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Video-EEG and Adult Seizures

Video-EEG can provide a definitive diagnosis of epilepsy and separate epileptic seizures from nonepileptic “spells.” It is performed to answer a particular question that cannot be addressed adequately by EEG recording alone. It is usually performed to record seizures, and encompasses one to several days of continuous EEG telemetry. An associated video signal is synchronized with the EEG so that the EEG may be precisely correlated with behavior, improving diagnostic accuracy. High-resolution video is now standard and may be coupled with either scalp or intracranial electrodes for seizure monitoring. This can be accomplished during outpatient recording sessions in the EEG laboratory, with ambulatory equipment so that video-EEG is recorded at home (aka home telemetry), or in an inpatient setting when it is necessary to record video-EEG for extended periods of time (days to weeks). Video-EEG also helps to classify the type of seizure recorded and is useful in identifying an epilepsy syndrome. Furthermore, it may quantify the seizure and spike burden relative to a prescribed duration of time. Importantly, it helps localize the source of recurrent seizures for the purposes of characterizing the focal epilepsy syndrome during presurgical evaluation. It is therefore useful not only for diagnosis, but also for planning medical and surgical treatments, and may assist in providing a prognosis when it helps establish the diagnosis of an epilepsy syndrome.

With video recording, the clinical neurophysiologist can study the recorded ictal behavior, which may itself be virtually diagnostic at times. For example, the cry heralding the start of a tonic–clonic seizure followed by characteristic tonic stiffening and then the gradual evolution of clonic jerking is a classic sign of an epileptic seizure (whether the onset is focal or generalized), and a trained observer can confirm a video-EEG based diagnosis of epilepsy in many patients based on semiology alone. Similarly, other behaviors, such as a “Jacksonian march” with spreading focal clonic movement, certain oral, hand, or leg automatisms, hypermotor behavior, and faciobrachial dystonic movements are also characteristic and nearly pathognomonic for epileptic seizures, even in the absence of ictal change in the scalp EEG. Other behaviors, such as arching of the back with closed eyes and side-to-side head shaking, are typical of psychogenic nonepileptic attacks, and when accompanied by lack of ictal EEG changes, provide confirmatory evidence for that clinical diagnosis. Moreover, response testing protocols, additional electrodes, and non-EEG sensors can be implemented in the EEG laboratory and inpatient epilepsy monitoring units to supplement information gained from observable behaviors. Neurological testing can be performed during seizures to assess memory and cognition, speech, and language, in addition to evaluating the degree of awareness. Postictal testing can determine whether elements of aphasia, disordered mentation, sensorimotor abnormalities, and visual field deficits are present. These signs can confirm an organic neurological disorder and offer clues as to lateralization and localization of the epileptogenic zone.

The EEG during video-EEG recording can provide support for the diagnosis of epilepsy with analysis of interictal and ictal observations. Interictal epileptiform discharges (IEDs) provide indirect support for a clinical diagnosis of epilepsy. In addition, they may help classify seizures and whether a generalized or focal epilepsy syndrome exists. However, 166the presence of IEDs does not guarantee a diagnosis of epilepsy as these may occur in asymptomatic individuals. For example, a significant minority of people with generalized spike-and-wave discharges (3 Hz or greater), centrotemporal spikes, and occipital spikes are asymptomatic and have no history of seizures. These may reflect either a genetic trait or an underlying brain injury. The person who is reported to lose consciousness and “shake” might have convulsive syncope or psychogenic nonepileptic attacks (PNEA) instead of epilepsy. This may infrequently occur even in the presence of an interictal EEG demonstrating generalized spike-and-wave discharges when the discharges are coincidental.

Whether epileptiform activity appears in the scalp EEG is predicated upon whether a sufficient volume of cortical involvement in the ictal discharge as well as the solid angle of the dipole projecting to the recording electrode. The underlying seizure type greatly influences the likelihood of ictal EEG detection. Nearly all seizures that impair consciousness and produce bilateral movements will produce an electrographic change in the scalp EEG. In contrast, seizures that involve small volumes of cortex, or primarily involve buried cortex (e.g., from interhemispheric foci, orbitofrontal foci, mesial temporal foci) may not show in the scalp EEG, even when bilateral movements or loss of awareness occurs. Therefore, mesial frontal or orbitofrontal seizures may not appear as a seizure in the scalp EEG unless there is extensive spread of ictal discharges more broadly through the brain or additional or high-density EEG is recorded. Focal aware seizures appear in the EEG approximately 25% of the time, due to the restricted spatial extent of these seizures. Sometimes, myogenic and movement artifact may completely obscure the ictal EEG during a seizure. However, even in that circumstance, the pattern of myogenic artifact may help establish the diagnosis of an epileptic seizure by demonstrating evolution. At other times, the presence of postictal slowing or attenuation underscores a seizure diagnosis.

Focal seizures do not reliably appear localized in one area of the brain when recorded with scalp EEG. Indeed, the scalp EEG shows a clear focal onset in 25% to 66% of seizures. When a well-localized seizure onset is apparent on ictal EEG, it usually reflects the lobe of origin. For the remainder of seizures, the ictal onset is poorly localized. It may appear broadly distributed over one hemisphere or appear to involve both hemispheres when it is first seen on scalp video-EEG. This is presumably due to rapid or extensive propagation of the ictal discharge within the underlying epileptogenic network. Therefore, though some seizures appear in the EEG to involve both hemispheres at onset, the diagnosis may still be consistent with that of a focal seizure, even though the pattern of ictal onset usually provides the clue that seizures are focal or generalized. Overall interpretation of the ictal EEG during video-EEG monitoring may be aided by also considering the findings of the interictal EEG. It is important to remember that the interictal EEG might be discordant from the clinical manifestations and semiology and show an asymptomatic inherited trait in the EEG. In addition, some people have a dual diagnosis with both focal and generalized seizures.

