|Year : 2015 | Volume
| Issue : 2 | Page : 109-113
Nonglaucomatous optic atrophy in Benin City
Vivian B Osaguona, Valentina W Okeigbemen
Department of Ophthalmology, University of Benin Teaching Hospital, Benin City, Edo State, Nigeria
|Date of Web Publication||19-Feb-2015|
Vivian B Osaguona
Department of Ophthalmology, University of Benin Teaching Hospital, P.M.B. 1111, Benin City, Edo State
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Context: Optic atrophy is a clinical sign and not a disease. The etiology of optic atrophy is diverse, some of which may be life threatening.
Patients and Methods: A retrospective review of the medical records of all adult patients aged 16 years and above with nonglaucomatous optic atrophy at the eye clinic of the University of Benin Teaching Hospital over a 4-year period was conducted.
Results: One hundred and four patients had nonglaucomatous optic atrophy. There were 58 males and 46 females with a male:female of 1.3:1. Their ages ranged from 16 to 83 years with a mean age of 49.2 ± 17.74 years. Majority (75%) of the patients were in the age range of 31-70 years. One hundred and fifty-seven eyes were affected with bilateral involvement in 53 patients. The etiology was unknown in 47 (45.2%) patients. Choriodoretinal disease 24 (23.1%), trauma 14 (13.5%), toxic-nutritional 8 (7.7%) and compressive lesions 5 (4.8%) were the most common among the known etiologies.
Conclusion: Optic atrophy is the end result of injury to the anterior visual pathway from a myriad of disease processes. A broad knowledge of the etiology of optic atrophy is needed to make a diagnosis .
| Abstract in French|| |
Contexte: L'atrophie optique est un signe clinique et non une maladie. L'ιtiologie de l'atrophie optique est diversifiιe, dont certaines peuvent κtre mortelles.
Patients et Mιthodes: Une ιtude rιtrospective des dossiers mιdicaux de tous les patients adultes βgιs de 16 ans et plus avec non glaucomateuse atrophie optique ΰ la clinique de l'œil d'un hτpital de soins tertiaires sur une pιriode de 4 ans a ιtι menιe.
Rιsultats: Cent quatre patients avaient non glaucomateuse atrophie optique. Il y avait 58 hommes et 46 femmes avec un mβle: femelle de 1,3:1. Leur βge variait de 16 ΰ 83 ans, avec un βge moyen de 49,2 17,74 annιes. La majoritι (75%) des patients ιtaient dans la tranche d'βge de 31-70 ans. Cent cinquante-sept yeux ont ιtι touchιs avec la participation bilatιrale chez 53 patients. L'ιtiologie ιtait inconnue dans 47 (45,2%) patients. Maladie Choriodoretinal 24 (23,1%), les traumatismes 14 (13,5%), toxiques nutritionnel 8 (7,7%) et des lιsions de compression 5 (4,8%) ιtaient les plus frιquents parmi les ιtiologies connues.
Conclusion: L'atrophie optique est le rιsultat d'une blessure ΰ la voie visuelle antιrieure d'une myriade de processus pathologiques de fin. Une connaissance approfondie de l'ιtiologie de l'atrophie optique est nιcessaire pour ιtablir un diagnostic.
Mots-clιs: Adultes, l'ιtiologie, disque pβleur, Nigeria
Keywords: Adults, etiology, disc pallor, Nigeria
|How to cite this article:|
Osaguona VB, Okeigbemen VW. Nonglaucomatous optic atrophy in Benin City. Ann Afr Med 2015;14:109-13
| Introduction|| |
Optic atrophy is a clinical sign. It results from disease processes that cause irreversible damage to the ganglion cells, and axons in the anterior visual pathway. The diagnosis is based on the findings of disc pallor, with associated changes in the integrity of the retinal nerve fiber layer and retinal vessels, and visual dysfunction (vision and/or visual field loss) attributable to the optic nerve.  The etiology is broad and may be a presentation of life-threatening processes. 
