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ICU EEG

Up to 20% of patients admitted to an ICU with altered mental status will have seizures, of which the majority are nonconvulsive seizures (NCSz) and can only be detected with continuous EEG (CEEG) monitoring. As many as half of these seizures fulfill the criteria for nonconvulsive status epilepticus (NCSE). An increasing number of studies indicate that frequent NCSz and NCSE are associated with, and very likely causing, secondary brain injury. A similar proportion of patients will have periodic or rhythmic discharges.

The detection of NCSz, periodic and rhythmic discharges, together with the assessment of the EEG background, is useful in monitoring the degree of cerebral dysfunction, especially when the clinical examination is of limited utility (e.g., in comatose patients), and provides important diagnostic and prognostic information. Lateralized periodic or rhythmic discharges may suggest a new focal abnormality of the brain that was not clinically evident and herald NCSz or NCSE at a later time during the CEEG. The use of quantitative EEG and display of long-term trends is particularly helpful for condensing the data to allow a better appreciation of slowly evolving variations and long-term trends that are difficult to notice at conventional “paper” speed. One example is the detection of delayed cerebral ischemia that develops days after aneurysmal subarachnoid hemorrhage. The EEG may occasionally suggest a specific diagnosis in specific clinical presentations such as, lateralized period discharges (LPDs) according to the American Clinical Neurophysiology terminology [f.k.a. “periodic lateralized epileptiform discharges (PLEDs)”] suggesting herpes encephalitis, 1-Hz generalized periodic discharges (GPDs) in Creutzfeldt-Jakob disease; and extreme delta brushes in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis.

To overcome the variability and, therefore, controversy, associated with the correct interpretation of critical care EEG and the clinical implications of background abnormalities and periodic and rhythmic patterns that occur in critically ill patients, the American Clinical Neurophysiology Society (ACNS) developed a consensus terminology. This terminology provides objective and well-defined terms for most patterns encountered in the ICU setting and has a high degree of inter-rater reliability. In the following text we will use this terminology to describe the relevant features of CEEG, but will also include the older terms that correspond.

Nonepileptic motor manifestations that are frequently misinterpreted as seizures in critically ill patients may include clonus triggered by stretch of the deep tendons, tremor, posturing, and other movement disorders. CEEG with video is useful to confirm the nonepileptic etiology to avert superfluous and potentially harmful treatment by excessive use of anti-seizure medications (ASMs).

One final difficulty is the frequent occurrence of artifacts in ICU EEG that interfere with proper interpretation of CEEG. Some are common to all techniques using EEG but are more frequent in the critically ill patient. Some artifacts are specific to the ICU setting. These artifacts may exhibit rhythmicity or periodicity and require some expertise to be recognized and not mistaken for periodic brain activity or seizures. Recording simultaneous video and audio are key to avoiding misinterpretation of many artifacts.

240GENERALIZED BACKGROUND ABNORMALITIES

Generalized background abnormalities are common in ICU EEG recordings and indicate diffuse or multifocal cerebral dysfunction affecting the gray and/or white matter. These abnormalities are nonspecific and are encountered in a variety of toxic-metabolic, postanoxic and structural processes. Structural processes causing generalized abnormalities in the EEG may be diffuse (e.g., widespread traumatic axonal damage or ischemic injury), focal with secondary generalized cerebral dysfunction (e.g., increased intracranial pressure from a space-occupying lesion or upper brainstem lesion with disruption of ascending pathways to the cortex), or multifocal.

When assessing EEG background, the following features are particularly important to assess the degree of cerebral dysfunction: continuity, voltage, predominant background frequency, reactivity to stimulation, and variability. Assessing the severity of encephalopathy should be done during the most awake portion of the recording. Severity scales have been proposed that correlate these EEG findings with clinical findings and, to some extent, prognosis after anoxic or traumatic brain injury, or during hepatic or septic encephalopathy. One common classification scheme is described below in Table 11.1 and includes a clinical correlation:

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Generalized polymorphic slowing is characterized by the disappearance of normal fast EEG activity (alpha and beta), which is replaced by generalized polymorphic slow (theta and/or delta) activity. This indicates diffuse or multifocal cerebral dysfunction, typically involving the subcortical white matter, though is a nonspecific finding. Clinical correlates range from subtle alteration of mental status to stupor (Figure 11.1).

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In the situation where an EEG contains generalized slowing, indicators of greater severity include pronounced low frequencies (delta vs. theta), poor variability, poor reactivity, low amplitude, and periods of attenuation (Figure 11.2). It should be remembered that the EEG indicates the degree of dysfunction at a given moment, and its prognostic value is dependent on the reversibility of the underlying disorder.

