Homonymous hemianopia (occipital lobe/optic tract lesion)

Key Points at a Glance

Homonymous hemianopia is a visual field defect in both eyes on the same side caused by a lesion in the retrochiasmal visual pathway.
Cerebrovascular disease (cerebral infarction, cerebral hemorrhage) is the most common cause, with posterior cerebral artery territory infarction being typical.
It can occur with lesions in the optic tract, lateral geniculate body, optic radiation, or occipital visual cortex.
Characteristic visual field patterns (e.g., quadrantanopia, macular sparing) appear depending on the lesion site.
Patients often complain of “difficulty seeing” rather than “decreased vision,” and may not notice it in the early stages.
In the acute phase, head MRI (DWI) is used to confirm the lesion site, and treatment of cerebrovascular disease takes priority.
Complete visual field recovery is difficult, but there is room for partial recovery and visual rehabilitation intervention.

1. Homonymous Hemianopia

Homonymous hemianopia is a condition in which the visual field on the same side (right or left) of both eyes is lost due to a lesion in the visual pathway posterior to the optic chiasm (optic tract, lateral geniculate body, optic radiation, visual cortex).

Since the visual pathway beyond the optic chiasm integrates and transmits information from both eyes, a unilateral lesion always affects both eyes. Basically, a lesion posterior to the optic chiasm always causes binocular visual field defects, while a monocular visual field defect suggests a lesion anterior to the optic chiasm.

Anatomy of the visual pathway

Information starting from the photoreceptors in the retina travels through the optic nerve and optic chiasm along the following pathways.

Optic chiasm: Nerve fibers from the nasal half cross to the opposite side, while those from the temporal half run on the same side.
Optic tract: After the optic chiasm. The right optic tract transmits information from the left visual field of both eyes, and the left optic tract from the right visual field of both eyes.
Lateral geniculate nucleus: A relay station from the optic tract.
Optic radiation: From the lateral geniculate nucleus to the visual cortex. It runs through the temporal and parietal lobes.
Calcarine sulcus visual cortex: Primary visual cortex on the medial surface of the occipital lobe

We capture visual targets with the fovea of the eye, and this information travels from the optic nerve, dividing into crossed and uncrossed fibers, enters the optic chiasm, optic tract, and lateral geniculate body where fibers are relayed, and reaches the visual center via the optic radiation.

Main causative diseases

Cerebrovascular disease (most common): Cerebral infarction or hemorrhage in the posterior cerebral artery (PCA) territory
Brain tumor: Tumors of the temporal, occipital, or parietal lobe
Trauma: Head injury
Demyelinating diseases: multiple sclerosis, etc.
Others: brain abscess, arteriovenous malformation, occipital lobe epilepsy

The posterior cerebral artery (PCA) perfuses the occipital visual cortex, and infarction in this area is the most common cause of homonymous hemianopia.

Q Is homonymous hemianopia a disease of one eye?

Homonymous hemianopia is a visual field defect that occurs in both eyes, not a disease of one eye. In right homonymous hemianopia, the right side (temporal side) of the right eye and the right side (nasal side) of the left eye are affected. Since the visual pathway posterior to the optic chiasm integrates information from both eyes, a unilateral lesion always affects both eyes.

2. Main symptoms and clinical findings

Subjective Symptoms

Subjective symptoms of homonymous hemianopia are diverse, and visual acuity itself is often preserved.

Complaints of “difficulty seeing”: Often not reported as decreased visual acuity
Bumping into things: Colliding with objects approaching from the blind side without noticing
Difficulty reading: In left homonymous hemianopia, finding the beginning of a line becomes difficult
Lack of awareness in early stages: Especially in right homonymous hemianopia, patients may not be aware. When left brain lesions cause aphasia, attention may not be directed to visual field defects.

Clinical Findings

Visual Field Defect Patterns (by Location)

Characteristic visual field patterns appear depending on the lesion location.

Complete Homonymous Hemianopia

Complete homonymous hemianopia: Complete loss of vision in one half of the visual field, divided vertically at the midline.

Macular sparing: In optic tract lesions, the central visual field is spared.

Incomplete Quadrantanopia

Incomplete homonymous hemianopia: Defect with incomplete density and extent.

Homonymous quadrantanopia: Defect only in the upper or lower quadrant. Characteristic of temporal and occipital lobe lesions.

Macular Sparing Type

Macular sparing: Homonymous hemianopia with preserved central visual field. Characteristic of lesions in the posterior pole of the occipital lobe.

