Aa
On "Wait and See" -- and ms as a clinical diagnosis.
I initially asked this in another thread, then decided I shouldn't hijack that one. Several people with ms had expressed frustration with all the "wait and see" going on in those of us undiagnosed.
So why does "wait-and-see" appear to be becoming the norm? Some of the mimics are NOT as slow moving as ms and should be treated. I suppose it would make sense if other mimics were explored during this time, but once that grinds to a halt with everything else ruled out, the patient, despite clinical signs and life altering symptoms, we are supposed to sit back and put up with it all?
Btw in my experience, ms is no longer fundamentally a clinical diagnosis. Otherwise I would have it, meeting DIS, DIT, neuro exam flunky, 5 relapses since 2013. I have some permanent issues now. My lesions are too small. In December neuro felt ms. My LP was clear. Therefore not ms.
Do you think it's a liability thing -- neurologists are so wary of misdiagnosing with ms, they don't? So you think there's a quota? (LOL). Unless every single test is textbook, they are unwilling. Have they seen enough cases end up being mimics that they can't be bithered? Is it a case of lack of funding to do active follow up? In which case should thy not refer you to a specialist in the area they think might be the issue?
Perhaps it's a Canadian thing -- although I know others here from other countries in the same boat.
I get that it still could be a mimic -- but unilateral sx in any of the mimics I have not yet been evaluated for are REALLY rare.
Anyway, this is not a practical question; would just love to hear other's thoughts on the why's behind wait and see when the ms neuro is done active testing. And whether anyone else senses a shift away from "ms is a clinical diagnosis."
Please, if there is an ms specialist out there reading the boards, please visit us incognito and weigh in :).
So why does "wait-and-see" appear to be becoming the norm? Some of the mimics are NOT as slow moving as ms and should be treated. I suppose it would make sense if other mimics were explored during this time, but once that grinds to a halt with everything else ruled out, the patient, despite clinical signs and life altering symptoms, we are supposed to sit back and put up with it all?
Btw in my experience, ms is no longer fundamentally a clinical diagnosis. Otherwise I would have it, meeting DIS, DIT, neuro exam flunky, 5 relapses since 2013. I have some permanent issues now. My lesions are too small. In December neuro felt ms. My LP was clear. Therefore not ms.
Do you think it's a liability thing -- neurologists are so wary of misdiagnosing with ms, they don't? So you think there's a quota? (LOL). Unless every single test is textbook, they are unwilling. Have they seen enough cases end up being mimics that they can't be bithered? Is it a case of lack of funding to do active follow up? In which case should thy not refer you to a specialist in the area they think might be the issue?
Perhaps it's a Canadian thing -- although I know others here from other countries in the same boat.
I get that it still could be a mimic -- but unilateral sx in any of the mimics I have not yet been evaluated for are REALLY rare.
Anyway, this is not a practical question; would just love to hear other's thoughts on the why's behind wait and see when the ms neuro is done active testing. And whether anyone else senses a shift away from "ms is a clinical diagnosis."
Please, if there is an ms specialist out there reading the boards, please visit us incognito and weigh in :).
Kyle, I have been referred back to a general neuro. It's my best option at this point. My neuro IS the ms specialist in this regions. Singular.
My previous general neuro retired, so hopefully this new neurologist is more communicative and can figure this mess out. I don't feel hopeful :P.
there are no other clinics within a few hours, and I will lose my mind if I have to start at the beginning again. I just can't even fathom that.
My previous general neuro retired, so hopefully this new neurologist is more communicative and can figure this mess out. I don't feel hopeful :P.
there are no other clinics within a few hours, and I will lose my mind if I have to start at the beginning again. I just can't even fathom that.
I understand what you are saying. It is clarifying for me that IF my ms neuro felt my lesions were large enough, I would meet the criteria (as neuro opth and radiologist believe.)
Yet I have things that are not ms-y, so even I am not certain!
You might be amused that the radiologist for my 2014 mris ruled out demyelinating disease of any sort because I did not meet barkhoff's criteria ... Ummm .. From my reading that was a while ago!! Lol. Unless I'm not understanding something.
Yet I have things that are not ms-y, so even I am not certain!
You might be amused that the radiologist for my 2014 mris ruled out demyelinating disease of any sort because I did not meet barkhoff's criteria ... Ummm .. From my reading that was a while ago!! Lol. Unless I'm not understanding something.
I expect that the chest x-Ray was a rule-out for systemic
Sarcoidosis. It can be a pretty impressive ms
Mimic. It can present with neurological symptoms.
Generally though , more systems are affected.
I've learned that sarcoidosis can effect BOTH peripheral and CNS -- for those of us with too much peripheral stuff going on, it's an important mic to rule out.
