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Anesth Analg 2003;96:449-455
© 2003 International Anesthesia Research Society

ANESTHETIC PHARMACOLOGY

Propofol Impairs the Central but Not the Peripheral Part of the Motor System

Michael H. Dueck, MD, DEAA*, Aloys Oberthuer, MD*, Christoph Wedekind, MD{dagger}, Matthias Paul, MD, DEAA*, and Ulf Boerner, MD*

Departments of *Anesthesiology and Intensive Care Medicine and {dagger}Neurosurgery, University of Cologne, Cologne, Germany

Address correspondence and reprint requests to Michael H. Dueck, MD, DEAA, Department of Anesthesiology and Intensive Care Medicine, University of Cologne, Joseph-Stelzmann-Str. 9, D-50924 Cologne, Germany. Address e-mail to m.dueck{at}uni-koeln.de


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Propofol provides some degree of muscle relaxation. Previous studies have investigated the effects of propofol on either the central or peripheral parts of the motor system. In this study, we simultaneously assessed both central (spinal) and peripheral effects. In 15 patients, general anesthesia was induced and maintained with fentanyl and midazolam. Neuromuscular blocking drugs were not administered. To investigate the central portion of the motor system, we monitored spinal F waves, an electrophysiologic variable of {alpha}-motoneuron excitability. Direct electrophysiologic muscle responses (M waves) and mechanomyography were studied to detect the peripheral effects of propofol on neuromuscular transmission or muscle contraction strength. After baseline recordings, 3 IV boluses of propofol (2 times 1 mg/kg followed by 2 mg/kg) were administered at 5-min intervals. Mean F-wave amplitudes were significantly reduced compared with baseline measurements (mean ± SD, 0.22 ± 0.13 mV) after the first (0.13 ± 0.08 mV; P < 0.05), second (0.08 ± 0.09 mV; P < 0.05), and third (0.03 ± 0.04 mV; P < 0.01) propofol injections. M-wave amplitudes and mechanomyography signals remained unchanged. Our data suggest that the central part, but not the peripheral part, of the motor system is impaired after bolus administration of propofol.

IMPLICATIONS: Propofol bolus administration provides some degree of muscle relaxation in humans. We demonstrated a decrease of motoneuron excitability in the spinal cord, measured by F-wave analysis, a late electromyographic signal. No effects on neuromuscular transmission or muscle contractility, measured by electromyography and mechanomyography, were observed.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Propofol is a widely used IV anesthetic that provides some degree of muscle relaxation. Several studies reported good tracheal intubating conditions after propofol-induced induction of anesthesia without the use of neuromuscular blocking drugs (1), as well as facilitation of laryngeal mask insertion (2). Propofol also reduces the pathologically increased muscle tone in patients with tetanus (3).

The underlying mechanisms of propofol’s muscle relaxing properties are not completely understood. They could be peripheral and/or central in origin and could affect any part of the motor pathway, from cortical motoneurons down to the muscle cells. A significant decrease in masseter muscle tone after succinylcholine was reported for propofol, but not thiopental, suggesting the involvement of a peripheral effect of propofol-induced muscle relaxation (4). Haeseler et al. (5) found that propofol inhibited human skeletal muscle sodium channels and suggested that this muscle cell-related mechanism may contribute to a clinically relevant reduction in muscle tone. Propofol does not appear to interfere with neuromuscular transmission, because it does not augment the neuromuscular blockade induced by neuromuscular blockers (6). Other authors recently demonstrated a central (spinal) effect of propofol with use of electromyographic (EMG) criteria (7,8): a reduction of H-reflex amplitudes and a decrease in F-wave persistence showed a decrease of spinal {alpha}-motoneuron excitability. However, the mechanical muscle contraction response was not assessed in these studies. F-wave analysis is a noninvasive electrophysiologic technique to evaluate the effects of anesthetics on motoneurons in the spinal cord (9,10). For volatile anesthetics, F-wave analysis showed a decrease in {alpha}-motoneuron excitability, and the authors proposed that this is an underlying mechanism for anesthesia-induced surgical immobility (11).

