VBI is a general term for any reduction in blood flow affecting the vertebral or basilar arteries. Distinct brain portions may be affected by vertebrobasilar ischemia and thus, symptoms may vary between VBI patients. The majority of symptoms may usually be ascribed to restricted brainstem functionality, but other symptoms result from limited perfusion of cerebellum and occipital cortex [6] [7]. In this line, the most common symptoms are dizziness and vertigo. Nausea and vomiting may result from vertigo. Also, patients may lose balance and coordination, experience ataxia, drop attacks and syncopes. Further common symptoms are visual disturbances and motor and sensory alterations. Visual impairment may consist in diplopia or even unilateral or bilateral complete loss of vision. Dysarthria, difficulties to swallow, paresthesia and confusion possibly result from VBI.

Symptoms may be transient and subside after as little time as a few minutes, other symptoms may become permanent.

VBI symptoms mimic and may indeed result from ischemic stroke. Therefore, they require urgent medical attention. Immediate treatment largely improves the outcome for stroke patients.

Initially, bedside tests are carried out to evaluate the overall condition of the patient and to establish a list of possible differential diagnoses. Maigne's test shall be mentioned as an example. Vertebral artery bruits can be detected non-invasively and may help to localize the problem. TCD monitoring may also be used bedside, is non-invasive and permits the visualization of hemodynamic conditions prevailing in vertebral and basilar arteries as well as the circle of Willis. It allows for the distinction between permanent artery stenosis and transient, posture-dependent occlusion. Findings should be thoroughly considered before further cervical manipulation is realized [8].

Additional imaging techniques are available to verify the diagnosis of VBI and to assess the extent of ischemia and cerebral damage. Magnetic resonance imaging, xenon-enhanced computed tomography, positron emission tomography and single photon emission computed tomography may be applied in VBI diagnosis [6] [9] [10] [11], but cerebral angiography is considered the gold standard to evaluate cerebral blood flow and identify the exact site causing VBI [12] [13]. In order to carry out cerebral angiography, contrast agents have to be administered by means of a catheter.

VBI treatment largely depends on the underlying cause of ischemia. Recommendations regarding head and neck movements may be sufficient in mild cases of transient, posture-dependent ischemia. More severe cases may require surgery. In other patients, surgical interventions are mainly performed to avoid relapses [14].

Surgery may consist in inserting a vascular bypass and thus in bridging the occluded site, in direct arterial anastomosis or plaque removal by means of endarterectomy. Such surgical interventions require highly skilled surgeons with years of experience in manipulating such small blood vessels. Perioperative morbidity and mortality remain rather high.

If VBI is caused by an occlusion located in the extracranial parts of the vertebrobasilar circulation system, endovascular therapeutic measures may be applied to treat the patient. Percutaneous transluminal angioplasty may allow for the restoration of blood flow. In general, morbidity and mortality ascribed to percutaneous transluminal angioplasty are significantly lower than in the aforementioned surgical approaches. Risks increase if more distal parts of the vertebral arteries have to be accessed because small vessels branching off the initially affected artery may be occluded by angioplasty. Another therapeutic option that avoids open surgery and the risk of occlusion of smaller branches is the insertion of stents.

Furthermore, anti-coagulants such as warfarin and acetylsalicylic acid are often administered in VBI to prevent recurrence of ischemia. A retrospective study that considered more than 150 patients suffering from intracranial artery occlusions found warfarin to be significantly more effective in preventing stroke than aspirin. Although VBI occurs due to extracranial artery stenosis or occlusion, these findings may be helpful when choosing an anti-coagulative therapy.

Prognosis of VBI depends on the severity of ischemia and resulting symptoms, on the patient's general and cardiovascular condition and their age. Asymptomatic VBI or those associated with mild symptoms are considered favorable prognostic factors. This also applies for otherwise healthy, young patients if they are willing to adopt a certain lifestyle in order to diminish their risk for further bouts of VBI. VBI. In contrast, outcome is poorer in patients suffering from severe cerebral ischemia and symptoms, as well as in frail and elder individuals.

Any generalized pathological condition of the cardiovascular system as well as local mechanical alterations may trigger VBI.

In rare cases, congenital abnormalities trigger VBI. By far the most common cause of VBI is atherosclerosis. Vertebral artery plaques may develop in situ. They are often hard and present a smooth surface without any signs of ulceration. However, embolism has to be considered as a possible cause of VBI, too. Embolism accounts for up to 40% of vertebrobasilar infarctions. Therefore, risk factors for atherosclerosis such as smoking, hypertension, diabetes mellitus, age and genetic predisposition may also be considered risk factors for VBI. Fibromuscular dysplasia differs pathogenetically from atherosclerosis, but results in similar narrowing of blood vessel diameters. Lateral flexion of the neck may provoke mechanical occlusion of the vertebral artery at the vertebral joint of atlas and axis. This movement reminds of an archer, which is why the corresponding type of VBI is also called bow hunter's stroke. Dolichoectasia, dissection or aneurysm of the vertebral arteries also result in reduced perfusion of the posterior parts of the brain.

