Evoked potential monitoring in anaesthesia and analgesia

REVIEW ARTICLE

Evoked potential monitoring in anaesthesia and analgesia

A. Kumar, A. Bhattacharya and N. Makhija*

Department of Anaesthesiology & Critical Care, University College of Medical Sciences & G.T.B. Hospital, Shahdara,Delhi-110095, India

SummaryElectrophysiological monitoring of selected neural pathways of the brain, brainstem, spinal cordand peripheral nervous system has become mandatory in some surgery of the nervous systemwhere preventable neural injury can occur. Evoked potentials are relatively simple methods oftesting the integrity of various aspects of the nervous system. This review covers the variety ofevoked potentials that can be monitored and outlines the principles of their measurement. Theiruse in specific situations and how factors such as anaesthesia might affect them is presented.

Keywords Anaesthesia. Central nervous system; complications. Monitoring; evoked potentials.

......................................................................................Correspondence to: Dr A. Kumar, Flat No. 5, Parivar Apartments, PlotNo. 30, I.p. Extn., Patparganj, Delhi-110092, India

Accepted: 24 June 1999

Electrophysiological monitoring of selected neural path-ways of the brain, brainstem, spinal cord and peripheralnervous system has become mandatory in some surgery ofthe nervous system where preventable neural injury canoccur. It is also useful in understanding the neurophysiolo-gical basis of chronic pain mechanisms. It is of benefit inmeasuring depth of anaesthesia and to determine adequatesedation for patients admitted to the intensive care unit(ICU). Advances in electrophysiological monitoring tech-nology have brought us to a stage where we can visualisesensations, thoughts and emotions in the brain as they occur.

The technology used in electrophysiological monitor-ing is relatively sophisticated but the evoked potentials arerather simple in concept with regard to their clinicalapplication for diagnostic testing and intra-operativemonitoring [1–5].

Evoked potentials

Evoked potentials are a measurement of the electricalpotentials produced in response to stimulating the nervoussystem (evoked) by sensory, electrical, magnetic or cogni-tive stimulation [6]. Sensory evoked potentials (SEPs) are

evoked potentials that are produced by stimulation of thesensory system. These responses arise from action poten-tials or graded polysynaptic potentials during the propaga-tion of an electrical impulse from the periphery to thebrain, and can be recorded over the scalp, as well as at thevarious sites along the anatomic pathway, using surfaceelectrodes (e.g. Ag/AgCl electrodes) or subdermal needleelectrodes. Since the amplitudes of evoked electricalpotentials are small compared with EEG, computer aver-aging is used to extract the SEP signals from the back-ground EEG noise. SEPs are pathway specific, stimulusspecific and event related. They therefore differ from EEG,which is random in nature.

It is interesting to note that monitoring guidelines havebeen well documented by the American Electroencepha-lographic Society [7]. The American Academy of Neurol-ogy has also published an assessment of intra-operativemonitoring, concluding that ‘considerable evidence favorsthe use of monitoring as a safe and efficacious tool inclinical situations where there is a significant nervoussystem risk, provided its limitations are appreciated’ [8].

Among the SEPs, the largest experience is withmonitoring of somatosensory-evoked potentials (SSEP,

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*Present address: Department of Cardiac Anaesthesia, Cardiothoracic &Neuroscience Centre, All India Institute of Medical Science, Ansari Nagar,New Delhi-110029, India

Fig. 1) during operations on the spine or spinal cord[9–14] and during chronic pain management [15].Brainstem auditory-evoked potentials (BAEP, Fig. 2) arerecorded during procedures in the posterior cranial fossa[16–21], to assess recovery from pre-operative sedationin regional anaesthesia [22] and during chronic painmanagement [23]. Visual-evoked potentials (VEP, Fig. 3)are recorded during operations involving the optic nerve,

optic chiasm and during cranial base surgery [24, 25].With SEP monitoring, deteriorating neurologicalfunction can be detected early, so that the anaesthetistand/or surgeon can intervene to minimise the chances ofpermanent damage to the nervous system.

Another variation is motor-evoked potentials (MEP)which assess the function of the motor cortex anddescending tracts. In MEP recording, muscle activity isrecorded after stimulation of the motor pathway.

Event-related potentials (ERPs) have long been thoughtto hold great promise as a window into the cognitiveprocesses of the brain. However, unlike SEPs or MEPs,ERPs are recorded only when the subject is selectivelyattentive to the stimulus. These are elicited only when thesubject can distinguish one stimulus (target) from a groupof other stimuli (non-targets). Because of the relationshipbetween P300-ERPs or P3 ERPs and cognitive processes,P300-ERPs have been widely used to evaluate cognitivefunctions in ageing [26], in chronic pain syndromes [27],including low back pain [28] and in awakening fromanaesthesia [29].

Neural generators of evoked potentials

Evoked potentials are usually described in terms of thepost-stimulation latency in ms (time between applicationof a stimulus and the occurrence of a peak in the EPwaveform) and peak-to-peak amplitude (in mV or nV) ofindividual peaks in the waveform. It is well established thatpeaks and valleys arise from specific neural generators.

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Figure 1 Short-latency somatosensory-evoked potentialsproduced by stimulation of the median nerve at the wrist (fromRef. 32).

Figure 2 Neuroanatomical correlates of the auditory-evoked response (AER). The symbols above the waves represent the standardelectrophysiological nomenclature (from Ref. 82).

Neural generators of individual SEP peaks have beenproposed on the basis of clinical studies in humans,clinico-pathologic correlations, studies in animals andintra-operative recordings from neural structures inhumans. Although these neural generators have not beenestablished definitely, the designations are useful clinically(Figs 1–3, 5).

