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Relevant bibliographies by topics / Eye; Retinitis pigmentosa

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Academic literature on the topic 'Eye; Retinitis pigmentosa'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Eye; Retinitis pigmentosa"

1

Bhattarai, D., N. Paudel, P. Adhikari, S. Gnyawali, and S. N. Joshi. "Unilateral retinitis pigmentosa." Nepalese Journal of Ophthalmology 7, no. 1 (September 17, 2015): 56–59. http://dx.doi.org/10.3126/nepjoph.v7i1.13171.

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Objective: To report a rare case of unilateral retinitis pigmentosa and to present the clinical features, and ¿ndings of multifocal ERG and visual field of this case.Case: A 70-year-old-female diagnosed as Retinitis Pigmentosa in right eye 7 years back, presented with further gradual painless diminution of vision in the very eye and without any similar symptoms in left eye. On examination, the findings (including multifocal ERG and visual field) suggested the features of retinitis pigmentosa in her right eye, while the other eye being unaffected.Conclusion: In this rare case, the distinct features of retinitis pigmentosa are seen only in one eye, and this can be further confirmed from multifocal ERG and visual field.

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Bromeo, Albert John, Sweet Jorlene Lerit, Amadeo Veloso, and Gary John Mercado. "Retinal vasoproliferative tumour secondary to retinitis pigmentosa sine pigmento." BMJ Case Reports 14, no. 5 (May 2021): e240878. http://dx.doi.org/10.1136/bcr-2020-240878.

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Retinitis pigmentosa can be associated with exudative vasculopathy in rare instances, which can manifest as retinal vasoproliferative tumours. We present the case of a 33-year-old woman previously diagnosed with retinitis pigmentosa sine pigmentosa in both eyes. She was asymptomatic and just came in for a routine follow-up eye examination. Thorough examination of the peripheral retina on the right eye revealed a dome-shaped retinal tumour with a feeder vessel and surrounding exudative changes at the superotemporal periphery, consistent with a secondary retinal vasoproliferative tumour from retinitis pigmentosa. She subsequently underwent focal laser photocoagulation of the tumour which resulted in tumour stabilisation. While exudative vasculopathy is very uncommon in retinitis pigmentosa, ophthalmologists need to be aware of its occurrence in such patients. Vision loss may occur from exudation, haemorrhage, retinal detachment and neovascularisation. A thorough examination of the peripheral retina is warranted in these cases.

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Aragao, Ricardo Evangelista Marrocos de, Ieda Maria Alexandre Barreira, Ariane Sa Vieira Bastos, Gustavo Jose Arruda Mendes Carneiro, and Talles Peterson Cavalcante Oria. "Unilateral retinitis pigmentosa: case report." Revista de Medicina da UFC 55, no. 2 (December 31, 2015): 54. http://dx.doi.org/10.20513/2447-6595.2015v55n2p54-58.

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Unilateral retinitis pigmentosa (URP) is a rare tapetoretinal dystrophy affecting only one eye. Criteria are necessary to make a correct diagnosis of URP: exclude all infective etiologies, check that the clinical signs of retinitis are present in the affected eye and the total absence of any signs or symptoms of retinitis pigmentosa in the fellow eye. Electroretinogram (ERG) and electro-oculogram (EOG) are useful for the correct diagnosis. In this paper we report one case.

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Bozic, Marija, Vujica Markovic, Ivan Marjanovic, and Vesna Maric. "Coincidence of retinitis pigmentosa and pseudoexfoliative glaucoma." Srpski arhiv za celokupno lekarstvo 145, no. 5-6 (2017): 294–95. http://dx.doi.org/10.2298/sarh160408051b.

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Introduction. This is an observational case report presenting retinitis pigmentosa associated with pseudoexfoliative glaucoma. Case outline. A 69-year-old man presented with retinitis pigmentosa. On examination, pseudoexfoliative material was detected on anterior segment structures, and intraocular pressure was 26 mmHg in the right and 24 mmHg in the left eye. The patient was commenced on topical antiglaucomatous therapy (timolol + dorzolamide twice daily, latanoprost once in the evening) to both eyes. Conclusion. To the best of our knowledge, this is the first reported case of retinitis pigmentosa associated with pseudoexfoliative glaucoma. Although rare, retinitis pigmentosa and glaucoma can occur in the same eye.

