Medical topics with questions, information and discussion related to Lyme disease and other tick-borne diseases.
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Postby Yvonne » Fri 25 Jul 2008 15:07

Lyme may present as a MS-like illness, but on many occasions the pathology is not actually in the CNS. Since Lyme symptoms are often predominantly neurological and vague, 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
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 which should not be present with 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.

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 exacerabating 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 infectioon by Lyme bacteria would cause a high production of cytokines that would mediate the demyelination and destruction of oligodendrocytes
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Re: Lyme/MS

Postby Yvonne » Fri 25 Jul 2008 15:10

Chronic Lyme borreliosis at the root of multiple sclerosis – is a cure with antibiotics attainable?

Markus Fritzsche,

Clinic for Internal and Geographical Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland

Received 15 September 2004; accepted 17 September 2004. Available online 11 November 2004.

Apart from its devastating impact on individuals and their families, multiple sclerosis (MS) creates a huge economic burden for society by mainly afflicting young adults in their most productive years. Although effective strategies for symptom management and disease modifying therapies have evolved, there exists no curative treatment yet. Worldwide, MS prevalence parallels the distribution of the Lyme disease pathogen Borrelia (B.) burgdorferi, and in America and Europe, the birth excesses of those individuals who later in life develop MS exactly mirror the seasonal distributions of Borrelia transmitting Ixodes ticks. In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable. As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted. The immunomodulating anti-inflammatory potential of minocycline and hydroxychloroquine may furthermore reduce the Jarisch Herxheimer reaction triggered by decaying Borrelia at treatment initiation. Even in those cases unrelated to B. burgdorferi, minocycline is known for its beneficial effect on several factors considered to be detrimental in MS. Patients receiving a combination of these pharmaceuticals are thus expected to be cured or to have a longer period of remission compared to untreated controls. Although the goal of this rational, cost-effective and potentially curative treatment seems simple enough, the importance of a scientifically sound approach cannot be overemphasised. A randomised, prospective, double blinded trial is necessary in patients from B. burgdorferi endemic areas with established MS and/or Borrelia L-forms in their cerebrospinal fluid, and to yield reasonable significance within due time, the groups must be large enough and preferably taken together in a multi-centre study. ... 840ed64c1c
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Re: Lyme/MS

Postby Yvonne » Fri 25 Jul 2008 15:12

1: Med Hypotheses. 2006 Dec 29; [Epub ahead of print] Links

Lyme borreliosis and multiple sclerosis are associated with primary effusion lymphoma.Batinac T,

Petranovic D, Zamolo G, Petranovic D, Ruzic A.
Department of Dermatovenerology, Rijeka University Hospital, Kresimirova 42, 51000 Rijeka, Croatia.

Multiple sclerosis (MS) is a chronic disease of the central nervous system characterized by chronic inflammation and demyelination. Studies suggested that the viral, especially Epstein-Barr virus infection, and bacterial infections, especially Borrelia burgodorferi infection, play a role in etiology of MS. MS prevalence parallels the distribution of the Lyme disease pathogen B. burgdorferi. Criteria used for diagnosis of MS can also be fulfilled in other conditions such as Lyme disease, a multisystem disorder resulting from infection by the tick-borne spirochete, B. burgdorferi. In the late period of Lyme disease demyelinating involvement of central nervous system can develop and MS can be erroneously diagnosed. A Lyme borreliosis can mimick central nervous system lymphoma. Also, B. burgdorferi has been implicated not only in etiology of MS, but also in etiology of lymphoma. Studies suggested that there is an increased risk of non-Hodgkin lymphoma in patients, who had a history of autoimmune diseases such as MS and that both non-Hodgkin's lymphomas and Hodgkin's disease were associated with Epstein-Barr virus infection. A small group of lymphomas called primary effusion lymphomas (PEL) is a recently individualized form of non-Hodgkin's lymphoma (WHO classification) that exhibit exclusive or dominant involvement of serous cavities, without a detectable solid tumor mass. These lymphomas have also been linked to Epstein-Barr virus and human herpes virus type 8 infections but virus negative cases have been described. Therefore, we propose that MS and neuroborreliosis are linked to central nervous system primary effusion lymphomas. As a first step in confirming or refuting our hypotheses, we suggest a thorough study of CSF in the patients suspected for the diagnosis of MS and Lyme borreliosis.

