Ligamentous hyperlaxity and dorsal wrist ganglions

Purpose To determine whether symptomatic dorsal wrist ganglions are associated with generalized ligamentous hyperlaxity. Methods Ninety-six patients (61 females) presenting to hand surgeons for a symptomatic dorsal wrist ganglions were prospectively enrolled in this case-control investigation. Beighton scores were calculated to quantify generalized ligamentous laxity in each patient, and a scaphoid shift test (scapholunate capsuloligamentous laxity evaluation) was performed. A positive scaphoid shift test was defined by both pain and a palpable clunk. Ninety-six individuals without ganglions were then enrolled to form an age and sex frequency-matched control cohort. The control group was similarly assessed for Beighton score and scaphoid shift test. Binary logistical regression was performed to assess the association of ganglions with generalized ligamentous hyperlaxity (Beighton score ≥ 4) while accounting for effects of age and sex. Results Patients with symptomatic dorsal wrist ganglions demonstrated significantly increased rates of generalized ligamentous hyperlaxity. Among those with ganglions, 27 of 96 (28%) patients exhibited generalized ligamentous hyperlaxity, compared with 12 of the 96 (13%) age- and sex-matched individuals in the control group. Patients with symptomatic dorsal wrist ganglions were also significantly more likely to demonstrate localized scapholunate hyperlaxity with a positive scaphoid shift test (25% positive scaphoid shift test with ganglions vs 1% in controls). In logistical modeling, patients with dorsal wrist ganglions had 2.9 (95% confidence interval [CI] 1.3-6.2) times greater odds of generalized ligamentous hyperlaxity compared with patients without a dorsal wrist ganglion after accounting for patient age and sex. Conclusions Symptomatic dorsal wrist ganglions were associated with both generalized ligamentous hyperlaxity and a positive scaphoid shift test. Although an association between wrist ganglions and ligamentous hyperlaxity does not prove causation, the possibility of the same underlying pathological entity causing both can be envisioned (ie, abnormal formation or organization of dense regular connective tissue). Type of study/level of evidence Prognostic III.