Several in vitro, animal, and clinical studies have reported on the effects of propofol on parts of the motor system (5,7,8,12). However, we are not aware of an investigation in humans that assessed both the central and peripheral effects of propofol simultaneously. In our study, we monitored lower central (spinal) and peripheral effects of bolus administrations of propofol by using EMG and mechanomyography (MMG). We analyzed the effects on the spinal motoneuron, axonal conduction velocity, neuromuscular transmission, and muscle contractility.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After obtaining approval from our IRB (Ethics Committee of the University of Cologne) and written, informed consent, we studied 15 patients, ASA physical status I–III, aged 49.8 ± 18.4 yr (mean ± SD), weighing 72.4 ± 14.4 kg, measuring 170.2 ± 9.8 cm, who had an elective craniotomy for intracranial tumor surgery. None of these patients had a history of peripheral neurological disorders, stroke, or neuromuscular diseases.

Midazolam 7.5–15 mg was given orally 1 h before the induction of anesthesia. After IV induction of anesthesia with fentanyl (7 µg/kg) and midazolam (0.2 mg/kg), the trachea was intubated without the use of neuromuscular blocking drugs. Anesthesia was maintained with mean hourly doses of 160.4 µg/kg of midazolam (range, 79.4–285.8 µg/kg) and fentanyl 9.0 µg/kg (range, 4.0–15.6 µg/kg). Patients were ventilated with 30%–50% oxygen without nitrous oxide, which interferes with F-wave monitoring (13). Routine monitoring included electrocardiogram, direct blood pressure measurement, pulse oximetry, end-expiratory CO2, central venous pressure, urine output, and blood gas analysis. Ventilation was adjusted to maintain a PaCO2 of 35–37 mm Hg. Body temperature was maintained between 36.0°C and 37.0°C by using a patient warming system.

F-wave monitoring is often used in the electrodiagnostic evaluation of disorders of peripheral nerves and parts of the central nervous system. The presence of a regular F wave requires the integrity of a motor axon from its axon hillock to the motor endplates (9,10). Briefly, peripheral stimulation of a motor nerve results in both orthodromic and antidromic impulse conduction (Fig. 1). The antidromic excitation reaches the motor cell soma, where it initiates an orthodromic reexcitation, which evokes a small muscle potential that is visible as a bi- or polyphasic voltage signal called the F wave. The F-wave signal is modulated by the motoneuron excitability, which depends on the balance of spinal excitatory versus inhibitory afferent input to that motoneuron. F waves are always preceded by a direct muscle response (M wave), which is evoked by the orthodromic neural excitation, because a stimulus threshold equal to or exceeding that for eliciting an M wave is required to generate an F wave. The most frequently reported variables of F-wave analysis are amplitude, latency (time from stimulus application to F-wave onset), and persistence (number of measurable F waves divided by the number of stimuli) (9,10).



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  		Figure 1. Stimulation of a peripheral motor nerve leads to orthodromic and antidromic impulse conduction. The orthodromic potential quickly results in an electromyographic signal known as the M wave. Simultaneously, the antidromic excitation reaches the motor cell soma, where it initiates a recurrent discharge, which is orthodromically conducted and evokes a small muscle potential that is visible as a bi- or polyphasic voltage signal called the F wave.

 
In our study, F waves and M waves were recorded from the abductor pollicis muscle after transcutaneous median nerve stimulation at the wrist, with constant-current square-wave pulses (duration, 0.1 ms) at an interstimulus interval of 1 s. Responses were gathered with surface AgCl cup electrodes filled with conducting gel. The active electrode was placed halfway between the midpoint of the distal wrist crease and the volar surface of the first metacarpophalangeal joint. The reference electrode was placed slightly distal to the joint (electrodes were placed 2–3 cm apart from each other). Filters were set at 20 and 3000 Hz. Amplification was 100–200 µV/1.25 cm for F-wave recording and 0.5–2.0 mV/div for M-wave recording. We used a commercially available electrophysiologic stimulation and recording device. Stimulation current was gradually increased to exceed that needed to evoke a maximum M wave (range, 10–25 mA). This supramaximal current was used for all subsequent stimulations. We identified the F wave by using the following criteria: 1) stimulus threshold greater than M-wave threshold, 2) voltage signal reaching a plateau with increasing nerve stimulation, 3) variable morphology (Fig. 2A) (4) increase of M-wave latency and decrease of F-wave latency after proximal shift of stimulus site (9,10). Two series with different amplifications for F-wave and M-wave analysis of eight consecutive stimuli were delivered, and responses were hard-copied by means of a thermoprinter for off-line analysis.



