Consistent Best Effort

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Posted on 4th April 2008 by Gordon Johnson in Uncategorized

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This week I have been discussing the basic principles of neuropsychological assessment, and its two foundational assumptions: the ability to reconstruct pre-morbid IQ and the need for “consistent best effort”. Yesterday’s blog dealt with the pre-morbid IQ. Today, we will discuss the issue of “consistent best effort.”

The number side of the neuropsychological assessment is based upon the theory that a neuropsychologist can make certain conclussions about pathology based upon an examination of the pattern of test scores. The process of doing this is called “discrepancy analysis”, meaning that if there is a discrepancy in certain areas, this points to pathology. Two other terms are important: “relative weakness” and “intraindividual comparison”. If while doing the intraindividual comparision (mean comparing the patient, only to his or her own scores versus the population as a whole) a “relative weakness” shows up, then that means something.

In a perfect world, it is a beautiful theory. You chart the scores, the “relative weakness” jumps out at the neuropsychologist, you look to the part of the brain that controls that area of function, and thus, make a diagnosis. The fundamental problem is that you must be able to presume that the test subject was making the same effort during the test where he or she did poorly, as across the entire battery of tests. But can we make that assumption?

I like to quote from depositions I have done to make these type of points, and I will do that again. My apologies to my son for my references to his middle school running career.


12 Q (By Mr. Johnson) Do you still have your Exhibit Number 1
13 before you?
14 A I do.
15 Q Page 6?
16 A Yes.
17 Q Now, as I understand what you’re saying in the first
18 paragraph of Page 6, what you’re saying is that because you
19 cannot be sure that the patient did not give optimum effort,
20 that you can’t reach conclusions based on the data in those
21 testing — in that testing; is that correct?
22 A I can make certain conclusions, but not on her current
23 status, on that date. That’s what I’m — all I’m trying to say
24 is this set of data had serious reservations because of lack of
25 effort.

54
1 Q Now, there are any number of things — strike that. Let’s
2 talk about the continuum of effort when you’re giving someone a
3 test; all right? I’ll give you an example.
4 My son, who is a 13 year old, goes out and runs a six-
5 minute mile, and he gave better effort than anyone else in the
6 class if you judge it just based on his performance, because he
7 won the race; okay?
8 A Got you.
9 Q Now, would that be considered best effort?
10 A It was certainly a sufficient effort to be recorded, yes.
11 Q Two months later in a track meet in his conference meet,
12 he’s able to run a five-minute, six-second mile without
13 significant change in this training status. In comparison to
14 the gym class — in comparison to the conference meet time of
15 five minutes and six seconds, did he give best effort in gym
16 class?
17 A There are other variables that have to be considered, and
18 I’d have to know other things. I’m not really following you.
19 Q Okay. Tell me what the variables would be.
20 A Like the environmental conditions, the contingencies if he
21 won or if he didn’t win, the particular mood or attitude that he
22 had on that day, how his physical health was, if he had a cold,
23 if he had some sort of limitation.
24 Q Now, we always have all of those limitations anytime we
25 give someone any type of test; is that correct?

55
1 A Exactly right.
2 Q If we were going to pick an example of when we might get
3 the highest percentage of people giving maximal effort or
4 optimal effort, is there a better example than the law school
5 admission test?
6 A Well, I’ve never seen the law school admission test, but if
7 it’s like the test that I took to get to graduate school, then
8 one certainly has to do well, as best as they can, yes.
9 Q And can we — if there ever — can we ever presume a higher
10 likelihood of maximum effort in an academic test than we would
11 in something like a law school or a medical college admissions?
12 A Well, I agree. I mean, one can’t do better than one can
13 do.
14 Q But what’s unique about the law school and the medical
15 school admission test, is people’s whole lives revolve around
16 how they do on this test; correct?
17 A Well, that’s probably their interpretation, but it’s not
18 real. They probably think —
19 Q And that thinking that would convince them at least
20 relative to other variables to give it their best shot?
21 A I would think so, yes.
22 Q Despite that, sometimes people who are testing in high-
23 pressure situations like a law school admissions test or a
24 medical college entrance exam, do not wind up at their optimum
25 performance level; correct?

