Commentary: Consensual ophthalmotonic reaction.

Intraocular pressure (IOP) change in the untreated fellow eye accompanied by a corresponding IOP reduction in the operated eye has been identified as the “consensual ophthalmotonic reaction” (COR), and the terminology was coined by Weekers in 1924.[1] This response was initially observed after contusion, ocular compression, tonography, and cauterization of the sclera.[2] In 1927, Wilmer published the first report on COR after a fistulating surgery in experimental animals.[3] After that, multiple studies have reported the possibility of IOP variation in the fellow eye following unilateral glaucoma surgery, including not only trabeculectomy, but glaucoma drainage device implantations, filtering canaloplasty, and microshunt implantations as well.[4] However, whether there is an IOP increase, decrease, or no change in the fellow eye after glaucoma surgery is still controversial. These contrasting results could be due to differences in the type of glaucoma, preoperative IOP, surgical technique, antimetabolite dosage and duration, time point of observation, and outflow facility of the untreated fellow eye. The postulated mechanisms behind COR include neuronal, hormonal, and cytokine regulation of aqueous flow dynamics.[5] Nevertheless, the exact mechanism is yet to be elucidated. A decrease in IOP in the fellow eye could be associated with improved patient compliance to the antiglaucoma therapy or the effect of systemic absorption of the medications. Also, it could result from a “regression to the mean” effect, as trabeculectomy is often planned when the IOP is high on the variation curve.[6] Regarding COR with topical medications, Newman et al.[7] observed that the IOP reduction in contralateral eyes was found to be associated with timolol only and not prostaglandins or carbonic anhydrase inhibitors. A similar decrease in IOP in the fellow eye has also been reported after laser trabeculoplasty, which might be due to the effects of the systemic release of humoral agents, such as matrix metalloproteinase, and improved medication compliance.[8] An increase in the fellow eye IOP following glaucoma surgery has been observed in the present study. We have also observed an IOP rise in a significant number of patients in the unoperated eye in the early postoperative period after unilateral trabeculectomy, though we do not have published data. Different theories have been postulated that may explain this finding. Weekers[1] explained the possible existence of COR in which activation of the nervous system increased the fellow eye aqueous production. Diestelhorst and Krieglstein[5] also postulated that unilateral filtration surgery triggers a central nervous system-mediated reflective increase in aqueous flow in the unoperated fellow eye to maintain physiological stability. In an animal experiment, a supraoptic controlling pathway has been suggested to lead to an IOP rise in response to water drinking after unilateral optic nerve sections.[9] A few studies described that underperfusion of the trabecular meshwork by aqueous humor in the operated eye and increased extracellular trabecular meshwork material deposition induces a reflex mechanism mediated by specialized cells in the scleral spur that can lead to decreased outflow in the fellow eye.[10] Another hypothesis was an increase in the prostaglandin level in response to the inflammation in the operated eye.[11] Other possible explanations include a postoperative presumed steroid response or withdrawal of antiglaucoma medications.[12] No studies have attributed the increase in IOP in the fellow eye to one factor. In the literature, post-surgical COR is found to occur at an earlier time frame than post-laser COR, which might suggest the role of mechanical triggers rather than chemical triggers in post-surgical COR. The predominance of one mechanism occurring due to a particular intervention may guide the IOP varia tion in the contralateral eye. Further prospective studies and a much more detailed macroscopic overview are needed to delineate the underlying mechanisms and the exact biological role of post-surgical COR. The take-home message is that the fellow eye needs to be carefully monitored after unilateral glaucoma surgery. The fellow eye may be the only eye with vision or the better eye of the two. Also, fellow eyes may be already glaucomatous, that failure to monitor and recognize IOP rise may delay appropriate management leading to glaucoma progression. It is recommended to inform the patient about the possibility of IOP variation in the other eye after glaucoma surgery and the need for multiple visits, especially in the early postoperative period. Another relevant message is that the fellow eyes should not be preferably used as a control in studies assessing the IOP outcomes of a particular treatment or intervention.