Acute Vision Loss  

Acute Vision Loss  

Introduction

• Acute vision loss can be defined as vision loss occurring over a period ranging from a few seconds to a day or two. The vision is generally reduced to 20/200 or worse and usually affects one eye.

Epidemiology & Demographics

• •Incidence of acute vision loss: NA.
• •Estimates of the prevalence of blindness from all causes vary between industrialized and developing countries. ¹ In developed countries, the major causes of overall blindness are primarily cataract, glaucoma, and retinal disease (mostly macular degeneration and diabetic retinopathy), all of which are strongly related to advancing age. The prevalence rate for blindness in any society is typically 100-fold greater among individuals older than 65 yr than among children in the same country. ²
• •The major causes of acute vision loss not related to trauma include vascular occlusion, retinal detachment, vitreous hemorrhage, macular disorders, neuro-ophthalmologic disease, and hysteria.

Etiology & Risk Factors ³

• •Acute central retinal artery occlusion: Acute central retinal artery occlusion occurs most commonly in those aged 50 to 70 yr. Risk factors include hypertension, cardiac disease, diabetes, collagen vascular disease, vasculitis, cardiac valvular abnormality, and sickle cell disease. Patients with increased orbital pressure are also at risk, including patients with acute glaucoma, retrobulbar hemorrhage, and endocrine exophthalmos.
• •Acute central retinal vein occlusion: There are two types of central retinal vein occlusion, ischemic and nonischemic. The nonischemic type involves mild fundus changes and does not include an afferent pupillary defect. ⁴
• •Retinal detachments: Retinal detachment affects about 1 in 300 people over the course of their lifetime. ⁵ Rhegmatogenous retinal detachment, the most common type of retinal detachment, generally occurs in patients older than 45 yr, is more common in men than in women, and is associated with degenerative myopia. Posterior vitreous detachment occurs most frequently in patients older than 60 yr.
• •Macular disorders: Degenerative maculopathies occur as a result of trauma, radiation exposure, inflammatory or infectious disease, vascular disease, toxins, or hereditary disease. They may also be idiopathic in nature. The most common form is AMD after the age of 65 yr. It is a leading reason for legal blindness in the United States. If left untreated, hemorrhage, transudation, scar formation, or exudative detachment of the retina can result. If a large hemorrhage occurs from the neovascular membrane, it can cause severe central visual loss and may break through the retina into the vitreous, causing peripheral visual loss. About 10% of patients with AMD have the neovascular form manifested by an often rapid decrease in central visual acuity caused by bleeding and scarring secondary to choroidal neovascularization. Inflammatory processes involving the retina may also cause visual loss, especially if the macula is involved. Bacterial, viral, and protozoal agents have been shown to cause maculopathy.
• •Optic neuritis is an inflammatory response associated with an infection or autoimmune disease (such as collagen vascular disease, granulomatous disease, MS, or neuromyelitis optica). There is acute monocular vision loss caused by focal demyelination of the optic nerve. The patients’ ages range from 15 to 45 yr. Approximately 30% of patients with acute optic neuritis develop multiple sclerosis within 5 yr. ⁶
• •Ischemic optic neuropathy is the most common optic neuropathy and one of the most common causes of visual loss past middle age. It is extremely rare in people younger than 50 yr, but the incidence rises with each subsequent decade. A significant proportion of patients sustain visual loss, which can be sudden, severe, and bilateral. Occasionally, visual loss is preceded by episodes of amaurosis fugax.
• •Primary angle closure glaucoma: Primary angle-closure glaucoma occurs when elevated intraocular pressure is associated with closure of the filtration angle or obstruction in the circulating pathway of the aqueous humor.
• •Giant cell arteritis (GCA) is a segmental systemic granulomatous arteritis affecting medium and large arteries in individuals >50 yr. Inflammation primarily targets branches of the extracranial head and neck blood vessels (external carotids, temporal arteries, ciliary and ophthalmic arteries).
• •Nonarteritic ischemic optic neuropathy (NION): These patients lack the classic symptoms of giant cell arteritis and do not have an elevated ESR. Most of these patients have systemic vascular disease, diabetes, or hypertension, and they tend to be younger.
• •Toxic and metabolic neuropathies: Common toxic causes include barbiturates, chloramphenicol, emetine, ethambutol, ethylene glycol, isoniazid, heavy metals, and methanol. Causes of metabolic optic neuropathies include thiamine deficiency and pernicious anemia.

