Generalized EEG Waveform Abnormalities

Updated: May 21, 2014
  • Author: Jane G Boggs, MD; Chief Editor: Selim R Benbadis, MD  more...
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Generalized EEG abnormalities typically signify dysfunction of the entire brain, although such dysfunction may not be symmetric in distribution. Generalized patterns thus may be described further as maximal in one region of the cerebrum (eg, frontal) or in one hemisphere compared to the other. Identification of an abnormality as generalized may require analysis of the EEG by several montages to determine lack of focal point. Careful elimination of external and bioelectric artifact is important to avoid misinterpretation of noncerebral activity (eg, ECG), which can contaminate multiple channels, appearing as generalized abnormalities.

This article discusses EEG patterns that usually are generalized and are not considered primarily ictal. Many of these patterns occur in encephalopathic states, which themselves can lower a patient's threshold for seizures. Some patterns can be considered epileptiform since they contain spikes, sharp transients, or rhythmic paroxysmal patterns. Remember that the term epileptiform is descriptive of an EEG's appearance only and does not necessarily imply that the pattern is epileptogenic. One must always consider how the patient appears clinically while the EEG is recording. Certainly, correlation with episodic behavior, reactivity, or changes in level of response may indicate that even a vague slow generalized pattern may imply seizures. [1]

The American Clinical Neurophysiology Society recently created a system of objective nomenclature for the various generalized and focal EEG patterns frequently encountered in EEGs of encephalopathic patients. In this terminology, "generalized" refers to bilateral, bisynchronous, and symmetric patterns, even if the pattern is restricted to a particular area of the brain (eg, bifrontal). Further modifiers specify whether a generalized pattern is predominant in a particular area of the EEG (eg, occipitally predominant) and whether it is periodic, rhythmic, spike/sharp, and wave. The prevalence, duration, frequency, number of phases, sharpness, amplitude, polarity, and whether the pattern is stimulus-induced are also noted in this new terminology. [2]

Patient education

For excellent patient education resources, see eMedicineHealth's patient education article Electroencephalography (EEG).


Slow Activity

Alpha coma

See the image below.

Alpha coma. This 29-year-old man sustained a close Alpha coma. This 29-year-old man sustained a closed head injury in an automobile accident. The patient was on a respirator, was deeply comatose, and responded to painful stimulation with decerebrate posturing. Later, he improved to a neurovegetative state. He could open his eyes and could breathe without the respirator, but he could not follow commands and made no purposeful movements. The EEG at 1 week contains high-voltage frontally predominant relentless alpha activity that was minimally responsive when stimulated. In this patient, reactivity did not suggest a good prognosis.

Unremitting 8- to 13-Hz EEG activity that is unresponsive to eye opening or other stimulation has been termed alpha coma. [3] This activity differs in appearance from alpha rhythm (normal background activity) in its lack of reactivity and its spatial distribution. It is monorhythmic or diffuse, or it may have anterior or posterior accentuation. Only minor fluctuations in amplitude occur, and minimal to no reactivity to external stimulation can be elicited. [4]

Spindle coma is similar in appearance and implications but consists of monorhythmic 11- to 14-Hz activities, occurring paroxysmally on a delta background, without reactivity. Such patterns often are seen in anoxia, head trauma, and diffuse cerebral insults. Prognosis is usually that of the underlying etiology, although reactivity portends a better prognosis than unreactivity on these EEGs. [5] This pattern must be distinguished from normal alpha rhythm in the locked-in state and from slower segments of 10- to 18-Hz rhythms observed in various intoxications. See the image below.

Spindle coma. This 14-year-old male patient suffer Spindle coma. This 14-year-old male patient suffered a closed head injury. At the time of the EEG (3 d after the injury) the patient was comatose, but respirations were spontaneous and he responded appropriately to painful stimulation. There is a generalized high-voltage delta activity with sleep spindles superimposed. The spindles are more widespread than normal sleep spindles, although they are of similar morphology. The patient gradually improved to normal neurologic function.

When alpha coma is found in comatose patients with brainstem lesions, it is often more posterior, varies with external painful stimulation, and the prognosis is poor. In severe anoxic encephalopathies, alpha appears more diffusely and is typically less reactive. Although this pattern also indicates a poor prognosis, with mortality rates exceeding 90%, instances of recovery have been reported occasionally [6] .

