Evolution of hippocampal CA-1 diffusion lesions in transient global amnesia
Article first published online: 13 AUG 2007
Copyright © 2007 American Neurological Association
Annals of Neurology
Volume 62, Issue 5, pages 475–480, November 2007
How to Cite
Bartsch, T., Alfke, K., Deuschl, G. and Jansen, O. (2007), Evolution of hippocampal CA-1 diffusion lesions in transient global amnesia. Ann Neurol., 62: 475–480. doi: 10.1002/ana.21189
- Issue published online: 27 NOV 2007
- Article first published online: 13 AUG 2007
- Manuscript Accepted: 15 JUN 2007
- Manuscript Revised: 4 JUN 2007
- Manuscript Received: 4 MAY 2007
Selective focal MR-Signal (diffusion-) changes in the CA-1 sector of the hippocampus have been described in transient global amnesia (TGA), but the pathophysiological substrate of these lesions is largely unknown. As several imaging and epidemiological findings point to a vascular origin an analysis of the temporal evolution of the hippocampal apparent diffusion coefficient (ADC) changes may offer new understanding of the pathomechanisms of TGA.
The time course of the ADC of hippocampal DWI lesions in TGA patients was studied using serial 3 T high-resolution MR-imaging within 1-10 days as well as 4-6 months after TGA. ADC values from 76 MR-studies were analyzed and expressed as ratio ADC (rADC) in reference to the unaffected hemisphere.
Twenty-nine patients with TGA showed 34 DWI lesions with corresponding T2 lesions in the CA-1 sector of the hippocampal cornu ammonis within a time window of 24-72 h after onset. Ratio ADC decreased below 1.0 (0.66 ± 0.08) 24 h after the acute TGA episode and did show a further significant decrease to 0.57 ± 0.1 after 3 days (p < 0.05). After 72 h, rADC increased and normalized around day 10 with rADC values of 1.0 (p < 0.05).
The temporal evolution of the rADC in hippocampal signal changes in TGA shows a time course previously described for ischemic lesions in human stroke patients. This might imply a vascular origin of diffusion changes leading to a transient perturbation of memory relevant circuits in the hippocampus. Ann Neurol 2007