Introduction. Materials and Methods. Subjects

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3 Abstract Introduction - We tested the hypothesis that a bifid median nerve predisposes to development of carpal tunnel syndrome (CTS) and investigated differences in electrophysiological findings and outcome. Methods consecutive patients with clinically defined CTS were included and investigated clinically, electrophysiologically, and ultrasonographically. 54 healthy asymptomatic volunteers were investigated ultrasonographically. Results - The prevalence of bifid median nerves is equal in patients with CTS and controls. Electrophysiological and ultrasonographic abnormalities are more pronounced in patients with non-bifid median nerves. Some outcome data are better in patients with non-bifid median nerves, but others do not show significant differences. Discussion - A bifid median nerve is not an independent risk factor for development of CTS. Some of our data suggest outcome after surgical decompression to be different, but others do not. The surgical technique in these patients may therefore have to be reevaluated.

4 Introduction The use of imaging studies such as ultrasonography and magnetic resonance imaging for diagnostic purposes in carpal tunnel syndrome (CTS) has led to an increase in the recognition of bifid median nerves and other anatomic or morphological anomalies in patients with CTS and in healthy controls. It is suggested that the presence of a bifid nerve is associated with the occurrence of carpal tunnel syndrome. 1-3 Some suggest that a bifid nerve may facilitate compression of the nerve in the carpal tunnel because of larger summated crosssectional areas (CSA) compared to the CSA of non-bifid nerves. 1 However, data about the frequency and association with CTS are ambiguous. The reported frequency of bifid median nerves varies from 0.8% to 21% in patients with CTS, 1,4-6 and up to 18% were found in a retrospective study with MRI scans performed for various medical reasons. 7 The frequency in healthy subjects is reported to be about 8-15%. 8,9 However, no significant association between the prevalence of bifid median nerves and CTS was found in a recent study among a large population of manual workers. 9 In addition to variable data on frequency, data about electrophysiologic findings and outcome in patients with CTS and bifid median nerves are scarce. The aim of this study is to test our hypothesis that a bifid median nerve, as demonstrated by ultrasonography, predisposes to development of carpal tunnel syndrome. The second aim is to investigate whether there are differences in clinical symptoms, electrophysiologic findings, and treatment outcome between patients with bifid and those with non-bifid median nerves. Materials and Methods Subjects 259 consecutive patients with clinically defined CTS were included in this study. Carpal tunnel syndrome was considered to be present clinically in patients with pain and/or paresthesias in the sensory distribution of the median nerve or in a glove distribution, and if patients met 2 or more of the following criteria: (1) nocturnal paresthesias; (2) reproduction or aggravation of paresthesias or pain by provocative tests (Tinel or Phalen signs); (3) aggravation of paresthesias by activities such as driving, bike riding, or holding a book or a telephone; or (4) relief of symptoms by shaking the hand. These clinical criteria have been used previously in other studies. 10,11 Patients were excluded if they had any of the following: clinical signs of polyneuropathy or known hereditary neuropathy 8 129

5 Chapter 8 Bifid median nerve in CTS with liability to pressure palsy; history of trauma or previous surgery of the symptomatic wrist; pregnancy; severe atrophy of the abductor pollicis brevis muscle; history of rheumatoid arthritis or arthrosis of the wrist; or known diabetes, thyroid disease, or alcoholism. In case of bilateral complaints compatible with clinical CTS, only the most symptomatic hand was included. All candidates gave written informed consent, and the study was approved by the local medical ethics committee. Control subjects The control group consisted of 54 healthy asymptomatic volunteers, 29 women and 25 men. Both hands were examined. Reference values for the nerve conductions studies were derived from 47 healthy, asymptomatic volunteers who were tested in the same laboratory. Electrodiagnostic evaluation All patients underwent standardized motor and sensory nerve conduction studies (NCS) in accordance with the American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) guidelines. 12 NCS were performed using a Viking Myograph type IV (Nicolet Biomedial Inc., Madison, WI, USA). Skin temperature at the site of recording was warmed and maintained at a minimum of 31.0 C by means of hot packs and was measured before and after each test with an infrared thermometer (62 Mini IR thermometer, Fluke Biomedical, Cleveland, OH, USA). Electrophysiological studies were all performed by the same examiner (JM), who was not informed of the preceding clinical examination results. Ring electrodes were applied for recording sensory nerve action potentials (SNAP). The proximal electrode was placed at the first interphalangeal joint and the distal recording electrode at a distance of at least 3 cm, if feasible. The ground electrode was placed between the proximal recording electrode and the stimulation site and, if necessary, repositioned in order to reduce stimulus artifacts. In case of disturbing stimulus artifacts, the anode was repositioned without changing the position of the cathode by turning the stimulator to reduce the stimulus artifact. The hand was fixed manually by the examiner to reduce movement artifacts. The optimal stimulation site was determined carefully, and stimulus current was adjusted to obtain supramaximal stimulation. Signal averaging was applied on all SNAPs. 130

