Archives of Physical Medicine and Rehabilitation
Volume 90, Issue 11 , Pages 1846-1852, November 2009

Analysis of Clinical Motor Testing for Adult Patients With Diagnosed Ulnar Neuropathy at the Elbow

  • Sarah B. Goldman, PhD

      Affiliations

    • United States Army Research Institute of Environmental Medicine, Natick, MA
    • Corresponding Author InformationReprint requests to MAJ Sarah B. Goldman, PhD, United States Army Research Institute of Environmental Medicine, Military Performance Division, 15 Kansas St, Building 42, Natick, MA 01760
  • ,
  • Teresa L. Brininger, PhD

      Affiliations

    • Telemedicine and Advanced Technology Research Center, Fort Detrick, MD
  • ,
  • John W. Schrader, HSD

      Affiliations

    • Department of Kinesiology, School of Health, Physical Education, and Recreation, Indiana University, Bloomington, IN
  • ,
  • Richard Curtis, MD

      Affiliations

    • Hand Care Center, Orange Park, FL
  • ,
  • David M. Koceja, PhD

      Affiliations

    • Department of Kinesiology, School of Health, Physical Education, and Recreation, Indiana University, Bloomington, IN

Article Outline

Abstract 

Goldman SB, Brininger TL, Schrader JW, Curtis R, Koceja DM. Analysis of clinical motor testing for adult patients with diagnosed ulnar neuropathy at the elbow.

Objective

To compare the dichotomous results for 7 ulnar nerve clinical motor tests (Froment's sign, Wartenberg's sign, finger flexion sign, Jeanne's sign, crossed finger test, Egawa's sign, presence of clinical fasciculations) with motor nerve conduction velocity findings.

Design

A static group comparison design assessed for differences among dichotomous test outcomes with respect to motor nerve conduction velocity.

Setting

Five medical facilities throughout the United States provided data for this study.

Participants

Records from participants (N=26) with diagnosed ulnar neuropathy at the elbow were included for data analysis.

Interventions

Not applicable.

Main Outcome Measures

Demographic data included age, sex, handedness, duration of symptoms, and the number of days between the clinical and electrodiagnostic exam. Other dependent variables included motor conduction velocity of the ulnar nerve, compound muscle action potential amplitude, and the dichotomous clinical motor test outcomes.

Results

Two motor signs, the presence of clinical fasciculations and a positive finger flexion sign, were identified more frequently (each present in 11 patients) than the other motor signs. An analysis of covariance revealed significant differences in motor nerve conduction velocity between positive and negative results for all the clinical motor tests except for the finger flexion sign. Significant chi-square analyses were found for the following comparisons: the presence of clinical fasciculations and Froment's sign, the finger flexion sign and the crossed finger test, Egawa's sign and Froment's sign, Warteberg's sign and Froment's sign, the crossed finger test and Froment's sign, and Egawa's sign and Wartenberg's sign.

Conclusions

Some clinical motor tests are better than others at identifying early motor involvement, providing the rehabilitation professional some insight regarding the relative decrement of motor nerve conduction velocity when a selected test is positive.

Key Words: Rehabilitation, Ulnar nerve

List of Abbreviations: ANCOVA, analysis of covariance, IP, interphalangeal, MP, metacarpophalangeal

 

CLINICAL MOTOR TESTING is an important component of a comprehensive assessment for patients with diagnosed ulnar neuropathy at the elbow. Timely identification of motor dysfunction may reduce the need for surgical intervention and minimize long-term functional deficits. According to Lund and Amadio,1 the purposes of the physical examination in patients with suspected ulnar neuropathy at the elbow are 3-fold: to confirm the diagnosis, to rule out differential diagnoses, and to clinically assess the severity of nerve compression. For diagnostic purposes, clinical motor testing alone is insufficient and should be combined with other important information such as a thorough patient history, sensibility testing, and provocative testing. In order to rule out differential diagnoses, clinical motor testing can help discriminate among several conditions associated with ulnar neuropathy at the elbow, such as a C8/T1 nerve root lesion, lower trunk brachial plexopathy, or a more distal ulnar nerve compression at Guyon's canal.2 Finally, clinical motor testing can greatly assist the rehabilitation professional in assessing the relative severity of motor unit involvement; however, more empirical evidence is needed to quantify the relationship between test outcome and electrophysiologic indicators of ulnar nerve dysfunction.

