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Corneal Changes in Neurosurgically Induced Neurotrophic Keratitis

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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. A longer duration of NK was associated with lower endothelial cell density (P = .046; R = −0.715).

CONCLUSIONS AND RELEVANCE Corneal morphology and function were impaired even years after neurosurgical trigeminal damage, suggesting that assessment of tear film and corneal sensitivity as well as in vivo confocal microscopy examination should be performed in all patients with trigeminal impairment.

Author Affiliations: Department of

Ophthalmology, University of Rome, Campus Bio-Medico, Rome, Italy (Lambiase, Mastropasqua, Bonini); Ospedale San Raffaele di Milano, Istituto di Ricovero e Cura a Carattere Scientifico, Milan, Italy (Sacchetti).

Corresponding Author: Stefano

Bonini, MD, Department of Ophthalmology, University of Rome, Campus Bio-Medico, Via Alvaro del Portillo, 200, 00128 Rome, Italy ([email protected]).
JAMA Ophthalmol. 2013;131(12):1547-1553. doi:10.1001/jamaophthalmol.2013.5064 Published online October 24, 2013.

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Research Original Investigation

Corneal Changes in Neurotrophic Keratitis

  • he cornea is the most densely innervated human tis-
  • rosurgical damage to the trigeminal nerve as well as their con-

sue. Corneal sensory nerves provide protective and tro- tralateral unaffected eyes were included in the study. Twenty

T

  • phic support to the cornea by regulating corneal epi-
  • eyes of 20 healthy subjects (mean [SD] age, 53 [15] years; 15 fe-

male, 5 male) were also included as a control group.
The diagnosis of NK was based on the history of trigemithelium integrity, proliferation, and wound healing.1,2 Experimental and clinical data have clearly demonstrated that the impairment of corneal sensitive nerve function induces nal damage after neurosurgical interventions for brain neofunctional and morphological changes of the corneal epithe- plasia associated with ipsilateral corneal hypoesthesia or anlium, leading to epithelial defects with poor tendency to spon- esthesia. taneous healing.1-3 In humans, injury of the trigeminal nerve leads to a decrease or absence of corneal sensation and to development of neurotrophic keratitis (NK).1,2 This condition is
All patients underwent evaluation for best spectaclecorrected visual acuity as well as complete eye examination.
Mechanical corneal sensation was measured at the cencharacterized by impairment of corneal sensitivity, corneal epi- tral cornea with the Cochet-Bonnet esthesiometer (Luneau thelial changes ranging from superficial punctate keratopa- Ophtalmologie). This uses nylon monofilaments that have a thy to corneal ulcer and perforation, stromal scarring, neovas- diameter of 0.027 mm (Toray Industries, Inc), range from 0 to cularization, tear function impairment, and decreased blink 6 cm in length, and apply different pressures to the cornea, reflex.
Currently, corneal changes observed in NK are considshortening in steps of 1.0 cm if a positive response is not obtained. If a positive response is obtained, the thread is adered a consequence of epithelial breakdown, but some evi- vanced by 0.5 cm. The longest filament length resulting in a dence suggests that corneal nerve damage may also induce positive response was considered the corneal sensitivity threshchanges of keratocytes and corneal endothelium. In fact, the recent introduction of in vivo corneal confocal microscopy old, which was verified twice.2
Tear function was evaluated by the Schirmer I and break-up
(IVCM) has allowed for investigation of the entire corneal struc- time tests.13 Corneal fluorescein staining was graded from 0 ture including epithelium, subbasal nerve plexus, keratocytes, and endothelium in healthy and pathological human corneas.4,5 Specifically, decreased corneal sensation in diato 5 according to the Oxford scale.13
In vivo slit scanning confocal microscopy examination
(Confoscan 4; Nidek Technologies) was performed bilaterally betic patients was associated with decreased subbasal nerve in the central cornea of all subjects with a 40×/0.75 objective and basal epithelium density as well as changes in corneal stro- lens. All Confoscan 4 examinations were performed by the mal keratocytes and endothelium.6-8 Patients with herpes sim- same operator (M.S.) using a Z-ring and an internal fixation tarplex virus keratitis also showed a relationship between de- get to stabilize images. Eyes were anesthetized with 1 drop of creased corneal sensation and changes in subbasal nerve plexus oxybuprocaine hydrochloride,0.4% (benoxinate hydrochloand endothelium morphology.9-11 This evidence suggests that ride). The objective lens of the microscope was disinfected with alteration of corneal sensitivity may affect all corneal struc- isopropyl alcohol (70% vol/vol, with swabs). Then, a large drop tures; however, both diabetic keratitis and herpes simplex vi- of Viscotears liquid gel (Carbomer 940; Novartis Pharma) was rus keratitis result from a combination of different mechanisms including decreased innervation and metabolic, thickness automated scanning mode with a 5-μm scan step was immune, and cytopathic effects. used during each examination. Each image represents a coroapplied to the tip of the lens as an immersion substance. Full-
In this study, we evaluated corneal structures by IVCM in nal section of approximately 425 × 320 μm with magnificapatients with monolateral NK after neurosurgical trigeminal tion of ×500 and a lateral resolution of 1 μm/pixel. Corneal damage to assess long-term changes of corneal sensitivity and thickness was assessed and a minimum of 3 representative im-

