Homonymous hemianopia (loss of vision in corresponding halves of the visual fields) signifies a lesion of the visual pathway behind the chiasm. When a homonymous hemianopia is complete, it is difficult to discern the localization within the retrochiasmal visual pathways on the basis of the field loss alone. In contrast, incomplete homonymous hemianopia has more localizing value. If the field defects in the two eyes are identical (congruous), the lesion is likely to be posterior, in the calcarine cortex and subcortical white matter of the occipital lobe. In contrast, if the incomplete homonymous deficit has a different pattern in each eye (with one eye showing greater field loss than the other, but both on the same side of the vertical meridian), the pattern is incongruous, and the localization is more anterior within the retrochiasmal pathways, with the optic tract or proximal optic radiations most likely to be implicated. In this portion of the visual pathways, the crossing axons from one eye are in the process of becoming juxtaposed with their paired axon from the fellow eye, and a partial lesion may disproportionately affect more of the fibers from one eye than the other. Absolute congruity of field defects is actually infrequent, even with occipital lesions.
The lower fibers of the geniculocalcarine pathway (from the inferior retinas) swing in a wide arc over the temporal horn of the lateral ventricle and then proceed posteriorly to join the upper fibers of the pathway on their way to the calcarine cortex (see Fig. 12-2). This arc of fibers is known variously as the Flechsig, Meyer, or Archambault loop, and a lesion that interrupts these fibers will produce a contralateral superior homonymous quadrantanopia (upper temporal deficit in the contralateral eye and upper nasal deficit in the ipsilateral eye; Fig. 12-2E), or in incomplete cases, a homonymous superior wedge defect respecting the vertical meridian. This clinical effect was first described by Harvey Cushing, so that his name also was in the past applied to the loop of temporal visual fibers. Parietal lobe lesions are said to affect the inferior quadrants of the visual fields more than the superior ones.
Just as with the contralateral representation of the visual fields in respect to the vertical meridian, the representation of the upper visual field is in the bank of neurons below the calcarine fissure and vice versa. As to the localizing value of quadrantic defects, the report of Jacobson is of interest; he found, in reviewing the imaging studies of 41 patients with inferior quadrantanopia and 30 with superior quadrantanopia, that in 76 percent of the former and 83 percent of the latter the lesions were confined to the occipital lobe.
If the entire optic tract or calcarine cortex on one side is destroyed, the homonymous hemianopia is complete. However, with infarction of the occipital lobe as a result of occlusion of the posterior cerebral artery, the macular region, represented in the most posterior part of the striate cortex, may be spared by virtue of collateral circulation from branches of the middle cerebral artery. In this circumstance, there is a 5to 10-degree island of vision around the fixation point on the side of the hemianopia (macular sparing). With other types of destructive lesions, this effect is not seen. Lesions of both occipital poles result in bilateral central scotomas. If all the calcarine cortex or all the subcortical geniculocalcarine fibers on both sides are completely destroyed, the bilateral hemianopias cause cerebral, or “cortical,” blindness (see the following text and Chap. 21).