Genome Wide Association Study of Neuropathic Ocular Pain

Huang, Jaxon J.; Rodriguez, Daniel A.; Slifer, Susan H.; Martin, Eden R.; Levitt, Roy C.; Galor, Anat

doi:10.1016/j.xops.2023.100384

Cited by 3 publications

(3 citation statements)

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“…Genetic polymorphisms can alter corneal neurophysiology and inflammation by changing the expression of neurokines and neuromediators, thereby modulating the clinical presentation of corneal neuropathic pain and its severity (He et al., 2019; López‐de la Rosa et al., 2021; Puja et al., 2021). A recent report showed single nucleotide polymorphism (rs140293404), an intronic variant located in gene ENSG00000287251 met genome‐wide significance threshold for corneal neuropathic pain (Huang et al., 2023). Other important and promising genes identified from gene‐based tests are MMP19 , SRP19 , REEP5 , CTC‐487M23.8 , and ZRSR1 (Huang et al., 2023).…”

Section: Mechanisms Involved In the Pathophysiology Of Neuropathic Painmentioning

confidence: 99%

“…A recent report showed single nucleotide polymorphism (rs140293404), an intronic variant located in gene ENSG00000287251 met genome‐wide significance threshold for corneal neuropathic pain (Huang et al., 2023). Other important and promising genes identified from gene‐based tests are MMP19 , SRP19 , REEP5 , CTC‐487M23.8 , and ZRSR1 (Huang et al., 2023). Current genome‐wide association studies are limited to caucasians and males potentially limiting their usefulness in applying to other populations, but still remains a promising area of corneal neuropathic pain research.…”

Section: Mechanisms Involved In the Pathophysiology Of Neuropathic Painmentioning

confidence: 99%

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Neurophysiology of corneal neuropathic pain and emerging pharmacotherapeutics

Asiedu

2023

J of Neuroscience Research

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The altered activity generated by corneal neuronal injury can result in morphological and physiological changes in the architecture of synaptic connections in the nervous system. These changes can alter the sensitivity of neurons (both second‐order and higher‐order projection) projecting pain signals. A complex process involving different cell types, molecules, nerves, dendritic cells, neurokines, neuropeptides, and axon guidance molecules causes a high level of sensory rearrangement, which is germane to all the phases in the pathomechanism of corneal neuropathic pain. Immune cells migrating to the region of nerve injury assist in pain generation by secreting neurokines that ensure nerve depolarization. Furthermore, excitability in the central pain pathway is perpetuated by local activation of microglia in the trigeminal ganglion and alterations of the descending inhibitory modulation for corneal pain arriving from central nervous system. Corneal neuropathic pain may be facilitated by dysfunctional structures in the central somatosensory nervous system due to a lesion, altered synaptogenesis, or genetic abnormality. Understanding these important pathways will provide novel therapeutic insight.

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Section: Mechanisms Involved In the Pathophysiology Of Neuropathic Painmentioning

confidence: 99%

Section: Mechanisms Involved In the Pathophysiology Of Neuropathic Painmentioning

confidence: 99%

Neurophysiology of corneal neuropathic pain and emerging pharmacotherapeutics

Asiedu

2023

J of Neuroscience Research

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“…Finally, genetics, age, and gender-related differences likely contribute to the pain experience as these facets have been shown to impact pain sensitivity (e.g., proneness to react to standardized experimental stimuli) and have been noted to be risk factors for chronic pain development. [ 17 18 19 ]…”

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confidence: 99%

My eyes feel dry. Is it all in my head?

Galor

2024

Indian Journal of Ophthalmology

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Corneal neuropathic pain: a review to inform clinical practice

Watson,

2024

Eye

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Corneal neuropathic pain (CNP) is a poorly defined disease entity characterised by an aberrant pain response to normally non-painful stimuli and categorised into having peripheral and central mechanisms, with the former responding to instillation of topical anaesthetic. CNP is a challenging condition to diagnose due to numerous aetiologies, an absence of clinical signs and ancillary tests (in vivo confocal microscopy and esthesiometry), lacking the ability to confirm the diagnosis and having limited availability. Symptomatology maybe mirrored by severe and chronic forms of dry eye disease (DED), often leading to misdiagnosis and inadequate treatment. In practice, patients with suspected CNP can be assessed with questionnaires to elicit symptoms. A thorough ocular assessment is also performed to exclude any co-existent ocular conditions. A medical and mental health history should be sought due to associations with autoimmune disease, chronic pain syndromes, anxiety and depression. Management begins with communicating to the patient the nature of their condition. Ophthalmologists can prescribe topical therapies such as autologous serum eyedrops to optimise the ocular surface and promote neural regeneration. However, a multi-disciplinary treatment approach is often required, including mental health support, particularly when there are central mechanisms. General practitioners, pain specialists, neurologists and psychologists may be needed to assist with oral and behavioural therapies. Less data is available to support the safety and efficacy of adjuvant and surgical therapies and the long-term natural history remains to be determined. Hence clinical trials and registry studies are urgently needed to fill these data gaps with the aim to improve patient care.

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Genome Wide Association Study of Neuropathic Ocular Pain

Cited by 3 publications

References 59 publications

Neurophysiology of corneal neuropathic pain and emerging pharmacotherapeutics

Neurophysiology of corneal neuropathic pain and emerging pharmacotherapeutics

My eyes feel dry. Is it all in my head?

Corneal neuropathic pain: a review to inform clinical practice

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