Epilepsy Essentials: VideoEEG Analysis

The advent of digital videoEEG recordings has expanded our understanding of seizure semiology, and the diagnosis of epileptic and nonepileptic events. VideoEEG has also introduced complexities surrounding clinical indications, patient safety, and proper recording environment, equipment, and techniques. Those issues were covered in the Mar/Apr 2022 issue of Practical Neurology in the first part of this special report. Here, in the second part, we address how to interpret EEG data from videoEEG monitoring in adults. Most of the information covered in both parts of this special report is equally applicable to pediatric patients, especially school-age children and adolescents.

VideoEEG monitoring is a powerful diagnostic tool when used appropriately. Accurate and precise analysis allows distinction between epileptic seizures and nonepileptic events. A patient with known epilepsy benefits from appropriate characterization of the epileptic syndrome, and accurate localization allows progression to presurgical evaluation.

The EEG in Epileptic Seizures

Interictal and Ictal Discharges

The presence of interictal epileptiform discharges (IED) is valuable but cannot be interpreted in isolation. A small proportion of the general adult population exhibits epileptiform discharges on EEG without clinical seizures; the rate of these events varies with age, and they are more frequent in children.^1-4 Similarly, IEDs can be seen in individuals with neurologic disorders without epilepsy.⁴ IEDs may be focal or generalized. The type, frequency, and localization of discharges confer prognostic and diagnostic value. The converse is also true in that an absence of IEDs or EEG changes does not exclude the presence of epilepsy. It is thought that a large area of cortex (approximately 6 cm²) must be involved before a scalp discharge can be observed.⁵ A routine EEG in new-onset seizures is abnormal in only 12% to 50% of adults, and that rate decreases further with specific epilepsy types.⁶ For example in parietal lobe epilepsy, the scalp interictal recording is often noncontributory, and more invasive monitoring is often needed.⁷

The onset of a seizure characterizes the epileptic syndrome (Table).^8-14 Generalized ictal discharges include 3-Hz spike-and-wave paroxysms, bursts of atypical spike-and-waves or slow spike-and-waves; paroxysmal fast activity (generalized repetitive fast discharge); and electrodecrement.¹⁵ Focal seizure discharges include focal or regional repetitive spike or sharp waves; rhythmic or sinusoidal theta, alpha, or beta frequency discharges; rhythmic or arrhythmic delta waves; periodic discharges, and electrodecrement.¹⁶ The pattern of focal discharge at onset has some association with specific regions of the cerebral hemispheres (eg, the rhythmic theta discharge pattern in temporal lobe seizures differs from the repetitive epileptiform pattern in frontal convexity seizures¹⁷ or the regular 5- to 9-Hz inferotemporal rhythm in hippocampal-onset seizures vs irregular polymorphic 2- to 5-Hz delta activity in temporal neocortical onset).¹⁸ A particular combination of scalp discharge pattern and location has high localization and prognostic value. A fast discharge in the beta frequency range at the onset of frontal seizures is highly indicative of the location of the epileptogenic zone.¹⁹ Approximately 90% of persons with this frontal ictal beta discharge pattern at seizure onset became seizure-free after resection of the frontal lobe focus, even when the MRI findings are negative. In comparison, postsurgical seizure freedom occurred in only 16.7% of persons with negative MRI findings who did not have this focal ictal beta pattern.

The typical frequency and waveform evolution expected on EEG during a seizure occurred in 92% of seizures with clinical manifestations but only 44% of subclinical seizures.²⁰ Focal seizures may not have detectable EEG discharge, especially frontal lobe seizures and focal aware seizures.^18,21-23 Sphenoidal electrodes, anterior temporal scalp electrodes, subtemporal chain scalp electrodes, and closely spaced electrodes are minimally invasive options for increasing the chance of recording ictal discharges. If required, a subtemporal chain of electrodes can be considered and easily added to the standard EEG montage. The chain includes the anterior temporal electrodes and is 10%, instead of 20%, inferior to the temporal chain of electrodes in the 10–20 system of electrode placement.²⁴ Routine application of closely spaced electrodes for recording frontal lobe epilepsy may not be as useful in that it may not yield information that is lacking in the regular 10–20 system scalp coverage.²⁵ Nonetheless, strategic placement of additional electrodes within an area predefined by seizure semiology, neuroimaging, or interictal discharges may better localize seizures in select individuals, especially when the focus is at the perirolandic or occipital region.