In the early stages of ulnar neuropathy at the elbow with an insidious onset, sensory changes typically precede motor changes.3 Some evidence supporting this pattern of clinical presentation relates to mechanosensitivity differences between sensory and motor axons at the elbow. Clarke et al4 investigated responses to dynamic compression of the ulnar nerve and found that sensory axons had greater mechanosensitivity than motor axons; therefore, sensory symptoms such as paresthesias in the ulnar nerve distribution can be elicited without any ectopic motor activity such as fasciculations or cramps. Further evidence relates to the fact that sensory fibers to the hand are more superficial than motor fibers innervating the intrinsic muscles. Also, the motor axons innervating the hand are all superficial at the level of the medial epicondyle, while the axons to the extrinsic flexor carpi ulnaris and flexor digitorum profundus (ring and small fingers) are deep.5 The implications of this anatomic arrangement are 2-fold. First, it may explain the common clinical finding of hand weakness but infrequent flexor carpi ulnaris and flexor digitorum profundus (to the ring and small fingers) weakness.6, 7 Second, it may also explain why sensory changes are an early finding in cubital tunnel syndrome, often preceding motor axon compromise.3, 8

Sensory changes can be quantified through a variety of well-established assessments that evaluate specific components of sensibility such as light moving touch, vibration threshold, cutaneous pressure, and pain. Conversely, early motor changes are more difficult to quantify and may not be clinically detected in patients with mild nerve compression.9 When muscle atrophy is present, it can be broadly classified as mild, moderate, or severe.9 There have been other systems that categorize both preoperative and postoperative motor function, but they can be difficult to apply to intrinsic hand muscles.10, 11, 12 With severe nerve compression, muscle atrophy will take place, but it may take weeks for muscle atrophy to be visible during clinical observation. Once ulnar nerve motor units are involved, clinical manifestations may include loss of dexterity, muscle atrophy, and muscle weakness affecting grip and pinch strength,3 which ultimately affect the performance of daily activities including work-related tasks.13 Both the degree of nerve injury and duration of nerve compression are contributing factors in assessing the overall severity of ulnar neuropathy,14 which typically results from a combination of vascular factors (due to ischemia)15 in addition to mechanical factors.16, 17, 18

There have been a number of clinical motor manifestations described in the medical literature to detect ulnar nerve–innervated muscle weakness before visible muscle atrophy, some of which include Froment's sign,19 Jeanne's sign,20 motor Tinel sign,21, 22 Wartenberg's sign,23 finger flexion sign,24 Egawa's sign,25 crossed finger test,26 nail file sign,27 and for a more distal lesion, the palmaris brevis sign.28 Some researchers have suggested that the onset of fasciculations may be an early indicator of motor neuron pathology including entrapment neuropathies involving motor axons.29, 30 Caress and Walker31 report that fasciculations can be a sign of future peripheral nervous system hyperexcitability, while Strandberg et al32 suggest that they indicate acute and subacute denervation in the presence of nervous system pathology. Fasciculations are often overlooked during the evaluation process, occurring too infrequently to be recognized clinically, or occurring in either deep muscles or the inner fibers of superficial muscles.31 Testing for the presence of clinical fasciculations may have an important role in assessing early changes in motor unit function in patients with ulnar neuropathy at the elbow. Despite all of the aforementioned clinical maneuvers, there is little empirical research to quantify the relationship of clinical motor testing and electrophysiologic indicators of motor impairment.

In an effort to quantify the magnitude of dichotomous (ie, either present or absent) ulnar nerve clinical motor test outcomes, the purposes of this study were 4-fold: (1) to confirm whether positive results for selected ulnar nerve clinical motor tests correspond to significant decreases in motor nerve conduction velocity as compared with negative results; (2) to investigate whether the presence of clinical fasciculations is an indicator of motor unit dysfunction in patients with ulnar neuropathy at the elbow; (3) to examine the level of agreement among the selected set of clinical motor tests; and (4) to estimate the relationship between patient-reported duration of symptoms and severity of compression.

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Methods 

Twelve medical facilities were invited to participate in this study, which was approved by the human subjects institutional review board at Indiana University and local institutional review boards as required by the local facilities. Local hand surgeons and hand therapists identified patients who had received a diagnosis of cubital tunnel syndrome and had undergone both a clinical and electrodiagnostic examination. All local examiners provided the following demographic information to the principal investigator: patient's age, handedness, duration of symptoms (expressed in months) as reported by the patient, and the dates of the electrodiagnostic and clinical examinations.

Participants 

Of the original 12 medical facilities, 5 sites (3 military treatment facilities, 1 hospital, 1 private practice) contributed data (5, 5, 4, 2, and 10 participants, respectively), and 30 participants were identified as meeting the following experimental criteria: received a clinical diagnosis of ulnar neuropathy about the elbow (or cubital tunnel syndrome), underwent an electrodiagnostic examination performed by the local neurologist including ulnar nerve motor conduction velocity testing, and had no prior clinical or surgical history related to an ulnar nerve injury anywhere along its course. From the participant pool, 4 patients were excluded because of either unreported motor nerve conduction velocity values or the absence of an ulnar nerve lesion at the elbow, and a total of 26 participants (19 men, 7 women) were included in the study. The mean age ± SD of all participants was 47.6±16.6 years: 48.8±17.1 years for men and 44.3±15.5 years for women. Table 1 describes the demographic characteristics of the participants in this study.

Table 1. Summary of Participants
MenWomenTotal
Participants19726
Average age (y)48.8±17.144.3±15.547.6±16.6
Handedness (right/left)16/35/221/5
Side involved (right/left)6/134/310/16
Average NCV (m/s)41.3±9.647.7±8.643.0±9.6
Average below-elbow CMAP amp (mV)6.9±3.27.3±3.47.0±3.2
Average above-elbow CMAP amp (mV)6.1±3.67.0±3.46.3±3.5
Average CMAP amp difference (mV)0.8±2.30.3±0.20.7±2.0

NOTE. Values are n or mean ± SD.

