Thalamocortical circuits causing remote hypometabolism during focal interictal epilepsy

Abstract 

The functional circuit causing depression of cerebral glucose metabolism in brain areas remote from an epileptic focus was investigated in experiments on the cortex of the rat. Epileptic activity was induced by direct epicortical application of Na-penicillin onto the motor cortical area Fr1/Fr2. The increased neuronal activity was associated with an increase of metabolism in the focal area and a decrease in somatosensory cortical areas. Metabolism was also massively increased in the thalamus, predominantly in the posterior nucleus. Stereotactic radiofrequency lesioning of this nucleus, 30 days prior to the induction of the epileptic focus, restricted the area with increase of metabolism to the upper cortical laminae, and abolished the cortical hypometabolism in the sensory cortex. It is suggested that the primary functional circuit affected by the acute epileptic focus in the present model consists of the motor cortex, the thalamic nucleus posterior and the somatosensory cortex.

Keywords:  Epilepsy, Hypometabolism, Penicillin, Posterior nucleus, Thalamic lesion

Abbreviations:  aCSF, artificial cerebrospinal fluid, ECoG, electrocorticogram, Fr1/2, frontal cortex, area 1 and 2, FL, forelimb area, Pir, piriform cortex, Ai/Gi, agranular and granular insular cortex, Par 1, parietal cortex, area 1, VPL, ventroposterior lateral nucleus, VL, ventrolateral nucleus, VPM, ventro-posteromedial nucleus, PO, posterior nucleus, PET, positron emissions tomography