DOCSLIB.ORG

Neurotrophic Keratitis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Neurotrophic Keratitis Eye (2003) 17, 989–995 & 2003 Nature Publishing Group All rights reserved 0950-222X/03 $25.00 www.nature.com/eye 1;3 2 1 1;3 Neurotrophic S Bonini , P Rama , D Olzi and A Lambiase CAMBRIDGE OPHTHALMOLOGICAL SYMPOSIUM keratitis Abstract an impairment of corneal sensitivity.2 Systemic diseases such as diabetes, multiple sclerosis, Neurotrophic keratopathy is a degenerative and leprosy may decrease sensory nerve corneal disease induced by an impairment of function or damage sensory fibres leading to trigeminal nerve. Impairment of loss of corneal anaesthesia.3,4 The corneal epithelium is corneal sensory innervation is responsible for the first target of the disease showing corneal epithelial defects, ulcer, and dystrophic changes and defects with poor perforation. In the present report, we reviewed tendency to spontaneous healing. The the pathogenesis, diagnosis, and therapeutic progression of the disease may lead to corneal aspects of this disease. An accurate history and ulcers, melting, and perforation.5 While the clinical examination, including the function of clinical diagnosis is easily oriented from the cranial nerves, together with the clinical history and clinical findings, the management of features of the ocular surface are essential for a this condition is one of the most difficult and prompt diagnosis. The evaluation of the challenging among all corneal diseases. corneal sensitivity and tear film function are important diagnostic steps as well. Specific medical and surgical treatments, based on the Pathophysiology clinical staging of the disease, are often able to halt its progression. Future developments in The cornea is provided with the richest the medical treatment including the innervation of all body tissues (40 times more administration of neuropeptide and growth than the tooth pulp and 400 times more than 1 factors are presented. skin). It is generally accepted that corneal Laboratory of Ophthalmology Eye (2003) 17, 989–995. doi:10.1038/ sensory nerves play a key role in maintaining Interdisciplinary Center for sj.eye.6700616 the anatomical integrity and function of the Biomedical Research (CIR) cornea and particularly of the epithelium. Keywords: neurotrophic keratitis; pathogenesis; Several reports have shown that loss of corneal medical treatment; surgical treatment; growth sensory innervation leads to a decrease of the 2Department of factors; neuropeptides vitality, metabolism, and mitosis of epithelial Ophthalmology cells and consequently to an epithelial San Raffaele Hospital breakdown.6,7 The corneal epithelium thickness Milan, Italy is decreased and epithelial cells show Introduction 3 intracellular swelling, loss of microvilli, and an GB Bietti Eye Foundation Rome, Italy Neurotrophic keratitis is a rare degenerative abnormal production of the basal lamina.8,9 corneal disease caused by an impairment of Conjunctival changes include a decrease of Correspondence: trigeminal corneal innervation, leading to a goblet cell density and loss of cell-surface S Bonini 10 decrease or absence of corneal sensation. Many microplicae. Laboratory of ocular and systemic diseases can determine a Several studies have focused on the role of Ophthalmology lesion at different levels of the fifth cranial sensory neuromediators in the corneal Interdisciplinary Center for nerve: the nucleus in the pons, the Gasserian epithelium pathophysiology. These studies have Biomedical Research (CIR) University of Rome ‘Campus ganglion, the trigeminal ophthalmic branch, the shown the depletion of substance P (SP) and Bio-Medico’, Via Emilio nasociliary nerve, or the long ciliary nerve acetylcholine (Ach) in the rat cornea after Longoni 83 00155 (Table 1). The most common causes of corneal sensory nerve injury.11,12 In vitro,SP, Rome, Italy anaesthesia are viral infection (herpes simplex cholecystokinin gene-related peptide (CGRP), Tel: þ 39 0622 5413 42 and herpes zoster keratoconjunctivitis) followed and Ach induce epithelial proliferation.13–15 In Fax þ 39 0622 5414 56 E-mail: sbonini@ by chemical burns, physical injuries, and contrast, in animal studies, SP treatment failed mclink.it corneal surgery.1 Intracranial space-occupying to promote corneal epithelial healing.16 17 lesions such as neuroma, meningioma, and Chikama et al showed a complete recovery of Received: 28 February 2003 aneurysms may also determine a compression neurotrophic keratitis in one patient