As the fibers approach the occipital lobes, congruity becomes more important. Central fibers become separate from peripheral fibers; the central ones course to the occipital tip and the peripheral ones to the anteromedial cortex. Furthermore, there is cortical magnification of the area that corresponds to central vision in the posterior part of the striate cortex; the central 10° of visual field corresponds to approximately 50% of the visual cortex that extends from the posterior portion of the medial area to the occipital tip.
Because of the disparity in crossed versus uncrossed fibers, some of the peripheral nasal fibers leading to the anteromedial region are not matched with the corresponding uncrossed fibers. Therefore, the anteromedial region of the occipital lobe subserves a monocular “temporal crescent” of visual field in the far periphery (60°–90°). Finally, fibers localize within the occipital cortex superior and inferior to the calcarine fissure. Thus, visual field defects from occipital lobe lesions may have the following characteristics in the hemifields contralateral to the lesion:
congruous homonymous hemianopia, possibly sparing the fixational region (Fig 4-32; see also Fig 4-25)
monocular defect of the temporal crescent involving only the most anterior portion of the occipital lobe
homonymous lesion sparing the temporal crescent in the eye contralateral to the lesion (Fig 4-33); kinetic perimetry testing is required
homonymous quadrantanopia (superior or inferior) respecting the horizontal meridian
Most occipital lobe lesions encountered by ophthalmologists result from stroke (infarction in the territory of the posterior cerebral artery) and cause no neurologic deficits other than vision loss.
Figure 4-32 Occipital lobe infarction. A, B, Visual field patterns show congruous right homonymous hemianopia respecting the vertical meridian and sparing fixation. C, T2-weighted axial MRI scan showing left parieto-occipital stroke (arrows) sparing the occipital tip.
(Parts A, B courtesy of Michael S. Lee, MD; part C courtesy of Steven A. Newman, MD.)
A macula-sparing homonymous hemianopia suggests a stroke involving the portion of the primary visual cortex supplied by the posterior cerebral artery. The tip of the occipital lobe receives a dual blood supply from the middle cerebral artery and the posterior cerebral artery. Occlusion of the posterior cerebral artery damages the primary visual cortex, except for the region representing the macula at the posterior tip of the occipital lobe, which remains perfused by the middle cerebral artery.
Systemic hypoperfusion often damages the occipital tip because the tip sits in a watershed area supplied by distal branches of the posterior and middle cerebral artery systems. This highly vulnerable region may be the only injured area, causing homonymous hemianopic scotomata (Fig 4-34).
Figure 4-33 A 60-year-old woman presented with 3 episodes of transient visual loss to the left side. Her visual acuity was 20/20 bilaterally, but visual field patterns demonstrated a left homonymous hemianopia (A). Her temporal crescent was intact on the left side, and an MRI scan (B) confirmed the presence of a right occipital lobe stroke (straight arrow) compatible with an infarct and sparing of the anterior visual cortex (curved arrow).
(Part A courtesy of Steven A. Newman, MD; part B courtesy of Sophia M. Chung, MD.)
Cerebral blindness results from bilateral occipital lobe damage. Normal pupillary responses and optic nerve appearance distinguish cerebral blindness from total blindness caused by lesions anterior to the LGB. Anton syndrome (denial of blindness), although classically associated with cortical blindness, can be due to a lesion at any level of the vision system severe enough to cause blindness. Bilateral occipital lobe lesions occasionally permit some residual visual function.
Disturbances of the primary visual cortex due to neoplasms, migraine, or drugs may also cause unformed visual hallucinations. Formed hallucinations (see Chapter 6) are usually attributed to lesions of the extrastriate cortex or temporal lobe. Patients with injury to the occipital cortex sometimes perceive moving targets but not static ones; this Riddoch phenomenon may also occur with lesions in other parts of the visual pathway. The Riddoch phenomenon probably stems from cells in the visual system responding better to moving stimuli than to those that are static.
Barton JJ. Higher cortical visual deficits. Continuum (Minneap Minn). 2014;20(4 Neuroophthalmology): 922–941.
Riddoch G. Dissociation of visual perceptions due to occipital injuries, with especial reference to appreciation of movement. Brain. 1917;40:15–57.
Figure 4-34 An 18-year-old woman presented with an 8-day history of sharp, left-sided headaches. Visual acuity was 20/20 bilaterally. A, B, She missed letters on the right of the chart, and bilateral 10-2 programs demonstrated a tiny 1° homonymous scotoma just below and to the right of fixation in both eyes. C, Her angiogram revealed an arteriovenous malformation involving the occipital tip (arrow).
(Courtesy of Steven A. Newman, MD.)
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.