Blood, Brain Barrier

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Robin (see below)

LYME BBB

MMS

Allicin: The main agent--allicin--has a very small molecular weight

and can therefore penetrate the blood-brain barrier in order to

combat infections of the central nervous system, something that

conventional antibiotics are unable to do.

http://huiliacuherbclinic.com/lymedisease.html

Artemisinin:

Artesunate is water soluble and may be the most active and the least

toxic, but it has the shortest life within the body. Artemether is

oil or lipid soluble and has the longest half-life. It also has the

most toxicity (but this is related to rather high dosages, which are

unnecessary. Its big advantage is that it can cross the blood-brain

barrier to reach cancers in the nervous system. Artemisinin is the

active parent compound of the plant.

It has an intermediate half-life, is very safe, and also can cross

the bloodbrain

barrier. The first two are slightly altered semi-synthetic

derivatives of artemisinin, the concentrated and purified active

agent. Dr. Singh reports that a combination of the forms may be the

very best treatment due to these different properties (based on a lab

experiment). Thus, he feels the best preparation will contain

artemisinin and artemether to provide a dose of 0.5-2 mg/Kg of each

form once daily before bed (away from any residual iron left in the

stomach from the evening meal). Dr. Hoang reports that 500 mg

twice daily of oral artemisinin by itself is the dosage he has been

using with great success.

http://tst.kanker-actueel.nl/index.asp?blz=an_al.Artemisinin & nieuws=23

intravenous rocephin

Minoclycline (high dose) (200 to 400 a day)

Doxyclycline high dose (300 to 600 a day)

http://info.lymebook.com/matthewgoss.html

(Zithromax) may successfully accomplish blood-brain tissue barrier

penetration that is needed.

http://www.wellsphere.com/healing---recovery-article/bells-palsy-of-

the-gut-and-other-gi-manifestations-of-lyme-and-associated-

diseases/20512

Metronidazole inhibits anaerobic bacteria and protozoa. The exact

mechanism is not understood, but it is believed that it interferes

with the synthesis of DNA. It penetrates all tissues including those

found in the CNS (no link)

Possibility? because of low BBB threshold with lyme:

The role of the newer macrolides in the treatment of Lyme

Disease needs further assessment. Erythromycin has been regarded

as ineffective, despite its good in vitro sensitivities.

Azithromycin has been reported to be less effective in the

treatment of early Lyme Disease than amoxicillin (21). Some

physicians use clarithromycin and azithromycin in higher dosages

and for longer periods of time, but there have been no reports of

greater success with these drugs than with the tetracyclines or

beta-lactams. In our experience, all macrolides are effective

when combined with a lysosomotropic agent, especially

hydroxychloroquine(see below)(10).

In evaluating the possible factors, it would appear that

antibiotics that can achieve intracellular concentrations and

activity are the most efficacious drugs. The results of studies in

Klempner's laboratory using a tissue culture model of borrelia

infection demonstrated that ceftriaxone was incapable of eradicating

intracellular organisms (17); similar experiments in Raoult's

laboratory using an endothelial cell model

demonstrated that tetracycline and erythromycin were effective,

but beta lactam antibiotics were not (3). These results are in line

with our experience that the tetracyclines and macrolides achieve the

greatest success.

In contrast to beta lactams, antibiotics of the tetracycline and

macrolide classes are capable of good intracellular penetration.

Experience with the macrolide antibiotics has been disappointing,

however, when compared with

its in vitro activities against the Lyme borreliae, and with the

established efficacy of macrolides against other intracellular

parasites such as chlamydia, legionella, mycobacterium-avium

intracellulare, and toxoplasma. If, though, the Lyme borreliae reside

in intracellular vesicles that are acidic, the macrolides' activity

would be sharply decreased at the lower pH.

This is in contrast to the tetracyclines, which are active at acid

pH; even

so, the activity of doxycycline was shown to be further increased by

increasing the pH. In a tissue culture model of ehrlichia infection,

the use of lysosomotropic agents such as amantidine, NH4Cl, and

chloroquine increased the killing of intracellular organisms by

doxycycline (22).

Based on those studies, and the hypothesis that late Lyme Disease

symptoms are due to persisting intracellular infection, we have been

successfully treating patients using the combination of a macrolide

and hydroxychloroquine (10).

As regards " CNS " disease, there is no evidence that ceftriaxone

is more successful than either the tetracyclines or the combination

of macrolide and hydroxychloroquine; if our presumption that the

pathogenesis of the disease involves the localization of the borrelia

to the endothelial cells of the blood vessels serving the nervous

system or to glial or neural

cells is correct, then one would not need to have a drug that can

cross the blood-brain barrier to be effective. Indeed, the

tetracyclines can cross the blood-brain barrier to some extent, and

were used when initially introduced into clinical medicine for the

treatment of meningitis, with some success.

