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Vertebrobasilar insufficiency

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

Synonyms and keywords: Basilar artery insufficiency; Basilar artery ischemia; Basilar artery stenosis; Vertebral artery insufficiency; Vertebral artery ischemia; Vertebral artery stenosis; Vertebrobasilar dolichoectasia; Vertebrobasilar ischemia

Overview

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

Overview

Historical Perspective

The concept of “vertebrobasilar insufficiency” was first described in 1961 by Niedermeyer.[1]

Classification

There isn’t classification about the VBI yet, but there are three phenotypes of the basilar artery occlusion depending on the modal of initial symptoms.

Pathophysiology

Causes

The causes leading to VBI is primarily the vasulcar ones, like atherosclerosis and cardioembolism, etc. As the vertebral artery is in the cervical vertebra, the orthopedical lesion also contribute to part of the causes.

Differentiating Myocarditis from other Diseases

Epidemiology and Demographics

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Laboratory Findings

Treatment

Medical Therapy

References

  1. NIEDERMEYER E (1963)The electroencephalogram and vertebrobasilar artery insufficiency.Neurology 13 ():412-22. PMID: 13938491

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Historical Perspective

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

Overview

In a long time in history,the VBI didn’t arouse enough focus because it is suppoesd to present only relatively benign synptoms and better outcomes. With the development of the diagnosis and perception, the VBI is believed to present a high recurrent risk and deserve a positive treatment and prevention.

Historical Perspective

Development of Treatment Strategies

The first surgical correction of vertebral artery stenosis was published by Crawford and De Bakey in 1958.[1] Transposition of the proximal vertebral artery to the common carotid was described by Clark and Perry in 1966.[2] The saphenous vein was used to bypass vertebral artery origin stenoses during 1970s.[3] The approach to the distal vertebral artery was first described by Matas[4]and was used for the treatment of traumatic injury.And in 1978,the carotid endarterectomy was proved to produced relief of symptoms in 90% of the patients.[5] In 1981, Motarjeme et published the first case of vertebral artery origi angioplasty.[6] In the recent 30 years, different kinds of surgery was rapidly developed to treat the VBI, such as fenestration, passby surgery. With the development of interventional techniques, more and more attemps have been made to treat the VBI, but there isn’t enough comparative evidence to support the benefit of interventional therapy.

References

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Classification

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

Overview

There isn’t classification about the VBI yet, but there are three phenotypes of the basilar artery occlusion depending on the modal of initial symptoms.

Classification

  • phenotype 1: patients present progressive brain stemsymptoms(for example: vertigo, doublevision, dysarthria, hemiparesis, or paresthesia) without any prodromal symptoms.[1]
  • phenotype 2: patients present nonspecific, such as nausea, tinnitus, hearing loss, and vertigo, which can precede the onset of the monophasic, progressive deficits by days, but typically by several weeks.[2][3]
  • phenotype 3: patients present symptoms with onset of severe, often bilateral motor weakness, ophtalmoplegia, and coma. The patients may have a severe outcome if basilar artery cannot be recanalized fast.[1]

References

  1. 1.0 1.1 Lindsberg PJ, Sairanen T, Strbian D, Kaste M (2012) treatment of basilar artery occlusion. Ann N Y Acad Sci 1268 ():35-44. DOI:10.1111/j.1749-6632.2012.06687.x PMID:22994219
  2. Ferbert A, Brückmann H, Drummen R (1990)Clinical features of proven basilar artery occlusion. Stroke 21 (8):1135-42. PMID: 2389292
  3. Baird TA, Muir KW, Bone I (2004) Basilar artery occlusion. Neurocrit Care 1 (3):319-29. DOI:10.1385/NCC:1:3:319 PMID:16174929

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Pathophysiology

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

Overview

Pathophysiology

The vertebral and basilar arteries supply the brain stem, cerebellum, and in most cases also the inferior temporal lobe, occipital lobe, and thethalamus. Variaties of reasons lead to impress the vertebral artery directly or indirectly may reduce the blood stream of posterior circulation of the brain; stimulation caused by the pathologic changes excite the sympathetic nerve and lead to the spasm of vertebral artery finally. Normally, the reduction of blood supply of unilateral veterbrobasilar artery doesn’t arouse the ischemia of brain. However, beacuse of the pre-existing maldevelopment, stenosis, embolism or other reasons leads to the reduction of blood supply of contralateral veterbrobasilar artery, patient will suffer the symptoms of ischemia of conrresponding brain area. Sometimes, the reduction of unilateral vertebralbasilar is too serious that the compensation of blood from the unjuried side isn’t enough to maintain the normal function of brain, the patient also suffer the symptoms. The sense organs of the visual, vestibular, and proprioceptive systems are connected with the cerebellum by way of the vestibular nuclei in the brainstem. Any disease that interrupts the integration of these 3 systems may give rise to symptoms of vertigo and disequilibrium.[1]

References

  1. Schneider JI, Olshaker JS (2012)Vertigo, vertebrobasilar disease, and posterior circulation ischemic stroke.Emerg Med Clin North Am 30 (3):681-93. DOI:10.1016/j.emc.2012.06.004 PMID: 22974644

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Causes

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

Overview

The causes leading to VBI is primarily the vasulcar ones, like atherosclerosis and cardioembolism, etc. As the vertebral artery is in the cervical vertebra, the orthopedical lesion also contribute to part of the causes.

