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IV infusions given for MS but test results unclear of diagnosis

Hi everyone. I’ve been dealing with Optic Neuritis in my right eye since 2017, due to vision changes I’ve seen my Optometrist, 2 Opthamologists, a Retina Specialist and a Neuro-Opthamologist. All came to same conclusion that my changes in vision is not a problem with my eyes but that Optic Neuritis was the culprit. However 4 MRIs of my brain and cervical spine have showed no lesions only white matter hyperintensities on my last brain MRI. Due to having vision changes in my left eye my PCP sent me to see a regular Neurologist who upon exam stated he could see the chronic damage that the Optic Neuritis has done to my right eye but nothing in my left eye as of yet. I told him of my other symptoms such as: lightheadedness, fatigue, muscle weakness, tingling in my feet and hands, unexplainable muscle/joint aches, memory issues, brain fog, migraines/headaches, etc. he stated that he was going to order some tests and treat me as if I have MS and do an IV infusion of SoluMedrol. I went through the week long treatment, I had a Lumbar Puncture, Evoked Potentials, bloodwork for blood cultures, Mog Antibody, NMO Antibody. The only things that have come back not within normal range was on my MS panel through my LP showed 2 oligoclonal bands not found in the serum and the CSF igG index was high, my EVP showed demyelination of my optic nerve in both eyes, and I had elevated WBCs and RBCs in my CSF. I don’t have my follow up appt with Neuro until Nov 20, so now with results like mine and definite answers I’m nervous as to what could be going on and hoping that others have maybe seen similar results and what their outcomes ultimately were.
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987762 tn?1671273328
COMMUNITY LEADER
Ok from my understanding of these parts of your MRI:

"There has been interval development of an ovoid area of increased signal in the subcortical white matter of the right posterior frontal lobe near the frontoparietal junction without mass effect or enhancement, measuring 1.0 x 0.7 cm."

there was actually a newly developed lesion of meaningful size and shape and noted as it not being seen on prior MRI's by this comment...

"2. Nonspecific hyper-intensities are present in the white matter and pons, with development of a new hyperintensity in the right frontal lobe since the prior study. "

...and whilst it doesn't specifically point towards MS at this time, it may help to work out some possible alternatives but i would expect MS wouldn't be able to be ruled out until an alternative explanation for the totallity of your diagnostic evidence, clinical signs and symptom pattern becomes clear.

Repeat brain and spinal MRI's are typical but additional nerve conductor tests may be of help too, honestly couldn't even guess with any accuracy with what additional tests your neuro wants you to have sorry.

Sorry i couldn't be of more help.....JJ
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You have been so helpful explaining the MRI to me thank you so much that was very helpful!
987762 tn?1671273328
COMMUNITY LEADER
Hi and welcome,

If i understand the information you've provided correctly, your saying your main test evidence like your brain and spinal MRI's didn't clearly pin point towards a neurological condition like MS because none of the 4 found any brain or spinal cord lesions  but your LP MS panel might have or has....

Technically your last MRI did actually pick up lesions  ie "white matter hyperintensities on my last brain MRI" would actually be brain lesions. White matter lesions are exstremely common lesions and not necessarily abnormal depending on the brain locations they're in, micro sizes, your age, health history, smoking history etc etc but WMH are not the same type of lesions that demyelinating conditions like MS cause.

Do you know if your last MRI was a 3 T compared to the MRI's prior which were 1.5T's, its just without more detailed information to help clue in to the why of it, its possible that the only reasoning of the last MRI showing the WMH up could have more to do with a changingof  MRI strength (1T vs 1.5T vs 3T) or using narrower slices MS protocal (5mm vs 3mm) or software update etc so they;ve potentially been there the entire time and not newly developed between MRI no 3 and MRI no 4.

Your LP results (MS panel) aren't actually as suggestive or as consistent with MS as you might be thinking; LP results are generally more usefull in diagnosing MS when the results are added to all the other suggestive / consistent dianostic evidence simply because the same / similar LP results are also found in many other medical conditions too.  

Depending on the lab specifications its generally 2+ unique Obands or 4+ unique Obands for an LP to be classified as abnormal so its likely the Obands are still within normal range.  

You mentioned "I had elevated WBCs and RBCs in my CSF", the RBC means blood which could of been from the LP itself but elevated WBC could be pointing towards an infection, inflamation or even bleeding.

"What does IgG in CSF mean?

IgG stands for immunoglobulin G, a type of antibody. Antibodies are proteins made by the immune system to fight viruses, bacteria, and other foreign substances. A CSF IgG index measures the levels of IgG in your cerebrospinal fluid. High levels of IgG can mean you have an autoimmune disorder."
https://medlineplus.gov/lab-tests/csf-immunoglobulin-g-igg-index/

You mentioned "CSF igG index was high" which from my understanding if its high and theres also an elevated WBC, it can often be pointing towards there being an infection of some kind. Unfortunately the LP isn't unique to any specific medical condition so its useful as value added information when combined with all the other abnormal diagnostic evidence a patient has.

Optic Neuritis (ON) is very much associated with MS but it's also a stand alone optic condition ,as well as being associated with some other medical conditions too....

"Causes of optic neuritis
Some of the many conditions and diseases that can cause optic neuritis include:

cytomegalovirus
hepatitis B
herpes
HIV
Lyme disease
measles
multiple sclerosis
mumps
paranasal sinus infection
radiation therapy
syphilis
tuberculosis."
https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/eyes-optic-neuritis

Bilateral ON isn't as common with MS as unilateral ON is, but its possible for someone with MS to eventually develop  ON in their other eye. Bilateral though might help narrow down any alternative medical explanations and any further tests to help rule them in or out.

Your may not have a definitive answer for some time yet so try to keep an open mind on what it is you might be dealing with cause it may not be a neurological condition like MS in the end.

Hope that helps........JJ
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I don’t know enough about MRIs to know. Here is my most recent report of the brain:

TECHNIQUE:    Multiplanar multisequence magnetic resonance imaging of the brain was obtained before and after the administration of intravenous contrast.

FINDINGS:
VENTRICLES: No hydrocephalus.
HEMORRHAGE: None.
ACUTE INFARCT: No evidence of an acute or evolving infarct.
BRAIN: A punctate T2 and FLAIR hyper-intensity is present in the subcortical white mater of the right posterior parietal lobe on series 6, image 101.  This does not meet MRI criteria for dissemination in space and multiple sclerosis.  This was seen previously.  There has been interval development of an ovoid area of increased signal in the subcortical white matter of the right posterior frontal lobe near the frontoparietal junction without mass effect or enhancement, measuring 1.0 x 0.7 cm.  No juxtacortical hyperintensities are present.  No periventricular hyperintensities oriented perpendicular to the corpus callosum are seen.
VASCULATURE:  Flow voids of the major intracranial vessels are maintained
indicating patency.
SKULL:        Normal.
OTHER:            Normal.
ENHANCEMENT:  No abnormal enhancement in the brain or meninges.

CONCLUSION:
1. No intracranial mass, mass effect, hemorrhage or hydrocephalus.
2. Nonspecific hyper-intensities are present in the white matter and pons, with development of a new hyperintensity in the right frontal lobe since the prior study. These are non-specific and considerations include chronic microvascular ischemic changes, sequela of chronic migraine headaches, or a demyelinating process.  These do not meet MRI criteria, however, for dissemination in space of multiple sclerosis

What other testing do you think they may suggest having?
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