Pathophysiology

• •Monocular vision loss is due to a lesion in one eye or optic nerve. Binocular visual loss, on the other hand, can result from disease located anywhere in the visual pathways from the corneas to the occipital poles. Lesions involving the optic chiasm produce nonhomonymous visual abnormalities ( Fig. E1 ).FIG. E1Visual fields that accompany damage to the visual pathways .1, Optic nerve: unilateral amaurosis. 2, Lateral optic chiasm: grossly incongruous, incomplete (contralateral) homonymous hemianopia. 3, Central optic chiasm: bitemporal hemianopia. 4, Optic tract: incongruous, incomplete homonymous hemianopia. 5, Temporal (Meyer) loop of the optic radiation: congruous partial or complete (contralateral) homonymous superior quadrantanopia. 6, Parietal (superior) projection of the optic radiation: congruous partial or complete homonymous inferior quadrantanopia. 7, Complete parieto-occipital interruption of the optic radiation: complete congruous homonymous hemianopia with psychophysical shift of the foveal point, often sparing central vision and resulting in “macular sparing.” 8, Incomplete damage to the visual cortex: congruous homonymous scotomas, usually encroaching at least acutely on central vision. Lt, left; Rt, right.From Goldman L, Schafer AI: Goldman-Cecil medicine, ed 26, Philadelphia, 2019, Elsevier.
• •Acute central retinal artery occlusion: The ophthalmic artery is the first intracranial branch of the internal carotid artery, and the central retinal artery is the first intraorbital branch of the ophthalmic artery. Central retinal artery occlusion causes an ischemic stroke of the retina.
• •Retinal detachments: Retinal detachment is the separation of the neurosensory retina (NSR) from the retinal pigment epithelium (RPE). This results in the accumulation of subretinal fluid (SRF) in the potential space between the NSR and the RPE. The main types of retinal detachment are rhegmatogenous (caused by retinal tear with vitreous fluid passing through the defect), tractional (subretinal fluid caused by fibrous proliferation and pulling from vitreous gel), and exudative (accumulation of subretinal fluid due to inflammation or tumors). Ocular tumors and inflammation including posterior uveitis and scleritis are the most common causes of exudative retinal detachment. Trauma may be associated with rhegmatogenous detachment by causing tears in the retina or by causing a disinsertion of the retina from its attachment at the ora serrata anteriorly. Traumatic retinal detachment can occur at any age. There is greater risk with severe myopia. Exudative retinal detachment occurs as a result of fluid or blood leakage from vessels within the retina. Conditions leading to exudative retinal detachment include hypertension, toxemia of pregnancy, central retinal venous occlusion, glomerulonephritis, papilledema, vasculitis, and choroidal tumor. Traction retinal detachment is a consequence of fibrous band formation in the vitreous and contraction of these bands. These fibrous bands result from the organization of inflammatory exudates or blood from prior vitreous hemorrhage.
• •Macular degeneration, usually referred to as age-related macular degeneration (AMD), is an acquired degeneration of the retinal pigment epithelium and subsequently the neurosensory retina and choroid resulting in loss of central vision. The etiology is not known but a combination of genetic predisposition to immune- and complement-mediated inflammation and certain risk factors plays an important role. Nonexudative (or “dry”) AMD is the most common, but exudative (or “wet”) AMD is the most visually devastating. The main mediator of neovascularization in wet AMD is vascular endothelial growth factor (VEGF). It induces angiogenesis and increases inflammation and vascular permeability.
• •Vitreous hemorrhage results from bleeding into the preretinal space or into the vitreous cavity. The most common causes are diabetic retinopathy and retinal tears. Additional causes include neovascularization associated with branch vein occlusion, sickle cell disease, retinal detachment, posterior vitreous detachment, trauma, age-related macular degeneration (AMD), retinal artery microaneurysms, trauma, and intraocular tumor.
• •Primary angle closure glaucoma: Results from narrow angles with acute closure. The blockage of circulatory path of the aqueous humor causes increase in IOP. Acute closure glaucoma (ACG, primary angle closure glaucoma) occurs more commonly in eyes with shorter axial length (farsightedness), shallower anterior chamber, and a relatively larger lens (enlarging cataract).
• •Giant cell arteritis is a vasculitis of unknown etiology. An association with HLA-DRB∗04 has been identified. ⁷ Recent demonstration of varicella zoster virus virion, antigen, and DNA within the vessel walls of the temporal arteries on histopathologic specimens of giant cell arteritis suggest an association.
• •Nonarteritic ischemic optic neuropathy (NION): Most of these patients have systemic vascular disease, diabetes, or hypertension.
• •Optic neuritis: the potential etiology of optic neuritis includes inflammation, infections, ischemia, drugs, and hereditary disorders:
  • 1.Inflammatory: MS, neuromyelitis optica spectrum disorder (NMOSD), sarcoidosis, lupus, Sjögren, Behçet, postinfectious, postvaccination, neuroretinitis, acute disseminated encephalomyelitis, paraneoplastic, autoimmune optic neuropathy
  • 2.Infectious: Syphilis, TB, Lyme disease, Bartonella, HIV, cytomegalovirus (CMV), herpes, helminths, chickenpox, Q fever, periorbital infections, Toxocara spp.
  • 3.Ischemic: Anterior and posterior ischemic optic neuropathies, diabetic papillopathy, branch or central retinal artery or vein occlusion
  • 4.Drugs and toxins: Arsenic, methanol, ethambutol, cyclosporine, etc.
  • 5.Mitochondrial: Leber hereditary optic neuropathy, other mitochondrial
• •Compressive optic neuropathy occurs at any age and can be caused by tumor, aneurysm, sphenoid sinusitis or mucocele, blunt trauma, or thyroid disorders. Although defined as a prechiasmal disorder, compression can occasionally occur far enough posteriorly to affect the optic chiasm. Chiasmal compression can be secondary to pituitary tumors, craniopharyngioma, or meningioma. Postchiasmal vision loss may be caused by infarction, tumor, arteriovenous malformation, and migraine disorders.
• •Functional vision loss: These patients fall into two categories: Hysterical conversion reactions and malingering.

