I can't understand how can a damaged axon transduce the signal when you think positive and not transduce it when you think negative. Perhaps I am a technocratic, super-materialistic, dogmatic ass, who only accepts what has a cause and an explanation.
By assessing central brain NAA in a relatively large, clinically stable MS population with a wide range of disability and disease duration, we showed that diffuse cerebral axonal damage (1) begins in the early stages of MS, (2) develops more rapidly in the earlier clinical stages of the disease, and (3) correlates more strongly with disability in patients with mild disease than in patients with more severe disease.
Our results emphasize that significant axonal pathology is not confined to lesions and must occur early in the evolution of MS, ie, axonal injury and loss is not restricted to the end stages of the disease. Even complete clinical recovery from acute attacks in early MS does not mean that axonal damage has not occurred. In the initial stages of MS, in addition to functional recovery due to reversal of axonal conduction block associated with inflammation and release of soluble factors,26 functional impairment due to axonal damage and dysfunction may be compensated for by mechanisms such as sodium channel redistribution27, 28 and brain plasticity.29, 30 In fact, the presence of early axonal damage in MS has been suggested in recent histological studies that showed that (1) axon degeneration can accompany acute demyelination,31 (2) milder axonal changes can occur before inflammation,32 and (3) axon degeneration can be evident in MS lesions of individuals with no history of neurologic symptoms. 33, 34 These in vitro observations lend support to our in vivo findings in suggesting that axonal damage does accumulate and is relevant to disability from the early stages of MS.
An interesting finding reported herein is that the decreases in NAA/Cr ratio were faster with respect to EDSS score in earlier stages of MS than in later stages. This should not be interpreted as evidence that axonal damage contributes less to disability later in the course of MS. In fact, with the progression of the disease, other mechanisms of axonal damage may become important and be more sensitively assessed by other magnetic resonance measures.
sou wrote:Hi AC.
Your PDF and Zamboni's study have inspired me to question everything I have read so far about MS and the nervous system. I have never been a fan of the proof-pending autoimmune dogma and the vasoconstriction theory quite fits.
Here is a post by somebody called Bob, claiming to be a healthcare teacher. I don't think there are any reasons for not believing his claim.
http://forum.neurologychannel.com/hc-fo ... 39496.html
Perhaps, it should be posted to the CCSVI thread. It is a very interesting point of view.
PS for the moderators: How do I enter shortened URLs? Does the underlying phpBB engine do this automagically?
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