In posterior cerebral artery occlusion, the posterior pole is often spared due to collateral circulation from the middle cerebral artery.

Associated Findings

Conjugate gaze deviation: In paralytic lesions of the frontal eye field, conjugate gaze deviation toward the affected side occurs.
Pupillary light reflex: Usually normal in occipital lobe or optic radiation lesions. In optic tract lesions, a relative afferent pupillary defect (RAPD) may be observed.
RAPD (Wernicke hemianopic pupil): In optic tract lesions, the pupillary light reflex to light from the affected side is diminished.

3. Causes and Risk Factors

Underlying Diseases

The most common cause of homonymous hemianopia is cerebrovascular disease, which includes the following conditions.

Posterior cerebral artery (PCA) territory infarction: Infarction in the PCA territory that perfuses the occipital visual cortex is the most common.
Middle cerebral artery (MCA) territory infarction: Infarction in the temporal and parietal lobes involving the optic radiation.
Cerebral hemorrhage: Hemorrhage due to hypertension, amyloid angiopathy, etc.
Brain tumor: Compression by tumors arising in the temporal, occipital, or parietal lobes.
Trauma: Direct damage to the occipital lobe due to head injury.
Demyelinating diseases: Occipital lobe lesions such as multiple sclerosis
Others: Brain abscess, arteriovenous malformation, occipital lobe epilepsy (transient)

Risk factors

Risk factors for cerebrovascular disease are also risk factors for homonymous hemianopia.

Hypertension: The greatest risk factor
Diabetes mellitus
Atrial fibrillation: a cause of cardiogenic embolism
Dyslipidemia
Smoking
Advanced age: progression of arteriosclerosis with aging

4. Diagnosis and Examination Methods

Visual field testing is fundamental for diagnosing homonymous hemianopia, and brain MRI is used to confirm the lesion location.

Visual Field Testing

Goldmann kinetic perimetry: Quantitatively evaluates the extent and density of homonymous hemianopia. Useful for assessing congruity of the hemianopia and provides detailed evaluation of the peripheral visual field.
Humphrey static automated perimetry: Quantifies the depth of visual field defects using threshold testing. Also useful for follow-up.

Assessment of congruity:

High congruity (visual field defect patterns are similar in both eyes) → lesion near the occipital lobe
Low congruity (visual field defect shapes differ between eyes) → lesion near the optic tract

Correspondence between lesion location and visual field pattern

The visual field patterns for each lesion location are summarized below.

Lesion location	Visual field pattern	Characteristics
Optic tract	Homonymous hemianopia (macular sparing)	Low congruity, RAPD present
Lateral geniculate body	Various visual field defects	Depends on lesion location
Optic radiation (Meyer’s loop)	Contralateral upper homonymous quadrantanopia	Temporal lobe lesion
Occipital visual cortex (upper part)	Contralateral lower homonymous hemianopia	Lesion of the upper lip of the calcarine sulcus
Occipital visual cortex (posterior pole)	Homonymous hemianopia with macular sparing	Infarction in the posterior cerebral artery territory

Head MRI

DWI (diffusion-weighted imaging): Essential for early detection of acute infarction
FLAIR/T2: Confirms lesion extent, evaluates chronic lesions
MRA: Evaluation of responsible vessels, confirmation of vascular stenosis/occlusion

The patient’s eye movement characteristics are observed with the naked eye to infer the disorder, and the diagnosis is confirmed with neuroimaging.

OCT (Optical Coherence Tomography)

Evaluation of retrograde trans-synaptic degeneration: After occipital lobe lesions, hemi-thinning of the retinal ganglion cell layer (GCL) and nerve fiber layer (RNFL) may be observed over months to years
More useful for follow-up in the chronic phase than in the acute phase, and serves as a means of confirming the lesion

Pupillary light reflex and pupil examination

Occipital lobe / optic radiation lesion: Pupillary light reflex is normal
Optic tract lesion: RAPD (Wernicke hemianopic pupil) may be observed. Light stimulation from the affected side reduces the pupillary light reflex

Q What is macular sparing? Why does it occur?

Macular sparing is a condition where central vision is preserved despite homonymous hemianopia. Nerve fibers from the macula terminate at the posterior end of the calcarine sulcus (occipital pole). In posterior cerebral artery infarction, the occipital pole is perfused by collateral circulation from the middle cerebral artery, so the visual cortex corresponding to the macula is often spared. The presence or absence of macular sparing is an important clue for estimating the lesion site.

