Pearls, Perils, and Pitfalls In the Use of the Electroencephalogram

Omkar N. Markand, MD, FRCPC


Semin Neurol. 2003;23(1) 

In This Article

EEG In Paroxysmal Disorders

An EEG is the most common and most useful test performed in evaluating patients suspected of epilepsy. There are many areas where an EEG has unique contributions. The value of an EEG lies in the fact that it not only shows specific ictal discharges during a clinical seizure but also characteristic epileptiform abnormalities in a high proportion of epileptic patients even in the interictal period. Furthermore, an EEG may be the only test demonstrating focal abnormalities responsible for the patient's epileptic seizures. Specific patterns in the EEG make it possible to classify the seizure type, which is an essential prerequisite to institute proper antiepileptic medication. An EEG is indispensable for the diagnosis of nonconvulsive epileptic status presenting as prolonged "twilight" state or a prolonged episode of abnormal behavior. In a patient with bizarre motor activity, the recording of an EEG during such an episode may be the only way to establish whether the abnormal behavior is due to an epileptic seizure or a nonepileptic event, physiologic or nonphysiologic. Finally, the EEG is indispensable to localize the epileptogenic (seizure producing) zone before resective surgery (excision of the epileptogenic zone) is undertaken in a patient with medically refractory focal epilepsy.

Epileptiform Abnormalities

Paroxysmal EEG activities, whether focal or generalized, are often termed "epileptiform activities." They are the EEG hallmark of epilepsy as they are highly correlated with the occurrence of clinical seizures. Epileptiform abnormalities are usually divided into "interictal" discharges, which appear in the interval between clinical seizures, and "ictal" discharges, which accompany clinical seizures. The distinction is arbitrary because the designation "ictal" or "interictal" often depends on how closely the patient was clinically observed because minimal behavioral alterations associated with the EEG paroxysms can be easily missed. Morphologically, interictal epileptiform abnormalities consist of spikes and polyspikes, sharp waves, spike-slow wave complexes, multiple (poly) spike wave complexes, and sharp-slow wave complexes. Spike is defined as an EEG transient clearly distinguished from the background, with a pointed peak at conventional paper speed and a duration of 20 to 70 milliseconds. Sharp waves are transients of similar character as spikes but have a duration of longer than 70 milliseconds and less than 200 milliseconds. Spike-slow waves and sharp-slow wave complexes are constituted by spikes or sharp waves followed by a high-amplitude slow wave.

Morphologic characteristics of epileptiform discharges have little correlation with different types of epileptic seizures. The topographic distribution of these discharges are more important in the classification of epilepsies. Generalized discharges that are bilaterally synchronous and symmetrical are associated with generalized epilepsies, whereas focal or lateralized discharges constitute the EEG "signature" of partial (focal) epilepsies. Most patients do not have their epileptic seizures during the brief period of routine EEG; hence, the interictal epileptiform abnormalities are the ones heavily relied on for the diagnosis of epilepsy. Although the interictal epileptiform abnormalities have a high correlation with the occurrence of clinical seizures, they do not themselves mean that the patient has epilepsy. The irrefutable evidence of epileptic seizure is a clinical seizure associated simultaneously with ictal discharges in the EEG, although such evidence is often difficult to obtain except during prolonged video EEG monitoring.

"Ictal" or an electrographic seizure pattern is characterized by repetitive EEG discharges with relatively abrupt onset and termination, and characteristic pattern of evolution lasting at least several seconds. The commonest waves or complexes vary in form, frequency, and topography. The ictal pattern is generally rhythmic and frequently displays increasing amplitude, decreasing frequency, and spatial spread during the seizure. The three EEG characteristics of a focal "ictal" pattern, therefore, consist of sudden onset/termination, occurrence of a rhythmic pattern of activity during the epileptic seizure, and its characteristic evolution with respect to amplitude, frequency, and spatial distribution.

Proper Identification of Diagnostic Epileptiform Abnormalities in the EEG

In the evaluation of abnormalities in the EEG, one needs to be constantly aware that there are many EEG transients that morphologically resemble epileptiform discharges and that need to be distinguished from diagnostically crucial epileptiform abnormalities to avoid overdiagnosis or misdiagnosis. These include:

  1. Artifacts: for example, electrode pop, muscle potentials, eye movements, electrocardiogram (EKG), etc.

  2. Normal components of ongoing background activity: for example, vertex sharp transients of sleep, POSTs, mu rhythm, lambda waves, drowsy activity during sleep in children that may often be associated with sharp components, etc.