Rarely, neurosarcoidosis will exist on its own, and it seems this is very difficult to dx.
(Systemic sarcoidosis has been ruled out for me via chest x-Ray.)
Sarcoidosis. It can be a pretty impressive ms
Mimic. It can present with neurological symptoms.
Generally though , more systems are affected.
I've learned that sarcoidosis can effect BOTH peripheral and CNS -- for those of us with too much peripheral stuff going on, it's an important mic to rule out.
Rarely, neurosarcoidosis will exist on its own, and it seems this is very difficult to dx.
(Systemic sarcoidosis has been ruled out for me via chest x-Ray.)
This may be easier said than done, but you should look for another MS doc. If the current one says you're way past CIS but won't diagnose MS he lacks conviction. I don't want a doc that lacks conviction.
Just one man's opinion...
Kyle
Just one man's opinion...
Kyle
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Basically and I do mean basically.....the original Mcdonald Criteria (2001) was created because MRI's became available in general practice and it was predominantly an additional diagnostic tool to aid neurologist in dxing MS earlier but it was focused on MRI imaging criteria alone.
The Mcdonald actually superseded the Poser Criteria (1983) which was the criteria used before MRI's, even the original Mcdonald was better able to dx MS, something like 30% more than those still suspected of MS under the Poser criteria were able to be clinically dx using the Mcdonald, but the 'wait and see' limbo aspect has generally always played a roll in diagnosing MS....
The Poser Criteria pre-dates the first DMD (Betaseron) which was released in the US around 93 but didn't get into the UK until something like 2000-1, there are still countries who's dx MSers don't become DMD illegible, under their public benefit scheme until they've reach a particular level of disability eg MSNZ until last year was about 8yrs behind Ozzie MSers with DMD access......my point is that DMD's are a separate issue and not significant to the 'diagnostic issues' in MS worldwide.
The Mcdonald was revised in 2005, again in 2010 and published in the Annals of Neurology in Feb 2011 but the upgraded Mcdonald Criteria which is still used today was actually based on the 1.5T.....
"Refinements in Imaging Criteria
The McDonald Criteria were based on detection of lesions generally using 1.5T magnet strength in noncortical regions of the brain and spinal cord.........Magnet strengths >1.5T with tailored acquisition protocols may also enhance diagnosis, with improvements in image resolution, signal-to-noise ratio, and chemical shift."
http://onlinelibrary.wiley.com/doi/10.1002/ana.22366/full
......but this later version of the Mcdonald Criteria whilst still requiring a minimum of 2 attacks, it has opened the diagnostic window without the need to wait for additional data by allowing reasonable patient history of 1 prior attack.
What that actually means is clarified;
"a) An attack (relapse, exacerbation) is defined as patient reported or objectively observed events typical of an acute inflammatory demyelinating event of the CNS, current or historical, with duration of at least 24hours in absence of fever or infection.
It should be documented by contemporaneous neurological examination, but some historical events with symptoms and evolution characteristic for MS, but for which no objective neurological findings are documented can provide reasonable evidence of a prior demyelinating event.....
....before a definite diagnosis of MS can be made at least 1 attack must be corroborated by findings on neurological examination, visual evoked potential response in patients reporting prior visual disturbance, or MRI consistent with demyelination in the area of the CNS implicated in the historical report of neurological symptoms. "
http://onlinelibrary.wiley.com/doi/10.1002/ana.22366/full
What i understand that to mean is if the patients MRI isn't providing enough clinical evidence of 2 attacks, the neuro can use both the MRI evidence of 1 attack 'and' the patients historical physiological clinical evidence to dx MS.
Cheers............JJ
The Mcdonald actually superseded the Poser Criteria (1983) which was the criteria used before MRI's, even the original Mcdonald was better able to dx MS, something like 30% more than those still suspected of MS under the Poser criteria were able to be clinically dx using the Mcdonald, but the 'wait and see' limbo aspect has generally always played a roll in diagnosing MS....
The Poser Criteria pre-dates the first DMD (Betaseron) which was released in the US around 93 but didn't get into the UK until something like 2000-1, there are still countries who's dx MSers don't become DMD illegible, under their public benefit scheme until they've reach a particular level of disability eg MSNZ until last year was about 8yrs behind Ozzie MSers with DMD access......my point is that DMD's are a separate issue and not significant to the 'diagnostic issues' in MS worldwide.
The Mcdonald was revised in 2005, again in 2010 and published in the Annals of Neurology in Feb 2011 but the upgraded Mcdonald Criteria which is still used today was actually based on the 1.5T.....
