posted
As I understand it the lesions look the same, but the lyme lesions wax and wane.
Posts: 649 | From United States | Registered: Dec 2003
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posted
Hey there Lymetoo, I am not sure but I read that the lesions are on the sides of the brain for us and they are shaped just a little differently.??? I do know there is a new blood test that helps to diagnose MS my mom has it or should I say was dx. with it but now that I have researched lyme I would bet my life she has lyme disease. Her lesions are on the sides but the ducks here have no clue. Your friend's symptoms should be a good indicator. I never could understand why my mom's symptoms did not fit like they should when she was dx. I studied it long before I even knew what lyme disease was. If she has a lot of pain and mental issues without any true weakness during early dx. of MS. That's what a neurologist told me who is lyme literate. Nothing is certain with either of the 2. I know there is research on the lesions I'll try and find what I read for you. Take care, mimi
Posts: 343 | From usa | Registered: Dec 2004
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Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
From my Feb. 2005 MRI:
``There are multiple foci of signal alteration predominantly involving the subcortical deep white matter of both hemispheres possibly representing sequella of previous vasculitis or encephalomalacia from microinfarcts. Sequelae of previous infectious processes such as Lyme disease can also present with similar appearances. Patients with severe migraine headaches can also present with multiple deep white matter similar appearing lesions. Demyelinating plaques of multiple sclerosis usually exhibit more of a periventricular distribution as well as involvement of the corpus callosum.''
From the radiologist's mouth: He didn't think it was MS (thought the location was wrong).
He didn't think it was migraines (lesions were too big).
There were a total of 11 lesions, the biggest of which was 5mm.
He could hardly believe it himself, but he thought it was Lyme -- had recently attended some conference where they had studied about the presentation of Lyme, even though he didn't realize there was any Lyme around here. (Scary, considering this is an endemic area!!!)
What's funny is that usually he doesn't attempt any kind of differential diagnosis, just reports on what he sees.. But he thought this MRI was so odd that he went ahead and put his ideas into his report...a good thing he did, as Lyme hadn't even occurred to me -- this was my first clue that made me go "aha" and remember the tick bite and rash that I'd disregarded, thinking there was no Lyme in California.
Michelle
[ 03. December 2005, 11:17 AM: Message edited by: Michelle M ]
Posts: 3193 | From Northern California | Registered: Apr 2005
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posted
It might be worth having a look at the presentation by Dr. Britton on the video at this URL. Not sure it will tell you what the differences are, but might be of general interest on the subject of white matter lesions. (On dial up, all I get is audio, think broadband needed for video.)
Consider that almost all neuro's have some education and training in identifying MS systoms and have used MRI's to agument dx over time and almost no education and training for lyme and what it may look like in an MRI, I would have no confidence in any statement other than"I don't know" from a neuro. Untill someone sets out to study the difference from known sources of lyme and MS in the brain, that is studying the matter itself, I don't see how anyone can say anything definitive, one way or the other.
Lyme has been treated more sucessfully with abx than MS has with all of the drugs you can name.
Posts: 219 | From Aubur,Al. USA | Registered: Oct 2004
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posted
Someone on another thread said Dr. Fallon had been looking at this issue. Might try a search for other MS threads (recent).
Posts: 8430 | From Not available | Registered: Oct 2000
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quote:Originally posted by Lymetoo: Gathering info for an MS friend. What area of the brain is usually affected by lesions from Lyme and which area for MS.
Any way to tell the difference between the two diseases?
This is OT but hopefully you will find it interesting - Seeing your post brought back memories . . .
In 1992 I had an angiogram of the brain and was dx with a small anuerysm in a very rare location. I was referred to JHU and since it was in such a rare location (2 surgeries ever) the head of neuro-surgery at the time consulted with a doc in Switzerland to perform the surgery. After 9 hours of surgery, it was declared I didn't have an anuerysm. A repeat angio was done the day after surgery and there was no anuerysm.
My neuro at the time was trying to confirm a MS or epilepsy dx. The closest he could get was MS like symptoms or seizure like activity.
My LLMD believes it was LD the entire time.
-------------------- When I feel blue . . . . . . its time to take another breath Posts: 296 | From East Coast | Registered: Aug 2005
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posted
Here's a few abstracts I came up with on pubmed relating to white matter and Lyme:
Neurol Neurochir Pol. 2001 Sep-Oct;35(5):803-13.
[Neuroborreliosis: CT and MRI findings in 14 cases. Preliminary communication]
[Article in Polish]
Tarasow E, Ustymowicz A, Zajkowska J, Hermanowska-Szpakowicz T.
Zakladu Radiologii Akademii Medycznej w Bialymstoku.
