Aa
MS, Lyme, NOW VERY CONFUSED ABOUT THE REAL ANSWER
28, male, White. years old. Dx: Late Stage Lyme disease from 2 MDs.
Age 19 while on vacation in Pennsylvania I woke up with bilateral topical foot numbness, malaise and mild vertigo followed. This went of for a week.
After this ended I remained generally symptom free, but often very tired until the next attack. I was 26, living in Nebraska under arduous and taxing academic pressure. I woke up on Feb 14 2005 with topical numbness from the waist down after a few weeks of pain in my left lymph nodes, stomach troubles, profuse sweating and a feeling of sickness. The
Age 19 while on vacation in Pennsylvania I woke up with bilateral topical foot numbness, malaise and mild vertigo followed. This went of for a week.
After this ended I remained generally symptom free, but often very tired until the next attack. I was 26, living in Nebraska under arduous and taxing academic pressure. I woke up on Feb 14 2005 with topical numbness from the waist down after a few weeks of pain in my left lymph nodes, stomach troubles, profuse sweating and a feeling of sickness. The
You might not even be reading this board anymore, but I just wanted to say, I read your above posts in full and I think it takes a lot of courage for you to come on here and finally be true to yourself. I hope you are able to continue to do that, to become comfortable with who you really are, whether in your "internet" life or in your real life. That's really all I wanted to say.
Prognostication, and an actual plan are not possible on line..you need a referal to an MS specialist to examine you and review all your labs/MRIs and then sit and tell the further plans
Bob
Bob
Bob,
Thank you so much for reading my report and for working with me.The Lyme thing has always seemed unreal to me.
Something inside always said, "This is not MS. This is something sexually transmitted-something I did."
So, if I did not make this clear-let me add the following:
I suffer with homosexuality-something that I find very difficult to deal with. In early January (attack happened in Feb) I had a sexual encounter with a man that I did not know (me preforming oral copulation). I did not injest semen but did come into contact with some.
A few weeks (maybe less) later I became very sick with flu like symptoms, severe pain in my lymph nodes (which still comes and goes from time to time). I remember just feeling awful.
This "flu" carried on for several weeks (and at the time I was in a state of severe depressive guilt) until Valentines Day, Feb 14, 2005 a little over a month later.
I woke up numb (topical paresthesias) from the waist down. You already read how the rest followed. That neurologist was certain that I had, "A very lucky case of Acute Transverse Myelitis," and that I escaped. Gait problems followed. He estimated w/o MRI that it was at the Thoracic level. Due to my weight problems during a later MRI they were unable to find anything in the T-Spine.
So, if if its ADEM, what can I do now? 2 years later? Can I die? Can I be healed?
My last MRI of the BRAIN showed larger lesions, no lesions in the corpus callosum and no lesions in the c-spine.
Please Advise....you have no idea what you have done for me.
John.
Thank you so much for reading my report and for working with me.The Lyme thing has always seemed unreal to me.
Something inside always said, "This is not MS. This is something sexually transmitted-something I did."
So, if I did not make this clear-let me add the following:
I suffer with homosexuality-something that I find very difficult to deal with. In early January (attack happened in Feb) I had a sexual encounter with a man that I did not know (me preforming oral copulation). I did not injest semen but did come into contact with some.
A few weeks (maybe less) later I became very sick with flu like symptoms, severe pain in my lymph nodes (which still comes and goes from time to time). I remember just feeling awful.
This "flu" carried on for several weeks (and at the time I was in a state of severe depressive guilt) until Valentines Day, Feb 14, 2005 a little over a month later.
I woke up numb (topical paresthesias) from the waist down. You already read how the rest followed. That neurologist was certain that I had, "A very lucky case of Acute Transverse Myelitis," and that I escaped. Gait problems followed. He estimated w/o MRI that it was at the Thoracic level. Due to my weight problems during a later MRI they were unable to find anything in the T-Spine.
So, if if its ADEM, what can I do now? 2 years later? Can I die? Can I be healed?
My last MRI of the BRAIN showed larger lesions, no lesions in the corpus callosum and no lesions in the c-spine.
Please Advise....you have no idea what you have done for me.
John.
Hi,
I will not go into the debatesabout the serology tests of Lyme disease, and why WB is kept for those with weakly positive ELIZA? ...but a couple of things are not with MS
1- The long cervical lesion
2- the severe load of brain/brainstem/spine WM lesion disappearing in a short time on antibiotecs..which also could happen spontaneously in ADEM a monophasic demyelination occures mainly in kids , but if occured in your age group it will be very hard to differentiate from a first episode of MS (theuratically we add things together + some MR findings to lean toward ADEM)..
You also never had a spinal tap!!
