Scotomata

Arcuate scotoma An arc-shaped area of blindness in the field of vision. 

Nasal scotoma An area of blindness in the nasal portion of peripheral vision. 

Paracentral scotoma A blind spot near the center of the visual field. 

The vapor causes eye irritation at 15 ppm eye contact with the solid may result in conjunctivitis, superficial injury to the cornea, chorioretinitis, scotoma, and diminished visual... 

Visual disturbances There have been reports of visual disturbances associated with the use of nefazodone, including blurred vision, scotoma, and visual trails. 

Visual field defects - Central scotoma with decreased visual acuity field constriction (rare) pericentral or paracentral scotoma. 

The duration of treatment for skin diseases is often longer than it is for malaria, and therefore, dose-related toxicities are important. The most serious toxicities are ophthalmological. Reversible alterations include ciliary body dysfunction and corneal changes with edema and deposits. Irreversible retinopathy also occurs however, it is less common with quinacrine than with the other two drugs. Toxicity may be asymptomatic, but the earliest symptoms are night blindness, scotoma, or tunnel vision. 

Dominant optic atrophy [13, 14] The most prevalent hereditary optic atrophy resulting in a progressive loss of visual acuity, centro-cecal scotoma and bilateral temporal atrophy of the optic nerve. It has been ascribed to mutations in the OPA1 gene encoding a dynamin-related protein localized to mitochondria. Anomalies of mitochondrial integrity and distribution are suspected to result from impairment of protein function. 

In another study, the adverse effects of the antiestrogenic effects of clomiphene citrate were hot flushes (10%), mood swings, depression, headaches (1%), pelvic pain (5.5%), nausea (2%), breast tenderness (2-5%), dryness and loss of hair (0.3%), visual symptoms, halos and streaks around lights (particularly at night), blurring, and scotoma (1.5%) (3). 

CORDX usually begins within the first two decades of life and is progressive. Clinical features of the disorder include reduced visual acuity, poor colour vision, fundus abnormalities, central scotomas in the visual field, photophobia, myopia and low b-waves in ERG recordings (Jacobson et al., 1989 Brown et al., 2000). A single... 

Molybdenum deficiency in humans has rarely been observed. The presenting symptoms included tachycardia, tachypnea, headache, night blindness, nausea, vomiting, central scotomas, lethargy, disorientation, and ultimately coma. 

Characteristics of the vision loss can aid in the diagnosis of demyelinating optic neuropathy. The vision loss is progressive, is maximal in 1 week, and achieves variable recovery within 4 to 6 weeks. The reduction in vision frequently is accompanied or preceded by periocular pain on movement of the eye. Color vision often is severely impaired, and visual fields most commonly reveal a relative central scotoma. The ophthalmoscopic picture is usually one of a normal optic nerve head, because most commonly the optic neuropathy is behind the globe and thus is called retrobulbar optic neuritis. When there is optic disc swelling, it is known as papillitis. 

Prognosis for return of vision is good. Vision characteristically begins to improve within 2 to 3 weeks, with stabilization at near normal by the fourth to fifth week. Some patients improve rapidly to a moderate acuity level, stabilize, and then experience a return of vision to near normal over a prolonged period. Recmrences characterize the disease, and with each recurrence acuity and visual fields become further compromised. If visual acuity drops to no light perception in the first attack, approximately two-thirds of patients recover vision to 20/400 or better, whereas one-third maintain dense central scotomas with visual acuity of less than 20/400. Each attack of retrobulbar optic neuritis can produce optic atrophy, although the incidence is as low as 36%. 

The incidence of optic neuropathy in thyroid eye disease is 5% to 10%. The class 6 patient usually has mild to moderate proptosis and relatively shallow orbits. Thyroid optic neuropathy may be evidenced by papilledema, papillitis, or retrobulbar neuritis and usually is characterized by a painless and gradual loss of visual acuity. Common visual field defects include central scotomas, arcuate or altitudinal defects, paracentral scotomas, or generalized depressions. Thus visual field and optic disc examinations are the best diagnostic tools for early optic neuropathy. Occasionally, vision loss can occur precipitously over 1 or 2 weeks. Other features of optic nerve dysfunction frequently associated with the decreased visual acuity are color vision disturbances, afferent pupillary defects in the less proptotic eye in patients with asymmetric involvement, and prolongation of the pupil cycle time. 

However, it is, at present, the basis for most types of serial visual field analysis (e.g., progression analysis). It may take as many as five to eight visual fields to be able to statistically differentiate true change from the noise of test-retest variability, particularly in visual fields with scotomas. Figure 344 shows the gray scales of 5 years of visual fields. 

Visual field Central scotoma Peripheral contraction... 

Comeal deposits of chloroquine may be asymptomatic or may cause halos around lights or photophobia. These are not a threat to vision and reverse when the dmg is stopped. Retinal toxicity is more serious, however, and may be irreversible. In the early stage it takes the form of visual field defects late retinopathy classically gives the picture of macular pigmentation surrounded by a ring of pigment (the bull s-eye macula). The functional defect can take the form of scotomas, photophobia, defective colour vision and decreased visual acuity resulting, in the extreme case, in blindness. 

The resulting functional defects are varied difficulty in reading, scotomas, defective color vision, photophobia, light flashes, and a reduction in visual acuity. Symptoms do not parallel the retinal changes. By the time that visual acuity has become impaired, irreversible changes will have taken place. 

Little is yet known about the development of the retinopathy after withdrawal of treatment. Retinal changes in the early stages are probably reversible if the drug is withdrawn, and progression of a severe maculopathy to blindness seems to be less frequent than feared. In 1650 patients with 6/6 vision and relative scotomas there was no further decline in visual acuity after drug withdrawal, but 63% of patients who presented with absolute scotomas lost further vision over a median period of 6 years. 

The onset of visual loss can be sudden and dramatic, with color vision defects in the red-green or blue-yellow spectra, as well as variable field defects. In acute cases, disc edema is accompanied by sphnter hemorrhages. Retrobulbar neuritis with ethambutol can be predominantly axial, presenting with reduced visual acuity and central scotoma, or periaxial, with peripheral field defects. In non-acute tjrpes the fundi and discs appear normal (13). Visual defects can be unilateral or bilateral. 

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