  3. Epileptiform variants of dubious clinical significance: there are a large number of benign epileptiform variants that must be recognized, lest they be misinterpreted. Although morphologically similar, they are nonepileptogenic as they have no established relationship with the process responsible for generating epileptic seizures. Such sharp transients include 14 to 6 per second positive spikes, small sharp spikes or benign epileptiform transients of sleep, 6 Hz spike wave or phantom spike wave, wicket spikes, psychomotor variant pattern or rhythmic midtemporal discharges, breach rhythm, etc. Sleep not only activates diagnostically useful epileptiform EEG patterns, but also unmasks several types of nonepileptogenic sharp transients.

It is critical that the EEG interpreter has clear criteria for distinguishing diagnostically relevant epileptiform discharges from sharply contoured background activity or benign variants. Useful criteria have been formulated for identification of epileptiform events[68,69]:

  1. Epileptiform discharges (spikes, sharp waves, and spike wave complexes) should be unarguably discrete events, not just accentuation of part of an ongoing sequence of waves. They should be clearly separable from ongoing background activity, not only by their higher amplitude but also by their morphology and duration.

  2. Most epileptiform discharges have a bi- or triphasic waveform and they have a more complex morphology than even high-voltage background rhythms.

  3. The epileptiform events are not sinusoidal but rather show asymmetric, rising and falling phases.

  4. Most spikes and sharp waves are followed by a slow wave.

  5. Finally, they should have a physiological potential field involving more than one electrode that helps to distinguish them from electrode-related artifacts or muscle potentials.

Specificity of Interictal Epileptiform Abnormalities

Are "hard-core" epileptiform abnormalities encountered in normal children and adults who do not have a history of epileptic seizures? Different studies, some in children[70,71] and others in all age groups,[72,73,74] found an incidence of less than 2 to 4% of epileptiform abnormalities in the EEG of nonepileptic subjects. In an interesting study on EEG findings in 13,658 males ages 17 to 25 without a previous history of significant illness who were medically screened for training in the Royal Air Force of England, 69 (0.5%) had unequivocal epileptiform discharges.[75] Hence, the incidence of epileptiform abnormalities in the healthy population was significantly lower than the 2 to 4% noted in the nonepileptic patients referred to hospital EEG laboratories.

One can certainly conclude that if an individual has a "blackout spell" or episodic loss of consciousness, it is very likely to be an epileptic seizure if there are unequivocal epileptiform discharges recorded in the EEG. To reemphasize, interictal epileptiform discharges in the EEG are never diagnostic of epilepsy by themselves, but in the appropriate clinical setting, they provide important circumstantial evidence for the diagnosis of epilepsy.

Sensitivity of EEG and Techniques to Improve the Yield of Interictal and Ictal EEG Abnormalities in Patients with Epileptic Disorders

Some patients with unequivocal epilepsy, especially focal epilepsy, may have repeatedly normal or nonspecific EEG studies. A single routine EEG consisting of half an hour recording during wakefulness, hyperventilation, and intermittent photic stimulation (IPS) provides diagnostic findings in approximately half of the patients with epilepsy.[76] The following describes a few ways to increase the yield of epileptiform abnormalities in an interictal EEG study.

Serial EEG Studies. EEGs recorded on more than one occasion will increase the chance for recording a specific epileptiform abnormality. Research[76] has demonstrated that serial EEG studies increase the yield for epileptiform abnormalities from 50% in the first record to 84% by the third EEG, and in 92% by the fourth EEG. There was little additional yield to serial EEGs beyond this point.[76] Thus, four or five EEG studies spread over a few years provide diagnostic abnormalities in over 90% patients with epilepsy. An opposite corollary is also true; serial negative EEG studies in a patient with continuing paroxysmal events should raise suspicion of nonepileptic episodes. It is also well known that interictal epileptiform discharges markedly increase after a clinical seizure[77]; hence, obtaining an EEG promptly after a clinical seizure will increase the chances of capturing interictal epileptiform discharges.