Abbreviations: CMAP amp, compound muscle action potential amplitude; NCV, nerve conduction velocity (ulnar nerve, motor).

No. of participants that had NCV recorded is 26.

No. of participants that had CMAP amplitude is 24.

Clinical Tests 

Clinical motor testing was performed by either a hand surgeon (defined as holding a Certificate of Added Qualifications in Surgery of the Hand) or an occupational therapist holding advanced hand credentials (defined as possessing either the Certified Hand Therapist credential or the U.S. Army's “Upper Extremity Neuromusculoskeletal Evaluator” skill identifier). All local examiners were provided written instructions on how to perform the clinical tests and how to identify positive and negative tests. Participants in the study underwent the following selected clinical motor tests as part of their assessment: Froment's sign, Jeanne's sign, crossed finger test, Egawa's sign, finger flexion sign, and Wartenberg's sign. Participants were also assessed for the presence of clinically observable fasciculations after 4 seconds of manual muscle testing of the involved first dorsal interosseous muscle. The elbow flexion test, a provocative test for sensory axons, was performed in addition to all of the aforementioned motor tests.

Although not a motor manifestation, the elbow flexion test was performed as described in the study by Rayan et al,2 with the participant sitting, the glenohumeral joint in a neutral position, the elbow in maximum flexion, the forearm in supination, and the wrist in neutral. This position was actively sustained for 60 seconds, and a positive outcome was indicated by either participant-reported paresthesias or worsening of preexisting paresthesias in the ulnar nerve distribution.

Assessing for the presence of Froment's and Jeanne's signs19, 20 was performed with the participant sitting and the forearm in a neutral position. The participant was asked to use a lateral pinch to hold a piece of paper while the examiner pulled it distally along the longitudinal axis of the thumb. A positive Froment's sign was recorded if flexion of the thumb IP joint was used to maintain the paper in a lateral pinch.33 Examiners were instructed to ensure that MP hyperextension was not the method of stabilization in a positive Froment's sign. A positive Jeanne's sign was recorded if the patient hyperextended the MP joint of the thumb to maintain lateral pinch of the piece of paper when performing the test to detect a Froment's sign.33 The presence of a Froment's sign and a Jeanne's sign was mutually exclusive.

The presence of an Egawa's sign25 was assessed with the patient sitting and the forearm in pronation. The participant was asked to actively flex the MP joint of the middle finger and subsequently actively abduct it in both a radial and ulnar direction.33 Although the original reference did not specify the amount of MP flexion required to perform this test, the patients flexed the MP joint approximately 75° as part of the procedures. A positive Egawa's sign was recorded if the participant was unable to perform this action as compared with the uninvolved side. Contralateral examination was performed to help identify coordination deficits that may lead to a false-positive outcome.

Assessing for the presence of a Wartenberg's sign23 was performed with the participant sitting, the wrist in a neutral position, and the forearm in full pronation. The participant was asked to first actively extend all digital MP and IP joints. The examiner instructed the participant to maximally abduct all fingers and then adduct all fingers. A positive Wartenberg's sign was recorded if the participant could not fully adduct the small finger, with the small finger being held in a position of abduction.33

The finger flexion sign, described by Tsujino and Macnicol,24 evaluating interossei function, was assessed with the participant sitting and both forearms in the neutral position. The examiner placed a sheet of paper between the middle and ring fingers of both hands up to the interdigital web space. The participant was instructed to hold the paper firmly as the examiner pulled it distally along the longitudinal axis. A positive finger flexion sign was indicated when MP flexion was used on the involved side to stabilize the piece of paper.24

The crossed finger test was performed as described by Earle and Vlastou26 with the participant sitting with forearms in pronation. This test assessed the function of the first volar and second interossei muscles. The examiner instructed the participant to cross the middle finger over index finger of both hands. A positive outcome was recorded if the participant could not fully cross the fingers on the involved side.26

Finally, the participant was examined for the presence of clinically observable fasciculations in either the first dorsal interosseous or abductor digiti minimi. For this test the participant was sitting with the forearm in pronation. The participant then actively abducted the index finger against examiner resistance for 4 seconds, then released the contraction. A similar test was performed for the abductor digiti minimi through active small finger abduction against examiner resistance for 4 seconds. A positive outcome was recorded if the examiner visually observed at least 1 fasciculation in the first dorsal interosseous or the abductor digiti minimi within 15 seconds of releasing the muscle contraction.

