More on heat sensitivity or Uhthoff's phenomenon

#MSBlog: More on temperature sensitivity; how temperature blocks conduction in demyelinated axons!

Stutzer & Kesselring. Wilhelm Uhthoff: a phenomenon 1853 to 1927. Int MS J. 2008 Sep;15(3):90-3.

The name of Wilhelm Uhthoff is associated with several aspects of progress in neurology in the 19th and 20th Century but is best known for his contribution to the pathophysiology of transient visual disturbance in people previouslt affected by optic neuritis. Uhthoff was born on 31 July 1853 in Klein Warin, Germany and died on 21 March 1927 in Breslau, Germany. This ophthalmologist described for the first time that increased body temperature from physical exertion may lead to transient impairment of vision in MSers.

"This figure shows you the affect of temperature on conduction velocity for a normal nerve fibre (upper curve) and for fibres with increasing loss of myelin (lower curves). For each curve the last point on the right is for the highest temperature at which continuous electrical conduction is possible, the dashed lines and arrows indicate a block of conduction The amount of demyelination in this figure is expressed relative to normal. What this shows that if you have a demyelinated axon it becomes very susceptible to temperature, for example normal fibres only block above 44 degrees C and fibre that is 67% demyelinated blocks at temperature at or slightly above body temperature. What worries me is that these fibres that are maintaining conduction are vulnerable to degenerate in the future. This is why we need to protect them so that they can remyelinate and correct their temperature sensitivity."

"The following two videos demonstrate how a normal and demyelinated nerve fibre conducts. It is clear  that the demyelinated one uses a lot of energy to transmit an electrical signal. This in itself may damage and cause the nerve fibre to degenerate over time. For those of you who think remyelination strategies will be sufficient to cure or treat MSers need to think again. We think MS is an immune disease that attacks myelin, therefore without supressing the immune attack on myelin and new myelin t hat is formed will simply be damaged again and with time this process fails. This why we need three approaches to treat MS; (1) anti-infammatories, to suppress the inflammation, (2) neuroprotective agents to keep the axon and nerve cell alive so that (3) remyelination can occur. The evidence that we need to augment remyelination in MSers is weak; all the evidence suggests you can do it on your own provided the inflammation is suppressed and the axons are still there to remyelinate. This may be why we see improvements in disabilities occurring when you are treated with more effective treatments."

"Conduction in a normal axon; note how fast it conducts with minimal effort or energy!" 

"Conduction in a demyelinated axon. It has restored conduction by a process called axonal plasticity. The conduction is slow and laboured and requires a large amount of energy  to conduct the electrical impulse. This axon is very temperature sensitive and is liable to block with a rise or possibly a fall in temperature. This axons is also susceptible to degenerate unless we can protect it long enough so that the body can remyelinate it."

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