Controversies in Neuroborreliosis **********************************
Audrey Stein Goldings, M.D.
Updated October, 2002
The objectives of this article are to cover issues related to Lyme disease that are not even-handedly addressed in the current literature. It will:
Present a practical approach for making the diagnosis of neuroborreliosis,
Explore the other side of the post-Lyme syndrome (i.e. the likelihood of chronic ongoing infection),
Discuss the relationship between MS and Lyme,
Critique the current regimens published for treating neuroborreliosis, and
Present my own approach which may differ from some leading authorities.
``Anyone who, in discussion, relies upon authority uses not his understanding but rather his memory.'' --Leonardo da Vinci, Notebooks (c. 1500)
It is hoped this data will provide the reader with a broader understanding of neuroborreliosis so that he or she may better use current and evolving knowledge for clinical decision making.
I. NEUROBORRELIOSIS: MAKING THE DIAGNOSIS
Because of difficulties in making the diagnosis of neuroborreliosis, the physician will need a familiarity with the most common forms of presentations, which will be emphasized.
The following points will help evaluate the patient for neuroborreliosis:
For most patients, systemic features of disease coexist with, or predate, neurologic manifestations.
Both central nervous and peripheral nervous system involvement is frequent with Lyme disease and typically occur together.
Laboratory data may or may not confirm the diagnosis, and other disease in the differential diagnosis must be evaluated thoroughly in cases where diagnostic ncertainty exists.
Although history of exposure to B. burgdorferi should be sought, for various reasons, patients may not remember a history of a tick bite, or the pathognomonic rash particularly if the disease is presenting years after the exposure.
Early on, personality changes, psychiatric symptoms, or cognitive manifestations may be the first, and occasionally the only, symptoms that the patient or family is aware of.
CLINICAL DESCRIPTIONS OF NEUROBORRELIOSIS ******************************************
CENTRAL NERVOUS SYSTEM INVOLVEMENT
Meningismus with normal CSF Lymphocytic Meningitis Meningoencephalomyelitis Subacute Encephalopathy (SAE) PERIPHERAL NERVOUS SYSTEM INVOLVEMENT
Patients may present with headache and stiff neck without evidence of CSF inflammation.
Since early CNS seeding has been described, as well as culture positivity during latent disease without concurrent CNS inflammatory changes, these symptoms probably indicate active infection.
Stiff neck might alternatively be due to axonal degenerative changes of the cervical paraspinal musculature, but there should be other evidence of a more widespread neuropathy when this is the case.
LYMPHOCYTIC MENINGITIS
Lymphocytic Meningitis may appear to be indistinguishable from aseptic meningitis during early-disseminated disease (weeks to months after inoculation with B. burgdorferi).
Most patients will have headaches that will fluctuate in intensity. Associated features may include a cranial neuropathy in about one-third.
Low-grade encephalopathy is present in up to one-half, with mild memory concentration deficits, mood changes, and sleep disturbance.
MENINGOENCEPHALOMYELITIS
Rarely, focal parenchymal CNS lesions occur.
The MRI may show punctate white matter lesions best seen on T2-weighted images; larger lesions occur infrequently.
One brain biopsy showed increased numbers of microglia cells, rare spirochetes, and minimal inflammation. Transverse myelitis, movement disorders (extrapyramidal cerebellar, chorea and myoclonus), and hemiparesis can occur.
PSYCHIATRIC DISORDERS
Psychosis, mood swings (mild or bipolar), profound personality changes, depression, anorexia nervosa, obsessive-compulsive disorder, and panic attacks may occur. CSF may be normal.
SUBACUTE ENCEPHALOPATHY (SAE)
The most common chronic CNS manifestation is a SAE, characterized by memory problems and depression.
Many patients (or their families) will complain of their excessive daytime sleepiness and extreme irritability.
These patients generally come to the office disorganized (despite a supreme effort to be organized), unable to give a coherent history.
They will bring copious notes, which are invariably in the wrong order.
Most patients will complain of fatigue, and about one-half have headaches.
Coincident polyneuropathy is very common with spinal or radicular pain, or distal paresthesias.
Quantifiable deficits in memory, learning and retrieval, attention and concentration, perceptual-motor skills, and problem solving are common.
MMPI testing generally shows a stable psychological pattern without significant psychopathology, similar to other medically ill patients.
ADDITIONAL CNS TESTING: **********************
NEGATIVE TEST RESULTS DO NOT RULE OUT THE DIAGNOSIS OF NEUROBORRELIOSIS
Confirmation by CSF CULTURE is seldom practical because the organism is very fastidious, present in small numbers, takes a long time to grow out, and may undergo changes to forms which cannot be cultured easily.
CSF ANTIBODY TITERS may be present but are inconsistent and therefore their absence does not rule out CNS infection. The MRI is seldom abnormal and the findings, when present, are not specific for Lyme.
CSF PCR (test for spirochetal DNA) is a useful tool, but at present, because the capture of DNA is inconsistent, a few questions still need to be addressed.
OLIGLOCLONAL BANDS AND IGG INDEX -- Looking for evidence of an intrathecal immune response may be helpful, but it is not specific.
As a rule, oligoclonal bands and an elevated IgG index are not present in North American Lyme disease and their presence should suggest other diseases.
THE PERIPHERAL NERVOUS SYSTEM
Cranial neuropathy, painful radiculitis, distal neuropathy, and plexopathy are seen and generally reflect different clinical presentations of mononeuritis multiplex (polyneuropathy).