Motor Ulnar Nerve Conduction Velocity and Compound Muscle Action Potential Amplitude 

Motor ulnar nerve conduction velocity values were expressed in meters per second, and compound muscle action potential amplitude was expressed in millivolts. Both values were obtained from the patient's electrodiagnostic examination. All participants underwent an orthodromic motor ulnar nerve electrodiagnostic exam, where at least 3 ulnar nerve segments were measured and documented. The involved extremity was positioned at approximately 90° of shoulder abduction and 90° of elbow flexion, with the forearm supinated and the wrist in a neutral position. Participants were included if there was both clinical and electrodiagnostic evidence to confirm the diagnosis of cubital tunnel syndrome, and the investigators used the segment across the elbow for all subsequent data analysis. In 2 of the 26 cases, the conduction velocity was not present in the examination results and was subsequently calculated by dividing the distance (converted from centimeters to meters) by the latency (converted from milliseconds to seconds) for each segment. Compound muscle action potential amplitude was recorded for all participants.

Data Analysis 

Data analysis was conducted with SPSS version 15.0 statistical software.a Initially, a Pearson's correlation was used to estimate the relationship between motor ulnar nerve conduction velocity and the duration of symptoms. An ANCOVA was performed (with the number of days between the clinical and electrodiagnostic testing as the covariate) to assess the differences between positive and negative results for all of the clinical motor tests with respect to ulnar nerve motor conduction velocity and compound muscle action potential amplitude. Pearson chi-square tests were used to assess any differences among the percentages of positive or negative test outcomes for each of the motor tests. For purposes of this study, a 2 × 2 chi-square was performed on all possible combinations of clinical motor tests, yielding 15 separate chi-square statistics. Effect sizes, using an omega squared statistic, for the ANCOVAs were calculated according to procedures outlined by Keppel and Wickens.34 For the univariate analyses, a 1-tailed alpha level of .025 or less was used to protect against an increased type I error rate. For chi-square analyses, an alpha level of .05 or less was used.

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Results 

The mean ± SD motor nerve conduction velocity for all participants was 43.0±9.6m/s: 41.3±9.6m/s for men and 47.7±8.6m/s for women. The mean ulnar nerve motor conduction velocities and compound muscle action potential amplitudes for the positive and negative motor test outcomes are shown in Table 2A, Table 2B. Jeanne's sign was not included in the univariate or bivariate analyses because no participants displayed a positive Jeanne's sign during the clinical examination.

Table 2A. Electrodiagnostic Results for Each Motor Test Outcome: Ulnar Nerve Motor Conduction Velocity
Motor TestPositiveNegative
Fasciculations38.8±9.846.7±8.1
Finger flexion39.7±11.445.5±7.5
Froment's34.0±8.847.0±7.0
Egawa's30.0±8.846.1±6.9
Wartenberg's33.4±17.644.8±6.7
Crossed finger31.6±9.845.7±7.5

NOTE. Values are mean ± SD. Dependent variable is ulnar nerve motor conduction velocity (above the elbow to the wrist segment) expressed in meters per second.

Table 2B. Electrodiagnostic Results for Each Motor Test Outcome: Compound Muscle Action Potential Amplitude
Motor TestPositiveNegative
Fasciculations0.5±1.40.8±2.3
Finger flexion0.8±1.40.6±2.3
Froment's1.5±0.51.8±0.4
Egawa's1.7±0.51.9±0.3
Wartenberg's1.4±0.61.9±0.3
Crossed finger1.7±0.51.8±0.4

NOTE. Values are mean ± SD. Dependent variable is the compound muscle action potential amplitude difference (below-elbow segment minus the above-elbow segment) expressed in millivolts.

Considering that clinical and electrodiagnostic examinations did not take place on the same day for all participants, an ANCOVA was performed on all univariate tests to statistically control for the number of days in-between these 2 data points. The number of days was not statistically significant for any of the motor tests considered in this study (table 3). Analysis of variance revealed significant differences with regard to ulnar nerve motor conduction velocity for the fasciculations test (t23=2.24, P=.017, ω2=.13), Froment's sign (t23=3.93, P<.001, ω2=.36), Egawa's sign (t23= 4.33, P<.001, ω2=.40), Wartenberg's sign (t23=2.27, P=.016, ω2=.14), and the crossed finger test (t23=3.42, P<.001, ω2=.29). Specifically, for the fasciculations test, those participants who tested positive had a mean nerve conduction velocity of 38.8m/s, whereas the participants who tested negative had a mean value of 46.7m/s. This trend was similar for the Froment's sign (positive test=34.0m/s, negative test=47.0m/s), the Egawa's sign (positive test=30.0m/s, negative test=46.1m/s), Wartenberg's sign (positive test=33.4m/s, negative test=44.8m/s), and the crossed finger test (positive test=31.6m/s, negative test= 45.7m/s).

Table 3. ANCOVA for All Motor Tests: Statistically Controlling for the Period Between Electrodiagnostic and Clinical Testing
Motor TestdfMSF RatioPω2Covariate Sig
Fasciculations23411.615.02.017.13.452
Finger flexion23200.892.19.075.04.591
Froment's23917.8415.44<.001.36.701
Egawa's231027.1418.75<.001.40.750
Wartenberg's23418.595.15.016.14.656
Crossed finger23771.8811.70<.001.29.735

NOTE. Group membership is either a positive or negative outcome within each clinical motor test. The dependent variable is motor nerve conduction velocity (meters per second) for the across the elbow forearm segment. The covariate (time in units of days) was not significant in any of these comparisons.

