Skip Navigation LinksHome > September 2003 - Volume 99 - Issue 3 > Pharmacologic and Physiologic Influences Affecting Sensory E...
Review Article

Pharmacologic and Physiologic Influences Affecting Sensory Evoked Potentials: Implications for Perioperative Monitoring

Banoub, Mark M.D.*; Tetzlaff, John E. M.D.†; Schubert, Armin M.D., M.B.A.‡

Free Access
Article Outline
Collapse Box

Author Information

EVOKED potentials (EPs) are the electrophysiologic responses of the nervous system to sensory or motor stimulation. 1,2 Stimulating the nervous system initiates the transmission of neural signals that may be recorded as EPs from various points along the stimulated pathway. Intraoperative monitoring (IOM) of EP has gained popularity because EPs reflect the functional integrity of neural pathways in anesthetized patients undergoing surgical procedures that place nervous system structures in jeopardy. EPs monitored intraoperatively include somatosensory evoked potentials (SSEPs), brainstem auditory evoked potentials (BAEPs; also referred to as auditory brainstem responses), visual evoked potentials (VEPs), and motor evoked potentials. Additional EP modalities include dermatomal sensory evoked potentials, electrocochleography, and electromyography.
Intraoperative EP changes may result from surgical injury or ischemia of the specific neural pathway, or they may be due to nonspecific physiologic or pharmacologic influences. Physiologic factors that may influence EPs include temperature, blood pressure, hematocrit, acid–base balance, and oxygen and carbon dioxide tensions. Anesthetic drugs and sedatives are the most common pharmacologic causes of nonspecific EP changes.
This review discusses the physiologic and pharmacologic factors (including newer anesthetic agents and adjuncts) that influence sensory evoked potentials (SEPs), focussing on SSEPs, BAEPs, and VEPs. For ease of reference and to allow better comparisons between anesthetic agents, the discussion of anesthetic effects is separated from physiologic effects. The review intends to help clinicians recognize the important confounding perturbations so that intraoperative changes in SEPs can be interpreted optimally. It also aims to guide anesthetic planning so that reliable intraoperative EP monitoring can be accomplished during effective and safe anesthesia.
Back to Top | Article Outline

Describing Sensory Evoked Potential Waveforms

Fig. 1
Fig. 1
Image Tools
The single cortical sensory evoked response has a low amplitude (1–2 μV) compared with the much larger electroencephalogram waves (50–100 μV). Therefore, the EP wave has to be extracted from concurrent spontaneous electroencephalogram activity by repetitive stimulation and computer-signal averaging techniques. 3 The EP waveform consists of a series of peaks and valleys presented as a graph of voltage over time and described in terms of amplitude, latency, and morphology. For IOM, amplitude is commonly measured as the waves’ peak-to-peak voltage difference. Latency is the time from stimulus to the peak of the response. Interpeak latency is the interval between the peaks of interest (fig. 1).
Evoked potential waves can have either negative or positive polarity. A negative wave occurring at a latency of approximately 20 ms would be indicated as N-20. Generally, negative waves are shown as upward deflections, while positive waves are shown as downward deflections. Evoked potentials can be of cortical or subcortical origin. Responses recorded by electrodes located within 3–4 cm of the neural generator are termed near-field potentials (e.g., cortical SSEP waves recorded from scalp electrodes), whereas those recorded from electrodes farther from the neural generator are called far-field potentials (e.g., BAEP recorded over the vertex). 4,5 SEPs are also classified as short latency (< 30 ms), intermediate latency (30–75 ms), or long latency (> 75 ms). 6
For the purposes of this review, SEPs are considered recordable when reproducible waveforms are reported. An anesthetic regimen is described as compatible with IOM when it results in consistently recordable waveforms. Reliability of SEPs refers to their ability to detect potentially injurious conditions intraoperatively.
Back to Top | Article Outline

