Continuing Education Activity

Optic neuritis is a vision-threatening disorder and often the first symptom of demyelinating diseases such as multiple sclerosis. Infections, autoimmune diseases, and certain medications may also trigger this condition. Symptoms typically include sudden vision loss, eye pain (especially with eye movement), and changes in color perception. Some individuals may also experience the Marcus Gunn pupil, an abnormal response to light.

Diagnosis involves a thorough clinical evaluation and the use of advanced imaging modalities, particularly optical coherence tomography and magnetic resonance imaging. Blood tests may be taken to exclude other conditions. Management often starts with high-dose intravenous corticosteroids to reduce inflammation and accelerate recovery. For individuals with underlying conditions like multiple sclerosis, disease-modifying therapies may be introduced to help prevent future episodes. The prognosis is generally positive, with most people experiencing partial or full recovery of vision within weeks to months. However, some may face persistent visual impairment, and the risk of recurrence or developing multiple sclerosis varies based on individual factors.

This activity for healthcare professionals is designed to enhance learners' proficiency in evaluating and managing optic neuritis. Participants gain deeper insights into the condition's etiology, risk factors, pathophysiology, symptomatology, and best diagnostic and therapeutic practices. Clinicians will learn how to differentiate optic neuritis from other causes of vision loss and explore the relationship between this condition and systemic diseases. Increased competence enables healthcare practitioners to collaborate effectively within an interprofessional team caring for affected individuals, improving outcomes.

Objectives:

• Identify the signs and symptoms indicative of optic neuritis.

• Select the appropriate diagnostic techniques for the evaluation of optic neuritis.

• Apply individualized, evidence-based management strategies for optic neuritis.

• Collaborate with the interprofessional team to educate, treat, and monitor patients with optic neuritis to improve patient outcomes.

Introduction

A healthy optic nerve is a crucial conduit for impulses generated within the layers of the retina to leave the eye. The photoreceptors initiate electrical signals in response to incident light, modified by retinal bipolar cells and transmitted through the optic nerves to the lateral geniculate bodies. Damage to the retinal nerve fiber layer (RNFL) or optic nerve may compromise the quality of these signals.[1] Optic neuritis is an inflammatory condition that affects the optic nerve and can lead to vision impairment in 1 or both eyes. While optic neuropathies can result from various causes, including infections, trauma, vascular insufficiency, metastases, toxins, and nutritional deficiencies, this activity focuses on optic neuritis specifically.

Optic neuritis involves inflammation of the optic nerve, which disrupts its ability to transmit visual information from the retina to the brain, causing sudden and often severe vision loss. This condition is multifactorial, though it is most commonly associated with demyelinating diseases, particularly multiple sclerosis and neuromyelitis optica spectrum disorder (NMOSD).[2] Optic neuritis is often 1 of the first clinical signs of multiple sclerosis and can indicate the future progression of this neuroinflammatory disease. NMOSD is another significant autoimmune cause of optic neuritis involving the optic nerve and spinal cord inflammation.

Other potential etiologies include infections (eg, syphilis, Lyme disease, and viral infections such as herpes simplex and varicella-zoster) and systemic autoimmune diseases (eg, systemic lupus erythematosus and sarcoidosis). Idiopathic cases have also been reported. In rare instances, optic neuritis may be triggered by toxins or drugs, such as ethambutol and methanol.[3]

Patients with optic neuritis typically present with a sudden onset of vision loss in 1 eye, although bilateral involvement can occur. The degree of visual loss varies, ranging from mild visual blurring to complete blindness in the affected eye. Pain, especially with eye movement, is a hallmark symptom of optic neuritis and often precedes visual impairment by a few days. Besides visual loss, patients may experience reduced color vision (dyschromatopsia) and contrast sensitivity. A relative afferent pupillary defect (RAPD) is often present when the condition affects only 1 eye or presents asymmetrically in bilateral cases. During an ophthalmologic examination, the optic disc may appear normal, indicating retrobulbar neuritis, or show swelling, known as papillitis, if the inflammation involves the anterior part of the optic nerve.[4]

Diagnosis of optic neuritis involves both clinical evaluation and imaging studies. Magnetic resonance imaging (MRI) of the brain and orbits with gadolinium contrast is the imaging modality of choice. MRI can help visualize optic nerve inflammation and detect any demyelinating plaques in the brain, which may indicate a high risk for multiple sclerosis. Visual field testing is also performed to assess the extent and pattern of visual field loss. Optical coherence tomography (OCT) can measure RNFL thickness and assess damage to the optic nerve fibers. In cases where infectious or autoimmune etiologies are suspected, additional investigations such as serologic studies, lumbar puncture for cerebrospinal fluid analysis, and antibody testing (eg, anti-aquaporin-4 or anti-AQ4 antibodies for NMOSD) may be warranted.[5]

The mainstay of treatment for optic neuritis is high-dose corticosteroids, typically administered intravenously for a short course, followed by an oral taper. Intravenous methylprednisolone is commonly used to accelerate visual recovery, although it does not affect the long-term visual outcome. Steroids are also indicated for cases of optic neuritis associated with systemic autoimmune diseases such as NMOSD. Appropriate antimicrobial or antiviral treatment is necessary when infectious etiologies are identified. For patients with recurrent optic neuritis or underlying multiple sclerosis or NMOSD, long-term immunomodulatory therapies such as interferon β, glatiramer acetate, and monoclonal antibodies like rituximab may be considered to reduce the risk of further attacks.[6]

Recent trends in the management of optic neuritis have focused on improving diagnostic accuracy and exploring novel therapeutic options. OCT has become essential in monitoring optic nerve and retinal health, providing valuable insights into RNFL thinning and ganglion cell loss. Advances in imaging techniques have also enabled the earlier detection of optic nerve changes even before significant vision loss occurs.[7]

Neuroprotective therapies in optic neuritis are gaining increasing attention for their potential to preserve axonal integrity and prevent permanent vision loss, particularly in patients with multiple sclerosis or NMOSD. Agents such as phenytoin, which has shown some neuroprotective properties, are being investigated in clinical trials. Furthermore, research into remyelinating therapies, such as anti-LINGO-1 monoclonal antibodies, offers promising future options for reducing inflammation and promoting the repair of damaged myelin. These emerging therapies may be crucial to altering the natural course of demyelinating optic neuritis.[8]

Optic neuritis remains a significant clinical concern with profound implications for patients' vision and overall neurological health. The association of this condition with demyelinating diseases, particularly multiple sclerosis, underscores the importance of early diagnosis and appropriate management. With advances in diagnostic imaging and the potential for novel therapeutic options, the future of optic neuritis treatment may include strategies to manage acute episodes and prevent long-term neurodegeneration. Healthcare providers should remain vigilant about this condition, as timely intervention can lead to improved patient outcomes and preservation of vision.

