Total BBB Review
 

I have finally got all my information together in one place!!!
There is a lot of evidence that the Blood Brain Barrier (BBB) permeability plays a very significant part in PD. It also seems significant in ALS, (and they have less time than we have, fatal in 2 to 5 years), and in MS. It seems to be only part of the story in AD, (Alzheimers), but may improve matters somewhat.
Either we were born with defective BBB's, or we damaged it by some mechanism or other, during life. We did polls and surveys to try and find out what it is we all have in common, sweet tooth consuming too much sugar, stress while in the womb, anxiety complex, and the rest. However Prof Leenders in Holland has shown one thing we do all have, a defective BBB.
Below, there are statements quoted from the literature, such as
" BBB disruption is one of the hallmarks of Multiple Sclerosis", and
""Increased permeability of the BBB is a feature of many diseases of the CNS (Central Nervous System)" There is much more work we could do to make a more watertight case. Add to the list of substances that close the pores of the BBB, GDNF, alpha lipoic acid, curcumin, citicoline, bilberry extract, doesn't the list look familiar? What about Q10, ginko biloba or any others?
Have a look at the following and add to it, constructive negative facts welcomed too, which may help to crystallise our thoughts.

Ron
The role of the Blood- Brain Barrier in Neurological diseases
The BBB is a membrane which protects the delicate brain from toxic substances, which come from a number of sources, but in a person with a normal efficient BBB, the toxins circulate harmlessly in the blood. However, people can be born with defective organs, such as the heart, lungs,, kidney, liver or BBB, or they could be damaged during life.
Can a defective BBB be the major cause of PD, MS, ALS and AD (Alzheimer’s Disease).

In
http://lpi.oregonstate.edu/ss03/zinc.html
It states,
", Alterations or dysfunction of the BBB have been observed in many brain disorders. Free radicals may play an important role in damaging the BBB because it is especially sensitive to oxidative damage. This vulnerability may be due to the high polyunsaturated fatty acid content of the BBB membrane—fatty acids that are very susceptible to free radical attack—as well as the relatively low antioxidant capacity of the BBB. Oxidation of the membrane drastically compromises its barrier properties and may lead to subsequent brain tissue damage, resulting in a host of pathologies.”


The data below shows a strong connection between a defective or porous BBB on neurological diseases.

l. Parkinson’s Disease.

This article states that the BBB Blood Brain Barrier is defective in PD patients, and that it might in the course of years allow toxic compounds … to enter the brain.
http://www.imakenews.com/wemove/e_ar...m0s,b1QrWd7M,w
E-MOVE reports from the 9th International Congress of Parkinson’s Disease and Movement Disorders, New Orleans 5-8 March, 2005. Pages and abstract numbers are from Movement Disorders 2005;20(suppl 10).
Blood-brain barrier dysfunction in Parkinson’s disease
KL Leenders, R Kortekaas, AL Bartels, J Oostrom, A Willemsen, J Bart
S77, P257
The blood-brain barrier is defective in PD patients, according to this study. PET imaging of verapamil was used to measure activity of the P-glycoprotein system, which transports unwanted substances out of the endothelium back into the blood. Comparing five PD patients to five controls, the authors found significant differences in the brain penetration of verapamil (18% higher for PD patients, p=0.02) only in the midbrain region. All patient values were higher than all controls. The authors suggest, “A faulty BBB function on the basis of genetic predisposition might in the course of years allow toxic compounds—or compounds normally circulating in the blood but not passing the BBB—to enter the brain in certain regions and damage vulnerable cells.”
It could therefore be expected that treatments which open the BBB, would intensify symptoms, whilst treatments which close or tighten the BBB would improve the Parkinson’s sufferer.

