This is due to dryness leading to pain or irritation that results in intermittent excess tearing, or epiphora.

Intermittent is the main point.

If you ask the patient meticulously , they will tell you that the tearing is episodic. Unlike continuous tearing throughout the day as in nasolacrimal duct obstruction patients.

https://www.ncbi.nlm.nih.gov/books/NBK470411/

Sunny Chi Lik Au , thank you for your comment. Some experts tell that epiphora in a dry eye patient is a sign of evaporative problem, so this symptom is the reason to exclude lacrimal gland pathology. What is your opinion?

Tearing in dry eye disease is secondary to the unstable tear film, which triggers secretion from the lacrimal glands. Interesting would be to know if increased tear film height in these patients is associated with decreased tear break up time. Also, if the incidence of conjunctivochalasis in such patients is more? Let me know Dr Vasily, if an interesting research idea comes up.

concerning the statement [epiphora in a dry eye patient is a sign of evaporative problem] , i think that this symptom is non-specific for such a cause of dry eyes. For evaluation of evaporative problem, there are many other ways, as if Swati Singh mentioned on the tear film break up time (TFBUT) is one of them.

Lacrimal gland is different from nasolacrimal duct in terms of anatomical meaning and location. Lacrimal gland pathology cannot be excluded by simply on the tears production, which tear production is just one of the functional parameters of the lacrimal gland Vasily Yartsev

Dear Dr. Swati,

Generally speaking, dry eye disease, according to etiopathogenic classification, consists of two types: Aqueous-deficient dry eye and evaporative dry eye (EDE).

The latter is accompanied by increased tear evaporation. There are some intrinsic causes to EDE, including meibomian gland dysfunction (MGD) and low blink rate. Meibum secreted by meibomian glands is an essential component of the tear film, contributing to the stability of tear film. Dysfunction of the glands causes decreased meibum secretion and altered meibum quality leading to the dysfunctional tear film and increased tear evaporation. Instability of tear film and loss of tear film homeostasis leads to desiccation of the ocular surface, the increased osmolarity of the tear film /hyperosmolarity, ocular surface inflammation, and ocular surface damage. Reflex tearing occurs then as a compensatory mechanism, which leads to even more significant tear film instability.

I can recommend Reports of the International Dry Eye Workshop (DEWS) 2007 and 2017.

https://www.tearfilm.org/dettreports-tfos_international_workshop_on_meibomian_gland_dysfunction/83_30/eng/

Kind regards

Dr. Reza A. Badian

I completely agree with Dr Sunny. Lacrimal gland pathologies can be better studied by looking at the gland, and examining the direct tear secretion from it using fluorescein dye.

The exact pathogenesis of tearing in DED is not so well studied in detail, and adds to the plethora of non-specific symptoms of dry eye. Why only few patients complain despite similar dry eye diagnostic work up?

Dr Reza, you have depicted very well the sequence of events in EDE. I agree with Dr Sunny that tearing cannot be considered as a factor for ruling out lacrimal gland pathology.

Interesting discussions. Thanks for the question Vasily.

Could be related to ocular surface irritation or rapid tear film evaporation both of which coul induce a neurogenic feedback reflex to the major lacrimal gland to secrete tears.

Could be related to ocular surface irritation or rapid tear film evaporation both of which coul induce a neurogenic feedback reflex to the major lacrimal gland to secrete tears.