Abstracts

Rationale: The concern for dual pathology is generally raised when hippocampal atrophy is found ipsilateral to a neocortical lesion, which can be seen in up to 30% of cases. Li ( 1999) reported that in such patients resection of both the neocortical lesion and the atrophic hippocampus results in better surgical outcome. However, given the possibility of paradoxical mesial temporal lobe (MTL) epilepsy with normal hippocampal anatomy and the variability in detecting neocortical lesions with MRI, the concern for dual pathology may be raised using other aspects of the evaluation such as seizure semiology, EEG or other imaging modalities. In this report we present twelve patients in whom a broader consideration was made for dual pathology using magnetic resonance spectroscopic imaging (MRSI). Methods: Patients were recruited from the Yale Epilepsy Surgery Program and were included in this analysis on dual pathology if there was either: (A) imaging data demonstrated clear dual pathology with MRI-documented hippocampal atrophy (HA) or (B) no MRI evidence for HA but other data (including semiology, PET and EEG) suggesting limbic and temporal involvement. All patients also had to have participated in high resolution spectroscopic imaging studies of the medial temporal lobes. Twelve patients fulfilled these criteria (Table 1). Results: Of the 12 patients meeting inclusion criteria, 6 were classified as extratemporal epilepsy and 6 as neocortical-temporal epilepsy. Three patients were classified as group A and 9 as group B. Of the nine patients without clear MRI evidence for HA, MRSI demonstrated metabolic dysfunction of the hippocampus in 5 patients. In total, 8 of 12 patients showed MRSI-determined MTL abnormalities. Table 2 illustrates this subgrouping. Nine patients have gone on to surgery, 6 with more than one year post operative follow-up. Of the patients with metabolic abnormalities in the MTL on MRS, 7 had surgery. Of those 7 patients, 3 underwent surgical resection which did not include the entire extent of the metabolically dysfunctional region within the medial temporal lobe. These 3 patients had poor surgical outcome and are two years post surgery. Conclusions: We found that 55% (5/9 patients) without overt hippocampal atrophy seen on MRI had metabolic abnormalities in the medial temporal lobe. These findings are consistent with Mueller (2006) and likely reflects the general injury that can arise in the setting of intractable epilepsy. The presence of dual pathology in the temporal lobe can be based on metabolic abnormalities detected by MRSI and other factors beyond MRI structural imaging to provide outcomes prediction and therapeutic guidance.