Treatments which open the BBB, (and cause a worsening of symptoms)

1. Stress.

http://www.sciencenews.org/pages/pdf...4/15024-10.pdf

The effect of stress causing a worsening of symptoms in PD sufferers is well known and documented.
http://www.sciencenews.org/pages/pdf...4/15024-10.pdf
"After receiving a drug to protect them against chemical weapons,
many Israeli soldiers serving
in the Persian Gulf War suffered adverse side effects from the
inoculation. These reactions
puzzled physicians, who had expected the blood-brain barrier to keep
this drug—like many
other chemicals circulating in the blood—out of the brain.
Now, an Israeli study suggests that stress may have temporarily
opened the blood-brain barrier.
"It was surprising—we saw quite large amounts of brain penetration,"
says Hermona Soreq of
the Hebrew University in Jerusalem, a coauthor of the report in the
December NATURE MEDICINE."


http://www.blackwell-synergy.com/doi...8.2006.05223.x
European Journal of Neuroscience
Volume 24 Issue 12 Page 3393 - December 2006
“functional studies demonstrate that noradrenaline controls the permeability of the blood–brain barrier,”

2. Nitric oxide

http://64.233.161.104/search?q=cache...k&ct=clnk&cd=1

“Nitric oxide is a compound associated with causing a worsening of
the symptoms, and is a well known compound causing neurological damage. It is
reported that nitric oxide "promotes BBB dysfunction"

3. Carbon monoxide

Another known toxin to cause PD, carbon monoxide also opens up the
BBB.
http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
“Conclusion: Carbon monoxide, involving in the occurrence of hypo tension and the increase of blood-brain barrier permeability,”

4. Organic Phosphates(OP’s)

Organic in this context does not mean produced as in organic food. Organic here means a phosphate group in a molecule containing other groups consisting of carbon and hydrogen, and or a carbohydrate group. There chemicals are used in agriculture, which already has a reputation for an increased incidence of PD. I made and handled many organo phosphates when I worked as a research chemist.
http://www.foresight-preconception.o...oklet_agro.htm

“Chronic exposure to OPs has been found to result in a gradual loss
of brain stem cholinergic muscarinic and nicotinic (97-101) and
serotonergic (102,103) receptors, as well as to an increased
permeability of blood-brain barrier (104).”

5. Old Age

Although younger people can be afflicted, PD is predominantly an older person’s disease.
The reason for this could well be the fact that as the body ages, the BBB loses its ability to keep the brain free of toxins, and becomes more porous.
http://www.molmed.org/content/2001/810.pdf
“old age significantly increases BBB permeability”

6. Sarin
http://cat.inist.fr/?aModele=afficheN&cpsidt=13856336
“Acute exposure to sarin increases blood brain barrier permeability and induces neuropathological changes in the rat brain: Dose-response relationships.”



Treatments which close the BBB permeability (and improve symptoms?)
A, Citicoline (CPD Choline),
http://www.naturalproductsinsider.co...ngredient.html
“citicoline was found to reduce brain edema and decrease breakdown of the blood-brain barrier in rats at a dose of 400 mg/kg. (31)”


B. Alpha Lipoic Acid (LA)
A popular supplement amongst \PD sufferers, being a thio antioxidant, which recycles glutathione. It is made in the body, but decreases with age.

The Journal of Immunology, 2006, 177: 2630-2637.
Copyright © 2006 by The American Association of Immunologists
Lipoic Acid Affects Cellular Migration into the Central Nervous System and Stabilizes Blood-Brain Barrier Integrity1
Gerty Schreibelt*, René J. P. Musters , Arie Reijerkerk*, Lody R. de Groot*, Susanne M. A. van der Pol*, Esther M. L. Hendrikx*, Ed D. Döpp*, Christine D. Dijkstra*, Benjamin Drukarch and Helga E. de Vries2,*
“LA has a protective effect….by stabilization of the BBB”

