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Rapid Responses: Rapid Responses published:
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Carpal Tunnel? Check the neck!
- Dr A Breck McKay (18 August 2007)
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Carpal tunnel syndrome (CTS) is a clinical syndrome
- Sidha Sambandan (18 August 2007)
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Thoracic Outlet Syndrome Should Be Ruled Out in All Cases Diagnosed as Carpal Tunnel Syndrme
- Carlos A Selmonosky.MD (19 August 2007)
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carpal tunnel syndrome is a clinical diagnosis
- peter j mahaffey (22 August 2007)
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CTS no occupational disease?
- P. Paul F.M. Kuijer (22 August 2007)
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Carpal Tunnel Syndrome in Patients on Dialytic Therapy
- Chandra Mauli Jha (23 August 2007)
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Real life management of CTS in UK General Practice
- Stephen Longworth (28 August 2007)
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Authors reply
- Jeremy D P Bland (28 August 2007)
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Carpal Tunnel Syndrome (CTS)
- NAZAR R DESSOUKI (28 August 2007)
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Authors reply (2)
- Jeremy D P Bland (30 August 2007)
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Re: Authors reply (1) & (2)
- Sidha Sambandan (11 September 2007)
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Author's replly (3)
- Jeremy D P Bland (13 September 2007)
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Real life (surgical!)management of CTS in General Practice
- John P Rine (14 September 2007)
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Compression theorem is built on sand riddled with holes.
- Ibrahim,M. Khan (27 September 2007)
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Dr A Breck McKay, Family/Musculoskeletal Physicain Victoira Point, Brisbane, Australia
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My colleagues and I have found that many carpal tunnel syndromes are secondary to enthesis problems of the scalenes at the lateral processes of the C5 C6 C7 . These can be readily palpated and when tender, injection of local anaesthetic, cortisone (as preferred) via a 25G, 35mm needle (classical tennis elbow injection technique), can immediately begin the removal of hand swelling, numbness, pain and loss of function. The patients are amazed at the rapid response (often after months or years of symptoms), as have been many observing doctors. The mechanism involved is secondary activation of the dorsal horn (wind up)from enthesis damage, resulting in mid brain autonomic efferent responses which then increase the repair process (eg increased tissue fluid in synovia), in the distal parts of the limb as well as at the anthesis. I have published this explanation based on clinical observation and the model of resulting whole body function always occurring as a response to nociception/pain, in the Australasian Musculoskeletal Medicine Journal, Nov 2005 "Tennis Elbow Everywhere" p 128-130 I can forward .pdf copies for requests sent to <mckayab@bigpond.net.au> Competing interests: None declared |
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Sidha Sambandan, FP/GPwSI Orthopaedics/H.Sen.Lecturer. Yare Valley Medical Practice,202 Thorpe Rd,Norwich NR1 1TJ, UK
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Not wishing to be pedantic about semantics, I wish to comment on some of the contents of this interesting review of CTS. CTS is as the word syndrome implies, a clinical diagnosis made from the history and examination of the patient. The prevalence of asymptomatic individuals fitting the accepted electrophysiological diagnostic criteria is small but significant, as shown by population studies. False negative rates for neurophysiological examination of the median nerve has been estimated in several trials to be between 7 and 13%.