Vertebrobasilar insufficiency natural history, complications and prognosis

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Vertebrobasilar insufficiency

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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] Medical refractory disease of the vertebrobasilar system carries a 5% to 11% risk of stroke or death at 1 year.[4] Mortality associated with a stroke is high, ranging from 20% to 30%.[4] [5][6][7] Patients presenting with VB events are more likely to have a recurrent TIA than patients with carotid events.[4]

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. 4.0 4.1 4.2 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
  5. Jones HR, Millikan CH, Sandok BA (1980) Temporal profile (clinical course) of acute vertebrobasilar system cerebral infarction. Stroke 11 (2):173-7. PMID: 7368245
  6. 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
  7. Patrick BK, Ramirez-Lassepas M, Synder BD (1980) Temporal profile of vertebrobasilar territory infarction. Prognostic implications. Stroke 11 (6):643-8. PMID: 7210071

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