Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits

Butler CR, Bhaduri A, Acosta-Cabronero J, Nestor PJ, Kapur N, Graham KS, et al.; Brain 2009; 132 (Pt 2); 357-368. [Epub 2008 Dec 10]

Commented by Prof Serge Gauthier, 13 Mar 2009

Aim of the study

To establish if subjective measures of memory reflect objective performance on neuropsychological tests in subjects with transient epileptic amnesia (TEA), a subtype of temporal lobe epilepsy where episodes of amnesia are short (30-60 minutes), recurrent, and may be associated with accelerated long-term forgetting (ALF). Establish if TEA is associated with focal volume loss in the brain, and if memory function in TEA correlates with seizure variables or with regional brain volume.

Method

A cohort of 41 patients with TEA defined as recurrent episodes of transient amnesia, cognitive functions other than memory judged to be intact during these episodes, epileptiform abnormalities on EEG and/or other clinical features of epilepsy (lip-smacking, olfactory hallucinations) and/or response to anticonvulsants (carbamazepine, sodium valproate, lamotrigine, phenytoin, levetiracetam), seizure-free for at least 6 months, was compared to 20 age and education-matched healthy controls.

They underwent subjective memory assessments and formal neuropsychological assessments, and MRI. Neuropsychological and manual volumetric measurements were compared between groups and correlated. Voxel-based morphometry was also used.

Results

The mean age of patients was 67.7 (SD 8.9); significant differences (P<0.05) were found against controls on logical memory delayed recall, Rey figure delayed recall, recognition memory test for words and faces, hospital anxiety and depression scale, modified autobiographical memory interview semantic and episodic components.

Manual volumetric data showed significant differences for left and right hippocampus, but not for the amygdala. The overall anterograde memory score showed a significant positive correlation with the right hippocampal volumes on manual as well as voxel-based morphometry.

Professor Gauthier's comments

Patients with TEA have subtle volume loss in the hippocampus and show a mild deficit in performance on standard tests of anterograde memory. In this patient cohort with no seizure for at least 6 months the memory deficits reported by patients related more closely to ALF and autobiographical amnesia, and the authors conclude that this type of memory impairment is not clearly related to regional brain atrophy, suggesting that further studies using metabolic and functional imaging are required to determine their pathophysiological origins.

The authors documented that patients' subjective impression of memory impairment was partially predicted by mood, but not by standard measures of anterograde memory.

This is not an unusual situation in memory clinics were more and more persons consult alone for subjective memory complaints not detected by family or co-workers, and without objective decline on formal memory testing: this "Subjective Cognitive Impairment" (SCI) should be assessed for underlying depression and long-term follow-up is appropriate in persons with a family history of Alzheimer's disease (ref. 1).

Should epilepsy be suspected in patients with SCI? This article and others by Butler et al. suggest that this is the case. Certainly questions should be asked to observers about motor symptoms if symptoms occur in discrete episodes, and a routine EEG should be considered if symptoms are intermittent.

From a broader perspective, it should be said again that not all persons with memory complaints have an underlying neurodegenerative condition. This article is a useful reminder of one of the many conditions to be considered in the differential diagnosis of memory complaints. But this does not mean that all persons with memory complaints  should have a trial of an antiepileptic drug!

References

1. Reisberg B, Gauthier S. Current evidence for subjective cognitive impairment (SCI) as the pre-mild cognitive impairment (MCI) stage of subsequently manifest Alzheimer's disease. International Psychogeriatrics 2008; 20 (1); 1-16

Last updated: 13.03.2009