Eye movement artifacts are seen in virtually every awake and conscious individual during routine EEG. Most eyeball artifact is easy to recognize by its anterior location and its bilateral, synchronized appearance. When the eyes move, the electric dipole between the positively charged cornea and the negatively charged retina also moves, yielding a large potential depending on the direction and rate of the movement. In general, it is symmetric as long as lead placement is measured well, the patient is not missing an eyeball (Fig. 13.2), both retinas are functional, and the frontal bones are intact (6). Eye movement monitors placed above and below the eye using one to two channels help identify potentials that are in phase with cerebral, and out of phase with extracerebral, ocular sources (9). Eye movement artifact is important for the determination of the normal waking background as eye opening blocks the alpha rhythm and eye closure produces alpha. The artifact is produced by the Bell’s phenomenon as the eyeballs roll upward with the closure of the eyes, producing an upward movement of the positive dipole created by the cornea. Eye movements can be quite rapid with fluttering eyelids occurring at rates up to 13 Hz and appear abnormal (Fig. 13.3) especially if they are asymmetric (Fig. 13.4)! They can also be rather slow in the delta range mimicking abnormal patterns such as frontal intermittent rhythmic delta activity (FIRDA; Fig. 13.5). With horizontal eye movements, the artifact is generated over the lateral eye leads, F7 and F8 (Fig. 13.6). It can be quite striking as in the case of lateral gaze nystagmus, generally noted more from the side of the fast phase (10). The characteristic deflection that includes a rapid rise and more gradual fall with the corrective movement is quite easy to recognize. The side of the positive phase reversal of the rapid rise indicates the direction of the fast component of the nystagmus. With leftward eye movement, the F7 electrode has positive reversals at the same time
that the F8 electrode reveals negative reversals (Fig. 13.7). Additionally, eye movements are crucial to correctly identify the stages of sleep such as the slow roving subdelta in the lateral eye leads representing drowsy eyeballs during stage Ia and REM artifact also seen in F7 and F8 lateral eye leads during REM sleep (Fig. 13.8).

During photic stimulation, light from the flash stimulus may produce artifact in the frontopolar leads (Fp1/Fp2). This artifact can be mistaken for photic driving due to the entrainment with the stimuli, but is not located occipitally. The source may be the retina (ERG) or from a nonphysiologic source such as a frontopolar electrode with high impedance creating a photocell. Covering the eye with a towel will block the input to the retina (ERG) and this should not be confused with the photoelectric effect (11).

Muscle is another commonly observed artifact in the EEG. It is high-frequency activity noted to be very “spiky” but too fast to be an epileptic discharge. It is observed more while the patient is awake, and may obscure critical portions of the recording, for example, during hypermotor seizures. The frontalis and temporalis muscles are principal sites of myogenic artifact. Frontalis muscle becomes most involved with forced eye closure, and photic stimulation (10). Temporalis muscles become active with jaw clenching, chewing, or bruxism appearing as bursts of fast activity (Fig. 13.9). Technologists can ask the patient to open the mouth that relaxes the jaw and diminishes this artifact. Frontalis muscle contraction during periocular movement may elicit sustained or individual motor unit potentials that can appear like “railroad tracks” (Fig. 13.10). Lateral rectus muscle spikes representing motor unit potentials recorded from the lateral orbit may simulate small interictal discharges (i.e., F7/F8) (Fig. 13.11). During intermittent photic stimulation, eye flutter artifact at frequencies of < 6 Hz may mimic generalized spike-and-wave when coupled with myogenic potentials and create a “pseudo-photoparoxysmal response” (Fig. 13.12) when muscle spikes are time-locked to the flash frequency.

The tongue is a very large muscle centrally located inside the head. Similar to the eye, the tongue creates a bioelectric dipole with the tip of the tongue negative relative to the root (11). During oropharyngeal motion, a direct current (DC) potential is produced that is often diffusely seen with frontal and temporal predominance (11). Cephalad-caudad motions may be produced by tongue movements involuntarily while speaking or when swallowing (Fig. 13.13) producing delta frequency waves that may mimic FIRDA distinguishable by the superimposed muscle artifact. Similar artifact may be produced when patients are asked to say “lilt” or “ta ta ta,” identifying similar patterns as artifact more conclusively (Fig. 13.14). Horizontal tongue movements (i.e., tongue in
cheek) can create unilateral artifact on the EEG that may be confusing. Validation is possible through application of tongue movement monitors with electrodes placed above and below the mouth over the cheek and chin (10). Using a bipolar montage, positive phase reversals are evident with tongue movement in a similar fashion to those recorded during eye movements.