"Refinements in Imaging Criteria
The McDonald Criteria were based on detection of lesions generally using 1.5T magnet strength in noncortical regions of the brain and spinal cord.........Magnet strengths >1.5T with tailored acquisition protocols may also enhance diagnosis, with improvements in image resolution, signal-to-noise ratio, and chemical shift."
http://onlinelibrary.wiley.com/doi/10.1002/ana.22366/full
......but this later version of the Mcdonald Criteria whilst still requiring a minimum of 2 attacks, it has opened the diagnostic window without the need to wait for additional data by allowing reasonable patient history of 1 prior attack.
What that actually means is clarified;
"a) An attack (relapse, exacerbation) is defined as patient reported or objectively observed events typical of an acute inflammatory demyelinating event of the CNS, current or historical, with duration of at least 24hours in absence of fever or infection.
It should be documented by contemporaneous neurological examination, but some historical events with symptoms and evolution characteristic for MS, but for which no objective neurological findings are documented can provide reasonable evidence of a prior demyelinating event.....
....before a definite diagnosis of MS can be made at least 1 attack must be corroborated by findings on neurological examination, visual evoked potential response in patients reporting prior visual disturbance, or MRI consistent with demyelination in the area of the CNS implicated in the historical report of neurological symptoms. "
http://onlinelibrary.wiley.com/doi/10.1002/ana.22366/full
What i understand that to mean is if the patients MRI isn't providing enough clinical evidence of 2 attacks, the neuro can use both the MRI evidence of 1 attack 'and' the patients historical physiological clinical evidence to dx MS.
Cheers............JJ
This is an informative, insightful and outstanding thread. Thank you for initiating this chat aspentoo. :)))
Medhelp only allows hyperlinks for pages within their own website, so http://msj.sagepub.com/content/18/4/396.full has to be cut-and-pasted manually in order to read it. But this is more about waiting to treat when someone is already considered CIS rather than what you were getting at in your original post. I'm not sure how helpful or insightful you might find it. But I just checked. The link works.
Karen, this theory doesn't hold a lot of water here in Ireland. DMDs are free for everyone with MS. The government negotiates the prices themselves, and those with diagnoses avail of the long-term illness scheme which covers approved drugs and appliances. (ditto other conditions like cerebral palsy, epilepsy, Parkinsons, cystic fibrosis, muscular dystrophy, etc.)
The process means that new drugs take a little bit longer to be available to us, but it's usually FDA approval + a year or less. This timeframe is for the negotiations and whatever additional EU drug approval hurdles there may be.
The link I added above is my own local neurologist giving his case (at least a few years ago) as to why he doesn't treat CIS with DMDs. I posted it not because it is or isn't my own opinion, but just to give the perspective of a well-respected neurologist who actually doesn't have to give a darn about what the drugs cost.
Karen, this theory doesn't hold a lot of water here in Ireland. DMDs are free for everyone with MS. The government negotiates the prices themselves, and those with diagnoses avail of the long-term illness scheme which covers approved drugs and appliances. (ditto other conditions like cerebral palsy, epilepsy, Parkinsons, cystic fibrosis, muscular dystrophy, etc.)
The process means that new drugs take a little bit longer to be available to us, but it's usually FDA approval + a year or less. This timeframe is for the negotiations and whatever additional EU drug approval hurdles there may be.
The link I added above is my own local neurologist giving his case (at least a few years ago) as to why he doesn't treat CIS with DMDs. I posted it not because it is or isn't my own opinion, but just to give the perspective of a well-respected neurologist who actually doesn't have to give a darn about what the drugs cost.
COMMUNITY LEADER
I'll write more tomorrow, it's very late over my side of the world sorry.......I was referring to a standard 1.5T MRI which is typically a 5mm slice but there's a lot more complicated techno babble with MRI's i'll get into tomorrow
Katya,
It is my opinion a large reason they don't give drugs even when MS is suspected, is because they can't. In the US, the insurance companies won't let them, pure and simple. I don't know if you've read any of the recent articles on the web (there was even a piece on NPR) about the criminal rise in the prices of all MS drugs - even the old ones like Copaxone that are about to go generic, but it is happening. The price per script for Tecfidera that I was quoted by my last insurance company was $6250 per month's supply - and I know from my statements, that the price paid by that insurance company, to Biogen, ended up being in the low 5000s per month. A friend was on Tysabri, and she says her insurance was billed $10,000 per infusion. Yeah. I can hear you hurking up a lung from here. Every time I think of those prices, I am livid and nauseated in equal measure. As for the older meds, as I recall, the maker of Copaxone is paying the generic makers off to NOT make a generic Copaxone. Yes, it is more lucrative for both Teva (I think they hold the patent) to pay potential generic makers off, and for them to accept, than it is for someone to actually make a med that patients can reasonably afford.
There is no way that prices like those can be paid by an individual or society long term, especially when they are for drugs that do not cure and, at this point, have unknown long-term effectiveness.