Activity arising in the cerebral cortex, subcorticalstructures, cranial nerve, spinal cord, nerve root, plexusand even peripheral nerves can be recorded noninvasivelyfrom electrodes fixed to the skin or scalp [30]. Duringsurgery, electrodes can be placed within the surgical field.The location of electrodes (Fig. 4) is according to theinternational Ten-Twenty electrode placement system[30]. The parameters used for stimulation and recordingvary according to the type of evoked potential to berecorded. Finally, in the analysis of evoked potentialrecordings, there are no universally accepted standardcriteria for a significant change. Commonly used criteriaare an increase in latency> 1 ms or a decrease in amplitude> 50%.

‘Near-field’ and ‘far-field’ evoked potentials

‘Near-field’ potentials are SEPs recorded from electrodesplaced near their neural generators. For example, corticalSEP recorded from scalp electrodes or spinal SEP recordedfrom electrodes in bone, intraspinous ligaments or thespinal epidural space [6] are near-field SEP. In contrast,‘far-field’ potentials (e.g. potentials arising in peripheralnerves, spinal cord or subcortical structures and recordedfrom scalp electrodes) are smaller in amplitude. As thedistance from neural origin to recording electrodeincreases, the signal strength decreases and averaged

responses to several hundreds and thousands of repetitionsof the sensory stimulus may be needed to demonstrate‘far-field’ evoked potentials.

Somatosensory-evoked potentials (SSEPs)

The electrophysiological technique with the greatest clin-ical application is SSEP (Fig. 1). In this technique, a squarewave stimulus of 0.2–2 ms duration is delivered to theperipheral nerve (usually a mixed motor and sensorynerve) and the intensity is adjusted to produce a minimalmuscle contraction (the motor threshold). The rate ofstimulation varies from 2 to 3 Hz [31]. The common sitesof stimulation include the median nerve at the wrist, thecommon peroneal nerve at the knee, and the posteriortibial nerve at the ankle [32]. The tongue, trigeminal nerveand pudendal nerve have also been studied [32]. Accordingto Bromm & Treede [33] multiple sclerosis and otherdemyelinating disorders can affect SSEP, resulting in anabsence of late vertex potential with the appearance of anultralate response (probably transmitted via C-fibres).

PathwaySSEPs consist of both short- and long-latency evokedpotentials. The short-latency SSEPs are most commonlystudied intra-operatively because they are influenced lessby factors that may vary during the peri-operative period,for example anaesthetic depth. The pathways involved inthe generation of short-latency SSEPs include large-fibresensory nerves with their cell bodies in the dorsal rootganglia and central processes travelling in the ipsilateralposterior column of the spinal cord synapsing in the dorsal

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Figure 3 Normal visual-evoked potentials with two positivepeaks at 100 (here 109 ms after stimulation) and 200 ms (fromRef. 32).

Figure 4 Electrode placement according to the InternationalTen-Twenty electrode placement system (from Ref. 30). Thesepositions are based on measurement of head circumference,interaural distance and the distance from nasion to inion.

column nuclei at the cervicomedullary junction (firstorder fibres), secondary fibres crossing to the contralateralthalamus (ventroposterolateral nucleus of thalamus) via themedial lemniscus, and third-order fibres from the thalamusto the frontoparietal sensori-motor cortex [34]. Purportedgenerators of short-latency SSEPs are listed in Table 1.N13 is generated from the dorsal column nucleus cunea-tus, N14 from the medial lemniscus and N19, N20, P22and N35 from the region of the thalamus and parietalsensory cortex.

Primary cortical-evoked responses result from the earliestelectrical activity generated by the cortical neurones and arethought to arise from the postcentral sulcus parietalneurones. The secondary cortical potentials (longer latency)are thought to arise in the association cortex, are less stableand have greater variability of waveform than primarycortical responses [35]. Cortical-evoked potentials, otherthan the primary cortical response, are not recorded intra-operatively because they are severely altered by generalanaesthesia and are extremely difficult to record in theoperating theatre.

The SSEP responses from the upper extremity primarilyrepresent activity in the pathway of proprioception andvibration (posterior column). Gugino & Chabot [34]observed that recordings following stimulation of thelower extremity appear to include additional componentsthat pass in the spinocerebellar pathways.

The contribution of these pathways may explain whythe SSEP is altered in anterior cord ischaemia andmonitoring of the SSEP correlates well, but not always,with motor function [6].

Monitoring of sensory pathwaysIntra-operative recording of SSEPs has been used to assessthe functional integrity of the sensory pathways duringoperations that place these pathways at risk. However, oneimportant limitation of the SSEP is the sensitivity ofcortical responses to anaesthesia. As such techniques havebeen developed for stimulation or recording from thespinal cord, which is less susceptible to anaesthetic effects,

recording needle electrodes have been placed in the spinebony elements, intraspinous ligaments and subdural orepidural space [6]. Epidural electrodes have becomequite popular, particularly in Japan and the UK wherethey are used for stimulation as well as recording. Recentstudies have concluded that epidural recording and stimu-lation are superior to peripheral nerve stimulation becauseof the ability to record well-defined responses [36, 37].

SSEP monitoring during peripheral nerve surgerySSEP has been considered ‘indispensable’ for intra-operative evaluation and monitoring during surgeryinvolving peripheral nerves and plexus regions [38]. Forexample, stimulation of nerves allows the identificationof intact nerves or nerve trunks in injury areas whenperipheral function has been lost [6]. The SSEP responsehas been used to detect sciatic nerve injury during hipprocedures and to position-related nerve compromise [6].

SSEP monitoring during spinal surgerySSEP monitoring has commonly been used duringscoliosis corrective surgery. This SSEP monitoring hasbeen found to correlate with neurological outcome ofthe patient. Meyer and colleagues [9] observed that in 295patients undergoing stabilisation for spinal instability(trauma), the neurological injury rate decreased from 6.9to 0.7% with SSEP monitoring. With SSEP monitoring,Epstein et al. [10] noted a reduction in paraplegia from3.7% to 0 during 100 procedures on the cervical spine.Nuwer et al. [12] also noted that SSEP monitoring reducesneurological deficits after scoliosis surgery. It is importantto realise that false-negative results can occur becausemonitoring is pathway specific and an injury not involvingthis pathway will not be detected [11].