5. Standard treatment

Treatment of homonymous hemianopia consists of two main pillars: treatment of the underlying disease and visual rehabilitation.

Acute Phase (Cerebrovascular Treatment Priority)

When caused by cerebrovascular disease, acute treatment by a neurologist or neurosurgeon takes priority. The ophthalmologist observes eye movements at the bedside and provides information to aid the attending physician’s decision-making.

Acute treatment of cerebral infarction:

Intravenous t-PA therapy (alteplase): Indicated within 4.5 hours of onset. Administer 0.6 mg/kg intravenously.
Mechanical thrombectomy: Indicated for large vessel occlusion.
Antiplatelet therapy: Aspirin, clopidogrel, etc.
Anticoagulation therapy: Indicated for cardiogenic embolism such as atrial fibrillation

Treatment of cerebral hemorrhage:

Hematoma evacuation (in indicated cases)
Strict blood pressure control

Chronic phase and rehabilitation

After acute treatment, chronic phase management centered on visual rehabilitation is performed.

Saccade training: Train saccadic eye movements toward the side of visual field loss to improve visual search on the affected side.
Prism glasses:
- Fresnel prisms: Shift visual information from the side of field loss to the intact side.
- Peli prisms: Attached to the outer edge of the visual field on the affected side to expand the field.
Visual field expansion training: Consciously practice moving gaze toward the side of field loss.

Daily living guidance

Safety measures when walking: Be aware of people/objects approaching from the affected side. Choose a path along the wall.
Reading aids: For left homonymous hemianopia, it is difficult to find the beginning of a line, so use a ruler or finger as a guide.
Driving eligibility: Homonymous hemianopia may not meet the visual field requirements (e.g., horizontal visual field of 150 degrees or more) stipulated by road traffic law.

Q Can I drive with homonymous hemianopia?

Homonymous hemianopia may not meet the visual field requirements stipulated by the Road Traffic Law (e.g., horizontal visual field of 150 degrees or more) and can be a disqualifying condition for a driver’s license. Driving suitability must be determined by the ophthalmologist and the public safety commission’s aptitude test. Self-judgment to continue driving should be avoided.

6. Pathophysiology and Detailed Mechanism of Onset

Anatomy of the Visual Pathway and Mechanism of Homonymous Hemianopia

Nerve fibers from the nasal half of the retina cross to the opposite side at the optic chiasm, while those from the temporal half run on the same side. After the optic chiasm, the right optic tract transmits information from the left visual field of both eyes, and the left optic tract from the right visual field. Therefore, a unilateral lesion in the visual pathway causes contralateral homonymous hemianopia.

Visual information from the optic radiations reaches the visual cortex in the calcarine sulcus. Fibers from the lower retina form the Meyer loop and enter the lower lip of the contralateral calcarine sulcus.

Meyer Loop and Course of the Optic Radiations

The optic radiation is a bundle of nerve fibers that runs from the lateral geniculate body to the visual cortex in the occipital lobe.

Superior fibers (dorsal pathway): Pass through the parietal lobe to reach the upper lip of the calcarine sulcus. They transmit information from the superior retina (inferior visual field).
Inferior fibers (Meyer’s loop): Make a large detour through the temporal lobe to reach the lower lip of the calcarine sulcus. They transmit information from the inferior retina (superior visual field), so temporal lobe lesions cause contralateral superior quadrantanopia.

Mechanism of Macular Sparing

The nerve fibers from the macula project to the posterior tip of the calcarine sulcus (occipital pole). The occipital pole receives collateral blood supply not only from the posterior cerebral artery but also from the middle cerebral artery. Even with occlusion of the posterior cerebral artery, the occipital pole is often preserved, maintaining central vision (macular sparing).

Nerve fibers from the macula terminate near the posterior tip of the calcarine sulcus (occipital pole). The preservation of the macula even in large occipital lobe lesions is largely due to this distribution. When central vision is preserved despite homonymous hemianopia, it is called macular sparing.

Retrograde trans-synaptic degeneration

After damage to the occipital visual cortex, retrograde degeneration from the lateral geniculate nucleus to retinal ganglion cells can occur over months to years. This is detected on OCT as hemiretinal thinning of the GCL and RNFL. This finding is useful for chronic phase evaluation of the lesion and aids in lesion localization.