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Migliorini, Raffaele, Anna Maria Comberiati, Giovanni Galeoto, Manuela Fratipietro, and Loredana Arrico. "Eye Motility Alterations in Retinitis Pigmentosa." Journal of Ophthalmology 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/145468.

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Purpose. We evaluated a sample of individuals with retinitis pigmentosa (RP) with the aim of assessing the presence or absence of ocular motility (OM) disorders.Materials and Methods. We included 23 out of the 25 individuals from the sample (9 females and 14 males) with an average visual acuity of 6/10.Results. The cover test about the vertical deviation in near distance showed an r/l in 3.45% and an l/r in 6.9%. The assessment of OM showed that 39.1% of the sample had a severe hyperfunction of the IO of the right eye and a severe hyperfunction (34.5%) of the SO of the left eye; 21.8% had a moderate hypofunction of right SO with a moderate percentage of hypofunction of 17.5% for the SO of the left eye; 30.5%, however, showed a serious hypofunction of the SR of both eyes; 21.7% of the sample showed a hyperfunction in both eyes of the IR.Conclusion. This alteration, however, is not attributable to either a high refractive defect (medium-low myopia: −1 diopter±3 SD) or to a severely impaired binocular vision (visual acuity, motor fusion, and stereopsis are normal or within a range of values commonly accepted). Therefore, the disorders of OM lead to a genetic origin.

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Taniai, Mariko, Atsushi Mizota, Kazuyuki Ishikawa, Mitsuya Ikejiri, Emiko Adachi-Usami, Haruo Kuroki, and Masashi Yamazaki. "Retinitis pigmentosa with osteochondrodysplasia in siblings." Eye 15, no. 5 (September 2001): 669–71. http://dx.doi.org/10.1038/eye.2001.212.

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Dryja, Thaddeus P. "Rhodopsin and autosomal dominant retinitis pigmentosa." Eye 6, no. 1 (January 1992): 1–10. http://dx.doi.org/10.1038/eye.1992.2.

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Rich, Walter. "Advances in the understanding of retinitis pigmentosa." Eye 6, no. 1 (January 1992): vii. http://dx.doi.org/10.1038/eye.1992.1.

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Sayadi, Jihene, Alexandra Miere, Eric H. Souied, and Salomon Y. Cohen. "Type 3 Neovascularization Associated with Retinitis Pigmentosa." Case Reports in Ophthalmology 8, no. 1 (April 10, 2017): 245–49. http://dx.doi.org/10.1159/000471790.

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Purpose: To report a case of type 3 neovascular lesion in a patient with retinitis pigmentosa (RP) complicated by macular edema. Case Report: A 78-year-old man with a long follow-up for RP was referred for painless visual acuity decrease in the right eye. Best-corrected visual acuity was 20/125 in the right eye and 20/40 in the left. Fundus examination showed typical RP and macular edema in both eyes. In the right eye, spectral domain optical coherence tomography revealed a marked cystic macular edema associated with disruption of the Bruch membrane/retinal pigment epithelium complex overlying a pigmentary epithelium detachment, with a vascular structure which appeared to originate from the deep capillary plexus and to be connected with the subretinal pigment epithelium space. Optical coherence tomography angiography showed a high-flow vessel infiltrating the outer retinal layers in the deep capillary plexus segmentation, and a tuft-shaped, bright, high-flow network that seemed to be connected with the subretinal pigment epithelium space in the outer retinal layer segmentation. This presentation was consistent with an early type 3 neovascular lesion in the right eye. Conclusion: Type 3 neovascularization may be considered a possible complication of RP.

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Iovino, Claudio, Giamberto Casini, and Enrico Peiretti. "Bilateral noncalcified astrocytic hamartomas in retinitis pigmentosa: Multimodal imaging evaluation over 8 years of follow-up." European Journal of Ophthalmology 29, no. 5 (October 3, 2018): NP18—NP21. http://dx.doi.org/10.1177/1120672118804386.