Activating Procedures. Activating procedures (e.g., hyperventilation, IPS), recording during sleep, are very well known to activate epileptiform discharges not recorded in the awake tracing. Hyperventilation and IPS are potent activators of generalized spike wave discharges associated with primary generalized epilepsies. On the other hand, sleep tends to bring out focal epileptiform abnormalities in patients experiencing focal epileptic seizures. Sleep activates virtually all focal epileptiform abnormalities; therefore, every patient suspected of epilepsy should have a sleep recording unless there is an unequivocal and specific abnormality displayed optimally during wakefulness. One of the best ways to ensure a sleep EEG is to instruct the patient to come for the EEG test after remaining awake during the entire or at least a major part of the previous night. Sleep deprivation appears to have a further activating effect that is additive to natural sleep itself, particularly in patients with complex partial seizures and in patients with juvenile myoclonic epilepsy.

Normal response to IPS includes photic driving (photic following) at flash rate or at harmonics. In about 5% of patients, asymmetric photic driving response (>50% difference in amplitude) may occur, which by itself (without asymmetric awake and/or sleep activities) has no clinical significance. IPS is especially helpful in patients with primary generalized epilepsy in eliciting abnormal paroxysmal discharges. Photoparoxysmal response (PPR) has a high correlation with clinical epilepsy. It is characterized by the occurrence of generalized bilaterally synchronous spike wave or multiple spike wave discharges occurring with IPS. The most effective frequency is around 15 flashes per second but other frequencies may be equally effective. Reilly and Peters distinguished two types of PPR: prolonged (self-sustained), which continues for a short period after the stimulus has been withdrawn (Fig. 20), and self-limited, which cease before the flashes stop.[78] There is a much higher incidence of epilepsy in patients with prolonged (93%) compared with the self-limited (52%) PPR. A 1992 meta-analysis of the studies on PPR concluded: (1) PPR, prolonged or self-limited, had a significantly higher incidence of seizures than controls; (2) a prolonged PPR was associated with a much higher incidence of seizures (85%) than the self-limited group (50%); (3) patients with prolonged PPR more often had other epileptiform abnormalities in their resting EEG than the self-limited group; (4) the risk of epilepsy increased if the PPR was associated with epileptiform abnormalities in the resting EEG; (5) the seizure incidence associated with self-limited PPR without other epileptiform abnormalities was lower (30%) but still significantly higher than patients without PPR.[79]

Figure 20.

An EEG of a 15-year-old patient with primary generalized epilepsy, showing prolonged (self-sustained) photoparoxysmal response.

Another photic-induced response that may superficially resemble PPR but has no significant correlation with epilepsy is a photo-myoclonic response (PMR). It consists of frontally dominant polyspikes synchronous with the flash rate and accompanied by rhythmic jerking of the muscles of the forehead, eyelids, and face. The response is blocked when the eyes are opened and it promptly stops with withdrawal of photic stimulation. PMR is generally considered to be a muscular response without cerebral participation but some regard it to be an expression of cortical response within the spectrum of photic cortical reflex myoclonus. It is seen in some nervous or tense individuals or in patients with psychiatric troubles or elderly subjects. Its presence in an individual case has no diagnostic significance.

Besides photic driving, PPR, and PMR, other less common IPS-induced EEG responses include:

  1. Posterior hemispheric stimulus-dependent response: an anomalous steady state flash visual evoked potential (VEP) of unusually sharp waveform or high amplitude. This has no clinical correlation except when it represents very-high-amplitude and spiky VEPs in association with Batten's disease or neuronal ceroid lipofuscinosis.

  2. Rarely, IPS may activate a focal epileptiform discharge, usually an occipital spike focus.

  3. Less often IPS may induce a frank seizure with clinical correlates (e.g., an absence, absence with eyelid myoclonus, single random generalized myoclonic jerks, repeated myoclonic jerks, occipital onset focal seizure, and rarely even a generalized tonic-clonic seizure).

Remember than 10% of patients with all forms of primary generalized epilepsy show PPR, with the highest incidence (30 to 35%) in juvenile myoclonic epilepsy.[80] The incidence of PPR is about 15% in childhood absence epilepsy, <10% in juvenile absence epilepsy, and 10 to 15% in epilepsy with generalized tonic-clonic seizures on awakening. PPR is also common in infantile and childhood epilepsies with myoclonic seizures such as benign and severe myoclonic epilepsies of infancy and myoclonic-astatic epilepsy of childhood. PPR is rare in focal epilepsies and secondary generalized epilepsies (e.g., Lennox-Gastaut syndrome).

It must be emphasized that PPR can be detected, although rarely, among individuals with headaches or other complaints, during evaluation for aviation jobs, or as a genetic marker in a susceptible individual with a family history of idiopathic generalized epilepsy. PPR in nonepileptic subjects has a prevalence of 1 to 4%; the response then is usually brief and less prominent.

