BORRELIOOSI/PARKINSONIN TAUTI

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BORRELIOOSI/PARKINSONIN TAUTI

ViestiKirjoittaja soijuv » Ma Syys 06, 2010 15:12

Borreliabakteerin aiheuttama Parkinsonin tauti

Raportteja Parkinsonin taudille tyypillisten oireiden esiintymisestä borrelioosia sairastavilla, on olemassa. Seuraavassa tapaus, jossa asia on raportoitu vaihe vaiheelta ja vahvistettu ruumiinavauksessa.

Mies sai punkinpureman v. 1995. Hänelle tuli tyypillinen ihomuutos, luusto-lihaksistokivut, polven turvotus, kipua vasemmassa olkapäässä ja käsivarressa. Vuotta myöhemmin hän sai diagnoosiksi borrelioosin. Selkäydinnesteen borreliavasta-aineet ja PCR olivat positiiviset.Tänä aikana kivut ja käden vapina olivat lisääntyneet. Hän sai 3 vko iv keftriaksonia ilman mainittavaa hyötyä. MRI (pään/kaulan magneettikuva) oli normaali.

Vuonna 1997 uusi antibioottihoito: iv keftriaksoni 2 vko + 42 vrk iv kefotaksiimia. Hoito auttoi oireisiin jonkin verran. Vuonna 1997 selkäydinnesteestä löydettiin hoidoista huolimatta borreliabakteereita. Diagnoosi: neuroborrelioosi joka ilmeni Parkinsonin tautina.

Vuonna 1998 oireet: laihtuminen, krooninen fatiikki, vapinoita, kipuja kaulassa ja käsissä, liikket kankeat ja kivuliaat. Hoito: antibioottia suun kautta; klaritromysiini + ciprofloksasiini + hydroksiklorokiini. Vapina helpotti hoidon aikana.

Vuonna 1999 borreliavasta-aineet olivat edelleen positiiviset. Antibioottihoidosta huolimatta miehen tila heikkeni. Hänen muistinsa heikkeni, virtsanpidätyskyky heikkeni, kuolaamista, kykenemätön liikkumaan ilman apua tai huolehtimaan itsestään. Selkäydinnesteen borreliavasta-aineet + PCR positiiviset. Babesia negatiivinen. Borreliabakteereita löytyi punasoluista. Antibioottihoitoa jatkettiin.

Vuoden 2000 lopulla mies joutui sairaalaan keuhkokuumeen vuoksi. Antibioottihoito. Vuoden 2001 alussa uusi keuhkokuume. Sylkinäytteestä löytyi stafylokokkeja. Hoidoksi iv vankomysiiniä.

Kuukauden kuluttua sylkinäytteestä löytyi borreliabakteereita. Myös muut testit olivat positiivisia.
IV vankomysiiniä + azithromysiiniä + atovaquonea jatkettiin. Hoidoista huolimatta mies kuoli infektioon huhtikuussa 2001.

Ruumiinavauksessa todettiin borrelia-bakteerin aiheuttama, Parkinsonin taudille tyypillinen, aivojen surkastuminen.

Muita borrelia-bakteeria/Parkinsonin oireita käsitteleviä tutkimuksia:

Kuntzer, T. , J. Bogousslavsky , and J. Miklossy . et al. Borrelia rhombencephalomyelopathy. Arch Neurol 1991. 48:832?836.

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

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

Kohlhepp, W. , W. Kuhn , and H. Kruger . Extrapyramidal features in Lyme borreliosis. Eur Neurol 1989. 29:150?155.
C
Cadavid, D. , T. O'Neill , H. Schaefer , and A. R. Pachner . 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.

Alkuperäinen artikkeli julkaistiin v. 2003
:

Lyme-Associated Parkinsonism: A Neuropathologic Case Study and Review of the
Literature

Archives of Pathology and Laboratory Medicine: Vol. 127, No. 9, pp.
1204­1206. Accepted April 11, 2003

David S. Cassarino, MD, PhD,a Martha M. Quezado, MD,a Nitya R. Ghatak, MD,a
and Paul H. Duray, MDa
aFrom 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)

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.2­6 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 -synuclein, which can be identified
immunohistochemically in glial cells. To our knowledge, the presence of
glial cytoplasmic inclusions and -synuclein has not been previously reported
in the brains of patients with Lyme disease.

REPORT OF A CASE Return to TOC

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 burgdorferi­specific 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
burgdorferi­specific 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.

PATHOLOGIC FINDINGS Return to TOC

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 -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.

COMMENT Return to TOC

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 anti­Parkinson'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 anti­B 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 -synuclein­positive 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.

Acknowledgments

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; 1997:635­646.
2. Kuntzer T, Bogousslavsky J, Miklossy J. et al. Borrelia
rhombencephalomyelopathy. Arch Neurol 1991;48:832­836. [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;8:384­390.
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;37:43­51.
5. Kohlhepp W, Kuhn W, Kruger H. Extrapyramidal features in Lyme
borreliosis. Eur Neurol 1989;29:150­155. [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;80:1043­1054. [PubMed Citation]
7. Lowe JS, Leigh N. In: Graham DI, Lantos PL, eds. Greenfield's
Neuropathology. New York, NY: Oxford University Press; 2002:343­346.
------------------------------------------------------------------------

Tables Return to TOC


Table 1. Western Blot Results

Table 2. Enzyme-Linked Immunosorbent Assay
------------------------------------------------------------------------
Figures Return to TOC

Click on thumbnail for full-sized image.

Figure 1. Coronal section of the brain showing basal ganglia atrophy.Figure
2. Striatum with neuronal loss and gliosis (hematoxylin-eosin, original
magnification ¥100).Figure 3. Substantia nigra with neuronal loss and
gliosis (hematoxylin-eosin, original magnification ¥100).Figure 4.
Ubiquitin-positive glial cytoplasmic inclusions in the striatum
(hematoxylin-eosin, original magnification ¥400).Figure 5.
-Synuclein­positive glial cytoplasmic inclusions in the striatum
(hematoxylin-eosin, original magnification ¥200)

Presented as an abstract at the annual meeting of the American Association
of Neuropathologists, Denver, Colo, June 22, 2002.

Reprints: Paul H. Duray, MD, Laboratory of Pathology, National Cancer
Institute, National Institutes of Health, Bldg 10, Room 2N212, 10 Center Dr,
Bethesda, MD 20892)
Viimeksi muokannut soijuv päivämäärä Ke Touko 25, 2011 13:31, muokattu yhteensä 3 kertaa
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ma Syys 06, 2010 15:16

Nykyiset Parkinsonlääkkeet voivat parantaa oireita mutta eivät muuta itse taudinkulkua. Parkinsonin syynä voivat olla eri taudinaiheuttajat ja niiden aiheuttama infektio, tulehdus ja häiriö immuunipuolustuksessa. Tutkijat ovat löytäneet geenin joka saattaa olla linkkinä taudin syntyyn. (2010)

http://news.yahoo.com/s/nm/20100815/hl_ ... gene/print

Immune system gene linked with Parkinson's: study
By Julie Steenhuysen Julie Steenhuysen Sun Aug 15, 1:02 pm ET


CHICAGO (Reuters) ? A gene linked with the immune system may play a role in developing Parkinson's disease, researchers said on Sunday, marking a possible advance in the search for effective treatments.

They said a gene in the human leukocyte antigen region or HLA -- which contains a large number of genes related to immune system function -- was strongly linked with Parkinson's disease.

"That means the immune system probably plays a role in your body developing Parkinson's disease," said Dr. Cyrus Zabetian of the University of Washington and Veteran's Administration Puget Sound Health Care System, whose study appears in the journal Nature Genetics.

Zabetian said there had been hints that the immune system may be linked to Parkinson's disease, a neurodegenerative disease that affects 1 to 2 percent of people over age 65.

"This is the best evidence we've seen so far," Zabetian said in a telephone interview.

The finding came from a large, long-term study of more than 2,000 Parkinson's disease patients and 2,000 healthy volunteers from clinics in Oregon, Washington, New York and Georgia.

Parkinson's sufferers have tremors, sluggish movement, muscle stiffness and difficulty with balance.

Researchers looked at clinical, genetic and environmental factors that might contribute to the development and progression of Parkinson's disease and its complications.

"We found strong evidence that a gene within the HLA region is associated with Parkinson's disease," Zabetian said.

HLA genes play an important role in helping the body discern between foreign invaders and the body's own tissues.

"We don't know specifically which gene because there is a cluster of genes in that region, but it is the first really strong link that the immune system plays a role," he said.

That may mean infections, inflammation or an auto-immune response play some role in the development of Parkinson's disease, Zabetian said.

"What this allows us to do is to hone in on the immune system," he said.

Although current medical treatments may improve symptoms, none can slow or halt the progression of the disease.

The study was funded in part by the National Institute of Neurological Disorders and Stroke, one of the National Institutes of Health.

(Editing by Vicki Allen)
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ma Syys 20, 2010 19:01

Ovatko Parkinson oireet borrelia-bakteerin aiheuttamia? Artikkelissa vertaillaan oireita, kerrotaan 30-vuotiaan Michaelin tarina jne.

http://www.personalconsult.com/articles ... rlyme.html

Is It Parkinson's or Lyme?
Are Young Adults Regularly Misdiagnosed?

Michael was a smart man in his 30's who was an actor with moderate success. He was, however, a little too impressed with Ivy. Meaning, anyone who worked as part of an "Ivy League" faculty was like a great heavenly Gnostic sage, offering the great pearls of truth. If he only knew the reality.

He was from New York and had enjoyed a wide range of vacations in the past, including hiking in the lovely New York mountains.

Lets look at the simple basic symptoms of Lyme disease.
Primary Symptoms That Are Reported to
Diagnose Parkinson's Disease

* Slow intentional movement -- if you want to go to another room it is hard to initiate this action, and once you are moving it is hard to keep going and get to the kitchen.
* Tremors in almost any part of the body when you are resting.
* Rigid or Stiff muscles -- one of the reason's folks with Parkinson's have frozen expressions
* Poor balance -- my grandfather had Parkinson's from the influenza in the 1910's and this was a serious problem. He would finally get moving and he could not keep his balance and would fall.
* Eccentric walking -- features include a wide based gait, with poor arm movement and tiny steps.

Other Parkinson's Signs

The neurological dopamine damage in the brain can cause many other symptoms. Indeed, a very wide range. Here is just a sampling:

* Psychosis and agitation
* Eating trouble -- since the muscles of eating are acting poorly, food can collect in the back of the throat. Swallowing is a very complex muscle and nerve action.
* Excess sweating and excess saliva.
* Trouble with urine and stool control
* Depression and hopelessness -- I recall my grandfather telling me over the space of fifteen minutes that he was not always this way. I was sad he said, this since I knew he was a vital and active lead RCA engineer in his time, and an avid dancer and golfer.
* Skin dryness and other skin trouble
* Eccentric handwriting including tremor signs at the point of initiation before the writing started and then very tiny letters.
* Low volume speech

The Diagnostic Disaster

The heart of the Parkinson's diagnosis is ruling out other neurological disorders, since these symptoms are found in many disorders. Most importantly, the symptoms above can occur in neurological Lyme.

As has been very well described, neuroLyme can present in a hundred ways and is called the "Great Imitator." Yet many Neurologists do not take this seriously and never consider Lyme in Seizures, ALS, Migraines, MS, Strokes or hundreds of other neurology or psychiatric diagnoses.

Since Lyme is the leading vector illness in the US, and lab tests are commonly utter junk (See 20 articles on this fact on my web site), it is easy to miss. Lyme with Parkinson's symptoms looks exactly like real Parkinson's. Exactly!

Parkinson's is progressive over years. But so is Lyme.

Parkinson's waxes and wanes, and so do the spirochetes of Lyme.

****

Michael had four labs look at his blood and urine, and in conclusion it was felt he might have Lyme. After eight weeks these tests were repeated and he was clearly positive -- perhaps because some Lyme was killed and pieces caused a large immune response and some parts were found in both the urine and the blood.

