1. Atroshi, I., Gummesson, C., Johnson, R., Ornstein, E., Ranstam, J., Rosen, I. “Prevalence of carpal tunnel syndrome in a general population.” JAMA, 1999; 282:153.
Refutes the misguided concept of CTS as an infrequent problem, but rather suggests it occurs in about 1 out of 5 or 6 adults.
2. Barfred, T. and Ispen, T. “Congenital carpal tunnel syndrome.” JHS, 1985; 10A: 246-248.
Report on a series of young people presenting with CTS with no reason to blame repetitive motion/cumulative trauma etc.
3. Bleecker, M.L. “Medical surveillance for carpal tunnel syndrome in workers.” JHS, 1987; 12A: 845-848.
4. Caruso, G., Labianca, O., Ferrannini, E., “Effect of ischaemia on sensory potentials of normal subjects of different ages.” J Neurol, Neurosurg, & Psych, 1973; 36:455-466.
Shows the effects of nerve ischemia on NCS testing and then helps to substantiate that pressure upon a nerve cause symptoms by reducing circulation to the nerve. This ties in closely with research on compartment syndrome and research on experimental pressure elevation (Gelberman et al).
5. Casanova, J.E., Casanova, J.S., Young, M.J., “Hand function in patients with diabetes mellitus.” Southern Medical Journal, 1991; 84:9:1111-1113.
Points out the high incidence of multiple hand problems in people afflicted with diabetes. CTS occurs more commonly in diabetics.
6. Cobb, T.K., An, K., Cooney, W.P. “Externally applied forces to the palm increase carpal tunnel pressure.” JHS, 1995; 20A: 181-185.
Simple study creates a question as to whether tasks/jobs increasing external pressures on one’s palm might lead to increased chance of development of CTS. Provides food for thought only. Ties in with Durkan study. May be the foundation for future research.
7. Cobb, T.K., Dalley, B.K., Posteraro, R.H., and Lewis, R.L. “Establishment of carpal contents/canal ratio by means of magnetic resonance imaging.” JHS, 1992; 17A: 843-849.
Nice, simple study helping to establish that radiologic, non invasive studies may accurately predict the available space in the carpal tunnel that might allow predication of the person susceptible to developing it. Precursor to studies showing smaller carpal tunnel volume in those with CTS compared with normals.
8. Danta, G. “Familial carpal tunnel syndrome with onset in childhood.” Journal of Neurology, Neurosurgery and Psychiatry, 1975; 38: 350-355.
Suggests a specific pattern of CTS presentation in a large family tree with multiple members diagnosed with CTS.
9. Dekel, Papaioannou, T., Rushworth, G., Coates, R. “Idiopathic carpal tunnel syndrome caused by carpal stenosis.” British Medical Journal, 1983; 1297.
Ties in nicely with #7 above and #13 below. The authors involved in this hysteria about “cumulative trauma”.
10. Eakins, D., Kuzma, G., Siegel, D. “The significance of lumbrical muscles in carpal tunnel syndrome. (An anatomic investigation with clinical correlation.) AAOS poster exhibit, Bowman Gray School of Medicine, Winston-Salem, NC.
Reveals variable size and position of the lumbrical muscles and the possibility that this results in increased CT pressure.
11. Ferry, S., Pritchard, T., Keenan, J., Croft, P., Silman, A.J. “Estimating the prevalence of delayed median nerve conduction in the general population.” British Journal of Rheum, 1998; 37:630-635.
High incidence of CTS (15-20% of adults) using good techniques refutes the nonsense about CTS occurring in ~1:1000 as suggested by ignoramuses for years.
12. Fuchs, P.C., Nathan, P.A., Myers, L.D. “Synovial histology in carpal tunnel syndrome.” JHS, 1991; 16A: 753-758.
This is large series of CTS patients taken to surgery where tendon lining (synovium) was sent to pathology for evaluation. It confirms absence of inflammation in development of CTS in all but a tiny rheumatid subset of CTS patients. Hence, the lack of benefit anticipated from use of NSAIDs for CTS.
13. Gamstedt, A., Holm-Glad, J., Ohlson, C.G., Sundstrom, M., “Hand abnormalities are strongly associated with the duration of diabetes mellitus.” J of Internal Medicine, 1993; 234:189-193.
Ties into the well documented increase in all sorts of systemic pathologies in long standing diabetics. See also Casanova et al (above).
