Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Homonymous hemianopia

Valérie Biousse, MD
Sachin Kedar, MD
Nancy J Newman, MD
Section Editor
Paul W Brazis, MD
Deputy Editor
Janet L Wilterdink, MD


Homonymous hemianopia is a visual field defect involving either the two right or the two left halves of the visual fields of both eyes. It is caused by lesions of the retrochiasmal visual pathways, ie, lesions of the optic tract, the lateral geniculate nucleus, the optic radiations, and the cerebral visual (occipital) cortex (figure 1) [1-4]. Characteristics of the visual field abnormalities (type, form, size, and congruity), along with associated neurologic signs and symptoms, have been traditionally used for localizing pathologic lesions in the brain (table 1) [1-6].

Homonymous hemianopia is often disabling, causing difficulties with reading and visual scanning. Patients may fail to notice relevant objects or avoid obstacles on the affected side, causing collisions with approaching people or cars. They are not legally allowed to drive in most states. This has dramatic consequences on their vocational and private lives [1,7].

This topic will discuss homonymous hemianopia as a fixed deficit; it may be a transient phenomenon resulting from migraine, transient cerebral ischemia, or seizure. This is discussed separately. (See "Amaurosis fugax (transient monocular or binocular visual loss)", section on 'Causes of transient binocular visual loss'.)


Any type of intracranial lesion in the appropriate location can cause a homonymous hemianopia; however, vascular causes (cerebral infarction and intracranial hemorrhage) are the most frequent in adults, ranging from 42 to 89 percent, followed by brain tumors, trauma, surgical interventions, and other central nervous system diseases [1,8-13]. In children, neoplasms are the most common cause of homonymous hemianopia (39 percent), followed by cerebrovascular disease (25 percent) and trauma (19 percent) [14]. Homonymous hemianopia after head trauma may be under recognized; multifocal brain injury is more common in this setting, contributing to other neurologic deficits that may overshadow the visual field defect [13].

Uncommon causes of homonymous hemianopia include multiple sclerosis, infections (encephalitis, abscess), degenerative dementia (posterior cortical atrophy), Creutzfeldt Jakob disease, adrenoleukodystrophy, seizures, and severe hyperglycemia [12,15-21] (See "Clinical features and diagnosis of Alzheimer disease", section on 'Atypical presentations'.)

