How to make electrodiagnosis of carpal tunnel syndrome with normal distal conductions?

The purpose of this study is to investigate which electrodiagnostic techniques are better in clinically diagnosed patients with carpal tunnel syndrome (CTS) and patients with CTS with normal distal conduction study. A total of 230 clinically diagnosed patients with CTS and 100 normal control subjects were enrolled. All subjects were evaluated by eight electrodiagnostic techniques, including conventional conduction studies: median distal sensory latency and distal motor latency; short distance conduction studies across wrist, including wrist-palm sensory conduction time and wrist-palm motor conduction velocity; comparison of median sensory conduction across the wrist with radial or ulnar nerves in the same limb (median-radial sensory latency difference [M-R] or median-ulnar sensory latency difference [M-U]); and comparison of median wrist-palm and palm-index conduction, including distoproximal conduction time difference and distoproximal conduction time ratio. Normal limits were derived by calculating the mean ± 2 standard deviations from the data of the controls. The sensitivity, specificity, positive predictive value, negative predictive value, and the area under the receiver operating characteristic curve with 95% confidence interval of each test were calculated. In clinically diagnosed patients with CTS, M-R is the best diagnostic technique with significant difference in area under the receiver operating characteristic curve (0.912) compared with other tests except that of M-U. The sensitivity, specificity, positive predictive value, and negative predictive value of M-R were 84.3%, 98%, 99%, and 73.1%, respectively. Further evaluation of patients with CTS with normal distal latencies also revealed the best diagnostic value of M-R and M-U with significance to other tests in area under the receiver operating characteristic curve. In clinical practice, after conventional median distal sensory latency and distal motor latency studies, the authors suggest performing M-R or M-U studies instead of segmental conduction or comparative studies of median nerves in the patients with CTS with normal distal latencies.

Comparison of sensitivity of transcarpal median motor conduction velocity and conventional conduction techniques in electrodiagnosis of carpal tunnel syndrome.

OBJECTIVE: To compare the sensitivity of median wrist-palm motor conduction velocity (W-P MCV) with those of standard sensory conduction techniques in the electrodiagnosis of carpal tunnel syndrome (CTS). METHODS: This study included 280 consecutively suspected CTS patients (360 hands) referred for evaluation and 150 volunteers who served as controls. We determined and calculated (1) median W-P MCV, (2) median motor distal latencies (DL) and median sensory DL for (3) thumb (D1), (4) index (D2) and (5) ring finger (D4), (6) median wrist-palm sensory conduction velocity (W-P SCV) and sensory conduction time (W-P SCT) for index finger and sensory latency differences between (7) median-radial (M-R) for thumb and (8) median-ulnar (M-U) nerves for ring finger. The normal limits were calculated from the median of normal controls +/-2.5 standard deviations. The sensitivities of each test were determined and compared. RESULTS: Among the 360 hands with suspected CTS, 32 hands (8.9%) had normal electrodiagnostic studies and 328 (91.1%) had at least one abnormal electrodiagnostic study. Among the 328 hands with abnormalities, 234 (65%) had abnormal motor DL and 294 (81.7%) had abnormal W-P MCV. The sensitivity was 80.3% for D1, 72.5% for D2, 76.7% for D4, 86.7% for M-R (specificity, 98.7%), 87.2% for M-U (specificity, 96.7%), 80.8% for sensory W-P SCT and 73.6% for W-P SCV. CONCLUSIONS: W-P MCV is a valuable motor conduction technique for the diagnosis of CTS and it is confirmed again that W-P MCV is equal to or more sensitive than W-P SCV and W-P SCT. Furthermore, the findings of the present study are in agreement with the conventional wisdom that internal comparison of latency differences between median and ulnar or radial nerves is the best method for a diagnosis of patients with suspected CTS. Therefore, we recommend that CTS patients be studied according to the following steps: (1) routine sensory and motor DL, (2) if step 1 is negative, then perform and determine W-P MCV or SCT. This may increase the diagnostic yield of 10%, (3) if step 2 is negative, measure the M-U or MR. These are the final and more sensitive techniques in making a diagnosis with an additional diagnostic yield of 10%. SIGNIFICANCE: We provide the evidence of W-P MCV that could be a standard technique for electrodiagnosis of CTS. Furthermore, we make a reasonable flow chart and recommendation for electrodiagnosis of CTS for electromyographers.

Does retrograde axonal atrophy really occur in carpal tunnel syndrome patients with normal forearm conduction velocity?