56
1 A I presume that’s correct.
2 Q And what explanations for that would do?
3 A Again, we just went through some of them. They have a
4 cold, they’re worried about money, they have stress at home,
5 they have stress on the job, I mean, there are all kinds of
6 events that could influence particular effort on a particular
7 day.
8 Q Or actually the stress of the test itself?
9 A Well, yes, of course. There’s some people who don’t do
10 well on tests.
11 Q And there are some people who do worse the more the
12 pressure is?
13 A Right. It’s not really the pressure; it’s how the patient
14 manages the pressure that’s the issue.

Now as we consider this long introduction in the context of the search for “relative weaknesses”, what does that mean? What if our test subject was only using the gym class effort level, versus the conference meet effort level? Can we make statistical comparisons then? Or should we compare that performance to how people do in gym class, and not comparing how they do in more stimulating environments?

Neuropsychology is a science, right? They should have control out all of these variables, right? Guess again, not because they don’t want to, but because they are dealing with human beings, and in brain injury evaluations, human beings who prevented from doing what they are presumed to do, based upon the precise disability for which we are evaluating them: brain damage.

Next: The Scope of the Problem for Brain Injured Person in Giving Consistent Best Effort.

Understanding Neuropsychological Statistics in Diagnosing Brain Injury

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Posted on 2nd April 2008 by Gordon Johnson in Uncategorized

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Yesterday’s blog threw out a few numbers to illustrate some basic starting principles about neuropsychology. As an aid to our further discussion of this neuropsychology, today I will give some basic numerical principles to help in further understanding the numeric part of neuropsychological assessment.

First, neuropsych scores are typical given in one of three scoring methods: Standard score, percentile score and T scores. T scores are a little bit too complicated to try to explain to a laymen, so I will limit this discussion to standard scores and convert them to percentile scores.

Most people are somewhat familiar to standard scores, because IQ’s are given in them. Yesterday I used the example of our successful professional who had a post accident IQ of 135. An IQ of 100 is perfectly in the middle. Something below 70 is evidence of significant impairment. Each time you move down the standard score grid by 10 points, it represents a significant drop.

Here are the basic categories of Standard scores, with their percentile equivalents.

Very superior — 130 and above — 98% and above
Superior __ 120 to 129 — 92% to 97%
High Average — 110 to 119 — 76% to 91%
Average — 90 to 109 — 25% to 75%
Low Average — 80 to 89 — 8% to 24%
Borderline — 70 to 79 — 3% to 7%
Impaired — below 70 — 2% and below

T scores use the same basic concept, and again using 10 points as the break point, but with a T score, the mid point is 50. Some neuropsychologists may disagree as to the exact point that separates these categories, but this is certainly representative of the concept.

The second term to understand in terms of understanding the statistical analysis done by a neuropsychologist is the concept of “deviations”. While I am incapable of synthesizing the dozens of different explanations of this concept into one cohesive definition, in essence, when you move from one category like very superior, to superior, you have moved one deviation. When you move from very superior to high average, that would be two deviations. Movements of two deviations are deemed to be significant.

Yesterday’s example of an IQ score of 135, which was very superior, to an average processing speed score of 100, is a movement of three standard deviations. That could be quite significant, but of course is only one factor to be looked at in doing a full blown “assessment.”

Tomorrow: assessing premorbid IQ and other ability levels.

Neuropsychological Assessment to Establish Brain Injury

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Posted on 1st April 2008 by Gordon Johnson in Uncategorized

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In yesterday’s blog, I talked about the essentials prerequisites to proving to a jury that a plaintiff is disabled by brain injury. I said there:

  • “Now, we have more cases than we did in 1996 where the neuroimaging is abnormal. Yet, we still must show the same things: an accident with the potential to injure the brain, acute evidence that the brain was injured, deficits that can be determined in how a person functions and a CHANGED PERSON. Neuroimaging adds to the equation, but doesn’t eliminate any of the other issues. The only thing I would seriously change from what I said in 1996 is that there are other ways in addition to neuropsychological assessment, that deficits in ways in which the brain are working, can be identified.”
The big change in the way I look at the structure of a brain injury case than I did when I started in this field nearly 20 years ago, is that I don’t see pure discrepancy analysis within a neuropsychological test battery to show relative deficits, as the cornerstone to diagnosis. That is a lot of jargon; let me explain what I mean. First some terms:

Neuropsychologist: is a not an M.D., but a Ph.D. in psychology, who has typically finished a post doctoral fellowship and training in neuropsychology, which is essentially the field of brain behavior and assessment.

