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Pathology of the flexor tendon sheath in the spontaneous carpal tunnel syndrome
PATHOLOGY OF THE THE SPONTANEOUS
FLEXOR CARPAL
TENDON TUNNEL
SHEATH SYNDROME
IN
N. C. NEAL, J. McMANNERS and G. A. STIRLING From the North Staffordshire Medical Centre, Stoke-On-Trent
The histological features of the flexor tendon sheath in the spontaneous carpal tunnel syndrome were studied. The main differences between our findings and previous studies were twofold. Firstly a striking absence of inflammation in our material and secondly the diversity of the pathological changes encountered - alterations in the connective tissue especially the collagen; proliferation with thickening of the tissues of the tendon sheath; fibrosis; amyloid deposition; oedema; vascular lesions including thickening of vessels walls, intimal hyperplasia, and thrombosis; and a foreign body giant cell reaction. Although the lesions described here may not be significant in every case in which they are encountered, they do appear to support the view that pressure in the carpal tunnel and ischaemia are the important factors in a majority of cases of the spontaneous carpal tunnel syndrome. The carpal tunnel syndrome, consisting of pain and parasthesiae in the region of the palm and radial digits, is due to compression of the median nerve under the flexor retinaculum. Compression may be produced by a variety of factors including fractures, trauma, acromegaly, an anomalous artery accompanying the nerve, and abnormal insertions of the muscles (Vainio, 1957). The role of tenosynovitis as a cause of the syndrome has been emphasised by several authors (Nissan, 1952; McKee, 1953; Lipscomb, 1959; Hybbinette and Mannerfelt, 1975) and the importance of rheumatoid arthritis in this connection has been stressed (Michaelis, 1950; Vainio, 1957; Hybbinette and Mannerfelt, 1975). In addition to these, there are many cases where the cause of the compression is obscure and referred to as ‘spontaneous’. Histopathology reports on the synovial membrane in the spontaneous carpal tunnel syndrome usually reveal little, according to Phalen (1951). Since then, three reports listing microscopic findings have appeared (Lipscomb, 1959; Wilhelm, 1982; Faithfull, Hybbinette and Mannerfelt, 1975; Faithfull, Moir and Ireland, 1986). These differ in many particulars from our findings. This, and the absence of a comprehensive histological study in the spontaneous carpal tunnel syndrome, have prompted us to report the histopathological findings in 45 consecutive cases. Methods and Materials Patients from orthopaedic waiting lists for carpal tunnel release were reassessed clinically. The series comprised 45 consecutive patients aged 18 to 82 years, of which 30 were women and 15 were men. Numbers in each decade are shown in Table 1. Collagen disease was excluded by physical examination, erythrocyte sedimentation rate estimation and the latex agglutination test. All the operations were carried out under local anaesthetic. At Received for publication 14th January, Dr. G. A. Stirling, North Staffordshire
VOL. 12-B No. 2 JUNE
1987
1987. Medical Centre,
Stoke-On-Trent,
Staffs.
SP4 7LN.
operation, bony, vascular and muscle abnormalities in the carpal tunnel and its contents were excluded. Tissue was removed from the flexor tendon sheath, placed on cardboard and teased out flat before immersion in 10 per cent neutral formalin followed by dehydration and embedding in wax. Sections 5pm thick were cut and stained by the following methods - haematoxylin and eosin, James’ reticulin method, Millers elastic stain and van Gieson, combined alcian blue and periodic acid Schiff, and Congo red. The normal appearances of the flexor tendon sheath were studied in material obtained from 16 fresh cadavers of both sexes of subjects ranging from 33 to 86 years with no history of symptoms referral to the carpal tunnel. This material was prepared, processed and stained in the same manner as the definitive series. TABLE 1 Ages of patients 4% IO-19 20-29 30-39 40-49 50-59 60-69 70-79 80-89
Results There was no abnormality specimens.