SSEP monitoring during brainstem and corticalsurgeryThe SSEP can be used to monitor the viability ofthe pathways as they travel through the brainstem (e.g.posterior fossa surgery) and cerebral cortex [6]. SSEPmonitoring has also been used to detect cerebral well-being in order to minimise cortical injury from retractors,which may occur in 5% of intracranial aneurysmoperations and 10% of cranial base operations. SSEPmonitoring has also been used to detect cerebral ischaemiain subarachnoid haemorrhage associated with intracranialaneurysm rupture [6]. SSEPs have also been utilisedduring neuroradiological procedures, such as occlusionof vessels (e.g. A-V malformation), or during streptokinasedissolution of occluding blood clots [6]

The SSEP may be less useful than the EEG for thedetection of cerebral ischaemia, since the EEG can assess amuch larger scope of cortex. However, in contrast to the



Table 1 Generators of SSEPs after median nerve stimulation

Peak Generator

N9 (EP) Brachial plexusN11 Posterior columns or spinal rootsN13/P13 Dorsal column nucleus cuneatusN14,15 Medial lemniscusN19/P22 Parietal sensory cortex

SSEPs, somatosensory-evoked potentials. From R. D. Miller. Text Bookof Anaesthesia, 4th edn, Vol. 1, 1994, New York: ChurchillLivingstone.

EEG, SSEP can detect ischaemia in subcortical regions [5].According to Friedman [13] SSEPs are essential for loca-lisation of the sensory–motor strip in the exposed cortex.The gyrus separating the motor and sensory strips (rolan-dic fissure) is localised by phase reversal of the responsemeasured on the cerebral surface.

Both false-negative and false-positive results have beenreported with intra-operative SSEP monitoring. How-ever, the reliability of SSEP monitoring to predict post-operative somatic sensory function has been reported to beexcellent [31, 39, 40].

SSEP monitoring in the ICUProlongation of central conduction time (CCT) in coma-tose patients has been associated with a worse long-termprognosis [41]. The CCT is the difference between thelatencies of the response recorded over the cervical spineand the response recorded over the sensory cortex [6].Prolongation of CCT in patients following subarachnoidhaemorrhage is associated with transient neurologicaldeficits and precedes the development of these deficits.The changes in CCT are possibly related to cerebralischaemia [42]. The extent of CCT prolongation is usuallycorrelated with the extent of injury, and CCT decreaseswith clinical recovery. In comatose patients in whom SSEPmonitoring has shown absent cortical responses (N20), theoutcome has generally been poor [43]. If they are persistentlypresent, despite a poor overall condition of the patient,they can indicate some hope of recovery.

SSEP monitoring has been used as an adjunct to otherindices, and has helped in diagnosis, in predicting prog-nosis and outcome, and in monitoring the recovery of thecomatose patient. Ruijs et al. [44] noted, in children withmild to moderately severe closed head injuries, that long-latency SSEP findings correlated with long-term deficits inschool performance. More recently, the use of continuousmultimodality monitoring has been shown to have a highlypromising role, especially in the long-term monitoring ofcomatose and head-injured patients [45, 46].

SSEP monitoring in chronic painKumar et al. [15] observed that the absolute peak latency(APL) of N19 is significantly delayed in chronic painpatients suffering from musculoskeletal disorders. In thisstudy, following electroacupuncture (EA) therapy, theincrease in latency of N19 persisted after the first periodof EA treatment, tended to revert to normal after the fifthtreatment and returned to control values after the tenthtreatment [15]. These observations suggest an interactionbetween the EA neural mechanism and the thalamicgenerator of SSEP, i.e. N19. Hence, it was concludedthat SSEP could act as a reflector of the analgesic effect ofEA [15].

Following SSEP monitoring in herpetic neuralgiapatients, Mahajan et al. [47] observed a delay in the centralconduction process. In herpetic neuralgia, following thetopical application of an aspirin–diethyl ether (ADE)mixture for 4 weeks, the SSEP recordings showed adecreasing trend in APL and an increasing trend inamplitudes of different waves. This study indicated anelectrophysiological interaction of the antinociceptiveeffect of the topical application of the ADE mixturewith the generators of SSEP [47].

Bromm & Treede [48] observed that pain-related cere-bral potentials and its late (100–700 ms) and ultralate (1–2 s) components are supposed to coincide with secondarycortical processing and with the magnitude and characterof the pain. Bjerring & Arendt-Nielsen [49] used an argonlaser (via quartz fibre) induced evoked response as a newtechnique to assess pain intensity objectively, and thistechnique has shown promising results in relation to thelate and ultralate components of the laser-evoked response.

Brainstem auditory evoked potentials (BAEP)and event-related potential (P300)

There are two types of BAEP (Fig. 2), transient and steadystate. Transient BAEPs (Fig. 5) consist of a series of positiveand negative waves that represent the processes oftransduction, transmission and processing of auditoryinformation from the cochlea to the brainstem, theprimary auditory cortex and the frontal cortex. Steady-state BAEPs are discussed later.

BAEPs with short latencies (< 10 ms) assess only brain-stem function. Long-latency (> 10 ms) cortical waves are



Figure 5 Diagrammatic representation of the transient auditory-evoked response. The symbols above the waves representthe standard electrophysiological nomenclature. P3 or P300component represents the events-related potential at 300 msafter stimulation.

used to evaluate cortical function. They can be divided intowaves originating in the brainstem (1–10 ms), early corticalor middle latency waves (10–100 ms) and late cortical waves(> 100 ms), which include the event-related potential (P300or P3 component; Fig. 5). Early cortical (or middle latencywaves) No, Po, Na, Pa and Nb, are generated from themedial geniculate and primary auditory cortex [50]. Latecortical waves Pl, N1, P2, N2 and P3 are generated from thefrontal cortex and associated areas [51].