with a Accepted in revised form: of the trigeminal nerve or ganglion and produce combination of SP and insulin-like growth 28 February 2003 Neurotrophic keratitis S Bonini et al 990 Table 1 A etiology of corneal sensory deficits action24 and, in vitro, NGF promotes proliferation and differentiation of rabbit corneal epithelial cells.25 In our Genetic Riley–Day syndrome (familial dysautonomia) study, in 43 patients affected by neurotrophic ulcers, Goldenhar–Gorlin syndrome topical administration of NGF restored corneal integrity 19,20 M¨obius syndrome and improved corneal sensitivity. Familial corneal hypoestesia To summarize, corneal sensory nerve damage induces marked changes in the levels of neuromediators that lead Systemic F Diabetes to an impairment of epithelial cell vitality clinically Leprosy represented by the development of recurrent or Vitamin A deficiency persistent epithelial defects. Central nervous system Neoplasm Presentation Aneurysms Stroke The literature does not report data regarding the Postneurosurgical procedures epidemiology of neurotrophic keratitis. We have recently For acoustic neuroma followed 43 patients affected by neurotrophic keratitis For trigeminal neuralgia with epithelial defects or corneal ulcers.19 In six of these Other surgical injury to the trigeminal nerve patients (13.9%) we did not find any justification of Ocular corneal anaesthesia and they were classified as Post-herpes infections (herpes simplex and herpes zoster) idiopathic, all of them were female and the onset of the Chemical and physical burns disease was before the age of 6 years. The other 37 Abuse of topical anaesthetics patients were affected by neurotrophic keratitis as a Drug toxicity (timolol, betaxolol, diclofenac sodium, sulphacetamide 30%) result of: herpetic keratitis (27.0%); following repeated Postsurgical or laser treatment (trauma of ciliary nerves) corneal surgery (21.6%); anaesthetic abuse (16.2%); Corneal incisions chemical burns (13.3%); neurosurgery (10.8%) diabetes Chronic ocular surface injury or inflammation (8.1%); radiotherapy (2.7%). No significant difference Contact lens wear was observed among the sexes (17 males; 20 females). Orbital neoplasia Corneal dystrophies (lattice, granular) According to the Mackie classification, it is possible to classify neurotrophic keratitis into three stages (Table 2).1,5 Stage 1 is characterized by punctate factor-1 (IGF-1) eye drops. They hypothesized that the keratopathy, epithelial hyperplasia and irregularity, combination of SP and IGF-1 stimulates corneal epithelial superficial neovascularization, and stromal scarring cell migration and the expression of integrin a5 and b1 (Figure 1). essential for the attachment of epithelial cells to the Stage 2 is characterized by a persistent epithelial extracellular matrix proteins. defectFmost frequently localized in the superior half Experimental and clinical evidence suggests a cornea (Figure 2). Usually, around the epithelial defect, bidirectional control of corneal epithelium proliferation: there is an area of poorly adherent opaque and sensory neuromediators promote epithelial cell mitosis, oedematous epithelium that can spontaneously detach while, on the other hand, sympathetic mediators, leading to an enlargement of the defect. Epithelial epinephrine and norepinephrine, reduce epithelial cell healing is inadequate and the edges of the defect become mitosis.13 In addition, in animal studies, corneal smooth and rolled. Descemet’s membrane folds and epithelium changes induced by lesion of the sensory stroma swelling may also be observed with an nerves can be reduced by cervical sympathetic inflammatory reaction in the anterior chamber and, denervation.18 rarely, sterile hypopion may be observed. We have recently evaluated the potential role of nerve Stage 3 is characterized by stromal involvement with a growth factor (NGF) in the treatment of neurotrophic corneal ulcer that may progress to perforation and/or keratitis.19,20 stromal melting (Figure 3). Corneal melting and NGF induces in vitro and in vivo recovery of sensory perforation can be caused by inappropriate use of topical neurons and induces the production of Ach in the central steroids or secondary infections (Figures 4 and 5). nervous system and SP in the peripheral nervous system.21,22 In addition, NGF plays an important role in Diagnosis the balance between sensory and sympathetic innervation, by modulating their functions.23 In rodents, The diagnosis is frequently suspected on the basis of the corneal sensory innervation is dependent on NGF patient’s history. Systemic diseases such as diabetes Eye Neurotrophic keratitis S Bonini et al 991 Table 2 Clinical staging of neurotrophic keratitis Stage 1 Rose bengal staining of the palpebral conjunctiva Decreased break-up time Increased viscosity of tear mucus Punctate corneal keratopathy Dellen Small facets of drying epithelium (Gaule spots) Superficial vascularization Stromal scarring Epithelial hyperplasia and irregularity Hyperplastic precorneal membrane Stage 2 Epithelial deficit, usually in the superior half cornea Surrounding rim of loose epithelium Stromal oedema Anterior