Number
of Parients 1 6 6 10 9 5 6 2
in seven of the forty-five
In the remaining 38 specimens the following abnormalities were present, often two or more in the same specimen. 1. Connective tissue changes Thickening of collagen bundles present in seven specimens.
(Figure
1) was
229
STIRLING
Hyaline change reduced the collagen to an amorphous pale eosinophilic material (Figure 2) in three specimens. Less severe changes were present in ten more. A combination of collagen bundle thickening and hyaline change was seen in eight more specimens. Massive proliferation of the, synovilum was present in one specimen (Figure 3). This also showed extensive hyaline change and collagen thickening but no inflammation. Fibrosis with a substantial amount of fibrous tissue was present in only one specimen (Figure 4). Fig. 1
Thickening of collagen bundles of the tendon sheath. Van Gieson stain x220.
Fig. 2
Hyaline change in collagen of the tendon sheath. Note the thickened vessel. Haematoxylin and eosin x 220.
Fig. 3
Massive proliferation of the synovium with no evidence of inflammation. Haematoxylin and eosin x 10.
One specimen showed a marked increase in elastic fibres and an excess of reticulin fibres were present in two more. Amyloid deposits (Figure 5) were seen in the connective tissue in two cases. Congo red staining was positive and both showed green birefringence in polarised light. 2.
Vascularlesions Platelet thrombi (Figure 6) occluded small arteries in two cases, and in one of the these there was intimal hyperplasia (Figure 7). In an additional nine cases vessel lumens were narrowed by thickening of small vessel walls (arteriosclerosis).
3.
Oedema Oedema, manifest as separation of the connective tissue fibres (Figure 8) and/or small cystic spaces were present in ten cases. The significance of this finding is discussed below.
4.
Inflammation The only inflammation found was a foreign body giant cell reaction to birefringent material (Figure 9). No abnormality for mucin.
was present in the sections stained
Of the 16 control specimens, two showed arteriosclerosis as severe as that encountered in the series of patients. Six more showed connective tissue changes: thickening of the collagen bundles (l), hyaline change in the collagen (2), thickening of collagen bundles and hyaline change (l), and separation of connective tissue fibres (2). These changes, much less severe that those encountered in the series of patients, involved older subjects aged 50 to 79 years. Discussion
Spontaneous gradual compression neuropathy of the median nerve without evidence of injury or disease is 230
believed, in most instances, to result from a chronic nonspecific synovitis involving the flexor synovium in the carpal tunnel (Phalen and Kendrick, 1957). Most series support this view of chronic inflammation as an important causative factor (Hybbinette and Mannerfelt, THE
JOURNAL
OF HAND
SURGERY
PATHOLOGYOF FLEXOR TENDON SHEATH IN CARPAL TUNNEL SYNDROME
Fig. 4
Fibrous thickening of the tendon sheath. Haematoxylin and eosin x 220.
Fig. 5
Amyloid deposits in the connective tissue of the tendon sheath. Confirmed by green birefringence in polarised light. Congo red stain x 220.
Fig. 6
Occlusion of a small artery Haematoxylin and eosin x 220.
thrombus.
Fig. 7
Intimal hyperplasia narrows the lumen of a small artery. Haematoxylin and eosin x 220.
Fig. 8
Oedema separates the connective tissue fibres of the tendon sheath. Haematoxyhn and eosin x 140.
Fig. 9
Foreign body giant cell granulomatous reaction to birefringent material in the tendon sheath. Haematoxylin and eosin x 220.