  • morphology.
  • ages were evaluated for superficial and basal epithelium, sub-

basal nerve plexus, superficial and deep stromal layer, and endothelium.4,5
Two masked observers evaluated the confocal images (M.S. and A.M.). The epithelial, stromal, and endothelial cells were

Methods

This study was performed in accordance with the Declaration manually counted using Adobe Photoshop 6.0 software (Adobe of Helsinki. The study was approved by the institutional re- Systems). All the cells were counted within a 0.05-mm2 frame view board of the University of Rome, Campus Bio-Medico, and to calculate the cell density, which was expressed as the numwritten informed consent was obtained from the patients and ber of cells per square millimeter. Nerve density was assessed

  • healthy volunteers before examinations were performed.
  • by measuring the total length of the nerve fibers in microm-

Inclusion criteria were the diagnosis of monolateral NK at eters per frame. Main nerve trunks were defined as the total stage 1 after neurosurgery1,2 and a corneal scarring grade of 0.5 number of main nerve trunks in 1 image after analyzing the imor lower according to the Fantes scale.12 Exclusion criteria were ages anterior and posterior to the analyzed image to confirm

  • the presence of diabetes mellitus, previous intraocular sur-
  • that these did not branch from other nerves. Nerve branch-

gery, history of ocular trauma, herpetic keratitis, and/or other ing was defined as the total number of nerve branches in 1 ocular-associated diseases, use of topical treatments with the image.14 Tortuosity and reflectivity were classified according exception of ocular lubricants, and use of contact lenses.
Eight eyes of 8 consecutive patients (mean [SD] age, 49 [18] to criteria described by Oliveira-Soto and Efron.15
Statistical analysis was performed using Wilcoxon rank test years; 6 female, 2 male) with monolateral NK caused by neu- and Mann-Whitney Utest to assess differences between groups.

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Corneal Changes in Neurotrophic Keratitis

Original Investigation Research

Table 1. Clinical and Demographic Characteristics of the Patients With Neurotrophic Keratitis Included in the Study

Patient No.

