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» LymeNet Flash » Questions and Discussion » Medical Questions » Anyone diagnosed with MSA/Multiple Systems Atrophy?(Is NOT Multiple Sclerosis)

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Author Topic: Anyone diagnosed with MSA/Multiple Systems Atrophy?(Is NOT Multiple Sclerosis)
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I just saw a friend yesterday diagnosed with MSA/Myltiple Systems Atrophy (NOT MS/Multiple Sclerosis) which is very similar to ALS and is a rare form of Parkinson's. He is in bad shape and seems to be deteriorating quickly. He has a history of camping and hiking in some of the hot spots in New England and has a brother with Lyme.

I showed him and his wife the Under Our Skin DVD and afterwards, he said he had 95% of the symptoms. If they can muster the strength they say they would like to look a Lyme as the caustive agent. They really have notnhing to loose.

Anyone have this or know of anyone with it, that can be tracked back to Lyme, and was hopefully treated successfully?

[ 07. September 2008, 02:02 PM: Message edited by: Jellybelly ]

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This is a detailed discussion of the question: MS or lyme?


Audrey Stein Goldings, M.D.

Updated October, 2002


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I cannot get the link to go through or find in at the home site under the articles. If you need to see it at the link, contact the site manager of PHA - but I could not figure that out either.


The Patient as Diagnostician: How the Internet Helped an MS Patient Find Her True Diagnosis

by Ginger Savely, FNP-C

How many of you have surfed the Web to look for a diagnosis to fit the symptoms that you or one of your loved ones is experiencing?

As a nurse practitioner I often see patients who, when dissatisfied with a diagnosis (or lack of diagnosis) given to them by a health care provider, look to the Internet to discover what is really wrong with them.

Many of my colleagues scoff at this behavior, saying that the Internet is the worst thing that has ever happened to health care.

They are displeased when patients come in with a probable diagnosis already in mind and present a list of tests they are convinced are needed in order to prove or disprove their conclusion.

The concern of many health care providers is that the information on the Internet is unreliable and that it encourages patients to obsess over symptoms and even to imagine new symptoms in order to fit the criteria necessary for a certain diagnosis. ``A little bit of knowledge is a dangerous thing,'' they often say.

Most of the patients I see have been through the mill when it comes to doctors and testing and have lost their faith in the health care system that has failed them.

So, it comes as no surprise to me that these patients have learned to take their health care into their own hands, educating themselves to the point of being able to speak ``medicalese'' like a pro.

Time and time again I have observed that this tendency on the part of patients to become medically educated has been to their advantage, and many a life has been saved or bettered through the process. In my opinion this proactive behavior on the part of patients should be encouraged.

Maria: A Case in Point

Maria lives in Austin, Texas and is a petite, 49 year old lady who appears younger than her age. During our first encounter she explained that she was frustrated and unwilling to accept a recent diagnosis of multiple sclerosis (MS).

She had been experiencing recurrent right-sided facial pain (trigeminal neuralgia) for five years which had led her to consult a neurologist. An MRI brain scan had shown white patches indicative of nerve inflammation.

A spinal tap had revealed unusual proteins consistent with an MS diagnosis, and a recent repeat MRI had shown progression of the disease with increased number and size of the inflammatory lesions.

Based on her symptoms and these findings, her neurologist had diagnosed her with MS and advised her to begin immunosuppressive therapy in order to decrease inflammation.

Maria had been researching her symptoms on the Internet, and had become convinced that her problem was actually related to advanced neurologic Lyme disease.

She had been unable to convince her neurologist that this might be the case. He felt it was a clear-cut case of MS and was not inclined to consider the possibility of an illness that did not appear to be endemic to central Texas.

To placate her he had ordered a Lyme screening test, the ELISA test, which had come back negative.

Because Maria was convinced her problem was due to a bacterial infection, she refused to follow the advice of her neurologist to begin immunosuppressive therapy, fearing that this would affect her ability to fight the infection.

