Ординатура / Офтальмология / Английские материалы / Field of Vision A Manual and Atlas of Perimetry_Barton, Benatar_2003

DISCUSSION

Field description: Progressive inferior arcuate defect OD?

Localization: Optic disk.

Pathology: IIH.

Confrontation field testing was normal.

MRI of the brain and MR venogram were normal, but on spinal tap the patient’s opening pressure was elevated at 32 cm H2O, with otherwise normal CSF. She started 500 mg of acetazolamide twice a day and attempted weight reduction, with eventual loss of 8 lb. However, her papilledema remained unchanged.

The overview shows an inferior arcuate defect OD, which over these three sequential fields appears to enlarge. The change analysis shows some fluctuation in her pattern deviations. With the persistent papilledema despite treatment, does this indicate a need to pro-

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ceed to surgery, such as an optic nerve sheath fenestration? She was brought back for a repeat field 1 week later, shown on this page. Whereas the earlier fields were done in the afternoons, this newest field was done in the morning, at her insistence. The field shows a more subtle inferior arcuate depression, indicating that she has not really progressed.

This case illustrates the difficulties in trying to detect subtle changes in a preexisting defect on automated perimetry. Confirmation with repeated assessments is always wise if an important therapeutic decision hinges on the results.

HISTORY AND EXAM

Two months earlier this 39-yr-old woman had been diagnosed with IIH, after presenting with transient visual obscurations OS for 5 months. The opening pressure on spinal tap was 44 cmH2O. She had a history of recurrent fainting spells. Despite using 500 mg of acetazolamide twice a day, she noted a decrease in the nasal field of vision OS and

increasing occipital headaches in the 2 weeks prior to her visit. Acuity was 20/20 OD and 20/40 OS, with a clear RAPD OS. Ishihara color scores were 9/14 OD and 3/14 OS. Fundoscopy showed asymmetric papilledema, worse OS. There was a subtle esotropia in left gaze, and she had mild postural hypotension.

DISCUSSION

Field description: Inferior arcuate defect OS with enlargement of the blind spot, mild inferonasal step OD.

Localization: Bilateral optic nerve.

Pathology: IIH.

Added features: Left VI palsy.

While the enlarged blind spot is a minor refractive finding in this condition (see Case 46), the arcuate defect indicates that the swelling at the optic disk is causing axonal dysfunction. Her disks show asymmetric papilledema (76,77), worse on the left, the eye with more nerve fiber bundle loss. The fibrillary pattern of the disk edema in this eye indicates

that the papilledema is chronic. Papilledema is asymmetric in about 8% of cases (76). The asymmetry may be due to variation in the ability of the optic nerve sheaths to transmit intracranial pressure to the optic nerve head, given differences in the trabeculation and size of the subarachnoid space from one nerve to another (77).

The main risk in IIH is visual loss, and the goal of treatment is to prevent it. This patient developed visual loss early in the course despite compliance with medical treatment, which points to a need for more aggressive surgical management. The options are lumboperitoneal shunt or optic nerve sheath fenestration (78). Although there are no formal head-to-head trials, retrospective reviews suggest comparable efficacy (79). As with all shunts, the former may require episodic revision.

DISCUSSION

Field description: Bilateral inferonasal step defects with enlarged blind spots OU.

Localization: Optic nerve.

Pathology: Papilledema secondary to sagittal sinus thrombosis. Tangent screen perimetry showed an inferonasal step defect OS.

The gray-scale images on automated perimetry clearly show the inferior arcuate defects with their nasal steps. The difficulty in showing the nasal step defect OD with tangent screen perimetry illustrates how easily some field defects from optic neuropathy can elude detection at the bedside. What is less apparent from the gray-scale image is the enlargement of the blind spots. This is shown better on the probability maps, which show some depression of test locations adjacent to the blind spots.

VI nerve palsies may occur with increased intracranial pressure of any cause. This patient’s gender and age might suggest IIH, but seizures would be very unusual in this condition. Hormonal treatment can cause a hypercoagulable state, increasing the risk for dural sinus thrombosis, in which seizures are common (80). In addition, she had more severe papilledema and more hemorrhages than are seen in typical IIH. This likely reflects a more acute rise in intracranial pressure (81) from her sagittal sinus thrombosis. The best treatment of this condition is debatable, although there are some data in favor of anticoagulation (82). Her disk edema and fields improved over 4 months without treatment, and she remained seizure-free on phenytoin.