In six months he was the best he had been in four years, and was using a greatly reduced Parkinson's medication dose.

He had three SPECT Scans, which are nuclear exams of how the brain is eating.

The first SPECT Scan showed eight lobes with a patchy Lyme-like finding.

The second looked much worse. We suspect it was worse from the death of so many Lyme bugs and their release of toxins in their outer membrane increasing inflammation.

The third SPECT scan was markedly improved, but not yet normal.

Michael is planning on doing more work, and is pleased with his progress. He suspects he got Lyme while camping about eight years ago.

For more information on the link between Lyme and Parkinson's symptoms go to: www.lymeinfo.net/multiplesclerosis.html
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ma Loka 25, 2010 07:41

Mercury News 2010:

Kuukausi sitten Bart Fenoliolle kerrottiin hänen sairastavan ALS-tautia ja että hänellä oli n. kaksi kuukautta elinaikaa. Vaimoa kehotettiin viemään puoliso kotiin ja aloittamaan saattohoidot. Fenolio osoitti kuitenkin lääkäreiden olleen väärässä. Hän aloitti antibioottihoidot borrelioosiin ja voi nyt päivä päivältä paremmin.

Tri Stricker kertoo tapaavansa jatkuvasti borrelioosia sairastavia jotka ovat saaneet vääriä Parkinson-, krooninen väsymysoireyhtymä- jne. diagnooseja.Yhtenä päivänä vastaanotolleni tuli nainen jolla oli outoja oireita. Hän oli käynyt Mayo-klinikalla jossa hänelle oli tehty useita testejä. Lääkärit eivät osanneet sanoa muuta kuin että naisella on fibromyalgia. Tri Stricker ihmettelee että lääkärit eivät olleet lainkaan huomioineet sitä tosiasiaa että nainen oli elänyt elämänsä Cape Codissa jossa borreliabakteereja kantavia punkkeja esiintyy paljon. "Miten ihmeessä lääkärit jättivät huomioimatta niin tärkeän yksityiskohdan", Stricker ihmettelee.

Fenolio, 69, tietää tarkkaan miten hän sai borrelioosin. Kuusi vuotta sitten hän oli täysin terve. Hän sai punkinpureman ollessaan koiransa kanssa lammen rannalla. Pureman ympärille tuli ihomuutos. Hän näytti sitä lääkärille mutta koska borrelioositesti oli negatiivinen, asia unohdettiin.

Kolme vuotta myöhemmin hän alkoi oireilla ja neurologi kertoi syynä olevan ALS-taudin.

Fenolion poika kuitenkin muisti isällä olleen aikoinaan punkinpureman. He lähettivät borrelianäytteen laboratorioon. Se oli positiivinen. Borrelioosiin erikoistunut lääkäri kirjoitti Fenoliolle pitkän antibioottilääkityksen.

Taistelu ei kuitenkaan ollut ohi. Vaikka Fenolio alkoi tulla antibioottihoidolla parempaan kuntoon kotikunnan lääkärit halusivat lopettaa hoidon Tähän oli syynä se, että IDSA eli Amerikkalaisten infektiolääkärien yhdistys on sitä mieltä että kroonista borrelioosia ei ole eikä pitkistä antibioottihoidoista ole hyötyä.

Fenolioiden mukaan antibiooteista on ollut selkeä apu. Bart Fenolio on tullut päivä päivältä parempaan kuntoon. Hän on tällä hetkellä vielä hoitolaitoksessa mutta vaimo on toiveikas että hän on parissa kuukaudessa tarpeeksi hyvässä kunnossa tullakseen kotiin.

Vaimo toivoo ettei kukaan muu joutuisi käymään läpi samaa painajaista kuin he ovat joutuneet. "Mikäli minun kerrottaisiin sairastavan ALS-tautia haluaisin totisesti että minulle tehtäisiin ensin borrelioositesti."

http://www.mercurynews.com/columns/ci_1 ... ck_check=1
Fisher: Learning about Lyme disease the hard way

By Patty Fisher

pfisher@mercurynews.com
Posted: 01/21/2010 05:41:13 PM PST
Updated: 01/22/2010 11:34:54 AM PST

Click photo to enlarge
Bart Fenolio with his wife, Heidi, at A Grace Sub-Acute Care... (Nhat V. Meyer, Mercury News)

A month ago, Bart Fenolio was told he had Lou Gehrig's disease and had two months to live. Doctors advised his wife, Heidi, to take him home and call a hospice.

But Fenolio is proving the doctors wrong. Instead of getting worse, he's growing stronger each day, thanks to antibiotics. That's because he doesn't have Lou Gehrig's disease, which isn't curable. He has Lyme disease, which is.

Lyme disease, a bacterial illness spread by ticks, is a poorly understood and strangely controversial illness that has been sweeping the country since it was discovered in Connecticut in the 1970s. While still rare in California, there were 28,921 confirmed cases and 6,277 probable cases in the United States in 2008, nearly twice as many as in 1994.

But Lyme experts suspect there could be 10 times that many. That's because when not treated immediately, Lyme can hide in the body for years and then attack, masquerading as anything from heart disease to arthritis to lupus. Folks might not even know they'd been bitten. And the tests for Lyme disease are notoriously unreliable.

Dr. Raphael Stricker, a Lyme disease expert in San Francisco, regularly sees patients who have been misdiagnosed with chronic fatigue syndrome or Parkinson's disease.

"I saw a new patient the other day who had weird symptoms and had gone to the Mayo Clinic for a complete work-up," Stricker told me. "All they could come up with was fibromyalgia," a syndrome characterized
by chronic pain, fatigue and depression. Stricker learned that the woman had grown up on Cape Cod, where Lyme-carrying ticks are common.

"How could you miss that little tidbit of her history?" he wondered.

Bitten in Morgan Hill

Fenolio, 69, knows just how he contracted the disease. Six years ago a healthy and hearty Fenolio was playing with his dog Cody near a percolation pond in Morgan Hill and was bitten by a tick. When a circular rash appeared around the bite, he went to the doctor. A Lyme test came back negative, and he forgot all about it.

Three years later he retired from the tropical fish store ?Dolphin Pet Village ? he and his sister owned in Campbell. He and his wife moved to San Diego to be near their grandchildren and to enjoy playing lots of golf.

But his golf game slowly deteriorated. He couldn't seem to grip the club. Then, during a vacation in Hawaii, he was too weak to climb out of the pool. His doctor told him he was just getting old. His wife wasn't buying it.

"I said, 'This is not old age. My husband is disintegrating before my eyes, and something's going on.' "

Their Kaiser Permanente internist referred them to a neurologist, who diagnosed Lou Gehrig's disease. Then Fenolio's son remembered the tick bite.

Fighting for treatment

A laboratory that specializes in Lyme tests confirmed his suspicion, and a Lyme specialist in Redwood City prescribed a long-term course of antibiotics. But the ordeal wasn't over. Although Fenolio began to improve on antibiotics, his wife told me, Kaiser doctors wanted to discontinue them.

That's because the Infectious Disease Society of America still recommends against extended treatment using antibiotics, and it casts doubt on whether chronic Lyme disease exists at all, despite thousands of documented cases. Because of the IDSA's position, health insurers generally refuse to cover long-term antibiotics. In most states, though not in California, doctors can lose their licenses just for treating chronic Lyme.

Dr. Sara Cody of the Santa Clara County Health Department cautioned that Lyme disease is rare here, and Fenolio's case doesn't prove that there's rampant misdiagnosis going on.

"What he is experiencing is tragic but not common," she said.

Dr. Jonathan Blum, an infectious disease specialist at Kaiser Permanente Santa Clara, wouldn't discuss Fenolio's case. He confirmed that Kaiser follows the IDSA protocols.
Tri Jonathan Blum on KAiseri alueen infektiolääkäri. Hän vahvistaa alueella noudatettavan IDSA:n näkemyksiä. Hänen mielestään pitkillä antibiooottihoidoilla on vakavia sivuvaikutuksia eikä niitä tule käyttää ellei niistä ole osoitettavissa selkeää hyötyä.

"Long-term antibiotics can cause significant side effects," he said, "and should be used only if they are going to help the patient."

Fenolio's family is convinced that the antibiotics are helping. Today he is in a San Jose nursing home, improving each day. He knows there will be setbacks, but his wife hopes he'll be strong enough to go home in a couple of months.

"I just wouldn't want anyone else to go through this nightmare," she said. "If I had one of those diseases and was told there was no cure, I would definitely want to be tested for Lyme."

Contact Patty Fisher at pfisher@mercurynews.com or 408-920-5852.

# Named for the Connecticut town where it was identified in the 1970s, Lyme disease is carried by ticks, specifically deer ticks and Western black legged ticks.
# To prevent infection, wear long sleeves and trousers when hiking and do frequent tick checks.
# If you are bitten, remove the tick and see a doctor.

# For more about Lyme disease or to find a Lyme disease specialist, go to the International Lyme And Associated Diseases Society at www.ilads.org, or the California Lyme Disease Association at www.lymedisease.org
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Elo 26, 2011 11:10

Alla muutama tutkimus joissa antibiootti minosykliinin todettiin edesauttavan keskushermostovaurioiden paranemista.

Alinna Parkinson-oireisiin sairastuneen henkilön kokemus antibioottien vaikutuksesta.


Minocycline: neuroprotective mechanisms in Parkinson's disease http://www.ncbi.nlm.nih.gov/pubmed/14965330

Neuroprotection by minocycline facilitates significant recovery from spinal cord injury in mice http://brain.oxfordjournals.org/content/126/7/1628.full

Minocycline promotes remyelination in aggregating rat brain cell culture Neuroscience. 2011 Jul 28;187:84-92. Epub 2011 Apr 29. http://www.ncbi.nlm.nih.gov/pubmed/21549181
----------------
"81-vuotias Bentley on sairastanut Parkinson oireita 20v. Olemme vuosien aikana hoitaneet häntä useilla erilaisilla hoidoilla. Niistä on ollut jonkin verran hyötyä. Muutaman viikon ajan olemme hoitaneet häntä antibiooteilla. Huomasimme niistä olevan suunnattomasti apua sen jälkeen kun B. sai antibioottia mahahaavan hoitoon. Hoidon aikana B:n oireet hävisivät suurelta osin. Hän kykeni esim. kääntymään vuoteessa ilman apua, hymyilemään, syömään, olemaan hereillä koko päivän jne.
Näyttääkin siltä että lääkäri oli oikeassa epäillessään Parkinson oireiden johtuvan bakteereista ja antibiooteista olevan hyötyä taudin hoidossa."


Bentley is 81 years old, has been diagnosed with Parkinsons for 20 years and has been living with left side paralysis from a failed double sided DBS procedure since May 2004. We have looked at many different treatment options and have used several for years with some success.

Over the past few weeks we began a journey that we hope will help us truly stop the source of Bentley's Parkinson's. As I mentioned in past emails, a friend of ours brought Dr. Borody to our attention. He is the Nobel prize winning researcher and physician that discovered that H Pylori was the cause of some ulcers and could be treated with antibiotics. We tested Bentley for H Pylori and he was positive. He went through a 10 day treatment and within the first 72 hours had incredible improvement in his Parkinson's symptoms. Then it stopped and he stayed about the same. It has been a week since he finished the medication and he is retaining the gains he made to some degree but with less energy. Here is what we has happened for Ben. I have video which I will find a way to attach.

Within 24 hours he could roll over in bed, lift his head and smile on both sides of his mouth. This is very important because he did this with no Sinemet first thing in the morning. He also could not smile on both sides without using hyperbaric oxygen for several months regularly. I always thought it was the stroke, but it must have been also the PD.
Could easily point and flex his right foot.
Could smile, open his mouth wide and stick out his tongue.
Could control his right arm to feed himself.
Could look up.
Eyes wide open.
Very alert and awake all day.


It seemed like a miracle that he could do these things so immediately after starting treatment. This makes us believe that maybe this doctor is right and Parkinsons may start from a bacteria and can possibly be treated with antibiotics.

