Metabolic correlates of cognitive impairment in mesial temporal lobe epilepsy

The purpose of the study was to determine the correlations between brain metabolism and cognitive impairment in patients with drug-resistant mesial temporal lobe epilepsy (MTLE).

[¹⁸F]-FluoroDeoxyGlucose positron emission tomography ([¹⁸F]-FDG-PET) and neuropsychological assessment were performed in 97 patients with MTLE (53 females, 15-56 years old, mean: 31.6 years, standard deviation (SD) = 10.4) with unilateral hippocampal sclerosis (HS, 49 left). We compared brain metabolism and gray matter volume (GMV) between patients with cognitive impairment (intelligence quotient (IQ) and memory index <80) and patients with normal cognition, using statistical parametric mapping (SPM), in the whole population then in right and left HS (RHS, LHS) separately.

Intelligence quotient (40-121, mean: 83.7 ± 16.9) and memory index (45-133, mean: 80.7 ± 19.3) were impaired in 43% and 51% of the patients, respectively, similarly in RHS and LHS. We did not find any correlations between IQ and clinical factors related to epilepsy; however, there was a significant correlation between low memory index and early age of onset in LHS (p = 0.021), and widespread epileptogenic zone in the whole population (p = 0.033). Impaired IQ correlated with extratemporal hypometabolism, involving frontoparietal networks implicated in the default mode network (DMN), predominantly in the midline cortices. Metabolic asymmetry regarding HS lateralization included the precuneus (pC) in LHS and the anterior cingulate cortex (ACC) in RHS, both areas corresponding to key nodes of the DMN. Memory index correlated with the same frontoparietal networks as for IQ, with an additional involvement of the temporal lobes, which was ipsilateral in RHS and contralateral in LHS. A diffuse decrease of GMV including the ipsilateral hippocampus correlated with cognitive impairment; however, the structural alterations did not match with the hypometabolic areas.

Cognitive impairment in MTLE correlates with extratemporal hypometabolism, involving the mesial frontoparietal networks implicated in the DMN and suggesting a disconnection with the affected hippocampus. Asymmetric alterations of connectivity may sustain the predominant ACC and pC metabolic decrease in patients with cognitive impairment.