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Old 05-17-2008, 11:22 PM   #1
Quixotic1
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Default The McDonald Criteria

THE MCDONALD CRITERIA (revised 2005)

(The Myth of the 9 lesions)
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APPROACH TO THE DIAGNOSIS OF MS



First, you need to understand that MS always was, AND STILL IS, mainly a clinical diagnosis. The definition of “Clinical Diagnosis” is:

A diagnosis that can be made on the basis of the history and the physical exam alone.


Yes, that means that in some cases, the diagnosis of MS can be made without using the MRI or other test at all. It would be unusual for this to happen, but it points out clearly the need for a thorough history and physical at the beginning of the diagnostic process. Many of the clues to the disease will already be there. In countries where MRIs are available, they are always obtained. Unfortunately, in practice, the results of the MRI often overshadow the "clinical" findings from the patient's history and the neurological exam, especially if the MRI is negative or atypical. According the guidelines of diagnosis, this MRI would not have to be positive in order for the neurologist to be confident the person has MS. However, it takes a smart and very self-assured neurologist, usually an MS Specialist, to diagnose MS with a normal MRI. It does happen, though.

The categories of MS are also based solely on the patient's experience, that is, their history of symptoms, of resolution, and of accumulation of disability. The categories are discussed more fully in another Health Page (see "Categories of MS"). These are Relapsing Remitting MS (RRMS), Secondary Progressive MS (SPMS), Primary Progressive MS (PPMS), and Progressive Relapsing MS (PRMS). About 85% of people with MS will have the Relapsing Remitting form. For this reason, physicians begin looking a patient with suspected MS from the standpoint of attacks and remissions.

What is an Attack?

An attack (relapse, flair, exacerbation) of MS is the appearance of new neurological symptoms or the worsening of old neurological symptoms of the kind that are seen in MS. It may be a combination of old and new symptoms. An attack may be documented from the report of the patient. In this case it is "subjective". Or it may be observed by the doctor (as in discovering a new problem on the neuro exam), though usually it is a combination of the two. Anything problem observed by the doctor is said to be "objective." An attack must last at least 24 hours.

An attack does not include a pseudoattack, which is the temporary worsening of symptoms that can occur elevation of the body's core temperature (as with fever or overheating). It also does not include single paroxysmal events (sudden jerks, brief loss of vision, single spasms of a muscle, a single bout of dizziness). If the single event occurs mutliple times over a period of more than 24 hours it would qualify as an attack. As noted above an attack often does include more than one symptom.

How Often Can Attacks Occur?

The time between attacks must be at least 30 days, during which the symptoms improve, resolve, or are stable in their intensity. So, a second attack must be at least 30 days from the day the first attack began to improve or stabilized. An attack may not be the immediate improvement seen after a course of steroids. This period between attacks is called a remission. Clinically, a patient with RRMS is always either in an attack or in a remission.


THE IMPORTANCE OF THE HISTORY AND NEUROLOGIC EXAM

So, you can see that the whole diagnostic process must begin with a thorough history from the patient of their symptoms, when they started, how they progressed, whether they improved and how much they improved, and whether they ever returned. It must look for a pattern of waxing and waning of symptoms, noting when new symptoms appeared. The physician must put together a timeline of the patient's complaints and symptoms looking for a pattern of "Relapse and Remission." The history should include the things that make symptoms worse or improve them, the pattern of symptoms severity with respect to time of day, level of exercise, temperature, and whether the symptoms became worse after things like infections, pregnancy, severe life stressors, or overexertion. It should be complete in other respects including non-neurological symptoms and events especially just preceding any attacks.

The patient's Family History should be noted with respect to neurological illnesses, including MS, and for signs of MS Mimics in other members of the family. It is imperative that the neurologist pay close attention and devote time to hearing what the patient can offer. No patient should be comfortable with a doctor that does not take this time in one way or another.

The neurological exam is just as important! It should be a thorough exam, that takes a good amount of time. It should cover multiples tests in each part of the neurological system. It is a head to toe exam, and done well, can be exhausting and may take an hour or more to perform. It should cover the multitude of tests of the face muscles and eye movements. There is also a thorough check of the major muscle groups through the body comparing one side to the other for symmetry. There should be checks for balance and coordination. There should be some testing of the sensation throughout the body using 2 or more tests of sharp/dull, soft touch, hot/cold, vibration, two-point discrimination and joint/ position sense. The doctor should observe the patient walking a good distance (more than the 4 steps across the exam room), walking on the toes and on the heels. Finally, several tendon reflexes should be checked and compared side to side.

