Abstracts

RATIONALE: Previous studies suggest that 60 to 80% of patients fulfilling MRI criteria of mesial temporal sclerosis (MTS) can expect a good seizure outcome after temporal lobe surgery. Reasons for surgical failure in those satisfying the MRI criteria are poorly understood. Possibilities include presence of more widespread mesial temporal structural damage, bilateral MTS, and conservative amygdalohippocampal resection. Previous studies done by our group have found concurrent fornix atrophy in 86% with ipsilateral hippocampal atrophy. This reflects analogous pathologic changes to limbic circuit interconnected structures. The contribution of the fornix as an independent preoperative determinant of surgical outcome remains to be validated. This study evaluates the contribution of the fornix as a determinant of seizure outcome in patients with preoperatively detected hippocampal atrophy.
METHODS: Subjects: We selected patients who had undergone standard anterior temporal lobectomy for intractable temporal lobe epilepsy at the UAB Epilepsy Center between 1994 and 1995 and who had a final diagnosis of mesial temporal lobe epilepsy. Patients with foreign tissue lesions and MRI showing no evidence of hippocampal atrophy were excluded. MRI acquisition and analysis: Using criteria and technique previously published by Kuzniecky et al, 1.5 T MRI study was performed in each patient as part of the presurgical evaluation. Surgery and outcome: Subpial aspiration technique was used for temporal resections. Patients were assessed regularly for postoperative seizure control. All had at least 3 years of follow-up. Outcome was evaluated using Engel[scquote]s classification. Statistical analysis: Fisher[scquote]s exact test was used to compare categorical data.
RESULTS: Seventy-three patients (45 women, 28 men; mean age 32, range 13 to 58) were studied. Mean age of seizure onset was 9.7 years and mean duration of epilepsy was 21.3 years. Eight patients were excluded because of lack of follow up. Thirty-five (47.9%) patients had hippocampal atrophy on MRI volumetry, and 30 had hippocampal and fornix atrophy. Eighty percent in the hippocampal atrophy group were seizure free (Engel[scquote]s I) at last follow up, compared with 73% in the fornix and hippocampal atrophy group (p= 0.5668, Fisher[scquote]s exact test)
CONCLUSIONS: The existence of fornix atrophy may be secondary to wallerian degeneration from hippocampal cell damage, or as a result of abnormal excitotoxic damage to axonal flow. These findings suggest that identification of fornix atrophy on MRI, is not an important preoperative determinant of surgical outcome. To our knowledge, this finding has not been previously reported.