14. 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, 1981; 63A: 380-383. *** Must Read
Classic. This timely article from the Orthopaedic Department of UC San Diego, was the first objective verification that there is in fact elevated pressure in the carpal tunnel of patients with carpal tunnel syndrome and it helped to define wrist positions that might affect that pressure. They applied their pressure measurement techniques to patients with confirmed CTS. (Unfortunately their study population was predominantly men from a VA hospital with a small study population and the age was much older than the average age of patients who typically present for CTS in common clinical practice in the U.S. at this time, i.e. mean of 56 vs. a mean of 42). Nevertheless, they demonstrated that the technique utilized for measurement of compartment pressures in evaluating compartment syndrome (another area that they have made contribution to at UCSD in the past) were applicable to measuring the pressures within the carpal tunnel with a wick catheter. As have almost all studies published by the main author in this article, the “controls” had not been carefully tested with electrodiagnostics to rule out entrapment neuropathy, thus the study laid a foundation in thought without a foundation in fact, making way for another study upon which clinical decision making could be made. The main contribution of this research is in assisting us in understanding that elevated pressure within the carpal tunnel, rather than frequent use of one’s hands, etc., is responsible for precipitating the symptoms of CTS. They did clearly show the symptomatic improvement in the patients after surgery and that the pressures were immediately reduced postoperatively.
15. Gellman, H., Chandler, D., Sie, I., Petrasek, J., Waters, R., “Analysis of carpal tunnel syndrome in paraplegics: Contribution of carpal tunnel pressures.” Presented at American Hand Society meeting, Puerto Rico, 1992; 72.
No less than stellar results after CTR for CTS in paraplegics. No answers identified. Basis for further study. This ties in with Cobb et al, JHS, 1995.
16. Gelmers, H.J., “Primary carpal tunnel stenosis as a cause of entrapment of the median nerve.” Acta Neurochirurgica, 1981; 55: 317-320.
Another report demonstrating the frequently overlooked familial occurrence of CTS.
17. Gilliatt, R.W., Wilson, T.G., “Ischaemic sensory loss in patients with peripheral nerve lesions.” J. Neurol, Neurosurg, and Psychiat, 1954; 17:104:114.
18. Gordon, C., Johnson, E.W., Gatens, P.F., Ashton, J.J. “Wrist ratio correlation with carpal tunnel syndrome in industry.” American Journal Phys Med & Rehabil, 1998; 270-272.
These investigations show that liability to develop CTS is related to carpal canal size which may be predicted by external measurements. This correlates with Cobb et al JHS, 1992.
19. Gray, R.G., Poppo, M.J., Gottlieb, N.L. “Primary familial bilateral carpal tunnel syndrome.” Annals Int Med, 1970; 91:37-40.
Ties together many of the concepts of high bilaterality of CTS and strong genetic predisposition.
19. Kerr, C.D., Sybert, D.S., Albarracin, N.S. “An analysis of the flexor synovium in idiopathic carpal tunnel syndrome: Report of 625 cases.” JHS, 1992; 17A: 1028-1030.
Essentially corroborates the work of Nathan, et al (JHS, 1991), in excluding inflammation as a cause of CTS except in a rare patient. Hence, the lack of benefit from NSAIDs to treat CTS.
20. Luchetti, R., Schoenhuber, R., De Cicco, G., Alfarano, M., Deluca, S., Landi, A. “Carpal tunnel pressure.” Acta Orthop Scand, 1989; 60:4: 397-399.
Corroborated the work of Gelberman (1981) and that of Okutsu (1986).
21. Lundberg, G. and Dahlin, L.B. “The pathophysiology of nerve compression.” Hand Clinics, 1992; 8:2: 215-227.
Helps to understand why carpal tunnel size, carpal tunnel pressure, and relief of CTS symptoms with CTR are interrelated. Ties in closely with Gelberman article JBJS 1981.
22. Lundberg, G., Gelberman, R.H., Minteer-Convery, M., Lee, Y., and Hargens, A.R. “Median nerve compression in the carpal tunnel – functional response to experimentally induced controlled pressure.” JHS, 1982; 7:252-259.
A natural extension of the article by Gelberman, JBJS 1981. Helps to demonstrate the correlation between pressure on a nerve and symptom onset.