During the neurological exam the doctor is looking for "clinical lesions." A clinical lesion is an abnormality on the exam that is objective evidence that there is damage in the nervous system. Examples of "clinical lesions" are 1) hyperactive reflexes which show that there is damage in the spinal cord, 2) problems with the muscles that move the eyes indicating a problem in the brainstem, 3) spasticity, usually also from the spinal cord, 4) positive Babinksi or Hoffman's test, and 7) paleness of the optic disc at the back of the eye. These are just a few of many dozens that can found on MS patients.

Please note that the word "lesion" is used in two different ways throughoutt discussions of MS. There are "clinical lesions" as described above. These are areas of the CNS that must be damaged in order to cause the problems seen in the body. There are also the "MRI lesions" which are the abnormalities "seen" on the MRI images. The two are not always the same. One can have a clinical lesion that does not show up on the MRI. There can also be white spots on the MRI that don't appear to have a symptom associated with them.

So, it becomes clear that the neurologist must listen to and exam the patient carefully at some point early in the diagnostic process before making any judgment on the diagnosis. The first clues about whether this is MS, a mimic or something else will come from this process. Be wary of the neurologist who skips these steps.



THE MCDONALD CRITERIA

What is the Neurologist Looking For?

The actual terms used by MS Specialists in describing the diagnostic characteristics of MS are Dissemination in Space, Dissemination in Time, and the Exlcusion of Any Better Explanation for the patient's symptoms and findings. This section is going to define these terms and others that are used in the McDonald Criteria.

Dissemination in Space - This means that there is evidence that the disease has attacked more than one area of the Central Nervous System. The disease has "spread out" in its location.

Dissemination in Time - This means that there have been attacks on the Central Nervous System on more than one occasion, and that the subsequent attack was in at least one different spot than the first attack. The disease has spread out in time. (It has been active more than once.) The attacks must have occurred at least 30 days apart.

Exclusion of Better Explanations - To do this the neurologist will order many blood tests looking for MS mimics, such as causes of autoimmune vasculitis, CNS infections like Lyme Disease and syphillis, blood clotting disorders like Hughes Syndrome, deficiencies, and heavy metal poisoning. Also other tests may be done like an EEG, sleep study, EMG, and Nerve Conduction Studies.

The McDonald Criteria - 2001

In 2001, a new set of diagnostic criteria were proposed and accepted by the MS world of doctors and researchers. The McDonald criteria were very good, in that, for the first time they described criteria for the diagnosis of Primary Progressive MS. But, they also allowed for the definitive diagnosis of MS in it’s earliest form (often called the Clinically Isolated Syndrome), when there had been only one “attack” or onset of one symptom. The diagnosis of these two situations requires real thought and documented abnormalities on the lab and imaging tests. These criteria were superior to earlier diagnostic guides in that they were better at picking the MS cases accurately and eliminating the non-MS cases.

For the first time, neurologists could use the information from MRIs to substitute for an attack or for more evidence of clinical lesions when the clinical history and exam was not enough to show a pattern of the spread of the disease in time and space. This allowed many people to be diagnosed earlier. In the last 10 years, MRI has become more and more important in the diagnosis of MS. The problem is that some neurologists have come to rely solely on the MRI results and may neglect the patient's history and physical almost completely. As you examine the McDonald Criteria, you will see that the Criteria never intended that the MRI assume the first and only role.

By theMcDonald Criteria, patients fall into one of three categories: Definite MS, Possible MS and Not MS. The “type of MS” (RRMS, SPMS, etc) is determined after diagnosis and is based almost entirely on the patient's clinical course.

There were problems, though, in the practical use of the McDonald Criteria. The MRI criteria were very stringent and difficult to figure out. Also, new techniques in MRI imaging made visualizing spinal lesions easier. It was clear that spinal lesions needed a larger role in the diagnosis.



The Revised MCDONALD CRITERIA (2005)

In 2005, a group of MS specialists reconsidered the original criteria, loosened some of the MRI requirements, changed the role of the results of CSF testing and VEP in the diagnosis of PPMS, and increased the importance of spinal MRI lesions. These changes have been shown to be as good or better at picking up patients with MS and in excluding patients who do not have it.

Below are definitions used in the criteria and a chart summarizing the revised criteria. After the chart is a text description in more detail about the different scenarios a neurologist finds.

Table: here


DEFINITIONS

What Provides MRI Evidence of "Dissemination in Space"?

This is the description of a postive MRI for the purposes of showing that there has been "dissemination in space." This would be needed if there is only evidence on neurologic exam of one clinical lesion, that is there is only one abnormality that points directly to a damaged area in the CNS. This is also where the misunderstanding about always needing 9 lesions on the MRI. (Sometimes you do, but not always.) In general lesions should be larger than 3mm in cross-section.



