evoked potentials W EEG

[Clark5]

Hello:
Does anybody out ther have a better grip or understanding of this topic?

What do evoked potentials have to do with r/o or r/in of MS?

Anyone know if using McDonald criteria if negative MRI e persistant/ waxing and waying neurological

symptoms are considered MS or CIS?  If CIS, what is the next step?

Regards
clark5

[Clark5]

Hello:
Thank-you for your answer.  I was just trying to decifer CIS in (MS for Dummies).

Due to the finding so far, 2 events noted by neurological exam, yet not positive MRI ( just a MRI that states, something about high frequency signals from T2 and T1, in the frontal lobe)  I wish that I had the exact wording.

Additionaly I have no stage 4 sleep, and very litle stage 3 (the restoring types) I do experience REM.   I believe that insomnia can cause abnormal EEG's.

I also believe that Migrains can cause some abnormalities in brain MRI, however Ido not understand the pathology.

Well, thank-you for your wealth of knowledge and empathy for others.

Happy Easter to you and your family!

Regards
clark5

[marez]

OH my please put this in your essays I am so glad you talk a lot also when you do post for lay and fogged people can you please define CIS a little more? or maybe I need to re-read several more times when awake and not foggy?

great question and answer
signed another girl with too many questions and does lots of talking you can all pass the duct tape if you want, or put me in time out :-)

thanks
Mary

[Quixotic1]

Well..You've asked a wartload of questions there.

First the Evoked Potentials, when they are positive, give weight "toward" a diagnosis of MS.  If they are negative, then they don't offer a whole lot of info with regard to MS.  That is, when negative the EP's don't act to exclude MS - despite what a few misguided neurologists say.

The EP's measure the sensory signal from point of origin along its path all the way to the brain.  For the Visual EP they measure the length of time it takes a visual stimulus to reach the brain.  The normal time it should take is well known.  If the pathway is interrupted by damage to the myelin of the optic nerve, then the signal will be delayed in reaching the brain.  The conduction time (called the P-100 latency) will be longer, but the "waveform" of the signal will be well-preserved.  Other kinds of damage may also dealy the signal, but they also may mess up the form of the signal as it arrives.  In MS the VEP is the EP that is most often positive.

For the other EP's the same is true.  For the Audio, the stimulus is a series of clicks or sounds.  For the SomatoSensory the stimulus is direct stimulation and then measurement of how long it takes to reach the brain.

My next essays going up on the Health Pages will be explaining the McDonald Criteria and the concept of the Clinically Isolated Syndrome, CIS.

In short, though, in the absence of lesions on the MRI or other supporting test, in order to obtain a diagnosis of MS, you would need clear history of two separate attacks of symptoms - of the kind seen in MS.  Each would need to be accompanied by "clinical" evidence of at least one brain or spine lesion, and together the two attacks must involve more than one part of the brain or spine.

"Clinical evidence" here means an objective finding of an abnormality by a doctor on neurological exam.  Another term for clinical evidence is clinical lesion.  These are important terms to remember.  They come up over and over again in our discussions and in the reading.

Examples of clinical lesions would be hyperactive reflexes, + Babinski test, central nystagmus, spasticity, significant muscle weakness.  The catch here is that if the attacks are just of a sensory nature (like numbness or tingling) then there will be no findings on exam.  The patient saying, "It tingles right there," is not sufficient.

We have people here on the forum who have been diagnosed with a clear relapsing/remitting history (more than one clear attack), an exam positive for objective evidence of multiple parts of the CNS being attacked AND a negative MRI.  It takes a smart and confident neurologist to do this.  I would venture that most neuro's would not stick their necks out.  

For there to be a CIS with a negative MRI, one must have a very suggestive attack and clinical evidence on exam, plus a postive VEP, or (and I'm not sure of this) a significantly postive spinal tap.  In reality, very few CIS are diagnosed with a negative MRI and only one attack.  Depending on the study, the odds af developing MS after one attack with a negative MRI are about 1 in 20 up to 1 in 50.

If the docs do think the person has CIS, then the current recommendations would be to begin Disease Modifying Meds and do interval MRI's.  The catch is that if this is early MS and if the meds do their job, they will prevent or markedly delay the onset of definite MS.  The patient may always wonder if they were really going to develop clear-cut MS or not.  Looking at this from our perspective, it would be well worth it, I think, but some studies show that medication compliance is often a problem in CIS.

More - or less - than you wanted to know.  Sorry.  I do know there is a support group for people who talk too much and I do belong.  It's called

ON-AND-ON ANON

Quix, MD