Vertebrobasilar insufficiency

Vertebrobasilar insufficiency (VBI), or vertebral basilar ischemia, refers to a temporary set of symptoms due to decreased blood flow in the posterior circulation of the brain. The posterior circulation supplies blood to the medulla, cerebellum, pons, midbrain, thalamus, and occipital cortex (responsible for vision). Therefore, the symptoms due to VBI vary according to which portions of the brain experience significantly decreased blood flow (see image of brain [1]). In the United States, 25% of strokes and transient ischemic attacks occur in the vertebrobasilar distribution. These must be separated from strokes arising from the anterior circulation, which involves the carotid arteries.

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Epidemiology

The incidence of VBI increases with age and typically occurs in the seventh or eighth decade of life. Reflecting atherosclerosis, which is the most common cause of VBI, it affects men twice as often as women and is more prevalent in African Americans. Patients with hypertension, diabetes, smoking, and dyslipidemias also have a higher risk of developing VBI.

Signs and Symptoms

Vertigo (commonly described as the environment spinning or as if the person is twirling in space) is the most recognizable and quite often the sole symptom of decreased blood flow in the vertebrobasilar distribution. The vertigo due to VBI rarely is brought on by head turning, which could occlude the ipsilateral vertebral artery and result in decreased blood flow to the brain if the contralateral artery is occluded. When the vertigo is accompanied by double vision (diplopia), graying of vision, and blurred vision, patients often go to the ophthalmologist. If the VBI progresses, there may be weakness of the quadriceps and, to the patient, this is felt as a buckling of the knees. The patient may suddenly become weak at the knee and crumple (often referred to as a “drop attack”). Such a fall can lead to significant head and orthopedic injury, especially in the elderly.

Transient ischemic attacks due to VBI will, by definition, have symptoms resolved within 24 hours. More often, however, the symptoms are very brief, lasting a few seconds to half an hour. These symptoms are often provoked by sudden and temporary drops in blood pressure. Postural changes (see orthostatic hypotension), such as getting out of bed too quickly or standing up after sitting for extended periods of time, often provoke these attacks. Exercise of the legs may also bring on the symptoms of VBI. For the sedentary older subject, going up a flight of stairs or walking the dog may be enough to cause pooling of blood in the legs and a drop in blood pressure in the distal arteries of the head. Heat and dehydration may also be contributing causes.

Diagnosis

The evaluation for VBI starts with a history and physical exam, with great emphasis on the cardiovascular and neurologic exam. It also includes a work-up to exclude benign conditions (such as labyrinthitis, vestibular neuronitis, and benign paroxysmal positional vertigo) that have overlapping signs and symptoms. However, the exact work-up largely depends on the patient’s age and known risk factors. For middle-aged patients, a cardiovascular risk factor evaluation is important. This often includes a cholesterol level, lipid profile (see this [2] to determine what your cholesterol level means), ECG, and echocardiogram. If a person with VBI is under age 45 and has no evidence for atherosclerosis, a work-up for hypercoagulable states (Lupus anticoagulant, anti-cardiolipin antibodies, protein C, protein S, antithrombin III deficiencies) is indicated.

Imaging studies are rarely required to diagnose VBI, but sometimes computed tomography (CT) is performed first. The CT is extremely sensitive in detecting hemorrhage. However, magnetic resonance imaging (MRI) is superior to the CT in detecting ischemic changes in the vertebrobasilar distribution. Magnetic resonance angiography (MRA) also can be used to identify vertebrobasilar occlusions, but it can often overestimate the degree of occlusion.

Treatment

Patients should discuss with their physician possible causes for their VBI symptoms. As discussed above, postural changes, exercise, and dehydration are some of the likely culprits. Treatment usually involves lifestyle modifications. For example, if VBI is attributed mainly to postural changes, patients are advised to slowly rise to standing position after sitting for a long period of time. An appropriate exercise regimen for each patient can also be designed in order to avoid the excessive pooling of blood in the legs. Dehydrated patients are often advised to increase their water intake, especially in hot, dry climates. Finally, when applicable, patients are often advised to stop smoking and to control their hypertension, diabetes, and cholesterol level.

In the event that a patient suffers a “drop attack,” and especially for the elderly population, the most important action is to be evaluated for associated head or other injuries. To prevent drop attacks, patients are advised to “go to the ground” before the knees buckle and shortly after feeling dizzy or experiencing changes in vision. Patients should not be concerned about the social consequences of suddenly sitting on the floor, whether in the mall or sidewalk, as such actions are important in preventing serious injuries.

Sometimes, to prevent further occlusion of blood vessels, patients are started on an antiplatelet agent (aspirin, clopidogrel, or aspirin/dipyridamole) or sometimes an anticoagulant (warfarin) once hemorrhage has been excluded with imaging.

For treatment of vertebrobasilar stenosis due to atherosclerosis, researchers from Stanford University found that intracranial angioplasty can be performed with an annual stroke rate in the territory of treatment of 3.2% and 4.4% for all strokes, including periprocedural events. Randomized control trials need to be performed.^[1]

References

1. ^ Marks MP, Wojak JC, Al-Ali F, et al (2006). "Angioplasty for symptomatic intracranial stenosis: clinical outcome". Stroke 37 (4): 1016–20. doi:10.1161/01.STR.0000206142.03677.c2. PMID 16497979.

• Lang E and Afilalo M. Vertebrobasilar Atherothrombotic Disease. [3]
• Savitz SI and Caplan LR. Vertebrobasilar Disease. New England Journal of Medicine 2005; 352(25):2618-2626. [4]