Transient Loss of Vision

Etiology

The term "transient vision loss" is reserved for episodes of reversible visual loss lasting less than 24 hours.[3] Loss can be monocular or binocular. Transient monocular vision loss is commonly caused by a lesion anterior to the chiasm at the level of the eyes or optic nerve. Common causes of monocular transient vision loss include thromboembolic or stenotic vascular diseases, vasospasm, retinal migraine, closed-angle glaucoma, and papilledema. "Amaurosis fugax" is a term used to denote transient monocular vision loss attributed to ischemia or vascular etiology.[9]

Binocular vision loss could be of chiasmal or retro-chiasmal origin or be due to the bilateral involvement of the eyes or optic nerves. Bilateral TVL may be caused by occipital epilepsy, complex migraines, papilloedema, and hypoperfusion. TVL is a symptom with various ocular, vascular, neurological, and systemic etiologies. Understanding these causes is crucial for effective management and prevention of permanent visual impairment.[9]

Ocular Causes

• Amaurosis fugax: This condition is a temporary loss of vision in one eye caused by impeded blood flow to the retina. This obstruction is typically caused by an embolus originating from the carotid artery or heart, leading to retinal ischemia.
• Papilledema: Increased intracranial pressure can cause swelling of the optic disc, leading to transient vision loss. This condition is often associated with headaches and other neurological symptoms.
• Optic neuritis: Inflammation of the optic nerve can lead to sudden, temporary vision loss, often accompanied by pain during eye movement. Optic neuritis is commonly associated with multiple sclerosis.
• Retinal artery occlusion: Sudden occlusion of the central or branch retinal artery can cause transient or permanent vision loss, depending on the duration and extent of the obstructed blood flow.
• Retinal vein occlusion: Obstructed flow through the retinal veins can lead to retinal hemorrhage, ischemia, and accompanying transient visual disturbances.[11]

Vascular Causes

• Transient ischemic attack: TIAs can affect the visual pathways, causing temporary visual loss. These attacks are often precursors to strokes and require immediate medical attention.
• Giant cell arteritis: An inflammatory disease of the blood vessels that can cause optic nerve head ischemia and transient vision loss. Prompt diagnosis and treatment with corticosteroids are essential to prevent permanent loss.[12]

Neurological Causes

• Migraine with aura: Migraines can cause visual auras, including transient vision loss, flashing lights, or zigzag patterns. These symptoms typically precede the headache phase of a migraine.
• Seizures: Occipital lobe seizures can manifest as transient vision loss and are often accompanied by other neurological symptoms.
• Intracranial tumors: Tumors affecting the visual pathways can cause transient vision loss due to compression or vascular compromise.[13]

Mechanical Causes

• Elevated intraocular pressure: Conditions such as acute angle-closure glaucoma can cause transient vision loss due to sudden elevation of intraocular pressure.
• Positional factors: Certain head positions or activities that increase intra-thoracic pressure (Valsalva maneuver) can lead to transient vision loss due to changes in blood flow to the optic nerve or retina.[14]

Systemic Causes

• Hypotension: Systemic hypotension, especially when standing up quickly (orthostatic hypotension), can reduce blood flow to the brain and eyes, causing transient vision loss.
• Cardiac arrhythmias: Irregular heart rhythms can lead to episodic cerebral perfusion reductions, manifesting as transient vision loss.
• Anemia: Severe anemia can reduce oxygen delivery to the retina and optic nerve, leading to transient visual disturbances.[15]

Miscellaneous Causes

• Medication side effects: Certain medications, such as blood pressure or anticoagulant drugs, can cause transient vision loss as a side effect.
• Systemic diseases: Conditions like diabetes and hypertension can predispose individuals to vascular events affecting the eyes, which may involve transient vision loss.

Prompt identification and treatment of the underlying cause are crucial to prevent permanent visual impairment and other serious complications. A comprehensive evaluation, including a detailed history and appropriate diagnostic testing, is essential for accurate diagnosis and effective management of TVL.[16]

Epidemiology

TVL is a clinical symptom with multiple causes; the most concerning is retinal ischemia. Study results have shown that patients with monocular TVL associated with atheromatous carotid artery disease have a 1-year risk of recurrent stroke of 2%. In patients with associated severe internal carotid artery stenosis, the risk of ipsilateral stroke rises to 16% after 3 years. A proper assessment and urgent intervention are critical for patients presenting with TVL, especially due to vascular causes.[1] TVL can manifest in patients of various ages, sexes, and geographic regions. Understanding the epidemiological patterns associated with TVL helps identify at-risk populations and improve diagnostic and therapeutic strategies.[5]

Frequency in the United States

TVL is relatively common in the United States and is often associated with vascular and neurological conditions. The prevalence varies based on the underlying cause:

• Amaurosis fugax: This condition is characterized by temporary monocular vision loss due to retinal ischemia and is commonly seen in individuals with carotid artery disease. Amaurosis fugax predominantly affects adults older than 50 and is slightly more common in men due to a greater prevalence of vascular risk factors in this patient population.
• Migrainous visual auras: Migraines occur in approximately 12% of the population, with a higher prevalence in women. Migraines often begin in adolescence or early adulthood, peaking in individuals 30 to 39 years old.
• Optic neuritis: Inflammation of the optic nerve is more common in adults aged 20 to 40 and has a higher incidence in women. This condition is often associated with multiple sclerosis, with an incidence of 5 per 100,000 people annually.[17]

