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

DISCUSSION

Field description: Superior and inferior arcuate defects OD, more severe superiorly.

Localization: Optic nerve.

Pathology: Intraorbital cavernous hemangioma compressing optic nerve.

Confrontation fields were normal.

The patient has a prominent superior arcuate defect with a nasal step. Inferiorly there is a depression that points toward the blind spot, indicating a milder arcuate defect there also. Axial T1-weighted orbital MRI showed a soft-tissue mass in the right orbit, with marked speckled gadolinium enhancement on the fat-saturated image, and lateral displacement of the optic nerve (this aspect not shown). These findings are consistent with

See Color Plate

after page 180

an orbital cavernous hemangioma, which was confirmed on resection a month later. Over the ensuing months, her visual acuity remained 20/20 OU and her visual field defects resolved.

Cavernous hemangiomas of the orbit are benign vascular growths. They may remain asymptomatic or present with slowly progressive proptosis and/or visual loss due to compression of the optic nerve. Those with asymptomatic cavernous hemangiomas, discovered incidentally during neuroimaging, can be safely followed without surgery (186). Surgery should be considered once there is visual compromise but should be undertaken with caution, given that preexisting visual deficits may worsen following apparently uncomplicated surgical excision (102,187).

without gadolinium

with gadolinium

HISTORY AND EXAM

This 47-yr-old woman had presented with 4 months of increasing blurry vision in the right eye. Approximately 6 months prior she had resection of a right sphenoid wing meningioma that presented with headaches. Visual acuity at far was 20/30 OD and 20/25

OS. Ishihara color plates were 10.5/14 OD and 12/14 OS. There was an RAPD OD. Fundoscopy showed mild temporal optic disk pallor OD. She had mild limitation of elevation and adduction OD.

DISCUSSION

Field description: Right superior and inferior temporal wedge defects. Localization: Right intracranial optic nerve.

Pathology: Compression by residual sphenoid wing meningioma.

Confrontational field testing showed hesitancy to finger count in the inferotemporal paracentral region OD, but colored stimuli and hand appearance were normal.

The wedge defects pointing at the blind spot indicate loss of superior and inferior wedges of nerve fiber layer. The combination of a compressive optic neuropathy and a partial III nerve palsy points to a lesion at the superior orbital fissure or cavernous sinus. Enhanced T1-weighted coronal and axial MRI showed a mass at the cavernous sinus

tracking along the lateral wall of the orbit, and encasing the right optic nerve (arrow). Medial sphenoid wing meningiomas disturb vision by compressing the intracranial

optic nerve or chiasm. They arise from a number of structures, including the anterior clinoid process, medial sphenoid ridge, tuberculum sellae, and diaphragma sellae. They can extend into the cavernous sinus or the superior orbital fissure, causing cranial nerve palsies and/or Horner’s syndrome. Tumors from the diaphragma sellae and medial sphenoid ridge are least often completely removed and most commonly associated with postoperative visual deterioration (188). Worsening may be due to slow progression or malignant transformation of the meningioma. The latter is a rare event, occuring in 1.7% of cases (189).

HISTORY AND EXAM

This 68-yr-old woman with diabetes, congestive heart failure, and moderate left carotid stenosis had a right occipital stroke that left her with a left hemifield defect 3 years previously. Three days prior to evaluation, she noted a grayness in the far periphery of her

right lower field, which gradually improved over the next few days. Visual acuity was 20/25 OU and there was no RAPD. Optic disks were normal, as was the rest of the neurologic examination.

DISCUSSION

Field description: Congruous left inferior quadrantanopia plus, macula sparing. Localization: Right striate cortex, superior bank of calcarine sulcus, sparing occipital

pole.

Pathology: Posterior cerebral arterial infarct, parieto-occipital branch.

Confrontation field showed left inferior quadrantopia extending into the superior field to hand motion.

T1-weighted sagittal MRI showed the old right striate infarct (left image), causing the patient’s field defect. There was also a new left medial parieto-occipital infarct (arrow,

right image) just above the anterior extent of the striate cortex. There is no current field defect corresponding to this new lesion. The transient field defect she had noticed may have been due to edema or compression surrounding the infarct, which may have had secondary effects on the adjacent striate cortex. This lesion, which probably affects human homologues of areas V2 and V3, does not cause a field defect on conventional perimetry. It is possible that other specific visual functions such as perception of motion or illusory contours may be affected contralaterally by this lesion. The old and the new lesions in this patient nicely illustrate the difference between striate and extrastriate lesions in relation to perimetry.

HISTORY AND EXAM

Over the week prior to his visit, this 52-yr-old man with mild hypertension noted that the midportion of license plates in front of him would disappear transiently. He then became aware that car bumpers would intermittently develop a vertical discontinuity or step. He had some blurry vision in both eyes, more to the temporal sides. He recalled

bifrontal headaches present for a few months. Visual acuity was 20/30 OD and 20/20 OS. Ishihara plates were 10/14 OU, and he missed the temporal digits of the plates with twodigit numbers. There was no RAPD. Optic disks showed mild temporal pallor OU. The remainder of the neurologic examination was normal.

DISCUSSION

Field description: Bitemporal superior and central hemifield defects. Localization: Optic chiasm, inferior aspect.

Pathology: Pituitary adenoma. Other features: Hemifield slide.

Confrontation testing showed blurred images in the upper and lower temporal fields OU.

Every isopter tested shows a sharp demarcation at the vertical midline, with normal nasal hemifields. The vertical steps are predominantly in the superior fields, consistent

with compression of the inferior optic chiasm. Enhanced sagittal T1-weighted MRI demonstrated a homogeneously enhancing mass arising from the sella and compressing the optic chiasm from below. This proved to be a nonsecreting pituitary adenoma on resection 3 weeks later.

The patient’s hemifield slide resembles that of Case 57. Unlike that patient, his defect was not a complete bitemporal hemianopia, which is the defect typically associated with hemifield slide. This case shows that even partial loss of temporal fields can weaken the fusional registration of one eye’s field with the other.

DISCUSSION

Field description: Incongruous left homonymous superior quadrantanopia. Localization: Right anterior temporal optic radiations.

Pathology: Resected dysembryoplastic neuroepithelial tumor.

Confrontation testing showed very incongruous left superior quadrantanopia to hand motion, worse OD.

In general, the resections involved in temporal lobectomies begin at the anterior pole and extend a variable degree posteriorly. The retinotopy in Meyer’s loop is such that the

fibers representing the vertical meridian are most anterior, and those near the horizontal meridian most posterior (where they eventually merge with the parietal radiations). The consequence of these two facts is that the field defects associated with lobectomy always begin at the vertical meridian and extend a variable degree toward the horizontal meridian, likely depending on the extent of resection. In this patient’s case, the resection of 4.2 cm is consistent with some sparing of field near the horizontal meridian.

HISTORY AND EXAM

This 68-yr-old woman had a known glioblastoma multiforme diagnosed 1 year earlier and treated with surgery and radiation. In the week prior to evaluation, she had unusual morning headaches and then a single, generalized tonic-clonic seizure. Her family also reported that she was getting lost on routes around her home. Visual acuity was 20/20 OU,

Ishihara color scores were 13/14 OU, and there was no RAPD. Neurologic examination in the emergency room showed a visual field defect as well as left hemineglect, extinction of left-sided stimuli when touched simultaneously on both sides of her body, and a dressing apraxia.