Causes

Life Threatening Causes

Common Causes

The most common causes of VBI are cardioembolism, atherosclerosis, and small artery disease.[1]

Causes by Organ System

Cardiovascular Intracranial atherosclerosis , vertebral artery dissections , maldevelopment or absent of unilateral vertebral artery, arterial embolism , subclavian steal syndrome ,rotational VA occlusion,
Chemical / poisoning No underlying causes
Dermatologic No underlying causes
Drug Side Effect No underlying causes
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic Fabry disease
Hematologic No underlying causes
Iatrogenic physiatric cervical manipulation
Infectious Disease No underlying causes
Musculoskeletal / Ortho Cervical spondylosis , degenerative cervical spine changes , Spinal disc herniation , Cervical tuberculosis, Cervical injury,osteoporosis
Neurologic No underlying causes
Nutritional / Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy Takayasu disease, arteritides
Sexual No underlying causes
Trauma Cervical injury
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Postural changes,like head rotation or extension , fibromuscular dysplasia

Causes in Alphabetical Order

arterial embolism

fibromuscular dysplasia

arteritides

Spinal disc herniation

Cervical injury

Cervical spondylosis

Cervical tuberculosis

degenerative cervical spine changes

Intracranial atherosclerosis

maldevelopment or absent of unilateral vertebral artery

Osteoporosis

Postural changes

rotational VA occlusion

subclavian steal syndrome

Takayasu’s arteritis

vertebral artery dissections

vertebrobasilar aneurysm


References

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Differentiating Vertebrobasilar insufficiency from other Diseases

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

Overview

Differentiating Vertebral Artery Disease from other Diseases

It’s often challenging to make an accurate early differentia diagnosis between the high-risk posterior circulation ischaemic events and carotid artery events before brain imaging.The Digital subtraction angiography(DSA)is the gold standard to diagosis the VBI.

References

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]

Overview

Epidemiology and Demographics

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. And intracranial atherosclerosis is more common in individuals with black African[1]or East Asian ethnic origin than in Caucasian populations[2] The stroke caused by VBI account for approximately 20% to 30%21–23 of all strokes[3] A study indicates that prevalence of >50% vertebral and basilar arterial stenosis, and vertebrobasilar arterial stenosis was more often associated with multiple ischemic episodes and a higher risk of early recurrent stroke.[4]

References

  1. Markus HS, Khan U, Birns J, Evans A, Kalra L, Rudd AG et al. (2007) Differences in stroke subtypes between black and white patients with stroke: the South London Ethnicity and Stroke Study. Circulation 116 (19):2157-64. DOI:10.1161/CIRCULATIONAHA.107.699785PMID: 17967776
  2. Suri MF, Johnston SC (2009)Epidemiology of intracranial stenosis. J Neuroimaging 19 Suppl 1 ():11S-6S. DOI:10.1111/j.1552-6569.2009.00415.x PMID: 19807851
  3. Schneider JI, Olshaker JS (2012) Vertigo, vertebrobasilar disease, and posterior circulation ischemic stroke. Emerg Med Clin North Am 30 (3):681-93. [1] PMID: 22974644
  4. Marquardt L, Kuker W, Chandratheva A, Geraghty O, Rothwell PM (2009)Incidence and prognosis of > or = 50% symptomatic vertebral or basilar artery stenosis: prospective population-based study. Brain 132 (Pt 4):982-8. DOI:10.1093/brain/awp026 PMID: [2]

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]

Overview

The risk factors of VBI is similar to atherosclerosis. Sudden or excessive neck movement might increase the risk of vertebral artery dissection which might cause the VBI.[1]

Risk Factors

The atherosclerosis risk factors

References

  1. Kawchuk GN, Jhangri GS, Hurwitz EL, Wynd S, Haldeman S, Hill MD (2008)The relation between the spatial distribution of vertebral artery compromise and exposure to cervical manipulation. J Neurol 255 (3):371-7. [1] PMID: [2]

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Natural History, Complications and Prognosis

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

Overview

Natural History, Complications and Prognosis

Natural History

Some VBI is caused by the embolus from subclavian artery or atherosclerotic lesions and dissection, etc. Once the blocked vertebral artery doesn’t get enough compensation from the contralateral, obviously multiple and multifocal infarcts in the brain stem, cerebellum symptoms will be observed immediately,and quickly develop to a severe outcome. Some patients present nonspecific symptoms, such as nausea, tinnitus, hearing impairment, and vertigo, which can precede the onset of the monophasic, progressive deficits by days, but typically by several weeks.

Prognosis

The prognosis of VBI vary depending on the severity of symptoms the patients present, such as:

  • Severe stroke or TIA?
  • The type of stroke?Ischemic and hemorrhagic?
  • The size and location of infarction or hemorrhage?
  • If the patient get an early diagnosis and treatment or not?

