A fibrinolytic defect is common in chronic back pain syndromes. Its role in the chronicity of these conditions is not fully understood. To elucidate the possible mechanisms, 11 patients with acute low back pain were studied over 12 months and compared with controls. The patients showed prolongation of the euglobulin lysis time throughout the study; the fibrin plate lysis area was initially normal but became abnormal within 2 weeks. In five patients, the symptoms resolved and the initial fibrinolytic defect improved. In contrast, the fibrinolytic defect remained in six patients with persistent pain. These results suggest that the fibrinolytic defect is secondary to mechanical damage but, if persistent, may become a secondary pathogenic factor associated with the chronicity of some back pain problems.