Our findings suggest that irrespective of symptoms, when both Tinel’s and Phalen’s tests are negative, mean SNC velocity in the median nerve is little different from that in asymptomatic hands. Conversely, abnormal SNC is most likely to be found when both of these tests are positive. In the absence of physical examination, the strongest predictor of abnormal SNC in the median nerve was the occurrence of numbness or tingling in an extensive median distribution with no involvement of non-median parts of the hand. With the methods that we used, a cut-point of 8 m/s in the distribution of the difference between little and index finger SNC velocities appears a reasonable basis on which to define abnormality of median nerve function in epidemiological research.
Our study had the strength of being based on a large sample of patients, and although the response from potential participants was incomplete (73%), and information was partially missing on some others who agreed to take part (for example, because they attended hospital on a day when the research nurse was not present), we have no reason to expect that those included in analyses would have been atypical in the relation of SNC to symptoms and physical signs. Furthermore, the clinical department in which the study was conducted was the only provider of nerve conduction studies for almost all of a local population of some 440,000 people, referrals coming mainly from general practitioners and orthopaedic surgeons. Thus, we would expect that within the age range studied (20–64 years), the associations that we found between clinical findings and SNC will have been fairly representative of those in patients with suspected CTS in the community. However, they cannot necessarily be extrapolated to older populations, in which other causes of neurological symptoms in the hand may be relatively more frequent.
Many of the asymptomatic hands which we studied were in patients with symptomatic CTS in the other hand, and therefore, their prevalence of abnormal nerve conduction may have been higher than that in asymptomatic hands in the general population. To the extent that this occurred, it may have caused us to underestimate the ability of our proposed cut-point of 8 m/s to discriminate between asymptomatic hands and those with typical features of CTS.
Other strengths of our study were the systematic and detailed collection of data on symptoms and the performance of a standardised physical examination. Moreover, by treating SNC velocity as a continuous variable in most of our analysis, we avoided the potential for error from arbitrary dichotomous definitions of abnormality. The distribution of SNC velocities across all of the hands examined was unimodal, with reduced conduction in some hands that were totally asymptomatic. Thus, even if impaired nerve conduction occurred when a clinical test was negative, the finding would not necessarily imply that the test lacked sensitivity.
In a few analyses we did dichotomise SNC velocities, and the predictive values that we then found for abnormality could reasonably be extrapolated to other similar patient populations. However, they would not be expected to apply where the underlying prevalence of abnormality was substantially lower (e.g. when screening a workforce). Nor could sensitivities and specificities necessarily be extended to other settings in which the mix of cases differed (e.g. a higher proportion of hands with borderline as compared with severe abnormality of SNC) or there was a different prevalence of other pathologies that could give rise to the same symptoms. For this reason, and because SNC velocity cannot be regarded as a diagnostic gold standard, we did not calculate sensitivities or specificities.
Report of symptoms, including through use of hand diagrams, may not have been entirely reliable, and it is possible that this contributed to the absence of important associations between nerve conduction and the distribution of pain (Table 2). However, misclassification of symptoms should not have given rise to spurious associations with nerve conduction.
Implications for clinical practice
In our series of 908 patients, the mean difference between little and index finger SNC velocities in symptomatic hands that were negative for both Tinel’s and Phalen’s tests was no higher than that in hands which had no numbness or tingling (Table 3); and the prevalence of abnormal SNC velocity as we defined it (25%) was rather lower than that in hands without these symptoms (32%). This suggests that unless patients with suspected CTS have other objective evidence of impaired median nerve function (e.g. abnormality on sensory testing or wasting of the thenar muscles), there is little value in referring them for nerve conduction studies if they are negative on both Tinel’s and Phalen’s tests.
Other studies that have examined the utility of Tinel’s and Phalen’s tests in the diagnosis of CTS have generally reported low sensitivity in relation to nerve conduction abnormalities [9, 10, 12, 16–18, 21, 25–27, 31]. However, because SNC velocity can be abnormal in asymptomatic hands, an ideal test would have a sensitivity of less than 100% when assessed against nerve conduction as a standard. In a study which made allowance for this by latent class analysis, the sensitivities of Tinel’s and Phalen’s tests were 0.97 and 0.92 respectively .
Among the 788 patients in our case series who underwent physical examination, 228 (29%) were negative for both Tinel’s and Phalen’s tests in both hands. This suggests that screening out patients negative for both of these tests could materially reduce the workload of some neurophysiology services.
Implications for epidemiological research
A recent review highlighted wide variation in the case definitions that have been used for CTS in epidemiological research . When defining cases for epidemiological purposes, a balance must be drawn between sensitivity and specificity, and the choice that is made will depend in part on the purpose of the research. For example, when estimating population attributable burdens of disease, it may be preferable to adopt a more sensitive and less specific case definition, any inflation of total disease prevalence because of false positives tending to be offset by reductions in estimates of relative risk (because of bias towards the null). On the other hand, for hazard identification and characterisation, a more specific case definition may be advantageous. Another consideration is the types of data that are available. In some studies, information may be obtained only on symptoms or only on symptoms and physical signs.
Our findings suggest that where information is limited to symptoms (e.g. in a survey based on questionnaires), the most specific case definition would be numbness/tingling with an extensive median distribution, and also affecting part-median regions of the hand, but with no involvement of non-median regions. A more sensitive, but somewhat less specific definition would be numbness/tingling with an extensive median distribution, irrespective of other symptoms. We have not found previous studies that classified symptoms exactly as we did, but these conclusions accord broadly with earlier research. Thus, one study found that mean SNC velocity was lower when sensory symptoms occurred in at least three of the four radial digits as compared with when only one or two of these digits was affected , and another that neurophysiological abnormality was more prevalent when paraesthesiae were restricted to the median nerve distribution . At the same time, several investigators have observed that patients with abnormal nerve conduction often have sensory symptoms outside the distribution of the median nerve [11, 35, 36]. Some studies have suggested that report of pain in the hand also has diagnostic value [9, 13, 30], although an association with impaired nerve conduction has not always been found , and there was none in our study.
If Tinel’s and Phalen’s tests can be performed in addition to ascertainment of symptoms, then a relatively specific case definition for epidemiological studies would be numbness/tingling with an extensive median distribution, combined with a positive Tinel’s test and positive Phalen’s test. A more sensitive but less specific case definition would include anyone with symptoms in whom either Tinel’s or Phalen’s test was positive.
In some studies, there may be a need to distinguish between abnormal and normal nerve conduction. While the choice of a cut-point for abnormality will inevitably be somewhat arbitrary, our results suggest that with the method of testing that we employed, a reasonable definition for an abnormal difference between SNC velocities in the little and index fingers sufficient to cause symptoms would be a value of >8 m/s.