Transient Binocular Visual Loss Visual aura associated with migraine is the most common cause of transient binocular visual loss (▶ Fig. 6.1). The patient typically notes a small scotoma in homonymous portions of the visual field, surrounded by jagged, luminous, shimmering edges. The scotoma enlarges over several minutes, then gradually disappears. The visual loss may enlarge to a complete homonymous hemianopia. A hemicranial throbbing headache characteristically follows (see Chapter ▶ 19). Fig. 6.1 Progression of visual changes during migrainous visual aura (from top to bottom). Some patients experience the visual aura of migraine without associated headache. The vision and visual fields return to normal after the aura, usually within 20 to 30 minutes (always less than 1 hour). Pearls Although migrainous visual aura is binocular by definition (since it originates from the occipital lobe), many patients do not recognize the visual phenomena as being in both eyes, especially when they involve only one hemifield. The relatively long duration of visual phenomena, the progressive buildup of symptoms (“migrainous march”), and the richness of visual phenomena strongly suggest migrainous visual auras, even when the patient thinks the visual symptoms were only in one eye. In older patients, episodes of transient, complete binocular visual loss may represent a transient ischemic attack (TIA) in the distribution of the basilar artery or of the posterior cerebral arteries. A unilateral occipital TIA manifests as a transient homonymous hemianopia. As opposed to migraine, hemianopic events of ischemic origin are typically sudden in onset and last only a few minutes. There may be associated headache, especially over the brow contralateral to the visual field loss, but the pain is usually coincident with the visual loss, rather than following the visual loss as in migraine. TIAs in the anterior circulation produce ipsilateral monocular visual loss, whereas TIAs in the posterior circulation produce binocular visual loss (often contralateral homonymous hemianopia). This is explained by the anatomy of the blood supply to the brain (▶ Fig. 6.2 and ▶ Fig. 6.3). Fig. 6.2 Blood supply of the brain. (From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy, Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007. Illustration by Karl Wesker.) Fig. 6.3 Circle of Willis at the skull base. (From Schuenke M, Schulte E, Schumacher U, Ross LM, Lamperti ED, Voll M. THIEME Atlas of Anatomy, Head and Neuroanatomy. Stuttgart, Germany: Thieme; 2007. Illustration by Markus Voll.) The internal carotid arteries provide the blood supply to the anterior part of both cerebral hemispheres and to the eyes. The vertebrobasilar system provides the blood supply to the posterior part of both cerebral hemispheres (including the occipital lobes) and to the posterior fossa (brainstem and cerebellum) (▶ Fig. 6.2). The occipital lobes are vascularized by the posterior cerebral arteries, which originate from the basilar artery (▶ Fig. 6.3). Basilar artery stenosis or occlusion may result in bilateral occipital ischemia and bilateral complete visual loss (cerebral blindness). Posterior cerebral artery occlusion usually produces unilateral occipital ischemia with contralateral homonymous hemianopia. Occipital seizures can occur at any age but are more common in children. They may be primary or secondary to an occipital lesion. The patient typically complains of recurrent and brief, simple, positive visual phenomena, such as flashes of light or bubbles. They are binocular and they may be localized to a hemifield or diffuse within the entire field of vision. ▶ Table 6.1 compares the characteristics of migrainous visual aura, occipital TIA, and occipital seizure. Migrainous visual aura Occipital transient ischemic attack Occipital seizures Visual symptoms Positive; very rich, moving; often black and white, scintillating, shimmering, jagged edges Negative (hemianopia or blindness) Positive; simple visual phenomena (phosphenes, bubbles) Colored Ictal blindness Progression of symptoms Typical migrainous march, with progression of symptoms over time Sudden onset and disappearance Usually not progressive Duration of visual symptoms Typically 20 to 30 minutes A few minutes Usually brief (seconds) Often repeated Headache Migrainous headache typically follows the aura; may be absent Brow headache possible at the time of visual symptoms None Associated symptoms Headache follows; visual aura may be followed by other migrainous aura (mostly sensory) Vertebrobasilar ischemia: Vertigo, dizziness Imbalance Diplopia Bilateral extremity weakness Often none May be associated with other seizures Other less common causes of transient binocular visual loss are head trauma, especially in children; hypertensive encephalopathy; toxemia of pregnancy; and toxicity of drugs, such as cyclosporine, which may result in cerebral blindness lasting hours or days (see ▶ Fig. 5.25). Transient monocular visual loss (TMVL) is the preferred term for abrupt and temporary visual loss in one eye. TMVL most often results from transient ocular ischemia (so-called amaurosis fugax;), but it may also result from other mechanisms such as disc edema and numerous ocular diseases. See the discussion in Chapter ▶ 5. TMVL can be vascular (transient ischemia in the territories of the ophthalmic artery, central retinal artery and its branches, posterior ciliary arteries, or central retinal vein), can be ocular in origin (such as from dry eyes or attacks of angle closure glaucoma), or can result from optic nerve head anomalies. Pearls Transient visual obscurations (TVOs) are characterized by brief blackouts or “gray-outs” of vision and are precipitated by changes in posture, such as bending over. They usually indicate underlying optic nerve head edema or optic nerve anomalies causing high tissue pressure at the optic nerve head. Although disc edema results from a variety of disorders, the most likely cause of TVOs is papilledema from raised intracranial pressure. An orbital mass may produce gaze-evoked episodes of TMVL. The examination may be normal between episodes when the mass is relatively small. Movements of the eye result in stretching of the optic nerve and intermittent compression of the nerve or of its blood supply, with resulting transient loss of vision (▶ Fig. 6.4). Fig. 6.4 Axial computed tomographic scan of the orbits with contrast showing a mass in the left orbit. Eyes with a narrow anterior chamber angle may have episodes of angle closure glaucoma resolving spontaneously (▶ Fig. 6.5). During such episodes, the intraocular pressure is elevated, and patients complain of painful transient monocular blurry vision with the perception of halos around lights. Fig. 6.5 a, b (a) Shallow anterior chamber on slit lamp examination (b) narrow angle on gonioscopy in a patient with recurrent episodes of painful transient monocular visual loss.
6.1.1 Differential Diagnosis
Migrainous Visual Aura
Occipital Transient Ischemic Attack
Occipital Seizure
6.2 Transient Monocular Visual Loss
6.2.1 Differential Diagnosis
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
