▪ Eyeball acts as a dipole with positive polarity of 100 mV at the cornea with respect to the retina.
▪ Bell’s phenomenon (upward eye deviation during eye closure) causes positive electrical activity at Fp1 and Fp2.
▪ Lateral eye movement causes positivity to the side of which gaze is directed to (either F7 or F8).
▪ Oblique eye movement is more difficult and can be misinterpreted as a focal abnormality.
▪ Courses of asymmetric eye movements include:
▸ Decreased movement of one eye or eyelid
▸ Absence of an eye or retina
▸ Asymmetric electrode placement
▸ Frontal skull defect
▪ With lateral eye movements, the eyes are moving to the side where positivity is noted. This is caused by the positivity of the cornea (100 mV positive compared to retina) coming closer to the F7 or F8 electrodes making positive the one toward which the eyes are moving.
▪ Asymmetric waves with steeper rise than fall.
▪ REM stage in healthy children does not occur within the first cycle but after one complete cycle (stage 1 to 4 and then back from 4 to 1), usually 90 minutes after sleep onset. If REM sleep appears near the onset of sleep (early REM), narcolepsy must be considered. However, early REM can be seen in individuals withdrawing from CNS depressants such as barbiturates or alcohol.
Figure 2-1.
Early Rapid Eye Movement (REM); Narcolepsy. A 15-year-old girl with recurrent episodes of daytime drowsiness and brief paralysis precipitated by laughing. Routine EEG shows frequent REM occurring around 15 minutes into the recording. Subsequent sleep study (MSLT) confirmed the diagnosis of narcolepsy.
With lateral eye movements, the eyes are moving to the side where positivity is noted caused by the positivity of the cornea coming closer to the F7 or F8 electrode, making one of them positive, the one toward which the eyes are moving. If the eyes are moving to the left, then the positivity on the cornea is directed to the left side (F7), making F7 a positive polarity (double-head arrows) and F8 a negative polarity. If the eyes are moving to the right, the opposite effect is noted at F7 and F8 (asterisk).
REM stage in healthy children does not occur within the first cycle but after one complete cycle (stage 1 to 4 and then back from 4 to 1), usually 90 minutes after sleep onset. If REM sleep appears near the onset of sleep (early REM), narcolepsy or withdrawing from CNS depressants such as barbiturates or alcohol must be considered.1
▪ SEM is a sign of drowsiness in older children and adults.
▪ Opposite polarity of slowing (<1 Hz) in the left and right fronto-temporal regions (F7 and F8) associated with other signs of drowsiness including:
▸ Alpha dropout (earliest sign)
▸ Increased beta activity over the fronto-central regions
▸ Diffuse rhythmic theta activity with anterior predominance
Figure 2-2.
Slow Eye Movement (SEM); Drowsiness. EEG of a 10-year-old girl during drowsiness shows slow (roving) eye movement. With lateral eye movements, the positively charged cornea comes closer to either the F7 or F8 electrode, making the one toward which the eyes are moving more positive. If the eyes are moving to the left, then the positivity on the cornea is directed to the left side (F7 electrode), making F7 a positive polarity (pen separation) (double-head arrows) and F8 a negative polarity (pen coming together). If the eyes are moving to the right, the opposite effect is noted at F7 and F8 (asterisk). SEM is a sign of drowsiness in older children.
(Figures 2-3 to 2-6)
▪ Horizontal nystagmus normally occurs bilaterally, but it is often only recorded unilaterally at either F7 or F8 on the side of the direction of the fast nystagmus due to larger positive voltage generated by the proximity of the cornea to that electrode.
▪ Vertical and rotatory nystagmus are rarely detected at the Fp1 and Fp2 due to the low voltage.
Figure 2-3.
Eye Movement Artifact (Nystagmus); Holoprosencephaly. An 8-year-old boy, who developed constant horizontal nystagmus, with congenital hydranencephaly and microcephaly with severe global developmental delay. EEG shows flattening of the background activity with rapid lateral eye movements characterized by “out-of-phase” potentials between F7 and F8.
The cornea produces a potential of approximately 50–100 mV. When the eye moves to the left, the cornea comes closer to the F7 electrode, causing a positive phase reversal with maximal positive potential at the F7 electrode, and a negative phase reversal with maximal negative potential recorded at the F8 electrode (open arrow).2
This EEG supported that the nystagmus in this patient was nonepileptic. Ophthalmic findings in hydranencephaly include pupillary abnormalities, strabismus, nystagmus, ptosis, optic nerve hypoplasia, chorioretinitis, retinal vessel attenuation, and incomplete anterior chamber cleavage.3
Figure 2-4.
