Re: ANS probs or Hypercoagualtion?

[Guest guest]

I don't think 'autonomic nervous system dysfunction' gets us too

far, because it doesn't tell us anything about the specific

pathology or its proximate cause. Why should the autonomic nervous

system function abnormally? Does that then point us to specific

locations in the body or brain to investigate? I get that it's a way

of pointing out that processes which are ordinarily self-regulating

have broken down, but beyond that what does it tell us?

Hypercoagulation does specify a pathology, but one whose symptoms

can present almost anywhere, in any part of the body or its various

systems, where reduced flow of blood / oxygen / nutrients / immune

cells can do harm. The difficulty of diagnosing this appears to be

substantial. My LLMD was also quite skeptical about ordering the

Hemex tests, because their cost is high and not many clinicians seem

to take them seriously yet.

One form of hypercoagulation that is often discussed is

antiphospholipid syndrome. I believe this is often found in patients

with MS, and one of the symptoms is heat intolerance, which quite a

few of us seem to suffer. I have no idea, though, how it might

relate to the specific symptoms DM mentions.

Like DM, I would like to know more, and appreciate any online

resources others might like to point us to.

>

> OK, first off, I am (A) very sketchy as to the proposed symptoms

of

> hypercoagulation, and ( unclear as to how/why hypercoagulation

may

> be a consequence of chronic infection.

>

> With those caveats (and implicit questions!) in mind, bear with my

> query:

>

> Several symptoms that I have are being described as " autonomic

> nervous system dysfunction. " They include cold/bluish legs and

> occassionally hands, difficultly breathing, heart arrythmias,

chest

> pain, and orthostatic hypotension. Now, if what little I've been

> able to ascertain re: hypercoagulation symptoms is accurate, don't

> these overlap?

>

> And if they do overlap, how does one discriminate between ANS

> dysfunction and hypercoagulation in the absence of a blood test?

> I've heard about the HEMEX panel but I don't have a doc that is

> willing to go that far down the alternative explanation aisle

> (including the lyme doc consulting with my PCP).

>

> Again, am curious as well to seeing a list of symptoms and hearing

> about the how/why of this proposed dysfunction.

>

> Thanks.

[Guest guest]

--- In infections , " Schaafsma "

<compucruz@y...> wrote {IN PART}:

>

> I don't think 'autonomic nervous system dysfunction' gets us too

> far, because it doesn't tell us anything about the specific

> pathology or its proximate cause. Why should the autonomic nervous

> system function abnormally? Does that then point us to specific

> locations in the body or brain to investigate? I get that it's a

> way of pointing out that processes which are ordinarily self-

> regulating have broken down, but beyond that what does it tell us?

As for cause, I personally wouldn't be surprised if my ANS was

affected in addition to my CNS. I have had meningitis from Lyme

twice, complete with high CSF pressure, gobs of WBCs in my CSF, and

positive Lyme titers on the CSF fluid.

So I suspect my peripheral nervous system, in addition to my CNS,

could also be directly trounced by infection. Moreover, as the ANS

innervates blood vessels, affects heart rate, innervates internal

organs, etc, its effects are as potentially ubiquitous as the

proposed hypercoagulation issue.

In short, I see the ANS dysfunction hypothesis as valid (just as I

see CNS dysfunction as valid simply as a consequence of direct

infection). So my question was less about which hypothesis is valid

and more about how does one discriminate between these hypotheses in

the absence of a blood test. That may be your question too but

I think I'm seeing an additional one on your part regarding the

validity of the ANS dysfunction diagosis. Just want to make sure

I'm understanding your point!

And I'll add yet another Q to this discussion. Is there

a " conventional " blood test (e.g., non-HEMEX) that can be used to

assess for hypercoagulation? Is there a test that checks fibrin or

fibrinogen (that's what is upregulated supposedly, no?).

[Guest guest]

Duramater wrote in part:

" That may be your question too but I think I'm seeing an

additional one on your part regarding the validity of the ANS

dysfunction diagosis. Just want to make sure I'm understanding your

point! "

Good of you, I have bad mush-brain today. Actually, I wasn't

doubting the validity of the ANS dysfunction diagnosis, just asking

what its tangible implications are. Does it give you something to

treat? Does one assume that ANS dysfunction will be corrected with

antibiotic treatment? What do you do differently when you

characterize symptoms in this way?

Those questions are more an expression of ignorance on my part than

a critique. Doctors have made references to the ANS in talking about

my illness, but none has ever proposed ANS dysfunction as a

diagnosis, and I honestly wasn't sure (am still not sure) what it's

diagnostic meaning is.

About testing for hypercoagulation: There are specific antibodies

(including anti-phospholid antibodies) that can cause

hypercoagulation. I have no idea how reliable the tests are, but

notice that many studies refer to them. My LLMD thinks highly of

some panel that Quest offers on coagulation, but I don't know what

it is.