6 Sensory nerve conduction studies comprised 2 comparison tests and 1 short segment study. One motor nerve conduction study was performed in each individual. In all tests, onset latencies were measured for comparison tests or to compute nerve conduction velocities. All tests have previously been described in detail. 13,14 In summary: 1. Sensory median-radial comparison test [DIG1]: SNAPs from median and radial nerves recorded from the first finger after separate stimulation of the median and radial nerve at the wrist, with the same conduction distance. Sensory nerve conduction velocities and differences between onset latencies were computed. A difference in onset latency more than 0.6 ms or the absence of the median SNAP is considered to be consistent with CTS. 2. Sensory median-ulnar comparison test [DIG4]: SNAPs from median and ulnar nerves were recorded from the fourth finger after separate stimulation of the median and ulnar nerves at the wrist, with the same conduction distance. Sensory nerve conduction velocities and difference between onset latencies were computed. A difference in onset latency more than 0.4 ms or the absence of the median SNAP is considered to be consistent with CTS. 3. Sensory short segment study [PALM3]: Sensory nerve conduction studies of the median nerve in the wrist to palm and elbow to wrist segments were performed antidromically. SNAPs were recorded from the third finger after stimulation of the median nerve at the palm, wrist, and elbow, respectively. Differences in sensory nerve conduction velocities between wrist to palm segment and elbow to wrist segments were calculated subsequently. 13 Absence of SNAPs after stimulating the median nerve at the wrist, conduction block, or a difference in conduction velocity between the forearm and wrist segment greater than 17.6 m/s is considered to be consistent with CTS Median nerve distal motor latency [DML]: median motor nerve conduction studies were performed by stimulating the median nerve at the wrist and at the cubital fossa. Compound muscle action potentials (CMAP) were recorded from the abductor pollicis brevis muscle by means of surface electrodes at a distance of 6 cm from the stimulation site at the wrist. A distal motor latency of > 4.0 ms is considered to be consistent with CTS. 8 Ultrasonographic evaluation Ultrasonographic examination was performed by an experienced electrodiagnostic technician, using a Philips Diagnostic Ultrasound System (model iu22) with a 5-17 MHz linear array transducer. The technician was blinded to the results of 131

7 Chapter 8 Bifid median nerve in CTS Figure 1. Bifid median nerve at the right wrist with persistent median artery in the middle. Measurement of CSA by means of tracing method. the preceding physical examination and nerve conduction studies. All wrists were examined in neutral position with palm up and fingers semi-extended. The median nerve was visualized about 7 cm proximal to the carpal tunnel in longitudinal and transverse planes in order to confirm identification of the nerve. No pressure was applied. The distal wrist crease was used as an external landmark. At the inlet of the carpal tunnel, which is defined as the proximal margin of the flexor retinaculum between the scaphoid tubercle and the pisiform bone, the cross-sectional area was measured by means of the direct tracing method. The inner margin of the hyperechoic sheath was considered to be the margin of the nerve. CSA calculations were performed automatically by the local ultrasound software program. The CSA of the median nerve was also measured at one-third distance between the distal wrist and elbow crease. In all patients, the wrist circumference at the distal wrist crease was measured by a marking gauge and a measuring tape with a precision of 1 mm. Ultrasonographic and electrophysiologic studies were performed on the same day. The median nerve was defined as bifid when it branched into radial and ulnar fascicle bundles proximal to the carpal tunnel (Figure 1). Color Doppler imaging was used to identify persistent median arteries and bifid median nerves. When there was doubt whether as to the presence of a bifid median nerve, a second electrodiagnostic technician with experience in neuromuscular ultrasound was consulted. 132