Abbreviations: MS, mean squares; Sig, significance.

With respect to clinical motor tests, the most frequently occurring positive result was with the fasciculation test and the finger flexion sign, both of which were present in 11 patients. The least frequently occurring positive result was with Jeanne's sign, which was not present in any of these patients, followed by Wartenberg's sign (present in 4 patients). The frequency counts of all the testing results are shown in figure 1. Significant chi-square analyses, representing disagreement between the positive and negative results, were found for the following comparisons: the presence of clinical fasciculations and Froment's sign (χ2=3.87, P=.049), the finger flexion sign and the crossed finger test (χ2=8.44, P=.091), Egawa's sign and Froment's sign (χ2=13.93, P<.001), Wartenberg's sign and Froment's sign (χ2=4.34, P=.037), the crossed finger test and Froment's sign (χ2=7.04, P=.008), and Egawa's sign and Wartenberg's sign (χ2=9.47, P≤.002) (table 4).

Table 4. Pearson's Chi-Square Values Analyzing the Agreement Between Positive and Negative Outcomes for All 2 × 2 Motor Test Comparisons
TestsFasciculationsFinger FlexionFroment'sEgawa'sWartenberg'sCrossed Finger
FasciculationsNA
Finger flexion2.35NA
Froment's3.871.93NA
Egawa's2.850.7913.93NA
Wartenberg's0.032.074.349.47NA
Crossed finger2.858.447.041.722.88NA

NOTE. Bolded values indicate a significant difference among the percentage of positive and negative test outcomes.

Abbreviation: NA, not applicable.

Finally, there was a significant negative 2-tailed Pearson's correlation (r=–.551, P=.004) estimated between patient-reported duration of symptoms and ulnar motor nerve conduction velocity.

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Discussion 

This study is among the first to explore the relationships between clinical motor test outcomes and ulnar nerve motor conduction velocity, addressing the paucity of studies in this area. Although clinical motor testing can certainly help diagnose the presence of ulnar nerve dysfunction,35 the results of this investigation suggest that some clinical motor tests are better than others at identifying early motor involvement, providing the rehabilitation professional some insight regarding the relative decrement of motor nerve conduction velocity when a selected test is positive.

The presence of a positive Egawa's sign25 signifies weakness in the ulnar nerve–innervated second and third dorsal interosseous muscles that abduct the middle finger. By performing the test in the position of metacarpophalangeal flexion and interphalangeal extension and then asking the patient to abduct the finger, the dorsal interosseous muscles are isolated from the median nerve–innervated lumbrical muscle. Of all the clinical motor tests that were statistically significant in this investigation, Egawa's sign had both the largest effect size and the greatest mean difference between positive and negative results. Therefore, the presence of a positive Egawa's sign represented the most pronounced degree of electrophysiologic ulnar nerve motor involvement when compared with the other clinical motor tests examined in this study. Although a positive Egawa's sign represented advanced levels of ulnar motor conduction velocity, it did not commonly occur in this investigation. Many examiners verbally reported that Egawa's sign was difficult to elicit in patients, even on the unaffected side. Because this sign can be more difficult to detect and is not commonly found in patients with a mild ulnar nerve compression, other clinical assessments of interossei function are recommended to assess for ulnar neuropathy. The chi-square analyses support this recommendation, indicating agreement among Egawa's sign and the 2 other signs (finger flexion sign and crossed finger test) aimed at testing the integrity of interossei muscle function.

The results of this investigation regarding examination for the presence of clinical fasciculations confirm previous study findings of their existence in patients with a subacute mononeuropathy of the ulnar nerve.31, 32 The presence of clinical fasciculations and the finger flexion sign were the most frequently occurring positive outcomes among all motor tests studied. Of all the motor signs to achieve statistical significance, the finger flexion test had the least mean difference of nerve conduction velocity values, suggesting that it can be an early indicator of motor unit pathology, which is consistent with findings of previous studies. Additionally, the presence of clinical fasciculations was found to be in agreement with every other motor test except for Froment's sign, which was not in agreement with any of the other selected motor tests in this study. Although testing for the existence of clinical fasciculations is not frequently cited in the medical literature, the results of this investigation suggest that they commonly occur in patients with ulnar neuropathy at the elbow, and their presence is associated with a significant decrease in motor conduction velocity. Keeping in mind that the current study assessed only clinically involved patients, future research is indicated to determine the sensitivity of this test by comparing the presence of clinical fasciculations elicited with muscle testing between healthy persons and those with compromised ulnar nerve function.

The finger flexion sign was described in 1998 as a way to assess the dorsal interosseous muscles of the ring and middle fingers.24 The authors suggest that this sign is a way to assess early ulnar nerve involvement, and they specifically compare it to the Froment's sign. They maintain that the extrinsic finger flexors substitute for interossei weakness earlier than the flexor pollicis longus compensates for a weak adductor pollicis muscle.24 There is some evidence in this study to support the authors' claim. Along with the test for clinical fasciculations, a positive finger flexion sign was the most commonly reported motor finding in this investigation. In addition and consistent with the authors' suggestion, the finger flexion sign had the smallest effect size of selected motor tests. Although assessing the difference between positive and negative results did not achieve statistical significance with this sample, there was still a slight decrease in nerve conduction velocity.

