A problem with vision is one of the most common symptoms of MS, and often one of the first that people with MS notice. The symptoms can include blurred vision, double vision (diplopia), optic neuritis, involuntary rapid eye movement and occasionally, a total loss of sight. Problems with vision can result from damage to the optic nerve or from a lack of coordination in the eye muscles. The optic nerve connects the eye to the brain.
Inflammation or demyelination in the optic nerve causes optic neuritis, which is experienced as a temporary loss or disturbance in vision and possibly pain behind the affected eye. Typically, vision returns partially or fully within a few weeks. While it is quite rare for a person with MS to become totally blind, it is not at all uncommon for an individual to have recurrent episodes of optic neuritis over the course of the disease, usually in one eye at a time. Damage to the optic nerve
can result in a blurring of vision, which may or may not totally resolve over time. Colour vision requires a great many nerve fibres from the eye for accurate transmission and is particularly susceptible to changes from demyelination. Optic neuritis can cause a large, noticeable “blind spot” in the centre of the visual field, and the person experiences a visual image with a dark, blank area in the middle. This is called a central scotoma and is not correctable with either
eyeglasses or medication, although steroids may be helpful in the early, acute phase. Diplopia (double vision), the experience of seeing two of everything, is caused by weakening or incoordination of eye muscles. This symptom is typically treated with a short course of steroids. Patching one eye while trying to drive or read will stop the double image; however, permanent patching of the eye will slow the brain’s remarkable ability to accommodate to the weakness and produce a single image
in spite of the weakened muscles. Some physicians are prescribing eyeglasses with special prisms that help to minimise double vision. Upon examination, the physician may detect a rhythmic jerkiness or bounce in one or both eyes. This relatively common visual finding in MS is nystagmus. Nystagmus does not always cause symptoms of which the person is aware. In the event that it does become troublesome, clonazepan (Klonopin®) is sometimes effective in reducing this annoying but painless
problem. Optic Neuritis in Multiple SclerosisOptic neuritis is an inflammatory injury of the optic nerve that represents the best-characterized clinically isolated syndrome (CIS) associated with multiple sclerosis (MS). [1] Clinical features at presentation Many of the cardinal clinical features of typical optic neuritis associated with MS have been identified based on findings from the Optic Neuritis Treatment Trial (ONTT). [26, 27] The ONTT revealed that most patients with typical optic neuritis are White (85%) and female (77%), with a mean age of 32 years. [26, 27] Among adults, sporadic optic neuritis is typically unilateral; however, bilateral simultaneous vision loss may be observed. Nonetheless, in this setting, other demyelinating optic neuropathies and potential optic neuritis mimics must be considered, including NMOSD, MOGAD, and Leber hereditary optic neuropathy (LHON). From a clinical perspective, a comprehensive history is imperative for differentiating optic neuritis from its potential mimics. Patients with optic neuritis often report subacute onset of vision loss that worsens over hours to days. This mode of onset helps distinguish optic neuritis from nonarteritic anterior ischemic optic neuropathy (NA-AION). [28] In contrast, NA-AION is generally unaccompanied by pain, and symptoms are frequently noted on morning awakening. Patients with compressive optic neuropathies may report sudden-onset awareness of vision loss. However, a detailed discussion often reveals that these individuals have experienced sudden-onset awareness of a longer-standing problem, rather than sudden-onset vision loss itself. [28] Ninety-two percent of individuals with typical optic neuritis experience pain that is frequently provoked by eye movements within the first 2 weeks of symptom onset. [1, 2, 26, 27, 28] Patients may also report intermittent flashes of light in the affected eye, known as photopsias or phosphenes. [29] Patients with optic neuritis may also describe worsening vision with increased body temperature, referred to as the Uhthoff phenomenon. [2, 30] Common examination findings in patients with optic neuritis In patients with suspected optic neuritis, several features on initial examination can help verify the diagnosis. Initially, the severity of vision loss in the affected eye may range from mild (Snellen visual acuity equivalent of 20/20) to—in rare cases—no light perception with high-contrast letter acuity testing. [28] In patients with unilateral optic neuritis or bilateral optic neuritis with asymmetric involvement, a relative afferent pupillary defect (RAPD) is apparent in the affected or, in cases of bilateral involvement, the more severely affected eye. [28] Visual field loss in patients with optic neuritis tends to follow the topography of the retinal nerve fiber layer (RNFL), with cecocentral, altitudinal, and arcuate deficits frequently observed. Keltner and colleagues [31] classified visual field abnormalities observed during longitudinal follow-up of patients in the ONTT and reported that both the affected and fellow eyes in patients with optic neuritis showed visual field losses. [31] These findings illustrate the role of perimetry in detecting both clinically overt and clinically occult optic nerve involvement in patients with MS. Dyschromatopsia, or decreased color vision, is typical in eyes with optic neuritis. [28] This finding can be particularly helpful in confirming the diagnosis in patients with mild central vision loss who have disproportionate deficits in color vision function. [28] Often, patients continue to note subjective color desaturation in the affected eyes after high-contrast visual acuity function has returned to a Snellen equivalent of 20/20. Traditionally, in typical cases of retrobulbar optic neuritis, the optic nerve has been described as normal in appearance, whereas patients with anterior optic neuritis, or papillitis, present with mild to moderate optic disc swelling at presentation. [28] As exemplified in the ONTT, severe optic disc edema, [32] vitreous cells, and/or hemorrhage are uncommon in the setting of typical optic neuritis. [28] Therefore, the observation of these fundus features should prompt investigation for other potential causes of vision loss. Pediatric optic neuritis Several features of the clinical presentation and course differentiate pediatric optic neuritis from the adult-onset syndrome. Although both children and adults present with vision loss, pain on eye movement, dyschromatopsia, and visual field defects, children are more likely to present with severe vision loss. [33] Children with optic neuritis more frequently demonstrate papillitis or anterior optic neuritis than their adult counterparts. [33] Moreover, younger pediatric patients are more likely than adolescents or adults to experience bilateral simultaneous optic nerve involvement. [34] In retrospect, the phenotypic characteristics that have long distinguished pediatric optic neuritis from optic neuritis in adults have in fact reflected that many of these cases in children were part of the MOGAD spectrum. Notably, MOG antibodies are more commonly encountered than AQP4-IgG antibodies in pediatric patients. [35] In fact, among children with optic neuritis, 50% will have MOG antibodies. [35] As mentioned, involvement of the anterior optic pathway (papillitis) is more frequently seen in patients with MOGAD than in patients with NMOSDs who more often have lesions in the posterior pathway with both chiasmal and postchiasmal involvement. [35] In both patients with NMOSD and those with MOGAD, bilateral optic neuritis and the presence of longitudinal lesions in the anterior visual pathway are distinguishing features. [35]  Optic neuritis: Making the diagnosis In patients with a typical history and expected examination findings, optic neuritis can be reliably diagnosed based on clinical grounds; however, certain red flags should raise concern for a potential mimic and therefore prompt additional investigations. [28] For example, young men who present with painless bilateral sequential or simultaneous optic nerve dysfunction should undergo testing for LHON. Middle-aged women in whom unilateral or bilateral optic neuritis develops should be evaluated for NMOSD and MOGAD because the management of optic neuritis in patients with these CNS inflammatory disorders differs from that of patients with MS. Additional features that should increase the clinical suspicion for NMOSD include poor clinical recovery, lack of typical MRI findings for MS, cerebrospinal fluid (CSF) pleocytosis, and manifestations of transverse myelitis. As described in the sections to follow, some patients with recurrent optic neuritis harbor a diagnosis of NMOSD or MOGAD. [36] Table 6. Differential Diagnoses of Optic Neuritis (Open Table in a new window)
Optic neuritis: Ancillary studies In the setting of typical optic neuritis, laboratory studies are not generally useful in facilitating diagnosis [32] ; however, additional investigations can be helpful in detecting potential mimics, such as NMOSD, MOGAD, lupus-related optic neuropathy, and syphilitic optic nerve injury. Specific clinical features should prompt consideration of these alternate diagnoses. Therefore, ancillary investigations should be selected based on the history and physical examination findings and may include any of the following:
Cerebrospinal fluid analysis is not generally required to diagnose typical cases of optic neuritis. The presence of oligoclonal bands (OCBs) can assist with the diagnosis of MS in patients who meet dissemination in space criteria, but not dissemination in time criteria. Cerebrospinal fluid analysis can also assist with determining the presence of alternative entities, such as suspected infectious optic neuropathies secondary to syphilis, tuberculosis, or Lyme disease. Visual evoked potentials In clinical practice, visual evoked potential (VEP) testing is typically unnecessary to confirm the diagnosis of optic neuritis. When mild optic neuritis or subclinical optic nerve damage is suspected, VEP testing can be useful in capturing the effects of prior demyelinating injury. Abnormal VEP findings in this context include increased latencies and reduced amplitudes of waveform. However, VEP abnormalities are not restricted to optic neuritis and may also occur with other conditions, such as optic nerve compression, infiltration, and nondemyelinating inflammation. [38] Multifocal VEP can be a more sensitive and specific tool for detecting optic neuritis in suspected clinically overt or clinically occult cases of optic neuritis, although the technique is not widely available for routine clinical use. [38] Optical coherence tomography Optical coherence tomography (OCT) is a noninvasive ocular imaging technique that provides high-resolution images of retinal architecture in vivo. Changes in peripapillary retinal nerve fiber layer (RNFL) thickness represent axonal damage, whereas loss of macular volume and ganglion layer thickness provides an indirect measure of neuronal injury in the afferent visual pathway. [39] In the context of acute optic neuritis, OCT-measured peripapillary RNFL thickness tends to be elevated in the eye affected by optic neuritis initially, presumably because of axoplasmic flow stasis. [39] In contrast, macular volume and ganglion layer measures, as determined with OCT, are comparable between affected and unaffected eyes of patients at symptom onset but later decline for up to 12 months. [39] Visual outcomes after acute optic neuritis—including high- and low-contrast letter acuity, color vision, and visual field sensitivity—correlate with the amount of OCT-measured RNFL, ganglion layer, and macular volume loss detected 6 to 12 months after onset of optic neuritis. [39] Recurrent optic neuritis, such as that seen with NMOSD, has been associated with poorer OCT measures. In a study of pediatric patients with CNS demyelinating syndromes, there was a 9-μm (9%) decrement in RNFL thickness for each additional optic neuritis episode. [40] One disadvantage of OCT is that a so-called floor effect can complicate detection of new changes in RNFL thickness in the setting of pre-existing optic atrophy, since mean RNFL values do not decrease below a measure of approximately 30 μm, regardless of the extent of optic nerve injury. [39] Optic neuritis: Acute management The Optic Neuritis Treatment Trial (ONTT) showed that high-dose intravenous corticosteroids (250 mg administered every 6 hours for 3 days, followed by oral prednisone [1 mg/kg/day] for 11 days) accelerated visual recovery relative to oral prednisone (1 mg/kg/day) and oral placebo. [27] In the ONTT, the only benefit of corticosteroids was hastened visual recovery within the first 2 weeks, which is the primary indication for treatment. [41] Secondary analyses of the trial data suggest that this early benefit represents only about 1 or 2 lines of Snellen acuity. [41] Subsequent studies have shown that the bioavailability of 1250 mg of oral prednisone (or 500 mg, administered orally twice daily) is comparable to that of 1 g of intravenous methylprednisolone (IVMP). [28, 42, 43] Martinelli and colleagues compared the efficacy and safety of 1000 mg of IVMP and 1000 mg of oral methylprednisolone in patients experiencing MS relapse. [43] Both treatment groups demonstrated reduced gadolinium-enhancing MRI lesions over time with a noninferiority effect evident between the 2 routes of administration. Patients in both treatment groups also showed significant improvement in Expanded Disability Status Scale (EDSS) scores in this study. [43] Burton and colleagues compared the efficacy of oral and intravenous steroids for MS relapses and reported no significant differences in clinical, radiologic, or pharmacologic outcomes between the groups. [44] Therefore, in clinical practice, high-dose oral steroids are often substituted for intravenous treatment because they are a more convenient option for patients and their caregivers. Patient-related factors should be considered when a decision about whether to initiate or defer treatment with steroids is being made for a patient with optic neuritis. In 2000, the Quality Standards Subcommittee of the American Academy of Neurology (AAN) reviewed the role of high-dose corticosteroids in the treatment of acute optic neuritis. The recommendation from the AAN was that treatment should be given with the intention to hasten recovery but not to improve ultimate visual outcome. Moreover, treatment decisions should take other non–evidence-based factors into account, such as quality of life, risk to the patient, and visual function in the fellow eye. [45] In contrast to typical optic neuritis associated with MS, optic neuritis associated with NMOSD and MOGAD needs to be more aggressively managed, often with more prolonged steroid regimens. Because of the disparate levels of visual recovery observed with these conditions, acute treatment algorithms are being proposed based on expert opinion and findings from retrospective studies. [41] Findings from retrospective studies of the acute treatment of NMOSD optic neuritis also support the early use of plasma exchange as