8 Treatment Patients were treated either non-surgically by means of local steroid injection or volar wrist splints, or surgically. Knowledge of the presence of a bifid median nerve never influenced the choice of treatment. Surgical treatment consisted of outpatient standard open carpal tunnel release performed by an experienced neurosurgeon. In all patients, the flexor retinaculum was released. Outcome assessment At inclusion and at 6 to 9 months follow up, patients completed a functional status (FSS) and symptom severity scale (SSS) of the Carpal Tunnel Syndrome Assessment Questionnaire (CTSAQ). 15 Also, at 6 to 9 months follow up, patients completed a short questionnaire, which consisted of 4 final subjective outcome points: (1) full recovery; (2) partial recovery; (3) no recovery at all; or (4) deterioration. Statistical Analysis Data concerning clinical variables, nerve conduction studies, and ultrasonography were processed using Microsoft Office Excel and Access 2010, and all statistical analyses were performed using IBM SPSS Statistics 20. Frequencies of bifid median nerves in patients and controls were computed. Means, mean differences, and standard deviation (SD) of the CSA of the median nerve were computed for both wrists separately. In case of a bifid median nerve, the cross-sectional area of the extra branch was added to the cross-sectional area of the main branch, since the size criterion is assumed to be higher for bifid median nerves. 1 By using regression equations based on left/right side and wrist circumference, we calculated how the observed (summated) CSA differed from the mean in order to obtain a Z-score. By definition, a Z-score of > 2 would be an abnormal result. The following regression equations were used: right side, Z right = [measured CSA 0.86 * wrist circumference (cm)] / 1.45 left side, Z left = [measured CSA 1.06 * wrist circumference (cm)] / 1.55 For a more detailed description of the regression equations, we refer to a previous publication. 16 The upper limit of normal (ULN) of the CSA of the median nerve at the wrist, corrected for wrist circumference, is computed by the following equations: ULN right = 0.86 * wrist circumference (cm) 2.1 and ULN left = 1.06 * wrist circumference (cm) 5.4 for the right and left wrist, respectively

9 Chapter 8 Bifid median nerve in CTS Additionally, the difference between the CSA at the wrist and forearm 17 and the wrist-to-forearm ratio 18 were calculated. Comparison between patients and controls was performed with the Mann-Whitney U test for continuous variables or a χ 2 test for ordinal or dichotomous variables. P-values < 0.05 were considered statistically significant. Electrophysiological severity of CTS was assessed and based on the classification previously reported by Padua. 19 Results Ultrasonographic examination was performed on a total of 108 hands in 54 controls, 25 men and 29 women, mean age 39.8 years (SD, 14.0). Two-hundred-and-fifty-nine patients with clinical symptoms of CTS were included in this study, 50 men and 209 women. The mean age in this group was 50.0 years (SD, 13.7). The median duration of symptoms was 12 months. Of all patients, 139 (53.7%) had bilateral symptoms. The mean age and gender distributions were significantly different between patients and controls (P < 0.01). Incidence of bifid median nerves in patients and controls Forty-one patients (15.8%) had a bifid median nerve, 6 of whom were bilateral (14.6%). Thus, in patients, a bifid median nerve was found in 47 out of 518 wrists (9.1%). Ten control subjects (18.5%) had a bifid median nerve, all unilateral. A unilateral bifid median nerve on the left side was seen in 19 patients and 8 controls; however this difference was not statistically significant. Detailed data are listed in Table 1. A unilateral bifid median nerve was found in 27 patients (60.0%) in the non-dominant hand and 18 (40.0%) in the dominant hand. This distribution was equal in subjects with either symptomatic or asymptomatic bifid median nerves. In case of bilateral bifid median nerves (n = 6), complaints occurred in equal distributions either unilaterally or bilaterally. There was no association between the side of complaints (if occurring unilaterally) and the side of the bifid median nerve (data not shown). Of all bifid median nerves found in patients, 33 (80.5%) were symptomatic. In 23 (69.7%) of patients, complaints were present bilaterally, while both median nerves were bifid. 134

10 Table 1. Number of patients and controls with non-bifid vs. bifid median nerves Patients n = 259 Controls n = 54 Total n = 313 Bifid median nerve 41 (15.8%) 10 (18.5%) 51 (16.3%) Bilateral 6 (14.6%) 0 6 (11.8%) P -value Unilateral 35 (85.4%) 10 (100%) 45 (88.2%) Right 16 (45.7%) 2 (20.0%) Left 19 (54.3%) 8 (80.0%) 8 Figure 2. Electrophysiological severity according to Padua et al. 19 in CTS patients with non-bifid median nerve vs. bifid median nerve. 135