Load more

Recommended publications
  • Corneal Changes in Neurosurgically Induced Neurotrophic Keratitis
    Research Original Investigation | CLINICAL SCIENCES Corneal Changes in Neurosurgically Induced Neurotrophic Keratitis Alessandro Lambiase, MD, PhD; Marta Sacchetti, MD, PhD; Alessandra Mastropasqua, MD; Stefano Bonini, MD IMPORTANCE Neurotrophic keratitis (NK) represents a sight-threatening complication after trigeminal impairment. To our knowledge, the duration for which trigeminal injury may affect corneal structures and function has not been investigated previously. OBJECTIVE To describe the long-term clinical, morphological, and functional outcomes of NK after neurosurgical trigeminal damage. DESIGN, SETTING, AND PARTICIPANTS Observational case series performed at a corneal and ocular surface diseases referral center in 2010. Eight consecutive patients with monolateral NK from 1 to 19 years after neurosurgery and 20 age- and sex-matched healthy participants were included. MAIN OUTCOMES AND MEASURES Complete eye examination, tear film function tests, corneal staining, and Cochet-Bonnet esthesiometry were performed. The number and density of corneal nerves, number of hyperreflective keratocytes, and corneal epithelial, endothelial, and keratocyte cell densities were evaluated by in vivo slit scanning confocal microscopy. Clinical and morphological data were compared with the contralateral unaffected eyes and with the eyes of healthy control participants. RESULTS All patients showed superficial punctate keratitis and dry eye in the NK eye and a healthy contralateral eye. Decreased corneal sensitivity was observed in all affected eyes (mean [SD], 2.0 [1.9] mm in the affected eyes vs 5.8 [0.3] mm in the contralateral unaffected eyes; P = .01) and was related to decreased subbasal nerve length (P = .04; R = 0.895). Corneal epithelial and endothelial cell densities were significantly decreased and the number of hyperreflective keratocytes was significantly increased in NK eyes compared with contralateral unaffected eyes and with the eyes of healthy participants.
    [Show full text]
  • Ophthalmic Herpes Zoster
    OPHTHALMIC HERPES ZOSTER RONALD J. MARSH and MATTHEW COOPER London SUMMARY Fig. 1 shows the age and sex distribution, which is A current review of ophthalmic zoster is presented biased in favour of females and compares with 50.7% including its virology, immunology, epidemiology and males, 49.3% females in another series.5 The 1981 census pathogenesis. We give our findings in 1356 patients for Greater London recorded 48% males and 52% referred to the Zoster Clinic at Moorfields Ey e Hospital, females. London. The treatment of the disease and its ocular com­ ONSET plications is discussed. There is a prodromal influenza-like illness of varying Ophthalmic herpes zoster is a disease varying in severity duration, with headache, pyrexia, malaise, depression, and from devastating, threatening life and sight, to so mild that sometimes neck stiffness, which may last up to a week it may pass unnoticed. The ophthalmic division of the fifth before the rash appears. This is shortly followed by local­ cranial nerve is affected in 7-17.5% of herpes zoster ised pain over the distribution of the ophthalmic nerve, patients. 1-5 Ocular involvement complicates approxi­ lymph node swelling in the corresponding drainage areas mately 50% of these cases and very rarely cases of maxil­ and, occasionally, a red eye. The localised pain is well lary herpes zoster,l affecting many of the tissues of the known to precede the rash by several days in some cases. globe and orbit by highly varied types of lesions. This probably represents the replication and migration We felt it would be helpful to report our experience with phase of the disease and is possibly accompanied by a lim­ the disease because the large number of cases we have ited viraemia.