OBJECTIVE: The cause of decreased median forearm motor conduction velocity (FMCV) in carpal tunnel syndrome (CTS) is best ascribed to retrograde axonal atrophy (RAA); however, the relationships between the occurrence of RAA and electrophysiological or clinical severity remains controversial. We attempt to determine whether RAA really occurs in CTS patients with normal median FMCV and to investigate any relationships between RAA and severity of compression at the wrist. METHODS: Consecutive CTS patients were enrolled and age-matched volunteers served as controls. We performed conventional nerve conduction studies (NCS) and measured median and ulnar distal motor latencies (DML), FMCV, compound muscle action potential (CMAP) amplitudes, distal sensory latencies (DSL), and sensory nerve action potential (SNAP) amplitudes. Furthermore, palmar median stimulation was done to calculate the wrist-palm motor conduction velocity (W-P MCV). Patients included for analysis should have normal FMCV and needle examination. We compared each electrodiagnostic parameters between the patient group and controls. RESULTS: The mean+/-SD of the W-P MCV for patients and controls were 33.26+/-6.74 and 52.14+/-5.85 m/s and those of median FMCV were 55.26+/-3.56 and 57.82+/-3.9 m/s, respectively. There was a significant reduction in the W-P MCV (36.2%, P<0.00001), significant decrease in the median FMCV (4.43%, P<0.00001) and SNAP amplitudes, and an increase of the DML and DSL in the patient group (P<0.00001) compared to the controls; however, there were no differences in median and ulnar CMAP amplitudes, ulnar FMCV and DML between the controls and patients. CONCLUSIONS: RAA and relatively slowed median FMCV do occur in CTS patients with normal median FMCV, regardless of severity of clinical manifestations and electrophysiological abnormalities. SIGNIFICANCE: This article provides new information for research of the electrophysiological changes of the proximal nerve part at distal injury.

Forearm mixed nerve conduction velocity: questionable role in the evaluation of retrograde axonal atrophy in carpal tunnel syndrome.

The objective of this study was to determine whether forearm mixed nerve conduction velocity (Fmix) reflects the real conduction velocity of forearm motor nerve (Fmot) and forearm sensory nerve (Fsen) fibers passing through the carpal tunnel. Forearm mixed nerve conduction velocity is presumed to be indicative of the conduction velocity of the median nerve over the forearm. Therefore, Fmix is used widely to assess the causes of slowing forearm conduction velocity in carpal tunnel syndrome. However, some authors claim that Fmix comes chiefly from the undamaged fibers in carpal tunnel syndrome, and thus cannot replace Fmot or Fsen in the evaluation of retrograde axonal atrophy. Patients with clinical symptoms and signs of carpal tunnel syndrome confirmed with standard electrodiagnosis were included. Age-matched volunteers served as control subjects. Conduction velocities across the wrist and over the forearm were measured, including those of the wrist sensory (Wsen), wrist motor (Wmot), and wrist mixed nerves (Wmix); and forearm mixed (Fmix), forearm motor (Fmot), and forearm sensory nerves (Fsen). The authors compared and correlated Wsen, Wmot, and Wmix; and Fmix, Fmot, and Fsen respectively. The mean values of Wsen, Wmot, Wmix, Fmix, Fmot, and Fsen of the control subjects less those of corresponding conduction velocity of carpal tunnel syndrome patients were designated Wsen N, Wmot N, Wmix N, Fmix N, Fmot N, and Fsen N respectively and were compared and correlated again. Wrist motor nerve conduction velocity, Wsen, and Wmix were significantly lower in carpal tunnel syndrome patients, and Fmot and Fsen but not Fmix were reduced significantly when compared with control subjects. Mean wrist sensory nerve conduction velocity, Wmot N, and Wmix N; and Fsen N and Fmot N showed good correlation except for Fmix N, suggesting that Fmix reflects the conduction velocity of undamaged fibers in carpal tunnel syndrome. Forearm mixed nerve conduction velocity cannot replace Fmot or Fsen in the assessment of retrograde axonal atrophy in carpal tunnel syndrome. In the disease state, Fmix possibly represents the conduction velocity of the palmar cutaneous branch.

The reason for forearm conduction slowing in carpal tunnel syndrome: an electrophysiological follow-up study after surgery.

BACKGROUND: The exact cause of decreased forearm median motor conduction velocity (FMMCV) in carpal tunnel syndrome (CTS) is still a subject of controversy. A conduction block or an axonal loss in the large myelinating fibers upon wrist compression, or retrograde axonal atrophy, is suspected. METHODS: In order to attempt a determination of the cause, 10 patients with clinical symptoms and signs of CTS, confirmed using standard electrodiagnosis and with a slowed FMMCV <50m/s, were included in this study. Serial standard median motor conduction studies were performed at baseline, 1 week, 2 weeks, 4 weeks, 8 weeks, and 12 weeks after endoscopic ligament release. Serial median motor distal latencies (MMDL), compound muscle action potential (CMAP) amplitudes, and FMMCV, were determined and compared. RESULTS: Significant improvement in MMDL had occurred at the 1-week follow-up examination; however, no such improvement in FMMCV was observed. Furthermore, a significant increase in CMAP amplitude was evidenced beginning 4 weeks after surgery. The results revealed an improvement in median motor conduction, across the wrist segment, that did not parallel the increase in FMMCV, suggesting that a conduction block or axonal loss at wrist compression was not the likely cause of the decreased FMMCV. CONCLUSIONS: Retrograde axonal atrophy, not selective damage to the large myelinating fibers at the wrist, is the direct cause of decreased FMMCV in CTS.

