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

DISCUSSION

Field description: Mildly incongruous left inferior quadrantanopia, partial. Localization: Right parietal optic radiation.

Pathology: Primary lobar hemorrhage.

Confrontation testing with hand motion showed the quadrantic defect.

The patient has almost complete loss of the inferior quadrant, not quite reaching the horizontal meridian. This is much like an inversion of the defect in Case 74.

A CT scan showed a large right parietal lobe hemorrhage with a small amount of surrounding edema. Lobar hemorrhage is typically the result of either coagulopathy (most often iatrogenic from the use of coumadin) or an underlying amyloid angiopathy (140). Hypometria of contralateral saccades is sometimes reported with posterior parietal lesions (141) but is usually mild and hard to detect. It may indicate loss of the human homologue of the lateral intraparietal area studied in monkeys (142).

HISTORY AND EXAM

This 84-yr-old woman was referred to determine whether her vision was contributing to a problem with recurrent falls over the preceding 5 months. Visual acuity was 20/25 on

the right and 20/80 on the left, but the latter improved with pinhole to 20/25. Color vision was normal and there was no RAPD. Optic disks were normal.

DISCUSSION

Field description: Congruous relative left inferior quadrantanopia. Localization: Right parietal optic radiation.

Pathology: Infarct.

Confrontation testing showed a subtle mildly incongruous quadrantic defect, but only with a moving red target.

The patient’s field defect is less dense and extensive than that of Case 78, even though the size of her old, large, right parietotemporal infarct on CT is similar to that patient’s hemorrhage. Clearly the bulk of her lesion narrowly avoided most of her optic radiation, a stroke of luck not afforded to Case 78. In the brain, as in real estate, location is everything.

With an indeterminate history of onset of the visual problem and its subsequent course, one cannot exclude a neoplasm from the clinical information. A lesion of the superior bank of the calcarine sulcus is also possible.

Inferior quadrantanopia is often more troubling than superior quadrant defects. It obscures the view of the floor, and patients will stumble over objects. When driving, we fixate on the horizon, so that the road, sidewalks, pedestrians, and other cars are located more in the lower field than the upper. Since we read lines from the top to the bottom of the page, an inferior quadrantanopia obscures the coming text more than a superior defect does.

HISTORY AND EXAM

This 38-yr-old woman reported decreased vision in the right eye. She had a 10-year history of MS, treated with β-interferon injections. She had one distant episode of optic neuritis but could not recall in which eye. She was treated with steroids and apparently had a full recovery. Visual acuity was 20/100 OD and 20/25 OS. Ishihara color plates

were 0/14 OD and 4/14 OS. There was an RAPD OD. The right eye had diffuse optic atrophy and the left had temporal disk pallor. There was a mild spastic quadraparesis and diminished vibration sense in the hands and feet. She had left-right confusion and mild finger agnosia, but her writing and arithmetical performance were normal.

DISCUSSION

Field description: Incongruous right partial homonymous hemianopia, with general constriction OD and superior arcuate defect OS.

Localization: Right optic radiation, parietal lobe, and previous bilateral optic nerve. Pathology: Demyelination.

Confrontation fields showed decreased hand motion in the right hemifield and left superior quadrant OU.

This is a complex field. Part of the incongruity may stem from the patient’s prior optic neuropathies. From her color vision scores, acuity, RAPD, and optic disk appearance, the optic neuropathy is worse in the right eye and likely causes the general constriction of the nasal field, the side not affected by the cerebral hemifield defect. The curving arcuate

defect in the left eye (arrow) does respect the vertical meridian but its shape and location are much more suggestive of a nerve fiber defect. The optic atrophy in both eyes suggests that the nerve damage is old. Her new complaint is probably of decreased vision in the right hemifield, not the right eye, although the confusion and the false conclusion are common among new patients, let alone someone who has experienced visual loss in one eye.

Her MRI revealed a new large lesion of the left parieto-occipital area and extensive loss of occipital white matter, shown on this axial T1-weighted image (arrows). Finger agnosia and left-right confusion are two of the four features of Gerstmann syndrome (acalculia and agraphia being the other two), which is characteristic of damage to the left parietal region (143).

HISTORY AND EXAM

This 72-yr-old man described his vision immediately following a right carotid endarterectomy as “scrambled,” with the parts of objects spatially disjointed (e.g., hair displaced left of the eyes, and eyes placed one above the other). While reading he saw

words as blurred and fragmented. He saw four images of objects, even with either eye closed. He could not reach accurately for objects with his left hand. Visual acuity was light perception only OU. Fundi were normal, although he had a severe cataract OS.

DISCUSSION

Field description: Homonymous visual islands in right superior quadrant and left superior paracentral field.

Localization: Bilateral occipitoparietal radiations. Pathology: Watershed infarctions.

Confrontation fields showed the larger superior island OU with hand motion testing.

Axial T2-weighted MRI demonstrated bilateral watershed infarcts (arrows) with sparing of the striate cortex. His devastating visual loss is the result of bilateral optic radiation injury. Fortunately, 1 month later his vision had substantially recovered, with acuity of 20/40 OD and 20/200 OS. His improved fields (shown here) show mainly homonymous inferior losses in both hemifields, worse on the left side.

Cerebral diplopia or polyopia refers to the perseveration of a visual image in space (144). The number of images perceived may range from two to hundreds, and the multiple images persist with monocular vision irrespective of which eye is closed. Palinopsia refers to the temporal perseveration of an image (i.e., an image, or component thereof,

continues to be perceived, even though it is no longer present) (145). There is overlap between these two symptoms, and at times they may be difficult to distinguish. Polyopia may be accompanied by other signs including visual field defects, achromatopsia, or impaired visually guided reaching. This patient reported the latter. His report of fractured and disoriented vision may reflect a combination of preserved islands of vision and polyopia but may also indicate spatial disorientation secondary to his parietal lesions.

DISCUSSION

Field description: Congruous homonymous right horizontal sectoranopia. Localization: Left optic radiations, midzone.

Pathology: Infarct, secondary to head trauma.

Confrontation fields did not show a defect, but tangent screen perimetry with a 3-mm white target showed a right hemifield wedge defect extending to 20° on either side of the horizontal meridian OU.

The predominant feature of the patient’s defect from the gray scale and visual sensitivity plots is a severe reduction in thresholds in a zone straddling the horizontal meridian. There is also some depression along the inferior vertical meridian (which helps to

confirm a retrochiasmal location), but this is much milder compared to the sector defect. The sectoranopia in this patient resembles that seen with posterior choroidal arterial infarction affecting the LGN (124). However, geniculate lesions of this duration are usually accompanied by a pattern of optic atrophy not unlike that seen with lesions of an optic tract. Admittedly, such atrophy may be subtle with partial geniculate lesions (124). Damage to the middle of the optic radiations, at the converging boundary between the parietal and temporal fibers, can also create a sectoranopia without optic atrophy (146). Coronal T1-weighted MRI in this patient reveals a wedge defect fanning from the ventricular to the cortical surface, intersecting the optic radiations.