PMID: 17197115
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Re: Lyme/MS

Postby Yvonne » Fri 25 Jul 2008 15:13

Przegl Epidemiol. 2006;60 Suppl 1:39-45. Links

Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?[Article in Polish]
Drozdowski W.
Klinika Neurologii AM w Bialymstoku.

Multiple sclerosis is the most frequent multifocal disease of the central nervous system, but in a diagnosis of atypical cases about 100 other diseases should be considered. Neuroborreliosis plays a particular role among them, especially in endemic regions. Difficulties result from similarities of clinical symptoms and lack of specific diagnostic investigations. Diagnostic procedures in neuroborreliosis are mostly based on laboratory analyses and serologic examinations of serum and cerebrospinal fluid, in connection with a clinical picture and an epidemiological state. Since the year 2001, multiple sclerosis neurological diagnostic is based on the diagnostic criteria established under the auspices of The US National Multiple Sclerosis Society and International Federation of Multiple Sclerosis Societies. Those recommendations regarding relapsing-remitting MS and primary progressing MS are discussed in this paper. Current knowledge of those diseases warrants cautiousness in the diagnostic of atypical cases.

PMID: 16909774
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Re: Lyme/MS

Postby Yvonne » Fri 25 Jul 2008 15:14

Arq Neuropsiquiatr. 1994 Dec;52(4):566-71. Related Articles, Links

Multiple sclerosis and positive Lyme serology.

Lana-Peixoto MA.

Faculdade de Medicina da Universidade Federal de Minas Gerais, Brasil.

As Lyme neuroborreliosis (LNB) may clinically mimic multiple sclerosis (MS) the presence of antibodies to Borrelia burgdorferi in serum of patients with a MS-like disease in non-endemic areas for Lyme disease may be troublesome. We report the case of a 45-year-old white female with the diagnosis of relapsing/remitting form of MS due to a 15-year history of optic neuritis and recurrent episodes of motor and sensation disturbance in the upper right limb and in both lower extremities associated with bladder dysfunction. A magnetic resonance imaging of the brain revealed multiple high intensity periventricular white matter lesions. The patient had been exposed to ticks but did not recall the presence of erythema migrans. ELISA for Lyme disease was positive in two different laboratories and the positive serology was confirmed by Western blotting. No convincing response followed treatment with ceftriaxone. Although it is clear that the patient had been infect by Borrelia burgdorferi the relationship of this spirochetal infection with the neurological disease could not be ascertained.
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Re: Lyme/MS

Postby Yvonne » Fri 25 Jul 2008 15:17


A total of 769 adult neurological patients hospitalised in clinics and hospitals
situated in the Lublin region (eastern Poland) were examined during the years 1997-
Borrelia burgdorferi
2000 with ELISA test for the presence of anti- sensu lato
antibodies. A statististically significant (p = 0.0422) relationship was found between the
clinically confirmed diagnosis of multiple sclerosis and the positive serologic reaction
with antigen. Ten out 26 patients with multiple sclerosis (38.5%) showed
positive serologic reaction to , whereas among the total number of examined
neurological patients the frequency of positive findings was twice as low (19.4%). The
result suggests that multiple sclerosis may be often associated with infection .


A statististically significant (p=0.0422) relationship
was found between the clinically confirmed diagnosis of
multiple sclerosis and the presence of anti-Borrelia
antibodies in ELISA test (Tab. 1). Ten out 26 patients
with multiple sclerosis (38.5%) showed positive serologic
reaction to Borrelia, whereas among the total examined
neurological patients the frequency of positive findings
was twice as low (19.4%).
An example of the positive anti-Borrelia reaction in the
patient with clinically confirmed multiple sclerosis is
presented in Table 2. The patient had been observed from
October 1995–November 1998 and therefore the tests
made in the period preceding the main study (1995–1996)
were carried out with the simpler, semiquantitative
ELISA assay (Biomedica, Vienna, Austria). The presence
of IgG antibodies to Borrelia was found, indicating the
past infection, probably in summer 1995. The level of the
IgG anti-Borrelia antibodies increased during 1996 and
remained high also during following years (1997-1998).


