Inflammation of trigeminal ganglion may account for pain as well as associated symptoms of migraine.
Brainstem dysfunction is favored in consideration of the diverse symptoms associated with the pain of migraine. Specifically, symptoms such as extreme sensitivity to lights and sounds most are most likely to originate in the brainstem.
The publication briefly summarized below suggests spreading inflammation of the trigeminal ganglion and associated structures as one possible means by which to account for both the pain and associated symptoms of migraine.
Neuron-glia signaling in trigeminal ganglion: implications for migraine pathology.
Summary of the abstract
OBJECTIVE: The goal of this study was to investigate neuronal-glial cell signaling in trigeminal ganglia under basal and inflammatory conditions using an in vivo model of trigeminal nerve activation.
BACKGROUND: Activation of trigeminal ganglion nerves and release of calcitonin gene-related peptide (CGRP) are implicated in the pathology of migraine. Cell bodies of trigeminal neurons reside in the ganglion in close association with glial cells. Neuron-glia interactions are involved in all stages of inflammation and pain associated with several central nervous system (CNS) diseases. However, the role of neuron-glia interactions within the trigeminal ganglion under normal and inflammatory conditions is not known.
CONCLUSIONS: Activation of trigeminal neurons leads to changes in adjacent glia. It is likely that neuronal-glial communication are involved in the development of peripheral sensitization within the trigeminal ganglion and, thus, are likely to play an important role in the initiation of migraine. Furthermore, propagation of inflammatory signals within the ganglion may help to explain commonly reported symptoms of comorbid conditions associated with migraine.