(from Jameson & Sloan, Anes. Clin.,
SomatoSensory Evoked Potentials (SSEPs or SEPs)
Sensory (visual, auditory, tactile, or position) stimuli activate afferent nerves
that synapse in the spinal cord or brainstem and ultimately arrive in the contralateral area of the designated cerebral cortex.
Sensory evoked potential monitoring provides a standard stimulus with recording of the electrical neuronal response over the appropriate area of sensory cortex.
The most commonly used sensory tests are somatosensory evoked potentials (SSEPs or SEPs) electrical stimulation of a mixed motor/sensory nerve, and brainstem auditory evoked potentials (BAEPs), standard sound stimulation of the cochlear (VIII) nerve.
Visual evoked potentials are not commonly performed due to difficulties in obtaining reliable responses.
Motor Evoked potentials (MEPs)
Motor evoked potentials (MEPs) do not involve areas of sensory cortex but are produced by the electrical stimulation of the
motor cortex and measurement of the electromyoqraphic response (EMG) in skeletal muscle, usually abductor pollicis brevis (APB), tibialis anterior (TA), medial gastrocnemius (MG), and interphalangeal foot muscles,
It is common practice to record EMG responses in arms, APB, and two or more locations in the lower extremities, TA or MG and foot.
Stimulus and Analysis
For SEP and BAEP the stimulus/response cycle is repeated and averaged between 150 and 1,000 times to allow identification of the response.
The MEP response is a single skeletal muscle response produced by four to six stimuli.
All waveforms are analyzed for latency (time from stimulus to peak response), amplitude (absolute difference between negative and positive wave deflection), and configuration or shape.
Waveform changes that are considered to indicate possible functional change are a 50% decrease in amplitude or a 30% increase in latency.
Pathologic changes in shape, amplitude, and latency are caused by tissue ischemia in the nerve, spinal cord, brainstem, or subcortical or cortical neural structures.
Sources of tissue ischemia include:
• hypoperfusion from systemic or local hypotension
• blood vessel damage
• local compression of tissue and vessels with retraction
• stretching of nerve, spinal cord, or brain stem
• decreased blood flow
• inadequate oxygen-carrying capacity (anemia)
• local or systemic hypothermia (vasoconstriction)
Effects of Anesthetic Agents:
Anesthetic agents produce varying degrees of change in the evoked
• Increasing concentrations of volatile anesthetics produce a dose-dependent decrease in amplitude and increase in latency.
• Nitrous oxide effect can range from none to substantial decreases in amplitude and increases in latency.
• Opioids have little effect on evoked potentials.
• Hypnotic intravenous drugs such as propofol and dexmedetomidine also have little effect.
• Ketamine can cause increases in the amplitude but has little effect on the latency.
For intraoperative evoked potential monitoring to be effective, the anesthetic protocols must be designed to minimize the drug effect on the evoked potential response. Low stable concentrations of volatile anesthetics with intravenous hypnotic agents or just intravenous hypnotic agents alone are usually advocated. Supplementation with low-dose ketamine infusion will often increase the waveform amplitude making it easier to identify changes due to surgical manipulation, particularly in patients with significant underlying abnormalities. Since minimal concentrations of volatile anesthetics and nitrous oxide can make it impossible to obtain an MEP, intravenous techniques without muscle relaxants are used.
Recommended intraoperative monitoring tests and anesthetic management by surgical procedure are listed in Table 1.
A couple of reprints of good journal articles are available in the Library under "E" for Evoked Potentials .
Sloan (author) also has a good technical artticle on MEP in 2012.