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Vertebrobasilar insufficiency

Vertebrobasilar insufficiency
Classification and external resources
ICD-10 G45.0
ICD-9 435.3
DiseasesDB 29497
MedlinePlus 001423
eMedicine emerg/834
NCI Vertebrobasilar insufficiency
Patient UK Vertebrobasilar insufficiency
MeSH C10.228.140.300.150.956

Vertebrobasilar insufficiency (VBI), or vertebral basilar ischemia (also called Beauty parlour syndrome (BPS)), 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.

Signs and symptoms

Vertigo, the sensation of spinning even whilst a person is still, is the most recognizable and quite often the sole symptom of decreased blood flow in the vertebrobasilar distribution.[citation needed] The vertigo due to VBI can be 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 optometrist/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.[citation needed]


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, is indicated. Screening for Protein C, Protein S, Antithrombin III deficiency is sometimes recommended but these are more usually responsible for venous thrombosis than arterial problems.

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 stenoses or occlusions, but it can often overestimate the degree of stenosis, or wrongly show stenosis as an occlusion. Intracranial MRA is mostly sufficient to evaluate vertebrobasilar arteries, while extracranial vertebral arteries are better diagnosed using contrast-enhanced MRA, which is less dependent on flow phenomena and more accurate in evaluating stenosis.

CT angiography is also highly accurate in evaluation vertebrobasilar vessels, but ionizing radiation and use of nephrotoxic contrast media make it less suitable both in elderly with renal insufficiency and young adults because of radiation exposure. Moreover, vessel wall calcification and beam-hardening artifacts due to dense bones or metal fillings sometimes cause strong CT-image degradation.


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]


The incidence of VBI increases with age and typically occurs in the seventh or eighth decade of life.[citation needed] Reflecting atherosclerosis, which is the most common cause of VBI, it affects men twice as often as women and patients with hypertension, diabetes, smoking, and dyslipidemias have a higher risk of developing VBI.[citation needed]

VBI, often provoked by sudden and temporary drops in blood pressure, can cause transient ischemic attacks. 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, or the sudden cessation of leg exercises, may also bring on the symptoms of VBI.[citation needed] 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.

Mechanical forces acting upon the neck at any age can cause VBI by exacerbating arterial insufficiency or outright occluding one or both vertebrobasilar arteries. Internal forces include those caused by turning the head to an extreme angle to the side, especially with the neck extended. The patient can create this condition while practicing yoga, driving a vehicle in reverse, shooting a bow and arrow, bird watching, or stargazing.[citation needed] External forces include those caused by sports or other physical contact.


VBI was first reported in the early 1990s when an American neurologist identified five patients who suffered strokes as a result of prolonged distortion of their necks from sitting at salon wash basins.

In 1997 medical journal The Lancet published a report by two British doctors about a 42-year-old woman who suffered a stroke after having her hair washed.[2]

The experts said the stroke was due to

"dissection of her right internal carotid artery.[3] Her head had been extended backwards for about five minutes while being washed and after the treatment she felt numb and suffered slurred speech."

The doctors recommended that hairdressers use a cushion and that the neck is not overextended. As a result of this recommendation there have been several sink cushions developed including Nekeze, Hairtools Basin Neck Cushion and the Soft n Style cushion. Trainee Hairdressers are also being taught to make sure that their clients are comfortable.

Several recent studies of the causes of strokes have identified how salon washing basins exert stress on the neck, causing the carotid or vertebral arteries to tear.

David Bateman, a consultant neurologist at Cumberland Infirmary, said that

“salon hairwashing was an identifiable, if small, risk factor for people predisposed to arterial damage. If your neck is stretched and it kinks for a long time, as happens during hairwashing, you stretch the arteries and if you are unlucky you can tear them,” he added “Once you have got that tear in the lining, blood starts flowing between layers of tissue and that can cause blood clots to start building up, leading to a stroke.”[4]

Dr. Bateman went on to say

“stroke cases from neck overextension appeared only in people particularly vulnerable to arterial tears, although there was little way of telling who might be at risk. Other factors that contribute to strokes include high blood pressure, diabetes, smoking and raised cholesterol.”

Other such triggers, which normally require ten minutes of neck overextension, include fairground rides, dentists’ chairs, sit-up exercises and yoga. Another cause, known as Golden Gate Bridge Syndrome, is prompted by excessive strain of looking up.


  1. ^ Marks MP, Wojak JC, Al-Ali F et al. (2006). "Angioplasty for symptomatic intracranial stenosis: clinical outcome". Stroke 37 (4): 1016–20. PMID 16497979. doi:10.1161/01.STR.0000206142.03677.c2. 
  2. ^ BBC, Warning over 'hair salon stroke',, 2004
  3. ^ GMTV, Beauty Parlour Syndrome,, 2005
  4. ^ The Times, Beware a brush with death at the hair salon,, 2004
  • Lang E and Afilalo M. Vertebrobasilar Atherothrombotic Disease. [3]
  • Savitz SI, Caplan LR (2005). "Vertebrobasilar disease". N. Engl. J. Med. 352 (25): 2618–26. PMID 15972868. doi:10.1056/NEJMra041544.