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1eye wrote:Maybe some things affected by autonomic nerve pathology get more automatic, and some less. Then wouldn't it depend on individual physiological differences, and how they affect specific nerves? And be predictable, but only in a particular individual?

Not only genetic makeup, but life history as well?

1eye wrote:Does the vagus predominate in the symptoms? Is it involved in intention tremor, which was among my earliest symptoms? Where do eyeballs fit in? Vision is pretty voluntary, so not placebo. In fact, aren't most eyesight improvements very testable, outside of placebo concerns? You can't turn it off without blinking.

1eye wrote:I thought the autonomic nervous system was just that: autonomous, and so by definition not placebo.

It is a well established fact that the autonomic nervous system (ANS) can be influenced by the person and therefore in conjunction with a placebo (i.e., inactive) treatment (Ross & Buckalew, 1985). For example, Cowan, Kogan, Burr, Hendershot, and Buchanan (1990) found that cardiac patients could cognitively increase their HRV through biofeedback training. If the ANS is altered, this result will be shown in HRV measurements.

Anonymoose wrote:I was reading through CCSVI treatment improvement stories yesterday and saw one instance in which a man went in for his followup checkup and thought he would be given the thumbs up since all of his improvements from treatment were still there. He had restenosed and had to be re-ballooned.

Anonymoose wrote:I had posted a link about the hpa axis dysregulation (autonomic) that increased with progression of ms in my original Aldo thread. The question is...which came first? The dysregulation or the ms? Is dysregulation driving the ms? That would account for the variability in the way ms presents and progresses in different people.

This experiment supported the researchers' first hypothesis, that vagal nerve stimulation produces dramatic surges in norepinephrine in a brain area involved with memory storage, a finding that almost certainly generalizes to humans. What's more, Williams says, "The magnitude and time course of changes in amygdala norepinephrine almost mirrored the changes produced by the dose of epinephrine that has been shown to improve memory."

Vagal influence on the adrenocortical function of the rat.
González-Fernández I, Gonzalo-Sanz LM.
Source
Departamento de Anatomía, Facultad de Medicina, Universidad de Navarra, Pamplona, Spain.
Abstract

The vagal influence on the fasciculata's function was studied in 23 Wistar male rats. The corticoadrenal function was evaluated by means of karyometric and histological studies. After vagotomy, the fasciculata of the left adrenal (operated side) showed a significant increase of the nuclear area in comparison with the right (control) side. This side difference was maintained in the stressed rats. In these animals the nuclear area did not increase significantly in either of the two adrenals. These results lead to the following conclusions: the vagus nerve, in normal conditions, has an inhibitory influence on the adrenal cortex; the vagal participation in the corticoadrenal response to a neurogenic stressor is meagre; the inhibitory vagal action on the fasciculata must be direct since the corticoadrenal modifications were unilateral, whereas, if the vagal influence were exerted through the hypophysis, the adrenal reaction should be bilateral; and, finally, the participation of the vagus nerve in the adrenal vascular disorders, which appeared in the stressed rats, seems to be insignificant since both glands, vagotomized and non vagotomized, showed a similar appearance.

Role of the Vagus Nerve at the Neural-Immune Interface

Afferent vagal pathways transmit information to the brain related to peripheral inflammation so as to participate in the activation of adaptive reactions, including fever and sickness behavior. On the other side, efferent vagal pathways inhibit the synthesis and release of pro-inflammatory cytokines by peripheral immune cells. Because activation of afferent vagal pathways by immune stimuli leads to suppression of immune reactions, the term inflammatory reflex was introduced. The inflammatory reflex adjusts the intensity and duration of inflammatory reactions according to actual needs, thus protecting an organism from tissue damage induced by excessive inflammation. Both experimental and clinical studies suggest that inappropriate activation of the inflammatory reflex participates in the development of diseases characterized by excessive production of cytokines.', '

Intrinsic Factor Secretion and Cobalamin Absorption: Physiology and Pathophysiology in the Gastrointestinal Tract

1991, Vol. 26, No. s188 , Pages 1-7
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H. P. M. Festen†
Groot Ziekengasthuis,'s-Hertogenbosch, The Netherlands
†Correspondence: Dr. H.P.M. Festen, Dept. of Internal Medicine, Groot Ziekengasthuis, Nieuwstraat 34, 5211 NL's-Hertogenbosch, The Netherlands

Intrinsic factor is produced by the gastric parietal cell. Its secretion is stimulated via all pathways known to stimulate gastric acid secretion: histamine, gastrin, and acetylcholine. There is, however, a different mode of secretion for both substances: atropine, vagotomy, and H2 receptor antagonists inhibit both intrinsic factor and acid secretion, but secretin and the hydrogen-potassium ATPase antagonist omeprazole have no effect on intrinsic factor while substantially reducing acid secretion. Cobalamin in food is bound to animal protein. Cobalamin deficiency due to inadequate dietary intake is rarely seen in extreme vegetarians (vegans). In the stomach cobalamin is liberated from its protein binding by peptic digestion and bound to R-proteins. Hypochlorhydria or achlorhydria, whether medically induced or not, may impair cobalamin uptake. The cobalamin-R-protein complex is split by pancreatic enzymes in the duodenum, where cobalamin is bound to intrinsic factor. Pancreatic insufficiency may lead to cobalamin deficiency. Lack of intrinsic factor is the commonest cause of cobalamin deficiency; very rarely, aberrant forms of intrinsic factor are produced, but the clinical syndrome is similar. Gram-negative anaerobe bacteria bind the cobalamin-intrinsic factor complex, and bacterial overgrowth of the small intestine diminishes cobalamin resorption. Parasitic infections with fish tapeworm and Giardia lamblia are also associated with cobalamin malabsorption. The cobalamin-intrinsic factor complex binds to the ileal receptors in the terminal ileum. Cobalamin absorption may be impaired after resection or by diseases affecting more than 50cm of the terminal ileum, such as Crohn's disease, coeliac disease, tuberculosis, lymphoma or radiation. There is clearly a wide diversity in the aetiology of cobalamin deficiency, which requires a versatile diagnostic approach.

Read More: http://informahealthcare.com/doi/abs/10 ... 9109111222