Frequency Worldwide

Globally, the epidemiology of TVL mirrors the United States, with variations based on the prevalence of underlying conditions and healthcare access:

• Vascular: Amaurosis fugax and other ischemic causes of TVL are prevalent worldwide, particularly in regions with high rates of cardiovascular disease. Countries with aging populations, such as Japan and many European nations, report higher incidences due to the increased prevalence of atherosclerosis.
• Neurological: Migraines are a significant cause of TVL globally, affecting approximately 1 billion people. The prevalence of migraines demonstrates regional variations, with higher rates reported in Europe and North America compared to Africa and Asia.
• Infectious and inflammatory: Conditions like optic neuritis may have different prevalence rates globally due to variations in the incidence of multiple sclerosis and other autoimmune diseases. Higher rates of optic neuritis are reported in northern Europe and North America compared to Asia and Africa.[18]

Age and Sex Distribution

• Age: TVL can occur at any age but is more frequently reported in middle-aged and older adults due to the higher prevalence of vascular diseases in these age groups. However, conditions like migraines and optic neuritis are more common in younger populations.
• Sex: The sex distribution of TVL varies with the underlying cause. Migraines are a leading cause of TLOV and occur more commonly in women. In contrast, amaurosis fugax and other ischemic events are slightly more common in men due to the higher prevalence of cardiovascular risk factors.[19]

Global Health Impact

Transient vision loss can significantly impact a patient's quality of life and functioning, particularly when recurrent. TVL is often a warning sign of more severe underlying conditions, necessitating a thorough medical evaluation and appropriate management. The global burden of TVL is closely linked to the prevalence of its underlying causes, such as cardiovascular diseases, migraines, and neurological disorders. In regions with limited access to healthcare, the impact of TVL can be more pronounced due to delayed diagnosis and management, leading to higher rates of complications and permanent vision loss. Public health initiatives focusing on the prevention and early detection of vascular and neurological diseases are crucial in reducing the burden of TVL globally. TVL's prevalence is determined by the underlying causes, which vary with age, sex, and regional health profiles. Understanding the epidemiology of TVL is essential for developing targeted interventions to reduce its incidence and associated morbidity.[20]

Pathophysiology

Underlying conditions can cause the symptoms of transient visual loss, including thromboembolism originating from the internal carotid artery, heart, or aorta and local thrombosis of the blood vessels supplying the retina or optic nerve.[2][3] An embolus can also originate from a non-atheromatous carotid artery disease, like a dissection. Other causes include hypoperfusion, vasospasm, hypercoagulable states, giant cell arteritis, retinal migraine, and impending central retinal vein occlusion (CRVO).[21] These conditions cause hypoperfusion of the optic disc or retina. TVL may also be seen in patients with optic disc edema, orbitopathies, glaucoma, and even dry eye disease.

Transient vision loss often arises from a temporary disruption in blood flow to the retina or optic nerve, leading to ischemia and impaired visual function. Visual loss in patients with TVL typically occurs abruptly and is often accompanied by other neurological or systemic symptoms depending on the underlying cause.[22] Common pathophysiological mechanisms include embolic events, vasospasm, and inflammatory processes. In amaurosis fugax, for instance, emboli from carotid artery stenosis can transiently obstruct the central retinal artery, causing brief episodes of monocular blindness. Disrupted visual processing in patients with aura migraines occurs due to cortical spreading depression, a wave of neuronal and glial depolarization that causes a temporary suppression of brain activity. Additionally, optic neuritis involves demyelination and inflammation of the optic nerve, leading to episodic visual impairment.

Histopathology

Histopathological examination of biopsy samples from patients with transient vision loss typically reveals findings related to the underlying etiology, which may be vascular, inflammatory, or degenerative. For embolic causes, microscopy may show cholesterol crystals or fibrin-platelet aggregates within retinal arteries. For conditions like optic neuritis, analysis often reveals inflammatory infiltrates within the optic nerve, including lymphocytes and macrophages. Demyelination and axonal loss may also be evident, especially given the association with multiple sclerosis. Transient vascular changes may occur in patients with vasospastic conditions like migraines, although these are less commonly observed.[2]

History and Physical

History

Obtaining a detailed history is crucial when assessing a patient with TVL. Information regarding timing, pattern, provoking factors, and associated symptoms can help determine the cause of an episode involving transient vision loss.[3] Patients may describe sudden, temporary episodes of vision loss, which may last seconds to minutes. Vision loss might affect one or both eyes and can be partial or complete. Critical historical points to consider include: [5]

• Onset and duration: Accurate determination of the onset (sudden or gradual) and duration of vision loss is critical. Transient episodes typically last a short period, often less than 24 hours.
• Associated symptoms: Clinicians should ask about accompanying symptoms such as headache, eye pain, nausea, neurological symptoms (eg, weakness, numbness), and systemic symptoms (eg, fever, weight loss).
• Precipitating factors: Participation in activities or states that precipitate vision loss, such as physical exertion, stress, exposure to bright light, or changes in posture, should be documented.
• Medical history: A comprehensive medical history should be obtained, including cardiovascular risk factors (eg, hypertension, diabetes, hyperlipidemia), migraines, strokes or transient ischemic attacks, autoimmune disease, and recent infections.
• Medication use: The patient's current medications, particularly anticoagulants, antiplatelets, and any new medications that might cause ocular side effects, should be documented.
• Family history: A family history of similar symptoms or relevant conditions such as migraines, cardiovascular disease, or autoimmune disorders may prove beneficial.[5]

