Ординатура / Офтальмология / Английские материалы / Field of Vision A Manual and Atlas of Perimetry_Barton, Benatar_2003
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ATLAS / CASE #23 |
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DISCUSSION
Field description: Inferior arcuate defect OS.
Localization: Anterior optic nerve.
Pathology: Papillitis OS.
Confrontation fields showed an inferonasal step to color and hand comparison.
Perimetry shows a wide and dense arching defect that marches out of the blind spot and curves to end at the nasal horizontal meridian. These are the essential features of a complete arcuate defect. While there are a few scattered points of reduced sensitivity in the superior field on the total deviation plots, these drop out on the pattern deviation plot, and inspection of the sensitivity decibel numbers shows a marked drop from the top to the bottom nasal field, from the mid-twenties to mid-teens.
After presentation the patient also noted tingling and numbness in her right leg, which resolved. Her visual defect disappeared over the next 3 weeks (repeat OS field shown this page).
Optic neuritis may affect the optic disc (anterior optic neuritis, or papillitis) or the portion of the optic nerve behind the disc (retrobulbar optic neuritis), in which case the optic disc appears normal in the acute phase of the illness. The retrobulbar form is more common, accounting for about two-thirds of cases (31). Papillitis rarely causes severe disc edema or hemorrhage, and such findings should raise alternative diagnoses, such as ischemia, venous occlusion, asymmetric papilledema, or disc infiltration. In patients without brain lesions on MRI, the risk of developing MS over the next 5 years is about 8% in patients with papillitis, about half the risk in those with retrobulbar optic neuritis (32).
ATLAS / CASE #24 |
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HISTORY AND EXAM
This 44-yr-old woman noted decreased vision in the left eye during a cold. Over a few |
were 13/14 OD and 12/14 OS. There was a large RAPD OS but the optic discs were |
days she realized that she now could not see in the upper field of the left eye. She had no |
normal. The remainder of the neurologic examination was normal. |
other symptoms. Visual acuity 23 days later was 20/20 OU, and Ishihara color scores |
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ATLAS / CASE #24 |
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DISCUSSION
Field description: Incomplete superior altitudinal defect, bisecting the macula, OS.
Localization: Retrobulbar optic nerve.
Pathology: Retrobulbar optic neuritis OS.
Confrontation testing with hand motion showed the same characteristics of the defect.
This is the field defect that would occur if an arcuate defect like that in Case 23 widened a bit more temporally to impair half the papillomacular bundle and a bit more nasally to impair the adjacent temporal field wedge. Altitudinal defects are supposed to be more characteristic of ischemic optic neuropathy (see Case 33). However, the patient’s young age, lack of vascular risk factors such as diabetes or hypertension, and progression over a few days are unusual for ischemic cases. In addition, most ischemic optic neuropathies involve the disc (anterior ischemic optic neuropathy) and should cause disc edema that persists for at least 1–2 months. It is also clear now that, contrary to neurologic folklore, altitudinal defects make up 30% of focal defects on automated perimetry in optic neuritis, the single largest group (31). In fact, this is more than double the 15% figure for cecocentral and central defects combined.
At follow-up the patient’s defect had not improved 6 weeks after onset, atypical for optic neuritis, which generally begins to recover in the first month (33). The diagnosis should be questioned when there is progression or failure to improve over more than 1 month. She had an MRI of the orbit and sella, a spinal tap, and testing for vasculitis and Lyme disease. Her only finding was a positive anti-nuclear antibody (ANA), of unclear significance. Her brain MRI did show a hyperintense lesion in the pons (arrow), consistent with demyelination, shown in this T2-weighted axial image.
ATLAS / CASE #25 |
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HISTORY AND EXAM
This 43-yr-old woman developed pain with eye movement and progressive visual loss in the left eye over 10 days, about 3 weeks after a flu-like illness with a facial rash. Initial examination showed visual acuity of 20/20 OD and 20/25 OS, Ishihara color scores of 14/14 OD and 5/14 OS, and an RAPD OS. Maculae and optic discs were normal. Her
condition resolved over one month, but she presented 11 months later with new “foggy vision” OS, without change in acuity or color vision OS on examination. An overview program is presented for this eye. (The right eye remained normal throughout her care.)
ATLAS / CASE #25 |
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DISCUSSION
Field description: Initial cecocentral scotoma with superior nasal step OS, with inferotemporal wedge defect 1 year later.
Localization: Retrobulbar optic nerve. Pathology: Recurrent retrobulbar optic neuritis.
Confrontation testing with red targets at her first visit showed a superonasal step OS.
Note the change over serial perimetry results. The first episode combined a cecocentral defect and a superior arcuate defect, manifest as the abnormal points on the deviation plots arrayed just above the nasal horizontal meridian. This represents a combination of damage to the papillomacular bundle and arcuate fibers in the inferior disc. The second episode is clearly different from the first and represents a new inflammatory episode. The change analysis (this page) shows worsening of short-term fluctuation and MD with each episode, seen as dips below the dashed line representing p <5%, meaning that there is a 95% probability that the field is abnormal. There is also a marked decline in pattern standard deviations (pattern standard deviation and corrected pattern standard deviation) with the second episode, indicating greater distortion of the hill of vision. This is consistent
with the patient’s wedge defect, which was more focal than her first, more diffuse central and arcuate depression. Her reliability was excellent during the pathologic events.