C. Curcumin (Tumeric)
Another popular non prescription supplement, being a powerful antioxidant, anti inflammatory, and a chelator of heavy metals.
http://en.wikipedia.org/wiki/Turmeric
It is also said that turmeric can strengthen the blood-brain barrier against attacks that result from auto-immune diseases (such as Multiple sclerosis)[verification needed].
D. Bilberry extract
http://www.lef.org/magazine/mag2000/mar00-cover1a.html
“In addition, bilberry extract has been shown to enhance the blood-
brain barrier, which tends to become impaired with aging, showing a
decrease in vascular density, increased permeability and other
abnormalities. The normal functioning of blood-brain barrier is
important not only for keeping out toxins and undesirable compounds,
but also for glucose transport to the brain. Anthocyanins and
related compounds seem able to decrease capillary permeability
(possibly by stabilizing membrane phospholipids). Animal studies
have also shown that if the blood-brain barrier becomes damaged and
too permeable, anthocyanins help restore normal permeability”

E. GNDF
http://www.pdf.org/News/news.cfm?sel...005%26type%3D1

“Glial cell line-derived neurotrophic factor, or GDNF, was first identified in 1993. It is one of the most powerful naturally-occurring human factors known to nourish and foster the growth of dopamine-generating neurons.”
For their own reasons, Amgen halted their clinical trials with this material, but it does also reduce the porosity of the BBB.

http://www.ihop-net.org/UniPub/iHOP/gs/88604.html

“We previously reported that GDNF reduced the endothelial
permeability of the blood-brain barrier (BBB).”

================================================== =========================
ll. Multiple Sclerosis (MS

http://www.ncbi.nlm.nih.gov/entrez/q..._uids=17124345
“Blood-brain barrier (BBB) disruption is one of the hallmarks of multiple sclerosis (MS).”

In
http://www.mult-sclerosis.org/news/D...rrierinMS.html
it states,

"Increased permeability of the BBB is a feature of many diseases of the central nervous system (CNS), among them MS.3 BBB increased permeability is an early and critical event, often preceding symptoms, and, in most cases, being present in chronic lesions"

"MRI is used frequently by clinicians as a major criterion to define lesion activity, and is thought to reflect BBB damage. Although this is considered to be one of the earliest changes in observed MS lesions, neuropathological and immunocytochemical studies reveal that BBB leakage can be found to variable degrees in every MS lesion,"


lll. Amyotrophic Lateral Sclerosis (ALS) or Lou Gerhrigs Disease

ALS is a progressive neuromuscular disease that causes degeneration of some of the largest of all nerve cells, called motor neurons. Motor neurons control the movement of voluntary muscles. ALS results in fatality within two to five years from the first appearance of the symptoms.
In
http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract
it states
“These findings support the hypothesis that blood-brain barrier damage occurs in ALS.”
================================================== =====================================

lV Alzheimers Disease, (AD)

In both the reports below, a significant but low number of AD patients had defective BBB’s.

http://www.springerlink.com/content/061856503303q982/
“18% of patients with probable Alzheimer's disease showed BBB dysfunctions”

http://www.medicalnewstoday.com/medi...p?newsid=49999

“The study found BBB impairment in a significant minority of subjects with AD. Furthermore, BBB disruption may be clinically significant by allowing antioxidants to "diffuse down" their respective concentration gradient facilitating unabated oxidative processes in the brain that underlie AD pathology. The relationship between this phenomenon, BBB impairment and maintenance, and the neurodegenerative process remains to be clarified.”


CONCLUSIONS

In PD, the BBB plays a major and very significant part, and merits much more research into methods of controlling the permeability of the BBB. A process that locks down the BBB to all but the few allowed molecules, must be found. It then must be tried on newly diagnosed patients, to establish whether it stops progression of the disease. Then it needs to be tried with advanced sufferers, to establish whether neurogenesis, or birth of new cells, whilst preventing any influx of toxins causing loss of established cells, means that a gradual recovery takes place.
Similarly, the process to totally tighten the BBB needs to be tried on ALS and MS patients, in a similar manner.
BBB porosity does not seem to be the major cause of AD, but it may make a significant improvement in the quality of life of AD sufferers.

much appreciation
 

Thanks for all the hard work Ron, this makes it so easy just to send off in an email to researchers or anyone else we know who might take a serious look.


paula

BBB Barrier Possible Cause
 

HI Ron,

I carry 2 Parkin mutations and have a sister with PD, When she was about 17, she was thrown off a horse and had to be flown to the nearest large medical center. She had a fractured skull and was leaking spinal fluid.

