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NERVE CONDUCTION STUDIES FOR CARPAL TUNNEL SYNDROME: ESSENTIAL PRELUDE TO SURGERY OR UNNECESSARY LUXURY?
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NERVE CONDUCTION STUDIES FOR CARPAL TUNNEL SYNDROME: ESSENTIAL PRELUDE TO SURGERY OR UNNECESSARY LUXURY? N.J. SMITH From the Clinical Neurophysiology Department, University Hospital, Nottingham, UK
Although carpal tunnel syndrome is a relatively trivial condition, controversy surrounds the use of nerve conduction studies, and whether they are essential to make the diagnosis, or as a prelude to surgery. This is partly due to the lack of a generally agreed definition of the condition, and failure to recognize that the patient’s first priority is rapid relief of symptoms. If nerve conduction studies do not contribute to achieving that aim it would be better not to do them. Supporters of routine preoperative nerve conduction studies ignore their shortcomings, which include lack of standardization, absence of population-based reference intervals, and lack of sensitivity and specificity. Only a controlled trial, in which patients are randomized to receive treatment either with or without nerve conduction studies, will determine whether they improve the outcome in patients with a firm clinical diagnosis of carpal tunnel syndrome. Journal of Hand Surgery (British and European Volume, 2002) 27B: 1: 83–85 Compared with cancer or Creutzfeldt–Jakob disease, carpal tunnel syndrome is pretty trivial. That is not to deny the inconvenience and discomfort it causes; merely to put it in perspective – on a par with piles, varicose veins and in-growing toenails. It is remarkable that the management of such a relatively minor condition should have given rise to a vast literature and heated debate. Much of the heat surrounds nerve conduction studies, and whether they are essential, either to make the diagnosis or as a prelude to surgery. The controversy arises partly from the lack of a generally agreed definition of ‘‘carpal tunnel syndrome’’ (Franzblau and Werner, 1999). After all, according to medical dictionaries, a syndrome is merely a collection of clinical features that commonly occur together, so from this point of view the definition is entirely clinical and the only problem is which features to include. The definition might be stretched to include nerve conduction abnormalities, the operative findings, and the response to treatment, a definite diagnosis being made only when nerve conduction is abnormal, the nerve appears compressed at operation, and symptoms are relieved by decompression: the lower cross-hatched area in Figure 1. Many patients fall into other categories, particularly those who respond to non-operative treatment, and those in whom decompression relieves symptoms in spite of normal nerve conduction (the upper cross-hatched area in Fig 1), a group which provokes endless debate among electromyographers. Fascinating though these discussions may be, we must remember that the patient has one over-riding aim: prompt relief of symptoms. Doctors should share that aim, and ought to recognize that if nerve conduction studies do not improve the outcome, it would be better not to do them.
In many patients, a confident clinical diagnosis of carpal tunnel syndrome can and should be made (Bland, 2000; Kremer et al., 1953; Payan, 1988). These patients are woken in the middle of the night by pain and paraesthesiae in the hand, not necessarily confined to the median nerve distribution, and subsiding within twenty or thirty minutes, often aided by shaking the hand. Pain, paraesthesiae and numbness may also be present in the daytime, frequently precipitated by using the hand or holding the wrist flexed, as when driving or reading a newspaper. This is the characteristic history of carpal tunnel syndrome. Two important points should be noted. First, the only possible explanation for episodic nocturnal pain in the hand, sufficient to awaken the patient, but only lasting half an hour or so, is intermittent ischaemia of the median nerve which is compressed in the carpal tunnel (Payan, 1988). Second, the diagnosis is made on the history alone; no physical signs are necessary. In the presence of this history, neither lack of sensory impairment, absence of weakness of thumb abduction, negative Phalen’s test, failure to elicit Tinel’s sign, nor normal nerve conduction studies, cast the slightest doubt on the diagnosis, and recently described clinical tests make no further contribution to diagnostic accuracy (Kaul et al., 2001). Conversely, there are undoubtedly many patients whose symptoms are not typical, particularly those with continuous pain or numbness, not exacerbated by any activity, but these patients can only be described as suffering from ‘‘possible carpal tunnel syndrome’’, unless their continuous symptoms are associated with, or were preceded by, nocturnal episodes. If clinical diagnosis is so straightforward, why do many clinicians insist upon nerve conduction studies before operating (if they are surgeons), or referring the 83
84
THE JOURNAL OF HAND SURGERY VOL. 27B No. 1 FEBRUARY 2002
Fig 1 Venn diagram showing relationship of different features of the carpal tunnel syndrome. The four circles enclose patients with typical symptoms, abnormal nerve conduction studies, a nerve which appears compressed at operation and those whose symptoms are relieved by decompression. The upper crosshatched area includes those with normal nerve conduction who nevertheless obtain relief from decompression. The lower cross-hatched area includes patients with all four features (typical symptoms, abnormal nerve conduction, compressed nerve and relief of symptoms after decompression).