The possible relationship between multiple sclerosis
and Lyme borreliosis is a matter of controversy since the
years following the identification of LB agent, Borrelia
burgdorferi sensu lato. As early as in 1986, Kurtz [10]
expressed a view that this spirochete may be one of the
major causes of MS. The opposite view is presented by
Schmutzhard [18] and Coyle [3] who negated any
association between LB and MS. However, the latter view
has been challenged by Lana-Peixoto [11] and Garcia-
Monco et al. [5] who found serological evidence of the
infection with LB agent in MS patients. Stelmasiak et al.
[21] found the presence of anti-Borrelia antibodies in 87
out of 161 patients with suspected MS (54.0%).
In this study, a statistically significant relationship was
found between the clinical diagnosis of MS and the
presence of antibodies against LB agent, which supports
the view on the possible relationship between these two
clinical entities. The proportion of the MS patients
showing positive serological reaction to B. burgdorferi
(38.5%) was much higher compared to the earlier studies
by Coyle [3], Coyle et al. [4] and Schmutzhard et al. [19]
who found respectively 1.1%, 6.7% and 14.2% positive
reactions among MS patients. The difference may be
partly explained by the overall high positive rate of
serologic response to LB agent in eastern Poland, due to
frequent exposure to bite of tick vector, Ixodes ricinus.
The nature of the stated relationship between infection
with LB agent and MS disease remains obscure. In some
cases, neuroborreliosis may be misdiagnosed as MS. A
direct provoking of MS by B. burgdorferi does not look
probable, but it cannot be excluded that the LB agent may
aggravate the pathogenic processes in the initial stage of
MS and thus increase a number of the symptomatic,
clinically diagnosed cases. This hypothesis, similar to that
proposed by Karussis et al. [8], may be supported by the
resemblance of the pathologic processes in both diseases:
activation of the lymphocytic system [6], inducing of the
matrix metalloproteinases (MMPs) production [15],
inducing of the autoantibodies production, including
antibodies to neuronal proteins [7] and to myelin basic
protein [8, 23]. In the late period of neuroborreliosis,
demyelinating involvement of CNS can develop, similarly
as in MS [5].

Considering certain limitations of the present work
lack of detailed clinical analyses, relatively low number
of definite MS cases under study), it cannot therefore be a
basis for suggestions on the nature of the stated significant
relationship between LB and MS. Nevertheless, it does
indicate a need for further studies on this subject.
In conclusion, the result of this study suggests that
multiple sclerosis may be often associated with Borrelia
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Re: Lyme/MS

Postby Yvonne » Fri 25 Jul 2008 15:19

Multiple sclerosis and Lyme borreliosis
Erich Schmutzhard
Department of Neurology, University Hospital, Innsbruck, Austria

Summary. In a deductive approach the two disease
entities of multiple sclerosis and chronic progressive neu-
roborreliosis are discussed. Various clinical features, se-
roepidemiology, neuroimaging, CSF findings, CSF serolo-
gy, specific proteins within the CSF and antibodies
against neuronal structures as well as the most recent
findings of different dendritic cells within the CSF are
discussed as a means of differentiating these two disease

Multiple sclerosis is a relapsing/remitting or chronic/
progressive disease of presumably autoimmune origin af-
fecting mainly or exclusively the CNS, leading to demye-
linisation and remyelinisation. Many pathogenic agents
have been incriminated in being either directly involved in
the pathogenesis or indirectly, i.e. by triggering an auto-
immune process within the CNS [50].
Gay and Dick were the first to discuss spirochetes as
the possible causative agents of multiple sclerosis [15],
and Kurtz et al. proposed both relapsing fever and Lyme
disease borreliae as having the capacity to cause a central
nervous system disease equal or similar to multiple sclero-
sis [24]. Although these medical hypotheses have never
been substantiated by biological, biochemical or molecu-
lar-biological findings, other authors have continued to
postulate a causative relationship between multiple sclero-
sis and spirochetes [4, 10, 15, 27].
The etiology of multiple sclerosis is still a subject of
controversial discussion and it continues to cause consid-
erable uncertainty in the medical community, reflected by
a very recent Polish publication in which a causal relation-
ship between the agent of Lyme borreliosis and multiple
sclerosis is postulated [5].
We aim here to clarify this confusion within the med-
ical community by contrasting epidemiologic, clinical and
diagnostic findings of neuroborreliosis, and in particular
chronic neuroborreliosis, with multiple sclerosis. In addi-
tion we discuss the most recent developments in molecu-
lar biology and neuroimmunology with respect to these
two diseases. Using deductive methods we believe we have
achieved conclusive results, i.e. we hope to clarify
the relationship between these two diseases.

