Abstracts

Rationale: ¹⁸F-FDG-PET hypometabolism is often found beyond the epileptogenic cortex in focal epilepsy. However, the significance of this hypometabolism remains poorly understood. This study examined the relationship between quantified left temporal lobe hypometabolism and neuropsychological functioning in patients with occipital lobe epilepsy (OLE). It was hypothesised that left temporal lobe hypometabolism is correlated with verbal memory but not frontal/executive functioning. Methods: Nine right-handed patients were included in the study, all of whom had medically refractory OLE, had undergone epilepsy surgery and were followed up for at least one year. Eight patients became free of seizures. Presurgical ¹⁸F-FDG-PET was analysed voxel-by-voxel using statistical parametric mapping (SPM) to identify significant regions of glucose hypometabolism relative to normal controls. Pearson’s product-moment correlation was then used to correlate left temporal lobe hypometabolism with presurgical verbal memory (recall of short stories) and frontal/executive functioning (both a composite measure comprising various executive tasks (CompExec), and perseverative errors on the Wisconsin Card Sort Task (WCSTpe)). Results: Eight patients had temporal lobe hypometabolism (four left-sided). Verbal memory was significantly correlated with the volume of left temporal lobe ¹⁸F-FDG-PET hypometabolism (r = -.72, p<0.05, one-tailed). This correlation was significantly stronger than that between WCSTpe and left temporal lobe ¹⁸F-FDG-PET hypometabolism (r = -.281, p=0.23, one-tailed); and between CompExec and left temporal lobe ¹⁸F-FDG-PET hypometabolism (r = .219, p=0.32, one-tailed) based on the Williams test (z = 6.05, p=<0.01, one-tailed and z = 1.82, p=<0.05, one-tailed, respectively). Conclusions: The results reveal left temporal lobe ¹⁸F-FDG-PET hypometabolism to be significantly correlated with verbal memory, an ability widely accepted to be related to left temporal lobe integrity. This was detectable in a very small sample independent of cognitive functions thought to be served by extra-temporal regions. To the researchers’ knowledge, this is the first study to investigate the relationship between neuropsychological functioning and ¹⁸F-FDG-PET hypometabolism beyond the epileptogenic cortex in focal epilepsy, quantified with SPM. Given that memory impairment is not normally expected with occipital lobe epilepsy, the results support emerging findings of the link between cerebral glucose hypometabolism and cognitive dysfunction.