Neuropsychological assessment begins with the administration of a battery of psychometric tests. Then the neurospcyhologist will do an analysis of the pattern of the test scores, the clinical interview of the patient and known potential traumatic or disease processes, to make an assessment as to what pathology may exist in the brain, and from what potential causes.

Discrepancy analysis is the technical, statistical analysis of the neuropsychological test battery to determine whether there are relative weaknesses in an intraindividual comparison, upon which conclusions about pathology can be made.

An intraindividual comparison is a method of determining whether or not a portion of a brain is performing abnormaly for that person, based on the pattern of tests scores, primarily within the specific battery of tests that are being performed at that time.

A relative weakness is a test score on a specific test within the battery where the score is sufficiently lower than other tests, that it shows that a particular part of the brain may be functioning in a pathologically changed way.

All of these technical terms and approaches are usually necessary because only in rare cases does an individual have previous neuropsychological assessments that precede their injury or disease. It is thru these technical approaches to evaluations, that a neuropsychologist can make determinations of pathology, without prior batteries to contrast current testing with.

To demonstrate how the statistical part of the assessment would work lets assume a simple example – focusing on a small part of the test battery. Let us assume we are assessing a very smart professional, who had excelled throughout his or her academic life, obtaining an advanced degree and always testing at the high end of all standardized tests.

One of the key elements to all neuropsychological assessments is the administration of the IQ test. Our hypothetical individual does as expected and receives an IQ score of 135, which is considered very superior. (More on the categories of achievement levels in tomorrow’s blog.) In contrast, when given tests which measure this individuals processing speed, the score was 100, which is still average, but is more than 35 points lower than the IQ score. If this person’s processing speed was compared to all individual’s, the score would be considered normal. But if Discrepancy Analysis is used to make an intraindividual comparison of the IQ score to the processing speed score, that person would be found to have a relative weakness. That relative weakness could begin to form the basis of an opinion about pathology, and perhaps pathology related to a specific event.

The key issue in engaging in formal discrepancy analysis would be a determination of how rare it is for someone with a 135 IQ to have a 35 point difference between that score and the processing speed.

One piece of this puzzle that most neuropsychologists would not mention, but I personally find significant, is that if this individual had consistently been in the top few percentiles on standardized testing, we can almost presume that they were capable of fast thinking. If you don’t think fast, you don’t get high scores on college or graduate school admissions tests.

But my practical approach contrasted to the technical approach of most neuropsychologists, is symptomatic of another major schism in the field: the method used to determine pre-morbid (pre-injury or disease) abilities.

More on these issues later this week.

Advances in Neuroimaging – Value in Diagnosis of Brain Injury

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Posted on 31st March 2008 by Gordon Johnson in Uncategorized

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Last week’s blogs covered a series of articles about the advances in neuroimaging to assist in the diagnosis of subtle brain injury (otherwise called Mild Traumatic Brain Injury or concussion.) The key to looking back at those blogs, is the word “assist.” Imaging studies can only tell us what the structures of the brain look like. They cannot tell us how they got that way. They tell us very little about the function of the brain (although that may change dramatically with the continued development of fMRI.)

The first time a client of mine got an abnormal 3T MRI, I was so ecstatic, I thought my job had completely changed. It didn’t. The words “clinical correlation required” became an integral part of each case and frankly, it is a good thing it did. “Clinical correlation required” in essence means that did this person suffer a change in the way his brain was functioning, at a point in time consistent with the pathology that is being seen on the scan.

That is what being a brain injury lawyer is all about. Taking the technical findings of various subspecialist in the field of brain injury and putting them in front of a jury in a way that the jury can clearly see that the traumatic event, resulted in a change in this person, which is clearly related (correlated) to the brain damage that could be suffered in the accident. Without the real world picture of how this human being has been changed, with the line of demarcation of the accident, one can simply not make a diagnosis of brain injury.