Maria came to me because she had heard of my special interest in the diagnosis and treatment of Lyme disease. I reviewed her medical history and made special note of her report of a tick attachment to her right lower leg six years earlier, followed by a 5 inch bullseye-shaped rash. This had occurred while she was camping in a rural area of central Texas.

Symptoms had started soon afterward. Some of these symptoms were typical of both Lyme disease and MS, such as insomnia, anxiety, confusion, dizziness, weakness, numbness, blood pressure fluctuations, constipation, acid reflux, urinary urgency, and exhaustion.

She was also experiencing symptoms that were typical of Lyme disease but not of MS: joint pain, muscle aches, jaw and tooth pain, ringing in the ears, and a stiff neck.

Many classic MS symptoms were missing, such as optic nerve inflammation, double vision, abnormal eye movements, spasticity, muscle atrophy and balance problems.

Her in-office physical exam did not reveal any obvious abnormalities.

I was familiar with a study published by the Texas Department of Health in 1994 that had revealed that over 1% of ticks collected in eight Texas state parks had tested positive for borrelia spirochetes, the corkscrew-shaped causative agents
of Lyme disease.

In fact, per the International Lyme and Associated Disease Society (ILADS), borrelia-carrying ticks had been found in every state in the union. The rash Maria had described on her leg certainly sounded like erythema migrans, the classic ``bullseye'' rash that is diagnostic for Lyme disease.

Her negative result on the ELISA screening test that had been ordered by her neurologist didn't impress me; ELISA tests for Lyme borreliosis are notoriously insensitive. There is evidence that the ELISA has a sensitivity of only 30-40% and therefore does not meet the 95% sensitivity criteria necessary for a
screening test.

The Western blot is a better test to use for screening. Unfortunately most labs do not report the individual reactive bands on the blot but report only a positive or
negative end-result based on the presence of bands relevant for epidemiologic rather than diagnostic criteria. It is of utmost importance to choose a lab that reports ALL of the positive bands.

Diagnosis of a sick patient and qualification for epidemiologic inclusion are two different matters! I chose to use the highly
reputable IGeneX Laboratories in Palo Alto, California.

Through IGeneX testing the patient was positive for Lyme both by the Western blot IgM and by antigen captured in the urine. The history, symptoms, and now the lab results were pointing to a diagnosis of late-stage neurologic Lyme disease (neuroborreliosis) rather than MS.

After three months of intravenous (IV) and oral antibiotic treatment, Maria reported several subjective improvements. Her overall fatigue, urinary frequency, and discomfort were lessened. The numbness in her hands and feet was gone, as was her subjective sensation of weakness.

Maria continued to tolerate the treatment well. After six months of IV antibiotics a repeat MRI showed a 25% reduction in inflammatory lesions. She reported overall improvement, with continually decreasing fatigue, malaise, weakness, cognitive problems, and muscle pain.

She continues to improve on IV antibiotics.

MS is a progressive disease, and although remissions are common, a reduction in brain inflammation is not.

This improvement in the patient's MRI was quite a surprise for the neurologist and served to strengthen my belief that the patient's problem all along had been neuroborreliosis rather than MS.

Because of the many similarities in the two diagnoses, it is extremely important to pay attention to the patient's history and development of symptoms and to know how to test correctly for the presence of borrelia antibodies.

MS is a diagnosis based primarily on subjective symptoms, and according to the CDC, Lyme disease is as well.

The previously mentioned MRI and spinal tap findings in this patient were not diagnostic of MS per se, since they are often also present in Lyme patients with neurologic involvement.

When clinicians complain about the incorrect medical information patients come across on the Internet or the tendency for patients to self-diagnose based on this information, they need to look at the bigger picture and realize that the occasional enlightening discovery is well worth the inevitable false alarms.

I continue to support patients who research their symptoms on the Web, believing it empowers them to be proactive about their health care. Sometimes, as was the case with Maria, this kind of patient collaboration can prove to be a life-saver.

See also:

Fritzsche, M. Chronic Lyme Borreliosis at the Root of Multiple Sclerosis: Is a Cure with Antibiotics Attainable? Medical Hypotheses 2005; 64 (3): 438-448.