Etiology

The mechanism responsible for acute optic neuritis has not been definitively identified. However, an autoimmune reaction damaging the myelin sheath surrounding neurons within the optic nerve is considered a primary factor. Patients with documented autoimmune diseases have a greater propensity to develop optic neuritis, and a causal relationship between HLA DRB1, HLA-B27, and this condition has been observed.[9][10][11] Some studies suggest that viral illnesses, known to precipitate autoimmune reactions, may induce optic neuritis attacks. Optic neuritis may manifest as a demyelinating disease affecting several central nervous system areas. Optic neuritis is often the first clinical manifestation of demyelination.

Optic neuritis is characterized by nerve inflammation, which can lead to temporary or permanent vision loss. The condition is multifactorial, with autoimmune, infectious, toxic, and idiopathic mechanisms potentially contributing to its development, as explained below.

• Autoimmune conditions: Optic neuritis is commonly associated with multiple sclerosis, often serving as the first clinical manifestation of this demyelinating disease. The inflammation is attributed to the autoimmune destruction of the myelin sheath, which protects nerve fibers, including the optic nerve.[12] NMOSD is an autoimmune condition that affects the optic nerve and spinal cord and is distinct from multiple sclerosis. NMOSD is often characterized by bilateral optic neuritis and more severe vision loss. NMOSD is associated with antibodies against AQP4.[13] Systemic lupus erythematosus (SLE) and sarcoidosis may also cause optic neuritis as part of their systemic inflammatory process. SLE, in particular, can cause retinal vasculitis that may be mistaken for optic neuritis.[14]
• Infections: Viral agents such as herpes zoster, Epstein-Barr virus (EBV), and measles have been linked to optic neuritis. These viruses may directly invade the optic nerve or trigger an immune-mediated response, leading to inflammation.[15] Certain bacterial infections, including syphilis and Lyme disease, are also recognized causes of optic neuritis. In these cases, treatment of the underlying infection often resolves optic nerve inflammation. Tuberculosis and toxoplasmosis, which typically affect immunocompromised individuals, may damage the central nervous system. Optic neuritis is a secondary manifestation of central nervous system involvement in these infections.[16]
• Postviral or postvaccination mechanisms: In some cases, optic neuritis can develop after a viral illness, such as upper respiratory infections, or following vaccination, particularly against measles, mumps, rubella (MMR), and hepatitis B. Optic neuritis in these cases is thought to result from a dysregulated immune response triggered by the virus or vaccine, leading to optic nerve inflammation.[17]
• Toxic causes: Substances such as methanol and ethambutol, an antibiotic used to treat tuberculosis, have been associated with optic neuropathy and optic neuritis. The mechanism is thought to involve direct toxicity on the optic nerve and the rest of the visual pathways.[18]
• Idiopathic: Idiopathic optic neuritis refers to cases where no specific cause can be established. This diagnosis necessitates a thorough workup to investigate potential autoimmune, infectious, toxic, or systemic contributors.

Understanding the various causes of optic neuritis is essential for appropriate diagnosis, management, and prognosis. Many causes are treatable, and early intervention often prevents long-term visual complications. Identifying the underlying etiology also helps direct therapy and informs the potential for associated systemic conditions, especially in autoimmune diseases like multiple sclerosis or NMOSD.[19]

Epidemiology

The annual incidence of new-onset optic neuritis has been reported to be between 0.56 and 5.1 cases per 100,000.[20] Risk factors for this condition include age (20 to 40 years), sex (female: male = 2:1), and race (Caucasian). Children infrequently develop bilateral optic neuritis, but childhood disease is not believed to foreshadow the development of multiple sclerosis.[21]. An increased incidence of multiple sclerosis in temperate climates has been proposed. Studies have identified that the northern United States and western Europe have more cases than equatorial regions.[22]

Optic neuritis is an inflammatory condition of the optic nerve that leads to visual impairment and is often associated with multiple sclerosis and systemic autoimmune conditions. The frequency and demographics of optic neuritis vary by geographical location, sex, and age group.

• Incidence: Optic neuritis varies worldwide, with an estimated annual incidence of 1 to 5 cases per 100,000 individuals. However, the incidence may be higher in populations with a greater prevalence of multiple sclerosis, as optic neuritis is often a presenting feature of this demyelinating disease.[23]
• Sex distribution: Women are more commonly affected by optic neuritis than men, with a female-to-male ratio of approximately 3:1. This pattern is consistent with the gender distribution seen in multiple sclerosis, where women are also disproportionately affected. The higher incidence in women is thought to be related to the autoimmune nature of the disease, as many autoimmune disorders are more prevalent in female individuals.[24]
• Age distribution: Optic neuritis most frequently affects young adults, typically between the ages of 20 and 50. The average age of onset is around 32. While optic neuritis can occur in children or older adults, it is far less common in these age groups. In pediatric cases, optic neuritis may be more often associated with postinfectious and postvaccination syndromes rather than multiple sclerosis.[25]
• Geographic variations: The incidence of optic neuritis correlates with the geographic distribution of multiple sclerosis. Optic neuritis is more common in temperate climates and less common in regions near the equator. For instance, individuals of northern European descent tend to have a higher risk of developing optic neuritis, which mirrors the geographical prevalence patterns of multiple sclerosis.[26]
• Ethnicity: Optic neuritis is more common in Caucasians than in other ethnic groups. However, in Asian and African populations, optic neuritis may present differently and is often associated with conditions such as NMOSD rather than multiple sclerosis.[27]

This information on the epidemiology of optic neuritis provides a critical understanding of its demographic and geographical prevalence. The condition's epidemiology demonstrates frequent association with multiple sclerosis and underscores the importance of considering autoimmune and infectious etiologies in different populations.

Pathophysiology

Optic neuritis begins with inflammation within the central nervous system, leading to demyelination. Recurrent episodes of optic neuritis indicate a propensity toward developing more generalized diseases, including multiple sclerosis, NMOSD, and myelin oligodendrocyte glycoprotein-associated disease (MOGAD).[28][29] The extent of axonal damage due to optic neuritis differs depending on the causative condition.

Optic neuritis is the initial inflammatory event in 15% to 20% of individuals with multiple sclerosis, and approximately half of all patients with multiple sclerosis experience at least 1 episode of optic neuritis over 15 years (see Image. Optic Neuritis as an Indicator of Multiple Sclerosis).[30][31] As mentioned, multiple sclerosis occurs more commonly in temperate climates, with more cases seen in the northern United States and western Europe than equatorial regions.[32][33][34] Oligoclonal bands within the cerebrospinal fluid (CSF) are pathognomonic for multiple sclerosis.

