Somatosensory Evoked Potentials

Function

Somatosensory information gets relayed within the spinal cord via two main pathways: the dorsal column-lemniscal system and the spinothalamic system.[2] SEPs monitor the dorsal column-lemniscal system, which transmits mechanoreception and proprioception; they do not monitor the spinothalamic tracts.[2][3] SEPs have been used as surrogates of motor pathway function, though they are not as sensitive or specific for this purpose as motor evoked potential (MEP) monitoring.[4] Recommended use of SEPs for intraoperative monitoring include them as part of a multimodal approach; they are generally not the sole method employed.[1]

The pathway, from the periphery to the cerebral cortex, that a sensory stimulus takes through the dorsal column-lemniscal system is as follows: detection of the stimulus occurs via peripheral nerve terminals in the skin, joints, etc. These terminals are part of primary afferent nerves which travel from the periphery, through the dorsal horn of the spinal cord, and project to second-order neurons within the dorsal column nuclei in the brainstem.[2] The second order neurons decussate after leaving the dorsal column nuclei and project to third order neurons in the ventral posterior nucleus of the thalamus.[2] Third order neurons from the thalamus project to the somatosensory cortex and various other areas involved in sensory processing.[2]

Typically SEPs are recorded from an upper or lower extremity nerve, pending surgical location. Electrodes are placed at multiple sites along the sensory pathway and correspond with different aspects of that pathway (see description above) [2]. The evoked potentials transmit from the electrodes placed along the sensory pathway to the cortex, where the waveform is recorded. For example, when recording median nerve SEPs, electrodes may be placed at Erb's point, with its waveform representing peripheral components, over the cervical spine to reflect subcortical components, and over multiple areas of the scalp to capture parietal and frontal cortical components.[2] Tibial nerve SEPs get recorded similarly, with electrodes placed at locations to capture various spots along the sensory pathway. 

When reviewing SEP recordings, it is crucial to understand how they get reported and to have a knowledge of the anatomic origin of commonly used recordings. A SEP waveform reports as N or P followed by a number; N or P corresponds to "negative" or "positive" (the wave polarity) and the number represents the expected latency of the wave in milliseconds, determined from a healthy population.[2] Each spot monitored along a sensory pathway has a typical recording value; for example, an electrode placed at Erb's point during median nerve monitoring would have a value of N9 in a healthy patient.[2] Alternatively, SEP values can be used to infer the placement of the monitoring electrode and the underlying neurologic structure represented by that value.[2] To use the previous example, a SEP of N9 represents monitoring of the median nerve, specifically at/near Erb's point, which is where the brachial plexus component of the sensory pathway along the median nerve is best assessed.[2]

Following are summaries of commonly used nerves/pathways for SEP monitoring, along with their specific points of monitoring, corresponding waveform values, and what portion of the sensory pathway they reflect[2]:

• Median nerve SEPs: Erb's point (N9, peripheral nerves-brachial plexus), cervical spine (N13, the post-synaptic dorsal horn of the cervical spinal cord), scalp/parietal and frontal cortices (P14, cervico-medullary junction, and N20, primary somatosensory cortex)
• Tibial nerve SEPs: popliteal fossa (N8, peripheral nerves-tibial nerve, sciatic nerve), lumbar spine (N22, the post-synaptic dorsal horn of the lumbar spinal cord), scalp/cortex (P39, somatosensory cortex)

Issues of Concern

Though minimal class I evidence is available to support the use of SEPs or any form of intraoperative neuromonitoring, the use of such monitoring techniques has been shown to improve outcomes after surgeries that could lead to neurologic impairment.[1] Evidence suggests that employing neuromonitoring intraoperatively, which is the most common use of SEPs, can help avoid neurologic deficits after surgery.[5] The lack of class I evidence has likely contributed to a dearth of guidelines dictating the use of intraoperative neuromonitoring, though it is routine practice in neurosurgery and relevant vascular surgeries where neurologic structures may be at risk.[3] The likelihood is that the use of SEPs will most frequently be in combination with other neuromonitoring methods, such as motor evoked potentials.

During intraoperative monitoring, baseline SEP waveforms should be recorded for the patient. Then, the surgeon, anesthesia provider, and other surgical team members should be alerted if there are critical changes in the waveform. "Critical changes" include a decrease in the wave's amplitude by 50% or higher, and/or an increase in the waveform's latency by 10% or more.[4] The amplitude of a SEP waveform reflects intact axons within the neural pathway; when the amplitude decreases, there is a concern that axons are being compromised or functionally lost.[5] During surgery, there are multiple possible causes of decreased amplitude and/or increased latency of a waveform. These include medications, decreased blood flow, changes in blood pressure, changes in temperature, retraction, local pressure, cautery, and operative techniques such as surgical dissection.[4]

SEPs are less reliable and helpful in patients with preexisting damage to the spinal cord or the nerve(s) subject to monitoring.[5] In these patients, the current opinion is that their neurologic status prior to surgery more closely links to postop outcomes.[1] On occasion, a change in SEP can correlate with a specific temporal event, such as placing a pedicle screw into the spinal cord or a sudden drop in blood pressure. Rectifying the underlying cause in a timely fashion will often restore signal and perhaps prevent long term or permanent neurological injury. 

