Vertebrobasilar System Disease
The vertebrobasilar arterial system (posterior circulation) is composed of the vertebral, basilar, and posterior cerebral arteries. These blood vessels supply the occipital cortex, brainstem, and cerebellum.
Clinical presentation of vertebrobasilar insufficiency
Patients with vertebrobasilar insufficiency often present to the ophthalmologist first, because ocular motor and visual symptoms are prominent (Fig 14-13). Nonophthalmic symptoms of transient ischemic attacks (TIAs) in the vertebrobasilar system include
ataxia, imbalance, or staggering
vertigo combined with other brainstem symptoms such as deafness or vomiting
transient dysarthria and dysphagia
hemiparesis, hemiplegia, and hemisensory disturbances
drop attacks (patient suddenly falls to the ground with no warning and no loss of consciousness)
Bilateral blurring or dimming of vision occurs almost as frequently as vertigo. The patient may report sudden bilateral graying or whiting out of vision. These episodes of dimming may last seconds to minutes and may be accompanied by flickering or flashing stars. Photopsias may occur, closely mimicking the scintillating scotomata of migraine. These attacks are frequently repetitive and may occur alone or in combination with the other transient symptoms of vertebrobasilar insufficiency. Migraine (discussed in Chapter 12) can produce similar symptoms, with or without an associated headache.
Homonymous visual field changes without other neurologic symptoms suggest involvement of the posterior circulation. Highly congruous homonymous visual field defects without other systemic symptoms are typical of occipital lobe infarcts. Patients who report reading difficulties without an obvious cause should undergo a careful visual field and Amsler grid examination in search of centrally located congruous homonymous visual field defects.
Chapter 4 details the visual manifestations of cortical infarction. Cerebral and cortical blindness, caused by bilateral occipital lobe lesions, is characterized by amaurosis, normally reactive pupils, and an unremarkable fundus appearance. Frequently, patients with cerebral blindness will deny their blindness (Anton syndrome; see Chapter 6).
Figure 14-13 A 58-year-old woman had a sudden onset of diplopia and vertigo. Examination revealed a right CN III palsy and ataxia. Symptoms and signs resolved over 24 hours. This cerebral angiogram shows marked stenosis of the basilar artery (arrow).
(Courtesy of Karl C. Golnik, MD.)
Ocular motor disturbances are common with vertebrobasilar insufficiency, and diplopia is a frequent complaint. Examination may reveal horizontal or vertical gaze palsies, internuclear ophthalmoplegia, skew deviation, ocular motor CN palsies, or nystagmus. An ipsilateral, central Horner syndrome may be present with pontine or medullary infarcts (Wallenberg syndrome).
Levin LA. Topical diagnosis of chiasmal and retrochiasmal disorders. In: Miller NR, Newman NJ, Biousse V, Kerrison JB, eds. Walsh and Hoyt’s Clinical Neuro-Ophthalmology. Vol 1. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2005:539–554.
Etiologies of posterior circulation ischemia
The most frequent causes of vertebrobasilar TIAs and stroke are atheromatous occlusion, hypertensive vascular disease (lacunar infarction), microembolization (either from the vertebrobasilar system or from the heart), fluctuations in cardiac output, and arterial dissection. The following conditions have all been associated with symptoms and signs of vertebrobasilar ischemia: polycythemia, hypercoagulable states, anemia, vasospasm, and congenital aplasia or hypoplasia of a vertebral or posterior communicating artery. Mechanical factors such as cervical spondylosis and chiropractic manipulation of the cervical spine have also been implicated in vertebrobasilar occlusions resulting in severe neurologic deficits. A less common cause of vertebrobasilar dysfunction is a reversal of blood flow in the vertebral artery (subclavian steal); this reversal is caused by a proximal occlusion of the subclavian artery that produces an unusual alteration in the direction of flow in the ipsilateral vertebral artery. Lowered pressure in the distal segment of the subclavian artery can siphon, or “steal,” blood from the vertebral artery and produce fluctuating symptoms of vertebrobasilar artery insufficiency.
Investigation of posterior circulation ischemia
The evaluation for posterior circulation ischemia is similar to the medical workup for carotid system disease. Neuroimaging is typically performed on all patients with homonymous visual field defects and other signs of brainstem or cerebellar dysfunction. Magnetic resonance angiography (MRA) and computed tomographic arteriography (CTA) are the best noninvasive methods for evaluating the posterior circulation. Carotid Doppler imaging is not sufficient for evaluating suspected posterior circulation symptoms. Sometimes conventional angiography is necessary to visualize the aortic arch, the configuration of the vertebrobasilar vessels, and the extent of filling from the anterior circulation through the circle of Willis.
The clinician is much less likely to find a treatable structural vascular abnormality with posterior circulation ischemia than with carotid system disease. The evaluation of these patients generally emphasizes a search for underlying cardiac or systemic disorders, including hypercholesterolemia, hypertension, diabetes mellitus, and postural hypotension. Cardiac evaluation should also include echocardiography.
Markus HS, van der Worp HB, Rothwell PM. Posterior circulation ischaemic stroke and transient ischaemic attack: diagnosis, investigation, and secondary prevention. Lancet Neurol. 2013;12(10):989–998.
Treatment of vertebrobasilar ischemia
Most patients with vertebrobasilar TIAs are treated with statins and antiplatelet therapy or anticoagulants. Intravascular stent placement can be used in select patients with symptomatic vertebrobasilar stenosis who have failed maximal medical therapy.
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.