We are now getting another appointment with our GP to have Bentley tested for C Dif. They can isolate the bacteria and treat. Some people need multiple courses of antibiotics and some eventually need the feacal implant to restore the good flora. When you read about C Dif it will say that a patient has persistent diarrhea, but you can also have constipation or no apparent symptom at all. Bentley does suffer from severe constipation, so it will make it easier to get him tested and treated.

If you or your loved one does not have symptoms, you may still want to find a way to get tested for C Dif.

I will be posting more information on this subject over the next few days. They are starting a trial very soon in Australia specifically for Parkinsons and treating for bacteria. They have already had success with at least one patient.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » To Loka 13, 2011 07:36

Otteita artikkelista:

http://www.newswithviews.com/Howenstine/james26.htm

"Borrelioosissa esiintyy yleisesti neurologisia ongelmia sillä bakteerin erittämät neurotoksiinit sitoutuvat rasvakudoksiin. Rasvakudosta on runsaasti mm aivoissa ja äärihermostossa. Neurotoksiinit voivat aiheuttaa äkillisen kuuroutumisen, kasvohermohalvauksen, Parkinsonin oireet, MS oireet, hermotulehduksia, kroonista kipua ym neurologisia ongelmia. Kissankynsi näyttäisi korjaavan immuunipuolustuksen toimintaa, tuhoavan mikrobeja ja estävän hermomyrkkyjen vaikutuksen soluihin, entsyymeihin ja hormoneihin.

Tri Joanne Whitakerin potilailla lähes jokaisen Parkinson oireita sairastavan borrelia-testi on ollut positiivinen. Tri Louis Romero kertoo kolmen Parkinson potilaansa olevan lähes oireettomia (99%) TOA vapaan kissankynsihoidon jälkeen.

Tapausselostuksia:

Larry Powers sairastui Parkinson taudin oireisiin v.1990. Hän käytti taudin hoidossa yleisesti käytettyä Sinemet hoitoa kahdeksan vuoden ajan. Hoidosta huolimatta hänen tilansa heikkeni heikkenemistään. Lopulta hän joutui pyörätuoliin eikä kyennyt syömään ilman apua. Kun hän sai tietää että Parkinson voi johtua borrelia-bakteerista, hän alkoi käyttää TOA vapaata kissankynttä. Kolmessa viikossa hänen tilansa parani niin paljon että hän pääsi pois pyörätuolista ja kävi kalastamassa.

Tom Coffey sai ALS diagnoosin 34-vuotiaana. Kesäkuussa 2001 hän ei kyennyt nielemään sylkeä eikä syömään. Hänelle laitettiin ruokintaletku. Hänen painonsa putosi nopeasti. Tom konsultoi Borrelioosiin erikoistunutta lääkäriä. Tämä aloitti suonensisäisen Tomille antibioottihoidon (Rocephalin) ja Tom tuli kuntoon."



Dr. Joanne Whitaker relates that nearly every patient with Parkinson?s Disease (PD). has tested positive for Bb. Dr. Louis Romero reports that 3 patients with PD are 99 % better after TOA-free cat?s claw (Uncaria tomentosa) therapy.
....
Case Reports Illustrating The Critical Importance Of Establishing The Diagnosis Of Lyme Disease
Case 1 Larry Powers, a former Mr. America in 1962, became ill with the symptoms of Parkinson?s Disease in 1990. Sinemet therapy was taken for eight years but he gradually became worse. He became confined to a wheel chair and required help with eating. After learning that Lyme Disease might be causing his symptoms of PD he started taking TOA free cat?s claw (Uncaria tormentosa). Within three weeks he was out of his wheelchair and fishing for 100 pound tarpon.
Case 2 Tom Coffey at age 34 developed diplopia, severe hypertension uncontrolled by drugs, and impaired balance. A diagnosis of amyotrophic lateral sclerosis was made. Surgery was performed to correct the diplopia. By June 2001 he was unable to swallow saliva and feeding tube nutrition was begun. His weight had fallen by 100 pounds. Nutritional support from the tube feedings produced slow resolution of the swallowing problem. Consultation with a Lyme expert uncovered the history of a bulls-eye rash after a tick bite. Therapy with Rocephin led to complete recovery.
Case 3 A young male college student developed such severe cognitive difficulties he was forced to drop out of school. A RIBb test was positive for LD and he resumed a normal life after receiving 4 months of antibiotic therapy...
.....Lyme Disease frequently exhibits neurologic abnormalities because the Bb neurotoxins are drawn to the fatty tissue found in the brain and peripheral nerves. As a consequence sudden deafness, Bells palsy, Parkinson?s Disease, Multiple Sclerosis, reflex sympathetic dystrophy, peripheral neuritis, chronic pain, and a multitude of other neurologic disorders may appear.
....The Influence of Toxins from Bb On The Symptoms and Course of Lyme Disease
Nuorilla Parkinsonin oireisiin kuolleilla tehdyissä ruumiinavauksissa on toistuvasti huomattu että aivovauriot eivät ole samanlaisia kuin tyypillisissä Parkinson tapauksissa vanhemmilla henkilöillä. Osa potilaista on saanut vuosikausiksi virheellisen Parkinson, ALS, MS diagnoosin. Osa on saanut nopean avun kissankynsivalmisteesta. Nopea apu ei selity immuunipuolustuksen vahvistumisella eikä valmisteen bakteereja tuhoavasta ominaisuudesta. Borrelia-bakteeri erittää erilaisia hermomyrkkyjä. Kissankynsi (Uncaria tomentosa) näyttäisi estävän hermomyrkkyjen vaikutuksen rasvakudoksiin.
Autopsy examinations of young persons (30s) dying from what appeared to be Parkinson?s disease PD have frequently failed to confirm the basal ganglion damage that would be expected in the classic PD seen in the elderly. Some patients with illnesses of many years duration misdiagnosed as Amyotrphic Lateral Sclerosis, Multiple Sclerosis, and Parkinson?s Disease have made incredible recoveries within periods as short as 24 to 72 hours when placed on TOA-free uncaria tormentosa (cat?s claw) for LD.. This rapid response could not rationally be attributed to improved immune function or bacteriocidal effects on spirochetes. Bb is known to produce a group of neurotoxins. The most sensible explanation for this recovery lies in turning off or blocking the neurotoxic effects of Bb on the lipid containing structures that the Bb neurotoxins are attracted to (central nervous system, peripheral nerves, muscles, joints etc.). This sudden improvement appears to be the result of blockage and inhibition of the neurotoxins[5]. The most important example of a ?Biotoxin Illness? appears to be Lyme Disease[6]. Patients with symptoms of Parkinson?s Disease at a young age caused by neurotoxins would not be expected to show permanent structural destruction in the basal ganglia. These neurotoxins probably act at specific sites such as neurotransmitters-pre- and- post synaptic membranes, altering dopamine, serotonin, GABA, and acetylcholine molecules, thereby blocking surface membrane receptors of various kinds which would interfere with the proper action of enzymes, coenzymes and hormones. This is only one of the damaging mechanisms of action of the neurotoxins.
The TOA free form of cat?s claw (Samento) may have three direct beneficial effects in humans with LD:
Immune modulation (correcting immune dysfunction)
Direct broad spectrum anti-microbial effect on spirochetes. Quinovic acid glycosides found in TAO-free cat?s claw are similar to the quinilones widely used as antibiotics.
Blocking the adverse neurotoxic effects on cells, enzymes, and hormones
Whether the serious lack of energy and fatigue seen in LD are similar to the cyanate[7] induced damage to the mitochondria?s ability to produce energy in the motor neurone found in amyotrophic lateral sclerosis or is due to failure of proper calcium channel function is not clear.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ti Huhti 10, 2012 16:21

12 Borreliatapausta joissa potilailla esiintyi erilaisia neurologisia oireita kuten Parkinson, meningoradikuliitti, meningomyeliitti, kasvohermohalvaus, polyneuriitti jne. Vain 3 muisti punkinpureman ja ainoastaan yhdellä oli ollut ihomuutos. Useimmilla esiintyi kovaa kipua. Kipu hellitti suonensisäisellä antibioottihoidolla. Parkinson ja hydrokefalus oireet eivät parantuneet antibiooteilla vaan vaativat lisähoitoja.


Rev Neurol (Paris). 1989;145(5):362-8.
[Neurologic forms of Lyme disease. 12 cases].
[Article in French]
Viader F, Poncelet AM, Chapon F, Thenint JP, Dupuy B, Morin P, Lechevalier B.
Source

Service de Neurologie Dejerine, CHU de Caen.

Abstract


Twelve cases of Lyme's disease with neurological complications are reported. Seven patients had meningoradiculitis of the Garin-Bujadoux-Bannwarth type, with facial palsy in 2 cases. In 1 case the radiculitis involved only the cauda equina. Two more patients had meningomyelitis. Of the remaining 3, 1 had subacute inflammatory polyneuritis with albumino-cytologic dissociation, 1 had probable dorsal epiduritis, and the last one developed parkinsonism and communicating hydrocephalus after an otherwise classical meningoradiculitis. Three patients recalled a tick bite but only one a cutaneous eruption. No arthritis or cardiac involvement were observed. In 2 cases the CSF contained pseudo-neoplastic cells. Severe pain was a prominent feature in most cases. Pain consistently and rapidly improved on high-dose intravenous penicillin, while other signs or symptoms (e.g. paresthesias or fatigue) often lasted several months. Parkinsonism and hydrocephalus were not influenced by penicillin, and both required specific therapy. Isolated neurological (both central and peripheral) involvement is not unusual in Lyme's disease and may give rise to a wide range of signs and symptoms. This diagnosis is to be considered even when other features of Borrelia burgdorferi infection are lacking.

PMID:
2662339
[PubMed - indexed for MEDLINE]
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ma Touko 28, 2012 12:24

Muutamia tutkimuksia ja artikkeleita Bb:n ja Parkinson oireiden mahdollisesta yhteydestä:

Dr Bransfield's Article on the Neuropsychiatric Assessment of
Lyme Disease:

Neurological symptoms have been previously recognized as a component of Lyme
disease (31-46). Cranial nerve findings begin before the cognitive changes are
seen and can intensify again late in the
course of the illness. There are times when the cranial nerve findings are more
evident late in the day when the patient becomes tired and they acquire double
vision, choke on food, or lose their ability to talk. Grand mal seizures are
more significant with congenital Lyme cases, while complex partial seizures are
seen in a notable percent of other NPLD patients. These seizures are
effectively controlled with
both anticonvulsants and antibiotics. Some neurological findings are common
such as numbness, tingling, sensory loss, burning, weakness, tremors, myoclonic
jerks. torticollis, and fainting. Ataxia is common
in these patients who are often clumsy, which leads to frequent accidents.
Myotonia is uncommon but I have been this in a few patients, and PARKINSON'S
SYNDROME caused by Lyme disease can also seen, although it is uncommon. A
number of these patients have herniated discs after having Lyme disease for
several years. I suspect, but cannot prove, there is a causal relationship
between Lyme disease and herniated discs. Burning is quite specific to NPLD,
but is also seen in herpes infections. The patient describes a sensation that a
blowtorch is burning the skin. It can affect any part of the body. In some
patients the burning migrates, while in others it remains in a given area. Both
antibiotics and anticonvulsants relieve this symptom.
______________________________________________
Title: [Neuroborreliosis in a patient with progressive supranuclear
paralysis. An association or the cause?]
Authors: Garcia-Moreno JM, Izquierdo G, Chacon J, Angulo S, Borobio MV
Source: Rev Neurol 1997 Dec;25(148):1919-21
Organization: Departamento de Inmunologia, Hospital Universitario
Virgen de la Macarena, Sevilla, Espana. Ay...@arrakis.es
Abstract:
INTRODUCTION: Many different neurological conditions may be seen in the
later stages of Lyme's Disease, such as blindness, epileptic crises,
CVA, extrapyramidal disorders, amyotrophic lateral sclerosis, and
dementia may be yet another form of presentation of chronic infection
due to Borrelia burgdorferi (Bb). Progressive Supranuclear Paralysis
(PSP), a disorder of unknown aetiology, considered to be the commonest
cause of Parkinsonism-plus, one of the symptoms of which is dementia,
has never been mentioned in this type of differential diagnosis.
CLINICAL CASE: We present the case of a 78 year old man with sub-acute
mental deterioration, Bb positive serology in both plasma and CSF, and
with clinical and epidemiological features compatible with Lyme's
Disease. Complementary tests were negative. The syndrome corresponded
to Lyme's Disease and improved after treatment with ceftriaxona.
CONCLUSIONS: We consider aspects of the aetiology of PSP which are
still not clear. In our patient, the aetiology seemed to be Bb
infection, according to the criteria of the original description of the
disease and in view of the neuropathological findings which have shown
Bb in the substancia nigra of the mid-brain and the existence of an
animal model in which Bb shows a particular tendency to colonize
infratentorial structures.
Keywords:
Aged, Antiparkinson Agents, THERAPEUTIC USE, Borrelia burgdorferi,
ISOLATION & PURIF, Case Report, Ceftriaxone, THERAPEUTIC USE,
Cephalosporins, THERAPEUTIC USE, Dementia, ETIOLOGY,
Electroencephalography, English Abstract, Facies, Frontal Lobe,
RADIONUCLIDE IMAGING, Human, Lyme Disease, COMPLICATIONS, DRUG THERAPY,
Magnetic Resonance Imaging, Male, Parietal Lobe, RADIONUCLIDE IMAGING,
Substantia Nigra, MICROBIOLOGY, PATHOLOGY, Supranuclear Palsy,
Progressive, DIAGNOSIS, DRUG THERAPY, MICROBIOLOGY, Temporal Lobe,
RADIONUCLIDE IMAGING, Tomography, Emission-Computed, Single-Photon
Language: Spa
Unique ID: 98188456
________________________________
Relationship Lyme Parkinson
This article submitted by Alrch Herman G on 12/15/96.
Lyme Disease and the Nervous System
Our Price: $65.00
Availability: This title usually ships within 4-6 weeks. Please note
that titles occasionally go out of print or publishers run out of
stock. We will notify you within 2-3 weeks if we have trouble obtaining
this title.
This book contains information on many aspects of your dad's case!!!
Re: parkinson's Dr Reik writes the following:
"Parkinson's syndrome can also develop during stage 2[footnotes
omitted]. The physical findings, which are sometimes asymetric, include
global rigidity, akinesia, hypomimia, tremor, cogwheeling, and postural
instability. Symptoms can begin 3 to 12 months after primary infection,
develop over weeks to months, and usually improve after antibiotic
therapy, sometimes combined with L-dopa treatment. When Parkinson's
syndrome does develop during stage 2 Lyme Disease, there is typically
an accompanying pleocytosis, sometimes with menigismus, other CNS
symptoms or signs, or cranial or peripheral neuritis, all serving to
differentiate it from idiopathic Parkinson's disease."
He adds later "Parkinson's syndrome does not always resolve completely."
_______________________________________________________________
"..Parkinsonian symptoms were noted during his last year of
life. Neither patient had symptoms of the skin, joint, or cardiac disorders
described in Borrelia infection. ...."
source: JAMA, Oct. 24/31. 1986--Vol. 256, No. 1
Letters
Borrelia in the Brains of Patients Dying of Dementia
"To the Editor.--I have identified spirochetes in serial subculture of autopsy
brain tissues from two patients with dementia. Indirect immunofluorescence,
using monoclonal antibodies specific for Borrelia species, resulted in
fluorescence of spirochetes that had previously been identified by darkfield
microscope examination (figures 1 through 4).
"Case 1 was a 74-year old woman with mild dementia of less than one year's
duration. She had resided in New York and Florida. Case 2 was a 69-year-old man
who died in a nursing home in Texas after a four-to five- year history of
progressive dementia. Parkinsonian symptoms were noted during his last year of
life. Neither patient had symptoms of the skin, joint, or cardiac disorders
described in Borrelia infection.
"Recent reports have described patients with various chronic degenerative
disorders whose blood or cerebrospinal fluid contains antibodies against B.
burgdorferi (1) Individuals with cognitive impairment were found within the
larger group of patients with chronic borreliosis. (2, 3) Borrelia species seem
to share with Treponema pallidum " (syphilis) " the potential to survive in
host tissues for prolonged periods of time and to cause disease in various
organ systems after months or years of clinical latency. Pachner and Steere (4)
have classified the neurological manifestations of B. burgdorferi infection
into primary, secondary, and tertiary forms. If Borrelia infection can be
linked to cases of dementia by serology or culture, a group of patients will be
canidates for intensive parenteral" (iv) "antimicrobial therapy analogous to
the treatment now used for neurosyphilis."
Alan B. MacDonald, MD
Southampton Hospital (NY)
1. Kohler J, Kasper J, Kern U, et al: Borrelial encephalomyelitis. Lancet
1986;2:35.
2. Reik L. Jr, Smith LM, Khan A, et al: Demyelinating encephalopathy in lyme
disease. Neurology 1985;35:267-269.
3. Hansen K, Rechnitzer C, Pederson NS, et al: Borrelia meningitis and
demyelinating CNS disease, Int J Microbiol Hyg 1986: in press
4. Pachner AR, Steere AC, Tertiary Lyme disease: Central Nervous System
manifestations of long standing infection with Borrelia burgdorferi, Int. J
Microbiol Hyg 1986: in press.
_______________________________________________________________
"Extrapyramidal Feaures in Central Lyme Borreliosis", European
Neurology, 1989;29:15-155 by Willi Kohlhepp. et al.


"Lyme can present with encephalitis which responds to antibiotic
treatment but with acute onset of extrapyramidal features together with
diffuse pain and many symptoms listed which correlate with Parkinson's
disease. Typical Parkinson's symptoms listed were "rigor", "tremor",
"proximal muscle weakness", "Reflex" abnormalities, "Babinski's sign",
"ataxia", "cranial nerve palsy" as in the flaccid facial muscles that
reflect Parkinsons. "Bradydiadochokinesia" were noted in the case
histories presented with severe rigor, hypomimia. L-Dopa was used still
but also antibiotic therapy. Spinal fluid findings were discussed at
length as well as the loss of involuntary movements and hyperhydrosis.
Muscle reflexes showed cloniform Achilles tendon reflex in one and
reduced arm swing in another.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ti Touko 29, 2012 18:11

Tapausselostus Australiasta.

72-vuotiaalla miehellä Parkinson oireet yli 10v. Potilas joutui vatsavaivojen vuoksi sairaalaan jossa aloitettiin suonensisäinen antibioottihoito (metronidatsoli, keftriaksoni). Potilaan vuosia kestäneet Parkinson oireet hävisivät silloin äkillisesti. Potilas kykeni kääntymään vuoteessa, seisomaan yhdellä jalalla, puhumaan normaalilla äänellä ja kirjoittamaan sujuvasti.

Oireet palasivat vähitellen kun antibiootti lopetettiin. Suun kautta otetulla antibioottihoidolla ei saatu yhtä hyvää hoitovastetta.

This is a case report which describes a dramatic switch-like reversal of PD symptoms with short IV antibiotic usage.

In early 2011 following a hernia repair, a 72 year old male with Parkinson?s disease (PD) developed abdominal adhesions / obstruction with increasing diarrhoea, abdominal swelling and cramping, raised temperature and severe vomiting. Neither food nor medications would remain down. After five days (Day 5) he eventually presented to hospital (in the evening).

Background: PD>10 years with rigidity, bradykinesia, balance instability, mask face.

Grew up on a dairy farm in the Brisbane area with multiple tick bites, and worked in India, Canada, America, New Zealand and England exposing him to a plethora of pathogens.

Medications: levodopa100+carbidopa25 -2daily, levodopa100+benserazide25 -1daily, pramipexoleER 1.5g -1daily, esomeprazole 20mg daily, pravastatin 40mg daily, aspirin 100mg daily, atenolol 25mg daily).


Medications in hospital (Day 5 and 6): (NilByMouth) N.Saline infusion, IV hyoscine butylbromide 40mg ondansetron wafer (SL) 4mg (given twice, 8hrs apart), 30ml antacid via a nasogastric tube up to qid then IV esomeprazole 40mg daily (PPI) and IV metoclopramide 500mg.

Day 6 (afternoon): IV metronidazole 500mg TDS and IV ceftriaxone 1G BD were commenced (for 3 days) in preparation for abdominal surgery. Approximately 8 hours after commencing (at 2am and after only two doses of metronidazole and one dose of ceftriaxone), most of his PD symptoms disappeared. He was able to turn himself in bed, balance on one foot, speak with a normal tone of voice and write fluently. He was ?on top of the world?.

Day 8: Laparoscopic surgery and bowel adhesion division. Day 9: Discharge

The patient remained PD symptom free for 10 days. PD symptoms then gradually returned (heralded by small right hand tremor which he never had previously) over the next 3 months and where PD medication was conservatively reintroduced and eventually reinstated to previous levels.


In early 2012, an antibiotic regime was commenced to attempt to cause sustained PD symptom reversal. It included oral medications: metronidazole 200mg morning and night, vancomycin 500mg morning and night, rifaximin 500mg morning and night and colchicine 500mcg twice a day, (increasing to 1g three in week 8). Reversal of PD symptoms again occurred but more gradually.

Week 8: improvements plateaued. Over weeks 10-11. PD symptoms returned with additional tremor. (Normal PD medications have continued throughout.)

Week 12 (this week): Will recommence IV metronidaloze (500mg tds) and IV ceftriaxone (1G BD)
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ViestiKirjoittaja soijuv » Ti Touko 29, 2012 19:45

59v mies oli saanut vuosien aikana lukuisia punkinpuremia. Mies sai Parkinson oireet, extrapyramidaalioireet - ei muita oireita. Hän sai antibioottihoidon. Oireet paranivat. Kuukausien kuluttua oireet kuitenkin palasivat vähitellen.


Title Neuroborreliosis with extrapyramidal symptoms: a case report.

Author(s) Biesiada G, Czapiel J, Sobczyk-Krupiarz I, Garlicki A, Mach T
Institution Department of Infectious Diseases, Division of Gastroenterology, Hepatology, and Infectious Diseases, Jagiellonian University School of Medicine, Kraków, Poland. gbiesiada@op.pl
Source Pol Arch Med Wewn 2008 May; 118(5):314-7.
MeSH Anti-Bacterial Agents
Basal Ganglia Diseases
Borrelia burgdorferi
Humans
Lyme Neuroborreliosis
Male
Middle Aged

Abstract The disease of Lyme is a tick-borne infection. It involves skin, the nervous system, joints and the heart. Spirochaeta Borrelia burgdorferi is the etiologic agent of the disease. In the majority of cases, clinical symptoms, like migrating erythema, occur from 3 to 30 days, sometimes to 3 months after a bite from a tick.

The early disseminated infection involves multiple migrating erythema, neuroborreliosis, arthritis, myocarditis and other organ-related symptoms. The late stage of chronic infection involves chronic atrophic leg dermatitis, neurological and rheumatological symptoms, and other organ-related symptoms which persist for above 12 months. The diagnosis of the disease of Lyme is based upon specific clinical symptoms confirmed by serologic tests. The two-step diagnostic protocol including the ELISA method, confirmed by the Western-blot test, is optimal.


The present article describes a case of a 59-year-old man, a computer specialist, who often spends his free time walking in woods for recreation, and who was bitten by a tick 3 years before hospitalization. The bite resulted in migrating erythema that subsided without antimicrobial treatment. In spite of this, the man had not changed his hobby exposing himself to bites from ticks.

One year later, multiple migrating erythema and extrapyramidalis symptoms appeared without any other organ malfunctions. In the current year, the patient was admitted to the Infectious Diseases Hospital, and received antibiotics (ceftriaxon) with following neurological improvement. Several months later, extrapyramidal symptoms increased. On the day of admission to the hospital, the neurologic examination showed abnormalities of upper and lower limbs movements (propulsive walking and the right lower leg traction), the right hand tremor, pouts of the face, and sleepiness.