add-on therapy (Table 5). [41] Prognosis for visual recovery Visual recovery after typical optic neuritis (associated with MS or sporadic in nature) tends to be favorable and frequently occurs within 3 to 6 weeks of symptom onset. During this time, patients experience optic atrophy, with temporal optic disc pallor. In the ONTT, mean visual acuity 1 year after entry improved to 20/20 (Snellen equivalent), with less than 10% of patients having a visual acuity worse than 20/40. [46] Early features that may predict a less favorable recovery after optic neuritis include visual acuity of 20/50 or worse, contrast sensitivity less than 1.0 log units, and visual field mean deviation of -15 decibels or less 1 month after initial presentation. [47] Motion perception deficits have been shown to persist a year after optic neuritis, despite recovery of high- and low-contrast visual acuity, color vision, and visual field performance. [48] Persistent deficits in motion perception may partly explain why many patients with optic neuritis describe problems with visual tracking in the postacute phase. The risk of developing multiple sclerosis after optic neuritis Studies have shown that the risk of developing MS increases over time in patients who present with optic neuritis as a clinically isolated syndrome (CIS). In a study conducted by Rodriguez and colleagues, [49] the 10-year risk of clinically definite MS was 39%, the 20-year risk was 49%, and the 40-year risk was 60%. In the longitudinal follow-up from the ONTT, the 15-year risk of developing clinically definite MS was 25% in patients with no brain lesions on baseline MRI, compared with 72% in patients with 1 or more lesions. [50] The risk for MS was 3 times higher in women in the ONTT. [50] Moreover, MS was more than twice as likely to develop in patients with retrobulbar optic neuritis as in patients with papillitis. [50] However, in the ONTT era, MS was diagnosed based on clinical criteria, whereas MS can currently be diagnosed at the time of the first clinical event based on MRI evidence of dissemination of lesions in space and time. [8] Optic Neuritis Associated with Neuromyelitis Optica Spectrum Disorder and Myelin Oligodendrocyte Glycoprotein IgG–Associated DiseaseIn cases of neuromyelitis optica spectrum disorder (NMOSD), optic neuritis is often more bilateral and severe, with visual acuity at presentation being the Snellen equivalent of 20/200 or worse. [51] Altitudinal visual field defects are more likely to be observed, and recovery may be poor despite high-dose corticosteroid therapy. [51] During optic neuritis attacks, lesions within the optic nerves may be detected with fat-suppressed T2-weighted orbital magnetic resonance imaging (MRI) sequences. [51] Typically, gadolinium enhancement of the optic nerve is seen on T1-weighted sequences. Bilateral optic nerve involvement, with a posterior nerve predominance (especially with extension into the optic chiasm), or extensive lesions of the optic nerve (more than half of the nerve length involved) are all radiologic features suggestive of NMOSD. [51] Optic neuritis associated with myelin oligodendrocyte glycoprotein IgG-associated disease (MOGAD) typically occurs with or without other neurologic symptoms, and it is often recurrent.(ref66} Patients often report pain at symptom onset and manifest significant optic disc edema, which distinguishes these cases from optic neuritis associated with multiple sclerosis (MS). [52] The MRI features of MOGAD-associated optic neuritis include longitudinally enhancing intraorbital lesions of the optic nerve, seen best with T1-weighted fat-suppressed gadolinium-enhanced views. [41, 52] Fifty percent of patients with MOGAD optic neuritis will also manifest perineural involvement with contrast enhancement of the optic nerve sheath and surrounding orbital tissue. [52] Although MOGAD optic neuritis attacks tend to present with severe vision loss, the majority of patients show good clinical recovery, which is different from NMOSD-associated optic neuritis. [41] UveitisPatients with MS are known to experience various forms of ocular inflammation, including uveitis, retinal perivascular sheathing (periphlebitis), and retinitis. [53, 54] Uveitis refers to inflammation of the uveal tract and is 10 times more common in patients with MS (incidence of 1-2%) than in the general population. [53, 54] Intermediate uveitis, or pars planitis, is the most frequent form of uveitis seen in patients with MS. Among patients with pars planitis, 8-12% will be diagnosed with MS. [54] Patients with uveitis report blurred vision, floaters, photophobia, pain, and eye redness. Ocular complications include retinal neovascularization, cystoid macular edema, cataracts, retinal detachment, and epiretinal membrane formation. Although uveitis and complications thereof can occur as part of MS itself, they may also arise as a consequence of MS therapy. Specifically, patients with MS who are treated with fingolimod, a sphingosine-1-phosphate receptor modulator, may develop fingolimod-associated macular edema (FAME). The clinical features of FAME typically manifest within months of initiation of therapy, although patients may or may