If not the conductivity, then WHY?

Apparently this heat sensitivity phenomena now has a name - Uhthoff's phenomenon (also known
as Uhthoff's syndrome,

From Wikipedia: Uhthoff's sign, and Uhthoff's Symptom is the worsening

of neurologic symptoms in multiple sclerosis (MS) and other neurological, demyelinating conditions when the body gets overheated from hot weather, exercise, fever, or saunas and hot tubs. It is possibly due to the effect of increased temperature on nerve conduction. With an increased body temperature, nerve impulses are either blocked or slowed down in a damaged nerve but once the body temperature is normalized, signs and symptoms may disappear or improve. The etiology of HR may be multifactorial. This includes: heat itself, effects of serum calcium, blockade of ion channels, circulatory changes, heat shock proteins unidentified humoral substances.

Research techniques are suggested to continue investigations into the enigma of HR, hopefully to widen knowledge of demyelination. Davis SL, Frohman TC, Crandall CG, et al. (March 2008). "Modeling Uhthoff's
phenomenon in MS patients with internuclear ophthalmoparesis"

And there come the articles, proving that indeed my initial hypothesis was (is) true:
Mechanisms of lability of neurological symptoms in multiple sclerosis
[Article in Russian]
Peresedova AV, Badina EV, Trifonova OV, Azenberg IV, Gnezditski VV, Barkhatova VP, Chernikova LA, Zavalishin IA.
Zh Nevrol Psikhiatr Im S S Korsakova. 2002;Suppl:15-9.

(http://www.ncbi.nlm.nih.gov/pubmed/12418387)
Abstract Pathophysiological peculiarities of demyelinated axons determine their high sensitivity to different exogenous factors and are the reason of instability of neurological signs in MS. One of the typical MS sing is high sensitivity to elevated temperature of the body. Even temporary elevation in body temperature may cause changes in impulse conduction in demyelinated fibres, which was proved by studies of evoked potentials and stabilometric studies. These disturbances may be associated with

disorder of ions channels function. The role of other factors (metabolic and immunological disturbances, levels of cytokines and neurotransmitters) in temporary block of nerve conduction in MS is discussed. Further studies of the mechanisms of the lability of neurological sings in MS may lead to elaboration of new approaches to MS treatment.

On the temperature sensitivity of multiple sclerosis patients (author's transl)].

[Article in German]
Brenneis M, Harrer G, Selzer H.

http://www.ncbi.nlm.nih.gov/pubmed/256872 Abstract Aggravation of neurological symptoms in MS patients in heating is well known. This phenomenon is explained by the change of conduction in demyelinated nerve fibers. In raised temperature conduction block occurs. The threshold of conduction block dependent on temperature, is probably proportional to the degree of demyelination. It is possible to inhibit this effect by tyrosin. This model may present a view to a part of neurophysiological mechanisms of MS, on which we possibly can take therapeutical influence. By way of a questionnaire 125 MS patients were asked about changes of their symptoms in heating or cooling. 93% had marked sensitivity to heating. In 90% worsening of neurological symptoms or of general feeling occured in a hot bath. On the other hand about half the patients reported improvement in a cold bath. Therefore we suggest, that a noticeable part of neurological deficit is reversible, if we were able to raise the threshold of conduction block, which depends on temperature, ph, electrolytes and neurotransmitters.
Neurology. 2008 Mar 25;70(13 Pt 2):1098-106. doi: 10.1212/01.wnl.0000291009.69226.4d. Epub 2008 Feb

20.

Modeling Uhthoff's phenomenon in MS patients with internuclear ophthalmoparesis.

Davis SL, Frohman TC, Crandall CG, Brown MJ, Mills DA, Kramer PD, Stve O, Frohman EM.

Source: Institute for Exercise & Environmental Medicine, Presbyterian Hospital of Dallas, TX, USA. Abstract
OBJECTIVE: The goal of this investigation was to demonstrate that internuclear ophthalmoparesis (INO) can be utilized to model the effects of body temperature-induced changes on the fidelity of axonal conduction in multiple sclerosis (Uhthoff's phenomenon). METHODS: Ocular motor function was measured using infrared oculography at 10-minute intervals in patients with multiple sclerosis (MS) with INO (MS-INO; n = 8), patients with MS without INO (MS-CON; n = 8), and matched healthy controls (CON; n = 8) at normothermic baseline, during whole-body heating (increase in core temperature 0.8 degrees C as measured by an ingestible temperature probe and transabdominal telemetry), and after whole-body cooling. The versional disconjugacy index (velocity-VDI), the ratio of abducting/adducting eye movements for velocity, was calculated to assess changes in interocular disconjugacy. The first pass amplitude (FPA), the position of the adducting eye when the abducting eye achieves a centrifugal fixation target, was also computed.

RESULTS: Velocity-VDI and FPA in MS-INO patients was elevated (p < 0.001) following whole body heating with respect to baseline measures, confirming a compromise in axonal electrical impulse transmission properties. Velocity-VDI and FPA in MS-INO patients was then restored to baseline values following whole-body cooling, confirming the reversible and stereotyped nature of this characteristic feature of demyelination. CONCLUSIONS: We have developed a neurophysiologic model for objectively understanding temperature-related reversible changes in axonal conduction in multiple sclerosis. Our observations corroborate the hypothesis that changes in core body temperature (heating and cooling) are associated with stereotypic decay and restoration in axonal conduction mechanisms.