patient to a surgeon (if they are not)? Several reasons are advanced for this policy: 1. 2. 3. 4.
5. 6. 7.
It’s the right thing to do, like taking a chest radiograph in a patient with pneumonia (Johnson, 1993). To provide ‘‘objective confirmation’’ of the diagnosis (Nathan et al., 1993; Semple and Cargill, 1969). To detect an underlying diffuse neuropathy, particularly diabetic (Payan, 1988). To provide a baseline for comparison with postoperative nerve conduction studies in the minority of patients who obtain no benefit from surgery (Dawson et al., 1990; Payan, 1988). To prevent unnecessary operation in patients with normal nerve conduction (Boniface et al., 1994; Dawson et al., 1990). To comply with patients’ expectations, and avoid dissatisfaction if operation is proposed without the nerve having been assessed electrophysiologically. To assist in refuting an allegation of negligence if the result of surgery is unsatisfactory.
These arguments are disingenuously advanced by those who provide an electrophysiology service, and therefore have a vested interest in maximizing the number of tests performed. Aside from the question of self-interest, it is my view that none of the above reasons for routine nerve conduction studies stands up to critical
examination. No randomized controlled trial has been performed to compare the outcome in patients having carpal tunnel decompression with and without nerve conduction studies; we therefore simply do not know whether nerve conduction studies improve the outcome. The available evidence suggests that they do not, provided that the clinical diagnosis is made by an experienced clinician (Braun and Jackson, 1994; Finsen and Russwurm, 2001; Glowacki et al., 1996). Furthermore, reliance upon nerve conduction studies undoubtedly contributes to poorer results in some patients by delaying surgery, and by denying operation to those with characteristic nocturnal symptoms but normal nerve conduction in the daytime: false negatives. False negative results arise because nerve compression is sometimes only sufficient to cause intermittent ischaemia of the nerve, without permanent demyelination, so conduction velocities remain normal. False negatives are not confined to nerve conduction studies. No test is perfect, so sensitivity and specificity will never be 100%, unless the disease is defined by the test, like anaemia. When false negative nerve conduction studies are reported, a common criticism is that the most sensitive tests were not performed, but this ignores the fact that improved sensitivity (fewer false negatives) is rarely achieved without diminished specificity (more false positives). The occurrence of false positive nerve conduction studies is rarely admitted by electromyographers (Redmond and Rivner, 1988), but the finding of an ‘‘abnormal’’ conduction velocity in an asymptomatic hand is not an indication of sub-clinical disease, it is merely a false positive result. Contrary to a widelyheld belief, there is no evidence that the risk of an asymptomatic subject developing symptoms is greater if nerve conduction is abnormal (Nathan et al., 1998; Werner et al., 1997). Nerve conduction studies are bedevilled by two problems in relation to the carpal tunnel syndrome. First, there is no generally agreed ‘‘gold standard’’ diagnostic criterion against which tests can be compared (Brown et al., 1994). Although electromyographers understandably regard nerve conduction studies as the ‘‘gold standard’’ (Johnson, 1993), adopting abnormal nerve conduction as the diagnostic criterion sometimes leads to the regrettable conclusion that nocturnal pain is not the most characteristic symptom (e.g. D’Arcy and McGee, 