In agreement with the above mentioned risk factors, VBI incidence is increased among those suffering from atherosclerosis, hypertension and diabetes mellitus. Smokers have a higher risk for VBI than non-smokers. Also, VBI incidence augments with age and is most frequently diagnosed in patients over 60 years of age. Two out of three VBI patients are males. This fact may be due to the gender distribution of diseases classified as VBI risk factors.

It has been estimated that up to 30% of cerebrovascular accidents affect posterior parts of the brain [3] [4].

The left and right vertebral arteries provide blood to the vertebrobasilar circulation system, they merge to form the single basilar artery which subsequently connects to the circle of Willis. The latter may maintain perfusion of cerebral structures even though certain arteries are under mechanical pressure or even completely occluded, but certain vessels are end arteries whose function cannot be taken over by other arteries.

Medulla, brainstem, cerebellum and occipital cortex are largely perfused with blood provided by the vertebrobasilar circulation system. Vertebrobasilar ischemia may be caused by cardiovascular and cervical spine pathologies as well as by cervical movement and manipulation [2] [5]. Symptoms resulting from VBI depend on the specific brain portion affected by reduced perfusion, the involvement of end arteries or the presence of collaterals. Due to its neurological activity and association with cranial nerves, brainstem symptoms often dominate the clinical picture.

Preventive measures consist in preventing or avoiding risk factors, particularly smoking and atherosclerosis. While nothing can be done with regard to age, the risk for VBI is significantly lower in non-smokers, in individuals whose blood pressure and glucose levels do not exceed reference values and in those who maintain a healthy diet and do sports.

Vertebrobasilar insufficiency (VBI) describes the pathological condition of transient reduced perfusion of the posterior parts of the brain. The extend of blood flow reduction in any vertebral artery and subsequent cerebral ischemia associated with VBI varies greatly. The majority of VBI cases is limited to transient ischemia possibly triggered by head and neck movements and/or degeneration of spinal structures [1] [2]. Here, cerebral perfusion is largely maintained by the collateral vertebral arteries. Blood flow to the posterior cerebrum may also be supported by the anterior parts of the circle of Willis. However, more severe cases may readily be termed stroke and result in neurological symptoms. The latter depend on the cerebral structures that are affected by reduced perfusion. Brain stem symptoms such as dizziness, vertigo, visual impairment and dysarthria are most commonly observed in VBI patients. Imaging techniques such as magnetic resonance imaging, single photon emission computed tomography and cerebral angiography may be helpful in diagnosis of VBI and identification of its underlying causes. Treatment is adjusted to the causes of VBI and may consist in conservative therapy, conduct recommendations or surgical relieve of pressured arteries.

The term vertebrobasilar insufficiency (VBI) describes a pathological condition triggered by decreased blood flow to the posterior parts of the brain. There are several blood vessels that may be affected in VBI patients. These blood vessels irrigate distinct parts of the brain and symptoms thus depend on the precise location of artery occlusion. In some cases, arteries are merely narrowed and not completely occluded, so tissues supplied by these arteries still receive some blood. Here, symptoms are usually less severe than in those cases where arteries are completely occluded. Another factor that determines the severity of symptoms is the overall time of ischemia. VBI may be caused by certain movements of head and neck. In this cases, blood flow reduction is usually transient and restoration occurs after a very short time. However, if atherosclerotic plaques form inside the vessels or if they exist elsewhere and parts of them are carried here with the blood, vessels may be occluded for prolonged periods of time.

Causes
Any pathological process leading to the occlusion of blood vessels supplying oxygen and nutrients to the posterior parts of the brain may trigger VBI. The most common cause for VBI is atherosclerosis. Atherosclerosis is a chronic cardiovascular diseases associated with the development of atherosclerotic plaques inside of blood vessels. These plaques consist in lipids, blood clots, inflammatory and other types of cells and further components. They adhere to the intravascular wall and narrow the vessel's lumen. Plaques or parts of plaques may also detach from the intravascular wall and be carried away by the blood stream and cause embolism. VBI may be provoked by both scenarios: Atherosclerotic plaques may either develop in head and neck arteries or may be carried here.

Because atherosclerosis is more common in smokers than in non-smokers and in individuals suffering from hypertension, overweight, diabetes mellitus and/or elevated blood fat levels, these conditions may contribute to VBI.

Pathologic alterations of the blood vessels themselves, e.g. pathologic dilations, dissections or aneurysms may also trigger VBI. In general, the individual risk for VBI increases with age. However, in rare cases congenital abnormalities may provoke VBI.

