Migraine-like symptoms nearly always present with reduced systolic blood pressure (below 105), or with a sudden relative drop in blood pressure prior to the migraine onset. Although this connection is weakly documented in medical literature, it is easily verified.
Several theories describe migraine cause, Depolarization, Vascular, Neural and Unifying. Curiously, none of these theories suggests that tissue oxygen deprivation as a trigger or cause for migraine. Hypoxia conditions, relating to capillary performance, and functional oxygen delivery, are fully hidden in medical evaluation methods, except in advanced cases where the arteries are sufficiently degenerate and show occlusion or aneurysm.
A French study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early migraine stages. A disabled hypothalamus, controls blood flow, both victim and cause of poor oxygen during a migraine. The victim/cause pattern makes complicates recovery and explains why migraines tend to last a long time 4-72 hours.
The depression wave model results from the spreading hypoxic distress of brain tissue. We assert that the hypoxic (stress) triggers a portion of the brain to enter anaerobic glycolysis which causes local acidosis, which further inhibits the aerobic metabolism of nearby brain areas, which causes them to enter anaerobic glycolysis. The effect is a "wave" which puts a large region of the brain into distress.
We assert that migraine attacks are triggered by a blood desaturation failure from a stress event. This failure causes a drop in usable oxygen delivery to brain, directly or by triggering capillary edema. The drop below the migraine-trigger-threshhold causes a cascade effect of distress processes including potentially neurotransmitters, hormones, inflammation and so on.
Both Manfred von Ardenne and Dr. Emanuel Revici developed methods that reduce the severity and incidence of migraines, though different, but complementary mechanisms:
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