23. Masaer, V., “An industrial cause of carpal tunnel syndrome” JHS, 1986; 11A: 222-227.
What the authors really show is very high incidence of CTS in adults. Percentage correlates well with epidemiologic studies (see Atroshi, et al JAMA, 1999, Bingham et al JOM 1996, Ferry et al 1998) (~20%). They would like to you to believe that meat packing industry workers are at higher risk, but they don’t provide any information to support that contention. Only 52% had returned to work at one-year post op revealing the authors difficulty with patients treated under worker’s comp and their poor understanding of CTS pathophysiology.
24. Middleton, W.D., Kneeland, J.B., Kellman, G.M., Cates, J.D., Sanger, J.R., Jesmanowicz, A., Froncisz, W., Hyde, J.S. “MR imaging of the carpal tunnel: Normal anatomy and preliminary findings in the carpal tunnel syndrome.” American Journal of Radiology, 1987; 148:307-316.
Correlates with the work of Cobb et al (JHS, 1992 above).
25. Nathan, P.A., Meadows, K.D., Doyle, L.S. “Relationship of age and sex to sensory conduction of the median nerve at the carpal tunnel and association of slowed conduction with symptoms.” Muscle &Nerve, 1998; 11:1149-1153.
A simple listing of expected changes in NCS that accompanies aging.
26. Okutsu, I., Ninomiya, S., Hamanaka, I., Kuroshima, N., and Inanami H. “Measurement of pressure in the carpal canal before and after endoscopic management of carpal tunnel syndrome.” JBJS, 1989; 71A: 679-683.
Classic. The inventor of endoscopic carpal tunnel release! Corroborates the work of Gelberman, et al, and Gelberman and Lundberg regarding pathophysiology. Sets the stage scientifically for ECTR and the relief afforded by ECTR.
27. Osterman, A.L., “The double crush syndrome.” OCNA, 1988; 19:1:147-155.
Dr. Osterman in this timely, well thought out study, though retrospective pointed out the high frequency of multiple nerve entrapment problems within the same patient and the possibility of overlap of these problems. He queried that this was related to multi-level entrapment of the nerves throughout its course, i.e. from neck, brachial plexus, and down to more localized spots that carpal or cubital tunnel respectively. This data clearly shows better response to nerve decompression at the carpal tunnel in patients with isolated carpal tunnel syndrome, then those with multiple involvement such as cervical spondylosis with carpal tunnel syndrome, etc. These findings are consistent with what we see in the day-to-day treatment of patients who present with these problems. The more difficult one is having multiple comorbidities frequently related the nervous or musculoskeletal systems. No attempt was made to confirm or prove actual multiple level involvement of a particular nerve root.
28. Papaioannou, T., Rushworth, G., Atar, D., Dekel, S. “Carpal canal stenosis in men with idiopathic carpal tunnel syndrome. JBJS, 1971; 53A: 160.
Suggests that developmental (genetic) narrowness of the carpal tunnel is responsible for the symptoms.
29. Radecki, P., “The familial occurrence of carpal tunnel syndrome.” Muscle & Nerve, 1994; 17:325-330.
A prospective study was undertaken to determine the prevalence and significance of a positive family history of CTS. 75 of 253 women and 40 of 168 men with a confirmed diagnosis of CTS indicating that at least one relative had symptoms of or surgery for CTS. They determined that obtaining a positive family history for CTS was predictive of a median abnormality or prior surgery at the carpal tunnel. Of the 84 patients who had undergone carpal tunnel surgery, those who were felt to be the most well informed historically had a positive family history in 39%, compared with 13.3% of the 279 patients who did not demonstrate median latency slowing. Thus Dr. Radecki concluded that familial occurrence appears crucial in the epidemiological study of carpal tunnel syndrome and may be important in the selection of normal subjects for electrodiagnostic standards. He is suggesting that we must make certain that we are setting our standards correctly by not including those who are developing CTS in studying the values.
30. Rojviroj, S., Sirichativeapee, W., Kowsuwon, W., Wongwiattananon, J., Tamnathong, N., Jeeravipoolvarn, P., “Pressures in the carpal tunnel: A comparison between patients with carpal tunnel syndrome and normal subjects.” JBJS, British, 1990; 70: 516-8.
Corroborates the work of Gelberman et al JBJS 1981 with wrist position related changes in CT pressures.
31. Rosenbaum, R.B., Ochoa, J.L., Carpal tunnel syndrome and other disorders of the median nerve. Butterworth-Heinemann, MA, 1993.