To show Dissemination in Space on the MRI:

You need to have 3 of the following 4 things:

*** 1 (one) contrast-enhancing lesion of the brain or spinal cord. If no enhancing lesion, then need 9 T2 hyperintense lesions in brain or spine.

*** 1 infratentorial lesion or a cord lesion (this means under the tentorium, which is the membrane on which the larger cerebrum sits. Below the tentorium is the cerebellum, brainstem and spinal cord.)

*** 1 (one) or more juxtacortical lesions (this involves nerve fibers - called U-fibers - that extend from the white matter in the subcortical area through the thin boundary with the cortex of the gray matter)

*** 3 or more periventricular lesions (these are lesions sitting adjacent or very close to the ventricles)


note: Individual cord lesions can substitute along with individual brain lesions to reach the required number of T2 lesions.


What Provides MRI Evidence of "Dissemination in Time"?

1) A Contrast-Enhancing (therefore, new) MRI lesion seen in a scan done at least 3 months after the onset of the first attack and at a site that is different from the site of the inital clinical attack. (an example would be: first attack was with Optic Neuritis. 3 months later there is an enhancing lesion in the frontal lobe)

OR

2) A new T2 lesion detected in a scan done at any time compared to an earlier scan. The earlier scan must have been done at least 30 days after the beginning of the first clinical attack.



What is a Positive CSF (Spinal fluid) Result?

Two or more unique oligoclonal bands found in the CSF, but not in the serum OR an elevated IgG Index


What is a Positive VEP?

A delayed optic nerve signal (usually longer than 115msec), but a well-preserved wave form

A text description of the Criteria in action is next.

What Does the Chart Say in Real Words?

The neurologist is usually faced with one of several situations because patients arrive in various stages of their first symptoms. The neuro must begin looking at each patient with an analysis of the patients history of symptoms. He is looking for a pattern of attacks and remissions. As you have seen above he must do a thorough neurologic exam to look for clinical lesions. Ideally the patient would have seen a physician for each attack he has had, but this often is not the case. Then the picture becomes much murkier.



Each scenario below assumes that all other reasonable expalnations for the patient's problems has been ruled out. They are listed by ease of making the diagnosis.

First scenario


2 attacks
2 clinical lesions


The patient has had 2 or more attacks by history, with a clearcut remission between at least two of them. A doctor has found different neurologic abnormalities during at least 2 attacks. In order to make the diagnosis, no further evidence is really needed! In reality this rarely happens. It is recommended to get an MRI for further documentation and as a baseline. The dilemma occurs when the MRI is normal or very atypical. It takes a very confident neurologist to make the diagnosis at this point. This is the topic of a huge amount of discussion on the forum.



2nd Scenario


2 attacks
1 clinical lesion


The patient has had 2 or more clear-cut clinical attacks, by history, separated by remission. The doctor has found only one clinical lesion, that is one neurologic abnormality that can only be due to damage in the CNS. This same lesion may be found during both attacks. What the doctor knows is that there is "dissemination in time," because there have been two attacks. What is lacking to make the diagnosis is evidence of dissemination in space, because only one part of the CNS can so far be shown to be affected. An example of this is two attacks and the only abnormality each time is optic neuritis in the same eye. Dissemination in space can be determined one of in three ways


1) a Positive MRI for Space requirement (see definition above)


OR


2) 2 or more MRI lesions that appear consistent with MS in addition to Positive CSF findings (see above)


OR


3) The doctor can "wait and see" until the patient has a new attack with evidence that a new part of the brain or cord is damaged.


3rd Scenario

1 attack
2 clinical lesions


This patient has had only 1 clear attack and shows 2 abnormalities on neurologic exam that are consistent with MS. So, there is evidence that the disease has attacked more than one distinct part of the central nervous system, so we're okay on Dissemination in Space. There is no evidence that the disease has disseminated in time. This situation qualifies for the term Clinically Isolated Syndrome with a Multifocal Presentation. This person would qualify for early DMDs at this point, but most neurologists would want to see "2 or more MRI lesions" (this is not part of the Criteria) as well before they made the decision to start early meds. To establish the diagnosis of Definite MS, the doctor would have to wait for one of two things to happen:

1) Positive MRI for Time requirement (see above)

OR

2) "Wait and see" for a second clinical attack. Remember that, for the purposes of the Criteria, an attack must include objective evidence of damage.


