USED IN MIGRAINE用于偏头痛的药物课件.ppt

This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. A French study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early stages. Vascular theory ?Migraines can begin when blood vessels in the brain contract and expand inappropriately. This may start in the occipital lobe, in the back of the brain, as arteries spasm. The reduced flow of blood from the occipital lobe triggers the aura that some individuals who have migraines experience because the visual cortex is in the occipital area. ?When the constriction stops and the blood vessels dilate, they become too wide. The once solid walls of the blood vessels become permeable, some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation. With each heart beat, blood passes through this sensetive area causing a throb of pain. ?The vascular theory of migraines is now seen as secondary to brain dysfunction. Serotonin theory Serotonin is a type of neurotransmitter, or communication chemical which passes messages between nerve cells. It helps to control mood, pain sensation, sexual behaviour, sleep, as well as dilation and constriction of the blood vessels among other things. Serotonin levels in the brain may lead to a process of constriction and dilation of the blood vessels which trigger a migraine. Triptans activate serotonin receptors to stop a migraine attack. Neural theory When certain nerves or an area in the brain stem become irritated, a migraine begins. In response to the irritation, the body releas