Revision and submission (re:for your consideration)

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Posted by Michel L ( on November 04, 1999 at 06:49:06:

Questions have arisen that I think I can address and finally correct my hypothesis and make it truely sound. For this I must use the perfect CH model. This will address the questions about the circadian objection, the vasodilation and the pain itself.

There were to many causal effects in my previous post. There is only one cause for the myelin sheath injury in the perfect CH sufferer, and this cause is a virus or a class of virus. The damage caused to the neural system is more extensive than I tought at first. The virus also reduces the ability of the sufferer to produce normal quantity of serotonin and by this depletion reduces the necessary serotonin stimulation needed to produce sufficient neurosteroids.

The CH sufferer as a treshold or viable quantity of serotonin-neurosteroid most of the time until the suprachiasmatic nucleus decides that it this the right time to further reduce serotonin production. The suprachiasmatic nucleus as no sense of what compound is needed and in what quantities, so the serotonin level reduction inhibits production of the neurosteroids.

Inflamability of the defective nerve is already in its steady near firing range and the lack of neurosteroids permits it to inflame just enough to cross the treshold and so a cycle begins. The cycle will last until the SPN decides it is time to command the elevation of serotonin - neurosteroids levels. This will permit reduction of the inflamation just under the firing range of the damage nerves.

I submitted that the damaged nerves were using sodium-potassium as fuel. The brain as no knowledge that the nerve is defective. When a neural entity within the cervical-cranial region burns sodium as fuel, the only possible interpretation by the brain is that this nerve is dying. Sodium consumption by a cell only occurs when totally lacking oxygen. It is dying. In our case this is not true, but the brain puts is number one priority in saving the neural connection and to achieve this goal provokes an almost instantaneous vasodilation in the hopes of bringing maximum oxygen to the dying connection. Pain is not an object here, the brain will kill you to save the neural connection. The pain you feel comes from the extreme dilation combined with the neural impulses. Since the emergency of saving the neural connection can appear more than once per day, the sufferer will as many attacks as this impulse-dilation phenomenom occurs. The brain may be successfull in its attempt to bring enough oxygen and reduces the neural inflamation under the firing treshold; once the danger is passed, rapid vaso constriction occurs to limit heat loss and oxygen excess in the cranial area. The contrary is not valid. Even if oxygen is a powerfull vasoconstrictor, the brain will let the vessels contract only when the sodium signal from the nerve will stop.

This of course is a very basic interpretation, but it was depriving me of sleep to think about it, so I decided to submit it so we can close this chapter.

Michel L’Ecuyer

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