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  		Figure 2. A, Original set of eight tracings of F waves before the administration of propofol, showing a variable morphology of F waves. Arrows indicate amplitude and latency. The size of the M waves exceeds the limits of the graph. B, To detect a short fading effect at the neuromuscular junction, which might lead to a decrease in F-wave amplitudes, two M waves were elicited by a paired stimulus at an interstimulus interval of 25 ms. Both M waves have the same amplitude, which demonstrates the fast recovery of the neuromuscular junction and disproves a fading effect.

 
For MMG monitoring, the contralateral ulnar nerve was stimulated transcutaneously at the wrist with square-wave supramaximal stimuli of 0.2 ms duration, delivered in a train-of-four (TOF) mode at 2 Hz every 15 s. The resulting twitches of the thumb were recorded by using a force transducer and hard-copied on a thermoprinter for off-line analysis.

To assess the central (spinal) effects of propofol, we analyzed F-wave amplitudes and F/M ratios. F-wave latencies were measured to assess axonal conduction velocity. Neuromuscular transmission was evaluated by monitoring M-wave amplitudes and TOF ratios. Muscle contraction strength was assessed by measuring the amplitude of the first TOF response (T1).

Recommended doses of propofol for the induction of anesthesia vary from 1.0 to 2.5 mg/kg (14,15), and loss of consciousness is achieved at blood concentrations of 3.5–5 µg/mL (16). To meet this variation in suggested induction doses, we chose to standardize the bolus injection of propofol as a three-step procedure with a cumulative dose of 4.0 mg/kg. Because spinal {alpha}-motoneurons are a part of the central nervous system, equilibration of spinal cord propofol concentrations with plasma concentrations had to be considered (17). According to our preceding pharmacokinetic simulations, we chose 5-min intervals between bolus administrations of propofol at 3 time points (T0, T2, and T4): T0, 1 mg/kg body weight injected over 15 s; T2, 1 mg/kg over 15 s; and T4, 2 mg/kg over 30 s. Simulating this study design, peak plasma concentrations occurred within 15 s after the completed bolus application, and peak effect-site concentrations of propofol occurred approximately 2.5 min after each bolus injection. These values are in agreement with values reported by others (17,18). A simulated mean peak blood concentration of 5.83 ± 1.42 µg/mL (mean ± SD) was achieved within 15 s after the third propofol bolus. To minimize a possible influence of noxious stimuli, electrophysiologic monitoring was started after craniotomy and opening of the dura were completed and a hemodynamic plateau was achieved. A stabilization period of 15 min was allowed before EMG and MMG baseline measurements were recorded (TB). M-wave and F-wave recordings were performed every 2.5 min starting with the first bolus (T0–T6). MMG recordings were performed continuously throughout the study period.

In our study, the time intervals between M waves and F waves were 15–25 ms. Depression of the F-wave amplitude could result from a propofol-induced phenomenon of tetanic fade at the neuromuscular junction, occurring after the first synaptic transmission evoking the M wave. In five patients we therefore performed a double-stimulus pulse trial with an interstimulus interval of 25 ms to evoke two M responses (Fig. 2 B). If the two resulting M waves were of the same amplitude, fading could be excluded as a reason for a decreased F wave after a single stimulus. Blood and effect-site concentrations of propofol, as well as blood concentrations of fentanyl and midazolam, were simulated for each time point (TB and T0–T6) by using a three-compartment model (IVA-SIM, Version 3.01; Zeneca, Planckstadt, Germany).

The F wave is a variable EMG signal. Therefore, at each time point, two series of eight consecutive traces with different amplifications for M waves and F waves were recorded, and maximal M- and F-wave peak-to-peak amplitudes were determined (Fig. 2A). The resulting eight values for each wave form were averaged to provide single values for statistical analysis for each of the eight time points (TB and T0–T6). Accordingly, F/M ratios (F-wave amplitude divided by M-wave amplitude) and the F-wave latencies of eight consecutive traces were determined and averaged. For each time point, MMG amplitudes of the first twitch were normalized to baseline values (T1 amplitude), and TOF ratios were determined (amplitude of the fourth twitch divided by amplitude of the first twitch). In addition, the ratios of paired M-wave amplitudes of the double-stimulus pulse trial were calculated for each time point. All variables were compared by one-way analysis of variance with repeated measurements. Paired multiple comparison procedures with Bonferroni correction were conducted for F-wave amplitudes and F/M ratios. A P value of <0.05 was considered significant. Statistical analyses were performed by using a computer program (SPSS 10.0; SPSS Inc., Chicago, IL).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Both F-wave amplitudes and F/M ratios showed a significant overall decrease after bolus administration of propofol (P = 0.002 and P = 0.038, respectively). Multiple comparison analysis revealed that F-wave amplitudes were significantly lower 2.5 min after the first bolus of propofol (T1; P = 0.043), 5 min after the second bolus (T4; P = 0.021), and 2.5 min (T5; P = 0.002) and 5 min (T6; P = 0.001) after the third bolus compared with baseline values (Fig. 3A). At the largest simulated propofol concentrations (T5 and T6), each individual showed a clear decrease of F-wave amplitudes compared with baseline values (Table 1, Fig. 3B); a complete loss of F waves was observed in 6 (40%) of 15 patients at T5 (Table 1). The F/M ratio was significantly reduced 2.5 min (P = 0.032) and 5 min (P = 0.024) after the third bolus administration of propofol (Fig. 3A).