Clinical Significance

SEP monitoring is employed intraoperatively to identify, and ideally, avoid impending permanent damage to neurologic structures. SEP waveforms change in response to many different factors, some of which can cause permanent damage.

Anesthetic agents have varying effects on SEPs, which should be kept in mind by anesthesia providers. The anesthetic plan for intraoperative neuromonitoring should be one that will interfere the least with the consistency of recorded waveforms.[6] The following is a summary of the effects of common anesthetics on SEPs:

• Volatile anesthetics cause a dose-dependent decrease in SEP amplitude and an increase in latency.[7] If used during intraoperative neuromonitoring, maintaining MAC less than 0.5 is advisable, though permissive use of higher MAC values may be acceptable with sevoflurane and desflurane.[6] Nitrous oxide alone decreases SEP amplitude while having little effect on latency. However, nitrous oxide potentiates the effects of almost all anesthetics on SEPs, including other inhaled agents.[6][8]
• Barbiturates decrease the amplitude and increase the latency of SEPs, though they do not prevent SEPs from being recorded.[6]
• Benzodiazepines have a variable, but in general, mild effects on SEPs. They cause decreases in amplitude and increases in latency.[6]
• Opioids do not cause significant changes in SEPs, though small reductions in amplitude and increases in latency can present.[6] This scenario is more common when giving opioids as a bolus rather than as a continuous infusion.[6]
• Propofol can increase SEP latency and decrease amplitude, though these changes stabilize over time and do not preclude SEPs from being recorded.[6]
• Etomidate has varying effects on SEPs depending on the site of generation; it causes the increased amplitude of cortical SEPs but decreased amplitude in subcortical SEPs.[6][9] It can be used to increase cortical SEP amplitudes during surgery to better detect changes.[6]
• Ketamine, similar to etomidate, increases the amplitude of cortical SEPs.[6][8] It has not been found to affect latency or subcortical SEP amplitude.[6][8]
• Alpha-2 agonists such as clonidine and dexmedetomidine do not affect SEPs and are considered good agents to use when intraoperative neuromonitoring is needed.[6][10]
• Neuromuscular blocking agents have no direct effect on SEPs.[6]

Generally, an inferred total intravenous anesthetic (TIVA) is desirable when using SEPs intraoperatively when reviewing the above effects of various anesthetics on SEPs, which are most changed by inhaled agents. If TIVA is the chosen anesthetic plan, additional monitoring to assess the depth of anesthesia could be a consideration.

Many surgical factors can alter SEPs, though the most time-sensitive of these are ischemia, surgical manipulation of structures, cautery, and dissection. Ischemia could result from pressure, retraction, clipped vessels, etc.[11] Manipulating structures and dissecting in certain areas may compromise neurologic structures and/or tracts, leading to a loss or distortion of evoked potential signals that, if not corrected, could result in permanent neurologic deficits. Cautery, if used too liberally, could compromise blood flow and/or directly injure a nerve or spinal tract.

Various physiologic parameters influence SEPs. Examples of these include hypothermia, changes in PaCO2, decreases in PaO2, and decreases in arterial blood pressure. Hypothermia increases the latency of SEPs and has an inconsistent effect on SEP amplitude.[11] Decreases in PaCO2 primarily affect SEPs; for example, hypocapnia to PaCO2 values under 20 mmHg causes small decreases in SEP latency.[11] Hypercapnia does not have significant if any, effects on SEPs.[6] Progressive hypoxia to levels that can cause ischemia to neurologic tissues causes decreased SEP amplitude and increased latency, though changes are not apparent with mild decreases in PaO2.[6] Drops in mean arterial pressure (MAP) affect SEPs, primarily if MAP falls outside of the autoregulatory range and the involved neural tissue becomes ischemic.[6]

Management of critical SEP changes requires excellent communication amongst the surgical team and timely response to avoid any neurologic injuries. The anesthesia provider should review the patient's vital signs, paying close attention to MAP, SpO2, FiO2, and temperature. They should also review the medications the patient has received and any recent changes to the anesthetic management that may contribute to the SEP changes. The surgeon should pause and review the surgical site and any recent changes to it; this could include newly placed clips on the vasculature, retractors, or overly-aggressive dissection close to a neural structure. Ideally, quick identification of the cause(s) of changes will lead to action to address the problem and the return of the SEP signal to baseline.

Enhancing Healthcare Team Outcomes

Intraoperative neuromonitoring, specifically somatosensory evoked potentials, provides a valuable method of identifying impending neurologic injury and avoiding it in vulnerable patients. The entire surgical team should be aware of and involved in the use of SEPs and their management, as this will lead to better patient outcomes. This collaboration includes clinicians, nursing, and surgical assistants. Although it is the anesthesia provider and surgeon's roles to address physiologic and/or physical changes that could cause SEP changes, the other members of the surgical team, including nurses, neurophysiologists, and technicians, should be aware of and able to assist in doing this, as it will ensure the best outcome for the patient. Nurses should feel comfortable in identify abnormalities and immediately report their findings to the clinicians. [Level V]

The available evidence supporting the use of SEPs is primarily level III, IV, and V evidence. There are very few randomized controlled trials focused on SEP use. However, SEPs have been in use for decades; thus, there is a wealth of historical data available to support their use and efficacy.