Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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196 Visual Fields
6-3 ISCHEMIC OPTIC NEUROPATHY
This is defined as watershed infarction of the optic disc or, less commonly, the retrobulbar portion of the optic nerve. It may be nonarteritic (NAION) or arteritic (AAION). It is the most common cause of nonglaucomatous optic nerve disorder found in patients older than 50 years.17
6-3-1 Nonarteritic Ischemic Optic Neuropathy. NAION is the sudden, painless, usually nonprogressive visual loss of a moderate degree; initially it is unilateral but it may become bilateral. A minority of cases may be progressive, with a second decrease in visual acuity or visual field, days or weeks after the initial episode. It usually occurs in adults 40 to 65 years old. A second attack in the same eye is extremely rare.
Etiology usually includes vasculopathic causes such as hypertension, diabetes, and/or arteriosclerosis.
Signs include pale segmental disc swelling, flame-shaped hemorrhages, afferent pupillary defect (APD), normal erythrocyte sedimentation rate (ESR), decreased color vision, altitudinal or central visual field defects, and optic atrophy after the edema resolves. The fellow optic disc usually appears normal, but it is often congenitally full, with a small or absent physiologic cup.1723
Visual field findings include the following:
1.Altitudinal. These defects involve the field above or below the point of fixation but do not cross the horizontal midline, at least not initially. Altitudinal defects may involve or spare fixation, depending on the underlying pathology. Typically, this type of defect extends to the periphery.
2.Central. This is described in optic neuritis.
3.Nasal steps. It is the beginning of an arcuate scotoma, manifest only at the nasal edge where it respects the horizontal raphe.
4.Arcuate. This is actually a mild form of an altitudinal defect. It does not involve fixation but rather the areas just peripheral to it.17-19
5.Top/bottom
An altitudinal visual field defect and the optic disc (pallid edema) in a patient with NAION are shown in Figures 6-2 and 6-3, respectively.
There is no proved therapy for this entity. Several different treatment modalities have been tried without success. There should be control of vasculopathic risk factors and systemic diseases such as hypertension and diabetes.24,25
6-3-2 Arteritic Ischemic Optic Neuropathy. The visual loss is usually more profound (counting fingers or worse) and may rapidly become bilateral. It usually affects older patients (older than 70 years).
Systemic symptoms may include headache, jaw claudication, scalp tenderness, proximal muscle and joint aches (polymyalgia rheumatica), anorexia, weight loss, or fever.
Signs include pale swollen disc, often with flame-shaped hemorrhages, that progresses to atrophy when edema resolves; APD; decreased color vision; and sometimes a palpable, tender, and nonpulsatile temporal artery.17,26-29
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Figure 6-2. Altitudinal visual field defect in a patient with nonarteritic ischemic optic neuropathy.
Visual field findings include the same five types described earlier for NAION and severe global depression. Workup should include an immediate ESR (abnormal if greater than 40 mm/hr) and C-reactive protein. Temporal artery biopsy should be obtained if giant cell arteritis (GCA) is based on the symptoms, signs, and/or laboratory tests.
Systemic steroids should be administered immediately once GCA is suspected (intravenous methylpredinisolone 1 g/day for 3 days followed by oral prednisone 60-100 mg/day). The tapering should be very slow, and the goal is to maintain
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Figure 6-3. Nonarteritic ischemic optic neuropathy optic disc (pallid edema).
with the minimal oral dose that suppresses the symptoms and keeps the ESR under normal limits. Visual recovery and prognosis are poor.26-29
6-4 METABOLIC OPTIC NEUROPATHIES
Etiologies includes malnutrition, toxic exposure (ethanol, methanol, tobacco, chloramphenicol, ethambutol, amiodarone, isoniazid, digitalis, chloroquine, streptomycin, disulfiran, lead, and others), and vitamin deficiency (B group). Other vitamins deficiencies also play a role in the pathophysiology in this entity.30-34
In general, metabolic optic neuropathies involve some form of damage to functioning of the mitochondria.
Symptoms include a painless, progressive, usually slow, bilaterally symmetric loss of vision. Signs include moderate visual loss (20/50 to 20/400), decreased color vision, temporal disc pallor, optic atrophy, or even normal-appearing disc.35-38
Visual field findings are usually bilateral but symmetric and include:
1.Bilateral cecocentral. This defect extends from the physiologic “blind spot” through and into the point of fixation. Although a central scotoma may also encompass the blind spot, a cecocentral scotoma is smaller and typically dumbbell shaped.
2.Bilateral central. This is described in optic neuritis.30-38
Figure 6-4 shows a typical visual field findings in metabolic optic neuropathy bilateral symmetric visual field defect in metabolic optic neuropathy.
6-5 COMPRESSIVE OPTIC NEUROPATHY
Etiologies include optic nerve glioma (usually patients younger than 20 years; and positive association with neurofibromatosis), optic nerve sheath meningioma
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Figure 6-4. Cecocentral bilateral symmetric visual field defect in metabolic optic neuropathy.
