Spreading Depolarization May Link Migraine and Stroke
Clinical and experimental studies suggest cortical hyperexcitability as a mutual mechanism of migraine pathogenesis and increased vulnerability to cerebral ischemia in migraine-susceptible brains. Upon experimental stroke, genetic mouse models expressing neuronal or vascular migraine mutations (FHM1 and CADASIL) exhibit a faster onset of ischemia-triggered SD with more frequent, following SDs. At the same time, mutants show an accelerated lesion growth and develop larger infarcts and worse neurological outcomes, which could be prevented by anti-excitatory treatment. Increased vulnerability to ischemia may predispose migraineurs to stroke during mild ischemic events that would remain clinically silent or only manifest as transient ischemic attacks in non-migraineurs. Drugs suppressing SD may protect migraineurs at risk of stroke if results from animal experiments can be translated to the clinical situation.
Conclusion
Clinical and experimental studies suggest cortical hyperexcitability as a mutual mechanism of migraine pathogenesis and increased vulnerability to cerebral ischemia in migraine-susceptible brains. Upon experimental stroke, genetic mouse models expressing neuronal or vascular migraine mutations (FHM1 and CADASIL) exhibit a faster onset of ischemia-triggered SD with more frequent, following SDs. At the same time, mutants show an accelerated lesion growth and develop larger infarcts and worse neurological outcomes, which could be prevented by anti-excitatory treatment. Increased vulnerability to ischemia may predispose migraineurs to stroke during mild ischemic events that would remain clinically silent or only manifest as transient ischemic attacks in non-migraineurs. Drugs suppressing SD may protect migraineurs at risk of stroke if results from animal experiments can be translated to the clinical situation.