Physical Examination

A thorough physical examination is essential to assess the potential causes of TVL. The examination should include:

• Visual acuity: Each eye should be measured separately. The clinician should document any observable differences between the eyes and the extent of the patient's vision loss.
• Pupillary response: Size, shape, and reactivity to light should be assessed. An afferent pupillary defect is suggestive of optic nerve pathology.
• Fundoscopic examination: The retina and optic nerve head should be examined in detail. Clinicians should look for signs of retinal emboli, optic disc swelling, or other abnormalities.
• Neurological examination: Relevant deficits may only be observed during a comprehensive neurological examination, including assessing cranial nerves, motor and sensory function, coordination, and reflexes.
• Cardiovascular examination: The patient's blood pressure, heart rate, and any signs of carotid artery disease (eg, bruits) should be documented.
• Temporal artery examination: Tenderness or thickening noted while palpating the temporal arteries of an older patient suggests giant cell arteritis.[23]

By systematically gathering a detailed history and performing a thorough physical examination, clinicians can narrow down the differential diagnosis and identify the underlying cause of transient vision loss, guiding appropriate diagnostic testing and management.

Emboli 

The patient usually describes a curtain of darkness that rises or falls in 1 eye and lasts 20 to 30 minutes. TVL can occur due to embolic occlusion of the blood vessels supplying the retina, optic disc, or choroid. The emboli may consist of cholesterol, platelet-fibrin, or calcium and may be visible during an ophthalmoscopic examination. The presence of an embolus is an indication of a thorough vascular and cardiac evaluation.[24]

Retinal Vein Occlusion 

TVL is known to precede a central retinal vein occlusion. These episodes last 2 to 4 hours and are described as a visual "cloudiness" by the patient. Ophthalmoscopy demonstrates engorged retinal veins.[25]

Giant Cell Arteritis 

TVL commonly manifests in patients with giant cell arteritis. The visual loss typically lasts 2 to 4 minutes. Episodes may be postural, recur many times, and be accompanied by flashes or streaks of light (photopsia), headaches, jaw claudication, scalp tenderness, or fever.[21]

Ocular Ischemic Syndrome 

Unlike an embolism, the visual symptoms of carotid artery disease have a gradual onset and last seconds to minutes. They are often precipitated by exposure to bright light. Other signs of ocular ischemic syndrome include dilated conjunctival and episcleral vessels, an anterior chamber reaction, narrow retinal arteries, and dilated retinal veins.[26]

Hypoperfusion 

TVL caused by reduced cardiac output or systemic hypotension is characteristically binocular and may be accompanied by lightheadedness and confusion.[27]

Retinal Migraine

The International Headache Society criteria for diagnosing a retinal migraine require at least 2 attacks of fully reversible monocular positive visual phenomena (eg, flashing lights, scintillating scotoma) or negative symptoms associated with migraine without aura. The visual loss typically lasts 5 to 20 minutes and may recur several times in the same day.[28]

Retinal Vasospasm

Episodes of TVL in retinal vasospasm are similar to a retinal migraine but without the associated headache. Relative afferent pupillary defect may be associated, or retinal vasospasm may be seen using ophthalmoscopy during the attack. Other conditions associated with TVL include hypercoagulable states, orbitopathies, and dry eye disease.[29]

Evaluation

Objective testing also provides vital diagnostic information for patients with transient vision loss. Carotid Doppler ultrasound, computed tomography and magnetic resonance-guided angiography, conventional angiography, and cardiac echocardiography may aid localization of an embolus. The patient should also be evaluated systemically for hypertension, diabetes, and dyslipidemia. Retinal vein occlusion warrants additional evaluation for hypercoagulable and hyperviscosity states. Suspicion for giant cell arteritis warrants initial laboratory testing (ie, erythrocyte sedimentation count, C-reactive protein, platelet count) and confirmation by temporal artery biopsy.[30]

Patients with altitudinal TVL are likely to have a cardiac or carotid embolus compared to those with a diffuse or constricting pattern of visual loss.[1] Anterior segment examination may show dilated conjunctival and episcleral blood vessels, anterior chamber inflammation, and even iris neovascularization in patients with ocular ischemic syndrome. Determining the cause of transient vision loss may be aided by the following:

Laboratory Testing

• Complete blood count: This test is to detect anemia, infection, or inflammation that may contribute to vision loss.[31]
• Erythrocyte sedimentation rate and C-reactive protein: This test identifies inflammatory conditions such as giant cell arteritis.[32]
• Blood glucose levels: The blood glucose level helps rule out diabetic retinopathy or other diabetes-related complications.[33]
• Lipid profile: This test assesses for hyperlipidemia, a risk factor for vascular occlusive events.[34]
• Coagulation studies: Prothrombin time, activated partial thromboplastin time, and international normalized ratio to identify clotting disorders aid in finding the cause of TVL.[35]
• Antinuclear antibodies and rheumatoid factor: This test is used to investigate autoimmune conditions that might cause vasculitis.[36]
• Specific antibodies: Antibodies such as anti-cardiolipin antibodies or lupus anticoagulants for antiphospholipid syndrome help determine the cause of TVL.[37]

