Sensory and Motor Nerve Conduction Velocities Following Therapeutic Ultrasound

Sensory and Nerve Conduction Velocities Following Therapeutic Ultrasound Nineteen healthy volunteers each received six, five-minute ultrasound treatments at sonation intensities of 0.0, 0.5, 1.0, 1.5, 2.0 and 2.5 W/crrf, applied along the proximal forearm segment~pf the ulnar nerve, over an area of approximately 4.5 times the area of the ultasound application head. Sensory and motor nerve con-' duction velocities responded similarly, but not identically to ultrasound. All clinical intensities, with the exception of 0.5 W/cm 2 (p <0.10), were associated with significantly increased velocities. Subcutaneous tissue temperatures were directly related to sonation intensity, although significantly increased temperatures were not observed until 1.5 W/crrf intensity was used. The effectiveness of clinical applications of ultrasound in pain relief cannpt be attributed to a decrease in nerve conduction velocity of the faster conducting A-fibers, which are evaluated using standard nerve conduction techniques. JOHN F. KRAMER John F. Kramer, Ph.D., is an Associate Professor in the Department of Physical Therapy, Faculty of Applied Health Sciences, University of Western Ontario, London, Ontario, Canada. The effect of therapeutic ultrasound on motor and sensory nerve conduction velocities has come under increasing study as practitioners seek to account for the clinical effectiveness of ultrasound by documenting its physiological effects. Amongthe most readily documented physiological parameters are nerve conduction velocity and subcutaneous tissue temperature. Griffin (1966) speculated that if ultrasound could decrease nerve conduction velocity, thereby allowing fewer nerve impulses to be propagated per unit of time, this might help explain the means by which ultrasound could relieve pain. The conventional sensory and motor nerve conduction techniques focus on the fastest conducting A-fibers (Smorto and Basmajian 1979, Braddom and Schuchmann 1984, Schuchmann and Braddom 1984). However, pain is also transmitted via the C-fibers, which are unmyelinated and have slow conduction rates (Ganong 1983). Herrick (1953), using an animal model, reported that the C-fibers were more sensitive to ultrasound than were the A fibers. Although the extent to which. the responce of the A-fibers can be extrapolated to the C-fibers is presently unclear, the conventional nerve conduction techniques do offer a means of quantifying some of the physiological effects of ultrasound on mixed peripheral nerve. With respect to motor nerve conduction velocity, initial studies suggested that continuous ultrasound has an intensity dependent, or bipositive effect. Zankel (1966) and Farmer (1968) reported decreased ulnar motor nerve conduction velocities to be associated with sonation intensities of 1 to 2 WI cm 2, but increased velocities to be associated with sonation at other intensities. Madsen and Gersten (1963) reported decreased velocities, at three minutes, following sonation at 0.88 and 1.28 WIcm 2, but increased velocities following sonation at 1.92 WIcm 2 The slowing of motor nerve conduction velocity has been attributed to a mechanical effect (Farmer 1968), or a micromassage action (Zankel 1966), and the increased velocities to the heating effect of ultrasound (Madsen and Gersten 1963, Farmer 1968). These studies suggest that at the intermediate intensities, reduced nerve conductionvelocity is a plausible explanation for the pain relieving action of ultrasound. The in vestigations cited sonated the entire forearm, for five to 10 minutes, at various intensities, using ultrasound frequencies of 870 khz (Farmer 1968, Zankel 1966) and 1 MHz (Madsen and Gersten 1963). Not all investigations have supported the bipositive effect of ultrasound on motor nerve conduction velocity. Kramer (1985a) applied continuous ultrasound (870 khz) over a 12 cm long segment of the ulnar nerve in the proximal forearm and observed that the The Australian Journal of Physiotherapy. Vol. 33, NO.4, 1987 235

post-treatment motor velocities associated with five ultrasound applications ranging from 0.5 to 2.5 Wfcm 2 intensity, were all significantly greater than were the respective pre-treatment velocities. In another study, five minutes of ultrasound (870 khz) at 1.5 Wfcm 2 and ihfrared radiation, applied until a subcut\neous tissue temperature in" crease similar to that associated with ultrasound had been achieved, produced similar post-treatment ulnar motor nerve conduction velocities (Kramer 1984). It was concluded that when sonation is confined to an area of approximately 4.5 times the area of the soundhead, the cooling effect associated with the ultrasound transmission gel on the skin surface was not as pronounced, and the heating effect of the ultrasound was responsible for the increased conduction velocities. Investigators having