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  		Figure 3. A, Averaged F-wave amplitudes and F/M ratios decreased during the course of three propofol administrations of two times 1 mg/kg followed by 2 mg/kg at 5-min intervals. *P < 0.05 versus TB; **P < 0.01 versus TB. The F-wave amplitudes and F/M ratios shown are means ± 95% confidence intervals. B, Original tracings of a set of 8 F waves before (TB) and after 3 (T1, T3, and T5) bolus administrations of propofol in one patient.

 

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  		Table 1. Electromyographic (F-Wave Amplitudes; mV) and Mechanomyographic Values (T1 amplitudes; %)
 

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  		Table 1. Continued
 
The mechanical muscle contractility monitored by MMG as T1 amplitudes (Table 1) and TOF ratios (Fig. 4, upper panel) remained stable. Additionally, M-wave amplitudes, an EMG indicator of the condition of the neuromuscular junction and muscle, also remained unchanged after repeated administrations of propofol (Fig. 4, lower panel). No changes were observed regarding the paired M-wave amplitudes (Fig. 4, lower panel). F-wave latencies, used to estimate axonal conduction velocity, were also unaltered (Fig. 4, lower panel).



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  		Figure 4. (Upper panel) Assessment of peripheral neuromuscular competence after three bolus administrations of propofol. The T1 amplitude (amplitude of the first train-of-four (TOF) twitch) is expressed as a percentage of baseline values. The TOF ratio is defined as the amplitude of the fourth mechanomyography (MMG) response (T4) divided by the amplitude of the first MMG response (T1) after a TOF stimulation pattern and is expressed as a percentage. (Lower panel) M-wave amplitudes and F-wave latencies were normalized to baseline values. {dagger}Because of a complete loss of F waves in some patients, the numbers of individuals (n) for the determination of mean F-wave latencies at T4, T5, and T6 were 13, 9, and 11, respectively. Values of paired M waves indicate the ratio of the first M-wave amplitude divided by the second M-wave amplitude after a paired stimulus at an interstimulus interval of 25 ms. An unimpaired M-wave amplitude, an unchanged MMG TOF ratio, and a stable M-wave ratio indicate an unimpaired function of the neuromuscular transmission. The unchanged T1 amplitude demonstrates constant muscle contraction strength. A stable F-wave latency indicates unchanged conduction velocities of motoneurons after the administration of propofol. Values are means ± 95% confidence intervals.

 
Our simulations of propofol’s blood and effect-site concentrations resulted in a step-by-step increase after each propofol injection. Simulated propofol blood and effect-site concentrations 2.5 min after each injection for the time points T1, T3, and T5 were 1.09 ± 0.23 µg/mL, 1.47 ± 0.30 µg/mL, 2.95 ± 0.61 µg/mL and 0.79 ± 0.16 µg/mL, 1.38 ± 0.29 µg/mL, 2.54 ± 0.53 µg/mL, respectively. Simulated blood and effect-site concentrations of fentanyl and midazolam remained stable during the investigation period (data not shown).


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Our study demonstrates a depression of human central (spinal) {alpha}-motoneuron excitability after bolus administration of propofol, as shown by a decrease of spinal F-wave amplitudes. In addition, according to stable F-wave latencies and MMG values, axonal conduction velocity, signal transduction at the neuromuscular junction, and muscle contraction strength were not impaired by propofol, suggesting the lack of a peripheral effect of propofol on the motor system.