Radiographic and Imaging Studies

• Magnetic resonance imaging of the brain and orbits: Evaluates for structural brain abnormalities, optic neuropathy, or demyelinating disease [38]
• Magnetic resonance angiography or computed tomography angiography: Assesses cerebral and ocular vasculature for occlusions, aneurysms, or stenosis [39]
• Carotid Doppler ultrasound: Detects carotid artery stenosis, which could lead to transient ischemic attacks and affect vision [40]
• Optical coherence tomography: Visualize retinal layers and detect conditions like retinal detachment or macular degeneration [41]
• Fundus fluorescein angiography: Evaluates retinal and choroidal circulation for signs of vascular occlusion or leakage [42]

Other Diagnostic Tests

• Electrocardiogram: Identifies cardiac arrhythmias or myocardial infarction, which might contribute to embolic events [43]
• Echocardiogram: Detects cardiac sources of emboli, such as atrial thrombi or valvular heart disease [44]
• Holter monitoring: Used for patients with suspected cardiac arrhythmias contributing to transient vision loss [45]

Guidelines

The American Academy of Ophthalmology (AAO) and the European Society of Ophthalmology (ESO) provide the following national and international guidelines for assessing patients with transient vision loss. Adhering to these comprehensive evaluation guidelines allows clinicians to systematically identify and manage the underlying causes of transient vision loss, ensuring optimal patient outcomes.[46]

National Guidelines, AAO

• Initial Evaluation: A comprehensive ophthalmic examination, including visual acuity, pupillary reactions, intraocular pressure, and slit-lamp examination, is recommended.
• Imaging: Optical coherence tomography (OCT), computed tomography (CT), magnetic resonance imaging /magnetic resonance angiography (MRI/MRA), or computed tomography angiography, as indicated based on clinical suspicion of underlying causes, are recommended.
• Referral: Refer the patient to neurologists or cardiologists if systemic vascular or neurological conditions are suspected.[47]

International Guidelines, ESO

• Initial evaluation: Laboratory testing of erythrocyte sedimentation rate, C-reactive protein, complete blood count, and glucose levels is recommended.
• Imaging: Immediate MRI or OCT for acute presentation with visual disturbances is recommended.
• Follow-up: Regular monitoring and follow-up imaging are recommended for patients with identified risk factors, such as carotid artery stenosis or cardiac anomalies.

Treatment / Management

Determining whether a TVL episode is due to a high-risk or low-risk cause significantly influences the patient's prognosis. Managing embolic TVL requires treating the underlying cause; therapy for patients with a cardiac source includes anticoagulation and proper management of the underlying cardiac cause. Internal carotid artery stenosis may be managed with antiplatelet therapy, systemic risk factor reduction, carotid endarterectomy, or stenting. Giant cell arteritis is treated with corticosteroid therapy. Retinal vasospasm could be treated with aspirin or calcium channel blockers. A retinal migraine is managed with conventional migraine therapy. Angle-closure glaucoma is also managed with standard therapy.[48]

Managing TVL primarily hinges on identifying and addressing the underlying cause. This approach involves a combination of medical, surgical, and supportive interventions tailored to the specific etiology. A comprehensive overview of medical, surgical, and other interventions is provided below.[5]

Medical Interventions

• Antiplatelet:
• Indication: Transient ischemic attacks or retinal artery occlusion
• Medications: Aspirin, clopidogrel, or a combination of both
• Guidelines: Provided by the American Heart Association (AHA) and American Stroke Association (ASA) for secondary stroke prevention [49]
• Anticoagulation:
• Indication: Atrial fibrillation or other cardiac emboli
• Medications: Warfarin, dabigatran, rivaroxaban, or apixaban
• Guidelines: AHA and ASA suggest anticoagulation for stroke prevention in patients with atrial fibrillation [50]
• Blood Pressure:
• Indication: Hypertension is a risk factor (eg, cerebrovascular events)
• Medications: Angiotensin-converting-enzyme inhibitors, angiotensin receptor blockers, β-blockers, calcium channel blockers, diuretics
• Guidelines: Targeting blood pressure (per Joint National Committee 8 or ACC/AHA guidelines) reduces stroke risk [51]
• Lipid-lowering:
• Indication: Hyperlipidemia contributing to atherosclerosis
• Medications: Statins (eg, atorvastatin, rosuvastatin)
• Guidelines: ACC/AHA cholesterol guidelines recommend statin therapy if at risk for cardiovascular events [52]
• Anti-inflammatory:
• Indication: Conditions like giant cell arteritis
• Medications: High-dose corticosteroids (eg, prednisone)
• Guidelines: American College of Rheumatology recommends immediately initiating corticosteroids to prevent vision loss [53]

Surgical Interventions

• Carotid endarterectomy:
• Indication: Significant carotid artery stenosis
• Procedure: Surgical removal of atherosclerotic plaque from the carotid artery
• Guidelines: Recommended by AHA/ASA for patients (symptomatic) with 70% to 99% stenosis [54]
• Endovascular procedures:
• Indication: Alternative to carotid endarterectomy for patients at high surgical risk
• Procedure: Carotid artery stenting
• Guidelines: Provider consideration based on the patient's risk profile and anatomical suitability [55]
(A1)

Other Interventions

• Intravitreal injection:
• Indication: Retinal vein occlusion or macular edema
• Medications: Anti-vascular endothelial growth factor, agents (eg, ranibizumab, aflibercept), corticosteroids
• Guidelines: Recommended by the American Academy of Ophthalmology [56]
• Ocular surface protection:
• Indication: Ocular surface disease
• Medications: Lubricating eye drops, punctal plugs
• Guidelines: Recommended by AAO for dry eye conditions [57]
• Laser therapy:
• Indication: Retinal tears or diabetic retinopathy
• Procedure: Panretinal photocoagulation or focal laser treatment
• Guidelines: Recommended by AAO for proliferative diabetic retinopathy [58]
(A1)

