The most familiar clinical abnormality resulting from a lesion of one occipital lobe, a contralateral homonymous hemianopia, has already been discussed in Chap. 12. Extensive destruction abolishes all vision in the corresponding opposite half of each visual field. With a neoplastic lesion that eventually involves the entire striate region, the field defect may extend from the periphery toward the center, and loss of color vision (hemiachromatopsia) often precedes loss of black and white. Destruction of only part of the striate cortex on one side yields characteristic field defects that accurately indicate the loci of the lesion. A lesion confined to the pole of the occipital lobe results in a central hemianopic defect that splits the macula and leaves the peripheral fields intact. This observation indicates that half of each macula is unilaterally represented and that the maculae may be involved (split) in hemianopia. Bilateral lesions of the occipital poles, as in embolism of the posterior cerebral arteries, result in bilateral hemianopias and cortical blindness as detailed below. Unilateral quadrant defects and altitudinal field defects due to striate lesions indicate that the cortex on one side, above or below the calcarine fissure, is damaged. The cortex below the fissure is the terminus of fibers from the lower half of the retina; the resulting field defect is in the upper quadrant, and vice versa. Most bilateral altitudinal defects, either superior or inferior, are traceable to incomplete bilateral occipital lesions (cortex or terminal parts of geniculocalcarine pathways). Head and Holmes described several such delimited cases caused by gunshot wounds; embolic infarction is now the common cause.
As indicated in Chap. 12, the homonymous hemianopia that results from ablation of one occipital lobe is not absolute. In monkeys, visuospatial orientation and the capacity to reach for moving objects in the defective field are preserved (Denny-Brown and Chambers). In humans also, flashing light and moving objects can sometimes be seen in the blind field even without the patient’s full awareness. Weiskrantz and colleagues have referred to these preserved functions as blindisms or blindsight. It is useful as a practical matter to note that the optokinetic responses are usually spared in hemianopic deficits of occipital origin.
Many of the complex behavioral defects involving visual function are caused by lesions at the junctions of the occipital and parietal or temporal lobes. They are discussed here with the occipital lobe syndromes for convenience but should be considered as transcending the largely arbitrary boundaries of these three lobes of the brain.
With bilateral lesions of the occipital lobes (destruction of area 17 of both hemispheres), there is a loss of sight that can be conceptualized as bilateral hemianopia. The degree of blindness may be equivalent to that which follows severing of the optic nerves. The pupillary light reflexes are preserved because they depend upon visual fibers that terminate in the midbrain, but reflex closure of the eyelids to threat or bright light may, or may not, be preserved (see Fig. 13-9). No changes are detectable in the retinas. The eyes are still able to move through a full range and, if there is macular sparing as there usually is with vascular lesions, optokinetic nystagmus can be elicited. Visual imagination and visual imagery in dreams are preserved. With rare exceptions, no cortical potentials can be evoked in the occipital lobes by light flashes or pattern changes (visual evoked response), and the alpha rhythm is lost in the electroencephalogram (EEG; see Chap. 2).
Less-complete bilateral lesions leave the patient with varying degrees of visual perception. There may also be visual hallucinations of either elementary or complex types. The mode of recovery from cortical blindness has been studied carefully by Gloning and colleagues, who describe a regular progression from cortical blindness through visual agnosia and partially impaired perceptual function to recovery. Even with recovery, the patient may complain of visual fatigue (asthenopia) and difficulties in fixation and fusion.