by a platelet
1975) so that even in the absence of histological studies the term ‘tenosynovitis’ is frequently employed. Inflammation was absent from our material which, significantly enough, included no patient with rheumatoid arthritis. Foreign body granuloma (Figure 9) containing birefringent material, present in VOL. 12-B No. 2 JUNE 1987
one of our cases, is not regarded as ‘chronic synovitis’ in the usual meaning of the term. Although not strictly ‘spontaneous’ no history of trauma or disease was elicited at the time of presentation. Changes in the collagen of the connective tissue forming the flexor synovium consisted of thickening of the 231
STIRLING
collagen bundles (Figure 1) and degradation of the collagen to an amorphous hyaline material (Figure 2). The former was present in seven specimens and the latter in 13 while both occurred together in eight more specimens. Usually the changes were mild but in four specimens they were substantial, with the severest change associated with proliferation of the synovial tissues. Whether these collagen changes would produce an increase in volume and therefore pressure in the carpal tunnel is uncertain. There was only a limited relationship with ageing. The most marked changes occurred in a woman aged 48 years. The presence, although mild in degree, of collagen changes in four control cases indicates a need for caution before attributing the syndrome to alterations in the collagen. There is no detailed histological account in the literature of the synovial connective tissue although most authors have commented on thickening of the flexor synovium in the carpal tunnel syndrome (Phalen, 1951; Nissan, 1952; Phalen and Kendrick, 1957; Hybbinette and Mannerfelt, 1975). A large excess of synovial membrane was noted in only one case (Figure 3) although Lipscomb (1959) considered it a common cause of the carpal tunnel syndrome. Our case was not associated with inflammation but did show, as already noted, changes in the collagen. Surprisingly+ in view of the frequency of reports of both gross and microscopic fibrous thickening in the carpal tunnel syndrome, we encountered it in only one case (Figure 4). There was no residual chronic inflammation present but this cannot be dismissed as the initial cause. In two cases deposits of amyloid were present in the connective tissue of the tendon sheath (Figure 5). Although the association of amyloidosis and the carpal tunnel syndrome has been known for many years (Grokoest and Demartini, 1954) it is apt to be forgotten. Both of our cases suffered from multiple myelomatosis but this was not known either to the surgeon or pathologist. Vascular changes occluding or narrowing lumens of small arteries and arterioles were present in 11 specimens. In two specimens platelet thrombi (Figure 6) occluded small arteries and were almost certainly responsible for the patients’ symptoms. One of these specimens also showed pronounced intimal hyperplasia (Figure 7), probably a consequence of cessation of blood flow. In neither case was there systemic disease, which might induce platelet thrombi. The remaining nine cases with vascular changes showed arteriosclerosis and it is noteworthy that Phalen (1951) has described arteriosclerosis as an aggravating factor on the grounds that most cases of the carpal tunnel syndrome are over 50 years of age. The occurrence of arteriosclerosis in the young and middle-aged is more likely to be of significance than in the aged. In our series three patients with this lesion were in their thirties and three more in 232
their forties. On the other hand although these lesions narrowed vessel lumens there was no certainty that they produced ischaemia and were responsible for the syndrome or indeed that they themselves were not the result of pressure. Oedema of the flexor tendon sheath has been invoked as a cause of the carpal tunnel syndrome most notably by Faithfull, Moir and Ireland (1986), who reported it in 24 out of 29 patients. We considered that oedema, interpreted as separation of the connective tissue fibres (Figure 8) and the presence of small ‘cystic’ spaces, was present in ten out of 38 specimens. The microscopic diagnosis of oedema must be made with caution since it is difficult to distinguish that from the artefactual separation of the tissue fibres occurring during the injection of the anaesthetic. The ‘cystic’ spaces, may be due to trauma from forceps or even enlarged fat cells. This is underlined by similar changes, although of mild degree, in two of our controls. Although we have described a variety of microscopic changes and lesions in the flexor tendon sheaths of our series they nevertheless fall into two groups, those that may increase the volume of the structures in the carpal tunnel, and those capable of producing ischaemia. Acknowledgments We wish to express our sincere thanks to the histopathology technicians of the Central Laboratories, Stoke-on-Trent, for preparations of the sections, to Mr. T. R. Fisher for his help and encouragement and to Mrs. A. Stirling for assistance in the preparation of the manuscript.