National and International Guidelines

• American Academy of Ophthalmology provides comprehensive guidelines for diagnosing and managing ocular conditions leading to transient vision loss.
• American Heart Association/American Stroke Association provides guidelines on managing cerebrovascular risk factors, including hypertension, hyperlipidemia, and anticoagulation.
• European Society of Cardiology offers recommendations on cardiovascular risk management, including treating artery disease and atrial fibrillation.[59]

Prompt identification and management of the underlying causes of transient vision loss are crucial to prevent permanent visual impairment and other serious complications. Regular follow-up and adherence to national and international guidelines ensure evidence-based and effective management of this complex condition.[5]

Differential Diagnosis

Clinicians evaluating patients with transient vision loss should consider the following differential diagnoses:

• Central retinal artery occlusion
• Central retinal vein occlusion [60]
• Corneal abrasion [61]
• Dry eye syndrome [62]
• Giant cell arteritis
• Migraine headache with aura [63]
• Multiple sclerosis
• Orbital masses
• Partial epilepsies
• Sickle cell disease
• Idiopathic intracranial hypertension
• Amaurosis fugax
• Transient ischemic attack 
• Optic neuritis
• Retinal detachment [64]
• Papilledema
• Vitreous hemorrhage
• Hypoglycemia
• Drug-induced vision changes
• Acute angle-closure glaucoma
• Ocular ischemic syndrome
• Posterior reversible encephalopathy syndrome 
• Epileptic seizure 
• Anterior ischemic optic neuropathy 
• Posterior ischemic optic neuropathy 
• Retinal migraine
• Leber's hereditary optic neuropathy 
• Non-arteritic anterior ischemic optic neuropathy 
• Functional vision loss (psychogenic)
• Carotid artery dissection
• Intracranial hypertension
• Vertebrobasilar insufficiency
• Central serous chorioretinopathy
• Homonymous hemianopia (due to stroke or brain tumor)
• Optic chiasm lesion (eg, pituitary adenoma)
• Toxic optic neuropathy (eg, methanol poisoning)
• Vascular occlusion (branch retinal artery occlusion)
• Posterior uveitis
• Idiopathic intracranial hypertension (pseudotumor cerebri)
• Optic disc drusen
• Sarcoidosis affecting the optic nerve
• Tuberculosis affecting the optic nerve
• Syphilitic optic neuropathy
• Lyme disease affecting the optic nerve
• Systemic lupus erythematosus optic neuropathy
• Polyarteritis nodosa optic neuropathy
• Granulomatosis with polyangiitis (formerly Wegener's granulomatosis)
• Multiple sclerosis
• Cryptococcal meningitis affecting the optic nerve
• Cytomegalovirus retinitis
• Herpes simplex virus retinitis
• Human immunodeficiency virus-associated retinopathy
• Diabetic retinopathy
• Hypertensive retinopathy
• Sickle cell retinopathy
• Retinopathy of prematurity
• Behçet disease

Pertinent Studies and Ongoing Trials

These studies and trials collectively enhance our understanding of transient vision loss, guiding evidence-based clinical practice and highlighting the importance of timely intervention to prevent serious complications.

Reported Studies

• Amaurosis fugax and carotid artery stenosis: Results from several studies have demonstrated a strong correlation between amaurosis fugax and carotid artery stenosis. The North American Symptomatic Carotid Endarterectomy Trial showed that carotid endarterectomy significantly reduced the risk of stroke in patients with transient vision loss and significant carotid artery stenosis.[59]
• Migraine with aura: Research results have shown that migraines with visual aura can often mimic transient ischemic attacks. The Women’s Health Study and the Physicians’ Health Study both provided evidence supporting migraine with aura as a significant risk factor for cardiovascular diseases, including ischemic stroke.[65]
• Transient ischemic attack: The EXPRESS study's results (Early use of EXisting PREventive Strategies for Stroke) demonstrated that rapid intervention in patients with TIA (including those presenting with transient vision loss) can substantially reduce the risk of subsequent stroke.[12]
• Optic neuritis: The Optic Neuritis Treatment Trial demonstrated that corticosteroids can accelerate visual recovery in patients with optic neuritis and reduce the risk of developing multiple sclerosis during the following 2 years.[66]
• Ocular ischemic syndrome: Results from various studies by the American Academy of Ophthalmology have highlighted the importance of diagnosing and managing ocular ischemic syndrome early to prevent permanent vision loss. Treatment often involves addressing the underlying carotid artery disease.[67]
• Retinal artery occlusion: Results from the Branch Retinal Artery Occlusion studies have shown that this condition often presents as transient monocular vision loss. The study conclusions recommend immediate cardiovascular evaluation and management to prevent further ischemic events.[68]