Diffuse slowing

Diffuse or anteriorly prominent theta and delta patterns occur in comatose and encephalopathic states of multiple potential etiologies. [7] Patterns that fail to respond, either in amplitude or frequency, to noxious, auditory, or visual stimuli carry a poor prognosis for meaningful neurologic recovery. Similar patterns with preserved reproducible reactivity imply potential for some recovery and should be compared to recordings repeated several days later. These patterns must be distinguished from those of normal drowsiness and sleep.

Intermittent delta

Intermittent rhythmic delta activity (IRDA) usually occurs at frequencies of 2-2.5 Hz with relatively sinusoidal, stereotypic, bilaterally synchronous waveforms appearing in short bursts. The ascending phase is sloped more steeply than the descent, and waves are typically bilateral and widespread with peak amplitude frontally in older individuals (FIRDA) and occipitally in children (OIRDA). These patterns attenuate with alerting or eye opening. Eye closure, drowsiness, and hyperventilation accentuate IRDA. Although IRDA disappears in stage 2 and deeper non-rapid eye movement (REM) sleep, it may reappear in REM sleep. [8]

Multiple etiologies can result in IRDA, including metabolic, toxic, hypoxic, or various diffuse or focal intracranial diseases. [9] Even when IRDA occurs unilaterally in association with a focal cerebral lesion, the lateralization of IRDA may be ipsilateral or contralateral to the lesion. Thus, IRDA is a nonspecific nonlocalizing EEG pattern, unless associated with other focal findings on the EEG. Although the mechanisms for production of IRDA are understood incompletely, studies correlating with pathologic specimens suggest that IRDA is associated primarily with diffuse gray matter disease.

The degree of encephalopathy manifested appears to correspond to the proportion of IRDA on the EEG. This pattern must be distinguished from the frequently encountered frontally maximal intermittent delta that can be seen in drowsy elderly patients.


Periodic Abnormalities

Burst suppression

High-voltage bursts of slow, sharp, and spiking activity alternating with a suppressed background have been termed burst suppression. The duration of bursts or suppressed epochs is highly variable. Myoclonic jerking can occur concomitantly with the bursts and may be ictal. Chemical paralysis in the intubated ventilated patient is required to determine if the patterns of ictal potential persist after elimination of motion artifact. The endogenous pattern of burst suppression needs to be distinguished from pharmacologically induced patterns (eg, with etomidate, barbiturates, benzodiazepines). This pattern is encountered in deep coma and has been suggested as the final pattern in deterioration of generalized status epilepticus. [10, 11]

See the image below.

This pattern has traditionally been designated as This pattern has traditionally been designated as burst suppression. However, these patterns have become controversial and would be called generalized PEDs by some and have even been considered potentially ictal by others.This 54-year-old patient was seen 5 days after a coronary artery bypass complicated by a prolonged hypotension causing diffuse cerebral anoxia. The patient is deeply comatose and unresponsive to any stimulation. He has occasional episodes of rapid eye blinking. The EEG has high-voltage bursts of spikes and polyspikes lasting for less than 1 sec followed by low-voltage epochs. This type of abnormality is usually associated with anoxic encephalopathy. It carries a very poor prognosis.

Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs)

A pattern of various rhythmic periodic EEG patterns elicited by stimulation may occur in critically ill patients. Although these patterns may occur in patients with epilepsy, case series found that only half of patients with SIRPIDs had seizures, and there was no significant difference in the incidence of clinical seizures in patients with or without SIRPIDs. [12]

Subacute sclerosing panencephalitis

Subacute sclerosing panencephalitis (SSPE) is an inflammatory disease of children and adolescents caused by chronic infection with the measles virus. The characteristic EEG pattern, initially described by Radermecker and Cobb and Hill, consists of high-voltage (300-1500 µV), repetitive, polyphasic sharp and slow wave complexes of 0.5- to 2-second duration that recur every 4-15 seconds. [13, 14] Rarely, the complexes can occur at intervals of 1-5 minutes. The interval between complexes may shorten as the disease progresses.