Although, with all that said, I have to say, many in limbo would seem to meet the criteria for CIS at least, which would give them a better chance of being allowed to take certain of the older MS meds that have been approved for CIS - I recall Copaxone as one. But it seems like they often don't even get that. Maybe those drugs' approvals are so new that some docs are not aware than they can be given now. I don't know.
Karen
It is my opinion a large reason they don't give drugs even when MS is suspected, is because they can't. In the US, the insurance companies won't let them, pure and simple. I don't know if you've read any of the recent articles on the web (there was even a piece on NPR) about the criminal rise in the prices of all MS drugs - even the old ones like Copaxone that are about to go generic, but it is happening. The price per script for Tecfidera that I was quoted by my last insurance company was $6250 per month's supply - and I know from my statements, that the price paid by that insurance company, to Biogen, ended up being in the low 5000s per month. A friend was on Tysabri, and she says her insurance was billed $10,000 per infusion. Yeah. I can hear you hurking up a lung from here. Every time I think of those prices, I am livid and nauseated in equal measure. As for the older meds, as I recall, the maker of Copaxone is paying the generic makers off to NOT make a generic Copaxone. Yes, it is more lucrative for both Teva (I think they hold the patent) to pay potential generic makers off, and for them to accept, than it is for someone to actually make a med that patients can reasonably afford.
There is no way that prices like those can be paid by an individual or society long term, especially when they are for drugs that do not cure and, at this point, have unknown long-term effectiveness.
Although, with all that said, I have to say, many in limbo would seem to meet the criteria for CIS at least, which would give them a better chance of being allowed to take certain of the older MS meds that have been approved for CIS - I recall Copaxone as one. But it seems like they often don't even get that. Maybe those drugs' approvals are so new that some docs are not aware than they can be given now. I don't know.
Karen
Thank you Aspentoo for starting this conversation! Question to JJ regarding the use of mri's of the spine- when speaking of the "first" MRI, are you stating that it was used (in this scenario) on a 1.5 with ms protocol and still could not pick up the lesions that a 3t with ms protocol would? I know a 3t is better, but I've asked for one and was told it was up to the radiologist. Makes me so mad as I'm paying for it (insurance and deductible) and they were certain my spine is involved in all "this", so why not use the big guns?? Also, ever heard of getting a chest x-Ray as part of the diagnostic tool to locating spine lesions? I had one at the Mayo-it was "clear", but had never heard that as part of MS work up.
Thank you! Very informative conversation!!
Thank you! Very informative conversation!!
Katya, there is a huge difference between cancer and ms, because cancer tumours are obvious and textbook in most cases. Not all.
The problem is, lesions in a brain could be anything. It's not so clear cut as a tumour.
But the other difference? No wait and see. All last fall I was imaged to death searching out other possible areas ... Because cancer kills? I guess? Ms doesn't. Therefore we can wait. That's my take ... No idea really. But it seems that an outcome of death is definitely prioritized higher that an outcome of disability. As it should be.
On the other hand it's not a party for those that are losing function as they wait ... Never mind the emotional consequences .
Limbo ... Not fun ... :P.
The problem is, lesions in a brain could be anything. It's not so clear cut as a tumour.
But the other difference? No wait and see. All last fall I was imaged to death searching out other possible areas ... Because cancer kills? I guess? Ms doesn't. Therefore we can wait. That's my take ... No idea really. But it seems that an outcome of death is definitely prioritized higher that an outcome of disability. As it should be.
On the other hand it's not a party for those that are losing function as they wait ... Never mind the emotional consequences .
Limbo ... Not fun ... :P.
Thanks, JJ. Good explanation. I have/had juxtacortixal and periventicular lesions. But all but one are "too small". I have pyramidal signs, rhomberg etc. as you mentioned (objective clinical evidence) but they couldn't visualize anything on the corticospinal tract (save for an internal capsule lesion). My neuro-opth was certain they would find a brainstorm lesion -- but nothing seen. I've had trigeminal neuralgia (2013) and double vision (2014) - which can be associated with ms but not a shoo-in like ON.
There are no 3T machines for public use in our area. I'm told repeatedly that 1.5T is sufficient, and given that all but 1 of mine are too small, I imagine that anything that would show up via 3T would also be considered inconsequential, since it/they would be tinier. I've had one lesion shrink, and one periventricular one disappear, only to have two pv back a year later (done on different machines, so I'm told that was the explanation.
My neuro also believes in the +\- 1 theory -- changes if just one lesion are disregarded because it iss probably just a slice difference. This explanation doesn't make sense to me because one of the ones that disappeared was a 3 mm one ... With 1 mm slices, or even with 3 mm, it would be a feat to miss them.
