Sesek, University of Utah Robert P. Tuckett, University of Utah Donald S. Bloswick, University of Utah ABSTRACT Pressure on the median nerve at the wrist can lead to decreased tactile sensitivity in the fingertips. People with carpal tunnel syndrome may often experience numbness, tingling, and decreased sensitivity in their finger tips. Compared to a control group, subjects symptomatic of carpal tunnel syndrome had a greater mean shift (decrease) in tactile sensitivity than the control group when exposed to certain ergonomic risk factors. These factors include wrist flexion, direct pressure on the transverse carpal ligament area of the wrist, and tendon loading. Additionally, the effect of slight venous occlusion in the forearm was studied. Inability to show significance between the groups and provocations at this time is likely due to high variance and low sample size in the symptomatic group. There is an increase in threshold during the recovery period after each provocation.

INTRODUCTION Carpal tunnel syndrome (CTS) is caused by compression of the median nerve within the carpal tunnel. It is much more common (three times) in women than in men. It has been attributed to many conditions including anatomical anomalies, fractures, repetitive action, induced trauma, nerve sheath tumors, ganglions, circulatory disturbances, and others (Pećina et al., 2001). Due to its prevalence in occupations requiring repetitive motion, especially at high force or in awkward wrist postures, it is of interest to those studying ergonomics. If diagnosed and treated early, permanent damage to the nerve may be avoided. Treatment may include immobilizing the wrist with a splint, discontinuing repetitive motion, use of antiinflammatory medication, and corticosteroid injections. If symptoms continue, the transverse carpal ligament may be sectioned to allow for more space (hence less pressure) within the carpal tunnel (Pećina et al., 2001). Several common diagnostic procedures exist. Tapping on transverse carpal ligament (Tinel’s sign), placing the wrist in flexion (Phalen’s sign), or use of a tourniquet may cause paresthesia within a subject (Gilliat, 1953). Direct pressure on the carpal tunnel has also been suggested (Durkan, 1991). 139

No subjects were excluded from the study. specificity) while causing less discomfort (physical and psychological) and the ability to monitor changes in the sensory transmission of the median nerve over time. Improvements over nerve conduction studies may include improved accuracy (statistical sensitivity.Additionally. This requested information regarding current CTS symptoms. 2001. Subject Screening Common diagnostic procedures. as sensory deficit is an indicator of nerve compression. nerve conduction studies are often used in the diagnosis of CTS. The current research compares four modes of provocation: prolonged wrist flexion. and prolonged wrist flexion with venous occlusion at the forearm. selectivity. prolonged wrist flexion with direct pressure on the carpal tunnel region. The study was approved by the University of Utah Institutional Review Board (IRB). and none discontinued participation voluntarily. These mechanosensory threshold studies test the difference between the minimum distinguishable amplitude of vibration in the absence of the risk factors and the amplitude when these factors are present. sensory studies are preferable (Pećina et al. The purpose of the current research is to assess the effect of several ergonomic risk factors applied to the wrist. 6). though variance in results between examiners is beyond the scope of this study. Sensory studies seek to find the velocity of conduction of the compound action potential within the nerve. Vibrotactile studies may also require less expertise to perform. 140 . while motor studies seek to measure the recruitment of muscle fibers to a given stimulus (a twitch in the muscle). while two (33%) tested Tinel’s sign positive. They were also tested using Phalen’s sign (maximum wrist flexion for 60 seconds) and Tinel’s sign (gently tapping on the transverse carpal ligament area of the wrist/hand. In diagnosing CTS. Most of the test subjects to date were recruited by word of mouth. and subjects read and signed a consent form. risk factors. The control group consisted of 4 males and 6 females with a mean age of 29 years and a range of 21 to 60 years. PROCEDURE AND RESULTS Subjects were recruited by word of mouth and through flyers posted at medical clinics. prolonged wrist flexion with tendon loading on the index and ring fingers. Conduction velocity is either sensory or motor. Six symptomatic subjects have been recruited with a mean age of 45 and a range of 28 to 62. Each subject completed a questionnaire. Also. we hope to show a significant difference between how normal nerves react as opposed to those subjected to CTS and other peripheral neuropathys. and related injuries. The effect is measured using the tactile sensitivity of the finger tips. Four of the symptomatic subjects (67%) tested Phalen’s sign positive. None of the control subjects tested positive to either Phalen’s sign or Tinel’s. These require electrically stimulating nerves or muscles and using surface or imbedded electrodes to monitor nerve or muscle response.

