PDA is 1–2 Hz, high-amplitude, arrhythmic slow-wave activity that is generally seen in the later stages of coma than IRDA and triphasic waves, but may still attenuate with stimulation. As the coma deepens, the predominant frequency in PDA becomes slower and loses its reactivity to stimulation.

PDA is believed to be generated in pyramidal neurons in cortical layers II, III, and V. Schaul and colleagues found that this pattern was largely seen in dysfunctions of the subcortical white matter or with lesions which partially deafferented white matter [12, 13]. Further studies revealed that it could be seen with metabolic, toxic, or infectious encephalopathies [14], and less commonly with infratentorial lesions involving the thalamus and rostral brainstem [15, 16]. Occasionally, PDA or more frequently continuous RDA occurs with deep-seated epileptic foci that are remote from the scalp surface, with limbic encephalitis and with limbic status epilepticus.

Figure 9.3 shows bilateral waxing and waning medium-to-high voltage 1–3 Hz delta activity with some interspersed lower voltage theta frequencies. There is little alpha or beta activity. The patient had severe head trauma and remains alive but with little functional recovery.

GPEDs are generalized, usually high-voltage sharp or spike morphologies, occasionally polymorphic, occurring synchronously and bilaterally. The discharge frequency typically is 0.5 Hz or slower and occurs in an unreactive coma, sometimes with low-amplitude face or limb myoclonus. There is often little background activity between discharges, but theta and delta may occur. As the coma deepens, amplitude of the inter-GPED activity decreases.

There is a high association of clinical seizures or electrographic seizures before or after the recording of periodic discharges, more so with GPEDs. The most frequent cause is cerebral anoxia after cardiorespiratory arrest. A poor outcome (mortality or vegetative state) is >97%. Severe metabolic disease and overdoses of lithium and baclofen may also cause GPEDs. The EEG should raise the suspicion of CJD. Patients with later stages of subacute sclerosing encephalitis (SSPE) can have GPEDs with longer inter-GPED interval.

Figure 9.4 shows GPEDs at 1.2 Hz in a patient after cardiac arrest. The record showed little background and no reactivity to stimuli. There were no brainstem reflexes and the patient died.

Burst suppression pattern refers to synchronous bursts of high-voltage, mixed frequency activity, separated by periods of EEG suppression to less than 10 µV (Fig. 9.5). The bursts contain spikes and discharges of almost any other frequency. The duration of the suppression increases with deepening coma or anesthetic agent dose. Etiologies that are commonly associated with burst suppression pattern include anoxic encephalopathy, drug intoxication, anesthetics, and hypothermia. This pattern is generally reversible if induced by hypothermia or anesthetics, including barbiturates or benzodiazepines. However, if it occurs in the setting of anoxic encephalopathy, it is associated with poor prognosis. Indeed, this pattern occurs shortly before progression to electrocerebral inactivity.

Low-voltage records (<20 μV) without variability or reactivity occur with anoxia or less frequently with severe metabolic and ischemic disturbances. Following cardiac arrest, it carries a zero percent prognosis for return to consciousness, but care must be taken to exclude significant hypothermia and sedative or anesthetic agents. Low-voltage fast patterns conversely may be seen in ~5% of the normal population and with alcoholism and sometimes with benzodiazepine use, but will also possess normal variability and reactivity.

Electrocerebral inactivity (ECI) (Fig. 9.6) represents an EEG pattern where no activity of cortical origin can be seen. The EEG often shows many types of artifacts, such as EKG, respiration, and intravenous drips. The record must be run so as to conform to the Guidelines of the American Clinical Neurophysiology Society (ACNS) (http://​www.​acns.​org/​pdf/​guidelines/​Guideline-3.​pdf):

Once these criteria are satisfied, and if the presence of anesthetic or suppressant drugs is excluded, the finding of ECI in concert with an appropriate clinical examination (demonstrating the lack of brainstem reflexes) indicates “brain death.” These recordings are usually obtained after cardiorespiratory arrest, severe head trauma, and intractable malignant raised intracranial pressure.