Pharmacologic Effects of Anesthetics on Sensory Evoked Potentials

Somatosensory Evoked Potentials
Anatomic and Electrophysiologic Considerations.
Fig. 2
Fig. 2
Image Tools
The SSEP represents the reproducible electrical activity of cortical and subcortical structures time-locked to a peripheral nerve stimulus. For perioperative applications, electrical impulses are commonly delivered to the median nerve or posterior tibial nerves using needle or surface electrodes. The impulse propagates peripherally (resulting in muscle twitches) and centrally via the peripheral nerve and the dorsal root to the spinal cord. The nerve cell body of the first-order neuron lies in the dorsal root ganglion. Impulses then ascend primarily in the dorsal column fibers of the spinal cord, which synapse (fig. 2) in the lower medulla near the nucleus gracilis and cuneatus, respectively. Axons of the second-order neurons cross the midline at the cervicomedullary junction, from where they regroup to form the medial lemniscus and synapse in the ventroposterior–lateral nucleus of the contralateral thalamus. Third-order neurons from the ventroposterior–lateral leave the thalamus and travel through the posterior limb of the internal capsule as the thalamocortical radiation to synapse in the primary somatosensory cortex in the postcentral gyrus of the parietal lobe. The spinocerebellar pathways, located anteriorly in the spinal cord, contribute to the rostral conduction of SSEP signals. Therefore, SSEPs can assess the sensory system from the peripheral nerves through the spinal cord and brainstem to the cerebral cortex.
Fig. 3
Fig. 3
Image Tools
Somatosensory evoked potential waveform activity can be recorded at the popliteal fossa after posterior tibial nerve stimulation and at Erb's point above the clavicle after median nerve stimulation. Spinal potentials recorded over the cervical and lumbar spinous processes confirm the delivery of the stimulus to the central neural axis, after it is delivered in the arm or leg, respectively. The subcortical component of the SSEP is recorded over the second cervical vertebra as a negative deflection (N-14) 14 ms after median nerve stimulation. The earliest cortical (midlatency) component of the SSEP wave is generated by the primary somatosensory cortex and occurs approximately 20 ms after median nerve and 40 ms after posterior tibial nerve stimulation. Cortical SSEPs are recorded from scalp overlying the contralateral primary sensory cortex (fig. 3). A spinal sensory EP may be stimulated or recorded from epidural electrodes placed percutaneously or in the surgical field. The central conduction time (CCT) is the time needed for the signal to travel from the cervicomedullary junction to the contralateral cerebral cortex (CCT = N-20 to N-14 latency difference after median nerve stimulation).
The subcortical SSEP recorded over the second cervical vertebra can be very useful intraoperatively because it is not very susceptible to anesthetic effects. 7 Assuming an electromyography artifact is eliminated and technical problems are solved, the cervical response has a shorter acquisition time that allows faster feedback to the surgical team, which enhances its usefulness in surgical procedures that may jeopardize the spinal cord. The midlatency cortical SSEP is moderately sensitive to anesthetic depression, but clinically useful recordings can be obtained in most patients with modifications in anesthetic technique. Longer latency SSEP waves, which represent further neural processing of sensory inputs into the association cortex, are exquisitely sensitive to anesthetic drugs, and therefore, are not useful to monitor the integrity of the sensory pathway. 8
Back to Top | Article Outline
What Constitutes an Important SSEP Change?
Diagnostic criteria to evaluate intraoperative waveform changes diagnostic of spinal cord dysfunction have been difficult to establish. Latency changes of 7–10% and amplitude decreases of 45–50% may occur without changes in postoperative neurologic function. 9–11 The criteria for determining which event-related changes 10 should be considered significant are still empiric. 12 In patients undergoing surgical correction of neuromuscular scoliosis, sensitivity and specificity of IOM in the detection of new postoperative neurologic deficits was maximized with the use of a 50% amplitude reduction criterion. 13 An alternate criterion for sounding the alarm intraoperatively has been loss of cortical baseline amplitude greater than 30–40%. 14–16 Most, however, consider a decrease in amplitude of 50% or greater, an increase in latency of 10% or greater, or both to be significant changes reflecting loss of integrity of a neural pathway, provided these changes are not caused by anesthetics or temperature. 17–20 At least one study suggests that the use of amplitude criteria is associated with better sensitivity for detecting neurologic injury than latency criteria. 21
Back to Top | Article Outline
Volatile Anesthetics.
General anesthesia has an inhibitory effect on neurotransmission and, therefore, on the EP. The effect of anesthetics is greater on synaptic transmission than on axonal conduction. 22 For this reason, responses recorded from polysynaptic pathways (e.g., cortical recordings) are affected by anesthesia to a much greater extent than those recorded from oligosynaptic pathways (e.g., spinal cord and subcortical recordings). 23 For example, VEPs (which represent cortical activity) are very sensitive to the effects of anesthetics while BAEPs (representing brainstem and subcortical activities) are the least sensitive to drug effects.
Table 1
Table 1
Image Tools
Fig. 4
Fig. 4
Image Tools
All volatile anesthetics produce a dose-dependent increase in SSEP latency, an increase in CCT, and a decrease in amplitude 23–29 (table 1). They may also cause morphologic changes, such as contraction of early cortical waveforms (N-20) into a simple monophasic wave under deep isoflurane 30,31 or sevoflurane 32,33 anesthesia (fig. 4). The later cortical waveform components are most sensitive to volatile anesthetics, with marked attenuation at concentrations exceeding 0.5 minimum alveolar concentration (MAC). 30
Satisfactory monitoring of early cortical SSEPs is possible with 0.5–1.0 MAC halothane, enflurane, or isoflurane without nitrous oxide. 24,26 At 0.67 MAC halothane or less, SSEPs were recordable in 96% of cases but only in 91% with higher concentrations. 34 During deep (1.6 MAC) isoflurane anesthesia, however, the early cortical N-20 wave was recordable 35 in 94%, and amplitude decreased severely (table 1). 30 Yet, the later N-35 wave, which is also important in IOM, could only be recorded in 47%. 35
The effect of volatile anesthetics on cortical SSEP amplitude is compounded by nitrous oxide. Increasing isoflurane concentration from 0.5 to 1.0 MAC in the presence of nitrous oxide resulted in a 75% decrease in the cortical SSEP (from 1.2 μV to 0.3 μV). 36
The newer volatile anesthetics desflurane and sevoflurane affect SSEPs not unlike isoflurane but may permit the use of higher inhaled concentrations (table 1). Increases in cortical latency and decreases in amplitude occur at doses of 1.5 MAC sevoflurane and desflurane or less, with minimal effects on subcortical SSEP components. 37,38 Desflurane up to 1.0 MAC without nitrous oxide is compatible with cortical median nerve SSEP monitoring during scoliosis surgery. 38 Even at 1.5 MAC (without nitrous oxide), the amplitude of cortical SSEPs was preserved at 60% of baseline. 39 However, nitrous oxide added to desflurane 40 or sevoflurane 41 severely depresses amplitude. At 1.7–2.5 MAC sevoflurane, a high-amplitude early cortical SSEP waveform is found with absence of all later waves. 32,33
Table 2
Table 2
Image Tools
How volatile anesthetics differ quantitatively in their effects on the SSEP is not completely settled. Pathak et al.26 showed that halothane had a greater effect on both amplitude and latency of the SSEP at equipotent concentrations than either isoflurane or enflurane. On the other hand, Peterson et al.24 found that isoflurane and enflurane reduced SSEP amplitude and prolonged CCT more than halothane did. Sevoflurane and desflurane are associated with less amplitude reduction than isoflurane at a MAC range of 0.7–1.3. 29 In contrast to their effects on the cortical SSEP, all volatile anesthetics, even at concentrations above 1.0 MAC, only minimally affect the subcortical waveform, resulting in high recordability 35 and reliability (table 2).
Back to Top | Article Outline
Nitrous Oxide.
Nitrous oxide (60–70%) generally diminishes cortical SSEP amplitude by approximately 50% while leaving cortical latency and subcortical waves unaffected. 36,42 Nitrous oxide potentiates the depressant effect of volatile anesthetics 24,41 and most intravenous anesthetics, 12,43,44 producing greater amplitude depression than an equipotent concentration of volatile anesthetics administered alone 24,45,46 (table 1). For example, adding 50% (0.5 MAC) nitrous oxide to a fentanyl-based anesthetic resulted in a greater decrease in amplitude than adding 1% (0.8 MAC) isoflurane, especially in patients with abnormal preoperative SSEP. 25 Likewise, during opioid-based anesthetics, nitrous oxide depressed cortical SSEP amplitude to a greater extent than did propofol when substituted for nitrous oxide. 12,47–49
Back to Top | Article Outline
Intravenous Anesthetics.
Table 3
Table 3
Image Tools
Intravenous anesthetics generally affect SSEPs less than inhaled anesthetics (table 3). This is easily seen from the fact that the human SSEP is preserved even at high doses of narcotics and barbiturates (table 3) but abolished at high volatile anesthetic concentrations. Intravenous agents only modestly affect early and intermediate (< 40 ms for median nerve stimulation and < 80 ms for posterior tibial nerve stimulation) SSEP components. Low doses of intravenous agents have minimal effects on SSEPs, whereas high doses of most agents cause slight to moderate decreases in amplitude and increases in latency. With very few exceptions, subcortical potentials are unaffected (table 3).
Back to Top | Article Outline
Barbiturates produce a dose-dependent increase in latency and decrease in early cortical SSEP amplitude that does not preclude IOM. Changes in long-latency cortical waves are affected more than subcortical and midlatency waveforms. This is consistent with the notion that barbiturates, like volatile anesthetics, affect synaptic transmission more than axonal conduction. An induction dose of thiopental (5 mg/kg) increases latency 10–20% and decreases amplitude 20–30%, an effect that lasts less than 10 min. 43,50,51 Similar changes occur with thiamylal. 40 Even at much higher doses, such as those used for barbiturate coma, barbiturates allow recording of cortical SSEPs. 52–55
Back to Top | Article Outline
Unlike the barbiturates, etomidate dramatically increases cortical SSEP amplitude (N-20), up to 400% above preinduction baseline in some patients. 50,43 Subcortical amplitude is decreased by up to 50% (table 3). 50,56 Etomidate is associated with a high incidence of myoclonic movements. 57 Patients with familial myoclonic epilepsy are also known to have abnormally large EPs, 58 especially noted during myoclonic jerking episodes. It is tempting to speculate that myoclonus is an indication that sensory signals are being synchronized (pathologically or by etomidate), which then result in enhanced SSEP amplitude. However, Kochs et al.59 observed amplitude enhancement after etomidate whether or not myoclonic movements occurred. Based on careful electrophysiologic experiments in cats, SSEP amplitude enhancement with etomidate is thought to result from an altered balance between inhibitory and excitatory influences at the level of the cerebral cortex, 60 resulting in increased signal synchronization at the thalamic level. 56
Back to Top | Article Outline
Like etomidate, ketamine increases cortical SSEP amplitude, with the maximum effect occurring within 2–10 min of bolus administration. 61 No effect on cortical latency 61 or subcortical waveforms 62 was evident. However, the addition of nitrous oxide 44 or 1.0 MAC enflurane 61 to a ketamine background anesthetic depressed SSEP amplitude by approximately 50%. Ketamine, 3 mg/kg, followed by 2 mg · kg−1 · h−1 combined with 0.15 mg · kg−1 · h−1 midazolam and 60% nitrous oxide was compatible with satisfactory recordings during major spine surgery. 63
Back to Top | Article Outline
Propofol's effect on SSEPs is similar to that of the barbiturates. This is important because propofol can be infused in anesthetic concentrations during prolonged central nervous system (CNS) surgery and still effect rapid emergence for timely postoperative neurologic assessment. A dose of 2.5 mg/kg propofol produced no changes in the amplitude of the cortical (N-20) and subcortical (N-14) waves after median nerve stimulation. 62 Cortical latency and CCT increased by 8 and 20%, respectively. In scoliosis surgery, total intravenous anesthesia with propofol and sufentanil (table 3) prolonged cortical latency 10–15% and reduced the amplitude of the cortical posterior tibial nerve SSEP by 50%. However, SSEP waveforms stabilized within 30 min after anesthetic administration and were compatible with IOM. 48
When used as a sedative hypnotic in combination with opioids, propofol reduces SSEP amplitude less than nitrous oxide or midazolam. Cortical SSEP amplitude is approximately 50% lower during sufentanil–nitrous oxide 47,48 or alfentanil–nitrous oxide anesthesia 49 compared with sufentanil-propofol-opioid–based regimens. 47,48 Propofol was associated with higher cortical SSEP amplitude despite the use of anesthetic concentrations equivalent to nitrous oxide or sevoflurane. 64 Average cortical SSEP amplitude was higher and within-patient amplitude variability was less during propofol–alfentanil than during nitrous oxide–alfentanil anesthesia. 49 Amplitude was also greater than during midazolam–alfentanil anesthesia. 65 The typical W-shaped morphology of the cortical posterior tibial nerve SSEP was better preserved with propofol than with midazolam.
Back to Top | Article Outline
Benzodiazepines have only mild-to-moderate depressant effects on SSEPs (table 3). Diazepam, 0.1–0.25 mg/kg, produced mild and moderate decreases in N-20 and later wave cortical amplitude, respectively. Very long latency peaks (200–400 ms) were abolished. 66
In a dose of 0.2–0.3 mg/kg, midazolam is associated with modest 67 or no 43 reduction in amplitude and slight prolongation of median nerve SSEP latency (table 3). Adding opioids 43,68 or nitrous oxide 43 to midazolam or propofol 65 preserves the cortical SSEP better when compared to adding nitrous oxide or opioids to thiopental, etomidate, 43 or ketamine. 44 Benzodiazepines affect sensory pathways differentially. The significant decrease in the amplitude of the evoked electromyelogram response (a spinal cord response to somatosensory stimulation) after diazepam 69 indicates a peripheral action. Conversely, sedative doses of midazolam (60–70 μg/kg), while leaving the early cortical waveform (N-20) unaffected, depress late cortical waves generated in the association cortex. 69 This is consistent with the notion that sedative doses of benzodiazepines might blunt the emotional response to pain perception. 70
Back to Top | Article Outline
Most authors report clinically unimportant changes in SSEP latency and amplitude after the administration of opioids, whether given in analgesic or anesthetic doses (table 3).
McPherson et al.50 found minimal SSEP changes after 25 μg/kg fentanyl for induction of anesthesia in adults. A small increase (5–6%) in cortical median nerve SSEP latency and a variable decrease (0–30%) in amplitude resulted after 36–71 μg/kg fentanyl, which was compatible with IOM. 71 No significant effects on SSEP from fentanyl up to 130 μg/kg were observed during hypothermic cardiopulmonary bypass. The effect of fentanyl was greater with boluses compared to a continuous infusion 72 during maintenance of anesthesia.
A bolus dose of 5 μg/kg sufentanil produced 5% increases in early cortical SSEP latency and a 15% increase in CCT. 73 The 40% decrease in cortical amplitude did not interfere with waveform acquisition. 73 Sufentanil, 0.5–1.0 μg/kg, followed by 0.25–0.5 μg · kg−1 · h−1 with 50% nitrous oxide and 0.5% isoflurane prompted a 50% reduction in cortical amplitude and a 5–10% increase in cortical latency and CCT but no changes in subcortical waves. 74
Alfentanil is associated with only modest SSEP amplitude depression while leaving latency unchanged 43,75 (table 3). Three doses of remifentanil (table 3) combined with 0.4 MAC isoflurane produced a 20–30% decrease in early cortical amplitude that was not dose dependant. By contrast, late cortical waves showed a 10–30% increase in amplitude. 76 Compared with the combination of fentanyl and nitrous oxide, remifentanil reduces cortical amplitude less, with lower amplitude variability. 77
Pathak et al.72 reported posterior tibial nerve SSEP latency to increase by approximately 10–15% and amplitude to decrease by 20% after induction of anesthesia with 0.25 mg/kg morphine. Amplitude continued to decrease to approximately 10% of control during subsequent morphine infusion. This study could not isolate the effect of morphine from residual effects of the barbiturate used for induction and the effect of a background nitrous oxide anesthetic, but it shows that this regimen is not desirable for IOM. As with fentanyl, the magnitude of morphine's effect was greater with bolus administration than with continuous infusion.
The administration of subarachnoid meperidine produced a 60% decrease in cortical posterior tibial nerve SSEP amplitude and a 10% increase in latency. The response was abolished in 40% of patients. 78 This is attributed to the local anesthetic-like effect of meperidine in blocking voltage-dependent sodium channels. In contrast, subarachnoid fentanyl (25 μg), 78 morphine (20 μg/kg) combined with sufentanil (50 μg), 79 or morphine alone (15 μg/kg) 80 produced no significant changes in latency or amplitude of cortical posterior tibial nerve SSEPS in the awake or anesthetized states, nor did the lumbar epidural administration of 0.1 mg/kg diamorphine in adolescents undergoing corrective surgery for idiopathic scoliosis. 81
Back to Top | Article Outline
Droperidol is an acceptable anesthetic adjunct with minimal effects of SSEPs. 8
Back to Top | Article Outline
Clonidine and Dexmedetomidine.
Clonidine, an α2 receptor agonist, reduces anesthetic requirements. 82,83 However, clonidine administered alone 84 or added to 1 MAC isoflurane 85 did not change latency or amplitude of the cortical SSEP. At a dose of 10 μg/kg, subcortical amplitude decreased by 10%, and latency increased 2%. 86 Clonidine can be used as an anesthetic adjuvant without compromising SSEP monitoring. Dexmedetomidine affects SSEP amplitude minimally at sedative doses. During isoflurane anesthesia, it blunts isoflurane's effect on SSEP amplitude. 87 In two patients undergoing spinal surgery, dexmedetomidine maintained good conditions for SSEP monitoring. 88
Back to Top | Article Outline
During isoflurane–nitrous oxide anesthesia, adenosine triphosphate does not affect human SSEPs. 89
Back to Top | Article Outline
Neuromuscular Blocking Drugs.
Neuromuscular blocking drugs do not directly influence SSEP, BAEP, or VEP. 90 However, they may improve waveform quality by favorably increasing the signal-to-noise ratio through elimination of the electromyography artifact, 90 which introduces noise at higher frequencies, especially when EPs are acquired at lower stimulation frequency and higher frequency cutoffs. 90
Back to Top | Article Outline
Regional Administration.
Complete local anesthetic block of the sensory pathway abolishes SSEPs. Local infiltration of lidocaine eliminates the cortical evoked response to painful dental stimulation 91,92 as does bupivacaine 93 or lidocaine subarachnoid block. 78
On the other hand, epidural administration of bupivacaine 93,94 or clonidine 95 variably affects the lower-extremity SSEP depending on dose and dermatome stimulated. The SSEP response to L1 dermatome stimulation is reliably abolished by bupivacaine epidural blockade. By contrast, because the S1 nerve root is often incompletely blocked during epidural anesthesia, posterior tibial nerve stimulation can still generate an SSEP response. Thoracic epidural anesthesia (to T7) with 1.5% etidocaine was associated with decreased cortical amplitude (by 60–80%) and increased cortical SSEP latency, while 1% etidocaine resulted in less pronounced changes. 96 Similarly, bupivacaine (0.5–0.75%) injected into the lumbar epidural space significantly prolonged latency and decreased amplitude of posterior tibial nerve SSEPs, contrasted with only slight latency prolongation with 0.25% bupivacaine. 97 Therefore, neuraxial administration of local anesthetics at higher concentrations is not suitable to supplement general anesthesia in scoliosis surgery if SSEPs are to be monitored. 97
Intravenously administered lidocaine affects cortical SSEPs but is unlikely to interfere with IOM. Systemically administered lidocaine at therapeutic plasma concentrations (3–6 μg/dl) in patients anesthetized with sufentanil–nitrous oxide–low dose (< 0.5%) isoflurane further decreased amplitude of the cortical SSEP by approximately 25–30% and produced a small (5%) latency prolongation. 74
Back to Top | Article Outline
Implications for Perioperative Monitoring.
Table 4
Table 4
Image Tools
The volume of information about effects of anesthetics on SEP waveform morphology and metrics is daunting. Ideally, reliable multicenter evidence should be available for each major anesthetic and anesthetic technique to assess the specificity and sensitivity of SEPs in the identification of impending neural injury to allow prompt and successful intervention. Yet, much of the published data of anesthetic effects on SEPs were gathered in neurologically normal patients or were obtained before surgical trespass on the nervous system. Data such as those presented in tables 1–4 represent merely a proxy for assessment of the reliability of IOM in identifying and predicting neural injury during various anesthetics.
It stands to reason that an identifiable, reproducible waveform (which we refer to as recordable) must persist during the anesthetic for critical events to be detectable with IOM. Anesthetic regimens during which even a small number of neurologically normal patients’ waveforms disappear are not suitable for successful IOM. Similarly unsuitable are anesthetics that result in amplitude depression and latency prolongation on the order that would confuse the interpretation of SSEP changes and potentially risk either not detecting a critical event or providing excessive false-negative interpretations. Such regimens include volatile anesthetics alone at a dose greater than 1–1.3 MAC and volatile anesthetics at greater than 0.5 MAC in combination with nitrous oxide (table 1). Therefore, volatile anesthetics alone at up to 1.0 MAC can be used. Desflurane or sevoflurane may allow successful IOM at even higher (1.5–1.75) MAC. Some intravenous anesthetic regimens, such as propofol–sufentanil, reduce amplitude sufficiently to be of concern (table 3). In general, however, intravenous anesthetic techniques result in less amplitude and latency perturbation than volatile anesthetics.
Somatosensory evoked potential waveform reproducibility is directly related to amplitude and inversely related to amplitude variability. 10,12 The smaller the amplitude of the SSEP waveform, the more is it subject to baseline variation, electrical noise, and other confounding influences. Therefore, amplitude preservation should be one of the important goals of the intraoperative monitoring team. This is particularly important when baseline amplitude is low and variability is high, as occurs in elderly (> 50 yr) patients and those with congenital scoliosis, paralytic scoliosis, spinal stenosis, spinal tumor, or other preexisting neurologic deficits. 9,10,18