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: Jun 21, 2017.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Levin LA. Topical diagnosis of chiasmal and retrochiasmal disorders. In: Walsh and Hoyt Clinical Neuro-ophthalmology, 6th, Miller NR, Newman NJ, Biousse V, Kerrison JB (Eds), Williams & Wilkins, Baltimore 2005. p.503.
  2. Liu GT, Volpe NJ, Galetta SL. Retrochiasmal disorders. In: Neuro-ophthalmology: Diagnosis and Management, Liu GT, Volpe NJ, Galetta SL (Eds), W.B. Saunders, Philadelphia 2001. p.296.
  3. Trobe JD. Visual fields. In: The Neurology of Vision, Trobe JD (Ed), Oxford, Oxford 2001. p.109.
  4. Newman NJ, Galetta SL, Biousse V, et al. Disorder of vision. Continuum: Lifelong learning in Neurology. Neuroophthalmology 2003; 9:11.
  5. Harrington, DO. Localizing value of incongruity in defects in the visual fields. Arch Ophthalmol 1939; 21:453.
  6. HARRINGTON DO. Visual field character in temporal and occipital lobe lesions. Localizing values of congruity and incogruity in incomplete homonymous hemianopsia. Arch Ophthalmol 1961; 66:778.
  7. Pambakian AL, Kennard C. Can visual function be restored in patients with homonymous hemianopia? Br J Ophthalmol 1997; 81:324.
  8. Fujino T, Kigazawa K, Yamada R. Homonymous hemianopia: a retrospective study of 140 cases. Neuroophthalmology 1986; 6:17.
  9. SMITH JL. Homonymous hemianopia. A review of one hundred cases. Am J Ophthalmol 1962; 54:616.
  10. Trobe JD, Lorber ML, Schlezinger NS. Isolated homonymous hemianopia. A review of 104 cases. Arch Ophthalmol 1973; 89:377.
  11. Huber, A. Homonymous hemianopia. Neuroophthalmology 1992; 12:351.
  12. Zhang X, Kedar S, Lynn MJ, et al. Homonymous hemianopias: clinical-anatomic correlations in 904 cases. Neurology 2006; 66:906.
  13. Bruce BB, Zhang X, Kedar S, et al. Traumatic homonymous hemianopia. J Neurol Neurosurg Psychiatry 2006; 77:986.
  14. Liu GT, Galetta SL. Homonymous hemifield loss in childhood. Neurology 1997; 49:1748.
  15. Lee AG, Martin CO. Neuro-ophthalmic findings in the visual variant of Alzheimer's disease. Ophthalmology 2004; 111:376.
  16. Horton JC, Hoyt WF. Quadrantic visual field defects. A hallmark of lesions in extrastriate (V2/V3) cortex. Brain 1991; 114 ( Pt 4):1703.
  17. Rosenberg YJ, Parish CR. Ontogeny of the antibody-forming cell line in mice. IV. Appearance of cells bearing Fc receptors, complement receptors, and surface immunoglobulin. J Immunol 1977; 118:612.
  18. Schrauzer GN, Kiefer GW, Tano K, Robinson PR. Chemical evolution of a nitrogenase model. IX. Concerning the effects of adenosine 5'-triphosphate and of acids in the model system and the adenosine 5'-triphosphate requirement of nitrogenase. J Am Chem Soc 1975; 97:6088.
  19. Hughes S, Field CA, Kennedy MR, Dash CH. Cephalosporins in bone cement: studies in vitro and in vivo. J Bone Joint Surg Br 1979; 61:96.
  20. Shaw S, Kim P, Millett D. Status epilepticus amauroticus revisited: ictal and peri-ictal homonymous hemianopsia. Arch Neurol 2012; 69:1504.
  21. Strowd RE, Wabnitz A, Balakrishnan N, et al. Clinical reasoning: acute-onset homonymous hemianopia with hyperglycemia: seeing is believing. Neurology 2014; 82:e129.
  22. Kedar S, Zhang X, Lynn MJ, et al. Congruency in homonymous hemianopia. Am J Ophthalmol 2007; 143:772.
  23. Jacobson DM. The localizing value of a quadrantanopia. Arch Neurol 1997; 54:401.
  24. Isa K, Miyashita K, Yanagimoto S, et al. Homonymous defect of macular vision in ischemic stroke. Eur Neurol 2001; 46:126.
  25. Landau K, Wichmann W, Valavanis A. The missing temporal crescent. Am J Ophthalmol 1995; 119:345.
  26. Lepore FE. The preserved temporal crescent: the clinical implications of an "endangered" finding. Neurology 2001; 57:1918.
  27. Savino PJ, Paris M, Schatz NJ, et al. Optic tract syndrome. A review of 21 patients. Arch Ophthalmol 1978; 96:656.
  28. Newman SA, Miller NR. Optic tract syndrome. Neuro-ophthalmologic considerations. Arch Ophthalmol 1983; 101:1241.
  29. Biousse V, Newman NJ, Carroll C, et al. Visual fields in patients with posterior GPi pallidotomy. Neurology 1998; 50:258.
  30. Frisén L, Holmegaard L, Rosencrantz M. Sectorial optic atrophy and homonymous, horizontal sectoranopia: a lateral choroidal artery syndrome? J Neurol Neurosurg Psychiatry 1978; 41:374.
  31. Frisén L. Quadruple sectoranopia and sectorial optic atrophy: a syndrome of the distal anterior choroidal artery. J Neurol Neurosurg Psychiatry 1979; 42:590.
