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Visual Field Deficits - Overview

Case 1
Left optic nerve lesion.
  • The unilaterality of the injury localizes the deficit to a prechiasmatic lesion, either in the optic nerve or in the retina, itself.
  • Note that a relative afferent pupillary defect would almost certainly accompany this optic nerve injury (See the Pupillary Response to Light tutorial).
Case 2
Lesion of the left postchiasmatic pathway.
  • Disruption of fibers from both the nasal right hemiretina and temporal left hemiretina produces a right homonymous hemianopia.
  • These retinal fibers first bundle posterior to the optic chiasm within the optic tract; however, a lesion anywhere along the postchiasmatic pathway — in the left optic tract, left lateral geniculate nucleus, left optic radiations, or left visual cortex (calcarine sulcus) — will produce the described right homonymous hemianopia.
Case 3
Left superior optic radiation lesion.
  • The lateral geniculate nucleus projects through superior and inferior optic radiations to the visual cortex (calcarine sulcus).
  • These radiations maintain the same superior–inferior retinotopic organization found in the retina; therefore, a superior optic radiation lesion produces an inferior field defect.
  • The hemianopia lateralizes to the right side, which means that the lesion is postchiasmatic on the left.
Case 4
Left inferior optic radiation lesion.
  • As noted previously, projections from the lateral geniculate nucleus to the visual cortex (calcarine sulcus) maintain the same superior–inferior retinotopic organization as found in the retina; therefore, an inferior radiation lesion produces a superior field defect.
  • The hemianopia lateralizes to the right side, so the lesion is postchiasmatic on the left.
Case 5
Optic chiasm lesion.
  • The optic chiasm contains crossing fibers from the bilateral nasal hemiretinae, which receive the temporal visual fields.
  • Bitemporal hemianopia is an important exam finding because it often suggests the presence of a sellar mass, such as a pituitary adenoma or craniopharyngioma.
    • Often it is stated that this lesion produces a constriction of vision and a sensation of "wearing horse blinders"; however, more accurately, bitemporal hemianopia produces a loss of binocular fusion, which results in "hemifield slide."
Case 6
Left occipital lobe lesion.
  • Our current patient has a right homonymous hemianopia with preserved central vision through sparing of left macular cortical representation.
  • According to the vascular model for macular sparing, the posterior cerebral artery supplies the occipital cortex except for the occipital pole, which the middle cerebral artery supplies.
    • Therefore, in the setting of posterior cerebral artery infarction, the middle cerebral artery maintains perfusion of the occipital pole, which spares macular cortical representation.
  • Additionally, or alternatively, macular sparing is argued to occur from redundant macular representation in both occipital cortices in much the same way that auditory information is redundantly localized to both transverse temporal gyri (of Heschl).
Case 7
Left lateral optic chiasm lesion.
  • Again, the deficit is limited to one eye; therefore, the injury is anterior to the optic tract.
    • The deficit is in the visual field contralateral to the affected eye, which means that the temporal retinal fibers are selectively affected.
  • Note that this pattern of injury could also occur along the optic nerve, but it is in the optic chiasm that the nasal and temporal retinal fibers split apart: this case highlights the separation of the nasal and temporal retinal fibers within the optic chiasm.
Case 8
Left-side retinal lesion (specifically, a lesion within the macula).
  • The restriction of the deficit to one eye makes this a prechiasmatic lesion, localizing to either the retina or optic nerve.
    • However, the limited pattern of visual field defect strongly suggests a retinal lesion.
  • Retinal lesions typically parse into the following categories: central or cecocentral scotomas from injury to the papillomacular bundle; arcuate field defects, which obey the horizontal meridian; and temporal wedge defects from nasal retinal wedge fiber injury.
  • We must appreciate, however, that a partial optic nerve injury can potentially assume the same deficit pattern as any retinal layer injury, and we must go beyond visual field testing to distinguish the localization of a prechiasmatic lesion.
Case 9
Junctional scotoma.
  • To understand the pathogenesis of junctional scotoma, show a fiber project from the right nasal hemiretina through the optic chiasm, and then bend anteriorly into the contralateral optic nerve (the nerve on the left) before projecting posteriorly into the left optic tract.
  • Indicate that this bend is called Wilbrand's knee; it carries inferonasal fibers.
    • Wilbrand's knee is argued to be an artifact of pathologic processing and not a true anatomic entity. Although the bend into the optic nerve may not exist, it still teaches us about the separation of the inferior and superior nasal projections: The inferonasal fibers collect in the anterior optic chiasm and the superonasal fibers collect in the posterior optic chiasm.
  • The junctional scotoma occurs from injury to the anterior nasal fibers.
  • Junctional scotoma is a lesion at the junction between the optic nerve and optic chiasm.
    • Two forms of anterior junctional defect are commonly recognized: junctional scotoma (aka anterior junction syndrome) and junctional scotoma of Traquair.
    • Both forms of anterior junctional defect involve the ipsilateral optic nerve. Junctional scotoma results in an ipsilateral central scotoma (from subtotal involvement of the ipsilateral optic nerve) and contralateral superior temporal quadrantanopia from injury to the crossed inferonasal fibers from the opposite eye.
    • Whereas, junctional scotoma of Traquair is an anterior junction injury with isolated ipsilateral optic nerve deficit and results in an ipsilateral temporal hemifield defect, only.
    • Let's not let the differences of the junctional scotoma and junctional scotoma of Traquair distract us from a key similarity between the two: both syndromes are perichiasmatic, and yet they both can easily be mistaken for optic nerve lesions.
    • Distinguishing perichiasmatic from optic nerve lesions is important because perichiasmatic lesions are almost universally secondary to parasellar tumors or aneurysms, whereas optic nerve lesions occur from both compressive and also noncompressive causes.

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