Clinical Manifestations

Presenting Signs & Symptoms

• •The presenting signs and symptoms vary with the cause of the acute vision loss:
  • 1.Acute central retinal occlusion is usually painless. Patients report a severe loss of vision that develops over seconds.
  • 2.Central retinal vein occlusion is painless and may present with a wide spectrum of clinical appearances depending on the degree of venous obstruction present. Vision loss ranges from minimal to recognition of hand motion only. There are two types of central retinal vein occlusion, ischemic and nonischemic. The nonischemic type involves mild fundus changes and does not include an afferent pupillary defect. These patients tend to have less severe visual loss, with two thirds of the patients having 20/40 or better visual acuity without therapy. ⁴ Patients with ischemic central retinal vein occlusion have a marked decrease in visual acuity and often an afferent pupillary defect. Appearance can vary but classically includes dilated and tortuous veins, retinal hemorrhages, and disk edema. Hemorrhages can cover the entire fundus, giving a “blood and thunder” appearance ( Fig. E2 ).FIG. E2A, Central retinal vein occlusion. Note “blood and thunder” appearance. B, Topographic diagnosis of visual field defects.A, Image courtesy www.tedmontgomery.com and B, from Bradley WG, Duroff RB, Fenichel GM, Jankovic J: Neurology in clinical practice, ed 5, Oxford, 2007, Butterworth-Heinemann, in Marx JA et al: Rosen’s emergency medicine: concepts and clinical practice, ed 8, Philadelphia, 2014, Saunders.
  • 3.Retinal breaks and detachment: Typically, patients note flashes of light related to the traction on the retina, floaters related to vitreal blood or pigmented debris, and visual loss. The visual loss is commonly described as a filmy, cloudy, or curtainlike appearance. Pain is absent.
  • 4.Posterior vitreous detachment: Symptoms are similar to those of retinal break, vitreous hemorrhage, and retinal detachment.
  • 5.Vitreous hemorrhage: Symptoms begin with floaters or “cobwebs” in the vision and may progress over a few hours to severe visual loss without pain.
  • 6.Primary angle closure glaucoma: Although angle-closure glaucoma can present with an acute painful crisis associated with blurred vision, more than 75% of patients present with an asymptomatic course with progressive loss of the visual field (similar to that in patients with primary open-angle glaucoma; referred to as intermittent, subacute, or chronic angle closure).
  • 7.Inflammatory processes of retina: The presenting symptoms and signs vary according to the disease process and severity. Inflammatory debris from exudative processes may fill the vitreous, leading to a cloudy appearance. Infections within the eye can cause pain and redness.
  • 8.Optic neuritis: Symptoms include a progressive vision loss over several hours or days and ocular pain with eye movement.
  • 9.Giant cell arteritis is characterized by weight loss, malaise, jaw pain, headache, scalp tenderness, polymyalgia rheumatica, low-grade fever, and severe painless visual loss.
  • 10.Nonarteritic ischemic optic neuropathy (NION): Patients have painless visual loss, afferent pupillary defects, disk swelling, and visual field defects that respect the horizontal meridian.
  • 11.Compressive optic neuropathy: Patients with compressive optic neuropathy present with symptoms related to the cause of the compression and increased intracranial pressure (headaches, seizures, lethargy, vomiting) and have visual loss. Patients with postchiasmal compression report difficulty in performing a certain task, such as reading. Lesions can be located from the immediate postchiasmal optic tract to the occipital cortex. The classic visual field defect is homonymous hemianopsia, a visual field loss on the same side of both eyes.
  • 12.Functional (psychogenic) vision loss: One of the most common presentations of psychogenic blindness is monocular visual loss and ipsilateral hemiparesis. This combination defies the facts of neuroanatomy because the division of optic pathways at the optic chiasm dictates that a cerebral lesion causing hemiparesis will cause hemianopia—not monocular blindness. In another presentation, individuals with psychogenic blindness often needlessly wear sunglasses. This ploy seems to serve several purposes: it signals that they are blind, reduces visual distractions, and prevents observers from seeing when they establish eye contact.