(1) The majority of the patients can be diagnosed in the community setting when the typical symptoms and signs are present. Electrophysiological studies are used in British practice mainly in three situations – when there is a doubt about the diagnosis, for medico-legal reasons including work compensation issues and in situations where there is no response to steroids or surgery. Some of the important clinical pointers in addition to that described are gender, and the predictive value of 2 of the 3 tests performed: the Phalen’s test, Tinel’s sign and the compression test. The presence of objective numbness in the little finger is an important negative predictor. Nocturnal pain is due to the tendency for humans to move into the foetal position when sleeping, with the wrists going into flexion. For a clinician it is important to know whether the CTS is a dynamic compression with intermittent symptoms (especially nocturnal symptoms) in the earlier phase when nerve conduction studies could sometimes be normal or whether it is in a later phase with “hard” neurological signs with constant numbness subjectively and objectively; weakness and wasting of the thenar muscles especially Abductor Pollicis Brevis (APB). A further indicator of possibility of a later phase is the duration of symptoms being more than a year. A diagnosis in clinical medicine is a psychological construct in the mind of a clinician which has a utility value, in that a therapeutic intervention leads to relief of symptoms, and reduces the complications from progression of the problem. If hard neurological signs are present, patient should be referred for surgical decompression as soon as possible, to prevent further progression. As the NHS has waiting lists, splints and steroids are useful while the patients wait for surgery, to alleviate the symptoms. In dynamic compression, most patients respond well to splints , steroids and other conservative interventions , but need to be informed about the natural history and possible outcomes, and ideally monitored by the family practitioner. Kaplan(2) has described five important factors determining the success of non-surgical treatments. Structured clinical questionnaire for the diagnosis of CTS has been shown to have a positive predictive value of 90% compared to 92% by nerve conduction studies.(3) References: 1) Atroshi I, Gummesson C, Johnson R et al. Diagnostic properties of nerve conduction tests in population-based carpal tunnel syndrome. BMC Musculoskeletal Disord. 2003 May 7;4:9.Epub 2003 May 7. (www.hubmed.org/display.cgi?uids=12734018) 2) Kaplan SJ, Glickel SZ, Eaton RG; Predctive factors in the non- surgical treatment of Carpal tunnel syndrome. J.Hand Surg. 1990;15B:106 3) Kamath V, Stothard J. A clinical questionnaire for the diagnosis of Carpal tunnel syndrome. J Hand Surg (British Vol) 2003; 28B:45-459 Competing interests: None declared |
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Carlos A Selmonosky.MD, Phys Inova Fairfax Hospital.Falls Church. VA .USA
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The symptoms of Carpal Tunnel Syndome(CTS) are very similar to those of Thoracic Outlet Syndrome(TOS).Sensory disturbance of the whole hand,pain radiating to the arm and shoulder,perception of swelling of the hand or fingers are not explained by median nerve compression.Weakness of the fifth finger should be tested in all patients,if detected manually or by dynamometry ,a diagnosis of TOS should be considered.A diagnostic triad consisting of 1)weakness of the fifth finger,2)paresthesias and or paleness of the hand on elevation;marked paleness is called the White Hand Sign,3)Tenderness on palpation of the supraclavicular area will confirm the diagnosis(see www.tos-syndrome.com).Therefore if these signs are present in patients diagnosed as CTS,the diagnosis of TOS should be considered as an associated pathology or it could be the only diagnosis.In summary determination of the presence of weakness of the fifth finger should be a must in the physical examination of patients suspected of having Carpal Tunnel Syndrome. Selmonosky C.A.The white hand sign.A simple maneuver useful in the diagnosis of thotacic outlet syndrome(Abstract} South Med J.2002 Oct:85(10):S 57 Competing interests: None declared |
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peter j mahaffey, consultant plastic & hand surgeon bedford hospital mk42 9dj
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Jeremy Bland gives a useful review of carpal tunnel syndrome (CTS). However, one must surely ask, without any disrespect, whether the authorship by a neurophysiologist of an article strongly advocating nerve conduction studies in the diagnosis of this condition represents something of an undeclared competing interest? Fortunately not all Dr Bland's colleagues support his enthusiasm, and clinicians involved in the day to day hands-on management of CTS mostly agree that there is a significant rate of false negatives such that the test should only be advocated for cases of unusual diagnostic difficulty. Just as CTS usually presents in the early hours of the morning due to extra-circulatory shifts in body fluids, so nerve conduction tests would also need to be performed at 4am to be truly accurate. Until Dr Bland's department can provide a round the clock service, willy-nilly requests for nerve studies are likely to more effective in bankrupting the NHS than providing helpful pointers towards firm diagnosis! As for the article's guidance on treatments, splintage certainly helps with symptoms but does nothing for the underlying condition, and who (apart from the cash-strapped Secretary of State for Health) really wants us to go to bed every night wearing a cumbersome splint? As for steroids, as Dr Bland tells us, relapse is common. Am I therefore like him also at risk of a conflict of interest in declaring that expert surgery is really the only definitive solution?!!!! Competing interests: None declared |
