People who live with migraine usually arrive at the topic of vision already well-read. You've been through the patient leaflets, the headache-diary apps, the lists of triggers; you may have spent years working out which of fluorescent overheads, scrolling text, sunlight on water, and stripes on a polo shirt are bad for you on a given week. So this post will skip the introductory framing on what migraine is, and go directly to a quieter observation in the research literature: between attacks — interictally, in the term of art — many people with migraine show measurable differences in how their visual system processes contrast. The differences are subtle, they don't show up on the eye chart, and they aren't found in every patient. But they are real, replicated, and worth knowing about if you're trying to make sense of why your visual world sometimes feels different even when no attack is in progress.
This post is about that literature. What's documented, what's contested, what a home contrast-sensitivity measurement can and can't add to your picture, and where the neuroscience gets genuinely interesting.
A short refresher on what migraine actually is
Migraine is a complex neurological event, not a particularly bad headache. The headache phase — when it occurs — is one of several phases in a sequence that can include a prodrome (mood, energy, cognitive changes hours to days before), an aura (focal neurological symptoms, usually sensory and most often visual), the headache itself, and a postdrome (the "migraine hangover"). Not every attack has every phase, and a meaningful minority of people experience aura without subsequent headache at all. The underlying physiology spans brainstem, hypothalamus, cortex, meninges, and the trigeminovascular system; it is not localised to one structure.
Visual aura is the most common aura type. Population-based epidemiology puts visual aura in roughly 30% of people with migraine — the American Migraine Survey II reported 31%, a Copenhagen-based study reported 33.7%, and a more recent population study found 29.4% (Hadjikhani & Vincent, 2021). The classic visual aura is a slowly-expanding scintillating arc (the fortification spectrum) that drifts across the visual field over 20 to 30 minutes before fading, sometimes leaving a transient blind area behind it. Fortifications account for about 40% of reported visual auras; other forms include simpler photopsias, distortions of size or perspective, and partial visual-field disturbances.
The mechanism behind aura is one of the more remarkable findings in modern neurology. Aura is now well-established as the perceptual signature of a cortical spreading depression (CSD) — a slow wave of neuronal and glial depolarisation that propagates across the cortex at roughly 3–5 millimetres per minute, followed by an extended period of suppression of cortical activity (Lauritzen, 2001). Because CSD typically begins in or near the visual cortex (the cortical area most densely packed with excitable cells, and a frequent starting point in the susceptible brain), the perceptual march of the aura mirrors the spatial march of the wave across V1 and surrounding areas. That match — between a slowly-moving cortical event and a slowly-moving perceptual one — is one of the cleaner correspondences between brain activity and subjective experience that the field has.
What the contrast-sensitivity literature shows
The relevant question for this post is what happens to vision outside an attack, when there's no aura in progress and no headache. The literature here is smaller than the literature on the attack itself, but several findings have replicated across labs.
Reduced contrast sensitivity, especially with peripheral or temporally-modulated stimuli. McKendrick and colleagues, working with 15 people with migraine-with-aura and 15 matched controls, tested vision interictally on a battery of tasks designed to probe different visual mechanisms. Significant deficits showed up specifically on temporally-modulated stimuli (around 16 Hz), orientation discrimination at low spatial frequency, and global dot motion — patterns that implicate both cortical and pre-cortical involvement, with relatively spared parvocellular function (McKendrick, Vingrys, Badcock & Heywood, 2001). A follow-up study a few years later, testing 12 people with migraine and 17 controls with stimuli designed to isolate magnocellular versus parvocellular pathways, found contrast-sensitivity reductions at 10° peripheral eccentricity that were not selective to one pathway — both magno-tuned and parvo-tuned stimuli showed deficits — suggesting the underlying change is broader than the simpler "magnocellular dysfunction" story sometimes told (McKendrick & Sampson, 2009). The same study found no significant foveal difference, which matters for an at-home test: a central-vision contrast-sensitivity measurement may under-register the deficit if it's strongest in the periphery.
Reduced cortical responses, impaired habituation. A 2022 meta-analysis pooled 23 visual-evoked-potential studies of interictal migraineurs and controls. The pooled picture: slightly reduced P100 amplitudes (an early cortical response component that tracks roughly with magnocellular activity), and — more strikingly — substantially reduced habituation of the P100 and N135 to repeated visual stimulation (Sezai, Murphy, Riddell, Nguyen & Crewther, 2022). The habituation finding is the consistent one across studies. Healthy controls' cortical responses dampen with repeated presentation of the same stimulus, an efficient filtering of redundant input; migraineurs' do not, or do so less. The interpretation in the field is that the migraine brain has a baseline state of reduced intracortical inhibition — a kind of mild, persistent "hyperexcitability" — that shows up in many measurement modalities, of which contrast sensitivity is one.