Recording of transient BAEPTransient BAEPs are recorded with the help of a recordingelectrode placed near (mastoid), on or in the ear. Thereference electrode is placed at the top of head (CZ, vertex)and the ground electrode is placed at the forehead (FZ).Stimuli, consisting of clicks of alternating polarity, aredelivered in the frequency range 1000–4000 Hz, mono-aurally to each ear through shielded headphones, or smallearphone stimulators (intra-operatively).

Short-latency BAEP waveformPeaks in BAEP recordings are labelled by the romannumerals I–VII, and the purported neural generators forthese peaks are listed in Table 2 and Fig. 2. As with SSEP,amplitude, and absolute and interpeak latencies areevaluated to assess the integrity of the auditory system,localise the functional defect and assess peripheral andcentral conduction times. Because waves VI and VII areinconsistent, they are not routinely studied [32], and mostpapers reporting the use of BAEPs in the operating theatreuse up to wave V [18, 52]. Waves IV and V often blendtogether.

Intra-operative monitoring of short-latency BAEPBAEP monitoring is essential during surgery involving ornear to the auditory pathway, as well as in posterior fossa

surgery when brainstem function might be compromised.These include microvascular decompression of cranialnerves (especially V and VIII), resection of acousticneuroma, exploration for vascular or neoplastic lesions,basilar artery aneurysm, arterio-venous malformation andsection of nerve VIII for intractable tinnitus [16–21, 52].During microvascular decompression of the facial nerve inpatients with hemifacial spasm, hearing loss has beenreported in 15% of patients and this can be reduced furtherwith BAEP monitoring [53, 54]. Intra-operative changesobserved include increases in latency (transient orpermanent) on the operative side, obliteration of wave-form distal to the operative site (transient or permanent),and rarely, obliteration of BAEP contralateral to theoperative side [18, 40, 52]. Patients with completeirreversible loss of BAEP will most likely have completeor near complete loss of hearing in the ipsilateral earpostoperatively [39, 40, 52]. Occasionally false-positiveresults have been reported, however, false-positive resultsare extremely rare.

The cochlear nerve, which is responsible for hearing,has been labelled as one of the most fragile cranial nerves[17] and is commonly involved in tumours of the posteriorfossa. Various studies have shown an improvement inhearing outcome using BAEP monitoring in acousticneuroma [19–21]. Several variations of the BAEP havebeen developed to monitor the auditory system morespecifically. Cochlear microphonics, monitoring the intra-cranial portion of the eighth cranial nerve (cochlear nerveaction potentials) and the nerves present in the lateralrecess of the fourth ventricle, have also been used [6].

BAEPs are thought to be the simplest of the SEPs tomonitor intra-operatively and are the least sensitive tochanges in peri-operative variables. But pre-operativedeafness (conductive and sensorineural hearing disorder)on the operative side eliminates the possibility ofrecording intra-operative BAEPs. Preservation of BAEPintra-operatively indicates preserved hearing post-operatively and persistent changes indicate significantrisk for injury.

BAEP monitoring in ICUWhen no BAEP can be recorded from a comatose patient,it is necessary to demonstrate that the peripheral hearingmechanism is functional. Recently Garcia-Larrea et al.[55] observed that in comatose patients, prolongation ofBAEP brainstem transmission time in response toelevation of intracranial pressure (> 40 mmHg) wasalmost always followed by brain death, while lack ofBAEP change with raised intracranial pressure reflected ahigh probability of survival. Rumpl et al. [56] also notedthat, in 85 comatose patients, BAEP findings correlatedwith outcome status.



Table 2 Correlation between various BAEPs and area fromwhich these potentials are generated

Wave Generator

I Nerve VII contiguous with the spinal ganglia in the mastoidbone

II Intracranial acoustic nerve and/or cochlear nucleus (lowpons)

III Superior olive (low pons)IV Lateral lemniscus (middle pons)V Inferior colliculus (midbrain)VI Medial geniculate (thalamus)VII Thalamocortical radiations

BAEPs, brainstem auditory-evoked potentials. From R. D Miller. TextBook of Anaesthesia, 3rd edn, Vol. 1, 1990, New York: ChurchillLivingstone.

Middle latency auditory-evoked potential(MLAEP) and implicit memory during anaesthesiaMost studies on BAEP concentrate on early cortical ormiddle latency AEP (MLAEP, Pa and Nb latencies). Thereare now sufficient studies to substantiate claims thatunconscious processing of auditory information andimplicit memory of intra-operative events occur inpatients in whom the early cortical potentials of theMLAEP are preserved during general anaesthesia [57].Schwender and colleagues [58] studied patients under-going cardiac surgery who were anaesthetised with high-dose fentanyl and either flunitrazepam, isoflurane orpropofol. During anaesthesia, the story of RobinsonCrusoe was played to the patients and postoperativelythey were asked to recall the association with the word‘Friday’. Any association with the Robinson Crusoe storywas taken as evidence of implicit memory. Of the patientswho showed evidence of implicit memory, all demonstratedan increase in Pa latency< 12 ms. None of the patients whohad evidence of increase in Pa latency > 12 ms showedevidence of implicit learning [58].

In MLAEP, a short Nb latency is associated withwakefulness and conscious awareness with explicit recall[57]. As the latency increases, amnesia occurs, followed byloss of consciousness and ultimately loss of implicitmemory. Recently Roy & Huang [59] suggested that byutilising alterations in Pa and Nb latencies, one can devise afeedback loop to regulate sedation at a comfortable levelfor patients admitted to the ICU. Mantzaridis & Kenny[60] suggested that the auditory evoked potential index(AEP idx) could be used as a reliable indicator of potentialawareness instead of latencies and amplitudes.

The effects of anaesthetic agents on MLAEP are discussedbelow. Bailey & Jones [57] recommend that, to avoidawareness, it would be advisable to avoid techniques thatrely only on agents associated with preservation of theMLAEP, namely opioids, benzodiazepines and nitrousoxide, and to include agents that suppress the MLAEP(namely volatile anaesthetic agents and propofol). In aninteresting study Newton et al. [61] observed a correlationbetween Nb latency and response to command in volunteeranaesthetists who were given sub-MAC concentrations ofisoflurane (0, 0.1, 0.2. and 0.4 MAC) on four separate days.Loss of verbal response to command and eyelash reflexafter a bolus dose of midazolam has been associated with anincrease in Nb latency from 44 to 58 ms [62], and aftermidazolam and propofol infusion with an increase from44.3 to 55 ms [63].

