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The purpose of this study was to determine the frequency with which the palmar cutaneous branch of the median nerve passes through the palmaris longus tendon. Fifty-two wrists (27 cadavers) were dissected. In three wrists the palmaris longus tendon was absent. The palmar cutaneous branch was seen to course through the fibers of the palmaris longus in two specimens (different cadavers). The nerve passed through the tendon 1 and 1.5 cm proximal to its insertion into the palmar aponeurosis. In the presence of this anomaly the palmar cutaneous branch of the median nerve is at risk of injury during harvesting of the palmaris longus tendon for grafts. To avoid injury, we recommend transecting the tendon 2 cm proximal to its insertion into the palmar aponeurosis.

Having observed an anomalous insertion of the lumbrical muscle in 74 consecutive operations for correction of camptodactyly of the small finger, we have concluded that the loss of normal lumbrical action is the principal cause of the intrinsic minus deformity seen in this condition. Other anatomic abnormalities observed in this series of patients are those of the superficial tendon in 47%, the x-ray appearance of the proximal interphalangeal (PIP) joint in 15%, and a fixed flexion contracture of the PIP joint in 66%. Fifty-seven percent of our patients had PIP flexion contracture of more than 45 degrees. To determine the contribution of these anomalies to this deformity, we analyzed a series of 53 patients who had been followed up for at least 1 year. The study revealed that these conditions are interdependent and that each had an adverse effect on the final operative results. Treatment included a transfer of the superficial tendon of the ring or little finger to the extensor mechanism of the little finger in all cases and other procedures as dictated by the individual situation. Overall, the joint contracture was reduced from 49 degrees to 25 degrees, but only 33% of the patients regained full flexion of the small finger.

The present status of adjudication for workers claiming compensation for Dupuytren's disease is inconsistent and, therefore, unfair to both workers and employers. In some Eastern European countries Dupuytren's disease is classified as an industrial disease, whereas in other countries it is considered to have no relation to manual work or hand injury. In jurisdictions that sometimes award compensation, the reasons for acceptance or rejection of a claim vary from case to case and are not necessarily based on our present knowledge of the disease. The purpose of this communication is to highlight the features of Dupuytren's disease that are pertinent to manual work and hand injury and to suggest guidelines that would provide some consistency in the adjudication process. It is hoped that these guidelines would be valuable to the individual surgeon, insurance agencies, and compensation boards.

There has been little or no change in the methods of treating Dupuytren's disease in recent years. However, we are encouraged by the interest of cellular biologists and collagen chemists who have contributed to our understanding of the disease process. We can anticipate that sufficient knowledge will be gained in the near future so that surgeons can evolve a rational approach to the treatment of Dupuytren's disease.

The lateral antebrachial cutaneous nerve was used as a nerve graft to bridge a defect in a digital nerve, when with the digit in full extension the nerve ends could not be approximated without tension. Thirteen grafts have been followed from 7 to 23 months. Two patients did not regain two point discrimination and therefore had a poor result. The remaining 11 patients recovered two point discrimination between 7 and 20 mm.

The palmar aponeurosis and the palmaris longus tendon were examined in 33 hands of gestational age from 5 weeks to term. At 5 weeks both the longitudinal and transverse layers of the palmar aponeurosis and the palmaris longus tendon were present and in continuity. The palmaris longus tendon was absent in five specimens and in these the longitudinal fibers of the palmar aponeurosis blended into the antebrachial fascia. Otherwise the structure of the palmar aponeurosis was similar in the presence or absence of the palmaris longus tendon. The staining characteristics of the palmaris longus tendon were those of tendon whereas the palmar aponeurosis stained like fascia. These observations, as well as the fact that the palmar aponeurosis has never been reported to be absent, support the view of Kaplan that the palmar aponeurosis and the palmaris longus tendon are separate anatomic structures, which develop independently and are associated only by anatomic proximity.

The tissue from 38 patients with Dupuytren's contracture was submitted for light and electron microscopy. The clinical and pathological data were correlated so that three stages of disease were recognized: early, active, and advanced. The cell of early disease was the perivascular fibroblast; whereas, the cell of active disease was the myofibroblast. Because the myofibroblasts have cell-to-cell and cell-to-stroma attachments, the collagen not only becomes oriented as it is formed, but it also is subjected to a contractile force.

Although Dupuytren's disease is common it is still not fully understood. A series of patients has been assessed by multiple regression analysis from which "outcome standards" have been formulated. It is anticipated that this method of analysis will further our understanding of the disease when greater numbers of patients are added to the study. As well, the application of an "outcome standard" to a given patient should reduce the number of unexpectedly poor results obtained and expose errors in the primary management of those patients.

This study was designed to determine if structural changes in the palmar fascia in Dupuytren's disease, as viewed by the scanning electron microscope, might provide some information about the pathogenesis of this disease. The palmar fascia from seven uninvolved hands and from 21 patients with Dupuytren's disease was examined. There were distinct differences between normal and diseased collagen. The diseased tissue showed collagen that was more tightly bound and had a shorter wave pattern. In the Dupuytren's tissue the waves were frequently in a helix, but this was never seen in the normal tissue. The most striking differences were noted in the nodule, presumably because it appears first, followed by the cord proximal to the nodule (pretendinous cord). Similar but less obvious changes were noted in the cord distal to the nodule (central cord) presumably because it is last to form. These observations suggest a mechanism of contraction. The short wave length and helix formation of the collagen indicate shortening. If the concept of the myofibroblast as a contractile cell is accepted, the contraction of these cells in stepwise fashion could produce the changes in the structure of the collagen that have been observed and result in joint contracture.

Thirty-seven specimens from the hands of 30 patients with Dupuytren's disease were examined by light microscopy after immunohistochemical staining for the presence of desmin intermediate filaments. Results indicated that desmin-positive cells were present in the proliferative Dupuytren's nodules, and that the number of desmin-positive cells decreased significantly in the fibrous phase of the disease. Also, on the basis of the pattern of distribution of the desmin-positive cells around vessels, we postulate that the desmin-positive cells in Dupuytren's nodules were migrating perivascular smooth muscle cells from the vessel wall. The exact fate of these cells is uncertain, but we hypothesize that these displaced perivascular smooth muscle cells are capable of transforming into collagen-producing, desmin-negative myofibroblasts that form the cellular basis of Dupuytren's lesions.

Our observations support the view of Millesi that camptodactyly is due to an imbalance between the flexor and extensor forces acting upon the proximal interphalangeal joint. In 21 consecutive operations the insertion of the lumbrical muscle was abnormal. The muscle inserted into either the superficialis tendon (in three cases), the capsule of the metacarpophalangeal joint (in 15), or the extensor expansion of the adjacent finger (in four). The fourth palmar interosseous muscle was examined in the last 10 patients and was abnormal in five. It was absent in two patients, small in one, and inserted into the extensor expansion of the ring finger in two patients. Therefore, it is suggested that camptodactyly is an intrinsic minus deformity. It follows that treatment should consist of soft tissue release, as necessary, to correct the flexion deformity, followed by a tendon transfer to restore intrinsic action and maintain correction of the deformity.