heat

[Scott1]

Hi 1eye,

I don't envy what you have to deal with.

On the issue of demyelination, I find myself more troubled by the standard thinking since I had my Botox shots in the leg. The reason is that it did help but the action of the treatment is to temporarily "kill off" the ends of the dendrites that plate to the muscles. The idea being if there is no neurotransmitter triggering the muscle to tighten then it becomes possible to stretch it. Taking the thinking of why they did it, they are not influencing the axon. It is remote from the local action of the injection.
If you pretended that you were the neuron, imagine you have your arms extended in a T shape. Your right arm is an axon, your head is the cell and your left arm is the dendrite. All the botox does is chop off the fingers of the left hand. They grow back and, like new growth on a tree, are better than before. None of this has anything to do with the Axon except by accident.
So extrapolating from that, that nerve problems can't be just the fault of demyelination. There must be more to consider.

Even if antivirals are beyond your budget, I would try to influence the respiration of the cell using Q10 as a minimum. The dose would have to be at least 300mg daily. I take 750 mg. It's just a hunch it might help you with heat. Nothing more.

Regards

[NHE]

If the myelin paradigm of insulation on a wire is accurate, the wire itself (not the insulation) is what responds linearly and posiitively to temperature.

Wires don't have nodes of Ranvier and don't undergo saltatory conduction. The analogy is limited at best.

[NHE]

I found these...

Effect of passive whole body heating on central conduction and cortical excitability in multiple sclerosis patients and healthy controls.
J Appl Physiol. 2013 Jun 15;114(12):1697-704.

• Heat stress is associated with increased fatigue perception and decrements in function for individuals with multiple sclerosis (MS). Similarly, healthy individuals experience decrements in exercise performance during hyperthermia. Alterations in central nervous system (CNS) function during hyperthermia include reduced voluntary activation of muscle and increased effort perception. The purpose of this investigation was to test the hypothesis that passive heat exposure in MS patients will produce increased subjective fatigue and impairments in physiological measures of central conduction and cortical excitability compared with healthy individuals. Eleven healthy individuals and 11 MS patients completed a series of transcranial magnetic stimulation studies to examine central conduction and cortical excitability under thermoneutral and heat-stressed (HS) conditions at rest and after a fatiguing thumb abduction task. Passive heat stress resulted in significantly greater fatigue perception and impairments in force production in MS patients. Central motor conduction time was significantly shorter during HS in controls; however, in MS patients normal increases in conduction velocity with increased temperature were not observed centrally. MS patients also exhibited decreased cortical excitability during HS, evidenced by significant increases in resting motor threshold, decreased MEP amplitude, and decreased recruitment curve slope. Both groups exhibited postexercise depression of MEP amplitude, but the magnitude of these decrements was amplified in MS patients during HS. Taken together, these results suggest that CNS pathology in MS patients played a substantial role in reducing cortical excitability during HS.

From the discussion section...

For MS patients, the apparent inability of central pathways to increase conduction velocity during conditions of increased core temperature may reflect altered conduction characteristics due to demyelination in the CNS.

and...

Central conduction (CMCT) was significantly shorter during HS in healthy controls; however, in MS patients, normal increases in conduction velocity with increased temperature were not observed centrally. Both groups exhibited increased peripheral nerve conduction velocity, supporting the concept that differences between MS patients and controls were of central origin.

and...

In demyelinated neurons, studies have shown that increased temperature reduces the conduction safety factor and can produce conduction slowing and/or conduction block.

...which references the following three papers...

Influence of temperature changes on multiple sclerosis: critical review of mechanisms and research potential.
http://www.ncbi.nlm.nih.gov/pubmed/7751837

The effects of temperature on conduction in demyelinated single nerve fibers.
http://www.ncbi.nlm.nih.gov/pubmed/4696011

Note: This paper is from 1973 and no abstract is available.