I was beaten by my father. One of his blows was to the back of my head. It was hard enough to make me see stars and black out. A later FDOPA Scan showed I had already sustained damage to my brain.

Vicky

Maybe it will help
 

Here in the U.K there was a programme on t.v last night about the brave people who experimented on themselves to prove that certain diseases were caused by nutritional deficiency not germs.Whilst I am no way saying that P.D is nutritional I did think of contributors to this site who have experimented on themselves.Then along comes this posting by Ronhutton.Well I have already got my husband taking curcumin and ALC/ALA .We are both now drinking organic blackcurrant juice
(22% concentrated blackcurrant the rest concentrated apple).This may not do anything to slow the progression of the disease but it does no harm to try.

back to the BBB
 

There is one point about the BBB theory that poses a problem: If the increased permeability is the cause of our problem, why is damage limited to the substantia nigra? The same question in another form might be why is the BBB just leaking in the area of the SN? In other words why would the damage be localized there?

There is an answer if we cast a slightly wider net. First, is there something special about the SN compared to the rest of the brain? Yes, at least one thing. The SN has an unusually high number of the immune system defenders called microglia. Possibly the highest density in the entire brain, in fact.

One thing about microglia is that in certain circumstances they attack the neurons they are supposed to defend. If that happened in the high density SN there would be a problem.

The circumstances where this malfunction occurs is in an adult who was exposed to bacterial toxins during critical stages of development as a fetus. That exposure has three effects of relevance. First is a lower number of neurons in the SN at birth. We start out with one strike against us.

Second is the over reactive microglia in the adult. This self destructive reaction occurs when the "primed" microglia detect further traces of the bacterial toxin that started the problem years before. We are born with a loaded gun in our brain.

Third effect is an alteration in the part of our brain that controls our stress response. The result is that our cortisol levels are chronically elevated. This stress response has an important effect. It triggers chronic inflammation.

Chronic inflammation, among other things, opens the BBB, allowing toxins to enter.

And one of the most common of those toxins is the bacterial one that started the whole chain. The BBB leaks from inflammation, the toxin enters the brain, the microglia go berserk, and neurons begin to die.

That is one of the pillars of the multiple hit hypothesis that we are going to be hearing a lot about over the coming years. of course the leaky BBB lets in other toxins as well, but the bacterial one is the one that turns our own defenders into madmen.

One caveat is that the above has all been demonstrated on animal models and part on humans thus far. But many teams are working on the various parts and a lot of things are faling into place.

That's all well and good, of course, but we need help today, not tomorrow.
:D

These three studies show that green tea extracts not only calm down the microglia but also protect the BBB and the counterpart in the GI tract.


1: J Neurosci Res. 2004 Dec 1;78(5):723-31.

(-)-Epigallocatechin gallate inhibits lipopolysaccharide-induced microglial
activation and protects against inflammation-mediated dopaminergic neuronal
injury.

Li R, Huang YG, Fang D, Le WD.

Health Science Center, Shanghai Institute for Biological Science, Chinese
Academy of Science, Shanghai Second Medical University, Shanghai, Peoples
Republic of China.