The patient’s initial MRI showed two small white matter lesions, one shown on this FLAIR axial image (arrow), which did not change on repeated MRI 2 years later. The ONTT suggests that she has an intermediate risk of about 25% of another demyelinating event over the next 5 years (32). However, her story included a recurrent facial rash and a positive ANA, though she never developed other evidence of connective tissue disease. While the ONTT found little value in testing for vasculitis, syphilis, and sarcoidosis in typical optic neuritis (31), unusual features such as rash, uveitis, or arthritis do require more investigation. In this patient, the second episode of optic neuritis increased the suspicion of MS instead, and, indeed, 1 month later she returned with a right internuclear ophthalmoplegia. β-Interferon treatment was recommended.
ATLAS / CASE #26 |
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HISTORY AND EXAM
This 56-yr-old man had relapsing-remitting MS for 19 years. His only visual episode was a few months of monocular blurry vision 18 years earlier, but he could not recall which eye had been affected. Visual acuity was 20/30 OD and 20/25 OS, and Ishihara
color scores were 13/14 OU. There was no RAPD. He had mild temporal optic disc pallor OD and a normal optic disc OS. He also had spastic quadriparesis and an ataxic left arm.
ATLAS / CASE #26 |
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DISCUSSION
Field description: Superior temporal wedge defect OD, superior arcuate defect with enlarged blind spot OS.
Localization: Retrobulbar optic nerves, bilateral. Pathology: Retrobulbar optic neuropathy OU.
Confrontation testing found some red desaturation in both inferonasal fields.
Both of the patient’s defects are subtle and led to confusing results on confrontation testing (perhaps the darker color in the upper field was the abnormality!). The arcuate defect OS is confirmed by its presence on two isopters. The temporal wedge defect OD differs from physiologic baring of the blind spot by the prominent temporal shoulder (arrow), which clearly defines the narrow path of the defect. In addition, this eye has optic atrophy. Not surprisingly, these peripheral defects of demyelinating optic neuropathy spare central acuity and color vision and, like the defects in early glaucoma, can be hard to find on confrontation testing. Such asymptomatic defects are not uncommon in patients with MS (34) and represent a mild chronic optic neuropathy. When slowly progressive, or asymptomatic and therefore not readily dated, as in this patient, one must also consider the possibility of compressive or other optic neuropathies. Having MS does not immunize one against the other vagaries of life.
ATLAS / CASE #27 |
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HISTORY AND EXAM
Seven months earlier, this 27-yr-old woman had vertigo, imbalance, and blurred vision OD that recovered with iv methylprednisolone after 3 weeks. Two months later, she had visual blurring OS, was treated with steroids again, with recovery after 1 week. A spinal tap showed oligoclonal bands and MRI showed multiple periventricular white matter lesions. She then presented with 5 days of blurred vision OD along with new tingling in
the left arm and leg, clumsiness of the left hand, and imbalance. With this attack, her acuity was 20/60 OD and 20/20 OS. Ishihara color scores were 12/14 OD and 13/14 OS, but slower OD. There was an RAPD OD and new mild blurring of the optic disc margin OD. She had mild pyramidal weakness in the right arm.
ATLAS / CASE #27 |
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DISCUSSION
Field description: Central scotoma and incomplete superior altitudinal defect OD. Localization: Anterior optic nerve.
Pathology: Optic neuritis/papillitis.
Confrontation testing showed a superior nasal step to red targets and abnormal hand and face comparison in the superior and temporal paracentral fields.
Perimetry shows almost complete reduction of sensitivity in the superior field, with the exception of a few points just temporal to the optic disc. This could be either a severe arcuate or an incomplete altitudinal defect. Clarification of this point would require examination of the visual field beyond 30°, best with a Goldmann field, but also possible with confrontation testing. The distinction is not necessarily that crucial. Both defects have been described with optic neuritis, and the boundary between the two is more quantitative than qualitative.
With her prior neurologic episodes and abnormal MRI, the patient meets the criteria for MS. Prospective placebo-controlled trials show that β-interferon reduces the annual relapse rate in MS by approximately 30% (35–37) (figure). There is also some evidence that it slows the rate of accumulation of physical disability. At 2 years, 34% of placebotreated and 21% of β-interferon-treated patients had developed sustained progression of disability (36). β-Interferon also slows progression of disability in secondary progressive MS, but the effect is less impressive (38).
ATLAS / CASE #28 |
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HISTORY AND EXAM
This 31-yr-old woman with MS for 5 years presented with 1 day of decreased central and inferior vision in the left eye. Visual acuity was 20/20 OD and 20/60 OS. Ishihara color scores were 12/14 OD and 5.5/14 OS. There was an RAPD OS but the optic discs
were normal. She had mild spasticity and hyperreflexia in the left arm and leg, and an action and postural tremor of both hands.