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72: Somatosensory-Evoked Potentials and Spinal Surgery

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CHAPTER 72 Somatosensory-Evoked Potentials and Spinal Surgery

Daniel J. Janik, MD [Colonel (Retired), USAF, MC]

1 What are somatosensory-evoked potentials?

Somatosensory-evoked potentials (SSEPs) are the electrophysiologic responses of the nervous system to the application of a discrete stimulus at a peripheral nerve anywhere in the body. They reflect the ability of a specific neural pathway to conduct an electrical signal from the periphery to the cerebral cortex.

2 How are somatosensory-evoked potentials generated?

Using a skin surface disc electrode or subcutaneous fine-needle electrode placed near a major peripheral mixed function (motor and sensory) nerve such as the median, a square-wave electrical stimulus of 0.2 to 2 ms is applied to the nerve at a rate of 1 to 2 Hz. The stimulus intensity is adjusted to produce minimal muscle contraction (usually 10 to 60 mA). The resulting electrical potential is recorded at various points along the neural pathway from the peripheral nerve to the cerebral cortex.

3 What major peripheral nerves are most commonly stimulated?

In the upper extremity the common sites of stimulation are the median and ulnar nerves at the wrist. In the lower extremity the common peroneal nerve at the popliteal fossa and the posterior tibial nerve at the ankle are used. Less commonly the tongue, trigeminal nerve, and pudendal nerve have been studied.

4 Trace the neurosensory pathway from the peripheral nerves to the cerebral cortex

The axons of the peripheral sensory nerves enter the spinal cord via the dorsal spinal roots. These first-order neurons continue rostrally in the ipsilateral posterior column of the spinal cord until they synapse with nuclei at the cervicomedullary junction. Second-order neurons from these nuclei immediately decussate to the contralateral side of the brainstem, where they continue their ascent via the medial lemniscus through the midbrain, synapsing in the thalamus. Third-order neurons then travel via the internal capsule to synapse in the postcentral gyrus, the primary somatosensory cortex.

5 At what points along the neurosensory pathway are somatosensory-evoked potentials most commonly recorded?

After upper limb stimulation, potentials are recorded at the brachial plexus (Erb’s point, 2 cm superior to the clavicular head of the sternocleidomastoid muscle), the cervicomedullary junction (posterior midline of the neck at the second cervical vertebra), and the scalp overlying the somatosensory cortex on the contralateral side.

After stimulation of the lower extremity, potentials are recorded at the popliteal fossa, lumbar and cervical spinal cord, and somatosensory cortex. It is important to record nerve and subcortical potentials to verify adequate stimulation and delineate anesthetic effects.

6 Describe the characteristics of the somatosensory-evoked potential waveform

The SSEP is plotted as a waveform of voltage vs. time. It is characterized by:

image Amplitude (A), which is measured in microvolts from baseline to peak or peak to peak
image Latency (L), which is the time, measured in milliseconds, from onset of stimulus to occurrence of a peak or the time from one peak to another
image Morphology, which is the overall shape of the waveform, described as positive (P, below the baseline) or negative (N, above the baseline)

A waveform is identified by the letter describing its deflection above or below the baseline followed by a number indicating its latency (e.g., N20) (Figure 72-1).

image

Figure 72-1 Characteristics of the somatosensory-evoked potential waveform.

7 Name several characteristic peaks important for the evaluation of somatosensory-evoked potentials

See Tables 72-1 and 72-2.

TABLE 72-1 Characteristic Peaks for Evaluation of Median Nerve Stimulation

Peak Generator
N9 Brachial plexus (Erb’s point)
N11 Dorsal root entry zone (cervical spine)
N13, 14 Posterior column (nucleus cuneatus)
P14 Medial lemniscus
N20 Somatosensory cortex

TABLE 72-2 Characteristic Peaks for Evaluation of Posterior Tibial Nerve Stimulation

Peak Generator
N20 Dorsal root entry zone (lumbar spine)
N40 Somatosensory cortex

8 What is the central somatosensory conduction time?

The central somatosensory conduction time is the latency between the dorsal column nuclei (N14) and the primary sensory cortex (N20) peaks and reflects nerve conduction time through the brainstem and cortex.

9 What are the indications for intraoperative use of somatosensory-evoked potential monitoring?

SSEP monitoring is indicated in any setting with the potential for mechanical or vascular compromise of the sensory pathways along the peripheral nerve, within the spinal canal, or within the brainstem or cerebral cortex. SSEP monitoring has been used in the following:

image Orthopedic procedures

image Correction of scoliosis with Harrington rod instrumentation
image Spinal cord decompression and stabilization after acute spinal cord injury
image Spinal fusion

image Brachial plexus exploration
image Neurosurgical procedures

image Resection of a spinal cord tumor or vascular lesion
image Tethered cord release
image Resection of a sensory cortex lesion (e.g., aneurysm or thalamic tumor)
image Carotid endarterectomy

image Vascular surgery

image Repair of a thoracic or abdominal aortic aneurysm

10 What constitutes a significant change in the somatosensory-evoked potential?

Any decrease in amplitude greater than 50% or increase in latency greater than 10% may indicate a disruption of the sensory nerve pathways. The spinal cord can tolerate ischemia for about 20 minutes before SSEPs are lost.