Microglial activation is believed to play a pivotal role in the selective
neuronal injury associated with several neurodegenerative disorders, including
Parkinson's disease (PD) and Alzheimer's disease. We provide evidence that
(-)-epigallocatechin gallate (EGCG), a major monomer of green tea polyphenols,
potently inhibits lipopolysaccharide (LPS)-activated microglial secretion of
nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) through the
down-regulation of inducible NO synthase and TNF-alpha expression. In addition,
EGCG exerted significant protection against microglial activation-induced
neuronal injury both in the human dopaminergic cell line SH-SY5Y and in primary
rat mesencephalic cultures. Our study demonstrates that EGCG is a potent
inhibitor of microglial activation and thus is a useful candidate for a
therapeutic approach to alleviating microglia-mediated dopaminergic neuronal
injury in PD.

PMID: 15478178 [PubMed - indexed for MEDLINE]

1: World J Gastroenterol. 2007 Jan 21;13(3):349-54.

Red wine and green tea reduce H pylori- or VacA-induced gastritis in a mouse
model.

Ruggiero P, Rossi G, Tombola F, Pancotto L, Lauretti L, Del Giudice G, Zoratti
M.

Novartis Vaccines & Diagnostics s.r.l., Research Center, Via Fiorentina 1, Siena
I-53100, Italy. paolo.ruggiero@novartis.com

AIM: To investigate whether red wine and green tea could exert anti-H pylori or
anti-VacA activity in vivo in a mouse model of experimental infection. METHODS:
Ethanol-free red wine and green tea concentrates were administered orally as a
mixture of the two beverages to H pylori infected mice, or separately to
VacA-treated mice. Gastric colonization and gastric inflammation were quantified
by microbiological, histopathological, and immunohistochemical analyses.
RESULTS: In H pylori-infected mice, the red wine and green tea mixture
significantly prevented gastritis and limited the localization of bacteria and
VacA to the surface of the gastric epithelium. Similarly, both beverages
significantly prevented gastric epithelium damage in VacA-treated mice; green
tea, but not red wine, also altered the VacA localization in the gastric
epithelium. CONCLUSION: Red wine and green tea are able to prevent H
pylori-induced gastric epithelium damage, possibly involving VacA inhibition.
This observation supports the possible relevance of diet on the pathological
outcome of H pylori infection.

PMID: 17230601 [PubMed - in process]


1: Wien Klin Wochenschr. 1999 Apr 9;111(7):278-82.

The green tea extract epigallocatechin gallate is able to reduce neutrophil
transmigration through monolayers of endothelial cells.

Hofbauer R, Frass M, Gmeiner B, Handler S, Speiser W, Kapiotis S.

Department of Medical and Chemical Laboratory Diagnostics, University of Vienna,
Austria. roland.hofbauer@akh-wien.ac.at

Green tea is widely used in Asia and has also become popular in Western
countries. The influence of green tea extracts on leukocytes is not well
understood. Leukocytes play a crucial role in the process of inflammation. They
migrate from the intravascular space into the tissue to attack micro-organisms.
The aim of the current study was to investigate the influence of
epigallocatechin gallate on leukocyte transmigration through endothelial cell
monolayers and thereby evaluate its potential role in the inflammatory process.
Human umbilical vein endothelial cells were cultured on microporous membranes to
achieve a monolayer. Freshly isolated neutrophils from healthy subjects were
measured with a migration assay. The amount of untreated neutrophils migrating
through untreated endothelial cell monolayers was used as control and set as
100%. Neutrophils and/or endothelial cell monolayers were pre-treated with
epigallocatechin gallate using relevant, as well as higher and lower
concentrations. The relevant plasma concentration of epigallocatechin gallate
was able to significantly inhibit neutrophil migration through endothelial cell
monolayers (69 +/- 6.4% SD; p < 0.05 compared to control), when both cell types
(leukocytes and endothelial cell monolayer) were treated. This is similar to the
situation after resorption in-vivo. Treating either neutrophils or endothelial
cell monolayers alone led to significant reductions in migratory response (only
neutrophils treated: 86 +/- 8.1% SD, p < 0.05; only endothelial cell monolayers:
77 +/- 6.1%, p < 0.05). In conclusion, epigallocatechin gallate was identified
as a potent inhibitor of leukocyte migration through endothelial cell
monolayers. The treatment of both cell types showed an additive effect.
Endothelial cells seem to be more affected than neutrophils. Further clinical
investigations are necessary to understand the potential clinical consequences.

