Evoked Potentials

An evoked potential is the nervous system's electrical answer to a question you ask it repeatedly. Apply the same stimulus — a flickering checkerboard, a click in the ear, a tap of current to a nerve — hundreds of times, average the recorded responses, and the random background noise cancels out while the tiny, time-locked signal emerges. What you are left with is a reproducible waveform whose timing tells you how fast a specific pathway is conducting. Because demyelination slows conduction long before it abolishes it, evoked potentials are exquisitely sensitive to a delay you cannot see on examination — they can expose a lesion that is completely silent at the bedside. Beyond diagnosis, they earn their keep in the operating room, where they warn the surgeon when a pathway is in danger, and in the intensive care unit, where they help forecast recovery after catastrophic brain injury.

The unifying idea: averaging reveals a hidden signal

The voltages generated by a sensory pathway are a fraction of the size of the ongoing EEG and muscle artifact that bury them. The trick is that the evoked response is time-locked to the stimulus — it appears at the same latency after every stimulus — whereas the noise is random. Averaging many trials therefore reinforces the response and washes out the noise. Two features of the resulting waveform carry the clinical information:

• Latency — the time from stimulus to peak. A prolonged latency is the hallmark of slowed conduction, classically demyelination. This is the most clinically useful measurement.
• Amplitude — the size of the response. Reduced or absent amplitude suggests axonal loss or conduction block along the pathway.
• The common theme: evoked potentials quantify conduction along one defined pathway and can reveal a clinically silent lesion within it.

Visual evoked potentials (VEP): the optic nerve interrogated

The standard VEP uses a pattern-reversal checkerboard: a screen of black-and-white checks that swap colors several times per second while the patient fixates. Responses are recorded over the occiput. The waveform that matters is the P100 — a large positive peak occurring at roughly 100 milliseconds.

• What a delayed P100 means: a prolonged P100 latency indicates slowed conduction in the optic nerve and anterior visual pathway — the signature of demyelination.
• Optic neuritis: after an attack, the P100 is characteristically delayed, and — importantly — the latency often remains prolonged even after vision has clinically recovered. The eye sees normally; the nerve still conducts slowly.
• Multiple sclerosis: a delayed P100 is one of the most useful electrophysiologic findings, capable of documenting prior anterior visual pathway demyelination the patient may never have noticed.

Brainstem auditory evoked potentials (BAEP / BAER): a map of the brainstem

Repetitive clicks delivered to the ear generate a sequence of small waves, conventionally numbered I through V, each reflecting a successive relay in the auditory pathway as the signal climbs through the brainstem. The generators are reasonably well localized, which is what makes the BAEP a topographic tool:

• Wave I — distal cochlear nerve (CN VIII)
• Wave II — proximal CN VIII / cochlear nucleus
• Wave III — superior olivary complex (lower pons)
• Wave IV — lateral lemniscus
• Wave V — inferior colliculus (midbrain)

Clinically, the BAEP is used to assess the auditory nerve and brainstem in suspected vestibular schwannoma (acoustic neuroma), to test brainstem integrity in comatose patients, and as a tool in multiple sclerosis evaluation. Historically it was offered as supportive data in brain-death evaluation, but the 2023 AAN/AAP/CNS/SCCM consensus guideline lists auditory and somatosensory evoked potentials as unacceptable ancillary tests for brain death / death by neurologic criteria — so this is no longer a current US use.

Somatosensory evoked potentials (SSEP): from nerve to cortex

Stimulating a peripheral nerve — most often the median nerve at the wrist or the posterior tibial nerve at the ankle — sends a volley up the large-fiber sensory pathway. Recording electrodes placed sequentially over the plexus, spinal cord, and scalp capture the signal as it ascends through the dorsal columns and on to the somatosensory cortex. For median nerve stimulation, the key cortical response is the N20.

• Intraoperative monitoring: SSEPs continuously check the dorsal-column / spinal-cord pathway during spine surgery and procedures that threaten cord perfusion such as thoracoabdominal aortic surgery. A drop in amplitude or rise in latency warns the surgeon to act before injury becomes permanent.
• Prognosis after cardiac arrest: in a comatose post-arrest patient, bilaterally absent cortical N20 responses are a robust predictor of poor neurologic outcome and are a recognized component of multimodal prognostication.

Motor evoked potentials (MEP): the corticospinal counterpart

Where SSEPs test the ascending sensory pathway, motor evoked potentials test the descending one. Transcranial magnetic stimulation of the motor cortex elicits a response recorded from a target muscle, allowing assessment of corticospinal (central motor) conduction. Intraoperatively, MEPs complement SSEPs by monitoring the motor tracts directly — useful because the cord's sensory and motor pathways can be injured independently.

Comparison at a glance