INTRODUCTION

∗ For my father.

Much of the literature has concentrated on the intra-articular component of ulnar-sided wrist pain. Arthroscopy has revolutionized our understanding of the ulnar side of the wrist and is without doubt the gold standard for establishing the diagnosis of ulnar-sided wrist pain. Ulnar-sided wrist pain is not always attributable to a tear of the triangular fibrocartilage complex (TFCC), however. It has become increasingly clear that ulnar-sided wrist pain may also arise from an extra-articular group of disorders, which include ulnar styloid impaction and extensor carpi ulnaris (ECU) pathologies.

In 1999, Watson and associates described a new cause of ulnar-sided wrist pain, triquetral impingement ligament tear (TILT) syndrome. Patients presented with ulnar-sided wrist pain and swelling; mild to moderate decrease in wrist extension, flexion, and grip strength; and point tenderness to palpation over the dorsal ulnar aspect of the triquetral bone. Although this was described as an impingement of ulnar-sided soft tissue on the triquetrum, the nature of the impinging tissue remained unclear.

RELEVANT ANATOMY

The ulnar aspect of the wrist is bound by a number of tendons and ligaments, which have been delineated as separate anatomic structures in both classic textbooks and cadaver studies. The most simplistic classification separates the intrinsic and extrinsic carpal ligaments. Much of the support of the ulnocarpal joint is from the volar radiocarpal ligaments. Loads acting on the dorsal aspect of the ulnocarpal joint are transmitted to the volar ulnolunate and ulnotriquetral ligaments via the TFCC and articular disk. The dorsal ligaments of the ulnar wrist are considered weak stabilizers of the ulnocarpal joint. The dorsal wrist capsule is reinforced by the dorsal radiocarpal ligament, which is an extrinsic ligament that arises from the radius and passes distally and ulnarly to insert into the dorsal aspect of the lunate and triquetrum. In combination with the dorsal intercarpal ligament, this forms a V -shaped arrangement as described by Viegas and colleagues. The dorsal radiocarpal ligament, along with the extensor carpi ulnaris subsheath, attaches to the dorsal aspect of the TFCC and prevents volar subluxation of the ulnar carpus. The ulnar collateral ligament has been described as little more than a thickening of the wrist capsule and extends from the base of the ulnar styloid to the triquetrum. It is not clear whether this structure exists. The extensor retinaculum overlies and fuses with these structures. Although these structures can be anatomically separated, Taleisnik has described them as blending into a holistic mass.

PATHOGENESIS

When describing the underlying problem in TILT syndrome, Watson described a structure he termed the ulnar sling mechanism . It is unclear which structures are actually injured in the antecedent injury leading to TILT. The offending soft tissue could be intra-articular or extra-articular.

In a separate unpublished series, 12 consecutive patients with the clinical picture of TILT before surgery were evaluated by the authors. The purpose of this series was to better define TILT. All patients in this series had magnetic resonance imaging (MRI) performed, and five patients underwent wrist arthroscopy. Patients with previous wrist surgery and other ulnar wrist pathology were excluded. Of the patients undergoing arthroscopy, two patients had evidence of radial-sided degeneration with minimal synovitis. One patient had no clear degeneration but some generalized synovitis, and another patient had synovitis in the area of the scapholunate interosseous ligament with no tear. The ulnar side of the wrist was found to have a normal arthroscopic appearance.

On MRI, there was evidence of focal subchondral edema in the triquetrum in six patients, and two patients had cystic changes in the triquetrum. Four patients had evidence of ulnar capsular edema/focal synovitis adjacent to the triquetrum, and the MRI of one patient highlighted extensor carpi ulnaris tendon sheath edema ( Figs. 48-1 and 48-2 ). These data do not clarify the true pathologic tissue involved in TILT syndrome, but they do hint at an extra-articular pathology. The meniscal homologue is the inconstant soft tissue structure that variably fills the space between the ulnar capsule, disk, and proximal aspect of the triquetrum. It is possible that this is the tissue that is torn and consequently causes impingement in TILT syndrome.

MRI of triquetral impingement ligament tear (TILT) . The triquetrum shows focal subchondral edema ( white arrow ).

MRI of triquetral impingement ligament tear (TILT) . Subchondral edema ( black arrow) of the triquetrum.

The presence of a redundant, free soft tissue mass that can impinge on the dorsal triquetrum is probably the important factor in the pathogenesis of TILT syndrome. Chronic impingement of this interposed soft tissue causes inflammation and erosion of the triquetrum with chondromalacia. In their published series describing the results of an open repair, Watson and Weinzweig noted hyperemia of the triquetrum along with eburnation, cortical softening, and exposure of the subchondral bone. The observed pathology of these patients with TILT syndrome resembled that of ulnar impaction syndrome. They postulated that the impingement was caused by the introduction of excess tissue into the joint space causing increased pressure on and eventual wear of the triquetrum. In 11 of the 12 patients, we found synovium or loose connective tissue in the dorsal aspect of the wrist, and in one patient, an osteochondral fracture/flap was present, which was treated with debridement. In our unpublished series, some tissue was removed in all of the patients through an open approach. It was unclear where this soft tissue originated, but it was clearly in a dorsal and extra-articular position. The removed tissue was sent for pathologic evaluation and unanimously was read as nonspecific degeneration. In one specimen, hypertrophic synovium was reported.