Language eng
Pub Type(s) Case Reports
Journal Article
PubMed ID 18619183
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ViestiKirjoittaja soijuv » Ti Touko 29, 2012 19:55

2004. Antibiootista toivoa Parkinsonin taudin hoitoon.

Lepran ja tuberkuloosin hoidoissa yleisesti käytetty antibiootti, rifampisiini, esti laboratorio-olosuhteissa Parkinsonin taudissa esiintyviä aivosolukuolemia. Antibiootti myös liuotti jo syntyneitä proteiini fibrillejä. Jatkotutkimuksia on suunnitteilla.

http://news.bbc.co.uk/2/hi/health/4051951.stm

Antibiotic hope for Parkinson's

Pills

Could a simple pill ward off Parkinson's?

An antibiotic used to treat leprosy and tuberculosis is showing promise as a therapy for Parkinson's disease.

In laboratory tests, rifampicin was found to prevent the formation of protein fibrils associated with the death of brain cells in Parkinson's.

Researchers from the University of California, Santa Cruz, also found the drug dissolved existing fibrils.

The research, which is still at an early stage, is published in the journal Chemistry and Biology.


If it works in people, that would really open up the possibility of stopping the progression of Parkinson's disease when it is first diagnosed.
Professor Anthony Fink
The researchers studied the effects of rifampicin in test-tube experiments and are currently doing studies with cell cultures and mice to see if the same effects occur in living cells.

Researcher Professor Anthony Fink said: "Clearly more work is needed to determine if this would work therapeutically, but if it does it would probably be most useful as a prophylactic therapy used in the early stages of the disease, before there is general neurological damage.

"The disaggregation of existing fibrils is probably the most interesting and novel finding in this study.

"If it works in people, that would really open up the possibility of stopping the progression of Parkinson's disease when it is first diagnosed."

Parkinson's is a progressive movement disorder resulting from the death of nerve cells in the brain which produce a key chemical called dopamine.

Toxic clumps

It is thought a critical step in the development of the condition is the collection of a protein, known as alpha-synuclein, into insoluble fibrils.

Certainly, deposits called Lewy bodies, composed mostly of alpha-synuclein fibrils, appear in affected nerve cells.

Some people believe the fibrils themselves are toxic and cause brain cells to die, others that the toxic agents are smaller component parts formed earlier in the process.
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2006. Finkin tutkijaryhmä etsii rifambisiinia haitattomampaa hoitovaihtoehtoa.

2006-08-01. A. An Antibiotic Shows Promise in Fighting Parkinson's Disease

http://www.ucop.edu/sciencetoday/article/2747

Narrator: This is Science Today. An antibiotic that's long been used to treat tuberculosis and leprosy has shown promise fighting Parkinson's disease in lab tests. Tony Fink, a professor of chemistry and biochemistry at the University of California, Santa Cruz, says the drug, called rifampacin, prevented the formation of protein fibrils associated with the death of brain cells that occur in Parkinson's disease.

Fink: We're interested in finding compounds that may be potentially effective as therapeutic agents as drugs to combat the disease. It's believed that one of the key steps in Parkinson's disease, in its development, is the formation of fibrils by a protein called alpha synuclein.

Narrator: In lab tests, Fink's group found that rifampicin stabilized alpha synuclein.

Fink: This is very basic research. In one sense, the purpose would be to allow us to develop new, potential drugs. Rifampicin itself has some drawbacks, so we're actively looking at other related compounds that may be more effective.

Narrator: For Science Today, I'm Larissa Branin.
Previous research has found that rifampicin may also prevent the formation of the protein deposits associated with Alzheimer's disease.

The Parkinson's Disease Society welcomed the research as "very interesting".

Spokesman Robert Meadowcroft said: "The findings by the researchers studying the effects of rifampicin are currently at a very early stage but do seem quite positive.

"However, it is important to remember that more work in the lab is needed to determine how much real potential there is for rifampicin as a drug in the prevention of Parkinson's.

"If all goes well after further tests have been completed, including using animal models, then we could be looking at the possibility of patient trials in the future."
---------------------------------------------------------------------------
Valitettavasti Finkin tutkimustyö jäi kesken sillä hän kuoli v 2008 sairastettuaan vuoden ajan.

http://www.chem.ucsc.edu/faculty/fink.html


Remembering UCSC Professor Tony Fink
Tony Fink, UCSC's distinguished Professor of Chemistry and Biochemistry, passed away on March 3, 2008, following a year-long illness.

During Tony's forty-year career in academia, he made many contributions to the field of biophysical chemistry. With more than 200 scientific publications, 20 book chapters, and three books, he was a world authority on protein folding.

Mistakes in this molecular process lead to degenerative diseases such as Parkinson's, Alzheimer's, and bovine spongiform encephalopathy, or mad-cow disease. Tony's research was to understand what goes wrong and to design treatments to repair the damage or prevent it from happening. He worked tirelessly towards the goal of designing potential drugs and therapeutic methods to combat Parkinson's and Alzheimer's diseases. Tony was elected to the American Association for the Advancement of Sciences in 2004, won the BioSTAR Outreach Ambassador of the Year Award in 2002, as well as the Division of Physical & Biological Sciences' Outstanding Faculty Award in 2007.
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ViestiKirjoittaja soijuv » Ke Touko 30, 2012 04:16

2010. Antibioottien vaikutusta liikeratasairauksiin, kuten Parkinson ja dystonia, tutkitaan edelleen. Nyt tutkimuksissa havaittiin antibiootti ampisilliinin parantavan laboratoriotestiolosuhteissa solujen toimintaa.

Movement Disorder Symptoms Are Lessened by an Antibiotic: Treating Worms With Ampicillin Helps Restore Normal Movement

ScienceDaily (Mar. 10, 2010) ? Discovery of an antibiotic's capacity to improve cell function in laboratory tests is providing movement disorder researchers with leads to more desirable molecules with potentially similar traits, according to University of Alabama scientists co-authoring a paper publishing March 10 in the journal Disease Models & Mechanisms.

"It's our hope that this discovery serves as the impetus for a proper clinical trial to evaluate the potential of drugs like ampicillin for early-onset torsion dystonia," said Dr. Guy Caldwell, associate professor of biological sciences at The University of Alabama. Dystonia is, like Parkinson's disease, a movement disorder. Combined, this class of diseases affects millions worldwide. People with early-onset dystonia have one good copy of the gene DYT1, and one problematic copy, in their DNA. These genes contain the information to make a protein called torsinA.

"When proteins go bad, they often cause disease, but they always have a normal function in our cells," Guy Caldwell said. "We looked to find molecules -- not necessarily that reversed the mutated form of the protein -- but instead enhanced the normal activity of the protein, thereby overcoming the deficiency caused by the mutant."

The UA researchers discovered that ampicillin, a common antibiotic of the penicillin group, serves to activate torsinA, which, in its normal form, appears to protect cells from stresses, such as protein misfolding -- a problem known to impact various movement disorders.

Using a nematode animal model designed to evaluate torsinA activity, the UA lab rapidly screened through hundreds of compounds to identify those that were most effective at enhancing torsinA's normally protective function.

"From there, we collaborated with researchers at Harvard and UAB to validate our findings in human patient cells and mice," said Dr. Kim Caldwell, associate professor of biological sciences at UA.

"In human dystonia patient cells, ampicillin was efficacious and restored the patient cells back to the normal function," Kim Caldwell said. "And, the drug restored normal movement to mice that were genetic mimics of dystonia."

Collaborators in the UA-led study were Drs. Xandra O. Breakefield and her colleagues at Harvard and Yuqing Li and his colleagues at The University of Alabama at Birmingham, known as UAB. Dr. Songsong Cao, a former doctoral student in the Caldwell Lab, is the study's lead author; two UA doctoral students, Alexander J. Burdette and Pan Chen; and one former UA student, Amber Clark Buckley, are among the co-authors.

Furthermore, the research shows ampicillin enhances the capacity of torsinA to protect, within animal models, the neurons which produce dopamine from dying. The death of these neurons in human brains leads to the hallmark symptoms of Parkinson's disease.

In a statement accompanying the paper, the researchers caution against the long-term use of an antibiotic in disease treatment.

"We have taken ampicillin and used that as a base structure to find things that work like ampicillin but which aren't ampicillin," Guy Caldwell said. "Finding molecules that are not antibiotic and still have the capacity to activate torsinA has been an ongoing effort of our lab, and we have some exciting leads in that direction."

UA filed patents covering the use of antibiotics and other novel chemicals as activators of torsinA for treatment of dystonia and other diseases, including Parkinson's disease. The University has also entered into a collaborative research and licensing agreement with QRxPharma, a clinical stage pharmaceutical company, to identify, develop and commercially exploit new torsinA activator drugs.

The UA/QRxPharma research program is directed at re-engineering existing drug therapies for new clinical applications and identifying new drug candidates for uses including the treatment of dystonia, Parkinson's disease and other neurological disorders.

The project exemplifies, the researchers said, how disease model systems can be used to accelerate the development of gene and drug discovery and bring pharmaceuticals more quickly to the clinical trial stage.

Bringing a drug that does not already have FDA approval from the research and development stage to a patient takes an estimated 12 years and $800 million dollars, said Kim Caldwell. By evaluating the potential of molecules already pre-screened for toxicity and that have FDA approval provides a potentially quicker route to clinical trials.

"What we were hoping to do was circumvent a lot of the cost in bringing pharmaceutical help to dystonia patients," Kim Caldwell said.

The research was supported by the Bachmann-Strauss Dystonia and Parkinson Foundation, Dystonia Medical Research Foundation, the Jack Fasciana Fund for Dystonia Research and the National Institutes of Health.
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ViestiKirjoittaja soijuv » Ke Touko 30, 2012 04:48

2008. Antibiootti minosykliini ja kreatiniini , näyttivät tutkimuksessa hidastavan Parkinsonin taudin etenemistä.

http://www.msnbc.msn.com/id/11516953/#.T8V6-FIRk90

An antibiotic and a muscle-related compound are leading candidates for a major government study of whether certain compounds could slow the worsening of Parkinson?s disease.

A pilot study, unveiled Thursday, suggests the two ? the antibiotic minocycline and creatine, a substance produced in muscle tissue ? may have some benefit.

?We are not concluding that these agents are useful, just that they are not useless,? cautioned Dr. Karl Kieburtz of the University of Rochester, who led the study.

It?s far too early for patients to seek the pills, stressed Dr. Diane Murphy, who oversees Parkinson?s research at the National Institutes of Health, which funded the work.

But in the study of 200 patients in the earliest stages of the disease?they didn?t yet require medication for its symptoms?those who took either of the two pills didn?t seem to decline quite as rapidly as those given a dummy pill, scientists said Thursday at Parkinson?s meeting in Washington.

The compounds are thought to lessen a type of cellular stress or fight inflammation that may damage cells.

About 1.5 million Americans have Parkinson?s disease, which gradually destroys brain cells that produce dopamine, a chemical crucial for the cellular communication that controls muscle movement. As dopamine levels drop, symptoms increase: tremors in the arms, legs and face; periodically stiff or frozen limbs; slow movement; impaired balance and coordination.
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Standard treatments are to replace lost dopamine with the drug levodopa, and a brain implant to control tremors. Both work for a while, but can?t stop the disease?s inevitable march.

So NIH?s National Institute of Neurological Disorders and Stroke is on a hunt for drugs that might protect patients? remaining dopamine-producing cells, a so-called neuroprotector. The holy grail would be a simple, easy-to-take pill that would lower the risk of worsening Parkinson?s much like an aspirin a day can lower people?s risk of heart attacks.

?We?re looking for the aspirin of Parkinson?s disease,? is how Murphy puts it. ?We don?t have a drug like that right now, and we don?t know of such a drug,? she cautions.

That?s where the pilot study comes in. NIH asked Parkinson?s specialists for a list of potential neuroprotective compounds ? substances that could enter the brain and seemed promising in animal studies. From an initial list of 60, they settled on four to pilot-test. The minocycline and creatine results are first in, published in the journal Neurology online this week and announced Thursday at the World Parkinson Congress. Now being analyzed is a similar study on the dietary supplement coenzyme Q-10 or CoQ10 and an experimental drug thought to help repair damaged nerves.