Optic neuritis-related vision loss in patients with NMOSD and MOGAD is usually more severe and results in larger scotomas. Bilateral vision loss is common since both disorders affect the optic nerve, chiasm, and tracts. Damage often extends longitudinally into the spinal cord in both conditions. NMOSD is characterized by frequent optic neuritis attacks that cause severe bilateral vision loss with little chance of functional improvement. Spinal cord lesions that extend beyond 3 vertebral segments are typical of NMOSD, and debilitating transverse myelitis often limits physical activities. The detection of AQP4 immunoglobulin G (IgG) antibodies confirms the diagnosis of NMOSD.

MOGAD correlates with significant bilateral visual impairment, but severe optic neuritis-related papillitis occurs less frequently than NMOSD. Marked enhancement of the optic nerve, nerve sheath, and periocular tissues is evident in neural imaging studies. Compared to individuals with NMOSD, patients with MOGAD are more likely to experience improved visual function after optic neuritis and may have less spinal cord involvement. Male and female individuals are affected with equal frequencies.[35][36]

Histopathology

Histopathological analysis in optic neuritis typically reveals findings indicative of optic nerve inflammation. The histopathological examination can provide insights into the mechanisms of demyelination and inflammation, particularly in cases associated with multiple sclerosis and systemic autoimmune conditions.

• Inflammatory infiltrate: Histologically, optic neuritis is characterized by perivascular infiltration of inflammatory cells, mainly T lymphocytes and macrophages, into the optic nerve. This inflammation primarily affects the optic nerve's white matter, damaging the myelin sheath that insulates the nerve fibers. The inflammatory process may release cytokines and other immune mediators, contributing to the destruction of myelin and subsequent neural injury.[37]
• Demyelination: One of the hallmark histopathological findings in optic neuritis is the demyelination of the optic nerve, especially in patients with multiple sclerosis. The loss of the myelin sheath disrupts nerve signal conduction, leading to visual dysfunction. Demyelination can be patchy or widespread, depending on the severity of inflammation. In chronic cases, axonal loss may also be observed, which is linked to poor visual recovery.
• Axonal loss and gliosis: Evidence of axonal degeneration in the optic nerve may be found in longstanding cases of optic neuritis. Axonal loss contributes to irreversible damage and permanent vision loss, particularly in severe or recurrent cases. Gliosis, or the proliferation of astrocytes in response to injury, is commonly observed in chronic optic neuritis. This finding indicates the nerve's attempt to repair itself, but extensive gliosis often results in optic atrophy.[38]
• Vascular changes: In some cases, vascular changes such as the thickening of blood vessel walls and perivascular cuffing may be evident in the optic nerve. These changes reflect the underlying immune-mediated process and inflammation and can contribute to ischemia or hypoperfusion of the nerve tissue.[39]

Histopathological findings are crucial to understanding the extent of optic nerve damage, especially in atypical optic neuritis cases linked to systemic, autoimmune, or infectious conditions.

Toxicokinetics

Toxicokinetics is not typically a central consideration in the context of optic neuritis, a condition that is largely due to optic nerve inflammation from demyelinating diseases, dysregulated immune responses, or underlying autoimmune disorders. However, optic neuropathy or conditions that mimic optic neuritis may also be induced by toxic substances or medications, making an understanding of toxicokinetics important in these cases.

Medication-Induced Optic Neuritis

Certain drugs can cause optic neuropathy, and toxicokinetics helps in understanding how these drugs interact with the body. Examples of these drugs include ethambutol, amiodarone, and linezolid.

The antituberculosis drug ethambutol can cause dose-dependent optic neuropathy. Toxicokinetics involves understanding how the drug is absorbed, distributed, metabolized, and excreted. Ethambutol toxicity is often linked to prolonged use at high doses, as the drug accumulates in the body and particularly targets the optic nerve. Once detected, drug discontinuation usually halts further damage, though recovery may not be complete, depending on the level of damage.

The antiarrhythmic amiodarone may also lead to optic neuropathy. Its long half-life increases the risk of accumulation and toxicity. Amiodarone deposits in tissues, including the optic nerve, can produce bilateral optic neuropathy. Understanding its prolonged elimination is vital to managing such toxic effects.

Linezolid, an antibiotic, is another agent that can cause optic neuropathy, particularly with prolonged use. The toxic effects are thought to be related to mitochondrial toxicity. Toxicokinetic considerations for linezolid involve the duration of therapy, and dose adjustments are essential in preventing neuropathies in long-term treatments.[40]

Toxic Substances Leading to Optic Neuropathy

Optic neuropathy may also result from exposure to toxins like methanol and heavy metals. Toxicokinetic information is crucial to understanding how the body processes these agents.

Methanol poisoning is a well-known cause of toxic optic neuropathy. Methanol is metabolized in the liver to formaldehyde and formic acid, which are highly toxic, particularly to the optic nerve. The toxicokinetic concerns for methanol include its rapid absorption through the gastrointestinal tract, with subsequent conversion to toxic metabolites. Treatment aims to inhibit the formation of these metabolites (eg, with ethanol or fomepizole) and enhance methanol elimination via dialysis.

Lead poisoning is another example of toxicokinetics being essential to understanding optic neuropathy. Chronic exposure leads to lead accumulation in tissues, including the nervous system, potentially damaging the optic nerve. Toxicokinetic factors impacting lead toxicity management involve its long half-life and storage in bones, from which the heavy metal may be released into the bloodstream over time, causing delayed toxicity. Chelation therapy is used to enhance lead excretion and limit its toxic effects.[41]

Steroid Use in Optic Neuritis

Corticosteroids are the mainstay of treatment for typical demyelinating optic neuritis, but their pharmacokinetics and potential toxicities are critical to managing their side effects. High-dose corticosteroids, such as methylprednisolone, are often used to hasten visual recovery. These drugs have a well-defined pharmacokinetic profile, with rapid absorption and action. However, the toxicokinetic issues of these drugs include adverse effects like hyperglycemia, mood changes, and increased infection risk. The duration of treatment and tapering strategies are vital to minimizing toxicity.

Immunosuppressants and Disease-Modifying Therapies

Immunosuppressants, like azathioprine, and disease-modifying therapies (DMTs) used for multiple sclerosis, like natalizumab and rituximab, may be involved in recurrent or atypical optic neuritis cases. The toxicokinetics of these drugs need to be carefully considered, particularly when deciding on long-term use, as they can cause hepatotoxicity, leukopenia, or progressive multifocal leukoencephalopathy (PML), a rare but serious viral brain infection.

Toxicokinetics plays an essential role in diagnosis and management in cases where toxic substances or medications cause optic neuritis or produce conditions resembling this eye disease. By understanding how toxins or medications are processed by the body—absorbed, distributed, metabolized, and excreted—clinicians can anticipate potential toxicities and adjust treatments to mitigate harm. Effective management involves timely cessation of the offending agent, dose adjustments, and supportive treatments to prevent permanent vision loss.[42]

History and Physical

Optic neuritis usually presents with acute monocular eye pain and vision loss in young adults. Pain is usually associated with eye movements and often precedes loss of vision. Patients often report having had similar events in the same or the fellow eye. The degree of vision impairment may range from near-normal acuity to no light perception.[43] Nearly any visual field defect may be seen on automated visual field testing, but central scotomas are the most common. Color perception is significantly impaired (red hues are notably desaturated), and contrast sensitivity is diminished. Patients may experience recurring photopsia. Vision loss may be exacerbated after exercise or elevation of body temperature (Uhthoff phenomenon).