The muscle-relaxing properties of propofol are not completely understood. Propofol may influence different parts of the motor pathway, from cortical motoneurons to the muscle cell. In this study, we investigated the lower (spinal) portion of the central part of the motor system as well as the peripheral part. The observed decrease in F-wave amplitudes in our study can be attributed to a decreased {alpha}-motoneuron excitability indicated by the lack of effect of propofol on the orthodromically conducted M-wave amplitude, even when stimuli were repeated at 25-ms intervals (paired M waves). This finding is in agreement with observations by other authors (7,8,19). Kerz et al. (7) found a concentration-dependent effect of propofol on the H reflex, another electrophysiologic variable to assess the excitability of motoneurons. However, in that study, depression of the H reflex occurred at larger propofol concentrations compared with our study; this may be due to the different physiology of the two signals. The H reflex includes an afferent input from large, fast conducting type Ia fibers and is modulated by inhibitory interneurons (Renshaw cells), whereas the F wave results from a recurrent discharge of antidromically activated motoneurons. Kakinohana et al. (19) reported a significant reduction in F-wave persistence after a propofol bolus of 2 mg/kg followed by a propofol infusion at a rate of 6 mg · kg-1 · h-1. Recently, these authors demonstrated a dose-dependent decrease of spinal motoneuron excitability at clinically relevant propofol blood target concentrations of 0.5 to 1.8 µg/mL (8). These values overlap with the simulated blood concentrations in our study. Other IV anesthetics did not lead to a decrease of {alpha}-motoneuron excitability; thiopental did not depress spinal F waves in rats (20) or humans (21), and ketamine and etomidate were found to increase the {alpha}-motoneuron excitability determined by increases of the H reflex (22,23). However, volatile anesthetics, e.g., isoflurane (24) and nitrous oxide (13), were shown to decrease F-wave amplitudes. This depression of {alpha}-motoneuron excitability during general anesthesia with volatile anesthetics was proposed to contribute to surgical immobility (11).

Depression of the {alpha}-motoneuron excitability either may be the result of a direct influence of propofol on the soma of the {alpha}-motoneuron or may be induced by a changed excitatory versus inhibitory afferent input to that motoneuron (11). In an animal model with spinal cord sections from turtles, propofol suppressed the plateau potentials mediated by L-type calcium channels, demonstrating a direct influence on the motoneuron soma (25). Zhou and Zhu (24) reported that isoflurane (0.5%) almost abolished motor evoked potentials, but not F waves, suggesting that spinal cord motoneuron excitability is not dependent predominantly on the input from higher central levels. These results support the hypothesis that a direct anesthetic effect on the {alpha}-motoneuron is more likely.

In our study, we could not detect a peripheral effect of propofol. F-wave latencies, M-wave amplitudes, and paired-pulse stimulation signals remained unaltered, suggesting that nerve conduction in the peripheral nerve and the neuromuscular transmission were not affected by propofol. These EMG findings are in agreement with results reported by Kakinohana et al. (8) and Kerz et al. (7). In addition to those studies, we also monitored muscle contractility by MMG with a TOF stimulation pattern. Our MMG findings of unchanged T1 amplitudes combined with a stable TOF ratio demonstrate that muscle contraction strength was not impaired in our study. However, Fujii et al. (12) detected a reduction of diaphragmatic contractility in dogs after propofol administration. These differences may be explained by different interspecies drug sensitivities, use of the diaphragm versus the adductor pollicis muscle, and use of a deviant method to determine contractility (inflated esophageal balloon). Blockade of heterologously expressed human skeletal muscle sodium channels by propofol determined in vitro was reported by Haeseler et al. (5). However, the effective concentrations applied in that study appear to be above the clinically relevant range. The stability of all signals in our study that would indicate a peripheral effect of propofol suggests that propofol’s influence on the motor system is more likely a central than a peripheral one. Accordingly, in contrast to volatile anesthetics, maintenance of anesthesia with propofol does not reduce the doses of neuromuscular blocking drugs required to maintain adequate muscle paralysis (6).

