This Is MS Multiple Sclerosis Community: Knowledge & Support

A basic lateral cervical x-ray view would help. The cervical MRI or the radiologists report would be better.

Brain. 2010 February; 133(2): 433–447.

Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment

...Although a few studies have shed light onto the possible roles of immune cells in the injured central nervous system, the underlying mechanisms are complex and remain unclear. Growth factors and protease inhibitors released by macrophages or T cells are thought to promote neuro regeneration (Cantini and Carraro, 1995; La Fleur et al., 1996; Jameson et al., 2002; Yin et al., 2006). Conversely, conditioned-media collected from PMNs or macrophages has been shown to promote neurotoxicity in vitro (Flavin et al., 1997; Brana et al., 1999; Nguyen et al., 2007). Although specific macrophage-derived neurotoxic factors have not been identified, we have shown that matrix metalloproteinases, reactive oxygen species and tumour necrosis factor-α released by PMNs all promote neurotoxicity in vitro (Nguyen et al., 2007). Additionally, physical PMN-to-neuron contact has been shown to enhance neurotoxicity (Dinkel et al., 2004). As similar mechanisms are likely to be involved in immune cell function after spinal cord injury, understanding the kinetics of cellular inflammation after spinal cord injury is essential for the development of effective therapeutic interventions...

European Journal of Neurology
Volume 9 Issue 1 Page 101 - January 2002
doi:10.1046/j.1468-1331.2002.00336.x

MR findings in subacute combined degeneration of the spinal cord caused by nitrous oxide anaesthesia - two cases
S. Ilniczky a , I. Jelencsik a , J. Kenéz b & I. Szirmai a

Discussion

The SCD may be the only manifestation of cobalamine deficiency in one-third of the patients (Hensing, 1981; Lindenbaum et al., 1988). Patients with mild haematological findings are often misdiagnosed. This is illustrated in Case 1, with borderline anaemia and the slightly elevated MCV. Although the second patient presented the typical haematological findings, the link with the neurological symptoms was simply overlooked. Surgical anaesthesia, as a pathogenetic factor was not considered.

Nitrous oxide may provoke symptoms of vitamin B12 deficiency because of the impairment of the methylcobalamin-dependent methionine synthetase reaction (Beltramello et al., 1998; Giron et al., 1998). It seems likely that patients having subclinical vitamin B12 deficiency are candidates for the N2O provoked SCD (Schilling, 1986; Filippo and Holder, 1993). Some patients respond poorly to vitamin B12 supplementation, but methionin therapy may be successful (Stacy et al., 1992).

High intensity signals in the posterior columns of cervical or thoracic spinal cord on T2 weighted MR scans in SCD were already described in five cases (Berger and Quencer, 1991; Murata et al., 1993; Wolansky et al., 1995). In one of these cases SCD also developed after N2O anaesthesia (Timms et al., 1993).

Inspite of the clinical evidences of corticospinal tract involvement hyperintense changes in the lateral columns could not be seen, but it may be because of the resolution limits of the MRI (Timms et al., 1993). The MR changes after N2O narcosis may indicate demyelination, which is proved to be reversible after B12 vitamin substitution. In our cases - with regards to the short latencies after the N2O exposure - surgical anaesthesia may only have been a provoking factor of the manifestation of subclinical B12 vitamin deficiency.

CN,
Notice in the study above that the connection between SCD and anemia in one of the cases was simply overlooked despite the presence of positive lab blood work signs indicating anemia. The key to the cure is catching the condition early before it does permanent damage.

What tests should she have doctor?
We ll need to go to a private hospital, that's for sure. What do you think? Should we wait for her results to come out?

The cord should be checked for symmetrical hyperintensity lesions. She needs a thorough case history to include digestion and elimination to check for indications of possible digestive problems such as hydrochloric acid and pancreatic enzyme deficiencies in the upper GI tract, and inflammatory bowel and malabsorption signs in the lower GI. Lab work should include a Complete Blood Count (CBC) with differential and indices, as well as SMA 25. More importantly, she also needs someone to go through the results with a fine tooth comb to check for borderline anemia, and she should get the Schilling test to check for problems with Vitamin B12 utilization.

I hate tests. Sounds more than I can handle, let me tell you...
Blood and lab tests will go first. One step at a time.

"...Patients with mild haematological findings are often misdiagnosed..."

The standard blood and chemistry tests are easy to do and should be just as easy to get even in Greece. You should also have them include a liver panel as well if possible. The Schilling test is slightly inconvenient but easy to do and it includes treatment. The inconvenience is you have to see a doctor frequently in the initial stages for the B12 injections.

Below is an interesting case posted on the comments page of my blog on intracranial hypertension and an autoimmune-inflammatory condition that was triggered by antibiotics ...

I have had Intracranial Hypertension for 8 years since taking Tetracycline antibiotics. It did not reverse afterwards.
But, I also have a variety of autoimmune disorders, including vasculitis. If I take diuretics it makes the condition tolerable. But, as my general blood pressure is normal, the diuretics drop it and I have side-effects from that.
I have now developed permanent poor memory, and a M.R.I. reveals ischaemia in the cerebral white matter. I am keen for this not to continue worsening!!!

How can I work out which could be what? I am limited to testings, as anything injected into my veins triggers an autoimmune flare, which then causes more irreversible damages.

Anything injected into the bloodstream, including vaccines and local anesthetics, bypass important parts of natural immunity and trigger the compliment immune system. Left unchecked, the compliment immune system can be very destructive.

Hi Dr, thanks for posting this, I missed it on your Blog.