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Purpose: To report the evolution of optic disk noncalcified astrocytic hamartomas in a patient with retinitis pigmentosa throughout 8 years of follow-up. Methods: Case report. Results: A 42-year-old white man with a diagnosis of retinitis pigmentosa was referred to our medical retinal center for the first time in 2010, for the development of a new optic nerve head lesion in the right eye. Fundus examination, fundus autofluorescence, fluorescein and green indocyanine angiography, spectral-domain optical coherence tomography were performed and confirmed the presence of a papillary noncalcified astrocytic hamartoma in the right eye. Four years later, multimodal imaging evaluation revealed in the left eye the presence of a first optic disk benign tumor, and in 2018, a second in the nasal retina, while in the right eye the sole papillary lesion increased slightly in size. Conclusions: Noncalcified astrocytic hamartomas can occur in patients with retinitis pigmentosa and can increase in size and number in time. A complete multimodal imaging evaluation is necessary to identify and classify any kind of new lesion that, as known, are associated with these group of hereditary retinal degenerations.

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Dissertations / Theses on the topic "Eye; Retinitis pigmentosa"

1

Nash, Mark Simon. "Melatonin and serotonin receptors associated with cultured human, and normal and Royal College of Surgeons rat retinal pigment epithelium." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282157.

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Clemson, Christine Moulton. "Development of a Multi-Site Phase II Clinical Trial of Valproic Acid for Retinitis Pigmentosa." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/470.

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The body of work presented here is a compendium of the multiple steps required for an investigator initiated trial of an existing medication (Valproic Acid- VPA) for a new indication (Retinitis Pigmentosa – RP). The chapters are listed in logical and chronological order of the process. In order to access patient records an expedited Institutional Review Board (IRB) application for retrospective chart review was submitted (Chapter 1). These records enabled the statistical analysis which not only laid the framework for the trial design, but also became the basis for two manuscripts (Chapter 2). Protocol development informed by the preliminary human studies (Chapter 3) was an instrumental part of the Investigational New Drug (IND) application (Chapter 3.5). This protocol along with the extensive case report forms that detail the intended data to be collected are included in the IND application. Because the Phase II clinical trial proposed attempting to identify the specific RP mutations of the subjects utilizing a National Eye Institute (NEI) study that enabled free genotyping services, two IRB applications were submitted (Chapter 3.6). The first was for approval of the NEI genotyping protocol, the second involved the VPA intervention. Two very different sources of funding for this trial were attempted (Chapter 4) – the NIH via the Challenge Grant mechanism and a private eye disease foundation (Foundation Fighting Blindness). In Chapter 5 I detail the alternate study designs that were considered and developed for this trial (and ultimately abandoned). Finally, in Chapter 6, I formally detail my suggestions to aid in the development of a comprehensive investigator initiated core facility at UMMMC. The goal of this project was two-fold. The first was to learn the entire process of trial and protocol design both from a Umass Institutional perspective as well as from the perspective of the FDA. The second goal was the very real prospect of helping patients with a blinding disease. This work was successful on both counts. IRB approval was received for all the submitted applications. The complexity and uniqueness of many aspects of these submissions culminated in a comprehensive learning experience. The process of working with the Umass Research Pharmacy as well as developing the industry contacts and know-how to develop a workable and financially feasible placebo were both particularly important learning experiences. FDA approval of the IND submission was also received, and the process of pre-communication and delving into the considerable and ever-changing rules and regulations resulted in an extensive and valuable knowledge base. While the practicality of funding has limited the ability of this trial to move forward at this point, given the extensive framework laid by this body of work, we are actively pursuing other opportunities. The third outcome of this work, while not as intentional, was the considerable process of determining the specific competencies and infrastructure that exist at UMMMC to enable investigator initiated drug intervention studies. While this institution is clearly moving rapidly in the direction of translational research, the many needs of these studies are often only clearly understood when the process is specifically undertaken. In completing the approval of this Phase II clinical trial, I was not only able to better understand and define the existing capabilities of UMMMC for this kind of research, I was able to add to that infrastructure when the existing knowledge or skill set was not available. In this manner, I was able to inform and guide many of the support personnel who guided me and have become a part of the strategic direction of UMMMC towards clinical translational research.