Eye Movement Artifact (Horizontal Nystagmus and Eye Closure). Another example of horizontal nystagmus. Cornea produces a potential of approximately 50–100 mV. When the eye moves to the left, the cornea comes closer to the F7 electrode, causing a positive phase reversal with maximal positive potential at the F7 electrode, and a negative phase reversal with maximal negative potential recorded at the F8 electrode (double-head arrow).
When the eyes are closed (open arrow), the eyeballs are in a neutral position (Bell’s phenomenon), and this upward eye movement is detected by a maximal positive potential recorded at the Fp1 and Fp2 electrodes with a falloff potential recorded at the next electrodes (F3 and F4). These cause downward deflections of EEG at Fp1-F3 and Fp2-F4 channels. When the eyeball moves in a downward direction, the inverse occurs.
Figure 2-5.
Eye Movement Artifact (Nystagmus). Constant horizontal nystagmus. EEG shows flattening of the background activity with rapid lateral eye movements characterized by “out-of-phase” potentials between F7 and F8.
The cornea produces a potential of approximately 50–100 mV. When the eye moves to the left, the cornea comes closer to the F7 electrode, causing a positive phase reversal with maximal positive potential at the F7 electrode, and a negative phase reversal with maximal negative potential recorded at the F8 electrode.2
Figure 2-6.
Eye Movement Artifact (Nystagmus). Horizontal nystagmus with fast component to the left side. Horizontal nystagmus normally occurs bilaterally, but it is often only recorded unilaterally at either F7 or F8 on the side of the direction of the fast nystagmus due to a larger positive voltage generated by the proximity of the cornea to that electrode.2
▪ Low-voltage (<50 mV) response to light stimulus of the retina.
▪ Synchrony with the flashes of light.
▪ Most commonly seen in, but does not invalidate, the diagnosis of brain death.
▪ The artifact disappears over the blocked eye with an opaque card.
▪ Consists of two peaks.
▪ Amplitude of ERG is usually low and obscured by normal EEG activity in Fp1 and Fp2
▪ ERG can be confused with an electrode artifact generated by the exposed silver metal of chipped EEG electrode during photic stimulation (photocell artifact).
▪ These physiological and artifactual potentials can be differentiated by using high photic stimulus frequencies. With 30-Hz photic stimulus frequency, amplitude of ERG diminishes while amplitude of electrode artifact is constant.
Figure 2-7.
Electroretinogram (ERG). Amplitude of ERG is usually low and obscured by normal EEG activity in Fp1 and Fp2. ERG can be confused with an electrode artifact generated by an exposed silver metal of chipped EEG electrode during photic stimulation. These physiological and artifactual potentials can be differentiated by using high photic stimulus frequency. With 30-Hz photic stimulus frequency, the amplitude of ERG diminishes while the amplitude of electrode artifact is constant.
(Figures 2-8 to 2-10)
▪ EEG shows biphasic sharp theta activity in bilateral prefrontal regions that simulate frontal sharp transients.
▪ Eye lead channels can differentiate between cerebral activity and eye movement artifact. When activity points to the different directions (out-of-phase), it indicates that it is eye movement artifact rather than cerebral activity.
▪ When the dipole axis of the EEG generator is oriented perpendicular to the skull defect, the defect usually increases the EEG voltage as seen in the breach rhythm. On the other hand, when the dipole axis of the EEG generator is parallel to the skull defect, as seen in the eye movement, the skull defect decreases the EEG voltage.
Figure 2-8.
Eye Movement Artifact. A 38-week CA infant with apnea. EEG shows biphasic sharp theta activity in bilateral prefrontal regions, which simulate frontal sharp transients. Eye lead channels can differentiate between these two conditions. When activity points to different directions as in this EEG, it indicates that this is eye movement artifact rather than brain waves.
Figure 2-9.
Skull Defect; Effect on Eye Blinking Artifact. A 17-year-old boy with a skull defect in the right frontal region. EEG shows asymmetric eye blinking artifact (asterisk) with lower voltage in the right prefrontal region and breach rhythm over the right hemisphere, especially parasagittal region.