2000), for reasons explained above. Second, nerve conduction studies are not standardized. They were introduced into clinical practice without anyone having confirmed that repeatable and reproducible results could be obtained (Eisenhart, 1963; Holland & Whitehead, 1974), and many variations in technique have arisen with questionable justification. Although a standardized approach has been proposed for the carpal tunnel syndrome (American Academy of Neurology, American Association of Electrodiagnostic Medicine and American Academy of Physical Medicine and Rehabilitation, 1993), many electromyographers do
NERVE CONDUCTION STUDIES
not follow the protocol in its entirety (Corwin and Kasdan, 1998), and widely different methods may be used within the same department. Furthermore, there is no general agreement as to what constitutes an abnormality, because no-one has determined reliable population reference intervals for nerve conduction values, corrected for age, sex, height, body weight, wrist circumference and occupation; to do so would mean testing hundreds of healthy subjects, an undertaking which has never been funded. Electromyographers therefore either use rules of thumb (‘‘over 50 m/s in the upper limb, 40 m/s in the lower’’), or copy reference limits from reports of small numbers of subjects, without allowing for differences in technique or the different populations studied (Smith, 2000). Consequently, results of nerve conduction studies are no more objective than clinical assessment, they just transfer the subjectivity to someone else, and whether or not they are reliable depends upon who does them (Bralliar, 1981; Corwin and Kasdan, 1998; Szabo and Madison, 1992). This unsatisfactory state of affairs is exacerbated by the fact that, until recently, many electromyographers were self-taught (Payan, 1996), and in many hospitals nerve conduction studies are still performed by medical staff whose primary interest is in some other specialty: neurology, rheumatology, rehabilitation, or even medical physics. Should nerve conduction studies ever be performed in patients with carpal tunnel syndrome? Yes, certainly, if the history is not typical, but the symptoms could nevertheless be explained by median nerve compression, particularly if a steroid injection into the carpal tunnel has had no effect. (Incidentally, relief of symptoms by steroid injection proves the diagnosis, which is not cast into doubt by subsequent relapse.) Of course, a selective policy for nerve conduction studies invites clinicians to say that every patient is atypical in some way. Indeed, many clinicians give the impression of never having seen a typical case, but they need better clinical skills, not nerve conduction studies. It must not be forgotten that nerve conduction studies will occasionally produce a false positive result purely by chance in a patient whose non-specific hand symptoms are not due to median nerve compression. Although this possibility is rarely considered, it may be the explanation for lack of response to decompression in some patients. In the age of evidence-based medicine it is impossible to justify either the continuing lack of standardization and reproducibility of nerve conduction studies, or the absence of a well-designed randomized trial to determine whether they improve the outcome in patients with carpal tunnel syndrome (Sackett et al., 2000). In the meantime, clinicians would be well advised to recognize the shortcomings of electrodiagnostic assessment, and to remember that Sir Sydney Sunderland regarded nerve conduction studies as an unnecessary luxury in patients with a firm clinical diagnosis of carpal tunnel syndrome (Sunderland, 1978).