  • Characteristic
  • 1
  • 2
  • 3
  • 4
  • 5
  • 6
  • 7
  • 8

  • Age, y
  • 38
  • 52
  • 42
  • 61
  • 32
  • 69
  • 77
  • 25

  • Sex
  • M
  • F
  • F
  • F
  • M
  • F
  • F
  • F

Disease for neurosurgery
Acoustic neuroma

  • Meningioma
  • Acoustic

neuroma

  • Chondroma
  • Meningioma
  • Meningioma
  • Meningioma
  • Meningioma

Time from trigeminal damage, y

  • 6
  • 5
  • 7
  • 7
  • 1
  • 8
  • 7
  • 19

  • Duration of NK, y
  • 5
  • 5
  • 5
  • 5
  • 1
  • 7
  • 7
  • 18

Previous NK treatments

  • Tarsorrhaphy
  • CL
  • CL
  • AMT
  • Autologous

serum, CL

  • Tarsorrhaphy
  • Tarsorrhaphy,

CL
Tarsorrhaphy

  • Symptoms
  • Mild redness
  • Mild dryness
  • None
  • Visual

impairment

  • None
  • Visual

impairment
Mucous secretion
None

  • Lagophthalmos
  • Mild

0.7 1
Absent
0.8

  • Moderate
  • Absent

0.3
Absent
0.6
Absent
0.4

  • Moderate
  • Mild

0.8 4

  • BCVA, decimal units
  • 0.8

4
0.7

  • 4
  • Central corneal sen-

sitivity threshold, cm

  • 0
  • 0
  • 0
  • 3

  • Break-up time, s
  • 8
  • 5

9
43
27

  • 6
  • 7

7

  • 2
  • 6

Schirmer test, mm/5 min

  • >10
  • >10
  • >10
  • >10

  • Oxford score
  • 1
  • 1
  • 1
  • 2
  • 1
  • 2
  • 1
  • 3

Abbreviations: AMT, amniotic membrane transplantation; BCVA, best-corrected visual acuity; CL, contact lens; NK, neurotrophic keratitis.

  • Spearman ρ test was used to correlate clinical, demographic,
  • No significant correlations were observed between cor-

and morphological parameters. We used SPSS version 18 sta- neal sensitivity and the tear function test and corneal staintistical software (SPSS Inc). P < .05 was considered statisti- ing results (P = .52 and P = .20, respectively), while the higher

  • cally significant.
  • corneal sensitivity was significantly correlated with a longer

history of NK (P = .048; R = 0.712).
Results of IVCM evaluations are showed in Table 2. Eyes with NK showed a significant decrease of superficial and basal epithelial cell densities when compared with both contralateral unaffected eyes (mean [SD] superficial epithelial cell den-

Results

Clinical characteristics of the patients are summarized in Table 1. At the inclusion, all patients showed a stage 1 mono- sity, 1068 [567] vs 1877 [490] cells/mm2, respectively; P = .047; lateral NK according to criteria described by Mackie1 with mild mean [SD] basal epithelial cell density, 3241 [600] vs 4366 [794] to severe superficial punctate keratitis and were being treated cells/mm2, respectively; P = .04) (Figure 1) and with healthy only with preservative-free artificial tears. All contralateral eyes eyes of control participants (mean [SD] superficial epithelial showed absence of pathological changes and normal corneal cell density, 2145 [401] cells/mm2; P = .04; mean [SD] basal episensitivity, Schirmer test results, and break-up times.
Patients underwent neurosurgery in the past 1 to 19 years thelial cell density, 5732 [1358] cells/mm2; P = .004).
Subbasal nerves were also significantly reduced as com-
(mean [SD], 7.5 [5] years) and were diagnosed as having NK from pared with both contralateral unaffected eyes (mean [SD] num1 to 24 months after neurosurgery. All patients also had a his- ber of nerve trunks, 1.0 [1.2] vs 4.4 [1.1], respectively; P = .04; tory of corneal ulcer 1 to 18 years (mean [SD], 6.6 [5] years) af- and mean [SD] total nerve length, 1814 [2614] vs 11 606 [5175] ter the onset of NK. Four patients had damage of the seventh cranial nerve with mild facial hemipalsy (Table 1). μm/mm2, respectively; P = .04) (Figure 2) and healthy eyes (mean [SD] number of nerve trunks, 4.5 [0.9]; P = .003; mean

  • [SD] total nerve length, 15 250 [2440] μm/mm2; P = .001). In
  • All affected eyes showed a significant decrease in me-

chanical corneal sensitivity evaluated by Cochet-Bonnet es- NK eyes, the lower subbasal nerve length directly correlated thesiometry when compared with the contralateral unaf- with lower corneal sensitivity values (P = .04; R = 0.895).

