Catamenial migraine cerebral vasomotor reactivity and role of oxidative stress

SUMMARYMigraine, is defined as a neurovascular disease having complex pathophysiology, where the peripheral and central components of the trigeminal nerve play a role.Cerebrovascular factors and hemodynamic changes play an important role in the pahtophysiology of migraine. Many migraine patients, had also increased headache during menses and this led to the notion of Menstrual Migrain. Hormonal changes occuring during premenstrual period decrease the threshold of migraine. İn this period the sudden decrease of estrogen levels after the its peak is not a cause but thought of as a trigger. The mechanism by which the decrease a estrogen triggers migraine is not well understood. İn premenopausal women, one of the primary mechanisms of transient change of arterial reactivity is probably the change in the production of NO.NO causes vasodilation in the vascular structure and this has unfavorable effects on the vasomotor reactivity. Transcranial doppler(TCD) is a noninvasive, easily used procedure, utilized, in functional tests to evaluate the hemodynamics of migraine.Because, vasoactivity shows the potential of artery dilatation, it is closely related to otoregulation and therefore it indicates the potential of tissue to keep constant, decrease or increase the blood flow as required.In the literatüre, althought there are publications about the vasomotor acitivity and oxidative stress patrameters in migraine patients, there are no studies examining menstrual migraine. In our study, we used transcranial doppler measurements in menstrual migraine patients and we aimed at evaluating the cerebrovascular reactivity with BHI and VEBF. We also studied the relationship of menstrual migraine with serum estrogen, NO, MDA, SOD, GSH, GSH-Px and GSH-Rd.In our study, 20 menstrual migraine patients (diganosed based on IHS- 2004 diagnosis criteria) and 20 healthy volunteers participated. Criteria for exclusion included irregularities in menstrual cycle, oral contraceptive use, migraine prophylaxis therapy, smoking, infection, other drug usages, alcohol and caffeine intake during in the last 24 hours.Participants had their blood tested for the levels of estrogen, NO, MDA, SOD, GSH, GSH-Px and GSH-Rd in the follicular (3-8 days of the menstrual cycle) and luteal (18-23 days of the menstrual cycle) phases and then were tested for cerebral vasomotor reactivity, BHI and VEBF measurement. There was no statistical significant difference between the control and the patient groups in according to age and menstrual cycle. In contrast, looking at the worked oxidative stress indicators in the follicular and luteal phases, the patient group had significantly more GSH-Px in the follicular phase than the control group. İn the vasomotor reacitivity findings however, except for the left BHI follicular phase values, all vasomotor reacitivity values were significantly lower in the follicular and luteal phases. The values of antioxidants, GSH-Rd and SOD increased significantly in the leuteal phase only in the patient group but not in the control group. In the control group, however, NO and GSH-Px increased significantly in the follicular and luteal phases respectively.There was no correlation between oxidative indicators and vasomotor reactivity. Vasomotor reactivity responses, which were low in the follicular phase, high in the luteal phase, in the control group, were low in menstrual migraine patients.In this condition, cerebral otoregulation in menstrual migraine patients, led us to think it was out of order but there is less than enough literatüre and data about this subject.On the other hand, looking at oxidative stress parameters, the fact that higher NO levels were found in the follicular phase than in the luteal phase, was compatible with existing literature. In migraine patients, GSH-Rd and SOD were higher in the control group in the luteal phase, and low in the follicular phase. This result was explained in terms of defence mechanism of antioxidant system in response to the release of free radicals because of the domination of estrogen in the luteal phase. GSH-Px was higher in the follicular phase in the control group relative to the patient group.Looking at follicular phase data, it is noticed that GSH-Px is lower in migraine patient group than in the control group. It can be concluded that the antioxidant system in the follicular phase in inadequate relative to healthy subjects.Also, there was no increase, physiologically, of vasomotor reactivity in the luteal phase in the control group. This condition leads to the idea that cerebral otoregulation in menstrual migraine patients in out of order.The relationship between menstrual migraine pathophysiology and cerebral otoregulation can be further clarified and new treatment strategies can be devised with further research and studies.