Neurology -- Correspondence for Galton et al., 57 (2) 216-225

Correspondence published:

Differing patterns of temporal atrophy in Alzheimer’s disease and semantic dementia: Dennis Chan, "Nick Fox, Martin Rossor" (6 November 2001)

Differing patterns of temporal atrophy in Alzheimer’s disease and semantic dementia 6 November 2001

Dennis Chan
Institute of Neurology London UK,
"Nick Fox, Martin Rossor"
Send Correspondence to journal:
Re: Differing patterns of temporal atrophy in Alzheimer’s disease and semantic dementia

d.chan{at}dementia.ion.ucl.ac.uk Dennis Chan, et al.

We read with interest the article by Galton et al. [1]. Their results complement those obtained in our study, in which quantitative MRI analysis was also used to measure the volumes of the temporal lobe structures in semantic dementia (SD) and Alzheimer’s disease (AD). [2]. There is a reassuring level of agreement between the two sets of results. Both studies revealed that there was marked hippocampal atrophy in the SD patients. The degree of right-sided hippocampal atrophy was comparable between the SD and AD groups, whereas the atrophy of the left hippocampus was more severe in the SD group.
Episodic memory is relatively preserved in SD, as evidenced by the demonstration in both studies that the SD patients were less impaired on tests of episodic memory than the AD patients. Given the role of the hippocampus in episodic memory, [3] these observations of hippocampal atrophy in SD appear somewhat surprising at first sight.
Galtonet al. suggested several possible explanations for this apparent discrepancy. [1] First, there is the possibility that episodic memory function in the SD patients is maintained by the right hippocampus. However, in both studies the right hippocampus in the SD patients was found to be at least as atrophied as in the AD patients. A second option is that there is a greater degree of frontal lobe dysfunction in the AD patients, and that this additional dysfunction may exacerbate the memory problem in AD. This argument, though, is weakened by the knowledge that the frontal lobes are frequently affected in SD, as Galton et al. point out. [1] Finally, the difference in episodic memory performance between SD and AD might be attributed to different effects of the two diseases on neurotransmitter systems.
We would like to propose an alternative explanation. We undertook an assessment of the anteroposterior gradient of hippocampal atrophy by measuring cross-sectional areas through both hippocampi along their rostrocaudal extents. In SD the hippocampal atrophy was predominantly anterior in location, with relative preservation of the posterior hippocampi. On this basis, we hypothesise that the relative sparing of episodic memory in SD is attributable to the sparing of the posterior hippocampi. This would be in keeping with functional imaging studies that show greater activation of the hippocampus posteriorly during episodic encoding and retrieval. [4, 5] Taken together, these data have implications for our understanding of the role of the hippocampus in episodic memory.
We would welcome further discussion on this intriguing subject.
References:
1. Galton CJ, Patterson K, Graham KS, et al. Differing patterns of temporal atrophy in Alzheimer's disease and semantic dementia. Neurology 2001;57:216-225.
2. Chan D, Fox NC, Scahill RI, et al. Patterns of temporal lobe atrophy in semantic dementia and Alzheimer's disease. Ann Neurol 2001;49:433-442.
3. Squire LR, Zola-Morgan S. The medial temporal lobe memory system. Science 1991;253:1380-1386.
4. Fernandez G, Weyerts H, Schrader-Bolsche M, et al. Successful verbal encoding into episodic memory engages the posterior hippocampus: a parametrically analyzed functional magnetic resonance imaging study. J Neurosci 1998;18:1841-1847.
5. Schacter DL, Wagner AD. Medial temporal lobe activations in fMRI and PET studies of episodic encoding and retrieval. Hippocampus 1999;9:7- 24.