Page 3 of 4: neuroradiology

syndrome_xy · Credits: 10937 My Scrapbook

hey i remember chand.. y has he gone out of this forum >>> think he got annoyed with few of them here...
thats great. so what do u do sonia ?? u both from US ?

wil try reading that book and wil give u a reply.

sandiv · Credits: 390 My Scrapbook

Hi,
About the oedema q
I think oedema is the right answer.
As -
Flowing blood is flow void and not hypointense
Hemosiderin is iso-intense (Diagnostic neuroradiology - Osborn 2nd Ed page 170)
Only oedema hypo
Sandiv (Radiology)

syndrome_xy · Credits: 10937 My Scrapbook

yes ur rite... Oedema is the answer.

soniadr25 · Credits: 2072 My Scrapbook

Dr Sandiv has raised an important point about hemosiderin. I think textbooks differ on this. Dahnert perhaps puts hemosiderin as hypointense.

To understand it logically let me put some basics of MRI here.

As we all know that our body is mostly water and therefore we have lots of H+ ions, simply put as proton henceforth. Now these protons are spinning around their own axis (like earth does). If we apply a magnetic field they start to precess like a toy top precesses. This precession is of definite angular frequency which is decided by the type of atom (eg hydrogen, sodium or phosphorus etc) and the magnetic field strength. This precessing proton is basically precession of a charged molecule and therefore it gives rise to some magnetic moment. Putting it in terms of quantum, some magnetic moments (majority) are directed in the direction of magnetic field and some against it. This gives rise to a net magnetisation vector in the direction of magnetic field.

Now our patient is in the core of the magnet and his/her net magnetisation is in the direction of magnetic field (usually towards head end). Now since we know the precession frequency of our proton, we can deliver required amount of energy with a radiofrequency wave of similar frequency. Since the frequencies match there is effect of resonance and hence large energy transfer takes place. (Does anyone remember that march break of sodiers on bridge so that the bridge may not break due to resonance effect!). Our this radiofrquency wave therefore flips the magnetisation vector to 90 degree. And now the wave is stopped. We use the same coil that transmitted the wave as a receiver coil. Our protons now want to relax back to their original state (in the direction of large magnetic field of our MRI magnet). While doing this they lose energy in two ways. One is the spin-spin relaxation or T2 and the other is spin-lattice relaxation or T1.

Now to make the long story short, T1 is basically gain in magnetization vector towards the main magnetic field (This is measured in a direction transverse to main magnetic field). T2 is basically loss in transverse magnetization (this magnetization we gained after flipping...remember that resonance effect). T2 is always smaller than T1. Now we set our sequences such that with small TE and small TR we catch the T1 times and with large TE and TR we catch the T2 times.....This itself is a long story. But if I apply a heuristic approximation, then the things which relax faster are hyperintense on T1W image and those that relax late are hyperintense on T2W image.

For learning I simply see the independence of water. Free water is really free (in our case CSF). Then the water becomes entangled in cell boundaries and hence a little bound (as in gray matter). It becomes more bound in small axons covered with myelin sheath (as in white matter). And finally fat holds protons closest to it than all these. So ultimately the intensities follow the same sequence. Free water relaxes last and is therefore hyperintense on T2 and hypointense on T1.

I am skipping all other details on image aquisition (for which laterbur got nobel) so that we can come back to our point on hemosiderin. Hemosiderin is a superparamagnetic substance. It has very high magnetic susceptibility that deteriorates our main magnetic field locally. The blood clot evolutes from intracellular oxyhemoglobin to intracellular deoxyhemogloin to extracellular deoxyhemoglobin to hemosiderin. Oxyhemoglobin is diamagnetic. The deoxyhemoglobin and methemoglobin are paramagnetic. Since these paramagnetic, superparamagnetic and ferromagnetic compounds kill the local magnetization, they basically enhance the relaxation. So anything having a magnetic susceptibility of its own will try to increase T1W signal and reduce the T2W signal. (There are lots of fallacies here with respect to concentration of paramagnetic contrast dyes, but for time being lets forget that). Diamagnetic substance have opposite effect.

