The visual field test maps the vision in each eye by measuring the entire scope (central and peripheral) of vision when attention is focused on a central point. A visual field deficit can help to localize a lesion along the visual pathway. These deficits are divided, taking into consideration if they are unilateral or bilateral. Unilateral deficits are caused by retinal and optic nerve disease. Bilateral deficits are caused by chiasmal lesions or lesions affecting the retrochiasmal pathways.
Homonymous superior quadrantanopia, also called “pie in the sky,” causes a field deficit in the superior field of both eyes for the same side. This visual field deficit is bilateral and involves retrochiasmal pathways.
Homonymous superior quadrantanopia deficit can be seen in a large variety of disorders:
Superior homonymous quadrantanopia is not a disease; rather, a clinical finding that points towards a lesion of the optic radiations coursing through the temporal lobe. Scarce information is available regarding the frequency of this visual defect in the general population. However, studies documenting the frequency of a superior quadrantanopia following temporal lobe injury have been published. The most common cause of the visual field defect is an ischemic stroke, comprising 69% of the cases. Most patients show homonymous hemianopia, but a third of the cases exhibit a superior quadrantanopia. Most lesions are localized in the occipital lobe, while 32% of lesions were found at the optic radiations.
The presence of a mild visual field deficit may go unnoticed in a patient. However, severe superior quadrantanopia can cause significant loss of peripheral vision and can impede activities such as driving. The incidence of a visual field defect increases with age as the older population has an increased incidence of strokes and traumatic injuries. The prevalence of a visual field defect in the Australian population 49 years or older is 0.8%. There is a statistically significant relationship between age, hypertension, diabetes, and renal insufficiency. However, only about half of the patients with visual defects had a history of stroke.
The optic radiation and cortex on one side of the brain contain the visual information from the contralateral binocular visual hemifield.
Homonymous superior quadrantanopia is caused by damage to the contralateral inferior parts of the posterior visual pathway: the inferior optic radiation (temporal Meyer loop), or the inferior part of the occipital visual cortex below the calcarine fissure. For normal visual acuity, you only need “half a macula”; hence, these patients have normal visual acuity.
The nerve fiber bundles of the geniculocalcarine tract are topographically distributed in a dorsal to the ventral array as they project from the lateral geniculate nuclei to the occipital lobe.
A lesion involving the V2 and V3 extrastriate cortex may also cause a quadrantic visual field defect. Bilateral superior quadrantanopsias, although rare, may occur for bilateral strokes of hemorrhages in both occipital lobes below the calcarine fissure.
If homonymous hemianopia develops slowly, it is usually caused by a compressive etiology, but when it presents acutely, it is caused by hemorrhage, ischemia, and inflammation.
Even if confrontation visual field testing is normal, perimetry performing formal visual field testing is an essential part of the assessment of any patient with possible visual pathway disease. The baseline field can be established to monitor the stability of the deficit or the efficacy of treatment. If there is complete homonymous hemianopia, no further localization is possible. Partial homonymous field loss can help localize the lesion in two ways. However, neither is entirely reliable:
Magnetic resonance imaging (MRI) of the brain is the best modality to identify if there is a lesion in the brain, causing the deficit. On rare conditions, the MRI may have no identifiable lesion. In the acute emergent cases from intracerebral hematomas and trauma, head computed tomography will adequately show the lesion.
Specific etiologies may require further laboratory tests, non-invasive and invasive studies, and invasive studies.
If a patient presents a superior quadrantanopia, treatment is directed toward the underlying pathology as the visual field deficit does not affect the quality of life. As the deficit in homonymous superior quadrantanopia is toward one side and only the superior quadrant, most patients do not need correction.
For patients with complete homonymous hemianopia, several techniques can be used and are described.
Patients with chronic, dense homonymous hemianopias can be offered optical assistance from prisms, but only a minority of them will find it beneficial.
Children with congenital or early-onset hemianopia may develop a rare compensatory phenomenon with an exotropic eye and head turn, both toward the field defect, an adaptive mechanism to increase the useful visual field.
Visual occupational therapy and rehabilitation can be helpful. Compensatory oculomotor strategies, designed to enhance visual saccades into and exploration within the defective hemifield, may be tried. Training of blindsight and recovering some lost visual field have also been attempted. Vision restoration therapy is a costly home-based computerized treatment with repetitive stimulation on both sides of a border of a visual field defect. Many patients seem to benefit from these types of therapies in terms of reading and watching television.
The following should be kept in mind while making a diagnosis:
The visual field lost is usually permanent, with less than 20% of the patients regain the missing field. If improvement occurs, it is within 3-6 months after the insult. Rehabilitation involves improving or expanding the existing visual field. Reading and driving are not markedly affected as the inferior field is intact.
An interprofessional team consisting of ophthalmologist, neuro-ophthalmologist, neurosurgeon, neurologist, and visual occupational therapy and rehabilitation can help in evaluation and management of the disease.
Prevention and modification of factors involved in the primary etiology should be instructed to the patient. Affected patients are cautioned that they must turn the head to see into the defective field, but most of them learn to do that anyway. As a superior quadrantanopia usually does not affect the quality of life of the patient, they have to make only minimal adjustments to their daily routine.
In patients with dense homonymous hemianopias, crossing the street independently may be challenging. Also, the defect makes driving problematic. Many have difficulty reading, because left hemianopia may hamper their ability to find the beginning of the next line, and right hemianopia may not allow them to appreciate the entire line of words (hemianopic alexia). Family members are instructed to approach the patient from within the intact hemifield and keep food, utensils, and beverages within the patient’s intact hemifield when eating.
While the neuro-ophthalmologist is almost always involved in the care of patients with homonymous superior quadrantanopia, it is important to consult with an interprofessional team of specialists that include a neurologist, neurosurgeon, and neuroradiologist. The nurses are also a vital member of the interprofessional group as they will monitor the patient during the treatment of the causative injury and assist with the education of the patient and family. The neuroradiologist also plays a vital role in determining the cause. Without providing a proper history, the neuroradiologist may not be sure what to look for or what additional radiologic exams may be needed. Some patients are sent for visual occupational therapy and rehabilitation. An interprofessional team that provides a holistic and integrated approach to postoperative care can help achieve the best possible outcomes.
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