IPS is not a totally benign activating procedure. One can induce a generalized tonic-clonic convulsion (often the first one) if photic stimulation is continued over a long duration in a patient who shows prominent PPR. It is recommended that the photic stimulation be limited to short periods (1 to 5 seconds) and terminated promptly as soon as generalized spike wave activity is recorded (Fig. 20).

Special Electrodes. Although the standard 10 to 20 international system of electrode placement provides reasonable coverage of the whole head, certain areas that have high epileptogenicity, such as the mesial temporal lobes in patients with mesial temporal sclerosis, are not fully explored by conventional placement and may require additional electrodes. Nasopharyngeal electrodes have been widely used in the past in patients suspected to have with temporal lobe epilepsy. They are associated with variable degrees of discomfort and may prevent the patient from attaining sleep during the EEG recording. They have now been largely replaced by the use of anterior temporal electrodes, which are placed 1 cm above and one third the distance along the line from the external auditory meatus to the external canthus of the eye.[81]

In a comparison of the percentages of spikes detected by standard scalp electrodes, anterior temporal, mini-sphenoidal, surface sphenoidal, and nasopharyngeal electrodes in patients with suspected complex partial seizures, the anterior temporal electrodes provided significant improvement in detecting epileptiform abnormalities.[82] Recordings from standard scalp electrodes detected 58% of the discharges. Anterior temporal electrodes were the best; they detected 70% of all the discharges by themselves, and 81% in combination with standard scalp electrodes. It can be concluded that recordings from anterior temporal electrodes must be done to improve the detection of interictal epileptiform abnormalities in patients suspected of having temporal lobe epilepsy. Sphenoidal electrodes are almost invariably employed during video EEG monitoring as a part of the presurgical evaluation of patients with medically intractable complex partial seizures. The yield of abnormality from sphenoidal recordings is certainly greater than that with nasopharyngeal or anterior temporal electrodes, but it is difficult to justify the use of invasive electrode placement in routine EEG study for paroxysmal disorders.

Activation of an Actual Seizure During Routine EEG Study. All efforts must be made to capture the patient's habitual episode during a routine EEG. If precipitating factors are known, these are appropriately exploited. Hyperventilation, a potent precipitator of an absence seizure in a child with primary generalized epilepsy, must always be utilized for at least 5 minutes, once in the beginning and again at the end of a routine EEG study. In rare patients with reflex epilepsy, playing specific music in musicogenic epilepsy, asking a patient to read from a book in reading epilepsy, bathing the patient in bathing epilepsy, asking the patient to eat his meals (eating epilepsy), smelling gasoline, and so on, may all be carried out to promote an ictal event.

In patients with possible pseudoseizures, suggestion protocols are often useful in precipitating episodes and demonstrating EEG changes.[83] It is important to emphasize that induced seizures must be clinically typical of a patient's habitual episodes before the diagnosis of pseudoseizures is strongly considered.

Some Interpretive Challenges of EEG Findings During Paroxysmal Events

Some of the pitfalls regarding ictal EEG changes during an actual seizure need to be stressed. All epileptic seizures are not associated with distinctive concomitant surface EEG changes. Seizures that remain very localized, including epilepsia partialis continua and simple partial seizures (focal seizures with preserved consciousness), may not have changes in the scalp EEG because the diagnostic discharge may be deep-seated or involve only a small pool of neuronal tissue. However, epileptic seizures manifested by loss of consciousness, on the other hand, are accompanied by demonstrable changes in the scalp EEG. Therefore, absence of such changes during a clinical episode of "unconsciousness" or bilateral widespread motor activity (resembling grand mal seizure) can be particularly important in making the diagnosis of nonepileptic events or pseudoseizures. Ten to 20% of patients with pseudoseizures do have epileptic seizures as well. The most one can say is that at least some of the clinical episodes appear to be functional, and this must be considered within the context of the entire clinical picture.

In evaluating patients with muscle jerks or other brief motor events, it needs to be established whether these represent epileptic phenomena. Simultaneous recording by placing two electrodes over the involved muscle may be very helpful in establishing the relationship of, or lack of, the EEG and the motor recordings. In patients with myoclonic seizures, it is not always easy to establish whether an electrical event synchronous with the motor jerk is indeed a cerebral discharge or simply a movement artifact. The presence of morphologically similar EEG discharges in other portions of the tracing but unassociated with obvious motor activity will establish that they represent a genuine cortical discharge rather than an artifact generated by sudden movement.


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