For testing information:


And cross search MS, borrelia - and MS, lyme - and MS, tick-borne at PubMed's site:

- ILADS for the Treatment Guidelines and articles


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Thanks Keebler for taking the time to post that, but this is NOT MS/Multiple Sclerosis. I know there is a connection between MS and Lyme, in fact my mom has Lyme with an MS diagnosis attached.

I also know there is already at least one reported patient with the MSA who did not survive and was found to Lyme positive at autopsy.

It is really a newer classification of Parkinson's and is very similar to ALS, and can kill you in a relatively short period of time.

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Sorry - I guess I was being lazy with the homework.

I was inclined to think that the articles about MS and lyme might still be of help.

However, seeing that you emphasized that this " . . . can kill in a relatively short period of time . . ." advances it to finding more specific information right now.

I hope you find what you need. I've not seen anything exactly about this. Marnie may have as she is an avid researcher.

I hope your friend can get to a LLMD ASAP as that might be the best avenue even if you don't find literature connecting the dots. It often takes a long time for such literature to show up.

You said: " . . .I also know there is already at least one reported patient with the MSA who did not survive and was found to Lyme positive at autopsy. "

Do you have an article or link about that? It would be good to save here on this thread or to a file in case others need it.

And, I would hope that other case would help convince your friend to call a LLMD and explain the urgency and perhaps get in as soon as possible or get another referral.

Your friend is lucky you have you. Good luck.


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Good idea Keebler. Here is the report on MSA Multiple Systems Atrophy and the Lyme connection:
Archives of Pathology and Laboratory Medicine: Vol. 127, No. 9, pp. 1204-1206.

This link will not work as it appears, all you need to do is go into the address above and put parenthesis around the year 2003 with no spaces on either side. With those parenthesis left in I am not able to make it work, don't know why????

Lyme-Associated Parkinsonism: A Neuropathologic Case Study and Review of the Literature
David S. Cassarino, MD, PhD; Martha M. Quezado, MD; Nitya R. Ghatak, MD; Paul H. Duray, MD

From the Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Md (Drs Cassarino, Quezado, and Duray); and the Departments of Pathology and Neuropathology, Virginia Commonwealth University, Richmond (Dr Ghatak)

Accepted April 11, 2003

Neurological complications of Lyme disease include meningitis, encephalitis, dementia, and, rarely, parkinsonism. We present a case of striatonigral degeneration, a form of multiple system atrophy, in Lyme-associated parkinsonism. A 63-year-old man presented with erythema migrans rash, joint pains, and tremors. Serum and cerebrospinal fluid antibodies and polymerase chain reaction for Borrelia burgdorferi were positive. Clinical parkinsonism was diagnosed by several neurologists. Despite treatment, the patient continued to decline, with progressive disability, cognitive dysfunction, rigidity, and pulmonary failure. At autopsy, the brain showed mild basal ganglia atrophy and substantia nigra depigmentation, with extensive striatal and substantia nigral neuronal loss and astrogliosis. No Lewy bodies were identified; however, ubiquitin-positive glial cytoplasmic inclusions were identified in striatal and nigral oligodendroglia. There were no perivascular or meningeal infiltrates, the classic findings of neuroborreliosis. To our knowledge, this is the first report of striatonigral degeneration in a patient with B burgdorferi infection of the central nervous system and clinical Lyme-associated parkinsonism.

Lyme disease is an infection caused by Borrelia burgdorferi, a spirochete transmitted by Ixodes ticks in the United States. Patients often initially present with the classic erythema migrans rash, a macular, erythematous, circular area with central clearing that expands around the site of the tick bite. The rash usually begins within 3 to 30 days after the bite, but is only found in about 60% of patients.1 Patients with long-standing Lyme disease may develop myocarditis, oligoarthritis of large joints, and central nervous system involvement (typically meningitis, encephalitis, and cranial neuropathy, and, rarely, basal ganglia and cognitive dysfunction) in the tertiary phase of the disease. There have also been reported cases of patients with Lyme disease developing clinical parkinsonism.2-6 We describe what to our knowledge is the first such case with autopsy follow-up.