examined' the effect ofcontinuous ultrasound on sensory nerve conduction have generally reported sonation to be associated with decreased antidromic sensory latencies, which would indicate increased conduction velocities (Currier et al 1978, Halle et al 1981, Currier and Kramer 1982, Kramer 1985b). In two studies, infrared radiation was used to produce an increase in subcutaneous tissue temperature similar to that associated with ultrasound (1 MHz), at 1.0 Wfcm 2 for a mean 13.2 minutes (Halle et a1198l) and at 1.5 Wfcm 2 for five minutes (Currier and Kramer 1982). Because the infrared radiation and the ultrasound treatments were associated with similar decreases in sensory latencies, the authors concluded that the heating effect of ultrasound was responsible for the increased sensory conduction velocities (Halle et a11981, Currier and Kramer 1982). Cosentino et al (1983), however, observed increased orthodromic sensory latencies to be associated with 10 minutes sonation (1 MHz) at intensities ranging from 0.0 to 1.5 Wf cm 2 The magnitudes of the associated decreases in sensory nerve conduction velocities were not statistically significau-t, and no significant difference was reported between any of their four intensity groups. In this study, the median nerve in the mid-forearm, for a distance of 25 to 40 em was sonated, whereas, the previous sensory conduction studies sonated a smaller length, approximately 12 em, of the lateral cutaneous branch of the radial nerve (Currier et al 1978, Halle et al 1981, Currier and Kramer 1982). Kramer (1985b) sonated (870 khz) a 12 em segment of the ulnar nerve in the proximal forearm and measured antidromic sensory latencies, using two stimulation sites that bordered the treatment area, to calculate sensory nerve conduction velocities. Five minutes sonation at intensities ranging from 0.5 to 2.5 Wf cm 2 was associated with increased sensory nerve conduction velocities at all intensities. When the investigations exammmg the effect ofultrasound on sensory and motor nerve conduction velocity are classified according to the size of the area sonated, the pattern appears to be one in which those having sonated large areas have reported decreased conduction velocities, whereas, those having sonated smaller areas have reported in creased conduction velocities. Currently, the appropriate area of sonation, as well as the rate of movement of the ultrasound application head, the treatment duration and the ultrasound transmission medium, are not precisely agreed upon. Several authors have recommended limiting the area of sonation to less than five times the area of the ultrasound application head during a typical five minute treatment (Faris 1969, Reid and Cummings 1973, Oakley 1978, Wadsworth and Chan mugan 1980). However, experimental evidence was not provided to substantiate this suggestion. That the cooling effect of the ultrasound transmission gel provides a decrease in the associated velocity measures is strongly suggested by the observation that all investigators who used a placebo, 0.0 Wf cm 2, ultrasound treatment, reported decreased velocities (Madsen and Gersten 1963, Farmer 1968, Cosentino et al 1983, Kramer 1984, 1985a and 1985b). At other intensities, the cooling effect of the ultrasound transmission gel on the skin surface of the forearm may confound the heating effect associated with ultrasound. This cooling effect may be further complicated by the course of the ulnar nerve in the forearm: lying deep within a muscular bed in the proximal aspect, but lying more superficial within the distal as" pect. To date, individual investigations have focused on either sensory or on motor conduction studies. Consequently, the precise ultrasound application technique and the area of sonation differed between studies, making a direct comparison ofsensory and motor velocities difficult. Although Kramer reported a similar sonation technique and a similar area of treatment during sensory (1985b) and motor (1985a) conduction studies, different subjects were treated. This difference introduces complications associated with the location and depth of the ulnar nerve, the degree of homogeneity of the tissues sonated, ultrasound attenuation and penetration. To minimize the effects of these factors, the present study measured both sensory and motor conduction velocities following the same therapeutic ultrasound applications, at intensities ranging from 0.0 to 2.5 Wfcm 2 To minimize measurement errors related to the determination of nerve conduction latencies, the sensory and motor latencies were determined using the Same electrical stimulus to simultaneously evoke both sensory and motor nerve action potentials in a mixed peripheral nerve, where it courses in a relatively homogeneous tissue bed. The purpose of the present study was to compare sensory and motor nerve conduction velocities associated with identical ultrasound treatments, at clinical intensities, applied to the same subjects; thereby contributing to the overall understanding of the physiological effects of ultrasound. 236 The Australian Journal of Physiotherapy. Vol. 33, No.4, 1987