Clinical presentation of multiple sclerosis and
thevarious forms of neuroborreliosis
There is little doubt about the clinico-neurological
presentation of MS with either a relapsing/remitting
course of disease or a chronic/progressive form [39, 50].
It is only the latter that ñ in a very rare instance ñ could
be mistaken for a progressive borrelial encephalomyelitis
[2, 13, 18, 44, 53]. Whereas the progressive form of MS in
most instances is confined to a chronic myelitis, with
frequent relapses and remittances in the early days of
disease before finally becoming progressive [13, 50], the
progressive borrelial encephalomyelitis, as defined by
Ackermann et al. [2], begins with a progressive (chronic)
myelitic disease [18]. In contrast to progressive borrelial
encephalomyelitis, early neuroborreliosis, as seen in
Bannwarthís syndrome includes the clinical entities of
meningitis, radiculoneuritis and peripheral polyneuritis
cranialis [30, 39]. None of these 3 syndromes is ever seen
in MS. In recent years neuroophthalmic manifestations of
Lyme disease have been discussed [3, 29, 38], however
both the oculomotor presentations and manifestations in-
volving the optic nerve are clearly different in MS, pre-
senting either as optic neuritis or as a pontomesencephalic
nuclear lesion of the oculomotor system leading to double
vision [50]. In contrast, Rothermel et al. [38] and Balcer
etal. [29], describing neuroophthalmic manifestations of
Lyme disease, saw in children either peripheral oculomo-
tor disturbances or compression of the optic nerves. Gold
et al. (1990), Lyon-Caen et al. (1994) and Karussis et al.
(1999) published, rather outspokenly, clear guidelines to
delineate the two disease entities of MS and Lyme borre-
liosis [16, 23, 26].

From this approach of deductive argumentation it is
without doubt that acute neuroborreliosis is a clearly dis-
tinct disease entity. Similarly without doubt is the fact that
any form of chronic neuroborreliosis, e.g. progressive
borrelial encephalomyelitis, may present as an MS-like
disease; however, there are many ways to clearly differen-
tiate multiple sclerosis from any form of chronic neu-
roborreliosis. It is not the task of this deductive outline to
discuss either the treatment protocols for the various
forms of multiple sclerosis or the distinct treatment proto-
col for neuroborreliosis (the reader is referred to the pub-
lished practice guidelines for the treatment of Lyme dis-
ease by Wormser et al. [52] and Steere et al. [45]).
Since both treatment options and prognosis are differ-
ent in these two disease entities (multiple sclerosis and
chronic neuroborreliosis) it is necessary to distinguish
them as early as possible and with maximum possible certainty,
keeping in mind the treatment options and their
prognostic aspects ... d%20MS.pdf
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Re: Lyme/MS

Postby Yvonne » Fri 25 Jul 2008 15:21

Treatment of Amyotrophic Lateral Sclerosis and Multiple Sclerosis With Antibiotics


In 1994, I saw two cases of classic severe far advanced MS that followed documented Lyme disease that they had suffered many years before. I treated both of these with ceftriaxone with indifferent results

In 2001, I saw in close succession, two patients who had exposure to tick bites that had resulted in a classic Lyme disease dermatologic reaction.
The first patient had been sick for a year with fatigue, fever, paresthesia, and unsteadiness on her feet. An MRI of her brain had revealed findings consistent with MS. Her search of “the web” convinced her that she had Lyme disease because she had been exposed to ticks and had a bull’s-eye rash just before becoming ill. Serologic tests were equivocal. I agreed with her diagnosis and arranged for her to have a 21-day course of ceftriaxone 2 grams intravenously. She became afebrile, her joint pain disappeared and she became essentially asymptomatic. Within several months she was able to resume her fulltime employment from which she as on disability leave. MRIs done yearly since then have shown no progression of the abnormalities that were considered consistent with MS. She remains on suppressive doxycycline therapy.

