[Mristudio-users] Absence of CST in subcortical motor cortex

Rajagopalan, Venkateswaran rajagov2 at ccf.org
Wed Apr 14 10:22:04 EDT 2010


Dear Dr.Mori,
 
Thanks very much for your informative and insightful answer. As you mentioned i don't see any CST abnormality i.e absence of CST in controls, so this relieves me from being worried as processing error.
 
Thanks very much.
 
Regards
venkat
 

________________________________

From: mristudio-users-bounces at mristudio.org on behalf of susumu mori
Sent: Tue 4/13/2010 4:25 PM
To: DTI Studio, ROI Editor, DiffeoMap Questions/Support
Subject: Re: [Mristudio-users] Absence of CST in subcortical motor cortex


Hi Venkat,

If you apply the same method to both groups and only one of the groups show the truncated CST, it tells there is some difference between the two groups detected by DTI.

I think this is a fact. Our interpretation, on the other hand, may not be a fact and there are many ways to interpret the same data. I believe this is the source of your question.

When we do MRI and find something (e.g. FA drops, ADC increases, fibers thinner, etc), we try to directly relate it to underlying neuroanatomy. For example, FA tells something about myelination and tractography about connectivity. However, MRI/DTI measures water properties at each pixel, which is a decidedly indirect indicator of any cellular entity. The level of biological question we are asking often require astronomical amount of data. For example, if we want to know myelination status, we are asking questions in micrometer scale of 100 billion axons. On the other hand, DTI data is merely 20 MB of information. This is a huge degeneration problem. You can predict what would happen in DTI/MRI if you know the anatomy, but it's much tougher to define what really happens from DTI/MRI results. 

By applying the same tractography protocol, you found consistent difference between two groups. If you use Wakana's protocol, there are more subjects in the patient group that return "null". If you quantify the results in some way (e.g. the number of "null" subjects, the average number of pixels, etc), you may be able to find a statistical difference. So far so good. However, you have to interpret this data, where the difficulty arises. If you literary take the results and claim, "there are more patients who lack the CST", that may not be true. This is because there could be multiple reasons that lead to the same tractography results; there is one area with low FA, enlargement of the ventricle made the CST trajectory more tortuous, thinning of one anatomical area made the tractography less reproducible (partial volume effect), reduction of the CST axon leads to the higher contribution of a small population of crossing fibers, and so on.

By having only 20 MB of the data, MRI/DTI/tractography can only be a screening tool, I think. To obtain more information, you may need to do more analysis to come closer to the true reason of your results. You can modify the CST protocol so that you can get more fibers. If you lower the second ROI away from the motor cortex, you get more fiber with an expense of less specificity to the CST. You can monitor FA values along the fiber. You can do voxel-based analysis to find a group of pixels that accounts for the different tractography results. If you can identify the reason (e.g. locations of pixels with different FA/vector values), you have more specific information about the difference between the two groups.

Sorry that I'm not providing a solution to your answer. If your control group shows good CSTs, then I think you are not making a mistake. It's possible that the corona radiata has lower FA in the patients. I would try to find out the reason of the truncated CST.

Susumu


On Tue, Apr 13, 2010 at 12:16 PM, Rajagopalan, Venkateswaran <rajagov2 at ccf.org> wrote:



	Dear All,
	
	In our study we tried to evaluate changes in CST between our patient and control groups using DTI metrics. We reconstructed CST using tracography and measured changes in DTI metrics.
	
	We used same protocol for DTI imaging and the DTI images were processed the same way in DTI studio like setting same the FA threshold for tracking in all the subjects, tracts reconstructed using Wakana et al's two ROI approach i.e we placed our first ROI in cerebral peduncle and then the second ROI in subcortical Motor cortex, used cut operation in all the subjects, then similar kind of outlier rejection of bad DW images.By this i mean same processing steps.
	
	
	The question i have is in some of these patients CST doesn't go all the way up to motor cortex i.e.after reconstruction CST is available only between cerebral peduncle to top of lateral ventricle and after that ( i.e. higher up) CST is absent, this is seen only in some of our patients not in all the cases. Can i attribute this to the disease process or is there somewhere i am making mistake in my image processing steps.
	
	Thanks in advance.
	
	venkat 

	

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