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Abstracts & Commentary
Sources: Helmstaedter C, et al. Chronic epilepsy and cognition: A longitudinal study in temporal lobe epilepsy. Ann Neurol. 2003;54:425-432; Duncan JS, Thompson PJ. Editorial. The cognitive consequences of epilepsy. Ann Neurol. 2003;54:421-422.
Helmstaedter and colleagues addressed the question of whether temporal lobe epilepsy (TLE) may be associated with cognitive decline. They retrospectively reviewed their experience over 8 years with TLE patients who had undergone temporal lobectomy (TLX; 72 left, 75 right) vs medical management (n = 102) alone. The duration of epilepsy was 17-19 years and not statistically significant between the surgically and medically treated groups. The study included 3 time points: T1 at initial evaluation baseline, T2 at 1-year status post-TLX for surgical patients, and T3 at 2-10 years follow-up for both TLX and medically treated patients. Unfortunately, surgical vs medical treatment was not randomized, and an age-matched control group was not included in the analysis.
Taking these deficiencies into account, Helmstaedter et al reported that 50% of TLX patients and 60% of medically treated patients showed significant memory decline at T3. Left TLX patients did worse in memory functions than right TLX patients. Patients who achieved seizure-free outcome after TLX improved in non-memory cognitive functions at T2 and in memory testing at T3. Epilepsy surgery accelerated memory dysfunction at T2, but this improved at T3 if patients were cured of their seizures.
Any neurologist who treats epilepsy will inevitably be told by their patients that they are having problems with memory. The problem in evaluating this complaint, and what we usually tell these patients, is that it is likely multifactorial: a function of the patient’s continuing seizures, medication effects, and affective issues (ie, depression and pseudo-dementia that the patient is unwilling to acknowledge). Neurologists for their part are unable to acknowledge that some forms of epilepsy may be progressive, in terms of seizure-control and/or cognitive function. The minority1 of patients who can achieve a seizure-free outcome with medical management typically do not complain of cognitive decline, but most medically refractory patients typically sense their memory problems.
The current study demonstrates that 1) refractory TLE patients’ complaints of memory impairment can be objectively substantiated, particularly when seizures originate from the left temporal lobe, and 2) improvement in seizure control with epilepsy surgery may arrest and even improve cognitive decline. Helmstaedter et al are appropriately cautious when it comes to recommending epilepsy surgery. Specifically, they recognize that there are, in their words, "double winners" (seizure-free patients who stabilize or improve cognitively) and "double losers" (who do not achieve seizure freedom and experience significant cognitive decline as a result of surgery).
Given the fact that left TLE is associated with a higher risk of cognitive decline after TLX and that epilepsy may be more commonly a left rather than right hemispheric disorder,2,3 one needs to be especially careful in counseling patients about the potential morbidity of treatment options. Nonetheless, epilepsy surgery affords a better chance of seizure freedom than medical management in this study, as well as in the only prospective randomized, controlled trial of medical vs surgical management of epilepsy.4 What is the evidence-based bottom-line in advising medically refractory epilepsy patients? The answer is patient-specific counseling and informed consent: Until further data are available (particularly regarding early surgical intervention),5 potential benefit always entails potential risk. — Andy Dean, Assistant Professor of Neurology and Neuroscience, Director of the Epilepsy Monitoring Unit, Department of Neurology, New York Presbyterian Hospital—Cornell Campus.
1. Mattson RH, et al. Neurology. 1996;47:68-76.
2. Dean AC, et al. Epilepsia. 1997;38:503-505.
3. Labar D, et al. Seizure. 2001;10:570-572.
4. Wiebes S, et al. N Engl J Med. 2001;345:311-318.
5. Engel J Jr. Arch Neurol. 1999;56:1338-1341.