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Updated: Apr 16, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
Published on: June 2, 2014
Vision and migraine
1Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Background:
Migraine, a common brain disorder, disrupts vision more than any other motor or sensory function. The possible visual aura symptoms vary from occasional small flashes of light to complex visual hallucinations, the stereotyped teichopsia being the most typical pattern. It is unclear as to why aura occurs serendipitously, sometimes preceding, but also occurring after the headache, and why aura can present with multiple phenotypes.
Methods:
To better understand the nature of visual disturbances in migraine, 4 aspects must be considered: What are the visual perceptions in migraine; why vision is affected in migraine; the role of cortical spreading depression (CSD); how does vision could affect migraine. Evidence supporting each of these topics is reviewed.
Results:
CSD travels at a similar pace as the march of symptoms in the visual field. Functional neuroimaging studies show spreading changes compatible with CSD regardless of aura. Computerized models reproducing the CSD march on the visual cortex predict a sensory experience compatible with naturally occurring visual auras. Rather than spreading in all directions, these models suggest that CSD moves preferentially in one direction. Migraine-preventive drugs increase the CSD threshold and reduce CSD velocity. Blind migraineurs may present atypical visual aura, with more colors, shorter duration, different shapes, and atypical symptoms, such as auditory experiences.
Conclusions:
CSD is the underlying phenomenon in migraine with and without aura. In migraine without aura, CSD probably does not run over silent areas of the cortex, but rather does not reach symptomatology threshold. Normal vision is important in migraine, as lack of sight may change the visual experience during migraine aura, probably due to cortical reorganization and changes in local susceptibility to CSD.
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