Bitemporal, homonymous and monocular field defects

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The visual field describes the area seen while the eyes remain directed towards a fixed target. Its pattern often localises disease more accurately than a nonspecific complaint of blurred vision. Information from each eye passes through the optic nerve, is partially crossed at the chiasm and then reaches the opposite hemisphere for each half of visual space. Testing the two eyes separately reveals whether the disturbance is monocular, bitemporal or homonymous.

Localisation and urgency are separate judgements. A slowly progressive bitemporal defect and a sudden homonymous defect both demand investigation, but their likely causes and immediate pathways differ. Normal central acuity does not exclude a substantial field deficit, and a patient may adapt by turning the head or omit the missing region from awareness. Ask about collisions, reading difficulty, missing food on one side of the plate and problems navigating familiar spaces.

Key points

Monocular field loss usually localises to the retina or optic nerve before the chiasm.
Bitemporal loss suggests optic-chiasm dysfunction and requires assessment for a sellar or suprasellar lesion.
A homonymous defect affects the same side of visual space in both eyes and localises behind the chiasm on the opposite side.
Patients may describe a homonymous defect as loss in one eye; testing each eye separately is essential.
Resolved sudden monocular or homonymous loss can be a TIA and still requires immediate referral for assessment within twenty-four hours.
For suspected TIA, NICE recommends aspirin 300 mg daily immediately unless contraindicated; persistent suspected stroke follows a different imaging-led acute pathway.
Formal fields document the deficit, but emergency referral must not wait for a scheduled visual-field machine test.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Prechiasmal ocular disease

Retinal vascular disease, detachment and optic-nerve injury can produce monocular field loss. The particular pattern reflects which retinal region or optic-nerve fibres are damaged, while time course helps distinguish acute from chronic causes.

Chiasmal compression

Sellar or suprasellar masses may compress crossing visual fibres and create bitemporal loss. Pituitary hormone disturbances or sudden haemorrhage into a lesion can add systemic and ocular motor features.

Retrochiasmal brain disease

Stroke, tumour, inflammation and trauma can interrupt visual pathways beyond the chiasm. These lesions generally affect the same side of visual space in both eyes, opposite to the damaged hemisphere.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Partial crossing at the chiasm
Fibres from the nasal retina cross to the opposite side while temporal retinal fibres remain uncrossed. The crossing arrangement brings information from the same half of visual space together beyond the chiasm.
2
Temporal fields and nasal retina
The outer visual fields project onto the nasal halves of the retinas. Compression involving their crossing fibres therefore produces temporal field loss in both eyes, although real defects may be asymmetric or incomplete.
3
Retrochiasmal organisation
Each optic tract, radiation and visual cortex carries information about the opposite half of space from both eyes. Injury can therefore preserve central acuity while removing a corresponding hemifield or quadrant.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Monocular loss before the chiasm

Check whether a missing area remains confined to one eye when tested separately. Retinal detachment, retinal vascular occlusion, glaucoma and optic neuropathy can create monocular defects. Pain, flashes, floaters, disc findings and an afferent pupil defect help distinguish causes but do not remove urgency from sudden loss.

Bitemporal loss at the chiasm

Loss of the outer field in each eye suggests involvement of crossing fibres. Ask about headache, menstrual or sexual changes, galactorrhoea, altered facial or hand size and symptoms of hormone deficiency. Pituitary lesions can progress gradually enough for substantial loss to go unnoticed.

Homonymous loss behind the chiasm

The same right or left half of space is missing with either eye tested alone. A left-sided brain lesion generally affects the right visual field and vice versa. Sudden onset raises concern for stroke, including an occipital stroke with few other obvious neurological signs.

Time course and associated phenomena

Establish whether the deficit was maximal at onset, gradually enlarged, fluctuated or fully resolved. Spreading shimmering visual symptoms can suggest migraine aura, but an abrupt negative curtain, persistent missing field or accompanying weakness requires assessment for ischaemia or another structural cause.