When the dipole axis of the EEG generator is oriented perpendicular to the skull defect, the defect usually increases the EEG voltage as seen in the breach rhythm. On the other hand, when the dipole axis of the EEG generator is parallel to the skull defect, as seen in the eye movement, the skull defect decreases the EEG voltage.4
Figure 2-10.
3-Hertz Spike-and Wave Discharges in Absence Epilepsy. EEG shows rhythmic 3- to 4-Hz spike-and-wave discharges in the anterior head region simulating eye blink artifact. Widely distributed activity, not limited to only F3 or F4, helps to distinguish these two wave forms. Eye lead recording showing in-phase activity supports 3-Hz spike-and-wave discharges.
(Figures 2-11 and 2-14)
▪ Occurs in 0.1% of normal population and 1% of patients with epilepsy.
▪ Most prominent in the frontal regions as a result of orbicularis oculi and frontalis muscle twitching during eye closure. Stops with flash.
▪ Immediate cessation of the response at the end of stimulation and prominent electromyographic activity help to distinguish this photomyoclonic response from photoparoxysmal response.
▪ Photomyoclonic response is considered a normal variant, although it can coexist with photoparoxysmal response or rarely progress to GTCS.
Figure 2-11.
Eye Fluttering During Photic Stimulation. A 9-year-old girl with well-controlled idiopathic generalized epilepsy. EEG shows spikes of muscle origin time-locked to the flash stimuli, which is confined exclusively to the prefrontal electrodes (Fp1, Fp2). This so-called “photomyoclonic response” occurs in 0.1% of normal population and 1% of patients with epilepsy. It is most prominent in the frontal regions as a result of orbicularis oculi and frontalis muscle twitching during eye closure and stops with flash. Immediate cessation of the response at the end of stimulation and prominent electromyographic activity help to distinguish this photomyoclonic response from photoparoxysmal response. Photomyoclonic response is considered a normal variant, although it can coexist with photoparoxysmal response or rarely progress to GTCS.
In this case, the involvement was limited to only frontalis and orbicularis oculi and did not involve temporalis muscles.
Figure 2-12.
Eye Flutter. Eyelid flutter is usually associated with a rhythmic 5–8 Hz activity at Fp1 and Fp2 with or without falloff of the voltage detected at F3, F4, or Fz because of the low voltage of the flutter.
Eye lead electrodes help to distinguish this artifact from intermittent rhythmic slow activity by showing out-of-phase potentials.
Figure 2-13.
Eye Flutter During Photic Stimulation. Eye flutter in the alpha frequency range without falloff of the voltage detected at F3, F4, or Fz due to low voltage of the flutter can be seen during photic stimulation. Alpha frequency activity restricted to the frontopolar electrodes is eye movement (flutter) artifact until proven otherwise.
Figure 2-14.
Eye Fluttering During Photic Stimulation. An 8-year-old girl with recurrent headaches and numbness of arms. EEG shows spikes of muscle origin time-locked to the flash stimuli, which is confined exclusively to the prefrontal electrodes (Fp1, Fp2). This so-called “photomyoclonic response” occurs in 0.1% of normal population and 1% of patients with epilepsy. They are most prominent in the frontal regions as a result of orbicularis oculi and frontalis muscle twitching during eye closure and stops with flash. Immediate cessation of the response at the end of stimulation and prominent electromyographic activity help to distinguish this photomyoclonic response from photoparoxysmal response. Photomyoclonic response is considered a normal variant, although it can coexist with photoparoxysmal response or rarely progress to GTCS. In this case, the involvement was limited to only frontalis and orbicularis oculi and did not involve temporalis muscles.
Figure 2-15.
Lateral Rectus Spikes. A lateral rectus spike (open arrows) is a single motor unit potential, best seen in frontal electrodes during lateral eye movement. It is characterized by a short-duration spike overriding a slow wave resulting from rapid lateral eye movement. Immediately after the lateral rectus spike (open arrows), a leftward lateral eye movement is noted. As the cornea has a positive electrical potential, it causes F7 to be positive with opposite polarity at F8.
Figure 2-16.
Lateral Rectus Spikes. A lateral rectus spike is a single motor unit potential, best seen in frontal electrodes during lateral eye movement. It is characterized by a short-duration spike overriding a slow wave resulting from rapid lateral eye movement. Eye lead channels (not shown) demonstrate eye movement time-locked with lateral rectus spikes.