Given the negative correlation between cortical SSEP amplitude and within-patient amplitude variability, the highest possible SSEP amplitude should be maintained. High-pass 30-Hz digital filtering significantly reduced cortical SSEP amplitude variability in patients undergoing spine surgery and improved amplitude. 12 During nitrous oxide–isoflurane anesthesia, intense surgical stimulation may increase cortical amplitude by more than 45%, contributing to amplitude variability. 98 The substitution of propofol for nitrous oxide increases cortical SSEP amplitude by up to 100% during an opioid-based anesthetic. 47–49 Eliminating nitrous oxide from the background anesthetic has been shown to improve cortical amplitude sufficiently to make IOM more reliable. 25,42 Substitution of remifentanil for fentanyl and nitrous oxide during a low-dose isoflurane anesthetic also decreased SSEP waveform variability, which should improve reliability. If nitrous oxide is to be used in situations in which amplitude needs to be maximized, it should be used in combination with midazolam, where it depresses amplitude the least (16 vs. 40–50% with opioids). 43 Anesthetic adjuncts with little or no effect on SSEPs, such as dexmedetomidine, clonidine, and neuroaxial opioids (table 3), may also be considered. Their MAC-reducing effect should allow lower doses of anesthetics to be used, with less depression of SSEP waveforms.
Alternatively, using agents known to increase the EP amplitude, such as etomidate or ketamine, can be beneficial. 99,44 Several investigators 99,100 were able to use etomidate to improve IOM in patients with abnormally small SSEP waves due to preoperative pathology. Bolus administration of etomidate, 0.5–1 mg/kg, followed by the infusion of 20–30 mg · kg−1 · min−1 augmented waveforms and allowed clinical monitoring that otherwise would not have been possible. Transient increases in the amplitude of SSEP (“injury current”) may represent an early warning sign of CNS hypoxia, 101,102 and etomidate theoretically could interfere with early detection of CNS hypoxia. 50 Nevertheless, Sloan et al.99 were able to detect intraoperative events leading to spinal cord compromise in patients in whom etomidate had been used to enhance the SSEP recordings, indicating that etomidate did not mask neural tissue ischemia.
Limiting the inspired volatile anesthetic concentration in an attempt to optimize IOM may be associated with undesirable consequences. Low concentrations of volatile anesthetics are often used during IOM, and anesthesia may be insufficient to prevent awareness and recall. Practitioners should consider using strategies or devices that assist in the assessment of anesthetic depth. Adding etomidate or propofol is preferable to beginning nitrous oxide or increasing volatile anesthetic concentrations when anesthetic depth is inadequate. Volatile anesthetics are also used to control blood pressure and myocardial stress. Vasodilator and β-adrenergic receptor blocker therapy may need to be substituted when IOM contraindicates the use of higher volatile anesthetic concentrations. Optimal airway resistance should be achieved through nonanesthetic pharmacologic means in bronchospastic patients because high volatile anesthetic concentrations are incompatible with successful IOM. If a volatile anesthetic is nevertheless needed rapidly, sevoflurane permits faster SSEP recovery after the acute need for volatile anesthetic has been resolved. 103
Several strategies can be used to enhance the amplitude and reproducibility of SSEPs during volatile anesthesia. Recording quality depends in large measure on the technical skill and knowledge of the monitoring team. Technical strategies such as keeping electrode impedance low and using appropriate bandpass filters 12 are important. Increasing the rate of stimulation in patients with normal baseline SSEPs may improve the preservation of SSEP waves, particularly at higher volatile anesthetic concentrations. Reliance on far-field subcortical waveforms for IOM, if technically feasible, allows the use of higher volatile anesthetic doses. 104 The robust subcortical SSEP responses are still adequately recorded at up to 1.6 MAC isoflurane alone 30 or 1.0 MAC in the presence of nitrous oxide 27 (fig. 4). Subcortical potentials can also be recorded near field epidurally or from spinous processes rostral to the area of surgical trespass. 17,18
The effects of anesthesia on the EP can be greater in neurologically impaired patients than in patients without preoperative deficits. 25,47,105 The baseline waveform is often diminished 10 and may become completely abolished with the combination of nitrous oxide and low-dose volatile anesthetics. 25,47 In patients with preexisting stroke, ipsilateral cortical SSEPs were of lower amplitude but could be used effectively for IOM during carotid endarterectomy. 106 Eliminating nitrous oxide can restore SSEP amplitude sufficiently to allow useful IOM. Slowing the stimulus presentation rate increased SSEP amplitude in this situation, which suggests a fatigue effect in abnormally responding neurons. 107
Data showing the effect of anesthetic regimens on the specificity and sensitivity of SSEPs in detecting reversible neurologic compromise are scarce. This limitation arises from small sample sizes in reported studies and from the low incidence of intraoperative neurologic injury for most surgical interventions (table 2). Only studies with large populations, such as might be gathered in a prospective multiinstitution trial, would have the capability to demonstrate reliable predictive information for IOM under different anesthetic conditions. 12 Nevertheless, available data suggest a relation between anesthetic techniques and good IOM conditions. Some techniques seem to minimize distraction from “false-positive” SSEP changes and possibly enhance the ability to detect neurologic injury more efficiently (table 2).
In an attempt to relate reliability of IOM to anesthetic regimen, table 2 summarizes sensitivity and specificity for a number of representative reports. Postoperative neurologic deficit has been used as the outcome against which SSEP changes are assumed, but it is useful to consider another dimension. Many intraoperative SSEP changes prompt surgical and circulatory interventions (such as changing the degree of spinal distraction or increasing blood pressure), which reverse potential neurologic injury and consequently result in the absence of postoperative neurologic deficits. In addition to calculating sensitivity and specificity, we therefore also present the incidence of SSEP changes unexplained by perioperative pathology (e.g., spinal distraction or hypotension) in table 2. It seems that the use of subcortical recordings is associated with a high (> 90% specificity) and low rate of unexplained SSEP changes. The same is true for anesthetic techniques that either carefully limit the concentration of volatile anesthetics to less than 1 MAC or avoid nitrous oxide. Interestingly, carefully controlled conditions associated with a general anesthetic seem to result in higher specificity of SSEP monitoring than during local anesthesia. Still, the incidence of “false negatives” and “true positives” is very low, and it is difficult to discern a relation between sensitivity and anesthetic regimen.
In summary, volatile anesthetics at up to 0.5 MAC with nitrous oxide or up to 1.0 MAC without nitrous oxide are compatible with IOM of cortical SSEPs. The newer volatile anesthetics, desflurane and sevoflurane, seem to allow IOM at even higher concentrations. Baseline recordings should be obtained after induction of anesthesia when a steady anesthetic state has been reached. The postinduction latency and amplitude values then serve as a new baseline with which to compare subsequent event-related changes. It is critical to avoid sudden changes in volatile anesthetic depth or bolus administration of intravenous anesthetics during surgical manipulations that could jeopardize the integrity of the neural pathways being monitored. If step changes in volatile anesthetic concentration are undertaken, it must be appreciated that cortical SSEP latency will take 5–8 min after the change to stabilize. 108 The use of continuous infusions of intravenous anesthetics and opioids, 72 as well as the use of constant low doses of volatile anesthetics, is therefore recommended. 72 Modifications in recording technique and anesthetic regimen can improve IOM. Anesthetic regimens consisting primarily of intravenously administered drugs, without the addition of nitrous oxide, are associated with reliable SSEP monitoring. The combination of propofol and an opioid, administered by continuous infusion, is particularly appealing because of favorable emergence characteristics. 68,77 Remifentanil's relative lack of depression of cortical SSEP amplitude and lower amplitude variability make it an attractive choice for IOM. A midazolam–opioid anesthetic may be preferable if intraoperative wake-up testing is contemplated. 109 When such strategies still fail to allow satisfactory IOM, anesthetic regimens known to enhance SSEP amplitude should be considered.
Back to Top | Article Outline
Brainstem Auditory Evoked Potentials
Anatomic and Electrophysiologic Considerations.
The short-latency brainstem components of the auditory evoked potential are referred to as the brainstem auditory evoked potential (BAEP) or the auditory brainstem response. The stimulus is a loud, repetitive click delivered to the external auditory canal. Computer signal averaging allows the response to be extracted from the background electroencephalogram, time-locked to the stimulus. Signals are recorded from electrodes placed over the vertex with the reference electrodes over the mastoid process. BAEPs are considered far-field potentials because their neural generators are far from the recording electrodes. 110–113
Fig. 5
Fig. 5
Image Tools
Brainstem auditory evoked potentials are particularly useful in assessing the structural integrity of the brainstem during certain surgical procedures in the posterior cranial fossa, e.g., resection of acoustic neuromas and other cerebellopontine tumors, as well as microvascular decompression of the trigeminal and facial nerves. 114–116 BAEPs have also been used to monitor brainstem function in comatose patients and those receiving high-dose barbiturates. 117 The BAEP is generated in the brainstem. It represents auditory sensory electrophysiologic activity starting with the eighth cranial nerve and extending through the medulla and pons. Seven waveform peaks occur within the first 10 ms after stimulus presentation 118 (fig. 5). Of primary importance for IOM are waves I, III, and V. The interpeak latency (IPL) I–III provides information regarding the integrity of the peripheral component of the auditory pathway including the eighth cranial nerve, while IPL III–V reflects central brainstem conduction pathways. 119 Waves VI and VII are more sensitive to anesthetics and are not routinely used for IOM. 116,120,121 IPL is less influenced by hearing impairment, stimulus rate, or stimulus intensity than are individual wave latencies.
Transient increases in wave I–V IPL are generally without clinical significance. However, persistent prolongation by more than 1 ms is associated with neurologic injury and auditory impairment. 16
Back to Top | Article Outline
Inhaled Anesthetics.
Potent volatile anesthetics are associated with small increases in BAEP latency but do not affect wave I–V amplitude 122–130 (table 4). The prolongation of wave I–V latency and IPL reflects the depressant effect of volatile anesthetics on brainstem neuronal activity.
Fig. 6
Fig. 6
Image Tools
Duncan et al.131 reported no changes in BAEP in children anesthetized with halothane. In adults, the effect of volatile anesthetics on BAEP latency is dose dependent 122,123 up to 0.9 MAC enflurane 124 and 0.85–1.3 MAC isoflurane. 125,126 The IPL III–V, reflecting brainstem conduction time, was also prolonged with isoflurane 125,126 (fig. 6). Sevoflurane at 0.5–1.5 MAC with 66% nitrous oxide produced a minor prolongation of wave III and V latencies as well as IPL I–III, III–V, and I–V. These changes are similar to those produced by isoflurane. 37
In contrast to cortical SSEPs, the action of volatile anesthetics on BAEP latency or amplitude is not affected by 50–70% nitrous oxide. Ten to 50% nitrous oxide alone also had no effect on the latency, interpeak latency, or amplitude of waves I–V in healthy volunteers. 132 However, in patients with certain forms of hearing impairment, BAEP latency was increased by nitrous oxide, perhaps due to nitrous oxide–induced increases in middle-ear pressure. 133,134
Back to Top | Article Outline
Intravenous Anesthetics.
Barbiturates in doses used for induction of anesthesia do not affect the BAEP, even when thiopental was administered to children already anesthetized with halothane and nitrous oxide. 131 At higher doses (up to 77.5 mg/kg), thiopental prolonged individual waveform latencies as well as interpeak latencies by approximately 10%. 53 Amplitude was unchanged in doses used for induction of anesthesia, and BAEP waveforms were easily recorded even in the presence of an isoelectric electroencephalogram. 53 Similar results were reported with pentobarbital. 54,55
Propofol (2 mg/kg followed by a continuous infusion) increased wave I, III, and V latencies by less than 5 % without changing amplitude. 135,136 In volunteers exposed to stepped blood concentrations of propofol, wave V amplitude did not change, but latency was slightly prolonged. 137 In patients anesthetized with thiopental and nitrous oxide, etomidate infusions of 10–50 μg · kg−1 · min−1 had no effect on individual wave, interpeak latencies, or the amplitude of BAEP 138 (table 4), nor did 2 mg/kg ketamine. 139,140 Fentanyl, 141,142 alfentanil, 142 sufentanil, 143 morphine, 142,144 and benzodiazepines do not change the amplitude or latency of BAEP. 145 Likewise, BAEPs do not change in humans receiving chronic therapy with pheno-barbital. 146
Back to Top | Article Outline
Midlatency Auditory Evoked Potentials.
Fig. 7
Fig. 7
Image Tools
Fig. 8
Fig. 8
Image Tools
The midlatency auditory evoked potential (MLAEP) consists of waves (Na, Pa, Nb, and P1) occurring 10–80 ms after stimulation (fig. 7). It represents processing of the auditory stimulus by the primary auditory cortex and can be monitored when that area is at risk. 147 MLAEPs have a characteristic periodic waveform with a large peak-to-peak amplitude. The major energy of the power spectrum is in the 30- to 40-Hz frequency range, which is why they are sometimes referred to as “40-Hz potentials” (fig. 8).
Back to Top | Article Outline
Inhaled Anesthetics.
Because BAEP signals are preserved with all volatile anesthetics, initial signal transduction remains intact, and auditory stimuli can be further processed rostral to midbrain level. Volatile anesthetic agents produce predictable dose-dependent increases in MLAEP latency and decreases in amplitude. 128–130 All volatile anesthetics suppress MLAEP components to a similar extent at equi-MAC. 119,121,122 At approximately 1 MAC, MLAEP components are markedly attenuated, indicating suppression of cortical auditory processing such as auditory perception, intraoperative wakefulness, and explicit or implicit recall of intraoperative events. 148–151
Nitrous oxide decreases cortical auditory evoked potential wave amplitude in a progressive, dose-related manner. 133,134,152,153 The auditory EP changes may be the result of a nitrous oxide–induced increase in the auditory threshold. 133
Back to Top | Article Outline
Intravenous Anesthetics.
Fig. 9
Fig. 9
Image Tools
Induction of anesthesia with barbiturates, propofol 135,136,154 and etomidate, 138,155 but not with benzodiazepines 145,156 (see next paragraph) causes complete suppression of MLAEPs. Amplitudes and latencies of MLAEP returned to the awake values 4–6 min after thiopental induction as motor signs of wakefulness appeared. 157 Etomidate caused dose-dependent decreases in amplitude and increases in latency of the Pa and Nb waves. Maintenance of anesthesia with propofol at a dose of 3–5 mg · kg−1 · h−1 caused MLAEP latency prolongation and amplitude reduction that was comparable to 0.4–0.8% isoflurane. 154 Stepwise increases in the dose of propofol caused graded changes in MLAEP (decrease in Pa and Nb amplitude and increase in latency), which correlated well with the level of sedation. The addition of alfentanil decreased the mean propofol concentration required for the same endpoint. 137 Pa and Nb latency had the best correlation with propofol concentration and sedation level 137 (fig. 9).
Induction of anesthesia with midazolam (0.2–0.3 mg/kg), diazepam (0.3–0.4 mg/kg), or flunitrazepam (0.03–0.04 mg/kg) did not affect waves Na, Pa, Nb, and P1 of the MLAEP, except for an isolated 15% increase in P1 latency with midazolam and a 40% decrease in Na/Pa amplitude with flunitrazepam. 145 Maintenance of anesthesia with flunitrazepam and fentanyl preserved MLAEP latency and amplitude and was associated with a high incidence of motor signs of wakefulness. 155 Induction doses of racemic ketamine (2 mg/kg) or S (+)-ketamine (1 mg/kg) likewise did not affect the MLAEP 140 Primary cortical processing of auditory stimuli therefore seems to be preserved with ketamine 140 and benzodiazepine 145 “anesthesia.”
Opioids produce partial suppression of the MLAEP without a clear dose dependence. Even at the highest opioid doses, early cortical MLAEPs (waves Na and Pa) are only slightly suppressed. Induction of anesthesia with alfentanil (100–500 μg/kg), fentanyl (10–50 μg/kg), or morphine (1–3 mg/kg) produced no changes in the (early) Na wave latency or Na/Pa and Pa/Nb amplitudes. However, Pa, Nb, and P1 latencies were prolonged by 5–25%, and the (later) Nb/P1 amplitude was reduced by 50–75%. 142 With sufentanil, 1–5 μg/kg, Na latency increased 10%, while Pa, Nb and P1 latencies increased 20–33%. 143 Nb/P1 amplitude decreased 60% after 3–5 μg/kg sufentanil. 143 In contrast to other opioids, remifentanil's effects on MLAEP showed mild dose dependence. 76 Remifentanil combined with 0.4 MAC isoflurane produced a 20% in-crease in Pa and Nb amplitude at a low dose (1-μg/kg bolus and 0.2-μg · kg−1 · min−1 infusion). The medium dose (2.5 μg/kg and 0.5 μg · kg−1 · min−1) left ampli-tude unchanged, while the high dose (5 μg/kg and 1 μg · kg−1 · min−1) decreased Pa and Nb amplitude by 10–20%. 76
The inability of opioids to suppress the MLAEP indicates that perception, processing, and, possibly, the explicit or implicit encoding of auditory information do not cease completely during opioid anesthesia. 142,143 Opioids, even in very large doses, are less reliable in suppressing consciousness and sensory information processing than are volatile anesthetics. 142,158,159 This is consistent with clinical reports of intraoperative awareness and perception of auditory stimuli if opioids are used exclusively for general anesthesia. Dexmedetomidine did not influence the suppressant action of volatile anesthetics on MLAEP. 87 Succinylcholine activated the MLAEP during isoflurane–nitrous oxide anesthesia, as evident from its ability to enhance Na and Nb amplitudes by 50%, possibly through increased neuronal traffic from muscle afferents. 160
Back to Top | Article Outline
Implications for Perioperative Monitoring.
Brainstem auditory evoked potential waves I–V can be adequately monitored under deep volatile anesthesia, even exceeding 1 MAC, whether in the presence or absence of nitrous oxide. 125 BAEP monitoring can also be successfully performed during deep levels of intravenous anesthesia, even at electroencephalogram burst suppression, 54,55 and does not impose limitations on anesthetic technique.
The MLAEP is affected by anesthetic agents in a manner similar to the cortical SSEP. Therefore, monitoring the MLAEP to assess the integrity of cortical brain areas requires modification of the anesthetic technique. In particular, the use of benzodiazepines, opioids, or ketamine and volatile anesthetics at less than 0.5 MAC would preserve MLAEPs for IOM. Current evidence suggests that MLAEPs are a sensitive indicator of residual cortical information processing and cognitive function during general anesthesia. 148,149 They may be useful for recognizing periods of insufficient anesthesia and intraoperative awareness. 148 The auditory evoked potentialIndex, a mathematical derivation from the MLAEP waveforms, has been used successfully as the input signal in a closed-loop system to control the administration of propofol 161 and volatile anesthetic 162 anesthesia. The auditory brainstem response has been used to differentiate brainstem anesthesia from other states affecting consciousness. 163
Back to Top | Article Outline
Visual Evoked Potentials
Anatomic and Electrophysiologic Considerations.
Fig. 10
Fig. 10
Image Tools
The visual pathway includes the retina, optic nerve, optic chiasm (where half the fibers cross to the contralateral side), optic tracts, lateral geniculate nucleus in the thalamus, optic radiation, and occipital visual cortex. Stimulating the retina produces an evoked electrical response in the occipital cortex, which may change with impairment of the visual apparatus and associated neural pathways. VEPs are recorded from scalp electrodes placed over the occipital, parietal, and central areas. 1 They are cortical near-field potentials with long latencies. In anesthetized patients, flashes of red light are delivered through closed eyelids using light-emitting diodes. 121 The characteristic waves of the flash VEP are a negative wave with 70-ms latency (N-70) and a positive wave with 100-ms latency (P-100). In the VEP waveform complex, the P-100 wave has been evaluated for IOM (fig. 10).
Back to Top | Article Outline
Inhaled Anesthetics.
Table 5
Table 5
Image Tools
Fig. 11
Fig. 11
Image Tools
In general, all volatile anesthetics markedly prolong VEP latency and decrease amplitude in a dose-dependent manner 164,165 (table 5). At 1.5 MAC, the VEP could not be interpreted (fig. 11). Nitrous oxide alone severely attenuates VEP amplitude, 132,166 and its addition to volatile anesthetics can make waveforms unrecordable. 27
Back to Top | Article Outline
Intravenous Agents.
Induction doses of thiopental decrease the amplitude and prolong the latency of VEP waves, 167 while etomidate produces a small increase in latency with no change in amplitude 168 (table 5). However, etomidate transiently decreased amplitude by as much as 50% when administered to patients already anesthetized with fentanyl and nitrous oxide. An induction dose of fentanyl (10–60 μg/kg) produced a 30% amplitude reduction beyond that associated with premedication 169 and was independent of dose.
Back to Top | Article Outline
Implications for Intraoperative Monitoring.
Visual evoked potentials are very sensitive to the effects of anesthetics and physiologic factors because they represent polysynaptic cortical activity. Because flashlight stimulation activates both temporal and nasal parts of the retina and the nasal fibers cross to the contralateral side at the level of the optic chiasma, retrochiasmatic lesions cannot be monitored. 170 In addition, VEPs are highly dependent on appropriate stimulation of the retina and may be unduly affected by narcotic-induced pupillary constriction. 169
The available data indicate that opioid and ketamine or propofol-based anesthetic techniques, as well as regimens using low-dose volatile anesthetics without nitrous oxide, allow intraoperative recording of VEPs. Although satisfactory intraoperative recordings can be obtained in the majority of patients, clinical observations suggest a high incidence of false-positive and false-negative results. 170 Anesthetic technique can affect the incidence of false-positive VEP changes. A propofol–nitrous oxide technique was associated with a 10–15% incidence of false positives compared to none with ketamine. 171 Up to 80% of intraoperative changes in VEP are not followed by postoperative neurologic deficits. 172,173 VEP monitoring has been largely abandoned for intraoperative applications because of these many limitations. However, VEPs have been recently used to assess the safety of peribulbar and retrobulbar blocks for regional anesthesia of the orbit. 174
Back to Top | Article Outline

