Abstracts

Patients with non-lesional temporal lobe epilepsy (NLTLE) commonly show prominent imaging abnormalities on magnetic resonance imaging (MRI) and flurodeoxyglycose positron emission tomography (FDG-PET) in the ipsilateral temporal lobe in the absence of hippocampal atrophy. The rat amygdala electrical kindling model shows many of the characteristics of NLTLE, including a relative lack of cell loss in the hippocampus. It is unknown if the imaging changes seen in NLTLE also are present in this model. The present study aimed to determine whether imaging changes seen on MRI and FDG-PET in NLTLE are also detectable in the hippocampus in the rat amygdala kindling model, and then utilise this model to investigate the pathophysiological processes underlying these changes. MRI compatible stimulating, ground and reference electrodes were developed to enable imaging without the induction of [lsquo]artefacts[rsquo] created by magnetic components within the magnetic field. Surgeries were performed according to well established methods. Following one week of recovery, FDG-PET and T[sub]2[/sub] weighted images were acquired every two weeks for six weeks on dedicated small animal imaging scanners. Electrical stimulations were started the day following the first imaging session and continued six days a week for four weeks. MRI demonstrated the development of focal regions of hyper intense T[sub]2 [/sub]signal in the rostral hippocampus during kindling (n=4/5) both ipsilaterally (n=3) and bilaterally (n=1) specifically in CA1 and dentate gyrus. FDG-PET demonstrated progressive development of hypometabolism (n=4/4) compared with control animals (median change in ipsilateral/contralateral ratios from pre-kindling to fully kindled: 5.6% vs. -1.6%, p[lt]0.05).[figure1] We have developed a method for acquiring high quality serial MR and FDG-PET images in amygdala kindled rats. Results demoonstrate that amygdala kindling produces progressive changes in T[sub]2[/sub] MRI and FDG-PET images similar to those seen in NLTLE. This model will provide a powerful tool to investigate the pathophysiological basis of the imaging changes and epileptogenesis in this common form of epilepsy.