not have symptomatic vision loss. [55] Patients with MS who have coexisting diabetes or a history of uveitis may be at an increased risk for development of FAME. [55] Dilated fundus examination, optical coherence tomography (OCT), and fluorescein angiography are the primary diagnostic tools in the evaluation of FAME. Treatment may consist of cessation of fingolimod therapy, observation, nonsteroidal anti-inflammatory agents, and/or corticosteroids. [55] Treatment typically starts with cessation of fingolimod treatment, which is often enough to alleviate manifestations of FAME. If development of FAME is suspected, referral of the patient to a general ophthalmologist, neuro-ophthalmologist, or retina specialist is appropriate. Orbital DiseaseAlemtuzumab is a humanized monoclonal antibody that targets cells expressing CD52. As a disease-modifying therapy (DMT), this agent effectively decreases relapse rate and disability progression in patients with relapsing forms of multiple sclerosis MS (Table 2). However, secondary autoimmune disorders complicate therapy in nearly 50% of patients being treated with alemtuzumab, with Graves disease being the most common. [37] Affected patients may have mild to severe manifestations of Graves disease–related eye disease/orbitopathy characterized by proptosis, lid lag, lagophthalmos, corneal exposure, a restricted pattern of ocular misalignment, and optic nerve impingement. [37] Thus, MS specialists treating patients with alemtuzumab should have a low threshold for referral of patients with suspected thyroid-related eye disease for consultation with an ophthalmologist. Posterior visual pathway lesionsLesions in the retrochiasmal and retrogeniculate visual pathways also affect patients with MS and other central nervous system (CNS) inflammatory disorders, albeit not with the same reported frequency as optic neuritis events. These lesions can be more difficult to diagnose because affected patients do not experience pain and may not be aware of deficits. If central vision is affected, patients with retrochiasmal or retrogeniculate lesions may describe missing parts of words of sentences with a binocular view, which is a hint that the visual deficit affects both eyes. Vision loss is characterized by homonymous visual field deficits, which may or may not completely resolve over time. Homonymous defects can impair a patient’s ability to drive safely, particularly when he or she is unaware of the deficit. Furthermore, homonymous field deficits represent a potential red flag among patients with MS who use natalizumab, since they are at risk for development of progressive multifocal leukoencephalopathy (PML), a CNS infection caused by John Cunningham (JC) virus. This condition occurs more frequently in patients with MS who have previously used immunosuppressant drugs, who have serum positivity for JC virus, and who have a longer duration of immunosuppressant therapy. [10] Natalizumab-associated PML is typically heralded by cognitive, motor, and language deficits; but vision loss and homonymous visual field deficits have been reported in 1 study as presenting features in 8 of 28 (29%) and 5 of 28 (18%) patients, respectively. [10] Progressive multifocal leukoencephalopathy has also been reported in the context of dimethyl fumarate use. [14] Therefore, new onset of homonymous visual field loss in patients with MS who have a history of treatment with natalizumab (or immunosuppression due to combination therapies or newer disease-modifying agents) should prompt consideration of PML, in part because of the high rates of morbidity and mortality associated with this diagnosis. Which ocular or vision related finding is a complication of multiple sclerosis?A common visual symptom of MS is optic neuritis — inflammation of the optic (vision) nerve. Optic neuritis usually occurs in one eye and may cause aching pain with eye movement, blurred vision, dim vision, or loss of color vision.
Which findings is consistent with a diagnosis of multiple sclerosis?Criteria for a diagnosis of MS
Find evidence of damage in at least two separate areas of the central nervous system (CNS), which includes the brain, spinal cord and optic nerves AND. Find evidence that the damage occurred at different points in time AND. Rule out all other possible diagnoses.
What is the complication of multiple sclerosis?The complications of MS range from mild to severe. They can range from fatigue to the inability to walk. Other problems include loss of vision, balance, and bowel or bladder control. Depression can result from the difficulty of living with a chronic condition.
What are the important ocular features of multiple sclerosis?Ocular motor deficits in multiple sclerosis include internuclear ophthalmoplegia and nystagmus, resulting in diplopia, oscillopsia, blurred visual, loss of stereopsis, and reading fatigue. Multiple sclerosis also may be associated with ocular inflammatory diseases, in particular pars planitis and retinal periphlebitis.
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Which ocular or vision related finding is a complication of multiple sclerosis quizlet?
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