Letters RESEARCH LETTER

Disablement-Based Nomenclature for Vision and Function Zhang et al1 recently reported that visual function loss but not visual acuity was associated with depression. In an accompanying editorial, Morse2 further described how the loss of functional vision (ie, actual task-related visual performance) leads to depression. The article and editorial raise important questions about the terminology of vision and function. To explore understanding of these terms, we informally discussed the abstract with 20 ophthalmologist colleagues. Based solely on the abstract, 6 participants (30%) believed that the study focused on conversion symptoms (ie, a somatoform disorder). According to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSMIV-TR), “The common feature of somatoform disorders is the presence of physical symptoms that suggest a general medical condition… and are not fully explained by a general medical condition, by the direct effects of a substance, or by another mental disorder.”3 Psychiatrists have replaced the term functional with the more specific DSM-IV-TR classification. Ophthalmologists appear to lack a clear sense of the term functional when describing vision and function. How should loss of visual function (ie, physical decline in the ocular system), self-reported loss of function due to poor vision, and functional vision loss (ie, perceived vision loss in the absence of organic pathology) be described? The disablement literature provides a unique framework for separating organic and somatoform loss of vision, and their functional sequelae. Verbrugge and Jette posited in 1994 the “disablement process,” a sociomedical model of disability that describes “how chronic and acute conditions affect functioning”4 and how “personal and environmental factors speed or slow disablement.”4 In this model, pathology leads to impairment (dysfunctions and structural abnormalities in specific body systems), which leads to functional limitations (restrictions in basic physical and mental actions) and then disability (difficulty performing activities of daily life). Ophthalmologists might best adhere to this model when describing eye disease and its consequences, invoking vision loss, visual impairment, loss of visual function, and visual disability. This schema will improve communication between clinicians and in the medical literature and provide a clearer conception of the impact of vision loss on function. As to our patients who report high levels of disability due to vision loss, perhaps beyond what we might expect based on what we see in their eyes, we should abandon any deprecatory terms, recognize their distress, and direct treatment to the whole person.5 Timothy V. Johnson, MD Barry W. Rovner, MD jamaophthalmology.com

Author Affiliations: Wills Eye Institute, Philadelphia, Pennsylvania (Johnson); Department of Psychiatry, Thomas Jefferson University, Philadelphia, Pennsylvania (Rovner); Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania (Rovner). Corresponding Author: Timothy V. Johnson, MD, Wills Eye Institute, 840 Walnut St, Philadelphia, PA 19107 ([email protected]). Author Contributions: Drs Johnson and Rovner had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Johnson, Rovner. Acquisition of data: Johnson. Analysis and interpretation of data: Johnson. Drafting of the manuscript: Johnson, Rovner. Critical revision of the manuscript for important intellectual content: Johnson. Administrative, technical, and material support: Johnson, Rovner. Study supervision: Johnson, Rovner. Conflict of Interest Disclosures: None reported. 1. Zhang X, Bullard KM, Cotch MF, et al. Association between depression and functional vision loss in persons 20 years of age or older in the United States, NHANES 2005-2008. JAMA Ophthalmol. 2013;131(5):573-581. 2. Morse AR. Vision function, functional vision, and depression. JAMA Ophthalmol. 2013;131(5):667-668. 3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed, text revision. Washington, DC: American Psychiatric Association; 2000. 4. Verbrugge LM, Jette AM. The disablement process. Soc Sci Med. 1994;38(1):1-14. 5. Tasman W, Rovner B. Age-related macular degeneration: treating the whole patient. Arch Ophthalmol. 2004;122(4):648-649.

OBSERVATIONS

Varicella-Zoster Virus Detection in Varicella-Associated Stromal Keratitis Stromal keratitis is a well-known development in herpes zoster ophthalmicus but is uncommonly noted following varicella, the primary infection with varicella-zoster virus.1 Keratitis typically occurs several weeks to months following varicella and is often described as disciform in nature. We describe a case of varicella-associated stromal keratitis in which the cornea was positive for varicella-zoster virus by polymerase chain reaction (PCR) testing. We believe that this is the first case of varicella-associated stromal keratitis documented by identification of varicella-zoster virus in the cornea. Report of a Case | A healthy 9-year-old girl presented with a 3-month history of redness and blurring of the right eye. A history of varicella 3 months prior to the onset of symptoms was elicited. Best-corrected visual acuity was 20/60. There was a central 5-mm circular area of full-thickness nonsuppurative stromal inflammation. The epithelium was intact. Serologic testing revealed elevated IgM and IgG levels for varicella-zoster virus. Antibodies to herpes simplex virus were negative. Epstein-Barr viral antibodies were consistent with JAMA Ophthalmology April 2014 Volume 132, Number 4