Both generalized and focal seizures display characteristic behaviors and EEG patterns. Both the onset and the evolution are distinctive for most seizure types, so knowledge of typical stereotyped patterns helps in understanding the diagnosis. Focal seizures display a wide variety of paroxysmal EEG patterns that express a change in frequency, amplitude, distribution, and rhythmicity in the electrographic pattern. Generalized seizures similarly display an evolution of these same features but do so differently. Sometimes, it is difficult to clearly separate an ictal or interictal pattern in the EEG because of the similarity of the electrographic features that are present. When this occurs in the ICU, this is referred to an ictal–interictal continuum, particularly when rhythmic spikes or rhythmic periodic discharges are present. These patients may have subtle stereotyped or repetitive movements that indicate a diagnosis of nonconvulsive status epilepticus, but other patients may be stuporous 167or comatose in which case the diagnosis is ambiguous. Lastly, the EEG may sometimes show electrographic seizures in the absence of behavioral correlate. These may be genuine epileptic phenomena, with the ictal discharge presumably confined to “silent” noneloquent cortex. This chapter will review various seizure types and their associated EEG findings.

GENERALIZED SEIZURES

Multiple types of generalized seizures have been described, some associated with genetic generalized epilepsies (GGE), others with epileptic encephalopathies and developmental disorders, and some with both. Throughout this book we refer to GGE as a broader category that comprises idiopathic generalized epilepsies (IGE) and other epilepsy syndromes (e.g., neonatal familial seizures, epilepsy with myoclonic absences, Jeavon’s syndrome etc.) in addition to four syndromes associated with IGE: CAE, JAE, JME and GTC-alone.

Tonic–Clonic Seizures

Generalized tonic–clonic (GTC) seizures begin with either generalized fast activity at 10- to 15-Hz or generalized spike-and-wave discharges at 3- to 5-Hz. The EEG shows diffuse, continuous myogenic artifact during the tonic phase, though sometimes ictal fast activity in the beta bandwidth may first appear. The tonic phase ends as slow waves begin to interrupt the intercurrent spikes, transitioning into the clonic phase with progressively greater intervals between successive spikes. Myogenic artifact typically obscures (“contaminates”) the EEG. However, myogenic “spikes” may also be synchronized in relationship to cortical spike frequencies to establish a clinical correlation. The EEG shows postictal background suppression and then evolves to manifest diffuse slowing. These EEG features may occur in both the GGEs and epileptic encephalopathies.

Absence Seizures

Absence seizures, found most often in childhood absence epilepsy, juvenile absence epilepsy, and juvenile myoclonic epilepsy, start with a generalized, bisynchronous, frontally predominant spike-and-wave discharge. They begin at a frequency of 3-Hz (range 3.4–4.5 Hz) and slow to approximately 2.5-Hz as the seizure ends. No postictal slowing occurs. On rare occasions, absence seizures may begin with ictal fast activity ranging from 10- to 14-Hz rather than spike-and-wave discharges as opposed to the “typical” appearance seen with absence seizures.

Atypical Absence Seizures

Atypical absence seizures, seen in epileptic encephalopathies and developmental disorders that include patients with the Lennox–Gastaut syndrome, are characterized by bilaterally synchronous 1.5- to 2.5-Hz spike-and-wave discharges. The “slow” spike-and-wave discharges are less monomorphic, the spikes appear more blunted (and often as sharp waves) and may appear in prolonged runs. These bursts may be difficult to distinguish from the patient’s interictal slow spike-and-wave pattern. Testing responsiveness may also be limited, though it provides the best means of differentiating between atypical absence seizures and interictal discharges present in the EEG.

Myoclonic Seizures

The EEG displays a brief, often single, generalized spike-wave or typically generalized polyspike-and-wave discharge during myoclonic seizures. Myogenic artifact may interfere with interpretation of the EEG by camouflaging the IED beneath the artifact. Usage of fast 168display speeds may help establish a relationship between the two signal sources as well as demonstrating a nonphysiological generator in the case of artifact alone.

Drop Attacks

Tonic Seizures

Drop attacks reflect tonic and atonic seizures due to the difficulty in differentiating them precisely but with the ultimate effect of producing a fall. Tonic seizures begin with generalized, frontally predominant fast activity at 10- to 25-Hz, which is often preceded by either a spike-and-wave discharge, a spike (and no wave), a slow wave (and no spike), or by background voltage attenuation. Continuous sustained myogenic artifact usually appears in all leads. While tonic posturing usually lasts several seconds or a little longer, a second phase with altered awareness may last for 10 to 30 seconds with semi-rhythmic delta appearing in the EEG during that time. These seizures typically occur in the epileptic encephalopathies and developmental disorders but rarely appear in GGEs. It is important to distinguish generalized tonic seizures from focal to bilateral tonic seizures since both may also produce bilateral tonic posturing. In general, the semiology differs somewhat as does the interictal and ictal EEG in patients with focal seizures.

Atonic Seizures

Atonic seizures appear similar to tonic seizures in the ictal EEG. While the EEG appearance is often indistinguishable, there is no superimposed myogenic artifact as there is with tonic seizures.

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The 3-Hz spike-wave complexes at the start of this seizure are typical for absence seizures. The evolution to polyspike-wave discharges is less common, although the gradual diminution in repetition rate is characteristic for absence seizures (Figure 8.1).

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Magnetoencephalography Abnormal EEG: Epileptiformt Technical Aspects of EEG Electrocorticography Normal EEG Artifacts of Recordings

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