শুক্রবার, ২৯ জুন, ২০১২

VASCULAR DAMAGE, HEADACHE AND MIGRAINE ? Regional ...

Serotonin, 5-hydroxytryptamine?-HT) is released from a number of non-neuronal cells such as platelets and mast cells and can produce excitation of nociceptive afferents via the activation of its large number of receivers, for example, 5-HT1A, 5-HT2 and 5HT3, and awareness of nociceptors, especially to bradykinin. The key role, but not the mechanisms of action of 5-HT in pain associated with migraine and other well-established, but little is known about the actions of this mediator in other non-cranial pain . The aura of neurological symptoms and / or signs of migraine is thought to be caused by vascular disease or a neural mechanism, or a combination of both. One theory suggests that changes in the vascular system are causing the migraine while a second theory proposes that the vascular changes that mediate pain and symptoms of migraine. A third theory suggests that the primary defect is neuronal and comes into the brain itself. The assumption was that the vasoconstriction of intracranial vessels leads to reduced blood flow, resulting in cerebral hypoxia. If the arteries are narrowed sufficiently to cause a reduction in regional cerebral blood flow? CBF), brain tissue is hypoperfused, which can cause neurological deficits believed to be responsible for the `will '. Wolff, who proposed the idea, said that following the vasoconstriction of cranial vessels, vasodilation of these vessels have occurred which resulted in pain? Ia stretching of nerve endings in the vessel walls), and has also led to a change in regional cerebral blood flow. There are some weaknesses in the theory that the main problem is in the vasculature. As the progression of symptoms does not respect vascular territories, it is unlikely to be mainly due to a spasm in the vasculature. Changes in blood flow are more consistent with a primary neuronal event causing secondary vascular changes. Another factor that makes the theory of a primary vascular abnormality untenable is that the headache may begin while the cortical blood flow is further reduced.

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