(Figure 2-11 to 2-14)
▪ Associated with a rhythmic 5- to 8-Hz activity at Fp1 and Fp2 with or without falloff of the voltage detected at F3, F4, or Fz because of the low voltage of the flutter.
▪ Alpha frequency activity restricted to the frontopolar electrodes is eye movement (flutter) artifact until proven otherwise.
▪ Eye lead electrodes help to distinguish this artifact from intermittent rhythmic slow activity by showing out-of-phase potentials.
▪ More rapid, more rhythmic, and lower amplitude appearance than eye blink.
▪ When periocular muscle contractions accompany the eye movements, bifrontal liked may be noted.
▪ May be falsely diagnosed as focal frontal delta activity in prosthetic eye, 3rd nerve palsy, or unilateral eye movement artifact.
(Figures 2-17 and 2-18)
▪ Most prominent when the neck is short and wide.
▪ Diphasic is the most common wave form.
▪ Maximal in the temporal region, greater on the left side.
▪ Most obvious in referential montage.
▪ Dipole with A1 positive and A2 negative in referential montage run.
▪ Regularity and bilateral synchronous nature distinguish EKG artifact from PLEDs.
▪ Location distinguishes EKG artifact (temporal) from GPEDs (bifrontal).
▪ Irregular heartbeats can be mistaken for cerebral activity.
Figure 2-17.
Electrocerebral Inactivity (ECI); Severe Hypoxic Ischemic Encephalopathy (HIE) with Central Herniation Synodrome. A 4-day-old girl who was born full term with Apgar scores of 0, 3, 3, and 5. Cord arterial gas was 6.91/66/-20. Initial venous blood gas 7.15/13/123/9/-22. She had a seizure described as tonic posturing. She was placed in a head-cooling device. She developed another clinical seizure with rhythmic head twitching and tongue thrusting lasting 10 minutes. She received treatment with phenobarbital and levetriacetam. No EEG was performed until the fourth day of life.
MRI performed at the fourth day of life shows severe global abnormality involving cerebellum, brainstem, thalamus, basal ganglia, deep white matter, and cortical gray matter. DWI MRI shows markedly increased signal intensity that suggests severe injury with liquefaction. Cardiorespiratory support was withdrawn 1 day after the EEG. EEG shows no cerebral activity (potentials > 2 μV when reviewed at a sensitivity of 2 μV/mm) consistent with electrocerebral inactivity (ECI). EKG artifact was noted with a dipole between A1 and A2. Although A1 is usually positive and A2 is usually negative, the opposite is noted in this EEG.5
ECI is indicative of death only of the cortex, not the brainstem; therefore, a newborn can have prolonged survival despite having an EEG of ECI.6
(Figures 2-19 and 2-20)
▪ Mechanical movement caused by pulsation artifact that occurs when an EEG electrode is placed over the pulsating blood vessel.
▪ The mechanical movement caused by pulsation of an artery can cause a rhythmic smooth or sharply contoured slow wave (sawtooth) that sometimes simulates EEG activity.
▪ Time-locked with the EKG but is delayed by approximately 200 msec after the R wave, because the pulse requires time to travel from the heart to the blood vessel.
▪ Occurs in any lead but most commonly at frontal and temporal regions, and less commonly over the occipital region.
▪ Identified by touching the electrode generating it. If the patient is lying on the involved electrode, the artifact sometimes may be eliminated by moving the head slightly.
▪ Relocation of electrode may eliminate the artifact.
Figure 2-19.
Pulse Artifact; Electrocerebral Inactivity (ECI). Pulse artifact (open arrow) is caused by mechanical movement resulting from pulsation artifact that occurs when an EEG electrode is placed over the pulsating blood vessel. The mechanical movement caused by pulsation of an artery can cause a rhythmic smooth or sharply contoured slow wave (sawtooth) that sometimes simulates EEG activity. Pulse artifact is time-locked with the EKG but is slightly delayed by approximately 200 msec, since the pulse requires time to travel from the heart to the blood vessel. Pulse artifact can occur in any lead but most commonly in frontal and temporal regions, and less commonly over the occipital region. Pulse artifact can be identified by touching the electrode generating it. If the patient is lying on the involved electrode, the artifact sometimes may be eliminated by moving the head slightly. Relocation of electrode may eliminate the artifact.5,7,8
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