Scotoma
Scotoma: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
Michael J. Puk
Scotoma is defined as a blind or partially blind area in the visual field. A basic understanding of neuroanatomy helps to localize the visual field defect. Simply put, pathology anterior to the optic chiasm produces monocular scotomas, whereas chiasmal or posterior chiasmal lesions form binocular field defects (1,2). Caveats apply here: bilateral retina or optic nerve disease will produce scotomas in each eye.
Approach
Determination of monocular versus binocular vision loss helps to localize the lesion. Patients often confuse a homonymous field loss to one eye (i.e., “can’t see in my right eye” with a right homonymous field loss). Inquire about vision loss while each eye is covered. Check for a Marcus Gunn or afferent pupillary defect (APD) to distinguish between an optic nerve or a retina problem. Example: central scotoma in a right eye with a afferent pupillary defect in the same eye equals optic nerve disease; if no prominent APD, then retina disease is more likely.
A. Special concerns. Sudden vision loss in one eye with an APD in an elderly patient is giant cell arthritis, unless proved otherwise, which requires immediate treatment. Sudden binocular field loss in a patient is a stroke unless proved otherwise and requires prompt evaluation and treatment by the stroke team.
History
A. Nature of the scotoma. Try to establish whether the field loss is monocular or binocular. Binocular scotomas, which imply chiasmal or posterior chiasmal lesions, are vascular (stroke, transient ischemic attack, migraine, ruptured arteriovenous malformation) or compressive in nature (pituitary mass, meningioma, glioma). Establish with the patient the location of the defect. Scotomas that migrate through the visual field include vitreous floaters, vitreous hemorrhage, scintillating scotoma of migraine, and so forth. An altitudinal field loss is likely a prechiasmal lesion [i.e., optic nerve disease (e.g., ischemic optic neuropathy, glaucoma) or retina disease (e.g., detached retina, retina vascular occlusion)]. Central scotomas are commonly seen in optic nerve and macular lesions with macular degeneration by far the most common in the elderly. Macular holes, optic neuritis, toxic or metabolic optic neuropathy, central serous choroidopathy, maculopathy secondary to medications (hydroxychloroquine, thioridazine, chlorpromazine, quinine, tamoxifen), and others are examples of macular-induced central scotomas. Peripheral vision loss, if bilateral and homonymous, indicates a stroke opposite the side of field loss. Tumors, arteriovenous malformations, and migraines can cause hemianopias. Glaucoma, detached retina, retinitis pigmentosa, chronic papilledema, and previous laser treatment for diabetes are also common entities affecting peripheral vision.
B. Onset and timing of scotoma. A scotoma of sudden onset will be secondary to some kind of vascular event: embolic, hypoperfusion, inflammatory, or hemorrhagic. Transient vision loss lasting seconds can occur with temporal arteritis, papilledema, or vertebrobasilar insufficiency. Visual loss lasting minutes to hours occurs in temporal arteritis or amaurosis fugax. Visual changes lasting weeks to months represent retinal vein occlusion, expanding compressive lesion, papilledema, and if associated with pain on eye movement, optic neuritis. Gradual progressive visual field loss occurs with compressive masses; however, acute expanding lesions from infectious, inflammatory (e.g., sarcoid, Tolosa-Hunt), aneurysmal, or apoplexy of a pituitary mass can cause rapid vision loss. Monocular vision loss after head trauma suggests injury to the intracanalicular portion of the optic nerve, compressive fracture of the sphenoid bone, or edema to the optic nerve. Emergent computed tomography (CT) scan with neurosurgical or ophthalmic consultation and high-dose intravenous steroids are needed.
C. Associated symptoms. The presence of neurologic signs or symptoms can localize the area of the pathology. Amaurosis fugax implies ipsilateral internal carotid disease or cardiac disease. History of vertigo, diplopia, and urinary incontinence in a young patient with a monocular central scotoma implies multiple sclerosis. Older patients with acute monocular vision loss associated with periorbital pain and headaches, fatigue, jaw claudication, or muscle aches strongly suggests temporal arteritis. Transient dimming or loss of vision in one or both eyes with orthostatic changes can be seen with papilledema of intracranial hypertension. Progressive monocular visual loss with proptosis obviously implies an orbital mass (optic nerve glioma, meningioma, cavernous hemangioma), but asymmetric thyroid-related orbitopathy can present a similar picture. Monocular loss progressing over time without orbital signs can be seen with an intracanalicular or intracranial optic nerve mass.