I have been saying that same thing since I first wrote a web page on brain injury in 1996. Here is the words and the graphics I said at that time:

They are:

1.
Sufficient Biomechanical Force;

2.
One of the Four Acute Symptoms of the Rehab Congress’s definition, i.e.:

a) any period of loss of consciousness,
b) a change in mental state as a result of the accident,
c) amnesia, or
d) focal neurological deficits;

3. Neuropsychological Deficits; and

4.
A Changed Person.

Click here for those words I first wrote in 1996.

Now, we have more cases than we did in 1996 where the neuroimaging is abnormal. Yet, we still must show the same things: an accident with the potential to injure the brain, acute evidence that the brain was injured, deficits that can be determined in how a person functions and a CHANGED PERSON. Neuroimaging adds to the equation, but doesn’t eliminate any of the other issues. The only thing I would seriously change from what I said in 1996 is that there are other ways in addition to neuropsychological assessment, that deficits in ways in which the brain are working, can be identified.

Dilated Perivascular Spaces in Identifying Mild Brain Injury

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Posted on 26th March 2008 by Gordon Johnson in Uncategorized

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We began our series on “Advances in Neuroimaging” with yesterday’s blog on Increased Field Strength – the improvement from the 1.5 Tesla MRI’s to the 3 Tesla MRI’s. Today’s blog will discuss the evolving research that seemingly insignificant evidence of abnormalities on lower field strength scans, can illuminate evidence of traumatic injury. This is particularly true of what is technically called dilated perivascular spaces, also called Virchow Robbin Spaces. In essence, these are areas surrounding blood vessels in the brain, where myelin sheath or other brain tissue is missing, and thus show up as holes (white spots – also called UBO’s – unidentified bright objects) on the MRI scans. The technical term in an MRI report would be “areas of abnormal increased signal intensity.” Myelin sheath is the insulation type substance that protects the length of most multilevel axons in the brain.

Even though the 3T scans allow us to see these bright spots much clearer, this one term, “dilated perivascular spaces”, is still being used to describe lots of very different types of pathology. Again, excerpts from a recent deposition I conducted:

10 Q. We have the term called dilated
11 perivascular spaces that we’ve talked about.
12 Peri meaning?
13 A. Around the vessels. It’s the
14 spaces around blood vessels of the brain.
15 Q. And in a normal brain, what is in
16 those — why are there no spaces?
17 A. Well, there actually are spaces.
18 There’s spaces in everybody. It’s just that
19 they’re very, very small. And in some
20 patients you really see very few, or you
21 don’t really see hardly any, but they’re
22 there.
23 And then if they enlarge, because
24 you have lost substance in the brain around
25 them, then you refer to them as dilated
1 perivascular spaces, or enlarged spaces. And
2 what they fill in with is basically water;
3 cerebrospinal fluid is water.
4 Q. What type of brain matter is lost
5 in these, in the dilated perivascular
6 situation?
7 A. It’s basically a white matter
8 substance of the brain predominantly, because
9 that’s where you — that’s where these
10 perivascular spaces tend to be is mostly in
11 the white matter. So basically what you’ve
12 lost is some of the connecting fibers.
13 Q. Now, white matter is the axonal
14 part of the brain; is that fair?
15 A. Right. It’s the connecting fibers
16 of the brain. I made the analogy earlier of
17 the telephone systems. Telephone systems on
18 the surface of the brain, they’re basically
19 neurons. The connecting fibers are the
20 axons. And those connecting fibers are what
21 make up the white matter.
22 Q. And they call it white matter
23 because it’s white when you autopsy the
24 brain?
25 A. Depending on how you fix the
1 brain, yes.
2 Q. What is it that you’re seeing
3 that’s white? Is it the axons themselves or
4 the insulation around it?
5 A. It’s the insulation around them,
6 the myelins.
7 Q. And when we see dilated
8 perivascular spaces, are we seeing absence of
9 axons or absence of the insulation?
10 A. It could be both. We’re seeing an
11 absence of one or the other.
12 Q. Is the insulation considerably
13 larger in scale than the axons are?
14 A. Yes.
15 Q. Do you have any sense of the
16 magnitude of the difference?
17 A. An axon is on the order of about
18 50 microns. And then it has a mild sheath
19 around it. So that covering around that. So
20 the whole thing is really small.
21 Q. How small is a micron relative to
22 a millimeter?
23 A. It’s a thousandth of a millimeter.
24 Really tiny.
25 Q. So 50 microns would be 1/20th of a
1 millimeter?
2 A. Pretty small.
3 Q. Can you see axons in a human
4 macroscopically?
5 A. Only collections of them. Only
6 bundles of them. Large groups of them. You
7 can’t see 50 micron scales.
8 Q. And relative to the 3-Tessla MRI,
9 what is its resolution in terms of pathology
10 and the smallest pathology you see?
11 A. I think that depends on the type
12 of pathology. I would say in general you’re
13 in the 1 millimeter resolution range.
14 Depending on the pathology, you could go
15 smaller. Some pathology you might have to go
16 a little bigger. I feel very confident
17 calling 1 millimeter lesions.
18 Q. How many axons grouped together do
19 you think you would have to see to be able
20 to see it on the MRI?
21 A. Well, at the very least hundreds,
22 and probably thousands.
23 Q. Some are thicker than others?
24 A. Right.