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Diffuse attenuation is seen with widespread low-voltage electrocerebral activity (Figure 11.3). It is defined as all or most activity lower than 20 μV that is measured peak to peak, in a standard longitudinal bipolar montage. Typically, most or all of the activity is delta or lower frequency that is often poorly reactive. This is a nonspecific finding that indicates severe global brain dysfunction, including the cortex diffusely, often due to anoxic injury or toxic, metabolic, ischemic, or inflammatory-infectious encephalopathies.

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In burst-suppression, periods of voltage attenuation (10–20µV) or suppression (<10µV), termed interburst intervals and present for more than 50% of the recording, alternate with bursts (>0.5s) of activity. Burst-suppression can be caused by deep sedation with barbiturates, propofol, or inhalational anesthetics (Figure 11.4A). If not caused by sedatives, it represents severe brain dysfunction and injury. The bursts are variable but typically consist of high-voltage polymorphic activity. A peculiar pattern of burst-suppression with identical bursts has been described in patients with severe anoxic brain injury (Figure 11.4B). Bursts that contain epileptiform or periodic discharges are called highly epileptiform bursts (Figure 11.4C).

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Electrocerebral inactivity (ECI) is defined as the absence of cerebral activity on a carefully performed EEG using an ECI protocol (Figure 11.5). The assessment of ECI for the diagnosis of brain death requires a very specific protocol, including reading EEG at high sensitivity (2 μV/mm), using a double distance montage (inter-electrode distance ≥10 cm), and maintaining electrode impedances between 100 and 10,000 ohms. There is a risk of amplifying artifacts in the EMG, EKG, and so on that should not be misinterpreted as brain rhythms. For use as an adjunctive test for the determination of brain death, all reversible causes of ECI should be excluded, including high doses of sedating medications, hypothermia, and marked metabolic dysfunction. The prognosis associated with ECI is mainly determined by the underlying etiology. It is invariably poor in predicting the outcome in a case of postanoxic encephalopathy, but is less so in cases of drug overdose, toxic-metabolic encephalopathy, and severe hypothermia where the cause may have a reversible component.

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Alpha coma is a unique and striking EEG pattern characterized by the presence of widespread prominent activity in the alpha frequency range (Figure 11.6). Unlike a normal alpha rhythm, the alpha rhythm in alpha coma has an anterior (frontal) predominance and displays no or minimal reactivity to stimulation. It is most commonly seen in postanoxic encephalopathy and with lesions of the middle to upper brainstem. Alpha coma typically indicates a poor prognosis when it is due to anoxia, though it probably does not have independent predictive value when the clinical course and etiology are taken into account. For example, it may be encountered in severe toxic or metabolic encephalopathy and has a much better prognosis in these situations. At times, reactivity is preserved and this carries a more favorable prognosis. There are variants of alpha coma, with similar significance, where the rhythmic activity lies in the theta or beta range (termed theta and beta coma). All three forms may coexist in the same patient.

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Spindle coma denotes the association of coma with EEG features that resemble N2 sleep. It is another form of coma with abundant faster frequencies (similar to alpha coma) in which the background consists of prominent poorly reactive low-voltage beta activity that resembles sleep spindles (Figure 11.7). It is seen with traumatic and atraumatic etiologies similar to those identified in patients with alpha coma, though spindle coma tends to carry overall a more favorable prognosis.

250PERIODIC AND RHYTHMIC DISCHARGES

Up to 20% of critical care EEG recordings will show the presence of repetitive waveforms that recur with some degree of regularity. These discharges include periodic (sometimes epileptiform) discharges (PDs), with return to background between discharges (an inter-discharge interval) and rhythmic discharges, which occur continuously with no inter-discharge interval. Periodic and rhythmic discharges can be conveniently and reliably described using the standardized ACNS terminology. An abbreviated version is presented below. Discharges are defined by two main terms, specifying the localization and type of discharge, and further features, such as frequency, morphology, or prevalence, can be further described with additional modifiers (Table 11.2).

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Lateralized PDs (formerly known as PLEDs) usually reflect the presence of an acute (or subacute) focal brain lesion, though they may reappear with acute reactivation of a chronic lesion (Figure 11.8). LPDs are most commonly associated with cerebral infarction, though intracranial hemorrhage, brain tumor, or infection may act as predisposing etiologies. They may also follow seizures in the absence of a structural lesion. They are transient and usually disappear after a few days to two weeks, rarely persisting for months or longer.

Patients with LPDs often display impaired consciousness and focal neurological signs and the majority of them will manifest seizures during the acute phase of their illness.

LPDs are usually felt to represent an interictal pattern. However, they may be occasionally associated with transient clinical manifestations, including time-locked motor features such as clonic jerks where they represent a form of focal SE.

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