Physiologic Influences on Sensory Evoked Potentials

In clinical practice, cooling to 33°–34°C may occur passively or represent a protective strategy for patients at risk of neurologic injury who at the same time may be undergoing IOM of EP (e.g., during thoracic aortic aneurysm repair). Even lower temperatures may occur during cardiopulmonary bypass. A clear understanding of the effects of hypothermia on EP is therefore necessary for the appropriate interpretation of the intraoperative SEPs.
Back to Top | Article Outline
General Physiologic Considerations: Hypothermia.
Mild hypothermia (33°–34°C) may produce cerebral stimulatory effects as reflected by arousal phenomena, increased EP amplitude, and hyperresponsive reflexes. 175 It is associated with increased amplitude and duration of nerve action potential but decreased conduction velocity, § brought about by enhanced neurotransmitter release leading to higher miniature endplate potentials. 176 Resting electroencephalogram at 33°C is characterized by a small shift to lower frequencies without changes in amplitude. These general electrophysiologic observations explain the small increase in EP latency and inconsistent effect on amplitude seen with mild hypothermia.
Neuronal function is decreased at temperatures less than 32°C (moderate hypothermia) because of reduced neurotransmitter release and impaired synaptic transmission. 177–179 Electrophysiologic changes are characterized by decreased resting membrane potential, decreased amplitude, increased nerve action potential duration, and decreased nerve conduction velocity. The slowing of axonal conduction has been linked to decreases in resting membrane potential and increases in sodium–potassium channel activation time across the membrane. 180 Synaptic transmission is more sensitive to the effects of hypothermia than axonal propagation. 178,181,182 Both peripheral and central conduction are significantly delayed by hypothermia decreasing by 5%183 and 15%184 per degree Celsius, respectively. The effects of temperature on the axon and synapse are additive, compounding temperature effects on multisynaptic pathways. For example, the more pronounced effect of hypothermia on cortical than on spinal SSEP is attributed to the additional suppression of synaptic transmission in the lemniscal–thalamic pathway. 185 Similarly, hypothermia progressively depresses both the resting electroencephalogram and late cortical SSEP components that involve an increasing number of interposed synapses. 183
Back to Top | Article Outline
Effect of Temperature on SSEP.
Back to Top | Article Outline
The site of temperature monitoring is important in assessing the relation between SSEP waves and body temperature. In patients undergoing hypothermic cardiopulmonary bypass, posterior tibial nerve SSEP latency correlated best with nasopharyngeal temperature. 186 Local extremity hypothermia also delays conduction along peripheral nerves in anesthetized patients, 187 but cortical SSEP amplitude and CCT are not affected by extremity temperature. 188 In acquired poikilothermia, hypothermia to 33.5°C decreased central and peripheral nerve conduction velocities. 189 SSEP latencies and CCT increased by 10–20%. The latency of the first cortical SSEP wave increased by 9–12% for every degree Celsius decrease in temperature in humans 186 as well as rats. 183 During hypothermic cardiopulmonary bypass, all SSEP components could be consistently recorded at esophageal temperatures as low as 19°C. 186 This level of hypothermia results in cessation of cortical electrical activity and, hence, electroencephalogram silence. 190 Cooling to a nasopharyngeal temperature of 27°C was associated with a linear increase in the latency of cortical and subcortical SSEP components. Latency to the first positive cortical median nerve SSEP peak N-20 increased by 1.5 ms/°C (or approximately 15%/°C) in nasopharyngeal temperature. Posterior tibial nerve SSEP latencies increased with nasopharyngeal temperature by 1.05 ms/°C for the subcortical P-27 peak and by 1.47 ms/°C for the cortical P-40 peak (approximately 4%/°C). 191 Human central conduction time increases linearly by 8–12% per degree reduction in temperature from 37–28°C. 186,187 Other authors have found an exponential relation between CCT 28,192 or median nerve SSEP latency 28 and temperature during hypothermic cardiopulmonary bypass.
Hypothermia-induced SSEP changes return to baseline after 30 min of rewarming. 186 However, a hysteresis exists in the relation between temperature and EP latency, 193 indicating that cooling and rewarming curves should be considered separately. 184 In one report, the latency of the primary cortical N-20 response increased by 1.7ms/°C during cooling but decreased by only 1 ms/°C during rewarming. The CCT increased linearly by 0.85 ms/°C during cooling and decreased by 0.46 ms/°C during rewarming. 183
While hypothermia-induced changes in SSEP latency are well defined, amplitude behaves unpredictably, 189,191 with reports of no change, decreased amplitude, and even increases in amplitude. 194 In one study, N-20 and N-13 amplitudes decreased by 3.5% and 1.3%, respectively, for each 1°C temperature reduction 195
Back to Top | Article Outline
Raising body temperature from 37.5° to 40.5°C produced a decrease in latency and increase in conduction velocity of rat spinal and cortical SSEP. 185 Compared with 37°C, mild hyperthermia to 39°C caused human cortical and subcortical SSEP latencies to decrease by 5–7%, with no changes in amplitude. 185 Further increases in temperature prolong SSEP latency. Hyperthermia beyond the temperature at which reversal of latency changes occurs (41.4°–42.1°C) alters rat SSEPs permanently, shortens survival time, and is associated with histologic evidence of neuronal damage. 196 For example, SSEP amplitude decreased to 15% of baseline 194 at 42°C.
Back to Top | Article Outline
Effects of Temperature on BAEP.
Back to Top | Article Outline
Brainstem auditory evoked potentials are more resistant than SSEPs to the effects of mild hypothermia. In humans undergoing cardiopulmonary bypass, BAEP latency was prolonged by 33% at 29°C and returned to baseline with rewarming. 197 Wave V was the most affected, while wave I showed the least change. As is the case with SSEPs, hysteresis exists in the temperature-versus-latency relation of the BAEP. 198
Brainstem auditory evoked potential amplitude is variably affected by hypothermia. In some studies, amplitude increased during progressive hypothermia, reaching a maximum at 28°–32°C. 189,199 At lower temperatures, BAEP amplitude decreased (as is the case with other EPs) until the waves disappeared at 20°–23°C. Other studies report a decrease in BAEP amplitude with progressive cooling without an initial increase. 197 This discrepancy may be related to differences in stimulus intensity, rate of temperature change, or both. Hypothermia-related amplitude increases were observed at stimulus levels of 75–90 dB but not with stimuli of lower intensity, which is at the high end of the stimulus-intensity range for IOM. 200 BAEP amplitude has also been shown to increase initially when temperature decreased rapidly but to decrease steadily with the slow and gradual development of hypothermia. 201
Back to Top | Article Outline
Several animal studies demonstrated that increases in temperature from 36° to 40°C to decrease BAEP amplitude, latency, and IPL. 202–204 Persistence of hyperthermia beyond a critical level was associated with increases in latency, further decreases in amplitude, loss of waves V and VI, and the appearance of new abnormal peaks. These changes likely indicate damage to neural tissue in the brainstem region. In rats, exposure needed to produce injury was 60 min at 41°C, 30 min at 42°C, and 15 min at 42.5°C. 202 Therefore, changes in BAEP during hyperthermia may serve as a noninvasive indirect estimate of regional brainstem temperature. Because BAEPs reflect the functional state and integrity of the brainstem, BAEP monitoring may have potential clinical utility in guiding the use of hyperthermic therapy of malignant diseases of the CNS, especially brainstem gliomas.
Back to Top | Article Outline
Effects of Temperature on VEP.
In conscious humans, VEP latency is 10–20% longer at 33°C than at 37°C. 203 Russ et al.204 reported progressive latency prolongation and amplitude reduction of VEP with hypothermia leading to complete loss of waves at 25°–27°C. With faster cooling, VEP disappeared at a higher temperature than with slower cooling.
Back to Top | Article Outline
Carbon Dioxide.
Clinically relevant levels of induced hypocapnia (arterial carbon dioxide tension [Paco2] 20–25 mmHg) do not compromise SSEP monitoring but shorten SSEP latencies by 2–4% in isoflurane-anesthetized patients 205 and awake volunteers. 206 In contrast to the 70% cortical amplitude enhancement seen in hyperventilating awake volunteers, 206 no changes in amplitude occurred in anesthetized hypocapnic patients. 205 The hypocapnia-related decrease in latency reflects an increase in conduction velocity, perhaps attributable to changes in pH, ionized calcium concentrations, and ionic equilibrium across neural membranes leading to enhanced neuronal excitability. It does not seem to be related to changes in anesthetic depth. 206
Hypercapnia to a Paco2 of more than 100 mmHg was associated with an increase in feline SSEP latency by 15–30% and a decrease in amplitude by 60–80%. 188 Hypercapnia to a Paco2 of 50 mmHg had no effect on human SSEPs. 207
Enflurane-induced increases in BAEP latency are mildly (< 5%) potentiated by hyperventilation to a Paco2 of 25–30 mmHg. 208
Back to Top | Article Outline
Mild hypoxemia (to an end-tidal pressure of oxygen [Peto2] of 48 mmHg) does not affect human 206 SSEPs. Severe progressive hypoxia 209 or cerebral ischemia 210 is associated with a decrease in SSEP amplitude and an increase in latency, eventually resulting in complete loss of cortical SSEP waves. 102 Grundy et al.211 reported a decrease in SSEP amplitude as a manifestation of intraoperative hypoxemia in patients. Cortical SSEPs are more sensitive to hypoxia than the electroencephalogram. 212 Because SSEP changes due to hypoxia correlate with reductions in brain high-energy phosphate concentrations, changes in SSEP may represent an indicator of CNS ischemia. Cortical evoked responses also seem to be more sensitive to hypoxia than spinal and subcortical responses, presumably because the latter are more tolerant of hypoxia than the cerebral cortex, because of their lower metabolic rate. 213 Early responses to ischemia or hypoxia can manifest as a transient increase in SSEP amplitude (“injury potential”) before the occurrence of amplitude reduction and latency prolongation. 102 This may be related to the phenomenon of anoxic activation, which is attributed to the early loss of function by inhibitory cortical interneurons. 214
No changes in BAEP were observed with arterial oxygen tension (Pao2) values ranging from 60 to 570 mmHg. 141 In sleep apnea patients, BAEP did not change with mild hypoxemia (arterial oxygen saturation as low as 45%). 215 However, acute severe hypoxemia (Pao2 20–30 mmHg) depressed the feline BAEP. 216,217 Rabbit peak and interpeak latencies increased before the complete loss of BAEP waves. 218 With normal mean arterial pressure, severe hypoxemia depressed BAEP waves but left cortical EPs unaffected. Early hypoxia-induced changes in BAEP result from failure of the cochlear mechanism and not from brainstem dysfunction, suggesting that the cochlea is exquisitely sensitive to hypoxia. 216,217 Hypoxia to Pao2 of 20 mmHg results in a transient increase followed by a decrease in feline VEP amplitude. 212
Back to Top | Article Outline
A decrease in mean arterial pressure (MAP) to levels below the autoregulatory threshold progressively decreased SSEP amplitude without changing latency. Such changes, which may be reversible or irreversible (in the case of permanent tissue injury), 219 likely reflect reduced oxygen delivery to neural tissues. A rapid decrease in MAP within the autoregulatory range is also associated with transient changes in SSEP that resolve despite the persistence of hypotension, presumably reflecting autoregulation at work to restore blood flow. The rapid reduction of MAP from 140 mmHg to 50 mmHg decreased canine SSEP amplitude to 58% of control. Within 15 min, SSEP recovered to 70% of control, and by 60 min, the amplitude had recovered to baseline despite continued hypotension.
Hemorrhagic shock has been associated with a transient increase in the amplitude of SSEP probably related to the phenomenon of anoxic activation followed by reduced amplitude and loss of SSEP. 220
Clinically encountered levels of hypotension have little effect on BAEP. Animal studies have shown the BAEP to be well preserved with profound levels of induced hypotension (MAP of 20–40 mmHg). 221 In children, the BAEP became abnormal with a reduction in cerebral perfusion pressure to less than 30 mmHg. 222 Concomitant hypotension and hypoxemia, on the other hand, severely depressed all EP modalities. 217
Back to Top | Article Outline
In primates, acute isovolemic hemodilution to a hematocrit of 11–15% for 1 h was associated with decreased SSEP amplitude, which recovered when the hematocrit was restored to baseline. 199,223 In another study, SSEP and VEP amplitude increased at a hematocrit of 16–20%, as seen with anoxic activation. A hematocrit less than 10% decreased amplitudes even more, an effect that reversed at a hematocrit of 22%. Hematocrit below 15% also prolonged the latencies of SSEP and VEP.
Back to Top | Article Outline
Concomitant Hypotension and Hemodilution.
Simian cortical SSEP amplitude was attenuated to 25–50% of control by the combined effect of hypotension (to a MAP of 25 mmHg) and hemodilution (to a hematocrit of 14%). 199 Latency was not affected. None of the surviving monkeys that maintained an SSEP amplitude greater than 60% of baseline had neurologic damage. The probability of brain injury was greater than 50%199 if the SSEP amplitude decreased below 60% of baseline. SSEP may be useful as an intraoperative monitor to avoid neurologic injury under conditions of combined hypotension and hemodilution.
Brainstem auditory evoked potentials were unchanged in monkeys that survived the stress of combined hemodilution (hematocrit of 16%) and hypotension (MAP of 30 mmHg). However in the nonsurviving monkeys, BAEPs recorded before death were diminished substantially or abolished, indicating the occurrence of extensive brainstem damage, which may have contributed to the mechanism of death. 199 BAEP alone may not be a useful predictor of impending brainstem injury during combined hemodilution and hypotension because of the absence of early warning criteria.
Back to Top | Article Outline
Implications for Intraoperative Monitoring.
Somatosensory evoked potentials may be recorded reliably at temperatures as low as 20°C and can be useful as indicators of neurologic function during a variety of surgical procedures that require hypothermic cardiopulmonary bypass and circulatory arrest (e.g., basilar aneurysm clipping). The relation between the latency of SSEP and temperature assists in SEP interpretation during cardiopulmonary bypass. Pathologic prolongation of SSEP latency can be presumed if latencies lengthen substantially beyond the level predicted by temperature changes (1.5 ms/°C for the early cortical SSEP), particularly if asymmetric changes are detected. This assumes that sufficient time for equilibration of SSEP latency is available and hysteresis-related uncertainty about latency changes is eliminated. The latter may be especially an issue if there is repeated cooling and warming because the direction of temperature manipulation determines the expected SSEP change concomitant with the magnitude of the temperature difference. This is analogous to the problems encountered with electroencephalogram interpretation during rapidly occurring temperature fluctuations. 224 Acute, dramatic, unilateral changes in SSEP amplitude may therefore be a more reliable indicator of intraoperative stroke in patients undergoing hypothermic cardiopulmonary bypass. 225
Somatosensory evoked potential waves disappear at different temperatures in individual patients, which argues against using a fixed temperature endpoint as an indicator of optimal cooling depth. Presence of the P-14 wave implies persistence of brainstem metabolic activity. Disappearance of the P-14 wave (which represents brainstem activity) has been used as the criterion for reaching satisfactory deep hypothermia. 226
Only severe hypercapnia degrades SSEP waveforms, 188 whereas the effects of hypocapnia are clinically insignificant. Cortical but not subcortical SSEPs are quite sensitive to hypoxemia. 213 BAEP are not a reliable warning sign for intraoperative brainstem hypoxemia because early hypoxia-induced changes in BAEP result from failure of the cochlear mechanism, not from brainstem dysfunction. 216,217
Transient SSEP changes in response to blood pressure reduction presumably reflect slow adaptation of cerebral blood flow autoregulation. Changes in SSEP after spinal distraction have resolved in some instances when the MAP was raised above the patient's normal blood pressure range. Therefore, during surgical manipulations, a degree of hypotension otherwise considered safe could result in spinal cord ischemia. 227 Monitoring of SSEP may help to determine the safe limits of hypotension in individual patients. During hypotension or hemodilution, cerebral oxygen delivery is maintained by compensatory cerebral vasodilation. The compensatory vasodilatory reserve is exhausted at higher perfusion pressures if hemodilution is combined with hypotension. 228 The exact safe thresholds for blood pressure and hematocrit during combined elective hypotension and isovolemic hemodilution (as used during scoliosis surgery) cannot be precisely defined but should probably be higher than they would be if either hypotension or hemodilution were used alone. Synergistic adverse effects of hemodilution and hypotension are evident in SSEP waveforms. 199 Hence, IOM of SSEP but not BAEP in this setting may be helpful in determining whether neuronal tissue oxygen demands are being met. An SSEP amplitude reduction greater than 40% from baseline may be cause for alarm in the setting of combined hypotension and hemodilution. 199
Back to Top | Article Outline


