CLINICAL NEURO-OPHTHALMOLOGY
poral and has a midline hemianopic character that extends to the periphery of the field. When only the macular crossed fibers from one eye are damaged, the resultant field defect is still monocular and temporal but is scotomatous and lo- cated in the paracentral region. If there is extensive damage to the visual fibers in an optic nerve, an extensive field defect or total blindness develops in the ipsilateral eye. In such cases, but also in less severe cases, the crossed ventral fibers that originate from ganglion cells inferior and nasal to the fovea of the contralateral eye may also be damaged, produc- ing a defect in the superior temporal field of the contralateral eye (Fig. 12.1).
This contralateral field defect, which occurs in an eye without other evidence of visual dysfunction, may be over- looked when kinetic perimetry is performed unless the supe- rior temporal region of the ‘‘normal’’ eye is carefully tested by the examiner, but it is almost always detected when auto- mated static perimetry is used (Fig. 12.1). Bird (5) detailed the findings in eight patients with the anterior chiasmal syn- drome. In each case, a central scotoma was present in the visual field of the eye on the side of the lesion, and there was temporal field loss in the contralateral eye. In five cases, the contralateral field loss was in the superior temporal field only, and in two of these five cases, the peripheral field was normal by kinetic perimetry, with the defect being scotoma- tous and detectable only in the paracentral upper temporal field with small test objects. In the remaining three patients, the contralateral field loss was in the paracentral temporal region, without preferential loss above or below the horizon- tal meridian.
The mechanism by which the fibers from the contralateral eye are damaged was ascribed to their anterior extension
into the affected ipsilateral optic nerve to form the structure called Wilbrand’s knee (6,7) (see Chapters 1 and 4). Horton
(8) suggested that this eponymous structure is more likely an artifact that develops during atrophy of the ipsilateral optic nerve. Against this are findings of superior temporal visual field defects in patients with acute avulsion injuries of the anterior chiasm (9,10). Whatever the mechanism, the importance of identifying the usually asymptomatic field de- fect cannot be sufficiently stressed, because it is at this point that the examiner can make an absolute diagnosis of an ante- rior optic chiasmal (distal optic nerve) syndrome, at a stage at which treatment of the underlying lesion is most likely to result in improvement in visual function.
Lesions that Damage the Body of the Optic Chiasm
Lesions that damage the body of the optic chiasm charac- teristically produce a bitemporal defect that may be quad- rantic or hemianopic and that may be peripheral, central, or a combination of both, with or without so-called splitting of the macula (Fig. 12.2). In most cases, visual acuity is normal. In some patients, however, visual acuity is diminished, even though no field defect other than a bitemporal hemianopia is present (11). When the lesion compresses the chiasm from below, such as occurs with a pituitary adenoma, the field defects follow a stereotyped pattern (12). When the periph- eral fibers are principally affected, the field defects usually begin in the outer upper quadrants of both eyes (Fig. 12.3). In the field of the right eye, the defect usually progresses in a clockwise direction and in the left eye in a counterclockwise direction (13).
The field defects may be unequal in the two eyes: one
Figure 12.2. Optic chiasmal syndrome. A, Kinetic pe- rimetry in a patient with a large pituitary adenoma reveals a complete bitemporal hemianopia. B, Static perimetry, using a Humphrey 24-2 Threshold Test, in another patient with a pituitary adenoma, reveals an incomplete bitemporal hemianopia.