Ongoing Research

• Assessment of novel antiplatelet therapy for TIA: This multicenter trial is investigating the efficacy of new antiplatelet drugs in preventing recurrent ischemic events in patients with TIA, including those with transient vision loss.[49]
• Evaluation of neuroprotective agents in optic neuritis: This ongoing study is assessing the efficacy of various neuroprotective agents in reducing long-term visual impairment in patients with optic neuritis.[69]
• Stroke prevention in carotid artery disease: Several ongoing trials are evaluating the role of carotid artery stenting versus endarterectomy in preventing recurrent ischemic events in patients with significant carotid artery stenosis and symptoms like transient vision loss.[70]
• Exploring the Role of Antioxidants in Preventing Retinal Ischemic Events: This trial is evaluating the effect of antioxidant therapy on the frequency and severity of retinal ischemic events in patients with underlying vascular diseases.[71]
• Multicenter Study on Amaurosis Fugax and Cardiovascular Outcomes: This study is exploring the relationship between amaurosis fugax, carotid artery disease, and long-term cardiovascular outcomes, focusing on optimizing management strategies.[72]

Treatment Planning

Prescription

Dosing: The treatment plan for transient vision loss varies depending on the underlying cause. Antiplatelet or anticoagulant therapy (aspirin [81-325 mg daily] or clopidogrel [75 mg daily]) may be prescribed for patients with a history of ischemic events. Corticosteroid therapy, such as intravenous methylprednisolone (1 g daily for 3 days) followed by oral prednisone (1 mg/kg/d), may be administered to patients with optic neuritis.[49]

Simulation

Diagnostic imaging:

• Magnetic resonance imaging: Identifies ischemic changes, demyelinating lesions, or structural abnormalities
• Carotid Doppler ultrasound: Assesses carotid artery stenosis, which may contribute to transient ischemic attacks
• Echocardiography: Detects cardiac sources of emboli in cases of suspected cardioembolic events
• Optical coherence tomography: High-resolution retina and optic nerve images, aiding diagnosis of optic neuritis or retinal artery occlusion
• Fluorescein angiography: Visualizing retinal and choroidal circulation [73]

Targets

Ischemic events:

• Carotid arteries: Endarterectomy or stenting may be considered for patients with significant carotid artery stenosis.
• Cardiac sources: Anticoagulation therapy targeting the heart is crucial for patients with atrial fibrillation or other conditions that may contribute to the development of an embolus.[74]

Optic neuritis:

• Optic nerve: High-dose corticosteroids can reduce inflammation and prevent further demyelination.[75]

Retinal conditions:

• Retinal arteries: Antiplatelet therapy and managing risk factors like hypertension and diabetes are essential.
• Choroidal circulation: Vascular anomalies occurring here may cause transient vision loss.[76]

Radiation Techniques

Radiation therapy is generally not a treatment modality for transient vision loss. However, in rare cases of ocular tumors causing TVL, radiation treatment planning typically involves:

• Prescription: Determining the total radiation dose and fractionation schedule
• Simulation: Using CT or MRI scans to simulate the treatment area and plan the precise delivery of radiation
• Targets/volumes: Tumor volume must be defined to ensure minimal exposure to surrounding healthy tissues [77]

Additional Considerations

Rehabilitation:

• Vision therapy: For patients with residual vision issues post-treatment, vision therapy can help improve visual function.
• Occupational therapy: This therapy assists patients in adapting to any lasting visual impairments.[78]

Follow-up and Monitoring:

• Patients should follow up with an ophthalmologist and possibly a neurologist or cardiologist, depending on the underlying cause.
• Clinicians should monitor visual acuity, vision fields, and retinal health with regular eye exams and imaging studies.

Lifestyle Modifications:

• Providers should recommend smoking cessation, regular exercise, and a healthy diet to manage vascular risk factors.
• Patients must remain compliant with prescribed medications to prevent the recurrence of ischemic events.[79]

By addressing the underlying cause and tailoring the treatment plan to individual patient needs, effective management of transient vision loss can be achieved, minimizing the risk of permanent visual impairment

Toxicity and Adverse Effect Management

Transient vision loss can arise from many causes associated with specific treatment protocols. Understanding each medication's potential toxicity and adverse events is crucial for optimizing patient outcomes. Effective management strategies are essential to mitigate these adverse effects and ensure patient safety.[5]

Common Treatments and Associated Toxicities

Antiplatelets and anticoagulants:

• Medications: Aspirin, clopidogrel, warfarin, direct oral anticoagulants 
• Toxicities:
• Bleeding: Gastrointestinal bleeding, intracranial hemorrhage, increased risk of bruising
• Management:
• Regular monitoring of international normalized ratio for patients on warfarin
• Dose adjustment based on bleeding risk factors
• Use of proton pump inhibitors to prevent gastrointestinal bleeding in high-risk patients
• Immediate intervention for patients with signs of severe bleeding [80]

Corticosteroids:

• Medications: Prednisone, methylprednisolone
• Toxicities:
• Hyperglycemia: Increased blood sugar levels, particularly in those with diabetes
• Osteoporosis: Long-term use can lead to bone density loss
• Infection: Increased susceptibility to infections due to immunosuppressive effects
• Weight gain and hypertension: Common side effects of systemic corticosteroid use
• Management:
• Blood sugar monitoring and management in diabetic patients
• Calcium and vitamin D supplementation to prevent osteoporosis
• Prophylactic antibiotics for patients at high risk of infection
• Regular blood pressure monitoring and lifestyle modifications [81]

Ocular Medications:

• Medications: Topical antibiotics, mydriatics, anti-glaucoma medications
• Toxicities:
• Ocular surface irritation: Dryness, redness, and discomfort
• Systemic absorption: Common during β-blocker therapy for glaucoma, may cause bradycardia or bronchospasm.
• Management:
• Use of preservative-free formulations to reduce irritation
• Educating patients on the correct application technique to minimize systemic absorption
• Monitor for systemic side effects (eg, patients receiving chronic therapy)[82]