On July 4, 2001, the second patient had a tick bite followed by a bull's eye rash. The rash persisted for a month and her mild arthritis flared to the point that she was becoming unable to work. She concluded that she might have Lyme disease and I agreed. She was given a 21-day course of ceftriaxone 2 grams intravenously with gradual improvement and she returned to work. She was maintained on oral doxycycline, azithromycin, and cefuroxime. After the initial clinical response she developed paresthesias and balance difficulty, and in July 2003, became so ataxic that she had difficulty in standing. She was hyperreflexic. Her MRI showed findings compatible with MS. At that time, I decided to treat her with glatiramer acetate and another course of intravenous ceftriaxone.25 She stated five days after the start of glatiramer acetate that her balance greatly improved. She is now back to work fulltime but she is still somewhat ataxic and has joint pains more typical of Lyme disease then of MS. She is being maintained on oral doxycycline and azithromycin. A delay in getting the intravenous ceftriaxone started, allowed her to observe a rapid clinical response of her ataxia that possibly was because of the glatiramer acetate. The tantalizing aspect of this part of her history is that it raises the speculation that in cases of Lyme disease with autoimmune features, glatiramer acetate might be worthwhile as part of the initial preventive therapy.

There are articles in the medical literature that are consistent with the hypothesis that Lyme disease can cause a clinical picture almost identical to MS. Pachner has called Lyme disease the great imitator.3 Chmielewska-Badora has questioned whether there is a connection between Lyme disease and MS.10 Lakos has stated that Lyme disease may imitate MS.11 Lana-Peixoto has reported positive serology for Lyme disease in MS.12 Garcia-Monco has found antibodies to myelin basic protein in Lyme disease.13 Martin has demonstrated that Borrelia burgdorferi can act as a trigger for autoimmune T-cell reactions within the central nervous system.14 A possible explanation for this phenomenon is that Borrelia burgdorferi exhibits molecular mimicry with human nervous tissue.16 Molecular mimicry might evoke antimyelin T-cells against myelin basic protein.14 Baig, et al demonstrated cells secreting antibodies to myelin basic protein in cerebrospinal fluid in patients with Lyme neuroborelliosis.17 Gay and Dick have referred to literature that suggests that Borrelia burgdorferi can cause demyelination as a sequel Lyme disease.18,19,20 They stated, “It seems inevitable that some patients, especially in area where Lyme disease is endemic, who have been labeled as “possible MS”, will ultimately be shown to have Lyme demyelinating encephalopathy.” They further suggested that, “A search for these patients should be undertaken in endemic areas.”18 The endeavors reported here appear to have supported their suggestions.

If there are physicians who feel that the possibility of ALS and MS syndromes are worthy of a trial of ceftriaxone therapy, there are some caveats that should be kept in mind.
The patients and their families must be made aware that there is only a possibility that being treated with ceftriaxone might be beneficial. It must be emphasized to the patient that this is an attempt to help them and not an experiment. The relative safety of the ceftriaxone can be emphasized. The patient should have possible exposure to Lyme disease, but serologic tests do not have to be positive to be considered for treatment. In addition, they are now medications that have been shown to have utility in the treatment of ALS and MS. They must eventually be included in the treatment plan. Riluzole has been found by some to be helpful in ALS and glatiramer acetate and beta interferon have utility in the treatment of MS.25,26 When and how ceftriaxone should fit into the treatment program must be considered. In most cases a 30-day trial of ceftriaxone before using riluzole or glatiramer acetate does not seem unreasonable.
Kuhn has expressed the opinion that good hypothesis must be innovative enough to create an interest and open ended enough to invite further study.27 The further study suggested by our hypothesis could be a mega analysis of patients treated for ALS and MS with ceftriaxone. These patients might be found through reports on the internet and in reports made to the societies dedicated to ALS and MS. These national ALS and MS organizations might be willing to act as a clearinghouse to find patients in whom a relationship between ALS or MS and Lyme disease seems likely. They might also be willing to solicit reports regarding the results of ceftriaxone therapy in patients with ALS and MS. This could be done by a questionnaire sent to patients in data banks

The caveat regarding trying to evaluate treatment of ALS with ceftriaxone is that more than one precipitating cause of ALS probably exists. They include geographic, genetic, electrical and other microbial influences. 28,29,30 It may well be that only a minority of ALS syndromes are involved with Borrelia organisms. If so, only a small number of cases may respond to ceftriaxone. Treatment of only those patients with solid serologic evidence of disease or those from heavily infected areas may be most fruitful. Since ALS is almost inevitably fatal, only a few long-term survivors who received ceftriaxone will be of particular interest.