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Ropelewski, Philip Edward. "Light-Independent Pathology of Rhodopsin Mislocalization." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1586965687533716.

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4

Venkatesh, Aditya. "Activation of mTORC1 Improves Cone Cell Metabolism and Extends Vision in Retinitis Pigmentosa Mice: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/822.

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Retinitis Pigmentosa (RP) is an inherited photoreceptor degenerative disease that leads to blindness and affects about 1 in 4000 people worldwide. The disease is predominantly caused by mutations in genes expressed exclusively in the night active rod photoreceptors; however, blindness results from the secondary loss of the day active cone photoreceptors, the mechanism of which remains elusive. Here, we show that the mammalian target of rapamycin complex 1 (mTORC1) is required to delay the progression of cone death during disease and that constitutive activation of mTORC1 is sufficient to maintain cone function and promote cone survival in RP. Activation of mTORC1 increased expression of genes that promote glucose uptake, retention and utilization, leading to increased NADPH levels; a key metabolite for cones. This protective effect was conserved in two mouse models of RP, indicating that the secondary loss of cones can be delayed by an approach that is independent of the primary mutation in rods. However, since mTORC1 is a negative regulator of autophagy, its constitutive activation led to an unwarranted secondary effect of shortage of amino acids due to incomplete digestion of autophagic cargo, which reduces the efficiency of cone survival over time. Moderate activation of mTORC1, which promotes expression of glycolytic genes, as well as maintains autophagy, provided more sustained cone survival. Together, our work addresses a long-standing question of non-autonomous cone death in RP and presents a novel, mutation-independent approach to extend vision in a disease that remains incurable.

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Venkatesh, Aditya. "Activation of mTORC1 Improves Cone Cell Metabolism and Extends Vision in Retinitis Pigmentosa Mice: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/822.

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Retinitis Pigmentosa (RP) is an inherited photoreceptor degenerative disease that leads to blindness and affects about 1 in 4000 people worldwide. The disease is predominantly caused by mutations in genes expressed exclusively in the night active rod photoreceptors; however, blindness results from the secondary loss of the day active cone photoreceptors, the mechanism of which remains elusive. Here, we show that the mammalian target of rapamycin complex 1 (mTORC1) is required to delay the progression of cone death during disease and that constitutive activation of mTORC1 is sufficient to maintain cone function and promote cone survival in RP. Activation of mTORC1 increased expression of genes that promote glucose uptake, retention and utilization, leading to increased NADPH levels; a key metabolite for cones. This protective effect was conserved in two mouse models of RP, indicating that the secondary loss of cones can be delayed by an approach that is independent of the primary mutation in rods. However, since mTORC1 is a negative regulator of autophagy, its constitutive activation led to an unwarranted secondary effect of shortage of amino acids due to incomplete digestion of autophagic cargo, which reduces the efficiency of cone survival over time. Moderate activation of mTORC1, which promotes expression of glycolytic genes, as well as maintains autophagy, provided more sustained cone survival. Together, our work addresses a long-standing question of non-autonomous cone death in RP and presents a novel, mutation-independent approach to extend vision in a disease that remains incurable.

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6

Choi, Eun-Jung. "Comparison of the effects of a processing sequence and a nuclear export element on ribozyme activity in transfected cells." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0007401.

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Thesis (M.S.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 68 pages. Includes Vita. Includes bibliographical references.

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Roberts, Paul Allen. "Mathematical models of the retina in health and disease." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:385f61c4-4ff1-45d3-bdb2-41338c174025.

