Neurobiology of epilepsy

The causes of epilepsy are not fully known, but it has been indicated that genetic factors, infections, brain and head injuries, brain tumours and hypoxic brain damage during childbirth or stroke may play a role [1]. Epileptic seizures can be divided into two main types - focal seizures, during which excessive neuronal activity is confined to only a specific part of the brain, and generalised seizures, where excessive neuronal discharges occur throughout the brain.

An epileptic seizure may result in injuries, both of a milder nature, such as soft tissue trauma or fractures [2], but also of a far more serious nature, such as respiratory problems and cardiac arrest [3]. Obtaining a correct diagnosis, pharmacotherapy and elimination of the triggers of an epileptic seizure are therefore key to improving the quality of life of patients with epilepsy and protecting them from danger.

However, providing appropriate treatment is not that simple. As the WHO indicates, some 50 million people worldwide suffer from epilepsy, and nearly 80 % of these people are from low- and middle-income countries [1]. Due to limited access to medical care, these patients do not receive tailored treatment and their frequency of epileptic seizures is not reduced. This is referred to as the Epilepsy Treatment Gap (ETG).

Antiepileptic drugs such as carbamazepine, phenobarbital, phenytoin, valproic acid and benzodiazepines are typically used to treat epilepsy [4]. They exert inhibitory effects on neurons by blocking sodium channels, increasing the influx of chloride ions into neurons or inhibiting the breakdown of gamma-amino-butyric acid (GABA) at synapses.

Correctly selected pharmacotherapy can be really effective, but there are also cases where pharmacotherapy does not improve (drug-resistant epilepsy). Other forms of treatment are then available, such as surgical excision of the epileptic focus, vagus nerve stimulation, transcranial magnetic stimulation or a ketogenic diet [4].