85
References American Association of Electrodiagnostic Medicine, American Academy of Neurology, American Academy of Physical Medicine and Rehabilitation (1993) Practice parameter for electrodiagnostic studies in carpal tunnel syndrome (summary statement). Neurology, 43: 2404–2405. Bland JDP (2000) The value of the history in the diagnosis of carpal tunnel syndrome. Journal of Hand Surgery, 25B: 445–450. Boniface SJ, Morris I, Macleod A (1994) How does neurophysiological assessment influence the management and outcome of patients with carpal tunnel syndrome? British Journal of Rheumatology, 33: 1169– 1170. Bralliar F (1981) Electromyography: its use and misuse in peripheral nerve injuries. Orthopedic Clinics of North America, 12: No. 2, 229–238. Braun RM, Jackson WJ (1994) Electrical studies as a prognostic factor in the surgical treatment of carpal tunnel syndrome. Journal of Hand Surgery, 19A: 893–900. Brown WF, Dellon AL, Campbell WW (1994) Electrodiagnosis in the management of focal neuropathies: the ‘‘WOG’’ syndrome. Muscle and nerve, 17: 1336–1342. Corwin HM, Kasdan ML (1998) Electrodiagnostic reports of median neuropathy at the wrist. Journal of Hand Surgery, 23A: 55–57. D’Arcy CA, McGee S (2000) Does this patient have carpal tunnel syndrome? Journal of American Medical Association, 283: 3110–3117. Dawson DM, Hallett M, Millender LH. Entrapment neuropathies, 2nd edn. Boston, Little, Brown, 1990: 60. Eisenhart C (1963) Realistic evaluation of the precision and accuracy of instrument calibration systems. Journal of Research of National Bureau of Standards – C. Engineering and Instrumentation, 67C: 161–187. Finsen V, Russwurm H (2001) Neurophysiology not required before surgery for typical carpal tunnel syndrome. Journal of Hand Surgery, 26B: 61–64. Franzblau A, Werner RA (1999) What is carpal tunnel syndrome? JAMA, 282: 186–187. Glowacki KA, Breen CJ, Sachar K, Weiss A-PC (1996) Electrodiagnostic testing and carpal tunnel release outcome. Journal of Hand Surgery, 21A: 117– 122. Holland WW, Whitehead TP (1974) Value of new laboratory tests in diagnosis and treatment. Lancet, 2: 391–394. Johnson EW (1993) Diagnosis of the carpal tunnel syndrome. The gold standard. American Journal of Physical Medicine and Rehabilitation, 72: 1. Kaul MP, Pagel KJ, Wheatley MJ, Dryden JD (2001) Provocative clinical tests and carpal tunnel syndrome. Muscle and Nerve, 24: 107–111. Kremer M, Gilliatt RW, Golding JSR, Wilson TG (1953) Acroparaesthesiae in the carpal-tunnel syndrome. Lancet, 2: 590–595. Nathan PA, Keniston RC, Meadows KD, Lockwood RS (1993) Predictive value of nerve conduction measurements at the carpal tunnel. Muscle and Nerve, 16: 1377–1382. Nathan PA, Keniston RC, Myers LD, Meadows KD, Lockwood RS (1998) Natural history of median nerve sensory conduction in industry. Muscle and Nerve, 21: 711–721. Payan J (1988) The carpal tunnel syndrome: can we do better? Journal of Hand Surgery, 13B: 365–367. Payan J (1996) Some reflections on approaching retirement. Journal of Neurology, Neurosurgery and Psychiatry, 61: 573–578. Redmond MD, Rivner MH (1988) False positive electrodiagnostic tests in carpal tunnel syndrome. Muscle and Nerve, 11: 511–518. Sackett DL, Straus SE, Richardson WS, Rosenberg W, Haynes RB. Evidencebased medicine. How to practice and teach EBM. 2nd edn Edinburgh, Churchill Livingstone, 2000: 105–135. Semple JC, Cargill AO (1969) Carpal tunnel syndrome. Results of surgical decompression. Lancet, 1: 918–919. Smith NJ (2000) What is normal? American Journal of Electroneurodiagnostic technology 40: 196–214. Sunderland S. Nerves and nerve injuries 2nd edn. Edinburgh, Churchill Livingstone. 1978: 719. Szabo RM, Madison M (1992) Carpal tunnel syndrome. Orthopedic Clinics of North America, 23: 103–109. Werner RA, Franzblau A, Albers JW, Buchele H, Armstrong TJ (1997) Use of screening nerve conduction studies for predicting future carpal tunnel syndrome. Occupational and Environmental Medicine, 54, 96–100. Dr N J Smith, Clinical Neurophysiology Dept, University Hospital, Nottingham NG7 2UH, UK. # 2002 The British Society for Surgery of the Hand doi: 10.1054/jhsb.2001.0669, available online at http://www.idealibrary.com on
NERVE CONDUCTION STUDIES FOR CARPAL TUNNEL SYNDROME: ESSENTIAL PRELUDE TO SURGERY OR UNNECESSARY LUXURY? N.J. SMITH From the Clinical Neurophysiology Department, University Hospital, Nottingham, UK