References FAITHFULL, D. K., MOIR, D. H. and IRELAND, J. (1986). The micropathology of the typical carpal tunnel syndrome. The Journal of Hand Surgery, 11: 131-132. GROKOEST, A. W. and DEMARTINI, F. E. (1954). Systemic disease and the carpal tunnel syndrome. Journal of the American Medical Association, 155: 635-637. HYBBINETTE, C. H. and MANNERFELT, L. (1975). The carpal tunnel syndrome. A retrospeclive study of 400 operated patients. Acta Orthopaedica Scandinavica, 46: 610-620. LIPSCOMB, P. R. (1959). Tenosynovitis of the hand and the wrist: Carpal tunnel syndrome, de Quervain’s disease, trigger digit. Clinical Orthopaedics, 13: 164-180. MCKEE, G. K. (1953). Acroparaesthesiae in the carpal tunnel syndrome. Lancet, 2: 732. MICHAELIS, L. S. (1950). Stenosis of the carpal tunnel, compression of the median nerve and flexor tendon sheaths, combined with rheumatoid arthritis elsewhere. Proceedings of the Royal Society of Medicine, 43: 414-417. NISSAN, K. I. (1952). Etiology of carpal tunnel compression of the median nerve. The Journal of Bone and Joint Surgery, 34B: 3: 514-515. PHALEN, G. S. (1951). Spontaneous compression of the median nerve at the wrist. Journal of the American Medical Association, 145: 1128-1133. PHALEN, G. S. and KENDRICK, J. 1. (1957). Compression neuropathy of the median nerve in the carpal tunnel. Journal of the American Medical Association, 164: 524-530. VAINIO, K. (1957). Carpal canal syndrome caused by tenosynovitis. Acta Rheumatologica Scandinavica, 4: 22-27. WILHELM, K., FELDMEIER, Ch., BRIEGEL, J., MEISTER, P. (1982) Genese des karpal tunnel syndroms. Munchener Medizinische Wochenschrift, 124: 28: 661-662. THE JOURNAL OF HAND SURGERY
FLEXOR CARPAL
TENDON TUNNEL
SHEATH SYNDROME
IN
N. C. NEAL, J. McMANNERS and G. A. STIRLING From the North Staffordshire Medical Centre, Stoke-On-Trent
The histological features of the flexor tendon sheath in the spontaneous carpal tunnel syndrome were studied. The main differences between our findings and previous studies were twofold. Firstly a striking absence of inflammation in our material and secondly the diversity of the pathological changes encountered - alterations in the connective tissue especially the collagen; proliferation with thickening of the tissues of the tendon sheath; fibrosis; amyloid deposition; oedema; vascular lesions including thickening of vessels walls, intimal hyperplasia, and thrombosis; and a foreign body giant cell reaction. Although the lesions described here may not be significant in every case in which they are encountered, they do appear to support the view that pressure in the carpal tunnel and ischaemia are the important factors in a majority of cases of the spontaneous carpal tunnel syndrome. The carpal tunnel syndrome, consisting of pain and parasthesiae in the region of the palm and radial digits, is due to compression of the median nerve under the flexor retinaculum. Compression may be produced by a variety of factors including fractures, trauma, acromegaly, an anomalous artery accompanying the nerve, and abnormal insertions of the muscles (Vainio, 1957). The role of tenosynovitis as a cause of the syndrome has been emphasised by several authors (Nissan, 1952; McKee, 1953; Lipscomb, 1959; Hybbinette and Mannerfelt, 1975) and the importance of rheumatoid arthritis in this connection has been stressed (Michaelis, 1950; Vainio, 1957; Hybbinette and Mannerfelt, 1975). In addition to these, there are many cases where the cause of the compression is obscure and referred to as ‘spontaneous’. Histopathology reports on the synovial membrane in the spontaneous carpal tunnel syndrome usually reveal little, according to Phalen (1951). Since then, three reports listing microscopic findings have appeared (Lipscomb, 1959; Wilhelm, 1982; Faithfull, Hybbinette and Mannerfelt, 1975; Faithfull, Moir and Ireland, 1986). These differ in many particulars from our findings. This, and the absence of a comprehensive histological study in the spontaneous carpal tunnel syndrome, have prompted us to report the histopathological findings in 45 consecutive cases. Methods and Materials Patients from orthopaedic waiting lists for carpal tunnel release were reassessed clinically. The series comprised 45 consecutive patients aged 18 to 82 years, of which 30 were women and 15 were men. Numbers in each decade are shown in Table 1. Collagen disease was excluded by physical examination, erythrocyte sedimentation rate estimation and the latex agglutination test. All the operations were carried out under local anaesthetic. At Received for publication 14th January, Dr. G. A. Stirling, North Staffordshire
VOL. 12-B No. 2 JUNE
1987
1987. Medical Centre,
Stoke-On-Trent,
Staffs.