For a more detailed explanation of the pathology of diffuse axonal injury, see http://subtlebraininjury.com/Neuropath

A dilated perivascular space on a 3T scan is no longer a vague bright dot but now has definition, measurable size and distinguishable shape. A neuroradiologist may be able to distinguish between such dilated spaces that can be caused by trauma, from other disease processes. .


25 Q. Is there weighting that goes into
1 your differential diagnosis when you look at
2 a dilated perivascular space in terms of more
3 likely trauma, more likely aging, more likely
4 microvascular? Is there — can you look at
5 the character in relation to the location of
6 perivascular spaces and shift a probability of
7 one diagnosis versus another?
10 THE WITNESS: Well, one of the
11 things that I’m looking at right now are
12 different types of perivascular spaces. And
13 we have a study that we’re conducting where
14 we’re looking at — I actually think there
15 are two types of perivascular spaces. There
16 are perivascular spaces that I would refer to
17 pathologic, and perivascular spaces that would
18 I would consider developmental.
19 So I’m going to eliminate the ones
20 that have — and what you’re asking me I’m
21 going to separate out the developmental ones.
22 The developmental ones, I think are
23 very round. They’re usually in the deep
24 basal ganglion region of the brain. They’re
25 very common. They can be extremely large.
1 They’ve been described in literature to be
2 well over a centimeter in size. Very big.
3 But I don’t think they ha ve any clinical
4 significance at all.
5 Then there are dilated perivascular
6 spaces that I think are pathologic, meaning
7 that something caused them, whether that is
8 aging, whether that is a disease process,
9 whether that’s trauma.
10 I think that differentiating
11 between those requires you to look at a
12 variety of factors. And that is, does the
13 patient have any other disease condition?
14 What is the age of the patient? What are
15 the size of these perivascular spaces relative
16 to the age of the patient? Are they greater
17 than you anticipate for that patient’s age?
18 Is the location predominately in areas of the
19 brain where those particular disease processes
20 are most common? Do they fit together in that
21 way?
22 So my opinion is that we probably
23 will be able to over time improve our
24 differential diagnosis. I think we can put
25 it into two categories right now. Andhttp://www.blogger.com/img/gl.link.gif then
1 I think beyond that it really requires
2 correlating it with clinical information, the
3 age, and the locatihttp://www.blogger.com/img/gl.link.gifon of the perivascular
4 spaces.

In summary, we have now covered improved field strength and dilated perivascular spaces. In tomorrow’s blog, we will address the need for tailored protocols in properly investigating Mild Brain Injury and the existence of Post Concussion Syndrome, aka, Subtle Brain Injury.

Advances in Neuroimaging

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Posted on 25th March 2008 by Gordon Johnson in Uncategorized

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My topic for the rest of this week is advances in diagnosing brain injury thru improved neuroimaging. A recent study out of BYU, highlights some of the exciting changes that occurring, “New study shows brain changes from concussion
By Elaine Jarvik, Deseret Morning News Published: Monday, March 17, 2008.
See http://deseretnews.com/dn/view/0,5143,695262379,00.html

The Deseret article begins:

“Even after a severe concussion, a brain can look normal and healthy on a traditional brain scan. But now a study co-authored by a Brigham Young University psychology professor, using a new kind of MRI technique, reveals brain changes that are subtle but significant.”

This article is talking about a technology called DTI imaging, but to fully understand the advances in neuroimaging, it is necessary to understand some basics about the science of neuroimaging and improvements in both the magnets and the software to interpret the raw information has changed.

