BACKGROUND: Epilepsy is a common chronic neurological disorder, usually 
requiring long-term treatment with anti-epileptic drugs (AED). Many studies have 
reported that AED therapy is associated with metabolic bone disease and is a 
major iatrogenic risk factor for fractures. There remains uncertainty about the 
type(s) of bone disease due to AED treatment, and the pathogenesis of 
AED-associated fractures.
RATIONALE: Deficits in bone mineral density (BMD) are widely reported in 
AED-treated patient populations. However, much of the research conducted to date 
has been limited by factors such as small sample size, potentially biased 
subject selection, a lack of selection of appropriate control data, and failure 
to take account of important confounding influences. The pathogenesis of 
AED-associated fractures is likely to be multifactorial, due to factors 
including reduced BMD, impaired bone quality (due to osteoporosis and/or 
osteomalacia), increased propensity to fall, and fractures associated with 
seizures or loss of consciousness.
RECOMMENDATIONS: Patients receiving long-term AED should be monitored for 
indices of bone health, including BMD and vitamin D status. Lifestyle factors 
should be optimized, vitamin D status maintained, and fall prevention strategies 
introduced as appropriate. Good seizure control is important. The use of 
additional, specific osteoporosis therapy is not evidence-based in this setting, 
but would appear reasonable in patients with clinically significant decreases in 
BMD, applying current treatment guidelines for osteoporosis.
CONCLUSION: There is a pressing need for improved understanding of the 
pathogenesis of AED-associated bone disease, for better definition of the risk 
associated with specific AED regimens, and for the development of evidence-based 
preventive and treatment approaches in this common but neglected disorder.