Next up, NIH plans to test the top candidates in a large study to prove whether any of them truly work.

Minocycline is a prescription-only antibiotic, but creatine is available in dietary supplements. Murphy cautioned that over-the-counter preparations of creatine or CoQ10 may not be the same strengths as are under study.
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ViestiKirjoittaja soijuv » Ke Touko 30, 2012 13:09

Yhden henkilön kokemus. Miehellä 20v Parkinson. Bentlylle aloitettiin helikobakteeriin antibioottihoito. 3vrk:n kuluttua hoidon aloituksesta hänen Parkinson oireensa alkoivat vähetä merkittävästi; hän hymyilee, kääntyy vuoteessa, nostaa päätään jne.

http://health.groups.yahoo.com/group/in ... ssage/2319

Dear Friends,

It has been a long journey on our quest for healing Bentley from both Parkinsons and Stroke. Bentley is 81 years old, has been diagnosed with Parkinsons for 20 years and has been living with left side paralysis from a failed double sided DBS procedure since May 2004. We have looked at many different treatment options and have used several for years with some success.

Over the past few weeks we began a journey that we hope will help us truly stop the source of Bentley's Parkinson's. As I mentioned in past emails, a friend of ours brought Dr. Borody to our attention. He is the Nobel prize winning researcher and physician that discovered that H Pylori was the cause of some ulcers and could be treated with antibiotics. We tested Bentley for H Pylori and he was positive. He went through a 10 day treatment and within the first 72 hours had incredible improvement in his Parkinson's symptoms. Then it stopped and he stayed about the same. It has been a week since he finished the medication and he is retaining the gains he made to some degree but with less energy. Here is what we has happened for Ben. I have video which I will find a way to attach.

Within 24 hours he could roll over in bed, lift his head and smile on both sides of his mouth. This is very important because he did this with no Sinemet first thing in the morning. He also could not smile on both sides without using hyperbaric oxygen for several months regularly. I always thought it was the stroke, but it must have been also the PD.

Could easily point and flex his right foot.
Could smile, open his mouth wide and stick out his tongue.
Could control his right arm to feed himself.
Could look up.
Eyes wide open.
Very alert and awake all day.

It seemed like a miracle that he could do these things so immediately after starting treatment. This makes us believe that maybe this doctor is right and Parkinsons may start from a bacteria and can possibly be treated with antibiotics.

We are now getting another appointment with our GP to have Bentley tested for C Dif. They can isolate the bacteria and treat. Some people need multiple courses of antibiotics and some eventually need the feacal implant to restore the good flora. When you read about C Dif it will say that a patient has persistent diarrhea, but you can also have constipation or no apparent symptom at all. Bentley does suffer from severe constipation, so it will make it easier to get him tested and treated.

If you or your loved one does not have symptoms, you may still want to find a way to get tested for C Dif.

I will be posting more information on this subject over the next few days. They are starting a trial very soon in Australia specifically for Parkinsons and treating for bacteria. They have already had success with at least one patient.

What we have seen with Bentley makes us believe that this is definitely worth trying. We will keep you updated on the testing and treatment as soon as we get started.
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Re: BORRELIOOSI/PARKINSONIN TAUTI

ViestiKirjoittaja soijuv » To Huhti 10, 2014 21:19

bakteeri- ja virusinfektioiden merkitys neurologisissa sairauksissa kuten Alzheimer, Parkinson, MS jne.
[/b]

http://www.bjmp.org/content/role-chroni ... hiatric-au

Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1

Garth L. Nicolson and Jörg Haier
Cite this article as: BJMP 2009:2(4) 20-28
Download PDF


Abstract

Chronically ill patients with neurodegenerative, neurobehavioral and psychiatric diseases commonly have systemic and central nervous system bacterial and viral infections. In addition, other chronic illnesses where neurological manifestations are routinely found, such as fatiguing and autoimmune diseases, Lyme disease and Gulf War illnesses, also show systemic bacterial and viral infections that could be important in disease inception and progression or in increasing the number and severity of signs and symptoms. Evidence of Mycoplasma species, Chlamydia pneumoniae, Borrelia burgdorferi, human herpesvirus-1, -6 and -7 and other bacterial and viral infections revealed high infection rates in the above illnesses that were not found in controls. Although the specific roles of chronic infections in various diseases and their pathogeneses have not been carefully determined, the data suggest that chronic bacterial and/or viral infections are common features of progressive chronic diseases.
Abbreviations: Ab beta amyloid; AD Alzheimer’s disease; ADHD attention-deficit/hyperactivity disorder; ALS amyotrophic lateral sclerosis; ASD autism spectrum disorders; EBV Epstein-Barr virus; CFS chronic fatigue syndrome; CFS/ME chronic fatigue syndrome/myalgic encephalomyopathy; CI confidence interval; CMV cytomegalovirus; CSF cerebrospinal fluid; CNS central nervous system; ELISA enzyme linked immunoabsorbant assay; GWI Gulf War illnesses; HHV human herpes virus; HSV herpes simplex virus; PCR polymerase chain reaction; PD Parkinson’s disease


Introduction

Chronic infections appear to be common features of various diseases, including neurodegenerative, psychiatric and neurobehavioral diseases, autoimmune diseases, fatiguing illnesses and other conditions.1-4 Neurodegenerative diseases, chronic degenerative diseases of the central nervous system (CNS) that cause dementia, are mainly diseases of the elderly. In contrast, neurobehavioral diseases are found mainly in younger patients and include autism spectrum disorders (ASD), such as autism, attention deficit disorder, Asperger’s syndrome and other disorders.5 For the most part, the causes of these neurological diseases remain largely unknown.2 Neurodegenerative diseases are characterized by molecular and genetic changes in nerve cells that result in nerve cell degeneration and ultimately nerve cell dysfunction and death, resulting in neurological signs and symptoms and dementia.2,3 On the other hand, neurobehavioral diseases are related to fetal brain development but are less well characterized at the cellular level and involve both genetic and environmental factors.6, 7 Even less well characterized at the cellular and genetic level are the psychiatric disorders, such as schizophrenia, paranoia, bipolar disorders, depression and obsessive-compulsive disorders.

Genetic linkages have been found in neurodegenerative and neurobehavioral diseases, but the genetic changes that occur and the changes in gene expression that have been found are complex and usually not directly related to simple genetic alterations.2, 6-8 In addition, it is thought that nutritional deficiencies, environmental toxins, heavy metals, chronic bacterial and viral infections, autoimmune immunological responses, vascular diseases, head trauma and accumulation of fluid in the brain, changes in neurotransmitter concentrations, among others, are involved in the pathogenesis of various neurodegenerative and neurobehavioral diseases.2, 3, 5-16 One of the biochemical changes found in essentially all neurological, neurodegenerative and neurobehavioral diseases is the over-expression of oxidative free radical compounds (oxidative stress) that cause lipid, protein and genetic structural changes.9-11 Such oxidative stress can be caused by a variety of environmental toxic insults, and when combined with genetic factors could result in pathogenic changes.14

Neurodegenerative diseases

Infectious agents are important factors in neurodegenerative and neurobehavioral diseases and may enter the brain within infected migratory macrophages. They may also gain access by transcytosis across the blood-brain-barrier or enter by intraneuronal transfer from peripheral nerves.15 Cell wall-deficient bacteria, such as species of Mycoplasma, Chlamydia (Chlamydophila), Borrelia and Brucella, among others, and various viruses are candidate brain infectious agents that may play important roles in neurodegenerative and neurobehavioral diseases.16-19 Such infections are systemic and can affect the immune system and essentially any organ system, resulting in a variety of systemic signs and symptoms.4, 15, 16, 19, 20

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is an adult-onset, idiopathic, progressive neurodegenerative disease that affects both central and peripheral motor neurons.21 Patients show gradual progressive weakness and paralysis of muscles due to destruction of upper motor neurons in the motor cortex and lower motor neurons in the brain stem and spinal cord. This ultimately results in death, usually by respiratory failure.21, 22 The overall clinical picture of ALS can vary, depending on the location and progression of pathological changes.23

The role of chronic infections has attracted attention with the finding of enterovirus sequences in a majority of ALS spinal cord samples by polymerase chain reaction (PCR).24 However, others have failed to detect enterovirus sequences in spinal cord samples from patients with or without ALS.25-26 In spite of the mixed findings on enterovirus, infectious agents that penetrate the CNS could play a role in the aetiology of ALS. Evidence for transmission of an infectious agent or transfer of an ALS-like disease from man-to-man or man-to-animals has not been found.27

Using PCR methods systemic mycoplasmal infections have been found in a high percentage of ALS patients.28, 29 We found that 100% of Gulf War veterans from three nations diagnosed with ALS had systemic mycoplasmal infections.28 All but one patient had M. fermentans, and one veteran from Australia had a systemic M. genitalium infection. In nonmilitary ALS patients systemic mycoplasmal infections of various species were found in approximately 80% of cases.28 Of the mycoplasma-positive civilian patients who were further tested for various species of Mycoplasma, most were positive for M. fermentans (59%), but other Mycoplasma species, such as M. hominis (31%) and M. pneumoniae infections (9%) were also present. Some of the ALS patients had multiple infections; however, multiple mycoplasmal infections were not found in the military patients with ALS.28 In another study 50% of ALS patients showed evidence of systemic Mycoplasma species by PCR analysis.29

ALS patients who live in certain areas often have infections of Borrelia burgdorferi, the principal aetiological agent in Lyme disease. For example, ALS patients who live in a Lyme-prevalent area were examined for B. burgdorferi infections, and over one-half were found to be seropositive for Borrelia compared to 10% of matched controls.30 In addition, some patients diagnosed with ALS were subsequently diagnosed with neuroborreliosis.31 Spirochetal forms have been observed in the brain tissue of ALS patients and in patients with other neurodegenerative diseases.32 In general, however, the incidence of Lyme infections in ALS patients is probably much lower. In one recent study on 414 ALS patients only about 6% showed serological evidence of Borrelia infections.33 Some Lyme Disease patients may progress to ALS, but this is probably only possible in patients who have the genetic susceptibility genes for ALS as well as other environmental toxic exposures.34, 35

Additional chronic infections have been found in ALS patients, including human herpes virus-6 (HHV-6), Chlamydia pneumoniae andother infections.36, 37 There is also a suggestion that retroviruses might be involved in ALS and other motorneuron diseases.38 McCormick et al.39 looked for reverse transcriptase activity in serum and cerebrospinal fluid of ALS and non-ALS patients and found reverse transcriptase activity in one-half of ALS serum samples tested but in only 7% of controls. Interestingly, only 4% of ALS cerebrospinal fluid samples contained reverse transcriptase activity.39

Although the exact cause of ALS remains to be determined, there are several hypotheses on its pathogenesis: (1) accumulation of glutamate causing excitotoxicity; (2) autoimmune reactions against motor neurons; (3) deficiency of nerve growth factor; (4) dysfunction of superoxide dismutase due to mutations; and (5) chronic infection(s).24, 27-40 None of these hypotheses have been ruled out or are exclusive, and ALS may have a complex pathogenesis involving multiple factors. 28, 36

It is tempting to propose that infections play an important role in the pathogenesis or progression of ALS.28, 40 Infections could be cofactors in ALS pathogenesis, or they could simply be opportunistic, causing morbidity in ALS patients. For example, infections could cause the respiratory and rheumatic symptoms and other problems that are often found in ALS patients. Since the patients with multiple infections were usually those with more rapidly progressive disease,28 infections likely promote disease progression. Indeed, when Corcia et al.41 examined the cause of death in 100 ALS patients, the main causes were broncho-pneumonia and pneumonia. Finally, there are a number of patients who have ALS-like signs and symptoms but fall short of diagnostic criteria. Although a careful study has not been attempted on these patients, there is an indication that they have the same infections as those found in patients with a full diagnosis of ALS (personal communication). Thus ALS-like diseases may represent a less progressive state, in that they may lack additional changes or exposures necessary for full ALS.

