Vertebrobasilar insufficiency history and symptoms

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Vertebrobasilar insufficiency

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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 often required to diagnose VBI, computed tomography (CT) is performed first. The CT is extremely sensitive in detecting hemorrhage. Duplex ultrasound is widely used to identify carotid stenosis, but is much less sensitive in the detection of vertebral artery stenosis. The vertebral origin can be often, but not always, visualised, but the more distal segments of the vertebral artery cannot be directly seen. 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.

History

Symptoms

Manifestations of TIAs affecting the vertebrobasilary territory tend to be more prolonged and diverse than those affecting the anterior circulation. The hallmark symptoms include vertigo, diplopia, dysarthria, numbness, ataxia, and weakness of one or both sides of the body.

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.

Dysarthria should also raise suspicion for VBI.[1]And there are also some nonspecific symptoms such as unilateral weakness; disturbances of respiration, anomalous hemodynamic change; and confusion, and memory loss. The most frequent symptoms were dizziness (47%), unilateral limb weakness (41%), dysarthria (31%), headache (28%), and nausea or vomiting (27%). The most frequent signs were unilateral limb weakness (38%), gait ataxia (31%), unilateral limb ataxia (30%), dysarthria (28%), and nystagmus (24%).[2] Some person with vertebralbasilar insufficency are asymptomatic. In a recent hospital-based study of 3717 patients with clinically manifest atherosclerotic arterial disease, 7·6% of patients (95% CI 6·8–8·5) had an asymptomatic vertebral artery origin stenosis of at least 50% or occlusion on duplex ultrasound.[3]

References

  1. Otto V, Fischer B, Schwarz M, Baumann W, Preibisch-Effenberger R (2008)Treatment of vertebrobasilar insufficiency--associated vertigo with a fixed combination of cinnarizine and dimenhydrinate. Int Tinnitus J 14 (1):57-67. PMID: 18616088
  2. Searls DE, Pazdera L, Korbel E, Vysata O, Caplan LR (2012)Symptoms and signs of posterior circulation ischemia in the new England medical center posterior circulation registry. Arch Neurol 69 (3):346-51. DOI:10.1001/archneurol.2011.2083 PMID:22083796
  3. Compter A, van der Worp HB, Algra A, Kappelle LJ, Second Manifestations of ARTerial disease (SMART) Study Group (2011)Prevalence and prognosis of asymptomatic vertebral artery origin stenosis in patients with clinically manifest arterial disease. Stroke 42 (10):2795-800. DOI:10.1161/STROKEAHA.110.612903 PMID:21852605

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