Oculofacial Pain: Corneal Nerve Damage Leading to Pain Beyond the Eye

Abstract

The cornea is supplied principally by the ophthalmic branch of the trigeminal nerve and is the most densely innervated organ in the human body. Under normal conditions, the corneal nerve terminals incorporate sensors that monitor the thickness and integrity of the tear film, which are essential for meaningful vision. A disrupted tear film or direct noxious stimulation of these corneal nerves can produce discomfort or pain limited to the affected surface. Damage to these nerves can sometimes lead to a chronic neuropathic condition, where pain persists months following the initial insult, long after the nerves appear to have healed in the cornea itself following treatment. Neuropathic pain appears to persist indefinitely in a few patients.

Figure

Trigeminal convergence pathway for oculofacial pain. Temperature, mechanosensitive, and polymodal nociceptors transduce noxious input from acute injury or inflammation into neural signals. Innervation of the cornea supplies afferents through branches of the ophthalmic division of the trigeminal nerve. These first-order neurons converge with afferent inputs from the other two divisions of the trigeminal nerve (maxillary and mandibular) and are somatotopically organized within the trigeminal ganglion. The neuronal bodies of the trigeminal nerve, located in the ganglion, have central projections that synapse in the trigeminal nucleus. Second-order neurons cross over in their ascending pathway (trigeminothalamic tract) to nuclei within the thalamus (e.g., ventroposteriormedial thalamus). From here, third-order neurons project to the primary somatosensory cortex where the cornea is functionally represented. The boxes below show referred pain (left) to the cornea from orofacial somatic and visceral structures and (right) to orofacial viscera from the cornea and skin. Such convergence may occur within the central nervous system, potentially involving the trigeminal nucleus and/or thalamus.