The aim of this study is to determine the causes of optic atrophy among adults seen at the eye clinic of the University of Benin Teaching Hospital.
| Patients and Methods|| |
Approval for this study was obtained from the Ethics and Research Committee of the University of Benin Teaching Hospital. A retrospective review of the medical records of all cases of unilateral or bilateral optic atrophy at first presentation to the eye clinic at the University of Benin Teaching Hospital from May 2009 to June 2013 was performed. Inclusion criteria for the study were: (1) All adult patients aged 16 years and above, (2) ophthalmoscopic findings of optic atrophy, (3) visual dysfunction (visual acuity, color vision and/or visual field loss) attributable to the optic nerve (e.g. relative afferent pupillary defect) and (4) normal intraocular pressure. Exclusion criteria were: (1) Children below the age of 16 years and (2) patients with glaucoma whether primary or secondary glaucoma. Data on age, gender, laterality of optic atrophy, visual function, and etiology of optic atrophy were obtained. The causes of optic atrophy were classified into choroidoretinal disease, inflammatory, ischemic, toxic-nutritional, compressive, traumatic, hereditary processes, and unknown. The results were analyzed using Microsoft Office Excel (Microsoft Corporation, 2010, Louisville KY) software.
| Results|| |
There were 104 patients with bilateral or unilateral optic atrophy. These included 58 males and 46 females with a male: female of 1.3:1. The age range was from 16 to 83 years with a mean age of 49.2 ± 17.74 years. Most of the patients were in the 31-50 years (38.5%) and 51-70 years (36.5%) age groups [Table 1]. One hundred and fifty-seven eyes were affected, with bilateral involvement in 53 patients. The etiology of optic atrophy seen in this study is presented in [Table 2]. [Table 3] shows the visual acuity in the affected eyes.
| Discussion|| |
Optic atrophy is a known cause of both unilateral and bilateral visual impairment and blindness. ,, It may also be the presentation of life-threatening conditions such as intracranial mass lesions (e.g. intracranial aneurysms). Optic atrophy was the most common (23.9%) ocular sign among patients with intracranial tumors in Ile-Ife, Nigeria.  In India, it was a presentation in 18% of patients with intracranial space occupying lesions.  Compression of the anterior visual pathway by mass lesions may result in optic atrophy. In our study, compressive optic neuropathy (evident on computed tomography) was seen in 5 (4.8%) patients. Eight (8%) cases of optic atrophy due to orbitocranial tumors were reported in a study by Oluleye et al. 
The etiology of optic atrophy is diverse. It may result from a myriad of disease processes that include ischemia, inflammation, compression, infiltration, trauma, and hereditary which cause irreversible damage to the ganglion cells, and axons in the anterior visual pathway. In our study, choriodoretinal disease (23.1%) was the most common known etiology. Similarly, in an earlier work by Ayanru  on the etiology of optic atrophy in Benin City, Nigeria, choriodoretinal disease was also the most common known etiology seen in 45 (24.7%) of the study population. Retinitis pigmentosa was a cause of optic atrophy in 3% of the sample population studied by Oluleye et al.  in Ibadan, Nigeria. In an earlier study in India, chorioretinal diseases accounted for 9 (9%) cases of optic atrophy. Choroidoretinal diseases cause optic atrophy from damage to the retinal ganglion cells and axons.
Trauma 14 (13.5%) was the second most common known etiology in our study. Trauma was also among the common known etiologies in other studies in Nigeria accounting for 1.3-15.4%. ,, In India, it was responsible for 7 (7%) cases of optic atrophy.  Optic atrophy may result either from indirect injury to the optic nerve due to transmitted shear forces to the nerve in closed head injury such as blunt trauma, or from direct injury to the optic nerve in penetrating injuries.  The most common form of injury to the optic nerve is by indirect injury with an incidence of 0.5-5% of all closed head injuries. , Common causes of traumatic optic neuropathy include road traffic accidents and falls; other less common causes include assaults, stab wounds, gunshots, and trivial injuries.  The patient with traumatic optic neuropathy commonly presents with a history of visual loss following head trauma and may have other injuries such as fracture to the base of the skull and multiple facial fractures with associated ocular motor nerve palsies as was the case in three of our patients. Optic atrophy usually results 8 weeks after injury. 