In cases of MS who are treated for the possibility of Lyme disease, evaluation of serial studies of the number of anti-myelin T-cells in their blood might be helpful.14 In the case of ALS, molecular mimicry between the polypeptide in Borellia and in the lateral nerve cells will be worthwhile to ascertain.
A physician and his/her patient who consider treatment of ALS and MS with ceftriaxone must weigh pros and cons. The pros are that there are some rational reasons to do this and these patients have enough to lose for them to “grasp at safe straws”. The cons are that hearsay evidence is always suspect, although one only has to hark back to the discovery of digitalis to realize that paying attentions to hearsay evidence has yielded results in the past
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Re: Lyme/MS

Postby Yvonne » Wed 13 Aug 2008 19:24

Med Clin (Barc). 1990 May 12;94(18):685-8.Links

Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion [Article in Spanish]

García-Moncó JC, Miró Jornet J, Fernández Villar B, Benach JL, Guerrero Espejo A, Berciano JA.
Department of Pathology, SUNY, Stony Brook.

There is no diagnostic biological marker in multiple sclerosis. Thus, its diagnosis is based on clinical criteria. These criteria can also be found in other conditions. Lyme disease is currently among them. In a late period of the disease demyelinating involvement of central nervous system can develop, and multiple sclerosis can be erroneously diagnosed. We have evaluated a series of 55 patients with a definite diagnosis of multiple sclerosis, and we have found evidence of infection by the causative organism of Lyme disease in three. We describe the three patients and we discuss the relationship between both conditions. We conclude that it is important to consider Lyme disease as a diagnostic possibility in patients with neurological disease of unknown etiology such as multiple sclerosis.

PMID: 2388492
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Re: Lyme/MS

Postby Yvonne » Sat 27 Dec 2008 20:04 ... yqfutj.pdf

Confounding Issues in the Diagnosis of Multiple Sclerosis: Lyme Disease Testing

Monte S. Willis, MD, PhD, Yu Bai, MD, PhD
Department of Pathology, University of Texas Southwestern, Dallas, TX

Clinical Presentation

A 28-year-old female presented to
the emergency department with bilateral
lower extremity weakness, which began
acutely 15 months previously and had
progressed to the point that she now required
a wheel chair. After the initial
onset, her weakness improved within
weeks and she was able to walk with the
use of a walker; however, she began a
variable course during the next 13
months which left her unable to mobilize
without assistance most of the time. She
reported intermittent blurred vision, and
denied back pain, fever, chills, and
cough. Upon further questioning, she remembered
an acute episode 2 years prior
that included decreased vision in her right
eye which lasted for a period of weeks
before it recovered spontaneously.
The only medications the patient was
taking were multivitamins, and she reported
that she had been under the care of
a chiropractor on a regular basis since the
episodes began without improvement.
The patient reported a penicillin allergy
(rash), denied smoking, alcohol or illicit
drug use, and had a family history of
breast cancer (grandmother) and
lymphoma (grandfather). Her past medical
history included a tick bite 2 years
prior (no characteristic Lyme disease rash
noted at any time), depression, anxiety,
and multiple motor vehicle accidents.
Magnetic resonance imagint (MRI) taken
2 years prior to admission after a motor
vehicle collision was reviewed and
demonstrated a normal brain and spinal
cord at that time (no central nervous system
(CNS) lesions identified).
The patient’s physical exam was
found to be normal except for decreased
strength in the flexor and extensor muscles
of the lower extremities, as well as
deficits of light touch and pinprick in the
right upper extremity and bilateral lower
extremities. Her principal laboratory findings
at the time of admission and during
her subsequent hospitalization are shown
in T1 and T2. Significant laboratory findings
during her hospitalization included a
positive Lyme index (antibody) with a
negative Lyme Western blot, an increased
CSF (cerebral spinal fluid) index and IgG
synthetic rate, and the presence of oligoclonal
bands in her CSF (not seen in her
plasma) [I1]. Moreover, a T2-weighted
MRI demonstrated scattered, abnormal
hyperintensities in the periventricular
areas of the brain and cervical spinal cord
compatible with a demyelinating process
[I2]. In the context of her clinical findings,
the laboratory and radiological findings
suggest the diagnosis of MS in this patient.