4th Scenario

1 attack
1 clinical lesion


The patient has had only one clinical attack. The doctor finds clinical evidence of 1 lesion on the neurologic exam. This is also called a Clinically Isolated Syndrome, with a Monosymptomatic presentation. In order to make a diagnosis of Definite MS, the doctor must find evidence that there is both dissemination of space of the disease AND must also find evidence that there has been dissemination in time. The MRI and the LP become very important in this case, because there is no pattern yet of Relapsing and Remitting.

Note: At this point the patient has a Clinically Isolated Syndrome with a monosymptomatic presentation. The decision to treat early with DMDs may be made here without a Definite Diagnosis.

Dissemination in Space can be shown by;

1) Positive MRI (see definition above for (Space)

OR

2) 2 or more MRI-detected lesions consistent with MS in addition to Positive CSF results (see above)


Dissemination in Time can be shown by:

1) Positive MRI ( acording to the chart above for Time)

OR

2) The doctor can "wait and see" for the patient to have a second clinical attack

Note: At this point with both time and space requirements fulfilled the patient can be diagnosed with Definite MS. Note that quite a bit of time may need to pass (sometimes many years) before both of the requirements above is taken care of.



5th Scenario

Insidious neurological progression of symptoms and signs suggestive of MS


These patients present the hardest case for the doctor. They do not have the clear-cut attacks and remissions of the RRMS patients, so their history looks much like other chronic neurologic diseases. The doctor must rely on long-term deterioration and accummulation of disability. In this case spinal lesions and a positive CSF become more important. In fact, the two of them together can substitute for brain lesions completely. In PPMS the majority of the disease is often found in the spinal cord. But the spinal fluid does not have to be positive as it was required to be by the first McDonald Criteria. This is in acknowledgement that there seems to be less inflammatory disease in PPMS, thus less of a tendency to form inflammatory antibodies (O-Bands) The diagnostic requirements for PPMS are:

*** One year of disease progression. This can be done looking back at the patient's history, or by following the patient for a year and observing progression, or a combination of both.

AND

*** 2 out of the 3 following requirements:

1) Positive Brain MRI - this would consist of 9 T2 lesions or (4 or more T2 lesions + Positive VEP)

2) Positive Spinal cord MRI with 2 or more focal T2 lesions

3) Positive CSF (either +Oligoclonal Bands or +IgG Index)


SUMMARY

Diagnosis is often an art, and doctors vary in their skill, their interpretation, their curiosity and their creativity. It is clear that MS can be daunting to diagnose. But, the process needed to begin the diagnosis is very clear. The neurologist must take a thorough history and physical, doing what is possible to make a timeline of the appearance of symptoms and their course. He/She must insert the observed "clinical lesions" into this timeline and make a judgment of whether the requirement that a disease has shown both dissemination in space and in time. From there he is ready to assess the MRI and decide which supporting tests need to be done and which tests will help add evidence in cases that are atypical and do not fit nicely into the patterns above.


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Old 05-18-2008, 12:14 PM   #2
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Hmmmm.. Too long? Too wordy?? Not Clear?? Not needed?? Quix
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Old 05-18-2008, 12:18 PM   #3
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I read part of it last night, and the rest of it this morning.

I dont think it was too long or wordy, only reason it took me so long to read is because my boyfriend called me while I was reading, and so I just went back to reading it this morning.

I thought it was good...it explained a few things for me, and in a way I could understand it too.
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Old 05-18-2008, 02:20 PM   #4
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Thanks, Erin.

As I was thinking about it last last there are two points about the Criteria I want to emphasize.

First, the neurologist must have a clear view of the pattern of symptoms and emerging neuro exam abnormalities before he ever approaches the MRI for additional evidence.

Second, is that the Criteria only deal with the T2 Hyperintense or enhancing lesions. That is also to say that they only deal with the immune-inflammatory part of our disease. This is the part that is directly responsible for our relapses and remissions (via demyelinationa and repair). But, we know that there is a separate and unclearly related part of direct nerve cell and nerve fiber degeneration/death that is more likely responsible for our accumulation of permanent dsability. There is also the destruction of gray matter via T2 lesions.

So when we are able to see the cellular degeneration via our imaging techniques, the Criteria will have to change to include them.

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Old 05-18-2008, 02:51 PM   #5
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Originally Posted by Quixotic1 View Post

Second, is that the Criteria only deal with the T2 Hyperintense or enhancing lesions. That is also to say that they only deal with the immune-inflammatory part of our disease. This is the part that is directly responsible for our relapses and remissions (via demyelinationa and repair). But, we know that there is a separate and unclearly related part of direct nerve cell and nerve fiber degeneration/death that is more likely responsible for our accumulation of permanent dsability. There is also the destruction of gray matter via T2 lesions.

