Page 392 - ILAE_Lectures_2015

Chapter 40

Bone health in epilepsy

HANNAH R. COCK

Epilepsy Group, Atkinson Morley Regional Neuroscience Centre, St Georges University
Hospitals NHS Foundation Trust, and Institute of Medical and Biomedical Education, St
George’s University of London, Cranmer Terrace, London
_________________________________________________________________________

The first case reports addressing bone health in epilepsy, specifically an association between
antiepileptic drug (AED) use and abnormalities in bone metabolism, were some 40 years ago1,2
and prevalence rates of 50% or more have been reported for clinical and sub-clinical bone
disorders in patients chronically treated with antiepileptic medication (comprehensively
reviewed in Petty et al3). Interest has since escalated, particularly over the last decade, but
despite this, a US-based survey in 20014 suggests that this was an area largely neglected by
treating neurologists in both adult and paediatric practice. Following this, editorials and
reviews have been published on a regular basis, all highlighting what was hitherto a lack of
familiarity with the current literature and urgent need for evidence-based guidelines. There
seems now to be little doubt that epilepsy patients are at increased risk of fractures and
metabolic bone disease, to an extent that we should be at least discussing with our patients.
Recent studies also support that at least some of this risk is AED associated, and thus
potentially preventable. However, many issues remain unresolved, including which of multiple
mechanisms are most important, whether newer drugs offer advantages over older in this
context, how best we should identify those most at risk, and what preventive treatment should
be offered. National guidance in the UK does now recommend vitamin D supplementation.
This chapter will review the currently available literature, and discuss recommendations based
on this.

Definitions and assessment

The primary symptom of metabolic bone disease is an increased incidence of fracture. Both
low bone mineral density (BMD) or bone mass5 and vitamin D deficiency6 are established
independent risk factors for fracture.

Bone mineral density
Low BMD without fracture is usually referred to as osteopenia, whereas osteoporosis is
traditionally defined as the occurrence of non-traumatic fractures, commonly of the spine, hip
and wrists, in the setting of a low BMD7. In the healthy population BMD increases throughout
childhood and adolescence, peaks at around 20 years of age, remains stable until age 40, and
then steadily declines. There is considerable individual variability, of which 80% is due to
hereditary factors including sex and ethnicity (Caucasian women have the highest incidence of
osteopenia, with Afro-Americans relatively protected)8. Low levels of physical activity,
smoking, alcohol and hormonal status (postmenopausal women, testosterone deficient men)
are also known be associated with reduced BMD.

The agreed gold standard for assessing BMD is dual energy X-ray absorptiometry (DEXA),
which has an accuracy of 12% at any given site9,10. Values can be obtained for whole bones
or joints, or bone cortex or trabecular bone alone. Values taken from sites of potential fracture,
ideally the total hip score, are considered the most valid. The spine is not suitable for diagnostic
purposes, but can be used to follow treatment effects. Results are usually expressed as T scores,