Title: Migraine: Early life stress and dysfunctional brain circuitry.
Presenter: Micah Johnson, PhD student, University of Iowa, US
Methodology, findings and conclusions of the research
In our study, we wanted to determine how brain-wide neural activity is coordinated during migraine-related sensory hypersensitivity. To accomplish this, we used a mouse model of migraine to induce migraine attacks in mice. After inducing migraine in mice, we recorded brain activity by measuring electrical activity transmitted across groups of neurons, or local field potentials. We also wanted to determine whether early life stress increases migraine susceptibility in mice. For this experiment, we separated mice from their mothers for the first few weeks of life (maternal separation stress) and when they were adults, tested migraine-like behavior including light aversion (light sensitivity) and mechanical allodynia (pain response to non-harmful touch).
We found that animals exhibited changes in limbic system activity indicated by a directional flow of information from the amygdala to the thalamus and increased activity in several thalamic nuclei groups (posterior thalamus and ventral posteromedial thalamus). For our early life stress experiment, we found that animals undergoing early life stress exhibited increased light aversion and mechanical allodynia during adulthood after being treated with a migraine-inducing compound, compared to those that didn’t experience early life stress. Overall, we concluded that sensory hypersensitivity brain states during a migraine attack are defined by changes in the limbic system. Endogenously, early life stress predisposes mice to a migraine-susceptible brain state.
Implications of the research for understanding migraine and/or its comorbidities
Our research suggests that the amygdala-to-thalamus circuit can potentially be manipulated to alter sensory hypersensitivity symptoms during migraine attacks. We also discovered that early life stress can be used as a way to endogenously probe brain activity prior to the occurrence of migraine and can thus be used to determine therapeutic brain circuits of interest. Most people can’t change that they’ve experienced early life stress, but if we can find a way to target early life stress-related brain circuits, we might be able to decrease susceptibility to migraine in this population. Overall, our research has shed light on central mechanisms underlying migraine and holds promise for new avenues to explore in attempts to improve outcomes for migraine patients by means of individualized treatment.