Does Epilepsy Surgery Accelerate Cognitive Aging?
Abstract number :
K.07
Submission category :
Year :
2001
Submission ID :
129
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
C. Helmstaedter, PhD, Epileptology, University, Bonn, NRW, Germany; M. Reuber, MD, Epileptology, University, Bonn, Germany; C. Elger, MD, Epileptology, University, Bonn, Germany
RATIONALE: Long term studies of memory in chronic temporal lobe epilepsy spanning ip to 10 years show surprisingly stable performance over time. Cross sectional data indicates that initial lesions and physiological aging are more likely causes of memory disability in advanced age than duration of epilepsy. Therefore we evaluated whether and how epilepsy surgery alters the course of cognitive aging with respect to memory.
METHODS: Age regression of verbal learning and memory was evaluated in 187 patients before and one year after left temporal lobe surgery (80 selective amydalo hippocampectomies SAH, 107 2/3 anterior temporal lobe resections ATL). Age regression of verbal memory in 272 healthy persons served as control. Memory was evaluated with respect to its cortical and mesial aspects (learning vs. consolidation retrieval)
RESULTS: Patients showed significant preoperative memory impairment. Surgery had additional negative effects on all aspects of verbal learning and memory. Age regression of preoperative learning paralled that observed in controls. Postoperative data demonstrated accelerated aging, particularly after ATL and less severly after SAH. In controls and in patients with SAH no significant age regression was found for consolidation retrieval. Patients with ATL had accelarated decline of mesial consolidation/retrieval preoperatively which was even greater after surgery.
CONCLUSIONS: The data supports our previous findings that age regressions of memory in patients with TLE are similar to those seen in healthy controls. Thus no general accelerating effect of chronic epilepsy on memory decline was observed. Patients treated with 2/3 ATL were the exception with age regressions of measures of mesial consolidation/retrieval showing a steeper decline than in healthy controls. These patients often had no hippocampal pathology. One could speculate that these patients have a cumulative mesial functional imepiarment caused by an extrahippocampal focus over time. Surgery worsenes verbal memory and brings patients closer to disability. After left ATL accelerated cognitive aging becomes particularly evident in cortical aspects of verbal memory.
Support: Deutsche Forschungsgemeinschaft (DFG EL 122/6-2)