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Visual disturbance usually falls into one of several categories but sometimes it is in more than one category, depending on whether visual loss is accompanied by other deficits.
Types of visual loss include
Monocular loss,
Binocular loss,
Hemianopia,
Diplopia, and
Positive visual disturbance.
Monocular visual loss is due to a lesion of the eye or of the optic nerve.
Pupillary response can help to distinguish between these locations, although imperfectly. If there is an afferent pupillary defect (APD), then optic neuropathy is more likely than ocular etiology, although severe ocular damage can produce APD.
Disc appearance varies depending on etiology. If the disc shows swelling or especially if there is hemorrhage, the neurologist should consider Giant cell arteritis (GCA), nonarteritic ischemic optic neuropathy, infections, and other etiologies with inflammatory or infiltrative features (e.g., tumor). If the disc is normal or shows mild swelling, optic neuritis or neuromyelitis optica (NMO) are possible causes. If the disc is absolutely normal, the neurologist should consider posterior ischemic optic neuropathy.
If there is no APD, or even mild relative defect, then the neurologist should consider retinal arterial or venous ischemia, although those should have fundus findings. The neurologist should also consider central serous maculopathy.
Subacute to acute binocular visual loss has a broad differential diagnosis with some differences from monocular.
Full-field binocular visual loss of recent onset can be due to bilateral occipital ischemia, bilateral retinal dysfunction, or bilateral optic nerve dysfunction. Cortical blindness from occipital ischemia should result in preservation of pupillary responses; if there is bilateral retinal or optic nerve pathology, then there should be apparent bilateral APD. Papilledema suggests idiopathic intracranial hypertension (IIH) as a cause, but bilateral optic neuritis should be considered. Methanol poisoning can produce bilateral visual blurring and blindness.
Hemifield binocular visual loss is most commonly due to stroke and often is incomplete because of the complex vascular supply to the optic radiations and cortex. In a transient ischemic attack (TIA), this loss would not be persistent. Migraine can produce hemifield visual loss, although often there are also associated visual phenomena. Similarly, seizure can produce hemifield visual loss and can be associated with transient positive visual symptoms. Related, posterior reversible encephalopathy syndrome (PRES) presents with similar symptoms.
In macular sparing with a hemianopia, there is damage to the occipital primary visual (calcarine) cortex around the calcarine sulcus. If stroke or other structural lesion spares the most posterior/occipital portion of this sulcus, which serves the macula, then the hemianopia is macular sparing. This is most common with posterior cerebral artery (PCA) stroke because the posterior macular region of the cortex receives at least some supply from the middle cerebral artery (MCA).
Binocular superior quadrant visual loss (quadrantanopia) is typically due to damage to the optic radiations as they pass through the temporal lobes.
Binocular inferior quadrantanopia is usually due to damage in the contralateral parietal region, affecting visual projections to the super side of the visual cortex.
The deficits affecting the quadrants are not exact because the optic tract projections are not perfectly organized.
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