11 Chapter 8 Bifid median nerve in CTS Clinical features There were no differences in clinical features in patients with non-bifid vs. bifid median nerves (gender, age, median duration of symptoms, atrophy of abductor pollicis brevis muscle, sensory loss, weakness of abductor pollicis brevis muscle, symptom severity, and functional status scale at inclusion), except for the higher frequency of weakness of the opponens pollicis muscle in patients with bifid median nerves (4.6% vs. 16.7% in patients with non-bifid vs. patients with bifid median nerves, respectively, P < 0.05). Electrophysiology DIG1: there were no significant differences in the number of abnormal tests, nerve conduction velocities or latency differences. DIG4: Median nerve SNAP was more frequently not recordable (from dig IV) in patients with non-bifid median nerves compared to patients with bifid median nerves [101 (41.9%) vs. 3 (16.7%), respectively; P = 0.035]. Recorded from dig IV, there were no significant differences in nerve conduction velocities and latency differences. PALM3: there were no significant differences in nerve conduction velocities of the palm-to-wrist segment. However, mean NCV of the digit-to-palm segment was significantly lower in patients with non-bifid median nerves compared to patients with bifid median nerves (47.8 ± 7.4 vs ± 8.5, respectively; P = 0.033). DML: In patients with non-bifid median nerves, DML was more frequently abnormal compared to patients with bifid median nerves [181 (75.7%) vs. 9 (50.0%), respectively; P = 0.016]. Moreover, mean DML was longer in patients with non-bifid median nerves (5.3 ± 1.7 vs. 4.6 ± 1.8, respectively; P = 0.044). Detailed data are listed in Tables 2 and 3. Distribution of electrophysiological severity according to Padua et al. 19 in patients with CTS with bifid vs. non-bifid median nerve is shown in Figure 2. The distribution was not significantly different between the two groups of patients. Ultrasonography Figure 3A and B show the spread of the summated CSA of bifid and non-bifid median nerves according to the regression equation in controls for right and left wrists, respectively. 16 In controls, mean summated CSA at the wrist (9.14 ± 1.98 vs ± 1.46) 136

12 Figure 3. Summated CSA of the median nerve in controls with non-bifid vs. bifid nerves according to wrist circumference 16. CSA = cross-sectional area. A. Right. Dashed bold line: ULN = 0.86 * wrist circumference (cm) 2.1. Dotted line: regression line equation y = 0.86 * wrist circumference (cm) B. Left. Dashed bold line: ULN = 1.06 * wrist circumference (cm) 5.4. Dotted line: regression line equation y = 1.06 * wrist circumference (cm) Dashed lines: 95% prediction lines

13 Chapter 8 Bifid median nerve in CTS Figure 4. Summated CSA of the median nerve in patients with non-bifid vs. bifid nerves according to wrist circumference. 16 CSA, cross-sectional area. A. Right. Dashed bold line: ULN = 0.86 * wrist circumference (cm) 2.1. Dotted line: regression line equation y = 0.86 * wrist circumference (cm) B. Left. Dashed bold line: ULN = 1.06 * wrist circumference (cm) 5.4. Dotted line: regression line equation y = 1.06 * wrist circumference (cm) 8.5. Dashed lines: 95% prediction lines. 138

14 Table 2. Mean of nerve conduction parameters of median sensory and motor conduction studies in patients with non-bifid vs. symptomatic bifid median nerves Non-bifid n = 241 Bifid n = 18 Nerve conduction study n* Mean ± SD n* Mean ± SD P - value DIG1 Median sensory NCV (m/s) ± ± 6.8 n.s. Onset latency difference (ms) ± ± 0.46 n.s. DIG4 Median sensory NCV (m/s) ± ± 8.3 n.s. Onset latency difference (ms) ± ± 0.88 n.s. PALM3 Median sensory NCV palm (m/s) ± ± Median sensory NCV wrist (m/s) ± ± 10.7 n.s. Median sensory NCV forearm (m/s) ± ± 3.7 n.s. Difference NCV forearm-wrist (m/s) ± ± 8.8 n.s. DML Median DML (ms) ± ± APB CMAP amplitude (mv) ± ± 4.1 n.s. * Number of patients may vary due to missing values or unrecordable SNAPs or CMAPs. n.s., not significant; NCV, Nerve conduction velocity; DML, Distal motor latency; APB, Abductor pollicis brevis muscle; CMAP, Compound muscle action potential; SNAP, Sensory nerve action potential 8 139

