Evoked potentials are the electrical manifestations generated by the nervous system in response to a brief external sensory stimulus.

During orthopaedic surgery for spinal deformities the most feared complication is postoperative paraplegia. For adults undergoing correction of scoliosis the loss of motor function in the lower extremities ranges from 1 to 1.7 per cent. A lesser rate of loss occurs in children. In over one-half of these cases the paraparesis is permanent. This impairment may be caused by such correctable factors as circulatory impairment, compression of the cord from bony structures or haematomas, trauma during fitting of orthopaedic instrumentation, or mechanical stretching of the spinal cord and peripheral nerve. Evoked potentials provide a way to identify the neurological impairment early enough to allow prompt correction of the cause.

Until the advent of evoked potential monitoring the main alternative was the wake-up test. The patient is awakened at the end of instrumentation while on the operating room table and with the surgical site still opened. The patient is asked to wiggle his or her toes as a test of motor function. First, an experienced anaesthesiologist is needed, one capable of quickly reversing the anaesthesia, awakening the patient, and then reanaesthetizing the patient. In addition, there are false-negative results in which, despite a normal wake-up test, the patient has permanent postoperative neurological impairment. The greatest inherent problem with the wake-up test, however, is that it is a single test in time and fails to identify problems that may develop before or after wake-up. In contrast, evoked potential monitoring does not require awakening the patient and can be performed safely throughout the operation as well as in the recovery room. In 1991 state-of-the-art spinal cord surgery should include intraoperative evoked potential monitoring.

Somatosensory evoked potentials are initiated by electrical stimulation of any peripheral sensory nerve. This stimulus excites the largest myelinated afferent fibres and travels to the dorsal root ganglion, then ipsilateral in the posterior column to synapse in the dorsal column nuclei of the nucleus cuneatus and nucleus gracilis. The potential crosses in the medial lemniscus to the ventral posterior lateral nucleus of the thalamus. After a second synapse in the thalamus the third sensory fibre travels directly to the sensory cortex. The central nervous system has a built-in amplifier effect, increasing the signal as it progresses rostrally. Abnormalities of the evoked potential are most commonly associated with a disorder of touch, vibration, and conscious proprioception.

With this understanding, one immediately questions why we would monitor a sensory tract to evaluate for a potential motor complication. The great assumption in evoked potential monitoring is that most insults to the spinal cord significant enough to cause a motor deficit also affect the sensory tract and therefore would be identified by evoked potential monitoring. There are excellent laboratory data recorded to substantiate this assumption.

Evoked potentials cannot be seen with routine EEG recordings because of their low amplitudes (0.1–20 mV) and their admixture with normal background brain &agr; wave activity. Separation of these waves can only be accomplished by signal averaging. Stimulation is given repetitively, and measurements are averaged by computer as they arrive at the recording site. In addition, common mode signal rejection, filtering, amplification amplifiers, and multichannel recordings systems are required. Electrode placement uses the international EEG 10–20 system.

Equipment standards are detailed by the American Electroencephalographic Society and the American Association of Electromyography and Electro-diagnosis. Voltage is recorded on the vertical axis and is reported as an amplitude or the size of the wave state in microvolts baseline to peak. Time is recorded on the horizontal axis and is reported as a latency or the time it took from stimulus to recording measured in milliseconds. In the upper extremity this is usually 19 to 20 ms while in the lower it is usually 37 to 40 ms. The morphology of a wave refers to its general appearance.

There are several common areas of confusion regarding these waveforms. The first involves the nomenclature for identifying waveforms. Unfortunately, there is no international standard. The two used most commonly involve numbering the waves sequentially P&sub1;, P&sub2;, P&sub3;, (positive 1, positive 2, etc.) or by the expected normal latency N19, P40 (negative 19 ms, positive 40 ms, etc.). A second confusing aspect involves polarity or whether a wave is positive up or positive down. Again there is no consensus on how to arrange polarity. Generally, electromyographers have adopted a convention of having negativity in the electrode produce an upward deflection. Nonetheless, there is no standard nomenclature. It does not matter if the wave is up or down, and if upper extremity waves take 19 to 20 ms to arrive, while lower extremity waves take 37 to 40 ms. Consistency during surgery is the key factor.

The development of a programme first involves establishing protocols. We have found stimulation of the posterior tibial nerve to be the most convenient. Preoperatively we place our electrodes bilaterally and then carry out unilateral stimulations periodically. During the critical stage, as determined by the orthopaedic surgeon (usually during wire placement and/or distraction) we monitor continuously. Bilateral stimulation has the advantage of increasing the amplitude of the evoked potential generated, but the disadvantage of missing unilateral changes and/or technical problems. An electrical burn can result from a short circuit.

Electrode placement is based upon the international 10–20 system. We have found electrode placement over Cz′–Fz′ and C4′–C5′ provides the best reproducible results. Lueders describes a technique of recording from high cervical intraspinous ligaments to be less affected by anaesthesia. Tamaki stimulates in the posterior epidural compartment while recording in the conus medularis. We, however, have not found it necessary to use additional recording sites.

In the operating room we have found the following technical points useful. All electrical wires should be taped down. The pre-amplifier should be covered to avoid drips. The machinery should be as far away from the operating table as possible. X-ray lights should be turned off and electrical outlets should be isolated during runs to decrease interference. Cephalic recording wires should be kept away from the site of X-ray plates. A bovie should not be used during runs.

