Cerebrovascular reactivity in interictal phase of migraine

Objective: To study the cerebrovascular reactivity in patients with migraine. Background: Migraine is an episodic disorder commonly encountered in daily practice. Multiple hypothesis have been proposed for the pathophysiology of migraine. It is a state of altered excitability capable of activating trigeminovascular system. It is a neurovascular coupling disorder where the cerebrovascular reactivity is malfunctioning. The neuronal hypersensitivity to different external and internal stimuli is the primary pathophysiological changes in these patients. The migraineurs show maladaptation to environmental stimuli owing to loss of adaptability compared to normal people. Several transcranial doppler studies have reflected the altered reactivity with varying outcomes in migraineurs. Study design: This study was conducted over a period of six months at tertiary hospital, RGGGH, chennai. We included 30 patients who satisfied criteria for migraine (with and without aura) as per IHS criteria and 30 age and sex matched controls. Transcranial doppler was performed on all patients. Cerebrovascular reactivity was assessed by repetitive photic stimulation. Average peak systolic velocity in middle cerebral artery and posterior cerebral artery was measured before and after photic stimulation. Results: The mean PSV in MCA in controls was 75.48±9.183 before and77.55±9.180 after stimulation PSV in patients before photic stimulation was 78.80±13.745 and 80.40±12.719 after stimulation. The change in PSV MCA was not significant(p<0.006).The PSV PCA in patients before photic stimulation was 59.47±10.345 and 63.13±11.013 after photic stimulation the increase in PSV was statistically significant(p<.001).The increase in PSV PCA in patients with aura was significant compared to those without aura(p<.002). Discussion: The study demonstrated an increased PSV levels of PCA after photic stimulation and significantly higher in migraine with aura. We found an altered cerebrovascular reactivity in interictal phase of migraineurs, being more pronounced in migraine with aura. Conclusion: There was maladaptation of cerebrovascular reactivity in migrainuers, more so in patients with aura causing a disturbance in neurovascular homeostasis possibly inducing migraine attacks.