Bell's Palsy occurs in almost 11% of all Lyme patients and is bilateral in up to 1/3.
Therefore, a bilateral Bell's Palsy is very suspicious for Lyme in an endemic area.
Painful radiculitis or cranial neuropathy can be seen with meningitis but also with normal CSF due to axonal neuropathy.
Myositis may occur with Lyme as well as polymyalgia rheumatica.
Symptoms of chronic involvement of the peripheral nervous system in a series of patients with chronic neurologic manifestations of Lyme disease developed a median of 16 months after the onset of infection, while CNS involvement began a median of 26 months after the onset of disease.
PERIPHERAL NERVOUS SYSTEM TESTING
Electrophysiological testing may show evidence of a mild peripheral neuropathy.
Axonal degeneration and perivascular inflammatory infiltrates are noted on pathological specimens.
THE MOST COMMON PRESENTATION IS SAE, POLYNEUROPATHY, AND ARTHRITIS
Most typically, patients present with SAE, most often combined with polyneuropathy.
Brief episodes of arthritis, primarily involving the knees, generally predate the symptoms and may persist after onset of neurological abnormalities.
The TRIAD OF SAE, POLYNEUROPATHY, AND ARTHRITIS IS HIGHLY SUSPICIOUS FOR NEUROBORRELIOSIS.
Since serologies may be contradictory or negative, the physician will have to settle for treating if clinical suspicion is strong enough and assess whether the patient has ``possible'' or ``probable'' neuroborreliosis.
Vigilant attempts to rule out other disorders should be undertaken.
Screening should be done for collagen vascular disease, other infections, cancer, metabolic or endocrinological disturbances, etc. when a definite diagnosis cannot be made.
II. CURRENT MEDICAL MYTHOLOGY *********************************
``YOU HAVE FIBROMYALGIA. YOU MIGHT HAVE HAD LYME DISEASE IN THE FIRST PLACE, AND EVEN IF YOU DID, YOU WERE GIVEN ENOUGH ANTIBIOTICS. RETREATMENT WILL NOT HELP.''
PERSISTENT INFECTION VERSUS POST-LYME SYNDROME ********************************************
Many patients are sent home with antidepressants, muscle relaxers, but no antibiotics from doctors' offices because they have symptoms of fibromyalgia.
Pictures similar, or identical, to fibromyalgia may be part of the constellation of symptoms of Lyme; it may occur more rarely as an isolated symptom, or surface after what would otherwise be considered successful treatment.
Symptoms of fibromyalgia due to Lyme disease have not been cured with short-term oral or intravenous antibiotics, so some argue fibromyalgia is not due to active infection.
I would question whether those particular antibiotic regimens were adequate to eliminate the infection, rather than assume the patient has developed ``Post-Lyme Syndrome'' (some yet to be defined immunologically triggered disorder).
THE SCOPE OF THE PROBLEM
Bujak et al. evaluated patients a mean of almost five years after treatment.
15% of these patients had symptoms of fatigue and arthralgia.
Almost one-half met criteria for fibromyalgia or chronic fatigue syndrome.
Fibromyalgia is thought to be a variant of the chronic fatigue syndrome.
Of note, nearly all patients continued to complain of memory loss or concentration difficulties.
One quarter had objective evidence of cognitive impairment, and 15% manifested depression.
SYMPTOMS OF FIBROMYALGIA AND CHRONIC FATIGUE SYNDROME IN LYME DISEASE MAY BE ATTENUATED FORMS OR CHRONIC MANIFESTATIONS OF THE FLU-LIKE SYMPTOMS ASSOCIATED WITH EARLY DISSEMINATION
All physicians experienced with treating Lyme disease have had patients who present with a recurrence of flu-like symptoms, months to years after they have completed the usual antibiotic course of therapy, oral or intravenous, and re-exposure had not occurred.
These patients describe their flu-like symptoms as identical to their early-disseminated stage of Lyme disease.
The flu-like symptoms may reoccur following what appears to be a trivial stressor, such as an uncomplicated viral URI.
Patients may be able to ``contain'' their symptoms without specific antimicrobial therapy, but many will have to resume antibiotics.
These patients complain of having to go to bed due to excessive fatigue or hypersomnolence.
They cannot think straight, their muscles and joints ache, and they may have a low-grade fever.
Do these symptoms sound like a ``fibromyalgia-like syndrome'' or ``acute fatigue syndrome?''
Prior medical experience suggests reactivation of infection.
Despite what may appear to have been a previous ``cure,'' relapse of symptoms in this context would appear to be due to failure to eradicate the infection and with reactivation after a period of dormancy.
Reoccurrence of symptoms due to immunologically triggered disease, INDEPENDENT of persistent infection seems unlikely.
In reality, DISTINCTIONS BETWEEN FLU-LIKE SYNDROME, FIBROMYALGIA, AND CHRONIC FATIGUE BLUR.
It seems more logical to postulate that fibromyalgia and chronic fatigue syndrome, when seen with Lyme disease, may be attenuated forms of chronic manifestations of earlier flu-like symptoms associated with early dissemination.