Patients with Lyme meningitis usually show increased numbers of lymphocytes and plasma cells in the pia and arachnoid, with some atypical lymphocytes.1 In Lyme encephalitis, there is edema, microglial activation, and intraparenchymal lymphoplasmacytic infiltrates in a predominantly perivascular distribution.1 These findings were lacking in the current case. Instead, the brain showed neuronal loss, gliosis, and glial cytoplasmic inclusions in the striatum and substantia nigra, leading to the diagnosis of striatonigral degeneration (SND).

Striatonigral degeneration is now recognized to be a subtype of multiple system atrophy (MSA), a relatively uncommon neurodegenerative disease characterized by neuronal loss and astrocytosis of the basal ganglia and substantia nigra, with characteristic ubiquitin-positive glial cytoplasmic inclusions.7 These inclusions contain α-synuclein, which can be identified immunohistochemically in glial cells. To our knowledge, the presence of glial cytoplasmic inclusions and α-synuclein has not been previously reported in the brains of patients with Lyme disease.


The patient was a previously healthy, 63-year-old white man who presented with an erythema migrans rash on his left inner thigh in June 1995. He developed diffuse musculoskeletal pain, swelling of the left knee, tremor of the left hand, and pain in the left shoulder and arm during the subsequent year. In June 1996, the diagnosis of Lyme disease was made based on a serum Western blot showing B burgdorferi-specific immunoglobulin (Ig) G bands. The patient's musculoskeletal pains and hand tremor worsened during the next few months, with loss of function. He was treated with 3 weeks of intravenous (IV) ceftriaxone without improvement in August 1996. A magnetic resonance imaging scan of the head and neck was reportedly normal in February 1997. He resumed antibiotic therapy with 2 weeks of IV ceftriaxone and then 42 days of IV cefotaxime sodium, with little improvement in his condition. In May 1997, a neurology consult was obtained, at which time a spinal tap cerebrospinal fluid (CSF) was found to be positive by enzyme-linked immunosorbent assay (ELISA) for B burgdorferi-specific IgG. Neurological examination documented parkinsonism, which was attributed to Lyme neuroborreliosis. Pharmacological treatment was initiated, without apparent benefit.

By July 1998, the patient had lost 20 kg and had developed symptoms, including chronic fatigue, tremors, and neck and bilateral hand pain; his movements were stiff and painful. He also developed cogwheel rigidity in August 1998. Due to continued clinical deterioration, he was started on oral antibiotics, including clarithromycin, ciprofloxacin, and hydroxychloroquine. His tremors seemed to improve after treatment; however, his other symptoms continued unabated. Western blots for B burgdorferi-specific IgM (30, 34, 41, and 93 kd) and IgG (30, 39, 41, 58, 66, and 93 kd) antibodies were positive in November 1999. Despite continued antibiotic treatments, the patient's movement disorder continued to progress. By May 2000, he exhibited decreased memory, incontinence, drooling, and inability to ambulate independently or to care for himself. Cerebrospinal fluid and blood polymerase chain reaction (PCR) tests at that time for Borrelia species were positive, and PCR for Babesia species was negative. A red blood cell culture showed classic spirochetes in his red cells. Oral multiagent antibiotic therapy was continued.

In December 2000, the patient was admitted to the hospital for aspiration pneumonia and was treated with antibiotics and parenteral nutrition. He was readmitted in January 2001 for another episode of aspiration pneumonia. He had a sputum culture that was positive for Staphylococcus aureus, and he was treated with IV vancomycin. In February 2001, a sputum culture was reportedly positive for B burgdorferi. A repeat serum Western blot for Borrelia IgM and IgG was positive, and PCR for Babesia organisms was also positive. Despite continued antibiotic treatments (IV vancomycin, azithromycin, and atovaquone), the patient's neurological status continued to decline, and he finally succumbed to infection and respiratory failure in April 2001. A full autopsy was performed.