Impulse conduction in multiple sclerosis: a theoretical basis for modification by temperature and pharmacological agents.
http://jnnp.bmj.com/content/37/2/152.long

[Scott1]

Hi,

I don't doubt heat is an issue in MS as I have experienced it. I'm just not sure, even allowing for these articles, that the relationship with demyelination is as closely correlated as we think. Those articles, particularly the last one, use mathematical models to develop the relationship but PH levels are also mentioned.
I have a pretty good chunk of myelin missing around C7 , for example, but heat doesn't trouble me now. It can't be only the demyelination. Where is my correlated outcome?
Should we just assume that demyelination causes fatigue and heat intolerance? They are only working from models.
Why do we ignore other relationships that look at the exchange of calcium in and out of cell or sodium or potassium?

I know what demyelination feels like due to how it affects my hands. The tightness in my legs could just as easily be reperfusion injury. They don't feel anything like my hands yet they are affected.

1eye has raised a really important topic - do the people like me who have demyelination but no heat intolerance present an opportunity to explore a better option than just avoidance?

This article is not about MS but looks at heat from Sauna in healthy controls - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4042662/


Regards

[NHE]

I have a pretty good chunk of myelin missing around C7 , for example, but heat doesn't trouble me now. It can't be only the demyelination. Where is my correlated outcome?
Should we just assume that demyelination causes fatigue and heat intolerance? They are only working from models.

That modeling paper is from 1974. I only mentioned it because it was one of the references cited for the quoted statement from the discussion section. The first paper took measurements on both MS patients and healthy controls.

[1eye]

I'm not saying it would be conclusive, but wouldn't it be very valuable to actually test demyelinated neurons in vitro rather than show off the size of one's intellect with a lot of theorizing? Empirical evidence works for me. I think we have a murine model using CSF from actual MS patients that probably includes demyelination.

Incidentally, had another trike ride of 15km yesterday, in more bloody heat, but was OK with the coolers and wet do-rag. I realize from hard experience that I risk my life, but I regularly omit the helmet. Will probably get a ticket eventually. The best cooler is this thing with water-absorbing crystals, worn around my neck, but it really is better on my trike because of the moving air, which cools, even when it is hot air. The wet do-rag gets too hot. I guess that's because heat rises.

Again incidentally last night the air conditioner was left off accidentally. Sweating seems to be noticeable around my neck. Woke up grouchy.

[pawel96]

Lupus and rheumatoid arthritis are some (but not all) examples of autoimmune diseases that get worse by heat but they do not affect the neurons. So I do not accept slowed conduction velocities due to demyelination as an only explanation why MS symptoms get worse with increasing heat. It is too much rocket science when there are far more obvious reasons: increased inflammation, edema around lesions, pressure on tissue, restricted blood flow to some parts of brain (due to edema).

P.

[1eye]

I have one sibling with lupus, one with RA and Reynauds.

To me, the most obvious reason in my MS, is my cooling system's gerfunckt. Why?

Has anyone done studies to prove or disprove this? The human body has an incredible cooling system. We use a large part of our energy budget contracting and expanding our 60,000 miles of blood vessels so as to redistribute blood, among other reasons, to control local temperature. The contracting and expanding of the diameters of these vessels results in a change of flow which uses a fourth-power mathematical relationnship of diameter to flow -- one of the most powerful mechanisms in living things. The result is a precision of temperature control not found in even very sophisticated household devices: 3 digits of accuracy as we measure it, probably 4 or more as the body sees it. Your household thermometer usually has only two.

But body temperature is only measured with instruments usually in mouth, armpit or rectum. I would think there is a range of "normal" temperatures depending on where you do the measuring, what the ambient conditions are, and what activities the body is engaged in. I used to try to fool my mother into thinking I was sick by waving the thermometer near a hot-air duct. I think there is a possibility the prime failure in MS is the failure of our blood vessels to expand and contract properly to redistribute heat via our blood vessels. Can it be that all of my symptoms that are variable can be traced to failure to control local brain, nerve, and muscle temperatures? How can we find this? Are there accurate enough temperature imaging devices?