I think a lot of patients just end up experimenting with

anticoagulants like bromelain, warfarin, etc., to see if their

symptoms improve. I've thought about it myself, always seem to be

waiting for an opportunity to try it while other things remain

constant, so I can try to evaluate the effect.

I hope we'll hear from others - the board's been quiet lately, but I

know there are many who've considered, and some who've pursued, anti-

coagulation treatment. They will probably have better answers about

testing.

Duramater wrote in part:

In short, I see the ANS dysfunction hypothesis as valid (just as I

see CNS dysfunction as valid simply as a consequence of direct

infection). So my question was less about which hypothesis is valid

and more about how does one discriminate between these hypotheses in

the absence of a blood test.

[Guest guest]

“unclear as to how/why hypercoagulation may be a consequence of chronic infection.”

I think this is approximately what’s going on

Macrophages ,have a number of roles , in simple terms they react inappropriately to our type of infection… the response is to injury …laying down fibrin rather than adopting a killing engulfing role .

The motor is inflammation

“However, in inflammatory reactions initiated by the immune system, the ultimate control is exerted by the antigen itself, in the same way as it controls the immune response itself. For this reason, the cellular accumulation at the site of chronic infection, or in autoimmune reactions (where the antigen cannot ultimately be eradicated), is quite different from that at sites where the antigenic stimulus is rapidly cleared”

In general, lymphocytes are involved in the adaptive response to inflammation, and the early events of inflammation are mediated in part by molecules produced by cells of the innate arm of the immune system.

Early phase mediators are produced by mast cells and platelets. They are especially important in acute inflammation and include mainly histamine, serotonin and other vasoactive substances. Platelets may contribute to inflammatory responses resulting as a consequence of tissue injury, through a variety of mechanisms including:

the release of vasoactive amines and other permeability factors,

the release of lysosomal enzymes,

the release of coagulation factors which lead to localized and generalized fibrin deposition, and

the formation of platelet aggregates or trombi which result in the blocking of vessels and capillaries.

http://nic.sav.sk/logos/books/scientific/node25.html

http://www.anapsid.org/cnd/diffdx/hypercoagulation.html

-----Original Message-----From: duramater27 [mailto:spam-barb@...]Sent: 06 April 2005 17:28infections Subject: [infections] ANS probs or Hypercoagualtion?OK, first off, I am (A) very sketchy as to the proposed symptoms of hypercoagulation, and ( unclear as to how/why hypercoagulation may be a consequence of chronic infection.With those caveats (and implicit questions!) in mind, bear with my query:Several symptoms that I have are being described as "autonomic nervous system dysfunction." They include cold/bluish legs and occassionally hands, difficultly breathing, heart arrythmias, chest pain, and orthostatic hypotension. Now, if what little I've been able to ascertain re: hypercoagulation symptoms is accurate, don't these overlap?And if they do overlap, how does one discriminate between ANS dysfunction and hypercoagulation in the absence of a blood test? I've heard about the HEMEX panel but I don't have a doc that is willing to go that far down the alternative explanation aisle (including the lyme doc consulting with my PCP).Again, am curious as well to seeing a list of symptoms and hearing about the how/why of this proposed dysfunction.Thanks.

[Guest guest]

Hi guys,

Ken Lasessen (or is it Lassesen?!) who moderates the

group has a ton of experience and information regarding hypercoagulation tests,

studies, etc..

Dan

>

> Duramater wrote in part:

>

> " That may be your question too but I think I'm seeing an

> additional one on your part regarding the validity of the ANS

> dysfunction diagosis. Just want to make sure I'm understanding your

> point! "

>

> Good of you, I have bad mush-brain today. Actually, I wasn't

> doubting the validity of the ANS dysfunction diagnosis, just asking

> what its tangible implications are. Does it give you something to

> treat? Does one assume that ANS dysfunction will be corrected with

> antibiotic treatment? What do you do differently when you

> characterize symptoms in this way?

>

> Those questions are more an expression of ignorance on my part than

> a critique. Doctors have made references to the ANS in talking about

> my illness, but none has ever proposed ANS dysfunction as a

> diagnosis, and I honestly wasn't sure (am still not sure) what it's

> diagnostic meaning is.

>

> About testing for hypercoagulation: There are specific antibodies

> (including anti-phospholid antibodies) that can cause

> hypercoagulation. I have no idea how reliable the tests are, but

> notice that many studies refer to them. My LLMD thinks highly of

> some panel that Quest offers on coagulation, but I don't know what

> it is.

>

> I think a lot of patients just end up experimenting with

> anticoagulants like bromelain, warfarin, etc., to see if their

> symptoms improve. I've thought about it myself, always seem to be

> waiting for an opportunity to try it while other things remain

> constant, so I can try to evaluate the effect.

>

> I hope we'll hear from others - the board's been quiet lately, but I

> know there are many who've considered, and some who've pursued, anti-

> coagulation treatment. They will probably have better answers about

> testing.