[page 2]
III. THE ASSOCIATION BETWEEN MULTIPLE SCLEROSIS AND LYME DISEASE:
THREE DIFFERENT SCENARIOS
1) LYME CAN LOOK LIKE MS BUT SYMPTOMS AND PATHOLOGY RESIDE OUTSIDE THE CENTRAL NERVOUS SYSTEM
Lyme may present as a MS-like illness, but on many occasions the pathology is not actually in the CNS.
Since chronic Lyme symptoms often are predominantly shifting, vague, behavioral-psychological, psychiatric, and, as mentioned, neurological, they are likely to conjure up the diagnosis of MS in patients and physician alike.
However, the existence of pathology outside the CNS should rule out the diagnosis of MS.
Some of the vague symptoms that can be mistaken for MS include those that are better attributed to peripheral nervous system damage, as part of the mononeuritis multiplex that may occur.
This might cause numbness, tingling, facial weakness, diplopia, etc.
The diagnosis of MS cannot be made in the absence of CNS symptoms and signs.
MRI and CSF findings would also help support the diagnosis of MS.
In addition, a significant CSF pleocytosis may occur with Lyme disease, which should not be present with MS.
2) OTHER LYME PATIENTS DO HAVE CNS LESIONS, BUT THESE ARE GENERALLY DISTINCTLY DIFFERENT, CLINICALLY, AND PATHOLOGICALLY FROM MS
Patients can have CNS lesions in the brain or spinal cord with Lyme disease.
The European literature includes many more cases than the American for encephalomyelitis, strokes, etc.
In those cases where there is focal involvement of the brain or spinal cord, it may be more difficult to distinguish neuroborreliosis from MS.
Again, a brisk CSF pleocytosis would help diagnose Lyme and the specific aforementioned test for CNS Lyme antibodies.
Simultaneous appearance of peripheral nervous system abnormalities or arthritis should suggest the diagnosis of Lyme.
3) ANOTHER GROUP OF PATIENTS HAS MULTIPLE SCLEROSIS AND LYME
There are some patients who have a clear-cut preexisting history of MS before the onset of Lyme disease.
The Lyme appears to accelerate their clinical course.
For others, it appears to be the initiating infection that triggers the MS.
These patients are most likely genetically predisposed to MS and the Lyme bacteria exerts its major effect by ``turning on'' immunologically directed CNS injury.
It is not uncommon to get a history of the onset of an exacerbation of MS related to infections, so Lyme exacerbating MS would be expected.
HLA Class II molecules determine the intensity of the immune response to pathogenic foreign or self-antigens.
With MS, the HLA-DR4 DQw8 haplotype has been associated with chronic progressive MS and the HLA-DR2 DQw6 haplotype has been associated with susceptibility to both chronic progressive and relapsing or remitting MS.
It is possible that in genetically predisposed patients of certain HLA types that infection by Lyme bacteria would cause a high production of cytokines that would mediate the demyelination and destruction of oligodendrocytes.
Most recently, researchers are studying positive outcomes when antibiotics that are most useful in treating Lyme disease are used to treat ``MS.''
IV. WHAT'S WRONG WITH ``CURRENT GUIDELINES FOR TREATMENT'' OF NEUROBORRELIOSIS?
First, read the fine print.
It is interesting to note that recommendations for treatment in the medical literature may carry provisos in small print that can easily be overlooked but are instrumental to understanding how important individualization of therapy is at the current time.
For instance, in the past and in small print, Dr. Alan Steere has written, ``treatment failures have occurred in all these regimens, and retreatment may be necessary; the duration of therapy is based on clinical response, and the appropriate duration of therapy with late neurological abnormalities may be longer than two weeks.''
A more recent article written by Rahn and Malawista states ``these guidelines are to be modified by new findings.
It should always be applied with close attention to the clinical course of individual patients.''
Dr. Katzel surveyed several Lyme Borreliosis conferences, including international ones. He finds a trend towards the use of antibiotics for longer periods than previously described and lack of standardization of care worldwide.
50% of physicians responding considered using antibiotics for time periods greater than one year in symptomatic seropositive patients, with almost as many extending therapy up to one and a half years when necessary.
THE CASE FOR PERSISTENT INFECTION
Studies have shown that Lyme bacteria can be an intracellular pathogen and may evade the normal host immune response.
The causative spirochete, B. burgdorferi, for instance, may persist within fibroblasts and survive at least 14 days of exposure to ceftriaxone.
In addition, B. burgdorferi has been cultured from CSF more than a half year after a standard regimen of IV antibiotics, according to Preac-Mursic.
Logigian and Steere looked at patients with chronic neuroborreliosis, evaluating them six months after two weeks of IV ceftriaxone.
Over one-half of the patients had already been treated with therapy that was thought appropriate for their stage of illness, yet the illness progressed.
The majority of patients studied had subacute encephalopathy and polyneuropathy.
Most had persistent fatigue, and almost one-half had headaches.
One-third of these patients had to stop working or had to go part-time, underscoring the disability that may be seen with Lyme disease on an individual and societal level.
After therapy, two-thirds of patients improved markedly, but seldom completely. Twenty-two percent improved but then relapsed, and fifteen percent had no change in their condition.
This study suggests that additional antibiotics greatly helped the majority with neuroborreliosis but they were insufficient to cause long lasting remission in those patients who subsequently relapsed.
Persistent residual or irreversible disease may explain the fifteen percent who had no change in their condition.
For those clinicians who have had extensive experience with chronic neuroborreliosis, more recent recommendations suggesting that a regime of only 20 to 28 days or even 6 weeks of intravenous antibiotics is sufficient for cure proved contrary to clinical experience.