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P. Paul F.M. Kuijer, consultant for work-related musculoskeletal disorders Academic Medical Center, Coronel Institute, Netherlands Center for Occupational Diseases
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In his clinical review on Carpal Tunnel Syndrom (CTS), Bland (BMJ 2007;335:343-346), states that ‘The role of occupational and recreational hand use in causation remains controversial. If overuse of the hands does contribute, it may be a relatively minor factor, though most patients report that heavy use of the hands aggravates the symptoms’. No reference is given by Bland to support this remark. As a consultant for work-related musculoskeletal disorders at the Netherlands Center for Occupational Diseases, I was surprised to read this remark, because CTS can be diagnosed as an occupational disease in the Netherlands. The diagnosis is based on the criteria-document for evaluating the work-relatedness of upper extremity musculoskeletal disorders (Sluiter et al. 2001). More recent, Melchior et al. (2006) concluded that a significant risk ratio of 2.1 between manual and non-manual female workers (n=1107, 44 cases) for physician-diagnosed CTS could for 96% be explained by exposure to three risk factors: repetitive movements, vibration and extreme wrist flexion. Dr P Paul FM Kuijer, Netherlands Center for Occupational Diseases, Coronel Institute of Occupational Health, Academic Medical Center, Universiteit van Amsterdam, PO Box 22700, 1100 DE Amsterdam Melchior M, Roquelaure Y, Evanoff B, Chastang JF, Ha C, Imbernon E, Goldberg M, Leclerc A; Pays de la Loire Study Group. Why are manual workers at high risk of upper limb disorders? The role of physical work factors in a random sample of workers in France (the Pays de la Loire study). Occup Environ Med. 2006; 63(11):754-61. Sluiter JK, Rest KM, Frings-Dresen MHW. Scand. J. Work Environ. Health. 2001; 27 suppl 1: 1-102. Competing interests: None declared |
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Chandra Mauli Jha, Incharge Nephrologist Rusatq Regional Hospital, Rustaq, Oman
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I enjoyed the concise review article. I would like to draw attention to an etiological subgroup of patients who are not less important. Patient of end-stage renal failure on maintenance haemodialysis are a special risk group for development of CTS (carpal tunnel syndrome). Development of carpal tunnel syndrome in patients on long term dialysis may be as high as 50%.(1) In personal experience I have encountered a few patients with CTS involving both hands mimicking a symmetrical polyneuropathy. Amyloid deposits composed mainly of ß2-microglobulin (ß2- M) fibrils are considered the pathology behind in such patients.(2) More recently, local inflammatory process in the carpal tunnel due to infiltration of peripheral monocytes which has increased adhesion capacity to fibronectin due to increased expression of VLA-4 on them has been suggested as another pathomechanism.(3) Management options remain those mentioned in the review article - splinting, local steroid injection, surgery etc. Surgical technique requires modification as the pneumatic tourniquet may not be used in such patient with AV-fistula at wrist or forearm. Subcutaneous Endoscope system under local anaesthesia without a pneumatic tourniquet has been noted to be effective.(4) In some of the patients there may be recurrence of symptoms at around 2 years after successful surgery. 1. C. Chazot, I. Chazot, B. Charra, J.C. Terrat, T. Vanel, E. Calemard, M. Ruffet, and G. Laurent. Functional study of hands among patients dialysed for more than 10 years. Nephrol. Dial. Transplant: 1993; 8: 347 - 351. 2. T. B. Drüeke. ß2-Microglobulin and Amyloidosis. Nephrol. Dial. Transplant. Mar 2000; 15: 17 - 24. 3. M Ogino, S Namie, Y Ozono, M Miyazaki, T Harada, and S Kohno. Expression of VLA-4 on peripheral mononuclear cells in patients on chronic haemodialysis with carpal tunnel syndrome. Nephrol. Dial. Transplant., Dec 1998; 13: 3126 - 3131. 4. I. Okutsu, I. Hamanaka, S. Ninomiya, Y. Takatori, K. Shimizu, and Y. Ugawa. Results of endoscopic management of carpal-tunnel syndrome in longterm haemodialysis versus idiopathic patients. Nephrol. Dial. Transplant. 1993; 8: 1110 - 1114. Competing interests: None declared |