Diagnosis

• •Comprehensive history and physical examination, direct ophthalmoscopy, laboratory evaluation, and diagnostic imaging.
• •The pattern of a patient’s visual loss is invaluable in localizing neurologic lesions. Routine examination at the bedside can detect large visual field defects, but more subtle abnormalities may require formal visual field evaluation. Most of these patients need ophthalmic or neurologic referral for a complete workup.

Diagnostic Criteria

• •Vision loss occurring over a period ranging from a few seconds to a day or two. The vision is generally reduced to 20/200 or worse.
• •Physical findings (see below) will confirm the diagnosis.

History & Physical Examination

• •Central retinal occlusion: Examination reveals a markedly reduced visual acuity with a prominent afferent pupillary defect. On funduscopic examination, the retina is edematous with a pale gray-white appearance, and the fovea appears as a cherry-red spot.
• •Retinal breaks and detachment: Visual acuity can be minimally changed to severely decreased. Visual field cuts relate to the location of the retinal detachment, and an afferent pupillary defect occurs if the detachment is large enough. When the detachment is visualized by ophthalmoscopy, the retina appears out of focus at the site of the detachment. In large retinal detachments with large fluid accumulation, the bullous detachment, with retinal folds, can easily be seen.
• •Vitreous hemorrhage: Direct ophthalmoscopy reveals a reddish haze in mild cases to a black reflex in severe cases. Details of the fundus are usually difficult to visualize. The hemorrhage may be evenly distributed throughout the vitreous or focal. Long-standing preretinal hemorrhage can become a white mass that may be misdiagnosed as a tumor, exudate, or infection.
• •Macular disorders: Patients have either a gradual or rapid onset of visual loss. Funduscopy reveals scattered drusen. Drusen are small, sharply defined yellow-white masses. Some patients with AMD and drusen develop a choroidal (subretinal) neovascular membrane, which appears as a grayish-green membrane beneath the retina.
• •Inflammatory processes of retina: Infections within the eye are often associated with severe pain, redness, and periocular edema.
• •Optic neuritis: Visual acuity can range from minimal loss to no light perception. An afferent pupillary defect is usually present, and direct ophthalmoscopic examination reveals a normal or swollen disk. The natural history of optic neuritis is for visual acuity to reach its poorest within 1 wk and then slowly improve over the next several weeks.
• •Giant cell arteritis: Signs include a large afferent pupillary defect, visual loss, and a visual field defect that may respect the horizontal meridian. The optic disk shows pallor and swelling. Tenderness and nodularity of affected temporal artery may be present.
• •Toxic and metabolic neuropathies: These processes are bilateral, progressive, and symmetric. Visual loss can be severe, and visual field testing reveals central defects.
• •Chiasmal neuropathy: Visual loss is gradual and progressive. Although formal visual field testing is necessary to stage the condition, the diagnosis can usually be made by confrontation visual field testing. The classic defect is a bitemporal hemianopsia; however, tumors often compress the optic chiasm and optic nerves asymmetrically, resulting in combined central and temporal defects.
• •Functional vision loss: Patients with hysterical conversion reactions have a nondeliberate, imagined visual loss. The patient has a flatter affect than one would expect. The patient might appear completely unaffected emotionally by the vision loss. The malingerer, on the other hand, is a patient who is well aware that no vision loss exists, yet deliberately feigns visual loss for secondary gain. This patient is typically overemotional concerning the visual loss. Normal pupillary reflexes and the absence of an afferent pupillary defect, together with normal funduscopic examination findings, point toward functional visual loss.