Quix
What about black holes? If a person has CIS and the MRI comes back showing T2 lesions, enhanced lesions, and black holes (like me!) isn't that a dissemination in time even without a second clinical attack?
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Old 05-18-2008, 03:12 PM   #6
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Thanks Quix, good post.

I think it would be a good idea for all of you limbolanders to make a copy of this and hand it to your Neuro, when he/she, somehow, conveys to you, or writes a little note in your records, that you find later, that it's all in your head.
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Old 05-18-2008, 04:55 PM   #7
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What about black holes? If a person has CIS and the MRI comes back showing T2 lesions, enhanced lesions, and black holes (like me!) isn't that a dissemination in time even without a second clinical attack?
Natalie, the Black Holes are seen in the T1-weighted images. They are the accumulation of areas of direct axonal (nerve fiber) degeneration. These correlate very well with both the accumulation of disability and with brain atrophy. Interesting enough, they are not so much the product of the inflammatory demyelinating and remyelinating lesions. So the Black Holes are NOT just the progression of the T2 lesions that the neuros talk about.

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Old 05-18-2008, 09:43 PM   #8
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Natalie, the Black Holes are seen in the T1-weighted images. They are the accumulation of areas of direct axonal (nerve fiber) degeneration. These correlate very well with both the accumulation of disability and with brain atrophy. Interesting enough, they are not so much the product of the inflammatory demyelinating and remyelinating lesions. So the Black Holes are NOT just the progression of the T2 lesions that the neuros talk about.

Quix

Thanks Quix. So if the black holes are not the progression of T2 lesions (which would show change over time) is this a separate process? How can I be told I have a bunch of black holes with my diagnosis 9 months ago but I have absolutely no disability at all and just the one incident of mild optic neuritis (where I still had 20/20 vision)?? Or is this just another example of how the MRI doesn't necessarily correlate with what is going clinically?
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Old 05-18-2008, 09:58 PM   #9
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Thanks Quix. So if the black holes are not the progression of T2 lesions (which would show change over time) is this a separate process? How can I be told I have a bunch of black holes with my diagnosis 9 months ago but I have absolutely no disability at all and just the one incident of mild optic neuritis (where I still had 20/20 vision)?? Or is this just another example of how the MRI doesn't necessarily correlate with what is going clinically?
Natalie, this is exactly where the MRI doesn't necessarily correlate. The best way I can answer this is an excerpt from my blurb on "Lesions vs. Symptoms"



"First, lets talk about the BRAIN. Remember that about 90% or so of our brains are "unused." That means that we don't know what those areas do when they are healthy or might do if they are damaged. ALL of the scientific articles are clear that the majority of MS lesions in the brain are not "eloquent", that is, they don't "speak up" with actions or sensations in the body. The same is true that those areas don't show symptoms if they are damaged. No good MS Specialist is going to try to map all the lesions with the symptoms that are showing up in the patient. It is almost impossible and it is a waste of time. It is well documented that some people with many, severe symptoms may have very few visible lesions. And some people who are diagnosed when they have just one symptom may have a whole brain full of lesions on their first MRI which had never before "spoken up."

This is the best way I have to explain your situation.

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Old 05-18-2008, 10:17 PM   #10
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What about black holes? If a person has CIS and the MRI comes back showing T2 lesions, enhanced lesions, and black holes (like me!) isn't that a dissemination in time even without a second clinical attack?
Sorry I missed this post. So you have a CIS with monosymptomatic presentation. You had one attack and one clinical lesion. Whether you fulfill the Criteria for Definite MS depends on the location and number of your lesions. I don't know the timeline (duration) from direct axonal damage to "Black Hole." But, the McDonald Criteria do not address the whole "Black Hole" issue at all. They are never mentioned.

A good neuro will set aside the stringent requirements of the Criteria and use his brain to see the whole picture. This is where I become so angry at either lazy or wishy-washy neuro's who do not attempt to put it all together. If you are being treated as a CIS, but actually are a Definite then there is no harm. Your treatment is pretty much the same. However, the visible black holes indicate you have some real progression in your disease. They represent brain loss - get enough of them and the brain will contract around them and you will have significant brain atrophy.

In putting this together I would think your neuro would want to be an the agressive side was far as watching and treating, but actually I don't know for sure. On my other forum we currently have three or four people with significant brain alterations (lesions), but few or no symptoms. I have not see a good description of how these people are treated or what the recommendations are. And I was not a neurologist in my prior life.

Again the whole neuro field of clinical treatment (as opposed to the research part) usually act as though the T2 lesion represents the sum total of our disease, when gads of research is showing that it is only a portion. It is the portion that seems to correspond to our RRMS the best, but not to the accrual of disability that runs along in so many of us.

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