I've had enough mris that I don't believe GAD is necessary -- having just read the recent report warning about GAD overuse I am going to turn it down next time.. I have had none show up as enhancing (mind you there is never a 5 minute wait after administration before they start up again, and I've never had an MRI when in the middle of issues)..
Again, I am not saying I have ms. Just trying to understand the process. Mostly impatient that something ... Anything ... gets figured out so there is a plan :p. At times I'm not sure how it COULDN'T be ... But who knows ....
There are no 3T machines for public use in our area. I'm told repeatedly that 1.5T is sufficient, and given that all but 1 of mine are too small, I imagine that anything that would show up via 3T would also be considered inconsequential, since it/they would be tinier. I've had one lesion shrink, and one periventricular one disappear, only to have two pv back a year later (done on different machines, so I'm told that was the explanation.
My neuro also believes in the +\- 1 theory -- changes if just one lesion are disregarded because it iss probably just a slice difference. This explanation doesn't make sense to me because one of the ones that disappeared was a 3 mm one ... With 1 mm slices, or even with 3 mm, it would be a feat to miss them.
I've had enough mris that I don't believe GAD is necessary -- having just read the recent report warning about GAD overuse I am going to turn it down next time.. I have had none show up as enhancing (mind you there is never a 5 minute wait after administration before they start up again, and I've never had an MRI when in the middle of issues)..
Again, I am not saying I have ms. Just trying to understand the process. Mostly impatient that something ... Anything ... gets figured out so there is a plan :p. At times I'm not sure how it COULDN'T be ... But who knows ....
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I think the later versions of Mcdonald Criteria, whilst being a lot better at dx MS earlier than ever before, still predominantly focuses on a patients MRI's to establish objective clinical evidence of demyelination eg 'both' Gad enhancing T2 lesion(s) 'and' non enhancing T2 lesion(s) in 2 or more MS specific locations (periventricular, juxtacortical, infratentorial, or spinal cord)
OR the addition of non enhancing T2 lesion(s) on subsequent MRI's in 2 or more MS specific locations (periventricular, juxtacortical, infratentorial, or spinal cord).
But wait there's more, unfortunately not a free set of steak knives but the Mcdonald criteria isn't as simplistic as it was intended to be, and the criteria is still open to neurologists professional interpretation. To meet the criteria the patient's MRI must demonstrate both dissemination in time (DIT) and Dissemination in space (DIS) which is why lesion locations and enhancing and non-enhancing lesions is important clinically objective MRI evidence.
Also a very common reason why a lot of patients get stuck in wait and see limbo, their basically waiting for additional objective clinical MRI evidence of enhancing lesion(s) or more T2 lesion(s) in another of the MS identified locations.
Objective clinical evidence isn't just the slam dunk MRI lesion location and demyelination evidence of MS though, it also includes the patients additional physiological 'objective clinical evidence' of lesion damage too eg ON, Nystagmus, Babinski's, Hoffmann, Hyperreflexia, Clonus etc etc etc
Technically the human body is still more accurate than the MRI's commonly used, a good example of this are spinal cord lesions. The 'physiological clinically objective evidence' of cord lesions will be there, the patient gets a standard 1.5T spinal MRI but no spinal cord lesions are evident, the same patient then gets a 3T full spinal MRI with MS protocol (thinner slices) and the spinal cord lesions become evident.
It's not that the spinal cord lesions were never there, the patients body demonstrated the clinical evidence of lesion damage but the 'first MRI' didn't objectively back up the patients objective clinical evidence, simply because the MRI strength and larger slices was not able to make visible what their body already showed....
Did that help explain things or did i make it as clear as mud again?
Cheers...............JJ
OR the addition of non enhancing T2 lesion(s) on subsequent MRI's in 2 or more MS specific locations (periventricular, juxtacortical, infratentorial, or spinal cord).
But wait there's more, unfortunately not a free set of steak knives but the Mcdonald criteria isn't as simplistic as it was intended to be, and the criteria is still open to neurologists professional interpretation. To meet the criteria the patient's MRI must demonstrate both dissemination in time (DIT) and Dissemination in space (DIS) which is why lesion locations and enhancing and non-enhancing lesions is important clinically objective MRI evidence.
Also a very common reason why a lot of patients get stuck in wait and see limbo, their basically waiting for additional objective clinical MRI evidence of enhancing lesion(s) or more T2 lesion(s) in another of the MS identified locations.