    [Show full text]
  • Diagnosis and Treatment of Neurotrophic Keratopathy
    An Evidence-based Approach to the Diagnosis and Treatment of Neurotrophic Keratopathy ACTIVITY DIRECTOR A CME MONOGRAPH Esen K. Akpek, MD This monograph was published by Johns Hopkins School of Medicine in partnership Wilmer Eye Institute with Catalyst Medical Education, LLC. It is Johns Hopkins School of Medicine not affiliated with JAMA medical research Baltimore, Maryland publishing. Visit catalystmeded.com/NK for online testing to earn your CME credit. FACULTY Natalie Afshari, MD Mina Massaro-Giordano, MD Shiley Eye Institute University of Pennsylvania School of Medicine University of California, San Diego Philadelphia, Pennsylvania La Jolla, California Nakul Shekhawat, MD, MPH Sumayya Ahmad, MD Wilmer Eye Institute Mount Sinai School of Medicine Johns Hopkins School of Medicine New York, New York Baltimore, Maryland Pedram Hamrah, MD, FRCS, FARVO Christopher E. Starr, MD Tufts University School of Medicine Weill Cornell Medical College Boston, Massachusetts New York, New York ACTIVITY DIRECTOR FACULTY Esen K. Akpek, MD Natalie Afshari, MD Mina Massaro-Giordano, MD Professor of Ophthalmology Professor of Ophthalmology Professor of Clinical Ophthalmology Director, Ocular Surface Diseases Chief of Cornea and Refractive Surgery University of Pennsylvania School and Dry Eye Clinic Vice Chair of Education of Medicine Wilmer Eye Institute Fellowship Program Director of Cornea Philadelphia, Pennsylvania Johns Hopkins School of Medicine and Refractive Surgery Baltimore, Maryland Shiley Eye Institute Nakul Shekhawat, MD, MPH University of California,
    [Show full text]
  • Herpetic Corneal Infections
    FocalPoints Clinical Modules for Ophthalmologists VOLUME XXVI, NUMBER 8 SEPTEMBER 2008 (MODULE 2 OF 3) Herpetic Corneal Infections Sonal S. Tuli, MD Reviewers and Contributing Editors Consultants George A. Stern, MD, Editor for Cornea & External Disease James Chodosh, MD, MPH Kristin M. Hammersmith, MD, Basic and Clinical Science Course Faculty, Section 8 Kirk R. Wilhelmus, MD, PhD Christie Morse, MD, Practicing Ophthalmologists Advisory Committee for Education Focal Points Editorial Review Board George A. Stern, MD, Missoula, MT Claiming CME Credit Editor in Chief, Cornea & External Disease Thomas L. Beardsley, MD, Asheville, NC Academy members: To claim Focal Points CME cred- Cataract its, visit the Academy web site and access CME Central (http://www.aao.org/education/cme) to view and print William S. Clifford, MD, Garden City, KS Glaucoma Surgery; Liaison for Practicing Ophthalmologists Advisory your Academy transcript and report CME credit you Committee for Education have earned. You can claim up to two AMA PRA Cate- gory 1 Credits™ per module. This will give you a maxi- Bradley S. Foster, MD, Springfield, MA Retina & Vitreous mum of 24 credits for the 2008 subscription year. CME credit may be claimed for up to three (3) years from Anil D. Patel, MD, Oklahoma City, OK date of issue. Non-Academy members: For assistance Neuro-Ophthalmology please send an e-mail to [email protected] or a Eric P. Purdy, MD, Fort Wayne, IN fax to (415) 561-8575. Oculoplastic, Lacrimal, & Orbital Surgery Steven I. Rosenfeld, MD, FACS, Delray Beach, FL Refractive Surgery, Optics & Refraction C. Gail Summers, MD, Minneapolis, MN Focal Points (ISSN 0891-8260) is published quarterly by the American Academy of Ophthalmology at 655 Beach St., San Francisco, CA 94109-1336.
