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

DISCUSSION

Field description: Complete left homonymous hemianopia, macula splitting. Localization: Right striate cortex, medial occipitotemporal lobe.

Pathology: Oligodendroglioma with surgical resection.

Other features: Prosopagnosia, topographagnosia, hemianopic dyslexia. Confrontation testing with hand motion showed complete hemianopia.

Complete macula-splitting hemianopia is the least localizing of all hemifield defects. A large lesion anywhere from the optic tract to striate cortex can do this. Optic radiation lesions with such severe defects tend to be associated with other motor, sensory, attentional, or language deficits, unless close to the LGN or to the termination of the radiations in the striate cortex. This patient has prosopagnosia (impaired recognition of familiar faces) and topographagnosia (getting lost in familiar surroundings), indicating dysfunc-

tion of extrastriate regions in medial occipitotemporal cortex. While it was previously thought that prosopagnosia required bilateral occipital damage (159), modern neuroimaging has shown that at least some cases may occur with only right-sided damage

(160–162).

His reading difficulty is a hemianopic dyslexia, which occurs when the central 5° of vision are affected (163). Subjects with left hemifield defects read a single line quickly but struggle to find the beginning of a new line because the left side of the page lies within the hemianopic field (164). As a result, they frequently skip or repeat lines and may begin to read midway through a line. A ruler with a marker to place at the left hand margin of text can be helpful when held under the line being read.

T1-weighted axial MRI with gadolinium showed residual tumor in the right occipital lobe involving the striate cortex and distal optic radiation.

DISCUSSION

Field description: Right homonymous paracentral scotomata.

Localization: Striate cortex, midzone (anteroposteriorly), in depth of calcarine sulcus. Pathology: Posterior cerebral arterial infarct secondary to platelet dysfunction. Confrontation testing with finger motion showed the homonymous scotomata.

Although the patient was referred with what was thought to be a unilateral problem, confrontation testing and perimetry both demonstrated that the problem was actually bilateral. This reinforces the point about not evaluating one eye’s field without seeing that of the other.

Axial FLAIR MRI (shown) confirms a midzone infarct sparing both the anterior and posterior striate cortex. The topography of the striate cortex proceeds from the macula posteriorly at the occipital pole to the far periphery anteriorly, just behind the splenium and parieto-occipital sulcus. In coronal section, the horizontal meridian lies in the depths of the calcarine sulcus, with the vertical meridians lying on the exposed banks.

She received steroids and plasmapheresis, which improved the thrombocytopenia. Over time the scotomata shrank but still persisted, at least 1 year later. The combination of hemolytic anemia, thrombocytopenia, and stroke makes thrombotic thrombocytopenic purpura the most likely diagnosis (165).

HISTORY AND EXAM

This 37-yr-old man lost consciousness briefly in a car accident but did not have an apparent head injury. Shortly after, he complained of difficulty reading and noted a shad-

owy fog in the left inferior field of both eyes. Visual acuity and color vision were normal, as was the remainder of the neurologic examination.

DISCUSSION

Field description: Congruous homonymous right inferior perifoveal scotoma. Localization: Left superior occipital pole.

Pathology: Infarct/contusion.

Other features: Hemianopic dyslexia.

Confrontation fields were normal, but tangent screen perimetry showed a small homonymous left inferior quadrantic defect to finger motion.

The automated perimetry shows central defects in both eyes. Are these central scotomata from bilateral optic nerve injury or from striate injury? In the left eye, the defect clearly respects the vertical meridian, consistent with striate damage. In the right eye, there is a mild depression in the total and pattern deviation maps on the other side of the vertical meridian. However, this is a borderline defect (28–30 dB in the visual sensitivity plot), compared with the drastic reduction to 0 and 16–24 dB for the two locations flagged in the right field. The similarity of the defects in the two eyes and the concentration of the

severe defects within one hemifield must outweigh this slight depression in the left quadrant of the right eye and lead one to conclude that a striate lesion is present. This was confirmed on axial T2 MRI (shown, arrow), as a faint occipital pole lesion.

Patients are frequently aware of defects within the central 5° because they impair tasks requiring high spatial resolution, such as reading. Loss of the right perifoveal field is more disabling to reading than loss of the left side (163,166). Since we read from left to right, the text ahead of fixation is always obscured by a right perifoveal field defect. This is especially vexing because we tend to fixate slightly left of the center of each word we look at. By contrast, subjects with left hemifield defects read quickly but encounter difficulty when they need to move to the next line (see Case 88).