Optic disc swelling is seen on fundoscopy in 1/3 of patients during the active phase. In the absence of observable papillitis, the signs and symptoms of optic neuritis are usually sufficient to diagnose retrobulbar neuritis. Bilateral presentation, profound loss of vision, and absence of eye pain before vision loss, together with atypical neurologic findings, should prompt the search for an alternative etiology. Visual symptoms due to optic neuritis tend to resolve over several weeks to months, and visual function improves to near-normal levels after 6 months in most cases. Nonetheless, some individuals may have persistent qualitative visual changes that last a lifetime.[44][45]

Patients with optic neuritis typically present with a sudden onset of unilateral visual loss, though bilateral involvement can occur, especially in children or individuals with conditions like NMOSD. Key historical features include the following:

• Visual symptoms: Patients often describe a rapid decline in visual acuity in 1 eye, progressing over hours to days. This manifestation is frequently accompanied by central vision loss or a scotoma (area of vision loss).
• Pain with eye movement: One of the hallmark symptoms is periocular pain, particularly exacerbated by eye movements. Pain is due to the inflammation of the optic nerve sheath.
• Color desaturation: Many patients experience difficulty perceiving colors, particularly red, which appears "washed out" or desaturated.
• Visual recovery: After the acute phase, vision typically begins to recover spontaneously within a few weeks, although some patients may experience residual deficits.
• Systemic symptoms: In patients with multiple sclerosis, other neurological symptoms, such as limb weakness, numbness, and difficulty with coordination, may be present. In NMOSD, patients may have a history of transverse myelitis or, more severe, recurrent optic neuritis episodes.

A thorough ophthalmologic examination is critical for diagnosing optic neuritis. Key findings include the following:

• RAPD: Also known as the Marcus Gunn pupil, RAPD occurs when the affected eye shows a diminished direct pupillary response compared to the unaffected eye.[46]
• Visual acuity: Reduced visual acuity in the affected eye, ranging from mild impairment to complete vision loss, depending on the severity of the inflammation.
• Fundoscopic exam: In typical optic neuritis, the optic nerve head may appear normal during the acute phase (retrobulbar optic neuritis). The optic disc may sometimes be swollen and hyperemic, termed "papillitis." However, optic disc edema is less common and is often seen in children or in atypical cases.
• Visual field defects: Central scotomas (blind spots) are frequently identified on visual field testing. These defects correspond to the area of optic nerve damage.
• Color vision testing: Decreased ability to differentiate colors, particularly red, which diminishes brightness and intensity (red desaturation test).
• Contrast sensitivity: Reduced contrast sensitivity, where patients have difficulty distinguishing between subtle shades of grey, may also be present.

Understanding these history and physical findings allows clinicians to differentiate optic neuritis from other causes of vision loss, such as ischemic optic neuropathy and retinal detachment, and initiate appropriate management.

Evaluation

Initial Assessment

The evaluation of optic neuritis involves a comprehensive clinical assessment, including laboratory tests, imaging, and other diagnostic procedures, to determine the underlying cause and guide appropriate management. The process includes ruling out associated conditions, particularly demyelinating conditions, such as multiple sclerosis and systemic autoimmune diseases. Clinical evaluation of suspected optic neuritis should include the following:

• Best-corrected visual acuity: Reduced visual acuity is a hallmark of optic neuritis. A complete visual function test, including Snellen visual acuity, color vision testing (Ishihara plates), and contrast sensitivity testing, is critical.
• Automated visual field testing: Automated perimetry can detect central scotomas or other visual field defects common in optic neuritis.
• Color vision testing: Particular attention should be given to red desaturation.
• Pupillary examination: The presence of RAPD should be determined. Eliciting RAPD using the swinging flashlight test indicates optic nerve dysfunction. However, RAPD may not be present in bilateral, symmetric optic nerve involvement cases. 
• Optic nerve examination: Although optic disc swelling (papillitis) may be seen in some cases, particularly when anterior optic neuritis is present, a normal fundoscopic examination is common in retrobulbar neuritis.

If clinical findings are consistent with optic neuritis, additional testing should include an MRI of the brain and orbits and IgG testing for NMOSD. MRI can help look for demyelinating disease with and without contrast enhancement. MRI of the brain and orbits with gadolinium contrast is the gold-standard imaging technique for diagnosing optic neuritis. MRI helps visualize optic nerve inflammation and identify demyelinating lesions in the brain that may suggest an association with multiple sclerosis. The affected optic nerve is enhanced in the active phase.

Demyelinating lesions within the brain confirm the diagnosis of multiple sclerosis. Optic neuritis with 2 or more typical lesions (1 of which is contrast-enhancing) is sufficient to diagnose the condition (McDonald criteria). White matter lesions on MRI increase the risk of developing multiple sclerosis. This finding is particularly important in patients with clinically isolated syndromes, including optic neuritis. MRI also helps rule out compressive lesions, tumors, or other structural abnormalities that may mimic optic neuritis.

NMOSD-specific IgG testing is useful if the clinical findings suggest this condition. This modality helps confirm that NMOSD is the cause of optic neuritis.[47]

Laboratory Tests

Laboratory tests that may be considered to evaluate optic neuritis include an autoimmune panel, infectious workup, and CSF analysis. The choice should depend on the clinical findings. Testing for autoimmune markers, such as antinuclear antibodies (ANA) for SLE, anti-AQ4 antibodies for NMOSD, and myelin oligodendrocyte glycoprotein-IgG (MOG-IgG) for MOGAD, is essential in patients with atypical presentations or recurrent optic neuritis. If an infectious cause is suspected, screening for infections such as syphilis, Lyme disease, or tuberculosis may be performed. CSF analysis may reveal oligoclonal bands, a finding supporting the diagnosis of multiple sclerosis associated with optic neuritis.[48]

Visual Evoked Potential Testing

This neurophysiological test measures the brain's electrical response to visual stimuli. Delayed visual evoked potential (VEP) latency indicates slowed conduction in the optic nerve, often seen in demyelinating conditions. While not always necessary for diagnosis, VEP testing can confirm the presence of optic nerve dysfunction.[49]

Optical Coherence Tomography

This noninvasive imaging modality is increasingly used to assess RNFL thinning, indicative of optic nerve damage. OCT can help monitor disease progression and recovery, particularly in cases associated with multiple sclerosis.[50][51]

National and International Guidelines

Guidelines from the American Academy of Neurology (AAN) and the American Academy of Ophthalmology (AAO) emphasize the importance of MRI with gadolinium contrast for patients with optic neuritis, especially when assessing multiple sclerosis risk. In uncertain cases, these organizations recommend early MRI and additional testing, such as OCT and VEP, to confirm the diagnosis and guide prognosis. In cases associated with NMOSD or other systemic conditions, targeted antibody testing, such as AQP4 and MOG-IgG, should follow national guidelines for autoimmune testing.

