Fluctuations of Corneal Sensitivity in Dry Eye Syndromes—A Longitudinal Pilot Study

Nepp, Johannes; Wirth, Magdalena A.

doi:10.1097/ico.0000000000000566

Cited by 17 publications

(18 citation statements)

References 21 publications

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“…A longitudinal study of corneal sensitivity in patients with DES found that, notwithstanding highly variable results, corneal sensitivity was found to be lowered in severe dry eye 37 . Bourcier and coauthors also found that subjects with dry eye can have reduced mechanical, chemical and corneal thermal sensitivity 26 .…”

Section: Regulation Of Basal Tear Production and Lacrimationmentioning

confidence: 99%

“…Apart from ageing-related reduced corneal sensitivity, 36 dry eye symptoms may be accompanied by a decrease in corneal sensitivity such as may be associated with refractive surgery, diabetes 18 . herpetic keratitis, topical pharmacological agents and long-term contact lens wear 37 . In addition, dry eye-induced alterations to the properties of corneal afferent neurons and the central processing of corneal input may have significant consequences for both the regulation of tearing and ocular pain 18 …”

Section: Regulation Of Basal Tear Production and Lacrimationmentioning

confidence: 99%

“…Each class of primary corneal afferent neuron has the potential to induce tear secretion by responding to different environmental stimuli and, according to the type or combinations of different types of neurons involved, tear composition may vary 18 as may the quantity of tears with associated variations in their homeostatic functions. For example, deprivation of afferent neurological stimulation signifies dysfunction of reflex tearing due to a decrease in corneal sensitivity 37 . Topical anaesthesia reduces basal tearing, suggesting that background activity in corneal nerve fibres is required to maintain a tonic stimulation of the lacrimal gland 4 .…”

Section: Regulation Of Basal Tear Production and Lacrimationmentioning

confidence: 99%

“…Neurological dysfunction can be classified according to whether it is influenced by the hypothalamus and the limbic system, the decrease of afferent neurological stimulation, or the deprivation of efferent neurological stimulation 41 . Hypothalamic and limbic influences can be due to stress, anxiety, or psychological imbalances, which may interfere with the physiological circadian rhythm of basal tear production 37 . For example, management of stress due to psychosocial causes should be an integral part of treatment plans 50 for cases of neuropathic pain.…”

Section: Treatment Of Chronic Pain or Irritationmentioning

confidence: 99%

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The potential role of neuropathic mechanisms in dry eye syndromes

McMonnies

2017

Journal of Optometry

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Dry eye syndromes can involve both nociceptive and neuropathic symptoms. Nociceptive symptoms are the normal physiological responses to noxious stimuli. Neuropathic symptoms are caused by a lesion or disease of the somatosensory nervous system and can be the result of hypersensitisation of peripheral or central corneal and conjunctival somatosensory nerves. For example, inflammation could induce neuroplastic peripheral sensitisation of the ocular surface or lid wiper and exacerbate nociceptive symptoms. Neuropathic symptoms may explain the incommensurate relation between signs and symptoms in some dry eye syndromes although absence of signs of a dry eye syndrome may also be a consequence of inappropriate methods used when examining for them. Involvement of neuropathic mechanisms may also help explain dry eye symptoms which occur in association with reduced corneal sensitivity. This review includes a discussion of the potential for ocular symptoms involving neuropathic mechanisms to contribute to psychosocial problems such as depression, stress, anxiety and sleep disorders as well as for these types of psychosocial problems to contribute to neuropathic mechanisms and dry eye syndromes. Failure to consider the possibility that neuropathic mechanisms can contribute to dry eye syndromes may reduce accuracy of diagnosis and the suitability of treatment provided. Dry eye symptoms in the absence of commensurate evidence of tear dysfunction, and unsatisfactory response to tear dysfunction therapies should prompt consideration of neuropathic mechanisms being involved. Symptoms which persist after local anaesthetic instillation are more likely to be neuropathic in origin. Reducing inflammation may help limit any associated neuroplastic hypersensitivity.

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Section: Regulation Of Basal Tear Production and Lacrimationmentioning

confidence: 99%

Section: Regulation Of Basal Tear Production and Lacrimationmentioning

confidence: 99%

Section: Regulation Of Basal Tear Production and Lacrimationmentioning

confidence: 99%

Section: Treatment Of Chronic Pain or Irritationmentioning

confidence: 99%

See 2 more Smart Citations

The potential role of neuropathic mechanisms in dry eye syndromes

McMonnies

2017

Journal of Optometry

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“…While subject numbers are frequently low in individual studies, corneal sensitivity to a pure mechanical stimulus, such as the Cochet Bonnet instrument, is consistently reduced in DED [372,447–453]. Of the different subclasses of DED patients, those presumed as demonstrating aqueous deficient DED consistently present with reduced corneal sensitivity using the Cochet Bonnet instrument, and this has been attributed to the greater corneal epithelial disruption assessed by corneal staining [454].…”

Section: Evaluation Of Ocular Surface Neurobiologymentioning

confidence: 99%

TFOS DEWS II pain and sensation report

et al. 2017

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Pain associated to mechanical and chemical irritation of the eye surface is mediated by trigeminal ganglia 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.

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