While many artifacts “contaminate” the EEG, some (i.e., the EKG) are essential for interpreting physiologic functions that may occur during the recording session. The heart is another key source of EEG artifact and is variably present on recordings depending on the montage used and the size of the patient. Referential montages often accentuate EKG artifact (Fig. 13.15), especially using ipsilateral ear reference with the larger intra-electrode distances. Linked ears montage can reduce the artifact (Fig. 13.16). Overweight patients with short stocky necks as well as babies may be predisposed to EKG artifact because the dipole is situated closer to the recording electrodes and better able to transmit the current (10). This may be reduced by altering head position. Recording the EKG during routine EEG is essential to enable recognition of the cardiac-cerebral relationship. Channel I of the EKG is approximated with electrodes linking the left and right chest using bipolar recording to identify the QRS. EKG interference may be noted as a small spike at 1/sec that in isolation mimics an interictal spike or in succession and on a low-amplitude record mimics periodic lateralized or generalized periodic epileptiform discharges (PLEDs or GPEDs). Bipolar montages may reveal apparent interictal epileptiform discharges (IEDs) that are “focal” diphasic waveforms predominately in the temporal derivations of the left hemisphere due to the vector created by the electric conduction of the heart. Opposite polarities of the R-wave from the EKG may be seen at the left (negative) and right (positive) ear electrodes. EKG can be readily identifiable as the source because of the regularity and time-locked waves synchronous with the EKG. Importantly, when an electrode is positioned over an artery, the blood pulsing through the vessel moves it regularly to produce a periodic and smooth waveform time-locked to the cardiac rhythm appearing approximately 200 msec after the QRS complex (Fig. 13.17) (10, 11 and 12). Pulse artifact can be eliminated by moving the electrode off the artery.

Scalp perspiration will also produce artifact by creating unwanted electric connections between electrodes. Perspiration artifact appears as very low-frequency (<0.5 Hz) low-amplitude undulating waves. Changes in the DC electrode potential from perspiration may result in an unstable baseline (sweat sway) and crossing of tracings in adjacent channels (Fig. 13.18). Perspiration artifacts are usually seen in multiple adjacent channels or over the entire scalp and poses a risk for bridging between electrodes (see also the section “Electrode and Input Lead Artifacts”). They can be reduced somewhat by increasing the low-frequency filter, and by drying the scalp and reapplying electrodes, or by cooling the patient with a fan.

Patient movements cause the leads or electrodes to move, and thus can provide a large source of “physiologic” artifact on
recordings. This is especially true for the awake and ambulatory patient (13), but is also quite notable in those who are agitated and confused. Synchronous video has been inordinately helpful in distinguishing the varieties of patient movements when a technologist is not present for the recording. Regular appearing patient movements such as tremor may manifest at different frequencies and amplitudes such as the 6-Hz tremor of Parkinson disease (Fig. 13.19) or scratching near an electrode. During bipolar recording, extra adjacent electrodes placed on the suspected limb are helpful to confirm tremor artifact but they may be readily apparent in the EKG lead. Sudden or rapid patient movements such as shivering (Fig. 13.20) can mimic the paroxysmal quality of an electrographic seizure, but usually do not show progression. Additional artifact that leads to regular movement of the head or body from large pulses through the aorta or ballistocardiographic artifact gives rise to delayed pulses that can appear more generalized but still linked to the EKG (14). During electrocerebral inactivity recordings at sensitivities of 2 µV/mm, ballistocardiographic artifact and pulse artifact may be more prominent with small scalp arteries causing repetitive movements of electrodes. Stabilizing the head with towels under the neck often eliminates this artifact. Artifact due to respiration is also generated by the movement of the body or the head (Fig. 13.21). This can be seen during hyperventilation over posterior head regions. A technologist can observe the breathing and annotate the recording to indicate where inhalation and exhalation occur (11). In the epilepsy monitoring unit (EMU), the technologist is away from the patient but continuous video and the ability to transmit and display the time-locked behavior with EEG usually leads to accurate interpretation. Technical guidelines for recording in the EMU have been developed by the American Clinical Neurophysiology Society (15). For further discussion, see Chapter 37. Long-term monitoring provides a greater likelihood of deterioration of the patient-electrode interface with drying out of the electrolytic gel or nonadherence of the electrodes to promote artifact that may override interpretation during behavioral events. In the EMU, approximately 20% to 25% of patients with episodes will be manifesting psychogenic nonepileptic attacks (PNEA) (16). These are described in more detail in Chapter 33. The importance of recognizing behavioral sources in addition to historic information is crucial to recognizing nonepileptic events especially if there is “pseudo-evolution” simulating an ictal recording (Fig. 13.22) (4).