Method Nineteen informed volunteers (7 men, 12 women), ranging in age from 20 to 36 years (mean 24.5 years), were examined. All subjects reported no history of major ulnar nerve trauma, nor any neurological, or other condition which' \{light modify ulnar sensory or motor i\erve conduction. Ultrasound treatments and nerve conduction testing were completed with the subject supine, and the dominant arm supported by pillows and toweling, in the following position: approximately 70 shoulder abduction, 50 shoulder external rotation, 70 elbow flexion and 45 forearm pronation. A four-channel TECA TE-42 Electromyograph, with fiber optic recorder (TECA Corporation, 3 Campus Drive, Pleasantville, New York 10570), was used to perform simultaneous antidromic sensory and motor (orthodromic) nerve conduction studies on the ulnar nerve, proximal forearm segment. For the sensory studies, a ring ground electrode, 2 mm coil diameter, was first positioned around the proximal phalanx of the little finger. Then two ring electrodes were positioned approximately 2 cm apart on the middle and distal phalanges of the small finger. For the motor conduction studies, two, 1 cm diameter surface electrodes were positioned, 2 cm apart, over the abductor digiti quinti muscle and the associated ground electrode was positioned over the dorsal surface of the hand. All skin contact areas were prepared by massaging the skin withelectrode gel. The electrodes were secured in position by means of stretch adhesive tape, which also served to prevent the subject from altering the finger position during testing and treatment. The EMO amplifiers were set at the frequency response ranges of 32 to 1600 Hz for the sensory channel and 1.6 to 3200.Hz for the motor channel. The motor action potential was positioned in the top one-half of the oscilloscope screen and the sensory action potential in the bottom one-half. A timing Distal Stimulation Site Proximal Stimulation Site 4.275ms 4.250ms 6.225ms 6.175ms amplification: 2mV/cm 3 1cmI Timing Channel (0.1 ms/dot) Sensory Timing Channel (0.1 ms/dot) Sensory Sensory amplification: 20p.v/cm F!gtlre 1: COpy of the sensory and motor action potentials associated with the ~Istal ~nd the proximal electrical stimulation sites (3 was the code number for the ImmedIate post-treatment velocity determination for this subject). marker channel, composed of diagonal rows of dots, with each dot representing 0.1 milliseconds (ms), was positioned between the two action potential traces and was used in measuring the latencies (Figure 1). Theelectrical stim ulus was a rectangular pulse of 0.1 fis duration, delivered at a frequency of two impulses per second, at supramaximal intensity. The intensity was set approximately 20 per cent greater than that required to elicit a supramaximal motor response at the least sensitive stimulation site. The stimulus intensity was approximately 1.5 times that required to obtain a supramaximal sensory response. The electrical stimulus intensity and amplifier settings were adjusted during the pretreatment nerve conduction determinations, and were not changed during that treatment. None of the subjects complained of discomfort associated with the electrical stimulation procedure. The action potentials on the oscilloscope were used to help determine the location and course of the ulnar nerve in the proximal forearm. The nerve was first identified at the ulnar notch and was then traced distally along its course by applying the stimulating electrodes (fixed 2 cm apart) over the skin. A satisfactory distal stimulation site was identified approximately 12 cm distal to the ulnar notch, and marked on the skin with permanent ink. A satisfactory proximal stimulation site was then identified by measuring approximately 12 cm back, or proximally from the distal stimulation site, and then confirming the location of the nerve by applying the stimulating electrodes again. The proximal site was also marked with permanent ink. In the case of poor quality sensory and/ or motor action potential recordings, the appropriate electrodes were repositioned, and if the quality of the re The Australian Journal of Physiotherapy. Vol. 33, No.4, 1987 237