Multiple sclerosis

Multiple sclerosis (MS) is the most common demyelinating neurological disease. It can occur in young or older people and is a cyclic (relapsing-remitting) or progressive disease that continues progressing without remitting.42 Inflammation and the presence of autoimmune antibodies against myelin and other nerve cell antigens are thought to cause the myelin sheath to break down, resulting in decrease or loss of electrical impulses along the nerve fibers.42, 43 In the progressive subset of MS neurological damage occurs additionally by the deposition of plaques on the nerve cells to the point where nerve cell death occurs. In addition, breakdown of the blood-brain barrier in MS is associated with local inflammation caused by glial cells.42, 43 The clinical manifestations of demyelinization, plaque damage and blood-brain barrier disruptions cause variable symptoms, but they usually include impaired vision, alterations in motor, sensory and coordination systems and cognitive dysfunction.43

There is strong evidence for a genetic component in MS.44, 45 Although it has been established that there is a genetic susceptibility component to MS, epidemiological and twin studies suggest that MS is an acquired, rather than an inherited, disease.46

MS has been linked to chronic infection(s).46, 47 For example, patients show immunological and cytokine elevations consistent with chronic infections.48-50 An infectious cause for MS has been under examination for some time, and patients have been tested for various viral and bacterial infections. 44, 45,47, 48, 51 One of the most common findings in MS patients is the presence of C. pneumoniae antibodies and DNAin their cerebrospinal fluid.51-53 By examining relapsing-remitting and progressive MS patients for the presence of C. pneumoniae in cerebrospinal fluid by culture, PCR and immunoglobulin reactivity Sriram et al.52 were able to identify C. pneumoniae in 64% of MS cerebrospinal fluid versus 11% of patients with other neurological diseases. They also found high rates (97% positive) of PCR-positive MOMP gene in MS- patients versus 18% in other neurological diseases, and this correlated with 86% of MS patients being serology-positive patients by ELISA and Western blot analysis.52 Examination of MS patients for oligoclonal antibodies against C. pneumoniae revealed that 82% of MS patients were positive, whereas none of the control non-MS neurological patients had antibodies that were absorbed by C. pneumoniae elemental body antigens.53 Similarly, Contini et al.54 found that the DNA and RNA transcript levels in mononuclear cells and cerebrospinal fluid of 64.2% of MS patients but in only 3 controls.

Using immunohistochemistry Sriram et al.55 later examined formalin-fixed brain tissue from MS and non-MS neurological disease controls and found that in a subset of MS patients (35%) chlamydial antigens were localized to ependymal surfaces and periventricular regions. Staining was not found in brain tissue samples from other neurological diseases. Frozen tissues were available in some of these MS cases, and PCR amplification of C. pneumoniae genes was accomplished in 63% of brain tissue samples from MS patients but none in frozen brain tissues from other neurological diseases. In addition, using immuno-gold-labeled staining and electron microscopy they examined cerebrospinal fluid sediment for chlamydial antigens and found that the electron dense bodies resembling bacterial structures correlated with PCR-positive results in 91% of MS cases.55 They also used different nested PCR methods to examine additional C. pneumoniae gene sequences in the cerebrospinal fluid of 72 MS patients and linked these results to MS-associated lesions seen by MRI.56

MRI was used by Grimaldi et al.57 to link the presence of C. pneumoniae infection with abnormal MRI results and found linkage in 21% of MS patients. These turned out to be MS patients with more progressive disease.58 In addition, higher rates of C. pneumoniae transcription were found by Dong-Si et al.58 in the cerebrospinal fluid of 84 MS patients. The data above and other studies strongly support the presence of C. pneumoniae in the brains of MS patients,59-61 at least in the more progressed subset of MS patients.

Other research groups have also found evidence for C. pneumoniae in MS patients but at lower incidence. Fainardi et al.62 used ELISA techniques and found that high-affinity antibodies against C. pneumoniae were present in the cerebrospinal fluid of 17% of MS cases compared to 2% of patients with non-inflammatory neurological disorders. They found that the majority of the progressive forms of MS were positive compared to patients with remitting-relapsing MS. The presence of C. pneumoniae antibodies was also found in other inflammatory neurological disorders; thus it was not found to be specific for MS.62

In contrast to the studies above, other researchers have not found the presence of C. pneumoniaeor other bacteriain the brains of MS patients.63-65 For example, Hammerschlag et al.66 used nested PCR and culture to examine frozen brain samples from MS patients but could not find any evidence for C. pneumoniae. However, in one study C. pneumoniae was found at similar incidence in MS and other neurological diseases, but only MS patients had C. pneumoniae in their cerebrospinal fluid.64 Swanborg et al.67 reviewed the evidence linking C. pneumoniae infection with MS and concluded that it is equivocal, and they also speculated that specific genetic changes may be necessary to fulfill the role of such infections in the aetiology of MS.

Another possible reason for the equivocal evidence linking MS with infections, such as C. pneumoniae, is that multiple co-infections could be involved rather than one specific infection. In addition to C. pneumoniae found in most studies, MS patients could also have Mycoplasma species, B. burgdorferi and other bacterial infections as well as viral infections.68 When multiple infections are considered, it is likely that >90% of MS patients have obligate intracellular bacterial infections caused by Chlamydia (Chlamydophila), Mycoplasma, Borrelia or other intracellular bacterial infections. These infections were found only singly and at very low incidence in age-matched subjects.68 In spite of these findings, others did not find evidence of Mycoplasma species in MS brain tissue, cerebrospinal fluid or peripheral blood.69

Viruses have also been found in MS. For example, HHV-6 has been found at higher frequencies in MS patients, but this virus has also been found at lower incidence in control samples.70 Using PCR Sanders et al.70 examined postmortem brain tissue and controls for the presence of various neurotrophic viruses. They found that 57% of MS cases and 43% of non-MS neurological disease controls were positive for HHV-6, whereas 37% and 28%, respectively, were positive for herpes simplex virus (HSV-1 and -2) and 43% and 32%, respectively, were positive for varicella zoster virus. However, these differences did not achieve statistical significance, and the authors concluded “an etiologic association to the MS disease process [is] uncertain.” They also found that 32% of the MS active plaques and 17% of the inactive plaque areas were positive for HHV-6.70 Using sequence difference analysis and PCR Challoner et al.71 searched for pathogens in MS brain specimens. They found that >70% of the MS specimens were positive for infection-associated sequences. They also used immunocytochemistry and found staining around MS plaques more frequently than around white matter. Nuclear staining of oligodendrocytes was also seen in MS samples but not in controls.71 Using immunofluorescent and PCR methods HHV-6 DNA has also been found in peripheral leukocytes in the systemic circulation of MS patients.72, 73 However, using PCR methods, others did not found herpes viruses in the peripheral blood or CSF of MS patients.74, 75 Evidence that prior infection with EBV could be related to the development of MS was proposed; however, EBV infects more than 90% of humans without evidence of health problems and 99% of MS patients.76 The difference in MS patients could be the presence of multiple infections, including EBV. Recently Willis et al.77 used multiple molecular techniques to examine MS tissue but failed to find EBV in any MS tissues but could find EBV in CNS lymphomas.

Current reviews and the information above points to an infectious process in MS.47, 48, 75, 76, 78-80 Although a few studies did not come to this conclusion,74, 75 most studies have found infections in MS patients. It is interesting that it is the progressive rather than relapsing-remitting forms of MS which have been associated with chronic infections; therefore, infections might be more important in MS progression than in its inception. Various infections may also nonspecifically stimulate the immune system.47, 48 Infections may also invade immune cells and alter immune cell function in a way that promotes inflammation and autoimmune activity.78 If infections like C. pneumoniae and Mycoplasma species are important in MS, then antibiotics effective against these infections should improve clinical status. Although preliminary, that is in fact what has been seen, but not in all patients.81 As in other neurodegenerative diseases, multiple factors appear to be involved in the pathogenesis of MS.

Alzheimer’s disease

Alzheimer’s Disease (AD) is a family of brain disorders usually found in elderly patients and is the most common cause of dementia. AD is characterized by slow, progressive loss of brain function, notable lapses in memory, disorientation, confusion, mood swings, changes in personality, language problems, such as difficulty in finding the right words for everyday objects, loss of behavioral inhibitions and motivation and paranoia. The course of AD varies widely, and the duration of illness can range from a few years to over 20 years. During this period the parts of the brain that control memory and thinking are among the first affected, followed by other brain changes that ultimately result in brain cell death.82

AD is characterized by distinct neuropathological changes in brain tissues and cells. Among the most notable are the appearance of plaques and tangles of neurofibrils within brain nerve cells that affect synapses and nerve-nerve cell communication. These structural alterations involve the deposition of altered amyloid proteins.83, 84 Although the cause of AD is not known, the formation of the amyloid plaques and neurofibrillary tangles may be due to genetic defects and resulting changes in the structure of beta amyloid proteins. This in turn may be caused by chemicals or other toxic events, inflammatory responses, excess oxidative stress and increases in reactive oxygen species, loss of nerve trophic factors and reductions in nerve cell transmission.83-87

Recently AD brain infections have become important.88-90 For example, one pathogen that has attracted considerable attention is C. pneumoniae.91, 92 As mentioned above, this intracellular bacterium has a tropism for neural tissue, and it has been found at high incidence in the brains of AD patients by PCR and immunohistochemistry.92 C. pneumoniae has also been found in nerve cells in close proximity to neurofibrillary tangles.92, 93 Similarly to Mycoplasma species, C. pneumoniae can invade endothelial cells and promote the transmigration of monocytes through human brain endothelial cells into the brain parenchyma.94 C. pneumoniae has been found in the brains of most AD patients,91 and it has been cultured from AD brain tissue.95 Injection of C. pneumoniae into mice stimulates beta amyloid plaque formation.96 Although the data are compelling, some investigators have not found C. pneumoniae infections in AD.97, 98

AD patients also have other bacterial infections, such as B. burgdorferi.99 Using serology, culture, Western blot and immunofluorenscence methods this Lyme Disease infection has been examined in AD.100, 101 Not all researchers, however, have found evidence of B. burgdorferi in AD patients.102, 103 The presence of intracellular infections like B. burgdorferi in AD patients has been proposed to be a primary event in the formation of AD beta amyloid plaques. This is thought to occur by the formation of “congophilic cores” that attract beta amyloid materials.104 Multiple reports indicate that AD nerve cells are often positive for B. burgdorferi, indicating that this intracellular bacteria could be important in the pathogenesis of AD.99, 100, 104, 105

The hypothesis in AD that intracellular microorganisms could provide “cores” for the attraction of beta amyloid materials is appealing, but other factors, including the induction of reactive oxygen species, lipid peroxidation and the breakdown of the lysosomal membranes releasing lysosomal hydrolases, are also thought to be important in beta amyloid deposition.105 That infections may be important in AD pathogenesis is attractive; however, some negative reports have not confirmed the presence of infections like B. burgdorferi in AD patients.99-101 This suggests that the infection theory, although compelling, remains controversial.102, 105

Herpes virus infections have also been found in AD,especially HSV-1.106, 107 Previously it was determined that HSV-1 but not a related neurotrophic virus (varicella zoster virus) is present more often in AD brains, and this could be linked to AD patients who have the risk factor ApoE e4 allele.108, 109 HSV-1 is thought to be involved in the abnormal aggregation of beta amyloid fragments within the AD brain by reducing the amount of full-length beta amyloid precursor protein and increasing the amounts of their fragments.110 HSV-1 infection of glial and neuronal cells results in a dramatic increase in the intracellular levels of beta amyloid forms, whereas the levels of native beta amyloid precursor protein are decreased.111 This is similar to what has been found in mice infected with HSV-1, indicating that HSV-1 is probably involved directly in the development of senile-associated plaques. Another herpes virus, HHV-6, has also been found in AD patients, but it is thought that this virus is not directly involved in AD pathogenesis. HHV-6 may exacerbate the effects of HSV-1 in AD ApoE e4 carriers.112

