Timothy C. Hain, MD, Chicago IL. Page last modified: March 17, 2019
Photophobia means "abnormal sensitivity to light". It is a common symptom with diverse causes. Photophobia is supposedly distinguished from "dazzle", meaning an unpainful though uncomfortable sense of glare. Dazzle is attributed to either diffusion of light in the ocular media or on a lack of adaptation. (Chronicle and Mulleners, 1996) Some also use the term "glare" by itself. We ourselves would find it a little difficult to distinguish between "painful" and "uncomfortable", and also find it difficult to describe the difference betwen "dazzle" and "glare". So perhaps these are really the same.
There are numerous sensory inputs that are endorsed by migraine patients as being provocative, as well as being enhanced during migraine including
Digre and Brennan (2012) listed roughly 50 "causes" of photophobia, from a review of the literature. Major groups include:
Migraine is associated with photophobia in roughly 80% of individuals having a migraine headache (Harriott and Schwedt, 2014) . Patients with migraine are more light sensitive both during and between attacks. Unilateral photophobia is possible in migraine variants, but practically this is almost never encountered.
Vanagaite (1997) suggested that "Photophobia seems to be an intrinsic property of migraineurs."
There is not a big literature. 10 migraine patients complained of more glare than controls when light was combined with facial pain, (Drummond, 1997). It is difficult to be sure what this means, but perhaps there is an "overload" phenomenon at work. It would also seem rather reasonable to us that should one in pain, everything that adds more distress would be considered more annoying. This paper does suggest a potential role for "multimedia" testing for migraine sufferers - -perhaps sound and light together would be more sensitive than either one alone ?
Salvesen et al (2000) noted that migraines are more likely during the bright artic summer season.
Light sensitivity per se:
There are lower thresholds for light found in migraine, tension and cervical headaches. Chong et al (2015) reported that "Relative to migraineurs without interictal photosensitivity, migraineurs with interictal photosensitivity have thicker cortex in several brain areas including the right lingual, isthmus cingulate and pericalcarine regions, and the left precentral, postcentral and supramarginal regions". This suggests that photosensitivity in migraine can be "hard wired" into the cortex, or alternatively and more simply, that these groups represent different disorders, both called "migraine". Recent genetic studies of "migraine" showing a myriad of genes associated with "migraine" lends more support to this idea.
Light wavelength also alters photosensitivity. Blue light is more uncomfortable according to some, and red light according to others. Treatment efforts usually just boil down to trying out colored classes until one is found that helps. This again suggests that there may be a myriad of underlying mechanisms all being called "migraine".
Migraine patients often endorse sensitivity to flicker, such as in fluorescent lighting, and prefer "natural lighting" that does not flicker.
From Kovacs et al (2005), migraine patients critical fusion frequency.
It would be reasonable then to suppose that migraine patients "see" more flicker. Oddly enough however, migraine patients have a lower "critical fusion frequency" than normal subjects -- one would think that this would make them percieve less flicker than normal subjects. According to Kowacs et al (2005), the "mean flickering fusion threshold" was 40.45 +- 6.38 vs 44.33 +- 6.49 Hz, in migraines vs controls. The difference between migraine patients and controls was small and certainly not sufficient to identify migraine patients as a group. The difference seems to be driven by a few outliers in the controls rather than a systemic difference. It would seem from this single paper that timing differences in visual processing in migraine patients is not the explanation for sensitivity to fluorescent lighting. A reasonable alternative is that Migraine patients simply are more annoyed by flicker than normal persons, in the same way that migraine patients are more annoyed by loud noises that they hear equally as well as normal subjects.
Marcus and Soso (1989) reported that "stripes" caused discomfort for 82% of 17 people with migraine compared with 18% of a control group. They judged discomfort as "grimace with eye narrowing and head withdrawal, turning away, or refusing to look at pictures of stripes. The stripes were vertical, viewed at 43 cm, black and white were equal width, and spacing was "3 or 4 cycles per degree of visual arc". There are no illustrations of their stimulus in the article - -we would think this would be more of a "grating" than "stripes" -- we would say stripes might reasonably occupy a degree or more of the visual arc. The small number of subjects and the judgement calls needed to score patients are obvious weaknesses of this paper. It is also implausible that any test should show a 4:1 sensitivity, given that Migraine is such a diverse entity. Still, we think it is true that patients with migraines complain more about stripes.
Harle et al (2006) performed a similar test using gratings, but called it the "pattern glare" test. They presented gratings varying between 0.5 cycles/degree to 12 cycles per degree, and provided participants a list of suggested "visual perceptual distortions (illusions)" to choose from. They found that 25 migraine patients were different than 25 controls, with higher "pattern glare score". The most succesful grating to separate between controls and patients was 3 cycles/degree. There was considerable overlap. The small number of subjects as well as the methodology where subjects had answers suggested to them is a weakness of this study.
Stripe stimuli are also used to elicit optokinetic nystagmus (OKN). The "duty cycle" of OKN -- black vs white -- is much higher than gratings. Much more about OKN can be found here.
Surprisingly, the body of published research done on stripes or gratings or whatever in migraine is rather small, considering the huge number of individuals that have migraine and also the relative ease of doing these psychophysical tests. What about horizontal vs vertical ? Wavy lines ? Speed of movement ? Spirals and rotation ? Lots of material here for more studies.
According to Shepard (2006), "visual after-effects are illusions that occur after prolonged viewing of visual displays (pattern adaptation). The motion after-effect (MAE), for example, is an illusory impression of motion that is seen after viewing moving displays. " Motion after effects last longer in migraine patients compared to controls.
Luedtke et al (2019) recently reported on the duration of after-images in healthy controls compared to patients with migraine. Although there was a gigantic overlap, after-image duration was shorter in migraine patients(roughly 8-9 sec) than healthy controls (about 12 seconds). Because of the gigantic overlap, this observation would not be likely to be useful for diagnosis. After-image duration increased on headache days, but nevertheless, did not reach the duration of healthy controls. After-images are correlated with long-range inhibition in visual cortex. This would imply that migraine patients have less long-range inhibition in visual cortex.
The term visual snow was recently coined to describe continuous static-like flickering dots in the entire visual field, sometimes combined with palinopsia or photophobia (Simpson et al, 2013). This syndrome is thought to overlap with migraine aura. Since migraine is so broad -- it would also seem fair to just call it another type of migraine aura. Eren et al (2018) found that visual evoked potentials in patients with visual snow and migraine had subtle changes in their VEP latencies and amplitudes. The data was very scattered and overlapping (as is nearly always true when one is studying migraine). Yildiz reported reduced thresholds for occipital magnetic stimulation, and loss of habituation.
Proposed treatments for visual snow include the migraine treatiemtns of lamotrigine, acetazolamide, and verapamil (Bou Ghannam and Pelak, 2017)
Pain from the eye is transmitted by the ophthalmic division of CN-5 to the brain. This is likely the mechanism for photophobia from ocular sources.
After light signals activate the eye, pain circuits can be activated through conventional vision circuits, through IPRGC's, or "intrinsicially photosensitive retinal ganglion cells", and similar cells outside the retina. Circuits include through the optic nerve, to the olivary pretectal nucleus, and through direct connections to the trigeminal ganglion.