That brief dosing does not appear to prevent relapse or improve long-term outcome dramatically in many cases.
Perhaps, as recent information has instructed, that is because the immune system does not begin to repair itself until the beginning of the fourth month of antibiotic treatment.
A trial of prolonged use of oral antibiotics seems more reasonable in many cases, given these circumstances.
Antibiotics used for chronic neuroborreliosis should be able to penetrate the blood-brain barrier, express activity against intracellular organisms, and assure good intraphagocytic penetration.
It is anticipated that the microbe during late disease has achieved maximal adaptation to its host environment. Also, because of the long generation time of the organism, lengthier therapy is warranted.
V. WE DON'T HAVE ALL THE ANSWERS BUT HERE'S WHAT IS RECOMMENDED
If a patient has meningitis or appears acutely ill, particularly with possible arrhythmia, admit him or her to the hospital for intravenous antibiotics and observation.
Generally, however, in patients with stable late disease, oral antibiotics can be tried first.
The majority of patients will have some improvement or gradual resolution of encephalopathic symptoms with a better energy level.
After a six-week trial of appropriate antibiotics, the patient is re-evaluated.
If there is no Herxheimer response or some clinical improvement during this interval, it is worrisome, and the physician needs to be concerned about:
1) misdiagnosis, 2) noncompliance, and/or 3) permanent end organ damage.
These possibilities should be addressed with the patient before proceeding with intravenous antibiotics since they may not be maximally beneficial either
Over the long haul, whether intravenous antibiotics are used for two weeks or longer, with chronic refractory disease, ultimately other methods are necessary.
A lengthier use of oral antibiotics seems more logical than intravenous antibiotics for some patients.
Unfortunately, there are no current tests that adequately measure disease activity with neuroborreliosis in all patients.
We are sorely in need of a test similar to the CSF VDRL for syphilis that would give us a measure of disease activity.
Culture negativity or disappearance of a specific immune response in the serum or CSF has not been useful at this time to establish cure. CSF antibodies may persist for years after otherwise successful treatment.
Particularly in the CNS, judging response of therapy is problematic because pathological changes may incompletely or, at least, very slowly reverse.
Any clinical improvement would be expected to occur in a delayed fashion after therapy is given.
Likewise, one would expect neuropathy related to axonal degeneration to remit slowly and/or incompletely.
Formal neuropsychiatric testing is of value in documenting pathology and following the patient.
It also helps delineate what the patient can and cannot do.
It also can help to define the disease for the patient, family, insurer, and the employer.
The patient needs to be told that his or her symptoms should remit slowly and incompletely, when on antibiotic treatment.
This is particularly important when the symptoms have been chronic.
VI. IN SUMMARY ****************
The premise of this approach to diagnosing and treating neuroborreliosis needs to be reinforced.
There is no current laboratory test that makes or breaks the diagnosis of neuroborreliosis.
It is a clinical diagnosis substantiated by laboratory data when possible.
Fortunately, the majority of cases are fairly uniform in their lack of uniformity, and other diagnoses are easily ruled out.
In situations where the physician simply cannot achieve diagnostic certainty, he or she should notify the patient that the diagnosis is ``possible'' or ``probable'' neuroborreliosis.
This has been done previously with MS (i.e., possible, probable, and definite MS), another disease where laboratory testing does not make the diagnosis in and of itself.
There is no perfect current laboratory test to monitor success of therapy, and this is critically needed.
Until better testing is available, assessing progress, or lack thereof, will largely be determined with clinical acumen.
The infection is difficult to eradicate and may require long-term treatment.
The spirochete, particularly in later stages, becomes well adapted to survival within its host environment.
There are some patients that we may not be able to cure, but will be able to palliate with currently available antibiotics.
Although immunopathogenic factors may play a crucial role in disease presentation, the presence of chronic infection appears necessary to perpetuate the process and play a causative role in persistence of immunologically triggered symptoms.
There is no Diagnostic and Statistic Psychiatry Manual (DSM IV) category for ``antibiotic seeking behavior.''
It is common for physicians who are unable to explain patients' symptoms or effect their cure to ascribe a psychiatric cause to their malady.
This is easily done with Lyme since objective findings may be subtle or non-existent.
Because neuropsychiatric symptoms may pre-dominate, it is easy in some patients to attribute their symptoms to depression or secondary gain.
These patients do not in any other way seek other medication that would be associated with habituation or addiction (i.e., pain medicine).
Many patients suffer unfairly at the hands of physicians who refuse to make the diagnosis because blood tests are either contradictory or negative.
``Lyme bashing,'' for instance, referring to Lyme disease as ``yuppie flu,'' is demeaning.
The ``just say no'' attitude of certain physicians towards Lyme patients who request retreatment with antibiotics should not be condoned in the face of continuing experience with this potentially chronically disabling infectious disease.
Audrey Stein Goldings, MD is a private practice neurologist in Dallas.
She is member of ILADS and a founding member of the Board of Directors.
_________________
Posts: 48021 | From Tree House | Registered: Jul 2007
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Keebler
Honored Contributor (25K+ posts)
Member # 12673
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Backing up a bit, I see this is your first post here.
Welcome. Sorry you had to find us, but I hope this will help in your journey back to health.
Here's some background information so that you understand why only a few doctors can diagnose and treat lyme - most will discount it. The first article explains all that.
