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Progressive bone deficit in epilepsy
Raj D Sheth1, Neil Binkley, Bruce P Hermann
1Department of Neurology, University of Wisconsin-Madison, 600 Highland Ave-H6/574 CSC, Madison, WI 53792-5132, USA. sheth@neurology.wisc.edu
Insights
Children with epilepsy experience reduced bone mineral density (BMD) starting within 1-5 years of treatment. This bone deficit worsens over time, increasing fracture risk and potentially accelerating osteoporosis.
Area of Science:
- Pediatrics
- Neurology
- Endocrinology
Background:
- Antiepileptic drug (AED) therapy in children is linked to decreased bone mineral density (BMD) and elevated fracture rates.
- Understanding the onset and progression of BMD deficits in pediatric epilepsy is crucial for intervention.
Purpose of the Study:
- To investigate the timing of bone mineral density (BMD) reduction in ambulatory children undergoing chronic antiepileptic medication treatment.
- To correlate the duration of epilepsy and AED treatment with BMD levels in children.
Main Methods:
- A cross-sectional study involving 82 ambulatory children with epilepsy (aged 6-18 years) and 32 healthy controls.
- Participants were grouped by epilepsy duration: <1 year, 1-5 years, and ≥6 years.
- Total body BMD Z-scores were measured and compared between groups, adjusting for age and sex.
Main Results:
- Children with epilepsy exhibited significantly lower total body BMD Z-scores compared to healthy controls.
- A progressive reduction in BMD was observed with increasing duration of epilepsy.
- BMD deficits were significant in children with epilepsy for 1-5 years and ≥6 years, but not in those with epilepsy for <1 year.
Conclusions:
- Children with epilepsy develop significant bone mineral density (BMD) deficits within 1-5 years of antiepileptic treatment.
- The BMD deficit progressively worsens with longer treatment durations.
- This bone loss may contribute to increased fracture risk and accelerated osteoporosis in pediatric epilepsy patients.
Objective:
Chronic treatment with antiepileptic medication is associated with reduced bone mineral density (BMD), which may underlie the two- to sixfold increase in fracture rates observed in patients with epilepsy. The objective was to determine the timing of the BMD deficit in ambulatory children with epilepsy.
Methods:
A cross-sectional evaluation was conducted in 82 ambulatory children aged 6 to 18 years (12.4 +/- 3.3 years) with epilepsy for <1 year (n = 18), 1 to 5 years (n = 37), and 6 or more years (n = 27). Controls were 32 healthy children aged 12.8 +/- 2.6 years. Age- and sex-corrected total body BMD Z-score was measured.
Results:
Total BMD Z-score was lower in children with epilepsy (0.10 +/- 0.96; CI = -0.08, 0.34) compared to controls (0.57 +/- 0.74; CI = 0.3, 0.84; p = 0.03). Increasing duration of epilepsy was associated with a progressive reduction in BMD compared to controls (Spearman r = -0.197; p = 0.03). Compared to controls, those with epilepsy for 1 to 5 years had a mean BMD Z-score of 0.13 +/- 0.78 (CI = -0.13, 0.39; p = 0.04) and in those treated for 6 or more years BMD was 0.06 +/- 1.11 (CI = -0.38, 0.5; p = 0.04). For those with epilepsy for <1 year BMD was 0.23 +/- 1.1 (CI = -0.31, 0.77; p = 0.21).
Conclusions:
Children treated for epilepsy sustain significant bone mineral density (BMD) deficit compared to controls during the initial 1 to 5 years of treatment which progressively worsens thereafter. This progressive BMD deficit may be a contributing factor to the increased fracture risk observed in patients with epilepsy and may accelerate aging-related osteoporosis.
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