15 Chapter 8 Bifid median nerve in CTS Table 3. Number of positive median sensory and motor nerve conduction study tests in patients with non-bifid vs. symptomatic bifid median nerves Non-bifid n = 241 Bifid n = 18 Nerve conduction study n* # Positive tests n* # Positive tests P -value DIG1 Number of positive tests (84.5%) (88.9%) n.s. Median nerve SNAP unrecordable (24.4%) 18 2 (11.1%) n.s. DIG4 Number of positive tests (90.9%) (88.9%) n.s. Median nerve SNAP unrecordable (41.9%) 18 3 (16.7%) PALM3 Number of positive tests (63.8%) (61.1%) n.s. SNAP unrecordable (wrist) (19.2%) 18 1 (5.6%) n.s. SNAP unrecordable (forearm) (25.4%) 18 3 (16.7%) n.s. DML Number of positive tests (75.7%) 18 9 (50.0%) m. APB CMAP unrecordable (2.1%) 18 0 (0%) n.s. * Number of patients varies due to missing values; including number of patients with unrecordable SNAPs or CMAPs; n.s., not significant; SNAP, Sensory nerve action potential; APB, Abductor pollicis brevis muscle; CMAP, Compound muscle action potential 140

16 Table 4. Ultrasonographic measurements in patients with CTS; non-bifid vs. bifid median nerves Non-bifid n = 362 (wrists) Bifid n = 36 (wrists) n * Mean ± SD n * Mean ± SD P - value Mean Z ± ± Mean CSA ± ± Right ± ± Left ± ± 3.01 n.s. Mean CSA forearm ± ± 1.21 n.s. Right ± ± 1.45 n.s. Left ± ± 0.96 n.s. Mean CSA Wrist - Forearm ± ± Right ± ± Left ± ± 0.96 n.s. Wrist to forearm CSA ratio ± ± Right ± ± 0.55 n.s. Left ± ± 0.54 n.s. * Numbers due to missing values; According to regression equation 16 ; n.s., not significant; CSA, cross-sectional area 8 141

17 Chapter 8 Bifid median nerve in CTS Figure 5. Boxplot: Summated CSA of the (non-)bifid median nerve in patients with CTS vs. controls. Figure 6. Outcome according to short questionnaire in CTS patients with non-bifid vs. bifid median nerve. 142

18 Table 5. Outcome in patients with non-bifid vs. bifid median nerves Non-bifid Bifid n* Mean ± SD n* Mean ± SD P - value Symptom Severity Score At inclusion ± ± 0.57 n.s. At follow up ± ± 1.02 n.s. Difference ± ± 1.19 n.s. Functional Status Scale At inclusion ± ± 0.45 n.s. At follow up ± ± 1.00 n.s. Difference ± ± 0.78 n.s. * Number of patients varies due to missing values; n.s., not significant and mean Z-scores (-0.03 ± 0.96 vs ± 1.00) did not differ significantly between non-bifid and bifid median nerves. The same applies to the CSA difference between the wrist and the forearm (2.27 ± 1.66 vs ± 1.77) and the wrist-to-forearm ratio (1.35 ± 0.28 vs ± 0.41) for non-bifid and bifid median nerves, respectively. In Figure 4A and 4B, for the right and left sides, respectively, the spread of the summated CSA of bifid and non-bifid median nerves according to wrist circumference in patients with CTS is shown. Mean summated CSA (13.6 ± 4.01 vs ± 3.56; P = 0.007) and Z-score according to the regression equation 16 (2.94 ± 2.65 vs ± 2.31; P = 0.008) are significantly higher in patients with non-bifid median nerves compared to patients with bifid median nerves. The difference in mean CSA was more pronounced for the right side (Table 4). The boxplot in Figure 5 shows the spread of the summated CSA of the bifid vs. non-bifid median nerves in patients with CTS and controls. None of the healthy controls had a persistent median artery. A persistent median artery was present between the two branches of the bifid median nerve in two patients, both asymptomatic. One persistent median artery was seen in a patient who did not have a bifid median nerve, also asymptomatic