11 Summarize the effects of anesthetic agents on the amplitude and latency of somatosensory-evoked potentials

See Table 72-3.

TABLE 72-3 Effects of Anesthetic Agents on Amplitude and Latency of Somatosensory-Evoked Potentials

Drug Amplitude Latency
Premedication
Midazolam (0.3 mg/kg) ↓ 0
Diazepam (0.1 mg/kg) ↓ ↑
Induction agents
Thiopental (5 mg/kg) ↑/0 ↑
Etomidate (0.4 mg/kg) ↑↑↑ ↑
Propofol (0.5 mg/kg) 0 ↑
Ketamine (1 mg/kg) ↑ *
Opioids
Fentanyl   ↑
Sufentanil   ↑
Morphine   ↑
Meperidine ↑/↓ ↑
Inhaled anesthetics
Nitrous oxide ↓ ↑
Isoflurane ↓ ↑
Halothane ↓ ↑
Enflurane ↓ ↑
Desflurane ↓ ↑
Sevoflurane ↓ ↑
Others
Droperidol ↓ ↑
Muscle relaxants 0 0

↑, increase; ↓, decrease; 0, no change; *, not known.

12 What is the take-home message of the effects of anesthetic agents on somatosensory-evoked potentials?

image All of the halogenated inhaled anesthetics probably cause roughly equivalent dose-dependent decreases in amplitude and increases in latency that are further worsened by the addition of 60% nitrous oxide. It is best to restrict the use of volatile anesthetics and nitrous oxide to levels below 1 minimum alveolar concentration (MAC) and not to combine the two.
image If possible, bolus injections of drugs should be avoided, especially during critical stages of the surgery. Continuous infusions are preferable.

13 What other physiologic variables can alter somatosensory-evoked potentials?

image Temperature: Hypothermia increases latency, whereas amplitude is either decreased or unchanged. For each decrease of 1° C, latency is increased by 1 ms. Hyperthermia (4° C) decreases amplitude to 15% of the normothermic value.
image Hypotension: With a decrease of the mean arterial blood pressure (MAP <40 mm Hg), progressive decreases in amplitude are seen. The same change is also seen with a rapid decline in MAP to levels within the limits of cerebral autoregulation.
image Hypoxia: Decreased amplitude caused by hypoxia has been reported.
image Hypocarbia: Increased latency has been described at an end-tidal CO2 <25 mm Hg.
image Isovolemic hemodilution: Latency is not increased until the hematocrit is <15%, and amplitude is not decreased until the hematocrit is <7%. This effect is likely caused by tissue hypoxia.

KEY POINTS: Somatosensory-Evoked Potentials and Spinal Surgery image

1. SSEPs are used when spinal cord or brain parenchyma is at risk for ischemia during surgery.
2. Volatile anesthetics have the most profound effects on SSEP waveforms.
3. An anesthetic technique that minimizes volatile anesthetic exposure is best—an opiate-based technique with low-dose (<1 MAC) volatile or a total intravenous anesthetic.
4. During distraction of the spinal column in scoliosis surgery (or other critical parts of surgery), minimize interventions that will lower mean arterial blood pressure or deepen anesthetic levels acutely to allow differentiation of changes in SSEP waveforms from anesthetic effect.

14 If somatosensory-evoked potentials change significantly, what can the anesthesiologist and surgeon do to decrease the insult to the monitored nerves?

image The anesthesiologist can:

image Increase mean arterial blood pressure, especially if induced hypotension is used.
image Correct anemia, if present.
image Correct hypovolemia, if present.
image Improve oxygen tension.
image Correct hypothermia, if present.

image The surgeon can:

image Reduce excessive retractor pressure.
image Reduce surgical dissection in the affected area.
image Decrease Harrington rod distraction, if indicated.
image Check positioning of associated instrumentation (e.g., screws, hooks).

If changes in the SSEPs persist despite corrective measures, a wake-up test may be performed to confirm or refute the SSEP findings. The patient’s anesthetic level is lightened, and a clinical assessment of neurologic function is performed.

15 Despite normal somatosensory-evoked potentials, can patients awaken with neurologic deficits?

Although SSEP monitoring is a useful tool in preventing neurologic damage during spinal surgery, it is by no means foolproof. Because motor tracts are not monitored, the patient may awaken with preserved sensation but lost motor function. However, the reported incidence of false-negative monitoring in a large (>50,000) series of cases is 0.06% (1/1500). The monitoring of motor-evoked potentials along with SSEPs provides a more complete assessment of neural pathway integrity.

SUGGESTED READINGS

1. Jameson L.C., Janik D.J., Sloan T.B. Electrophysiologic monitoring in neurosurgery. Anesthesiol Clin. 2007;25:605-630.

2. Jameson L.C., Sloan T.B. Monitoring of the brain and spinal cord. Anesthesiol Clin. 2006;24:777-791.

3. Mahla M.E., Black S., Cucchiara R.F. Neurologic monitoring. In Miller R., editor: Anesthesia, ed 6, Philadelphia: Churchill Livingstone, 2005.

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