1. Barfred, T., Ipsen, T., “Congential 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.
2. Behse, F., Buchthal, F., Carlson, F., Knappeis, G.G., “Hereditary neuropathy with liability to pressure palsies.” Brain, 1972; 95:777-794.
Genetic tendencies to have symptoms of nerve entrapment at multiple nerves. A rare condition localizable ton chromosome analyze.
3. Cruz-Martinez, A., Conde, C. P., Cajal, S.R.Y., Martinez, A., “Recurrent familial polyneuropathy with liability to pressure palsies. Special regard to electrophysiological aspects of twenty five members from seven families.” Electromyogr Clin Neurophysiol, 1977; 17:101-124.
4. Danta, G. “Familial carpal tunnel syndrome with onset in childhood.” J 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.
5. Earl, C.J., Fullerton, P.M., Wakefield, G.S., Schutta, H.S., “Hereditary neuropathy with liability to pressure palsies.” Quarterly J of Med, 1964; 33:132:481-498.
Very limited value.
6. 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 Rheumatol, 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. Must Read
7. Florack, T.M., Miller, R.J., Pellegrini, V.D., Burton, R.I., Dunn, M.G., “The prevalence of carpal tunnel syndrome in patients with basal joint arthritis of the thumb.” JHS, 1992; 17A: 624-630.
Review of literature and study of their own patients reveals greater than 50% incidence of CTS in association with basilar thumb arthritis.
8. Gelmers, H.J. “Primary carpal tunnel stenosis as a cause of entrapment of the median nerve.” AN, 1981; 55: 317-320.
Another report demonstrating the frequently overlooked familialism of CTS.
9. Gibson, C.T., Manske, P.R., “Carpal tunnel syndrome in the adolescent.” JHS, 1987; 12A: 279-281.
10. Gordon, C., Johnson, E.W., Gatens, P.F., Ashton, J.J., “Wrist ratio correlation with carpal tunnel syndrome in industry.” Am J of Phys Medicine and Rehabil, 1988; 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.
11. Gossett, J.G., Chance, P.F., “Is there a familial carpal tunnel syndrome? An evaluation and literature review.” Muscle & Nerve, 1998; 21: 1533-1536.
They reviewed the reports of families proposed to have the familial carpal tunnel syndrome (FCTS). The demographic features of sporadic carpal tunnel syndrome (CTS) differ from FCTS, where an earlier onset and increased bilateral involvement is seen. They also identify seven new potential FCTS pedigrees on the basis of their having four or more members with symptoms suggesting CTS. In all but two pedigrees an explanation other than FCTS was felt to be present. They conclude that the FCTS is a rare, but genetically distinct disorder.
12. Gray, R.G., Poppo, M.J., Gottlieb, N.L., “Primary familial bilateral carpal tunnel syndrome.” Annals of Intern Med, 1979; 91:37-40.
Ties together many of the concepts of high bilaterality of CTS and strong genetic predisposition. Suggests this is specific subgroup of patients with CTS.
13. Lagos, J.C., “Compression neuropathy in childhood.” Dev Med and Child Neurol, 1971; 13:4:531-532.
Lettin, A.W., “Carpal tunnel syndrome in childhood.” Proceedings of the Royal Society of Medicine, 1966; 59:8:705.
14. McArthur, R.G., Hayles, A.B., Gomez, M.R., Blanco, A.J., “Carpal tunnel syndrome and trigger finger in childhood.” Am J Dis Child, 1969’; 117:463-469.
15. 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.
16. Pareyson, D., et al, “Detection of hereditary neuropathy with liability to pressure palsies among patients with acute painless monneuropathy or plexopathy.” Muscle & Nerve, 1998; 21:1686-1691.
17. 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.
18. Roos, D., Thygesen, P., “Familial recurrent polyneuropathy.” Brain, 1972; 95:235 248.
19. Rosen, S.A., Wang, H., Cornblath, D.R., Uematsu, S., Hurko, O., “Compression syndromes due to hypertrophic nerve roots in hereditary motor sensory neuropathy type 1.” Neurology, 1989; 39:1173-1177.
20. Staal, A., de Weerdt, C.J., Went, L.N., “Hereditary compression syndrome of peripheral nerves.” Neurology, 1008-1017.
21. Stoll, C., Maitrot, D., “Autosomal dominant carpal tunnel syndrome.” Clin Genet, 1998; 54: 345-348.
A family with autosomal dominant heritage of carpal tunnel syndrome was identified unassociated with systemic disease. Careful literature review was discussed regarding presentation of familial carpal tunnel syndrome. The family herein demonstrated an interesting pattern of inheritance with earlier onset of symptoms in subsequent generations, but this trend was also identified in 4 other published reports that were also reviewed. They queried that further analyses would be needed to determine whether the severity of the disease can be shown to increase in subsequent generations. Must read for those believing in cumulative trauma!
22. Vallat, J.M., Dunoyer, J. “Familial occurrence of entrapment neuropathies.” Letters to the Editor, Acta Neurol, 1979; 36:323.
23. Werner, C.O., Elmqvist, D., Ohlin, P., “Pressure and nerve lesion in the carpal tunnel.” Acta Orthop Scand, 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. 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 stimulation was done galvanic stimulation 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.
24. Wilson, K.M., Buehler, M.J., “Bilateral carpal tunnel syndrome in a normal child.” JHS, 1985; 10A: 246-248.
Nothing new, just a child with bilateral CTS. No way to blame CTS on work!
25. Windebank, A.J., “Inherited recurrent focal neuropathies.” Diseases of the Peripheral Nervous System, 70:1656-1679.