SE-EPI DWI is predominantly T2-weighted because of the 180-degree refocusing pulse, which corrects for dephasing due to field inhomogeneities. T2* effects from the EPI readout are minor.
I wanted to ask this, because he repeatedly stated that the image was T2*-weighted. But it should be T2-weighted because of the rephasing 180° RF Pulse, right?
i think vlogger is correct, because DWI has the same bad geometric distortion and signal loss (e.g. at air/tissue interface) as T2* fMRI does, but that 180 pulse throws me off too. so it would be nice if he clarified.
Why is the B0 a T2* image if there is a 180 degree RF pulse used and a longer TE? - would the 180 degree RF pulse counter the T2* effects and make a T2 image?
Definitely need to review your spin echo video, but wow, this was explained so well. It definitely is like a physics brain teaser and very cool to see how diffusion weighted imaging can be used. Thank you so much for this.
Thanks to this 27-minutes lesson I finally understood DWI, you're my hero. A question: why do you keep saying that the b0 image is T2*-weighted and not simply T2-weighted? If a SE sequence was used in your example, shouldn't the signal be closer to the tissue's T2? I'll try to answer myself, but I'm not sure if I'm getting the point: could it be that the T2* is an effect of the inhomogeneity created by the EPI gradients?
First off, superb video series. What an amazing achievement to put all this together. I am slightly confused here. Does the frequency encoding gradient come BEFORE the phase encoding gradient when we are doing B0? If so, why? Or is the phase, and then frequency encoding gradient? maybe its a bit late at night here, and I am oversaturated with coffee?
Excellent series, your videos have been invaluable for FRCR revision. Do you mind sharing whether the question bank will be made available to radiopaedia all access pass holders, and roughly what time frame this might be? Thanks
Even though we confirm with ADC that restriction is true why do we still value dwi more than ADC and dwi together? Like in pirads we can count high signal on dwi even with normal ADC. In general hyperintensity on dwi even without hypo on ADC should be at least suspicious.
Ive a question . How do Diffusion gradients in same directions lead to rephasing? If they were in opposite directions id get it cuz laggers become leaders but it is in the same direction so the leader will still be going faster than the lagger on the second gradient? I am considering a voxel with all in phase and then gradient along one plane in my model and applying the previous leader lagger model.
The 180 degree RF pulse causes the ‘leaders’ to become the ‘laggers’. If there was no RF pulse the diffusion gradients would need to be in opposite directions. However the 180 degree RF pulse means that the two diffusion gradients will effectively be equal and opposite.
You’re right. Diffusion is movement across a concentration gradient. Diffusion weighted imaging isn’t actually measuring diffusion rather the ability of particles to move freely/without restriction. These particles move with Brownian motion. Thanks for pointing out the difference
@@radiologytutorials Thank you so much for actually answering. I do apologise for the bluntness of my comment but yesterday I was going mad with this situation. I have yet not resolved the issue. To give you a little bit of context: - I am currently working in stroke, it’s why I got entangled with this. At the beginning I was assuming DWI measured diffusion, hence I was trying to explain the physiopathology of cytotoxic oedema from DWI point of view. Almost went mad. Actually, with cytotoxic oedema there is a net movement, a diffusion of water from extracellular space to intracellular space. In normal conditions net movement is 0, there is dynamic equilibrium. But in cytotoxic oedema, there is ischaemia → reduction in NaKATPase → intracellular Na accumulation → increase of IC osmotic pressure → diffusion (net movement) of water through acuaporines to the IC space. The absolute opposite of “restricted diffusion in DWI”. I was going beyond mad at this point. Then it’s when I discovered that actually diffusion sequences do not measure diffusion but freedom of movement. I went from mad to angry. This is when I posted the comment in your video. Sorry about that. I am still trying to clarify why the diffusion sequences were called diffusion on the very first place. I am researching, I will eventually find out. I’m sure there must be an explanation, probably related with the “experiment” itself of doing an MRI, perhaps the MRI actually creates by itself a difference in concentration of water with the magnetic fields (like pulling the molecules of water towards one direction like a magnet) in relation to non polarised molecules and then it let goes and measures the capability of the water to diffuse back? There must be an explanation for sure. If not, I am starting a revolution. - But then, then there is another issue. DWI measures free movement of water. In stroke in cytotoxic oedema there is restriction of free movement, according to DWI. However, is this really the case? I mean the extracellular space in between cells in the brain is so small in comparison with cellular volume. Cells are like sardines in a can. How is freedom of movement better outside than inside? Even worse, how is reduction in freedom of movement even more reduced when actually there is increase in intracellular water due to cytotoxic oedema and therefore an increase in volume allowing more space for the molecules of water to move? For a moment I though… may be it’s the lack of vascular flow, as intravascular volume accounts for extracellular volume? But no, as DWI is used also in other conditions that don’t have restriction in blood supply. I will keep researching. I will find out and let you know. Thank you for your videos, though. Finding your channel is one of the good outcomes of this battle.
