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Epidemiology of Degenerative Lumbar Disk Disease in Children

This page was last updated on May 9th, 2017

Incidence and Prevalence

  • From 1.1–66% children have LBP: Up to 66% of school children report a history of generalized LBP (6,25,28).
  • 26% of children < 16 years of age have degenerative disk disease (DDD): DDD is more prevalent than previously suspected, with 26% of asymptomatic children < 16 years old demonstrating disc degeneration on MRI (27). In patients with symptomatic DDD, the pain is most often radicular (68%) versus diffuse (32%), 56% have a motor deficit, 60% have sensory involvement, 24% have a family history of lumbar disk disease, and only 8% recall a primary causative injury (15).
  • 50% of children ≤ 15 years old with back complaints have disease: Of children age 15 or younger with nontraumatic back complaints, more than 50% were found to have a diagnosis specific for their back symptoms (31).

Age Distribution

  • Age of LBP onset: The mean age of onset of LBP in children is 13.6 years (6).
  • The mean age of presentation for DDD is 16 years: The mean presenting age for DDD is 16 years for those less than 20 years old. It is after the age of 10 years that spondylolysis and spondylolisthesis begin to present, as the incidence of LBP increases between 12 and 15 years of age.
  • Non-DDD etiology in children < 10 years with LBP: In patients younger than 10 years, look for diskitis, tumor, or other causative mechanisms, since DDD is quite rare in this age group.

Sex Predilection

  • Gender distribution for LBP: A meta-analysis found no significant difference in gender distribution of LBP in children (51.1% male) (6).
  • Gender distribution for disk herniations: In the largest pediatric series reported to date, 60% of children with disk herniations were female (5).

Risk Factors

  • Body weight and sports: Risk factors for pediatric DDD include obesity and high-strain sports activities like football, weightlifting, and cheerleading. There appears to be a complex, variably penetrant genetic component as well. Patients with a positive family history are up to five times as likely as are those without to have a herniated lumbar disk before the age of 21, and small series have reported several children with disk herniations (24, 32). Animal and human studies have linked mutations in collagen, aggrecan, matrix metalloproteinase 3, and vitamin D receptors with an increased risk of disk degeneration (2, 12-14, 18, 19, 34, 36, 37).

Relationships to Other Disease States and Syndromes

  • Differential diagnoses for LBP: Several diseases may present with LBP. Diagnoses that may mimic axial back pain (11) include infection/diskitis, sickle cell disease/crisis, inflammatory disease, seronegative spondyloarthropathy, neoplasms, myelodysplasia, and kidney, pancreas, or splenic problems.
  • Red flags: Alarming symptoms such as rapidly progressive back pain, age < 4 years, night-time pain with the inability to return to sleep should lead to a faster and more aggressive evaluation as they are suggestinve of a tumor, an infection, or an inflammatory condition until proven otherwise. ,Other symptoms suggesting a diagnosis are functional limitation/limb favoring, systemic complaints/symptoms (e.g., fevers, weight loss), neurological deficits, immediate pain relief with NSAIDs (consider osteoid osteoma, ankylosing spondylitis, or juvenile rheumatoid arthritis).

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