Objective clinical evidence isn't just the slam dunk MRI lesion location and demyelination evidence of MS though, it also includes the patients additional physiological 'objective clinical evidence' of lesion damage too eg ON, Nystagmus, Babinski's, Hoffmann, Hyperreflexia, Clonus etc etc etc
Technically the human body is still more accurate than the MRI's commonly used, a good example of this are spinal cord lesions. The 'physiological clinically objective evidence' of cord lesions will be there, the patient gets a standard 1.5T spinal MRI but no spinal cord lesions are evident, the same patient then gets a 3T full spinal MRI with MS protocol (thinner slices) and the spinal cord lesions become evident.
It's not that the spinal cord lesions were never there, the patients body demonstrated the clinical evidence of lesion damage but the 'first MRI' didn't objectively back up the patients objective clinical evidence, simply because the MRI strength and larger slices was not able to make visible what their body already showed....
Did that help explain things or did i make it as clear as mud again?
Cheers...............JJ
Wow, that's awful.
The point of medical advancement is to catch and PREVENT damage in its early stage, not irresponsibly watch it happen, and decide after, "Oh gee, this is MS, or blah blah disease". And it seems to me quite a few people who still are not Dx, are well beyond 'early stage' and MS looks absolutely obvious.
We don't wait to see if a tumor spreads, before diagnosing a person with Cancer. I don't see a difference.
I am curious why doctors do not try to treat people with suspected MS, for MS with the drugs, to see if it helps them. This is a widely used practice for many other 'suspected' issues. (IE: for Lyme, some providers trial the patient on the antibiotics, to see if symptoms improve, if they do Great, Dx lyme and treat, if not, discontinue and keep searching.)
I wonder what is the reason, Are the drugs dangerous? Is there some specific reason?
I'm genuinely very curious.
The point of medical advancement is to catch and PREVENT damage in its early stage, not irresponsibly watch it happen, and decide after, "Oh gee, this is MS, or blah blah disease". And it seems to me quite a few people who still are not Dx, are well beyond 'early stage' and MS looks absolutely obvious.
We don't wait to see if a tumor spreads, before diagnosing a person with Cancer. I don't see a difference.
I am curious why doctors do not try to treat people with suspected MS, for MS with the drugs, to see if it helps them. This is a widely used practice for many other 'suspected' issues. (IE: for Lyme, some providers trial the patient on the antibiotics, to see if symptoms improve, if they do Great, Dx lyme and treat, if not, discontinue and keep searching.)
I wonder what is the reason, Are the drugs dangerous? Is there some specific reason?
I'm genuinely very curious.
I'm glad your neurologist was able to be gutsy in your diagnosis, and that his intuition was spot-on.
So, getting back to "what does clinical actually mean."
If you look at the McDonald Criteria, the first line is if there are "2 or more clinical attacks" and then:
"Objective clinical evidence of 2 or more lesions or objective clinical evidence
of 1 lesion with reasonable historical evidence of a prior attack."
I would like to know what they mean by "objective clinical evidence of lesions". Only later in the chart, where there have not been 2 relapses, do they mention T2 lesions and CSF analysis.
Anybody here know for sure what "objective clinical evidence of lesions means"?
So, getting back to "what does clinical actually mean."
If you look at the McDonald Criteria, the first line is if there are "2 or more clinical attacks" and then:
"Objective clinical evidence of 2 or more lesions or objective clinical evidence
of 1 lesion with reasonable historical evidence of a prior attack."
I would like to know what they mean by "objective clinical evidence of lesions". Only later in the chart, where there have not been 2 relapses, do they mention T2 lesions and CSF analysis.
Anybody here know for sure what "objective clinical evidence of lesions means"?
http://www.mindbodygreen.com/0-5756/10-Reasons-Why-We-Need-at-Least-8-Hugs-a-Day.html
Definitely need more hugs going round.
Nx
Definitely need more hugs going round.
Nx
Limbo is a weird place, really. The first year is awful, but at some point you accept it on a day to day basis (or else you would go crazy). Only occasional bouts of insanity generally revolving around neurologist appointment dates ;).
We have a lot more time to process different outcomes than someone hoodwinked by a fast clinical course and diagnosis. That would be scary.
When things even out, denial is our friend ;).
I'll take the hugs, and (((hugs))) back <3.
We have a lot more time to process different outcomes than someone hoodwinked by a fast clinical course and diagnosis. That would be scary.
When things even out, denial is our friend ;).
I'll take the hugs, and (((hugs))) back <3.
Katya, I am a prime example of that. I had a concurrent symptom for 2 of my journey. Neuro was waiting and watching, other docs were assuming ms (bladder related and bladder related issues are ms, right?). Mine was completely unrelated and should not have waited 2 years in to be found accidentally.
NOT everything is ms, especially if you don't officially have it yet. And even after ...
My permanent stuff is frustrating. Even if I were to end up with ms at this point, there is no saying that anything would be any different had I been dxed immediately. Perhaps DMT's would have delayed things? Maybe not. But yes, if it isn't ms, many of the other disease processes do have some sort of earlier intervention that may help ... and for that we wait.