Although carpal tunnel syndrome is a relatively trivial condition, controversy surrounds the use of nerve conduction studies, and whether they are essential to make the diagnosis, or as a prelude to surgery. This is partly due to the lack of a generally agreed definition of the condition, and failure to recognize that the patient’s first priority is rapid relief of symptoms. If nerve conduction studies do not contribute to achieving that aim it would be better not to do them. Supporters of routine preoperative nerve conduction studies ignore their shortcomings, which include lack of standardization, absence of population-based reference intervals, and lack of sensitivity and specificity. Only a controlled trial, in which patients are randomized to receive treatment either with or without nerve conduction studies, will determine whether they improve the outcome in patients with a firm clinical diagnosis of carpal tunnel syndrome. Journal of Hand Surgery (British and European Volume, 2002) 27B: 1: 83–85 Compared with cancer or Creutzfeldt–Jakob disease, carpal tunnel syndrome is pretty trivial. That is not to deny the inconvenience and discomfort it causes; merely to put it in perspective – on a par with piles, varicose veins and in-growing toenails. It is remarkable that the management of such a relatively minor condition should have given rise to a vast literature and heated debate. Much of the heat surrounds nerve conduction studies, and whether they are essential, either to make the diagnosis or as a prelude to surgery. The controversy arises partly from the lack of a generally agreed definition of ‘‘carpal tunnel syndrome’’ (Franzblau and Werner, 1999). After all, according to medical dictionaries, a syndrome is merely a collection of clinical features that commonly occur together, so from this point of view the definition is entirely clinical and the only problem is which features to include. The definition might be stretched to include nerve conduction abnormalities, the operative findings, and the response to treatment, a definite diagnosis being made only when nerve conduction is abnormal, the nerve appears compressed at operation, and symptoms are relieved by decompression: the lower cross-hatched area in Figure 1. Many patients fall into other categories, particularly those who respond to non-operative treatment, and those in whom decompression relieves symptoms in spite of normal nerve conduction (the upper cross-hatched area in Fig 1), a group which provokes endless debate among electromyographers. Fascinating though these discussions may be, we must remember that the patient has one over-riding aim: prompt relief of symptoms. Doctors should share that aim, and ought to recognize that if nerve conduction studies do not improve the outcome, it would be better not to do them.
In many patients, a confident clinical diagnosis of carpal tunnel syndrome can and should be made (Bland, 2000; Kremer et al., 1953; Payan, 1988). These patients are woken in the middle of the night by pain and paraesthesiae in the hand, not necessarily confined to the median nerve distribution, and subsiding within twenty or thirty minutes, often aided by shaking the hand. Pain, paraesthesiae and numbness may also be present in the daytime, frequently precipitated by using the hand or holding the wrist flexed, as when driving or reading a newspaper. This is the characteristic history of carpal tunnel syndrome. Two important points should be noted. First, the only possible explanation for episodic nocturnal pain in the hand, sufficient to awaken the patient, but only lasting half an hour or so, is intermittent ischaemia of the median nerve which is compressed in the carpal tunnel (Payan, 1988). Second, the diagnosis is made on the history alone; no physical signs are necessary. In the presence of this history, neither lack of sensory impairment, absence of weakness of thumb abduction, negative Phalen’s test, failure to elicit Tinel’s sign, nor normal nerve conduction studies, cast the slightest doubt on the diagnosis, and recently described clinical tests make no further contribution to diagnostic accuracy (Kaul et al., 2001). Conversely, there are undoubtedly many patients whose symptoms are not typical, particularly those with continuous pain or numbness, not exacerbated by any activity, but these patients can only be described as suffering from ‘‘possible carpal tunnel syndrome’’, unless their continuous symptoms are associated with, or were preceded by, nocturnal episodes. If clinical diagnosis is so straightforward, why do many clinicians insist upon nerve conduction studies before operating (if they are surgeons), or referring the 83
84
THE JOURNAL OF HAND SURGERY VOL. 27B No. 1 FEBRUARY 2002
Fig 1 Venn diagram showing relationship of different features of the carpal tunnel syndrome. The four circles enclose patients with typical symptoms, abnormal nerve conduction studies, a nerve which appears compressed at operation and those whose symptoms are relieved by decompression. The upper crosshatched area includes those with normal nerve conduction who nevertheless obtain relief from decompression. The lower cross-hatched area includes patients with all four features (typical symptoms, abnormal nerve conduction, compressed nerve and relief of symptoms after decompression).