PMID: 10355038 [PubMed - indexed for MEDLINE]

bbb
 

Also, the brain consists of dozens of cell types, each one of which deals with a different function, and whose deficiency or damage would lead to a different medical disorder. If a deficiency of the blood brain barrier had a primary effect in Parkinson's Disease then somebody would simultaneously suffer from dozens of neurological disorders. The selective insufficient function in Parkinson's Disease shows that there is a specific insufficient function of the dopaminergic neurons rather than dozens of cell types.


most people don't come in to contact with sufficient quantities of toxins in order to cause Parkinson's Diseae. For example, carbon monoxide, the most widespread of the toxins would have to cause a coma for it to cause Parkinson's Disease. The general tendency in Parkinson's Disease is a very gradual decline. If this were due to toxicity this would only be explained by persistent exposure over many years or even decades to a known toxic cause of Parkinson' Disease. However, if exposure does occur it is usually sporadic rather than persistent.

The study that claims that there is a defective blood brain barrier in Parkinson's Disease used only five subjects. Due to the small number of subjects and the low level of increased permeability found, statistically it would not be considered as significant. Although it used five subjects as controls, there is no indication that these were age controlled. So all that they may have shown is that there is a tendency for the blood brain barrier to deteriorate with age, which is something that was already known. Also, if the blood brain barrier deteriorated with age and thereby made Parkinson's Disease more likely, why is it that amongst the oldest of people - those between 110 and 120 years old - Parkinson's Disease is virtually unknown.

Neuro-inflammation end result?
 

Whether Parkinson's is a result of a defective blood brain barrier or some other cause, the ongoing process could be due to neuro-inflamation as in the report below. The authors go into the mechanisim of this inflammation (which is beyond my understanding). They also believe they have found a class of compounds, opioid antagonists, used at a very low dose to slow or even halt the progression of PD. Even if stem cells can restore dopamine cells, the disease process would still probably continue. So maybe treatment with these opioid compounds would be still necessary to to prevent ongoing inflammation as well as to treat early stage PD. I am in this latter catagory and I have been takin 4.5mg of naltrexone for 32 months. Maybe it's the PD drugs I also take but I don't think I have progressed over this time.
Ashley

http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract

ABSTRACT
Inflammation has been increasingly recognized to contribute to the pathogenesis of Parkinson’s disease. Several compounds are neuroprotective at femtomolar concentrations through the inhibition of inflammation. However, the mechanisms mediating femtomolar-acting compounds are poorly understood. Here we show that both gly-gly-phe (GGF), a tri-peptide contained in the dynorphin opioid peptide, and naloxone are neuroprotective at femtomolar concentrations against LPS-induced dopaminergic neurotoxicity through the reduction of microglial activation. Mechanistic studies demonstrated the critical role of NADPH oxidase in the GGF and naloxone inhibition of microglial activation and associated DA neurotoxicity. Pharmacophore analysis of the neuroprotective dynorphin peptides and naloxone revealed common chemical properties (hydrogen bond acceptor, hydrogen bond donor, positive ionizable, hydrophobic) of these femtomolar-acting compounds. These results support a common high-affinity site of action for several femtomolar-acting compounds, where NADPH oxidase is the critical mechanism governing neuroprotection, suggesting a novel avenue of anti-inflammatory and neuroprotective therapy.—Qin, L., Block, M. L., Liu, Y., Bienstock, R. J., Pei, Z., Zhang, W., Wu, X., Wilson, B., Burka, T., Hong, J.-S. Microglial NADPH oxidase is a novel target for femtomolar neuroprotection against oxidative stress.