The evaluation of optic neuritis is multifaceted, requiring a thorough clinical and radiographic assessment, supplemented by laboratory investigations where necessary. Timely diagnosis and differentiation from other causes of optic neuropathy are essential for guiding treatment and improving long-term outcomes.[52]

Treatment / Management

Medical Treatment

High-dose intravenous corticosteroids (eg, methylprednisolone 1g/day for 3–5 days) followed by an oral prednisone taper is the cornerstone of treatment for acute optic neuritis. Steroids help reduce inflammation, accelerate visual recovery, and lessen the severity of symptoms. However, studies like the Optic Neuritis Treatment Trial (ONTT) indicate that steroid use does not alter the long-term visual prognosis, though it can shorten the recovery period. Oral corticosteroids alone without an intravenous lead-in are generally not recommended as they may increase the risk of recurrence.

Immunosuppressive therapies, such as rituximab, mycophenolate mofetil, and azathioprine, may prevent recurrence in patients with underlying autoimmune conditions like NMOSD and SLE. Plasma Exchange (PLEX) can be a rescue therapy for patients with severe optic neuritis who do not respond to corticosteroids, particularly in cases associated with NMOSD. This treatment helps by removing pathogenic antibodies and other inflammatory mediators.[53]

Immunomodulatory and disease-modifying therapies

DMTs, such as interferon β, glatiramer acetate, and newer agents like natalizumab and ocrelizumab, may benefit patients with a high risk of developing multiple sclerosis, particularly those with abnormal brain MRI findings. These agents help reduce the risk of future demyelinating events and slow the progression of multiple sclerosis. In NMOSD, monoclonal antibodies like eculizumab and rituximab target specific immune pathways involved in disease pathogenesis.[54]

Adjunctive Therapies

Although still under investigation, agents like citicoline and brimonidine are being explored for their potential neuroprotective effects in optic neuritis. Additionally, growing evidence supports Vitamin D's role in immune regulation and its potential to reduce multiple sclerosis risk in patients with optic neuritis. Individuals with optic neuritis should thus be advised to maintain adequate Vitamin D levels.[55]

Surgical Interventions

Surgical decompression is rarely needed in typical optic neuritis but may be indicated if a mass or tumor compresses an optic nerve. In these cases, surgical decompression of the optic nerve sheath could be considered to relieve pressure and potentially preserve vision.[56]

Management of Vision Loss

Visual rehabilitation services are essential for patients with significant residual visual impairment. These services include low-vision aids, occupational therapy, and strategies to enhance quality of life despite visual loss. Continuous monitoring of visual acuity, color vision, and contrast sensitivity over time is critical, especially in cases where visual recovery may be prolonged or incomplete.[57]

National and International Guidelines

Guidelines provided by the American Academy of Neurology, the American Academy of Ophthalmology, and the National Multiple Sclerosis Society (NMSS) recommend the use of high-dose intravenous corticosteroids for managing optic neuritis and emphasize the importance of early neuroimaging, particularly MRI, to assess the risk of multiple sclerosis. For NMOSD, updated guidelines endorse the early use of immunosuppressive therapies to prevent relapses and mitigate the risk of optic neuritis recurrence.

Prognosis and Follow-up

Visual function returns to near-normal levels over weeks to months whether or not treatment is initiated. However, visual recovery is hastened when treated with corticosteroid therapy. Based on the long-term results of the ONTT, the protocol widely accepted throughout the medical community for treating optic neuritis involves intravenous administration of methylprednisolone 500 to 1,000 mg once daily for 3 days, followed by oral prednisone (1 mg/kg once daily) for 11 days. Importantly, using oral prednisone alone was found to increase the rate of recurrent optic neuritis attacks.[58] If lesions characteristic of multiple sclerosis are evident on an MRI, then immune-modulating therapies should be considered to delay subsequent attacks.

While most patients experience significant visual recovery within 3 to 6 months, some may be left with subtle deficits, such as impaired contrast sensitivity or color vision. Long-term follow-up is essential, particularly in individuals at risk of developing multiple sclerosis or recurrent episodes of optic neuritis.

Interprofessional Care

Optimal management of optic neuritis requires an interprofessional approach involving neurologists, ophthalmologists, and immunologists, especially in systemic autoimmune diseases or multiple sclerosis cases. Coordination between these specialties ensures comprehensive care, better outcomes, and individualized treatment strategies for each patient. This comprehensive approach to treatment ensures that patients with optic neuritis receive the most appropriate and effective care tailored to the underlying cause and the severity of their presentation.[59]

Differential Diagnosis

The differential diagnosis of optic neuritis includes the following conditions:

• Inflammatory, demyelinating disease (classic)
• Idiopathic optic neuritis
• Multiple sclerosis
• NMOSD [60]
• MOGAD
• Ischemic optic neuropathy
• Autoimmune disorders
• SLE 
• Giant cell arteritis
• Sarcoidosis
• Behcet disease
• Infectious
• Viral
• Herpes simplex 1 and 2
• Varicella zoster
• Cytomegalovirus
• Less frequent: Human immunodeficiency, Epstein-Barr, dengue fever, West Nile, chikungunya, measles, mumps, rubella, influenza
• Bacterial
• Bartonella henselae (cat-scratch disease)
• Treponema pallidum (syphilis)
• Borrelia burgdorferi (Lyme disease)
• Mycobacterium tuberculosis (tuberculosis)
• Less frequent: Rickettsioses, Coxiella burnetti (Q fever), Tropheryma whippleii (Whipple disease), Leptospira, Brucella, Mycobacterium leprae (leprosy)
• Fungal
• Cryptococcus neoformans (Cryptococcosis)
• Candidiasis
• Histoplasma capsulatum (Histoplasmosis)
• Aspergillus fumigatus (Aspergillus)
• Mucormycosis
• Parasitic
• Toxoplasma gondii (Toxoplasmosis)
• Toxocara canis (Toxocariasis)
• Diffuse unilateral subacute necrosis
• Drugs
• Ethambutol
• isoniazid
• Chloramphenicol
• Sulfonamides
• Amiodarone
• Digitalis
• Quinine
• Chloroquine
• Hydroxychloroquine
• Methotrexate
• Vincristine
• Tamoxifens
• Nutritional: Vitamin B deficiencies, particularly vitamin B12
• Toxic
• Alcohols like methanol
• Tobacco
• Compressive optic nerve lesions: Most often associated with a slow, subtle onset of signs and symptoms [61]

Proper management requires a thorough clinical assessment and optimal use of diagnostic examination.