The 40-Hz steady-state response (steady-state BAEP)It is well established that the amplitude of the evokedresponse increases with increasing click frequency, with apeak at a frequency of , 40 Hz. This is known as the steady-

state response (SSR) and is due to superimposition of thetwo main waves of the transient BAEP Pa and Pb (Fig. 5)[64, 65]. Jeffreys et al. [66] observed that fast, ‘40 Hz’ orgamma rhythms, are also involved in higher cognitivefunctions. They range from 30 to 100 Hz and may overlapwith the beta band (15–30 Hz). The significance of the‘40-Hz’ rhythm is to bind together the many discontinuouscortical networks required in the conscious process [66].

Plourde & Picton [29] showed that the 40-Hz SSRdisappears following the induction of anaesthesia andre-emerges upon recovery [29]. Plourde & Boylan [67]also demonstrated this pattern with high-dose opioidanaesthesia [67]. Munglani et al. [68] showed that, withincreasing concentration of isoflurane, the coherentfrequency decreases from , 40 Hz awake to just less than20 Hz when consciousness is lost. Jeevaratnam et al. [69]recently showed that the coherent frequency correlateswith word list recognition performance and can be used asa test of cognitive function during propofol sedation.

Recording the event-related potential (P300)The current utility of P300 is in research rather thanclinical monitoring. P300 is measured from the vertex(CZ and PZ, Fig. 4) in response to two types of soundstimuli presented binaurally through shielded headphonesor small earphones applied to the patient’s ears. A standardauditory ‘oddball’ paradigm is used to apply two types ofsound stimulus and the patient is asked to respond bypressing a button whenever an infrequent target stimulus ispresented [70]. The auditory threshold of each patient isdetermined before starting the procedure.

Active electrodes are placed at CZ and PZ with referenceelectrodes at the ear lobules (A1 and A2). The groundelectrodes are placed at FZ (Fig. 4). The input impedance iskept at < 5 kQ. Alternating tone bursts with a startingcondensation phase of 10 ms rise/fall time, 100 ms duration(plateau time) and intensity 70 dB above the normalhearing limit and at the rate of one every 2 s are used astarget stimuli. Eighty per cent of a total 160 tones are of1 kHz (frequent) and 20% are of 2 kHz (rare). The stimulussequence is random, is in phase in two ears and evokedresponses are averaged simultaneously for 32 responses[70, 71].

P300 waveform and clinical applicationThe P300 or P3 component of the evoked potential(Fig. 5) has a peak latency of < 300–400 ms, followingthe onset of the rare stimulus, and its amplitude is maximalin the midline over the central and parietal regions of thescalp. Neural generators of this P300 response are supposedto be located subcortically in the limbic structures, inparticular the hippocampus [70]. The extensive presenceof both endogenous opioids and mono-aminergic systems



in the hippocampus and its circuitry with other limbicstructures are suggested to be involved in P300 generation.The P300 component is not influenced by stimulusintensity, but is altered by the ratio of target to nontargetstimuli, by shifts in the attention of the subject or bychanges in the ease with which targets can be distinguishedfrom nontargets [70]. It is important to realise that inolder persons one can observe an age-related increase inlatency and a reduction in peak amplitude of cerebralevent-related potential (CERP) components [72].

Thornton et al. [73] showed that BAEP is not suitable asan indicator of the depth of anaesthesia because it isaffected differently by different anaesthetics. There isvery limited work regarding anaesthetic action on thelate cortical potentials. Jessop et al. [74] noticed that theP300 component of the evoked potential is reduced in adose-dependent manner by nitrous oxide, reaching 0 at62% end-tidal nitrous oxide, but its reappearance isdelayed following awakening from anaesthesia [75]. Thisis probably because such event-related potentials (ERP)require the attention of the subject. In a recent study,Tandon et al. [28] observed an increase in the APL of theP300 component in chronic low-back pain patients whichmight be due to a delay in the sensory perceptive process inaddition to the cognitive process in the cortex. Tandonet al. also reported the presence of maladaptive cognitionand cognitive–behavioural deterioration in chronic painpatients as their attention is focused exclusively on pain [27].Following epidural methylprednisolone administration,this APL of P300 was significantly reduced on the 5thand 10th day of the epidural injection (Fig. 6). Since theclinical relief of low-back pain and improvements incognitive function go hand in hand, it has been suggestedthat P300 ERP may be used as an objective parameter toassess pain relief in chronic low-back pain patients [28].

Visual-evoked potential (VEP)

Monitoring of VEP appears to have very limited applica-tion in the operating theatre. Basically VEPs monitor thefunction of the retina, optic chiasm, optic radiation andoptic cortex [24]. VEPs are recorded after monocularstimulation with recording electrodes over the occipital,parietal and central scalp [32]. VEPs are recorded inresponse to visual stimuli, such as a checker board patternor flashing light-emitting diode ‘goggles’. For surgery onthe anterior cranial fossa, the goggles interfere with theapproach to the operative field. Hence smaller stimulatorsmade of contact lenses or scleral caps are sometimes moreuseful. Stechison [25] believes that VEP can be of value,particularly with skull base surgery, by using scleral cap orcontact lens stimulation.

Normally in VEP recording, two positive peaks at

< 100 and 200 ms are observed in response to a flashstimulation of 1–3 Hz and 3–5 ms duration [31]. Thenormal P100 (here 109 ms after stimulation, Fig. 3)arises in the occipital cortex and is the most importantmarker for intra-operative monitoring. Factors affectingVEPs are conditions such as optic neuritis and lens defectssuch as cataract.