26 m/sec (Oh. Since some subjects have longer hands. Pennington. The amplitude was decreased to find the smallest vibration sensed. Then the threshold measurement was begun at the start of flexion (time 0) and at each 2. so no age correction was used. but requires a 14 cm distance between the active electrode (placed on the middle finger) and the stimulator cathode. This smallest vibration is the vibrotactile threshold. 1993). a longer distance was used and the instrument’s report was not used.Nerve conduction studies. 141 .. where ∆T is the difference between the desired skin temperature and the temperature at the time of the measurement (Oh. Instead. Antidromic sensory nerve conduction latency was tested on each of the subjects using surface electrodes (Brevio manufactured by NeuMed. the signal amplitude for the only subject over 60 (symptomatic) was not high enough to record the latency. 1).26 m/sec limit when temperature was corrected to 32 0C. Inc. Two of the six symptomatic subjects exceeded this limit. and one correction to 32 0C. 0 Two of the control group subjects had low temperature and low conduction velocities. This value was compared to 41. Thus all control subjects and two symptomatic subjects were sNCV negative. amplitude. The vibrotactile threshold was tested during four separate sessions with at least 24 hours between visits. shake. sensory nerve conduction velocity (sNCV) was found by dividing the distance by the latency. The timing of probe vibration.e0. It is suggested that a 2 m/sec per decade over 60 years allowance be given for subjects over 60 years old (Oh. The subject pressed a button when a stimulus was sensed. However. Some of the subjects. but exceeded the 41. This nerve conduction instrument reports whether the latency is within the normal range. NJ). and duration between stimuli (50 Hz) were controlled by the computer.5 min interval while the wrist was placed in one of four provocations for 15 minutes. the subject was instructed to massage. Test hand selection. Three recovery measurements were then taken at 2. one without correction. had less than the recommended (31 to 34 C) skin temperature.0419∆T. despite washing in warm water. 1993). The test hand for the control group was the least symptomatic (or nondominant if both were equally asymptomatic). the nerve conduction velocity was corrected using a correlation suggested by DeJesus: Vcorrected = Vmeasured. the most symptomatic (or dominant if both were equally symptomatic) hand was chosen unless there were previous injuries on this hand unrelated to CTS. For these people. Following the measurement at 15 min. Vibrotactile Studies Mechanical sensitivity of the middle finger is measured using a computer-controlled vibrometer. For the symptomatic group. Several factors can affect conduction velocity including age and temperature.5 min intervals with the wrist in a neutral posture. 1993). or otherwise relieve pressure and numbness for one minute. At each session. a baseline threshold was found with the wrist in neutral posture (see Fig. The rest of the control group had velocities in the normal range.

C) wrist flexion with tendon loading (Fig. and D) wrist flexion with venous occlusion (Fig. presented to the subject in randomized order. B) wrist flexion with direct pressure on the carpal tunnel (Fig. 5). Test B: Wrist flexion with direct pressure Figure 4. Durkan Gauge in fixture 142 . 6). 2). were A) wrist flexion (Fig. Baseline measurement with wrist in neutral posture Figure 2. Test A: Wrist flexion The four provocations.Figure 1. 3). Figure 3.