Pertinent Studies and Ongoing Trials

The collaborative, multicenter ONTT attempted to clarify the role of corticosteroids in acute optic neuritis treatment.[62] More than 450 patients were enrolled at 15 sites between 1988 and 1991. The average age of enrolled subjects was 32. Most participants were Caucasian (85%) and female (77%). Subjects were randomized to receive oral prednisone 1 mg/kg daily for 2 weeks or intravenous methylprednisolone 250 mg every 6 hours for 3 days, followed by either oral prednisone or an oral placebo for the remainder of the 2 weeks.

Most subjects in each cohort recovered visual function in the first 1 to 3 months. Visual improvement occurred more rapidly in subjects treated with intravenous methylprednisolone, but no difference was observed in the cohorts receiving oral corticosteroids and placebo. Visual acuity did not fully return in many subjects, with initial visual acuity of 20/200 or worse. Visual outcomes at 6 months were similar in all cohorts, but optic neuritis recurred twice as often in subjects who received prednisone. 

At 1 year, no differences were found in visual function (ie, acuity, visual field, color discrimination, and contrast sensitivity) between subjects who received placebo and corticosteroids [visual acuity of 20/40 or better: placebo (95%), intravenous methylprednisolone (94%), and oral prednisone (91%)].[63] Visual recovery, visual field results, and neurologic consequences of optic neuritis have been reported at 3 years and 15 years.[64][65][66][67][68][69][70][71][72][73][74][75][76][77] Diagnostic and treatment guidelines for optic neuritis have evolved to help physicians differentiate typical cases from the atypical variants associated with more complex neurologic disorders.[78][79][80][81]

Treatment Planning

Treatment planning is essential for optimal recovery from optic neuritis and for preventing complications. Below is an outline of the treatment planning process.

• Initial assessment: The treatment begins with a thorough clinical assessment, including detailed history taking and ophthalmic examination, which includes visual acuity, color vision, visual fields, and fundoscopy to assess for optic disc swelling or pallor.[82]
• Corticosteroid therapy: Intravenous methylprednisolone is the 1st-line treatment to accelerate visual recovery. The regimen typically includes a 3-day course of high-dose intravenous methylprednisolone followed by oral prednisone. The goal is to reduce inflammation quickly and prevent further optic nerve demyelination.[83]
• Follow-up and monitoring: After initial treatment, patients require close follow-up to monitor visual recovery and potential side effects of corticosteroids, such as hyperglycemia, hypertension, immunosuppression, and infection. Visual fields and acuity should be reassessed periodically.
• Long-term management: DMTs should be considered in patients with multiple sclerosis or NMOSD to prevent future optic neuritis relapses. MRI scans of the brain and spine are often recommended to assess for demyelinating lesions, guiding long-term care and treatment planning.[84]

This comprehensive approach helps minimize visual loss while managing the conditions underlying optic neuritis.

Toxicity and Adverse Effect Management

Monitoring for toxicity and managing adverse effects are crucial when using corticosteroids to treat optic neuritis. Below is a detailed overview of the potential adverse effects of optic neuritis treatment and the management strategies that can address them.

• Corticosteroid toxicity: Intravenous methylprednisolone carries the typical risks associated with steroid therapy, such as hyperglycemia, hypertension, insomnia, mood changes, and gastrointestinal upset. Blood glucose and blood pressure should be monitored to manage these adverse reactions, particularly in patients with preexisting conditions. Proton pump inhibitors or H2 blockers may be prescribed to prevent gastric irritation, and patients should be advised on proper sleep hygiene and monitored for psychiatric symptoms.
• Osteoporosis and avascular necrosis: Long-term use or high doses of corticosteroids increase the risk of bone density loss and avascular necrosis. Patients should be counseled on calcium and vitamin D supplementation. Weight-bearing exercises may also be recommended. Bone density testing should be considered in high-risk patients.[85]
• Infection risk: Immunosuppression from corticosteroids can increase the risk of infections. Before initiating treatment, patients must be screened for latent infections like tuberculosis and hepatitis B. Prophylactic antimicrobial therapies may be needed for patients on long-term immunosuppressive therapies.
• Cataracts and glaucoma: Chronic corticosteroid use can lead to cataract formation or steroid-induced glaucoma. Regular ophthalmologic examinations, including intraocular pressure monitoring, should be performed if prolonged steroid use is anticipated.[86]

By anticipating these complications, healthcare professionals can mitigate toxicity risks while optimizing outcomes for patients with optic neuritis.[87]

Staging

Optic neuritis does not typically follow a formalized staging system like other diseases. However, the condition may be described in stages based on the clinical presentation and progression. These stages can be loosely defined as follows:

• Acute stage: Usually occurs over a few days, during which patients experience sudden vision loss, often accompanied by eye pain, particularly with movement. Visual acuity can decrease rapidly during this stage, and color vision is frequently impaired. RAPD is commonly observed.
• Subacute stage: Occurs after the acute episode and involves gradual stabilization of visual symptoms over a few weeks. Eye pain typically subsides, and patients may notice slight improvements in their vision, but this experience varies from person to person.
• Recovery stage: Recovery begins around 4 to 6 weeks after the initial onset, with many patients regaining most of their lost visual acuity by 6 months. However, subtle deficits in contrast sensitivity, color vision, and visual field may persist.
• Chronic or recurrent stage: Optic neuritis can sometimes recur, particularly when associated with multiple sclerosis and NMOSD. Recurrent episodes can lead to cumulative optic nerve damage and a poorer visual prognosis, sometimes resulting in permanent visual deficits.

This staging can help clinicians understand the condition's progression, manage patients' symptoms, and provide appropriate follow-up care.

Prognosis

The prognosis of optic neuritis can vary significantly depending on the underlying cause, the presence of recurrent episodes, and associated systemic conditions like multiple sclerosis or NMOSD. Pain with eye movement usually resolves within days to weeks. Visual acuity and color perception improve over 2 weeks to 3 months, and nearly 90% of patients achieve near-normal function by 6 months. Only 3% of patients have a best-corrected visual acuity of 20/200 or worse after 5 years. In 15% to 20% of cases, optic neuritis precedes the development of multiple sclerosis, and recurrence increases the risk of developing multiple sclerosis or NMOSD. Approximately 50% of patients with multiple sclerosis have had at least 1 optic neuritis attack within the prior 15 years.

When optic neuritis is associated with multiple sclerosis, future neurological episodes are likely, and the disease course may become more progressive. Studies show that about 50% of patients with a first episode of optic neuritis develop multiple sclerosis over 15 years, particularly if brain MRI shows lesions at the time of the optic neuritis episode. In NMOSD-related optic neuritis, the prognosis is often worse, with a higher likelihood of recurrent episodes and permanent visual impairment.