🤦 I FINALLY understand this! Thank you so much!
Wow! Thank you so much. That’s very generous. So glad this helped!
SE-EPI DWI is predominantly T2-weighted because of the 180-degree refocusing pulse, which corrects for dephasing due to field inhomogeneities. T2* effects from the EPI readout are minor.
I wanted to ask this, because he repeatedly stated that the image was T2*-weighted. But it should be T2-weighted because of the rephasing 180° RF Pulse, right?
I had the same understanding.
Same question
Same question ~ In the previous lecture, he said it includes both T2* and T2. I didn’t fully understand, but I assumed it was beyond our scope.
i think vlogger is correct, because DWI has the same bad geometric distortion and signal loss (e.g. at air/tissue interface) as T2* fMRI does, but that 180 pulse throws me off too. so it would be nice if he clarified.
Most awaited lecture❤❤
Why is the B0 a T2* image if there is a 180 degree RF pulse used and a longer TE? - would the 180 degree RF pulse counter the T2* effects and make a T2 image?
Definitely need to review your spin echo video, but wow, this was explained so well. It definitely is like a physics brain teaser and very cool to see how diffusion weighted imaging can be used. Thank you so much for this.
Why is B0 a T2* W image when there is a 180 degree pulse applied at TE/2, shouldn’t it be a T2WI ?
Thanks brother...because of you I understand MRI Physics...keep it up❤
Thank you, much awaited
Thanks to this 27-minutes lesson I finally understood DWI, you're my hero. A question: why do you keep saying that the b0 image is T2*-weighted and not simply T2-weighted? If a SE sequence was used in your example, shouldn't the signal be closer to the tissue's T2? I'll try to answer myself, but I'm not sure if I'm getting the point: could it be that the T2* is an effect of the inhomogeneity created by the EPI gradients?
First off, superb video series. What an amazing achievement to put all this together.
I am slightly confused here. Does the frequency encoding gradient come BEFORE the phase encoding gradient when we are doing B0? If so, why? Or is the phase, and then frequency encoding gradient? maybe its a bit late at night here, and I am oversaturated with coffee?
Excellent series, your videos have been invaluable for FRCR revision.
Do you mind sharing whether the question bank will be made available to radiopaedia all access pass holders, and roughly what time frame this might be? Thanks
Excellent series
Really helpful
Thank you for your great explanations! Helps a lot!! Could you please do a video about diffusion tensor imaging?
Just amazing
Kindly make videos of nuclear imaging.stay blessed.
B0 creates T2 not T2* because of 180 pulse, correct?
Please can u make a detail lecture on ct scan...❤
Simply the best. As always.
Thank you ☺️
Nicely understood…..please make a video on ct and mri anatomy of orbit
Thank you!!❤
Thank you so much! This was very helpful
Can you do a SWI susceptability weighted imaging tutorial please? Thanks so much for your work, or ngaa mihi nui as we say in Aotearoa, NZ.
thanks so much!
