Migraine as a Cortical Brain Disorder

TAKE-HOME MESSAGE

  • Migraine has been a difficult condition to fully understand
  • Advanced neuroimaging data and neurophysiological research indicate that fluctuating excitability, plasticity, and metabolism of cortical neurons represent the pathophysiological substrate of the migraine cycle.
  • Migraine disorder stems, in part, from an imbalance in inhibitory/excitatory cortical circuits
  • Spinal Manipulative Therapy (SMT) has been found to have an effect on the pre-frontal cortex and this may explain why some migraine patients improve with SMT.
  • Physicians with interest in migraine headache should be informed by this important article.

Abstract

PURPOSE

Migraine is an exclusively human chronic disorder with ictal manifestations characterized by a multifaceted clinical complexity pointing to a cerebral cortical involvement. The present review is aimed to cover the clinical, neuroimaging, and neurophysiological literature on the role of the cerebral cortex in migraine pathophysiology.

OVERVIEW

prefrontal cortex

Converging clinical scenarios, advanced neuroimaging data, and experimental neurophysiological findings, indicate that fluctuating excitability, plasticity, and metabolism of cortical neurons represent the pathophysiological substrate of the migraine cycle. Abnormal cortical responsivity and sensory processing coupled to a mismatch between the brain’s energy reserve and workload may ignite the trigeminovascular system, leading to the migraine attack through the activation of subcortical brain trigeminal and extra-trigeminal structures, and driving its propagation and maintenance.

DISCUSSION

The brain cortex emerges as the crucial player in migraine, a disorder lying at the intersection between neuroscience and daily life. Migraine disorder stems from an imbalance in inhibitory/excitatory cortical circuits, responsible for functional changes in the activity of different cortical brain regions encompassing the neurolimbic-pain network, and secondarily allowing a demodulation of subcortical areas, such as hypothalamus, amygdala, and brainstem nuclei, in a continuous mutual crosstalk.

Citation: https://headachejournal.onlinelibrary.wiley.com/doi/epdf/10.1111/head.13935