The EEG is the most single important ancillary test for the diagnosis of epilepsy. Epileptiform discharges include spikes (< 70 ms), polyspikes, sharp waves (70-200 ms), spike-and-slow-wave complexes, sharp-and-slow-wave complexes. Other nonspecific findings in epilepsy include focal polymorphic slowing and intermittent rhythmic delta activity.

Not only can the presence of epileptiform discharges (EDs) confirm a clinical suspicion of epilepsy, but the localization and type of discharge also helps to identify the diagnosis of a specific syndrome (Table 25.1). A proper syndromic classification is paramount to ensure adequate management, as different syndromes may call for different treatments. It should be noted that EDs may occasionally be absent in a minority of patients who have epilepsy. The first routine EEG obtained after an inaugural seizure demonstrates EDs in approximately 30% to 50% of cases. This proportion increases to a maximum of 80% to 90% after the third routine EEG and subsequent EEGs do not raise this proportion further. Longer recordings, sleep recordings, and so-called activation procedures, such as hyperventilation, intermittent photic stimulation, and sleep deprivation can be performed to increase the sensitivity of the EEG.

Conversely, EDs are seen in 1% to 2% of EEGs of individuals without a history of epilepsy. This proportion is higher in children and in siblings of patients with epilepsy.

In addition to diagnosis, EEG results also help with the management of epilepsy. A finding of interictal EDs after a single seizure increase the likelihood of seizure recurrence and therefore influences the decision about whether to treat with antiepileptic drugs. Similarly, the presence of interictal EDs increases the likelihood of seizure recurrence when consideration is being given to discontinuing antiepileptic drugs after a period of seizure control. Finally, in the setting of convulsive status epilepticus, EEG can be extremely helpful in determining whether individuals with prolonged postictal cognitive impairment (usually >30 minutes) are experiencing electrographic seizures (up to 50%) or nonconvulsive status epilepticus (up to 14%).

Finally, so-called benign epileptiform variants should not be confused for bona fide EDs. These variants are physiologic activity with a somewhat sharp morphology that may resemble spikes or sharp waves but can be readily dismissed after careful inspection. This distinction is important, as it is not uncommon to encounter patients who carry a diagnosis of medically refractory epilepsy but turn out to have nonepileptic spells and in whom a normal variant has been mislabeled as an ED.

With the advances of brain imaging, the usefulness of EEG for the diagnosis of focal brain injury has significantly decreased. However, EEG remains the only way to assess the epileptogenic potential of a cerebral lesion. The hallmark of focal brain injury is the presence of localized nonrhythmic delta (1 to 4 cps) or theta (5 to 7 cps) activity, referred to as focal polymorphic slowing (Fig. 25.3). As a rule of thumb, delta activity is associated with more destructive lesions than theta activity. Focal attenuation of fast activity, the absence of normal alpha or beta (14 to 30 cps) activity over a region of the scalp indicates focal cortical injury. Both focal slowing and attenuation can be seen in the absence of a focal lesion (Fig. 25.4). In this case, they represent the presence of focal cerebral dysfunction as a result of a postictal state or, rarely, migraine. Lateralized periodic discharges (LPDs; also referred to as periodic lateralized epileptiform discharges or PLEDs) usually indicate the presence of an acute destructive lesion with a high epileptogenic potential, usually stroke, neoplasm, or encephalitis, as up to 85% of patients will experience seizures during the acute phase of their illness (Fig. 25.5). They
can occasionally be seen in the aftermath of a seizure in patients with chronic epilepsy or with a remote brain injury. Rarely, LPDs are associated with clinical manifestations (time-locked contralateral myoclonus, visual hallucinations, etc.).

Toxic, metabolic, diffuse hypoxic-ischemic, and other global insults to the brain result in generalized nonspecific EEG changes. Mild encephalopathy is characterized by slowing of the posterior dominant rhythm and a generalized excess of polymorphic theta activity. With more pronounced brain dysfunction, the posterior dominant rhythm is lost and replaced by a mixture of theta and delta activity. These changes are described as generalized polymorphic slowing. In more severe cases, cerebral activity consists mostly of delta activity, which may become monotonous. At this point, reactivity to external stimulation (noise, noxious stimuli) may be lost. In the most severe forms of encephalopathy, there is attenuation (< 20 µV) or even suppression (< 2 µV) of all cerebral activity.
A suppression-burst pattern in which periods of suppression alternate with bursts of high amplitude activity, can also be seen in severe cases (Fig. 25.6). Generalized rhythmic delta activity (GRDA; often frontal and intermittent; FIRDA) is another nonspecific finding of encephalopathy, although it can be seen with lesions in the frontal lobes. Generalized periodic discharges (GPDs) are repetitive waveforms that occur either at periodic or quasiperiodic intervals of 0.5 to 3 cps. They can be encountered in any type of encephalopathy, at a moderate to severe stage, and are associated with an increased risk of seizures. Triphasic waves are a subtype of GPDs with a typical morphology (Fig. 25.7). They were initially thought to be specific of hepatic encephalopathy. They can in fact be seen in most metabolic or toxic encephalopathies and even during or after status epilepticus. A major role of the EEG in patients with acute confusion and obtundation is to identify those who suffer from nonconvulsive status epilepticus.