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Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report
INTRODUCTION: Monocular hemianopia is a visual field defect with an uncommon pattern. The etiology of monocular temporal hemianopia has been well-evaluated and has been suggested to result from an optic nerve or chiasmal lesion. However, the etiology of monocular nasal hemianopia remains unclear. PA...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Wolters Kluwer Health
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7386976/ https://www.ncbi.nlm.nih.gov/pubmed/32791737 http://dx.doi.org/10.1097/MD.0000000000021352 |
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author | Lin, Hsin-Le Yen, Ju-Chuan |
author_facet | Lin, Hsin-Le Yen, Ju-Chuan |
author_sort | Lin, Hsin-Le |
collection | PubMed |
description | INTRODUCTION: Monocular hemianopia is a visual field defect with an uncommon pattern. The etiology of monocular temporal hemianopia has been well-evaluated and has been suggested to result from an optic nerve or chiasmal lesion. However, the etiology of monocular nasal hemianopia remains unclear. PATIENT CONCERNS: Here, we present the case of a 41-year-old male who was punched on the head with fists during a fight and then suffered from painless blurred vision in the left eye after mild traumatic brain injury. An ophthalmic examination revealed a conjunctival chemosis, periorbital hematoma, and a relative afferent pupillary defect in the left eye. Automated perimetry indicated there was a left side nasal hemianopia along the vertical meridian. DIAGNOSIS: Examination of the fundus showed there was a normal appearing retina and disc bilaterally. Fluorescein angiography revealed no delayed filling of the vessels. Computed tomography and magnetic resonance imaging showed unremarkable findings of the visual pathways, orbit, and brain. A diagnosis of left traumatic optic neuropathy was made. INTERVENTIONS: Systemic steroid pulse therapy (1 gram of intravenous methylprednisolone per day) was given to the patient for 3 days. OUTCOMES: An ophthalmologic examination after treatment indicated there was no obvious improvement in the relative afferent pupillary defect, best corrected visual acuity, and color sense. A second set of automated perimetry results showedno changes after 3 months. CONCLUSION: Monocular nasal hemianopia caused by traumatic optic neuropathy is uncommon. In this case, monocular nasal hemianopia was likely due to ischemic changes from impairment of the prechiasmal arterial anastomotic network or indirect injury to the lateral prechiasmal nerve fiber. |
format | Online Article Text |
id | pubmed-7386976 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Wolters Kluwer Health |
record_format | MEDLINE/PubMed |
spelling | pubmed-73869762020-08-05 Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report Lin, Hsin-Le Yen, Ju-Chuan Medicine (Baltimore) 5800 INTRODUCTION: Monocular hemianopia is a visual field defect with an uncommon pattern. The etiology of monocular temporal hemianopia has been well-evaluated and has been suggested to result from an optic nerve or chiasmal lesion. However, the etiology of monocular nasal hemianopia remains unclear. PATIENT CONCERNS: Here, we present the case of a 41-year-old male who was punched on the head with fists during a fight and then suffered from painless blurred vision in the left eye after mild traumatic brain injury. An ophthalmic examination revealed a conjunctival chemosis, periorbital hematoma, and a relative afferent pupillary defect in the left eye. Automated perimetry indicated there was a left side nasal hemianopia along the vertical meridian. DIAGNOSIS: Examination of the fundus showed there was a normal appearing retina and disc bilaterally. Fluorescein angiography revealed no delayed filling of the vessels. Computed tomography and magnetic resonance imaging showed unremarkable findings of the visual pathways, orbit, and brain. A diagnosis of left traumatic optic neuropathy was made. INTERVENTIONS: Systemic steroid pulse therapy (1 gram of intravenous methylprednisolone per day) was given to the patient for 3 days. OUTCOMES: An ophthalmologic examination after treatment indicated there was no obvious improvement in the relative afferent pupillary defect, best corrected visual acuity, and color sense. A second set of automated perimetry results showedno changes after 3 months. CONCLUSION: Monocular nasal hemianopia caused by traumatic optic neuropathy is uncommon. In this case, monocular nasal hemianopia was likely due to ischemic changes from impairment of the prechiasmal arterial anastomotic network or indirect injury to the lateral prechiasmal nerve fiber. Wolters Kluwer Health 2020-07-24 /pmc/articles/PMC7386976/ /pubmed/32791737 http://dx.doi.org/10.1097/MD.0000000000021352 Text en Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc. http://creativecommons.org/licenses/by/4.0 This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0 |
spellingShingle | 5800 Lin, Hsin-Le Yen, Ju-Chuan Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report |
title | Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report |
title_full | Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report |
title_fullStr | Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report |
title_full_unstemmed | Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report |
title_short | Acute monocular nasal hemianopia following a mild traumatic brain injury: A case report |
title_sort | acute monocular nasal hemianopia following a mild traumatic brain injury: a case report |
topic | 5800 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7386976/ https://www.ncbi.nlm.nih.gov/pubmed/32791737 http://dx.doi.org/10.1097/MD.0000000000021352 |
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