Fredrickson and colleagues set out to define the natural history of isthmic spondylolysis and spondylolisthesis through childhood and adolescence by radiographing unselected first‑graders and their families over time.
Prospective radiographic cohort of 500 unselected first‑graders from a small New York–Pennsylvania community, followed for 25 years to 1979, with family and neonatal ancillary studies.
Methods
Design
Prospective radiographic cohort
Three ancillary studies run alongside
Data source
AP, lateral and oblique lumbar radiographs
All films taken by the same technician
Consensus review with a radiologist
Tomography when a defect was unclear
Patients
500 unselected first‑grade children from local public schools
Families of 23 children with a defect on initial films
500 normal neonates from the same community
32 consecutive families of children born in 1955 or 1956
Exposure
27 subjects with an L5 pars defect vs 116 defect‑free subjects with complete films
Follow-up
Repeat films at ages 10 to 12, 15 to 16 and 18 or older
Reached by 85%, 37% and 34% of the 500
Study ended in 1979 after 25 years
Outcomes
Incidence of spondylolysis
Slip percentage (Taillard method, modified)
Lumbar index
Spina bifida occulta, sacralization and lumbarization
Key Findings
Spondylolysis was found in 4.4% of the original 500 children at age 6, and 8 more defects on later films brought the total to 30 (6%) by adulthood.
L5 was the site in 27 of the 30 patients (5.4% of the cohort), and the 3 defects at other levels were unilateral and never slipped.
Slip developed in 20 of the 27 adults with an L5 defect, ranged from 0% to 30%, and never reached spondyloptosis.
No slip progressed after age 18, and the largest changes came in the early teenage years.
No child had pain while a defect formed or a slip progressed, and the 4 patients with a defect who later reported low back pain were not attributed to the slip by the authors.
The authors found a hereditary tendency toward the defect and a strong link with spina bifida occulta.
Board pearl
The authors read their data as supporting an origin of the pars lesion in a defect of the vertebra's cartilaginous anlage.
Authors' conclusion
Progression of a slip was unlikely after adolescence and the slip was never symptomatic in the population that we studied.
Fredrickson and colleagues set out to define the natural history of isthmic spondylolysis and spondylolisthesis through childhood and adolescence by radiographing unselected first‑graders and their families over time.
Prospective radiographic cohort of 500 unselected first‑graders from a small New York–Pennsylvania community, followed for 25 years to 1979, with family and neonatal ancillary studies.
Methods
Design
Prospective radiographic cohort
Three ancillary studies run alongside
Data source
AP, lateral and oblique lumbar radiographs
All films taken by the same technician
Consensus review with a radiologist
Tomography when a defect was unclear
Patients
500 unselected first‑grade children from local public schools
Families of 23 children with a defect on initial films
500 normal neonates from the same community
32 consecutive families of children born in 1955 or 1956
Exposure
27 subjects with an L5 pars defect vs 116 defect‑free subjects with complete films
Follow-up
Repeat films at ages 10 to 12, 15 to 16 and 18 or older
Reached by 85%, 37% and 34% of the 500
Study ended in 1979 after 25 years
Outcomes
Incidence of spondylolysis
Slip percentage (Taillard method, modified)
Lumbar index
Spina bifida occulta, sacralization and lumbarization
Key Findings
Spondylolysis was found in 4.4% of the original 500 children at age 6, and 8 more defects on later films brought the total to 30 (6%) by adulthood.
L5 was the site in 27 of the 30 patients (5.4% of the cohort), and the 3 defects at other levels were unilateral and never slipped.
Slip developed in 20 of the 27 adults with an L5 defect, ranged from 0% to 30%, and never reached spondyloptosis.
No slip progressed after age 18, and the largest changes came in the early teenage years.
No child had pain while a defect formed or a slip progressed, and the 4 patients with a defect who later reported low back pain were not attributed to the slip by the authors.
The authors found a hereditary tendency toward the defect and a strong link with spina bifida occulta.
Board pearl
The authors read their data as supporting an origin of the pars lesion in a defect of the vertebra's cartilaginous anlage.
Authors' conclusion
Progression of a slip was unlikely after adolescence and the slip was never symptomatic in the population that we studied.