Special features of optic tract lesions

Optic tract lesions have the following characteristics:

RAPD (relative afferent pupillary defect): Occurs with optic tract lesions because the pupillary light reflex pathway passes through the optic tract. In occipital lobe lesions, the pupillary light reflex remains normal.
Incongruous visual field defects: Due to intermixing of fibers within the optic tract, the shape of the visual field defect differs between the two eyes.
Macular splitting: The central visual field is split (opposite pattern to macular sparing)

7. Prognosis and Course

The prognosis of homonymous hemianopia depends on the underlying disease.

Possibility of Visual Field Recovery

Homonymous hemianopia due to occipital lobe infarction: Partial recovery may occur within weeks to months after onset
Complete visual field recovery is difficult: Visual field defects persist in many cases
Factors associated with better recovery:
- Incomplete hemianopia (more likely to recover than complete hemianopia)
- Early intervention after onset (first 1–3 months are the golden period for recovery)
- Relatively younger age at onset

Chronic phase adaptation

Unconscious saccade strategy: The patient unconsciously shifts gaze toward the blind side, improving adaptation in daily life.
Long-term impact on QOL: Reading difficulties, collisions while walking, and driving restrictions become long-term issues.

8. Latest Research and Future Prospects (Research-stage Reports)

Research on Visual Field Recovery Mechanisms

Research on the natural recovery mechanisms and prognostic factors of homonymous hemianopia after stroke is progressing from the perspective of neuroplasticity. Identification of biomarkers for cortical reorganization involved in visual field recovery is being attempted, and the construction of recovery prediction models is expected.

Evaluation by OCT/OCT-A

Research is progressing on quantitative evaluation of retrograde trans-synaptic degeneration after occipital lobe lesions using OCT/OCT-A. Studies continue to investigate whether thinning patterns of GCL and RNFL can serve as indicators for lesion site estimation and prognosis prediction.

Evidence for Visual Rehabilitation

Multiple RCTs have been conducted on the effectiveness of saccade training and prism therapy, and evidence is accumulating. However, the quality of evidence for intervention effects varies at present, and a standard protocol has not yet been established.

Non-invasive Brain Stimulation Methods

Attempts at visual field recovery using transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) have been reported. Research continues at the study stage as neural rehabilitation utilizing plasticity of the visual cortex.

9. References

Rowe FJ, Wright D, Brand D, et al. A Prospective Profile of Visual Field Loss following Stroke: Prevalence, Type, Rehabilitation, and Outcome. BioMed Research International. 2013;2013:719096. PMID: 24089687. PMCID: PMC3782154. https://pmc.ncbi.nlm.nih.gov/articles/PMC3782154/
Gilhotra JS, Mitchell P, Healey PR, Cumming RG, Currie J. Homonymous visual field defects and stroke in an older population. Stroke. 2002;33(10):2417-2420. PMID: 12364731. https://pubmed.ncbi.nlm.nih.gov/12364731/
Goodwin D. Homonymous hemianopia: challenges and solutions. Clinical Ophthalmology. 2014;8:1919-1927. PMID: 25284978. PMCID: PMC4181645. https://pmc.ncbi.nlm.nih.gov/articles/PMC4181645/
Glisson CC. Visual Loss Due to Optic Chiasm and Retrochiasmal Visual Pathway Lesions. Continuum (Minneapolis, Minn). 2014;20(4 Neuro-ophthalmology):907-921. PMID: 25099100. PMCID: PMC10564022. https://pmc.ncbi.nlm.nih.gov/articles/PMC10564022/
Giorgi RG, Woods RL, Peli E. Clinical and Laboratory Evaluation of Peripheral Prism Glasses for Hemianopia. Optometry and Vision Science. 2009;86(5):492-502. PMID: 19357552. PMCID: PMC2680467. https://pmc.ncbi.nlm.nih.gov/articles/PMC2680467/
Sahraie A, Cederblad AMH, Kenkel S, Romano JG. Efficacy and predictors of recovery of function after eye movement training in 296 hemianopic patients. Cortex. 2020;125:149-160. PMID: 31982700. https://pubmed.ncbi.nlm.nih.gov/31982700/
Hokazono K, Monteiro MLR. Homonymous quadrantic macular ganglion cell complex loss as a sign of trans-synaptic degeneration from occipital lobe lesion. American Journal of Ophthalmology Case Reports. 2018;13:76-79. PMID: 30582077. PMCID: PMC6299126. https://pmc.ncbi.nlm.nih.gov/articles/PMC6299126/

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