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The retina is the ocular tissue responsible for the detection of light. Its extensive demand for oxygen, coupled with a concomitant elevated supply, renders this tissue prone to both hypoxia and hyperoxia. In this thesis, we construct mathematical models of the retina, formulated as systems of reaction-diffusion equations, investigating its oxygen-related dynamics in healthy and diseased states. In the healthy state, we model the oxygen distribution across the human retina, examining the efficacy of the protein neuroglobin in the prevention of hypoxia. It has been suggested that neuroglobin could prevent hypoxia, either by transporting oxygen from regions where it is rich to those where it is poor, or by storing oxygen during periods of diminished supply or increased uptake. Numerical solutions demonstrate that neuroglobin may be effective in preventing or alleviating hypoxia via oxygen transport, but that its capacity for oxygen storage is essentially negligible, whilst asymptotic analysis reveals that, contrary to the prevailing assumption, neuroglobin's oxygen affinity is near optimal for oxygen transport. A further asymptotic analysis justifies the common approximation of a piecewise constant oxygen uptake across the retina, placing existing models upon a stronger theoretical foundation. In the diseased state, we explore the effect of hyperoxia upon the progression of the inherited retinal diseases, known collectively as retinitis pigmentosa. Both numerical solutions and asymptotic analyses show that this mechanism may replicate many of the patterns of retinal degeneration seen in vivo, but that others are inaccessible to it, demonstrating both the strengths and weaknesses of the oxygen toxicity hypothesis. It is shown that the wave speed of hyperoxic degeneration is negatively correlated with the local photoreceptor density, high density regions acting as a barrier to the spread of photoreceptor loss. The effects of capillary degeneration and treatment with antioxidants or trophic factors are also investigated, demonstrating that each has the potential to delay, halt or partially reverse photoreceptor loss. In addition to answering questions that are not accessible to experimental investigation, these models generate a number of experimentally testable predictions, forming the first loop in what has the potential to be a fruitful experimental/modelling cycle.

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Ohashi(Arai), Yuuki. "Retinitis Pigmentosa with EYS Mutations Is the Most Prevalent Inherited Retinal Dystrophy in Japanese Populations." Kyoto University, 2016. http://hdl.handle.net/2433/217740.

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Kruczek, P. M. "Characterisation of interacting partner(s) for EYS, a major gene implicated in autosomal recessive retinitis pigmentosa." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1473377/.

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Mutations in EYS are a common cause of autosomal recessive retinitis pigmentosa (arRP). EYS is one of the largest genes expressed in the retina and the role of the protein it encodes is presently unclear. It has been shown, however, that EYS localises to the outer segments of porcine photoreceptors and that the Drosophila orthologue of EYS is essential in the biogenesis of the ommatidium, where it interacts with prominin, a highly conserved protein implicated in retinopathies. The aim of this project was to examine the role of EYS in the retina by investigating its subcellular localisation and by identifying its interacting partners. Characterisation of the genetic structure of EYS has revealed that it has at least four isoforms expressed in the retina and testis. Immunocytochemistry studies have shown that EYS isoforms predominantly localise to the cytoplasm of cultured cells whereas immunohistochemistry studies in the primate retina have revealed that it localises to the photoreceptor ciliary axoneme. Yeast 2-hybrid screening has resulted in identification of one potential interacting partner of EYS, AIPL1, which is a molecular chaperone required for the proteostasis of the retina. Further analysis by co-immunoprecipitation and immunofluorescence has confirmed that AIPL1 interacts with the N terminal fragment of EYS isoforms 1 and 4 as well as EYS isoforms 2 and 3. Furthermore, co-immunoprecpietation assays and immunofluorescence studies have suggested that the human orthologues of EYS and Prominin-1 do not interact. The mutation screening of PROM1 has resulted in identification of seven heterozygous novel variants in six unrelated arRP patients; however, pathogenicity of the changes could not be established. Altogether, the results of the study have demonstrated that EYS may be a novel protein associated with the photoreceptor ciliary axoneme, where it could play a role in maintenance of the photoreceptor outer segments. Furthermore, the analysis of the interacome of EYS has demonstrated that it may require the activity of AIPL1 for correct folding and trafficking, and that the functional link of EYS and Prominin-1 described in Drosophila is unlikely to be conserved in humans. The knowledge gained from the study presented herein has brought us closer to unravelling the molecular mechanisms underlying arRP and adds to the overall understanding of the physiology of the retina in health and disease.

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10

Hirashima, Takako. "Choroidal Vasculature in Bietti Crystalline Dystrophy With CYP4V2 Mutations and in Retinitis Pigmentosa With EYS Mutations." Kyoto University, 2020. http://hdl.handle.net/2433/253205.

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Books on the topic "Eye; Retinitis pigmentosa"

1

Byers, W. Gordon M. An atypical case of retinitis pigmentosa. [S.l: s.n., 1985.