Zaaroor et al. [76], using steady-state VEPs recordedduring neurosurgical procedures or in the ICU, showedchanges within seconds of surgical and/or medicaldecompression of intracranial hypertension.

Limitations of VEPsIn the opinion of the author of one of the largest series ofpatients studied using intra-operative VEP monitoring withcurrent techniques, VEPs cannot be reliably interpretedintra-operatively [40]. Recently, Cedzich & Schramm [77]concluded that this lack of consistency makes VEP a lesseffective monitor than other modalities.

Influence of anaesthetic drugs on SEPs

There are multiple drugs used in the peri-operative periodthat can affect the intra-operative monitoring of SEPs(Table 3). Different groups of drugs have different effects.In general, VEPs are the most sensitive and BAEPs themost resistant to drug effects. In addition, early waves(brainstem) are affected less by drugs than are latepotentials (cortical). With inhalational agents, the spinaland subcortical waves are affected less than the corticalpotentials [78, 79].

Both inhalational and intravenous anaesthetic agents



Figure 6 P300 (P3) tracings in a patient with chronic low backpain (baseline and on days 5 and 10) following epidural injectionof methylprednisolone (from Ref. 28).

result in an increase in latency and a reduction in amplitudeof the Pa and Nb waves of the MLAEP [73, 80–82]. It isbelieved that the change in MLAEP reflects the hypnoticcomponent of anaesthesia as opposed to an analgesic effect.Thornton et al. [83] observed that nitrous oxide, a stronganalgesic but weak hypnotic agent, produces less effecton Pa and Nb latencies and amplitudes than MACconcentration of isoflurane. Similarly, Schwender et al.[84] demonstrated that opioids producing powerfulanalgesia have little or no effect on the MLAEP. However,benzodiazepines do not result in marked changes in theamplitudes and latencies within the MLAEP [85],although midazolam (at high bolus doses) has beenshown to produce transient attenuation of the MLAEP.Midazolam causes a decrease in amplitude withoutchanges in latency of SSEPs [86].

Schwender et al. have shown that a bolus injection ofthiopental suppresses the MLAEP, but as the patientbegins to awaken, the latencies within the responsereturn to their awake values [87]. When propofolinfusion produces unconsciousness (as judged by lossof both the eyelash reflex and the response to com-mand), Davies et al. [88] observed an increase in thelatencies of Na, Pa and Nb, which is reversible andreproducible during alternating periods of consciousnessand unconsciousness. Schwender et al. [89] also observedthat during anaesthesia for Caesarean section, a prominentMLAEP is associated with intra-operative wakefulness,purposeful movements and postoperative recall of surgicalmanipulation.

Recently Schwender et al. [90] also observed that a high

incidence of motor signs of wakefulness and consciousnessassociated with preserved MLAEP indicate a high levelof cortical neural activity and responsiveness duringanaesthesia with midazolam (induction with midazolam0.3 mg.kgÿ1 and maintenance with midazolam 0.3–0.9 mg.kgÿ1.hÿ1).

In a recent study, Kumar et al. [22] observed that pre-operative sedation with oral clonidine (5 mg.kgÿ1) causesno significant increase in the interpeak latencies and APLof BAEP waves I–V on recovery from cataract extractionunder regional block. In this study, in the diazepam (oral)group there was a significant increase in interpeak latenciesand APL of waves I–V. A few other authors have alsodemonstrated significant changes in evoked potentialsfollowing the administration of diazepam [91, 92].

In general, narcotics cause dose-dependent increases inlatency and decreases in amplitude of SSEPs. Fentanylcauses dose-dependent increases in the latency of all waves,with cortical or late waves affected more than earlierwaves, and decreases in amplitude. The changes inamplitude are more variable than the increases in latency[93, 94]. Even at high doses of fentanyl (up to 60 mg.kgÿ1)reproducible SSEPs can be recorded [94]. RecentlyLangeron et al. [95] observed that fentanyl (induction dose6 mg.kgÿ1 and maintenance dose 3mg.kgÿ1.h) induces amodest alteration in CSEP (cortical SSEP) amplitude andlatency [95]. Various authors have recommended monitor-ing CSEP signals with different doses of fentanyl duringspinal surgery [86, 96–98, 150]. Morphine causes similardose-dependent changes in SEPs to fentanyl [99]. Pethidinecauses increases in latency, but may also result in increases in



Table 3 Drug effects on sensory and motor-evoked potentials

SSEPs BAEPs VEPs Transcranial MEPs

Lat Amp Lat Amp Lat Amp Lat Amp

Isoflurane ↑ ↓ ↑ 0 ↑ ↓ ↑ pEnflurane ↑ ↓ ↑ 0 ↑ ↓Halothane ↑ ↓ ↑ 0 ↑ 0 ↑ ↓↓Nitrous oxide 0 ↓ 0 0 ↑ ↓ ↑ ↓↓*Barbiturates ↑ ↓ ↑ 0 ↑ ↓ P† P†Etomidate ↑ ↑ ↑ ↓ ↑ 0Propofol ↑ ↓ ↑ ↓ p P†Droperidol ↑ ↓ ↓↓‡Diazepam ↑ ↓ 0 0Midazolam 0 ↓ p pKetamine 0 ↑ 0‡Fentanyl ↑ ↓ 0 0 0 0Morphine ↑ ↓Meperidine ↑ ↑/↓

SSEPs, somatosensory evoked potentials; BAEPs, brainstem auditory evoked potentials; VEPs, visual evoked potentials; MEPs, motor evokedpotentials; Lat, latency; Amp, amplitude; p, prohibitive in clinically useful doses. *P if inspired concentration > 50%. †Following bolusadministration; low-dose infusions may be acceptable in some cases. ‡Drug not given during general anaesthesia; volunteers awake followingadministered dose. From R. D Miller. Text Book of Anaesthesia 4th edn, Vol. 1, 1994, New York: Churchill Livingstone.

the amplitude of SSEPs [100]. BAEPs are resistant to doses offentanyl up to 50 mg.kgÿ1 with no changes observed in APL,interpeak latency or amplitude [99].

