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Beyond Neurovascular: Migraine as a Dysfunctional Neurolimbic Pain Network

Authors

  • Morris Maizels MD,

    Corresponding author
    1. From the Blue Ridge Headache Center, Asheville, NC, USA (M. Maizels); Swedish Neuroscience Institute – Swedish Headache Center, Seattle, WA, USA (S. Aurora); Oregon Health & Science University – Neurological Surgery, Portland, OR, USA (M. Heinricher).
      M. Maizels, Blue Ridge Headache Center, 1998 Hendersonville Road, Suite 45, Asheville, NC 28803, USA, email: morris.maizels@gmail.com
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  • Sheena Aurora MD,

    1. From the Blue Ridge Headache Center, Asheville, NC, USA (M. Maizels); Swedish Neuroscience Institute – Swedish Headache Center, Seattle, WA, USA (S. Aurora); Oregon Health & Science University – Neurological Surgery, Portland, OR, USA (M. Heinricher).
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  • Mary Heinricher PhD

    1. From the Blue Ridge Headache Center, Asheville, NC, USA (M. Maizels); Swedish Neuroscience Institute – Swedish Headache Center, Seattle, WA, USA (S. Aurora); Oregon Health & Science University – Neurological Surgery, Portland, OR, USA (M. Heinricher).
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  • Conflict of Interest: The authors report no conflicts of interest.

M. Maizels, Blue Ridge Headache Center, 1998 Hendersonville Road, Suite 45, Asheville, NC 28803, USA, email: morris.maizels@gmail.com

Abstract

No single model of migraine explains all of the known features of the disorder. Migraine has recently been characterized as an abnormality in pain-modulating circuits in the brainstem. The periaqueductal gray appears to have a critical role in migraine genesis and has been labeled the “migraine generator.” The concept of a “pain matrix,” rather than a specific locus of pain, is widely accepted in the pain literature and offers a new dimension to understanding migraine. Recent neuroimaging studies of migraineurs suggest altered functional connectivity between brainstem pain-modulating circuits and cortical (limbic) centers. Numerous clinical observations suggest that limbic influences play an important role in migraine expression. We propose a model of migraine as a dysfunction of a “neurolimbic” pain network. The influence between brainstem and cortical centers is bidirectional, reflecting the bidirectional interaction of pain and mood. Neurolimbic dysfunction may increase as migraine becomes more chronic or refractory. The neurolimbic model expands the model of migraine as a dysfunction of brainstem nuclei. A neurolimbic model may help bridge a gap in understanding the migraine attack, the interictal dysfunctions of episodic migraine, the progression to chronic migraine, and the common comorbidities with other disorders (such as fibromyalgia, irritable bowel syndrome, and mood and anxiety disorders), which may also be considered neurolimbic. A neurolimbic model of migraine may be a useful heuristic that would impact both clinical treatment and research agendas, as well as education of physicians and patients.

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