SP4 7LN.
operation, bony, vascular and muscle abnormalities in the carpal tunnel and its contents were excluded. Tissue was removed from the flexor tendon sheath, placed on cardboard and teased out flat before immersion in 10 per cent neutral formalin followed by dehydration and embedding in wax. Sections 5pm thick were cut and stained by the following methods - haematoxylin and eosin, James’ reticulin method, Millers elastic stain and van Gieson, combined alcian blue and periodic acid Schiff, and Congo red. The normal appearances of the flexor tendon sheath were studied in material obtained from 16 fresh cadavers of both sexes of subjects ranging from 33 to 86 years with no history of symptoms referral to the carpal tunnel. This material was prepared, processed and stained in the same manner as the definitive series. TABLE 1 Ages of patients 4% IO-19 20-29 30-39 40-49 50-59 60-69 70-79 80-89
Results There was no abnormality specimens.
Number
of Parients 1 6 6 10 9 5 6 2
in seven of the forty-five
In the remaining 38 specimens the following abnormalities were present, often two or more in the same specimen. 1. Connective tissue changes Thickening of collagen bundles present in seven specimens.
(Figure
1) was
229
STIRLING
Hyaline change reduced the collagen to an amorphous pale eosinophilic material (Figure 2) in three specimens. Less severe changes were present in ten more. A combination of collagen bundle thickening and hyaline change was seen in eight more specimens. Massive proliferation of the, synovilum was present in one specimen (Figure 3). This also showed extensive hyaline change and collagen thickening but no inflammation. Fibrosis with a substantial amount of fibrous tissue was present in only one specimen (Figure 4). Fig. 1
Thickening of collagen bundles of the tendon sheath. Van Gieson stain x220.
Fig. 2
Hyaline change in collagen of the tendon sheath. Note the thickened vessel. Haematoxylin and eosin x 220.
Fig. 3
Massive proliferation of the synovium with no evidence of inflammation. Haematoxylin and eosin x 10.
One specimen showed a marked increase in elastic fibres and an excess of reticulin fibres were present in two more. Amyloid deposits (Figure 5) were seen in the connective tissue in two cases. Congo red staining was positive and both showed green birefringence in polarised light. 2.
Vascularlesions Platelet thrombi (Figure 6) occluded small arteries in two cases, and in one of the these there was intimal hyperplasia (Figure 7). In an additional nine cases vessel lumens were narrowed by thickening of small vessel walls (arteriosclerosis).
3.
Oedema Oedema, manifest as separation of the connective tissue fibres (Figure 8) and/or small cystic spaces were present in ten cases. The significance of this finding is discussed below.
4.