  32. Papageorgiou E, Ticini LF, Hardiess G, et al. The pupillary light reflex pathway: cytoarchitectonic probabilistic maps in hemianopic patients. Neurology 2008; 70:956.
  33. Barton JJ, Hefter R, Chang B, et al. The field defects of anterior temporal lobectomy: a quantitative reassessment of Meyer's loop. Brain 2005; 128:2123.
  34. Yogarajah M, Focke NK, Bonelli S, et al. Defining Meyer's loop-temporal lobe resections, visual field deficits and diffusion tensor tractography. Brain 2009; 132:1656.
  35. Çelebisoy M, Çelebisoy N, Bayam E, Köse T. Recovery of visual-field defects after occipital lobe infarction: a perimetric study. J Neurol Neurosurg Psychiatry 2011; 82:695.
  36. Weisberg LA, Wall M. Alexia without agraphia: clinical-computed tomographic correlations. Neuroradiology 1987; 29:283.
  37. Pandit RJ, Gales K, Griffiths PG. Effectiveness of testing visual fields by confrontation. Lancet 2001; 358:1339.
  38. Kerr NM, Chew SS, Eady EK, et al. Diagnostic accuracy of confrontation visual field tests. Neurology 2010; 74:1184.
  39. Wong AM, Sharpe JA. A comparison of tangent screen, goldmann, and humphrey perimetry in the detection and localization of occipital lesions. Ophthalmology 2000; 107:527.
  40. Parisi JL, Bell RA, Yassein H. Homonymous hemianopic field defects and driving in Canada. Can J Ophthalmol 1991; 26:252.
  41. Gray CS, French JM, Bates D, et al. Recovery of visual fields in acute stroke: homonymous hemianopia associated with adverse prognosis. Age Ageing 1989; 18:419.
  42. Tiel, K, Kolmel, HW. Patterns of recovery from homonymous hemianopia subsequent to infarction in the distribution of posterior cerebral artery. Neuroophthalmology 1991; 11:33.
  43. Zhang X, Kedar S, Lynn MJ, et al. Natural history of homonymous hemianopia. Neurology 2006; 66:901.
  44. Gilhotra JS, Mitchell P, Healey PR, et al. Homonymous visual field defects and stroke in an older population. Stroke 2002; 33:2417.
  45. Racette L, Casson EJ. The impact of visual field loss on driving performance: evidence from on-road driving assessments. Optom Vis Sci 2005; 82:668.
  46. Pambakian A, Currie J, Kennard C. Rehabilitation strategies for patients with homonymous visual field defects. J Neuroophthalmol 2005; 25:136.
  47. Pollock A, Hazelton C, Henderson CA, et al. Interventions for visual field defects in patients with stroke. Cochrane Database Syst Rev 2011; :CD008388.
  48. Bowers AR, Keeney K, Peli E. Community-based trial of a peripheral prism visual field expansion device for hemianopia. Arch Ophthalmol 2008; 126:657.
  49. Bowers AR, Keeney K, Peli E. Randomized crossover clinical trial of real and sham peripheral prism glasses for hemianopia. JAMA Ophthalmol 2014; 132:214.
  50. Pameijer JK. Reading problems in hemianopia. Ophthalmologica 1970; 160:322.
  51. Schuett S, Heywood CA, Kentridge RW, Zihl J. Rehabilitation of hemianopic dyslexia: are words necessary for re-learning oculomotor control? Brain 2008; 131:3156.
  52. Pambakian AL, Mannan SK, Hodgson TL, Kennard C. Saccadic visual search training: a treatment for patients with homonymous hemianopia. J Neurol Neurosurg Psychiatry 2004; 75:1443.
  53. Spitzyna GA, Wise RJ, McDonald SA, et al. Optokinetic therapy improves text reading in patients with hemianopic alexia: a controlled trial. Neurology 2007; 68:1922.
  54. Roth T, Sokolov AN, Messias A, et al. Comparing explorative saccade and flicker training in hemianopia: a randomized controlled study. Neurology 2009; 72:324.
  55. Bouwmeester L, Heutink J, Lucas C. The effect of visual training for patients with visual field defects due to brain damage: a systematic review. J Neurol Neurosurg Psychiatry 2007; 78:555.
  56. Sabel BA, Kasten E. Restoration of vision by training of residual functions. Curr Opin Ophthalmol 2000; 11:430.
  57. Sabel BA, Trauzettel-Klosinksi S. Improving vision in a patient with homonymous hemianopia. J Neuroophthalmol 2005; 25:143.
  58. Schreiber A, Vonthein R, Reinhard J, et al. Effect of visual restitution training on absolute homonymous scotomas. Neurology 2006; 67:143.
  59. Koch G, Bonnì S, Giacobbe V, et al. θ-burst stimulation of the left hemisphere accelerates recovery of hemispatial neglect. Neurology 2012; 78:24.
  60. Cazzoli D, Müri RM, Hess CW, Nyffeler T. Treatment of hemispatial neglect by means of rTMS--a review. Restor Neurol Neurosci 2010; 28:499.