Unmasking Photophobia and Blepharospasm Mechanisms: The Role of Optic Chiasm and Trigeminal Nerve Compression in a Giant Pituitary Adenoma Case.

Blepharospasm, characterized by abnormal blinking and sensory hypersensitivity such as photophobia and ocular pain, is thought to arise from pathological sensorimotor integration. We report a rare case of a male teenager with a growth hormone-secreting giant pituitary adenoma compressing both the optic chiasm and bilateral trigeminal nerves. Initially, the patient presented with visual disturbances and bitemporal hemianopia, without photophobia or ocular pain. Following partial tumor resection, which relieved compression of the optic chiasm but not the trigeminal nerves, he developed severe photophobia, deep ocular pain, and bilateral secondary blepharospasm. These symptoms persisted despite pharmacologic interventions, including pregabalin and topical rebamipide. A second surgery, which decompressed the trigeminal nerves, led to the complete resolution of all symptoms. The clinical course suggests that trigeminal nerve compression, particularly of the ophthalmic branch (V1), may induce hypersensitivity states resulting in neuropathic pain, photophobia, and secondary blepharospasm. We hypothesize that initial optic chiasm compression suppressed photophobia by disrupting non-visual photophobia circuits through the suprachiasmatic nuclei to pulvinar nuclei. After decompression, restoration of this pathway unmasked the hypersensitivity induced by ongoing trigeminal compression. The complete resolution of symptoms following trigeminal decompression supports the role of peripheral sensory nerve compression in the pathogenesis of photophobia and secondary blepharospasm. This case provides novel clinical evidence for the interrelationship between the trigeminal and visual pathways in sensorimotor disorders.