Neuroimaging the epileptogenic process

Abstract

Epilepsy is one of the most common chronic neurological conditions worldwide. Anti-epileptic drugs (AEDs) can suppress seizures, but do not affect the underlying epileptic state, and many epilepsy patients are unable to attain seizure control with AEDs. To cure or prevent epilepsy, disease-modifying interventions that inhibit or reverse the disease process of epileptogenesis must be developed. A major limitation in the development and implementation of such an intervention is the current poor understanding, and the lack of reliable biomarkers, of the epileptogenic process. Neuroimaging represents a non-invasive medical and research tool with the ability to identify early pathophysiological changes involved in epileptogenesis, monitor disease progression, and assess the effectiveness of possible therapies. Here we will provide an overview of studies conducted in animal models and in patients with epilepsy that have utilized various neuroimaging modalities to investigate epileptogenesis.

Fig. 1

Volumetric and [18F]FDG–positron emission tomography (PET) changes in kainic acid model of temporal lobe epilepsy and fluid percussion injury model of traumatic brain injury (TBI). There is persistent hypometabolism, and progressive degeneration after kainic acid-induced status epilepticus (A–C; adapted from [29]). Although all rats suffer progressive neurodegeneration after fluid percussion injury (D–F), rats that develop post-traumatic epilepsy display persistent hypometabolism at 3 months after TBI (G–I; adapted from [11])