptiform discharges observed in as many as 45% of patients

Gliomas

Slowly growing gliomas such as oligodendrogliomas and fibrillary astrocytomas (excluding tumors of deep structures) often can be distinguished from the more rapidly growing anaplastic astrocytoma and glioblastoma multiforme.

• With the more benign tumors, which are comparatively circumscribed, the abnormalities tend to be localized and within the theta range.
• In rapidly growing tumors, relatively more overall abnormality is present, and the background (particularly the alpha rhythm) is more impaired and disorganized.
• Glioblastomas produce the most widespread, slowest (often 1 Hz or less), and largest (100-200 µV) delta waves. These tumors cause prominent PDA, with marked alteration of background rhythms. Also, the high incidence of necrosis makes "flat PDA" (low-amplitude slow delta with diminished fast activity) more likely.
• Indolent gliomas commonly cause seizures, and epileptiform activity may appear before significant slowing occurs. Later, delta appears, often intermittently and at 2-3 Hz. Still later, focal PDA becomes persistent.

Metastases

Metastatic tumors to the brain occur commonly with carcinomas of lung, kidney, and breast and with melanomas and chorionic carcinomas. When metastases are present bilaterally, slowing often appears diffuse, although it is often asymmetric; slowing from multiple bilateral lesions is often difficult to distinguish from a toxic-metabolic disturbance. Meningeal carcinomatosis usually causes changes that correlate with the clinical situation; when deposits are widespread and cause an encephalopathy, slowing is usually diffuse.

Isolated metastases usually cause less prominent abnormalities than gliomas of similar size and location. Slow waves show higher frequency, lower amplitude, and less persistence than with high-grade gliomas, and normal background rhythms are more likely to be preserved.

EEG CHANGES OVER TIME

Section 7 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

Because of improvements in neuroimaging and neurosurgery and recognition of the benefits of early resection, serial EEG studies now are rarely performed prior to surgery. Older studies suggest that EEG evolution during tumor growth is characterized mainly by increased slowing—lower frequency, higher amplitude, more persistence, and wider distribution—with rate of change depending mainly on rate of tumor growth. In addition, epileptiform discharges are more likely to occur as the tumor grows.

Occasionally, successful treatment with steroids or chemotherapy can cause reduction in slowing and epileptiform activity.

Following resection, dramatic changes may occur in the EEG; these usually stabilize over periods of weeks to months. Since screening for tumor recurrence now depends on neuroimaging, serial EEGs usually are reserved for patients with clinical changes that are not explained by imaging, particularly when seizures are suspected.

EEG changes after neurosurgery

EEG changes after neurosurgery usually exhibit the following features:

• In the immediate postoperative period, the EEG frequently deteriorates, with prominent focal and sometimes generalized slowing. Localized PDA can occur if, for example, the temporal or frontal lobe was retracted to provide access to a deep tumor.
• After a week or so, EEG abnormalities improve, and slow waves diminish, although much individual variation exists.
• In most patients, the residual EEG abnormality becomes stable 3-4 months after craniotomy.
• Abnormalities seldom resolve completely; residual abnormality depends largely on completeness of tumor excision.
• Subsequent localized or generalized increase in slowing or loss of background activity strongly suggests tumor recurrence.
• With further progression, delta activity increases in voltage while frequency becomes slower and distribution wider.
• Emergence of epileptiform activity without changes in focal or generalized slowing may occur and does not necessarily imply tumor recurrence.
• Appearance of a postoperative breach rhythm is almost universal. This consists of a localized increase in theta and faster frequency activity, usually 6-11 Hz, which shows a sharp, often arciform contour. Decrease in the filtering effect of the intact skull on higher frequency activity after a breach (break) in the cranium is the major cause of these changes, which generally persist despite replacement of the bone flap and healing of the craniotomy. Preoperative and postoperative recordings on a patient with an oligodendroglioma illustrate these changes (see Images 1-2). At times, such rhythmic activity can suggest a seizure pattern, but it does not have the characteristic evolution of frequency, amplitude, and distribution of an ictal discharge.