CONTROVERSY CONTINUES TO FUEL THE "LYME WAR" -(author's details at link)
As two medical societies battle over its diagnosis and treatment, Lyme disease remains a frequently missed illness. Here is how to spot and treat it.
Excerpts:
Meet the players
The opponents in the battle over the diagnosis and treatment of Lyme disease are the Infectious Diseases Society of America (IDSA), the largest national organization of general infectious disease specialists, (and)
and the International Lyme and Associated Diseases Society (ILADS), an organization made up of physicians from many specialties. ( www.ilads.org )
ILADS, by contrast, asserts that the illness is much more common than reported, underdiagnosed, easier to contract than previously believed, difficult to diagnose through commercial blood tests, and difficult to treat, (especially)
especially when treatment is delayed because of commonly encountered diagnostic difficulties ( http://www.ilads.org/guidelines.html - Accessed April 6, 2007).
. . .
" . . .To treat Lyme disease for a comparable number of life cycles, treatment would need to last 30 weeks. . . ."
`` . . .Patients with Lyme disease almost always have negative results on standard blood screening tests and have no remarkable findings on physical exam, so they are frequently referred to mental-health professionals for evaluation.
"...If all cases were detected and treated in the early stages of Lyme disease, the debate over the diagnosis and treatment of late-stage disease would not be an issue, and devastating rheumatologic, neurologic, and cardiac complications could be avoided..."
. . . * Clinicians do not realize that the CDC has gone on record as saying the commercial Lyme tests are designed for epidemiologic rather than diagnostic purposes, and a diagnosis should be based on clinical presentation rather than serologic results.
- Full article at link above, containing MUCH more detailed information.
-===
Co-infections (other tick-borne infections or TBD - tick-borne disease) are not discussed in the Savely article due to space limits. Still, any LLMD you would see would know how to assess/treat if others are present.
May 2008 Volume 39 Number 5 LABMEDICINE www.labmedicine.com - American Society for Clinical Pathology
CHRONIC BACTERIAL AND VIRAL INFECTIONS IN NEURODEGENERATIVE AND NEUROBEHAVIORAL DISEASES
- by Garth Nicolson, Ph.D.
===========================
AFTER reading the articles above this will make more sense and, sadly, shows the state of treatment (and - with the new committee gathered, it is still a horrible situation for there are no real experts on the new panel):
Attorney General Richard Blumenthal today announced that his antitrust investigation has uncovered serious flaws in the Infectious Diseases Society of America's (IDSA) process for writing its 2006 Lyme disease guidelines and the IDSA has agreed to reassess them with the assistance of an outside arbiter.
You should also be evaluated for coinfections. Not all tests are great in that regard, either, but a good LLMD can evaluate you and then guide you in testing. One of the top labs is:
There are a couple other good labs for certain tests: Fry; Clognen; Focus. Your LLMD will know. Some say MDL does good work (but I don't know if they test all the bands).
The International Lyme and Associated Diseases Society (ILADS) provides a forum for health science professionals to share their wealth of knowledge regarding the management of Lyme and associated diseases.
- In the menu to the left of their home page, you can order DVDs of past ILADS seminars. You might also be able to borrow some from your local lyme support group.
This are invaluable to understanding how these infections work. And, none of this is taught in medical schools. None.
In addition to the usual coinfections from ticks (such as babesia, bartonella, ehrlichia, RMSF, etc.), there are some other chronic stealth infections that an excellent LLMD should know about:
TF
Frequent Contributor (5K+ posts)
Member # 14183
posted
I agree. No steroids, and skip the lumbar puncture. I had one. It was a waste and can be dangerous and leave you with problems. Per Burrascano, the steroids can cause permanent damage in someone with lyme. So, look into the "MS shots" and find out what they are in medical terminology and if they are a steroid, do NOT take them.
I had two areas of hypoperfusion (UBOs--unidentified bright objects--which you may be calling "white spots.") Both MS and lyme can cause these spots on the brain. I was treated only for lyme, and my mental function returned to normal. The UBOs have disappeared.
MS and lyme are virtually identical on a brain scan, so it is highly likely that MS is actually lyme disease. Did you know that some MS doctors are now treating MS patients with antibiotics and are getting rid of MS in people that way?
I had a coworker who got treated with antibiotics by her MS doctors for her so-called MS, and she got cured! So then her docs said that it must not have really been MS all along.
So, my advice is to treat only the lyme. If that doesn't make the MS symptoms go away, the MS doctors will always be there offering you their help. I really doubt you will ever need their help.
Treat the lyme disease.
Posts: 9931 | From Maryland | Registered: Dec 2007
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Keebler
Honored Contributor (25K+ posts)
Member # 12673
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As you find a LLMD for diagnostics, there are a few things that can help with some of the common symptoms:
Magnesium is multi-purpose and can help relieve pain, calm an over-excited neurological system but also lift depression -- while also helping with relaxation and also help your liver to be able to better detox some of the toxins from lyme, etc.
From Carol in PA, here's a great form of magnesium:
Source Naturals Ultra-Mag, because it has four kinds of the more easily absorbed:
Magnesium 200 mg each tablet, (as magnesium citrate, taurinate, malate, glycinate and succinate)
Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
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With apologies and promise of this being my last post, I just went back to read your post to see if I missed anything.
I did.