Confounding Issues in the Diagnosis of MS: Lyme Disease Testing

Positive serological testing for Lyme
disease can confound the diagnosis of MS,
as was the case in our patient. It should be
noted, however, that an emphasis on clinical
and specific laboratory findings can
often differentiate the 2 diseases.
Lyme borreliosis is a multisystem
disease caused by the spirochete Borrelia
burgdorferi. The clinical hallmark of infection
is an early, expanding lesion of
the skin, termed erythema migrans (EM,
also referred to as a ‘target lesion’),
which is recognized in 90% or more of
patients with Lyme disease. Several
weeks to months after the development
of EM, approximately 15% of patients
develop frank neurologic abnormalities,
including meningitis and encephalitis. A
more common pattern of disease is fluctuating
meningoencephalitis with cranial
nerve (especially facial) palsy, and peripheral
radiculoneuropathy, although a Bell’s
palsy-like symptomatology may occur by
itself. Patients with meningitic symptoms
generally have a lymphocytic pleocytosis
(~100 cells/mm3) in their CSF and diffuse
slowing on encephalogram. Neck stiffness
is rare (ie, Kernig’s and Brudzinski’s signs
are absent) and neurologic abnormalities
generally last for months but resolve until
late neurologic complications occur.
Chronic neurologic findings can be seen
many years after the onset of disease;
however, they are rare and include
demyelinating lesions in the CNS

The clinical manifestations of Lyme
disease are highly variable, but most patients
experience an acute illness at the
onset. Additional clinical history that is
suggestive of Lyme infection includes
living in endemic areas, confirmed exposure
to ticks, as well as objective signs of
characteristic skin (target) lesions from
tick bites. The clinical course of the CNS
findings in Lyme borreliosis occur in
stages involving remissions and exacerbations
similar to MS. However, in general,
meningitis and facial nerve paralysis
tend to appear relatively early in Lyme
infection compared to MS. Moreover,
radiculoneuropathy, cranial neuropathies,
and less fulminant forms of peripheral
nerve-, nerve plexuses-, or CNS-involvement
may present later in the course of
Lyme disease. While encephalomyelitis is
relatively rare, a far more common finding
in Lyme disease is a mild to moderate
chronic encephalopathy, presenting as a
state of confusion or mild dementia that
tends to occur in patients with evidence
of systemic Lyme disease.

CSF cell count in Lyme disease:

Although the pathogenesis of Lyme borreliosis
and MS is not clear, considerable
data suggests that both diseases are mediated
by a T-cell process.23 Therefore,
under both conditions, analysis of the
CSF may show lymphocytic cell
infiltrates.23 The total leukocyte count in
the CSF is generally <50 cells/µL in MS
patients, but is generally significantly
higher in the acute stage of Lyme
infection.23 Unfortunately, this test was
not performed in this patient to use as a
means of differentiation.

Serum/CSF immunological tests in Lyme disease:

The determination of B.
burgdorferi-specific antibodies is
commonly used as the most important tool
for the diagnosis of Lyme exposure. The
second national conference on serological
diagnosis of Lyme disease has
recommended a 2-step testing system toward
standardizing laboratory serologic
testing for B. burgdorferi. Initially, a sensitive
enzyme immunoassay (EIA) or immunofluorescent
assay (IFA) using either
whole B. burgdorferi organisms or purified/
recombinant antigens should be utilized
followed by a standardized Western
immunoblot if the EIA or IFAis positive.24
While this testing procedure supports a
diagnosis of Lyme disease, the Western
immunoblot does NOT constitute a “confirmatory”
test and still requires a clinical
diagnosis (history of exposure, symptoms,
and signs) to be correlated with laboratory