Immunosuppressants:

• Medications: Azathioprine, cyclosporine
• Toxicities:
• Nephrotoxicity: Renal impairment, particularly during cyclosporine use
• Hepatotoxicity: Liver function abnormalities
• Myelosuppression: Reduced bone marrow activity (anemia, leukopenia, thrombocytopenia)
• Management:
• Regular monitoring of renal and liver function tests
• Complete blood counts to monitor bone marrow function
• Dose adjustments based on laboratory findings, clinical assessment [83]

General Management Strategies

Patient Education:

• Patients should be informed about the potential side effects of their medications and the importance of adherence to prescribed therapies.
• Additionally, patients should be educated on alarming symptoms that are indications for immediate medical attention.[84]

Regular Monitoring:

• Frequent follow-up appointments are critical for monitoring the efficacy and safety of treatments.
• Treatment regimen adjustments should be based on patient response and the development of adverse events.[85]

Multidisciplinary Approach:

• Collaboration between ophthalmologists, primary care physicians, endocrinologists, and other specialists is necessary to provide comprehensive care.
• A team-based approach allows for improved management of complex cases and ensures optimal patient outcomes.[86]

Effective management of toxicity and adverse effects in patients experiencing transient vision loss involves a thorough understanding of the treatments used and their potential side effects. Through vigilant monitoring, patient education, and a multidisciplinary approach, healthcare providers can mitigate these risks and improve overall patient care.

Staging

Staging transient vision loss is essential for determining the underlying cause, severity of the condition, and appropriate management strategies. Although various conditions can cause TVL, the staging process involves a thorough clinical assessment to categorize the episode's nature, duration, and potential etiologies. A general approach to staging transient vision loss is outlined below.[87]

Stage 1: Initial Presentation

• History taking: Take a detailed patient history, including the onset, duration, frequency, and any precipitating factors or associated symptoms (eg, headache, neurological deficits).
• Symptoms: TVL is characterized by an abrupt vision loss that resolves within minutes to hours. Patients may describe it as a curtain falling or a shadow moving over their vision.
• Duration: TVL typically resolves within seconds or minutes but can last for several hours.[88]

Stage 2: Clinical Examination

• Visual acuity: Assess visual acuity before and after the episode.
• Ophthalmoscopy: Examine the retina and optic nerve to identify any underlying pathology.
• Slit lamp examination: Evaluate the anterior segment to rule out ocular surface or anterior chamber abnormalities.

Stage 3: Diagnostic Evaluation

• Imaging: Various modalities, including MRI, CT, or ultrasound (B-scan), may be indicated based on the suspected cause.
• Ocular Doppler ultrasound: This modality assesses the blood flow in the retinal and choroidal vessels.
• CT/MRI: These imaging modalities provide a neurological assessment of a suspected central cause (eg, transient ischemic attack, migraine).
• Electrocardiogram: The presence of cardiac arrhythmia should be established if amaurosis fugax (monocular TVL due to retinal ischemia) is suspected.[89]
• Laboratory testing:
• Blood: Blood tests help rule out differential diagnoses or identify systemic conditions (eg, diabetes, hyperlipidemia).

Stage 4: Etiology-Based Staging

• Vascular:
• Amaurosis fugax: This staging is based on the extent of carotid stenosis.
• Migraine: This condition is often associated with an aura (ie, transient visual phenomena preceding or accompanying the headache).
• Neurological:
• Transient ischemic attack: Transient vision loss due to posterior circulation ischemia requires prompt evaluation and management to prevent stroke.
• Papilledema: Staging is based on the severity and underlying cause.
• Ocular:
• Retinal vein occlusion: Staging is based on the extent of occlusion and retinal involvement.
• Central serous chorioretinopathy: This condition may cause intermittent blurring of vision. Staging is based on chronicity and recurrence.[90]

Stage 5: Management and Prognosis

• Immediate management: Management is determined by the etiology (eg, anticoagulation for embolic events).
• Long-term management: Treatment for underlying risk factors, such as hypertension, diabetes, and hyperlipidemia, is provided. Regular follow-up is necessary to monitor for recurrence.
• Prognosis: The prognosis is determined by the underlying cause and treatment response. Prompt diagnosis and intervention can prevent long-term visual and systemic complications.[91]

Staging transient vision loss involves a comprehensive approach that integrates patient history, clinical examination, diagnostic evaluations, and identification of the underlying cause. Appropriate staging is crucial for timely and effective management, improving patient outcomes, and preventing recurrent episodes.

Prognosis

While alarming to the patient, transient vision loss is typically associated with positive outcomes if the cause is a benign condition (eg, ocular migraine). However, if TVL is a symptom of a more serious underlying condition (eg, transient ischemic attack, retinal artery occlusion), the prognosis depends heavily on the underlying pathology, timely recognition and intervention, and the patient's response to treatment.

