by Martin Rakusa
Migraine—with and without aura—is one of the most common neurological disorders, affecting millions worldwide. In the past few years, several new studies have been finished and we have got a better insight into the pathophysiology of migraine.
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Prof. Margarita Sanchez Del Rio from Spain opened this Symposium on Migraine Cortical Spreading Depression at EAN 2022 with the lecture ‘Pathophysiology Cortical Spreading Depression’. Cortical spreading depression was first studied in rabbits’ brains. After electrical stimulation, activity slowly expanded at a rate of 2-5mm per minute, concentrically, regardless of functional or vascular territories. Cortical spreading depression collapses ion homeostasis, releases neurotransmitters, changes blood flow, and induces neuroinflammatory response. In humans, we can find cortical spreading depression after seizures, traumatic brain injury, intracerebral haematoma, subarachnoidal haemorrhage and malignant hemispheric stroke. There is growing evidence that cortical spreading depression also underlies migraine aura. The first study was done on a patient who could self-induce visual aura during fMRI. During aura, cortical activity in the visual cortex was stopped.
The second lecture was ‘Cortical Spreading Depression is the main clinical initiation wave for all migraine types’. Prof. Anna Andreou from the UK reminded the audience that migraine pathophysiology involves persistent cortical activation. Therefore, cortical spreading depression can be used as a model to study cortical excitation in migraine. Both cortical activation and depression may (de)sensitise third-order thalamic neurons and, possibly through corticothalamic modulation, influence the ascending trigeminothalamic pathways and cause pain. However, we may modulate cortical excitation with transcranial magnetic stimulation. Therefore, we may use it for migraine treatment.
In the last lecture, Prof. Astrid Gendolla from Germany explained clinical expression, headache classification and possible therapeutic possibilities. Up to one third of patients with migraine experience aura. The lifetime prevalence of migraine with aura is 5%, and females are affected twice as frequently as males. Clinical symptoms develop gradually and usually precede the headache phase. They are fully reversible and, in most patients, begin in the visual system, followed by sensory, speech/language, motor, brainstem and retinal symptoms.
In some cases, the aura may persist for several days. Patients usually report visual phenomena and several well-known syndromes such as ‘Alice in wonderland syndrome’, ‘visual snow’, and seeing afterimages of objects. Prof. Gendolla also pointed to comorbidities. Patients with migraine are more likely to experience depression, anxiety disorder and stroke. Women who use combined oral contraception have a 2-4 times higher risk for stroke. An important question for a clinician is how we can treat aura and when to start the treatment for headaches. All clinical trials with triptans taken during aura were negative. However, positive results were seen when triptans were taken at the headache onset. An alternative possibility would be transcranial stimulation, which can also treat aura. However, it is unlikely that patients would be able to receive it before the aura is over. For the prevention of aura, similar therapy can be used as for the prevention of migraine. The treatment of migraine with or without aura may differ. However, which strategy we should use for patients with both types of migraine is still unresolved.