patient to a surgeon (if they are not)? Several reasons are advanced for this policy: 1. 2. 3. 4.
5. 6. 7.
It’s the right thing to do, like taking a chest radiograph in a patient with pneumonia (Johnson, 1993). To provide ‘‘objective confirmation’’ of the diagnosis (Nathan et al., 1993; Semple and Cargill, 1969). To detect an underlying diffuse neuropathy, particularly diabetic (Payan, 1988). To provide a baseline for comparison with postoperative nerve conduction studies in the minority of patients who obtain no benefit from surgery (Dawson et al., 1990; Payan, 1988). To prevent unnecessary operation in patients with normal nerve conduction (Boniface et al., 1994; Dawson et al., 1990). To comply with patients’ expectations, and avoid dissatisfaction if operation is proposed without the nerve having been assessed electrophysiologically. To assist in refuting an allegation of negligence if the result of surgery is unsatisfactory.
These arguments are disingenuously advanced by those who provide an electrophysiology service, and therefore have a vested interest in maximizing the number of tests performed. Aside from the question of self-interest, it is my view that none of the above reasons for routine nerve conduction studies stands up to critical
examination. No randomized controlled trial has been performed to compare the outcome in patients having carpal tunnel decompression with and without nerve conduction studies; we therefore simply do not know whether nerve conduction studies improve the outcome. The available evidence suggests that they do not, provided that the clinical diagnosis is made by an experienced clinician (Braun and Jackson, 1994; Finsen and Russwurm, 2001; Glowacki et al., 1996). Furthermore, reliance upon nerve conduction studies undoubtedly contributes to poorer results in some patients by delaying surgery, and by denying operation to those with characteristic nocturnal symptoms but normal nerve conduction in the daytime: false negatives. False negative results arise because nerve compression is sometimes only sufficient to cause intermittent ischaemia of the nerve, without permanent demyelination, so conduction velocities remain normal. False negatives are not confined to nerve conduction studies. No test is perfect, so sensitivity and specificity will never be 100%, unless the disease is defined by the test, like anaemia. When false negative nerve conduction studies are reported, a common criticism is that the most sensitive tests were not performed, but this ignores the fact that improved sensitivity (fewer false negatives) is rarely achieved without diminished specificity (more false positives). The occurrence of false positive nerve conduction studies is rarely admitted by electromyographers (Redmond and Rivner, 1988), but the finding of an ‘‘abnormal’’ conduction velocity in an asymptomatic hand is not an indication of sub-clinical disease, it is merely a false positive result. Contrary to a widelyheld belief, there is no evidence that the risk of an asymptomatic subject developing symptoms is greater if nerve conduction is abnormal (Nathan et al., 1998; Werner et al., 1997). Nerve conduction studies are bedevilled by two problems in relation to the carpal tunnel syndrome. First, there is no generally agreed ‘‘gold standard’’ diagnostic criterion against which tests can be compared (Brown et al., 1994). Although electromyographers understandably regard nerve conduction studies as the ‘‘gold standard’’ (Johnson, 1993), adopting abnormal nerve conduction as the diagnostic criterion sometimes leads to the regrettable conclusion that nocturnal pain is not the most characteristic symptom (e.g. D’Arcy and McGee, 