Attention and awareness

Assess whether the patient notices the missing field and explores that side of space. Visual neglect can coexist with a hemianopia and increase functional danger. A normal conversation or ability to read selected chart letters does not establish safe mobility or driving.

Red flags requiring action

Abrupt persistent loss of one side of the visual world requires emergency stroke assessment even when speech and limb strength are normal.
Severe sudden headache with visual loss, diplopia, reduced consciousness or hypotension requires urgent assessment for pituitary apoplexy and other intracranial emergencies.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Immediate bedside visual and neurological examinationFirst step
Why
Localise the deficit and identify emergency pathways without waiting for formal testing.
Interpretation and limitations
Measure acuity in each eye, pupils, confrontation fields, eye movements and relevant neurological signs. Record onset or last-known-well time. A reproducible homonymous pattern supports retrochiasmal disease but does not by itself establish whether the lesion is ischaemic, haemorrhagic or another cause.
02
Urgent brain imaging for acute persistent neurological loss
Why
Identify stroke or another intracranial lesion and guide time-sensitive treatment.
Interpretation and limitations
Use the acute stroke pathway and appropriate CT, vascular imaging or MRI selected by the receiving team. Do not delay emergency assessment because central acuity is good or the field defect is the only recognised deficit.
03
Formal perimetry with ophthalmic structural assessment
Why
Map the extent of loss and establish a reproducible baseline for follow-up.
Interpretation and limitations
Automated or kinetic fields should be interpreted alongside fixation, reliability, acuity and the optic-disc or retinal examination. An unreliable field requires careful reassessment; it should not be used to dismiss a consistent emergency history.
04
Pituitary MRI and endocrine assessment
Why
Investigate chiasmal compression and associated hormone excess or deficiency.
Interpretation and limitations
MRI defines the relationship of a sellar lesion to the optic nerves and chiasm. Severe headache, reduced consciousness, hypotension or rapidly worsening vision changes this from a routine mass investigation to an emergency apoplexy assessment, including urgent consideration of cortisol deficiency.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Migraine visual aura

A typical aura often spreads gradually with positive shimmering phenomena and then resolves. First, atypical, strictly monocular or persistent symptoms require assessment for vascular, retinal or structural alternatives before reassurance.

Visual neglect

Impaired attention to one side of space can coexist with or resemble a field deficit after brain injury. Examination of awareness and exploration helps distinguish attention failure from loss of visual input.

Unreliable perimetry

Poor fixation, fatigue, misunderstanding and reduced attention can distort a formal field test. Correlation with bedside examination, repeat testing and structural findings is necessary before accepting or dismissing a neurological pattern.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01EmergencySudden persistent visual-field lossFirst stepA new monocular or homonymous deficit remains present or accompanies acute neurological symptoms.

1Activate emergency assessment, document symptom timing and ensure the patient does not drive to hospital.
2Distinguish monocular from homonymous loss at the bedside while preserving rapid access to stroke and ophthalmic expertise.
3Arrange cause-appropriate imaging or urgent dilated retinal examination through the receiving team.
4If severe headache and chiasmal or ocular motor signs suggest pituitary apoplexy, involve endocrinology and neurosurgery immediately and stabilise circulation.

02UrgentResolved suspected visual TIAA sudden negative visual deficit has completely resolved and a retinal or cerebral ischaemic event is suspected.

1Offer aspirin 300 mg orally daily immediately unless contraindicated and refer immediately for specialist assessment within twenty-four hours of symptom onset.
2Do not use a low ABCD2 score or symptom resolution to lower referral urgency.
3Assess for giant-cell arteritis in the appropriate older patient and arrange simultaneous urgent treatment if that diagnosis is suspected.
4After specialist confirmation, establish cause-specific vascular prevention and a clear plan for any recurrent or persistent symptoms.

03SpecialistProgressive chiasmal or established field deficitA non-acute field abnormality suggests compression or remains after the acute cause has been treated.