A perifoveal defect may be missed on kinetic perimetry or confrontation fields if done without care. With the normal acuity, this may lead the unsuspecting examiner to the false conclusion that vision is normal. Automated perimetric tests that focus on the central 10 or 30° of vision are best at detecting this visual field defect.

HISTORY AND EXAM

This 14-yr-old girl reported that over the last year there were repeated times when she could not see clearly in the right inferior field. She would be aware of this only briefly, for about a minute. Her birth had been difficult with shoulder dystocia, meconium aspiration, a seizure, and subarachnoid hemorrhage. At age 3 days, an examination had found vitreous hemorrhage OS and retinal and preretinal hemorrhages OD (i.e., a neonatal

Terson’s syndrome). She had developed well, though, and only reported occasional headaches, with no other neurologic problems. At evaluation, her acuity was 20/20 OD and 20/25 OS, with normal color scores of 13/14 OD and 12/14 OS. There was no RAPD. Fundoscopy showed normal optic disks and some peripheral pigment clumping OS, consistent with old choroidal infarction. She had a comitant intermittent exotropia.

DISCUSSION

Field description: Congruous homonymous right inferior scotomata OU. Localization: Striate cortex.

Pathology: Occipital hemorrhage.

Confrontation fields were full, including color comparisons.

Despite the patient’s extensive earlier retinal history, her small field defect was present in both eyes and highly congruous. The lesion respected the vertical meridian, insofar as it did not cross it, but it did not abut this to cause a definitive vertical step. Nevertheless, the congruity stamps this as retrochiasmal and most likely striate in origin. Sagittal and coronal T1 MRI (shown) demonstrate the lesion above the calcarine fissure and well anterior to the pole.

Why had she only intermittently noted the scotoma? It is not uncommon for small defects outside of the perifoveal region to go unnoticed. Furthermore, in her case the exotropia may have helped hide the defect. Because of her ocular misalignment, most of the time the defects were not overlapping in her view of the world. Hence, they would come to light only during moments when she was intermittently orthotropic, suppressing the vision of one eye, or just closing one eye.

Note on the sagittal image that the distances from the lesion to the parieto-occipital fissure (arrow) and to the occipital pole are about the same. On the field, this volume of spared striate cortex corresponds to 60° of peripheral vision and a mere 10° of central vision—a graphic illustration of cortical magnification (see Chapter 2).

HISTORY AND EXAM

This 77-yr-old man noted the sudden onset of several visual problems. He bumped into things, especially on the right. He had trouble reading newspapers and seeing objects on the floor. He had a history of coronary artery disease, hypertension, diabetes, a previous stroke, and resection of a right occipital meningioma 7 years earlier. On examination 3

weeks after onset, visual acuity was 20/25 OD and 20/20 OS. Ishihara color plates were 6/12 OD and 5/12 OS, with a tendency to miss digits on the right. There was no RAPD and disks appeared normal. The remainder of the neurologic examination was normal.

DISCUSSION

Field description: Relatively congruous homonymous inferior defects involving the two hemifields asymmetrically, with probable vertical step.

Localization: Occipital cortex bilaterally.

Pathology: New left infarct, old right meningioma resection.

Confrontation testing showed no hand motions in the left lower quadrant and decreased vision to hand comparisons in the right lower quadrant OU.

Bilateral inferior defects might also be the result of bilateral optic neuropathy, particularly AION (see Case 33). However, altitudinal defects from optic nerve disease should always extend to the nasal horizontal meridian in each eye, which is not the case here. In addition, the similarity of the defects in the two eyes and the vertical steps at the center of vision in both eyes here are best explained by a retrochiasmal problem.

While Goldmann perimetry showed the full peripheral extent of the defect, it does not show the central vertical step as well as the automated field did.

Without knowing whether the left hemifield defect dates to the patient’s resection, it is not clear whether his new event is unilateral or bilateral. Tumor recurrence is a possibility, but MRI ruled this out. Rather, T1 and T2 axial MRI showed, in addition to a large area of right occipital encephalomalacia, a new area of abnormal signal in the left occipital lobe.

HISTORY AND EXAM

This 38-yr-old man was shot in the head at age 20, with subsequent evacuation of an intracranial hematoma. Since that time he has been unable to recognize faces, gets lost in familiar surroundings, and notes that colors are faded and grayish. Visual acuity was

20/20 OU. He saw 10/14 Ishihara pseudo-isochromatic plates OU. Eye movements were normal. He had mild difficulty recognizing visual objects, particularly when seen in unusual views. He had a mild verbal memory impairment.