cordings could not be improved through skin preparation or technical adjustments, the subject was not used for testing. Subcutaneous tissue temperature was recorded using a 24-gauge needle probe (YSI ]No. 524 Hypodermic Temperature Prope, Yellow Springs Instrument Company, Yellow Springs, Ohio 45387) inserted diagonally into the mid-portion of the treatment area so that its temperature-sensitive tip lay in the subcutaneous tissue, over the previously identified course of the ulnar nerve. The area of insertion was initially cleansed with isopropyl alcohol and the temperature probe was sterilized through gas autoclaving prior to each insertion. The probe remained in position from approximately five minutes before treatment until one minute after treatment. Temperatures were:recorded from a digital telethermometer (YSI Model 49TA Digital Telethermometer, Yellow Springs Instrument Company, Yellow Springs, Ohio 45387) which had been previously calibrated for temperature conversion. Continuous ultrasound was applied using an ultrasound (Burdick UTI 4300 Ultrasound, Burdick Corporation, Milton, Wisconsin 53563) with an output frequency of 870 khz and a 4.1 cm diameter soundhead. The unit was calibrated for intensity prior to the study and after every 50 treatments. The conventional circular sonation technique, with the soundhead moving at approximately 3 cm/s and each circle overlapping approximately 50 per cent of the previous circle, was used. The area of treatment was restricted to approximately 12 cm in length by 5cm in width, and lay precisely between the two stimulation sites and over the course of the nerve. Both the ultrasound application head and the transmission gel (Aquasonic 100, Parker Laboratories, 307 Washington St., Orange, New Jersey 07050) were at room temperature prior to treatment. The gel was applied only once, at the start of the treatment. Following insertion of the temperature probe, the subject was allowed approximately two minutes to rest, and for nerve conduction and temperature values to stabilize. Thereafter, temperatures were recorded at one-minute intervals, until two successive temperatures were within 0.1 C ofone another. At that time, the one-minute pre-treatment nerve conduction velocity measures were completed and the temperature recorded. One minute later, the immediate pre-treatment nerve conduction and temperature data were gathered. If the three temperatures did not differ from one another by more than 0.1 C, the subject was considered to have stabilized and the assigned ultrasound treatment was administered. Temperatures were recorded every minute during treatment. Nerve conduction and temperature data were again collected immediately post-treatment and at one-minute post-treatment. The ultrasound transmission gel was gently wiped from the skin surface of the treatment area immediately after the initial poshreatment recordings. No toweling or other material was placed over the exposed treatment area during the one-minute recovery period. Approximately three stimulation impulses were required at each site for 'each latency determination, in order to confirm electrode location and to obtain satisfactory action potentials for analysis. Approximately 10 seconds were required to complete both the proximal and distal latency recordings associated with each time of measurement. Prior to applying the electrical stimulus immediately post-treatment, sufficient transmission gel was wiped from the stimulation sites, to prevent the formation of an electrical bridge between the two stimulating electrodes. The four nerve conduction recordings were each coded with a number, separated from the fibre-optic recording paper and randomly attached to a blank page. One examiner evaluated all the nerve conduction records and recorded the latencies relative to the code number. In this way the examiner did not know which of the four conduction time periods was being measured. Latencies were measured to the initial negative deflection of the motor action potential and to the peak negative deflection on the sensory action potential. The sensory and the motor action potentials were identified by their characteristic shape, amplitude and location. Generally, the sensory latency was shorter than was the associated motor latency. Consequently, the action potential on the sensory channel, the electrodes for which were positioned 2 cm distal to the motor electrodes, could not be attributed to motor overflow from the abductor digiti quinti muscle. One of the following six sonation intensities was randomly administered during each treatment period: 1) 0.0, 2) 0.5, 3) 1.0,4) 1.5, 5) 2.0 and 6) 2.5 W/cm 2 A minimum of 48 hours was required between successive treatments and the subjects were not advised as to the sonation intensity until after treatment. Room temperatures ranged from 22.0 to 25.0 C during the course of the study, but did not vary more than 1 C during anyone treatment period. Door, windows and ventilation ducts were closed during the treatments, so as to limit any effect that air currents might have on temperatures. Once adjusted, the electrical stimulus and the recording parameters were not changed during a testing session. Data Analysis A priori planned contrasts (Brecht and Woodward 1984) were used to compare the absolute sensory and motor nerve conduction velocities at oneminute pre-treatment and immediately pre-treatment, for each of the six sonation sessions (12 tests). Pearson Product Moment Correlation Coefficients (Winer 1971) were calculated between the absolute sensory and motor velocities immediately pre-treatment and immediately post-treatment (six coeffi cients for each time of measurement) for the six sonation sessions,and between the one-minute pre-treatment 238 The Australian Journal of Physiotherapy. Vol. 33, No.4, 1987