Interictal, Ictal, and Postictal Slowing

Interictal temporal delta slowing also suggests the location of the seizure focus. Only temporal intermittent rhythmic delta activity (TIRDA), however, has a high association with an ipsilateral temporal lobe seizure focus, because temporal intermittent polymorphic delta activity (TIPDA) is present in 20% of people with extratemporal epilepsy.²⁶

Unequivocal onset of background slowing during or after a spell excludes psychogenic nonepileptic seizures (PNES) for a particular spell. The remaining major differential diagnoses are epileptic seizures, syncope, or migraine. Much less common possibilities are drug effects, acute metabolic disturbance, and strokes. These nonepileptic conditions usually have more prominent slowing during the spell, rather than following resolution of the clinical spell. Relatively more prominent EEG slowing following resolution of clinical symptoms is more compatible with an epileptic seizure event.

The presence of lateralized postictal polymorphic delta activity (PPDA) in temporal lobe epilepsy is also highly suggestive of the hemisphere of seizure origin. Lateralized PPDA is concordant with the side of eventual temporal lobe epilepsy surgery in 96% of EEGs.²⁷

The ECG Recording

Every effort should be made to ensure that the electrocardiogram (ECG) channel in the EEG recording montage is recording properly. The ECG is invaluable in recognizing cardiac-related artifacts; determining seizure occurrence, even when the EEG is indeterminate; and diagnosing potentially fatal cardiac events.²⁸ It is not uncommon for ictal tachycardia to be the only convincing objective evidence of an epileptic mechanism, because an EEG discharge may not be observable, often because of muscle and movement artifacts from the clinical seizure activity. The degree of tachycardia that suggests an epileptic mechanism in focal seizures with impaired awareness is 120% to 218% of baseline heart rate but only 84% to 126% during nonconvulsive PNES.²⁹ Heart rate during epileptic convulsive seizures is 136% to 236% of baseline heart rate, compared with 101% to 137% during convulsive PNES. These findings alone are not very useful clinically because of overlap in the values. A derivation from these findings, however, that heart rate increases of at least 1.5 times above baseline are highly sensitive and specific for an epileptic seizure mechanism, strongly indicates an epileptic explanation for the spell. Ictal tachycardia is also characteristically abrupt in onset,³⁰ and often precedes seizure onset on EEG.³¹ Figure 1 demonstrates diagnosis of epileptic seizures and treatment with antiseizure medication based on EEG and ECG findings when EEG seizure discharges are undetectable.

Ictal bradycardia/asystole syndrome is a potentially serious disorder that can present as syncopal spells.^32-34 Epileptic seizures from the right or left temporal lobe induce hemodynamically significant slowing or arrest of heart rhythm in this syndrome. The diagnosis is established with videoEEG with ECG channel recording. The risk of sudden unexplained death in epilepsy (SUDEP) with this syndrome is not known, but on-demand cardiac pacing may be required when these seizures are refractory to medical treatment and the ictal bradycardia/asystole causes falls that are reduced with cardiac pacing.³⁵

The EEG in PNES

Absence of discharges on EEG during a spell is often considered the hallmark of nonepileptic spells. As discussed, however, epileptic seizures may not be accompanied by discernible EEG discharges. PNES is differentiated from epileptic seizures by 4 other EEG features. First, although PNES may occur when an individual appears to be asleep, the EEG typically has an awake rhythm (ie, EEG shows sleep activity at onset in less than 1% of PNES).^36,37 Second, ictal tachycardia favors an epileptic mechanism as discussed. Third, a normal awake rhythm in a mentally unresponsive person is not physiologic and therefore favors a psychogenic cause. Note that an EEG may appear normal in a mentally confused person due to epileptic seizure occurrence, but EEG findings are not normal when the patient is unresponsive and appears to be comatose. Other rare conditions in which the EEG may be normal in an unresponsive person are locked-in syndrome and generalized motor paralysis such as pharmacologic neuromuscular blockade or Guillain-Barré syndrome. Finally, postictal slowing precludes PNES also, as discussed.