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Stephen Longworth, GP Principal and Hospital Practitioner in Orthopaedics The East Leicester Medical Practice, 131 Uppingham Road, Leicester, LE5 4BP, UK
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As a GP with a special interest in Musculoskeletal Medicine I would like to make the following observatons about Jeremy Bland's review of carpal tunnel syndrome (CTS). In General Practice I see many cases with classical/typical clinical features and diagnosis is straightforward. In cases of diagnostic doubt the first step is a thorough history and clinical examination which may realistically mean bringing the patient back for a longer appointment. If the diagnosis is doubtful, then before organising nerve conduction studies (NCS) it makes sense (given the logistics of arranging NCS as a UK GP) to arrange screening blood tests for the common causes of neuropathy (diabetes, thyroid disease, B12 and folate deficiency, hypercalcaemia, alcohol excess) and a test such as ESR/CRP (plus a FBC?) as a pointer to other rarer causes. Bland says that milder cases may be treated with local steroid injection before further investigation and points out that The American Academy of Neurology guidelines suggest NCS and therapeutic trials of non-invasive treatments (the only evidence based one being splinting) as the strategies of choice when clinical diagnosis is uncertain. Injecting steroid into the carpal tunnel is useful diagnostically as well as being a therapy that is easy to administer in Primary Care. If symptoms and signs disappear after a CTS injection then it was probably CTS. Given the less than impressive specificity and sensitivity of NCS in correctly diagnosing CTS and that Bland reports the risk of median nerve damage from injection as <0.1% in competent hands then it can be argued that a trial of injection is a reasonable strategy in cases of diagnostic uncertainty. My current management strategy in this situation is to take blood tests and then offer the patient a choice of NCS (waiting time of weeks to months and not 100% reliable) or immediate diagnostic/therapeutic injection (very low probabilty of causing any harm) and let them decide. I suspect that no response to a CTS inection points strongly away from the diagnosis and this is an issue that might be easily explored in a prospective trial. Bland rightly points out some of the unknowns surrounding injection therapy for CTS (long term outcomes, frequency and timing of injections). Further unknowns include which steroid, what dosage and volume, which injection technique, the best injection site (radial or ulnar side of the median nerve), post-injection advice (e.g. rest afterwards, and if so for how long) and the benefit of adding other treatments (exercises, splints, oral NSAIDs etc). A real life dilemma in UK General Practice surrounds the management of patients who are waiting for a surgical appointment for their CTS. Should you inject them to give them symptom relief while they are waiting to be seen and risk them being discharged from their first outpatient appointment because there is nothing to be treated, or should you ask them to soldier on with their symptoms so that they have something to show the surgeon? Again, my strategy is to explain the dilemma to the patient and let them choose. Competing interests: Co-author of a textbook on joint and soft tissue injection techniques |
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Jeremy D P Bland, Consultant Neurophysiologist Kent and Canterbury Hospital, Canterbury CT2 9BB
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I would like to thank all the correspondents for taking the trouble to engage in discussion. Drs Sambandan and Mahaffey both argue for the pre -eminence of ‘clinical diagnosis’. It is frequently stated that ‘Carpal tunnel syndrome is a clinical diagnosis’ often as an article of faith. I think that this statement now deserves a rather more critical analysis. If all we mean by this phrase is that the entity we are describing is absolutely defined by the coincidence of a cluster of symptoms and signs then it allows us to assign a name to a group of patients in a manner which cannot be argued with, though even then I would point out that there is not universal agreement on exactly what symptoms and signs constitute the syndrome nor how many of them must be present, though there have been suggestions such as those by Rempel et al.