The last three years have been an exciting time to be a brain injury lawyer because the implementation of 3 Tesla MRI scanners for clinical diagnosis of mild brain injury has resulted in an exponential increase in the number of abnormal scans for our clients. But increased field strength is part of the equation.

INCREASED FIELD STRENGTH

Tesla is the measurement of the strength of a magnet. 1.5 Tesla (1.5 T) is the current prevalent maximum field strength of MRI scanners found in US hospitals, with many facilities having scanners with weaker field strengths. While research facilities have been using considerably stronger field strengths than the 1.5 for at least five years, it wasn’t until mid 2004, that 3 T MRI scanners began to appear for clinical use. As I write this in March of 2008, there is likely a 3T MRI scanner at most major university medical centers, although many of these may still be restricted to research only applications.

One way to conceptualize the improvement in scanners is to compare such to similar improvements in the mega pixel capacity of a digital camera. An 8 mega pixel camera has roughly twice the resolution of a 4 mega pixel camera, and while the difference in MRI scanners don’t quite track a pure arithmetic improvement, the analogy holds quite nicely. After all, MRI scanners are essentially cameras, that use as the contrast agent, the vibrations of magnetized protons, instead of light.

My examination of a leading neuroradiologist, will a bit technical, will assist those who want to understand the details of these new advances:

My examination of a leading neuroradiologist in a recent case, may be helpful to understand the basic principles:

23 Q. My understanding is that MRI
24 imaging essentially uses an especially powerful
25 magnet with respect to 3-T to make the
1 molecules inside the brain resonate; is that
2 correct?
3 A. Correct.
4 Q. Explain what’s really going on
5 there.
6 A. What happens with an MRI
7 examination — for example, you mentioned
8 specifically 3-T. Well, the T stands for
9 Tesla. The more — the higher the Tesla
10 number, the more power the magnet. Which
11 really translates to your ability to see
12 smaller things.
13 So in many ways it’s analogous to
14 a microscope. If you have a higher powered
15 microscope you can see things better than you
16 can a lower powered microscope. An MRI
17 scanner is a higher powered. An MRI scanner
18 you can see things — many things you can
19 see better.
20 It’s not absolutely universal that
21 you see everything better, but for the most
22 part you see things much better on a higher
23 field strength magnet.
24 No matter what field strength
25 magnet you’re in, if I put you in an MRI
1 machine, basically what happens is that the
2 protons, which are part of the water
3 molecule, tend to line up with a magnetic
4 field.
5 So right now your water molecules
6 and your protons are just random in the
7 direction. They have a direction, and that
8 direction is random all over the place.
9 When I put you in an MRI machine,
10 they all line up. They all line up with a
11 magnetic field. And then what we do is we
12 give a radio frequency pulse. And it’s
13 basically very, very similar to an FM radio
14 wave. It’s almost the same energy as an FM
15 radio wave.
16 And basically what we do is we hit
17 your body with what’s called a radio
18 frequency pulse, which is really similar to
19 an FM radio wave. So it’s not dangerous.
20 There’s nothing bad about it. But what it
21 does do is it knocks those protons out of
22 that alignment.
23 And then as those protons come
24 back into alignment, they come back into
25 alignment at different rates, different speeds
1 based on the tissue, which is referred to as
2 a relaxation time.
3 So that the time it takes for
4 those protons to come back into alignment is
5 different for the skin, for the bone, for the
6 skull, for the cerebrospinal fluid. They all
7 have different rates.
8 The computer then assigns a gray
9 scale. So it’s kind of like paint by numbers.
10 If the relaxation rate has a certain number,
11 then it gets a certain color.
12 So basically, the computer does
13 something that’s completely analogous to paint
14 by numbers, and creates a picture out of
15 that.
16 And we do that with different
17 settings, depending on what we’re looking for.
18 And we can emphasize different tissues.

Increased field strength is only part of the breakthrough in neuroimaging. As more and more pathology is seen on these scans, neuroradiologists are realizing that what were considered to be insignificant findings on lower field scans, are of the pattern and nature most likely explained by traumatic forces, not disease processes or normal variants.
Tomorrow:

Dilated Perivascular Spaces in Identifying Mild Brain Injury