    [Show full text]
  • Herpes Zoster Ophthalmicus—Diagnosis and Management
    Herpes Zoster Ophthalmicus—Diagnosis and Management Antoine Rousseau, MD1, Tristan Bourcier, MD PhD2, Joseph Colin, MD, PhD3, Marc Labetoulle, MD PhD4 1 Ophthalmologist, Ophthalmology Department, Bicêtre Hospital, South Paris University, Le Kremlin-Bicêtre, France, 2. Head, Ophthalmology Department, Nouvel Hôpital Civil, Strasbourg University Hospital, Strasbourg, France, 3. Head, Ophthalmology Department, Bordeaux University Hospital, Bordeaux, France, 4. Head, Ophthalmology Department, Bicêtre Hospital, South Paris University, Le Kremlin-Bicêtre, France, and Herpes Team leader, laboratory of molecular and structural virology, National Center for the Scientific Research, Gif-Sur-Yvette, France. Abstract Varicella-zoster virus (VZV) infections are widely distributed in the general population. The lifetime risk of herpes zoster is estimated to be 10–20 %, increasing with age (1–4). Since herpes zoster ophthalmicus (HZO) accounts for 20 % of all locations of shingles, the lifetime risk of HZO is about 1–2 %. The management of ocular complications of VZV infection is now well codified, but sequellae still can occur, despite an armamentarium effective in limiting viral replication and its immune consequences. Keywords Herpes zoster ophtalmicus (HZO), keratitis, post herpetic neuralgia Disclosure: The authors have no conflicts of interest to declare. Received: November 18, 2012 Accepted: December 20, 2012 Citation: US Ophthalmic Review, 2013; 6(2):[ePub ahead of print] DOI: 10.17925/USOR.2013.06.02.1 Correspondence: Pr Marc Labetoulle, Service d’Ophtalmologie, CHU de Bicêtre, Assistance Publique – Hôpitaux de Paris, Université Paris-Sud, 94275 Le Kremlin-Bicêtre, France E: [email protected] Pathophysiology: The three Phases of Varicella sites of latency for VZV, the sensory neurons of the trigeminal and spinal Zoster Virus Infection sensory ganglia seem particularly concerned.7 The Primary Infection This mostly occurs during childhood and early years of adult life.
    [Show full text]
  • Herpes Zoster-Shingles Review
    Herpes Zoster Ophthalmicus: More than Meets the Eye Guillermo Rocha, MD, FRCSC; Mercedes Muzychuk, OD ABSTRACT The varicella virus is common; in recent decades the In this paper, a review of the basics of the herpes infection was found to affect 50% of Canadians by age 5 zoster virus will be covered. Aspects of ophthalmic and 90% by age 12. 6 Although the rate of infection with complications and postherpetic neuralgia will be VZV is high, the reported incidence of herpes zoster discussed. Finally, the recent advent of the zoster ranges from 2.2-3.4/1000 people per year. 2 Incidence and vaccine will be discussed. severity increase with age. Along with variation of incidence with age, there INTRODUCTION appears to be a disparity between males and females. In a The varicella zoster virus (VZV) causes two distinct study examining the epidemiology of shingles in Alberta clinical manifestations: varicella (chickenpox) and from 1986-2002, the rate of herpes zoster was found to be zoster (shingles). 1 After primary infection with VZV increasing, with more females being affected than males (chickenpox), the virus becomes latent in the sensory at every age group, with the disparity between females ganglia. 2 Herpes zoster occurs when the virus reactivates and males being highest in the 50 to 54 year age group. 7 from the sensory ganglia and spreads to the corresponding The incidence of herpes zoster is also higher in dermatome, 2 producing the characteristic zoster rash. It is immunocompromised individuals. 4 Most immuno- thought that the likelihood of reactivation increases with compromised individuals present with distinct inflam- age because of an age-related decrease in cell mediated mation, hemorrhages, and necrosis that follows a multi - immunity to the VZV.