Laboratory Tests

• •Fasting glucose, HBA1c
• •Lipid panel
• •Erythrocyte sedimentation rate (ESR), CRP
• •Toxicology screen when suspecting toxic neuropathy
• •Thiamine, vitamin B ₁₂ level when suspecting metabolic neuropathy
• •CBC, antinuclear antibody (ANA), ACE
• •Consider HIV Ab, Lyme titer, rapid plasma reagin (RPR), other autoimmune or infectious causes in patients with bilateral or recurrent optic neuritis (ON); neuromyelitis optica (NMO), immunoglobulin (IgG), myelin oligodendrocyte glycoprotein (MOG IgG), paraneoplastic CRMP-5-IgG

Imaging Studies

• •Contrast enhanced brain MRI when suspecting optic neuritis or compressive neuropathy
• •Brain MRA when suspecting aneurysm
• •Ocular ultrasonography—useful in confirming the presence of a retinal detachment
• •Laser scan of nerve fiber layer and optic nerve, optical coherence tomography (OCT) in suspected angle closure glaucoma
• •Nerve fiber analysis, OCT, Heidelberg retinal tomography in suspected angle closure glaucoma
• •Fundus photography (optic nerve photos)—helpful for comparing changes in optic nerve shape
• •Fluorescein angiography for neovascular disease such as diabetic retinopathy, retinal vein occlusions
• •OCT in suspected macular degeneration

Diagnostic Procedures

• •Direct funduscopy
• •Visual field testing
• •Measurement of intraocular pressure in angle closure glaucoma (IOP can be extremely high, >60 mm Hg)
• •Gonioscopy for direct visualization of the chamber angle and slit-lamp examination in angle closure glaucoma
• •Optic nerve evaluation
• •Indirect ophthalmoscopy to visualize the more anterior portions of the retina in suspected retinal detachment
• •Temporal artery biopsy in suspected giant cell arteritis

Differential Diagnosis

The differential diagnosis of acute visual loss not related to trauma includes vascular occlusion, retinal detachment, vitreous hemorrhage, macular disorders, neuro-ophthalmologic disease, and hysteria. The differentiation between each of them is described in the sections on clinical presentation and physical examination; listed below is the differential diagnosis of acute painful, acute painless, and transient vision loss.

Vision Loss, Acute, Painful

• 1.Acute angle-closure glaucoma
• 2.Corneal ulcer
• 3.Uveitis
• 4.Endophthalmitis
• 5.Factitious
• 6.Somatization syndrome
• 7.Trauma

Vision Loss, Acute, Painless

• 1.Retinal artery occlusion
• 2.Optic neuritis
• 3.Retinal vein occlusion
• 4.Vitreous hemorrhage
• 5.Retinal detachment
• 6.Exudative macular degeneration
• 7.CVA
• 8.Ischemic optic neuropathy
• 9.Factitious

Vision Loss, Monocular, Transient

• 1.Thromboembolism
• 2.Vasculitis
• 3.Migraine (vasospasm)
• 4.Anxiety reaction
• 5.CNS tumor
• 6.Giant cell arteritis
• 7.Multiple sclerosis

Treatment

Treatment varies with the cause of the acute vision loss.