>

>

> Duramater wrote in part:

>

> In short, I see the ANS dysfunction hypothesis as valid (just as I

> see CNS dysfunction as valid simply as a consequence of direct

> infection). So my question was less about which hypothesis is valid

> and more about how does one discriminate between these hypotheses in

> the absence of a blood test.

[Guest guest]

I posted a reply to your question on the Lyme site.

I will give the link here since I have done it before.

http://cure2003.conforums.com/index.cgi

There is a whole topic on hypercoagulation, lots to read.

[Guest guest]

It was Jelly's information and Ken's site that helped me get my head

around the ISAC issue, living in the UK I had to self treat so I

needed to be sure of what I was doing. Berg was very helful

too, it soon became clear it had been a long standing problem for me,

since my childhood in fact. I used bromelain.

Until I started herxing on my so-called gentler lyme protocol I

became aware of the differences between what seemed to be applicable

to the ISAC and what could be attributed to neuroborreliosis, like

S I am significantly affected and disabled by it, I have been

for many years.

Cheers, Tansy

>

> I posted a reply to your question on the Lyme site.

>

> I will give the link here since I have done it before.

>

> http://cure2003.conforums.com/index.cgi

>

> There is a whole topic on hypercoagulation, lots to read.

[Guest guest]

> >

> > I posted a reply to your question on the Lyme site.

> >

> > I will give the link here since I have done it before.

> >

> > http://cure2003.conforums.com/index.cgi

> >

> > There is a whole topic on hypercoagulation, lots to read.

[Guest guest]

Just to add some background to my reply post on

“unclear as to how/why hypercoagulation may be a consequence of chronic infection.”

Because the immune system does not recognise our [stealth] pathogens as presenting antigens……. The IS is not switched on at the time of infection onset …the IS is switched on in response to the toxins & tissue damage our pathogens create , But as macrophages have several roles…. infection recognition & eradication , wound clearance & injury healing the macrophages are misdirected into stimulating the laying down of fibrin ….as there are many sites of inflammation [chain reaction of Angiotensin II] those sites attract fibrin production . The ARB’s {Benicar] close down the chain reaction production of Ang II removing one method the pathogens use to hide from the IS .

-----Original Message-----From: Jaep [mailto:Jaep@...]Sent: 06 April 2005 19:39infections Subject: RE: [infections] ANS probs or Hypercoagualtion?

“unclear as to how/why hypercoagulation may be a consequence of chronic infection.”

I think this is approximately what’s going on

Macrophages ,have a number of roles , in simple terms they react inappropriately to our type of infection… the response is to injury …laying down fibrin rather than adopting a killing engulfing role .

The motor is inflammation

“However, in inflammatory reactions initiated by the immune system, the ultimate control is exerted by the antigen itself, in the same way as it controls the immune response itself. For this reason, the cellular accumulation at the site of chronic infection, or in autoimmune reactions (where the antigen cannot ultimately be eradicated), is quite different from that at sites where the antigenic stimulus is rapidly cleared”

In general, lymphocytes are involved in the adaptive response to inflammation, and the early events of inflammation are mediated in part by molecules produced by cells of the innate arm of the immune system.

Early phase mediators are produced by mast cells and platelets. They are especially important in acute inflammation and include mainly histamine, serotonin and other vasoactive substances. Platelets may contribute to inflammatory responses resulting as a consequence of tissue injury, through a variety of mechanisms including:

the release of vasoactive amines and other permeability factors, the release of lysosomal enzymes, the release of coagulation factors which lead to localized and generalized fibrin deposition, and the formation of platelet aggregates or trombi which result in the blocking of vessels and capillaries.

http://nic.sav.sk/logos/books/scientific/node25.html

http://www.anapsid.org/cnd/diffdx/hypercoagulation.html

-----Original Message-----From: duramater27 [mailto:spam-barb@...]Sent: 06 April 2005 17:28infections Subject: [infections] ANS probs or Hypercoagualtion?OK, first off, I am (A) very sketchy as to the proposed symptoms of hypercoagulation, and ( unclear as to how/why hypercoagulation may be a consequence of chronic infection.With those caveats (and implicit questions!) in mind, bear with my query:Several symptoms that I have are being described as "autonomic nervous system dysfunction." They include cold/bluish legs and occassionally hands, difficultly breathing, heart arrythmias, chest pain, and orthostatic hypotension. Now, if what little I've been able to ascertain re: hypercoagulation symptoms is accurate, don't these overlap?And if they do overlap, how does one discriminate between ANS dysfunction and hypercoagulation in the absence of a blood test? I've heard about the HEMEX panel but I don't have a doc that is willing to go that far down the alternative explanation aisle (including the lyme doc consulting with my PCP).Again, am curious as well to seeing a list of symptoms and hearing about the how/why of this proposed dysfunction.Thanks.