Epilepsy in Southeast Asia, how much have we closed the management gap in past two decades?

@#The last review on epilepsy in Southeast Asian (SEA) countries was reported in 1997. This review aimed to update the understanding of epilepsy management in this region over the past 23 years. There has been significant increase in the epidemiological studies which reported a prevalence of 4.3-7.7 per 1,000 populations in this region. Reversible aetiologies of epilepsy such as head injury, birth trauma, cerebrovascular disease, and intracranial infections (neurocysticercosis or meningoencephalitis) are still prevalent, with a surge in autoimmune encephalitis. There was a surge in genetic studies which suggest ethnic variation. Treatment gap is still high especially in the rural and less developed areas, and the availability and affordability of newer anti-epileptic drugs (AEDs) is still a major challenge in SEA. Alternative medicine is a common practice but varies among different ethnic groups. AEDs hypersensitivity especially on the association between HLA-B*1502 and carbamazepine-related severe cutaneous reaction had been extensively studied and proven in nearly all SEA countries. However, HLA-B*1502 screening is not widely available in SEA and the cost-effectiveness of the screening is questionable. Stigma and its psychosocial consequences are still a major concern despite enormous efforts to study the public attitudes towards epilepsy and change of epilepsy naming in a few countries. The number and complexity of epilepsy surgery are progressing, but it is still under-utilized in many SEA countries, related to cost, cultural perception and lack of facilities. More resources should also be channelled in training adequate number of epileptologists who can spearhead epilepsy care around the region, as well as public education and research in epilepsy. In conclusion, there is an increase in epilepsy research in this region, gradual increase in trained neurologists and facilities, and efforts to reduce the knowledge and treatment gap, but the epilepsy management gap is still a battle to fight.

Peripheral neuropathy induced by drinking water contaminated with low-dose arsenic in Myanmar

BACKGROUND@#More than 140 million people drink arsenic-contaminated groundwater. It is unknown how much arsenic exposure is necessary to cause neurological impairment. Here, we evaluate the relationship between neurological impairments and the arsenic concentration in drinking water (ACDW).@*PARTICIPANTS AND METHODS@#A cross-sectional study design was employed. We performed medical examinations of 1867 residents in seven villages in the Thabaung township in Myanmar. Medical examinations consisted of interviews regarding subjective neurological symptoms and objective neurological examinations of sensory disturbances. For subjective neurological symptoms, we ascertained the presence or absence of defects in smell, vision, taste, and hearing; the feeling of weakness; and chronic numbness or pain. For objective sensory disturbances, we examined defects in pain sensation, vibration sensation, and two-point discrimination. We analyzed the relationship between the subjective symptoms, objective sensory disturbances, and ACDW.@*RESULTS@#Residents with ACDW ≥ 10 parts per billion (ppb) had experienced a "feeling of weakness" and "chronic numbness or pain" significantly more often than those with ACDW  50 ppb). These data suggest a threshold for the occurrence of peripheral neuropathy due to arsenic exposure, and indicate that the arsenic concentration in drinking water should be less than 10 ppb to ensure human health.