The known effects of anesthetics and anesthetic adjuvants on the major SEP modalities used for IOM have been reviewed, along with the influences of body temperature, blood gas tensions, blood pressure, and hematocrit. Practical conclusions are summarized that reflect the relative importance of these effects on the ability to reliably monitor neurologic pathways at risk during the perioperative period.
The authors thank Tanya Callaway (Secretary, Department of General Anesthesiology, The Cleveland Clinic Foundation, Cleveland, Ohio) for her excellent work in manuscript preparation and Nadia Kolta, M.B.A., M.L.I.S. (Librarian, Program Coordinator, Department of General Anesthesiology, The Cleveland Clinic Foundation, Cleveland, Ohio), for her expert assistance with library resources.
Back to Top | Article Outline


§ The velocity of conduction in human nerve fibers varies from 5 to 100 m/s. It is directly proportional to myelinated fiber diameter and exponentially related to unmyelinated fiber diameter. A decrease in conduction velocity results in a proportionately increased latency of the EP wave. EP latency can be affected to a greater extent than conduction velocity if the corresponding latency assesses a neural pathway with multiple synapses. Cited Here...
Back to Top | Article Outline


1. Chiappa KH, Ropper AH: Evoked potentials in clinical medicine (first of two parts). N Engl J Med 1982; 306: 1140–50

2. Chiappa KH, Ropper AH: Evoked potentials in clinical medicine (second of two parts). N Engl J Med 1982; 306: 1205–12

3. Nakamura M, Nishida S, Shibasaki H: Deterioration of average evoked potential waveform due to asynchronous averaging and its compensation. IEEE Trans Biomed Eng 1991; 38: 309–12

4. Grundy BL: Monitoring of sensory evoked potentials during neurosurgical operation: Methods and applications. Neurosurgery 1982; 11: 556–75

5. Greenberg RP, Ducker TB: Evoked potentials in the clinical neurosciences. J Neurosurg 1982; 56: 1–18

6. Chiappa KH. Pattern-shift visual evoked potentials: Interpretation, Evoked Potentials in Clinical Medicine, 2nd edition. Edited by Chiappa KH. New York, Raven Press, 1990, pp 111–3

7. Sebel PS, Erwin CW, Neville WK: Effects of halothane and enflurane on far and near field somatosensory evoked potentials. Br J Anaesth 1987; 59: 1492–6

8. Sloan TB: Anesthetic effects on electrophysiologic recordings. J Clin Neurophysiol 1998; 15: 217–26

9. LaMont RL, Wasson SL, Green MA: Spinal cord monitoring during spinal surgery using somatosensory spinal evoked potentials. J Pediatr Orthop 1983; 3: 31–6

10. Lubicky JP, Spadaro JA, Yuan HA, Fredrickson BE, Henderson N: Variability of somatosensory cortical evoked potential monitoring during spinal surgery. Spine 1989; 14: 790–8

11. York DH, Chabot RJ, Gaines RW: Response variability of somatosensory evoked potentials during scoliosis surgery. Spine 1987; 12: 864–76

12. Kalkman CJ, ten Brink SA, Been HD, Bovill JG: Variability of somatosensory cortical evoked potentials during spinal surgery: Effects of anesthetic techniques and high-pass digital filtering. Spine 1991; 16: 924–9

13. Noordeen MH, Lee J, Gibbons CE, Taylor BA, Bentley G: Spinal cord monitoring in operations for neuromuscular scoliosis. J Bone Joint Surg Br 1997; 79: 53–7

14. More, RC, Nuwer MR, Dawson EG: Cortical evoked potential monitoring during spinal surgery: Sensitivity, specificity, reliability, and criteria for alarm. J Spinal Discord 1988; 1: 244–5

15. Sbarigia E, Schioppa M, Misuraca M, Panico MA, Battocchio C, Maraglino C, Speziale F, Fiorani P: Somatosensory evoked potentials versus locoregional anaesthesia in the monitoring of cerebral function during carotid artery surgery: Preliminary results of a prospective study. Eur J Vasc Endovasc Surg 2001; 21: 413–6

16. Burke D, Nuwer MR, Daube J, Fischer C, Schramm J, Yingling CD, Jones SJ: Intraoperative monitoring. The International Federation of Clinical Neurophysiology. Electroenceph Clin Neurophysiol Suppl 1999; 52: 133–48

17. Brown RH, Nash CL, Berilla JA, Amaddio MD: Cortical evoked potential monitoring: A system for intraoperative monitoring of spinal cord function. Spine 1984; 9: 256–61

18. Nuwer MR, Dawson E: Intraoperative evoked potential monitoring of the spinal cord: Enhanced stability of cortical recordings. Electroencephalogr Clin Neurophysiol 1984; 59: 318–27

19. McTaggert Cowan RA: Somatosensory evoked potentials during surgery. Can J Anesth 1988; 45: 387–92

20. Faberowski LW, Black S, Trankina MF, Pollard RJ, Clark RK, Mahla ME: Somatosensory-evoked potentials during aortic coarctation repair. J Cardiothorac Vasc Anesth 1999; 13: 538–43

21. Lam AM, Manninen PH, Ferguson GG, Nantau W: Monitoring electrophysiologic function during carotid endarterectomy: A comparison of somatosensory evoked potentials and conventional electroencephalogram. A nesthesiology 1991; 75: 15–21

22. Richard CD: Actions of general anaesthetics on synaptic transmission in the CNS. Br J Anaesth 1983; 55: 201–7

23. Samra SK, Vanderzant CW, Domer PA, Sackellares JC: Differential effects of isoflurane on human median nerve somatosensory evoked potentials. A nesthesiology 1987; 66: 29–35

24. Peterson DO, Drummond JC, Todd MM: Effects of halothane, enflurane, isoflurane, and nitrous oxide on somatosensory evoked potentials in humans. A nesthesiology 1986; 65: 35–40

25. McPherson RW, Mahla M, Johnson R, Traystman RJ: Effects of enflurane, isoflurane and nitrous oxide on somatosensory evoked potentials during fentanyl anesthesia. A nesthesiology 1985; 62: 626–33

26. Pathak KS, Amaddio BS, Scoles PV, Shaffer JW, Mackay W: Effects of halothane, enflurane, and isoflurane in nitrous oxide on multilevel somatosensory evoked potentials. A nesthesiology 1989; 70: 207–12

27. Sebel PS, Ingram DA, Flynn PJ, Rutherfoord CF, Rogers H: Evoked potentials during isoflurane anaesthesia. Br J Anaesth 1986; 58: 580–5

28. Hume AL, Durkin MA: Central and spinal somatosensory conduction times during hypothermic cardiopulmonary bypass and some observations on the effect of fentanyl and isoflurane anesthesia. Electroencephalogr Clin Neurophysiol 1986; 65: 46–58

29. Rehberg B, Ruschner R, Fischer M, Ebeling BJ, Hoeft A: Concentration-dependent changes in the latency and amplitude of somatosensory-evoked potentials by desflurane, isoflurane and sevoflurane. Anasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie 1998; 33: 425–9

30. Porkkala T, Kaukinen S, Hakkinen V, Jantti V: Median nerve somatosensory evoked potentials during isoflurane anaesthesia. Can J Anaesth 1997; 44: 963–8

31. Porkkala T, Jantti V, Kankinen S, Hakkinen V: Somatosensory evoked potentials during isoflurane anesthesia. Acta Anesthesiol Scand 1994; 38: 206–10

32. Rytky S, Huotari AM, Alahuhta S, Remes R, Suominen K, Jantti V: Tibial nerve somatosensory evoked potentials during EEG suppression in sevoflurane anaesthesia. Clin Neurophysiol 1999; 110: 1655–8

33. Jantti V, Sonkajarvi E, Mustola S, Rytky S, Kiiski P, Suominen K: Single-sweep cortical somatosensory evoked potentials: N20 and evoked bursts in sevoflurane anaesthesia. Electroencephalogr Clin Neurophysiol 1998; 108: 320–4

34. Salzman SK, Beckman AL, Marks HG, Naidu R, Bunnell WP, MacEwen GD: Effects of halothane on intra-operative scalp-recorded somatosensory evoked potentials to posterior tibial nerve stimulation in man. Electroencephalogr Clin Neurophysiol 1986; 65: 36–45

35. Porkkala T, Jantti V, Kaukinen S, Hakkinen V: Nitrous oxide has different effects on the EEG and somatosensory evoked potentials during isoflurane anaesthesia in patients. Acta Anaesthesiol Scand 1997; 41: 497–501

36. Wolfe DE, Drummond JC: Differential effects of isoflurane/nitrous oxide on posterior tibial somatosensory evoked responses of cortical and subcortical origin. Anesth Analg 1988; 67: 852–9

37. Kameyama Y: Effect of isoflurane and sevoflurane on evoked potentials and EEG. Jpn J Anesth 1994; 43: 657–64

38. Bernard JM, Pereon Y, Fayet G, Guiheneuc P: Effects of isoflurane and desflurane on neurogenic motor- and somatosensory-evoked potential monitoring for scoliosis surgery. A nesthesiology 1996; 85: 1013–9

39. Schindler E, Muller M, Zickmann B, Osmer C, Wozniak G, Hempelmann G: Modulation of somatosensory evoked potentials under various concentrations of desflurane with and without nitrous oxide. J Neurosurg Anesthesiol 1998; 10: 218–23

40. Shimoji K, Kano T, Nakashima H, Shimizu H: The effects of thiamylal sodium on electrical activities of the central and peripheral nervous systems in man. A nesthesiology 1974; 40: 234–40

41. da Costa VV, Saraiva RA, de Almeida AC, Rodrigues MR, Nunes LG, Ferreira JC: The effect of nitrous oxide on the inhibition of somatosensory evoked potentials by sevoflurane in children. Anaesthesia 2001; 56: 202–7

42. Schindler E, Muller M, Zickmann B, Osmer C, Wozniak G, Hempelmann G: Modulation of somatosensory evoked potentials under various concentrations of desflurane with and without nitrous oxide. J Neurosurg Anesth 1998; 10: 218–23

43. Koht A, Schutz W, Schmidt G, Schramm J, Watanabe E: Effects of etomidate, midazolam, and thiopental on median nerve somatosensory evoked potentials and the additive effects of fentanyl and nitrous oxide. Anesth Analg 1988; 67: 435–41

44. Schubert A, Licina MG, Lineberry PJ: The effect of ketamine on human somatosensory evoked potentials and its modification by nitrous oxide. A nesthesiology 1990; 72: 33–90

45. Thornton C, Creagh-Barry P, Jordan C, Luff NP, Dore CJ, Henley M, Newton DE: Somatosensory and auditory evoked responses recorded simultaneously: Differential effects of nitrous oxide and isoflurane. Br J Anaesth 1992; 68: 508–14

46. Lam AM, Sharar SR, Mayberg TS, Eng CC: Isoflurane compared with nitrous oxide anaesthesia for intraoperative monitoring of somatosensory-evoked potentials. Can J Anaesth 1994; 41: 295–300

47. Schwartz DM, Schwartz JA, Pratt RE Jr, Wierzbowski LR, Sestokas AK: Influence of nitrous oxide on posterior tibial nerve cortical somatosensory evoked potentials. J Spine Disord 1997; 10: 80–6

48. Borrissov B, Langeron O, Lille F, Gomola A, Saillant G, Riou B, Viars P: Combination of propofol-sufentanil on somatosensory evoked potentials in surgery of the spine. Ann Francaises d Anesth et de Reanimation 1995; 14: 326–30

49. Kalkman CJ, Traast H, Zuurmond WW, Bovill JG: Differential effects of propofol and nitrous oxide on posterior tibial nerve somatosensory cortical evoked potentials during alfentanil anaesthesia. Br J Anaesth 1991; 66: 483–9

50. McPherson RW, Sell B, Thaystman RJ: Effect of thiopental, fentanyl and etomidate on upper extremity somatosensory evoked potentials in humans. A nesthesiology 1986; 65: 584–9

51. Ikuta T: Effects of thiopental on the human somatosensory evoked response. Folia Psychiatr Neurol Jpn 1966; 20: 19–31

52. Ganes T, Lundar T: The effect of thiopentone on somatosensory evoked responses and EEGs in comatose patients. J Neurol Neruosurg Psychiatry 1983; 46: 509–14

53. Drummond JC, Todd MM, U HS: The effect of high dose sodium thiopental on brainstem auditory and median somatosensory evoked responses in humans. A nesthesiology 1985; 63: 249–54

54. Sutton LN, Frewen T, Marsh R, Jaggi J, Bruce DA: The effects of deep barbiturate coma on multimodality evoked potentials. J Neurosurg 1982; 57: 178–85

55. Drummond JC, Todd MM, Schubert A, Sang H: Effect of acute administration of high dose pentobarbital on human brainstem auditory and median nerve somatosensory evoked responses. Neurosurgery 1987; 20: 830–5

56. Russ W, Thiel A, Schwandt HJ, Hempelmann G: Somatosensory evoked potentials under thiopental and etomidate. Anaesthesist 1986; 35: 679–85

57. Ghoneim MM, Yameda T: Etomidate: A clinical and electroencephalographic comparison with thiopental. Anesth Analg 1977; 56: 479–85

58. Halliday AM: Cerebral evoked potentials in familial progressive myoclonic epilepsy. J R Coll Physicians 1967; 1: 123–7

59. Kochs E, Treede RD, Schulte J: Increase in somatosensory evoked potentials during anesthesia induction with etomidate. Anaesthesist 1986; 35: 359–64

60. Samra SK, Sorkin LS: Enhancement of somatosensory evoked potentials by etomidate in cats: An investigation of its site of action. A nesthesiology 1991; 74: 499–503

61. Stone JL, Ghaly RF, Levy WJ, Kartha R, Krinsky L, Roccaforte P: A comparative analysis of enflurane anesthesia on primate motor and somatosensory evoked potentials. Electroencephalgr Clin Neurophysiol 1992; 84: 180–7

62. Scheepstra GL, deLange JJ, Booij LH, Ross HH: Median nerve evoked potentials during propofol anaesthesia. Br J Anaesth 1989; 62: 92–4

63. Langeron O, Lille F, Zerhouni O, Orliaguet G, Saillant G, Riou B, Coriat P: Comparison of the effects of ketamine-midazolam with those of fentanyl-midazolam on cortical somatosensory evoked potentials during major spine surgery. Br J Anaesth 1997; 78: 701–6

64. Boisseau N, Madany M, Staccini P, Armando G, Martin F, Grimaud D, Raucoules-Aime M: Comparison of the effects of sevoflurane and propofol on cortical somatosensory evoked potentials. Br J Anaesth 2002; 88: 785–9

65. Laureau E, Marciniak B, Hébrard A, Herbaux B, Guieu JD: Comparative study of propofol and midazolam effects on somatosensory evoked potentials during surgical treatment of scoliosis. Neurosurgery 1999; 45: 69–74

66. Loughnan BL, Sebel PS, Thomas D, Rutherfoord CF, Rogers H: Evoked potentials following diazepam or fentanyl. Anaesthesia 1987; 42: 195–8

67. Sloan TB, Fugina ML, Toleikis JR: Effects of midazolam on median nerve somatosensory evoked potentials. Br J Anaesth 1990; 64: 590–3

68. Langeron O, Vivien B, Paqueron X, Saillant G, Riou B, Coriat P, Lille F: Effects of propofol, propofol-nitrous oxide and midazolam on cortical somatosensory evoked potentials during sufentanil anaesthesia for major spinal surgery. Br J Anaesth 1999; 82: 340–5

69. Kaieda R, Maekawa T, Takeshita H, Maruyama Y, Shimizu H, Shimoji K: Effect of diazepam on evoked electrospinogram and evoked electromyelogram in man. Anesth Analg 1981; 60: 197–200

70. Coulthard P, Rood JP: Midazolam and somatosensory evoked potentials. Br J Oral Maxillofac Surg 1993; 31: 28–31

71. Schubert A, Drummond JC, Peterson DO, Saidman LJ: The effect of high-dose fentanyl on human median nerve somatosensory-evoked responses. Can Anaesth Soc J 1987; 34: 35–40