Assessing for a Froment's sign is commonly used to identify weakness in the adductor pollicis muscle during lateral pinch through compensation with the flexor pollicis longus innervated by the anterior interosseous nerve.19 In this study, the presence of a Froment's sign was the third most commonly occurring positive motor sign, and it represented significantly decreased motor nerve conduction velocity compared with the absence of this sign. It also had the second largest effect size for all tests considered in this investigation, suggesting that it is a clinically important identifier of ulnar neuropathy. Jeanne's sign, although identified in the medical literature as an indicator of ulnar neuropathy,20 did not occur in any of these patients, and it may have little added value in assessing patients with ulnar neuropathy. Altered thumb biomechanics that occurs during lateral pinch because of a weak adductor pollicis muscle may take time to develop in chronic ulnar neuropathy, potentially resulting in a delayed onset of a positive Jeanne's sign.

The crossed finger test is a simple way to assess the first volar and second dorsal interossei muscles.26 Earle and Vlastou26 suggest that in comparison with the first dorsal interosseous muscle, the median nerve seldom innervates these muscles. The results of this study indicate that a positive crossed finger test represented a significant decrease in ulnar nerve motor conduction velocity test as compared with a negative test in an involved population. It also had a large effect size, suggesting that it is a robust indicator of ulnar nerve involvement; however, unlike the other tests that were both statistically significant and had a large effect size, a positive crossed finger test did not occur as frequently in this sample. The chi-square analyses indicated agreement with one test of interossei function (Egawa's sign) but not the other (the finger flexion sign). This difference can be because the finger flexion sign represented an earlier clinical indicator of ulnar nerve dysfunction.

The findings of this study confirm those of previous studies indicating that the presence of a positive Wartenberg's sign is a late sign of ulnar nerve involvement.23 With the notable exception of Jeanne's sign, a positive Wartenberg's sign occurred the most infrequently among all motor tests. However, when a positive Wartenberg's sign was present, it was significant. Because of the limited number of participants with a positive sign, homogeneity of variance was significant and the effect size was relatively low compared with other tests that had mean differences greater than 10m/s. More participants are needed to reanalyze this test with the homogeneity of variance assumption met.

The results of this research support those of previous studies regarding the significant correlation between the patient-reported duration of ulnar nerve compression and the electrodiagnostic results. Studies using a blood pressure cuff to the elevated arm simulating experimental ischemia identified both clinical36, 37 and electrophysiologic38, 39, 40 effects over a period. Similarly, histologic studies indicate progressive myelin and axonal changes with longer durations of compression.41 A study by Chang et al42 showed that the duration of vibration exposure significantly resulted in decreased nerve conduction velocity and amplitude in rats. These studies are all consistent with the estimated correlation in this study.

Anomalous innervations in the upper extremity have been widely reported; therefore, patients with ulnar nerve lesions may present with slight variations of typical motor findings. Rowntree43 reported that approximately 20% of 225 patients with median or ulnar nerve lesions had an anomalous nerve supply of some kind. He identified many patterns of variability including both complete ulnar (in 1 patient) and complete median innervation (in 4 patients) of the hand.43 Murphey et al44 reported that 4 of 698 patients with ulnar nerve lesions had a median nerve–innervated first dorsal interosseous muscle. In addition, some of these innervations patterns may relate to an anomalous anastomosis in the forearm. A Martin-Gruber anastomosis is a median to ulnar nerve connection of motor fibers in the forearm resulting in ulnar nerve–innervated muscles being innervated from both the crossed over median fibers and the ulnar nerve fibers. This anomaly may account for some of the variability in intrinsic motor innervation patterns.45 The prevalence rates vary slightly in the medical literature; Gruber46 originally reported 20%, and Mannerfelt's findings33 are consistent with those of McCabe and Kleinert47 in which 15% of subjects had a Martin-Gruber anastomosis. Alternately, a Riche-Cannieu48, 49 anastomosis, a connection between the deep branch of the ulnar nerve and the recurrent branch of the median nerve, can account for other variability patterns within the population.33 These anomalous innervations may contribute to varying patterns of motor unit dysfunction in some patients with ulnar neuropathy. As a result, hand therapy practitioners need to exercise some caution in generalizing the findings of this investigation.

Study Limitations 

One of the inherent methodological constraints was that clinical examination and electrodiagnostic testing could not be performed on the same day; however, an analysis of covariance was performed to statistically control for the time difference, which was not found to be a significant covariate in this study. In this regard, some research has shown that ulnar motor nerve conduction velocity can significantly change within a single day for healthy persons performing work activities associated with ulnar neuropathy.50, 51 Therefore, any future replication of this study should ensure that electrodiagnostic testing immediately follow the clinical motor examination at the same time of day for all participants. Also, there were more men than women in the sample, because 3 of the 5 data collection sites were military facilities. Although sex was not considered as an independent variable in this study, future research at nonmilitary medical facilities might allow more direct comparisons between men and women.

