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The migraine headache is considered a vascular headache, although the precise mechanism and etiology remain unknown. There are several known triggers some of which include food allergies, blood sugar disturbances, stress load, mechanical injury, and hormonal fluctuations. The vascular hypothesis of migraine, first proposed by Wolff, theorizes that the aura of migraine is caused by intracerebral constriction followed by extracranial vasodilation resulting in headache pain.(1)
Migraine may be classified as migraine without aura, formerly called common migraine, or migraine with aura, formerly known as classic migraine, and is based upon the presence or absence of focal neurologic symptoms prior to the onset of headache. The aura may consist of flashing lights, or zigzag lines, or may manifest as blind spots in the vision. Patients may even experience speech difficulty, tingling in the face or hands, confusion, or weakness of an arm or leg. The majority of patients suffering from classic migraine have an aura that develops 10-30 minutes prior to development of the actual headache. According to recent studies, the aura is believed to be the response to a trigger that creates a neuronal depression. This may result in as much as a 25-35 percent reduction in cerebral blood flow, and is certainly enough to cause the symptoms associated with the aura.
Auras are experienced by approximately 10 percent of migraineurs.(2) The International Headache Society has developed a classification system of migraine headaches that includes six subdivisions under the heading migraine with aura. These include the following:
- Migraine with typical aura (Aura lasting less than one hour)
- Migraine with prolonged aura (aura lasting more than one hour but less than one week)
- Familial hemiplegic migraine
- Basilar migraine
- Migraine aura without headache
- Migraine with acute onset aura (aura develops fully in less than 5 minutes)(3)
Migraine without aura, or common migraine, occurs in approximately 85 percent of patients. Scientists have devised one theory, which explains blood flow changes, and also biochemical changes, which may be involved in the headache process. According to this theory, migraine pain is believed to be the result of activity in the trigeminovascular system. Axons within this system originate from the trigeminal ganglia and upper cervical dorsal root. They surround cerebral blood vessels in close proximity to all vessel layers to allow for constant monitoring of the microenvironment of the vessel wall. Arteries and venous sinuses have the highest degree of trigeminal innervation.(4) Trigeminal nerves act as important initiators and promoters of tissue inflammation. When neuronal activation occurs, vasoactive neuropeptides are released which interact with dural blood vessels. The result is vasodilation and extravasation of plasma proteins, which initiates a sterile, neurogenic inflammatory response.
The inflammation sensitizes surrounding tissues and produces a hyperalgesic state that prolongs headache pain. Additionally, activation of unmyelinated C fibers of the trigeminovascular system stimulates pain-transmitting neurons within the brain stem and upper spinal cord. Activity within the trigeminovascular system is regulated by noradrenergic and, more importantly, serotonergic neurons within the brainstem. Brainstem mechanisms that lead to activation of the nociceptive trigeminovascular system may be stimulated by the cerebral cortex, thalamus, or hypothalamus in response to emotion or stress, excessive afferent stimulation (e.g., glare, noise, smells), or changes in the internal clock or environment.(5)
Serotonin is thought to be an important mediator of migraine. Of the seven classes of 5-HT receptors that have been identified, 5-HT1 receptors, presynaptic autoreceptors that<
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