To optimize monitoring conditions and to reduce patient discomfort due to painful continuous MMG monitoring, electrophysiologic recordings were performed in patients under general anesthesia maintained with fentanyl and midazolam. An underlying contribution of midazolam and fentanyl cannot be completely excluded. The concentrations of propofol required to cause a decrease in F-wave amplitude might be smaller because of the coadministered drugs. However, simulated blood levels of midazolam and fentanyl during the study remained stable during the investigation period, and F waves were reproducibly recorded in all patients until propofol was administered, indicating that the changes in F-wave amplitudes were produced by propofol. Further, we reported earlier that facial nerve F-wave monitoring for certain neurosurgical procedures was not impaired under this anesthetic regimen (26) and that fentanyl given as a bolus of 5 µg/kg was found to have no effect on F-wave amplitudes (19). However, other investigators used propofol for the maintenance of anesthesia to study the effect of volatile anesthetics on {alpha}-motoneuron excitability (24). According to our results and those of Kerz et al. (7) and Kakinohana et al. (19), we recommend that propofol be used with caution if F-wave monitoring is intended for clinical or study purposes.

Our data suggest a dose-dependent effect of propofol on spinal {alpha}-motoneuron excitability because mean F-wave amplitudes decrease with successive propofol dose increments corresponding to increasing simulated blood and effect-site concentrations. This is consistent with the dose-dependent effect of propofol on H reflexes reported by Kerz et al. (7). However, dose dependency cannot be proven in our study because steady-state conditions of propofol levels were not achieved because of the study design. We chose a repeated-bolus design, achieving large transient propofol concentrations, to model the anesthesia induction conditions for which the muscle-relaxing properties were reported (1,2).

In summary, our study demonstrates a substantial decrease of human F-wave amplitudes after bolus administration of propofol during general anesthesia with fentanyl and midazolam. No effect of propofol on signal transduction at the neuromuscular junction and no direct effect on muscle contraction strength could be detected. Therefore, the mechanism of propofol’s muscle-relaxing properties is probably a central effect, namely, the depression of spinal {alpha}-motoneuron excitability. Further, propofol may impair F waves unpredictably, even at smaller concentrations, and should therefore be used with caution if F-wave monitoring is intended for clinical or study purposes.


   Acknowledgments
 
The authors would like to thank K. Tamer and D. Wiegand for advice and assistance with the electrophysiologic recording.


   Footnotes
 
Presented in part at the annual meeting of the American Society of Anesthesiologists, San Francisco, CA, October, 2000, and published in abstract form [Propofol depresses spinal {alpha}-motor neurons in man: an F-wave study. Anesthesiology 2000;93(Suppl):A60].


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication October 9, 2002.




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T. M. Hemmerling, N. Le, P. Decarie, J. Cousineau, and D. Bracco
Total intravenous anesthesia with propofol augments the potency of mivacurium: [L'anesthesie intraveineuse totale avec le propofol augmente la puissance du mivacurium]
Can J Anesth, June 1, 2008; 55(6): 351 - 357.
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 Br J AnaesthHome page
B. S. von Ungern-Sternberg, F. J. Frei, J. Hammer, A. Schibler, R. Doerig, and T. O. Erb
Impact of depth of propofol anaesthesia on functional residual capacity and ventilation distribution in healthy preschool children
Br. J. Anaesth., April 1, 2007; 98(4): 503 - 508.
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 Br J AnaesthHome page
J. H. Baars, S. Tas, K. F. Herold, D. A. Hadzidiakos, and B. Rehberg
The suppression of spinal F-waves by propofol does not predict immobility to painful stimuli in humans{dagger}
Br. J. Anaesth., January 1, 2006; 96(1): 118 - 126.
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 Anesth. Analg.Home page
S. Manikandan, P. K. Sinha, P. K. Neema, and R. C. Rathod
Severe Seizures During Propofol Induction in a Patient with Syringomyelia Receiving Baclofen
Anesth. Analg., May 1, 2005; 100(5): 1468 - 1469.
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 Anesth. Analg.Home page
M. H. Dueck, M. Paul, P. Sagawe, A. Oberthuer, C. Wedekind, and U. Boerner
Different F-Wave Recovery After Neuromuscular Blockade with Pancuronium and Mivacurium
Anesth. Analg., November 1, 2004; 99(5): 1402 - 1407.
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 Anesth. Analg.Home page
J. Ahrens, G. Haeseler, M. Leuwer, B. Mohammadi, K. Krampfl, R. Dengler, and J. Bufler
2,6 Di-tert-butylphenol, a Nonanesthetic Propofol Analog, Modulates {alpha}1{beta} Glycine Receptor Function in a Manner Distinct from Propofol
Anesth. Analg., July 1, 2004; 99(1): 91 - 96.
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press