NOT everything is ms, especially if you don't officially have it yet. And even after ...
My permanent stuff is frustrating. Even if I were to end up with ms at this point, there is no saying that anything would be any different had I been dxed immediately. Perhaps DMT's would have delayed things? Maybe not. But yes, if it isn't ms, many of the other disease processes do have some sort of earlier intervention that may help ... and for that we wait.
I'm sorry you are stuck in this journey as well. My babinski, reflexes etc. are all right side as well.
Do you have the option of another opinion? Someone who might "have an idea?"
Do you have the option of another opinion? Someone who might "have an idea?"
I'm glad someone finally asked the question. That whole "it's a clinical diagnosis" thing has not been squaring with so many tales of docs' over reliance on MRIs, etc (see "Lies My Neuro Told Me). I did not feel comfortable asking it, possibly because I have a rather jaundiced view of neurologists, and I know it, and it likely would have turned into a rant. I am perhaps being a bit unfair to them, (well...no, not really) but my experiences with them personally when my I was trying to get my mother diagnosed (she died of ALS) and now from reading almost a year's worth of horror stories here, of endless limbo even with lesions, etc, confirm character traits that were presented to me decades ago by a physician friend of mine.
He said that most neurologists have crap people skills and are all about the patient being an interesting clinical case, and NOT about the patient as a person. (Which is a bit ironic since my friend - NOT a neuro - was ranting recently about how med schools now are too touchy-feely and that the personality traits that make excellent diagnosticians don't often come in the same package as decent people skills. He himself was actually moaning about the good old days when the doc could come in, be an unfeeling d*ck in his delivery of tragic news, but hey! he was RIGHT, and what do you want, right OR nice, because you don't get both. *eyeroll* Anyway, as we see with Alex's situation, docs' personal aversions to taking even the tiniest risk of being wrong, can have very real and detrimental consequences for the patient. The insurance issues with the cost of DMDs, etc, is a whole topic unto itself, but again, forces that have little to do with what is actually best for the uncomfortably human patient, are in play.
As an aside, I was diagnosed last Nov - and I thought MAYBE it should have been a CIS, and asked the doc if he was sure - given that this was only a single attack and all. He firmly said that he was sure, or he'd not be giving me that dx. However, when I had my first relapse in the following January, I could tell he was a bit taken aback that he'd made the right call, not only from the relapse so soon, but because my presentation had been "uncommon".
I'm not sure what was so uncommon other than my age, or perhaps because I did not appear to have spinal involvement ? (yet) or optic involvement. But he had clearly gone out on some internal diagnostic limb, and was feeling a bit vindicated. Thus I saw the neurologist ego quite clearly on display.
My doc is a young buck and making his reputation at this point - as an MS specialist, so he may be more willing to take risks at this point in his career? I'm glad he took what even he perceived as that risk of wrong - although how risky it actually was with 3 oval lesions, 8 o-bands and all mimics ruled out, is debatable - because his diagnostic instincts, however much leaping was involved, were right, and had me diagnosed in 2 months. It could have dragged on and don't I know it....
He said that most neurologists have crap people skills and are all about the patient being an interesting clinical case, and NOT about the patient as a person. (Which is a bit ironic since my friend - NOT a neuro - was ranting recently about how med schools now are too touchy-feely and that the personality traits that make excellent diagnosticians don't often come in the same package as decent people skills. He himself was actually moaning about the good old days when the doc could come in, be an unfeeling d*ck in his delivery of tragic news, but hey! he was RIGHT, and what do you want, right OR nice, because you don't get both. *eyeroll* Anyway, as we see with Alex's situation, docs' personal aversions to taking even the tiniest risk of being wrong, can have very real and detrimental consequences for the patient. The insurance issues with the cost of DMDs, etc, is a whole topic unto itself, but again, forces that have little to do with what is actually best for the uncomfortably human patient, are in play.
As an aside, I was diagnosed last Nov - and I thought MAYBE it should have been a CIS, and asked the doc if he was sure - given that this was only a single attack and all. He firmly said that he was sure, or he'd not be giving me that dx. However, when I had my first relapse in the following January, I could tell he was a bit taken aback that he'd made the right call, not only from the relapse so soon, but because my presentation had been "uncommon".
I'm not sure what was so uncommon other than my age, or perhaps because I did not appear to have spinal involvement ? (yet) or optic involvement. But he had clearly gone out on some internal diagnostic limb, and was feeling a bit vindicated. Thus I saw the neurologist ego quite clearly on display.