    [Show full text]
  • Oral Pharmaceuticals in Anterior Segment Disease
    Oral Pharmaceuticals in Anterior Segment Disease Blair Lonsberry, MS, OD, MEd., FAAO Pacific University College of Optometry [email protected] 1 Disclosures Paid consultant for: Maculogix: Honoraria-Advisory Board Sun: Honoraria: Advisory Board 2 Case • 20 year old male presents with a red painful eye – Started that morning when he woke up – reports a watery discharge, no itching, and is not a contact lens wearer • SLE: – See attached image with NaFl stain 3 Herpes Simplex Virus (HSV) Keratitis: Clinical Features • Characterized by primary outbreak and subsequent reactivation – Primary outbreak is typically mild or subclinical (90% of people are asymptomatic) – Most clinical ocular infections are manifestations of virus reactivation; ocular involvement occurs in fewer than 5% of primary infections • After primary infection, the virus becomes latent in the trigeminal ganglion or cornea – The majority of ophthalmic HSV cases are unilateral, with recurrences affecting the same eye. Bilateral disease (not necessarily concurrent) occurs in 1-12% of cases and is more common in patients with atopy or other immune abnormalities • Stress, UV radiation, and hormonal changes can reactivate the virus • Lesions are common in the immunocompromised (i.e. recent organ transplant or HIV patients) 4 Herpes Simplex Keratitis • Epithelial Keratitis: – Symptoms: • Ocular irritation, redness, photophobia, watering, blurred vision – Signs: • Swollen opaque epithelial cells arranged in a course punctate or stellate pattern • Central desquamation results
    [Show full text]
  • Neurotrophic Keratitis Recurrent Corneal Erosion Syndrome
    Neurotrophic Keratitis Dr Sue Ormonde Learning objectives: 1. Describe the aetiologies of recurrent corneal erosions 2. Understand the therapeutic options for recurrent corneal erosions 3. Identify the causes of exposure keratopathy 4. Understand management strategies for exposure keratopathy 5. Recognise and discuss the management of neurotrophic corneal ulcers Suggested reading: Davis EA. Dohlman CH. Neurotrophic keratitis. International Ophthalmology Clinics. 41(1):1-11, 2001. Das S. Seitz B. Recurrent corneal erosion syndrome. Survey of Ophthalmology. 53(1):3-15, 2008 Jan-Feb. Neurotrophic or neuropathic keratopathy occurs in anaesthetic cornea Corneal sensory nerves key to corneal metabolic activity & epithelial health Loss of neural influence promotes oedema & exfoliation of epithelial cells Acquired causes: - Herpes Simplex - Herpes Zoster - Transection CN 5 - Diabetes - Leprosy - Acoustic neuroma Congenital causes: - Familial dysautonomia (Riley-Day) - Anhidrotic ectodermal dysplasia - Congenital insensitivity to pain Diagnosis: - Often presents late as painless initially - Early - punctate keratopathy, epithelial irregularity - Later - persistent epithelial defect, round/oval, usually central/superior half, surrounding opaque epithelium with smooth rolled edges, may progress to corneal melt esp. if secondary infection or steroid use Treatment: - Preservative free lubricants, prophylactic preservative free antibiotics - Tarsorrhaphy or botulinum toxin ptosis. Patching ineffective. Recurrent corneal erosion syndrome • Epithelial
    [Show full text]
  • Prevalence of Ocular Manifestations and Visual Outcomes in Patients with Herpes Zoster Ophthalmicus
