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

DISCUSSION

Field description: Congruous bilateral superior quadrantanopia, with extension into right inferior quadrant.

Localization: Bilateral striate cortex, inferior calcarine banks. Pathology: Gunshot wound.

Other features: Prosopagnosia, topographagnosia, partial dyschromatopsia. Confrontation fields showed no hand motion vision in any superior quadrant, with

impaired color discrimination in the lower right quadrant.

Bilateral superior altitudinal defects could also be the result of bilateral optic neuropathy, particularly the ischemic variety. While there is no obvious step at the vertical meridian, the congruous nature of the defect, especially in the right hemifield, stamp this

as bilateral quadrantanopia rather than bilateral altitudinal nerve fiber layer defects. The defect in the left eye is particularly revealing; the defect aligns more along the horizontal meridian on the temporal side and not the nasal side, the opposite of what is seen with optic neuropathy.

Coronal MRI showed the trajectory of the bullet, causing bilateral posterior ventral occipitotemporal lesions, extending more anteriorly on the right. Bilateral medial occipitotemporal lesions are associated with a classic tetrad of superior field defects, prosopagnosia, topographagnosia, and dyschromatopsia (159). While the patient does not have complete loss of color vision, subsequent testing showed that he was severely impaired on judgments of color saturation.

HISTORY AND EXAM

This 52-yr-old man was resuscitated from a cardiac arrest due to an inferolateral myocardial infarction. Five days later he lost consciousness briefly in the hospital and on recovery was blind in both eyes. Over the following few days vision gradually improved, and he began to experience episodic hallucinations of flashes of light and colors. His

examination 2 years later showed visual acuity at only count fingers OU, without RAPD or optic atrophy. He continued to report hallucinations of colored clouds or people in his central vision, and sometimes saw objects such as television images a few minutes after they had disappeared from view.

DISCUSSION

Field description: Fairly congruous, large bilateral central scotomata with inferior extension and vertical steps.

Localization: Bilateral striate cortex, posterior.

Pathology: Bilateral posterior cerebral arterial infarction, calcarine branches, probably embolic (“top of the basilar” syndrome).

Other features: Release hallucinations, palinopsia, initial cerebral blindness.

These are fairly complex fields at first glance. One starts by visualizing the shape of the holes, which have transformed the hill of vision into a volcano. The deepest part of the valley (dark gray shading) is a central zone in which the II4e target is not seen. (However, the perimetrist has indicated that a III4e target can be seen here; thus, it is a relative, not an absolute, scotoma.) Surrounding this is a shallow slope, with a zone in which the II4e but not the I4e can be seen (light gray shading). The defect is less severe superiorly, where it rises to a preserved crescent in which the I2e target can be seen. This represents

the lip of the volcano’s crater, as it were. Having visualized the overall shape of the defect, the key then is to search for localizing clues. In this example, the two main features are

(1) relative congruity of the complex margins of the scotomata (mild incongruity may be due to difficulty maintaining fixation at center, given the patient’s acuity of counting fingers only); and (2) the numerous vertical steps in the isopters defining the central holes, indicating pathology behind the chiasm.

Bilateral central defects can occur with either bilateral cerebral disease (167) or bilateral optic neuropathy. Bilateral striate lesions are more common than bilateral optic radiation damage, especially when simultaneous and in the absence of other neurologic defects. His hallucinations are release phenomena (Charles Bonnet syndrome) and lack localizing value, since they can occur with bilateral visual loss ranging from cataracts to striate lesions. Sagittal and axial FLAIR MRI showed bilateral occipital pole infarcts (arrows), with some change to the white matter also, seen on the axial image.

HISTORY AND EXAM

Immediately after a prostatectomy, this 69-yr-old man with hypertension and asthma was completely blind and had slurred speech, drowsiness, right gaze deviation, and right hemiparesis. He gradually improved to only a mild right-sided weakness and a visual field defect. Visual acuity was 20/30 OU, and Ishihara color scores were 11/14 OD and 13/14

OS. There was no RAPD and optic disks were normal. Pursuit was impaired in all directions and saccades were inaccurate in both fields, requiring multiple saccades to locate a target. He had a right hemiparesis. Reaching for targets with either hand was inaccurate; this improved when the targets were parts of his own body.

DISCUSSION

Field description: Congruous homonymous bilateral hemianopia, with sparing of macula and left inferior island of vision, respecting the vertical meridian.

Localization: Bilateral striate cortex, sparing occipital pole. Pathology: Bilateral posterior cerebral artery infarction.

Confrontation testing with hand motion showed a residual island of vision in the left inferior quadrant OU.