1972). Direct pressure is hypothesized to increase the interstitial pressure on the median nerve above that of flexion alone. 6). OR. especially in the region of swelling in CTS subjects (Gelberman. Loops were placed on the middle segment of the index and ring fingers. In this test. 2001. 2). Sesek et al. causing hypoxia. thereby increasing the pressure on the median nerve. 1972). 1981. Test D: Wrist flexion with venous occlusion. Test B: Wrist flexion with direct pressure. Phalen suggested wrist flexion as a diagnostic procedure (Phalen. A gauge reading of 9 psi (this assumes a certain surface contact area. Pressure was applied with a rounded (approx. Understanding the effect of decreased blood flow on nerves is important. 3).Figure 5. submitted). 5). Test D: Wrist flexion with venous occlusion Test A: Wrist flexion. however. Test C: Wrist flexion with tendon loading. see Fig. submitted). the wrist was place in flexion as before and a pressure cuff was placed on the forearm. a 9 psi gauge reading was found to correspond to about 16.8 lbf) was maintained throughout the 15 min of testing. 143 . Phalen. Hood River. much as edema. The force was intended to increase tension on the tendons running through the carpal tunnel. Kempe studied the effect of tendon loading on fingertip sensory deficit (Kempe. often in the tip of the middle finger. Flexion of the wrist increases the pressure within the carpal tunnel. The pressure was raised to 15 mm Hg to slightly occlude the veins (see Fig. One of the provocations was simply placing the wrist in flexion. These loops were connected by a system of strings and pulleys to weights (see Fig. tendon loading was coupled with wrist flexion. It may be important also in distinguishing between CTS and other peripheral neuropathies such as that caused by diabetes. 4). This has been studied in previous research (Khalighi. 2cm diameter) probe on a Durkan Gauge (Gorge Medical. Hence.. Another provocation combined wrist flexion with the application of pressure directly on the carpal tunnel region (see Fig. In this test. and is thought to be part of the reason that people with CTS experience pain at night (Sesek. 2002). Test C: Wrist flexion with tendon loading Figure 6.8 N or 3. The result is decreased sensation within the region of the hand innervated by the median nerve. The vibrometer was elevated and the elbow was supported by a foam pad (see Fig.

the next measurement was skipped so that the following one could be started on time.03 for each).5 min to run. When this occurred. This was followed by a reduction at the first recovery point then another general increase in threshold over the last two recovery points.Results Figure 7 shows the trend in the data with error bars representing the standard error of the mean at each time. Comparing the mean threshold at each time to the baseline showed significant difference at all times for each test except for test B at 0 (p = 0.051). A generally increasing trend was seen among both groups during the fifteen minutes of provocation. few comparisons were significant. C. 2. The data were compared to see if the differences in the means at each time were significant. Further.5 min period among symptomatic subjects (with particularly high thresholds) during Test B. and 12. The data plots (see Fig. Because all groups of data (for each test at each time within each study group) passed normality tests. Then the mean threshold at each time was compared to the threshold for the previous time.5 (p = 0. However. so a valley appeared on the plot at 12. The symptomatic data were compared using a nonparametric ANOVA because of the significant differences in variance among the groups. all among symptomatic subjects.0036).0001. Repeated measures ANOVA showed that there was significant difference in the normal data (for A. 144 . 7.0969). Exclusion of these points caused the mean threshold to drop drastically between the 10 and 15 min means. the mean threshold at each time was compared to the baseline. for each test. but the variance in the symptomatic group is reduced. This contributed to large variance in the symptomatic group data. This occurred twice at the 12. Some threshold measurements took much longer than 2. it shows the expected trend. None of the control group thresholds exceeded 39 µm on any test. and D p < 0. several in the symptomatic group exceeded the limit of the machine (over 400 µm).2889). This accounts for 21 observations.5 min (p = 0. Because of this. paired t-tests were performed when making comparisons within study groups. While this prevents demonstrating statistical significance. The data were adjusted such that thresholds above 50 µm were set equal to 50.5min. the Test B data for these two subjects were excluded from the plots. In the symptomatic group.1048) for the control group. 8) show the same trend. for B p = 0. The values of these comparisons are shown in Tables 1-4.5 (p = 0. The difference between times in each test was once again significant (p < 0.

5 Tim e (m inutes) 30 25 20 15 10 5 0 Base 0 2.5 5 7.5 15 17.5 20 22.5 Tim e (m inutes) Figure 7.5 15 17.5 5 Threshold (microns) Provocation D 7.5 15 17.5 5 Provocation D 7.5 20 22.5 15 17.5 10 12.5 10 12.5 20 22.5 Provocation B Threshold (microns) Tim e (m inutes) Provocation C 35 Threshold (microns) 30 Threshold (microns) 25 20 15 10 5 0 Base 0 2.5 5 7. Symptomatic data are represented by the top line.5 20 22.5 10 12.5 5 7.5 10 12.Provocation A 350 Threshold (microns) 300 Threshold (microns) 250 200 150 100 50 0 Base 0 2.5 10 12.5 5 7.5 Tim e (m inutes) 40 35 30 25 20 15 10 5 0 -5 Base 0 2. Adjusted data.5 Tim e (m inutes) Provocation C 250 Threshold (microns) 200 150 100 50 0 Base 0 2.5 15 17.5 10 12. 145 .5 20 22.5 5 Provocation B 7.5 15 17. time for each provocation.5 10 12.5 5 7. Values over 50 were assigned a value of 50.5 15 17.5 20 22.5 20 22. The top line in each represents the symptomatic group. Provocation A 45 40 35 30 25 20 15 10 5 0 Base 0 2.5 Tim e (m inutes) Figure 8.5 Tim e (m inutes) 80 70 60 50 40 30 20 10 0 Base 0 2.5 10 12. Threshold vs.5 Tim e (m inutes) 30 25 Threshold (microns) 20 15 10 5 0 -5 Base 0 2.5 15 17.5 20 22.

