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Abnormal EEG: Nonepilept

Interictal EEG provides useful information about the presence of nonepileptiform neurophysiological dysfunction. When abnormalities are encountered, they are not specific for an underlying etiology, and as such represent abnormalities without further differentiation of the pathological process. While neuroimaging demonstrates anatomical definition of an abnormality, the EEG provides evidence of abnormal neurophysiological function when neuroimaging is normal.

The EEG is sensitive to cerebral dysfunction but may have a lag during clinical improvement or lead relative to maximal clinical symptomatology. Many of the patterns that are nonepileptiform are due to a nonspecific etiology. Still, the presence of a nonepileptiform abnormality reflects the clinical presence of abnormality and often parallels the degree of dysfunction. Acuity is unable to be demonstrated by EEG in nonepileptiform abnormalities, although serial tracing may further help to define the trend of neurological improvement or deterioration. Therefore, the EEG is objectively able to substantiate and quantify the degree or depth of encephalopathy when diffuse nonepileptiform abnormalities are encountered. Furthermore, they may lateralize (or even localize) abnormalities when focal areas of slowing are evident. Many nonepileptiform and epileptiform abnormalities may help characterize the encephalopathy when the two features are identified on the EEG. This chapter will discuss and focus on generalized and focal nonepileptiform abnormalities.

76DIFFUSE ABNORMALITIES

Diffuse slowing on the EEG may have various morphologies, and occur intermittently or continuously, to reflect abnormal cerebral function. The presence of diffuse slowing suggests a bilateral disturbance of cerebral function and represents an encephalopathy that is nonspecific for etiology.

Intermixed diffuse intermittent theta in the most alert state is normal in young adults. When theta frequencies are seen in the frontal or frontocentral regions and voltages are greater than 100 µV or when theta is present greater than 10% of the time in an adult (not in childhood or elderly), then theta may reflect a nonspecific abnormality similar to diffuse intermittent slowing or background slowing. The slower the frequency, the higher the amplitude, and the greater the persistence, the more likely intermittent theta is abnormal (Figure 4.1).

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Diffuse (or generalized) slowing of the background electrocerebral activity reflects a nonspecific abnormality (Figure 4.2). It is indicative of a bilateral disturbance of cerebral function. With progression of cerebral dysfunction, the degree of generalized abnormal nonepileptiform abnormalities increases. Abnormally intermixed intermittent slowing that is manifest initially as intermittent theta (sometimes normal as discussed above) progresses to involve a greater degree of intermittent slowing, first becoming continuous theta slowing that is subsequently replaced by greater amounts of higher amplitude delta frequencies.

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Background slowing is defined as slowing of the posterior background activity to a frequency slower than the lower limits of a normal alpha rhythm frequency of 8 Hz (Figure 4.3). Diffuse slowing of the posterior dominant rhythm is a feature of encephalopathy. The degree of slowing of the background reflects the degree of cerebral dysfunction. The greater degree of background slowing reflects a more severe encephalopathy. Abnormality is defined when a posterior dominant rhythm that is present and that is normally reactive appears too slow for the patient’s age. The lower limits of normal for an alpha rhythm is 5, 6, 7, and 8 Hz at ages 1, 3, 5, and 8 years, respectively. Often times diffuse slowing of the background is associated with other stigmata of mild diffuse encephalopathy, such as intermittent bursts of generalized theta or delta activity.

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Diffuse intermittent slowing is characterized by intermittent bursts of diffuse slow activity. This usually appears in the delta range and often appears in addition to background slowing of the posterior dominant rhythm (see Figure 4.4). Like background slowing, with which it frequently coexists, it is indicative of a diffuse encephalopathy. The bursts are usually irregular or polymorphic but can occasionally be rhythmic. As the severity of the encephalopathy increases, the bursts will increase in duration and frequency and merge into or become continuous generalized slowing (see continuous generalized slowing, page 60). Like other encephalopathic patterns, the presence of diffuse intermittent slowing is nonspecific relative to an etiology and may reflect either the presence of cortical or subcortical cerebral dysfunction.

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Frontal intermittent rhythmic delta activity (FIRDA) appears as bursts of intermittent delta. These intermittent bursts are often high voltage, bisynchronous, and monomorphic waveforms (Figure 4.5). FIRDA may rarely appear asymmetric, especially when a focal structural lesion is present. However, FIRDA typically has a bilaterally symmetric electrophysiological field. FIRDA may appear normally during the buildup associated with hyperventilation (see Chapter 1). An abnormal pattern exists when FIRDA occurs in the waking adult EEG consisting of bilateral rhythmic monomorphic delta waves. The frequency is usually consistent throughout the EEG when it appears. Bifrontal predominance is typical in adults, and occipital predominance is more typically seen in children, shifting with brain maturation. FIRDA is most often associated with encephalopathies of toxic or metabolic origin. It also occurs with subcortical lesions, such as a deep midline lesion, or increased intracranial pressure.

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Occipital intermittent rhythmic delta activity (OIRDA), like FIRDA, is a nonspecific finding in the EEG relative to etiology but in children often associated with generalized epilepsies. OIRDA is demonstrated as a posterior predominant bisynchronous rhythmic delta slowing appearing in bursts (Figure 4.6). OIRDA has the same features as FIRDA but occurs almost exclusively in children as a maturation-related spatial feature in EEG. OIRDA appears maximal over the occipital region instead of appearing with frontal predominance. OIRDA has been noted to occur in association with generalized (absence) epilepsy but is not an epileptiform abnormality unless intermixed spikes are present.

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