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Continuing Education Activity

Hemianopsia (hemianopia) is a clinical term used to describe the loss of one half of a vertical visual field. A careful history and physical examination may provide valuable information regarding the location of the pathologic lesion. This activity outlines the evaluation and management of hemianopsia and reviews the role of the clinician managing patients with this condition.


  • Identify the pathophysiology of hemianopsia and its association with neurological emergencies.
  • Review the evaluation process for hemianopsia.
  • Outline the management options available for hemianopsia.
  • Summarize some interprofessional team strategies for improving care coordination and communication to advance the treatment of hemianopsia and associated pathologic conditions to improve patient outcomes.


Hemianopsia results from the disruption of visual pathways within the central nervous system. Understanding the functional anatomy of the visual pathway can help localize pathologic lesions. In brief, visual stimuli are received by each retina and transmitted along the optic nerves to the optic chiasm. Grossly, the retinal fibers divide into nasal and temporal fibers. The nasal fibers decussate at the optic chiasm allowing information about the right and left visual fields to split into their respective pathways for processing in the contralateral side of the brain.[1] For example, the right visual field is made up of information from the right nasal retina and left temporal retina. After decussation in the optic chiasm, visual information travels along the optic tract, and then the optic radiations to the ipsilateral primary visual cortex located in the occipital lobe. 

Lesions may classify as prechiasmal, chiasmal, or retrochiasmal. Prechiasmal lesions impact the optic nerve and produce monocular blindness in the affected eye.[1] Lesions of the optic chiasm disrupt the medial decussating nasal fibers producing bitemporal hemianopsia. Lesions posterior to the chiasm may disrupt the optic tract, optic radiations, or primary visual cortex. Disruption of the optic tract and primary visual cortex classically produce homonymous hemianopsia, whereas damage to the optic radiations results in an inferior or superior quadrantanopia.[1]

Homonymous hemianopsia, in conjunction with an afferent pupillary defect, localizes the lesion to the optic tract.[2] The pupillary defect will be present on the side opposite of the lesion, resulting from damage to afferent nasal fibers that cross at the optic chiasm, continue on the optic tract, and synapse on the pretectal nuclei, followed by the Edinger-Westphal nuclei as part of the afferent pupillary light reflex pathway. 

Homonymous hemianopsia with preservation of the central visual field, otherwise known as macular sparing, is suggestive of damage to the primary visual cortex, which receives dual vascular supply from the middle and posterior cerebral arteries.[1]


Homonymous hemianopsia may result from stroke, head trauma, mass occupying lesions, invasive surgical procedures, or neurologic conditions such as multiple sclerosis, Alzheimer disease, and epilepsy.[3][4] Bitemporal hemianopsia is most often associated with mass occupying lesions such as pituitary adenomas, craniopharyngiomas, and meningiomas.[5] Basilar skull trauma or vascular lesions, such as anterior communicating artery aneurysms, have also been identified as causes of bitemporal hemianopsia.[6][7]


The epidemiology of hemianopsia depends on the type of pathologic insult. Stroke is the most common cause of homonymous hemianopsia.[3][8] A review published in the Journal of Neuro-Ophthalmology included 904 cases of homonymous hemianopsia. Stroke accounted for 69.7% of patients with homonymous hemianopsia. Stroke patients had a mean age of 58. Patients with homonymous hemianopsia from other causes (head trauma, surgery, inflammatory conditions) tended to be younger with a mean age of 36. Lesions of the occipital area were most common in stroke patients (54%) followed by lesions of the optic radiations (33%), and optic tract (6%).

In contrast, homonymous hemianopsia in non-stroke patients was a result of damage to the occipital lobe (24%, optic radiations (31%), optic tract (19%), or multiple locations along the visual pathway (25%).[3] Pituitary adenomas are the most frequently encountered cause of bitemporal hemianopsia. A systematic review based on radiographic and autopsy studies estimated the overall prevalence of pituitary tumors to be 16.7%.[9]

History and Physical

Patients presenting with visual complaints should undergo a complete physical examination, including a thorough neurologic evaluation. Signs and symptoms of neurologic emergencies, such as an acute change in mental status or the presence of new focal neurologic deficits, should prompt rapid acquisition of vital signs and appropriate airway, circulation, and breathing management.