72. Pathak KS, Brown RH, Casorbi HF, Nash CL: Effects of fentanyl and morphine on intraoperative somatosensory cortical-evoked potentials. Anesth Analg 1984; 63: 833–7

73. Kimovec MA, Koht A, Sloan TB: Effect of sufentanil on median nerve somatosensory evoked potentials. Br J Anaesth 1990; 65: 169–72

74. Schubert A, Licina MG, Glaze GM, Paranandi L: Systemic lidocaine and human somatosensory-evoked potentials during sufentanil-isoflurane anaesthesia. Can J Anaesth 1992; 39: 569–75

75. Kalkman CJ, Rheineck Leyssius AT, Bovill JG: Influence of high-dose opioid anesthesia on posterior tibial nerve somatosensory cortical evoked potentials: Effects of fentanyl, sufentanil, and alfentanil. J Cardiothoracic Anesth 1988; 2: 758–64

76. Crabb I, Thornton C, Konieczko KM, Chan A, Aquilina R, Frazer N, Dore CJ, Newton DE: Remifentanil reduces auditory and somatosensory evoked responses during isoflurane anaesthesia in a dose-dependent manner. Br J Anaesth 1996; 76: 795–801

77. Samra SK, Dy EA, Welch KB, Lovely LK, Graziano GP: Remifentanil- and fentanyl-based anesthesia for intraoperative monitoring of somatosensory evoked potentials. Anesth Analg 2001; 92: 1510–5

78. Fernandez-Galinski SM, Monells J, Espadaler JM, Pol O, Puig MM: Effects of subarachnoid lidocaine, meperidine and fentanyl on somatosensory and motor evoked responses in awake humans. Acta Anaesthesiol Scandinavica 1996; 40: 39–46

79. Goodarzi M, Shier NH, Grogan DP: Effect of intrathecal opioids on somatosensory-evoked potentials during spinal fusion in children. Spine 1996; 21: 1565–8

80. Schubert A, Licina MG, Lineberry PJ, Deers MA: The effect of intrathecal morphine on somatosensory evoked potentials in awake humans. A nesthesiology 1991; 75: 401–5

81. Loughman BA, Yau KW, Ransford AO, Hall GM: Effects of epidural diamorphine on the somatosensory evoked potential to posterior tibial nerve stimulation. Anaesthesia 1991; 46: 912–4

82. Goyagi T, Tanaka M, Nishikawa T: Oral Clonidine premedication reduces induction dose and prolongs awakening time from propofol-nitrous oxide anesthesia. Can J Anesth 1999; 46: 894–6

83. Katoh T, Ikeda K: The effect of clonidine on sevoflurane requirements for anaesthesia and hypnosis. Anaesthesia 1997; 52: 377–81

84. Lorenz M, Verner L, Hartmann M, Gaab MR: SEP monitoring during clonidine therapy of alcohol delirium. EEG EMG Z Elektroenzephalogr Elektromyogr Verwandte Geb 1991; 22: 168–71

85. Porkkala T, Jantti V, Hakkinen V, Kaukinen S: Clonidine does not attenuate median nerve somatosensory evoked potentials during isoflurane anesthesia. J Clin Monit Comput 1998; 14: 165–70

86. Gabriel AH, Faryniak B, Sojka G, Czech T, Freye E, Spiss CK: Clonidine: An adjunct in isoflurane N2O/O2 relaxant anesthesia: Effects on EEG power spectra, somatosensory and auditory evoked potentials. Anaesthesia 1995; 50: 290–6

87. Thornton C, Lucas MA, Newton DE, Dore CJ, Jones RM: Effects of dexmedetomidine on isoflurane requirements in healthy volunteers: 2. Auditory and somatosensory evoked responses. Br J Anaesth 1999; 83: 381–6

88. Bloom M, Beric A, Bekker A: Dexmedetomidine infusion and somatosensory evoked potentials. J Neurosurg Anesthesiol 2001; 13: 320–2

89. Andoh T, Ohtsuka T, Okazaki K, Okutsu Y, Okumura F: Effects of adenosine triphosphate (ATP) on somatosensory evoked potentials in humans anesthetized with isoflurane and nitrous oxide. Acta Anaesthesiol Scand 1993; 37: 590–3

90. Sloan TB: Nondepolarizing neuromuscular blockade does not alter sensory evoked potentials. J Clin Monit 1994; 10: 4–10

91. Gehrig JD, Colpitts YH, Chapman CR: Effects of local anesthetic infiltration on brain potentials evoked by painful dental stimulation. Anesth Analg 1981; 60: 779–82

92. Chartrain GE, Canfield RC, Knauss TA, Lettich E: Cerebral responses to electrical tooth pulp stimulation in man: An objective correlation of acute experimental pain. Neurology 1975; 25: 745–57

93. Lund C, Selmar P, Hansen OB, Hjortsu NC, Kehlet H: Effect of epidural bupivacaine on somatosensory evoked potentials after dermatomal stimulation. Anesth Analg 1987; 66: 34–8

94. Saugbjerg P, Asoh T, Lund C, Kuhl V, Kehlet H: Effects of epidural analgesia on scalp recorded somatosensory evoked potentials to posterior tibial nerve stimulation. Acta Anaesthesiol Scand 1986; 30: 400–3

95. Lund C, Hansen OB, Kehlet H: Effect of epidural clonidine on somatosensory evoked potentials to dermatomal stimulation. Eur J Anaesthesiol 1989; 6: 207–13

96. Lund C, Hansen OB, Kehlet H, Mogensen T, Qvitzau S: Effects of etidocaine administered epidurally on changes in somatosensory evoked potentials after dermatomal stimulation. Reg Anesth 1991; 16: 38–42

97. Loughman BA, Fennelly ME, Henley M, Hall GM: The effects of differing concentrations of bupivacaine on the epidural somatosensory evoked potential after posterior tibial nerve stimulation. Anesth Analg 1995; 8: 147–51

98. Rundshagen I, Kochs E, Schulte am Esch J: Surgical stimulation increases median nerve somatosensory evoked responses during isoflurane-nitrous oxide anaesthesia. Br J Anaesth 1995; 75: 598–602

99. Sloan TB, Ronai AK, Toleikis JR, Koht A: Improvement of intraoperative somatosensory evoked potentials by etomidate. Anesth Analg 1988; 67: 582–5

100. Agarwal R, Roitman KJ, Stokes M: Improvement of intraoperative somatosensory evoked potentials by ketamine. Paediatr Anaesth 1998; 8: 263–6

101. Nagao S, Roccoforte P, Moody RA: The effects of isovolemic hemodilution and reinfusion of packed erythrocytes on somatosensory and visual evoked response. J Surg Res 1978; 25: 530–7

102. Colin F, Bourgain R, Manil J: Progressive alteration of somatosensory evoked potential waveforms with lowering of cerebral tissue pO2 in the rabbit. Arch Int Physiol Biochem 1978; 86: 677–9

103. Ku ASW, Irwin MG, Chow B, Gunawardene S, Tan EE, Luk KDK: Effect of sevoflurane/nitrous oxide versus propofol anaesthesia on somatosensory evoked potential monitoring of the spinal cord during surgery to correct scoliosis. Br J Anaesth 2002; 88: 502–7

104. Guerit JM, Witdoeckt C, Rubay J, Matte A, Dion R: The usefulness of the spinal and subcortical components of the posterior tibial nerve SEPs for spinal cord monitoring during aortic coarctation repair. Electroencephalogr Clin Neurophysiol 1997; 104: 115–21

105. Gillerman R, Duncan J, Boltan J: Prolonged somatosensory evoked potential depression following a brief exposure to low concentrations of inhalation anaesthetic in a 3-year-old child. Paediatr Anaesth 2000; 10: 336–8

106. Manninen PH, Tan TK, Sarjeant RM: Somatosensory evoked potential monitoring during carotid endarterectomy in patients with a stroke. Anesth Analg 2001; 93: 39–44

107. Schubert A, Drummond JC, Garfin SR: The influence of stimulus presentation rate on the cortical amplitude and latency of intraoperative cortical somatosensory evoked potential recordings in patients with varying degrees of spinal cord injury. Spine 1987; 12: 969–73

108. Mason DG, Higgins D, Boyd SG, Lloyd-Thomas AR: Sequential measurement of the median nerve somatosensory evoked potential during isoflurane anaesthesia in children. Br J Anaesth 1992; 69: 567–9

109. Koscielniak-Nielsen ZJ, Stens-Pedersen HL, Hesselbjerg L: Midazolam-flumazenil versus propofol anaesthesia for scoliosis surgery with wake-up tests. Acta Anaesthesiol Scand 1998; 42: 111–6

110. Achor LJ, Starr A: Auditory brain stem responses in the cat: I. Intracranial and extracranial recordings. Electroencephalogr Clin Neurophysiol 1980; 48: 154–73

111. Jewett DL, Williston JS: Auditory-evoked far field averaged from the scalp of humans. Brain 1971; 94: 681–96

112. Picton TW, Hillyard SA, Krausz HI, Galambos R: Human auditory evoked potentials: I. Evaluation of components. Electroencephalogr Clin Neurophysiol 1974; 36: 179–90

113. Chiappa KH, Gladstone KJ, Young RR: Brain stem auditory evoked responses: Studies of waveform variations in 50 normal human subjects. Arch Neurol 1979; 36: 81–7

114. Grundy BL, Lina A, Procopio PT, Jannetta PJ: Reversible evoked potential changes with retraction of the eighth cranial nerve. Anesth Analg 1981; 60: 835–8

115. Sloan TB: Evoked potential monitoring. Int Anesthesiol Clin 1996; 34: 109–36

116. Grundy BL, Jannetta PJ, Procopio PT, Lina A, Boston JR, Doyle E: Intraoperative monitoring of brain-stem auditory evoked potentials. J Neurosurg 1982; 57: 674–81

117. Sloan TB: Electrophysiologic monitoring in head injury. New Horizons 1995; 3: 431–8

118. Rockoff MA, Marshall LF, Shapiro HM: High-dose barbiturate therapy in humans: A clinical review of 60 patients. Ann Neurol 1979; 6: 194–9

119. Starr A, Achor LJ: Anatomical and physiological origins of auditory brainstem responses, Human Evoked Potentials: Applications and Problems. Edited by Lehmann D, Callaway E. New York, Plenum Press, 1979, pp 415–29

120. Symon L, Hargadine J, Zawirshi M, Branston N: Central conduction time as an index of ischaemia in subarachnoid haemorrhage. J Neurol Sci 1979; 44: 95–103

121. Grundy BL: Intraoperative monitoring of sensory-evoked potentials. A nesthesiology 1983; 58: 72–87

122. Thornton C, Heneghan CP, James MF, Jones JG: Effects of halothane or enflurane with controlled ventilation on auditory evoked potentials. Br J Anaesth 1984; 56: 315–23

123. Thornton C, Catley DM, Jordan C, Lehane JR, Royston D, Jones JG: Enflurane anaesthesia causes graded changes in the brainstem and early cortical auditory evoked response in man. Br J Anaesth 1983; 55: 479–86

124. Sato S, Chassy J, Macnamara TE: Effects of enflurane on brainstem auditory evoked responses in humans. Anesth Analg 1982; 61: 898–902

125. Manninen PH, Lam AM, Nicholas JF: The effects of isoflurane-nitrous oxide anesthesia on brainstem auditory evoked potentials in humans. Anesth Analg 1985; 64: 43–7

126. Stockard JE, Stockard JJ, Westmoreland BF, Corfits JL: Brain-stem auditory-evoked responses. Arch Neurol 1979; 36: 823–31

127. Madler C, Keller I, Schwender D, Poppel E: Sensory information processing during general anaesthesia: Effect of isoflurane on auditory evoked neuronal oscillations. Br J Anaesth 1991; 66: 81–7

128. Heneghan CP, Thornton C, Navaratnarajah M, Jones JG: Effect of isoflurane on the auditory evoked response in man. Br J Anaesth 1987; 59: 277–82

129. Schwender D, Klasing S, Conzen P, Finsterer U, Poppel E, Peter K: Midlatency auditory evoked potentials during anaesthesia with increasing end expiratory concentrations of desflurane. Acta Anaesthesiol Scand 1996; 40: 171–6

130. Schwender D, Conzen P, Klasing S, Finsterer U, Poppel E, Peter K: The effects of anesthesia with increasing end-expiratory concentrations of sevoflurane on midlatency auditory evoked potentials. Anesth Analg 1995; 81: 817–22

131. Duncan PG, Sanders RA, McCullough DW: Preservation of auditory evoked brainstem responses in anesthetized children. Can Anaesth Soc J 1979; 26: 492–5

132. Sebel PS, Flynn PJ, Ingram DA: Effect of nitrous oxide on visual, auditory and somatosensory evoked potentials. Br J Anaesth 1984; 56: 1403–7

133. Houston HG, McClelland RJ, Fenwick PBC: Effects of nitrous oxide on auditory cortical evoked potentials an subjective thresholds. Br J Anaesth 1988; 61: 606–10

134. Harkins SW, Benedetti C, Colpitts YH, Chapman CR: Effects of nitrous oxide inhalation on brain potentials evoked by auditory and noxious dental stimulation. Prog Neuropsychopharmacol Biol Psychiatry 1982; 6: 167–74

135. Thornton C, Konieczko KM, Knight AB, Kaul B, Jones JG, Dore CJ, White DC: Effect on propofol on the auditory evoked response and oesophageal contractility. Br J Anaesth 1989; 63: 411–7

136. Chassard D, Joubaub A, Colson A, Guiraud M, Dubreuil C, Banssillon V: Auditory evoked potentials during propofol anaesthesia in man. Br J Anaesth 1989; 62: 522–6

137. Iselin-Chaves IA, El Moalem HE, Joo Gan TJ, Ginsberg B, Glass PS: Changes in the auditory evoked potentials and the Bispectral Index following propofol or propofol and alfentanil. A nesthesiology 2000; 92: 1300–10

138. Thornton C, Heneghan CP, Navaratnarajah M, Bateman PE, Jones JG: Effect of etomidate on the auditory evoked response in man. Br J Anaesth 1985; 57: 554–61

139. Bobbin RP, May JG, Lemoine RL: Effects of pentobarbital and ketamine on brain stem auditory potentials. Arch Otolaryngol 1979; 105: 467–70

140. Schwender D, Faber-Zullig E, Fett W, Klasing S, Finsterer U, Poppel E, Peter K: Mid-latency auditory evoked potentials in humans during anesthesia with S (+) ketamine: A double-blind, randomized comparison with racemic ketamine. Anesth Analg 1994; 78: 267–74

141. Samra SK, Lilly DJ, Rush NL, Kirsh MM: Fentanyl anesthesia and human brainstem auditory evoked potentials. A nesthesiology 1984; 61: 261–5

142. Schwender D, Rimkus T, Haessler R, Klasing S, Poppel E, Peter K: Effects of increasing doses of alfentanil, fentanyl and morphine on mid-latency auditory evoked potentials. Br J Anaesth 1993; 71: 622–8

143. Schwender D, Weninger E, Daunderer M, Klasing S, Poppel E, Peter K: Anesthesia with increasing doses of sufentanil and midlatency auditory evoked potentials in humans. Anesth Analg 1995; 80: 499–505

144. Samra SK, Krotak-Krol H, Pohereck R, Domino EF: Scopolamine, morphine and brainstem auditory evoked potentials in awake monkeys. A nesthesiology 1985; 62: 437–41

145. Schwender D, Klasing S, Madler C, Poppel E, Peter K: Effects of benzodiazepines on mid-latency auditory evoked potentials. Can J Anaesth 1993; 40: 1148–54

146. Verrotti A, Trotta D, Cutarella R, Pascarella R, Morgese G, Chiarelli F: Effects of antiepileptic drugs on evoked potentials in epileptic children. Pediatr Neurol 2000; 23: 397–402

147. Knight RT, Brailowsky S: Auditory evoked potentials from the primary auditory cortex of the cat: Topographic and pharmacological studies. Electroencephalogr Clin Neurophysiol 1990; 77: 225–32