241 0.84 ± 36.5 10.0014 0.0016 0.51 0.6 7.08 ± 1. Time (min) 0.22 ± 0.333 ± 4.56 9.093 38.88 13.3709 0.88 8.35 ± 1.5 15.0743 0.7167 ± 1.45 ± 1.5 5.12 P .5 15.003 0.0 17.7 ± 0.3159 128.35 ± 2.0709 0.0 12.35 7.1048 0.0019 <.09 4.49 8.6 ± 1.15 ± 2.0007 Symptomatic Group Difference (µm ± SEM) P .23 2. Time (min) 0.11 ± 0.0 7.0 12.2889 0.417 ± 1.3066 133.01 0.0001 0.05 ± 1.75 ± 126.04 ± 1.16 0.833 ± 1.0001 41.3381 148.0001 0.0 2.5 20.0 17.74 ± 0.0 22.96 6.52 5.0211 0.78 ± 124.Value 0.85 4.82 3.62 20.57 0.5 Control Group Difference (µm ± SEM) 3.4 6. Threshold relative to baseline: Flexion.0118 <.01 3.09 ± 1.0168 0.Value 1.95 ± 11.77 ± 0.0 7.0014 0.0 17.2405 67.49 6.07 123.0001 0.5 5.5 Control Group Difference (µm ± SEM) 0.16 235.75 ± 1.Value 0.Table 1.72 ± 1.Value 0.3324 0.5 10.0001 0.51 5.86 ± 0.58 ± 0.84 8.0017 0.0035 0.4776 0.29 136.83 ± 1.34 ± 2.5 15.005 0.72 3.2783 0.11 5.29 ± 2.3575 146 .5 5. Time (min) 0.0077 Symptomatic Group Difference (µm ± SEM) 3.062 Table 3.0078 0.38 8.47 4.55 ± 1.71 ± 2.55 1.0001 <.85 ± 0.0 12.4 ± 2.38 ± 57.4 ± 122.5 10.4 < 0.01 6.0124 0.75 ± 3.18 ± 1.2 ± 27.65 9.002 0.28 3.93 3.52 ± 1.71 6.95 3.1932 0.0356 0.67 P .Value 0.5 20.67 ± 1.0 22.93 ± 1.28 P .44 ± 1.42 4.0018 0.02 6.0026 0.0787 0.0184 <.Value 0.66 17.5 Control Group Difference (µm ± SEM) 2.76 0.31 6.85 6.52 0.65 ± 3.4 P .54 0.0082 Table 2.54 132.051 0.3376 133.37 ± 1.44 3.44 ± 1.98 ± 119.0 2.317 ± 4.54 P .0251 0. Threshold relative to baseline: Flexion and tendon loading.2793 7.36 ± 1.1226 0.0 22.74 0.09 3.59 0.58 ± 1.43 0.0019 Symptomatic Group Difference (µm ± SEM) 0.6 ± 101.3716 5. Threshold relative to baseline: Flexion and direct pressure.07 7.6404 0.14 ± 2.5 3.82 ± 99.67 8.0014 0.38 ± 0.0005 0.0969 0.375 ± 6.0519 0.6 ± 1.28 ± 122.66 2.3 ± 0.4959 0.1215 0.0 2.19 ± 1.5 20.367 ± 6.53 6.58 ± 123.0 7.

