This article includes discussion of transient visual loss, cerebral visual loss, monocular visual loss, and visual loss involving central pathways. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Clarification of the mechanism and cause of transient visual loss first depends on separating monocular and binocular symptoms and signs. Binocular transient visual loss usually reflects cerebrovascular vertebrobasilar circulation thromboembolism, systemic hypoperfusion, or migraine. Monocular transient visual loss is often attributable to arteriostenotic disease of the internal carotid artery in the cervical or intracranial segment, or stenosis of the ophthalmic artery or its central retinal artery branch. However, reports show that migrainous vasoconstriction and various nonvascular mechanisms are also common causes of monocular transient visual loss and that familial hemiplegic migraine can be associated with multiple daily episodes of transient monocular vision loss in families with SCN1 mutations. Case reports also document that Whipple disease with bilateral optic disc edema and the use of latanoprost for glaucoma have both been associated with transient monocular vision loss in individual patients. In this article, the author cites case reports in which acute glaucoma led to transient vision loss in one or both eyes, which is important for the neurologist to include in the differential diagnosis so that an appropriate ophthalmologic referral can be made in order to prevent permanent vision loss.
• Transient binocular visual loss usually results from cerebrovascular vertebrobasilar circulation thromboembolism, systemic hypoperfusion, or migraine.
• “Reversible posterior leukoencephalopathy” refers to transient cortical binocular blindness with occipital white matter edema that is most commonly associated with acute systemic hypertension and eclampsia or preeclampsia. It has also been associated with various immunosuppressive and cytotoxic drugs.
• Transient monocular visual loss usually results from arteriostenotic disease of the internal carotid artery in the cervical or intracranial segment, or stenosis of the ophthalmic artery or its central retinal artery branch.
Historical note and terminology
The complaint of transient visual loss or simply difficulty seeing can be related to any disorder that temporarily perturbs the afferent visual system. The disorder can affect the eye, retina, optic nerve or tracts, lateral geniculate body, geniculocalcarine tract, or the calcarine visual striate and peristriate cortices. Conditions that affect the oculomotor system can also cause difficulty focusing, double vision, oscillopsia, and other eye movement disorders that compromise binocular vision and are interpreted by the patient as sight difficulties. The alert clinician can usually determine from patient history and examination that these disorders are due to eye movement abnormalities: paresis of movement of an eye muscle, a conjugate gaze or internuclear gaze abnormality, or nystagmus. This article will limit the detailed discussion to disorders that affect visual perception, that is, those that affect the afferent visual system.
Visual loss can be located in 1 eye (monocular) or both eyes (binocular), or may be referable to a portion of 1 homonymous visual field, in which case the defect is detectable in both eyes. In other patients, the disorder is caused by dysfunction of the visual cortex on both sides of the brain, and there is a loss of vision in both eyes and both visual fields. Many patients fail to distinguish between eye and visual field. They have never thought of vision as being brain-related and do not understand the concept of a visual field. Many have not attempted to localize the visual deficit. Because monocular and visual field abnormalities that cause transient visual loss have different clinical manifestations, causes, diagnostic strategies, and treatments, the discussion will be divided sharply between visual loss related to the eyes and visual loss related to the brain and the tracts that connect the eye to the brain.
The clinical importance of monocular visual loss (ie, amaurosis fugax, transient monocular blindness, transient visual obscuration) was described in detail by Miller Fisher (Fisher 1951; Fisher 1952), who emphasized that transient visual loss in a single eye often provided a clue to the presence of severe occlusive disease of the ipsilateral internal carotid artery in the neck, especially if patients with attacks of monocular visual loss had transient attacks of dysfunction of the contralateral limbs as well. Fisher also described and illustrated the funduscopic findings in a patient that he observed during an attack of transient monocular blindness (Fisher 1959). Pessin and colleagues subsequently showed that nearly all patients who had episodic transient monocular visual loss and transient hemispheric dysfunction referable to the ipsilateral cerebral hemisphere had severe stenosis or occlusion of the ipsilateral internal carotid artery (Pessin et al 1977).
Bilateral loss of vision referable to the brain (cortical blindness) had been recognized for centuries, but Sir Charles Symonds and Mackenzie deserve credit for demonstrating that the cause was usually infarction of the calcarine visual cortices, most often caused by an embolus that reached the rostral basilar artery and moved into both posterior cerebral arteries (Symonds and Mackenzie 1957).
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