TFOS DEWS II pain and sensation report

Carlos Belmonte*, Jason J. Nichols, Stephanie M. Cox, James A. Brock, Carolyn G. Begley, David A. Bereiter, Darlene A. Dartt, Anat Galor, Pedram Hamrah, Jason J. Ivanusic, Deborah S. Jacobs, Nancy A. McNamara, Mark I. Rosenblatt, Fiona Stapleton, James S. Wolffsohn

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

Pain associated to mechanical and chemical irritation of the eye surface is mediated by trigeminal ganglion mechano- and polymodal nociceptor neurons while cold thermoreceptors detect wetness and reflexly maintain basal tear production and blinking rate. These neurons project into two regions of the trigeminal brain stem nuclear complex: ViVc, activated by changes in the moisture of the ocular surface and VcC1, mediating sensory-discriminative aspects of ocular pain and reflex blinking. ViVc ocular neurons project to brain regions that control lacrimation and spontaneous blinking and to the sensory thalamus. Secretion of the main lacrimal gland is regulated dominantly by autonomic parasympathetic nerves, reflexly activated by eye surface sensory nerves. These also evoke goblet cell secretion through unidentified efferent fibers. Neural pathways involved in the regulation of Meibonian gland secretion or mucins release have not been identified.In dry eye disease, reduced tear secretion leads to inflammation and peripheral nerve damage. Inflammation causes sensitization of polymodal and mechano-nociceptor nerve endings and an abnormal increase in cold thermoreceptor activity, altogether evoking dryness sensations and pain. Long-term inflammation and nerve injury alter gene expression of ion channels and receptors at terminals and cell bodies of trigeminal ganglion and brainstem neurons, changing their excitability, connectivity and impulse firing. Perpetuation of molecular, structural and functional disturbances in ocular sensory pathways ultimately leads to dysestesias and neuropathic pain referred to the eye surface. Pain can be assessed with a variety of questionaires while the status of corneal nerves is evaluated with esthesiometry and with in vivo confocal microscopy.

Original languageEnglish
Pages (from-to)404-437
Number of pages34
JournalOcular Surface
Volume15
Issue number3
Early online date20 Jul 2017
DOIs
Publication statusPublished - Jul 2017

Keywords

  • central nervous system
  • cold receptors
  • corneal esthesiometry
  • dry eye disease
  • in vivo corneal confocal microscopy
  • mechano-nociceptors
  • neuropathic pain
  • ocular surface dryness
  • pain
  • peripheral sensory nerves
  • polymodal nociceptors
  • sensation
  • trigeminal brainstem nuclear complex
  • TRP channels

Fingerprint Dive into the research topics of 'TFOS DEWS II pain and sensation report'. Together they form a unique fingerprint.

  • Cite this

    Belmonte, C., Nichols, J. J., Cox, S. M., Brock, J. A., Begley, C. G., Bereiter, D. A., Dartt, D. A., Galor, A., Hamrah, P., Ivanusic, J. J., Jacobs, D. S., McNamara, N. A., Rosenblatt, M. I., Stapleton, F., & Wolffsohn, J. S. (2017). TFOS DEWS II pain and sensation report. Ocular Surface, 15(3), 404-437. https://doi.org/10.1016/j.jtos.2017.05.002