Inflammation The only inflammation found was a foreign body giant cell reaction to birefringent material (Figure 9). No abnormality for mucin.
was present in the sections stained
Of the 16 control specimens, two showed arteriosclerosis as severe as that encountered in the series of patients. Six more showed connective tissue changes: thickening of the collagen bundles (l), hyaline change in the collagen (2), thickening of collagen bundles and hyaline change (l), and separation of connective tissue fibres (2). These changes, much less severe that those encountered in the series of patients, involved older subjects aged 50 to 79 years. Discussion
Spontaneous gradual compression neuropathy of the median nerve without evidence of injury or disease is 230
believed, in most instances, to result from a chronic nonspecific synovitis involving the flexor synovium in the carpal tunnel (Phalen and Kendrick, 1957). Most series support this view of chronic inflammation as an important causative factor (Hybbinette and Mannerfelt, THE
JOURNAL
OF HAND
SURGERY
PATHOLOGYOF FLEXOR TENDON SHEATH IN CARPAL TUNNEL SYNDROME
Fig. 4
Fibrous thickening of the tendon sheath. Haematoxylin and eosin x 220.
Fig. 5
Amyloid deposits in the connective tissue of the tendon sheath. Confirmed by green birefringence in polarised light. Congo red stain x 220.
Fig. 6
Occlusion of a small artery Haematoxylin and eosin x 220.
thrombus.
Fig. 7
Intimal hyperplasia narrows the lumen of a small artery. Haematoxylin and eosin x 220.
Fig. 8
Oedema separates the connective tissue fibres of the tendon sheath. Haematoxyhn and eosin x 140.
Fig. 9
Foreign body giant cell granulomatous reaction to birefringent material in the tendon sheath. Haematoxylin and eosin x 220.
by a platelet
1975) so that even in the absence of histological studies the term ‘tenosynovitis’ is frequently employed. Inflammation was absent from our material which, significantly enough, included no patient with rheumatoid arthritis. Foreign body granuloma (Figure 9) containing birefringent material, present in VOL. 12-B No. 2 JUNE 1987
one of our cases, is not regarded as ‘chronic synovitis’ in the usual meaning of the term. Although not strictly ‘spontaneous’ no history of trauma or disease was elicited at the time of presentation. Changes in the collagen of the connective tissue forming the flexor synovium consisted of thickening of the 231
STIRLING
collagen bundles (Figure 1) and degradation of the collagen to an amorphous hyaline material (Figure 2). The former was present in seven specimens and the latter in 13 while both occurred together in eight more specimens. Usually the changes were mild but in four specimens they were substantial, with the severest change associated with proliferation of the synovial tissues. Whether these collagen changes would produce an increase in volume and therefore pressure in the carpal tunnel is uncertain. There was only a limited relationship with ageing. The most marked changes occurred in a woman aged 48 years. The presence, although mild in degree, of collagen changes in four control cases indicates a need for caution before attributing the syndrome to alterations in the collagen. There is no detailed histological account in the literature of the synovial connective tissue although most authors have commented on thickening of the flexor synovium in the carpal tunnel syndrome (Phalen, 1951; Nissan, 1952; Phalen and Kendrick, 1957; Hybbinette and Mannerfelt, 1975). A large excess of synovial membrane was noted in only one case (Figure 3) although Lipscomb (1959) considered it a common cause of the carpal tunnel syndrome. Our case was not associated with inflammation but did show, as already noted, changes in the collagen. Surprisingly+ in view of the frequency of reports of both gross and microscopic fibrous thickening in the carpal tunnel syndrome, we encountered it in only one case (Figure 4). There was no residual chronic inflammation present but this cannot be dismissed as the initial cause. In two cases deposits of amyloid were present in the connective tissue of the tendon sheath (Figure 5). Although the association of amyloidosis and the carpal tunnel syndrome has been known for many years (Grokoest and Demartini, 1954) it is apt to