Macrolide antibiotics do not cross the blood-brain barrier, but have

been

effective in treating other CNS infections (e.g., toxoplasmosis), and

in our experience have been effective in reversing the

neuropsychiatric symptoms and signs (eg SPECT scans) of Lyme Disease

(10). With regard to the issue of bactericidal vs bacteristatic

effects, any such effect in vivo has not been demonstrated.

Finally, there have been no reports showing any change in antibiotic

resistance patterns during the course of treatment. Ultimately, the

determination of efficacy of therapy depends on the clinical

response.

clinical response.

http://www.prohealth.com/library/showarticle.cfm?id=3579 & t=CFIDS_FM

Lyme Disease and Autism

Other neurogenic strains of Borrelia that cause Relapsing Fevers in

Africa can be deadly within mere weeks of entering the brain. While

Lyme disease may be a bit more subtle upon penetrating the brain,

its

silent and insidious invasion may be the reason that brain

involvement

can and is often be overlooked by physicians for months or even

years

in neurological Lyme patients.

Just as the spirochete that causes syphilis can remain active

within

the brain for decades in tertiary Syphilis, there is equal cause for

concern that the Lyme bacteria can also become a sequestered

unwelcome

interloper to the central nervous system. How does the Lyme bacteria

enter the brain when the blood brain barrier fights against foreign

invasion?

Once the Lyme spirochete enters the peripheral blood circulation

through an infected tick bite, the bacteria fights to escape the

confines of the blood vessel walls. The spirochete's motility allows

it to swim in the blood stream until it lodges a wiggling tip into a

endothelial cell junction, where it bores between endothelial cells

lining the capillaries and causes a specific inflammation and

irritation that causes the endothelial cells to release digestive

proteins that create holes within the capillary bed.

In 1989, experiments were done using umbilical cord vein to show

that Borrelia burgdorferi attaches tip first to endothelial cells

and

microscopic examination found holes near the areas of attachment. If

these vessels were within the heart or brain, it would be clear that

there is nothing to stop Borrelia and other blood stream components

from entering those sites. In the case of the brain, allowing

bacteria

and white blood cells access to the brain is setting up the brain

for

a series of events to occur which we can call neurocascade events.

This is where one event will trigger another, which in turn will

trigger another and so on until a small nonsymptomatic event becomes

noticeable.

To see if Borrelia burgdorferi truly breaks down the blood brain

barrier, several animal experiments were done. Since blood albumin

protein should not be in the cerebral spinal fluid (CSF),

researchers

tagged normal albumin with radioactive Iodine. In mice, hamsters,

and

dogs without infection the radioactive Iodine never penetrated into

the CSF of the normal control animals. But when the animals were

infected with Lyme disease, within mere hours the blood brain

barrier

became permeable and radioactive iodine was found within the CSF of

infected animals usually for about two weeks following initial

infection. This window of permeability certainly gives ample time

for

the Lyme bacteria to establish itself within the brain. Detailed

collection of CSF from recently bitten Lyme patients reveals that

sub

clinical infections of the CNS occurs often before the infection in

the body is even detected.

Before we talk about the neurotoxic effects of Borrelia

burgdorferi

within the brain, let's first look at some other neurocascade events

that occur in acute brain trauma and repeated brain trauma such as

in

sports accidents like soccer, football and boxing. Repeated

concussions in football players and boxers can cause a slow onset

of a

syndrome sometimes called Pugilistic Dementia, or Sports-Related

Encephalopathy. Common symptoms begin months to years after injury

occurs and usually includes: headaches, muscle twitches, tics,

sensitivity to bright lights and loud noises, inability to retrieve

words, loss of time, depression, suicidal thoughts. Later these

symptoms can progress to fatigue, lethargy, loss of interest, severe

depression, Parkinson-like tremors, loss of motor control, and

overall

slowness, and finally dementia.

An interesting comparison between Lyme encephalitis and Pugilistic

dementia besides sharing similar symptoms is that both patients can

have global-cerebral-atrophy years after their initial trauma. In

other words, the brain shrinks, and appears to have lost the ability

to properly repair damage that accumulates over many years. These

abnormal MRIs of the brains of boxers and Lyme patients may be

caused

by different mechanisms, but the end result can appear similar in

both

the symptoms and pathology of the two conditions.

http://findarticles.com/p/articles/mi_m0ISW/is_285/ai_n19170369/print?

tag=artBody;col1