2000), for reasons explained above. Second, nerve conduction studies are not standardized. They were introduced into clinical practice without anyone having confirmed that repeatable and reproducible results could be obtained (Eisenhart, 1963; Holland & Whitehead, 1974), and many variations in technique have arisen with questionable justification. Although a standardized approach has been proposed for the carpal tunnel syndrome (American Academy of Neurology, American Association of Electrodiagnostic Medicine and American Academy of Physical Medicine and Rehabilitation, 1993), many electromyographers do
NERVE CONDUCTION STUDIES
not follow the protocol in its entirety (Corwin and Kasdan, 1998), and widely different methods may be used within the same department. Furthermore, there is no general agreement as to what constitutes an abnormality, because no-one has determined reliable population reference intervals for nerve conduction values, corrected for age, sex, height, body weight, wrist circumference and occupation; to do so would mean testing hundreds of healthy subjects, an undertaking which has never been funded. Electromyographers therefore either use rules of thumb (‘‘over 50 m/s in the upper limb, 40 m/s in the lower’’), or copy reference limits from reports of small numbers of subjects, without allowing for differences in technique or the different populations studied (Smith, 2000). Consequently, results of nerve conduction studies are no more objective than clinical assessment, they just transfer the subjectivity to someone else, and whether or not they are reliable depends upon who does them (Bralliar, 1981; Corwin and Kasdan, 1998; Szabo and Madison, 1992). This unsatisfactory state of affairs is exacerbated by the fact that, until recently, many electromyographers were self-taught (Payan, 1996), and in many hospitals nerve conduction studies are still performed by medical staff whose primary interest is in some other specialty: neurology, rheumatology, rehabilitation, or even medical physics. Should nerve conduction studies ever be performed in patients with carpal tunnel syndrome? Yes, certainly, if the history is not typical, but the symptoms could nevertheless be explained by median nerve compression, particularly if a steroid injection into the carpal tunnel has had no effect. (Incidentally, relief of symptoms by steroid injection proves the diagnosis, which is not cast into doubt by subsequent relapse.) Of course, a selective policy for nerve conduction studies invites clinicians to say that every patient is atypical in some way. Indeed, many clinicians give the impression of never having seen a typical case, but they need better clinical skills, not nerve conduction studies. It must not be forgotten that nerve conduction studies will occasionally produce a false positive result purely by chance in a patient whose non-specific hand symptoms are not due to median nerve compression. Although this possibility is rarely considered, it may be the explanation for lack of response to decompression in some patients. In the age of evidence-based medicine it is impossible to justify either the continuing lack of standardization and reproducibility of nerve conduction studies, or the absence of a well-designed randomized trial to determine whether they improve the outcome in patients with carpal tunnel syndrome (Sackett et al., 2000). In the meantime, clinicians would be well advised to recognize the shortcomings of electrodiagnostic assessment, and to remember that Sir Sydney Sunderland regarded nerve conduction studies as an unnecessary luxury in patients with a firm clinical diagnosis of carpal tunnel syndrome (Sunderland, 1978).