Other infections have been found in AD patients, for example, C. pneumoniae, Helicobacter pylori amongst others.113 It has been proposed that such infections may act as a trigger or co-factor in AD.114 Although experimental evidence that pathogens can elicit the neuropathological changes and cognitive deficits that characterize AD is lacking, this approach may yield interesting and important results. These authors also stressed that systemic infections must be considered as potential contributors to the pathogenesis of AD.114

Parkinson’s disease

Parkinson’s disease (PD) is characterized by akinesia, muscular rigidity and resting tremor.103 In addition, autonomic dysfunction, olfactory disturbances, depression, sensory and sleep disturbances and frequently dementia characterize this disease.115 The pathology of PD indicates a progressive loss of the dopamine neurons of the substantia nigra together with the presence of Lewy bodies and alpha-synuclein. More extensive brain degeneration also occurs, from the medulla oblongata to the cerebral cortex.116, 117

Age-related inclusion bodies and protein aggregations or defects in their degradation characteristically occur in PD, but their role in PD pathogenesis remains unclear.117, 118 Some evidence suggests a relationship between PD and specific genetic changes, such as changes in the genes affecting mitochondria, protein degradation, organelle trafficking and vesicular fusion, and in proteins involved in oxidative stress or antioxidant function.102 Inflammation has also been associated with PD pathology.119

The pathogenesis of PD has been proposed to be due to multiple genetic and neurotoxic events that produce oxidative damage and cell death. In the case of PD the relevant targets of toxic events are neuromelanin-containing dopaminergic neurons of the substantia nigra.118, 120 A case-control study indicated that multiple environmental factors and genetic background were statistically related risk factors for PD.121 Prominent among these were long-term toxic exposures and trauma early in life.122 For example,early life exposure to brain injury, chemicals and/or infections may initiate a cyclic inflammatory process involving oxidative damage, excitotoxicity, mitochondrial dysfunction and altered proteolysis that later in life results in substantia nigra neuron death.123, 124

A role for chronic infections in PD pathogenesis has been proposed.123, 124 One infection found in PD that has aroused considerable interest is the presence of chronic gastrointestinal Helicobacter pylori.125 Indeed, treatment of this infection offers relief to late stage cachexia in PD patients receiving L-dopa.126 Helicobacter pylori-infected PD patients showed reduced L-dopa absorption and increased clinical disability,127 whereas treatment of this infection increased L-dopa absorption and decreased clinical disability.128 H. pylori may not be directly involved in the pathogenesis of PD, but its systemic presence could affect the progression and treatment of PD, probably by stimulating inflammation and autoimmunity.128

Chronic infections in PD have been linked to inflammation and autoimmune responses.129-131 Experimental models of PD have been developed using neurological viral or bacterial infections to initiate the pathogenic process.132, 133 Spirochetes have also been found in Lewy bodies of PD patients.30 Other infections, such as viral encephalitis,134 AIDS-associated opportunistic infections of the basal ganglia,135 coronavirus,136 among other infections,68, 137, 138 have been found in PD and could be important in stimulating inflammation and autoimmune responses. It has been stressed that additional research will be necessary to establish whether a causal link exists between PD and chronic infections.139

Neurobehavioral diseases

Autism spectrum disorders

ASD, such as autism, Asperger’s syndrome, etc., are neurobehavioral diseases of primarily the young where patients generally suffer from an inability to communicate properly, form relationships with others and respond appropriately to their environment. Such patients do not all share the same signs and symptoms but tend to share certain social, communication, motor and sensory problems that affect their behavior in predictable ways. These patients often display repetitive actions and develop troublesome fixations with specific objects, and they are often painfully sensitive to certain sounds, tastes and smells.140, 141

ASD cases are likely to be caused by multiple factors, including genetic defects, heavy metal, chemical and biological exposures, among other important events, which are probably different in each patient. ASD patients appear to have similarities in genetic defects and environmental exposures that are important in patient morbidity or in illness progression.5-8, 140-142

Chronic infections appear to be an important element in the development of ASD.6, 16, 143, 144 In ASD patients more than 50 different bacterial, viral and fungal infections have been found,6 some apparently more important than others in causing symptoms. It has been known for some time that ASD patients have a number of nonspecific chronic signs and symptoms, such as fatigue, headaches, gastrointestinal, vision problems, occasional intermittent low-grade fevers and other signs and symptoms that are generally excluded in the diagnosis of ASD but are consistent with the presence of infections.143 Indeed, increased titres to various viruses as well as bacterial and fungal infections have been commonly seen in ASD patients.6, 16, 19, 143-145 Not withstanding these reports, epidemiological evidence for an association of childhood infections in the first two years of life and ASD has been mixed.146

Environmental exposures to chemicals and heavy metals also appear to be important in the development of ASD.140, 141, 147, 148 The relationship between ASD and heavy metals may involve the role of multiple vaccines in ASD pathogenesis.130, 141 ASD patients often show their first signs and symptoms after multiple childhood immunizations, and the sharp increase in Autism rates occurred only after the multiple MMR vaccine came into widespread use.141 In some states in the U.S. children receive as many as 33 vaccines before they can enroll in school.140 Such vaccines can contain mercury and other toxic preservatives, and some may also contain contaminating bacteria, as found in veterinary vaccines.149

There are very few studies that have followed the transmission of infections and subsequent autism. Previously we found that veterans of the Gulf War with chronic fatiguing illnesses (Gulf War illnesses, GWI) exhibited multiple nonspecific signs and symptoms similar to chronic fatigue syndrome/myalgic encephalomyopathy (CFS/ME).150, 151 After returning to the home with GWI, their children subsequently became symptomatic, and these children were often diagnosed with ASD.152, 153 Symptomatic children (mostly diagnosed with ASD) were infected with the same Mycoplasma species, M. fermentans, that was found in the veterans and their symptomatic family members, and this was not seen in aged-matched control subjects or in military families without GWI. In the GWI families some non-symptomatic family members did have mycoplasmal infections (~10%), but this was not significantly different from the incidence of mycoplasmal infections in healthy control subjects.152, 153

Subsequently ASD patients who were not in military families were examined for systemic mycoplasmal infections.153 The majority (~54%) were positive for mycoplasmal infections. However, in contrast to the children of GWI patients who for the most part had only M. fermentans, the civilian children tested positive for a variety of Mycoplasma species. We also tested a few siblings without apparent signs and symptoms, and for the most part few had these infections.153 In another study we examined the blood of ASD patients from Central and Southern California and found that a large subset (>58%) of patients showed evidence of Mycoplasma infections compared to age-matched control subjects (Odds Ratio=13.8, p<0.001).19 ASD patients were also examined for C. pneumoniae (8.3% positive, Odds Ratio=5.6, p<0.01) and HHV-6 (29.2% positive, Odds Ratio=4.5, p<0.01). The results indicated that a large subset of ASD patients display evidence of bacterial and/or viral infections (Odds Ratio=16.5, p<0.001).19

ASD patients have been examined for B. burgdorferi infections.154 Various studies revealed that 22-30% of ASD patients (N=76) have Borrelia infections.6, 154 The incidence of Borrelia infections in ASD patients may be related to Lyme disease distribution, with some Lyme-intense areas having high prevalence, and other areas having a low prevalence. Other infections, such as Lyme-associated Bartonella, Babesia, Ehrlichia and non-Lyme-associated CMV, Plasmodium species, Toxoplasma species and Treponema species may also be associated with ASD.6


Final comments to part 1

When neurological symptoms are present, infections of the CNS must be considered. Brain infections can stimulate glial responses, and the presence of viral and bacterial infections in nerve cells, can stimulate autoimmune responses against nerve cell antigens as well as the infections within them.155 For example, in MS some 20 different bacterial and viral infections have been found, but the link between these infections and the pathogenesis of MS is still being debated.16, 47, 75 One or even a few types of infections cannot be causally linked to MS, and the reason for this is that there may be too many possibilities. No one infection or a group of infections needs to be the trigger in MS to be important in the pathogenesis of MS. In time combinations of certain infections may eventually be identified at least in a subset of MS patients, and this will allow the development of new therapeutic approaches for many MS patients that are not recognized today.

One problem that is rarely discussed is the apparent disparity between the laboratory results from different laboratories. Often different laboratories cannot agree on types of infections found in various chronic diseases.47 There are a number of reasons for this, including differences in the source of materials, qualities of reagents and techniques used.16 Some procedures, such as PCR, have specific challenges that must be overcome in the handling of specimens, their stability, presence of interfering substances, contamination, sensitivity and specificity of the tests and interpretation of the results. Variability in results from different laboratories will remain a problem unless research groups work closely together to solve these problems. One example of how this has been overcome is a multi-centre research study on the presence of C. pneumoniae in the cerebrospinal fluid of clinically defined, mono-symptomatic MS patients.156 Sriram et al.156 conducted this diagnostic trial with good concordance of results between different laboratories. Cooperative studies such as this should eventually alleviate discrepancies in the types of infections found by different research groups.

This review continues in Part 2 with psychiatric diseases, autoimmune diseases, fatiguing illnesses, and other infectious diseases with neurological aspects and an overall discussion of the topic. 157



Competing Interests
None Declared
Author Details
GARTH L. NICOLSON, Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, California 92647, USA JORG HAIER, Department of General and Visceral Surgery, University Hospital, Münster 48149, Germany
CORRESSPONDENCE: Prof. Garth L. Nicolson, Office of the President, The Institute for Molecular Medicine, P.O. Box 9355, S. Laguna Beach, California, 92652 USA
Email: gnicolson@immed.org

References

1.Nicolson GL, Nasralla M, Haier J, et al. Mycoplasmal infections in chronic illnesses: Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis. Med Sentinel1999; 4: 172-176.
jne
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

Re: BORRELIOOSI/PARKINSONIN TAUTI

ViestiKirjoittaja soijuv » La Touko 31, 2014 14:08

Bob Cowartilla diagnosoitiin Borrelioosi v 2006 ja Parkinsonin tauti v. 2009. Hännen epäillään sairastaneen borreliosia jo 40v ajan.

http://bobcowart.blogspot.fi/p/about-bob.html


He has had Lyme disease for an estimated 40 years, according to his diagnosis in 2006. It was probably contracted in PA, where he grew up and was often exposed to ticks. He was subsequently diagnosed with Parkinson's disease in 2009. The debate continues between his Lyme and Parkinson's doctors as to which diagnosis is accurate.

Most of his creative activities have been suspended due to symptoms of neurological disease. Unable to work very effectively, he is currently receiving Social Security Disability Insurance (SSDI) benefits.

Although this blog began as a vehicle for articles and commentary about high-tech matters such as hybrid cars and computer-related topics, it has morphed to be largely about Lyme disease research and Bob's personal experiences with treatment for these strange, debilitating, and politically-charged medical conditions. Lyme disease newly infects an estimated 200,000+ Americans every year.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

Re: BORRELIOOSI/PARKINSONIN TAUTI

ViestiKirjoittaja soijuv » La Touko 31, 2014 14:08

Bob Cowartilla diagnosoitiin Borrelioosi v 2006 ja Parkinsonin tauti v. 2009. Hännen epäillään sairastaneen borreliosia jo 40v ajan.

http://bobcowart.blogspot.fi/p/about-bob.html


He has had Lyme disease for an estimated 40 years, according to his diagnosis in 2006. It was probably contracted in PA, where he grew up and was often exposed to ticks. He was subsequently diagnosed with Parkinson's disease in 2009. The debate continues between his Lyme and Parkinson's doctors as to which diagnosis is accurate.

Most of his creative activities have been suspended due to symptoms of neurological disease. Unable to work very effectively, he is currently receiving Social Security Disability Insurance (SSDI) benefits.

Although this blog began as a vehicle for articles and commentary about high-tech matters such as hybrid cars and computer-related topics, it has morphed to be largely about Lyme disease research and Bob's personal experiences with treatment for these strange, debilitating, and politically-charged medical conditions. Lyme disease newly infects an estimated 200,000+ Americans every year.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16


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