A visual acuity test and complete cranial nerve assessment should be performed in all individuals to assess for visual deficits. The examiner should place particular attention on the pupillary examination as well as visual field testing. A bitemporal visual field defect localizes the pathologic lesion to the optic chiasm, whereas the presence of a homonymous visual field defect suggests damage to the areas posterior to the optic chiasm such as the optic tract, optic radiations, or primary visual cortex in the occipital lobe. Homonymous hemianopsia, in conjunction with an afferent pupillary defect, localizes the lesion to the optic tract.[2] Homonymous hemianopsia with macular sparing suggests damage to the primary visual cortex.


Neuroimaging, in conjunction with physical examination findings, may be used to characterize the cause of hemianopsia and guide clinical management.

Patients with focal neurologic findings suggestive of stroke and within the window for intervention (chemical or mechanical thrombectomy) should receive prompt imaging per institutional protocols or the AHA Stroke Guidelines. 

MRI of the brain best evaluates both bitemporal hemianopsia and homonymous hemianopsia with contrast. In the case of bitemporal hemianopsia, special attention should focus on the structure of the optic chiasm and sellar region. With homonymous hemianopsia, the retrochiasmal structures, including the optic tract and occipital lobe, should be well characterized.

Diffusion-weighted imaging is preferable for detecting vasogenic edema associated with acute ischemic changes. Note that CT may be employed in emergent scenarios to evaluate for ischemia, mass lesions, or vascular aneurysms. CT angiogram is helpful in the case of large vessel pathologies, such as a middle cerebral artery or posterior cerebral artery occlusion.[10]

Treatment / Management

The results of physical examination and imaging studies should guide clinical management. Patients with cerebral infarct or hemorrhage require management accordingly. Consultation with neurology and neurosurgery should take place when appropriate. Patients with mass lesions or signs of increased intracranial pressure may also require admission for medical or surgical therapy.

Patients with visual field deficits may not realize the limitations of their condition and should be advised not to drive.[11] Patient recovery may benefit from a multifaceted approach that includes visual training, visual assist devices (prism correction), occupational therapy, and psychological rehabilitation.[12]

Differential Diagnosis

The differential diagnosis of hemianopsia relates closely to the underlying etiology. It, therefore, should include vascular pathology (cerebral infarct, intracranial hemorrhage, aneurysm, dissection), mass lesions, trauma, inflammatory, and degenerative neurologic conditions.


Visual loss in the setting of stroke suggests a poor prognosis. Studies suggest that only 17 to 18% of patients with homonymous hemianopsia regain their vision within 28 to 30 days of the inciting event. Opportunities for visual recovery decrease over time.[13][12] Patients with bitemporal hemianopsia as a result of pituitary tumors often have visual field improvement (79 to 95%) following resection; however, the extent of the recovery depends on preoperative and operative factors.[14]


Visual field impairment has a significant impact on patient quality of life. Failure to recognize patterns of hemianopsia may delay definitive treatment and opportunities for rehabilitation.

Deterrence and Patient Education

Patients should receive education regarding risk factors for stroke, including hypertension, diabetes, hyperlipidemia, vascular disease, and smoking. Importantly, patients with visual field deficits may not recognize the extent of their functional impairment and should be instructed not to drive.

Enhancing Healthcare Team Outcomes

Hemianopsia is a debilitating condition. Patients with visual impairment may have difficulty navigating environments or performing essential tasks such as reading, writing, and driving. Consequently, patients with visual field deficits may suffer from depression and anxiety. A team-based and patient-centered approach for rehabilitation may improve patient quality of life. Occupational, physical therapy, and psychological therapy are essential resources for facilitating recovery.[12]

Article Details

Article Author

Jonah Ruddy

Article Editor:

Alfonso C. Cardenas


8/8/2022 8:58:12 PM

PubMed Link:




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