Pearl

Tumors that arise from positions inferior to the chiasm, such as those arising from the pituitary gland, initially produce deficits with a bitemporal component in the superior quadrants, close to the midline. Other tumors, like the craniopharyngiomas that approach the chiasm from above, are more likely to cause early bitemporal deficits that first appear in the lower quadrants (see Chaps. 3 and 4).

More important for the nature of early visual field defect, however, is the positional relationship between the chiasm and the diaphragma sellae. This varies significantly from one person to the next (■ Fig. 12.3). Compression of the chiasm by masses approaching from the anterior aspect are more likely to cause monocular or highly asymmetric visual field loss, while tumors that compress the posterior aspect of the chiasm are more likely to cause homonymous patterns of loss by damaging the optic tract(s). Tumor types are summarized in ■ Table 12.4 (particularly frequent types are in italics).

The extent of visual field loss at the time of diagnosis varies from (1) minimal deficits that the patient has not yet noticed to (2) complete bilateral loss of the temporal hemi-fields to (3) catastrophic, binocular loss of all light perception. The latter presentation is seen when necrosis of and subsequent hemorrhage into a rapidly growing pituitary adenoma results in pituitary apoplexy, an abrupt enlargement of the tumor that causes intense headache and acute, severe compression of the chiasm from below. Rapid surgical decompression of the chiasm by evacuating the mass often allows for substantial recovery of the acutely lost vision. Bilateral loss of the temporal hemifields causes a loss of depth perception, with a completely blind area beyond the object of regard and loss of fusional vergence control (due to loss of all binocular areas of visual field). The loss of motor control of ocular alignment due to the loss of all binocular areas of the visual field results in sensory disturbances that include absolute blind areas between separated nasal hemifields (in patients with antecedent esode-viations), diplopia with overlapping nasal hemifields (antecedent exodeviations), or splitting and relative vertical displacement of image halves in those with vertical hetero-phorias (the so-called hemifield slide phenomenon described in Chaps. 2 and 15). Acuity is not necessarily reduced but will more likely to appear the longer the process lasts and the deeper the visual field loss grows. Even in the early stages of chiasmal progression, the acuities of both eyes may be reduced. Compression of the chiasm is usually blunt, with large masses with smooth surfaces, and damage is done to both crossing and uncrossed axons within the chiasm. This explains the loss of acuity in chiasmal disease and retention of normal acuity in patients with complete, retrogeniculate, homonymous hemianopias.

Optic atrophy may or may not be seen at the time of presentation, but is usually affecting both eyes (one exception: anterior junction syndrome, discussed in Chap. 3), a sign that the chiasmal damage is part of a long-standing disease process.

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