Adenosine kinase and adenosine receptors A1 R and A2A R in temporal lobe epilepsy and hippocampal sclerosis and association with risk factors for SUDEP.

Reduced cortical A2A R suggests glial dysfunction and impaired adenosine modulation in response to seizures in patients at higher risk for SUDEP. Increased neuronal A1 R in the high-risk group could contribute to periictal amygdala dysfunction in SUDEP.