Now let me say something which is the most difficult of all this...... (most of this that follows is borrowed from internet)

Many factors influence the appearance of intracranial hemorrhage on MRI. Intrinsic factors include macroscopic structure of clot, hemoglobin oxidation state, red blood cell morphology, protein concentration/clot hydration, size/ location of hematoma, and edema. Extrinsic factors that may influence the appearance of intracranial hemorrhage on MRI include pulse sequences and field strength.

*

All the above metioned acute events are a bit fuzzy in reality. We use diffusion weighted imaging and T2*W echoplanar imaging to visualize acute condition in stroke. The echoplanar sequence makes the hypointense T2W signal to hyperintense T2*W signal by its short TR and TE. Actually T2* is always less than T2, this time comes into picture due to the magnetic inhomogenity. This inhomogenity is present always and is taken care by using spin echo sequence.

I am not sure if I have been able to convey anything in this long post of mine.....I hope Dr Sandiv would tell the true picture seen clinically...but theoretically hemosiderin can be either hypointense or isointense on T1W image.

sandiv · Credits: 390 My Scrapbook

Thanks for the long post.
Clinically, well, it may look hypo or iso.
Grienger Allison and Bradley say that it can look iso to slightly hypo to brain parenchyma on T1.
So, the answer becoming confusing. Why I said oedema because of their prperties. Flowing blood causes an artefact which look very black rather than hypo (In fact, we say signal void or flow void rather than to call it hypo, and hemosiderin laden macrophages may cause suceptibility ), but oedema looks hypo. But it can be argued that anything blacker than parenchyma is hypo.
Actually, the hemosiderin signal may reach to that of CSF on T1 ! so, is it the 'd' or last answer ?
Sandiv

soniadr25 · Credits: 2072 My Scrapbook

Thanks Dr Sandiv for replying!! My point was not to argue about the answer but just to put a different perspective.... As you said the flow voids occur because there is no return signal from the excited protons as by the time signal is collected back, the protons have changed the position with the flowing blood, and so they appear hypo .... Hope to learn lot more from you!!

sandiv · Credits: 390 My Scrapbook

Your perspective is right.
Flow void happens because the 'saturated' protons by RF pulse have moved away from the slice, so no signal generation. Second, hemosidering, being paramagnetic, produces loss of T1 signal and may look hypo so, all of the above can also be the answer.
Of course, MCQs must have only one answer, and because of it I was never good at them
Anyway, Thanks

soniadr25 · Credits: 2072 My Scrapbook

Hello Dr Sandiv,

I do not know if you would ever be reading this thread again but today I came across a wonderful concept on fMRI. I thought of sharing that with you.

I hope you know about MR spectroscopy in which a voxel in brain is checked for specific metabolites. This kind of work has been done in India by Head of NMR department in AIIMS , Prof Jagannathan.

Actually as you know, the MRI is derived from NMR spectroscopy (after laterbur's innovation on gradients). The NMR spectroscoy determines the chemical structure through frequency shifts in proton resonance frequency in relation to the nearby atoms eg. carbon in glucose. This part has been made use in imaging as we can check for specific metabolites in an area and can predict the local chemical nature thereby predicitng whether the lesion is tuberculosis or tumor and in case of tumor it can tell apporximate spread. Although this field is still evolving but it is promising.

Today I came across this concept being used in fMRI. For use in fMRI (and also otherwise) the signal from water (which is huge in comparison to others) is crushed with the help of complex sequences (VAPOR etc). Now as we know that increased neural activity in an area means increased neural transmission. Glutamate is one of the neurotransmitters which is abundant in cortex. Now glucose with C13 is injected to the patient. Nomal C12 is not MR active (as the mass number is even and the spins are cancelled). This MR active carbon is only 1% abundant in normal beings. So this injected C13 is taken up by active neural cells and converted to glutamate locally. Now two sequences are run. In one the intensity of frequency shift from glutamate is measured and in other the frequnecy shift coming from C13 is inverted. These two types of frequency shifts on subtraction kills all other frequnecy shifts and the glutamate signal stands up which can be easily measured.

This gives the area of increased activity. This is akin to PET in terms of increased glucose uptake but it has more anatomical details and it is nerual specific as only glutamate is measured.....

I hope you would find this fascinating....

-sonia

soniadr25 · Credits: 2072 My Scrapbook

This concept I think came from Schulman's group way back in 2003....

fia · Credits: 412 My Scrapbook

i guess its melanin

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