Recently McGregor et al. [101] observed that remifentanil(bolus dose of 1 mg.kgÿ1 followed by infusion) incombination with either propofol 6 mg.kgÿ1.hÿ1 or0.6% end-tidal isoflurane obtunded the early corticaleffects of intubation and incision [101]. Remifentanilalso reduces auditory and somatosensory evoked responsesduring isoflurane anaesthesia in a dose-dependant manner[102]. Brunner et al. [103] observed that alfentanil obtundsthe increase in the Pa amplitude associated with intubationin a dose-dependent fashion.

Increasing doses of thiopental in patients result inprogressive dose-dependent increases in latency anddecreases in amplitude in median nerve SSEPs, andprogressive increases in latency in BAEPs [104]. Thechanges in SSEPs are more pronounced than the changesin BAEPs. Following bolus administration and intravenousinfusions, etomidate causes increases in the latency of allwaves and prolongation of central conduction time inSSEPs, as well as increases in the amplitude of corticalwaves, but a slight decrease in the amplitude of cervicalpotentials [95]. This effect seems to be present in thecortex but not in the spinal cord [105]. The effects ofetomidate on BAEPs are dose-dependent increases anddecreases in amplitude [97]. Propofol reduces the amplitudeand increases the latency of Pa and Nb waves of earlycortical auditory-evoked responses [98, 106, 107]. Doi et al.[108] tried to relate blood concentrations of propofol tovarious electrophysiological variables during emergencefrom anaesthesia. Petersen-Felix et al. [109] observed thatboth propofol and alfentanil induce similar decreases in theamplitude of the evoked potentials elicited by nociceptiveand non-nociceptive (auditory) stimuli, but only alfentanilreduced perceived pain, therefore reflecting that thedecrease in amplitude of the vertex potential by propofolwas not caused by an analgesic effect.

The effects of currently used volatile agents on SSEPsare dose-dependent increases in latency and conductiontimes and decreases in amplitude [78, 79, 110, 111]. Therelative effects are somewhat controversial: some evidencesuggests that halothane has a greater impact on SSEPs thaneither isoflurane or enflurane [79], other evidence supportsa greater effect by enflurane and isoflurane than halothane[78]. Up to 0.5–1 MAC isoflurane in the presence ofnitrous oxide is compatible with adequate monitoring ofcortical SSEPs [78, 79, 110–112].

Halothane, enflurane, isoflurane (Fig. 7) and desfluranereduce the amplitude and increase the latency of Pa andNb waves of early cortical AEP in a dose-related manner[113–116]. In a recent study, Sharpe et al. [116] concludedthat AEP may be a more sensitive indicator of anaesthetic

depth at low desflurane doses and the EEG more sensitiveat higher concentrations.

Use of volatile agents during monitoring of VEPs resultsin dose-dependent increases in latency with or withoutchanges in amplitude [111]. Nitrous oxide causes decreasesin amplitude without changes in latency in SSEPs whenused alone or when added to a narcotic-based or volatileanaesthetic [78, 79, 117]. Use of nitrous oxide alone causesno change in BAEPs [117]. Use of nitrous oxide aloneresults in an increase in latency and a decrease in amplitudein VEPs, but when added to a volatile anaesthetictechnique it causes no further changes in VEPs [117].

Svensson et al. [118] observed changes in the amplitudeand latency of argon laser-evoked cortical responsesfollowing the application of Eutectic local anaesthetic(EMLA) cream.

Influence of electroacupuncture on SEPs

Kumar et al. have studied the effects of EA on BAEP [23]and SSEP [15] in chronic pain patients. The effects of EAon SSEPs have been discussed above. The results of theeffect of EA on BAEP indicate a significant delay in theAPL of waves I, II and III, and a significant reduction inthe amplitude of wave V [23]. As both the descendinginhibitory pain pathways and some of the generators ofBAEP lie close to each other, they might interact inmodulating BAEPs. Hence, the modulating effect ofanalgesic mechanisms of EA seems to be located mainlyin the lower brainstem [23], as shown by significant delay



Figure 7 Auditory-evoked responses in relation to end-tidalisoflurane concentrations (from C. Thornton, PhD thesis,London University, 1990).

in the APL of waves I, II and III. In an interesting study,Shen et al. [119] showed an inhibitory effect of EA onsplanchnically evoked potentials in the orbital cortex of thecat, thereby indicating the involvement of descendinginhibition in the effect of EA.

Influence of physiological factors on SEPs

A number of physiological factors including systemicblood pressure, temperature, blood-gas tension and iso-volaemic haemodilution can influence SEP recordings.With a decrease in mean arterial blood pressure to levelsbelow cerebral autoregulation (due to either blood loss orvasoactive agents), SSEP changes are a progressive decreasein amplitude until loss of waveform with no change inlatency [120, 121]. BAEPs are relatively resistant to evenprofound levels of hypotension (MAP of 20 mmHg indogs) [120]. Cortical (synaptic) function appears to bemore sensitive to ischaemia than spinal cord transmission[121]. SSEP changes resolved with increase of bloodpressure to slightly above the patient’s normal pressure,suggesting that the combination of surgical manipulationand levels of hypotension generally considered ‘safe’ couldresult in spinal cord ischaemia [122].

Hypothermia causes an increase in latency and adecrease in amplitude, with loss of waves at 25–278C inVEPs [123], and an increase in latency and an alteration inmorphology of BAEPs with late waves affected more thanearly waves [124, 125]. Hyperthermia also alters SEPs,with increases in temperature leading to decreases inamplitude in SSEPs and loss of evoked potentials at 428Cduring induced hyperthermia [126, 127].

Changes in arterial blood-gas tension have beenreported to alter SEPs, probably in relation to changesin blood flow or oxygen delivery to neural structures[128, 129]. SSEP changes (decreased amplitude) resultingfrom hypoxia have been reported [129].