and the immediate pre"treatment velocities within each nerve conduction" intensity combination (l2coefficients). Because nerve conduction and tern" perature change scores (immediate~post treatment minus immediate pre-treatment) were of major interest in the present study, the one"minute and immedia\e pre"treatment values were first compwed to determine if these values were similar within and across the six intensities associated with that nerve conduction measure. Three two-way analysis of variance (ANOVA) procedures (two levels of time by six levels of intensity), with repeated measures on both factors, were used to examine the absolute sensory and motor nerve conduction velocities, and the absolute temperatures. Following non statistically significant interaction and main effects on the three ANOVA's, the pre" treatment values were considered to be similar and further analysis was conducted on the change scores. A twoway ANOVA procedure (two levels of nerve conduction by six levels of intensity) with repeated measures on both factors, was used to examine the nerve conduction change score data. A one" way ANOVA, with repeated measures over intensities, was used to examine the changes in subcutaneous tissue temperatures. One sample, non"directional, I-tests (Ferguson 1972) were used to determine if the magnitude of the velocity and temperature change score associ" ated with each of the six sonation intensities was significantly greater than zero, the expected score if the ultra~ sound treatment had no effect. Pearson Product Moment Correlation Coefficients were calculated between the changes in subcutaneous tissue temperatures and theasosciated changes in motor and sensory velocities, and between the changes in sensory and motor conduction velocities. The analysis of variance tests were computer based (Brecht and Woodward 1984). Following statistically significant F-ratios associated with the ANOVA procedures, a Newman-Keuls technique (Winer 1971) was used to compare selected pairs of means. The 0.05 level of significance was adopted throughout analysis. Results All subjects completed the full five minute treatments, using each of the six ultrasound intensities. The subjects did, however, report an increasing sen" sation of heatifig as the sonation in" tensity increased - particularly so at sonation intensities of 2.0 and 2.5 Wf cm 2 Based on the subjects comments, heating ranged from imperceptible to mild, at intensities of 0.0 through 1.5 Wfcm" and from mild to very warm, at 2.5 Wfcm 2 None of the subjects reported the heating at 2.5 Wfcm 2 to be hot or painful - the criteria for discontinuing treatment. Absolute Scores: Nerve Conduction Velocity On the twelve a priori contrasts, the sensory velocities were all observed to be significantly greater than were the associated motor velocities (p<0.05) at one"minute pre-treatment and immediately pre"treatment, for the six sonation sessions, with the exception of the one"minute pre-treatment velocity Sensory Change Scores: Nerve Conduction Velocity On the absolute nerve conduction velocities, no statistically significant difference was observed between the one-minute and the immediate pretreatment velocities, within or across the six ultrasound intensities, for either the sensory or the motor data. For this reason, the subjects were considered to have stabilized prior to each sonation session and the immediate pre-treatment values were considered to be simprior to sonation at 2.0 Wfcm 2 (Figure 2). The correlations between the sensory and the motor velocities, imme" diately pre-treatment, were all statistically significant (p < 0.05) (Table 1). However, at the immediate post-treatment comparison, the correlations at 1.0 (p:=0.35) and 2.5 (p:=0.24) Wfcm 2 were non significant, while the correlations at the other four intensities were significant (p < 0.02). The correlation between the one-minute and the immediate pre-treatment velocities, within each nerve conduction"intensity combination, was significant (p<0.02) in 11 of 12 cases, the exception being the sensory velocity associated with the 2.0 W/cm 2 session (r:= 0.42; p:= 0.07). W/cm' 66 ~ a 65.,~~ 2.5 111// 64 t Ii III 63~o~ Nerve :j {j,. Conduction / ~. 59 2.0 1.5 1.0 Velocity 62 ~ '" ~ o (m/s) I::::::::". 0.5 58 0.0 =r " " " II Pre 1 Pre 0 Post 0 Post 1 " Time of Recording (minutes pre and post sonation) Figure 2: Absolute sensory and motor nerve conduction velocities. W/cm' The Australian Journal of Physiotherapy. Vol. 33, No.4, 1987 239