148. Schwender D, Klasing S, Madler C, Poppel E, Peter K: Depth of anesthesia: Midlatency auditory evoked potentials and cognitive function during general anesthesia. Int. Anesth Clin 1993; 31: 89–106

149. Thornton C, Barrowcliffe MP, Konieczko KM, Ventham P, Dore CJ, Newton DE, Jones JG: The auditory evoked response as an indicator of awareness. Br J Anaesth 1989; 63: 113–5

150. Newton DE, Thornton C, Konieczko KM, Jordan C, Webster NR, Luff NP, Frith CD, Dore CJ: Auditory evoked response and awareness: A study in volunteers at sub-MAC concentrations of isoflurane. Br J Anaesth 1992; 69: 122–9

151. Schwender D, Klasing S, Madler C, Poppel E, Peter K: Mid-latency auditory evoked potentials indicate wakefulness during caesarean section. Eur J Anaesth 1994; 11: 147–8

152. Jarvis MJ, Lader MH: The effects of nitrous oxide on the auditory evoked response in a reaction time task. Psychopharmacologia 1971; 20: 201–12

153. Fenwick P, Bushman J, Howard R, Perry I, Gamble T: Contingent negative variation and evoked potential amplitude as a function of inspired nitrous oxide concentration. Electroencephalogr Clin Neurophysiol 1979; 47: 473–82

154. Schwender D, Daunderer M, Mulzer S, Klasing S, Finsterer U, Peter K: Midlatency auditory evoked potentials predict movements during anesthesia with isoflurane or propofol. Anesth Analg 1997; 85: 164–73

155. Schwender D, Faber-Zullig E, Klasing S, Poppel E, Peter K: Motor signs of wakefulness during general anaesthesia with propofol, isoflurane and flunitrazepam/fentanyl and midlatency auditory evoked potentials. Anaesthesia 1994; 49: 476–84

156. Brunner MD, Umo-Etuk J, Sharpe RM, Thornton C: Effect of a bolus dose of midazolam on the auditory evoked response in humans. Br J Anaesth 1999; 82: 633–4

157. Schwender D, Klasing S, Madler C, Poppel E, Peter K: Midlatency auditory evoked potentials and purposeful movements after thiopentone bolus injection. Anaesthesia 1994; 49: 99–104

158. Plourde G, Picton TW: Human auditory steady-state response during general anesthesia. Anesth Analg 1990; 71: 460–8

159. Plourde G, Boylan JF: The auditory steady state response during sufentanil anaesthesia. Br J Anaesth 1991; 66: 683–91

160. Brunner MD, Nathwani D, Rich PA, Thornton C, Dore DJ, Newton DE: Effect of suxamethonium on the auditory evoked response in humans. Br J Anaesth 1996; 76: 34–7

161. Kenny GNC, Mantzaridis H: Closed-loop control of propofol anaesthesia. Br J Anaesth 1999; 83: 223–8

162. Nayak A, Roy RJ: Anesthesia control using midlatency auditory evoked potentials. IEEE Trans Biomed Eng 1998; 45: 409–21

163. Yamashiro H: Differentiation of brain stem anesthesia from high spinal anesthesia using auditory brain stem response. Masui 1990; 39: 1704–7

164. Chi OZ, Field C: Effects of isoflurane on visual evoked potentials in humans. A nesthesiology 1986; 65: 328–30

165. Uhl RR, Squires KC, Bruce DL, Starr A: Effect of halothane anesthesia on the human cortical visual evoked response. A nesthesiology 1980; 53: 273–6

166. Church MW, Gritzke R: Effects of ketamine anesthesia on the rat brain-stem auditory evoked potential as a function of dose and stimulus intensity. Electroencephalogr Clin Neurophysiol 1987; 67: 570–83

167. Chi OZ, Ryterband S, Field C: Visual evoked potentials during thiopentone-fentanyl-nitrous oxide anaesthesia in humans. Can J Anaesth 1989; 36: 637–40

168. Chi OZ, Subramoni J, Jasaitis D: Visual evoked potentials during etomidate administration in humans. Can J Anaesth 1990; 37: 452–6

169. Chi OZ, McCoy CL, Field C: Effects of fentanyl anesthesia on visual evoked potentials in humans. A nesthesiology 1987; 67: 827–30

170. Raudzens PA: Intraoperative monitoring of evoked potentials. Ann NY Acad Sci 1982; 388: 308–26

171. Hou WY, Lee WY, Lin SM, Liu CC, Susceto L, Sun WZ, Lin SY: The effects of ketamine, propofol and nitrous oxide on visual evoked potentials during fentanyl anesthesia. Ma Tsui Hsueh Tsa Chi Anaesthesiologica Sinica 1993; 31: 97–102

172. Cedzich C, Schramm J, Fahbusch R: Are flash-evoked visual potentials useful for intraoperative monitoring of visual pathway function? Neurosurgery 1987; 21: 709–15

173. Cedzich C, Schramm J, Mengedoht CF, Fahlbusch R: Factors that limit the use of flash visual evoked potentials for surgical monitoring. Electroencephalog Clin Neurophysiol 1988; 71: 142–5

174. Lavinsky J, Gus PI, Ehlers JA, Roehe D, Nora DB: Visual evoked potentials: Assessment of retrobulbar and peribulbar anesthesia. J Cataract Refract Surg 2000; 26: 1529–32

175. Blair E: A physiologic classification of clinical hypothermia. Surgery 1965; 58: 607–18

176. Lundberg A: Potassium and the differential thermosensitivity of membrane potential, spike and negative after-potential in mammalian A and C fibers. Acta Physiol Scand Suppl 1948; 50: 1–67

177. Fay T: Early experiences with local and generalized refrigeration of the human brain. J Neurosurg 1959; 16: 239–60

178. Hubbard JI, Jones SF, Landau EM: The effect of temperature change upon transmitter release, facilitation and post-tetanic potentiation. J Physiol 1971; 216: 591–609

179. Benita M, Conde H: Effects of local cooling upon conduction and synaptic transmission. Brain Res 1972; 36: 133–51

180. Klee MR, Pierau FK, Faber DS: Temperature effects on resting potential and spike parameters of cat motoneurons. Exp Brain Res 1974; 19: 478–92

181. Anderson P, Gjerstad L, Pasztor E: Effect of cooling on synaptic transmission through the cuneate nucleus. Acta Physiol Scand 1972; 84: 433–77

182. Sohmer H, Gold S, Cahani M, Attias J: Effects of hypothermia on auditory brain-stem and somatosensory evoked responses: A model of a synaptic and axonal lesion. Electroencephalogr Clin Neurophysiol 1989; 74: 50–7

183. Russ W, Sticher J, Scheld H, Hempelmann G: Effects of hypothermia on somatosensory evoked responses in man. Br J Anaesth 1987; 59: 1484–91

184. Zeithlhofer J, Steiner M, Bousek K, Fitzal S, Asenbaum S, Wolner E, Deecke L: The influence of temperature on somatosensory-evoked potentials during cardiopulmonary bypass. Eur Neurol 1990; 30: 284–90

185. Oro J, Haghighi SS: Effects of altering core body temperature on somatosensory and motor evoked potentials in rats. Spine 1992; 17: 498–503

186. Aren C, Badr G, Feddersen K, Radegran K: Somatosensory evoked potentials and cerebral metabolism during cardiopulmonary bypass with special reference to hypotension induced by prostacyclin infusion. J Thorac Cardiovasc Surg 1985; 90: 73–9

187. Reynolds PC, Antoine JA, Bettencourt J, Starck TW: Regional hypothermia affects somatosensory evoked potentials. Anesth Analg 1991; 73: 653–6

188. Browning JL, Heizer ML, Baskin DS: Variations in corticomotor and somatosensory evoked potentials: Effects of temperature, halothane anesthesia, and arterial partial pressure of CO2. Anesth Analg 1992; 74: 643–8

189. MacKenzie MA, Vingerhoets DM, Colon EJ, Pinckers AJ, Notermans SL: Effect of steady hypothermia and normothermia on multimodality evoked potentials in human poikilothermia. Arch Neurol 1995; 52: 52–8

190. Woodhall B, Sealy W, Hall K, Floyd WL: Craniotomy under conditions of quinidine-protected cardioplegia and profound hypothermia. Ann Surg 1960; 152: 37–42

191. Takaki O, Kuro M, Nakajima T, Hayashi Y, Kitaguchi K, Shibata H: Effects of hypothermia with cardiopulmonary bypass on posterior tibial nerve somatosensory evoked potentials in man. Jpn J Anesth 1992; 41: 1119–24

192. Kopf GS, Hume AL, Durkin MA, Hammond GL, Hashim SW, Geha AS: Measurement of central somatosensory conduction time in patients undergoing cardiopulmonary bypass: An index of neurologic function. Am J Surg 1985; 149: 445–8

193. Markland ON, Warren C, Mallik GS, King RD, Brown JW, Mahomed Y: Effects of hypothermia on short latency somatosensory evoked potentials in humans. Electroencephalogr Clin Neurophysiol 1990; 77: 416–24

194. Strenge H: Somatosensory evoked potentials in moderate hyperthermia. EEG-EMG Zeitschrift fur Elektroenzephalographie Elektromyographie und Verwandte Gebiete 1991; 22: 157–63

195. Schron V, Lennon V, Bickford R: Temperature effects on the brainstem evoked responses (BAERS) of the rat. Proc San Diego Biomed Symp 1977; 16: 313–8

196. Panjwani GD, Mustafa MK, Muhailan A, Aneja IS, Owunwanne A: Effect of hyperthermia on somatosensory evoked potentials in the anaesthetized rat. Electroencephalogr Clin Neurophysiol 1991; 80: 384–91

197. Markland ON, Warren CH, Moorthy SS, Stoelting RK, King RD: Monitoring of multimodality evoked potentials during open heart surgery under hypothermia. Electroencephalogr Clin Neurophysiol 1984; 59: 432–40

198. Kochs E: Electrophysiological monitoring and mild hypothermia. J Neurosurg Anesth 1995; 7: 222–8

199. Dong WK, Bledsoe SW, Chadwick HS, Shaw CM, Hornbein TF: Electrical correlates of brain injury resulting from severe hypotension and hemodilution in monkeys. A nesthesiology 1986; 65: 617–25

200. Butler RA, Konishi T, Fernandez C: Temperature coefficients of cochlear potentials. Am J Physiol 1960; 199: 688–92

201. Williston JS, Jewett DL: The Q10 of auditory brain stem responses in rats under hypothermia. Audiology 1982; 21: 457–65

202. Ahmed B, El-Wafai S, Bana L: Effect of elevation of body temperature on the electroretinogram of the rat. Int J Hypertherm 1989; 5: 675–82

203. FitzGibbon T, Hayward JS, Walder D: EEG and visual evoked potentials of conscious man during moderate hypothermia. Electronencephalogr Clin Neurophysiol 1984; 58: 48–54

204. Russ W, Kling D, Loesevitz A, Hempelmann G: Effect of hypothermia on visual evoked potential (VEP) in humans. A nesthesiology 1984; 61: 207–10

205. Schubert A, Drummond JC: The effect of acute hypocapnia on human median nerve somatosensory evoked responses. Anesth Analg 1986; 65: 240–4

206. Ledsome JR, Cole C, Sharp-Kehl JM: Somatosensory evoked potentials during hypoxia and hypocapnia in conscious humans. Can J Anasth 1996; 43: 1025–9

207. Kalkman CJ, Boezeman EH, Ribberink AA, Oosting J, Deen L, Bovill JG: Influence of changes in arterial carbon dioxide tension on the electroencephalogram and posterior tibial nerve somatosensory cortical evoked potentials during alfentanil/nitrous oxide anesthesia. A nesthesiology 1991; 75: 68–74

208. Dubois MY, Sato S, Chassy J, Macnamaara TE: Effects of enflurane on brainstem auditory evoked responses in humans. Anesth Analg 1982; 61: 898–902

209. McPherson RW, Zeger S, Traystman RJ: Relationship of somatosensory evoked potentials and cerebral oxygen consumption during hypoxic hypoxia in dogs. Stroke 1986; 17: 30–6

210. Branston NM, Lodds A, Symon L, Wang AD: Comparison of the effects of ischemia on early components of the somatosensory evoked potentials in brainstem, thalamus and cerebral cortex. J Cereb Blood Flow Metab 1984; 4: 68–81

211. Grundy BL, Heros RC, Tung AS, Doyle E: Intraoperative hypoxia detected by evoked potential monitoring. Anesth Analg 1981; 60: 437–9

212. Kayama Y: Evoked potentials of the cortical visual system during and after hypoxia in cats. Electroencephalogr Clin Neurophysiol 1974; 36: 619–28

213. Kobrine AI, Evans DE, Rizzoli HV: Relative vulnerability of the brain and spinal cord to ischemia. J Neurol Sci 1980; 45: 65–72

214. Iwayama K, Mori K, Sakai S, Yamashiro K, Iwamoto K: Changes of somatosensory evoked potential accompanying ischemia and hypoxia in cats. Neurol Res 1986; 8: 157–63

215. Mosko SS, Pierce S, Holowach J, Sassin JF: Normal brain-stem auditory evoked potentials recorded in sleep apneic patients during waking and as a function of oxygen saturation during sleep. Electroencephalogr Clin Neurophysiol 1981; 51: 477–82

216. Sohmer H, Gafni M, Chisin R: Auditory nerve-brainstem potentials in man and cat under hypoxic and hypercapnic conditions. Electroencephalogr Clin Neurophysiol 1982; 53: 506–12

217. Sohmer H, Freeman S, Gafni M, Goitein K: The depression of the auditory nerve brain-stem evoked response in hypoxemia: Mechanism and site of effect. Electroencephalogr Clin Neurophysiol 1986; 64: 334–8

218. Pierelli F, Rizzo PA, Romano R, Mattioli GL, Pauri F, Affricana C, Morocutti C: Early auditory evoked potential changes during hypoxic hypoxia in the rabbit. Exp Neurol 1986; 94: 479–88

219. Mead CO, Moody RA, Ruamsuke S, Mullan S: Effect of isovolemic hemodilution on cerebral blood flow following experimental head injury. J Neurosurg 1970; 32: 40–50

220. McCutcheon EP, Frazier DT, Boyarsky LL: Changes in the somatosensory cortical evoked potential produced by hypovolemic shock. Proc Soc Exp Biol Med 1971; 136: 1063–71

221. Dong WK, Bledsoe SW, Eng DY, Heavner JE, Shaw CM, Hornbein TF, Anderson JL: Profound arterial hypotension in dogs: Brain electrical activity and organ integrity. A nesthesiology 1983; 58: 61–71

222. Goitein KJ, Fainmesser P, Sohmer H: Cerebral perfusion pressure and auditory brain-stem responses in childhood CNS diseases. Am J Dis Child 1983; 137: 777–81

223. Merton PA, Morton HB, Hill DK, Marsden CD: Scope of a technique for electrical stimulation of human brain, spinal cord and muscle. Lancet 1982; 2: 597–600

224. Bashein G, Nessly ML, Bledsoe SW, Townes BD, Davis KB, Coppel DB, Hornbein TF: Electroencephalography during surgery with cardiopulmonary bypass and hypothermia. A nesthesiology 1992; 76: 878–91

225. Stecker M, Cheung AT, Patterson T, Savion JS, Weiss SJ, Richards RM, Vavaria JE, Gardner TJ: Detection of stroke during cardiac operations with somatosensory evoked responses. J Thorac Cardiovasc Surg 1996; 112: 962–72

226. Doyle WJ, Fria TJ: The effects of hypothermia on the latencies of the auditory brain-stem response (ABR) in the rhesus monkey. Electroencephalogr Clin Neurophysiol 1985; 60: 258–66

227. Grundy BL, Nash CL, Brown RH: Arterial pressure manipulation alters spinal cord function during correction of scoliosis. A nesthesiology 1981; 54: 249–53

228. Borgstrom L, Johannson H, Siesjo BK: The influence of acute normovolemic anemia on cerebral blood flow and O2 consumption in anesthetized rats. Acta Physiol Scand 1975; 73: 505–14

