erythrocyte sedimentation rate and C-reactive protein concentration are included. Particularly in younger patients, hyperviscosity syndrome and hypercoagulable states should be considered, and serologic testing may include tests for anticardiolipin antibody, antiphosphatidyl choline and serine, antinuclear antibody, serum protein electrophoresis, partial thromboplastin time, VDRL, treponema pallidum hemagglutination assay (TPHA), protein S, and protein C. Whether vasospasm can truly cause transient visual loss is debated, but calcium channel blockers that prevent vasospasm seem to provide relief from attacks of amaurosis fugax in some patients.

Hyperviscosity is a rare cause of transient visual loss. Approximately 10% of patients with polycythemia vera complain of episodes of TMVL.

Winterkorn JMS, Burde RM. Vasospasm—not migraine—in the anterior visual pathway. Ophthalmol Clin North Am. 1996;9:393–405.

Transient Binocular Visual Loss

Common causes of transient binocular visual loss include

migraine

occipital mass lesions: tumor, arteriovenous malformation occipital ischemia: embolic, vasculitic, hypoperfusion occipital seizures

Migraine

The most common cause of transient binocular visual loss is the homonymous hemianopic defect caused by migraine. On occasion, this may progress to a fixed visual field defect called a “complicated” migraine, and MRI is mandatory in such instances. Evaluation of migraine is discussed in Chapter 12.

Occipital Mass Lesions

In a patient with episodic headaches and transient binocular visual loss, if attacks always occur on the same side or if visual symptoms follow rather than precede the onset of headache, a structural lesion—usually an occipital arteriovenous malformation or tumor—must be ruled out. Such patients require contrast-enhanced cranial MRI and possibly cerebral angiography.

Occipital Ischemia

As the patient with migraine ages, the intensity of headaches may diminish, or headaches may not occur at all after visual symptoms. A diagnostic dilemma is presented by the elderly patient who experiences a migraine-like aura for the first time but no headache. Differentiating between migrainous vasospasm and vertebrobasilar insufficiency may be difficult. Treatable causes of cerebrovascular disease or a source of emboli should be excluded. Patient evaluation should include hematologic studies (eg, complete blood count, erythrocyte sedimentation rate, and C-reactive protein

concentration), as well as MRI and MRA to evaluate the vertebrobasilar circulation. If the results of these studies are negative, the prognosis is usually good, and treatment of a presumed migrainous syndrome may be warranted.

Transient recurrent bilateral visual blurring is among the most frequent symptoms of vertebrobasilar insufficiency. Composed of the vertebral, basilar, and posterior cerebral arteries (see Chapter 1), the vertebrobasilar system supplies the occipital cortex, brainstem, and cerebellum. Patients with vertebrobasilar insufficiency often see the ophthalmologist first because of prominent ocular motor and visual symptoms. Nonophthalmic symptoms of TIAs in the vertebrobasilar system are discussed in Chapter 14.

Occipital Seizures

Occipital seizures typically produce unformed positive visual phenomena, such as colored or swirling lights or a whiting out of vision, “like a flashbulb going off.” However, some patients experience purely negative visual symptoms, typically described as a blacking out of vision. These episodes usually last 1–2 minutes, although they may persist for many hours (termed status epilepticus amauroticus). Most adults with occipital seizures harbor a structural lesion (eg, tumor, arteriovenous malformation, or trauma); in children, such seizures are more often benign. A normal electroencephalogram (EEG) does not rule out an underlying seizure disorder, and, in appropriate cases, prolonged EEG monitoring may be required. Treatment consists of anticonvulsant therapy.

Kun Lee S, Young Lee S, Kim DW, Soo Lee D, Chung CK. Occipital lobe epilepsy: clinical characteristics, surgical outcome, and role of diagnostic modalities. Epilepsia. 2005;46(5):688–695.