85
References American Association of Electrodiagnostic Medicine, American Academy of Neurology, American Academy of Physical Medicine and Rehabilitation (1993) Practice parameter for electrodiagnostic studies in carpal tunnel syndrome (summary statement). Neurology, 43: 2404–2405. Bland JDP (2000) The value of the history in the diagnosis of carpal tunnel syndrome. Journal of Hand Surgery, 25B: 445–450. Boniface SJ, Morris I, Macleod A (1994) How does neurophysiological assessment influence the management and outcome of patients with carpal tunnel syndrome? British Journal of Rheumatology, 33: 1169– 1170. Bralliar F (1981) Electromyography: its use and misuse in peripheral nerve injuries. Orthopedic Clinics of North America, 12: No. 2, 229–238. Braun RM, Jackson WJ (1994) Electrical studies as a prognostic factor in the surgical treatment of carpal tunnel syndrome. Journal of Hand Surgery, 19A: 893–900. Brown WF, Dellon AL, Campbell WW (1994) Electrodiagnosis in the management of focal neuropathies: the ‘‘WOG’’ syndrome. Muscle and nerve, 17: 1336–1342. Corwin HM, Kasdan ML (1998) Electrodiagnostic reports of median neuropathy at the wrist. Journal of Hand Surgery, 23A: 55–57. D’Arcy CA, McGee S (2000) Does this patient have carpal tunnel syndrome? Journal of American Medical Association, 283: 3110–3117. Dawson DM, Hallett M, Millender LH. Entrapment neuropathies, 2nd edn. Boston, Little, Brown, 1990: 60. Eisenhart C (1963) Realistic evaluation of the precision and accuracy of instrument calibration systems. Journal of Research of National Bureau of Standards – C. Engineering and Instrumentation, 67C: 161–187. Finsen V, Russwurm H (2001) Neurophysiology not required before surgery for typical carpal tunnel syndrome. Journal of Hand Surgery, 26B: 61–64. Franzblau A, Werner RA (1999) What is carpal tunnel syndrome? JAMA, 282: 186–187. Glowacki KA, Breen CJ, Sachar K, Weiss A-PC (1996) Electrodiagnostic testing and carpal tunnel release outcome. Journal of Hand Surgery, 21A: 117– 122. Holland WW, Whitehead TP (1974) Value of new laboratory tests in diagnosis and treatment. Lancet, 2: 391–394. Johnson EW (1993) Diagnosis of the carpal tunnel syndrome. The gold standard. American Journal of Physical Medicine and Rehabilitation, 72: 1. Kaul MP, Pagel KJ, Wheatley MJ, Dryden JD (2001) Provocative clinical tests and carpal tunnel syndrome. Muscle and Nerve, 24: 107–111. Kremer M, Gilliatt RW, Golding JSR, Wilson TG (1953) Acroparaesthesiae in the carpal-tunnel syndrome. Lancet, 2: 590–595. Nathan PA, Keniston RC, Meadows KD, Lockwood RS (1993) Predictive value of nerve conduction measurements at the carpal tunnel. Muscle and Nerve, 16: 1377–1382. Nathan PA, Keniston RC, Myers LD, Meadows KD, Lockwood RS (1998) Natural history of median nerve sensory conduction in industry. Muscle and Nerve, 21: 711–721. Payan J (1988) The carpal tunnel syndrome: can we do better? Journal of Hand Surgery, 13B: 365–367. Payan J (1996) Some reflections on approaching retirement. Journal of Neurology, Neurosurgery and Psychiatry, 61: 573–578. Redmond MD, Rivner MH (1988) False positive electrodiagnostic tests in carpal tunnel syndrome. Muscle and Nerve, 11: 511–518. Sackett DL, Straus SE, Richardson WS, Rosenberg W, Haynes RB. Evidencebased medicine. How to practice and teach EBM. 2nd edn Edinburgh, Churchill Livingstone, 2000: 105–135. Semple JC, Cargill AO (1969) Carpal tunnel syndrome. Results of surgical decompression. Lancet, 1: 918–919. Smith NJ (2000) What is normal? American Journal of Electroneurodiagnostic technology 40: 196–214. Sunderland S. Nerves and nerve injuries 2nd edn. Edinburgh, Churchill Livingstone. 1978: 719. Szabo RM, Madison M (1992) Carpal tunnel syndrome. Orthopedic Clinics of North America, 23: 103–109. Werner RA, Franzblau A, Albers JW, Buchele H, Armstrong TJ (1997) Use of screening nerve conduction studies for predicting future carpal tunnel syndrome. Occupational and Environmental Medicine, 54, 96–100. Dr N J Smith, Clinical Neurophysiology Dept, University Hospital, Nottingham NG7 2UH, UK. # 2002 The British Society for Surgery of the Hand doi: 10.1054/jhsb.2001.0669, available online at http://www.idealibrary.com on