Migraine pathogenesis involves a complex interaction between hormones, neurotransmitters, and inflammatory pathways, which also influence the migraine phenotype. The Mediterranean fever gene (MEFV) encodes the pyrin protein. The major role of pyrin appears to be in the regulation of inflammation activity and the processing of the cytokine pro-interleukin-1β, and this cytokine plays a part in migraine pathogenesis. This study included 220 migraine patients and 228 healthy controls. Eight common missense mutations of the MEFV gene, known as M694V, M694I, M680I, V726A, R761H, K695R, P369S, and E148Q, were genotyped using real-time polymerase chain reaction with 5′ nuclease assays, which include sequence specific primers, and probes with a reporter dye. When mutations were evaluated separately among the patient and control groups, only the heterozygote E148Q carrier was found to be significantly higher in the control group than in the patient group (P=0.029, odds ratio [95% confidence interval] =0.45 [0.21–0.94]). In addition, the frequency of the homozygote and the compound heterozygote genotype carrier was found to be significantly higher in patients (n=8, 3.6%) than in the control group (n=1, 0.4%) (P=0.016, odds ratio [95% confidence interval] =8.57 [1.06–69.07]). However, there was no statistically significant difference in the allele frequencies of MEFV mutations between the patients and the healthy control group (P=0.964). In conclusion, the results of the present study suggest that biallelic mutations in the MEFV gene could be associated with a risk of migraine in the Turkish population. Moreover, MEFV mutations could be related to increased frequency and short durations of migraine attacks (P=0.043 and P=0.021, respectively). Future studies in larger groups and expression analysis of MEFV are required to clarify the role of the MEFV gene in migraine susceptibility.

Summary: Cyclic vomiting syndrome (CVS) is a disorder characterized by recurrent, stereotypic episodes of nausea, vomiting, and other symptoms, separated by intervals of comparative wellness. These episodes carry on for hours or days. The patient is healthy between the episodes and has no clinical finding. For the treatment of the CVS, antiemetic, antimigraine and sedative medications were used. However, in some cases CVS treatment is very difficult. We report about a young patient, who did not respond to many agents, but was succesfully treated with chlorpomazine

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ÖzetAmaç: Hipoksi-iskemi ve reperfüzyon sonrasında gelişen apopitozisin şiddeti, beyin hasarının bir göstergesidir. Serebral iskemide hücre ölümüne uzanan olayları başlatan birçok faktör bulunmaktadır. En önemli faktörlerin başında hücre içi kalsiyum konsantrasyonundaki aşırı artış gelmektedir. N-metil-D-aspartat (NMDA) reseptörlerindeki iyon kanalları Ca ++ 'nın hücreye girişini artırarak hücre ölümüne neden olmaktadırlar. Memantin, NMDA reseptörünün nonkompetitif eksitatör aminoasid blokörüdür. İskemi öncesi veya sonrası memantin uygulamasının nöronal hasarı azalttığını ileri süren çalışmalar yayınlanmıştır. Bu çalışmada; memantinin iskemi sonrası, özellikle penumbra alanındaki apopitoz ile sonuçlanan nöronal hasarı azaltıcı ve beyin dokularında antioksidan ve oksidan düzeylerine olan etkilerinin araştırılması amaçlandı. Sum maryObjective: The severity of apoptosis developing after hypoxia-ischemia and reperfusion is an indicator of cerebral injury. In cerebral ischemia, there are many factors initiating the events progressing to cell death. The most common leading cause is excessive increase in intracellular calcium concentration. Ion channels in NMDA receptors cause cell death by increasing Ca ++ entries into the cell. Memantine is a non-competitive excitatory amino acid blocker of the NMDA receptor. Studies suggesting administration of memantine before and after ischemia decreasing the neural injury have been published. In this study we aimed to examine the memantine could have a decreasing effect on neuronal injury resulting with apoptosis especially in the penumbra region after ischemia and its effects on antioxidants and oxidants in brain tissues. Ma te ri al and Met hod: Experimental study was performed in three groups; each of them including 7 rats. The control group (without any intervention) was used for evaluation of the normal brain tissue. Transient focal cerebral ischemia was performed by clipping the right common carotid arteries of the rats in ischemia and ischemia-drug groups. Ten mg/kg intraperitoneal memantine was administered in ischemia-drug group 30 minutes after ischemia and for 5 days thereafter. All of the rats were sacrificed after the experiment. Antioxidant and oxidant levels of the cerebral tissues were measured. Apoptotic cells were determined immunohistochemically using TUNEL method. Re sults: When the memantine administered group was compared with the ischemia group, we observed that memantine decreased apoptotic cells in the brain tissue and there was an improvement in the oxidant levels (p<0.05). Dis cus si on: In conclusion, memantine may be effective in prevention of apopitosis and neuronal injury in cerebral ischemic tissue via decreasing cerebral oxidant formations. (Turkish Journal of Neurology 2013; 19:85-9)

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