In Southern Nigeria, bilateral optic atrophy is a feature of the tropical amblyopia syndrome or tropical ataxic neuropathy (which is characterized by bilateral optic atrophy, bilateral sensorineural deafness, myelopathy, and polyneuropathy). ,, Typically, these patients have a diet consisting mainly of cassava (Mannihot) products, eaten at least twice a day with very little first-class protein in the diet.  Three of our patients had presumed tropical amblyopia syndrome, although laboratory testing of the blood thiocyanate levels was not done. Chronic cyanide intoxication from cassava products causes segmental demyelination of nerve fibers.  Other known toxic-nutritional causes include anti-tuberculous medications such as ethambutol and isoniazid, methanol, tobacco, amiodarone, deficiencies of Vitamin B12 or folate, lead, quinine, tamoxifen, cafergot among many others. ,,
In our study, no case of optic atrophy was related with multiple sclerosis or hereditary optic atrophy, which was the situation in other reports on optic atrophy in Nigerians. ,, Multiple sclerosis is documented to be rare in Nigerians and only very few cases in Nigerians have been reported. ,, The diagnosis of hereditary optic atrophy may be made, perhaps, if patients' relatives are examined and genetic studies done in those suspected of having familial optic atrophy (bilateral, symmetric visual loss, bilateral optic atrophy and probable family history of vision loss). It is notable, however, that facilities for genetic studies are not readily available or affordable in this environment.
Similar to other studies in which the etiology of optic atrophy could not be determined in 109 (59.8%),  62 (62%)  and 9 (69.2%)  cases respectively, the etiology could also not be determined in the majority 47 (45.2%) of our patients. However, a lower percentage of undiagnosed cases is reported in our study. This may be due, in part, to the fact that facilities for neuroimaging were relatively more available during our study period than in theirs. The challenges in making a diagnosis in our center include the fact that many of our patients are poor historians, and the lack of access to previous medical records. Moreover, many of the patients were seen once in consultation and were subsequently lost to follow-up. Patient education on their case and management plan may help to reduce the rate of loss to follow-up. Some other patients were unable to have neuroimaging done due to financial constraints. In a study of 91 patients with isolated unexplained optic atrophy, magnetic resonance imaging with contrast showed a compressive etiology in 18 (20%) of them.  We recommend that neuroimaging should be covered by the National Health Insurance Scheme in order to take care of the problem of the huge cost of neuroimaging, and that the National Health Insurance Scheme should be made accessible to all. It is noteworthy that even with thorough clinical evaluation and investigations, some cases of optic atrophy still remain of unknown etiology.
Our study has some limitations in that (1) it is a retrospective study, which does not allow for a standardized protocol. (2) It is a hospital-based study, which may not be a true representation of the etiology in the community, and (3) the etiology could not be determined in 45.2% of the patients, some of whom were not fully evaluated for various reasons as earlier stated. Had the etiologies been known they would have been spread among other specific etiologies.
A patient with optic atrophy should be thoroughly evaluated as it may be a treatable condition or a presentation of a life-threatening condition. , With thorough history and examination the etiology of optic atrophy can be determined in most cases.  The level of optic nerve function should be determined by visual acuity, color vision, brightness sensitivity testing, confrontation and a formal perimetry. There is usually a relative afferent pupillary defect in unilateral disease or bilateral, asymmetric disease. The area of disc pallor (segmental or diffuse pallor), retinal nerve fiber layer loss and the integrity of the retinal vessels should be assessed. A full neurologic examination should also be done to exclude other neurologic deficits. Laboratory investigation should be done as indicated from the clinical evaluation.  Patients' relatives should be examined, and genetic testing done in those suspected of having hereditary optic neuropathy. In cases of unexplained optic atrophy, neuroimaging with contrast of the orbit and brain with attention paid to the course of the optic nerve, chiasm and retrochiasmal visual pathway should be done. Follow-up should be with visual acuity, color vision, quantitative visual field tests and fundus photographs. If after evaluation, the etiology remains undiagnosed, or there is progression, a neuro-ophthalmic referral should be sought.
| Conclusion|| |
Optic atrophy is the end result of injury to the anterior visual pathway from a myriad of disease processes. A broad knowledge of the etiology of optic atrophy is needed to make a diagnosis. A patient with optic atrophy should be thoroughly investigated as it may be the presentation of a life or vision threatening disease. Cases of unexplained or progressive optic atrophy should be referred to a neuro-ophthalmologist.
| References|| |
Miller NR, Newman NJ, Biousse V, Kerrison JB, editors. Walsh and Hoyt′s Clinical Neuro-ophthalmology: The Essentials. Philadephia, USA: Lippincott Williams and Wilkins; 2008. p. 104.
Lee AG. Neuro-ophthalmic afferent system diagnoses a general ophthalmologist should (almost) never make alone. Middle East Afr J Ophthalmol 2009;16:41-5.
Adegbehingbe BO, Majengbasan TO. Ocular health status of rural dwellers in South-Western Nigeria. Aust J Rural Health 2007;15:269-72.