Table 1: Absolute pre-treatment nerve conduction velocities (m/s) and subcutaneous tissue temperatures (OC) and sensory motor correlation Nerve Ultrasound Intensity (W/crrf) Conduction 0.0 0.5 1.0 1.5 2.0 2.5 Sensory 62.61" 61.19 61.12 62.83 62.24 62.08 VeloC,ity (4.01)b (3.78) (3.61) (4.34) (3.65) (4.90) 60.37 59.40 59.16 61.11 60.64 60.24 Velocity (4.35) (3.57) (2.86) (3.13) (2.84) (5.23) Temperature 32.7 33.0 32.8 33.0 32.9 32.8 (0.7) (0.8) (0.8) (0.7) (0.8) (0.8) Sensory 0.68 0.58 0.49 0.66 0.55 0.72 r" Sensory 0.54 0.52 0.23 0.57 0.79 0.28,n " Mean b Standard deviation C Based on absolute values fbr immediate pre-treatment velocities d Based on absolute values for immediate post-treatment velocities Critical values for two tailed test of significance: r (0.05,17) = 0.46, r (0.02,d =0.53, r <0.01,17) =0.58 Table 2: Change scores" for the sensory and the motor nerve conduction velocities (m/s), and subcutaneous tissue temperature (Oc) Ultrasound Intensity (Wlcrrf) 0.0 0.5 1.0 1.5 2.0 2.5 Sensory -1.74 b 0.87 1.93 2.78 3.47 3.20 Velocity (3.13)C (2.00) (2.38) (3.68) (3.28) (3.61) -1.46 1.04 2.17 3.06 3.19 3.24 Velocity (1.82) (2.59) (2.68) (2.59) (2.85) (3.65) Temperature -2.8-1.6-0.5 0.5 1.8 2.8 (1.0) (0.7) (0.7) (0.8) (0.9) (0.7) " Immediate post-treatment minus immediate pre-treatment b Mean C Standard deviation main effect, the change associated with the 0.0 Wfcm' intensity was observed to be significantly different from those changes associated with the other five intensities (p<0.01). Similarly, the change score associated with the 0.5 Wfcm' intensity was significantly less than that associated with the 2.5, 2.0 and the 1.5 Wfcrn' intensities (p<0.05), but was not significantly different from that associated with the 1.0 Wf cm' intensity. The change scores associated with the 1.0, 1.5, 2.0 and 2.5 Wfcm' intensities did not differ significantly among one another. The magnitudes of the changes in nerve conduction velocity associated with the sensory and the motor tests were significantly different from zero (the expected value under the null hypothesis) for all intensities (p<0.01); p<0.05 for the 0.0 Wfcm' sensory velocity), with two exceptions: 0.5 Wf cm 2 for both the sensory and motor velocities, which were narrowly not significant (p<0.1o). Change Scores: Subcutaneous Tissue Temperature Because no significnat differences were observed between the one-minute and the immediate pre-treatment temperatures, within or across the six sonation intensities (Figure 3), analysis was confined to change scores. The F-ratio for change in subcutaneous tissue temperature was significant on the oneway ANOVA (p<0.0l). The change in temperature associated with each ultrasound intensity (Table 2) was significantly different from the changes observed for the other intensities (p<0.0l). The magnitude of the change in tissue temperature was significantly different from zero for all intensities (p<0.01). Har across intensities, and to provide an acceptable baseline from which to determine change scores (Table 2). On the change scores ANOVA, the main effect for nerve conduction velocity and the nerve conduction velocity by intensity interaction were not statistically significant, whereas the main effect for intensity was significant (p<0.01). When the change scores for the sensory and the motor velocities were combined to examine the intensity Change Scores: Correlation Coefficients No statistically significant relationships were observed between the changes in either sensory or motor nerve conduction velocity and the associated changes in subcutaneous tissue 240 The Australian Journal of Physiotherapy, Vol. 33, No.4, 1987

temperature, for any of the six sonation intensities (Table 3). The relation" ship between the changes in sensory and the changes in motor nerve conduction velocities was statistically significant for only two of the six intensities, 2.0 and 2.5 W/cm 2 (p<o.ol). Discalssion Absolute Velocities The absolute sensory nerve conduc tion velocities were greater than were the associated motor velocities, being significantly so in 11 of the 12 pretreatment comparisons. The direct comparison of sensory and motor velocities has not been extensively reported in the available literature. Dawson (1956) reported significantly greater sensory orthodromic than motor velocities for the median and ulnar nerves, whereas Buchthal and Rosenfalck (1966) reported no consistent difference. The correlation coefficient between the absolute sensory and the absolute motor velocities was statistically significant in all six immediate pre-treatment comparisons and in four of six immediate post-treatment comparisons (Table 3). Generally, the magnitudes of the coefficients observed in the present study were not as high as those reported by Melvin et of (1973), r=0.76, based on distal latencies of the median nerve. The present study supports the suggestions