19 Chapter 8 Bifid median nerve in CTS Outcome Figure 6 shows the distribution of the outcome according to the short questionnaire in patients with CTS and a bifid median nerve vs. non-bifid median nerve. 51.5% of patients with non-bifid vs. 28.6% of patients with CTS associated with a bifid median nerve had clinically full recovery after 6 months (P = 0.003). The difference in treatment outcome according to the symptom severity score and functional status scale between patients with bifid and non-bifid median nerves did not reach the level of statistical significance (Table 5). Discussion The prevalence of bifid median nerves has been described previously in surgical, 2,6,20 MR 7, and ultrasound studies. 1,9,21,22 Our study showed that the occurrence of bifid median nerve is equal in patients with CTS (15.8%) and controls (18.5%). This is consistent with data from a recent study by Granata et al. 8 and indirectly from data from Walker et al. 9 In contrast, however, Bayrak et al. found a higher prevalence of bifid median nerves in patients with CTS compared to controls (19 vs. 9%, respectively). 1 Hunderfund et al. found the opposite: a greater number of bifid median nerves in the control group compared to patients (12 vs. 1.8%, respectively). 23 Although they suggested that a bifid median nerve might be a risk factor for developing CTS, obviously our prospectively collected data do not support this hypothesis. We have no explanation for these observed differences. In healthy controls, the mean of the summated CSA of bifid median nerve was within our previously assessed upper and lower limits of normal for non-bifid median nerves. 16 However, among CTS patients, the mean summated CSA was smaller in patients with bifid median nerves compared to those with non-bifid median nerves. This was also found in a previous study. 24 This may be explained by the fact that only 1 branch of the bifid median nerve is enlarged and that, as a result, the sum of their CSA may be within normal limits and produces a lower mean grand average in groups of patients. The summation of the components of a bifid configuration may thus cause underestimation. The results of Bayrak et al. differ from those of our study in that they indicate that CSA of bifid median nerve in controls is higher than of non-bifid median nerves. 1 They suggest that, to diagnose CTS, higher cut-off values should be used in case a bifid median nerve is found. Our data do not support this suggestion. 144

20 We did not find any relevant difference in clinical presentation of complaints in patients with and without bifid median nerves. However, in patients with a bifid nerve there was a higher frequency of opponens pollicis weakness. We do not have a satisfactory explanation for this observation. As demonstrated by others, we found a bifid median nerve relatively more frequently in the non-dominant hand. 1 Patients in the non-bifid group showed more profound electrophysiological abnormalities (more often absent dig IV SNAP; significantly lower mean NCV of median palm segment; more frequently abnormal DML; significantly larger DML values) as well as ultrasonographic abnormalities (larger mean CSA values). Bayrak et al. did not observe atypical electrophysiological presentation in patients with a bifid median nerve. 1 Comparison of electrophysiological data between patients with bifid vs. non-bifid nerves was not shown in that study. However, Granata et al. suggested that an atypical electrophysiological distribution may suggest the presence of a bifid median nerve. 8 In contrast to the more profound electrophysiological abnormalities in patients with non-bifid median nerves, outcome according to the short questionnaire seems to be better, but not according to the differences in the symptom severity score and functional status scale before and after treatment. Because of the small number of patients with a bifid median nerve and available data of the symptom severity score and functional status scale before and after treatment, it is not possible to draw definite conclusions about outcome according to these measurements. In our cohort prior to surgery, the neurosurgeon was not informed about the presence of a bifid median nerve. All patients were treated according to the local protocol. Therefore, knowledge about the presence of a bifid median nerve did not influence the procedure. A potentially better outcome in the non-bifid group with more profound electrophysiological and ultrasonographic findings would be remarkable. One may speculate that in case of a bifid configuration, 1 branch is relatively spared and the other is compromised, leading to typical CTS complaints. As onset latency of evoked compound sensory and motor action potentials are determined by the fastest conducting fibers, the fibers with slow or blocked conduction in the compressed branch may be overshadowed by the first. As a consequence, in these patients conduction abnormalities may remain undetected. This is also illustrated in a case report in which preoperative electrophysiological studies suggested sparing of the thenar motor branch, which was confirmed perioperatively. 25 The observation that outcome seems to be worse in patients with bifid median nerves may be an indication that the surgical approach in 8 145