0002 <.Value 0. Comparisons were made using unpaired t-tests.0 22.0107 0.0271 0. significant difference was seen in test C between 0 and 2.1442 0.5 min and in test D between 0 and 2.35 5.5 and 20 min.0791 0. allowing for unequal variance.5 Control Group Difference (µm ± SEM) 2.0039 0.0043 0.99 ± 0.58 8. the mean difference between symptomatic and control (symptomatic minus control) is 0.37 5. at the 5 min measurement.73 7.5 min and 15 and 17.0281 0.5 min.0872 When mean thresholds at each time were compared to the threshold at the time before.60 ± 1.2174 0.5 10. significant difference was seen in test A between 0 and 2. there does appear to be a difference between tests when comparing symptomatic mean thresholds to control thresholds for each test (see Table 5).59 6.28 ± 19. 3. We hope that increasing the symptomatic sample size will allow this to be statistically demonstrated.5 min. Though there are large differences between the groups at many of the time intervals during provocation. As discussed above.28 ± 5. This indicates that adding risk factors to flexion causes a greater separation between symptomatic and control data.84 ± 1. This does not statistically demonstrate that adding other risk factors to flexion causes a substantial change in the effect on the median nerve.84 56.00 ± 0.45 ± 2. 147 .53 ± 1. Threshold relative to baseline: Flexion and venous occlusion.76 ± 3. However.558 µm for Test D.08 12.5 5.62 3.0323 0.0 7.2344 0. For instance.53 26. 35.19 5.44 18. potentially because of the small sample size and large variance in symptomatic data.001 0. For the symptomatic group. statistical tests do not show significance in these differences.0001 Symptomatic Group Difference (µm ± SEM) 3. Control data for each provocation were compared to symptomatic data at each time interval.84 5.9003 µm for Test A.2478 0.0472 0.06 ± 40.5 15. This may also be attributed to the large variance in symptomatic data.73 8. the mean thresholds were compared at each time.28 ± 2.3705 0.46 ± 8.57 ± 1.02 ± 3.61 13.15 ± 0.36 15.5 20. The results are tabulated in Table 5.0 17.778 µm for Test C.89 P . Significant difference was seen between tests A and C at 2.0 12. there is not a significant difference when comparing mean thresholds between groups for each provocation at each time. and between B and C at 7. Between each test (provocation). Time (min) 0.5 five min for the control group.0001 0.48 8.0033 0.504 µm for Test B.0 2. Likewise.58 ± 6.56 52.5 min and in test C between 5 and 7. comparing within subject groups (symptomatic or control).11 5.Value 0.11 ± 1.42 ± 35.Table 4.04 P . and 11.88 ± 3.0007 0.78 ± 2. there was not a significant difference between provocations at each time.

4494 4.0 17.851 0.6 -0.1335 0. Perhaps the data will show significance between provocations when more symptomatic subjects are tested.2926 37. This may be concluded because of lack of significance in most comparisons between each provocation at each time.478 0.06 0.504 0.778 0. However.278 0.4903 Flexion + Tendon Loading Difference P(µm) Value 2. and the mean thresholds at these times are significantly different from baseline in each test for the control group and for tests A at 22.278 0. better comparisons may be made. The trend of increasing tactile thresholds during recovery may be due to reactive effects.11 0. Without extending recovery measurements.3628 142.558 0.03 0.3585 0.0 7.3853 Flexion + Venous Occlusion Difference P(µm) Value 1.3171 124.6815 0.5 20.93 0.1697 0.5 10.3084 3.2767 5. It is more pronounced in some of the provocation.Table 5.0 12.2738 35.873 -0. but is common to both control and symptomatic data.1419 11.668 0.738 0.418 0.0968 44.818 0. it is unknown how long the trend will continue before the thresholds again approach the baseline.5 5.749 0. Threshold Comparisons: Symptomatic minus control Flexion Time (min) Baseline 0.5 min interval data show a decrease in tactile threshold from the 15 min threshold. and may have importance when considering work/rest cycles.5216 1.178 0. We hope that testing more symptomatic subjects will also show which combination of risk factors will cause the greatest difference in tactile threshold shift between study groups.5 min.467 3. The 17.6906 0.9291 0.838 0.0 22.9602 2.3073 8.2819 49.0469 8. though not statistically significant.1082 0.3894 123. CONCLUSIONS While the data show the expected trend during provocation—that the tactile threshold gradually increases but more for symptomatic subjects—statistical significance cannot be shown between the study groups because of extreme variance among the symptomatic subjects. B at 20 min.087 1.3645 127.4121 2.2178 117.23 0.97 129.3984 3.47 0.538 0.2703 PValue 0.54 0. 148 .13 0.8936 Flexion + Direct Pressure Difference P(µm) Value -0.2365 22.4538 0.4602 0.5 15.43 227. This may be caused by reactive hyperemia. It appears from the data collected thus far that the most effective risk factor in compromising tactile sensitivity in the fingertips is wrist flexion.972 0.1888 An unexpected but noteworthy trend occurred during recovery.9 0.44 0.5 data show a trend of increasing thresholds.2976 14. the 20 and 22.0507 1. and D at 20 min for the symptomatic group.3659 128.9003 1.5 Difference (µm) 1.874 0.191 0.028 0.448 0.71 15.523 0.7594 4.3037 61.34 0.0 2.54 0.408 0.2828 8.438 0.4609 8.1097 0.1272 5. With an increased sample size.64 0.3126 1.