Early treatment with high-dose corticosteroids may shorten the duration of symptoms, but it does not necessarily affect the long-term visual outcome. In cases of recurrent optic neuritis, particularly if associated with a demyelinating condition, preventive treatments like DMTs are recommended to reduce the risk of future attacks and progression.

In cases of idiopathic optic neuritis, most patients experience a favorable recovery of visual acuity within 6 months, although some visual deficits, such as contrast sensitivity and color vision, may persist. About 90% of patients recover to near-normal visual acuity, although visual quality may not fully return to pre-episode levels.[88]

Complications

Optic neuritis can present with various complications, especially when associated with underlying conditions such as multiple sclerosis and systemic autoimmune disorders. The most common and concerning sequelae include the following:

• Permanent vision loss: While many patients recover their vision partially or fully after an episode of optic neuritis, some may suffer from permanent optic nerve damage. This nerve injury can result in persistent visual deficits, such as decreased visual acuity, color vision loss, and visual field defects. Despite treatment, about 3% to 5% of patients may not fully recover their vision.
• Recurrence: Patients with a history of optic neuritis, particularly those with demyelinating diseases, are at a higher risk of recurrence. Recurrent episodes can lead to cumulative damage to the optic nerve, exacerbating vision loss over time. The recurrence rate can be as high as 35% within 10 years in patients with multiple sclerosis.
• Multiple sclerosis: Optic neuritis is often the first symptom of this demyelinating condition. Studies indicate that around 50% of patients with optic neuritis develop multiple sclerosis within 15 years of their initial episode. Patients with lesions detected on MRI at the time of the 1st optic neuritis episode are at an even higher risk of developing multiple sclerosis.
• Steroid-related side effects: High-dose corticosteroids are commonly used to accelerate recovery. However, these drugs have potential side effects, including increased blood pressure, elevated blood glucose levels, weight gain, mood changes, and, in rare cases, avascular necrosis of the hip.
• NMOSD: In some cases, optic neuritis may be associated with NMOSD, a condition characterized by more severe optic neuritis and a higher risk of bilateral visual loss. NMOSD requires specific treatments that differ from multiple sclerosis, and missing this diagnosis can lead to inappropriate management.
• Psychosocial impact: Episodes of optic neuritis, especially if associated with chronic diseases like multiple sclerosis, can lead to significant psychological distress. Patients may suffer from anxiety, depression, and decreased quality of life due to the uncertainty of vision recovery and the potential for future episodes or systemic disease progression.[89]
• Visual fatigue: Some patients experience persistent visual fatigue even after the acute episode of optic neuritis has resolved. This symptom can interfere with daily activities, particularly tasks requiring prolonged focus, such as reading or computer work.
• Uveitis: Though rare, optic neuritis may sometimes be associated with uveitis, an eye's middle layer inflammation. This combination increases the complexity of the disease and can contribute to further vision complications.[90]
• Optic atrophy: Recurrent or severe episodes of optic neuritis can lead to permanent damage to the optic nerve, resulting in optic atrophy. A pale optic disc and permanent visual impairment characterize this condition, which may be evident in clinical examinations and imaging studies, such as OCT.
• Decreased contrast sensitivity: Contrast sensitivity deficits may linger even in patients who recover visual acuity after an episode of optic neuritis. This symptom makes it difficult for patients to perceive differences in shades of gray, particularly in low-light conditions.
• Blind spots: Some patients may experience persistent central or paracentral scotomas in their visual field, which can make reading and fine visual tasks more challenging.
• Pain with eye movement: One of the hallmark features of optic neuritis is pain with eye movement. While pain improves as the inflammation subsides, some patients may experience persistent or recurrent discomfort, especially during flare-ups.[91]
• Color desaturation: Even after recovery from optic neuritis, patients often report a reduced ability to perceive colors (color desaturation), particularly reds and greens. This symptom can persist long after the resolution of the acute episode.[92]
• Phosphenes (light flashes): Some patients experience visual phenomena, such as seeing flashes of light (phosphenes) or flickering in their visual field, particularly when moving their eyes or visualizing objects in dimly lit environments. These symptoms can be distressing and difficult to manage.[93]
• Double vision (diplopia): Ocular alignment issues that lead to double vision may develop in more severe or bilateral cases of optic neuritis, particularly when associated with central nervous system demyelinating disorders.
• Visual field loss: Partial or complete loss of visual fields may occur, especially in patients with recurrent optic neuritis or underlying autoimmune conditions such as NMOSD. The extent and location of the field loss depend on the degree of optic nerve damage.
• Glaucoma risk: While optic neuritis itself does not cause glaucoma, patients who require long-term corticosteroid treatment for recurrent episodes are at an increased risk of developing steroid-induced glaucoma, which can further compromise vision if not managed appropriately.
• Impaired quality of life: Beyond the physical aspects of vision loss, optic neuritis can significantly reduce the patient's overall quality of life. Difficulty with daily activities such as driving, reading, and working can lead to frustration, anxiety, or depression, necessitating psychological support or rehabilitation services.

Early recognition and appropriate management of optic neuritis are crucial to minimize these complications and improve patient outcomes. Regular follow-up and MRI monitoring are recommended to identify potential underlying causes, such as multiple sclerosis or NMOSD, which can alter the course of treatment.

Postoperative and Rehabilitation Care

Optic neuritis typically does not require surgical intervention, but rehabilitation care and follow-up are essential after initial treatment. Posttreatment recovery focuses on restoring visual function and monitoring for recurrence or progression to multiple sclerosis. Patients should have regular ophthalmological check-ups to assess visual acuity, color vision, and visual fields, which can take several months to improve. Steroid therapy is often used in acute management, and patients may require tapering doses, with follow-up to monitor for side effects such as elevated blood sugar or blood pressure.

