A 42-year-old woman noted sudden onset of severe headache and increased sensitivity to light. Although she had a history of migraine headaches in the past, she was certain that these symptoms were unlike her usual migraines, especially the photophobia, which was persistent rather than episodic. Her neuro-ophthalmic examination and Goldmann visual field results were normal. MRI revealed a pituitary mass with bright T2 signal consistent with apoplexy. There was parasellar extension and chiasmal contact without distortion by this tumor. Endocrine evaluation disclosed low cortisol and thyroid levels. Following replacement therapy, the patient noted improvement of headaches and photophobia.
Our five patients with chiasmal compressive lesions (three pituitary adenomas, one craniopharyngioma, one clivus chordoma) all reported an increased sensitivity and intolerance to ordinary light, often described as objects looking “too bright” or “glarey.” The duration of the photophobia from onset to diagnosis ranged from 1 week to 1 year (see Table 1). Two patients experienced photopsias as well—peripheral heatwaves (Case 4) or central sparkling (Case 2). The only other visual symptom at onset was mild blurring of vision in one eye of one patient (Case 2); an additional patient (Case 4) developed blurred vision in one eye 9 months after onset of photophobia. Four patients had headaches. Examination showed subtle visual dysfunction. There was no loss of visual acuity in 7 of 10 eyes, one line of loss in 1 eye, two lines of loss in 1 eye, and three lines in 1 eye. Visual field testing results were normal in one patient. Two patients had a bitemporal visual field defect; one patient had mild central defects. The fifth patient had extensive preexisting field losses from congenital chorioretinal scarring. The MRI scans always showed large lesions involving the sellar region. Following surgical decompression, photophobia remitted in all five patients.
Lesions that compress the optic chiasm typically produce progressive dimming and loss of vision. Especially in the early stages, when visual acuity is normal or nearly normal, visual symptoms are nonspecific, including such descriptions as “foggy,” “dim,” “hazy,” or “fuzzy.” Other less common visual symptoms include loss of depth perception, objects appearing and disappearing from view, and intermittent diplopia.
Positive visual phenomena may also be associated with compressive lesions of the optic nerves and chiasm. Safran and colleagues  prospectively obtained a detailed symptom history from 45 consecutive patients with optic nerve or chiasmal diseases such as optic neuritis, ischemic optic neuropathy, and compressive lesions. They divided symptoms of positive visual phenomena into two groups: photopsias and photophobia. They defined symptoms such as sparks, flashes, or colored lights as “photopsias” and sensations of dazzling or glaring light, a general visual discomfort in bright light, and an awareness of improved visual function in conditions of dim illumination as “photophobia.” They found that 30 of 62 visually symptomatic eyes had photopsias or photophobia or both. Of 13 eyes affected by a mass lesion (pituitary adenoma, meningioma, glioma, aneurysm), 9 eyes had photopsia, photophobia, or both. Only three patients had onset of photopsia or photophobia before onset of visual loss. These three patients were subsequently found to have compressive lesions, two patients with pituitary adenoma compressing the optic chiasm (similar to three of our five patients) and one patient with a unilateral perioptic meningioma.
Walsh and Hoyt  observed photophobia in one patient with a hypophyseal tumor and in another patient with a recurrent craniopharyngioma. Such small numbers of reported cases suggest that photophobia is a rare symptom of chiasmal compression. Photophobia, an intolerance to ordinary light such that pain may result, is more frequently encountered in diseases of the anterior structures of the eye or meninges. Photoreceptor disease is also associated with photophobia. The mechanism for the light intolerance in cases of corneal disruption, iritis, meningitis, and migraine remains unclear and is presumably related to irritation of the trigeminal afferent pathway.
The mechanism producing photophobia is even less clear in our patients. One possibility is release of blood or cystic contents from the suprasellar tumor causing meningeal irritation, thus producing headache and photophobia. This is a plausible explanation for Cases 2 and 5, whose MRI scans were consistent with previous pituitary apoplexy, and Case 3, whose tumor, a craniopharyngioma, contained cystic areas. Such a `chemical meningitis' would be less likely in the remaining two patients, especially Case 1 who had no accompanying headache. Case 4 did experience headache, but only after the onset of the photophobia. In these two patients, and perhaps the others as well, photophobia may be related to stretching of pain-sensitive structures at the base of the brain, those associated with meninges or blood vessels, transmitted via trigeminal afferents and processed centrally.
Because photosensitivity and photopsias are more commonly associated with ocular disease such as inflammation, corneal disruption, or photoreceptor degeneration, examiners may dismiss the symptoms as psychogenic if the eye examination is normal or mistakenly attribute them to ocular abnormalities. In fact, two of our patients who experienced photopsias as well as photophobia were initially suspected to have an outer retinal inflammatory syndrome, and retinal studies were undertaken before neuroimaging. We advise clinicians to consider compressive lesions of the anterior visual pathway in patients who complain of photophobia, even when visual acuity or results of visual field evaluations are normal.
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