You said: " . . . already was diagnosed with late stage chronic lyme"
Hmm. So, are you currently being treated for late stage chronic lyme? Or - was this a while back in time?
The neurologist who wants to give you MS shots obviously does not know about the lyme ??? (Unless the shots address infection directly, they cannot possibly treat lyme disease.)
and your LLMD who is treating you for lyme ??? What does that doctor say about the MS shots ?
posted
Thanks for all your knowledge. I was told that if new white lesions appear on next MRI while still on abxs, that it is a sure sign of MS. That new ones wouldn't appear if it is lyme. I was showed in a MS textbook that my brain scan looks the same. If I go on treatment for MS, can the lesions be stopped? I tested positive for lyme & co-infections.I've had it for three yrs.I heard that MS treatment will make someone worse, because pulls back immune system, that if you have lyme you need. Any more info. would be great,I'm really confused?? My neurologist said if on the shots for ms, it won't mess me up. It will be o.k, but I don't know what to do???? I'm going to get more opinions.
Posts: 24 | From lymeland | Registered: Sep 2008
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lymeinhell
Frequent Contributor (1K+ posts)
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RUN FROM THE NEURO!!!!
MS SHOTS ARE STEROIDS.
AND YES I AM YELLING!!!
MS is a description of symptoms, not a disease.
MS treatment is immuno-suppressants (aka steroids), and you will undoubtedly get worse.
I too was in the same boat. Three lesions.
I've been treated and have my life back - off antibiotics more than 4 years now. The second neuro I saw (while trying to get dxd) wanted to do the obligatory spinal tap to 'rule out MS'. And despite completely normal evoked potentials testing, he refused to believe it could be lyme because I had a negative Quest PCR test. One day I'll have to go back there just so I can shove my clean MRI up his you-know-what.
THEY HAVEN'T A CLUE ABOUT LYME - RUN AWAY. SERIOUSLY. Stick with your LLMD. Treat the Lyme and coinfections. You'll see. It will suck for a while, but if you have the right treatment in the right order, you will get better.
-------------------- Julie _ _ ___ _ _ lymeinhell
Blessed are those who expect nothing, for they shall not be disappointed. Posts: 2258 | From a better place than I was 11 yrs ago | Registered: Sep 2003
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quote:Originally posted by lymeherx: Thanks for all your knowledge. I was told that if new white lesions appear on next MRI while still on abxs, that it is a sure sign of MS. That new ones wouldn't appear if it is lyme. I was showed in a MS textbook that my brain scan looks the same. If I go on treatment for MS, can the lesions be stopped? I tested positive for lyme & co-infections.I've had it for three yrs.I heard that MS treatment will make someone worse, because pulls back immune system, that if you have lyme you need. Any more info. would be great,I'm really confused?? My neurologist said if on the shots for ms, it won't mess me up. It will be o.k, but I don't know what to do???? I'm going to get more opinions.
Have you been treating for 3 years or had it untreated that long? Seems that if you had treated for 3 years and have new lesions it would really point to something other than just LD. It's a tough call. MS is nothing to play with, either.
Posts: 41 | From SC | Registered: Jan 2009
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Keebler
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You said: " . . .I was told that if new white lesions appear on next MRI while still on abxs, that it is a sure sign of MS. That new ones wouldn't appear if it is lyme. . . ."
NOT TRUE. Lyme is progressive and what what you write, it sounds as if you are not being treated for lyme.
You know lyme is a player. Lyme does not just go away. Even with 3 years of treatment, (did you have that ? ) . . . lyme can still be a connection.
Please come back and post the exact name of the medicine in those "MS shots" all the ingredients, active an inactive.
It sounds like you are not being treated for lyme. What happened with that? Where is your LLMD?
How long did your treatment last?
When did it end?
Was it combination? Were you on IV Rx for several months, at least?
Did you have an ILADS LLMD?
---
I would run, run, RUN for any neurologist who fed you that line of pooh about no new lesions from lyme. NOT TRUE. Not true at all.
You must have some one who is ILADS-educated about lyme to treat you, even if "MS" - please go back and read Goldings' article from top to bottom.
I guarantee that if you get more opinions from the regular world of medicine that you will not get the most knowledgeable answers.
posted
I'm being treated with cipro&ceftin for lyme&co-infections, but still feel dizzy and off balance a little. I have to find new llmd, because mine is annoying and hard to get a hold of. my neuro is also treating my sister and just started her on the low dose shot for ms. she has a couple spots on her brain too. I think she is on naltraxine or something. I just don't want to start treatment for ms and get worse, will I??Every neur is going to say ms. ms means many scars, but what brought it out, the lyme?Is it environmental???? there is no way millions of people have ms, but it's believable lyme, because there is ticks everywhere.Did anyone else go through this? did anyone get an mri and have spots on brain that a neuro says it ms if it gets worse???? she said that since I'm being treated for lyme, it should stop any new spots from happening&appearing, is that true? I don't want to listen to one dr. I know when you have lyme you need your immune system, and the ms shots suppress the immune system so I will definately get worse, right? the nuro showed me in a MS book that my MRI looks the same as a picture in that book, can lyme do that too?????Can the pictures look the same as the MS pictures??
Posts: 24 | From lymeland | Registered: Sep 2008
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posted
does the antibiotics stop new lesions from appearing? Can you get new ones even if being treated? Does that show it's MS???