    CLINICAL SCIENCE Prevalence of Ocular Manifestations and Visual Outcomes in Patients With Herpes Zoster Ophthalmicus Simon K. H. Szeto, MRCS,*† Tommy C. Y. Chan, FRCS,*† Raymond L. M. Wong, MRCS,*† Alex L. K. Ng, MRCS,‡ Emmy Y. M. Li, FRCS,*† and Vishal Jhanji, MD*† associated with increased health care utilization, impact on Purpose: To investigate the prevalence of ocular manifestations and daily social and physical functioning, and work place pro- visual outcomes in patients with herpes zoster ophthalmicus (HZO). ductivity.2 Zoster vaccine has been shown to reduce the 3 Methods: Consecutive cases diagnosed with HZO who attended 2 incidence of herpes zoster by 50%. According to the Centers for Disease Control and Prevention, routine vaccination is hospitals between July 1, 2011, and June 30, 2015, were retrospec- $ tively reviewed. Patient demographics, clinical presentations, and recommended to all immunocompetent individuals aged 60 management were reviewed. The logistic regression model was used years. Herpes zoster ophthalmicus (HZO) is caused by to estimate the odds ratio of visual loss with ocular manifestations. reactivation of latent varicella zoster virus. It presents as painful vesicular rashes along the skin supplied by the Results: A total of 259 patients were included. Of these, 110 (42.5%) ophthalmic branch of the trigeminal nerve. It is believed that patients were ,60 years old and 149 patients (57.5%) were $60 years viral reactivation occurs as a result of declining cell-mediated old. None of the patients had received zoster vaccination before immunity, which can be associated with aging, impaired presentation. Ocular manifestations were present in 170 (65.6%) immunity, trauma, and psychological stress.4 HZO is associ- patients with no difference between both age groups (P = 0.101).
    [Show full text]
  • Renewed Sensation
    234_AAO 2020 Enduring Monograph_8 pgs rev 2.qxp_Layout 1 3/5/21 1:52 PM Page 1 CME MONOGRAPH ReNewed Sensation IMPROVING AWARENESS, DIAGNOSIS, AND TREATMENT OF NEUROTROPHIC KERATITIS Original Release: April 1, 2021 Expiration: April 30, 2022 VISIT HTTPS://TINYURL.COM/NKCME2021 FOR ONLINE TESTING AND INSTANT CME CERTIFICATE INSTRUCTIONS FOR OBTAINING CREDIT FACULTY To obtain AMA PRA Category 1 Credit™ for this activity, please read the monograph, consult referenced sources as necessary, and complete the posttest and evaluation online. Upon Edward J. Holland, MD (Chair) passing with a score of 70% or higher, a certificate will be made available immediately. Professor of Clinical Ophthalmology University of Cincinnati DISCLOSURE POLICY Director, Cornea Services MedEdicus requires that anyone who is in a position to control the content of this educational Cincinnati Eye Institute activity disclose all relevant financial relationships with any commercial interest. Financial Cincinnati, Ohio relationship information is collected and resolved prior to the educational activity. FACULTY Preeya K. Gupta, MD Preeya K. Gupta, MD, is a consultant for Dompé US, Inc. Associate Professor of Ophthalmology Cornea & Refractive Surgery Edward J. Holland, MD, is a consultant for Aerie Pharmaceuticals, Inc, Akros Pharma Inc, Duke University Eye Center Alcon, Aldeyra Therapeutics, Allegro Ophthalmics, LLC, Allergan, Azura Ophthalmics Ltd, Durham, North Carolina BlephEx, BRIM Biotechnology, Inc, Claris Bio, CorneaGen, CorNeat Vision Ltd, Dompé US, Inc, Expert Opinion,
    [Show full text]
  • CORNEAL NEUROTISATION for NEUROTROPHIC KERATOPATHY: CLINICAL OUTCOME, in VIVO CONFOCAL MICROSCOPIC and HISTOPATHOLOGIC FINDINGS Darren S
