| Objective:Cerebrovascular disease has been rising for the first disease of the death and disability in china.And with the ageing of society, the number of cerebrovascular disease will be increased, which will bring heavy burden to the community and families. Ischemic cerebrovascular disease rate of 80 percent of all stroke. 10% ~ 39% patients of cerebral infarction suffer headache, which can occur before,after or onset of the disease.So it is very important to make clear the related factors of cerebral infarction headache and we may can discover the cerebral infarction earlier and study the pathological biochemistry changes of cerebral infarction further.CGRP is a bioactive peptide,made of 37 amino acid residues, which widely distribute in the nervous and cardiovascular systems and its receptors show the same distribution of CGRP nearly. CGRP possesses variety of biological functions, such as enormous vasodilatation, reducing blood pressure and positive inotropic effect, and it participate in the regulation of certain hormones as well. At prenzent,the information indicates that the plasma CGRP have changed in the cerebral infarction and migraine, but it is unclear the role and mechanism of plasma CGRP in cerebral infarction headache. So we observed the chang of plasma CGRP in cerebral infarction headache patients, compared with it in cerebral infarction patients without headache and normal people,and the chang of plasma CGRP in different system infarct at the same time,in order to explore the role of CGRP in the mechanisms of cerebral infarct headache further and understand pathological mechanism of cerebral infarct and headache.Methods:We choose cerebral infarction patients within 72 hours, proved by CT or MRI, whithout aphasia and disturbance of consciousness (Glasgow score> 14), and whithout similar headache history as well.Exclusion criteria: 1. Patients with elevated blood pressure, whose headache reduce when blood pressure adjust to normal;2. If infact lesions> 4 mm, headache relief afer using mannitol;3. Atrial fibrillation, as well as myocardial ischemia prompted by ECG;5.Electrolyte disturbance, such as hypomagnesemia ;6. Fever, temperature> 37.3℃;7.Female who use contraceptives long-term; 8.The patients who take nitroglycerin drugs;9. Anemia, polycythemia or hypolekocytosis;10. Patients with dysfunction of liver and kidney;11. Zung Depression Scale (Self-Rating Depression Scale, SDS) scores> 50 points or Hamilton Anxiety Scale (14 Table) score (HAMA)> 7 points. Cerebral infarction group make of 50 patients, aged 39 to 79, include 26 women and 24 men. According to wether infact patiets suffer headache or not, we divided them into two groups:1.Cerebral infarction headache group: 21 cases, including 9 women and 12 men, and the average age was 56.81±13.05 years; 15 patients feeled headache when cerebral infarction and 6 after;10 patients feeled gas pain, 2 feeled vague pain and 9 pulsatile headache; 9 patients feelde ipsilateral, 3 bilateralis, 3 forehead,3 all the head, 2 occipital part and 1contralateral ;2. cerebral infarction without headache group: 29 cases, including 17 female and 12 male, the average age was 60.76±9.45 years. According to infarct locus, we divided them into two groups another:1.Carotid artery infarction group: 27 cases, 17 women and 11 men, with an average age of 62.0±10.72 years; 2. Vertebrobasilar system infarction group: 23 cases, 10 women and 13 male, with an average age of 56.17±10.32 years. The control group of 40 patients, from the healthy medical center, rule out diseases of heart, liver, lung, kidney, brain and other organs by the clinical and laboratory examinations, without hypertension disease, diabetes, various inflammation, tumor, blood disease, autoimmune disease, anxiety and depression and fever. And both age and gender of control group match with cerebral infarction group. 2 ml venous blood was drew from cerebral infarction patients within 72 h, then injected into tube with 7.5% Disodium EDTA 30 ul and aprotinin 40 ul, and then centrifuged 3000 rpm for 10 min at 4℃after blending, and then we abstracted supernatant and put it into -70℃freezer to preserve. The blood of control group was done the same.CGRP was analyzed by radioimmunity.The data was analyzed by SAS software and the result was expressed by mean±standard ( x±S).Results: 1. The plasma CGRP level of cerebral infarction headache group (33.58±6.98 pg / nl) and the cerebral infarction headache without headache group (24.59±6.45 pg / nl) was lower than the control group (44.53±10.38 pg / nl), but the plasma CGRP level of cerebral infarction headache group (33.58±6.98 pg / nl) was higher than cerebral infarction headache without headache group (24.59±6.45 pg / nl),and there were significant differences between various groups(p <0.05). 2. There was no significant difference of the plasma CGRP level between carotid artery infarction group and the vertebrobasilar system infarction(p> 0.05).Conclusion: 1. The plasma CGRP level of cerebral infarction group was lower than the control group. 2. the plasma CGRP level of cerebral infarction headache group was higher than cerebral infarction headache without headache group, so we presume that CGRP take part in the pathophysiology of cerebral infarction headache.3.The plasma CGRP level shows no significant difference between carotid artery infarction group and the vertebrobasilar system infarction. |
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