Posts: 24 | From lymeland | Registered: Sep 2008
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Dawnee
Unregistered
posted
Yep, we thought I had MS too. Only one bright spot on my MRI at the time though and multiple neuro symptoms. I had to diagnose MYSELF with Lyme and then find a doctor to test and treat me. Came back CDC positive for Lyme. Thank GOD I didn't do any kind of treatment for MS... because it could have damaged me further.
I know you are confused, and this is a lot of info being posted for you. But PLEASE do not do any shots or any other kind of steroid treatment.
Who has been treating you for your chronic Lyme disease??? Is it an LLMD? ILADS member Lyme doctor? If not... find one pronto!
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posted
EVERY SINGLE PERSON i TALK TO SAYS THAT AFTER A NEUROLOGIST SEES their MRI they say it is MS. How can anyone tell the difference between the two? What is a sure sign of MS? I am seeing a LLMD but I want to change drs,I don't think he's that good. Are there good ones on here?
Posts: 24 | From lymeland | Registered: Sep 2008
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Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
-
lymeherx:
your post a couple up is hard for many to read. I'm breaking up the text here so you can have more answers.
It would really help if you could add more white space in your posts. Many here with neurolyme really need that to be able to sort out sentences.
thanks.
---------------
I'm being treated with cipro & ceftin for lyme & co-infections, but still feel dizzy and off balance a little. I have to find new llmd, because mine is annoying and hard to get a hold of.
my neuro is also treating my sister and just started her on the low dose shot for ms. she has a couple spots on her brain too.
I think she is on naltraxine or something.
I just don't want to start treatment for ms and get worse, will I??Every neur is going to say ms. ms means many scars, but what brought it out, the lyme?Is it environmental????
there is no way millions of people have ms, but it's believable lyme, because there is ticks everywhere.Did anyone else go through this?
did anyone get an mri and have spots on brain that a neuro says it ms if it gets worse????
she said that since I'm being treated for lyme, it should stop any new spots from happening&appearing, is that true? I don't want to listen to one dr.
I know when you have lyme you need your immune system, and the ms shots suppress the immune system so I will definately get worse, right?
the nuro showed me in a MS book that my MRI looks the same as a picture in that book, can lyme do that too?????Can the pictures look the same as the MS pictures??
====
then added:
does the antibiotics stop new lesions from appearing?
Can you get new ones even if being treated? Does that show it's MS???
======
EVERY SINGLE PERSON i TALK TO SAYS THAT AFTER A NEUROLOGIST SEES their MRI they say it is MS.
How can anyone tell the difference between the two? What is a sure sign of MS?
I am seeing a LLMD but I want to change drs,I don't think he's that good.
Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
-
Yes, lyme lesions can appear the same as "MS"
Yes, the right treatment for lyme can help the lesions shrink, sometimes disappear.
Yes, the right treatment for lyme can help prevent further lesions.
I still have not been able to determine how long you have been treated. For 3 years straight ?
-------------
* You need to find out what is in the shots they want you to take. You can call that doctor's office and ask the office manager for the name and then look it up on line.
* You need to find a new LL neurologist who would be familiar with the information that Goldings presents in the article above. Here's that link again:
" city and state: need LL Neurologist - or LLMD familiar with "MS" issues "
post a message similar to this:
"need to find a LL Neurologist (or a good LLMD) who is familiar with neuro-lyme and lesions in a lyme patient told they have MS from their MRI scans. "
Remember, none of this is to scare you but rather to help inform. Knowledge is power. I hope you find the best doctor with the best knowledge base to help you sort this out.
-
[ 03-05-2009, 01:34 AM: Message edited by: Keebler ]
Posts: 48021 | From Tree House | Registered: Jul 2007
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bettyg
Unregistered
posted
welcome herx to the board!
please post in SEEKING DR. forum for a LYME LITERATE MD, llmd,
show the show the LARGEST CITY CLOSEST TO YOU IN YOUR STATE IN SUBJECT LINE!!
copy KEEBLER'S BROKEN UP POSTS OF WHAT YOU WROTE HERE as majority of us, like me, can NOT read or comprehend anything you wrote due to our neuro lyme.
we'd like to help you if you'll help us please
thru keebler's broken up post, i caught this about lyme and MS MRIS LOOKING THE SAME.
look at my newbie package links, TABLE OF CONTENTS, and look in contents about a post i put there where a scientific link SHOWS BOTH MS/LYME MRIS and what they look like.
in future, please break up your text like keebler did for you ok; otherwise, neuro folks like me will scroll on by, sob, since we can't read as is. BIG THANKS!
Welcome; i'm so glad you found us!! You've come to the right place for education and support!
Dr. Burrascano's most recent "Diagnostic Hints and 2008 Treatment Guidelines for Lyme and Other Tick Borne Illnesses" @
please go to my newbie links, copy the entire thing, and then print this off....FINANCIAL BURDENS compiled by melanie reber print off pages 74 - 92; outstanding info there. i believe there are a few more general comments there without links!! print that off too as it's newer info from members thru their own personal, tragic experiences.
Betty's POSTING GUIDELINES . many of us have neuro lyme where we can NOT read long solid block text and be able to comprehend and read it as is.
please edit your post by CLICKING PAPER/PENCIL ICON to right of your name. that opens up BOTH subject line and body text.
now please break up your WORDY SENTENCES into one sentence paragraphs. Then hit ENTER KEY ``TWICE`` after each paragraph; we need that space for comprehension.