Does direct measurement of forearm mixed nerve conduction velocity reflect actual nerve conduction velocity through the carpal tunnel?

OBJECTIVES: The purpose of this study was to determine whether forearm (wrist-elbow) mixed nerve conduction velocity (W-Emix) represents the actual nerve conduction velocity (CV) of nerve fibers passing through the carpal tunnel. BACKGROUND: W-Emix is presumed to reflect the actual forearm CV through the carpal tunnel. However, it has been argued that W-Emix chiefly originates from the nerve fibers passing outside the carpal tunnel. Therefore, the direct measurement of W-Emix cannot be used to assess retrograde axonal atrophy in carpal tunnel syndrome (CTS). SUBJECTS AND METHODS: Thirty patients with clinical signs and symptoms of CTS were recruited and the diagnosis was confirmed with standard electrodiagnosis. Fifty age-matched volunteers served as control. Recording electrodes were placed over the elbow and index finger for mixed nerve and sensory nerve conduction studies, respectively. Stimulation was applied at the palm and wrist for the measurement of mixed nerve wrist-palm CV (W-Pmix), wrist-elbow CV (W-Emix), and elbow-palm CV (E-Pmix). Stimulation was applied at the elbow, wrist, and palm for the measurement of wrist-elbow sensory CV (W-Esen), wrist-palm CV (W-Psen), and elbow-palm CV (E-Psen). Comparisons were made between W-Pmix and W-Psen, W-Emix and W-Esen, and E-Pmix and E-Psen. RESULTS: Correlations between W-Emix and W-Esen, E-Pmix and E-Psen, and W-Pmix and W-Psen were good in the control. In the patient group, there was a strong positive correlation between W-Pmix and W-Psen, and between E-Pmix and E-Psen. However, W-Esen correlated weakly with W-Emix, suggesting that W-Emix chiefly represents the CV of fibers passing outside the carpal tunnel. Therefore, the direct measurement of W-Emix cannot be used to assess retrograde axonal atrophy. Furthermore, the reduction in W-Psen was more marked than the reduction in W-Esen, implying that a conduction block at the wrist is the least likely cause of proximal slowing in CTS. CONCLUSIONS: W-Emix does not reflect the actual CV of the nerve fibers passing through the carpal tunnel. In addition, retrograde axonal atrophy appears to be the primary cause of decreased forearm CV in CTS.

The cause of slowed forearm median conduction velocity in carpal tunnel syndrome: a Palmar stimulation study.

OBJECTIVES: To elucidate the etiopathogenesis of decreased forearm median motor conduction velocity (FMMCV) in carpal tunnel syndrome (CTS), we used segmental stimulation at the palm, wrist and antecubital fossa to determine conduction block at wrist and calculate and compare the segmental median motor conduction velocity (MMCV) to determine the pathogenesis. BACKGROUND: The cause of the decreased FMMCV in CTS remains unclear. Animal models have supported retrograde axonal atrophy as the cause. Some authors believe standard FMMCV, calculated by subtracting the distal latency, may not represent an exact assessment of FMMCV but rather the velocity of small fibers that persist throughout the carpal tunnel. SUBJECTS AND METHODS: Patients with clinical symptoms and signs of CTS which had been confirmed with standard electrodiagnosis, were included. The patients were divided into two groups: one with reduced FMMCV <50m/s (Group I, n=20) and the other with normal FMMCV>50m/s (Group II, n=40). Age-matched volunteers served as controls (n=60). We used palm, wrist and antecubital stimulation, and recorded compound muscle action potential (CMAP) amplitudes at the abductor pollicis brevis (APB) muscle. Based on a ratio of the CMAP amplitudes obtained from wrist and palm stimulation (W/P ratio) and the latency differences, we calculated the W/P ratio and the across wrist MMCV (AWMMCV) and FMMCV and compared and correlated them between two patient groups. RESULTS: There was no difference in median motor and sensory distal latency between Groups I and II. CMAP and sensory nerve action potential amplitudes were reduced in Group I compared with Group II, but the difference was only marginally significant. Four patients had a significant reduction of the W/P ratio in Group I, compared with 7 patients in Group II, which did not reach a significance. Sixteen patients (80%) in Group I demonstrated no conduction block. Furthermore, Group I showed significantly decreased FMMCV when compared with Group II; however, AWMMCV was not significantly reduced in Group I, suggesting that decreased FMMCV does not result from a decrease in AWMMCV. CONCLUSIONS: There was no significant motor conduction block and no correlation of the FMMCV and AWMMCV in CTS patients with a decrease of FMMCV, suggesting retrograde axonal atrophy, and not selective conduction block of the large fibers at the wrist, is the direct cause of decreased FMMCV in CTS.