Prostate surgery used to be followed by an acute confusional state in some patients, because the glycine used as a diluent was absorbed and gained access to the CNS, where it is an inhibitory neurotransmitter (168). Glycine is no longer used, however. In this patient, the event was an embolic “top-of-the-basilar” stroke (169). The nonvisual symp-

toms were likely due to brain stem ischemia, and the visual symptoms to propagation of emboli into both posterior cerebral arteries at the terminus of the basilar artery. Bilateral blindness with normal fundi after surgery might also represent posterior ischemic optic neuropathies (63), especially when hypotension or significant blood loss occurs, but the pupillary light reflexes would be impaired in PION, whereas they would be normal in cerebral blindness. His partial defects now are clearly congruous and have a step at the vertical meridian, indicating bilateral hemianopias rather than bilateral optic neuropathies. He has inaccurate saccades and misreaching to visual targets, signs reminiscent of the ocular motor apraxia and optic ataxia of Bálint syndrome. However, in this case, these are due to severely limited peripheral vision and not additional parietal damage. Axial T2 MRI shows the bilateral medial occipital infarctions.

HISTORY AND EXAM

This 67-yr-old woman got lost while driving familiar routes and struggled to find her desk at work, only succeeding when she recognized her coat on the chair. She had trouble remembering her daily schedule and began having severe headaches. Two months later a left hemianopia was found by an ophthalmologist, and MRI showed a mass, which was resected. She was stable for the next 4 months, but in the few weeks prior to examination

was having more trouble navigating and finding objects around her. Visual acuity was 20/30 OD and 20/40 OS. Ishihara color plates were 0/14 OU. Optic disks were normal. Line bisection showed left hemineglect and she drew the numbers on a clock face in reverse order. Cube construction was poor. The remainder of the neurologic examination was normal.

DISCUSSION

Field description: Complete left homonymous hemianopia and right inferior quadrantanopia with sparing of the monocular temporal crescent.

Localization: Bilateral occipitotemporal and right occipitoparietal lobes.

Pathology: Tumor.

Other features: Topographagnosia, achromatopsia, left hemineglect.

Confrontation fields showed no hand motion in the left hemifield and hand motion but not count fingers vision in the right inferior quadrant.

The homonymous nature and the vertical step at the meridian confirm that the patient’s fields represent bilateral hemifield defects. Achromatopsia indicates damage to the lingual and fusiform gyri in the occipitotemporal cortex, while the left hemineglect suggests right parietal involvement. The reverse ordering and scattering of left-sided numbers in her

clock drawing reveal severe spatial disorganization, again attributable to a right parietal lesion (170) and borne out in her attempt to copy a cube. The lesion must be bilateral and extensive. MRI showed enhancing tumor in the right occipital lobe with edema spreading into the temporal lobe on the right as well as faint enhancement in the left temporo-occip- ital white matter, (arrows), seen on these axial and coronal T1-weighted images.

Bilateral tumors are bad news, and are usually glioblastoma multiforme (GBM) or primary CNS lymphoma. The pathology from her partial resection showed GBM and she was treated with cranial irradiation. Factors predicting a better prognosis include: Grade III (anaplastic astrocytoma) rather than Grade IV (GBM), age under 50 yr, normal mental state examination, gross total surgical resection, and Karnofsky performance score over 70 (i.e., the patient is independent in his or her activities of daily living) (171). This patient died 2 months after her visit.

DISCUSSION

Field description: Congruous homonymous left upper and right lower quadrantanopias, with sparing of right temporal crescent.

Localization: Bilateral striate cortex.

Pathology: Bilateral partial posterior cerebral arterial infarctions, involving left parietooccipital branch and right posterior temporal branch.

Other features: Charles Bonnet syndrome (release hallucinations).

Confrontation fields showed a superior quadrantic defect extending into the lower quadrant to hand motion, but no defect apparent in the right hemifield.

The bilateral vertical meridian steps clearly stamp this as bilateral occipital rather than bilateral optic disease. T2-weighted axial MRI shows these lesions, despite the motion artifact.

Stroke after CABG is common, occurring in 2–6% of patients. A prospective study of 456 patients undergoing CABG identified five factors associated with an increased risk of intraoperative stroke: previous stroke, carotid bruit, hypertension, diabetes, and old age (172). Most strokes in this setting involve multiple vascular territories, as might be expected with emboli from the heart or aortic arch. Showers of emboli may result from manipulation of an atherosclerotic aorta. The deleterious effects of these emboli on the brain may be compounded by concurrent hypoperfusion from low mean arterial pressure or lack of pulsatile blood flow while on cardiac bypass (173).

The patient’s Horner’s syndrome is probably due to intrathoracic surgical manipulation (174). Vertebrobasilar brain stem ischemia could also cause a Horner’s syndrome, but he lacked other signs of midbrain or lateral medullary damage.

HISTORY AND EXAM

This 40-yr-old woman had decreased vision OS, trouble looking to the left, left-sided weakness, and fatigue 3 years earlier. An MRI showed a few spots in her white matter. Over the following year she continued to experience fatigue, blackouts, and “straining to see.” In the past 10 days, she had had intermittent diplopia and total body numbness and was given iv methylprednisolone for a presumed MS attack. Acuity was 20/80 OD and

20/50 OS, improving with pinhole and encouragement to 20/40 OD and 20/30 OS. There was no RAPD. Ishihara color scores were 7/14 OD and 10/14 OS. Optic disks were normal. Eye movements were normal, and she was orthotropic in all positions of gaze. Neurologic examination showed give-way weakness diffusely, and reduction of all sensory modalities in all body parts tested.