Oluleye TS, Ajaiyeoba AI, Akinwale MO, Olusanya BA. Causes of blindness in Southwestern Nigeria: A general hospital clinic study. Eur J Ophthalmol 2006;16:604-7.
Osaguona VB, Ukponmwan CU, Kayoma DH, Okojie OH. Ocular health status of patients seen at the screening centre of the University of Benin Teaching Hospital, Benin City, Nigeria - A preliminary report. J Med Biomed Res 2012;11:44-50.
Onakpoya OH, Komolafe EO, Akintomide F, Ajite K, Komolafe MA, Adeolu AA, et al
. Ophthalmic manifestations in patients with intracranial tumours. Afr J Neurol Sci 2009;28 (1). Available from: http://www.ajns.paans.org/article.php3?id_article=294
. [Last accessed 2014 April 29].
Raju KV, Khadder AA. Ocular manifestations of intracranial space occupying lesions - A clinical study. Kerala J Ophthalmol 2009;XXI: 248-52.
Oluleye TS, Ajaiyeoba AI, Fafowora OF, Olusanya BA. The aetiology of optic atrophy in Nigerians - a general hospital clinic study. Int J Clin Pract 2005;59:950-2.
Ayanru JO. Environment, culture, and eye disease in Nigeria (Experience at Benin-City, Bendel State of Nigeria). Proceedings African Eye Nairobi, Kenya; 1982. p. 41-63.
Omoti AE, Waziri-Erameh MJ. Pattern of neuro-ophthalmic disorders in a tertiary eye centre in Nigeria. Niger J Clin Pract 2007;10:147-51.
Chaddah MR, Khanna KK, Chawla GD. Optic atrophy (review of 100 cases). Indian J Ophthalmol 1971;19:172-6.
Steinsapir KD, Goldberg RA. Traumatic optic neuropathy. Surv Ophthalmol 1994;38:487-518.
Carta A, Ferrigno L, Salvo M, Bianci-Marzoli S, Boschi A, Carta F. Visual prognosis after indirect traumatic optic neuropathy. Am J Ophthalmol 2003;136:784.
Simon S, Torpy D, Brophy B, Blumbergs P, Selva D, Crompton JL. Neuro-ophthalmic manifestations and outcomes of pituitary apoplexy - a life and sight-threatening emergency. N Z Med J 2011;124:52-9.
Mavrakanas NA, Schutz JS. Feigned visual loss misdiagnosed as occult traumatic optic neuropathy: Diagnostic guidelines and medical-legal issues. Surv Ophthalmol 2009;54:412-6.
Ayanru JO. The tropical amblyopia syndrome (or tropical nutritional amblyopia) in the Mid-Western State of Nigeria. Afr J Med Med Sci 1976;5:41-8.
Williams AO, Osuntokun BO. Peripheral neuropathy in tropical (nutritional) ataxia in Nigeria. Light and electron microscopic study. Arch Neurol 1969;21:475-92.
Oluwole OS, Onabolu AO, Link H, Rosling H. Persistence of tropical ataxic neuropathy in a Nigerian community. J Neurol Neurosurg Psychiatry 2000;69:96-101.
Golnik K. Nonglaucomatous optic atrophy. Neurol Clin 2010;28:631-40.
Orssaud C, Roche O, Dufier JL. Nutritional optic neuropathies. J Neurol Sci 2007;262:158-64.
Miller NR, Newman NJ, Biousse V, Kerrison JB, editors. Walsh and Hoyt′s Clinical Neuro-Ophthalmology: The Essentials. Philadephia, USA: Lippincott Williams and Wilkins; 2008. p. 208.
Onwuekwe I, Ekenze O. Multiple sclerosis in a nigerian alcoholic male: A case report from Enugu, South East Nigeria. Ann Med Health Sci Res 2011;1:107-13.
Keme-Ebi IK, Asindi AA. Locked-in syndrome in a Nigerian male with multiple sclerosis: A case report and literature review. Pan Afr Med J 2008;1:4.
Ajayi AO, Olarinoye JK. Acute exarcebation of multiple sclerosis in pregnancy: A case report. Ann Afr Med 2006;5:209-11.
Lee AG, Chau FY, Golnik KC, Kardon RH, Wall M. The diagnostic yield of the evaluation for isolated unexplained optic atrophy. Ophthalmology 2005;112:757-9.
[Table 1], [Table 2], [Table 3]