Mid spatial-frequency changes are commonly reported but heterogeneous. Across the broader migraine literature, reductions tend to cluster in the mid spatial-frequency range — roughly 3 to 12 cycles per degree — though specific findings depend a lot on the stimulus, the protocol, the sub-population (aura vs no-aura), and how recently the last attack occurred (Hadjikhani & Vincent, 2021). Some studies find reductions only with peripheral testing; some only with temporally-modulated stimuli; some find paradoxically increased sensitivity in subgroups. The honest summary is that interictal contrast-sensitivity changes are real and replicable as a population finding, but the individual pattern is variable.
Not every migraine patient shows changes. The literature consistently reports group-level differences between migraineurs and controls. Within the migraine group, there is wide individual variation. Plenty of people with migraine have entirely typical contrast sensitivity between attacks. A normal CSF measurement does not say much about whether your migraine is real, severe, or worth tracking — it says only that the particular subtle population-level effect doesn't show up in your particular measurement on your particular day.
This is interictal, not during an attack. During an actual aura or headache, vision can change in ways that are obvious without any measurement: blurring, scotomata, photophobia, altered colour perception, transient hemianopia. Those experiences are real and important, but they are not what a contrast-sensitivity test is for. The interictal frame is the one where a quiet objective measurement adds something — because the perceived differences are subtle, the eye chart says everything is fine, and a CSF curve is one of the few places those subtle differences become legible.
Why it might matter to you
If you have migraine and the visual world sometimes feels slightly different between attacks — flat, or harsh, or more effortful to parse, or strangely fatiguing to look at — the literature gives that experience some grounding. You're not imagining it, and you're not pathologising a normal variation. There is a body of work documenting subtle visual-processing differences in interictal migraine, and a plausible neurophysiological mechanism (reduced intracortical inhibition / impaired habituation) behind them.
The practical use of a home contrast-sensitivity measurement, in that context, is as one piece of pattern data alongside everything else you already track. If you keep a headache diary — and if you have migraine, you almost certainly do — adding a CSF measurement at whatever rhythm survives gives you a numerical thread running alongside the diary's narrative thread. Over months, you may notice patterns: does your contrast sensitivity dip during clusters of frequent attacks? Does it sit lower in stretches of poor sleep, high stress, or hormonal phases that you already know are tough? Does a change in preventive medication coincide with a shift in your baseline?
For chronic migraine specifically, the value tends to be in the trend, not the snapshot. A single number on a single day is too noisy to carry much weight. A multi-month trajectory plotted alongside your headache diary is the kind of thing that can earn its place in a conversation with your neurologist — not as a diagnostic claim, but as the patient bringing observational data they collected themselves.
What it cannot tell you
Note. A contrast-sensitivity test is a screening and tracking measurement, not a diagnostic test.
It does not diagnose migraine. Migraine is a clinical diagnosis based on history — the pattern of attacks, the associated symptoms, the family history, the response to treatment — and on ruling out secondary causes when the picture warrants. No vision test, online or in a clinic, replaces that.
It does not reliably predict your next attack. The literature does not support using CSF as a short-term forecast for individual migraines. Some people may notice subjective visual changes hours before an attack; that's a different observation from anything a once-a-week home test can register.
It does not distinguish migraine from other things that affect contrast sensitivity. Refractive error, dry eye, fatigue, certain medications, early cataract, glaucoma, MS, post-concussion changes, and a long list of other conditions can all reduce contrast sensitivity. The test cannot tell them apart.
A single result is a snapshot. Test-retest variation is real even with carefully validated clinical instruments, and an online test on a consumer screen is noisier than that. A trend over time on the same setup is far more informative than any one session's number.
A reduced result is not a reason to change migraine medication. Medication decisions belong with your neurologist or headache specialist, who has the rest of your clinical picture. A reduced result is, at most, a piece of pattern data worth mentioning at your next appointment.
The framing we'd ask you to hold: this is one objective data axis you can add to a headache diary, no more and no less. It is not a verdict on whether your migraine is real, getting worse, or being managed well.