21 Chapter 8 Bifid median nerve in CTS these specific cases should be different, as has been suggested by others. 23,24,26 It is likely that, if 1 fascicle is not decompressed surgically, complaints persist. Another explanation may be iatrogenic injury to 1 of the compressed fascicles. 27 To our knowledge, however, prospectively performed studies are published on different surgical approaches in CTS associated with bifid median nerve have not yet been published. First, the potential difference in treatment outcome and second, benefits of different surgical approach in patients with bifid vs. patients with non-bifid median nerves, should be confirmed in future studies. This study has several shortcomings. Given the multiple comparisons and the small numbers of patients with a bifid median nerve, it is difficult to draw definite conclusions about electrophysiological data and outcome. Moreover, not all patients were treated surgically. However, equal percentages of patients with a bifid median nerve vs. a non-bifid nerve were treated with surgery. Knowledge of the presence of a bifid median nerve never influenced the choice or method of treatment. Also, the neurosurgeon was not aware of the presence of a bifid median nerve preoperatively. So it does not appear that this explains the difference, if any. Another issue is that we have chosen to measure the CSA of the median nerve solely at 2 points. First, the median nerve was visualized about 7 cm proximal to the carpal tunnel in different planes. Second, the CSA was measured at the proximal margin of the flexor retinaculum at the inlet of the carpal tunnel where the nerve is visualized most easily 23 and where the measurement is easiest to perform. 28 It is known, however, that cut-off points, sensitivity and specificity values vary at different measurement locations. Moreover, measurement at the point of greatest enlargement has a risk of increased false positives. 29 Because we did not identify the median nerve distal to the flexor retinaculum, it is possible that the number of bifid median nerves in our study is relatively underestimated. Finally, in patients, only the most symptomatic hand was examined electrodiagnostically, whereas both were examined ultrasonographically. In summary, ultrasonography can effectively disclose the presence of a bifid median nerve. Measuring the summated CSA, however, does not add any additional data for diagnosis of CTS and may lead to false negative findings. Electrophysiological and ultrasonographic abnormalities are more pronounced in CTS patients with non-bifid median nerves. Some of our data suggest that treatment outcome may be better in these patients compared to patients with bifid median nerve. We hypothesize that a lesion of one branch of 146

22 the bifid median nerve may contribute to this phenomenon. It may also be an indication that surgical planning and the procedure should be different in this specific patient group. If so, it would be useful to know preoperatively whether a bifid configuration is present. Obviously, further study is required to determine this. At this moment, however, outcome data are inconclusive

23 Chapter 8 Bifid median nerve in CTS References 1. Bayrak IK, Bayrak AO, Kale M, Turker H, Diren B. Bifid median nerve in patients with carpal tunnel syndrome. J Ultrasound Med 2008; 27: Schultz R, Endler P, Huddleston H. Anomalous median nerve and an anomalous muscle belly of the first lumbrical associated with carpal-tunnel syndrome. J Bone Joint Surg 1973; 55A: Stancić MF, Eskinja N, Stosić A. Anatomical variations of the median nerve in the carpal tunnel. Int Orthop 1995; 19: Eiken O, Carstam N, Eddeland A. Anomalous distal branching of the median nerve: case reports. Scand J Plast Reconstr Surg 1971; 5: Tountas C, Bihrle D, MacDonald C, Bergman R. Variations of the median nerve in the carpal canal. J Hand Surg Am 1987; 12: Ahn D, Yoon ES, Koo S, Park S. A prospective study of the anatomic variations of the median nerve in the carpal tunnel in Asians. Ann Plast Surg 2000; 44: Pierre-Jerome C, Smitson RD, Shah RK, Moncayo V, Abdelnoor M, Terk MR. MRI of the median nerve and median artery in the carpal tunnel: prevalence of their anatomical variations and clinical significance. Surg Radiol Anat 2010; 32: Granata G, Caliandro P, Pazzaglia C, Minciotti I, Russo G, Martinoli C, et al. Prevalence of bifid median nerve at wrist assessed through ultrasound. Neurol Sci 2011; 32: Walker FO, Cartwright MS, Blocker JN, Arcury TA, Suk JI, Chen H, et al. Prevalence of bifid median nerves and persistent median arteries and their association with carpal tunnel syndrome in a sample of latino poultry processors and other manual workers. Muscle Nerve 2013; 48: Jablecki C, Andary M, So Y, Wilkins D. Literature review of the usefulness of nerve conduction studies and electromyography for the evaluation of patients with carpal tunnel syndrome. Muscle Nerve 1993; 16: Witt JC, Hentz JG, Stevens JC. Carpal tunnel syndrome with normal nerve conduction studies. Muscle Nerve 2004; 29: Jablecki CK, Andary MT, Floeter MK, Miller RG, Quartly CA, Vennix MJ, et al. Practice parameter: Electrodiagnostic studies in carpal tunnel syndrome: Report of the American Association of Electrodiagnostic Medicine, American Academy of Neurology, and the American Academy of Physical Medicine and Rehabilitation. Neurology 2002; 58:

24 13. Kasius KM, Claes F, Verhagen WI, Meulstee J. The segmental palmar test in diagnosing carpal tunnel syndrome reassessed. Clin Neurophysiol 2012; 123: Kasius KM, Claes F, Verhagen WI, Meulstee J. Ultrasonography in severe carpal tunnel syndrome. Muscle Nerve 2012; 45: Levine DW, Simmons BP, Koris MJ, Daltroy LH, Hohl GG, Fossel AH, et al. A self-administered questionnaire for the assessment of severity of symptoms and functional status in carpal tunnel syndrome. J Bone Joint Surg Am 1993; 75: Claes F, Meulstee J, Claessen-Oude Luttikhuis TT, Huygen PL,Verhagen WI, Usefulness of additional measurements of the median nerve with ultrasonography. Neurol Sci 2010; 31: Klauser A, Halpern E, De Zordo T, Feuchtner G, Arora R, Gruber J, et al. Carpal tunnel syndrome assessment with US. Value of additional cross-sectional area measurements of the median nerve in patients versus healthy volunteers. Radiology 2009; 250: Hobson-Webb LD, Massey JM, Juel VC, Sanders DB. The ultrasonographic wrist-toforearm median nerve area ratio in carpal tunnel syndrome. Clin Neurophysiol 2008; 119: Padua L, LoMonaco M, Gregori B, Valente EM, Padua R, Tonali P. Neurophysiological classification and sensitivity in 500 carpal tunnel syndrome hands. Acta Neurol Scand 1997; 96: Fernandez-Garcia S, Pi-Folguera J, Estallo-Matino F. Bifid median nerve compression due to a musculotendinous anomaly of FDS to the middle finger. J Hand Surg Br 1994; 19: Klauser AS, Halpern EJ, Faschingbauer R, Guerra F, Martinoli C, Gabl MF, et al. Bifid median nerve in carpal tunnel syndrome. Radiology 2011; 259: Szabo RM, Pettey J. Bilateral median nerve bifurcation with an accessory compartment within the carpal tunnel. J Hand Surg Br 1994; 19: Hunderfund AN, Boon AJ, Mandrekar JN, Sorenson EJ. Sonography in carpal tunnel syndrome. Muscle Nerve 2011; 44: Cartwright MS, Hobson-Webb LD, Boon AJ, Alter KE, Hunt CH, Flores VH, et al. Evidence-based guideline: neuromuscular ultrasound for the diagnosis of carpal tunnel syndrome. Muscle Nerve 2012; 46: Gregori B, Accornero N, Canero G. Electrophysiologic correlates of anomalous course of the median-nerve thenar motor branch. Muscle Nerve 2001; 24: Beekman R, Visser LH. Sonography in the diagnosis of carpal tunnel syndrome: a 149

25 Chapter 8 Bifid median nerve in CTS critical review of the literature. Muscle Nerve 2003; 27: Iannicelli E, Chianta GA, Salvini V, Almberger M, Monacelli G, Passariello R, Evaluation of bifid median nerve with sonography and MR imaging. J Ultrasound Med 2000; 19: Mondelli M, Filippou G, Gallo A, Frediani B. Diagnostic utility of ultrasonography versus nerve conduction studies in mild carpal tunnel syndrome. Arthritis Rheum 2008; 59: Ulaşli AM, Duymuş M, Nacir B, Rana Erdem H, Koşar U. Reasons for using swelling ratio in sonographic diagnosis of carpal tunnel syndrome and a reliable method for its calculation. Muscle Nerve 2013; 47:

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