Symptoms
Common symptoms are dizziness, vertigo, sudden falls due to loss of muscle tone and syncopes and result from limited perfusion of the brainstem. Loss of coordination and an unsteady, staggering gait reveal involvement of the cerebellum. The occipital cortex does contribute to processing visual impressions. If it is affected by VBI, double vision, blurred vision and even loss of vision may be experienced. These visual impairments may be unilateral or bilateral. Slurred speech, difficulties to swallow and abnormal sensations in hands and feet are further symptoms of VBI.

Diagnosis
Medical history and clinical examination will not be able to rule out stroke since the above mentioned symptoms may be provoked by cerebral infarction as well.

Physicians will usually first assess the exact condition of a patient and evaluate whether certain head and neck movements trigger transient reductions of blood flow to the cerebrum. This evaluation is necessary to take appropriate precautionary measures when vessels and cervical spine as well as cerebral blood flow and tissue damage are finally examined with diagnostic imaging techniques. In order to do so, ultrasound, magnetic resonance imaging, single photon emission computed tomography and other techniques may be applied. If the source of VBI is identified, adequate treatment may be provided.

Treatment
In mild cases, conservative treatment may be sufficient to prevent relapses. Such treatment may consist in instructions to avoid certain head and neck movements and drug therapy. Anti-coagulants are often administered to VBI patients.

More severe cases will require endovascular or surgical intervention. Physicians may try to re-open occluded vessels by inserting a small balloon into the artery and subsequently inflating it inside the vessel. Stents are small tubes that may be inserted into a vessel to keep it open. Surgery will be necessary if a bypass or an arterial anastomosis is required to bridge the site of lesion.

1. Fox MW, Piepgras DG, Bartleson JD. Anterolateral decompression of the atlantoaxial vertebral artery for symptomatic positional occlusion of the vertebral artery. Case report. J Neurosurg. 1995; 83(4):737-740.
2. Vates GE, Wang KC, Bonovich D, Dowd CF, Lawton MT. Bow hunter stroke caused by cervical disc herniation. Case report. J Neurosurg. 2002; 96(1 Suppl):90-93.
3. De Marchis GM, Kohler A, Renz N, et al. Posterior versus anterior circulation strokes: comparison of clinical, radiological and outcome characteristics. J Neurol Neurosurg Psychiatry. 2011; 82(1):33-37.
4. Schneider JI, Olshaker JS. Vertigo, vertebrobasilar disease, and posterior circulation ischemic stroke. Emerg Med Clin North Am. 2012; 30(3):681-693.
5. Albuquerque FC, Hu YC, Dashti SR, et al. Craniocervical arterial dissections as sequelae of chiropractic manipulation: patterns of injury and management. J Neurosurg. 2011; 115(6):1197-1205.
6. Doss A, Phatouros CC. Vertebrobasilar insufficiency. Curr Treat Options Cardiovasc Med. 2006; 8(2):111-119.
7. Otto V, Fischer B, Schwarz M, Baumann W, Preibisch-Effenberger R. Treatment of vertebrobasilar insufficiency--associated vertigo with a fixed combination of cinnarizine and dimenhydrinate. Int Tinnitus J. 2008; 14(1):57-67.
8. Cagnie B, Barbaix E, Vinck E, D'Herde K, Cambier D. Atherosclerosis in the vertebral artery: an intrinsic risk factor in the use of spinal manipulation? Surg Radiol Anat. 2006; 28(2):129-134.
9. Nakagawa T, Shigeta T, Takashima T, Tomiyama K. Magnetic resonance angiography evaluation of basilar artery stenosis in patients with vertebrobasilar insufficiency. Eur Arch Otorhinolaryngol. 2000; 257(8):409-411.
10. Agrawal D, Gowda NK, Bal CS, Kale SS, Mahapatra AK. Have cranio-vertebral junction anomalies been overlooked as a cause of vertebro-basilar insufficiency? Spine (Phila Pa 1976). 2006; 31(7):846-850.
11. Marti-Fabregas JA, Catafau AM, Mari C, et al. Cerebral perfusion and haemodynamics measured by SPET in symptom-free patients with transient ischaemic attack: clinical implications. Eur J Nucl Med. 2001; 28(12):1828-1835.
12. Frisoni GB, Anzola GP. Vertebrobasilar ischemia after neck motion. Stroke. 1991; 22(11):1452-1460.
13. Hanakita J, Miyake H, Nagayasu S, Nishi S, Suzuki T. Angiographic examination and surgical treatment of bow hunter's stroke. Neurosurgery. 1988; 23(2):228-232.
14. Hopkins LN, Martin NA, Hadley MN, Spetzler RF, Budny J, Carter LP. Vertebrobasilar insufficiency. Part 2. Microsurgical treatment of intracranial vertebrobasilar disease. J Neurosurg. 1987; 66(5):662-674.