(1) Unfortunately, using a diagnosis defined in this way does not lead to a logical approach to treatment because implicit in this use of ‘syndrome’ is the possibility that there may be several different underlying pathologies producing the same clinical picture. This definition only leads one to the following question – now I have a patient with carpal tunnel syndrome, what is causing it? This approach also underlies Dr Breck McKay’s assertion that in ‘many’ patients the symptoms are actually due to a problem with the scalene muscles adjacent to the C5/6/7 spinous processes. Given the wealth of experimental and clinical evidence that raised tissue pressure within the carpal tunnel produces functional, and ultimately pathological, change in the median nerve and results in this symptom complex I would argue, and I think Dr Sambandan at least would agree, that the term CTS should be restricted to those cases in which the pathophysiology lies in the carpal tunnel and that other causes of hand symptoms should have their own, explicit, diagnoses… such as Dr Selmonosky’s thoracic outlet syndrome (which I should perhaps have included in my list of differential diagnoses, though in my experience it is extremely rare in comparison to CTS). Such an approach, by which we attempt to limit the patient population to which we attach the label ‘CTS’ to those with a problem with the median nerve at the wrist, leads logically to treatment directed at the right place. If we accept that the definition of CTS includes the mechanism of increased carpal tunnel pressure impairing the median nerve then the issue becomes, ‘how can we most accurately identify patients with CTS?’ Dr. Mahaffey believes that except ‘in cases of unusual diagnostic difficulty’ ordinary history taking and physical examination provides enough certainty to embark on a surgical procedure and that laboratory investigation should be dispensed with as the results only interfere with the surgeons judgement. To do this is to wilfully discard a body of information about the patient in front of you which could contribute to diagnosis and prognosis. I am not merely a neurophysiologist. I run a busy carpal tunnel clinic with more than 2600 referrals for suspected CTS over the last three years and I both test and treat patients, though others perform surgery for me when necessary. The nerve conduction (NCS) results, supplement, but do not supplant clinical diagnosis. It remains unproven whether diagnosis of CTS with or without the aid of NCS is more accurate but ‘clinical diagnosis’ in other fields is notoriously inaccurate on post-mortem studies. I see no clear evidence that it is any more accurate in hand surgery and I am not encouraged by the number of patients I see who have been subjected to surgical carpal tunnel decompression with either no benefit or even to the detriment of their symptoms. Dr Mahaffey would be on safer ground in advocating surgery as the definitive treatment if surgery were 100% effective and if there was not a significant natural remission rate for the untreated syndrome. Profligate surgery at £916.45 per operation (NHS tariff) is much more likely to bankrupt the NHS than splinting at £3.70! I would however agree with him on one point, nerve conduction studies do need to be readily accessible if they are to be used and our local policy is that they should be performed within two weeks of general practitioner referral in order not to delay treatment. It is not necessary to record at night however. NCS do not measure the symptoms of CTS but rather a structural change in the median nerve which happens to be fairly well, but not perfectly, correlated with the presence of the syndrome. The focal demyelination which primarily produces conduction slowing persists night and day. Dr Kuijer takes issue with my reading of the tiresomely extensive literature regarding occupational causation of CTS, pointing out that CTS is recognised as an occupational disease in the Netherlands. This is also the case in the USA, but not generally in the UK. I have read over 500 of these papers and like authors who have attempted systematic reviews of this literature, (2-4) my predominant conclusion is that they tend to be of poor quality, frequently depending on inadequate diagnostic methods, failing to take account of non-occupational risk factors, and being biased by selective patient recruitment, follow up and compensation incentives. In the recent study by Melchior et al, to which Dr Kuijer refers, the diagnostic criteria for CTS used for the analysis are extremely vague. We are not told whether the analysis was performed for current diagnoses at the time of examination or for past diagnoses reported by the patient, both of which were sought in the protocol, and no NCS confirmation was used. The physicians making these diagnoses were not blind to the patient’s occupation and may well have been biased towards making the diagnosis of CTS where they expected to find it. The statistical methods used in this