Gross examination revealed few significant findings. Externally, there were multiple bruises and IV marks, and decubital ulcers over the sacrum. The chest cavities contained fluid and there were bilateral pleural effusions. The brain and spinal cord were externally unremarkable; on sectioning, the basal ganglia showed mild atrophy bilaterally (Figure 1 ), with greater changes on the left, and the substantia nigra showed depigmentation. The cerebellum also appeared to show mild atrophy.

Microscopic examination of the heart showed scattered lymphocytes and plasma cells, with areas of mild fibrosis, suggesting possible remote myocarditis. No significant inflammation was identified in any other organs. The brain showed extensive neuronal loss and severe astrogliosis in the striatum (Figure 2 ) and substantia nigra (Figure 3 ). Other brain regions were unaffected. No Lewy bodies were identified; however, there were ubiquitin-positive glial cytoplasmic inclusions in scattered oligodendroglia in the striatum (Figure 4 ) and substantia nigra, but not in the pons (including the olivary nuclei) or cerebellum. These glial cytoplasmic inclusions also stained positively with α-synuclein immunohistochemistry (Figure 5 ). Premortem Western blot and ELISA studies showed positive reactions for Borrelia-specific IgM and IgG antibodies in both serum and CSF samples (Tables 1 and 2 ). Polymerase chain reaction analysis for Borrelia-specific sequences in the substantia nigra and basal ganglia was performed; however, the results were not able to be confirmed on the postmortem tissue.


To the best of our knowledge, this report describes the first case of parkinsonism arising in association with Lyme disease to come to autopsy. Histological study of the brain displayed characteristic morphologic changes of SND, a variant of MSA. The patient's diagnosis of Lyme disease was well documented, confirmed by both serum and CSF ELISA, Western blots, and premortem PCR studies. The patient developed signs and symptoms of MSA after his presentation with the erythema migrans rash, and there was no prior history of neurologic dysfunction. Although it cannot be excluded that the SND could have developed independent of his Lyme disease, the temporal association with tertiary Lyme disease, the high titer of Borrelia antibodies in his CSF, and premortem PCR for B burgdorferi-specific sequences in the CSF favor an association. The fact that the classic inflammatory changes associated with Lyme disease were absent may indicate an atypical central nervous system infection in this patient, or merely that the infection and inflammation had resolved by the time of death (which occurred 5 years after infection and after multiple courses of antibiotics). In most cases, the organisms cannot be identified in histologic sections.1,6

Regardless of whether the infection had resolved by the time of death, we hypothesize that it was sufficient to cause ongoing neuronal loss and astrogliosis leading to SND. Therefore, the negative studies for organisms in the postmortem tissue may reflect either the absence of organisms or the persistence of low numbers of spirochetes and false-negative findings. Overall, we believe that the SND and resulting parkinsonism in this case might be related to direct infection by Borrelia organisms, or to the immune response against the organisms, and these findings are therefore of particular interest because the etiology of SND and MSA is unknown.

Clinical diagnosis of MSA is based on diagnostic criteria, including parkinsonism with poor or transient response to L-dopa therapy. Patients often develop progressive bulbar dysfunction leading to dysphagia and laryngeal stridor, eventually predisposing to aspiration pneumonia.7 Our patient's parkinsonism was resistant to traditional medications, and he developed classic signs of parkinsonism as well as dysphagia, consistent with the clinical course of MSA. In a previous report of Lyme-associated extrapyramidal features in 5 patients,5 all of the patients exhibited akinesia, pains, and rigidity, similar to our patient, although only 2 developed tremors. Four of the 5 patients also developed bulbar dysfunction, a characteristic finding in MSA. Although none of these patients came to autopsy, and therefore could not be definitively diagnosed with MSA, the clinical findings were consistent with this conclusion and were generally similar to findings in our case. One significant difference was that their patients responded to anti-Parkinson's medications, which is unusual in MSA, and they also improved on antibiotics. This dissimilarity may indicate a different underlying pathology compared to the present case, in which there was little or no improvement with anti-Parkinson's drugs and antibiotics. Alternatively, as our patient did not receive antibiotics until 14 months after initial infection, he may have suffered irreversible neuronal damage by the time treatment was initiated.

