The cornea is positively charged relative to the retina, with a voltage difference between 50 and 100 microvolts. This can result in a detectable electrical field with eye movements, including blinking. The electrical artifacts created by eye movements are generally better seen on anterior electrodes, due to the proximity of those electrodes to the eye. Blinking is associated with a brief upward movement of the cornea (known as Bell’s phenomenon.) This movement creates a positive (downward) symmetric deflection on the EEG that is most prominent in the frontal polar electrodes. Rapid blinking (often referred to as “eyelid fluttering”) can produce rhythmic activity in the anterior electrodes. The frequency of the artifact depends largely on the frequency of eyelid flutter. Slower 2–3 Hz eyelid flutter can resemble frontally predominant rhythmic delta activity, although it tends to be less uniform in size and appearance than most frontally predominant cerebral rhythmic delta activity (Fig. 4). Faster 6–13 Hz eyelid flutter can produce rhythmic activity that resembles an ictal pattern. If there is a clinical concern for eyelid flutter artifact, the use of electrooculogram recordings from the left and right outer canthus can aid in the identification of this artifact. Additionally, artifacts related to eyelid flutter can be distinguished from electrocerebral activity by close observation of the patient’s eyelids. If eyelid flutter or blinking artifacts are extremely disruptive to interpretation of the underlying EEG, the patient’s eyelids can be taped closed, but this is rarely necessary.

Both horizontal and vertical eye movements can also give rise to artifacts on the EEG. Lateral eye movements are often preceded by a less than 50 millisecond “lateral rectus spike” related to activation of the lateral rectus muscle with eye abduction. These low-voltage waveforms are typically more prominent in F7 and F8. They are typically followed by a slow potential related to eye movement. Dysconjugate gaze, brainstem injury, and cranial nerve palsies, which may be seen in ICU patients with neurologic injuries, can result in either unilateral or asymmetric artifacts from eye movement.

In addition, many ICU patients receive medications or have brainstem or cerebellar injuries that give rise to nystagmus. This artifact often has a “sawtooth” appearance related to the fast and slow components of the nystagmoid eye movements. In patients with horizontal nystagmus, the artifact is typically more prominent on the side of the fast movement, and a phase reversal may be seen at F7 or F8. In patients with vertical nystagmus, the artifact is usually most prominent in the frontal polar electrodes (Fig. 5).

The electroretinogram (ERG) potential is a potential seen at the frontal polar electrodes in response to sudden, flashing light stimulus. In the outpatient setting, this is commonly seen with photic stimulation. However, in the ICU setting, this can occasionally be seen on low-voltage EEGs when a flashlight is used to assess pupil reactivity. In patients who are being evaluated for electrocerebral inactivity (ECI), the presence of an ERG potential should not exclude the diagnosis of ECI.

Patients in the ICU are prone to a wide variety of abnormal movements including tremors, clonus, myoclonus, rigors, shivering, posturing, and other types of hypermotor activity. Many of these movements have a relatively stereotyped appearance on EEG. Tremors can produce a rhythmic, spiky appearing artifact that corresponds to the frequency of the tremor (commonly between 4 and 12 Hz for conditions such as essential tremor, cerebellar tremor, or Parkinsonian tremor). Artifacts related to tremor typically generate nonphysiologic phase reversals; tremor artifacts are often more prominent in ECG leads than they are in EEG leads (Fig. 6).

Myoclonus also produces an extremely brief, spiky appearing potential. This can be challenging to distinguish from epileptic spikes at a normal paper speed of 30 mm/s. However, by changing the paper speed to 60 or 120 mm/s, it becomes easier to see that these seemingly epileptic spikes demonstrate nonphysiologic phase reversals (Fig. 7). In some instances, myoclonic artifact can be caused by epileptic activity, which can make it particularly challenging to distinguish between electrocerebral activity and artifacts. Under those circumstances, it may be necessary to use neuromuscular blocking agents to better assess the underlying EEG activity.

In addition to patient movements, movements by nursing staff, EEG technologists, and physicians can generate artifacts. Suctioning the patient can create a rhythmic low-voltage artifact in the delta range; the artifact is often frontally predominant (Fig. 8). Rubbing a patient’s sternum can create a slightly faster 3–7 Hz, high-voltage artifact with irregular waveforms (Fig. 9). The waveforms can be diffuse or focal, depending on patient positioning.