The EEG in Syncopal Attacks

Syncopal attacks can produce EEG changes that may resemble those of epileptic seizures. A full sequence of EEG changes can be seen in a typical syncopal attack but not necessarily in a near-faint.³⁸ The earliest alteration on EEG in syncope is slowing of background rhythms. High-voltage delta slow waves follow, with the anterior head regions showing the highest amplitude. If cerebral perfusion is markedly compromised by hypotension, bradycardia, or asystole, the EEG may become suppressed or “flattened” (Figure 2). Such EEG suppression often accompanies convulsive syncope or decorticate/decerebrate-like posturing. Seizure discharges are not present, even in convulsive syncope. As the syncopal attack ends, the sequence of the EEG changes reverses. VideoEEG monitoring is especially suitable for tracking the development of clinical and EEG manifestations of syncope.³⁹

The ECG channel is necessary to detect cardiac arrhythmia as a cause of syncope, which, of all types of syncope, carries the most serious prognostic implications.⁴⁰ The ECG channel also helps detect bradycardia that can occur with noncardiac types of syncope (eg, neurocardiogenic syncope and carotid hypersensitivity). Figure 2 demonstrates the EEG changes seen during ventricular tachycardia followed by ventricular fibrillation.

Integration of Clinical and EEG Data

EEG has a reputation as a standard test for evaluating seizuress and seizure mimics; however, EEG has several limitations for evaluation of many types of events. Ictal EEG discharges are not always detectable on the scalp, and the absence of EEG discharge alone is not confirmation of the nonepileptic nature of an event. When EEG discharges are present, location or origin may be equivocal. In a study of unilateral mesial temporal lobe epilepsy,⁴¹ seizure onset could not be lateralized by EEG in 25% to 30% of recorded seizures. EEG localization of individual seizure episodes is often equivocal even in those who had successful temporal lobectomy.^42-44 Limitations of ictal EEG are even greater in extratemporal epilepsy. Approximately 35% to 50% of extracranially recorded seizures in extratemporal epilepsy are nonlateralizing.⁴² The nature and anatomic origin of seizures can be more confidently determined when EEG data are supplemented by other information.^45,46 Video-recorded seizure semiology improves the lateralization of seizures for temporal lobectomy.⁴⁷ With scalp EEG alone, approximately 65% of people who were candidates for temporal lobectomy had adequately lateralized foci, but with the addition of video-recorded seizure semiology, lateralization improved to almost 95%.

Ideally, the onset of an EEG seizure discharge should be earlier than or coincident with the clinical seizure onset. If EEG seizure onset is delayed, the possibility of false EEG localization should be entertained, because the EEG discharge detected could have been from a region of seizure propagation, rather than the region of seizure origination. Clinical seizures may not have developed until the EEG discharge has spread from the focus of onset to regions underlying the clinical semiology (ie, the symptomatogenic zone). In contrast, when ictal EEG onset precedes the clinical onset, EEG localization is generally accepted as correctly localizing, so long as the 2 localizations are not discordant, and there are no other conflicting clinical or neuroimaging data.

Discharge From the Epilepsy Monitoring Unit

It is imperative that recorded seizures be verified with patients and their relatives or friends to be certain that they are representative of habitual seizures. It is also important that enough seizure episodes are captured so any previously unrecognized seizure foci will more likely be recorded.

When phenytoin, phenobarbital, or carbamazepine is resumed or initiated as the primary antiseizure medication (ASM), we recommend serum concentrations be checked before discharge. This is especially important for those at risk for convulsive seizures. Serum concentrations of other ASMs may not be as useful because of less reliable correlation between their dose and their therapeutic effect. Nonetheless, if any of those ASMs are intended as the main antiseizure agent, it may be necessary to defer discharge until an appropriate target dose and steady state have been achieved.

Among the most difficult situations is in deciding whether ASM should be stopped in patients whose recorded seizures are nonepileptic in nature. It is best to verify the following situations before considering ASM discontinuance in such a case: 1) there are no other type of seizure or seizure-like events that have not been addressed; 2) the patient does not have risk factors for epilepsy (eg, intracranial epileptogenic lesion or history of meningoencephalitis); 3) the EEG shows no epileptiform discharges; 4) the ASM therapy had been ineffective; and 5) the consequences of seizures or seizure-like events are not particularly grave. If all 5 apply, patients may be counseled that the benefit of discontinuing the ASM may outweigh the risk of exacerbating unrecognized epilepsy. Their decision to discontinue an ASM would have been based on the best medical evidence available from a complete evaluation. If suspicion remains regarding the possibility of concomitant epilepsy, patients may be asked to continue at least 1 ASM while they undergo proper treatment for their nonepileptic events. When they are free of such events for at least a year, ASM withdrawal may again be considered. This approach is based on the practice of permitting ASM withdrawal in seizure-free patients with factors that are favorable for seizure remission following ASM withdrawal.^48,49