Autopsy brain studies on patients with Lyme disease are limited to single case reports or small case series. In addition to meningoencephalitis, multiple other neuropathologic findings have been reported. One patient was found to have rhomboencephalitis on autopsy, with microgliosis and obliterative inflammatory vasculopathy associated with ischemic infarcts.2 Another case showed multifocal inflammation, neuronal cell loss, demyelination, and astrocytosis in the cortex, thalamus, cerebellum, and spinal cord.3 Bertrand et al4 reported 3 cases, 1 of which showed cortical involvement, and all 3 of which showed cerebral and cerebellar white matter changes, with associated lymphocytic infiltrates, microglial activation, spongiform changes, diffuse astrogliosis, and demyelination. To date, however, no neuropathologic findings have been reported in the substantia nigra or basal ganglia. Clinically, Kohlhepp et al5 described 5 patients with Lyme disease with extrapyramidal symptoms and documented CSF infection by B burgdorferi. Interestingly, treatment of the patients with high-dose penicillin led to both normalization of their CSF and improvement in their extrapyramidal symptoms.5

In primates infected with B burgdorferi, brain autopsy and PCR analysis showed organisms in the leptomeninges, nerve roots, and dorsal root ganglia, but not in the brainstem, cerebellum, or basal ganglia.6 Histologic and immunohistochemical studies with polyclonal anti-B burgdorferi antibodies confirmed the PCR results in this study.6

In summary, this is the first published report of SND or MSA, with characteristic ubiquitin and α-synuclein-positive inclusions, in a patient with documented B burgdorferi infection of the central nervous system and clinically diagnosed Lyme-associated parkinsonism. Therefore, this case raises the possibility of a causal link between B burgdorferi infection of the central nervous system and SND.

We thank Robert G. Beitman, MD, and Gregory P. Bach, DO, for submitting this fascinating case to us.

References Return to TOC

1. Duray PH, Chandler FW. Lyme disease. In: Connor DH, Chandler FW, Schwartz DA, Manz HJ, Lack EE, eds. Pathology of Infectious Diseases. Stamford, Conn: Appleton and Lange; 1997:635-646.

2. Kuntzer T, Bogousslavsky J, Miklossy J. et al. Borrelia rhombencephalomyelopathy. Arch Neurol 1991;48:832-836. [PubMed Citation]

3. Kobayashi K, Mizukoshi C, Aoki T. et al. Borrelia burgdorferi-seropositive chronic encephalomyelopathy: Lyme neuroborreliosis?. An autopsied report. Dement Geriatr Cogn Disord 1997;8:384-390.

4. Bertrand E, Szpak GM, Pilkowska E. et al. Central nervous system infection caused by Borrelia burgdorferi: clinico-pathological correlation of three post-mortem cases. Folia Neuropathol 1999;37:43-51.

5. Kohlhepp W, Kuhn W, Kruger H. Extrapyramidal features in Lyme borreliosis. Eur Neurol 1989;29:150-155. [PubMed Citation]

6. Cadavid D, O'Neill T, Schaefer H, Pachner AR. Localization of Borrelia burgdorferi in the nervous system and other organs in a nonhuman primate model of Lyme disease. Lab Invest 2000;80:1043-1054. [PubMed Citation]

7. Lowe JS, Leigh N. In: Graham DI, Lantos PL, eds. Greenfield's Neuropathology. New York, NY: Oxford University Press; 2002:343-346.

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My husband had symptoms that were ALS; symptoms typically Parkinsons, and symptoms typical to MS.

There was a time when he was not walking at all, and where I literally just dragged him on the floor to certain rooms because home is not suitable for wheels everywhere.

He is also heavy metal toxic, did a lot of flying and had radiation exposure. And he had Lyme and all co-infections,

until just recently when he was successfully treated with the Bionic 880, which I have posted about. He is rapidly on his way to recovery, and we expect full recovery when his muscles will be back in full action with physical therapy. We still have some metal toxins to go, but all else -- all infections, co-infections, viral infections, etc. are gone after the treatment with Bionic photons.

Hope your friends will listen. I always hoped, but never expected what is really happening in our house now.

Take care.

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