Ocular migraine:

• Short-term: TVL usually resolves without long-term effects on vision. Patients may experience recurrent episodes, which may be managed with lifestyle modifications and medications.
• Long-Term: The prognosis is good, assuming appropriate management. Patients typically retain full visual function between episodes.[29]

Amaurosis fugax:

• Short-term: This condition is often a warning sign of carotid artery disease or other vascular conditions. Immediate evaluation and treatment are essential to prevent further ischemic events.
• Long-term: The prognosis can significantly improve with appropriate management of underlying vascular risk factors (eg, hypertension, hyperlipidemia, smoking cessation). The risk of stroke can be reduced with carotid endarterectomy or medical management.[59]

Transient ischemic attack:

• Short-term: Patients have an elevated risk of subsequent stroke, particularly within the first few days after the attack. Immediate medical evaluation and intervention are critical.
• Long-term: The prognosis improves with aggressive management of risk factors (eg, anticoagulation, antihypertensives, statins). Regular follow-up is necessary to monitor treatment response and adjust the patient's regimen.[40]

Retinal artery occlusion:

• Short-term: The prognosis is poor if not treated promptly. The window for effective intervention (eg, hyperbaric oxygen therapy, ocular massage) is very short, often only hours long.
• Long-term: Visual outcomes are generally poor if immediate intervention is unsuccessful. Preventive measures for underlying conditions such as atherosclerosis or cardiac emboli are essential to prevent recurrence.[92]

Papilledema:

• Short-term: Immediate intervention to reduce intracranial pressure is crucial. The prognosis depends on the cause of the increased intracranial pressure (eg, brain tumor, idiopathic intracranial hypertension).
• Long-term: The long-term prognosis can be good when effectively managing the underlying condition. Routine monitoring for changes in vision and intracranial pressure is necessary.[93]

Optic neuritis:

• Short-term: Some patients recover fully with or without treatment, while others may have persistent visual deficits.
• Long-term: Recurrence is possible, particularly in patients with multiple sclerosis. The long-term prognosis is improved with early intervention and management of underlying conditions.[94]

Factors influencing prognosis

• Timeliness of diagnosis and intervention: Early diagnosis and treatment significantly improve outcomes, particularly for patients with TVL caused by vascular conditions.
• Management of underlying conditions: Aggressive control of systemic diseases such as diabetes, hypertension, and hyperlipidemia is crucial.
• Patient compliance: Adherence to medical therapy, lifestyle modifications, and regular follow-up provider visits can improve the long-term prognosis.[95]

The prognosis of transient vision loss is highly variable and depends on the underlying etiology and promptness of medical intervention. While some causes have a benign prognosis, others are severe conditions requiring immediate and aggressive management to prevent significant morbidity and mortality. Regular follow-up and management of underlying risk factors are essential to improving patient outcomes and avoiding recurrence.

Complications

Transient vision loss can be a symptom of various underlying conditions, each with potential complications. Understanding these complications is crucial for timely intervention and management.

Stroke and cerebrovascular events:

• Transient ischemic attack: TIAs often precede more severe cerebrovascular accidents (ie, strokes). Approximately 10% to 15% of patients who experience a TIA have a stroke within 3 months. This risk is highest during the first 48 hours.
• Stroke: Permanent vision loss, hemiparesis, speech difficulties, and cognitive impairments are possible complications that may occur.[96]

Permanent vision loss:

• Retinal artery occlusion: If not promptly treated, this occlusion can cause permanent retinal damage and irreversible vision loss.
• Optic neuritis: Recurring optic neuritis, particularly in patients with multiple sclerosis, can lead to progressive and permanent visual impairment.[97]

Intracranial pathologies:

• Papilledema: Left untreated, elevated intracranial pressure can lead to chronic papilledema, which can cause permanent optic nerve damage and blindness. Papilledema may also be the result of severe conditions such as brain tumors, hydrocephalus, or intracranial hemorrhages.[93]

Systemic complications:

• Cardiovascular disease: Conditions such as carotid artery disease can cause amaurosis fugax and are associated with an increased risk of myocardial infarction and other cardiovascular events.
• Hypertension and diabetes: Poorly controlled hypertension or diabetes can exacerbate vascular conditions, leading to transient vision loss. These conditions may also result in additional systemic complications, including nephropathy, neuropathy, and cardiovascular disease.[98]

Recurrence and chronic conditions:

• Ocular migraine: While usually benign, ocular migraines can recur frequently. These migraines cause significant discomfort and may indicate underlying vascular conditions requiring treatment.
• Chronic inflammatory conditions: Diseases such as giant cell arteritis can cause repeated episodes of vision loss and require long-term immunosuppressive therapy, which adds additional risk and potential adverse events.[88]

Psychosocial impact:

• Anxiety and depression: Recurrent or idiopathic episodes of transient vision loss can cause significant anxiety and fear of future episodes, affecting the patient's mental health and quality of life.
• Lifestyle limitation: Persistent concern regarding vision loss may cause the patient to restrict daily activities, work, and social interactions, decreasing quality of life.[99]

Diagnostic and treatment-related complications:

• Pharmaceutical adverse events: Medications prescribed to treat underlying causes of transient vision loss (eg, anticoagulants for TIAs, corticosteroids for optic neuritis) can cause severe adverse events, including bleeding risks and immunosuppression.
• Surgical risks: Interventions such as carotid endarterectomy or vitrectomy carry surgical risks, including infection, bleeding, and anesthesia-related complications.[40]

Transient vision loss is a critical symptom that requires a detailed evaluation to identify and manage underlying conditions. Potential complications range from permanent vision loss and stroke to systemic cardiovascular events and psychological impacts. Early diagnosis and aggressive treatment are essential to prevent these complications and improve patient outcomes. Regularly monitoring and comprehensively managing associated risk factors are necessary to reduce the incidence of severe complications.[15]