229. Mason DG, Higgins D, Boyd SG, Lloyd-Thomas AR: Effects of isoflurane anesthesia on the median nerve somatosensory evoked potential in children. Br. J Anaesth 1992; 69: 562–6

230. Abel MF, Mubarak SJ, Wenger DR, Costello J, Hicks GE: Brainstem evoked potentials for scoliosis surgery: A reliable method allowing use of halogenated anesthetic agents. J Pediatr Orthop 1990; 10: 208–13

231. Prokop AM, Meyer GP, Walter M, Erasmi H: Validity of SEP monitoring in carotid surgery: Review and own results. J Cardiovasc Surg (Torino) 1996; 37: 337–42

232. Schweiger H, Kamp HD, Dinkel M: Somatosensory-evoked potentials during carotid artery surgery: Experience in 400 operations. Surgery 1991; 109: 602–9

233. Taniguchi M, Nadstawek J, Pechstein U, Schramm J: Total intravenous anesthesia for improvement of intraoperative monitoring of somatosensory evoked potentials during aneurysm surgery. Neurosurgery 1992; 31: 891–7

234. Haupt WF, Horsch S: Evoked potential monitoring in carotid surgery: A review of 994 cases. Neurology 1992; 42: 835–8

235. Russ W, Fraedrich G, Hehrlein FW, Hempelmann G: Intraoperative somatosensory evoked potentials as a prognostic factor of neurologic state after carotid endarterectomy. Thorac Cardiovasc Surg 1985; 33: 392–6

236. Kochs E, Blanc I, Werner C, Schulte am Esch J: The electroencephalogram and somatosensory evoked potentials following intravenous administration of 0.5 mg/kg ketamine. Anaesthesist 1988; 37: 625–30

237. Kano T, Shimoji K: The effect of ketamine and neuroleptanalgesia on the evoked electrospinogram and electromyelogram in man. A nesthesiology 1974; 40: 241–6

238. Lauer K, Munshi C, Larson S: The effect of midazolam on median nerve somatosensory evoked potentials. J Clin Monit 1994; 10: 181–4

239. Klasen J, Thiel A, Detsch O, Bachmann B, Hempelmann G: The effects of epidural and intravenous lidocaine on somatosensory evoked potentials after stimulation of the posterior tibial nerve. Anesth. Analg 1995; 81: 332–7

240. Chaves-Vischer V, Brustowicz R, Helmer SL: The effect of intravenous lidocaine on intraoperative somatosensory evoked potentials during scoliosis surgery. Anesth Analg 1996; 83: 1122–5

241. Freye E, Buhl R, Ciaramelli F: Opioids with different affinity for subreceptors induce different effects on early and late sensory evoked potentials (SEP) in man. NIDA Res Monogr 1986; 75: 551–4

242. Ueda S, Aso S, Watanabe Y, Mizukoshi K: Changes in auditory evoked responses during intravenous lidocaine. Acta Otolaryngol (Stockh) 1993; 504( suppl): 89–93
243. Kasaba T, Kosaka Y, Itoga S: Effect of intravenous lidocaine administration on auditory brainstem response. Masui Jpn J Anesthesiol 1991; 40: 931–5
244. Fenwick PBC, Stone SA, Bushman J, Enderby D: Changes in the pattern reversal visual evoked potential as a function of inspired nitrous oxide concentration. Electroencephalogr Clin Neurophysiol 1984; 57: 178–83

245. Russ W, Luben V, Hempelmann G: Der EinfluB der Neuroleptanalgesie auf das visuelle evozierte Potential (VEP) des Menschen. Anaesthesist 1982; 31: 575–8

246. Makela K, Harkainen K, Rorarius M, Jantti V: Suppression of F-VEP during isoflurane-induced EEG suppression. Electroencephalogr Clin Neurophysiol 1996; 100: 269–72

Cited By:

This article has been cited 42 time(s).

European Journal of Neuroscience
Effects of the a2-adrenergic receptor agonist dexmedetomidine on neural, vascular and BOLD fMRI responses in the somatosensory cortex
Fukuda, M; Vazquez, AL; Zong, XP; Kim, SG
European Journal of Neuroscience, 37(1): 80-95.
Journal of Neurophysiology
Analysis of stimulus-related activity in rat auditory cortex using complex spectral coefficients
Krause, BM; Banks, MI
Journal of Neurophysiology, 110(3): 621-639.
Expert Review of Medical Devices
Influence of intraoperative neurophysiologic monitoring on the development of surgical dissection techniques
Zielinski, P; Furtak, J
Expert Review of Medical Devices, 9(6): 571-575.
Plos One
Predictability of Painful Stimulation Modulates the Somatosensory-Evoked Potential in the Rat
Schaap, MWH; van Oostrom, H; Doornenbal, A; Baars, AM; Arndt, SS; Hellebrekers, LJ
Plos One, 8(4): -.
ARTN e61487
Brain Stimulation
Vagal Sensory Evoked Potentials Disappear Under the Neuromuscular Block - An Experimental Study
Leutzow, B; Lange, J; Gibb, A; Schroeder, H; Nowak, A; Wendt, M; Usichenko, TI
Brain Stimulation, 6(5): 812-816.
Increased risk of postoperative neurologic deficit for spinal surgery patients with unobtainable intraoperative evoked potential data
Thuet, ED; Padberg, AM; Raynor, BL; Bridwell, KH; Riew, KD; Taylor, BA; Lenke, LG
Spine, 30(): 2094-2103.

Pediatric Anesthesia
Neurophysiological monitoring under anesthesia to position a child with extreme lumbar spine flexion for MRI and CT scan
Gundlapalli, S; Anand, RS; Schwartz, DM; Wierzbowski, LR; Cohen, DE; Cook-Sather, SD
Pediatric Anesthesia, 16(2): 195-199.
Anesthesia and Analgesia
Dose-Dependent Suppression of the Electrically Elicited Stapedius Reflex by General Anesthetics in Children Undergoing Cochlear Implant Surgery
Crawford, MW; White, MC; Propst, EJ; Zaarour, C; Cushing, S; Pehora, C; James, AL; Gordon, KA; Papsin, BC
Anesthesia and Analgesia, 108(5): 1480-1487.
Distinct actions of etomidate and propofol at beta 3-containing gamma-aminobutyric acid type A receptors
Drexler, B; Jurd, R; Rudolph, U; Antkowiak, B
Neuropharmacology, 57(4): 446-455.
British Journal of Anaesthesia
Cortical somatosensory-evoked potentials during spine surgery in patients with neuromuscular and idiopathic scoliosis under propofol-remifentanil anaesthesia
Hermanns, H; Lipfert, P; Meier, S; Jetzek-Zader, M; Krauspe, R; Stevens, MF
British Journal of Anaesthesia, 98(3): 362-365.
Equine Veterinary Journal
Lumbosacral spinal cord somatosensory evoked potentials for quantification of nociception in horses
van Loon, JPAM; van Oostrom, H; Doornenbal, A; Hellebrekers, LJ
Equine Veterinary Journal, 42(3): 255-260.
Brain Research Bulletin
FTY720 sustains and restores neuronal function in the DA rat model of MOG-induced experimental autoimmune encephalomyelitis
Balatoni, B; Storch, MK; Swoboda, EM; Schonborn, V; Koziel, A; Lambrou, GN; Hiestand, PC; Weissert, R; Foster, CA
Brain Research Bulletin, 74(5): 307-316.
Anesthesia and Analgesia
Somatosensory evoked potentials by median nerve stimulation in children during thiopental/sevoflurane anesthesia and the additive effects of ketoprofen and fentanyl
Westeren-Punnonen, S; Ypparila-Wolters, H; Partanen, J; Nieminen, K; Hyvarinen, A; Kokki, H
Anesthesia and Analgesia, 107(3): 799-805.
Frequency-dependent neural activity, CBF, and BOLD fMRI to somatosensory stimuli in isoflurane-anesthetized rats
Kim, T; Masamoto, K; Fukuda, M; Vazquez, A; Kim, SG
Neuroimage, 52(1): 224-233.
Anesthesia and Analgesia
The effects of propofol, small-dose isoflurane, and nitrous oxide on cortical somatosensory evoked potential and bispectral index monitoring in adolescents undergoing spinal fusion
Clapcich, AJ; Emerson, RG; Roye, DP; Xie, H; Gallo, EJ; Dowling, KC; Ramnath, B; Heyer, EJ
Anesthesia and Analgesia, 99(5): 1334-1340.
Anasthesiologie & Intensivmedizin
Remarks on relevant CNS examination and monitoring techniques on the ICU, and the effectiveness of a basic course in imparting the necessary knowledge and skills
Maurer, E; Martin, J; Milewski, P; Dinkel, M
Anasthesiologie & Intensivmedizin, 46(): 84-+.

Medical Science Monitor
Effects of physiological parameters on intraoperative somatosensory-evoked potential monitoring: Results of a multifactor analysis
Cui, HY; Luk, KDK; Hu, Y
Medical Science Monitor, 15(5): CR226-CR230.

Suppressing the Mind: Anesthetic Modulation of Memory and Consciousness
Cortical Disintegration Mechanism of Anesthetic-Induced Unconsciousness
Hudetz, A
Suppressing the Mind: Anesthetic Modulation of Memory and Consciousness, (): 99-125.
Neurocritical Care
A functional near-infrared spectroscopy study to detect activation of somatosensory cortex by peripheral nerve stimulation
Niederhauser, BD; Rosenbaum, BP; Gore, JC; Jarquin-Valdivia, AA
Neurocritical Care, 9(1): 31-36.
American Journal of Veterinary Research
Use of epidurally derived evoked potentials for quantification of caudal nociception in ponies
van Loon, JPAM; Stienen, PJ; Doornenbal, A; Hellebrekers, LJ
American Journal of Veterinary Research, 70(7): 813-819.

Journal of Anesthesia
Mechanisms of anesthetic actions and the brain
Ishizawa, Y
Journal of Anesthesia, 21(2): 187-199.
Anasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie
Neuromonitoring for estimating the depth of narcosis
Schmidt, N; Bischoff, P
Anasthesiologie Intensivmedizin Notfallmedizin Schmerztherapie, 39(1): 33-60.

Anaesthesia, Pain, Intensive Care and Emergency Medicine
Choice of anaesthetics for neurosurgical anaesthesia
Patel, PM
Anaesthesia, Pain, Intensive Care and Emergency Medicine, (): 641-649.

British Journal of Anaesthesia
Effects of isoflurane and propofol on cortical somatosensory evoked potentials during comparable depth of anaesthesia as guided by bispectral index
Liu, EHC; Wong, HK; Chia, CP; Lim, HJ; Chen, ZY; Lee, TL
British Journal of Anaesthesia, 94(2): 193-197.
Pharmacology & Therapeutics
Interactions of anesthetics with their targets: Non-specific, specific or both?
Urban, BW; Bleckwenn, M; Barann, M
Pharmacology & Therapeutics, 111(3): 729-770.
Anaesthesia and Intensive Care
Comparison between sevoflurane/remifentanil and propofol/remifentanil anaesthesia in providing conditions for somatosensory evoked potential monitoring during scoliosis corrective surgery
Fung, NY; Hu, Y; Irwin, MG; Chow, BFM; Yuen, MY
Anaesthesia and Intensive Care, 36(6): 779-785.

Pediatric Anesthesia
Inhalational anesthesia vs total intravenous anesthesia (TIVA) for pediatric anesthesia
Lerman, J; Johr, M
Pediatric Anesthesia, 19(5): 521-534.
Brain Research Bulletin
Differences between somatosensory-evoked potentials recorded from the ventral posterolateral thalamic nucleus, primary somatosensory cortex and vertex in the rat
Stienen, PJ; de Groot, HNM; Venker-van Haagen, AJ; van den Brom, WE; Hellebrekers, LJ
Brain Research Bulletin, 67(4): 269-280.
Liver International
Neurophysiological investigations of hepatic encephalopathy: ISHEN practice guidelines
Guerit, JM; Amantini, A; Fischer, C; Kaplan, PW; Mecarelli, O; Schnitzler, A; Ubiali, E; Amodio, P
Liver International, 29(6): 789-796.
Annals of Thoracic Surgery
Perioperative management to improve neurologic outcome in thoracic or thoracoabdominal aortic stent-grafting
Weigang, E; Hartert, M; Siegenthaler, MP; Beckmann, NA; Sircar, R; Szabo, G; Etz, CD; Luehr, M; von Samson, P; Beyersdorf, F
Annals of Thoracic Surgery, 82(5): 1679-1687.
Regional Anesthesia and Pain Medicine
Stimulating catheter as a tool to evaluate peripheral nerve function during hip rotationplasty
Werdehausen, R; Braun, S; Hermanns, H; Krauspe, R; Lipfert, P; Stevens, MF
Regional Anesthesia and Pain Medicine, 32(6): 528-532.
Journal of Neuroscience Methods
Digit tapping model of functional activation in the rat somatosensory cortex
Schulte, ML; Li, SJ; Hyde, JS; Hudetz, AG
Journal of Neuroscience Methods, 157(1): 48-53.
Anesthesia and Analgesia
Perioperative management of patients undergoing transsphenoidal pituitary surgery
Nemergut, EC; Dumont, AS; Barry, UT; Laws, ER
Anesthesia and Analgesia, 101(4): 1170-1181.
Brain Research Bulletin
Vertex-recorded, rather than primary somatosensory cortex-recorded, somatosensory-evoked potentials signal unpleasantness of noxious stimuli in the rat
Stienen, PJ; van Oostrom, H; van den Bos, R; de Groot, HNM; Hellebrekers, LJ
Brain Research Bulletin, 70(3): 203-212.
Identification of Sensory Blockade by Somatosensory and Pain-induced Evoked Potentials
Schmidt, GN; Scharein, E; Siegel, M; Müller, J; Debener, S; Nitzschke, R; Engel, A; Bischoff, P
Anesthesiology, 106(4): 707-714.
PDF (851) | CrossRef
Desflurane Selectively Suppresses Long-latency Cortical Neuronal Response to Flash in the Rat
Hudetz, AG; Vizuete, JA; Imas, OA
Anesthesiology, 111(2): 231-239.
PDF (860) | CrossRef
General Anesthesia Increases Temporal Precision and Decreases Power of the Brainstem Auditory-evoked Response-related Segments of the Electroencephalogram
Scheller, BC; Daunderer, M; Pipa, G
Anesthesiology, 111(2): 340-355.
PDF (2612) | CrossRef
Motor and Somatosensory Evoked Potentials Are Well Maintained in Patients Given Dexmedetomidine during Spine Surgery
Bala, E; Sessler, DI; Nair, DR; McLain, R; Dalton, JE; Farag, E
Anesthesiology, 109(3): 417-425.
PDF (750) | CrossRef
Journal of Neurosurgical Anesthesiology
Anesthesia for Minimally Invasive Cranial and Spinal Surgery
Schubert, A; Deogaonkar, A; Lotto, M; Niezgoda, J; Luciano, M
Journal of Neurosurgical Anesthesiology, 18(1): 47-56.

PDF (625)
Journal of Neurosurgical Anesthesiology
An Unusual Arterial Waveform
Eipe, N; Bertram, S
Journal of Neurosurgical Anesthesiology, 20(1): 68-69.
PDF (133) | CrossRef
Journal of Neurosurgical Anesthesiology
A Comparison of Auditory Evoked Potentials Derived From a Monitor Integrated Module Versus Standard Technique
Fudickar, A; Kluzik, A; Weiler, N; Scholz, J; Tonner, PH; Bein, B
Journal of Neurosurgical Anesthesiology, 21(2): 120-126.
PDF (250) | CrossRef
Journal of Neurosurgical Anesthesiology
Unusual Waveforms During SSEP Monitoring—Facts and Artifacts
Adhikary, SD; Manickam, BP
Journal of Neurosurgical Anesthesiology, 20(3): 207.
PDF (95) | CrossRef
Back to Top | Article Outline

© 2003 American Society of Anesthesiologists, Inc.

Publication of an advertisement in Anesthesiology Online does not constitute endorsement by the American Society of Anesthesiologists, Inc. or Lippincott Williams & Wilkins, Inc. of the product or service being advertised.

Article Tools