(usually young women; orbital imaging may show an optic nerve mass, diffuse optic nerve thickening, or a railroad track sign, which is an increased contrast of the periphery of the nerve), any intraorbital or intracranial mass (schwannoma, hemangioma, pituitary adenoma, craniopharyngioma, or meningioma), or mass effect in Graves optic neuropathy, because of increased muscle volume or fat and, finally, by vascular compression as in intracranial aneurysm.39-47
Slowly progressive visual loss is the most common symptom.
Signs include RAPD, which may be seen in unilateral and/or asymmetric cases. The optic nerve may be pale, normal, or occasionally swollen. Proptosis and/or optociliary shunt vessels (small vessels around the optic disc that shunt blood from the retinal to the choroidal venous circulation) may be present.39-45
Figure 6-5 shows optociliary shunt vessels. Visual field findings include:
1.Central. This is described in optic neuritis.
2.Altitudinal. This is described in NAION.
Figure 6-5. Optociliary shunt vessels in compressive optic neuropathy.
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3.Junctional scotoma. This is the only situation in which unilateral optic nerve disease results in a bilateral field defect. Junctional scotoma is an ipsilateral central scotoma with a contralateral superior temporal quadrantanopsia. It results from damage to the most posterior optic nerve at the chiasmal junction, known as anterior genu of von Wilbrand. Its presence indicates a compressive lesion, most commonly a pituitary adenoma with a postfixed chiasm.
Workup should include orbital and cranial neuroimaging (computed tomography [CT] or MRI) and vascular studies such as magnetic resonance angiography (MRA).
Treatment is controversial, but in general these lesions may be irradiated or followed. If there is progressive proptosis, vision loss, discomfort/pain, or intracranial involvement with risk to the contralateral optic nerve or other vital structures, other treatment options should be considered.39-47
6-6 PAPILLEDEMA
Papilledema is defined as bilateral optic disc swelling produced by increased intracranial pressure. Rare exceptions of unilateral disc swelling are usually related to previous optic atrophy or to dysplastic discs.
Patients are usually asymptomatic but symptoms may include episodes of transient, usually bilateral, visual obscurations or losses lasting seconds, headaches, double vision, nausea, and vomiting.
Signs include bilateral hyperemic disc swelling with blurry margins and obscurations of blood vessels. The retinal nerve fiber layer is commonly involved. Peripapillary or papillary flame-shaped hemorrhages, loss of venous pulsations (may occur in up to 20% of normal population), and dilated, tortuous retinal veins may be observed. There is usually a normal visual acuity, pupillary response and color vision. Enlarged physiologic blind spot is the most common finding in visual field exam. Diplopia may develop and is usually due to increased intracranial pressure causing unilateral or bilateral abducens nerve palsies.48,49
Papilledema showing disc swelling with blurry margins and obscurations of blood vessels is represented in Figure 6-6.
In chronic papilledema, there is optic atrophy, the hemorrhages resolve, and narrowing of the peripapillary vessels and shunt vessels may develop. Decreased color vision and visual acuity may occur.48,49
Visual field findings include:
1.Enlarged blind spot (reversible)
2.Nasal step; when scotomata occur above and below the fixation point, they meet in the nasal field and form a horizontal steplike defect
3.Arcuate (defined in NAION)
4.Bi-arcuates
5.Generalized constriction
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Figure 6-6. Papilledema: disc swelling with blurry margins and obscurations of blood vessels.
6.Central depression plus items 1 through 5
7.Complete blindness
8.Peripheral field defect may occur; a temporal island of vision may be preserved before progression to complete blindness.50
Figure 6-7 shows generalized constriction in visual fields in a patient with papilledema.
Etiologies includes primary and metastatic intracranial masses, hydrocephalus, subdural and epidural hematomas (usually secondary to traumas), subarachnoid hemorrhage, brain abscess, meningitis, encephalitis, and idiopathic.
Workup should include brain neuroimaging, preferentially MRI. If the scan is normal, lumbar puncture should be performed with recording of opening pressure. Analysis of the cerebrospinal fluid is essential to exclude infectious or neoplastic processes. If this analysis is normal except for increased opening pressure, the patient probably has pseudotumor cerebri or IIH.
IIH has a peak incidence in the third decade and is twice as common in women as in men. The patient is often obese and complains of generalized headache, nausea, vomiting, dizziness, and tinnitus. IIH may also present with transient (lasting seconds) visual obscurations and horizontal diplopia (abducens nerve palsy).
The etiology is not known, but several disorders may be associated with it, such as obstructed intracranial venous drainage, endocrine and metabolic dysfunctions, exogenous agents (e.g., tetracycline antibiotics), and systemic diseases.
Intensity of management is based on severity of headaches, degree of visual field loss, and depth of visual acuity loss; it may include medical and surgical procedures.
Medical management options include weight loss, serial lumbar punctures, dehydrating agents, diuretics, and corticosteroids.
Surgical options include shunting procedures or optic nerve sheath decompression.51-53
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Figure 6-7. Generalized constriction in visual fields in a patient with papilledema caused by idiopathic intracranial hypertension.
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B
Figure 6-7. (Continued)
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