Abstracts

RATIONALE: In some patients with left temporal lobe epilepsy (TLE), resection of the left hippocampus poses a significant threat to verbal memory. In these cases, a resection which preserves as much hippocampal tissue as possible has been suggested as a way of avoiding or minimizing postoperative verbal memory impairment. Our previous observations, however, suggest that the left perirhinal region plays a role in verbal memory function¹. We examined verbal memory outcome in three patients with hippocampal-sparing left temporal lobe resections. OBJECTIVE: To test the hypothesis that left anterior temporal lobectomy involving the perirhinal/entorhinal cortices, but preserving normal hippocampus, causes verbal memory impairment.
METHODS: Pre- and post-operative performance on a range of verbal memory tests including arbitrarily- and semantically-related verbal paired associate learning was studied in three patients who underwent resection of epileptogenic lesions in the anterior temporal lobe. Post-operative T1-weighted MRI scans were placed in stereotaxic coordinate space and residual mesial temporal structures identified using previously described anatomical landmarks^2-3.
RESULTS: In two patients, the resection spared the amygdala and hippocampus but adjacent perirhinal/entorhinal cortices were resected. In the remaining case the perirhinal/entorhinal cortices, amygdala and hippocampus were spared. Both cases with perirhinal/entorhinal damage had postoperative impairments in the acquisition of unrelated paired associates which persisted over a 12 month follow-up period. Learning of semantically-related paired associates showed an early postoperative decrement, but returned to normal levels within twelve months. The case with sparing of the perirhinal region did not show a postoperative change in associative learning.
CONCLUSIONS: Hippocampal-sparing resections may result in verbal memory deficits when perirhinal/entorhinal tissue is resected. In these cases, the verbal memory deficit is task-specific and is similar to the dissociation observed pre-operatively in patients with left hippocampal sclerosis⁴. Whether this effect results from hippocampal deafferentation or is the result of perirhinal or entorhinal damage [italic]per se[/italic] remains to be determined.
1. Weintrob D, Saling MM, Berkovic SF, Berlangieri SU, & Reutens DC. Verbal memory in left temporal lobe epilepsy: Evidence for task-related localization. Ann Neurol 2002;51:442-447.
2. Watson C, Andermann F, Gloor P, Jones-Gotman M, Peters T, Evans A, Olivier A, Melanson D, & Leroux G. Anatomic basis of amygdaloid and hippocampal volume measurement by magnetic resonance imaging. Neurology 1992;42:1743-1750.
3. Insausti R, Juottonen K, Soininen H, Insausti AM, Partanen K, Vainio P, Laakso MP, & Pitkänen A. MR volumetric analysis of the human entorhinal, perirhinal and temperopolar cortices. AJNR Am J Neuroradiol 1998;19:659-671.
4. Wood AG, Saling MM, O[scquote]Shea MF, Berkovic SF, & Jackson GD. Components of verbal learning and hippocampal damage assessed by T2 relaxometry. J Int Neuropsychol Soc 2000;6:529-538.
[Supported by: NHMRC, Australia]