paper were so complex that the authors were unable to quote confidence limits for their estimate that 96% of the excess risk of CTS could be attributed to physical work factors and curiously this figure was higher for women than for men. Why should there be a sex difference? There was not space in my article to comprehensively review and reference this vexatious subject and my wording was carefully chosen. I would point out however that the majority of CTS cases I see have their onset in the non- employed population and, unless one posits a very delayed effect of work, the majority of CTS is clearly not an occupational disease. Dr Jha points out that there is a high incidence of CTS in patients on long-term renal dialysis. There is an extensive literature on this subject dating back at least to 1975,(5) and at first it was thought that having an arteriovenous shunt in situ might predispose to CTS. It has subsequently become apparent however that this is not the case and dialysis CTS is somehow connected with the process of haemodialysis itself. It may be more common with some dialysis membranes than others (6) and is indeed related to deposition of beta2 microglobulin in the carpal tunnel. It is notable for being one of the few forms of CTS in which recurrence after successful surgical decompression is relatively common (7) but overall, dialysis associated CTS constitutes only a very tiny majority of all cases. 1. Rempel D, Evanoff B, Amadio PC, de Krom M, Franklin G, Franzblau A, et al. Consensus criteria for the classification of carpal tunnel syndrome in epidemiologic studies. Am J Public Health 1998;88(10):1447- 1451. 2. Vender MI, Kasdan ML, Truppa KL. Upper extremity disorders: a literature review to determine work-rleatedness. J Hand Surg 1995;20A:534- 541. 3. Louis DS, Calkins ER, Harris PG. Carpal tunnel syndrome in the workplace. Hand Clinics 1996;12(2):305-308. 4. Stock SR. Workplace ergonomic factors and the development of musculoskeletal disorders of the neck and upper limbs: a meta-analysis. Am J Ind Med 1991;19(1):87-107. 5. Kumar S, Trivedi HL, Smith EKM. Carpal tunnel syndrome: a complication of arteriovenous fistula in haemodialysis patients. Can Med Assoc J 1975;113:1070-1072. 6. Aoike I. Long-term clinical experience with PMMA membrane. Contrib Nephrol 1999;125:205-212. 7. Hirasawa Y, Ogura T. Carpal tunnel syndrome in patients on long-term haemodialysis. Scand J Plast Reconstr Surg Hand Surg 2000;34(4):373-381. Competing interests: None declared |
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NAZAR R DESSOUKI, CONSULTANT SURGEON ST BERNARDS HOSPITAL GIBRALTAR
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Some people might think that carpal tunnel syndrome is a new condition of the information technology age, born from long hours of computer keyboarding. But carpal tunnel syndrome isn't new. Evidence of people experiencing signs and symptoms of carpal tunnel syndrome occurs in medical records dating back to the beginning of the 20th century. Bounded by bones and ligaments, the carpal tunnel is a narrow passageway — about as big as the thumb — located on the palm side of your wrist. This tunnel protects the median nerve and nine flexor tendons. Pressure placed on the nerve produces the numbness, pain and, eventually, hand weakness that characterize carpal tunnel syndrome. Fortunately, for most people who develop carpal tunnel syndrome, proper treatment usually can relieve the pain and numbness and restore normal use of the wrists and hands. Competing interests: None declared |
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Jeremy D P Bland, Consultant Neurophysiologist Kent and Canterbury Hospital CT1 3NG
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Dr Longworth has some interesting observations on management of CTS in primary care and I would like to reply to a few of them. He is quite correct that the diagnosis may be strongly suspected on clinical grounds but I am not sure about his list of screening investigations unless there are also clinical pointers to the presence of more widespread neuropathy. Even the association with thyroid disease, which appears in every textbook, turns out to be not as well founded in hard evidence as one might expect when examined critically.(1) I think there is room for a well conducted study of the cost/benefit ratio of such screening blood tests in patients with apparently idiopathic CTS and no clinical evidence of other disease. I agree absolutely about the diagnostic and therapeutic utility of steroid injection and faced with a long wait for NCS I too would offer injection. In my own local circumstances however we have long allowed GP direct referral for NCS and we try to keep the wait to 2 weeks. I still feel that it is quite acceptable to inject patients without performing nerve conduction studies but as I am studying the relationship of steroid responsiveness to NCS findings we find it convenient here to perform NCS in all cases. There is one comparative trial of different steroids which concluded there was little difference in effect(2) but there is also experimental evidence that some steroid preparations may be more neurotoxic than others on accidental intraneural injection.