First-Line Treatment

Giant Cell Arteritis

• •If there is clinical suspicion of GCA, treatment should be initiated without waiting for results of laboratory or imaging studies.
• •IV methylprednisolone (250 to 1000 mg for 1 to 3 days) is considered standard of care in patients with severe clinical manifestations such as visual loss from ischemic optic neuropathy.
• •Oral prednisone (1 mg/kg/day): High-dose oral regimen should be continued at least until symptoms resolve and ESR returns to normal; usually 3 to 4 wk after treatment initiation. Steroid taper is very slow (10% to 20% per mo) with monitoring of clinical features as well as ESR and CRP. When dose <10 mg/day, taper by 1 mg/mo. Treatment may last up to 2 yr or more.
• •Although corticosteroids have traditionally been the treatment of choice, tocilizumab, an IL-6 receptor blocker, was recently approved by the FDA for the treatment of GCA. ⁸ Patients treated with tocilizumab and prednisone achieved remission faster, had a greater reduction in steroid dosage, and had prolonged maintenance of remission when compared with those treated with prednisone alone.

Optic Neuritis

Treatment is with methylprednisolone (MP) 250 mg IV every 6 hr (or 1 g IV daily) for 3 days followed by an oral prednisone taper of 11 days.

Retinal Tear/Detachment

Immediate surgery. The three principal methods for reattachment of the retina in patients with primary retinal detachment are scleral buckling, vitrectomy, and pneumatic retinopexy. There is a paucity of randomized trials comparing these procedures, and the choice remains subjective. Some data suggest that vitrectomy may be preferable for detachment in pseudophakic eyes, whereas primary detachment in phakic eyes with complexity exceeding the original indications for pneumatic retinopexy may be treated with scleral buckling or vitrectomy. ⁹

Vascular Occlusion

Central retinal artery occlusion is an ischemic stroke and may be amenable to the use of thrombolytic agents. A 2011 study demonstrated that the effective therapeutic time window of opportunity for intraarterial thrombolytic therapy is likely less than 6 hr. ^8 , 10 A study found lack of efficacy of anterior chamber paracentesis, globe massage, and intraocular pressure–lowering agents, in acute central retinal artery occlusion. Treatment of central retinal vein occlusion also includes lowering of intraocular pressure, topical steroids, cyclocryotherapy, and photocoagulation. Patients with central retinal vein occlusion who develop macular edema may benefit with treatment with intraocular antivascular growth factor. ¹¹ Intravitreal injection of steroids also shows promise in the management of macular edema associated with central retinal vein occlusion. ¹²

Acute Angle Closure Glaucoma ¹³

Treatment consists of IV mannitol, pilocarpine, β-blockers, Diamox laser iridotomy, and anterior chamber paracentesis (as emergency treatment).

Macular Degeneration

• The introduction of therapies blocking VEGF has dramatically changed the management of AMD and is now the standard of care in the management of neovascular AMD.
• Intravitreal injections of anti-VEGF agents (ranibizumab, bevacizumab, and aflibercept) are first-line treatments for neovascular AMD.
• Intravitreal administration of ranibizumab, a humanized antibody fragment that neutralizes all active forms of VEGF A, was shown to stabilize or improve vision in 95% of patients compared to 65% of patients treated with verteporfin photodynamic therapy (PDT).
• Aflibercept is a soluble protein that acts as a VEGF receptor decoy and is the most recently FDA-approved intravitreal therapy.
• Randomized controlled trials showed it to be noninferior to ranibizumab. Bevacizumab, a full-length monoclonal antibody to VEGF, is used off-label as intravitreal therapy. Its cost per intravitreal dose is significantly lower than that of ranibizumab and aflibercept.
• However, several comparative effectiveness trials have shown bevacizumab to be noninferior to ranibizumab. ¹³

Vitreous Hemorrhage

• •Laser treatment may be indicated for certain retinal diseases (diabetic retinopathy, retinal vein occlusion, retinal macroaneurysm).
• •Treatment may be indicated for wet macular degeneration or diabetic retinopathy (intravitreal injection).
• •Treat underlying systemic disease.
• •Repair any damage from trauma.

Compressive Neuropathy (Neoplasm)

Traditionally, surgery has been the main treatment for craniopharyngioma. However, radiation treatment instead of surgery may be an option in selected cases. Intralesional 32P irradiation or bleomycin for unresectable tumors.

Functional Vision Loss

• •Education about illness including explanation and diagnosis. A multidisciplinary treatment team including a neurologist and psychiatrist can be helpful for some patients.
• •Medical providers who fail to explain the diagnosis, misattribute the symptoms, and/or continue to pursue medical investigations and procedures can contribute to the patient’s belief that there is an irreversible medical cause and thereby risk perpetuating the symptoms.

Referral

Ophthalmology, neurology

References

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