.T. (2002). H. subjects with diabetic neuropathy are also being tested to see if these ergonomic risk factors affect these subjects differently than CTS-symptomatic subjects and the normal subjects. The carpal tunnel syndrome: a study of carpal canal pressures. G. This data may help us understand the effects of the various ergonomic risk factors beyond during the period of provocation or exposure. Gilliat. REFERENCES Durkan. Hergenroeder. J. B. To date. 1991. The contents are solely the responsibility of the author(s) and do not necessarily represent the official views of the National Institute for Occupational Safety and Health. though this posture will require a different vibrometer configuration. Utah: University of Utah. Khalaghi.4. only two subjects with diabetic neuropathy have been tested. Journal of Bone and Joint Surgery 63A(3). As part of this study. Journal of Bone and Joint Surgery 73(A) No. Hargens. is supported by Training Grant No. The Rocky Mountain Center for Occupational and Environmental Health. To understand the effect of wrist posture on the median nerve. W. T42/CCT810426 from the Centers for Disease Control and Prevention/National Institute for Occupational Safety and Health.SUGGESTIONS FOR FURTHER RESEARCH Because of the unexpected trend in recovery data. Utah: University of Utah. A. (1981). W. A new diagnostic test for carpal tunnel syndrome. Lancet 2. future tests will extend the recovery threshold measurements until the threshold approaches baseline or level off. P. Investigation of Sensory Deficit Resulting from Finger Loading. 380-3.. but may not be as effective at provoking symptoms of CTS as flexion (Gelberman.. R. Lundborg. R. 535-8. (2001).. A. 1981. Wilson T. 1972). ACKNOWLEDGMENTS This research was supported in part by a pilot project research training grant from the Rocky Mountain Center for Occupational and Environmental Health at the University of Utah. Phalen. N. and Akeson. 595-7. Salt Lake City. R. Salt Lake City. M. Improving Vibrotactile Carpal Tunnel Syndrome Screening. Gelberman. extension should also be studied.. H. A pneumatic-tourniquet test in the carpal-tunnel syndrome. an Education and Research Center. 1953. Wrist extension has been shown to have greater effect on carpal tunnel pressure than extension. G. Kempe. 149 .

(1986). Clinical Electromyography: Nerve Conduction Studies. V. M. and Markiewitz.M.. clinical evaluation of 598 hands. 222-7. S. The carpal-tunnel syndrome: Orthopaedics 83. J.D. (1993). M. (Submitted)... Clinical Sesek. R. Phalen. S. P. Tunnel Syndromes: peripheral nerve compression syndromes. G..**Masear. G. Hayes. R. J. and Khalighi. (1972). Oh. F. M. FL: CRC Press LLC. Pećina. R. (2001). A.J. 150 . 3rd ed. Journal of Hand Surgery 11A(2). Bloswick. Krmpotić-Nemanić. Submitted to Journal of Hand Surgery.. Baltimore: Williams & Wilkins.. 2nd ed. and Hyde. Tuckett. S. Boca Raton. D. A. An industrial cause of carpal tunnel syndrome. 29-40. Effects of prolonged Wrist flexion on transmission of sensory information in carpal tunnel syndrome.

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