that sensory antidromic velocities are faster than are motor velocities and that there is a significant relationship between sensory and motor velocities. However, available information indicates that this relationship is not high. The lack of a statistically significant difference between the one-minute pretreatment and the immediate pre-treatment velocities, for either the sensory or the motor tests, or temperatures, was considered to indicate that sensory and motor nerve conduction velocities, and subcutaneous tissue temperatures, had stabilized prior to testing. If it is assumed that the true nerve conduction velocities did not change during the Subcutaneous Tissue Temperature (0G) 29 o Pre Treatment W/crn' Figure 3: Absolute subcutaneous tissue temperatures before, during and after five minutes ultrasound, at each of the six intensities indicated. Table 3: Correlation change scores Sensory Velocity Temperature Velocity Temperature Sensory Velocity 0.0-0.02 0.10 0.25 2 3 During Treatment Time of Measurement (minutes) Ultrasound Intensity (W/Crrf) 0.5 1.0 1.5 2.0-0.12 0.11 0.36 0.14 0.01 0.33 4 0.39 0.25 0.41 Immediate post-treatment minus immediate pre-treatment Critical values for two tailed test of significance: r (0.05,17)= 0.46 and r (o.d1,d = 0.58* pre-treatment time period, the significant correlations between the one-minute and the immediate pre-treatment velocities can be interpreted as a confirmation of an acceptable reliability of measurement. Nerve Conduction Velocity Change Scores On the change scores ANOVA, the nerve conduction by intensity interac- 5 Post Treatment 0.11-0.17 0.69* 2.5 2.0 1.5 1.0 0.5 0.0 2.5-0.37-0.17 0.65* tion was not statistically significant, suggesting that, overall, sensory and motor velocities responded similarly to ultrasound. The sensory and motor v~ locity changes were, therefore, considered to be similar and were combined for further analysis. All clinical in tensities of ultrasound were associated with increases in nerve conduction velocity. Only following sonation at 0.5 WIcm 2 was the magnitude of the in- The AUslralian Journal ofphysiolherapy. Vol. 33, No.4, 1987 241

crease, narrowly, not statistically signfkant (p < 0.10). The changes associated with sonation at 1.0, 1.5, 2.0 and 2.5 WIcm 2 were similar, generally being greater than those associated with sonation at 0.0 or 0.5 WIcm 2 (no significant difference was observed between the changes associated with the 0.5 and the 1.0,.WIcm 2 intensities). Placebo ultrasound, on the other hand, was associated with signficant decreases in velocity. The results of the present study are in agreement with those previously describing sensory (Currier et a/ 1978, Halle et a/ 1981, Currier and Kramer 1982, Kramer 1985b) and motor (Kramer 1984 and 1985a) responses, when treatment was confined to an area of less than five times the area of the Ultrasound application head. Thermal and Mechanical Effects of VItrasonnd Although the present study did not compare ultrasound with other therapeutic modalities known to have a heating effect, and no mechanical effect, the consistency of the changes observed suggests that the increased ve locities are attributable to the heating effect of ultrasound. Previous investigations which compared clinical ultrasound and infrared treatments, concluded that both modalities produced similar increases in sensory (Halle et a/ 1981, Currier and Kramer 1982) and motor (Kramer 1984) velocities. The decreased sensory (Cosentino et al 1983) and motor (Madsen and Gersten 1963, Zankel 1966, Farmer 1968) con duction velocities previously reported are attributed to methodological differences between previousand the present studies. Although the present study limited the area of treatment to less than five times the area of the ultrasound application head, experimental evidence, based on clinical applications of ultrasound, was not available to support this decision. It is thought that the smaller treatment area reflects the current clinical norm (Faris 1969, Reid and Cummings 1973, Oakley 1978, Wadsworth and Chanmugan 1980). Subcntaneous Tissue Temperature The subcutaneous tissue temperature changes observed in the present study were all significant and were directly related to the ultrasound intensity (Figure 3). The magnitudes and directions of the temperature changes observed in the present 'Study were similar to those reported previously, when using similar sonation techniques and.a similar area of treatment (Kramer 1984, 1985a and 1985b). The heating effect of ultrasound did not negate the cooling effect of the ultrasound transmission gel until sonation intensities of 1.5 WIcm 2, or greater, were used. The changes in subcutaneous tissue temperature rose linearly with the sonation intensity, with each temperature change being significantly different from all other temperature changes. At the clinical intensities of 0.5 and 1.0 WIcm 2 the