Any positive or equivocal results
from ELISA or IFA should be further
tested, or supplemented, by using a Western
blot method for detecting specific
antibodies to B. burgdorferi. Therefore,
in the present case, the positive B.
burgdorferi IFA reactivity was not supported
by a positive Western blot or by
clinical findings and should not be interpreted
as diagnostic for B. burgdorferi infection.
Furthermore, recommendations on
Lyme disease testing emphasizes that the
2-step positive results only provide supportive
evidence of exposure to B.
burgdorferi, which should support a clinical
diagnosis of Lyme disease but NOT be
used as criterion for diagnosis by itself.
Antibody detection methods do not provide
definitive results for establishing or ruling
out a diagnosis of Lyme disease, and the
predictive value of positive results is low
when specimens are tested from patients in
which the diagnosis is not supported by
history of exposure, symptoms, signs, and
laboratory data. Cases of seronegative active
Lyme disease have been reported, further
demonstrating the importance of the
clinical findings in the diagnosis of Lyme

Polymerase chain reaction (PCR) analysis:

PCR has been applied in an effort
to increase the sensitivity of detection
of B. burgdorferi. So far 17/18 tested
species of Borrelia can be detected using
this molecular technique.27 While no data
indicating an increase in sensitivity or
early detection compared to serology has
been reported,28 one study has claimed
that PCR results could accurately predict
clinical outcome by analyzing CSF obtained
before and after parenteral antimicrobial

MRI studies:
More than 85% of
patients with MS have demyelination
with typical changes of multifocal,
prominent hyperintensive lesions on
proton-weighted and T2-weighted MRIs,
and hypointensive lesions on T1-
weighted images in the periventricular
cerebral white matter, corpus callosum,
cerebellum, brain stem, and spinal cord.23
Patients with Lyme demyelinating
encephalopathy have been reported to
demonstrate multiple white matter lesions
that were also hyperintense on proton- and
T2-weighted images, but isointense on
T1-weighted images.30 Moreover, the
lesions in neuroborreliosis are generally
smaller than that of typical ones in MS
(ie, >5 mm).23 The MRI from this patient
demonstrated T2-weighted hyperintensities
which were hypointense on T1-
weighted MRI and were larger, more
typical for MS (>5 mm) [I1].

The diagnosis of B. burgdorferi CNS
infection can be challenging as well.
While there is rarely any doubt that the
CNS is involved, it is difficult to prove
that the CNS disease is directly caused by
B. burgdorferi. It is important to correct
for the amount of peripheral blood antibodies
that may cross the blood-brain
barrier. Moreover, CSF from MS patients
may show intrathecal antibody production
against measles, rubella, or mumps
virus, while neuroborreliosis patients
have been shown to have no intrathecal
virus antibody synthesis.

A Multiple Sclerosis-Lyme Disease Connection?

Multiple sclerosis has been
proposed to be caused by a CNS invasion
by treponemal spirochetes through
defects in the wall of the sphenoidal
sinus and subsequently inducing an antiself
response via molecular mimicry.
Evidence supporting this theory comes
from CNS immunological studies (ie,
including both ELISA/IFA and Western
immunoblot) that have demonstrated the
presence of B. burgdorferi in the CNS in
some patients with active MS.36 However,
since no significant clinical
improvement has ever been observed in
MS patients shown to have positive
Lyme immunological analyses after antimicrobial
treatment, many people think
that B. burgdorferi inoculation may lead
to only latent infection in many cases,
and such latent infections may coexist in
MS patients.40 Moreover, since 22% of
people acquired antibodies to B.
burgdorferi after a tick bite, some authors
suggested that the finding of reactive
Lyme serology in an MS patient
with no suggestive features of the infection
is unlikely to indicate neurological
Lyme disease.41-43

Since the relationship between Lyme
infection and MS exists, and B. burgdorferi
may occasionally cause demyelination
as a sequel to Lyme disease, it is
important to determine if the Lyme infection
is active by monitoring changes in
immunological analyses when Lyme versus
MS or coexistence of Lyme and MS
is in doubt, especially in endemic areas.30
A trial of antimicrobial therapy should be
granted to the cases where the immunological
analyses show the “possible” active
Lyme infection with the effort to
remove any possible insults and correct
reversible tissue damage as well as facilitate
the differential diagnosis.

Listen to all,
plucking a feather from every passing goose,
but follow no one absolutely

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