Since 1987 when Januszkiewicz and Kieda first described borreliosis, it is commonly recognized as infection of the nervous system in Poland, especially in north-east region. The diagnosis of the disease is mainly based on typical clinical signs, supported by serological testing. In 14 patients with clinical symptoms of neuroborreliosis CT and MR were performed to evaluate CNS changes. MR examinations were abnormal in 36%. Most patients (60%) presented cerebral atrophy. In 2 cases areas of abnormal signal were identified within cerebral white matter as well as within the brain stem. In the first case it was, recognized as demyelination focus, in second one MR showed evidence of or were suggestive of vascular involvement. In one case symmetrical calcifications were also found in internal capsules. Neuroradiological signs in Lyme disease are not specific. Neuroborreliosis has to be considered when patients present foci of hyperintense signal (T2-weighted images) in white matter and brain stem.
Publication Types: Case Reports
PMID: 11873593 [PubMed - indexed for MEDLINE] ~~~~~~~~~~~~~~~~~~~~~~~~
Differential diagnosis of multiple sclerosis: contribution of magnetic resonance techniques.
Triulzi F, Scotti G.
Department of Neuroradiology, Scientific Institute H S Raffaele, Milan, Italy. [email protected]
It is widely accepted that magnetic resonance imaging (MRI) findings are not totally specific for the diagnosis of multiple sclerosis. White matter lesions that mimic those of multiple sclerosis may be detected in both normal volunteers and patients harbouring different diseases. Virtually all the characteristic features of multiple sclerosis are sometimes encountered in other conditions affecting predominantly the white matter. Different conditions such as vasculitis, subcortical atherosclerotic leukoencephalopathy, Lyme disease, or acute disseminated encephalomyelitis can be virtually indistinguishable from multiple sclerosis on conventional MR images. Also the FLAIR technique adds little to the differential diagnosis. The calculation of magnetisation transfer ratio (MT ratio) may be useful to better characterise some entities, such as vasculitis, from multiple sclerosis.
Publication Types: Review Review, Tutorial
PMID: 9647278 [PubMed - indexed for MEDLINE] ~~~~~~~~~~~~~~~~~~~~~~~~~
Regional cerebral blood flow and cognitive deficits in chronic lyme disease.
Fallon BA, Keilp J, Prohovnik I, Heertum RV, Mann JJ.
The NYS Psychiatric Institute, New York, New York 10032, USA.
This study examined brain functioning in patients with Lyme encephalopathy. Eleven patients underwent neuropsychological tests and Xenon(133)-regional cerebral blood flow (rCBF) studies, using an external detector system. Each rCBF scan was age- and sex-matched to two archival, normal controls. While few differences were noted on gray-matter flow indices (ISI, fg), Lyme patients demonstrated significant flow reductions in white matter index (k(2)) (p=.004), particularly in the posterior temporal and parietal lobes bilaterally (p=.003). Flow reductions in white matter areas were significantly associated with deficits in memory (r=.66, p=.027) and visuospatial organization (r=.62, p=.041). Results suggest that Lyme encephalopathy may be a disease primarily affecting the cerebral white matter.
[New aspects of the pathogenesis of lyme disease] [Article in Polish]
Zajkowska JM, Hermanowska-Szpakowicz T.
Klinika Chorob Zakaznych i Neuroinfekcji AM w Bialymstoku.
Morphological changes of B. burgdorferi as well as changes in expression of surface proteins caused by environmental determinants are essential in pathogenesis of Lyme disease. Cysts, spherical form (spheroplasts, L-form) and "blebs" (gemmae) can be responsible for long lasting antigenic stimulation, signs of chronic borreliosis, and even probably connected with MS and Alzheimer disease. Mechanisms to avoid elimination and persistence in the host include: expression of low heterogenic Osp A, B replaced by polymorphic in sequence and antigenic reactivity OspC, the hindrance of access to some membrane proteins by other proteins on the spirochete's surface, effects of tick saliva proteins action. Hiding of spirochetes is possible by invagination into fibrocytes membrane as well as, coating by antigens derived from lymphocytes B. Distribution of spirochetes is facilitated by binding to platelets through integrin aIIb b3, and to the endothelial cells through integrins av b3 i a5b1, recognition of decorin by lipoproteins DbpA i DbpB, receptor for NAG (N-acetyl glucosamina). Endothelial cells, toxic products of granulocytes, monocytes, macrophages as well as phagocytosis counterpart in pathogenesis. Induced cytokines are connected with activation subsets of T lymphocytes involved in inflammatory response. Cytokines produced by Th1 as cytotoxic CD8 accompany the disease. Important are also dendritic cells regarded as initiators of Th1 response with participation of IL-12. In pathogenesis of Lyme disease participation of autoimmunity is notified, especially molecular similarities between OspA and human lymphocytic antigen (hLFA-1). Neurotoxin, produced by B. burgdorferi Bbtox1 was identified. Encephalopathy signs in Lyme borreliosis could be result of releasing toxico-metabolic products, ability of spirochetes to pass the blood-brain barrier as well as, effect of lymphocytes migration. Active invasion of brain endothelium as ability to adherence to endothelial wall could be the source of focused or disseminated inflammation of brain vessels. Antiaxonal antibodies could disturb axon conduction without damaging. But damage of white matter could be connected with damage of mielin production cells, probably by antibodies, induced in cross reaction.
