偏头痛的流行病学与治疗于生元课件.ppt

偏头痛的流行病学与治疗 解放军总医院神经内科 于生元 原发性与继发性头痛的年患病率 各种原发性头痛的年患病率 原发性头痛性别分布 原发性头痛年龄分布 城乡原发性头痛患者头痛诊疗费用 各种原发性头痛患者的收支状况 * Activation and sensitization of the trigeminovascular system (TGVS): a central event in the pathophysiology of migraine It is generally recognized that the development of migraine headache depends on the activation of sensory afferent fibers of the ophthalmic division of the trigeminal nerve1 Migraine has a strong (up to 50%) genetic component with a likely multifactorial polygenic inheritance1 Experimental evidence suggests that the cerebral cortex of patients with migraine with or without aura is hyperexcitable and exhibits enhanced responsiveness to external stimuli2 Mechanisms remain unknown and might be multifactorial Genetic mutations may contribute to hyperexcitability Abnormal cortical activity might lead to cortical spreading depression (CSD) when enhanced activation coincides with other triggering factors2 CSD is hypothesized to lead to the activation of the trigeminovascular afferents1 Substances like K+ ions, H+ ions, nitric oxide (NO), and arachidonic acid that are released during CSD may activate the perivascular trigeminal terminals in the meninges Dysfunctional brainstem nuclei involved in the central control of pain might exert a permissive role by favoring central trigeminal hyperexcitability2 Neuroimaging findings have shown that the once widely accepted “vascular theory of migraine” is untenable. According to this theory, migraine aura is caused by transient ischemia induced by vasoconstriction, and the headache arises from rebound abnormal vasodilation of intracranial arteries and consequent mechanical activation of perivascular sensory fibers1 Instead, it is now generally recognized that migraine arises from a primary brain dysfunction that leads to activation and sensitization of the TGVS1 References: 1. Pietrobon D. Migraine: new molecular mechanisms. Neuroscientist. 2005;11:373–386. 2. Pietrobon D, Striessnig J. Neurobiology of migrain