An additional concern identified in this investigation is that motor nerve conduction velocity used to assess motor unit dysfunction selectively stimulates only large-diameter and fast-conducting nerve fibers.32, 41 Neuropathies that affect only medium and small nerve fibers cannot be measured with nerve conduction velocity testing.35 Nerve injuries that result in muscle dysfunction may not result in slowing of conduction velocity if even one large-diameter nerve fiber survives. For these reasons, many authors report that some electrodiagnostic findings can be misleading and should be interpreted with caution.1, 8, 35 Regardless of the limitations of electrodiagnostic testing, clinical motor testing is not a substitute for an electrodiagnostic exam and vice versa.

A final limitation of this study was that both the electrodiagnostic and clinical exams were performed by different examiners; however, this was unavoidable because of the data collection process. Although the clinical examiners were provided instructions to control for interrater reliability concerns, future studies should control for this possible source of error. Future research is indicated to determine whether there are any significant differences among motor tests with a positive result. The low number of participants with independent positive test results precluded this analysis from occurring.

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Conclusions 

This study quantified the relative electrodiagnostic involvement between selected clinical motor test outcomes, as well as determined significant associations among pairs of motor tests. From the results, the finger flexion sign and the presence of clinical fasciculations were found to be clinical indicators of early ulnar nerve motor involvement and can provide useful information about motor unit function in the absence of observable muscle atrophy. The results also indicated that Froment's sign, Wartenberg's sign, and the crossed finger test represented a greater decrease of ulnar nerve motor conduction velocity in patients with ulnar neuropathy at the elbow. Further research should be conducted with a larger sample size using logistic regression models to determine how effective these clinical motor tests are at predicting motor nerve conduction velocity.