  • fected eye (mean [SD], 2.0 [1.9] vs 5.8 [0.3] mm, respectively;
  • The number of hyperreflective keratocytes was signifi-

P = .01). Fluorescein staining demonstrated mild to severe epi- cantly increased in NK eyes when compared with contralattheliopathy in NK eyes compared with unaffected eyes (mean eral unaffected eyes (mean [SD], 4.0 [2.2] vs 1.5 [2.2] hyperre[SD] Oxford score, 1.6 [0.7] vs 0, respectively; P < .001). Eyes flective keratocytes/frame, respectively; P = .04) and with with NK also showed a significant decrease in break-up time healthy eyes (mean [SD], 1.2 [1.2] hyperreflective keratocytes/ compared with contralateral unaffected eyes (mean [SD], 5.0 frame; P = .02) (Figure 3). [2.0] vs 7.5 [2.3] seconds, respectively; P = .004), while Schirmer test results were not significantly different between the contralateral and pathological eyes (P = .66).
Interestingly, corneal endothelial cell density was significantly reduced in NK eyes when compared with both contralateral unaffected eyes (mean [SD], 2187 [582] vs 3059 [352]

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Corneal Changes in Neurotrophic Keratitis

Table 2. Results of In Vivo Confocal Microscopy Evaluations in Patients With Monolateral Neurotrophic Keratitis Compared With Contralateral Unaffected Eyes and With Eyes of Healthy Participants
Table 2. Results of In Vivo Confocal Microscopy Evaluations in Patients With Monolateral Neurotrophic Keratitis Compared With Contralateral Unaffected Eyes and With Eyes of Healthy Participants (continued)

  • P
  • P

  • Variable
  • Mean (SD)
  • Value
  • Variable
  • Mean (SD)
  • Value

Central corneal thickness, μm
Beadlike formations, No./frame
Contralateral eyes NK eyes
530 (56) 560 (93) 551 (71)
Contralateral eyes NK eyes
7.4 (6.0) 2.5 (3.1) 5.9 (3.2)
.28a .39b
.14a .28b
Healthy eyes
Healthy eyes
Superficial epithelial cell density, cells/mm2
Nerve branching, No./frame Contralateral eyes NK eyes
2.7 (3.0) 0.3 (0.6) 3.1 (2.5)
Contralateral eyes NK eyes
1877 (490) 1068 (567) 2145 (401)
.03a .03b
.047a .04b
Healthy eyes
Healthy eyes
Endothelial cell density, cells/mm2

Contralateral eyes NK eyes
Basal epithelial cell density, cells/mm2
3059 (352) 2187 (582) 2960 (323)
.01a .004b
Contralateral eyes NK eyes
4366 (794) 3241 (600) 5732 (1358)
.04a .004b
Healthy eyes
Healthy eyes

Abbreviation: NK, neurotrophic keratitis. a Comparing NK eyes vs contralateral unaffected eyes (Wilcoxon rank test). b Comparing NK eyes vs healthy eyes (Mann-Whitney U test).

Anterior stromal cell density, cells/mm2

Contralateral eyes NK eyes
949 (243) 990 (274) 894 (250)
.60a .43b

cells/mm2, respectively; P = .01) and with healthy eyes (mean [SD], 2960 [323] cells/mm2; P = .004) (Figure 4A-C). Eyes with NK showed a significant correlation between the longer duration of NK and the lower endothelial cell density (P = .046; R = −0.715) (Figure 4D).
No significant difference in all morphological parameters were observed in the subgroup of patients with both NK and lagophthalmos.

Healthy eyes Hyperreflective keratocytes, No./frame

Contralateral eyes NK eyes
1.5 (2.2) 4.0 (2.2) 1.2 (1.2)
.04a

  • .02b
  • Healthy eyes

Posterior stromal cell density, cells/mm2

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  • Neurotrophic Keratitis Recurrent Corneal Erosion Syndrome

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    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
  • Prevalence of Ocular Manifestations and Visual Outcomes in Patients with Herpes Zoster Ophthalmicus

    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).
  • Renewed Sensation

    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,
  • 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

    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).
  • Advances in the Treatment of Neurotrophic Keratitis New Approaches for Corneal Healing

    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.