Most importantly, the surgeon must be prepared to respond to a warning from the monitoring team. One case highlighting this point involved loss of a potential almost immediately after initiating surgery and long before the critical period. When we reported this, the surgeon withdrew all instruments and detractors to investigate further. He discovered an anomalous blood vessel feeding the spinal cord, inadvertently occluded by a retractor. There is no question that had this remained undetected the patient would have suffered a postoperative complication even with a wake-up test.

Many factors can affect evoked potentials: examples are age, sex, and body size. These, however, can be accounted for by obtaining preoperative studies. Technical problems such as a loose wire or electrical interference from other equipment is usually self evident. Temperature is another variable, which is especially significant since it is not unusual for body temperature to be low during surgery. Hypothermia causes gradual prolongation of the latency (time) and should not be a cause for alarm.

Hypotension is also frequently used during scoliosis surgery to reduce blood loss; it too may diminish the amplitude. The degree of hypotension must be decided by the anaesthesiologist and the surgeon and is usually safely kept at 55 to 60 mmHg. From an evoked potential standpoint, it is especially important to keep hypotension at a steady state during the critical period. In two cases we had a sudden abolition of the evoked potential at a mean blood pressure of 55 mmHg. While we would expect the patient to tolerate this blood pressure, we insisted on raising it to 60 mmHg, where the evoked potential returned unchanged. The surgery proceeded at 60 mmHg and there was no postoperative sequel.

Probably the most significant patient-related factors affecting evoked potentials are drugs and anaesthetic agents. Some substantially impair ability to monitor cortical somatosensory evoked potentials. It is therefore important to understand the affects of these agents.

Barbiturates in low doses do not cause significant changes. Moderate to high doses and bolus doses may have a significant effect. In a low dose diazepam is not a problem, but high doses or boluses can cause substantial alterations. Narcotics cause unpredictable changes.

In general, however, low doses are tolerated while high doses or boluses are variable. Neuromuscular blocking agents do not affect evoked potentials, but, on the contrary enhance recordings by decreasing movement artefact. Nitrous oxide in concentrations less than 60 per cent is compatible with recordings of evoked potentials. Even at that concentration, however, we have identified a gradual shift in latency that occurs at 3 to 3.5 h. This is most probably due to tissue saturation. At higher concentrations (> 60 per cent) nitrous oxide may suppress evoked potentials. Halogenated agents in general are incompatible with evoked potential monitoring. This list includes halothane and ethrane.

Forane, although a halogenated agent, is not absolutely contraindicated if used in low concentrations (0.25–0.5 per cent).

These restrictions raise a major difficulty with intraoperating room monitoring. Obviously, proper anaesthesia is the most important issue. There are, however, many ways to obtain anaesthesia. In general we prefer high narcotic, low gas (forane < 0.5 per cent, nitrous oxide < 60 per cent).

There are numerous situations in which monitoring of evoked potentials might be beneficial. These include peripheral nerve releases, brachial plexopathies, thoracic outlet syndrome, radiculopathies, carotid endarterectomies, cardiac bypass surgery, and spinal cord tumour excision. Evoked potential monitoring, however, is most widely used in scoliosis surgery. Nash and Brown (Cleveland) and Gonzales (New York City) have been pioneers in the development of spinal cord monitoring. They report a series of 137 patients who underwent posterior spinal fusion of scoliosis with monitoring. One change in evoked potentials was identified among the 68 patients who received a Harrington rod without segmental spinal surgery. Twelve changes were noted in the 69 patients who received segmental spinal surgery with or without a Harrington rod. Loss of the evoked potential resulted in intervention and a correction of the evoked potential in each case. Spielholz et al. reported 55 consecutive cases of Harrington rod surgery and monitoring with no neurological complications. Mostegl and Bauer report two significant changes out of 61 cases during Luque wiring and loss of function was confirmed by an immediate wake-up test. The surgeons responded, the evoked potential returned, and there were no neurological sequelae.

We have now monitored 72 cases. Nine changes were due to technical problems (primarily loose wires), and 28 changes were due to anaesthesia. There were two significant changes due to hypotension, already discussed, and two changes during distraction that returned after reversal of distraction (Fig. 1) 2511. Interestingly, we have had two cases with diminished but present sensation in which we were not able to obtain preoperative studies. One patient was an achondroplastic dwarf and the other a child with a significant myelomeningoceal deficit. We could not monitor either case; one patient was paraparetic after surgery.

What constitutes a true change in evoked potential? Certainly a sudden abolition of the evoked potential in the lower extremity with preservation of the upper extremity evoked potential is a significant event. Many teams adhere to the 50 per cent rule. Simply stated a 50 per cent loss of amplitude is significant, but a loss of less than 50 per cent is probably not associated with a significant risk of impairment. In our experience major neurological events rapidly and significantly decrease the amplitudes more than 50 per cent, prolong the latency more than 50 per cent, and modify the wave morphology. Isolated changes in only one of these three parameters should provoke concern but not panic. I notify the surgeon when I am convinced that there is a significant wave form change. Our protocol for identifying changes is detailed in Table 1 619.

False-positive results or unnecessary alarm is a nuisance, but is substantially more common for inexperienced teams who do not know how to minimize technical problems and normal clinical variability. False-negative results are those in which the evoked potential remains stable, but there is a postoperative neurological deficit. Minor false-negative cases are those in which there is mild transient neurological postoperative sequelae.

While false-negative results are possible, they are usually associated with poor technique. I have seen cases where monitoring teams were following background noise or artefacts (paradoxical 60 Hz waves) not real evoked potentials. The incidence of false-negative results is extremely rare.

No discussion of medicine in 1993 can avoid the issue of cost analysis. Obviously this procedure is expensive: it involves highly-developed computer equipment, and is costly in terms of physician and technician man hours.

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