(3) At present I do not think there is sufficient evidence to formally recommend one preparation over another, nor to specify other details of technique, though it is notable that in Dammers study,(4) an injection performed several centimetres proximally in the forearm was effective. Both Dr Longworth and Dr Mahaffey seem to have the idea that I recommended NCS in all cases, which is not in fact what I said. I do feel that NCS should be performed before surgery, the incidence of ‘failed carpal tunnel decompression’ being quite significant and analysis of what has gone wrong afterwards being greatly facilitated by the availability of pre-operative NCS. I would suggest that, in a patient faced with a significant wait for both surgery and NCS and suffering from severe symptoms one should arrange all three – injection, NCS and a surgical appointment. If the symptoms then respond very well to injection, subsequent appointments can be cancelled and the patient has then been spared a modestly risky surgical procedure. 1. Bland JDP. Use of screening blood tests in patients with carpal tunnel syndrome. J Neurol Neurosurg Psych 2007;78:551. 2. O'Gradaigh D, Merry P. Corticosteroid injection for the treatment of carpal tunnel syndrome. Ann Rheum Dis 2000;59(11):918-919. 3. Mackinnon SE, Hudson AR, Gentili F, Kline DG, Hunter D. Peripheral nerve injection injury with steroid agents. Plast Reconstr Surg 1982;69:482-489. 4. Dammers JWHH, Veering MM, Vermeulen M. Injection with methylprednisolone proximal to the carpal tunnel: randomised double blind trial. Brit Med J 1999;319:884-886. Competing interests: None declared |
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Sidha Sambandan, GpwSI / H.Sen Lecturer Yare Valley Medical Practice,202 Thorpe Rd,Norwich NR1 1TJ
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I thank the author for his clarifications and comments. It is paramount to be mindful that "NCS supplements and does not supplant clinical diagnosis," as the author himself agrees. Due to the current waiting times in England, I would inject even those who do not have hard neurological signs. Those patients with a short history, intermittent symptoms that are not progressive, without hard neurological signs may have long remissions of their symptoms with a steroid and lidocaine injection. While those with long history and hard neurological signs will be referred at the same time for decompression, as they do not respond well to steroids. Diabetes is another predictor of poorer outcomes with conservative or surgical methods of treatment. Most of the patients presenting with CTS and thyroid disease in my experience have already been on thyroxine therapy for a long time. In UK, in order to do NCS, we have to refer to the neurologist first, (a further wait of about 10-12 weeks) and while some would do a NCS at the visit, others will then refer to a neurophysiologist. The latter will not take direct referral from GPs! Competing interests: None declared |
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Jeremy D P Bland, Consultant Neurophysiologist Kent and Canterbury Hospital CT2 9BB
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Dr Sambandan is unfortunate in practicing in an area of the UK where access to nerve conduction studies is clearly very poor. I would like to point out that, following considerable investment as part of the 18 week referral to treatment target, the majority of neurophysiology departments in the UK have dramatically reduced waiting times for NCS for CTS and many accept direct GP referrals. The Norwich sitautation should not be generalised to 'the UK'. Jeremy Bland Competing interests: None declared |
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John P Rine, GPwSI Surgery including Carpal Tunnel Surgery Herne Bay