Use of EEG to predict postoperative seizures

Because of the tendency of focally increased high-frequency activity after craniotomy to sharpen the contour of background waves, identification of interictal epileptiform discharges is difficult. A distribution other than the breach rhythm, asymmetric up-slope and down-slope, extremely sharp peak, and prominent after-coming slow wave suggest epileptogenicity. However, in a preliminary study, degree of slowing (predominantly delta rather than theta) was associated more closely with seizures than with amount of sharp activity. Similar lack of predictive value of interictal discharges has been noted in a recent series of meningiomas and in a mixed group of mainly low-grade temporal lobe tumors. Another recent study failed to show a correlation between spikes or slow waves and seizure recurrence after withdrawal of antiepileptic drugs in children with brain tumors several years after presentation.

Complications of brain tumors and their treatment

The possibility of perioperative stroke has been mentioned. Sizable ischemic infarcts typically exhibit increased slowing in the region of the stroke, with loss of fast activity if cortex is involved. Hemorrhagic stroke or hemorrhage into the tumor bed also is accompanied by increased slowing, which may be bilateral if deep structures are affected.

If chemotherapy or radiation is effective, slowing can diminish even without surgery. Conversely, late effects of radiation can result in increased slowing, as well as new epileptiform activity and clinical seizures in the case of radiation necrosis. EEG probably does not help in distinguishing recurrent tumor from radiation necrosis. In radiation-induced or chemotherapy-induced encephalopathies, including methotrexate leukoencephalopathy, slowing of the EEG usually parallels the clinical situation.

The clinician and electroencephalographer also must remember that patients with brain tumors can develop additional diseases, particularly when immunosuppressed, such as progressive multifocal leukoencephalopathy or herpes simplex encephalitis. In these patients, EEG changes such as focal slowing or periodic discharges reflect the new condition.

CONCLUSIONS

Section 8 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

The character and distribution of EEG changes produced by tumors depend primarily on lesion size, rate of growth, distance from the cortical surface, and specific structures involved.

In general, the following are true:

• PDA is the hallmark of tumor localization.
• Both metastatic tumors and gliomas commonly cause delta activity, often localized to the tumor site and neighboring zone, although bilateral slowing may occur. Changes are more marked with aggressive gliomas.
• Deep tumors are more likely to cause widespread hemispheric or bilateral slowing, often rhythmic (IRDA). Small deep tumors may cause no abnormalities, especially if the thalamus is not involved.
• When the tumor is growing rapidly and involves cortex, localized loss of background activity may occur.
• Slowing of the alpha rhythm is frequent in posterior supratentorial tumors.
• Spikes, sharp waves, or spike-wave discharges often are observed at the time of diagnosis in slowly growing tumors that are most likely to present with seizures. With more malignant neoplasms, both seizures and epileptiform discharges occur later. Location of discharges does not always correlate with tumor location; at least with dysembryoplastic neuroepithelial tumors, discordance of structural and EEG abnormalities does not predict a poor seizure outcome after surgery.
• Craniotomies and other interventions alter the EEG in usually predictable ways. Breach rhythm can complicate the interpretation of interictal epileptiform activity.

Despite advances in neuroimaging, EEG still offers a unique view of physiologic changes over time in patients with brain tumors.

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

Media file 1:  Preoperative EEG in a patient with a right temporal oligodendroglioma. Polymorphic delta activity is localized mainly over the right anterior-midtemporal region, with some centroparietal spread; alpha is preserved. (Longitudinal bipolar montage; right temporal chain is bottom 4 channels. Calibration: 1 second, 50 mV.)
	View Full Size Image
Media type:  Photo

Media file 2:  Patient with a right temporal oligodendroglioma after tumor resection. The patient is drowsy, and bilateral alpha is not present, but right posterior alphalike activity with intermixed sharp theta constitutes a breach rhythm. Beta also is increased on that side, and polymorphic delta activity is less prominent. (Irregular eye movement artifact is observed bilaterally in anterior derivations.)
	View Full Size Image
Media type:  Photo

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Background
• Types of EEG Abnormalities Associated With Brain Tumors
• EEG Changes in Tumors by Location
• Tumor Type and EEG
• EEG Changes Over Time
• Conclusions
• Multimedia
• References

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Article Last Updated: Sep 27, 2006