The International Association for the Study of Pain recently updated its definition of pain for the first time since 1979 to be “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”.¹
This definition is important for clinicians to understand, as pain is not only confined to tissue damage or injury, but also the experience associated with the stimulus.
Indeed, analgesia, which is commonly used to denote the management of pain, is more specifically defined as the reduction or absence of the sensation of pain in response to a typically painful stimulus.¹ Unfortunately, for a subset of patients, it is the system that signals pain through the nerves and gives the perception of pain that can be dysfunctional; this leads to neuropathic pain which can be quite different than pain associated with direct tissue damage.
Neuropathic pain is inherently a disease of the somatosensory system and as such, is referred to colloquially as “nerve pain”.² There are numerous aetiologies for neuropathic pain. In many instances the link between a disorder of the somatosensory system and the presence of neuropathic pain is apparent, while in other cases it is a secondary effect of the condition which may only occur in some instances. For example, in patients who have suffered injuries leading to paralysis or are afflicted with diseases of the nerves themselves, such as in multiple sclerosis, damage to the somatosensory system is part of the primary pathophysiology of the disease and the resulting pain is a manifestation of this harm.³
For other aetiologies, damage to the nerves and thus pain signalling may not always be present. Examples of this include diabetic neuropathy as well as herpes zoster, where the pathophysiology of the primary condition can lead to nerve dysfunction and cause pain sensation, but is not always a feature of these diseases.³ It is also important to note that “regular” pain caused by the stimulation of our pain receptors due to insults, can also be converted to neuropathic pain if it is not treated promptly and persists for long periods of time.
In the eye, common causes of neuropathic pain include dry eye, post corneal and refractive surgery, and herpetic infection. These neatly represent some of the possible locations along the trigeminal nerve through to the cornea that can be afflicted.2,4,5 Reactivation and replication of herpetic viruses in the nasociliary branch of the trigeminal nerve not only leads to viral shedding and the clinical manifestations of ocular herpes, but may also damage the nerves themselves and disrupt nerve signalling which leads to persistent pain.4
Anterior segment and refractive surgery damage nerves in an iatrogenic manner: corneal nerves can be cut or otherwise suffer trauma due to the procedure.5 Dry eye disease also involves neurosensory abnormalities, as found in the definition for the disease in the TFOS DEWS II report.6 Here, the thought is that there may be some link between the chronic inflammation induced by the disease that affects the health of nerves on the ocular surface.²
For the eyecare practitioner, identifying patients at risk of developing neuropathic pain is crucial to ensure prompt and appropriate management. Clinicians should identify patients who experience pain that is out of proportion to their clinical signs (hyperalgesia), pain from stimuli that are normally not painful (allodynia) or pain that persists after the causative insult has ceased to exist.³ Use of a questionnaires, including the Ocular Pain Assessment Survey (OPAS), is recommended to document the pain.7
Management of neurologic pain centres on controlling the primary condition as much as possible. Earlier involvement of the patient’s general practitioner or referral to a pain specialist should be considered, particularly for conditions such as herpes zoster ophthalmicus where post herpetic neuralgia can be severe and has the potential for long term impact on quality of life.4 For the ocular surface, management of neuropathic pain often begins with the use of anti-inflammatory therapy or autologous serum, as decreasing inflammation has been shown to have a positive impact on reducing pain.7
ABOUT THE AUTHOR:
Name: Adjunct A/Prof Alex Hui Qualifications: OD, PhD, GradCertOcTher, FAAO
Organisation: School of Optometry and Vision Science, Faculty of Medicine and Health, UNSW Sydney; Centre for Ocular Research and Education, School of Optometry & Vision Science, University of Waterloo
Position: Adjunct Associate Professor (UNSW); Head, Biosciences (Waterloo)
Location: Toronto, Canada
Years in profession: 12
1. International Association for the Study of Pain. Terminology. 2020 [cited 2022 19/07/2022]; Available from: https://www. iasp-pain.org/resources/terminology/.
2. Rosenthal, P. and D. Borsook, Ocular neuropathic pain. British Journal of Ophthalmology, 2016. 100(1): p. 128.
3. Jensen, T.S. and N.B. Finnerup, Allodynia and hyperalgesia in neuropathic pain: clinical manifestations and mechanisms. Lancet Neurol, 2014. 13(9): p. 924-35.
4. Sampathkumar, P., L.A. Drage, and D.P. Martin, Herpes zoster (shingles) and postherpetic neuralgia. Mayo Clin Proc, 2009. 84(3): p. 274-80.
5. Moshirfar, M., et al., Neuropathic Corneal Pain Following LASIK Surgery: A Retrospective Case Series. Ophthalmology and therapy, 2021. 10(3): p. 677-689.
6. Craig, J.P., et al., TFOS DEWS II Definition and Classification Report. Ocul Surf, 2017. 15(3): p. 276-283.
7. Nortey, J., et al., Topical Therapeutic Options in Corneal Neuropathic Pain. Frontiers in Pharmacology, 2022. 12.