subcutaneous tissue temperatures were observed to decrease significantly, while both the sensory and the motor nerve conduction veloc ities increased (narrowly not statistically significant for the 0.5 WIcm 2 intensity). Although the temperatures associated with sonation intensities of 1.0, 1.5, 2.0 and 2.5 WIcm 2 were each successively greater than the preceding values, no significant differences were observed between the associated changes in velocity. These observations suggest that subcutaneous tissue tern perature may not be a good predictor of velocity changes, relative to ultrasound treatments. This suggestion is further supported by the lack of a significant relationship between the changes in temperature and the associated changes in either sensory or motor velocities, for any of the six sonation intensities. Similar observations have been reported previously when using comparable ultrasound treatments (Kramer 1985a and 1985b). Other investigators,using 20 minutes, or more, heating or cooling via water bath, have reported significant relationships be tween changes in motor nerve conduction velocities and the associated changes in skin, subcutaneous tissue and intramuscular tissue temperatures (Abramson et a/1966, Halaret a/1980). Because the tissue temperature probe used in the present study was positioned in the subcutaneous tissue, while the ulnar nerve coursed beneath the body of the flexor carpi ulnaris muscle, the temperatures recorded were not nerve bed temperatures. Furthermore, ultrasound passes readily through fatty tissue with minimal heating, and has a selective heating effect on nerve tissue (Driffin 1966, Griffin and Karselis 1982, Lehman and de Lateur 1982). The combination of the deep heating effect of ultrasound, its selective effect on nerve tissue and the superficial cooling effect of the ultrasound transmission gel on the skin surface may have confounded any relationship between temperature and velocity. In addition, the short treatment time of five minutes, as opposed to 20 minutes, or more, may have prevented local tissue temperature from reaching a stable point, or achieving a relatively homogeneous state. Sonation at the Higher Clinical Intensities The greatest increases in sensory (Kramer 1985b) and motor (Kramer 1985a) velocities, following five minutes sonation, have been reported to occur following sonation at 2.0 WI cm 2, rather than following sonation at 2.5 WIcm 2 The present study is in agreement with this observation for sensory velocities. However, the motor velocity changes observed in the present study were directly related to sonation intensity, with the greatest changes being observed at 2.5 WIcm 2 When changes in the sensory and motor velocities observed in the present study were combined, the trend of greater changes associated with the 2.0 W/cm 2 intensity was again observed. Sonation at 2.5 WIcm 2 may restrict velocity increases, as the result of heating of the nerve beyond its physiolog- 242 The Australian Journal of Physiotherapy. Vol. 33, No.4, 1987

ical response range or the mechanical effects of ultrasound. However, this suggestion requires further study, as the changes associated withsonation intensities of 1.0, 1.5, 2.0 and 2.5 W/ cm 2, observed in the present study, did not differ significantly from one,another, and the intensity of 2.5 W/cm 2 repres~ts a relatively high clinical dosage. ' The effect of ultrasound on C-fibres has been reported to be greater than its effect on A-fibres (Herrick 1953). Consequently, the intensities which increased velocity in the A-fibres may block the C-fibres. In this event, a block or reduction of nerve impulses as originally speculated by Griffin (1966) may help explain the pain relief often associated with clinical ultrasound. Conclusions Sensory and motor nerve conduction velocities responded similarly, but not identically, to clinical ultrasound. The increased velocities associated with all clinical intensities ofultrasound are attributed to a heating effect of ultrasound and the decreased velocities associated with placebo ultrasound are attributed to the cooling effect of the ultrasound transmission gel. The presentstudy examined one sonation frequency (870 khz) and one ultrasound application technique. Under the treatment conditions described, therapeutic ultrasound did not have a bipositive effect on nerve conduction velocities, but was associated with increases in both sensory and motor velocities. The possibility that ultrasound, at the clinical intensities described, may relieve pain by reducing conduction velocities in A-fibres is not supported. Further studies might focus on other physiological parameters such as local circulation, metabolism, counter-irritation, or nerve conduction characteristics of C-fibres, as a means of helping to explain the clinical effectiveness of ultrasound. 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