Abstract

AbstractOcular infections such as herpes simplex virus (HSV) keratitis result in ocular sensitivity changes. During acute HSV episodes and eventually during postherpetic outbreaks, spontaneous pain and hyperalgesia are experienced, being reduced by treatment with Na+ channel blockers (not only by local anaesthetics but also by gabapentin, lacosamide or amitriptyline). At the same time, patients commonly develop hypoesthesia due to the decrease of sensitivity to mechanical stimulation, whose appearance could be due to the internalization of Na+ channels in trigeminal sensory neurons innervating the infected cornea.When explored using a gas esthesiometer that allows selective mechanical, chemical, heat and cold stimulation, HSV‐infected corneas showed those sensitivity disturbances to be expected when corneal polymodal nociceptor activity is altered. On the contrary, sensitivity to cold stimuli is not modified, which suggest that cold thermosensitive ocular neurons are not infected by the virus. A surprising result is the alteration, in the same sense although to a lesser degree, of the sensitivity of the contralateral eye. This contralateral altered sensitivity could be caused by a subclinical HSV infection of the contralateral side. Another possibility is that to be due to a neuroimmune interaction that ends up affecting the activity of sensory nerves of both eyes, in a similar way to what happens in non‐infectious inflammatory processes affecting only one eye.(PID2020‐115934RB‐I00 from DOI: MCIN/AEI/10.13039/50110001103)

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