Migraine understood as a sensory threshold disease

Abstract

Migraine encompasses a broader spectrum of sensory symptoms than just headache. These “other” symptoms, eg, sensory phobias, cognitive and mood changes, allodynia, and many others indicate an altered sensitivity to sensory input which can be measured, in principle, by quantifying sensory threshold changes longitudinally over time. Photophobia, for example, can be quantified by investigating the discomfort thresholds towards the luminance of light. The aim of this review is to look into how thresholds change in patients with migraine. We performed a PubMed search up to June 2018 targeting all peer-reviewed articles evaluating the changes in threshold, sensory phobia, or sensitivity in patients with migraine. Migraineurs, in general, exhibit lower sensory thresholds compared with healthy controls. These threshold changes seem to follow the different phases during a migraine cycle. In general, thresholds reach a nadir when the headache starts (the ictal phase), rise after the headache ends, and then gradually descend towards the next attack. The sensory modality of measurement—mechanical, thermal, or nociceptive—and the location of measurement—trigeminal vs somatic dermatome—also influence the sensory threshold. Functional imaging studies provide evidence that the hypothalamo-thalamo-brainstem network may be the driving force behind the periodic threshold changes. In summary, there is evidence in the literature that migraine could be understood as a periodic sensory dysregulation originating from the brain. Nevertheless, the interstudy discrepancy is still high due to different study designs and a lack of focus on distinct migraine phases. Further well-designed and harmonized studies with an emphasis on the cyclic changes still need to be conducted.

Longitudinal Neuroimaging over 30 Days: Temporal Characteristics of Migraine

“…24 Given the dense interconnection of various hypothalamic nuclei with the trigeminal pain processing and pain modulating system, 15 this might pose a possible mechanism for the precipitation of migraine pain. 13,[25][26][27][28][29] Internal and external processes 30,31 might lead to an alteration of hypothalamic activity, which in turn might influence pain processing pathways, thus facilitating trigeminal pain perception. Ultimately, these processes could result in a headache attack.…”

Premonitory symptoms in glyceryl trinitrate triggered migraine attacks: a case-control study

“…This chain of symptomology has led to the hypothesis of an oscillating system of complex brain networks influencing the susceptibility threshold of sensory signals and bodily functions toward the onset of migrainous headache. 8 , 34 , 38 …”

Redefining migraine phases – a suggestion based on clinical, physiological, and functional imaging evidence

“…Functional imaging evidence suggests certain regional activation in the brain even before the headache starts ( 2 , 3 ). Therefore, when a migraine attack starts, it comprises three different phases: i) preictal – the time before the headache starts, when the patient may develop prodromes, including appetite changes, thirst, yawning, or others; ii) ictal – when the patient experiences headache, which lasts by definition 4–72 hours ( 4 ); iii) postictal – the time following the cessation of the headache, characterized by non-headache symptoms such as cognitive deficits, fatigue, and others ( 5 ). The definition of prodromes may be traced back to John Fordyce in 1758 in his De Hemicrania where he observed polyuria and mood changes before the headache ( 6 ).…”