Parkinson’s disease (PD) is characterized by the specific and progressive death of dopaminergic neurons in the substantia nigra (SN); other neuronal cell types are much less affected. Recent reports have linked inflammation to neurodegenerative disease, where microglia, cells of myeloid lineage responsible for innate immunity in the brain, are considered to be the major cell type underlying the inflammation-mediated neurotoxicity (7 8 9) . The activation of microglia is a complex process involving the release of several soluble proinflammatory factors [tumor necrosis factor {alpha} (TNF-{alpha}), PGE2, IL-1] and free radicals (nitric oxide, superoxide) (7) . Current replacement therapy with L-dopa is able to alleviate disease symptoms, but is unable to alter the disease course. Thus, therapeutic interventions designed to inhibit the microglial inflammatory response offer hope for attenuation of the neurodegenerative disease process. The current anti-inflammatory treatments available, including steroids and nonsteroidal anti-inflammatory drugs, are limited by the ability to influence only a small portion of the microglial response (10) . Thus, identification of compounds acting on novel targets to inhibit the release of a wide range of proinflammatory factors from overactivated microglia is of paramount importance. In the ensuing study, we report that femtomolar concentrations of naloxone and the peptide fragment glycine-glycine-phenylalanine (GGF) attenuate a broad spectrum of the microglia inflammatory response (reactive oxygen species (ROS) and proinflammatory factors) and are neuroprotective with extremely potent efficacy through the inhibition of microglial NADPH oxidase.

As I have previously posted
 

I take dextromethorphan,DM, readily available in over-the-counter cough syrups as dextromethorphan HBr. It has the same activity decreasing glial cell-mediated inflammation and neurodegeneration as naloxone and naltrexone which are available only by prescription. I take 5 to 8 mg of DM each night just before bedtime. I also take 450 mg generic sinemet, 100mg amantadine and 1000mg of CoQ12 each day.

I began this regimen two years after Dx, after starting at Dx on sinemet and amantadine. I do not think my symptoms have progressed since that time

Robert

MOAB inhbitors and naloxone
 

anyone know if one can take dextromethorphan or naloxone with an MAOB inhibitor? seems I read once that it was contraindicated.

I have progressed too much for my liking over the past year, and recently felt as though I was ready for another med adjustment..Seems like as soon as my meds are working..its time to change something again..:confused: ..I had talked to my Dr about LDN a while ago, and he wouldnt prescribe it..and gave me this speach that I could still be swinging a golf club at age 60..(I dont play golf)..so I gave up on the idea for a while..Ashleyk has been persistant in sharing her experiences with LDN, and I figured that it must be benefiting her if she keeps posting about it..so three weeks ago I started taking CVS brand cough syrup 15% Dextromethorphan by volume @ 1/2 teaspoon before bed daily..well..the first two weeks werent daily because I couldnt remember to take it..but I noticed when I did that the next day I felt better than usual..I have taken it everyday now for 8 days in a row..and every single day Ive had a remarkable amount of movement, and I feel better than I have in 2 years..I am energetic, sleep better, and Im alot more confident in my daily endeavors, driving, walking, daily chores, etc..Pd was starting to creep in to the left side of my body, and I began to experience some changes in coordination in picking objects up, typing, handling a fork and knife..etc..It feels like movement has been restored, and I definately have more movement/coordination in my bad hand..I can get in my truck in the dark and get the key in the ignition first shot 8 out of 10 times..I was having trouble doing it in the daylight before..It feels premature to be saying this after only 8 days..but I havent had 8 consecutive days like this in I cant remember how long..Something has changed..I can feel it, and I know its not my imagination..a couple of people who know me well have noticed it as well..I feel the same way I felt the first time I took a brand name Sinamet..The way I figure it..For a lousy $5.00 for a bottle of cough syrup, what have I got to lose?