Publication Types: Review Review, Tutorial
PMID: 12194230 [PubMed - indexed for MEDLINE] ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Folia Neuropathol. 1999;37(1):43-51. Related Articles, Links
Central nervous system infection caused by Borrelia burgdorferi. Clinico-pathological correlation of three post-mortem cases.
Bertrand E, Szpak GM, Pilkowska E, Habib N, Lipczynska-Lojkowska W, Rudnicka A, Tylewska-Wierzbanowska S, Kulczycki J.
Department of Neuropathology, Institute of Psychiatry and Neurology, Warszawa.
The spirochete Borrelia burgdorferi (B. burgdorferi) may cause severe meningoencephalomyelitis as the sole manifestation of Lyme borreliosis. We would like to present three such cases, where definite neuroborreliosis was clinically diagnosed in two cases and possible neuroborreliosis was recognized in one case. Alive spirochetes were isolated and cultured from blood and cerebrospinal fluid (CSF) in both definite cases. B. burgdorferi as the causative agent of the infection was confirmed in CSF by polymerase chain reaction (PCR) in one definite case. In the possible case spirochetes were cultured from blood and CSF. Alive spirochetes were not isolated, however anti-B. burgdorferi antibody value in serum was significantly elevated. On necropsy gross examination brain edema without focal changes was detected in two cases. Cerebral atrophy was seen in Case 3. Microscopically, lymphocytic infiltrates, microglial diffuse and nodular activation, spongiform changes, diffuse demyelination of the cerebral and cerebellar white matter, and diffuse astrocytosis, were characteristic pathological features in all presented cases. Multifocal, perivascular degenerative changes in the cerebral and cerebellar white matter were observed in the first case. Inflammatory changes in the nuclei and roots of cranial nerves were present in the third case.
Publication Types: Case Reports
PMID: 10337063 [PubMed - indexed for MEDLINE] ~~~~~~~~~~~~~~~~~~~~~~~ Pediatr Neurol. 1992 Nov-Dec;8(6):428-31. Related Articles, Links
MRI findings in children infected by Borrelia burgdorferi.
Belman AL, Coyle PK, Roque C, Cantos E.
Department of Neurology, School of Medicine, State University of New York, Stony Brook 11794.
Cranial magnetic resonance imaging abnormalities were observed in 8 children (5 boys, 3 girls; ages 4-14 years) with neurologic problems following infection by Borrelia burgdorferi, the etiologic agent of Lyme disease. Neurologic features included headache (6), behavioral changes (5), facial palsy (2), papilledema (2), papilledema with diplopia (1), disturbance of sleep pattern (2), and carpal tunnel syndrome (1). Two MRI studies demonstrated multiple focal areas of increased signal intensity in white matter on long TR (both proton-density and T2-weighted) images.
PMID: 1476570 [PubMed - indexed for MEDLINE] ~~~~~~~~~~~~~~~~~~~~~~~ J Peripher Nerv Syst. 2004 Sep;9(3):165-7. Related Articles, Links
Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi.
Latov N, Wu AT, Chin RL, Sander HW, Alaedini A, Brannagan TH 3rd.
Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY 10022, USA. [email protected]
Neurological syndromes that follow vaccination or infection are often attributed to autoimmune mechanisms. We report six patients who developed neuropathy or cognitive impairment, within several days to 2 months, following vaccination with the OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment, one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense white matter lesions on magnetic resonance imaging. The similarity between the neurological sequelae observed in the OspA-vaccinated patients and those with chronic Lyme disease suggests a possible role for immune mechanisms in some of the manifestations of chronic Lyme disease that are resistant to antibiotic treatment.
PMID: 15363064 [PubMed - indexed for MEDLINE]
-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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GiGi
Frequent Contributor (5K+ posts)
Member # 259
posted
I will say it as I have seen it many times and been told many times by Dr. K.:
All of his MS patients that he has treated have Lyme Disease and many co-infections. All of them, without exception, are heavy metal and chemical toxic. All of them need treatments for other parasite infections. The majority of them need interventions for dental infections, cavitations, root canals, infected wisdom teeth sites, etc.
MS is a neurotoxin mediated disease, and all the problems mentioned here create neurotoxins as do any ongoing new exposures.
Metals, etc. have a synergistic effect with bacterial, viral, mold and other neurotoxins.
It's only the order or severity in which this needs to be done that changes from one patient to the next. The body does not reveal all of it at the outset.
His comments on brain lesions: "They all look alike" (whether MS, Parkinsons or Lyme).
Take care.
Posts: 9834 | From Washington State | Registered: Oct 2000
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-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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bettyg
Unregistered
posted
Tutu, I met another young 30ish woman online here from disinissues web site.
She was dx with exteme MS last year, and hers has attacked her mercilessly! She had mri showing brain lesions, etc., and did have lyme at one time earlier in her life.
She can NOT type on a computer, but has special computer equipment where she speaks now and pc types it up for her.
She's been hospitalized for long periods of time all of last year as well as having a 4-yr. old child with severe health problems too.
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