Abstract

Although lumbar spondylolysis (LS) is regarded as a stress fracture, the underlying pathomechanism has yet to be fully elucidated. Here, we present a case that casts doubt on the notion that LS is truly a stress fracture. An 11-year-old female basketball player was brought to our clinic with a 2-week history of persistent low back pain. Magnetic resonance imaging with short TI inversion recovery (STIR-MRI) showed high signal intensity changes at the L4 pedicles bilaterally. Computed tomography (CT) revealed a faint fracture line at the left pars interarticularis. We made a diagnosis of stress fracture and recommended conservative treatment, including cessation of sports activities and wearing of a hard brace. Compliance with treatment was excellent. As expected, the STIR-MRI findings at L4 gradually resolved and bone healing was achieved. However, a follow-up STIR-MRI scan 10 weeks later revealed high signal intensity at the left L5 pedicle. Conservative treatment was continued for the findings at L5, which were considered to indicate a stress fracture (spondylolysis). Five weeks later, CT revealed a bony defect in the lamina at L5 on the left and bone union at L4. Although LS is generally considered to be a stress fracture, there have been several reports of familial occurrence and genetic predisposition. This patient’s mother had also been treated for spondylolysis at L5. These observations suggest an underlying genetic etiology in this case.

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