My doc is a young buck and making his reputation at this point - as an MS specialist, so he may be more willing to take risks at this point in his career? I'm glad he took what even he perceived as that risk of wrong - although how risky it actually was with 3 oval lesions, 8 o-bands and all mimics ruled out, is debatable - because his diagnostic instincts, however much leaping was involved, were right, and had me diagnosed in 2 months. It could have dragged on and don't I know it....
I think MRIs changed MS diagnosing. Before MRIs doctors had decide on their wits alone. Now in the US the insurance companies want proof not just the doctors say so. Also at the time MRIs became the norm DMDs came in. Before that it was chemotherapy or nothing. They were sure it was MS before they used chemo on you.
Now the other issue is the DMDs are so expensive. Canada and the insurance companies do not want to pay for these meds unless they know you with out a doubt have MS.
I was pre MRIs and DMDs I saw dozens of neurologists growing up. All agreed I had "brain damage". Then in 2007 my MRI showed Dawson's fingers, my LP had 12 obands only in the CSF. I had the abnormal EP, abnormal neurological exam, A Neuro/Opth said my double vision was MS, and all my blood work was normal. 5 neurologists all said it looked like MS but no one would diagnose me. It took so long I lost all chance of disability because I could not work and my five years between not working and diagnosis ran out.
If they had diagnosed me as a kid I would have been on disability my whole life but they won't back track to when I got MS or when they saw it in 2007.
It is all subjective.If we all went to the same neurologist we would not all be diagnosed with MS even those who have been diagnosed. It is more art than science.
I am in a clinical trial to try to find a blood test. The truth is the only true way to find MS is to look at the brain of a dead person. Since they can't do it when we are living it is all guess work.
Alex
Now the other issue is the DMDs are so expensive. Canada and the insurance companies do not want to pay for these meds unless they know you with out a doubt have MS.
I was pre MRIs and DMDs I saw dozens of neurologists growing up. All agreed I had "brain damage". Then in 2007 my MRI showed Dawson's fingers, my LP had 12 obands only in the CSF. I had the abnormal EP, abnormal neurological exam, A Neuro/Opth said my double vision was MS, and all my blood work was normal. 5 neurologists all said it looked like MS but no one would diagnose me. It took so long I lost all chance of disability because I could not work and my five years between not working and diagnosis ran out.
If they had diagnosed me as a kid I would have been on disability my whole life but they won't back track to when I got MS or when they saw it in 2007.
It is all subjective.If we all went to the same neurologist we would not all be diagnosed with MS even those who have been diagnosed. It is more art than science.
I am in a clinical trial to try to find a blood test. The truth is the only true way to find MS is to look at the brain of a dead person. Since they can't do it when we are living it is all guess work.
Alex
Limbo land must be awful for those hanging there. Like Immi, my dx was pretty quick really, sight loss first week Jan, loads and loads of tests and confirmed end Feb.
I was 'lucky' also to have ON that started to come back in only 3 weeks, plus two MRIs only 2 weeks apart which showed new lesions, existing lesions, old lesions between that two week period! Plus lots of odd symptoms (to me) that were apparently classic signs.
My main frustration having been dx so quickly is not to have started meds yet due to NHS distribution problems!
I also felt like my brain was that ticking time bomb having loads of lesions and what seemed to be a very active progression. Thank goodness a recent MRI showed all silent with two shrinking - only on high Vit D, multivits and magnesium!
There really does need more help for Neuros I think, they have MacDonald but I guess they are concerned about giving what are essentially very strong meds to someone and damaging them if they haven't actually got it.
Sending warm hugs to everyone - I'm told everyone needs a maintenance dose of at least 8 hugs a day!!
Nx
I was 'lucky' also to have ON that started to come back in only 3 weeks, plus two MRIs only 2 weeks apart which showed new lesions, existing lesions, old lesions between that two week period! Plus lots of odd symptoms (to me) that were apparently classic signs.
My main frustration having been dx so quickly is not to have started meds yet due to NHS distribution problems!
I also felt like my brain was that ticking time bomb having loads of lesions and what seemed to be a very active progression. Thank goodness a recent MRI showed all silent with two shrinking - only on high Vit D, multivits and magnesium!
There really does need more help for Neuros I think, they have MacDonald but I guess they are concerned about giving what are essentially very strong meds to someone and damaging them if they haven't actually got it.
Sending warm hugs to everyone - I'm told everyone needs a maintenance dose of at least 8 hugs a day!!
Nx
"I'd be very confused by someone who presents me with an opinion that I'm in diagnostic purgatory between CIS and MS. I wasn't aware there were any stops between those two stations."
Thanks for the laugh :D.
He is on the older side, actually ... I've pmed you with some details.
Thanks for the input :).
Thanks for the laugh :D.
He is on the older side, actually ... I've pmed you with some details.
Thanks for the input :).
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