CAMPTODACTYLY CAUSED BY ABNORMAL INSERTION ORIGIN OF LUMBRICAL MUSCLE
AND
A. MINAMI and T. SAKAI From the Session of Hand Surgery, Department of Orthopaedic Surgery, Hokkaido University School of Medicine, Sapporo, Japan
A lZyear-old boy had camptodactyly of the little finger. Operative findings revealed an abnormal origin of the lumbrical muscle from the transverse carpal ligament, and abnormal insertion into the tendon sheath of the flexor digitorum superficialis tendon. No similar case has been reported in the literature. Journal of Hand Surgery
(British and European
Volume, 1993)
CASE REPORT
tendon was pulled proximally as far as possible. Passive extension of the PIP joint was not changed even after the FDS tendon was resected. The FDP tendon also looked normal, but there was a communication between it and the FDP tendon of the ring finger as a fibrous band. This was resected. The lumbrical muscle of the little finger originated from the flexor retinaculum at the palmar aspect of the wrist joint (Fig 3). The lumbrical muscle formed the muscle belly with the palmar interosseous muscle and gave rise to the tendinous portion. A small part of its tendon entered the fibrous flexor sheath and a major part of its tendon joined the third palmar interosseous muscle to the radial lateral band. The tendinous band which entered the tendon sheath was cut off at its insertion. After dividing this tendon the PIP joint could be extended. The divided tendon was passed through the subcutaneous tissue and attached to the lateral band. The finger was held with the MP joint flexed and the IP joint extended using a Kirschner wire. This was removed after 3 weeks and active exercise was begun. Six months after the operation, the active range of motion in the PIP joint was 80” in flexion and - 50” in extension. A palmar splint was fitted to support the little finger in extension, but there was no improvement in active extension. One year after the first operation the lumbrical muscle was completely removed at a second oper-
The PIP joint of the left little finger of a IZyear-old boy had become increasingly flexed from the age of 11 years. He felt pain in the palmar aspect of the PIP joint when it was passively extended. He received conservative treatment including massage and an extension splint, but the symptoms were not relieved. On examination, the left little finger rested in 50” of hyperextension at the metacarpophalangeal joint and was flexed to 100” at the PIP joint. It resembled a claw finger induced by intrinsic paralysis of the ulnar nerve (Fig 1). The PIP joint could be extended to 0” by a strong passive force when the MP joint was extended to 0” although the PIP joint could be extended to - 10” when the MP joint was hyperextended. He complained of pain in the palm. No X-ray changes were observed. He could not tolerate a palmar splint even for 1 day because of pain in the palm. In view of the duration and severity of his symptoms, surgical exploration was undertaken under general anaesthesia. The left little finger was explored through a palmar zig-zag skin incision. The flexor digitorum superficialis tendon seemed to be normal at the distal portion and also normal at the proximal portion; there was no connection to the flexors of the ring finger nor to transverse carpal ligament (Fig 2). However, the gliding of the FDS tendon could not be observed when the
Fig2 Fig 1
The left finger showed
a typical
18B: 310-311
camptodactyly. 310
Operative findings revealed that the flexor digitorum ficialis and profundus tendons were normal.
super-
311
CAMPTODACTYLY
Fig 3
Lumbrical muscle originated from the flexor retinaculum at the palmar aspect of the wrist joint. The lumbrical muscle
formed the muscle belly with the palmar interosseous muscle and gave rise to the tendinous portion. A small part of its tendon entered the fibrous flexor sheath and a major part of its tendon joined the third palmar interosseous muscle to form the radial lateral band.
ation and active exercises were begun. Six months later, the PIP joint had a full active range of motion although a flexion deformity of the PIP joint in - 10” extension remained.
camptodactyly of the little finger and concluded that the loss of normal lumbrical action is the principle cause of the intrinsic minus deformity seen in camptodactyly. The fourth lumbrical muscle was absent in 4% and the insertion was abnormal in the remainder. The most frequent abnormal insertion found at operation was that of muscle fibres into the soft tissue on the side of the MP joint, either completely or with some of the muscle fibres also attached to the free margin of the extensor mechanism. Whether the insertion onto the MP joint was complete or incomplete, traction on the belly of the muscle did not extend the PIP joint. There has been no report of an abnormality of the origin of the lumbrical in the English-language literature. Maeda and Matsui (1985) reported a case in which camptodactyly was caused by an abnormal. insertion of the lumbrical. In their case, almost complete correction was obtained by attachment of the tendon of the lumbrical into the lateral band. In view of their report and McFarlane’s report, we also attached the lumbrical muscle to the lateral band, but only slight improvement in flexion deformity was obtained. Subsequently, the lumbrical muscle of the little finger was totally removed leading to almost complete correction. However, it is still uncertain whether resection of the whole muscle is applicable to other cases. Acknowiedgement
DISCUSSIBN Camptodactyly has been attributed to a number of abnormalities, including contracture of the palmar skin, shortening of the flexor tendon, imbalance between flexor and extensor tendon forces, contracture of the collateral ligaments and the volar plate, changes in the size and shape of the head of the proximal phalanx, abnormal development of the lumbrical and interosseous muscles, and proximal tethering of FDS. Courtemanche (1969), Maeda and Matsui (1985) and McFarlane et al (1983, 1992) described an abnormal insertion of the lumbrical muscle as the cause of the camptodactyly. In particular, McFarlane et al (1992) analysed 74 consecutive operations for correction of
The authors thank Professor Kiyoshi Kaneda MD, Department of Orthopaedic Surgery, Hokkaido University School of Medicine, Sapporo, Japan.
References COURTEMANCHE, A. D. (1969). Camptodactyly: Etiology and management. Plastic and Reconstructive Surgery, 44: 5: 451-454. MAEDA, M. and M.4TSU1, T. (1985). Camptodactyly caused by an abnormal lumbrical muscle. Journal of Hand Surgery, lo&: 1: 95-96. McFARLANE. R. M., CLASSEN, D. A., PORTE. A. M. and BOTZ, J. S. (1992). The anatomy and treatment of calqtodactyly of the small finger. The Journal of Hand Surgery, 17A: 1: 35-44. McFARLANE. R. M., CURRY, G. I. and EVANS, A. B :1983). Anomalies of the intrinsic muscles in camptodactyly. The Journal of Hand Surgery, 8: 5(l): 531-544.
Accepted: 10 December 1992 Akio Minami MD. Department of Orthopaedic Medicine, Kita-IS-Jo, Nishi-7.Chome, Kita-Ku, G 1993 The Brltlsh
Soaety
for Surgery
Surgery, Hokkaido Sapparo 060, Japan.
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