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References 

  1. Lund A, Amadio P. Treatment of cubital tunnel syndrome: perspectives for the therapist. J Hand Ther. 2006;19:170–178
  2. Rayan G, Jensen C, Duke J. Elbow flexion test in the normal population. J Hand Surg [Am]. 1992;17:86–89
  3. Folberg C, Weiss P, Akelman E. Cubital tunnel syndrome: part I. Presentation and diagnosis. Orthop Rev. 1994;23:136–144
  4. Clarke EC, McNulty PA, Macefield VG, Bilston LE. Mechanically evoked sensory and motor responses to dynamic compression of the ulnar nerve. Muscle Nerve. 2007;35:303–311
  5. Sunderland S. Nerves and nerve injuries. New York: Churchill Livingston; 1978;
  6. Apfelberg D, Larson S. Dynamic anatomy of the ulnar nerve at the elbow. Plast Reconstr Surg. 1973;51:76–81
  7. Bozentka D. Cubital tunnel syndrome pathophysiology. Clin Orthop Relat Res. 1998;(351):90–94
  8. McPherson S, Meals R. Cubital tunnel syndrome. Orthop Clin North Am. 1992;23:111–123
  9. Novak C, Mackinnon S. Evaluation of nerve injury and nerve compression in the upper quadrant. J Hand Ther. 2005;18:230–240
  10. Birch R, Booney G, Wynn Parry C. Surgical disorders of the peripheral nerves. London: Churchill Livingstone; 1998;
  11. Kline D, Hudson A. Nerve injuries: operative results for major nerve injuries, entrapment and tumors. Philadelphia: WB Saunders; 2007;
  12. Medical Research Council of the UK. Aids to the examination of peripheral nervous system. Palo Alto: Pentagon House; 1976;
  13. Cutts S. Cubital tunnel syndrome. Postgrad Med J. 2007;83:28–31
  14. Mackinnon S. Pathophysiology of nerve compression. Hand Clin. 2002;18:231–241
  15. Powell H, Myers R. Pathology of experimental nerve compression. Lab Invest. 1986;113:433–455
  16. Dyck P, Lais A, Giannini C, Engelstad J. Structural alterations of nerve during cuff compression. Proc Natl Acad Sci U S A. 1990;87:9828–9832
  17. Ochoa J, Flowler T, Gilliatt R. Anatomical changes in peripheral nerves compressed by a pneumatic tourniquet. J Anat. 1972;113:433–455
  18. Rayan G. Compression neuropathies, including carpal tunnel syndrome. Clin Symp. 1997;49:2–32
  19. Froment J. La prehension dans les paralysies du nerf cubital et Le Signe du Pouce. Presse Med. 1915;23:409
  20. Jeanne M. La deformation du pouce dans la paralysie cubitale. Bull Mem Soc Chir Paris. 1915;41:703–719
  21. Kingery W, Park K, Wu P, Date E. Electromyographic motor Tinel's sign in ulnar mononeuropathies at the elbow. Am J Phys Med Rehabil. 1995;74:419–426
  22. Montagna P, Liguori R. The motor Tinel sign: a useful sign in entrapment neuropathy?. Muscle Nerve. 2000;23:976–978
  23. Wartenberg R. A sign of ulnar palsy. J Am Med Assoc. 1939;112:1688
  24. Tsujino A, Macnicol M. Finger flexion sign for ulnar neuropathy. J Hand Surg [Br]. 1998;23:240–241
  25. Egawa T. Electromyographic studies on finger motion. J Osaka Univ Med Sch. 1959;11:1739–1758
  26. Earle A, Vlastou C. Crossed fingers and other tests of ulnar nerve motor function. J Hand Surg [Am]. 1980;5:560–565
  27. Kapandji A. La defaillance du crochet ulnaire: ou encore “signe de la lime a ongles,” signe peu connu d'atteinte du nerf ulnaire. Ann Chir Main. 1999;18:295–298
  28. Pleet A, Massey E. Palmaris brevis sign in neuropathy of the deep palmar branch of the ulnar nerve. Ann Neurol. 1978;3:468–469
  29. Rosenfeld J. Fasciculations without fibrillations: the dilemma of early diagnosis. Amyotroph Lateral Scler Other Motor Neuron Disord. 2000;(1 Suppl 1):53–56
  30. Roth G, Magistris M. Neuropathies with prolonged conduction block, single and grouped fasciculations, localized limb myokymia. Electroencephalogr Clin Neurophysiol. 1987;67:428–438
  31. Caress J, Walker F. The spectrum of ectopic motor nerve behavior: from fasciculations to neuromyotonia. Neurologist. 2002;8:41–46
  32. Strandberg E, Mozaffar T, Gupta R. The role of neurodiagnostic studies in nerve injuries and other orthopedic disorders. J Hand Surg [Am]. 2007;32:1280–1290
  33. Mannerfelt L. Studies on the hand in ulnar nerve paralysis: a clinical-experimental investigation in normal and anomalous innervations. Acta Orthop Scand. 1966;S87(Supp):1–176
  34. Keppel G, Wickens T. Design and analysis: a researcher's handbook. Upper Saddle River: Pearson Prentice Hall; 2004;
  35. Hilburn J. General principles and use of electrodiagnostic studies in carpal and cubital tunnel syndromes: with special attention to pitfalls and interpretation. Hand Clin. 1996;12:205–221
  36. Lewis T, Pickering GW, Rothschild P. Centripetal paralysis arising out of arrested bloodflow to the limb, including notes on a form of tingling. Heart. 1931;1:1–31
  37. Weddell G, Glees P. “Pins and needles”: observations on some of the sensations aroused in a limb by the application of pressure. J Neurol Neurosurg Psychiatry. 1947;10:26–48
  38. Caruso G, Labianca O, Ferrannini E. Effects of ischemia on sensory potentials of normal subjects of different ages. J Neurol Neurosurg Psychiatry. 1973;36:455–466
  39. Nielsen V, Kardel T. Decremental conduction in normal human nerves subjected to ischemia. Acta Physiol Scand. 1947;92:249–262
  40. Seneviratne K, Peiris O. The effect of ischemia on the excitability of human sensory nerve. J Neurol Neurosurg Psychiatry. 1968;31:338–347
  41. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley and Belfus; 1995;
  42. Chang K, Ho S, Yu H. Vibration induced neurophysiological and electron microscopical changes in rat peripheral nerves. Occup Environ Med. 1994;51:130–135
  43. Rowntree T. Anomalous innervation of the hand muscles. J Bone Joint Surg Br. 1949;31:505–510
  44. Murphey F, Kirklin J, Finlayson A. Anomalous innervation of the intrinsic muscles of the hand. Surg Gynecol Obstet. 1946;83:15–23
  45. Martin F. Tal om nervers allmanna egenskaper I manniskans kropp. Stockholm: L Salvius; 1763;
  46. Gruber W. Ueber die Verbindung das nervus medianus mit dem nervus ulnaris am unterarme des menschen und der saugethiere. Arch Anat Physiol. 1870;37:501–522
  47. McCabe S, Kleinert J. The nerve of Henle. J Hand Surg [Am]. 1990;15:784–788
  48. Cannieu A. Note sur une anastomose entre le branche profunde de cubital et le median. Bull Soc Physiol Norm Pathol Bordeaux. 1897;17:339–342
  49. Richie P. Le nerf cubital et les muscles del l'eminence thenar. Bull Mem Anat Paris. 1897;251–252
  50. Patterson J, Jaggars M, Boyer M. Ulnar and median nerve palsy in long-distance cyclists: a prospective study. Am J Sports Med. 2003;31:585–589
  51. Rosencrance J, Anton D, Cook T, Merlino L. Effect of pneumatic power tool use on nerve conduction velocity across the wrist. Hum Factors Ergon Manuf. 2005;15:339–352
  • a SPSS Inc, 233 S Wacker Dr, 11th Fl, Chicago, IL 60606.

 Disclaimer: The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the official policy or position of the Department of the Army, the Department of Defense, or the U.S. Government.

 No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit on the authors or on any organization with which the authors are associated.

PII: S0003-9993(09)00441-9

doi:10.1016/j.apmr.2009.06.007

Archives of Physical Medicine and Rehabilitation
Volume 90, Issue 11 , Pages 1846-1852, November 2009