1Arrange ophthalmic assessment, formal fields and imaging matched to the suspected anatomical site.
2Coordinate endocrine and neurosurgical review when a sellar lesion affects vision or hormone function.
3Provide rehabilitation focused on scanning, reading, safe mobility and practical adaptation to the missing field.
4Advise cessation of driving until assessment; homonymous and complete bitemporal defects require DVLA notification in Great Britain and assessment against the visual-field standards. Northern Ireland licence holders use the DVA medical process.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Reduce early vascular risk when a resolved episode is clinically suspected to be a TIA.

Aspirin for suspected TIA

Give 300 mg orally once daily immediately unless contraindicated, pending urgent specialist assessment and the resulting secondary-prevention plan.

Check hypersensitivity, active bleeding and other relevant contraindications. This recommendation must not be transferred uncritically to persistent suspected stroke before haemorrhage has been excluded; discuss current anticoagulant treatment and bleeding risk urgently.

Provide urgent glucocorticoid cover in suspected apoplexy with haemodynamic instability, altered consciousness, reduced acuity or severe field loss.

Hydrocortisone for emergency pituitary apoplexy

The Society for Endocrinology emergency guidance includes 100 mg intramuscularly immediately, followed by 50–100 mg intramuscularly every six hours; continued route and dosing are directed by the emergency endocrine team.

Take endocrine blood samples before treatment if this causes no delay. Stabilise fluids and electrolytes, monitor glucose and blood pressure, and arrange urgent specialist care; steroid administration does not replace assessment for neurosurgical treatment.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Mobility and driving risk

Missing peripheral information can lead to collisions, falls and failure to detect traffic. The danger may be greater when the patient lacks awareness of the deficit or has associated neglect.

Permanent visual loss

Retinal infarction, optic-pathway stroke and prolonged chiasmal compression can leave lasting deficits. Rapid recognition of treatable causes and appropriate rehabilitation help preserve remaining function and reduce disability.

Endocrine collapse in apoplexy

Acute pituitary injury can impair cortisol production alongside visual-pathway compression. Hypotension and altered consciousness may therefore require urgent glucocorticoid replacement and resuscitation as well as neurological and ophthalmic assessment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat formal fields and acuity according to the cause and speed of change, retaining comparable tests to distinguish recovery from measurement variability.
For pituitary disease, link visual review with endocrine results and imaging because tumour control, hormonal function and field recovery can change independently.
Assess navigation, reading, falls, work demands and visual neglect, with rehabilitation tailored to the tasks the patient actually finds difficult.
After a suspected TIA or stroke, confirm completion of vascular assessment and prevention, and reinforce emergency action for recurrent symptoms.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

One eye may be an inaccurate description

A patient with right homonymous loss may feel that the right eye is responsible because the missing right temporal field is particularly noticeable. Ask them to describe the view with each eye covered rather than relying on the initial label.

Normal acuity can conceal major loss

A person may read the centre of a visual chart while missing most of one side of space. Acuity and field testing answer different questions, and neither can substitute for assessment of attention and functional navigation.

Quadrants refine but do not prove localisation

An upper homonymous quadrantic defect can reflect temporal optic-radiation involvement, while a lower defect can reflect parietal involvement. Real lesions and incomplete defects vary, so imaging must test the anatomical hypothesis.

Rehabilitation compensates for a deficit

Scanning strategies, reading adaptations and selected prisms can improve practical function. Explain their purpose without promising restoration of damaged visual pathways, and reassess associated neglect or cognitive difficulty that may limit benefit.

11Common pitfallsFrequent interpretation and management errors.

01
Reassuring a patient with sudden isolated hemianopia because there is no facial droop or arm weakness.
02
Labelling a transient monocular curtain as migraine without assessing retinal ischaemia or arteritis.
03
Using normal central acuity to exclude chiasmal compression or significant visual disability.
04
Waiting for formal perimetry before referring an acute persistent field defect.