Authors :
Presenting Author: Lynette Sadleir, MD, MBChB – University of Otago, Wellington
Ngaire Keenan, MBChB – University of Otago, Wellington; Suzanne Davis, PhD, MD – Te Whatu Ora Health New Zealand; Erik Andersen, MBChB – Te Whatu Ora Health New Zealand; Shayma Ali, BSc – University of Otago, Wellington; Jeannine Stairmand, MPH – University of Otago, Welligton; James Stanley, PhD – University of Otago, Wellington
Rationale:
Epilepsy is a serious neurological disorder which affects all ages, social classes, and ethnicities. In 2022, the World Health Organization adopted the Intersectoral Global Action Plan on Epilepsy and other Neurological Disorders 2022-2031 (IGAP). The aims of IGAP are to improve epilepsy healthcare, minimize health disparities, and ultimately reduce the burden of epilepsy with a specific emphasis on high-risk groups such as Indigenous people. Māori, the Indigenous peoples of New Zealand, make up 27% of the peadiatric New Zealand population and typically have worse health outcomes and access to healthcare. New Zealand studies have reported that, despite similar levels of treated epilepsy for Māori and non-Māori children, Māori people with epilepsy are more likely to present to the emergency department, more likely to be admitted to hospital, and have a higher mortality rate. We aim to identify the types, severity, and etiology of epilepsy in Māori children and compare these to non-Māori, non-Pasifika children with epilepsy.
Methods:
Population-based retrospective cohort study of 337 Māori children and 421 age and sex matched non-Māori, non-Pasifika children (< 18 years) with treated epilepsy. Medical records were examined to determine each individual’s epilepsy type, syndrome, and etiology.
Results:
Children in both cohorts were most likely to have a focal onset epilepsy (65.6% Māori; 59.4% non-Māori, non-Pasifika).
Māori children (relative to non-Māori, non-Pasifika children) had lower odds (OR=0.51, 95% CI 0.30-0.83) of having a self-limited epilepsy syndrome, were less likely to have a developmental and epileptic encephalopathy (OR=0.59, 95% CI 0.40-0.88), and were more likely to have intellectual disability and epilepsy (OR=1.65, 95% CI 1.18-2.32). Genetic epilepsy was the most common etiology in both groups. Māori were more likely to have a structural etiology (OR = 1.5, 95% CI 1.08-2.16), more likely to have an infectious etiology (OR=4.7, 95% CI 1.66-16.50), and less likely to have a genetic etiology (OR=0.70, 95% CI 0.52-0.95). A preventable etiology was identified in 18% of Māori children and 7% of non-Māor, non-Pasifika children. After adjustment for socioeconomic status and rurality, Māori children were 2.5 times (95% CI 1.49-4.22) more likely to have a preventable etiology. The most common preventable etiologies were pre and perinatal injury (5% Māori; 4% non-Māori, non-Pasifika), central nervous system infections (4% Māori; 0.7% non-Māori, non-Pasifika), and traumatic brain injury (2% Māori; 0.7% non-Māori, non-Pasifika).
Conclusions:
We identified significant disparities in the etiology of epilepsy in Māori children compared to non-Māori, non-Pasifika children. Understanding the type and causes of epilepsy is essential for the development of public health strategies that aim to improve epilepsy healthcare.
Funding:
Neurological Foundation, Health Research Council of New Zealand, Royal Australasian College of Physicians