The morphology of the waveforms tends to be consistent in a single recording but may be strikingly variable with disease progression. Although the complexes are usually symmetric and synchronous, they may be asymmetric with a time lag between hemispheres or lobes. [15] The EEG usually is not changed by stimuli except in the earliest stages of the disease or in remission, when the EEG pattern tends to be more inconstant. [16] The EEG background is slow and progressively more disorganized as the disease advances. The stages of sleep eventually become difficult to distinguish.

Abnormal movements, cognitive deterioration, and the diagnostic EEG characterize the clinical disease. Stereotypic jerking or other movement abnormalities occur with the periodic complexes. Rarely, the periodic complexes become apparent before the movements manifest. The movements often disappear in sleep, even though the complexes persist. [17] See the image below.

Subacute sclerosing panencephalitis. This is a 7-y Subacute sclerosing panencephalitis. This is a 7-year-old boy who is comatose and having myoclonic jerks. The onset of the illness began 14 months ago with deterioration of intellectual function and he has become progressively unresponsive. This EEG shows stereotyped high-voltage (300-400 mV) bursts of activity every 4-6 seconds.

Creutzfeldt-Jakob Disease

Creutzfeldt-Jakob disease is a long-latency infection caused by a prion. The characteristic EEG shows biphasic or triphasic discharges that are initially sporadic and may even be asymmetric. As the disease advances, the pattern becomes generalized and synchronous with continuous periodic stereotypic 200- to 400-millisecond sharp waves occurring at intervals of 0.5-1.0 seconds. [18, 19]

Myoclonic jerks often occur in association with the sharp waveforms, but the relationship is not constant. Late in the illness and during sleep, myoclonic jerks disappear, despite the persistence of the periodic EEG. The sharp waves typically react to external stimuli. Early in the disease, alerting the patient may elicit the periodic pattern; later, when the periodic pattern is readily apparent, rhythmic photic or other stimuli can "drive" the periodic frequency. Benzodiazepines or barbiturates can temporarily eliminate both myoclonic jerks and periodic patterns.

Creutzfeldt-Jakob disease. This is a 56-year-old f Creutzfeldt-Jakob disease. This is a 56-year-old female professor who became more withdrawn and increasingly forgetful. Over the next 4 months she deteriorated rapidly and became mute, bedridden, and unable to eat with myoclonic jerks of her arms. The EEG done 6 months into her illness shows a pseudoperiodic, well-organized 1- to 2-Hz biphasic and triphasic waves and very little other activity. In this clinical setting, this EEG is virtually pathognomonic of Creutzfeldt-Jakob disease and is regarded as a manifestation of severe gray matter disease involving the cortex and deep nuclei.

Electrocerebral Inactivity

EEGs are performed occasionally to provide supportive evidence of brain death. Although brain death is defined by clinical criteria, some situations preclude complete or definitive examination findings (such as severe open head or eye trauma). In such situations, a confirmatory test is often helpful. Cerebral angiography demonstrating no blood flow is the most sensitive and specific confirmatory test, but it also is time and labor intensive and may be refused by the family as it is highly invasive. An EEG may be a reasonable alternative, but it needs to be performed according to strict criteria for clinical as well as medical-legal determinations.

Electrocerebral inactivity (ECI), or electrocerebral silence (ECS), is defined as no cerebral activity over 2 µV using a montage that uses electrode pairs at least 10 cm apart with interelectrode impedances < 10,000 ohms and >100 ohms.

According to guidelines of the American Clinical Neurophysiology Society, the following are minimum technical standards for EEG recording in suspected brain death: [20]

  • A minimum of 8 scalp electrodes
  • Impedances between 100 and 10,000 ohms
  • Integrity of entire recording system tested by touching each electrode individually to obtain appropriately located artifact potential
  • Interelectrode distances of at least 10 cm
  • Sensitivity of at least 2 µV for 30 minutes of the recording, with appropriate calibrations documented
  • High-frequency filter (HFF) not set below 30 Hz and low-frequency filter (LFF) not set above 1 Hz
  • Additional monitoring techniques used as necessary to eliminate or prove waveforms are artifactual
  • No EEG reactivity to strong and thorough tactile, auditory, or visual stimulation
  • Recording performed by a qualified technologist working under the direction of a qualified electroencephalographer
  • If ECI in doubt, EEG repeated after an interval (suggested 6 h)