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2

M, LaVail Matthew, Anderson Robert E, Hollyfield Joe G, and International Congress of Eye Research (8th : 1988 : San Francisco, Calif.), eds. Inherited and environmentally induced retinal degenerations: Proceedings of the International Symposium on Retinal Degenerations, held in San Francisco, California, September 2 and 3, 1988. New York: Liss, 1989.

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3

D, Humphries Peter Ph, Bhattacharya Shomi, and Bird Alan C, eds. Degenerative retinopathies: Advances in clinical and genetic research : proceedings of the Sixth World Congress of the International Retinitis Pigmentosa Association (IRPA), Dublin, Ireland, July 20 to 22, 1990. Boca Raton: CRC Press, 1991.

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4

Marshall, Mildred H. Changing eyes, changing lives. [Toronto, Ont.]: M.H. Marshall, 1990.

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Inherited and environmentally induced retinal degenerations: Proceedings of the International Symposium on Retinal Degenerations, held in San Francisco, ... in clinical and biological research). Liss, 1989.

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6

Redfern, Robert. Improving Eye Disease in 30 Days : Reduce Your Risk of Eye Disease in 30 Days: Macular Degeneration, Retinitis Pigmentosa, and Diabetic Retinopathy Rehabilitation. Naturally Healthy Publications, 2015.

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Bird, Alan C., Peter Humphries, and Shomi Bhattacharya. Degenerative Retinopathies: Advances in Clinical and Genetic Research. CRC, 1991.

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8

Miller, Adam, Damon P Miller II MD, and Carlyle Coash MA. Stem Cells Heal Your Eyes : Prevent and Help: Macular Degeneration, Retinitis Pigmentosa, Stargardt, Retinal Distrophy, and Retinopathy. OrganicMD Media, 2014.

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Book chapters on the topic "Eye; Retinitis pigmentosa"

1

Bartlett, Hannah. "Retinitis pigmentosa." In Nutrition and the Eye, 123–27. Elsevier, 2006. http://dx.doi.org/10.1016/b978-0-7506-8816-1.50024-0.

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2

Ferreyra, Henry A., and John R. Heckenlively. "Retinitis Pigmentosa." In Genetic Diseases of the Eye, 381–92. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195326147.003.0023.

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3

"Syndromic Retinitis Pigmentosa." In Inherited Eye Diseases, 377–414. CRC Press, 2005. http://dx.doi.org/10.1201/b14269-15.

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O'Neill, Damian. "Retinitis pigmentosa." In Perkins and Hansell's Atlas of Diseases of the Eye, 91–92. Elsevier, 1994. http://dx.doi.org/10.1016/b978-0-7506-4063-3.50040-9.

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Ali, Mohsin H., Alessandro Iannaccone, and Lejla Vajzovic. "Retinitis Pigmentosa." In Handbook of Pediatric Retinal OCT and the Eye-Brain Connection, 105–9. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-323-60984-5.00023-8.

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"17 Retinitis Pigmentosa." In Wills Eye Handbook of Ocular Genetics, edited by Alex V. Levin, Mario Zanolli, and Jenina E. Capasso. Stuttgart: Georg Thieme Verlag, 2018. http://dx.doi.org/10.1055/b-0037-149040.

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"Isolated (Non-Syndromic) Retinitis Pigmentosa." In Inherited Eye Diseases, 301–76. CRC Press, 2005. http://dx.doi.org/10.1201/b14269-14.

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Aldred, M., M. Jay, and A. Wright. "X-Linked Retinitis Pigmentosa." In Molecular Genetics of Inherited Eye Disorders, 259–76. CRC Press, 1994. http://dx.doi.org/10.1201/b14734-11.

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Humphries, Peter, Paul Kenna, and G. Farrar. "Autosomal Dominant Retinitis Pigmentosa." In Molecular Genetics of Inherited Eye Disorders, 153–72. CRC Press, 1994. http://dx.doi.org/10.1201/b14734-7.

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Pennesi, M. E., P. J. Francis, and R. G. Weleber. "Primary Photoreceptor Degenerations: Retinitis Pigmentosa." In Encyclopedia of the Eye, 502–15. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374203-2.00210-4.

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