Initiating DMTs may be recommended for individuals at high risk of developing multiple sclerosis, requiring collaboration with a neurologist for long-term management. Visual rehabilitation may involve exercises, adaptive devices, or training with low-vision aids if recovery is incomplete. Patients should also receive education on the importance of follow-up MRI to assess for multiple sclerosis progression and the potential need for early intervention with immunomodulatory therapy. Finally, psychological support should be offered, as vision loss, even if temporary, can significantly impact patients' mental health and quality of life. An interprofessional approach ensures optimal recovery and addresses the complex needs of patients with optic neuritis.[94]

Consultations

For patients with optic neuritis, prompt involvement of multiple specialists is crucial for comprehensive care. First, a neurologist should be consulted, especially if an underlying neurological condition such as multiple sclerosis is suspected. Neurological evaluation, including a brain MRI, can help assess the risk of progression to multiple sclerosis. Additionally, an ophthalmologist is essential for the initial diagnosis and ongoing management of optic neuritis. Detailed visual assessments and follow-up visits ensure proper monitoring of visual recovery and identify any recurrence.[95]

In some cases, a neuro-ophthalmologist may be involved for more specialized care, particularly if the diagnosis is uncertain or complex neurovisual issues have developed. These experts can assist in refining the diagnosis and determining appropriate treatment pathways. Lastly, involving a rheumatologist may be necessary if systemic autoimmune diseases like SLE and sarcoidosis are suspected. These specialists can evaluate the patient for systemic signs and determine whether immunosuppressive therapies are needed beyond standard optic neuritis treatments. Collaborative care across these disciplines enhances diagnosis, treatment, and patient outcomes in optic neuritis.[96]

Deterrence and Patient Education

It is critical to educate patients about optic neuritis and its potential association with multiple sclerosis. While optic neuritis typically has a good prognosis with partial or full vision recovery, patients should be aware of the possibility of recurrent episodes or the development of non-visual neurological symptoms. Early diagnosis and treatment are essential to improving visual outcomes, so patients should be encouraged to seek prompt medical attention if they experience sudden vision loss or eye pain.[97]

Patients should also be informed about the role of MRI in identifying potential brain lesions that may indicate an increased risk of multiple sclerosis. For individuals at higher risk, long-term follow-up and monitoring for symptoms of this demyelinating disorder is advised. In some cases, preventive therapy of multiple sclerosis with DMTs may be discussed as part of the long-term management plan.

Besides medical management, educating patients on lifestyle factors, such as managing stress and maintaining a healthy lifestyle, may contribute to their overall well-being and reduce exacerbations, especially if they have multiple sclerosis. Providing psychological support and clear communication about prognosis and treatment options can improve adherence and empower patients to participate actively in their care. Ultimately, comprehensive patient education helps ensure early recognition of symptoms and appropriate treatment, which can significantly improve long-term outcomes in optic neuritis.[98]

Pearls and Other Issues

Important points to remember when managing optic neuritis include the following:

• To reduce the potential for visual impairment, neurologic disabilities, and physical limitations, optic neuritis must be recognized quickly and accurately.
• Optic neuritis is often an early sign of multiple sclerosis. Consequently, every case should be approached with an acute management plan and a long-term neurological perspective. MRI with gadolinium contrast is crucial for assessing the severity of optic nerve inflammation and ruling out other causes of optic neuritis. The presence of brain lesions on an MRI may predict the future development of multiple sclerosis.
• Treatment typically involves high-dose intravenous corticosteroids, which can speed up recovery but do not necessarily affect the long-term visual outcome. One pitfall is relying solely on oral steroids, which have been associated with a higher recurrence rate of optic neuritis. Clinicians should also be aware of the differential diagnoses, such as NMOSD, which may require a different treatment approach.
• Other causes of optic nerve disease should be considered when:
  • Vision loss is bilateral, especially in older patients.
  • Visual deterioration due to presumed optic neuritis persists without improvement after 5 weeks.
  • Vision loss is not accompanied by eye pain. 
  • Retinal hemorrhage or marked optic disc edema is present.
• Patients with acute optic neuritis tend to have a lower risk of developing multiple sclerosis if they demonstrate no demyelinating lesions on MRI, have optic disc swelling, and belong to the male sex.
• A key preventive measure involves long-term monitoring for demyelinating conditions like multiple sclerosis. Patients with optic neuritis should be educated about the potential for recurrence and the risk of developing multiple sclerosis. In some cases, initiating DMTs may be considered if the patient meets the criteria for multiple sclerosis based on imaging findings or clinical progression.
• Regarding disposition, early diagnosis and prompt optic neuritis treatment can lead to favorable visual outcomes in most patients. However, some may experience residual deficits like color desaturation or visual field abnormalities.
• An interprofessional approach involving neurologists and ophthalmologists is crucial to ensure comprehensive care.
• Close follow-up is essential to detect any future relapses or progression to multiple sclerosis.

These pearls and preventive strategies improve short-term visual recovery and long-term patient outcomes, highlighting the importance of an integrated, vigilant approach to managing optic neuritis.

Enhancing Healthcare Team Outcomes

Managing optic neuritis requires the close coordination of various healthcare professionals. The initial treatment is provided by a neuroophthalmologist or a neurology team familiar with the guidelines derived from the ONTT. The probability of developing multiple sclerosis within 15 years of the initial optic neuritis attack is 50%. For patients with multiple sclerosis or at high risk for developing this condition, various healthcare specialists should be consulted to provide comprehensive care. The healthcare team should render a wide range of services.

A complete optic neuritis management team should have a combination of the following providers:

• Neurology team: Tasked with making the diagnosis and formulating the treatment plan. Members include neurologists, advanced practice professionals, and advanced practice nurses.
• Rehabilitation specialists: In charge of enhancing strength, physical stability, and musculoskeletal function. Members include physical medicine and rehabilitation physicians (to manage this group), physical therapists (to facilitate strength, balance, and range of motion and alleviate musculoskeletal pain), and occupational therapists (to facilitate activities of daily living skills).[99]
• Medical specialists: Provide other services patients may need. Members include mental health specialists, such as psychiatrists and psychologists who manage mental health concerns, and clinical social workers who provide appropriate resources and advocate for patient rights. Neuro-ophthalmologists are needed to manage visual deficiencies related to neurological disease. Low vision specialists present aids to ameliorate the barriers inherent to diminished visual function. Urologists and gynecologists can help manage the urogenital complications of systemic conditions underlying optic neuritis.
• Pharmacists: Provide patient education and monitor the complex medication regimen.
• Primary care providers: Coordinate overall health status and manage concomitant conditions. 
• Well-being professionals: Provide lifestyle modifications that benefit nutrition, fitness, and resilience.[100]

Enhancing healthcare team outcomes in the management of optic neuritis requires a coordinated, interprofessional approach involving ophthalmologists, neurologists, advanced practitioners, nurses, and pharmacists. Early and accurate diagnosis, noting findings from imaging technologies such as MRI, is vital for optimizing treatment and improving patient outcomes. Ophthalmologists and neurologists should collaborate closely to identify underlying conditions such as multiple sclerosis.[101]

Nurses are critical in patient education, ensuring adherence to prescribed treatments and monitoring for adverse effects, particularly when using high-dose corticosteroids. Pharmacists contribute by managing medication therapies, preventing drug interactions, and counseling patients on potential side effects. Interprofessional communication ensures that all team members are informed of patient condition changes, medication adjustments, and diagnostic findings. Ethics and patient-centered care should guide decision-making, emphasizing the patient's preferences and values in treatment plans.

Healthcare teams can improve patient safety, optimize visual outcomes, and reduce long-term complications, such as multiple sclerosis and permanent vision loss, through effective coordination, clear communication, and shared responsibilities. These efforts contribute to a holistic approach that addresses the immediate and long-term needs of patients with optic neuritis.[102]