Isovolaemic haemodilution results in progressiveincreases in the latency of SSEPs and VEPs, whichbecome significant at haematocrits below 15%. Changesin amplitude were variable until very low haematocrits(< 7%) were reached when the amplitude of all waveformsdecreased [130].

Motor-evoked potentials

Motor-evoked potentials (MEPs) assess the function of themotor cortex and descending tracts. The ‘wake-up’ test is areliable and simple method for testing motor function,however this test is not feasible during some operations.The peripheral response of MEP is recorded by measuringcompound muscle action potentials (CMAPs) with thehelp of fine wire electrodes within muscles innervated by

the motor nerve or surface electrodes over the muscle afterdirect stimulation of the nerve in the operative field. SSEPmonitoring of the spinal cord has limitations, in that theyonly monitor the dorsal column (sensory pathways) andfalse-negative or false-positive results may occur. Hence itwould be interesting to have direct monitoring of themotor system. In the opinion of Owen [14], directmonitoring of the motor system (neurogenic MEP)can be carried out by stimulating the spinal cord withelectrodes placed near or in the vertebral bodies cephaladto the site of spinal surgery [14]. Phillips et al. [131]observed that neurogenic MEP was a more reliablemonitor of motor function than SEP. Motor nerveconduction studies are important in both the diagnosticlaboratory and the operating theatre.

Pure motor-tract monitoring is better achieved bymotor cortex stimulation using transcranial electrical[132–136] or magnetic stimulation [135–140], and theresults are more promising. These responses can berecorded in the spinal cord, peripheral nerve or asCMAPs. Deletis [141] suggested epidural recordings, asanaesthetic agents may affect at the anterior horn cells orneuromuscular junction and thus reduce the motorresponse in the nerve and muscle. Sood et al. [142]recommend that the transcranial MEP technique is safeand injury is unlikely with the present technique. Inrecording MEPs, narcotics have less effect than volatileanaesthetics. Neuromuscular blocking drugs may obtundthe responses completely. Hence newer multipulsestimulation techniques are being developed as theyappear to be less susceptible [143]. Currently MEPmonitoring is mainly an explorative tool.

EMG monitoring of cranial nerves

Since cranial nerve involvement is common with intra-cranial growths > 2 cm, monitoring of cranial nervefunction is essential in surgical management. It is impor-tant to realise that in posterior fossa surgery, one mustmonitor facial nerve function and hearing. Yingling [17],Apel et al. [144] and the National Institute of Health [145,146] have established an improvement in outcome inposterior fossa surgery with monitoring of cranialnerves. Taniguchi et al. [147] recommend facial nervemonitoring by placing closely spaced bipolar recordingelectrodes in the orbicularis oris and orbicularis oculi. TheEMG recordings are evident on an oscilloscope screen aswell as when played through an audio system with provi-sion for suppression during cautery.

Taniguchi et al. also emphasise monitoring of the motorcomponent of other cranial nerves, which has been usedextensively in surgery on the base of the skull, cavernoussinus and in the posterior fossa. Monitoring of cranial



nerves IX, X, XI and XII is essential during resectionof large low brainstem lesions. Monitoring of the vagalinnervations of the larynx has also been suggestedin the resection of tumours of the lower brainstem,thyroidectomy, parathyroidectomy and anterior cervicalspine surgery.

SEPs and brain death

SEPs have been used to help predict early brain death.SSEP findings usually show loss of cortical waves but theremay be preservation of the subcortical components. Find-ings with BAEP vary from having no waves present orhaving only 1 peak present, either unilaterally or bilateral,but delayed in latency.

SEPs and cardiopulmonary brain resuscitation(CPBR)

Another area where SEP has been used to predict outcomeis following CPBR. Madl et al. [148] recently observedthat, in patients who were successfully resuscitated fromcardiac arrest but were still unconscious and mechanicallyventilated, the SEP measurements (N70 between 74 and116 ms) correlate with good outcome and an absent ordelayed N70 (121–171 ms) correlates with poor outcome.

More recently, MEPs have also been added to thecontinuous multimodality evoked potential monitoringin the ICU. This has been used to help in predictingoutcome and estimating the extent of underlying braindysfunction in patients with ‘locked-in’ syndrome [149].

Conclusion

Evoked potential monitoring is remarkably useful duringsurgical procedures because it provides the ability tomonitor the functional integrity of sensory and motorpathways in the anaesthetised patient undergoing surgerythat places these pathways at risk. This unique monitoringis particularly helpful in understanding the central effectsof various anaesthetic agents and in monitoring theconcept of implicit memory, awareness and depth ofanaesthesia. It may also help in titrating sedation in ICUpatients. It is also significant in assessing the recoveryfrom pre-operative sedation used in regional blocks, inunderstanding the neurophysiological basis of chronicpain mechanisms and of various pain managementmodalities, and in assessing the cognitive response ofpain management techniques. It may help in diagnosisand in predicting prognosis and outcome in comatosepatients following cardiopulmonary brain resuscitation.However, the limitations of this technology must beduly understood. The equipment is very expensive and

interpretation is difficult. It is hoped that in the nextcentury monitoring technology may improve as additionalinformation is obtained from experimental and clinicalobservations.

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Additional reading

Chiappa KH. Evoked Potentials in Clinical Medicine. New York:Raven Press, 1990.

Cooper R, Osselton JW, Shaw JC. EEG Technology. Boston, MA:Butterworths, 1980.

Emerson RG, Turner CA. Monitoring during supratentorialsurgery [Review]. Journal of Clinical Neurophysiology 1993; 10:404–11.

Grundy BL. Intraoperative monitoring of sensory-evokedpotentials. Anesthesiology 1983; 58: 72–87.

Luders H. Advanced Evoked Potentials. Boston, MA: Kluwer, 1989.Moller AR. Intraoperative Neurophysiologic Monitoring. Luxem-

bourg: Harwood Academic Publishers, 1995.Nuwer MR. Evoked Potential Monitoring in the Operating Room.

New York: Raven Press, 1986.



Evoked potential monitoring in anaesthesia and analgesia

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