For patients who experience vertebrobasilar transient ischemic attack portends a 30%to 35% risk for stroke during a 5-year period, whicih is higher than patients with carotid events in the acute phase, but that this is reversed in the subacute and chronic.[1][2][3] In patients with clinically defi nite vertebrobasilar TIA, the absolute risk of stroke at 1 year was 17·1%.[4] Medical refractory disease of the vertebrobasilar system carries a 5% to 11% risk of stroke or death at 1 year.[5] Mortality associated with a stroke is high, ranging from 20% to 30%.[5] [6][7][8] Patients presenting with VB events are more likely to have a recurrent TIA than patients with carotid events.[5] If the basilar artery is occluated, the death or disability rate is close to 70%.[9] Algorithms using diffusion-weighted imaging(DWI) or CT-based scoring systems have been published for prognostic assessment of early ischemic injury in basilar artery occlusion to distinguish those patients who will most likely benefit from recanalization from those who will not.[10][11][12][13]

Complications

Complications of vertebrobasilar circulatory disorders are stroke and its complications. The complications of stroke include:

  • Respiratory (breathing) failure (which may require use of a machine to help the patient breathe)
  • Lung problems (especially lung infections)
  • Heart attack
  • Dehydration and swallowing problems (sometimes leading to the placement of tubes in the stomach for artificial feeding)
  • Problems with movement or sensation, including paralysis and numbness
  • Formation of clots in the legs

Complications caused by medications or surgery may also occur.

References

  1. Cartlidge NE, Whisnant JP, Elveback LR (1977) Carotid and vertebral-basilar transient cerebral ischemic attacks. A community study, Rochester, Minnesota. Mayo Clin Proc 52 (2):117-20. PMID: 609290
  2. Heyman A, Wilkinson WE, Hurwitz BJ, Haynes CS, Utley CM, Rosati RA et al. (1984) Risk of ischemic heart disease in patients with TIA. Neurology 34 (5):626-30. PMID: 6538654
  3. Whisnant JP, Cartlidge NE, Elveback LR (1978) Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence–a population study. Ann Neurol 3 (2):107-15. DOI:10.1002/ana.410030204 PMID: 655661
  4. Marquardt L, Kuker W, Chandratheva A, Geraghty O, Rothwell PM (2009) Incidence and prognosis of > or = 50% symptomatic vertebral or basilar artery stenosis: prospective population-based study. Brain 132 (Pt 4):982-8. DOI:10.1093/brain/awp026 PMID: 19293244
  5. 5.0 5.1 5.2 Flossmann E, Rothwell PM (2003)Prognosis of vertebrobasilar transient ischaemic attack and minor stroke.Brain 126 (Pt 9):1940-54. DOI:10.1093/brain/awg197 PMID: 12847074
  6. Jones HR, Millikan CH, Sandok BA (1980) Temporal profile (clinical course) of acute vertebrobasilar system cerebral infarction. Stroke 11 (2):173-7. PMID: 7368245
  7. MCDOWELL FH, POTES J, GROCH S (1961) The natural history of internal carotid and vertebral-basilar artery occlusion. Neurology 11(4)Pt2 ():153-7. PMID: 13773892
  8. Patrick BK, Ramirez-Lassepas M, Synder BD (1980) Temporal profile of vertebrobasilar territory infarction. Prognostic implications. Stroke 11 (6):643-8. PMID: 7210071
  9. van der Hoeven EJ, Schonewille WJ, Vos JA, Algra A, Audebert HJ, Berge E et al. (2013) The Basilar Artery International Cooperation Study (BASICS): study protocol for a randomised controlled trial. Trials 14 ():200. DOI:10.1186/1745-6215-14-200 PMID: 23835026
  10. Puetz V, Sylaja PN, Coutts SB, Hill MD, Dzialowski I, Mueller P et al. (2008) Extent of hypoattenuation on CT angiography source images predicts functional outcome in patients with basilar artery occlusion. Stroke 39 (9):2485-90. DOI:10.1161/STROKEAHA.107.511162 PMID: 18617663
  11. Cho TH, Nighoghossian N, Tahon F, Némoz C, Hermier M, Salkine F et al. (2009) Brain stem diffusion-weighted imaging lesion score: a potential marker of outcome in acute basilar artery occlusion. AJNR Am J Neuroradiol 30 (1):194-8. DOI:10.3174/ajnr.A1278 PMID: 18768716
  12. Renard D, Landragin N, Robinson A, Brunel H, Bonafe A, Heroum C et al. (2008) MRI-based score for acute basilar artery thrombosis. Cerebrovasc Dis 25 (6):511-6. DOI:10.1159/000131668 PMID: 18480603
  13. Terasawa Y, Kimura K, Iguchi Y, Kobayashi K, Aoki J, Shibazaki K et al. (2010) Could clinical diffusion-mismatch determined using DWI ASPECTS predict neurological improvement after thrombolysis before 3 h after acute stroke? J Neurol Neurosurg Psychiatry 81 (8):864-8. DOI:10.1136/jnnp.2009.190140 PMID: 20562433

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1


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