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Perry Rosenthal, James Bradley; Dry Eye-like Symptoms Without Dry Eyes Is A Neurological Disease. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3855.
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To identify and characterize a trigeminal pain syndrome defined by disabling dry eye-like symptoms disproportionate to external signs.
This retrospective chart review case series identified 58 patients with severe dry eye-like symptoms that were not mitigated by a vapor-sealed compartment of artificial tears (scleral lens).
Gender distribution favored females 4:1. The corneas of 88% of patients showed no fluorescein staining. Corneal confocal images revealed striking nerve morphometric changes in some eyes. Median Cochet-Bonnet filament threshold was 4.3 mm. 20% had indications of secondary hyperalgesia involving conjunctiva. Photophobia without visible cause was reported by 58%. 53% reported pain or altered sensory perception in the receptive fields of non-ophthalmic branches of the trigeminal nerve and 26% reported distorted responses of non-trigeminal sensory cranial nerves. 3 patients exhibited tactile allodynia of their face and forehead. Slit lamp examinations of corneas that had no corneal staining suggested a trend to lower tear metrics. LASIK was the neuropathic pain trigger in 4 patients and PRK in 1. Coexisting blepharospasm that began with or followed onset of dry eye-like pain was present in 5 patients and failed to respond to effective pain-mitigating interventions.
The scleral lens is a valuable clinical tool for distinguishing chronic dry eye-like symptoms due solely to evaporative corneal hyperalgesia which it completely suppresses, and ectopic (spontaneous) corneal or cornea-projected pain which, by definition, it does not suppress. Symptoms projected to the receptive fields of non-ophthalmic branches of the trigeminal nerve and other sensory cranial nerves suggested entrenched hyperexcitability of the brain stem pain circuitry with spread to adjacent uninvolved neurons (cross-talk). The co-existence of lid dystonia/ apraxia in 5 patients, including Meige’s syndrome in 2, indicate aberrant activity in the basal ganglia that was temporally associated with trigeminal neuropathic pain in all affected patients. Successful therapeutic interventions in these patients require suppression of ectopic (spontaneous) pain activity and/or lowering the entrenched elevated homeostatic excitability in the central pain-signaling network.
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