be forgotten. Both of our cases suffered from multiple myelomatosis but this was not known either to the surgeon or pathologist. Vascular changes occluding or narrowing lumens of small arteries and arterioles were present in 11 specimens. In two specimens platelet thrombi (Figure 6) occluded small arteries and were almost certainly responsible for the patients’ symptoms. One of these specimens also showed pronounced intimal hyperplasia (Figure 7), probably a consequence of cessation of blood flow. In neither case was there systemic disease, which might induce platelet thrombi. The remaining nine cases with vascular changes showed arteriosclerosis and it is noteworthy that Phalen (1951) has described arteriosclerosis as an aggravating factor on the grounds that most cases of the carpal tunnel syndrome are over 50 years of age. The occurrence of arteriosclerosis in the young and middle-aged is more likely to be of significance than in the aged. In our series three patients with this lesion were in their thirties and three more in 232
their forties. On the other hand although these lesions narrowed vessel lumens there was no certainty that they produced ischaemia and were responsible for the syndrome or indeed that they themselves were not the result of pressure. Oedema of the flexor tendon sheath has been invoked as a cause of the carpal tunnel syndrome most notably by Faithfull, Moir and Ireland (1986), who reported it in 24 out of 29 patients. We considered that oedema, interpreted as separation of the connective tissue fibres (Figure 8) and the presence of small ‘cystic’ spaces, was present in ten out of 38 specimens. The microscopic diagnosis of oedema must be made with caution since it is difficult to distinguish that from the artefactual separation of the tissue fibres occurring during the injection of the anaesthetic. The ‘cystic’ spaces, may be due to trauma from forceps or even enlarged fat cells. This is underlined by similar changes, although of mild degree, in two of our controls. Although we have described a variety of microscopic changes and lesions in the flexor tendon sheaths of our series they nevertheless fall into two groups, those that may increase the volume of the structures in the carpal tunnel, and those capable of producing ischaemia. Acknowledgments We wish to express our sincere thanks to the histopathology technicians of the Central Laboratories, Stoke-on-Trent, for preparations of the sections, to Mr. T. R. Fisher for his help and encouragement and to Mrs. A. Stirling for assistance in the preparation of the manuscript.
References FAITHFULL, D. K., MOIR, D. H. and IRELAND, J. (1986). The micropathology of the typical carpal tunnel syndrome. The Journal of Hand Surgery, 11: 131-132. GROKOEST, A. W. and DEMARTINI, F. E. (1954). Systemic disease and the carpal tunnel syndrome. Journal of the American Medical Association, 155: 635-637. HYBBINETTE, C. H. and MANNERFELT, L. (1975). The carpal tunnel syndrome. A retrospeclive study of 400 operated patients. Acta Orthopaedica Scandinavica, 46: 610-620. LIPSCOMB, P. R. (1959). Tenosynovitis of the hand and the wrist: Carpal tunnel syndrome, de Quervain’s disease, trigger digit. Clinical Orthopaedics, 13: 164-180. MCKEE, G. K. (1953). Acroparaesthesiae in the carpal tunnel syndrome. Lancet, 2: 732. MICHAELIS, L. S. (1950). Stenosis of the carpal tunnel, compression of the median nerve and flexor tendon sheaths, combined with rheumatoid arthritis elsewhere. Proceedings of the Royal Society of Medicine, 43: 414-417. NISSAN, K. I. (1952). Etiology of carpal tunnel compression of the median nerve. The Journal of Bone and Joint Surgery, 34B: 3: 514-515. PHALEN, G. S. (1951). Spontaneous compression of the median nerve at the wrist. Journal of the American Medical Association, 145: 1128-1133. PHALEN, G. S. and KENDRICK, J. 1. (1957). Compression neuropathy of the median nerve in the carpal tunnel. Journal of the American Medical Association, 164: 524-530. VAINIO, K. (1957). Carpal canal syndrome caused by tenosynovitis. Acta Rheumatologica Scandinavica, 4: 22-27. WILHELM, K., FELDMEIER, Ch., BRIEGEL, J., MEISTER, P. (1982) Genese des karpal tunnel syndroms. Munchener Medizinische Wochenschrift, 124: 28: 661-662. THE JOURNAL OF HAND SURGERY