I have a different thought pattern when I see this type of experience.
a. Firstly why was ABx used in the first place?

b. Did the time on the ABx generate any symptom changes?

c. What were the tests done to make the dx and decision to use ABx, and was there a retest after the ABx use. I would also add that retesting some months later is advisable to ensure the 'issue' is not a Stealth Bacteria http://beyondthebandaid.com.au/concept- ... nfections/ and all that has happened is that the Bacteria has gone dormant for the period that the ABx is in the patients system.

d. Have there been flairs of symptoms over time both before and since the ABx treatment and what was the cause of this, did bloods targeted at antibodies show any indications of immune activity?

e.What is really happening in regard to the current symptoms and how does that compare to the History'development of the patients symptoms?

Quote;"Anything injected into the bloodstream, including vaccines and local anesthetics, bypass important parts of natural immunity and trigger the compliment immune system. Left unchecked, the compliment immune system can be very destructive."

I totally agree with this comment, my insights to this are that the activation by introducing Immune System activators has lasting effects that are NOT understood.
There are pages of peer reviewed documents that assume the positive and the negative outcomes from use of 'introduced' man made products. The bottom line is that there are no studies that follow the action, of for instance, ABx because the life cycle of the, for instance, Bacteria is not known in detail.
The Bacteria CPn for instance has had some follow up studies on aspects of the life cycle (Stratton, Siriram and others http://www.CPn Help.org/?q=node/29 ) and it's presence in a patient. Any persistent infection or chronic infection is going to require a life long monitoring to manage the re-infection possibilities.
Re-infection of many MS related co-infections such as CPn, Lyme, Mycoplasma and other known bacteria are clouding the picture of the first infection and commencement of symptoms, the dx challenges for MS, the dx challenges for Bacterial infections and the treatment of both MS and Bacterial infections over a life span are all in the Ethers!
When flairs happen in MS for instance it is still not known what is activating the symptoms at a cellular level, until these changes are understood there will be no further progress. The Pharma industry wants to modify rather than find the cause so Research stops each time an opportunity to change the disease progression happens the research stops searching for the process cause and drifts off on the side track of changing symptoms rather than stopping symptoms at there cause.
I put a poster on my site ( https://www.facebook.com/pages/CCSVI-in ... 1636357984 ) that I think is worth pondering!
https://www.facebook.com/photo.php?fbid ... nt_count=1

Change is Eminent!

Have a Great Day,
Nigel

IIH is typically associated with overweight and pregnant females. There are many different causes such as the endocrine system. The dural sinuses and venous obstruction have also long been suspected as potential causes of IIH. I suspect it has to do with the design of the skull, spine and pelvis that predispose females to back pressure against the venous drainage system of the brain. Tetracycline, minocycline, doxycycline and hypervitaminosis A are known to trigger IIH but the signs and symptoms typically resolve after ceasing the antibiotic or vitamin A. The patient probably had a low grade or a tendency to IIH prior to taking the tetracycline. She also has an autoimmune-inflammatory condition. Antibiotics can cause inflammation of the gut. Excess vitamin A causes liver toxicity. It can also cause swelling in the brain. The increase in inflammation coupled with back pressure against the venous system most likely triggered the IIH.

Thanks Dr. Again I wonder if the action of ABx and also of 'auto-immune disease is understood at all.

The changes made by killing of for instance bacteria cause endo-toxins so that is a secondary effect that needs to be factored into the use of an ABx.

Obesity has now been linked to bacterial infections that alter the metabolism.

I like to look for primary causes rather than secondary effects.

If there is an imbalance caused by, for instance, Bacterial load then the entire system goes into imbalance in opposite directions, which of cause sends out red herring symptoms.

Since this morning there has been another clip on Health prospects for degenerative diseased folk,

For those of us with MS this video will start to connect the dots or fit the missing pieces of the infamous Puzzle.
Excellent presentation, hope it goes 'viral' real quick
Thank you to https://www.facebook.com/beyondthebandaid

http://www.youtube.com/watch?v=jpvLjJ4O ... e=youtu.be


Nigel

Good presentation Nigel. In addition to infections there are many different antigens and toxins that can trigger autoimmune-inflammatory conditions, including vaccines. The cause isn't clear when it comes to vaccines. It could be the viruses, the adjuvants or other elements in the vaccine. Bypassing mucosal immunity and injecting substances into the blood stream triggers the complement immune system, which can cause a cascade of autoimmune-inflammatory reactions due to molecular mimicry, bystander and fertile field effect etc.

Nat Rev Microbiol. 2003 Nov;1(2):151-7.

Microorganisms and autoimmunity: making the barren field fertile?

von Herrath MG, Fujinami RS, Whitton JL.
Division of Developmental Immunology, Immune Regulation Laboratory, La Jolla Institute for Allergy and Immunology, 10355 Science Centre Drive, San Diego, California 92121, USA. matthias@liai.org

Abstract

Microorganisms induce strong immune responses, most of which are specific for their encoded antigens. However, microbial infections can also trigger responses against self antigens (autoimmunity), and it has been proposed that this phenomenon could underlie several chronic human diseases, such as type 1 diabetes and multiple sclerosis. Nevertheless, despite intensive efforts, it has proven difficult to identify any single microorganism as the cause of a human autoimmune disease, indicating that the 'one organism-one disease' paradigm that is central to Koch's postulates might not invariably apply to microbially induced autoimmune disease. Here, we review the mechanisms by which microorganisms might induce autoimmunity, and we outline a hypothesis that we call the fertile-field hypothesis to explain how a single autoimmune disease could be induced and exacerbated by many different microbial infections.

Thanks Dr,
another example of what I am finding, assumed answers to puzzling theories!

Technology will give the tools, one day .........................


Nigel

In the meantime, a good case history, physical exam, imaging and lab work are the best approach. The problem is most doctors aren't very good at taking case histories and doing physical exams anymore. Most are mesmerized and blinded by technology.