Practical next steps
If you have migraine and new or changing visual symptoms — particularly anything that doesn't fit your usual aura pattern, persistent visual changes between attacks, or any sudden visual event — that's a reason to see a neurologist or headache specialist, not to start running a home test. The literature on interictal contrast-sensitivity changes is background context; an unfamiliar visual symptom in a person with migraine deserves a clinical look, including an ophthalmological exam to rule out structural problems first.
If you already have a stable migraine picture and you'd like to add CSF tracking to your existing diary, a workable rhythm:
- Take the curve once. Our free test runs in the browser, takes a few minutes, and keeps results on your device. Calibration at the start (screen size, viewing distance, brightness response) is what lets numbers compare across sessions on the same setup.
- Retake at a sustainable interval. Once a week or once a fortnight is enough for trend data and not so often that it becomes a chore. Test in similar lighting, on the same device, at a similar time of day — fatigue and ambient light both move the curve, and you want the variance to come from you, not your setup.
- Note context in your diary. Just a few words: attack in the last 24 hours, sleep, stress, medications, hormonal phase, any visual symptoms you've noticed that week. The context is what makes the numbers interpretable later.
- Bring the trend, not a single number. If you notice CSF sitting consistently lower during a stretch of frequent migraines, that's worth mentioning at your next neurology appointment as a descriptive observation. Bring the plot if you have one. Don't change medication on your own based on the curve.
Two cross-links worth keeping at hand. The conceptual background on what a CSF measurement actually is, and what makes it more informative than a simple eye-chart number, lives in the primer post on contrast sensitivity. For the broader pattern of how to integrate vision tracking with a chronic-illness diary, the post-concussion vision post walks through a similar framing for a different patient population — different condition, same respectful approach to noisy objective data as a thread alongside lived experience.
Take the test
Take the test now. Save the result. If migraine is part of your life and you already keep a headache diary, this is one more data point you can track alongside it — a quiet objective measurement that may, over months, surface patterns you can bring to the specialist who knows the rest of your picture.
A few minutes today, a few minutes next month. The first reading is a snapshot. The second is the start of a line.
References
- Lauritzen, M. (2001). Cortical spreading depression in migraine. Cephalalgia, 21, 757–760. A concise review by one of the leading investigators of cortical spreading depression — the slow propagating wave of cortical depolarisation that underlies migraine aura. Establishes CSD as the neurophysiological substrate of aura on the basis of converging clinical and experimental evidence.
- McKendrick, A. M., Vingrys, A. J., Badcock, D. R., & Heywood, J. T. (2001). Visual dysfunction between migraine events. Investigative Ophthalmology & Visual Science, 42(3), 626–633. Foundational interictal study comparing 15 people with migraine-with-aura against matched controls on multiple vision tasks. Found significant interictal deficits on temporally-modulated stimuli (16 Hz), low-spatial-frequency orientation discrimination, and global dot motion, with relatively spared parvocellular function.
- McKendrick, A. M., & Sampson, G. P. (2009). Low spatial frequency contrast sensitivity deficits in migraine are not visual pathway selective. Cephalalgia, 29(5), 539–549. Tested 12 people with migraine and 17 controls using stimuli designed to isolate magnocellular versus parvocellular pathways. Found peripheral (10° eccentricity) contrast-sensitivity reductions for both pathway-targeted stimulus types and no significant foveal difference — arguing that interictal contrast deficits in migraine are not selective to a single visual pathway.
- Sezai, T., Murphy, M. J., Riddell, N., Nguyen, V., & Crewther, S. G. (2022). Visual processing during the interictal period between migraines: a meta-analysis. Neuropsychology Review, 33(4), 765–782. Meta-analysis of 23 visual-evoked-potential studies comparing interictal migraineurs and controls. Pooled findings: slightly reduced P100 amplitudes and substantially reduced habituation of P100 and N135 to repeated visual stimulation, consistent with reduced intracortical inhibition / cortical hyperexcitability as the underlying interictal state.
- Hadjikhani, N., & Vincent, M. (2021). Visual perception in migraine: a narrative review. Vision (Basel), 5(2), 20. Comprehensive narrative review covering visual aura prevalence (~30% of people with migraine), cortical spreading depression as the substrate of aura, cortical hyperexcitability across multiple measurement modalities, and the heterogeneity of interictal contrast-sensitivity findings across the literature.