While the rest all are with MS , as the reliable symptomes of sensory level, brainsrtm paroxysm, motor heaviness of the legs..ext as all fullfill the definition of an MS attack plus the shape of the lesions and its direction on your MRI
If I examined you clinically and saw the MR myself, I would call your case CIS , clinically isolated syndrome and refer you to An MS specialist to
1- do the full battery of tests including a spinal tap and send labs for other illnesses which could give a long cervical lesion
2-to suggest the different palans of therapy,
3- and a follow up plan for what its called DIT (dissemination in time ) meaning a second possible attack at least > imonth from the first one, and DIS, dissemination in space, meaning a new anatomical deficits (since 2005 we can use a repeat MRI with GD for both DIT, & DIS while CSF is used for DIS only)
Hope this is helpful
Bob Hilton
I will not go into the debatesabout the serology tests of Lyme disease, and why WB is kept for those with weakly positive ELIZA? ...but a couple of things are not with MS
1- The long cervical lesion
2- the severe load of brain/brainstem/spine WM lesion disappearing in a short time on antibiotecs..which also could happen spontaneously in ADEM a monophasic demyelination occures mainly in kids , but if occured in your age group it will be very hard to differentiate from a first episode of MS (theuratically we add things together + some MR findings to lean toward ADEM)..
You also never had a spinal tap!!
While the rest all are with MS , as the reliable symptomes of sensory level, brainsrtm paroxysm, motor heaviness of the legs..ext as all fullfill the definition of an MS attack plus the shape of the lesions and its direction on your MRI
If I examined you clinically and saw the MR myself, I would call your case CIS , clinically isolated syndrome and refer you to An MS specialist to
1- do the full battery of tests including a spinal tap and send labs for other illnesses which could give a long cervical lesion
2-to suggest the different palans of therapy,
3- and a follow up plan for what its called DIT (dissemination in time ) meaning a second possible attack at least > imonth from the first one, and DIS, dissemination in space, meaning a new anatomical deficits (since 2005 we can use a repeat MRI with GD for both DIT, & DIS while CSF is used for DIS only)
Hope this is helpful
Bob Hilton
The GP there thought that is was neuropsychological but sent me for an MRI of my Brain. These were the results (Feb, 06):
BRAIN WITH & W/O CONTRAST
2/15/06
INDICATION:
Evaluate for MS. Parethesias, weakness, and visual changes.
TECHNIQUE:
Multiplanar T1, T2 weighted and FLAIR sequences were obtained prior to intravenous contrast. After intravenous Omniscan, T1 images were obtained.
FINDINGS:
There is no MRI evidence of midline shift or mass effect. Multiple round to ovoid foci of increased T2 weighted signal are noted in the periventricular and deep white matter of both cerebral hemispheres. Some foci within the centrum semi-ovale are oriented perpendicular to the plane of the corpus callosum and cingulate gyrus, suspicious for MS plaques. More ill-defined increased T2 weighted signal is noted in the periventricular white matter. Faint nodular areas of increased T2 weighted signal are noted within the corpus callosum. A small, 3-4 mm ovoid focus of increased T2 weighted signal is seen within the posterior aspect of the left middle cerebellar peduncle.
After IV contrast, at least five of the presumed plaques appear to enhance, the largest seen in the right frontal white matter, measuring 8 mm in maximum AP dimension.
Normal signal void is demonstrated in the major vasculature at the base of the brain. Visualized paranasal sinuses appear clear.
IMPRESSION:
Multiple round to ovoid foci of increased T2 weighted signal in the periventricular and deep white matter of both cerebral hemispheres, as well as within the left middle cerebellar peduncle and corpus callosum. Several lesions appear to enhance after IV contrast. Findings are non-specific, but are suspicious for MS plaques. Other etiologies, such as Vasculitis or Lyme disease, could produce similar findings. Clinical correlation advised.
--
And so, my freakish GP freaks out,
BRAIN WITH & W/O CONTRAST
2/15/06
INDICATION:
Evaluate for MS. Parethesias, weakness, and visual changes.
TECHNIQUE:
Multiplanar T1, T2 weighted and FLAIR sequences were obtained prior to intravenous contrast. After intravenous Omniscan, T1 images were obtained.
FINDINGS:
There is no MRI evidence of midline shift or mass effect. Multiple round to ovoid foci of increased T2 weighted signal are noted in the periventricular and deep white matter of both cerebral hemispheres. Some foci within the centrum semi-ovale are oriented perpendicular to the plane of the corpus callosum and cingulate gyrus, suspicious for MS plaques. More ill-defined increased T2 weighted signal is noted in the periventricular white matter. Faint nodular areas of increased T2 weighted signal are noted within the corpus callosum. A small, 3-4 mm ovoid focus of increased T2 weighted signal is seen within the posterior aspect of the left middle cerebellar peduncle.
After IV contrast, at least five of the presumed plaques appear to enhance, the largest seen in the right frontal white matter, measuring 8 mm in maximum AP dimension.
Normal signal void is demonstrated in the major vasculature at the base of the brain. Visualized paranasal sinuses appear clear.
IMPRESSION:
Multiple round to ovoid foci of increased T2 weighted signal in the periventricular and deep white matter of both cerebral hemispheres, as well as within the left middle cerebellar peduncle and corpus callosum. Several lesions appear to enhance after IV contrast. Findings are non-specific, but are suspicious for MS plaques. Other etiologies, such as Vasculitis or Lyme disease, could produce similar findings. Clinical correlation advised.
--
And so, my freakish GP freaks out,
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