    CORNEAL NEUROTISATION FOR NEUROTROPHIC KERATOPATHY: CLINICAL OUTCOME, IN VIVO CONFOCAL MICROSCOPIC AND HISTOPATHOLOGIC FINDINGS Darren S. J. Ting, FRCOphth1, Gustavo Figueiredo, MBChB, PhD1,2, Christin Henein, MBBS, MRes1,2, Eric Barnes, FRCOphth1,2, Omar Ahmed, FRCS (Plast)3, Hardeep S. Mudhar, FRCPath, PhD4, Francisco C. Figueiredo, FRCOphth, MD, PhD1,2 1Newcastle Eye Centre, Royal Victoria Infirmary 2Newcastle University, Newcastle upon Tyne, NE1 4LP, UK. 3Department of Plastic Surgery, Royal Victoria Infirmary, Newcastle upon Tyne, NE1 4LP, UK. 4National Specialist Ophthalmic Pathology Service, Royal Hallamshire Hospital, Sheffield, S10 2JF, UK. Corresponding author: Darren Shu Jeng Ting Email: [email protected] Conflict of interest: None Funding / support: None Key words: Corneal anaesthesia; corneal neurotisation; aesthesiometer; in vivo confocal microscopy; neurotrophic keratopathy; keratitis; meningioma 1 ABSTRACT (Word count: 288 words; max. 250 words) Purpose: To describe the long-term outcome, in vivo confocal microscopic (IVCM) and histopathologic findings following corneal neurotisation surgery for unilateral neurotrophic keratopathy. Methods: Two patients with severe unilateral neurotrophic keratopathy secondary to cerebellopontine angle meningioma were included. Corneal neurotisation surgery was performed at a tertiary referral centre. Corneal sensation was measured using Cochet-Bonnet aesthesiometer. IVCM was performed using Heidelberg HRT3 laser scanning technology combined with Rostock Corneal Module. Histopathologic examination was performed on the excised corneo-scleral disc of patient 2. Results: Preoperatively the corneal sensations of the affected eyes of patients 1 and 2 were 0.5mm and 0mm, respectively. Following the corneal neurotisation surgery, patient 1 noticed subjective improvement of corneal sensation at two months and objective improvement by thirteen months (60mm in 3 quadrants).
    [Show full text]
  • Advances in the Treatment of Neurotrophic Keratitis New Approaches for Corneal Healing
    CME MONOGRAPH VISIT HTTPS://TINYURL.COM/NKCME FOR ONLINE TESTING AND INSTANT CME CERTIFICATE. ADVANCES IN THE TREATMENT OF NEUROTROPHIC KERATITIS NEW APPROACHES FOR CORNEAL HEALING Original Release: June 1, 2020 Expiration: June 30, 2021 LEARNING METHOD AND MEDIUM FACULTY This educational activity consists of a supplement and ten (10) study questions. The participant should, in order, read the learning objectives contained at the beginning of this supplement, Kenneth A. Beckman, MD, FACS (Chair) read the supplement, answer all questions in the post test, and complete the Activity Evaluation/ Clinical Assistant Professor of Ophthalmology Credit Request form. To receive credit for this activity, please follow the instructions provided on Ohio State University the post test and Activity Evaluation/Credit Request form. This educational activity should take a Columbus, Ohio maximum of 1.0 hour to complete. Director of Corneal Surgery ACTIVITY DESCRIPTION Comprehensive Eye Care of Central Ohio The health of the corneal surface depends on a feedback mechanism that involves sensory Westerville, Ohio innervation. This feedback loop can be disrupted by both ocular and systemic conditions that damage trigeminal innervation of the cornea, leading to the corneal condition neurotrophic Mark S. Milner, MD, FACS keratitis, which is characterized by disrupted tearing and progressive corneal damage that does Associate Clinical Professor not readily heal. Until very recently, a lack of effective treatments to reinnervate and heal eyes Department of Ophthalmology affected by neurotrophic keratitis served to further hamper efforts toward timely diagnosis. Now that an effective treatment is available, clinicians must strive to identify patients who might Yale University School of Medicine benefit before the disease progresses to the point of corneal perforation and subsequent loss of New Haven, Connecticut visual acuity.
    [Show full text]