NOTE: you do NOT have to use "", just show the name of person you are responding to, and then type your comment.
IF you need to use "", PLEASE DELETE "BOLD" CODES so it's regular type text we read vs. the DARK, HARSH/PAINFUL BOLDING. delete the first 4 characters of 2ND LINE of a ""
[QB] just delete these 4 characters, and BOLDING is GONE! my eyes will really appreciate that; it's one very bad side effect of my having lyme for 38.5 years!! xox
then go to left hand corner and mark box to receive ALL REPLIES, and click EDIT SEND
we thank you for helping us; otherwise, we will SOB, SCROLL ON BY, since we can't read to help you. If I see posts like this, I SOB them; to hard on me. ------------------------------------------------------
People seeking doctors might be able to get help from their state online information and support group. Nearly 3,400 people belong to state groups. Some of the groups are small but more than 20 of them have 50 or more people and seven have over 100.
The groups are moderated and you have to apply. Most don't allow doctor names, but once on the group, you can ask for doctors in a certain area and ask people to email you privately. *******************************************
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Keebler
Honored Contributor (25K+ posts)
Member # 12673
posted
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Glad to see BettyG stopped by with her great links.
Medical Abstracts and much more. This is a great page for many links.
Excerpt:
When to Suspect Lyme
"Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP).
The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques.
Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination."
Note: These articles do not all insist that Lyme and MS are the same but keep in mind that MS means "multiple sclerosis". Multiple sclerosis simply put means "many lesions".
It is simply a DESCRIPTIVE NAME of a disease which causes the nerves to lose their myelin sheath and in particularto show lesions on the brain on MRI which Lyme does as well.
My readings and research have indicated that the brain lesions, the spinal fluid findings and the actual clinical manifestations of Lyme and MS cannot be distiguished one from the other, perhaps simply due to a strain variance of Lyme.
We know that Lyme causes an immunologic dysfunction including a component of autoimmune activity possibly causing this neuro-damage in the form of MS activity.
. . . .
================
NEUROBORRELIOSIS - Lyme Pathogenesis from Infection to Inflammation 12.19.07
Michelle M
Frequent Contributor (1K+ posts)
Member # 7200
posted
I have numerous brain lesions (11), as well as other abnormalities which caused my neurologist to diagnose me with probable MS. However, I also have lyme and babesia duncani, which is what caused them -- not MS.
I suggest you find a GOOD LLMD who will treat you aggressively. Perhaps even with IV. Your neurologist does not know anything about lyme - trust me. Very few do. Have you tested or treated for co-infections?
You are unlikely to see improvement from MS treatment. That is because you have an infection. MS drugs do not fight infection. Therefore, it will only get worse.
I've gotten much better with treatment. But we are talking about a couple YEARS' treatment. I can't imagine what shape I'd be in had I stayed with my neurologist. Perhaps dead.
Lesions may go away with antibiotic treatment. Or, they might not. Chances are about 50/50. An inability to vanquish them does not mean you have MS.
A good and experienced LLMD is key. One in whom you have confidence and trust. An ILADS doctor is a good choice.
Good luck!
Michelle
Posts: 3193 | From Northern California | Registered: Apr 2005
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-------------------- The fibromyalgia I've had for 32 years was an undiagnosed Lyme symptom.
"For I know the plans I have for you", declares the Lord, "plans to prosper you and not to harm you, plans to give you hope and a future". -Jeremiah 29:11 Posts: 6076 | From Pennsylvania, USA | Registered: Nov 2008
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TF
Frequent Contributor (5K+ posts)
Member # 14183
posted
You can go to "Seeking a Dr." forum and post for a lyme literate neurologist. See if anyone knows of any.
Posts: 9931 | From Maryland | Registered: Dec 2007
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posted
I treated "MS" from 1996-2006 and white spots on brain just increased year after year, treatment after treatment. I have been on abx for 3 years - this is my first year with lyme dr. and I was tested for lyme in 2008 and positive. If my llmd can get me out of the wheelchair it will be a miracle. Treat the Lyme first is my advise -
Posts: 128 | From MICHIGAN | Registered: May 2008
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posted
You go Wiggy. I, too, went through the "you have MS" thing. I only spent five weeks in a wheelchair though. I truly hope you get well.
Posts: 374 | From United States | Registered: Nov 2008
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posted
Thank-you Snailhead Working on it!!!!!!!!!!!!!!!
Posts: 128 | From MICHIGAN | Registered: May 2008
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richedie
Frequent Contributor (1K+ posts)
Member # 14689
posted
Keep in mind, most all researches realize that something kicks off MS. It doesn't just happen for the heck of it. A virus or infection plants the seed for MS. same thing with many such diseases. If you have Lyme for sure and you have MS, most likely they ARE linked!
-------------------- Mepron/Zith/Ceftin Doxy/Biaxin/Flagyl pulse. Artemisinin with Doxy/Biaxin. Period of Levaquin and Ceftin. Then Levaquin, Bactrim and Biaxin. Bactrim/Augmentin/Rifampin. Mepron/Biaxin/Artemisinin/Cat's Claw Rifampin/Bactrim/Alinia Plaquenil/Biaxin Posts: 1949 | From Pennsylvania | Registered: Feb 2008
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otherwise, we will SOB, SCROLL ON BY, since we can't read to help you. If I see posts like this, I SOB them; to hard on me. 
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