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Management of CTS in General Practice is not confined to splints and injections. I am a GP with a Special Interest in Surgery including performing Carpal Tunnel Decompression on a regular basis. Indeed, I receive referrals for surgical decompression from Dr Bland. An increasing proportion of patients referred for surgery in this scheme are treated in a community setting, which patients find convenient with less waiting time than was previously the case. For those of you who are concerned about the cost of NCS, surgery in this setting is also extremely cost efficient. It is the case that patients have NCS as part of their management, but all are in addition assessed clinically prior to any intervention. Having decompressed over 300 patients referred by Dr Bland in the past three years, I would say the correlation between the NCS results and the clinical picture is very good indeed. There are exceptions but these are few. Decisions about surgery are made taking all factors into consideration including past history,current history, current symptoms, past symptoms, response to injections or splinting, other risk factors, clinical examination and recent NCS results. As an operator I am reassured by having a baseline NCS. As Dr Bland points out this becomes very useful when a possible failure is being queried. Repeat NCS has helped to separate out those few geniune failures due to incomplete decompression, from those for example, who are undergoing a slow recovery phase. It also assists in informing the patient about expectations, as the result does have prognostic significance. Competing interests: I am contracted by the PCT to operate on cases including CTD. |
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Ibrahim,M. Khan, Orthopedic hand surgeon P.O.Box 7566, Beverly Hills-CA 90212
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In his clinical review on carpal tunnel syndrome(CTS),Bland ( BMJ 2007,335:343-346) would have us believe that CTS as a compressive neuropathy is an open & shut case.But I would argue that it's any thing but open& shut.Because compression theorem is built on sand riddled with holes.It is built on sand because the thinking behind compressive neuropathy is that isolated compatmental syndrome can occur in carpal tunnel.Which is infact a psuedologica fantastica because carpal tunnel is not a closed space.And closed space is a prerequisite for compatmental syndrome.Now,as I walk the readers of BMJ through the so called " evidence " the gapping holes will be self evident. For starters,the conclusion of 1981 study (1) dubbed the" bible of carpal canal pressures ", " It must be concluded that factors other than increases in pressure in the carpal tunnel play a significant role in the causation of signs & symptoms of this condition".Does this sound like open & shut? I don't think so.In the same article we are also told that vascular insufficiency rather than morphological changes within the nerve is the primary abnormality in the carpal tunnel syndrome.If that was true, one would expect a strong co-relation with smoking.But in a large study of risk factors for CTS (2),there is no such co-relation,driving another nail in the coffin of CTS as a compressive neuropathy. In science,we seek naturalistic explanations for our observations which is exacly why the natural history of diseases is so crucial in medicine. CTS as a compressive neuropathy not only can not square with the natural history of CTS but is diametrically opposed to it & this repudiation of the natural history of CTS is exactly what makes compression theorem counterfactual.Ignorance of the natural history of CTS is exactly why Bland is so lopsidedly pro remission.To top it all off,if increased pressure in the tunnel were the problem, decompression could have worked.But since decompression is not working (3),increased pressure in the carpal tunnel can not be the cause of idiopathic CTS. Compression group think obsession with CTS as a compressive neuropathy has led us up a blind alley when trying to explain the etiology,the histopathology,& the natural history of CTS,which is exactly what has brought on CTS"Trilemma"--a three horned dilemma 0f Idiopathy, Disingenuous histopathology, & Unaccounted natural history.Therefore,to rid the CTS of its trilemma, we have no choice but to kick our century old addiction to the fantasy of compression & avail ourselves the opportunity to my Universal theory (4)( based on median neurodesis to flexor pollicis longus sheath in the proximal carpal tunnel) which can & does solve the trilemma of CTS. References: (1)Gelberman,R.H;Hergenroeder,P.T;Hargens,A.R;Lundborg,G.N;Akeson,W.H: The Carpal Tunnel Syndrome. A study of carpal canal pressures. JBJS 63A # 3 pp 380-383. (2)Geoghegan,J.M;Clark,D.I;Bainbridge,L.C;Smith,C;Hubbard,R:Risk factors in carpal tunnel syndrome.J Hand Surg 29B #4,315-320. (3)Work-Related Upper Extremity problems at work place.How much do we know? US Department of health & human servuces.Agency for health care quality & research. AHRQ publication 2002. (4)Khan.M.I: Work-Related Arm Pain ( WRAP ).In proceedings of the 9th congress of IFSSH,2004. Sincerely,
Competing interests: None declared |
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