Insights into migraine pathology, progression, and treatment

Professor Paul Durham, Missouri State University, speaking during the Hot Topics in Basic Science plenary session at #AHSAM21 presented preclinical research highlights revealing current knowledge of the mechanisms of migraine pathology and treatment. Next, Dr Catherine Chong, Mayo Clinic, discussed evidence from brain imaging studies showing that migraine disease severity and burden can modify brain structure and function and that effective treatment may reverse or normalize brain alterations.

Migraine mechanisms and treatment

Migraine is a prevalent neurological disease characterized by unpredictable episodic attacks of intense head pain. The underlying pathology involves sensitization and activation of the trigeminal system.

Non-invasive vagus nerve stimulation (nVNS) is recommended for migraine treatment, and studies by Professor Durham and colleagues show that nVNS inhibits trigeminal activation to a similar degree as a triptan medication in animal models of episodic migraine, through mechanisms involving GABAergic and serotonergic descending pain signaling.1

Non-invasive vagus nerve stimulation and triptans inhibit trigeminal activation through mechanisms involving GABAergic and serotonergic descending pain signaling

In further studies of an animal model of chronic migraine, the researchers found that a combination of reported migraine risk factors (neck inflammation, sleep deprivation, and exposure to a pungent odor) promotes a state of sustained trigeminal hypersensitivity characteristic of chronic headache.2 In this model, daily nVNS was effective in inhibiting nociception and may represent a therapeutic option for other chronic pain disorders involving sensitization of the trigeminal system by promoting descending pain modulation.2,3

 

Migraine brain remodelling

Dr Catherine Chong presented evidence from brain imaging studies suggesting that migraine disease severity and burden may contribute to brain remodelling. Magnetic resonance imaging studies show that migraine is not a static brain state and cortical abnormalities in specific brain regions have been detected in people with migraine.4,5

Migraine risk factors promotes a state of sustained trigeminal hypersensitivity characteristic of chronic headache

Frequency of migraine attacks and the duration of the disorder has a significant impact on cortical thickness in the sensorimotor cortex and middle-frontal gyrus.4 Chronic migraine is associated with structural changes in brain regions involved in pain processing but also in affective and cognitive aspects of pain.5 Some grey matter alterations are correlated with headache frequency assessed in both episodic and chronic migraine.

These findings support the assumption that chronic pain alters brain plasticity. Grey matter volume increase may reflect a remodeling of the central nervous system due to repetitive headache attacks leading to chronic sensitization and a continuous ictal-like state of the brain in chronic migraine.5

Migraine disease severity and burden may contribute to brain remodeling

 

Effective treatment may halt migraine progression

Dr Chong highlighted emerging evidence that effective treatment for migraine may associate with recovery (reversibility) of brain alterations. Preliminary findings in a small number of migraine patients (N=16) suggest that external trigeminal neurostimulation induces a functional antinociceptive modulation in the right anterior cingulate cortex that is involved in the mechanisms underlying its preventive anti-migraine efficacy.6

Effective treatment for migraine may associate with recovery of brain alterations

These findings support the notion that migraine progression can modify brain structure and function and that effective treatment may reverse or normalize brain alterations, which require further exploration.

 

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Our correspondent’s highlights from the symposium are meant as a fair representation of the scientific content presented. The views and opinions expressed on this page do not necessarily reflect those of Lundbeck.

References
  1. Cornelison LE, et al. Front Neurol 2020;11:146.
  2. Cornelison LE, et al. Pain Rep 2020;5(6):e881.
  3. Cornelison LE, et al. Nutr Neurosci 2021 Feb 5:1–12.
  4. Magon S, et al. Cephalalgia 2019;39(5):665–673.
  5. Neeb L, et al. Headache 2017;57:400–416.
  6. Russo A, et al. Front Neurol 2019;8:282.
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