Abstract
Migraine is a neurological disorder characterized by paroxysms of head pain accompanied by trigeminovascular system activation and autonomic dysfunction. Diagnosis is currently based on clinical diagnostic criteria. Though physiological differences exist between migraineurs and non-headache controls, true physiological biomarkers have been elusive, especially for the full clinical spectrum of migraine, inclusive of chronic, episodic, and probable migraine. We used edge-light pupil cycle time (PCT) as a probe of the pupillary light circuit in migraine, paired with clinical assessment of migraine characteristics, and compared these to non-headache controls. We found significantly increased PCT in probable, episodic, and chronic migraine, compared to controls. Additionally, increased PCT correlated with the presence of craniofacial autonomic symptoms, linking pupillary circuit dysfunction to peripheral trigeminal sensitization. The sensitivity of PCT, especially for all severities of disease, distinguishes it from other physiological phenotypes, which may make it useful as a potential biomarker.
Highlights
Migraine is a common, recurrent headache disorder characterized by paroxysms of head pain accompanied by trigeminovascular system activation and autonomic dysfunction
There were no significant differences in age or sex-distribution between the NH and migraine groups
As expected, based on diagnostic criteria, headache days per month was significantly higher in chronic migraine (CM) subjects; Migraine Disability Assessment (MIDAS) and HIT-6 scores were significantly higher in CM than episodic migraine (EM) and probable migraine (PM)
Summary
Recurrent headache disorder characterized by paroxysms of head pain accompanied by trigeminovascular system activation and autonomic dysfunction. Diagnosis is currently based on clinical diagnostic criteria and may be diagnostically categorized as probable, episodic, or chronic migraine, based on duration, number of attacks, and associated symptoms. Far while clinical signs of migraine chronification (previously termed “transformation”) and central sensitization are recognized, such as cutaneous allodynia [1, 2], few human studies have shown abnormalities in physiology present across the full clinical spectrum of migraine inclusive of chronic, episodic, and especially probable migraine. Recent evidence supports the possibility of a disease gradient in the expression of pupillary responses to light, perhaps linked to the presence of photophobia [7], a well-recognized symptom of central sensitization most evident in chronic migraine (CM). Craniofacial autonomic signs and symptoms are recognized to be relatively common in migraineurs (37–73%) and often co-occur with photophobia and allodynia [8, 9]
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