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. 
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. 
For excellent patient education resources, see eMedicineHealth's patient education article Electroencephalography (EEG).
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Unremitting 8- to 13-Hz EEG activity that is unresponsive to eye opening or other stimulation has been termed alpha coma.  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. 
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.  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.
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  .
Diffuse or anteriorly prominent theta and delta patterns occur in comatose and encephalopathic states of multiple potential etiologies.  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 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. 
Multiple etiologies can result in IRDA, including metabolic, toxic, hypoxic, or various diffuse or focal intracranial diseases.  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.
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]
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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. 
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.  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.  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.  See the image below.
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.
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: 
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)