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Letters

Figure. Full-Thickness Corneal Scarring With Intact Epithelium Following Corticosteroid Therapy for Varicella-Associated Stromal Keratitis

keratitis was not described and no history of disciform keratitis was documented. We believe that our patient represents the first case of varicella-associated nonsuppurative stromal keratitis with PCR documentation of the presence of varicella-zoster virus in subepithelial tissue. Moreover, the 2-layered excision of the host cornea localized the virus to the deep cornea. Alice Y. Matoba, MD Beeran Meghpara, MD Paty Chevez-Barrios, MD Author Affiliations: Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas (Matoba, Meghpara); Department of Pathology and Genomic Medicine, Houston Methodist Hospital and Weill Medical College of Cornell University, Houston, Texas (Chevez-Barrios). Corresponding Author: Alice Y. Matoba, MD, Baylor College of Medicine, 6565 Fannin St, NC-205, Houston, TX 77030 ([email protected]).

past infection. The keratitis initially resolved with prednisolone acetate, 1%, 6 times per day, leaving a faint scar; however, the patient did not keep subsequent appointments. She returned after 6 months, having discontinued corticosteroid therapy, with recurrent inflammation. Despite more intense topical corticosteroid therapy, the cornea scarred with resultant best-corrected visual acuity of 20/80 (Figure). A penetrating keratoplasty was performed. At the time of surgery, an anterior lamellar button was dissected, followed by excision of the remaining 10% of stroma. The specimens were analyzed histopathologically and by PCR. Following keratoplasty, the patient initially did well, with improvement of visual acuity to 20/30. However, she was again lost to follow-up after 6 months. Results | A chronic lymphocytic infiltrate was scattered sparsely throughout both specimens. Endothelial cells were degenerated. Testing with PCR was negative for varicella-zoster virus in the anterior stromal specimen but positive in the specimen containing deep stroma and endothelium. Discussion | Stromal keratitis has been reported following varicella, herpes zoster ophthalmicus, and varicella-zoster virus vaccination.2 For herpes zoster ophthalmicus–related stromal keratitis, presence of varicella-zoster virus in the stroma has been well documented.3,4 However, documentation of the virus in the cornea following varicella is sparse. In 1974, Nesburn et al5 detected varicella-zoster virus by electron microscopy in epithelial scrapings from dendritic lesions of the cornea following varicella. Associated stromal edema was described, but no specimens were taken from the stroma. In 1997, Power et al6 described a 6-year-old boy with a recent history of varicella who underwent emergency penetrating keratoplasty for uncontrolled Staphylococcus epidermidis keratitis. Testing of the excised cornea by PCR was positive for varicella-zoster virus. Their report may be the first to show detection of the virus in a corneal stromal specimen following varicella. However, in their case, epithelium was likely included in the specimen. Also, the course of the eye disease prior to development of microbial 506

Author Contributions: Dr Matoba had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Acquisition of data: All authors. Analysis and interpretation of data: All authors. Drafting of the manuscript: All authors. Critical revision of the manuscript for important intellectual content: Matoba, Chevez-Barrios. Administrative, technical, and material support: Meghpara. Study supervision: Matoba, Chevez-Barrios. Conflict of Interest Disclosures: None reported. 1. Wilhelmus KR, Hamill MB, Jones DB. Varicella disciform stromal keratitis. Am J Ophthalmol. 1991;111(5):575-580. 2. Nagpal A, Vora R, Margolis TP, Acharya NR. Interstitial keratitis following varicella vaccination. Arch Ophthalmol. 2009;127(2):222-223. 3. Mietz H, Eis-Hübinger AM, Sundmacher R, Font RL. Detection of varicella-zoster virus DNA in keratectomy specimens by use of the polymerase chain reaction. Arch Ophthalmol. 1997;115(5):590-594. 4. Yu DD, Lemp MA, Mathers WD, Espy M, White T. Detection of varicella-zoster virus DNA in disciform keratitis using polymerase chain reaction. Arch Ophthalmol. 1993;111(2):167-168. 5. Nesburn AB, Borit A, Pentelei-Molnar J, Lazaro R. Varicella dendritic keratitis. Invest Ophthalmol. 1974;13(10):764-770. 6. Power WJ, Hogan RN, Hu S, Foster CS. Primary varicella-zoster keratitis: diagnosis by polymerase chain reaction. Am J Ophthalmol. 1997;123(2):252-254.

Rapid Progression of Uveitis and Alopecia Syphilitica in AIDS There has been recent renewed interest in the ocular manifestations of syphilis, likely owing to the increased prevalence of patients with human immunodeficiency virus (HIV) coinfections in recent years. Ocular complications due to syphilis in these immunocompromised patients have been noted not only to progress faster but also to be more severe.1,2 We describe a young man, ultimately diagnosed as having syphilis and AIDS, who presented with florid panuveitis in the setting of progressive, secondary syphilitic dermatologic findings including alopecia of the scalp, eyebrows, and eyelashes, oral ulcers, and maculopapular rash of the face. Report of a Case | A 28-year-old man with photophobia, conjunctival hyperemia, and rapidly progressing loss of vision in his left eye for approximately 10 days was referred from an optometrist. He had positive results on a rapid oral HIV test and

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Varicella-zoster virus detection in varicella-associated stromal keratitis.

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