D. Past medical and social history. Diabetes and hypertension are the two most common causes of ischemic optic neuropathy (ION). ION presents as a sudden painless monocular vision loss, altitudinal in nature, with an APD. The risk of retinal vascular occlusions is much greater in patients with diabetes mellitus or hypertension. The risk is greater with tobacco use. A history of rheumatic fever, heart murmur, or cardiomyopathy is significant for an embolic source. Sudden vision loss without an APD in a diabetic patient is most likely a vitreous hemorrhage. An acquired immunodeficiency syndrome patient with a CD4 count less than 50 × 103 with visual scotomas needs to be evaluated for cytomegalovirus retinitis. A history of alcohol abuse or a psychiatric patient with bilateral vision loss and change in mental status needs urgent chemistries for anion gap acidosis with hemodialysis if methanol ingestion is suspected. An intravenous drug user can suffer a vascular occlusion from talc.
Physical examination
A. Visual acuity. The vision of each eye should be assessed with spectacles or contact lenses in each eye independently. Central scotomas are seen with optic nerve, macular disease, or (rarely) an occipital tip lesion; and Snellen visual acuity will be decreased.
B. Visual fields. Confrontation field test is performed with each eye independently. Briefly flash several fingers in each of the four quadrants. Bilateral field loss in the same field of vision in each eye indicates injury posterior to the chiasm. Bitemporal field defects are seen with chiasmal lesions (pituitary masses, craniopharyngiomas, and others). Monocular field defects are seen in retina and optic nerve disease.
C. Pupil examination. The presence of a prominent APD, which implies optic nerve injury, will help to differentiate central scotomas caused by macular disease. An APD is commonly seen with optic neuritis, optic neuropathy (ischemic and traumatic), asymmetric glaucomatous damage, optic nerve tumors, and central retinal artery or vein occlusion. An APD is not seen in early papilledema and minimally with macular degeneration, macular holes, or choroidopathy.
D. Fundus examination. Direct ophthalmoscopy can give a quick assessment of the red reflex (i.e., a dim red reflex in a diabetic with vitreous hemorrhage). Vitreous floaters can occasionally be seen as shadows in the red reflex. Examine the nerve for edema, pallor, or glaucomatous cupping. Macular scarring or pigmentary change is most commonly seen with macular degeneration.
E. Other examinations. A neurologic assessment is needed for a patient with bilateral field loss, screening for contralateral paresis and other focal deficits, palpation of the temporal artery for tenderness or diminished pulse if the history suggests giant cell arteritis, as is auscultation of the carotids for bruits and the heart for a murmur in a patient with amaurosis fugax or stroke. Glaucoma can be screened with tonometry. Check arms and legs for signs of intravenous drug abuse.
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A. Laboratory tests. Erythrocyte sedimentation rate and C-reactive protein should be ordered urgently if giant cell arteritis is suspected. Vasculitis workup would include a serologic test for syphilis (VDRL), antinuclear antibody titer, Lyme disease titer, and complete blood count in young patients in whom optic neuritis or ION is suspected. Other laboratory testing is usually not warranted.
B. Imaging studies. CT scan to differentiate ischemic versus hemorrhagic stroke is required to promptly institute tissue-type plasminogen activator (tPA) treatment. A magnetic resonance imaging scan is best utilized in correlating demyelinating disease in patients with optic neuritis. Carotid Doppler ultrasound and an echocardiogram are indicated in amaurosis fugax and stroke to look for embolic sources.
Diagnostic assessment
Ophthalmic consultation can be helpful in confirming and further elucidating the cause of visual scotomas. Suspected giant cell arteritis needs to be aggressively pursued with temporal artery biopsy and steroid treatment. Cerebrovascular accidents, even if vision loss is the only neurologic deficit, need to be evaluated expediently by the stroke team to benefit from tPA treatment (Chapter 4.8). Other visual scotomas can be evaluated with ophthalmic consultation semiemergently.
References
1. American Academy of Ophthalmology. Basic and clinical science. Volume 5. 1993–1994. San Francisco: American Academy of Ophthalmology, 1993.
2. Friedberg MA, Rapuano CJ. Wills Eye Hospital office and emergency room diagnosis and treatment of eye disease. Philadelphia: JB Lippincott, 1990:1–2, 15–16.
3. Bajandas FJ, Kline LB. Neuro-ophthalmology review manual. Thorofare, NJ: Slack Inc., 1988:1–43.
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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