| Migraine, whose prevalence rate is high, is one kind of the most common headaches in children. Its main clinical manifestation is periodic, paroxysmal, plusatic and acute pain in one lateral or bilateral head, lasting several hours to more than ten hours, even to one day. During its attack, there are many symptoms of autonomic nervous system while portentous symptoms are relatively seldonm. The pediatric migraine in infant is vomiting periodically, abdominal pain in preschool age children and migraine in school age children. All in one word, the clinical characteristics of migraine in children is not so distinctive as that in adults, but the symptom of digestive is very prominent. The pathogen of migraine is extremely complicated, so the pathogenesis has not been clear yet. In recent years, the theories in mainstream include vein origin theory, trigeminal-vein theory, nerve origin theory, and so on. In vein origin theory, the vasoconstriction and vasodilator-dysfunction in cerebrovasa is considered of as the pathology base during its attack. Attributing to the physiologicoanatomical speciality of pediatric cerebaovasa, there is cerebral blood flow abnormality in both common and classic migraine during attack in transcranial dopplor evaluation. What's more, velocity increase of blood flow is principal which indicates that cerebrovasa spasm is often seen in migraine. Between attack, all coefficients of TCD recover normao. The fact suggests that there is no potential abnormality in cerebral blood flow. In trigeminal-vasa theory, the end of trigeminus centripetal fibres release substance P and other nerve transmitters, and centrifugal fibres affect cerebrovasa. Thus blood vessel expands and migraine takes place. In relation to trigeminal system, the most important transmitter is calcitonin gene-related protein, in the second place are substance P and nerve kinin A. Substance P is a kind of nerve transmitters that can transfer and decrease pain threshold together with nerve kinin A. Calcitonin gene-related protein through its high ability to expand vessel cause headache. In nerve oigin theory, variation of nerve during migraine attack is chief, and the blood volume variation is succeeding. The phenomen of cortical spreading depression is the base of migraine aura and nerve dysfunction. Besides, CSD will cause transmitters in relation to migraine, such as NO and CGRP, releasing. It also can produce gene transcripts in relation to hyperalgesic and inflammation, which maybe the important reason of headache and the clinical manefistation caused by CSD-like electric activity. In recent years, many studies have confirmed that there is tight link between migraine and platelet abnormality. Genes from platelets are upregulated in migraineurs blood, in which C-fos and cox-2 are especially high. The abnormalities of platelet function in migraineursare high activation and release, dyssecretion of platelet-product, hypofunction of MAO, the increase of adenosineproduct, substance P, β-thrombulin and platelet factor 4. P-selectin, previously also known as GMP-140, is a member of the selectin family of adhesion molecules. It's a component of the αgranules of platelets and also a component of the Weibel-Palade body. When the above-mentioned cells are in rest, levels of P-selectin in plasma are low. It is rapidly mobilised to the cell surface by various stimuli including LPS, thrombin, histamine, peroxids, protein-kinase C, completment system, ADP,IL-1β, TNF-α, oxygen radicals, and so on. Thus expression of P-selectin in blood is rapid and tansient. In addition, P-selectin-related genes can also be activated by LPS,IL-1β,TNF-α. Its expression is upregulated in 2-4 hours after stimulated. Attributing to the two kinds of expression fashions, P-selectin in blood will appear early and remain long after cell stimulation. After expressed in blood, P-selectin can lead to an interaction between those activated endothelium, platelets and neutrophycyts. P-selectin has two forms: the common and the soluble. The molecule of the latter is 3000KD smaller than that of the first. In the soluble form there is lack of transmembrane domain and several residues in cytoplasmic tail, which can be seen in the common. As P-selectin is a membrane constituent of both platelet αgranules and endthelial cell Weibel-Palade bodies, soluble levels may derive fromeither source. Failure of levels of soluble P-selectin to correlate with an established endthelial cell marker (von-willebrand factor) implies soluble P-selectin is derived from platelets. This is supported by preliminary flow cytometry experiments in non-human primates which indicate that a loss of surface membrane P-selectin from platelets is accompanied by a increase in soluble P-selectin. Failure of levels of soluble P-selectin to correlate with an established marker of platelet activity, βthromboglobulin, implies that it is related to a different aspect of platelet activity of physiology. Furthermore, the relative ease of measurement and stability of soluble P-selectin may be a considerable advantange overβthromboglobulin. Hence it may be that soluble P-selectin will prove to be more popular in platelet studies thanβthromboglobulin, especially in laboratories and clinics whose resource are limited. In the light of these considerations, we believe that cytometric analysis of P-selectin (either alone of in combination with other platelet antigens) cannot be an ideal marker for the detection of circulating activated platelets, particularly in clinical settings where a chronic stimulus is generally present, but should be limited to those case in which the activating stimulus acts immediately before sampling. Later, some studies suggest that soluble P-selectin correlates with platelet count. So plasma soluble P-selectin is an ideal marker for the function of platelets and can reflect the P-selectin secretion of the whole body, Its measurement may represent...
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