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ARTICLES:
V. N. Thijs, A. Adami, T. NeumannHaefelin, M. E. Moseley, M. P. Marks, and G. W. Albers
Relationship between severity of MR perfusion deficit and DWI lesion evolution
Neurology 2001; 57: 1205-1211
[Abstract][Full text][PDF]
Vincent.Thijs{at}uz.kuleuven.ac.be Vincent Thijs, et al.
We appreciate the comments of Parsons et al. The focus of our study
was not to predict final infarct volume using the lesion volumes
identified on baseline MTT, CBF or CBV maps, as was performed elegantly by
Parsons et al. [2] Our goal was to evaluate the predictive value of the
relative signal intensities identified on these hemodynamic maps, rather
than differentiate between the value of individual maps. Our results show
that the more hyperintense the MTT lesion, the more likely the diffusion
lesion was to grow to equal the size of the baseline MTT lesion. As
acknowledged in the paper, the lack of predictive value of our CBF ratios
may be due to the small sample size, the inclusion of regions of normal or
increased CBF within the “CBF lesion” or susceptibility artefacts.
The best functional MR method to predict final infarct volume in
hyperacute stroke patients is currently unknown. ADC, MTT, CBF and CBV,
separately or in combination have all been proposed as having a high,
although imperfect, predictive ability for detecting ischemic lesion
growth. [2, 4, 5, 6] We suspect that discrepancies between the results of
these studies are related to differences in MR acquisition technique,
mathematical analysis, and definition of PWI/DWI mismatch, variable
clinical inclusion criteria and inherent biological variability. To
resolve this issue, multicenter studies are needed that include large
numbers of patients and uniform criteria for data acquisition and
analysis. Different post-processing methods should be directly compared
to identify the method with the best predictive value. Until these
important studies are performed, the superiority of one approach over
another will remain unestablished.
References:
1. Thijs VN, Adami A, Neumann-Haefelin T, Moseley ME, Marks MP,
Albers GW. Relationship between severity of MR perfusion deficit and DWI
lesion evolution. Neurology 2001;57:1205-1211.
2. Parsons MW, Yang Q, Barber PA, et al. Perfusion magnetic
resonance imaging maps in hyperacute stroke: relative cerebral blood flow
most accurately identifies tissue destined to infarct. Stroke 2001;32:1581
-1587.
3. Barber PA, Darby DG, Desmond PM, et al. Prediction of stroke
outcome with echoplanar perfusion- and diffusion-weighted MRI. Neurology
1998;51:418-426.
4. Oppenheim C, Grandin C, Samson Y, et al. Is there an apparent
diffusion coefficient threshold in predicting tissue viability in
hyperacute stroke? Stroke 2001;32:2486-491.
5. Wu O, Koroshetz WJ, Ostergaard L, et al. Predicting tissue outcome
in acute human cerebral ischemia using combined diffusion- and perfusion-
weighted MR imaging. Stroke 2001;32:933-942.
6. Sorensen AG, Copen WA, Ostergaard L, et al. Hyperacute stroke:
simultaneous measurement of relative cerebral blood volume, relative
cerebral blood flow, and mean tissue transit time. Radiology 1999;210:519-
527.
Relationship between severity of MR perfusion deficit and DWI lesion evolution
18 February 2002
Mark W Parsons Royal Melbourne Hospital Victoria Australia, Alan Barber and Stephen M Davis
We were interested to read the article by Thijs et al. [1] examining
the relationship between severity of MR perfusion deficit and DWI lesion
evolution. We have recently published a similar analysis of sub-6 hour
ischemic stroke patients with acute PWI>DWI mismatch. [2] We also found
that MTT and CBV lesions closely predicted final infarct size. However,
the strong correlation between acute CBF lesions and final infarct size in
our 23 patients was not reproduced in the 12 patients studied by Thijs et
al. [1]
Perhaps the differing methodology explains the lack of agreement. It
would not be unreasonable to expect the CBF ratio to be similar to CBV
ratio/MTT ratio (as MTT = CBV/CBF at a pixel level). However, there are
three of the 12 patients (7, 11, and 12 in the Table) where the presented
CBF ratio exceeds the predicted CBF value by more than twenty-five per
cent. We wonder if reflecting the larger MTT lesion onto the CBF map has
led to inclusion of tissue with normal or increased CBF within the
‘lesion’, thus leading to a higher than anticipated CBF ratio.
Furthermore, as the current authors and others have shown, the
visually apparent acute MTT lesion almost always overestimates final
infarct size. [1, 2, 3] Therefore patient 2 in the Table, who has a final
infarct 65% greater than the acute MTT lesion, may have an artefactual
result. This could be due to the significant susceptibility artefact on
the PWI maps that the authors acknowledge.
We agree that MTT maps are the most practical of the PWI maps to use
in stroke and concur that thresholded MTT maps are reasonably accurate at
predicting tissue at risk of infarction. However, we believe that some
caution should be applied when interpreting the CBF results of the current
study, particularly in view of the small number of patients presented.
References
1. Thijs VN, Adami A, Neumann-Haefelin T, Moseley ME, Marks MP,
Albers GW. Relationship between severity of MR perfusion deficit and DWI
lesion evolution. Neurology 2001;57:1205-1211.
2. Parsons MW, Yang Q, Barber PA, et al. Perfusion magnetic resonance
imaging maps in hyperacute stroke: relative cerebral blood flow most
accurately identifies tissue destined to infarct. Stroke 2001;32:1581-1587
3. Barber PA, Darby DG, Desmond PM, et al, Prediction of stroke
outcome with echoplanar perfusion- and diffusion-weighted MRI. Neurology
1998;51:418-426.