After a long time, thnks a lot for the lectures. Love from india
Thank you so much Dr
Thank you very much indeed!
My pleasure 👍🏼
How many videos are there going to be in the MRI series?
Even though we confirm with ADC that restriction is true why do we still value dwi more than ADC and dwi together? Like in pirads we can count high signal on dwi even with normal ADC. In general hyperintensity on dwi even without hypo on ADC should be at least suspicious.
Wonderful
Ive a question . How do Diffusion gradients in same directions lead to rephasing?
If they were in opposite directions id get it cuz laggers become leaders but it is in the same direction so the leader will still be going faster than the lagger on the second gradient?
I am considering a voxel with all in phase and then gradient along one plane in my model and applying the previous leader lagger model.
The 180 degree RF pulse causes the ‘leaders’ to become the ‘laggers’. If there was no RF pulse the diffusion gradients would need to be in opposite directions. However the 180 degree RF pulse means that the two diffusion gradients will effectively be equal and opposite.
@@radiologytutorials somehow it makes sense now. Thank you. Master Sorcerer.
you're genius
You are my hero
Should I learn this as an aspiring neurosurgeon?
❤❤
😊😊
Yay! :)))
No. Wrong. Diffusion is not Brownian movement. Diffusion is not random movement of particles.
You’re right. Diffusion is movement across a concentration gradient. Diffusion weighted imaging isn’t actually measuring diffusion rather the ability of particles to move freely/without restriction. These particles move with Brownian motion. Thanks for pointing out the difference
@@radiologytutorials Thank you so much for actually answering. I do apologise for the bluntness of my comment but yesterday I was going mad with this situation. I have yet not resolved the issue. To give you a little bit of context:
- I am currently working in stroke, it’s why I got entangled with this. At the beginning I was assuming DWI measured diffusion, hence I was trying to explain the physiopathology of cytotoxic oedema from DWI point of view. Almost went mad. Actually, with cytotoxic oedema there is a net movement, a diffusion of water from extracellular space to intracellular space. In normal conditions net movement is 0, there is dynamic equilibrium. But in cytotoxic oedema, there is ischaemia → reduction in NaKATPase → intracellular Na accumulation → increase of IC osmotic pressure → diffusion (net movement) of water through acuaporines to the IC space. The absolute opposite of “restricted diffusion in DWI”. I was going beyond mad at this point. Then it’s when I discovered that actually diffusion sequences do not measure diffusion but freedom of movement. I went from mad to angry. This is when I posted the comment in your video. Sorry about that. I am still trying to clarify why the diffusion sequences were called diffusion on the very first place. I am researching, I will eventually find out. I’m sure there must be an explanation, probably related with the “experiment” itself of doing an MRI, perhaps the MRI actually creates by itself a difference in concentration of water with the magnetic fields (like pulling the molecules of water towards one direction like a magnet) in relation to non polarised molecules and then it let goes and measures the capability of the water to diffuse back? There must be an explanation for sure. If not, I am starting a revolution.
- But then, then there is another issue. DWI measures free movement of water. In stroke in cytotoxic oedema there is restriction of free movement, according to DWI. However, is this really the case? I mean the extracellular space in between cells in the brain is so small in comparison with cellular volume. Cells are like sardines in a can. How is freedom of movement better outside than inside? Even worse, how is reduction in freedom of movement even more reduced when actually there is increase in intracellular water due to cytotoxic oedema and therefore an increase in volume allowing more space for the molecules of water to move? For a moment I though… may be it’s the lack of vascular flow, as intravascular volume accounts for extracellular volume? But no, as DWI is used also in other conditions that don’t have restriction in blood supply.
I will keep researching. I will find out and let you know.
Thank you for your videos, though. Finding your channel is one of the good outcomes of this battle.
❤❤
❤❤
❤❤