This timely text is the most comprehensive source on carpal tunnel syndrome in print today. There is a lot left to be updated in terms of the actual genetic relationship to the development of carpal tunnel syndrome and the clinical management of the problem. Its greatest strong point is the explanation of the pathophysiology of nerve compression and the utilization of electrodiagnostic testing for it. Dr. Ochoa has been studying has been studying abnormalities of peripheral nerves for many years and his findings are the basis for a good deal of our understanding.
32. Rydivik, B., Lundberg, G., Bagge, U. “Effects of graded compression on intraneural blood flow.” JHS, 1981; 3-12.
Ties in closely with Gelberman, et al JBJS 1981 and Lundberg et al JHS 1982. Increased pressure on nerve leads to reduced blood pressure and abnormal nerve conduction. This helps to confirm that pressure, not occupational overload, is the cause of CTS.
33. Schottland, J.S., Kirschberg, G.J., Fillingim, R., Davis, V.P., Hogg, F. “Median nerve latencies in poultry processing workers: An approach to resolving the role of industrial “Cumulative trauma” in the development of carpal tunnel syndrome.” JOM, 1991; 33:5: 627.
Very limited value. Poorly performed NCS limits conclusions rom this study. This is a plea to thoroughly exam and critically analyze patients with hand symptoms alleged from their jobs.
34. Szabo, R.M., Gelberman, R.H., Williamson, R.V., Hargens A.R. “Effects of increased systemic blood pressure on the tissue fluid pressure threshold of peripheral nerve.” J Orthop Res, 1983; 1:172-178.
Basis for more research which has not been done regarding the effects of BP lowering, i.e. anti-hypertensive, med treatment on the development of CTS.
35. Sugimoto, H., Miuaji, N., Ohsawa, T., “Carpal tunnel syndrome: Evaluation of median nerve circulation with dynamic contrast-enhanced MR imaging.” Radiology, 1994; 1:2:459-466.
Suggests a technique albeit costly and indirect, is available that reflects circulation embarrassment in the median nerve in those with CTS.
36. Sunderland, S., “The nerve lesion in the carpal tunnel syndrome.” J of Neurol, Neurosurg, and Psychiat, 1976; 39:615-626.
Historical value from one of the most knowledgeable on peripheral nerve lesions.
37. Werner, C.O., Elmquist, D., Ohlin, P. “Pressure and nerve lesion in the carpal tunnel. Acta Orthop Scan, 1983; 54:312-316.
In this classic, elegantly performed study Dr. Werner, et al confirmed the elevated resting pressure in the carpal tunnel in patients with CTS previously demonstrated by Gelberman et al JBJS 1981. He went on to demonstrate the massive increase in pressure in the carpal tunnel upon forcible muscle contraction by using galvanic stimulation in patients under general anesthesia with carpal tunnel syndrome. The study was very nicely set up. Though the group of patients is limited and the muscle contraction was artificially induced as opposed to voluntary contraction there was a definite correlation in the small group of patients study (16) for linear association between prolongation of the sensory latency and elevation in carpal tunnel pressure. This study helps to explain the possibility of carpal tunnel symptom exacerbation by physical activity involving a lot of grasping and/or wrist motion. It does not, however, in any way confirm the association between activity and the development of carpal tunnel syndrome. For example, the patients studied here all averaged 46-year-old, 15 of the 16 studied were women, which is a classic group to develop CTS in the first place.
39. Werner, R.A., Albers, J.W., Franzblau, A., Armstrong, T.J., “The relationship between body mass index and the diagnosis of carpal tunnel syndrome.” Muscle & Nerve, 1994; 17:632-636.
Suggests a very high incidence of obesity in patients seen with CTS. Does not, however, help to make connections for the inadequacy/fallacy of the method used to determine “obesity” in the first place. Fails to account for the small CT volume and genetics and sex noted in prior, more enlightened research.
40. Willis, C.B., Alderman, A., Louis, D.S. “Anatomic anomalies and carpal tunnel syndrome: A review.” Tech Hand &Upper Extremity Surg, 1999; 3:2: 99-103.
A large variety of anomalies that may or may not have contributed to development of CTS were noted at the time of CTR. It’s noteworthy that the anomalies he cited are quite rare.
41. Yu, J., Bendler, E.M., Mentari, A., “Neurological disorders associated with carpal tunnel syndrome.” Electromyogr Clin Neurophysiol, 1979; 19:27-32.
Points out the frequency other neurologic disorders are present in a person with CTS. It does nothing to separate out cause and effect