HISTORY AND EXAM

After a few days of flu-like illness, this 39-yr-old man was brought to the emergency room because of confusion. An MR venogram showed a cerebral venous thrombosis. Hematologic investigations uncovered a platelet count of 700,000 and a prothrombin gene mutation. He was started on coumadin. On evaluation 6 months later, his acuity was 20/20

OU, and he had evidence of congenital dyschromatopsia. There was no RAPD. Fundoscopy (shown next page) showed papilledema, worse OD, with choroidal folds OD. He had a mild left VI nerve palsy. He weighed 160 lb and height was 6 ft. An overview shows fields at this time and 3 months later.

DISCUSSION

Field description: Enlarged blind spot OD, improving on follow-up.

Localization: Optic disk.

Pathology: Papilledema from increased intracranial pressure due to venous sinus thrombosis.

Confrontation fields were normal.

On Goldmann perimetry the marked enlargement of the patient’s blind spot is less with the brighter I3e target than with the I2e target, indicating a relative defect. In addition, the enlargement on the I2e isopter shrinks when retested with a +2.00 spherical lens, showing that it is partly the result of elevation of the peripapillary retina out of the plane of focus, a phenomenon also suggested by the choroidal folds shown on his fundus pictures (83). The plus lens restores focus on this retinal zone and the faint small target becomes visible (84).

Three months later his disk edema had resolved nearly completely and his fields normalized.

IIH is not the only cause of papilledema in the absence of a mass lesion. Venous occlusion by a small sinus mass or thrombosis can increase intracranial pressure; usually the posterior third of the sagittal sinus and/or the lateral sinuses are affected (85). The patient’s MR venogram shows absence of the sagittal sinus (contrasted with a normal MR venogram on the right, arrows). The presentation with confusion in a nonobese man clearly indicates that IIH is unlikely. However, venous thrombosis can present like IIH, with headache as the sole symptom and CSF contents normal (85). Hence, MRI and MR venography are being used more frequently to exclude sinus thrombosis in the work-up of IIH. Risk factors for thrombosis include systemic inflammatory diseases such as Behçet or lupus, the postpartum state, coagulopathies, and cancer.

HISTORY AND EXAM

This 48-yr-old man had 4 days of blurred vision OS. He had an aggressive neuroendocrine tumor of his colon resected 9 months earlier, treated with VP-16, carboplatin, and radiation, but with a metastasis to the pedicle of the T9 vertebral body 5 months later. For

2 weeks he had noted pulsatile tinnitus. He had recently tapered off dexamethasone. Acuity was 20/20 OU, with a small RAPD OS. Fundoscopy showed unilateral papilledema OS with engorged veins, but no hemorrhages. His legs were areflexic.

DISCUSSION

Field description: Partial inferior altitudinal and superior arcuate defect OS, with homonymous right superior quadrantic depression, respecting vertical meridian.

Localization: Left occipital lobe, left optic nerve.

Pathology: Sagittal sinus metastasis and thrombosis causing increased intracranial pressure.

Confrontation testing showed an inferior field decrease to red comparison OS, sparing the macular region.

The Goldmann field shows a subtle vertical meridian effect in both eyes, raising suspicion of a homonymous postchiasmal defect. If this had not been documented, one might have erroneously concluded that the patient also had a relative superior temporal wedge defect OD.

The significant subacute visual field loss OS with disk edema suggested first a compressive or infiltrative optic neuropathy, given his metastatic cancer. However, this would

not explain the mild homonymous defects. Instead, he had an occipital metastasis (arrow) causing both striate dysfunction and sagittal sinus thrombosis (arrowheads). The latter led to acutely raised intracranial pressure and rapid asymmetic papilledema with visual loss.

HISTORY AND EXAM

This 74-yr-old woman reported that for 2 weeks the top half of vision in the right eye was missing. She was uncertain about its tempo but had no eye pain or headache. She had hypertension and breast cancer, treated with mastectomy 3 years earlier, but complicated

by local recurrence and a solitary cerebellar metastasis that had been resected 7 months earlier. Visual acuity was count fingers OD and 20/25 OS. There was an RAPD OD and fundi were normal.