Synonyms

Scotoma; Visual field loss

Short Description or Definition

A visual field deficit refers to diminished or absent vision in circumscribed parts of the visual field.

Categorization

Visual field deficits are caused by lesions at different levels of the visual system. Lesions at the retinal level result in scotoma of the affected eye. Optic nerve lesions peripheral to the partial crossing of fibers at the optic chiasm usually cause visual field deficits for one eye only (i.e., unilateral or monocular, incongruent defect). Lesions of the chiasm, optic tract, lateral geniculate nucleus, optic radiations, and primary visual cortex produce deficits in the contralateral visual hemifield that are roughly congruent for both eyes (i.e., covering the same area when tested monocularly (Fahle 2003)).

There are four general types of visual field defects. Altitudinal defects occur with partial damage to an optic nerve and consist of a deficit in part or all of the nasal and temporal fields limited to the upper quadrants or to the two lower quadrants of vision. Central scotoma is the partial or complete loss of vision at the center of the visual field caused by injury of the portion of the optic nerve carrying fibers from the macular region usually owing to bilateral injury to the occipital poles. Paracentral scotoma is a small defect in the paracentral visual field. Hemianopsia occurs from lesions of the optic chiasm and refers to a visual field deficit respecting the vertical midline. When lesions affect the decussating fibers from the nasal retina of each eye (which carry information from the temporal fields), it results in the loss of both temporal visual fields, referred to as bitemporal hemianopsia. Binasal hemianopsia results from lesions of the decussating fibers from the temporal retina of each eye. Quadrantanopia is the loss of vision in superior or inferior visual field quadrants and can be bitemporal (or homonymous). For example, a bitemporal superior quadrantanopsia is usually caused by pituitary adenomas impinging on the optic chiasm that can evolve into full hemianopsia with growth of the adenoma. Homonymous (identical side) hemianopsia results from a lesion in the optic tract or the optic radiation of one eye causing a deficit in the temporal field of that eye and in the nasal field of the other eye. Homonymous superior quadrantanopsia can occur with lesions in the anterior temporal lobe where the fiber bundles of the optic radiation are most separate. Superior quadrantanopsia also results from a lesion of the lingual gyrus of the primary visual cortex; inferior quadrantanopsia is the result of a lesion in the cuneus (Gilman and Newman 2003) (Fig. 1).

Visual Field Deficit, Fig. 1
figure 222figure 222

Visual field deficits. The visual pathways carry information from the left visual field to the right visual cortex and from the right visual field to the left visual cortex. The figure depicts visual field defects (in the black areas) as patients with lesions at sites 1–6 experience them

Full size image
  1. 1.

    A lesion of the right optic nerve causes total loss of vision in the right eye.

  2. 2.

    A lesion of the optic chiasm causes bitemporal hemianopsia (loss of vision in the temporal halves of both visual fields).

  3. 3.

    A lesion of the optic tract causes contralateral homonymous hemianopsia (complete loss of vision in the opposite half of the visual field).

  4. 4.

    After leaving the lateral geniculate nucleus, the fibers representing both retinas mix in the optic radiation. A lesion of the optic radiation in the temporal lobe causes an upper contralateral quadrantanopsia (loss of vision in the upper quadrant of the opposite half of the visual field of both eyes).

  5. 5.

    Partial lesions in the primary visual cortex lead to partial defects on the opposite side. A lesion in the upper bank of the calcarine sulcus (5) causes a contralateral inferior quadrant deficit. A lesion in the lower bank of the calcarine sulcus (6) causes a contralateral superior quadrant defect. A more extensive lesion affecting both banks of the calcarine sulcus would cause more extensive contralateral visual field loss. The central area of the visual field is unaffected by cortical lesions (5 and 6), probably because the foveal region of the retina is represented so extensively that a single lesion is not likely to destroy the entire representation (from “Central visual pathways” by Wurtz, R.H. & Kandel, E.R. (pages 523–547) in Principles of Neural Science, 4th Edition (2000) Kandel, E.R, Schwartz, J.H. & Jessell, T.M. (Eds.) and by permission from McGraw-Hill Health Provisions Division).

Epidemiology

The most common visual field deficit is homonymous hemianopsia (65%), followed by quadrantanopsia and paracentral scotoma. Occipital cerebrovascular disease is the cause of most visual field defects (76.1%). Other causes include closed head trauma (11.3%), tumor (operated, 5.5%), hypoxia (3.9%), and others (Zihl 2000).

Evaluation

Perimetry is used to test visual fields. Perimetry can be kinetic, where points of light are moved from the periphery inward until the patient sees them, or static where points of light are flashed in the visual field and the patient indicates when they are detected. Visual fields can be screened “at bedside” using a confrontation method. For example, with one eye covered and visual fixation on the examiner’s nose, the patient indicates whether they detect movement of the examiner’s finger in each of the visual field quadrants.

Interventions

Visual field defects can have significant effects on one’s ability to perform daily activities and quality of life (e.g., loss of the ability to read and drive). Rehabilitation strategies that have been used to treat visual field deficits include (1) restitution training to increase the size of the remaining visual field, (2) compensation training to scan across the “seen” and “lost” visual field, and (3) substitution strategies such as the use of eye glasses with prisms. In a search of the Cochrane Stroke Group Trials Register, Pollock et al. (2011) found that there have been few studies comparing rehabilitation strategies with a placebo, control, or no treatment group in patients with visual field deficits following stroke. In the studies reviewed, they found limited evidence supporting the use of compensatory scanning training to improve scanning and reading outcomes, but with insufficient evidence for beneficial effects on other functional activities. There was insufficient evidence for any beneficial effects of restitution or substitution intervention strategies.